Rani Lill Anjum

Samantha Copeland
Elena Rocca Editors

Rethinking Causality,
Complexity
and Evidence for
the Unique Patient
A CauseHealth Resource for Healthcare
Professionals and the Clinical Encounter
Rethinking Causality, Complexity and Evidence
for the Unique Patient
Rani Lill Anjum • Samantha Copeland
Elena Rocca
Editors

Rethinking Causality,
Complexity and Evidence
for the Unique Patient
A CauseHealth Resource for Healthcare
Professionals and the Clinical Encounter

With contributions from

Brian Broom, Ivor Ralph Edwards,

Karin Mohn Engebretsen, Roger Kerry,
Anna Luise Kirkengen, Tobias Gustum Lindstad,
Matthew Low, Kai Brynjar Hagen, Christine Price
Editors
Rani Lill Anjum Samantha Copeland
NMBU Centre for Applied Ethics and Philosophy
Philosophy of Science of Technology Section
Norwegian University of Delft University of Technology
Life Sciences, Ås, Norway Delft, The Netherlands

Elena Rocca
NMBU Centre for Applied
Philosophy of Science
Norwegian University of
Life Sciences, Ås, Norway

ISBN 978-3-030-41238-8    ISBN 978-3-030-41239-5 (eBook)

https://doi.org/10.1007/978-3-030-41239-5

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In memory of Stephen Tyreman
vii
Preface

The Story of CauseHealth

This book is a result of the interdisciplinary research project CauseHealth,

Causation, Complexity and Evidence in Health Sciences, at the Norwegian
University of Life Sciences (NMBU) from 2015 to 2019. The core team of
CauseHealth during those years, located at NMBU, consisted of myself, Stephen
Mumford, Samantha Copeland, Elena Rocca and Karin Mohn Engebretsen. Our
international network of researchers and practitioners included more than 40 experts
from a wide range of specialities: general practice, pharmacology, surgery, oncol-
ogy, clinical psychology, experimental psychology, psychiatry, physiotherapy, oste-
opathy, immunology, cardiology, paediatrics, pharmacovigilance, nursing,
epidemiology, systems medicine, behavioural medicine, public health, medical
sociology, medical ethics, person-centred medicine and practice, evidence-based
medicine and practice, medical humanities, medically unexplained symptoms, phe-
nomenology and philosophy of medicine and causation.
The idea for CauseHealth was born back in 2011, after the first meeting of an
earlier research project, Causation in Science. This project addressed some practical
and methodological challenges for establishing causal relationships in science, by
tracing these challenges back to how to understand causality, philosophically. Four
broad areas were chosen: physics, biology, psychology and social science. Since
most of the collaborators were interested in biology, the first project event was on
this topic. We held an international conference: Causality and Reductionism in
Biology and Beyond. Coincidentally, a few of the talks were on medicine, and in the
afterthought of these, the first seed for the CauseHealth project was planted. After
all, if it is difficult to understand causality in physics, biology, psychology and
social science, then medicine must represent the ultimate challenge. The subject of
medicine, the human being, is the unity of them all: the physical, the biological, the
mental and the social. Our health affects, and is affected by, all these four dimensions.
There were three themes from the 2011 conference that inspired what later
became the CauseHealth project. First, Thor Eirik Eriksen discussed the practical

ix
x Preface

problem of dealing with so-called medically unexplained symptoms. In his presen-

tation ‘Waiting for an Explanation’, he mentioned how these chronic conditions
remain a challenge to the medical profession because of their heterogenic and com-
plex nature (Eriksen et al. 2013). Second, he used the term ‘medicalisation’, which
refers to a reductionist tendency in medicine to define more and more aspects of
human life as medical issues. Third, Roger Kerry gave a talk with the title ‘Causal
Dispositionalism in the Health Sciences’ where he argued that randomised con-
trolled trials, the gold standard for establishing causal relationships, have a strong
philosophical basis in the neo-Humean difference-making theory of causality.
Together, these ideas inspired the three pillars of CauseHealth, which are methodol-
ogy, ontology and practice:
–– The philosophical and conceptual motivation for choice of scientific methodol-
ogy in medicine (methods)
–– The reductionist tendency of treating complex psychosocial phenomena as bio-
medical ones (ontological model)
–– The practical challenge of establishing medical causes in cases of complexity
and individual variation (practice)
Initially, the CauseHealth project was directed towards medicine and health sci-
ences in general, without a particular focus on clinical practice. It turned out, how-
ever, that the philosophical themes and slogans capturing the essence of the project,
such as ‘One size does not fit all’, ‘Statistics don’t get me’ and ‘N=1’, struck a chord
with clinicians. We therefore wanted to create a resource specifically directed at
healthcare practitioners. The plan was to gather the philosophical ideas that are
most relevant to the clinical encounter, which can then be used as an intellectual
resource for anyone working with individual patients. We have made an effort to
present the philosophical material in a way that is accessible for nonphilosophers
and to include contributions from eight clinicians and one patient from the
CauseHealth network who show a practical way forward that is in line with the
philosophical ideas. By including these texts, we hope that the more abstract philo-
sophical ideas will become more concrete and useful for clinical practice.
This book is made possible by the generous funding from the Research Council
of Norway and the Uppsala Monitoring Centre, the WHO Collaborating Centre for
International Drug Monitoring. As for the contents of the book, this is entirely the
result of all those people who have engaged with the CauseHealth project and
shared their expertise and ideas with us over these past few years. Without the peo-
ple who helped me develop and pilot the project from initial idea to proposal –
Stephen Mumford, Svein Anders Noer Lie, Thor Eirik Eriksen and Roger
Kerry – there wouldn’t even have been a CauseHealth project.
CauseHealth has been fuelled by the intellectual power, professional experience
and personal engagement of so many. Ever since the beginning of CauseHealth, our
collaborators and project network, many of whom have contributed to this book,
have been vital sources of insights into the practical concerns and challenges facing
clinicians and other healthcare professionals in their daily practice. We have been
surprised and overwhelmed by the enthusiasm of practitioners participating in our
Preface xi

CauseHealth events or engaging with us on Twitter. So many of them have been

invaluable ambassadors for the project by spreading and translating the philosophi-
cal ideas of CauseHealth to colleagues around the globe through talks, blogs, pod-
casts, articles and social media.
This book is written for and because of them.

Ås, Norway Rani Lill Anjum

January 2020

Reference

Eriksen TE, Kerry R, Lie SAN et al (2013) At the borders of medical reasoning - aetiological
and ontological challenges of medically unexplained symptoms. Philos Ethics Hum Med
8:1747–1753
Contents

Part I Philosophical Framework

1 Introduction: Why Is Philosophy Relevant
for Clinical Practice? ������������������������������������������������������������������������������    3
Rani Lill Anjum, Samantha Copeland, and Elena Rocca
2 
Dispositions and the Unique Patient������������������������������������������������������   13
Rani Lill Anjum
3 
Probability for the Clinical Encounter��������������������������������������������������   37
Elena Rocca
4 
When a Cause Cannot Be Found������������������������������������������������������������   55
Rani Lill Anjum and Elena Rocca
5 
Complexity, Reductionism and the Biomedical Model������������������������   75
Elena Rocca and Rani Lill Anjum
6 The Guidelines Challenge�����������������������������������������������������������������������   95
Samantha Copeland

Part II Application to the Clinic

7 
The Complexity of Persistent Pain – A Patient’s Perspective�������������� 113
Christine Price
8 Above and Beyond Statistical Evidence. Why Stories
Matter for Clinical Decisions and Shared Decision Making���������������� 127
Matthew Low
9 
Causality and Dispositionality in Medical Practice������������������������������ 137
Ivor Ralph Edwards

xiii
xiv Contents

10 Lessons on Causality from Clinical Encounters

with Severely Obese Patients������������������������������������������������������������������ 149
Kai Brynjar Hagen
11 
Reflections on the Clinician’s Role in the Clinical Encounter ������������ 167
Karin Mohn Engebretsen
12 The Relevance of Dispositionalism for Psychotherapy
and Psychotherapy Research������������������������������������������������������������������ 179
Tobias Gustum Lindstad
13 
Causal Dispositionalism and Evidence Based Healthcare ������������������ 201
Roger Kerry
14 
The Practice of Whole Person-Centred Healthcare������������������������������ 215
Brian Broom
15  Broken Child – A Diseased Woman���������������������������������������������������� 227
A
Anna Luise Kirkengen
16 
Conclusion: CauseHealth Recommendations for Making Causal
Evidence Clinically Relevant and Informed������������������������������������������ 237
Rani Lill Anjum, Samantha Copeland, and Elena Rocca
Notes on Editors and Contributors

Editors and Contributors to Part I

Rani Lill Anjum is Researcher in Philosophy and Principal Investigator of

CauseHealth at the Norwegian University of Life Sciences (NMBU). She leads the
NMBU Centre for Applied Philosophy of Science together with Elena Rocca, where
she works on the philosophical foundations of science with focus on causality,
probability and dispositions. She has written four books with Stephen Mumford:
Getting Causes from Powers, Causation: A Very Short Introduction and Causation
in Science and the Methods of Scientific Discovery, published with Oxford
University Press, and What Tends to Be: The Philosophy of Dispositional Modality,
with Routledge.

Samantha Copeland is Assistant Professor in the Ethics and Philosophy of

Technology section at Delft University of Technology. She was a postdoctoral fel-
low with the CauseHealth project and is on the editorial board for the annual phi-
losophy thematic of the Journal of Evaluation in Clinical Practice. Copeland has
published on the ethics of addressing unexpected results in clinical research that
involves human subjects, including ‘The Case of the Triggered Memory:
Serendipitous Discovery and the Ethics of Clinical Research’ and ‘Unexpected
Findings and Promoting Monocausal Claims, a Cautionary Tale’. She is also
Coauthor of ‘Pharmacovigilance as Scientific Discovery: An Argument for Trans-­
disciplinarity’, written with Ralph Edwards and Elena Rocca.

Elena Rocca is an Interdisciplinary Researcher with background in pharmacy, biol-

ogy and theory of science at the Norwegian University of Life Sciences (NMBU).
She is Principal Investigator of the project CauseHealth Risk and Safety and leads
the Centre for Applied Philosophy of Science with Rani Anjum. She is on the edito-
rial board of the International Journal of Risk and Safety in Medicine. Rocca is
interested in the role of philosophical bias in the production and evaluation of evi-
dence. She is Author of ‘The Judgements that Evidence-Based Medicine Adopts’

xv
xvi Notes on Editors and Contributors

and ‘Bridging the Boundary Between Scientists and Clinicians’ and Coauthor of
‘Real or Ideal Risk? Philosophy of Causation Meets Risk Analysis’ with Rani Anjum.

Contributors to Part II

Brian Broom was until early 2019 a Clinical Immunologist at Auckland City
Hospital and is Adjunct Professor in Psychotherapy at Auckland University of
Technology. He is trained in internal medicine and psychotherapy and now works to
train clinicians to practice whole-person medicine and healthcare. He has written
three books addressing this issue: Somatic Illness and the Patient’s Other Story,
Meaning-Full Disease: How Personal Experience and Meanings Cause and
Maintain Physical Illness and Transforming Clinical Practice Using a MindBody
Approach: A Radical Integration.

Ivor Ralph Edwards is Professor of Medicine and Senior Advisor (Former

Director) at the Uppsala Monitoring Centre, the WHO Collaborating Centre for
International Drug Monitoring. He has worked in clinical toxicology in the fields of
drug abuse, acute and chronic poisoning, toxicity from industrial chemicals as well
as adverse drug reactions. He now works on medical and legal aspects of causality
evaluation, as well as issues of risk and benefit evaluation and data mining
approaches to support signal detection and evaluation. He is Coeditor of
Pharmacovigilance: Critique and Ways Forward and Author of ‘Causality
Assessment in Pharmacovigilance: Still a Challenge’.

Karin Mohn Engebretsen is a Gestalt Psychotherapist, with over 15 years of clini-

cal experience from private practice. Her doctoral dissertation is on phenomenology
and medically unexplained symptoms, with particular focus on burnout. She has
written ‘Suffering Without a Medical Diagnosis’, ‘Naked in the Eyes of the Public’
and ‘Burned Out or “Just” Depressed?’.

Kai Brynjar Hagen is Senior Consultant in the Regional Centre for Morbid
Obesity, North Norway. He is also General Practitioner, District Medical Officer for
Communicable Diseases and Advising Senior Consultant in the Norwegian Labour
and Welfare Administration (NAV). He is Specialist in Community Medicine and is
interested in ecological thinking in medicine, from individual to health policy. He is
interested in primary causes of obesity development and factors that contribute to
maintain obesity, such as trauma or other stressors.

Roger Kerry is Associate Professor in the Division of Physiotherapy and

Rehabilitation Sciences, Faculty of Medicine and Health Sciences, University of
Nottingham. He specialises on risks and adverse events of manual therapy, neck
pain and headache as well as clinical reasoning. He holds a PhD in Philosophy with
the doctoral dissertation Causation and Evidence-Based Medicine. He is Author of
Notes on Editors and Contributors xvii

‘Expanding Our Perspectives on Research in Musculoskeletal Science and Practice’

and Coauthor of ‘The Form of Causation in Health, Disease and Intervention’ and
‘Causation and Evidence-Based Practice’.

Anna Luise Kirkengen is Professor of General Practice in the Department of

Public Health and Nursing, Norwegian University of Science and Technology
(NTNU), and has worked as General Practitioner for 30 years. She specialises on
the health impacts of childhood violation and is Author of The Lived Experience
of Violation. How Abused Children Become Unhealthy Adults and Inscribed
Bodies. Health Impact of Childhood Sexual Abuse, ‘Creating Chronicity’ and
‘From Wholes to Fragments to Wholes—What Gets Lost in Translation?’.

Tobias Gustum Lindstad has extensive background as a Clinical Psychologist

both within secondary public mental healthcare and community-based primary care
services, as well as in private practice. His research concerns the relevance of phi-
losophy for psychology, psychotherapy research and mental healthcare. He is the
main Editor of the book Respect for Thought: Jan Smedslund’s Legacy for
Psychology, coedited with Erik Stänicke and Jaan Valsiner, under contract with
Springer.

Matthew Low is a Consultant Physiotherapist in Musculoskeletal Conditions at the

Royal Bournemouth and Christchurch Hospitals NHS Foundation Trust. He is a
Visiting Associate at the Orthopaedic Research Institute, Bournemouth University.
He also teaches on the topics of clinical reasoning and the management of spinal
conditions as well as spinal manipulative physiotherapy. He is Author of ‘A Novel
Clinical Framework: The Use of Dispositions in Clinical Practice. A Person-Centred
Approach’ and runs the blog Perspectives on Physiotherapy.

Christine Price is affected by neuropathic nerve pain, which she has lived with
since an injury in 2008. Recently she started to write, blog and talk about her experi-
ences of living well with pain, directed at both clinicians and patients. She has been
invited to sit on research advisory panels and is the first patient representative on the
executive board of the UK’s Physiotherapy Pain Association. She is Coauthor of ‘A
Person-Centered and Collaborative Model for Understanding Chronic Pain:
Perspectives from a Pain Patient, a Practitioner, and a Philosopher’ with Rani Anjum
and Matthew Low.
Abbreviations

ADHD attention deficit hyperactivity disorder

APA American Psychological Association
AUT Auckland University of Technology
BMI body mass index
CBT cognitive behavioural therapy
CT computed tomography
DSM Diagnostic and Statistical Manual of Mental Disorders
EBHC evidence-based healthcare
EBM evidence-based medicine
EBP evidence-based practice
GP general practice
HP helicobacter pylori
LBP lower back pain
MSK musculoskeletal
MUPS medically unexplained physical symptoms
MUS medically unexplained symptoms
OA osteoarthritis
OCD obsessive-compulsive disorder
PTSD posttraumatic stress disorder
RCT randomised controlled trials
RSSO Regional Centre for Morbid Obesity
SMT somatic mutation theory
SSRI selective serotonin reuptake inhibitors
TOFT tissue organization field theory
WHO World Health Organization
WPC whole person care

xix
List of Figures

Fig. 2.1 The original evidence hierarchy of EBM......................................... 16

Fig. 2.2 The vector model of causality.......................................................... 26
Fig. 2.3 Subtractive interference................................................................... 27
Fig. 2.4 Additive interference........................................................................ 28
Fig. 2.5 Dispositions with different strength of tendency............................. 28
Fig. 2.6 A threshold effect T......................................................................... 29
Fig. 4.1 A vulnerable situation, where R is close
to the threshold for illness................................................................ 60
Fig. 4.2 A robust situation, where R is far from the threshold
for illness.......................................................................................... 61
Fig. 5.1 The hierarchy of science.................................................................. 76
Fig. 5.2 A Venn diagram illustrating a reductionist ontology
of wholes and parts.......................................................................... 77
Fig. 5.3 A change in methods and practice must start
from a change in ontology............................................................... 83
Fig. 7.1 Dispositions on a good day.............................................................. 117
Fig. 7.2 Dispositions on a difficult day......................................................... 118
Fig. 7.3 A dynamic threshold for health........................................................ 120
Fig. 7.4 Threshold on a difficult day............................................................. 120
Fig. 7.5 Mind map illustrating the complexity of my pain........................... 124
Fig. 7.6 The main contributors and improvers of my pain in January.......... 125
Fig. 7.7 The main contributors and improvers of my pain in August........... 125
Fig. 12.1 The Medical model.......................................................................... 182
Fig. 12.2 The vector model part 1: patient and his/her
situational circumstances................................................................. 195
Fig. 12.3 The vector model part 1: patient, situational
circumstances and psychotherapist.................................................. 196

xxi
xxii List of Figures

Fig. 13.1 Randomised controlled trial methodology

The randomisation and allocation processes
create the counterfactual conditions
by which B(x) – B(y) would, under a counterfactual
account of causation, constitute a causal claim.
However, causation is happening in each group,
irrespective of the other group......................................................... 205
 Part I
Philosophical Framework
Chapter 1
Introduction: Why Is Philosophy Relevant
for Clinical Practice?

Rani Lill Anjum, Samantha Copeland, and Elena Rocca

1.1 Why Philosophy?

No practice takes place in a philosophical vacuum and medicine is no exception.

Health sciences and healthcare practice are enabled, shaped and restricted by some
tacit philosophical assumptions, of which practitioners should be aware. What, for
instance, does it mean to say that clinical practice should be based on the best avail-
able evidence? What counts as the best evidence? And what is the most relevant
evidence for the clinical encounter? Although the scientific evidence is itself largely
empirical, many normative aspects of evidence based practice are not, as we will
explain. In this sense medicine and health sciences, like all sciences, contain some
non-empirical elements. These could be concepts, methods, tools, or what we call
‘basic implicit assumptions’ or philosophical bias. We define philosophical bias as
Basic Implicit Assumptions in Science about how the world is (ontology), what we can
know about it (epistemology), or how science ought to be practiced (norms). (Andersen
et al. 2019, p. 1)

They count as biases because they skew the development of hypotheses, the design
of experiments, the evaluation of evidence and the interpretation of results in spe-
cific directions. How we think the world is (ontology) will be reflected in the way
we study it (epistemology) and how we think that science ought to be practiced
(norms). In medicine and healthcare, philosophical biases would typically influence

R. L. Anjum (*) · E. Rocca

NMBU Centre for Applied Philosophy of Science, Norwegian University of Life Sciences,
Ås, Norway
e-mail: rani.anjum@nmbu.no; elena.rocca@nmbu.no
S. Copeland
Ethics and Philosophy of Technology Section, Delft University of Technology,
Delft, The Netherlands
e-mail: s.m.copeland@tudelft.nl

© The Author(s) 2020 3

R. L. Anjum et al. (eds.), Rethinking Causality, Complexity and Evidence for the
Unique Patient, https://doi.org/10.1007/978-3-030-41239-5_1
4 R. L. Anjum et al.

choice of methods (e.g. the evidence hierarchy), norms of practice (e.g. standardised
treatment) or scientific framework (e.g. the biomedical model).
In the CauseHealth project, Causation, Complexity and Evidence in Health
Sciences, we wanted to show how philosophical assumptions motivate particular
norms, methods and practices in medicine and healthcare. If we want to see a change
in the way medicine and healthcare are practiced, we therefore cannot leave the
philosophical foundation on which they are based untouched. Any competing prac-
tices will require different methods, norms and philosophical assumptions:

PHILOSOPHICAL ASSUMPTIONS → NORMS → METHODS → PRACTICE

For instance, we might want a healthcare system that acknowledges the patient
as an integrative whole, where medical issues must be understood not only on the
physiological level, but also within a biographical, social and cultural context.
However, if the practice of medicine is premised on Descartes’ mind-body divide
(what is called dualism) then no such integration of the whole person can be
achieved. It seems, then, that any genuine and permanent change in practice and
methodology will have to be motivated by a change in how we think about the world
on the most fundamental level. In the words of osteopath Stephen Tyreman:
…progress and development is not simply a matter of making new discoveries. It is a com-
plex, multi-faceted process that involves good science, yes, but in the context of prevailing
socio-cultural ideas and, most importantly, of an individual’s world-view. (Tyreman 2018)

This book offers a guide for rethinking some of these more foundational assump-
tions, or world-views, within medicine and healthcare. Such a foundational rethink
seems timely and warranted. Since the introduction of evidence based medicine in the
1990s, there has been an increasing interest in methodological, conceptual and onto-
logical discussions among medical researchers, healthcare professionals and philoso-
phers of medicine. There are emerging movements, such as Person Centered Medicine
and Practice, the Campaign for Real Evidence Based Medicine and the Critical
Physiotherapy Network, to mention only a few. The historian of science, Thomas
Kuhn, saw it as a sign of a paradigm in crisis when its members start participating in
philosophical discussions (Kuhn 1962). We should not, however, characterise what
we see in medicine and healthcare as a scientific crisis so much as a crisis in the phi-
losophy that grounds it (Anjum 2016; Eriksen et al. 2013), as we now go on to show.

1.2 Philosophical Debates in Medicine and Healthcare

A number of concerns have already been raised in the profession about how medi-
cine is defined and practiced, especially when this affects the clinic. We now present
briefly some of the debates that are most relevant for the context of this book:
debates about medical models (ontology), scientific methodology (epistemology)
and clinical practice.
1 Introduction: Why Is Philosophy Relevant for Clinical Practice? 5

1.2.1 Debating Models (Ontology)

Beyond the Biomedical Model. The biomedical model of health and illness
assumes that all medical conditions should be explained as some physiological
abnormality. Conditions lacking such biomedical explanation are then characterised
as medically unexplained or psychosomatic (Wade and Halligan 2004). A criticism
of this is that health complaints must be seen as more complex, containing biologi-
cal, social and psychological elements. Even if it were desirable to separate the
psychosocial causes of health from the ‘medical’ ones, it might not even be possible
(Arnaudo 2017). The bio-psychosocial model proposed by Engel (1977) was thus
an attempt to move beyond the biomedical model, though many argue that the bio-
medical model is still dominating the paradigm in healthcare, both in medicine and
psychology (Engebretsen 2018; Engebretsen and Bjorbækmo 2019).

Fragmentation of Care. Although co- and multi-morbidity are the norm in the
clinic, medicine and healthcare tend to be organised according to single diseases
(Mercer et al. 2009; Parekh and Barton 2010; Vogt et al. 2014; Tómasdóttir et al.
2015). This specialisation of medical disciplines was brought about in order to
enhance and deepen the specialists’ skills and expertise. On the other hand, health-
care has been criticised for becoming increasingly compartmentalised, organised
into distinct and sometimes isolated ‘silos’. This means that patients with chronic
and complex health complaints must go through the healthcare system by moving
from specialisation to specialisation, treated as fragments, not as wholes
(Kirkengen 2018).

Medicalisation of Life. In current healthcare there is the hope that a biomedical

treatment, such as a drug, might ideally treat effectively even complex psychosocial
phenomena (Ballard and Elston 2005). On the other hand, the expansion of the
medical domain into most aspects of life, such as fertility, sexuality, sleeping pat-
terns, angst, ageing and grief, has been criticised. Some are worried about placing
experiences that all human beings are expected to have in the ‘healthy-unhealthy’
category. Ultimately, such a move suggests that it is imperative that we treat those
experiences medically rather than accepting or living through them (Burgess 1993;
Pilgrim and Bentall 1999; Moloney 2010).

1.2.2 Debating Methodology (Epistemology)

Information Gets Lost in Statistics. One ongoing debate is over what it means
that clinical decisions should be evidence based. In evidence based medicine and
practice, causally relevant evidence is taken to be statistical and population based,
generated from large clinical studies. The aim is thus to ground the care of individu-
als in general knowledge about what is the most effective intervention in a studied
6 R. L. Anjum et al.

population (Sackett et al. 2000). Critical voices have raised concerns about the ten-
sion between the public health interest in equality of care and the clinical needs of
individuals. While evidence based policy is widely informed about what happens
elsewhere, the worry is that causally relevant information about the unique local
context is disregarded or lost (Cartwright and Hardie 2012).

The Importance of Mechanistic Knowledge. In evidence based medicine and

practice, randomised controlled trials (RCTs) are seen as the gold standard for
establishing causality (Howick 2011). This is because, thanks to their experimental
design, a well conducted RCT is the best way to isolate one causal factor from
potentially confounding factors and see whether it makes a statistical difference in
outcome. In contrast, some argue that causal relationships cannot be established
without the use of unquantifiable factors such as the theoretical knowledge coming
from the laboratory and clinical science (Charlton and Miles 1998). This is parallel
to the ongoing debate in philosophy of medicine on whether statistical knowledge
must be accompanied by a theory of causal mechanism for the purpose of establish-
ing causality (Russo and Williamson 2007; Osimani 2013; Anjum and
Mumford 2018).

A Call for Phenomenology. For ethical reasons, it is not possible to establish

whether psychosocial factors causally affect health in a negative way using clinical
experiments. For instance, one cannot test the causal impact of childhood trauma,
abuse, grief, psychological stress or social stigmatisation using RCTs, the gold stan-
dard for establishing causal relationships. One way to overcome this problem is to
substitute RCTs with other statistical methods, such as cohort studies or case-­
control studies. This is still within the framework of evidence based medicine and
practice. Other approaches emphasise instead individual uniqueness and phenome-
nology, urging the profession to change its focus to the whole patient experiencing
the condition (Loughlin et al. 2018, see also Engebretsen, Chap. 11, Broom, Chap.
14 and Kirkengen, Chap. 15, this book).

Limited External Validity. In the health sciences, like in many natural sciences,
causality is studied through experimentation, within controlled and somewhat arti-
ficial settings. Because of the need to control for confounders, clinical trials use
strict inclusion and exclusion criteria for recruiting the participants. On one side,
such controlled conditions increase the reliability of the experimental results, and
the confidence that the observed result is actually due to the tested intervention. At
the same time, however, this limits the external validity of the studies. When facing
chronically ill patients, older patients, pregnant women, or even children, it is there-
fore not obvious that the results from clinical studies apply directly in respect to
dosage, efficacy or even safety (Rothwell 2005, 2006; Baylis and MacQuarrie 2016).
1 Introduction: Why Is Philosophy Relevant for Clinical Practice? 7

1.2.3 Debating Practice

Upgrading Clinical Judgement and Knowledge. One motivation for the intro-
duction of evidence based medicine and practice was to ensure that patients got the
best available treatment, independently of the experience or preference of their
healthcare practitioner. Rather than depending entirely on clinical judgement and
the authority of expertise, treatment should be given according to the best scientific
evidence, preferably from RCTs and meta-studies. Of concern among healthcare
practitioners is how this depreciation of clinical judgement affects the clinical
encounter. In particular, when practitioners are encouraged to use guidelines and
computational tools to diagnose and make decisions about treatment, this leaves
less room for their own clinical expertise and knowledge of the particular patient at
hand. A worry is that, in the process of decision making, data from other patients
will weigh more than the evidence from the person seeking care (Greenhalgh 2018).

Efficiency at the Cost of Individual Needs. New Public Management is an

increasingly popular global phenomenon that started in the late 70s, with the aim of
improving efficiency of public services by making them more similar to businesses
(Diefenbach 2009). The introduction of New Public Management has affected the
way in which healthcare is financed, organised and executed (Simonet 2008; Wyller
et al. 2013). Health service delivery is supposed to be time- and cost-efficient and
resources are allocated according to generic standards, such as type of diagnosis.
On the other hand, proponents of person centered healthcare worry about the cur-
rent trend towards package solutions and standardisation of care. This approach
often hinders the assessment of individual needs, they warn. An alternative manage-
ment ideology for the health services, according to these critical voices, could be
one where the suffering individual, and not societal needs, has priority in setting the
course of care. Calls for action have been raised among medical professionals, urg-
ing that the New Public Management approach is leading to a decay in healthcare,
rather than to an improved quality and efficiency (Wyller et al. 2013).

1.3 Aims and Overview of the Book

This book is intended as an intellectual resource for clinicians and healthcare pro-
fessionals who are interested in digging deeper into the philosophical foundations
of their daily practice. It is a tool for understanding some of the philosophical moti-
vations and rationality behind the way medicine and healthcare are studied, evalu-
ated and practiced, at the interface of science and the humanities. We will show how
a change in the ontological foundation could motivate a paradigmatic change in
8 R. L. Anjum et al.

scientific methodology and clinical practice towards a genuine person centred

approach, focusing on the whole person. In particular, this book illustrates the
impact that our thinking about causality, both philosophically and conceptually, has
on the clinical encounter.
By ‘clinical encounter’ we mean, in the broad sense, a consultation between the
healthcare professional and the individual person seeking care. This is not limited to
medical practice, but covers healthcare in general, including nursing, psychology,
physical therapy, clinical pharmacy, rehabilitation, homecare services, as well as
individual preventive care or any follow up of the patient. Although many of our
examples come from medicine and general practice, the philosophical ideas should
have a wider relevance also for these other parts of healthcare. If some of the philo-
sophical biases that dominate current medical thinking actually limit the notion of
evidence in a way that disadvantages the clinical encounter, then this needs to be
critically discussed. Being able to identify the non-empirical foundation of scien-
tific norms and practices is thus a first and necessary step for critically evaluat-
ing them.
In this book we want to prepare the ground for a genuine transdisciplinary dis-
cussion, not only between healthcare professionals and philosophers, but also one
that expands to decision-makers and patients (Rocca et al. 2019). The main aim of
this book is to engage and empower healthcare professionals to take part in chang-
ing and defining the premises for their own practice. After all, if clinical decisions
should be based on evidence, this ought to be evidence that is relevant and well-­
suited for the clinic.
We have organised the book into two parts, Philosophical Framework and
Application to the Clinic. The first part is written primarily from the philosophical
perspective, by philosophers, and presents a singular overall framework. The sec-
ond part is written primarily by clinicians who address some implications of the
philosophical framework for different aspects of their own practice. The philosophi-
cal framework will thus be presented from different angles throughout the book,
with more or less explicit focus on clinical practice. We hope that the diversity of
voices, focus and perspective reflected in the chapters will contribute to make the
philosophical ideas more accessible and relevant for practitioners with different
professional backgrounds.
In the first part, we give an overview of the philosophical framework and themes
of CauseHealth. In Dispositions and the Unique Patient we introduce the theory of
dispositionalism and explain how this offers a better foundation for understanding
causality in the individual case. In Probability for the Clinical Encounter we show
how dispositionalism challenges the way we think about probabilities and propose
an alternative – a singularist propensity theory – that we argue is better suited for the
clinic. In When a Cause Cannot be Found we discuss how dispositionalism can
throw some new light on medically unexplained symptoms, since this theory treats
causal complexity, individual variations and medical uniqueness as essential fea-
tures of causality rather than as problems for causality. Next, in Complexity,
Reductionism and the Biomedical Model, we argue that a dispositionalist approach
would deny any form of reductionism and render the biomedical understanding of
1 Introduction: Why Is Philosophy Relevant for Clinical Practice? 9

health and illness deeply problematic. Finally, in The Guidelines Challenge, we

discuss the tension between clinical guidelines, based on general medical knowl-
edge and aimed toward standardisation, and their use in the clinical encounter,
based on local knowledge about the patient and aimed toward tailored
interventions.
In Part II, eight practitioners and one patient from the CauseHealth network
translate the philosophical ideas into a clinical setting. In their contributions, they
show how philosophical reflections concerning foundational issues have influenced
their own practice and how they understand and deal with health and illness. This
part has nine chapters. The Complexity of Persistent Pain – A Patient’s Perspective
is written by Christine Price who suffers from chronic pain. Price explains how she
uses the dispositionalist framework to understand, model and manage her own
chronic pain after she learned about this from her physiotherapist Matthew Low.
Low is the author of Above and Beyond Statistical Evidence. Why Stories Matter
for Clinical Decisions and Shared Decision Making. In this chapter he explains
why patient narratives and dispositionalism are valuable resources for shared clini-
cal decision making. In Causality and Dispositionality in Medical Practice, gen-
eral physician and clinical pharmacologist Ivor Ralph Edwards discusses the
tension between the need of a full phenomenological, dispositional and causal
evaluation for making better diagnoses and the practical restrictions of the clinical
reality.
Following up on these challenges, Lessons on Causality from a Clinic for Patients
with Severe Obesity is written by senior consultant and general practitioner Kai
Brynjar Hagen. Hagen describes how conversations dedicated to the first encounter
with the patients allowed him to get closer to a causal diagnosis of their obesity,
suggesting a causal therapy rather than a purely symptomatic one. Next, in
Reflections on the Clinician’s Role in the Clinical Encounter, psychotherapist Karin
Mohn Engebretsen illustrates how the clinician’s own personal and professional
background influences the therapy in positive or negative ways and explains why
clinicians ought to be conscious about what they bring with them to the clinical
encounter. In The Relevance of Dispositionalism for Psychotherapy and
Psychotherapy Research, psychologist Tobias Gustum Lindstad explores the influ-
ence of the evidence based framework on psychotherapy and proposes a disposi-
tional revival of the profession. Causal Dispositionalism and Evidence Based
Healthcare, written by physiotherapist Roger Kerry, discusses whether a new evi-
dence based practice framework can be offered, one underpinned by a dispositional
ontology, and reflects on how this would look. Next, The Practice of Whole Person-­
Centred Healthcare, by immunologist and psychotherapist Brian Broom, is an
account of the emergence in New Zealand of a non-dualistic, whole person centred
form of clinical practice, particularly in relation to the treatment of physical disease
of all kinds. In A Broken Child – A Diseased Woman, general practitioner Anna
Luise Kirkengen contrasts the personal biography of a patient, which is a history of
violation, to her sickness histories as documented in the medical records. The chap-
ter is a powerful reminder of why medicine and healthcare must be genuinely
10 R. L. Anjum et al.

person centred in order to obtain crucial information for understanding, diagnosing

and treating patients.
In its totality, this book reinterprets what a genuine person centered approach
should entail; from ontological foundation to norms of methodology and practice.
This means that even those already educated within a person centered framework
might have some of their preconceptions challenged by the dispositionalist theory
presented here. We conclude the book by proposing a list of CauseHealth recom-
mendations for a paradigmatic change in medicine and healthcare.

References and Further Readings

Anjum RL (2016) Evidence-based or person-centered. An ontological debate. Eur J Pers Cent

Healthc 4:421–429
Anjum RL, Mumford S (2018) Causation in science and the methods of scientific discovery.
Oxford University Press, Oxford
Andersen F, Anjum RL, Rocca E (2019) Philosophical BIAS is the one bias that science cannot
avoid. eLife 8:e44929. https://doi.org/10.7554/eLife.44929
Arnaudo E (2017) Pain and dualism: which dualism? J Eval Clin Pract 23:1081–1086
Ballard K, Elston MA (2005) Medicalisation: a multi-dimensional concept. Soc Theory Health
3:228–241
Baylis F, MacQuarrie R (2016) Why physicians and women should want pregnant women included
in clinical trials. In: Baylis F, Ballantyne A (eds) Clinical research involving pregnant women.
Springer, Cham
Burgess M (1993) The medicalization of dying. J Med Philos 18:269–280
Cartwright N, Hardie J (2012) Evidence-based policy. A guide to do it better. Oxford University
Press, Oxford
Charlton BG, Miles A (1998) The rise and fall of EBM. Q J Med 91:371–374
Diefenbach T (2009) New public management in public sector organizations: the dark sides of
managerialistic ‘enlightenment’. Pub Adm 87:892–909
Engebretsen KM (2018) Suffering without a medical diagnosis. A critical view on the biomedical
attitudes towards persons suffering from burnout and the implications for medical care. J Eval
Clin Pract 24:1150–1157
Engebretsen KM, Bjorbækmo WS (2019) Burned out or “just” depressed? An existential phenom-
enological exploration of burnout. J Eval Clin Pract. https://doi.org/10.1111/jep.13288
Engel GM (1977) The need for a new biomedical model: a challenge for biomedicine. Science
196:129–136
Eriksen TE, Kerry R, Lie SAN et al (2013) At the borders of medical reasoning – aetiological
and ontological challenges of medically unexplained symptoms. Philos Ethics Humanit Med
8:1747–1753
Greenhalgh T (2018) Of lamp posts, keys, and fabled drunkards: a perspectival tale of 4 guidelines.
J Eval Clin Pract 24:1132–1138
Howick J (2011) The philosophy of evidence-based medicine. BMJ Books/Wiley-Blackwell, Oxford
Kirkengen AL (2018) From wholes to fragments to wholes—what gets lost in translation? J Eval
Clin Pract 24:1145–1149
Kuhn T (1962) The structure of scientific revolutions. University of Chicago Press, Chicago
Loughlin M, Mercuri M, Parvan A et al (2018) Treating real people: science and humanity. J Eval
Clin Pract 24:919–929
Mercer SW, Smith SM, Wyke S et al (2009) Multimorbidity in primary care: developing the
research agenda. Fam Pract 26:79–80
1 Introduction: Why Is Philosophy Relevant for Clinical Practice? 11

Moloney P (2010) ‘How can a chord be weird if it expresses your soul?’ Some critical reflections
on the diagnosis of Aspergers syndrome. Disabil Soc 25:135–148
Osimani B (2013) Until RCT proven? On the asymmetry of evidence requirements for risk assess-
ment. J Eval Clin Pract 19:454–462
Parekh AK, Barton MB (2010) The challenge of multiple comorbidity for the US health care sys-
tem. J Am Med Assoc 303:1303–1304
Pilgrim D, Bentall R (1999) The medicalisation of misery: a critical realist analysis of the concept
of depression. J Ment Health 8:261–274
Rocca E, Copeland S, Edwards IR (2019) Pharmacovigilance as scientific discovery: an argument
for trans-disciplinarity. Drug Saf. https://doi.org/10.1007/s40264-019-00826-1
Rothwell PM (2005) External validity of randomised controlled trials: “to whom do the results of
this trial apply?”. Lancet 365:82–93
Rothwell PM (2006) Factors that can affect the external validity of randomised controlled trials.
PLoS Clin Trials. https://doi.org/10.1371/journal.pctr.0010009
Russo F, Williamson J (2007) Interpreting causality in the health sciences. Int Stud Philos Sci
21:157–170
Sackett DL, Straus SE, Richardson WS et al (2000) Evidence-based medicine: how to practice and
teach EBM, 2nd edn. Churchill Livingstone, Edinburgh
Simonet D (2008) The new public management theory and European health-care reforms. Can
Public Adm 51:617–635
Tómasdóttir MO, Sigurdsson JA, Petursson H et al (2015) Self reported childhood difficulties,
adult multimorbidity and allostatic load. A cross-sectional analysis of the Norwegian HUNT
study. PLoS One 10:e0130591
Tyreman S (2018) Evidence, alternative facts and narrative: a personal reflection on person centred
care and the role of stories in healthcare. Int J Osteopath Med 28:1–3
Vogt H, Ulvestad E, Eriksen TE et al (2014) Getting personal: can systems medicine integrate
scientific and humanistic conceptions of the patient? J Eval Clin Pract 20:942–952
Wade DT, Halligan PW (2004) Do biomedical models of illness make for good healthcare sys-
tems? BMJ 329:1398
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133:655–659

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Chapter 2
Dispositions and the Unique Patient

Rani Lill Anjum

I have been working as a regular GP for many years and experienced how useful it is to
know patients as persons. Through repeated encounters over time, I became familiar with
many of my patients as persons—who they were and how they lived their lives—whether I
was aiming for it or not.

Although such information may be of medical relevance, it is rarely written down in the
medical records. In many aspects, it is tacit knowledge. Nevertheless, as General
Practitioners we use this kind of knowledge all the time in everyday medical practice, tai-
loring the approach and follow-up of individual patients, especially when we are dealing
with the patients we see the most.

There is also a growing body of research documenting that adverse life experiences can
have a decisive impact on people’s health. However, traditional biomedicine, the dominant
perspective through which today’s medical practice is conceptualised, has placed little
emphasis on expert findings, such as those within modern stress physiology, indicating that
biographical and person-related knowledge has medical relevance.

Bente Prytz Mjølstad, ‘Does your regular GP know you – as a person?’, CauseHealth blog
(https://causehealthblog.wordpress.com/2017/11/09)

2.1 The Similar and the Unique

From the biomedical perspective, medicine primarily deals with what is common
for all: cells, tissues, organs, anatomy and biological processes and interactions. In
the clinical encounter, however, one has to also deal with what is particular and
unique. But how much space should the practitioner give to evidence that is specific
to the single patient? Given that time and resources are limited, the highest priority
must be given to the clearly defined medical facts. Then, if there is time, one can talk
to the patient about other and more personal matters. Or so one might argue.

R. L. Anjum (*)
NMBU Centre for Applied Philosophy of Science, Norwegian University of Life Sciences,
Ås, Norway
e-mail: rani.anjum@nmbu.no

© The Author(s) 2020 13

R. L. Anjum et al. (eds.), Rethinking Causality, Complexity and Evidence for the
Unique Patient, https://doi.org/10.1007/978-3-030-41239-5_2
14 R. L. Anjum

In the quotation above, general practitioner Bente Prytz Mjølstad offers a differ-
ent perspective. She suggests that knowing the patient as a person might also help
the clinician to better understand their medical condition and medical needs.
Perhaps, then, knowledge of what is unique to a patient ought to be given a higher
priority in the clinic. Or would that take time and resources away from what is most
important: to understand, diagnose and treat the patient? In the CauseHealth project,
we have met a number of practitioners who emphasise the importance of patient
narratives, and who use the patient’s perspective and story as a source of valuable
medical information (many of these have contributed to Part II of this book).
Immunologist and psychotherapist Brian Broom describes this as follows:
Sometimes people wonder why I am so keen on the ‘story’. It is simply that we clinicians
who want to practice in a whole person way need practical doorways into the world of the
whole person, and especially that part of the person’s world not accessed by the normal
biomedical approach to disease. The latter, as currently practised, focuses on the expertise
of information-holding, the power of drugs and physical interventions, activities directed at
restoring, repairing and compensating for ‘mechanical’ deficits and distortions, and so on.
I greatly value the benefits of much of this.

But listening for the patient’s story opens up an entirely different world, and its power
derives from quite a different set of assumptions, attitudes and relational values. Asking for
a story may seem a simple matter but the implications are hugely important. In reality, most
of the stories implicated in illness are relational stories: of trauma, failure, loss, abuse,
abandonment, manipulation, and much more. We are all fundamentally relational…

We don’t need to be a psychologist or psychotherapist to start this process, or to make

simple connections, or to give the patient permission and encouragement to consider the
connections. The interaction doesn’t have to be perfect, or prolonged, or all done at once.
Patients know that we are persons too, and have limits on our capacities. We can be
good-enough.

Brian Broom, ‘Imagination and its companions’, CauseHealth blog (https://causehealth-

blog.wordpress.com/2017/07/03)

Clinicians might see an advantage in knowing more about their patients’ stories, for
the purpose of finding the causes of health and illness and for making predictions
about treatment and recovery. But there is little support for patient stories within
current medical thinking. In evidence based medicine and practice, information
from the single patient is not generally treated as strong evidence, at least not of
causality. One might even refer to the experience of individuals as ‘subjective’ or
‘anecdotal’, suggesting that their stories are relevant mainly for themselves and not
scientifically valid for claiming, for instance, that a certain factor contributed to a
certain condition. A question we should ask is then: at what point does information
from individual patients become causal evidence (see also Kerry, Chap. 13, this
book)? Is there a threshold at which anecdotes transform into evidence, for instance
when there is a sufficient number of individuals who report similar experiences?
Say a patient reports experiencing a possible side effect from a prescribed medi-
cine. If no one else using the medicine has reported the same side effect, one might
be reluctant to conclude that the medicine caused that effect, and for good reasons.
2 Dispositions and the Unique Patient 15

But if, after a few years on the market, a sufficient number of people using the medi-
cine report the same reaction, it might be concluded that it is a side effect after all.
From an epistemological perspective, meaning from the perspective of what we
can or cannot know, this is reasonable. If one knows little about the medicine’s
causal mechanisms, a single report is not itself sufficient evidence of causality. But
if one thinks that 10, 100 or 1000 reports amounts to sufficient causal evidence, then
didn’t causality happen within each of these individuals? So even if the first patient
reporting the effect was not sufficient evidence of this causal link, it does not follow
that causality did not happen also in that instant. Lack of evidence does not imply
lack of causality: we cannot conclude that there is no causality happening in that
particular person, ontologically, simply because we, epistemologically, lack evi-
dence of causality. Ontologically, meaning from the perspective of what does or
does not exist, if causality happens, it does so in the particular instance and does not
depend on what happens in other cases to similar patients.

Simply put…

Ontology concerns reality: what exists or happens in the world.

Epistemology concerns knowledge: what we can and cannot know about

reality.

Example: Ontologically, one might have a rare genetic disease even if one has
yet not discovered it. Lack of knowledge does, therefore, not entail lack of
reality. Ontologically, the disease exists, but epistemologically, we don’t have
any evidence or symptoms of it. In other situations, there might be symptoms
or evidence of some disease that is not actually there, such as when a cancer
screening gives a false positive. Epistemologically, there was evidence of can-
cer, but ontologically, there was no cancer.

Why is the distinction between epistemology and ontology important? First of

all, if causality happens in the particular case (ontologically), this means that each
individual patient represents a valuable source of evidence (epistemologically), also
for causality. Secondly, this distinction also points to a tension in how we under-
stand causality as a phenomenon. Philosophically it boils down to the question of
whether there in principle could be a case of a unique causal event. Could causality
happen only once and never be repeated throughout the whole history of time? This
is an ontological question and not the same as the epistemological question of
whether we could ever scientifically establish causality for such a unique case.
This question is relevant for the clinical encounter because it matters in terms of
how one deals with medical uniqueness and individual variation. Should we place
much weight on single case reports or patient stories of seemingly unique effects or
16 R. L. Anjum

Fig. 2.1 The original

evidence hierarchy of EBM
Systematic reviews

Randomised Controlled Studies

Observation studies

Mechanistic reasoning

Clinical judgement

experiences? Or must we wait for results from larger clinical studies to even con-
sider causality?
In the original evidence hierarchy of evidence based medicine (EBM) (Fig. 2.1),
patient narratives, or even case reports, do not count for much, at least not with
respect to causality. The idea is that unless there is repetition, and preferably many
repetitions, one simply cannot know if something is causally related. This places
EBM within the philosophical tradition of empiricism and its emphasis on the
observable. We will now see how empiricism has influenced our understanding of
causality.

2.2 Empiricism: Causality Requires Repeated Observations

Historically, empiricism is the most influential view for how we understand causal-
ity, in philosophy and science in general. This view has itself been largely shaped by
the empiricist philosopher David Hume and his famous work A Treatise of Human
Nature from 1739. Hume was critical of ontology: he was skeptical about making
claims about what ultimately exists. Indeed, he believed that all we can really know
about the world is restricted by what we can experience through our senses. This is
the empiricist assumption, namely that our observations are the only evidence we
can have of reality. Positivism is the idea that science should be strictly empirical,
and only deal with what can be observed and measured.
This scepticism toward ontology also meant that Hume was critical of any theory
that says more than what can be backed up by data. If we try to explain what we
observe by appealing to some general, underlying principle, this would be to say
more than what we have evidence of. In practice, however, this might mean that all
scientific theories have a speculative element to them, unless they simply report the
available data. For Hume, therefore, as for any empiricist, epistemology trumps
ontology.
2 Dispositions and the Unique Patient 17

Simply put…

Empiricism is the idea that we can only know what can be experienced
through our senses. This means that all scientific knowledge should ultimately
come from observation data.

Positivism is a strict empiricist view of science, stating that science should

only deal with what can be established through observation and measurement,
and that everything else is metaphysical speculations.

When analysing the concept of causality, Hume used the example of the billiard
ball table. Here, we think that hitting the object ball with the cue ball causes the
object ball to roll. But what do we actually observe on the table? Hume found three
observable features of causality:
1. The cause is perfectly correlated with its effect, so that every time the cause hap-
pens, the effect follows. He called this the constant conjunction of cause
and effect.
2. The cause always happens before the effect. He called this temporal priority.
3. There must be some contact between cause and effect in time and space, so that
the cause and effect meet. He called this contiguity.
What Hume could not observe, however, was any form of link or necessary con-
nection between cause and effect. We cannot observe that also the next time the
cause occurs, the effect will necessarily happen. If we have not observed this yet, we
cannot infer that it will happen, even if we are convinced that it will.
To assume that what we have observed until now will be what we observe also in
the future, is what Hume called an inductive inference. These inferences are logi-
cally invalid, since the conclusion goes beyond the premises. So we have seen
something happening in the past, but then we infer that it will be the same in the
future. This is something that we cannot know yet. When it comes to causality,
therefore, all we can know is that it is a form of regularity, as specified by 1–3
above. We cannot infer from this that there is a causal law that guarantees the same
pattern of regularity in the future, as this is yet to be observed.

Simply put…

Inductive inference is the process of drawing a conclusion by going beyond

the available evidence. For example, one could infer a conclusion for a whole
population from the results of a study conducted on a representative sample of
such a population. Since the conclusion goes beyond the premises, we cannot
be sure that inductive inferences are logically valid.
18 R. L. Anjum

Hume’s is a very strict form of empiricism. To follow it up scientifically, we

would have to constrain ourselves from making any form of general or theoretical
claims that also involve future events. The law of gravitational attraction, for
instance, might have worked in the past and the present, but whether it will work
tomorrow is not yet evident. A causal law is then nothing but a claim that the cause
and the effect have been repeatedly observed to follow one another in a certain way
in the past.
This is now known as the regularity theory of causality, in which repetition is the
key to calling something causality. From this perspective, the same cause should
always give the same effect, at least under the same or similar conditions. Hume was
quite insistent on this criterion for causality: ‘The same cause always produces the
same effect, and the same effect never arises but from the same cause’ (Hume 1739,
I, iii: 173). In the clinic, we might refer to a certain sub-population of patients that
share some important features, such as their diagnosis. If these patients are given the
same treatment, we might expect that they should also get the same effect from it.
But we know that this is not generally the case. How can this be explained
philosophically?
There is an important consequence of Hume’s principle, that same cause, gives
same effect. If the effect is different, it can only mean that something was different
in the cause, or in the background conditions. Hume seems to think of this as an
undeniable truth about causality:
The difference in effects of two resembling objects must proceed from that particular, in
which they differ. For as like causes always produce like effects, when in any instance we
find our expectation to be disappointed, we must conclude that this irregularity proceeds
from some difference in the causes. (Hume 1739, I, iii: 174)

Hume would then say that if two patients with the same diagnosis get different
effects from the same treatment, there must be some other difference between them
that is causally relevant. The question is which individual differences are causally
relevant for the effect and which are not. We might expect sex, age and weight to be
relevant, but many treatments work across these differences. One might still expect
that if everything were the same between two patients, the same intervention should
produce the same outcome. If so, this would be in accordance with Hume’s under-
standing of causality.
Another consequence of Hume’s theory is that there can be no unique instance of
causality. Without the possibility of repetition, one cannot check whether the same
cause always produces the same effect. Hume accepts this and even goes as far as to
say that if the creation of the universe happened only once, it could not count as
causal. The alternative to this view is the position called ‘causal singularism’, which
will be discussed in the next section.
Although many philosophers might disagree with Hume in one or more of these
features of causality, they might still agree with his empiricist starting point: (i) that
2 Dispositions and the Unique Patient 19

the causal link itself is not directly observable and (ii) that causality must therefore
be inferred from what we can actually observe. In science, however, there seems to
be a general acceptance of Hume’s idea that same cause gives the same effect, and
that any difference in the effect must come from a difference in the cause.
How does this relate to how we understand causality in clinical research?
Assuming the empiricist ideal of science, causal relations should then be estab-
lished from observation data, for instance of an intervention and its outcomes. From
such data, one might be able to observe regularities, difference-makers or probabil-
ity-raisers, all of which can be detected via statistical methods. If causality is acces-
sible via observation data in this way, causal hypotheses and theories could in
principle be generated directly from data.
Crucial for this understanding of causality is that one needs repetition. Statistical
methods require large samples, or at least more than one or two individuals. In cases
of individual variation, one at least needs an actual or assumed sub-population of
which this patient is thought to be representative. A problem with a view of causal-
ity based on repetition, is that it leaves no room for causal uniqueness, as will be
explained further in the next section. If all patients are different, having a unique
biology, biography, life-style, diet, and so on, then no sub-group will perfectly rep-
resent them.
If repetition is a requirement for establishing causality, all causally relevant dif-
ferences between individuals seem to fall outside the scope of a single study. From
the clinical perspective this is a practical problem. How to deal with causality in
cases of large individual variation? Or perhaps we should say in case of uniqueness
when N = 1? This question was one of the main drivers for the Cause Health project.

2.3 Dispositionalism: Causality Happens in the Single Case

There are two ways to think about causal uniqueness. One is to think of it as a prob-
lem of causality, because we are then lacking the possibility of confirmation from
other similar cases. The other way is to think of causal uniqueness as typical of
causality, and therefore as the default expectation in any causal assessment. Causal
dispositionalism represents the latter view, called ‘causal singularism’. This section
presents a brief overview of the dispositionalist theory of causality and explain why
it gives ontological and epistemological weight to the particular over the general.
The theory of causal dispositionalism was first introduced in Mumford and
Anjum (2010) and is described in detail in their book Getting Causes from Powers
(Mumford and Anjum 2011). We will now explain why the individual patient and
their narrative should be at the heart of causal matters from a dispositionalist
perspective.
20 R. L. Anjum

Simply put…

Causal singularism is the ontological view that causality happens in the par-
ticular case and does not require repetition.

Example: The first person to die from a rare disease is a single and unique
case up until the next person dies from it. But even in the first person, the
disease caused their death, ontologically. So even if one might need more
cases to establish causality, epistemologically, either in animal models or in a
clinical study, causality happens in each individual case.

2.3.1 Causes Are Dispositions

Dispositions are also referred to as ‘causal powers’, ‘abilities’ (Mumford 1998) or

‘capacities’ (Cartwright 1989). They refer to what something can do. A sharp knife
can cut, a medication can heal, and a virus can make an otherwise healthy person ill.
A disposition is a type of property, but one that can exist unmanifested. Examples
of dispositional properties are fragility, flammability, toxicity and fertility. A sub-
stance is toxic even when it is not harming anyone. And a person can be fertile
throughout their life without reproducing. Causality typically happens when dispo-
sitions manifest themselves. A fertile woman becomes pregnant, toxic arsenic kills
or some explosive substance explodes. In this sense, the dispositional property is a
cause and the manifestation is an effect.
Whether something or someone has a disposition is not always observable until
it is manifested. The ‘proof’ of a disposition’s existence thus lies in its manifesta-
tion. Empiricist philosophers have asked how we can even know that dispositions
are real if they cannot be observed. Some dispositions might be possible to tease out
by an intervention or a test, such as a fertility test. But there will always be disposi-
tions that we simply cannot know of until they are manifested, and perhaps not even
then. A person might have early stage cancer without manifesting any observable
symptoms, but the causal process has nevertheless started. A disposition is thus not
a pure possibility, like the possibility of flying cars in the future. It is a potentiality
that exits in the world here and now as a real possibility in the properties of things.
Since empiricists trust only what can be observed (observability being another
disposition), they take manifestations to be real but see dispositions as merely pos-
sibly real. This seems a plausible conclusion if we think that the dispositions are
nowhere until they are manifested. But many dispositions are clearly present also
before they manifest. For instance, a sharp knife has a disposition to cut through
skin in virtue of the shape and material of the knife. If a knife was made of a mate-
rial that was too soft to penetrate the skin, it would lack that disposition.
2 Dispositions and the Unique Patient 21

According to Hume, our knowledge about dispositions is inferred from what we

have already observed elsewhere. Hume and neo-Humean philosophers, such as
David Lewis, Stathis Psillos and Helen Beebee, are therefore sceptical of disposi-
tions. They would therefore not include dispositions in their ontology unless they
are analysed into something observable (Mumford 1998, 2004). The only reason
why we think a wine glass is fragile, one might say, is because we have seen other
wine glasses break from very little impact elsewhere. Whether a particular wine
glass is actually fragile is thus something we cannot know until it breaks.
Epistemologically, this might be the case for many dispositions. But ontologi-
cally, at least, once the glass actually breaks, doesn’t this mean that it was in fact
fragile? If we had to wait until a manifestation occurred in every case before we
believed in its dispositions, we could not say that a nuclear power plant was explo-
sive unless it explodes. Dispositionalists would therefore reject the strict empiricist
principle, and argue that some things could be real even if they are not directly
observable.
Dispositions are seen as plausibly real because they can explain what actually
happens – the underlying principles of the behaviour of things. Causal effects with-
out underlying dispositions would on this view be unaccounted for and remain an
ontological mystery. The Humeans, on the other hand, would rather see everything
that is not observable as representing the real mystery, but their motivation for say-
ing so is primarily epistemological: we could not possibly know of something’s
existence (ontology) unless we can observe it (epistemology).
Although some philosophers are sceptical of dispositions, these properties seem
to play an important role in our lives. That we take dispositions seriously can be
seen in how they influence our behaviour. We are careful around explosive, flam-
mable or poisonous substances, and we don't expose ourselves unecessarily to con-
tagious diseases or let our children play with sharp knives. As Stephen Mumford
puts it in the opening section of his book Dispositions (1998: 1), referring to Nelson
Goodman, this is a world of threats and promises. And our behaviour very much
reveals our understanding of dispositions as real and important.
How is this relevant for the clinic? One might from the observation of a heavy
smoker’s lungs see that they are disposed to emphysema, chronic bronchitis and
lung cancer. And if a person’s arteries are clogged by arterial plaques, aren’t they
disposed to reduced blood flow and therefore to heart attack and stroke? In this
sense, the current situation points toward a possible, or even likely, future. The dis-
positions might reveal the direction toward which the situation is heading: what
tends to be (Anjum and Mumford 2018a). Dispositions are thus useful for making
prognoses for illness and recovery, but also for making the correct diagnosis. Since
many symptoms could be the manifestations of a range of illnesses, it is important
for choosing the right treatment that it targets the right disposition. If a headache is
caused by stress, the treatment will be different from if the headache is caused by a
tumour in the brain. Similarly, if chronic depression is caused by a biological dispo-
sition or by childhood trauma or abuse, or both, the treatment scheme should reflect
this difference (see also Hagen, Chap. 10, this book).
22 R. L. Anjum

2.3.2 Causes Are Intrinsic

Dispositions are typically intrinsic properties, belonging to some particular indi-

vidual or entity. That dispositions are intrinsic is crucial for the purpose of causality,
since we should not say that a drug works unless it has an intrinsic property to bring
about its effect. This is why medical interventions are typically tested against a pla-
cebo, to check whether the effect on recovery comes from the intervention or from
the patient’s own expectations of recovery. We might say that the placebo effect is a
manifestation of the patient’s dispositions, and not of dispositions belonging to the
intervention.
That dispositions are intrinsic does not mean that they have to belong to an indi-
vidual. Many dispositions belong to entities that are higher-level or even abstract. A
community can be supportive, friendly, homophobic or xenophobic, for instance. A
family can be loving or dysfunctional. A work environment can be stimulating or
draining and a legal system can be racist. Some dispositions might only emerge at
group level. As a community of people, we have social dispositions related to com-
munication, relationships, politics and law. Arguably, none of these are intrinsic to
the individual but emerge as a result of interactions with others (Anjum and
Mumford 2017, see also Rocca and Anjum, Chap. 5, this book).

Simply put…

A disposition is an intrinsic property that can exist unmanifested and gives its
bearer a causal power, ability or capacity.

Example: Someone can have a disposition toward a disease that is never man-
ifested, just like a glass can be fragile without being broken.

2.3.3 Causality Is Complex

We said that whenever dispositions are manifested, causality happens. A fertile

woman becomes pregnant, a fragile glass breaks, a medicine cures an illness: these
are all examples of causality. It is, however, important to recognise that all such
manifestations are a result of multiple dispositions working together. It takes much
more than a fertile woman and her eggs to become pregnant. Without the sperm
from a fertile man, for instance, and a prepared uterus with the correct balance of
hormones, the pregnancy will not happen. All these are what we call the manifesta-
tion partners for pregnancy, a term initially used by Martin (2008). That something
is an appropriate manifestation partner for a disposition means that they can pro-
duce an effect together that neither of them could have produced on their own.
2 Dispositions and the Unique Patient 23

From a dispositionalist perspective, all causality is complex in this sense, requir-

ing the interaction of one or more mutual manifestation partners. When a match is
struck and lights, this effect is caused by the striking as well as the flammable match,
the dry wood and the oxygen. But rather than treating one of these as the cause and
others as background conditions, they are all causes of the effect in virtue of their
own dispositions. Some of these dispositions might be necessary for the effect,
while others might be thought of as triggers. Still, everything that contributes to
producing the effect are on the dispositionalist view causes.
Causal complexity is particularly important to recognise in the clinic, since one
cannot focus only on the medical intervention when treating a patient. What an
intervention does on population level is one thing, but in this case, it will be interact-
ing with a particular individual. Unless this individual is an appropriate manifesta-
tion partner for the intervention, it will not be able to do its causal work. For
example, antibiotics tend to treat infections, but only in interaction with a non-­
resistant bacterium and proper conditions for being absorbed by the patient’s body.
Since most medical interventions have more than one disposition, a patient might be
a non-responder to the targeted effect, but still a mutual manifestation partner for
one or more of the non-targeted effects (see Edwards, Chap. 9, this book).

Simply put…

Mutual manifestation partners are a pair or set of dispositions that can do

causal work in interaction with each other that they cannot do on their own.

Example: When a match is struck and lights, this is the manifestation of the
flammable tip, the dry wood, the presence of oxygen, and so on.

When choosing a treatment for a particular patient, therefore, one should try to
learn more about the dispositions of the patient who will be interacting with the
treatment, as well as looking into the dispositions of the treatment. Most of the caus-
ally relevant dispositions in a treatment situation will actually come from the patient
and their unique causal set-up, including medical history, genetics, diet, life situa-
tion and biography. This is why rich patient evidence is important, but it is also why
it is important to understand causal mechanisms. Such mechanisms will tell us how
the treatment works in the body, but also how the various dispositions of the patient
might interact with the treatment.
How important is it for the clinic to have mechanistic evidence? Evidence based
medicine and practice emphasise statistical evidence over mechanistic knowledge
for establishing whether an intervention works. One argument for this is that our
knowledge about pathophysiological mechanisms is at any time incomplete, and
might be wrong. Because of this, some EBM proponents argue (Howick 2011),
prediction about the effectiveness of an intervention should be based on population
24 R. L. Anjum

trials rather than on fallible mechanistic thinking. However, for the purpose of find-
ing out how an intervention works, knowledge of causal mechanisms seems neces-
sary. Russo and Williamson (2007) proposed what has been called the
Russo-Williamson thesis. This thesis says that in order to establish causality, one
needs both statistical evidence and evidence of mechanisms. Indeed, the correla-
tions that are yielded from population studies are not necessarily causal.
Let’s take an example. Use of paracetamol is correlated to a higher incidence of
asthma, but this association could be due to confounding by indication. This means
that the onset of asthma could be due to frequent infections rather than to the con-
comitant use of paracetamol. In order to establish whether the correlation is causal
or not, it is necessary to understand the mechanism by which the cause brings about
the effect.
Russo and Williamson (2007) also argue that mechanistic knowledge is needed
to plan the experimental design of clinical trials, as well as for the interpretation of
the results from such studies. Rocca (2018) adds to these that knowledge of the
causal mechanisms underlying medical phenomena is necessary to evaluate com-
plex evidence, and to judge which population study we need to trust when different
studies give conflicting results. Gillies (2018) argues that mechanistic knowledge is
needed, not only to establish causal hypotheses about the cause of illness, but also
to develop an appropriate treatment and for evaluating the safety of a treatment.
From a dispositionalist point of view, knowledge of causal mechanisms is crucial
for understanding causality. On this perspective, the mechanism is a complex and
contextual matter, and includes the types of dispositions that are involved in the
causal process, how they interact, and also a potential for dispositions interfering
with and altering the causal process.
Without any understanding of causal mechanisms, it is difficult to predict how a
treatment will affect a particular patient and their unique set of dispositions.
Statistical data from other patients might help reveal causal mechanisms, but there
will always be causally relevant differences between individual patients that influ-
ence the outcome of an intervention. The more knowledge we have of the disposi-
tions of an intervention (both beneficial and harmful) and of the patient (including
vulnerability), the better our predictions will be for how the treatment will work for
that patient. This is also why one always needs to know which other medications a
patient is taking. While two of the drugs might be appropriate mutual manifestation
partners for the desired outcome, there might be other drugs that interfere and alter
that outcome. This brings us to the context-sensitivity of causality.

2.3.4 Causality Is Context-Sensitive

A cause will tend to produce different effects in different contexts, depending on

what else it interacts with. We have seen that this is a problem for empiricism: in
order to define C as the cause of a certain outcome, we need to observe the same
outcome every time we have C. For Hume, if the outcome observed is different, then
2 Dispositions and the Unique Patient 25

we cannot talk about the same cause. This is why it is hard to define causes outside
of experimental isolation. However, the story changes if we think of a cause as an
intrinsic disposition that might exist without being manifested, something we saw
was unacceptable for Hume. The same disposition might tend to produce different
effects. In fact, anything else should be surprising. How?
Because effects are produced, not by single dispositions but multiple, we cannot
expect that the same causal intervention will always produce the same effect. Different
contexts will give different effects, and we should not expect that two contexts are
ever exactly the same. This is essential in the clinic. Assuming that all patients are
different in at least some dispositions, each patient will represent a unique set-up of
mutual manifestation partners for a treatment. One patient will therefore be a differ-
ent mutual manifestation partner for the treatment than another patient. So even if the
treatment works in the intended way in both patients, meaning that the treatment has
the same disposition in both, the two patients might get different side effects, or the
treatment might work with different strength or momentum in each of them. The
outcome, or manifestation, of a disposition can thus be different in different contexts,
but this does not mean that the disposition of the intervention (e.g. the drug) was dif-
ferent. This is why we urge that the same cause does not always give the same effect.
By thinking this way we need some additional strategies for making claims about the
disposition of the drug, other than Hume’s perfect regularity of cause and effect. For
instance, we might know the drug’s disposition because we know how it works.
We can illustrate this point with an example of extreme context-sensitivity, where
the same causal disposition tends to produce widely different effects in different
contexts. Antiarrythmic drugs have the disposition to calm irregular heartbeat, by
altering the electrophysiology of myocardial cells at a faster heart rate. Such altera-
tion is obtained by inhibiting the fast sodium channels. This in turn prolongs the
action potential refractory period in some of the myocardial tissues. This disposition
is an intrinsic property of the antiarrythmic drug, and since we are aware of this
property and how it works, we can say it is present also when it is not manifested.
In some patients, the same types of drugs can on the contrary worsen irregular heart-
beat, by inhibiting a different type of electric flow through the cell membrane, for
instance by blocking potassium channels. In this case, the manifestation is different
because of a different set up of mutual manifestation partners. However, we can still
say that the disposition of the drug to block the sodium channel was present and the
same. What is different is the way in which the disposition of the drug manifested
itself in patients with different sets of dispositions. This is what it means to say that
causality is context-sensitive from a dispositionalist approach.
Could we plausibly say that the same intervention amounts to the same treatment
in two different patients, if one patient’s symptoms are alleviated while the other
patient’s symptoms are aggravated? In the first case, the intervention produces the
effect it was intended to produce. But in the second case, another effect happened.
Was it a side effect of the drug? Or did the patient interfere with the drug, preventing
the effect from happening? In this case, it seems more accurate to say that the two
causal set-ups produced different effects because of the different mutual manifesta-
tion partners involved.
26 R. L. Anjum

2.3.5 Modelling Causality

We can model causality in the single case using the vector model (Fig. 2.2). The
model was developed in Mumford and Anjum (2011), adapted to the clinical sce-
nario in Low (2017, see also Low, Chap. 8, this book) and later used by Price (see
Price, Chap. 7, this book) to understand and manage the complexity of her chronic
condition. In the vector model, the current situation is represented by a vertical line,
on a quality space between two outcomes, F and G. In a patient with a chronic con-
dition, such as irritable bowel syndrome, F might represent lack of gastrointestinal
symptoms while G might represent continuous symptoms. Then we add the disposi-
tions which are in place simultaneously and contribute to either of these outcomes
as vectors. Vectors allow us to model two important features of dispositions: their
degree of strength and their direction. Say, for instance, that for this patient con-
sumption of fatty meals disposes toward gastrointestinal symptoms to a greater
degree than salt or sugar. In that case, this should be reflected in the length of the
vectors. One should not only include the dispositions that dispose toward the appear-
ance of symptoms, of course, but also those that dispose away from them. The
patient might experience less symptoms when he exercises regularly for instance, or
after a good night of sleep. The resultant vector R thus shows whether the overall
tendency disposes toward F or G, and how much.
An important feature of the vector model is the qualitative nature of the vectors.
The length of the vector is not reflecting a numeric or statistical tendency, of how
often the effect happens in a particular population. This means that the length of the
vectors, as well as the type of disposition represented by the vectors, will vary from
one individual to another. The reason for this is that the vector model should repre-
sent the singularism of causal dispositionalism: that causality happens in the unique
particular context. While one person will tend to an impoverished gastrointestinal
flora because of intensive pharmacological treatment, another person might not
share this disposition, while still being overall disposed to irritable bowel syndrome.
The length and direction of the vector should therefore be based on what is the case
for a particular person at a particular time. One thing is that general scientific knowl-
edge (generated by a plurality of evidence, including population studies) can be
useful to suggest which causal disposition might be at play in the case of this

Fig. 2.2 The vector model

of causality

F G

R
2 Dispositions and the Unique Patient 27

particular patient: in general, we know that symptoms might be caused by the type
of diet, emotional stress, etc. However, this general knowledge is not what the
model represents.
Note that in Fig. 2.2, it is assumed that the different dispositions compose in a
simple additive way, but this is not always or even usually the case. Some disposi-
tions interact in nonlinear ways, and produce synergistic or antagonistic effects.
This means that the total effect is greater than (synergistic) or smaller than (antago-
nistic) the sum of the individual factors. For example, knee pain can be improved or
worsened by exercise, depending on the individual context, but also on the amount
and type of exercise. We should therefore not expect exercise to be modelled with
the same intensity or even direction in two different individual situations, or even
for the same individual at two different moments in time. As physiotherapist
Matthew Low (2018: 26) notes: ‘When evaluating the evidence, one must ask one-
self, how does this study relate to my particular patient at this particular time?’.
What is relevant for one patient might not be relevant for another.
The vector model, therefore, is a way to describe the quality of a causal situation,
and not to measure and quantify it. Since we are used to thinking about vectors in
connection with units of measure, it might take some time to get used to dropping
such concerns in this case. But once this is left behind, it should become clear that
the vector model allows us to illustrate some central features of causality: different
types of causal interference, different degrees of tendency, threshold effects and tip-
ping points, in addition to causal complexity and causal sensitivity. We will present
these briefly, one by one.

2.3.6 Two Types of Causal Interference

The effect can be interfered with by removing a vector disposing toward the effect
(subtractive interference) or by adding a vector disposing away from the effect
(additive interference).
Suppose that in a patient, gastrointestinal symptoms can be counteracted subtrac-
tively (Fig. 2.3) by reducing the intake of alcohol, sugar or processed food. But one
can also use additive interference (Fig. 2.4), such as probiotic supplements to

Fig. 2.3 Subtractive

interference

F G

R
28 R. L. Anjum

Fig. 2.4 Additive

interference

F G

Fig. 2.5 Dispositions with

different strength of
tendency

F G

enhance the gut microbiota complexity. Additive interference can be used when
subtractive interference is not possible or sufficient to reduce the unwanted effect.
Typically, all causal processes can be counteracted by adding something to the situ-
ation that tends away from the effect, at least in principle. In fact, most medical
treatments are cases of additive interference, and even if an intervention has not
been found for all health conditions, the default expectation is that we should keep
looking for one.

2.3.7 Degree of Tendency

A disposition has a tendency towards its manifestation with a certain degree or

intensity.
All dispositions come in various strengths (Fig. 2.5). For instance, oral contra-
ception has a very strong disposition to prevention ovulation, but also a very weak
disposition to produce thrombosis. So even though the correlation between oral
contraception and thrombosis looks very weak, statistically, it still counts as causal-
ity because there is an intrinsic disposition in the pill toward thrombosis in combi-
nation with the appropriate manifestation partners. According to the dispositionalist
theory, it is therefore no requirement that a cause produces its effect regularly or
even ‘often enough’ in other similar circumstances, in order to count as causality.
What counts is that there is something in the intervention that contributes to the
outcome to a stronger or weaker degree.
2 Dispositions and the Unique Patient 29

2.3.8 Threshold Effects and Tipping Points

A threshold effect or tipping point is a stage in the causal process where something
conspicuous happens that we might be particularly interested in bringing about or
preventing.
The threshold effect (Fig. 2.6) is often a pragmatic and interest-relative matter,
but it could also be the point at which a disposition manifests itself into something
observable. In medicine and healthcare, a threshold effect might be the stage in the
process of an illness where a problem or symptom occurs, such as fever, pain or
anxiety attack. It could also represent a crucial stage toward recovery, such as in
rehabilitation, where the goals or threshold might change along the way according
to changes in the patient and their context.
Thresholds are useful because they can help show whether a situation is close to
or far from a tipping point. One patient can be more vulnerable than another, if they
are closer to the threshold for illness. In such a situation, a small change in the cause
might result in a vast change in the effect. In cases of burnout or chronic fatigue, for
instance, the trigger could have been something that might seem relatively harmless
from a medical point of view. This could be a conflict at work, an infection or a life-­
changing event such as a divorce. What triggers an illness is thus not always the
main cause of illness, but might simply be the ‘straw that broke the camel’s back’.
In the vector model, one could then illustrate how a small change could have a big
impact when the background conditions were already close to the threshold effect,
although the same change would not make a difference for a person in a more robust
stage of health (see also Price, Chap. 7, this book).

Fig. 2.6 A threshold T

effect T

F G

R
30 R. L. Anjum

2.4 Philosophy of Causality Influences Scientific Methods

We have seen some main features of causal dispositionalism. This is primarily an

ontological framework where causes are seen as dispositions. But how we think
about a phenomenon will necessarily influence how we approach it. In this sense at
least, ontology has an impact on practice. We will now see how ontological assump-
tions about the nature of causality influence even the scientific methods used for
generating causal evidence.
In the CauseHealth project, we have argued that scientific methods are not philo-
sophically neutral, but carry with them a number of assumptions about the nature of
causality (Anjum and Mumford 2018b). How does this work? Let us look at some
common methods and see how they attempt to establish causality, epistemologi-
cally. From this, we can see what type of features that causality needs to have,
ontologically, in order for the method to be a reliable way to test for causality.
Epidemiological and other statistical methods use correlation data to search for
causality. They also emphasise large amounts of data and proportion of outcomes.
The idea is that more data will lead to more accurate causal conclusions. Ideally,
one might think, if we had a complete set of correlation data — past, present, and
future — one would also have complete causal knowledge. Philosophically speak-
ing, this fits well with Hume’s regularity theory of causality and empiricist agenda.
Further, causality is established by observing as many repetitions as possible, where
the same cause is followed by the same effect. Some epidemiologists are sceptical
of making causal claims based on their observations, and prefer instead to speak of
correlations, raised probabilities or relative risk. This meets all the empiricist crite-
ria for not saying something that goes beyond the available observation data and
thereby avoiding inductive inference.
Other methods use comparisons of data to establish causality. Comparative
methods allow us to search for causes by looking at the difference between two set-­
ups: one in which the cause is present (test) and a second in which it is absent (con-
trol). In randomised controlled trials (RCTs), if the outcome is more frequent in the
test group than in the control group, one concludes that the increase is due to the
intervention rather than the background conditions, which should be evenly distrib-
uted between the groups. The cause is then understood as a difference-maker, as
suggested by Hume and Lewis (1973). Crucial for difference-making theory, is that
the cause is something that can make a difference to the effect. If no difference can
be observed, epistemologically, we have no reason to assume causality,
ontologically.
Most scientific methodologies will rely on both regularity and difference-­making.
In a lab experiment, one compares what happens in the case of intervention with
what happens without it, and usually with some repetition. Instead of randomisation
of background conditions, these are carefully controlled for. By isolating the cause
from interfering factors, one expects to better observe its causal role. Experimental
methods also involve an assumption of manipulability, which is the assumption that
a causal process can be manipulated in some way. This is crucial when we want to
2 Dispositions and the Unique Patient 31

bring about or prevent a certain effect. By manipulating the cause, one also manipu-
lates the effect. This is the basic idea of the interventionist theory of causality, with
Woodward (2003) as its main proponent. Note that interventionist theory can be
Humean or dispositionalist. If Humean, it would look for whether an intervention
makes a difference. If dispositionalist, one would be more interested in the intrinsic
properties of the intervention, its causal mechanisms and its influence across indi-
vidual variations. This tension between statistical and individual effects is also seen
in methodological approaches within psychology, as here discussed by psychologist
Tobias Gustum Lindstad:
A prevailing idea among psychologists is that, in order to make psychotherapy evidence based,
one has to prove the relevance of therapeutic models and the effects of specific techniques on
a group-level. Thus, hundreds of perspectives, models and theories have been thrown into
rivalry competing for the best mean results. However, this idea, that the only proper way to
uncover the relevant causes is to observe their regular effects (the regularity view) threatens to
throw the baby out with the bathwater. Since statistics does not take individual experiences into
account, information about aspects that are relevant in each case are lost. Thus, one size does
not necessarily fit all, and we must qualify our services locally and individually in any case.

Tobias Gustum Lindstad, ‘If statistics don’t get me, then what?’, CauseHealth blog (https://
causehealthblog.wordpress.com/2016/02/05/if-statistics-dont-get-me-then-what/)

2.5 Practical Implications for the Clinic

In this chapter, we have given a brief overview of the dispositionalist theory of cau-
sality. We have explained how ontology – how we think the world is – influences
epistemology – how we go about investigating the world. We saw that there are
ontological assumptions about causality in all scientific methods. But what about
clinical practice? What exactly are the practical and clinical implications of under-
standing causality in the dispositionalist way? We have already mentioned some
ways in which dispositionalism might be used as a normative basis for clinical
practice.

2.5.1 Causal Evidence Comes from the Patient

Emphasising causal singularism, mutual manifestation and interference, disposi-

tionalism suggests that a major part of causal knowledge will rely on insights into
the local context of a unique causal setup. In practice, this means that causal
inquiry – both for understanding the condition and deciding how best to treat it –
should begin from understanding the full complexity of the patient’s situation. This
is because the patient will represent most of the causally relevant information
needed to understand, diagnose or treat them. The patient’s context (the situation,
the history, the narratives) is an indispensable source of medical evidence. This is
32 R. L. Anjum

not to say that general theory and population studies are of little use for clinical
practice. Rather, local evidence about the patient context is needed in order to make
sense of all the other types of evidence and theory available to the clinician. A prac-
tice that overlooks it is likely to end up being bad practice, even when it relies on
good science and advanced technology. The question arising from this is how a
clinician can get a better insight into aspects of the patient’s unique history and
context that might influence their condition in positive or negative ways. One
straightforward answer, which we heard from many of the clinicians we met during
the project, is by listening to a patient’s narratives, and to the stories they have to
tell. This is for instance what physiotherapist Neil Maltby has to say about the matter:
You’re history! Literally. What would you be without it? A void. It is impossible to change
it. Your previous choice of job, degree, partner, hobby. Your exposure to family life,
upbringing, culture, sports, arts, influential others. Even your genetic make up. Our histo-
ries intertwined with previous generation. It would be hard to look at these historical
events without acknowledging their causal power in who you are now. What if I had been
born into a richer/poorer family, the opposite gender, part of a majority/minority group?
Would these not be causally relevant in who we become?

Say we randomly take 100 people off the street and show them the film Terminator. The
situation is the same for each person. Same cinema, same time, same popcorn. Will they
have the same reaction to the film? Of course not. Because history is more than just events.
History is about people. People have dispositions. The best history for me is where people
defy their circumstance. This is where we meet personal (or dispositional) attribution.

Dispositional attribution helps explain individual differences to the same stimulus or situa-
tion. This is not to say our situation has no impact on us. Clearly it does. It may help shape
future dispositions. In life we lean on our internalised dispositions, feelings, previous expe-
rience. Two people (or even a single person with a time gap) may internalise the same situ-
ation in very different ways. This means we cannot rely on humans reacting robotically
especially to complexity.

Is this even important?! Well I’d say so. It means as healthcare clinicians we are not striving
for uniformity in treatment (situational attribution) because, as research shows, not every-
one will respond to this. I think there is a lingering hope that one day we will come up with
perfect protocols for lower back pain, fibromyalgia, tendon pain, irritable bowel syndrome
and depression. This seems to be the aim in most research I read. Treatments based on
pathology tend ultimately to look at situational attribution and not the dispositions of the
individual.

Neil Maltby, ‘You’re history (hasta la vista, baby)’, CauseHealth blog (https://causehealth-
blog.wordpress.com/2016/02/19)

2.5.2 There Is No Standard or Average Patient

Assuming causal singularism and causal complexity, dispositionalism suggests that

there might never be two identical causal situations in practice. All patients are in
some sense medically unique, with different genetics, life situation and biography.
2 Dispositions and the Unique Patient 33

In practice, this means that we should not expect that there is a ‘normal’, ‘ideal’ or
‘standard’ patient or even a normal response to a treatment. If something happens in
one patient that cannot be backed up statistically or observed in other patients, this
does not rule out the possibility of causality. Causal singularism means that all
causal processes are intrinsic and particular. Effects happen in the single patient, as
the result of multiple dispositions, many of which are unique to that patient.
Physiotherapist and researcher Wenche Schrøder Bjorbækmo writes about
standardisation:
At the end of the 1990s I perceived standardised testing and standardised procedures as the
future. As a tester I became concerned with performing the tests correctly, which meant
following the standardised procedures. The tasks I asked the children to do, and the ques-
tions I asked the parents were guided by the instructions and the structure of the test. It was
important to remember the order of the tasks and questions. Several of the tests had many
tasks and questions, and there wasn’t just one test to learn, but many. Each test had been
adapted for different purposes and for different patient groups.

The test directs the professional view in particular directions, and thus away from anything
else. When something in this way is brought into the foreground, other aspects, of for
instance a child’s functioning, are disappearing into the background. In many ways this
experience led me to think that in testing I was actually gaining less knowledge about the
child and his or her functioning than in traditional clinical observations.

This experience of having ‘seen’ less and received less information frustrated and disturbed
me. The test “demanded” a special form of communication and being together. I experi-
enced the standardised framework of the test and administrative demands as framing the
communication and relation made possible between the child, parents and myself.

Wenche Bjorbækmo, ‘Glasses and blind spots: through the eyes of a tester, CauseHealth
blog (https://causehealthblog.wordpress.com/2017/11/20)

2.5.3 Unexpected Outcomes Are Valuable Causal Lessons

Dispositionalism stresses that all causal processes can be counteracted, subtrac-

tively or additively. So even when the effect typically follows from the cause, it is
still possible to have the cause together with some interferer that is preventing the
effect from happening. When this happens, one should aim to understand the dispo-
sitions involved and the causal mechanisms by which they interacted to produce or
inhibit the effect.
This type of causal knowledge is particularly important for predicting how a
patient will benefit from a treatment, or if there are any risks involved. While all
treatments have a targeted effect that is tested and established, one can learn some-
thing important about the treatment’s other dispositions from their side effects. Side
effects are often rare and unexpected, yet they point to dispositions in the patient
that were able to causally interact with the drug. From this, we can develop new
causal hypotheses for theory development, which are also relevant for basic research
34 R. L. Anjum

within medicine and biology (Rocca et al. 2019; Rocca et al. 2020). Ivor Ralph
Edwards, medical doctor and senior medical advisor of the WHO collaborating
Uppsala Monitoring Centre for International Drug Monitoring, has been dealing
with the problem of detecting unexpected effects of pharmaceutical interventions
for decades. In the following text, he explains why thinking of causes as disposi-
tions can be useful in pharmacovigilance:
There is an ongoing debate about how to analyse and evaluate the data we gain from large
data sets, and particularly what we can say about causality – after all, one is bound to find
correlations by chance in vast amounts of data and with multiple analyses; but all this
assumes that causality is a linear process which can be evaluated epidemiologically.
Causality in real life, however, is usually multifactorial and complicated, and pharmaco-
vigilance is concerned with data from complex healthcare systems in which multiple inter-­
relating factors evolve. The data we collect is affected by those changes over which we have
no control….

One different approach to causality in pharmacovigilance is causal dispositionalism and is

applicable to complex data. This approach considers the innate characteristics (the disposi-
tions) of both the medicinal product and the exposed patient – some property, state, or
condition that, under certain circumstances, gives the possibility of some further specific
state or behaviour. The relevant properties of the medicines would include its various phar-
macological actions (pharmacodynamics), its distribution in the body (pharmacokinetics),
and its interactions with other drugs. The relevant properties of the patient would include
specific susceptibilities, such as genetics, age, sex, physiological state such as body weight
or pregnancy, co-morbidities, drug-drug interactions, and social and environmental factors
that have affected the patient.

Consider a medication M, with a set of dispositions, M[d1], M[d2], and so on, known to be
able to cause benefits and harm, and patient P with dispositions P[d1], P[d2], and so on. We
may then begin to investigate the probabilities that any M[d] will produce beneficial or
adverse outcomes in a patient with any P[d], asking the questions ‘how?’, and ‘when?’,
using whatever information we have about the medicine M and the patient P to determine
the benefit to harm balance. This type of analysis is not merely probabilistic, but also takes
into account the strength – the power – of M to affect P, as well as any outside factor that
interacts with the causal link, e.g. drug-drug interactions. It also explicitly takes into
account the power of P to respond to M. A disposition may be present but not become mani-
fest until its power reaches a particular threshold, e.g. above a certain dose of a medication,
in combination with, for example, a certain degree of renal function impairment in the
patient.

Alternatively, a medicine with disposition M[d4] may have maximal effects in patient P1
with dispositions P1[d2,3,4,5,6,7], partial effects in Patient P2 with dispositions P2[d2&7], and
partial or maximum effects in other patients Pn with, say, dispositions Pn[d2,3,4,5,6,7,8,9], but
only in certain environment where the two extra dispositions d8 and d9 result in an addi-
tional influence, such as might occur when syncope from a vasodilator only happens when
a susceptible patient is dehydrated…

Let’s be very broad-minded about what new value we can find in the multiplicity of big
real-life data sets we can utilise to examine benefit and risk and thereby improve therapy.
(Edwards 2018: 28–29)
2 Dispositions and the Unique Patient 35

2.6 To Sum Up…

In this chapter we have argued that a genuine revision of the norms and practices in
clinical work needs to start from a revision of the way we think about the world, and
in particular the way we think about the most foundational concepts, such as causal-
ity. We have presented the dispositionalist theory of causality and explained why
this theory is better suited for the clinic than the orthodox Humean theory which
motivated the EBM framework. We have argued that causality ought to be under-
stood as something singular and intrinsic rather than as a pattern of regularity across
different contexts. From a dispositionalist perspective, causal knowledge ought to
start from the single case. In the clinic, this means that the more we know about the
multiple dispositions that are involved and how they interact in this specific context,
the better equipped we will be to make good and relevant explanations, predictions
and decisions for the individual seeking care.

References and Further Readings

Anjum RL, Mumford S (2017) Emergence and demergence. In: Paoletti M, Orilia F (eds)
Philosophical and scientific perspectives on downward causation. Routledge, London,
pp 92–109
Anjum RL, Mumford S (2018a) What tends to be. The philosophy of dispositional modality.
Routledge, London
Anjum RL, Mumford S (2018b) Causation in science and the methods of scientific discovery.
Oxford University Press, Oxford
Cartwright N (1989) Nature’s capacities and their measurements. Oxford University Press, Oxford
Edwards R (2018) Living with complexity and big data. Uppsala Rep 78:28–29
Gillies D (2018) Causality, probability, and medicine. Routledge, London
Howick J (2011) Exposing the vanities – and a qualified defense – of mechanistic reasoning in
health care decision making. Philos Sci 78:926–940
Hume D (1739) A treatise of human nature. In: Selby-Bigge LA (ed) Clarendon Press, Oxford, 1888
Lewis D (1973) Causation. In: Lewis D (ed) Philosophical papers ii. Oxford University Press,
Oxford 1986:159–213
Low M (2017) A novel clinical framework: the use of dispositions in clinical practice. A person
centred approach. J Eval Clin Pract 23:1062–1070
Low M (2018) Managing complexity in musculoskeletal conditions: reflections from a physio-
therapist. In Touch 164:22–28
Martin CB (2008) The mind in nature. Oxford University Press, Oxford
Mumford S (1998) Dispositions. Oxford University Press, Oxford
Mumford S (2004) Laws in nature. Routledge, London
Mumford S, Anjum RL (2010) A powerful theory of causation. In: Marmodoro A (ed) The meta-
physics of powers: their grounding and their manifestations. Routledge, London, pp 143–159
Mumford S, Anjum RL (2011) Getting causes from powers. Oxford University Press, Oxford
Rocca E (2018) The judgements that evidence based medicine adopts. J Eval Clin Pract
24:1184–1190
36 R. L. Anjum

Rocca E, Copeland S, Edwards IR (2019) Pharmacovigilance as scientific discovery: an argument

for trans-disciplinarity. Drug Saf 42:1115–1124
Rocca E, Anjum RL, Mumford S (2020) Causal insights from failure. Post-marketing risk assess-
ment of drugs as a way to uncover causal mechanisms. In: La Caze A, Osimani B (eds)
Uncertainty in pharmacology: epistemology, methods and decisions, Boston series for the his-
tory and philosophy of science, Springer, Dordrecht
Russo F, Williamson J (2007) Interpreting causality in the health sciences. Int Stud Philos Sci
21:157–170
Woodward J (2003) Making things happen: a theory of causal explanation. Oxford University
Press, Oxford

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Chapter 3
Probability for the Clinical Encounter

Elena Rocca

3.1 Uncertainty and Probability in the Single Case

‘Healthcare professional’ are words we use to describe a group of professionals

with a variety of different specialisations, approaches and backgrounds. And yet,
one can draw out some commonalities from this diversity. There are some aspects
that everyone working through consultation with suffering individuals will recog-
nise, in different degrees, as a daily part of their job. One of these aspects is
uncertainty.
No matter their specific field of expertise, every healthcare professional must
cope with the fact that all patients are different. Not only is every biological setup
unique; the multiplicity of contextual conditions, lives, habits and stories make
every patient a special case. Because of this, the practice of inferring information
from one patient (or group of patients or experimental model) to another patient
always entails some unknown margin of error. Uncertainty is intrinsic to all the
phases of the encounter with the single patient, from diagnosis to prognosis to treat-
ment. Some of these uncertainties must be accepted as such, but most of them need
to be somehow qualified. Even the most experienced healthcare professional needs,
in every single instance, to find an answer to the question:
What is the probability that this intervention will work this time, for this particu-
lar patient?
This question, we can say, is universal in the clinical encounter. However, there
are different ways to approach it, conceptually and philosophically.
We are used to think about probability as the way to deal with uncertainty.
Probability turns uncertainty into something more tangible by somehow giving it a
qualification, or even a quantification. For instance, we say that the chances that a

E. Rocca (*)
Centre for Applied Philosophy of Science, School of Economics and Business, Norwegian
University of Life Sciences, Aas, Norway
e-mail: elena.rocca@nmbu.no

© The Author(s) 2020 37

R. L. Anjum et al. (eds.), Rethinking Causality, Complexity and Evidence for the
Unique Patient, https://doi.org/10.1007/978-3-030-41239-5_3
38 E. Rocca

certain treatment will work in the single patient is 30%, fairly low or higher com-
pared to another treatment. This will inform the clinical choice in a more satisfac-
tory way than just acknowledging that “the outcome is uncertain”. Thinking in
terms of probability is then a useful tool for dealing with uncertainties for the single
patient. But what do these numbers mean? Can they be interpreted in only one way,
or in many?
Thinking in terms of probability offers multiple ways, rather than only one, for
dealing with uncertainty. Although we might assign similar probabilities to a certain
event, there are different ways to interpret what such assigned values, or descrip-
tions, mean. Think, for instance, about a healthcare professional who assures a
patient that the probability of recovery with a certain intervention is ‘very high’.
How should the patient understand such a statement? That the majority of the
patients, previously treated with the same intervention, finally healed? That the pro-
fessional has a high confidence in the positive outcome of this particular case? Or
does it mean that the patient’s condition at this moment is optimal to respond to this
particular treatment, considering its mode of action? Clearly, these are three differ-
ent types of statement, and might lead to different clinical decisions.
In this chapter, we will first explore the basic assumptions that hide behind the
usual conceptualisation of probability in evidence based approaches. One version of
probability is objective and the other is subjective. We then explore a dispositional-
ist concept of probability, which we think is most relevant for the clinical context.
We will show how this understanding of probability can help integrate evidence
from healthcare guidelines with evidence from the single patient.

3.2 Probability from Statistics: Frequentism

To understand the frequentist approach to probability, imagine that you see a coin
for the first time, and you notice that it is two-sided. You wonder what is the prob-
ability of the coin landing heads when tossed. One way to approach this question is
to toss the coin many times, and count how frequently you get a head. After a suf-
ficient number of repetitions you might calculate that about half the outcomes were
heads, and therefore you can infer that the probability of getting a head at the next
toss is ½ or 50%. Crucially, you would not be confident in drawing a conclusion
after only 3, 5, or 20 tosses. The more instances you have to base your calculation
on, the more you can trust the result to be accurate.
We see that the frequentist approach calculates the probability that a certain
event will happen by investigating how often it happened in the past. Philosophers
call this type of approach ‘empirical’, meaning that it is exclusively based on obser-
vation. Recall that David Hume only trusted knowledge that could be observed
through our senses, which was his empiricist starting point (see Anjum, Chap. 2,
this book). To know how probable it is for the coin to land heads or tails, you would
then not need to understand anything about the coin’s properties or hidden
3 Probability for the Clinical Encounter 39

dispositions. You simply toss the coin as many times as you can and count the dis-
tribution of outcomes.
In reality, the calculation of past events is usually much more elaborate than in
the coin example, which is why scientists use statistical models and tools to calcu-
late the relative frequency of a certain outcome in a sequence of events.
Note also that this approach was developed by thinking about games of chance,
similar to coin tossing, and as such it needs two important premises to count as suc-
cessful. First, the frequentist approach presupposes that there is the possibility (at
least theoretically) of an infinite number of repetitions. Second, one needs to repeat
many instances of the exact same conditions. As a consequence of this, it is not pos-
sible to calculate a frequentist probability for a single case if it cannot be repeated.
From a single case, all we know is the actual outcome, not the proportion of such
outcomes over a series of similar trials.

Simply put...

Frequentism means to calculate the objective probability that a certain event

will happen based on the proportion of positive outcomes in a sequence of
trials. To calculate probability, one then needs to observe how often the same
type of event happened in previous, similar cases.

3.2.1 Frequentism and Evidence Based Approaches

Now imagine that, instead of the coin toss, we are talking about an intervention for
the single patient. Clearly in this case, we are missing both premises that we saw are
important for the frequentist approach to be reliable. We only have one instance of
this particular patient meeting this particular intervention under some particular
conditions. How can a frequentist notion of probability possibly be applied to the
single patient? How can we say something about the probability of effect for this
individual case?
There is a way out, and it is one that is widely used in evidence based approaches.
By assuming that each single patient is a statistical average of a group of individuals
that are similar enough to the patient in question, one can use the group as a repre-
sentative for that patient. The probability that an intervention works for this patient
can then be derived from the calculation of the statistical frequency of successful
outcome in their patient group. This is the principle on which clinical studies are
based. To say that a patient has 30% probability of recovery from a certain interven-
tion based on clinical studies, means that 30% of sufficiently similar patients who
tried that intervention under sufficiently similar conditions, recovered (at least for
the patients who participated in those trials). These kinds of predictions are
40 E. Rocca

common in evidence based medicine and practice, which takes the best evidence to
be statistical evidence from clinical trials.
From a healthcare perspective, however, there are some problems with this type
of reasoning. By seeing the patient as an average of similar patients, one must be
able to define what counts as ‘similar’. Which pieces of information are relevant in
each case? Similar age, medical history, lifestyle or social status? We are normally
not aware of which factors play a causal role in the single process, which is why it
can be misleading to see a patient as an average of groups of other patients, even
within the appropriate patient group. This issue is well acknowledged, and it is
sometimes referred to as the ‘reference class’ problem. The reference class problem
influences the interpretation of statistical data from population studies for the pur-
poses of inferring the probability of an outcome for the single patient. Imagine for
instance having to calculate the probability of a patient to respond to a certain class
of anti-depressants. The patient has countless properties (woman, young, history of
eating disorders, wealthy, diabetic, highly educated, hyperactive…), but which of
these will have a role in her condition and in the therapeutic process? This is known
only partially. Our patient is a member of many different classes (young wealthy
women, diabetic patients, patients with eating disorders), for which the frequency of
recovery from the anti-depressant differs. However, it is not obvious how the patient
should be ‘classified’ in relation to her depression and its treatment, since we do not
have a complete knowledge of which of her properties will play a causal role in her
clinical development. A number of tactics have been suggested as a solution to this
problem, and many of these consist in moving away from a purely frequentist
approach to probability, and including different types of evidence in the calculation,
such as mechanistic evidence (Clarke et al. 2013, 2014; Wallmann and
Williamson 2017).

3.2.2 Randomisation, Inclusion Criteria and Exclusion

Criteria in Population Trials

Let us now look at the case of clinical trials, of which randomised controlled trials
(RCTs) are currently considered the most reliable. RCTs have the purpose to assess
the frequency of recovery in a group of patients that received a treatment, compared
to a group of patients that received only a control or placebo. Based on such fre-
quency, one can predict the probability for the treatment to have a positive outcome
for the single patient. This is a frequentist approach to probability, as we described
above. Recall the example of the coin toss. There are two important premises for
being able to infer the probabilities for the next toss, from the frequency of out-
comes of previous coin tosses: first, the repetitions should be many, and second,
they should all happen under similar conditions. How can these conditions be met
in an RCT?
3 Probability for the Clinical Encounter 41

The first requirement is served by including a large number of patients in the

trial. One criterion of quality for an RCT’s design is that the more patients included,
the better. This is however not sufficient. If we want to end up with many instances
in which the same treatment is tried out in similar contexts, we also need to cancel
out the influence of individual variations between different patients. This is pursued
with two strategies at the same time.
The first strategy is randomisation. The reasoning goes like this: if one randomly
assigns the patients to the two groups (the group of patients who receive the treat-
ment and the group of patients who receive the placebo) and the groups are large
enough, then there is greater probability that the relevant causal factors are distrib-
uted evenly across the groups. This way, the two groups can be considered homoge-
neous, or at least similar enough. This is important in case we detect a statistical
difference in the outcome among the two groups, since it allows us to infer that any
such difference is caused by the intervention we are testing, rather than by some
other factor. Note that the difference spotted in an RCT is at the population level, not
in single patients, since there will be many individual variations within both the test
group and the control group.
There is an additional strategy for cancelling out the influence of individual vari-
ation on an RCT. This is to define in advance strict inclusion and exclusion criteria
for selecting which patients qualify to take part in the study. Typically, the patients
included in the study belong to a certain age range and have a certain medical
profile.
When designing an RCT, it is important to define in advance inclusion and exclu-
sion criteria, so that the sample included in the study is representative enough for
the population we want to study. In other words, at the end of the study one wants
to use the results observed in the selected sample in order to say something general
about the population we wanted to study. If the aim of the RCT is to get some infor-
mation about Norwegian women of fertile age, for instance, the study sample should
not be imbalanced with respect to age, geography, income or health condition. As a
result of this knowledge, exceptional cases, outliers, patients with conditions that
could influence or confound the interpretation of the statistical results, or patients at
higher risk of adverse effects might be excluded.

3.2.3 Internal and External Validity of Causal Claims

from Randomised Controlled Trials

These two strategies (randomisation and predetermined inclusion and exclusion cri-
teria) are aimed at increasing the reliability of the trial’s results. We want the study
to allow us to detect the effect of the intervention, and not to be confounded with
other factors that could influence it. This is also called the internal validity, or reli-
ability, of a causal claim based on a certain study design. A different matter, how-
ever, is to figure out what use we may have for such causal claim, once we know
42 E. Rocca

they are valid for the experimental sample on average. How does the knowledge of
how often something happened to the participants of an RCT apply when predicting
what is going to happen in the single patient? This is the question of external valid-
ity, or relevance, of a causal claim based on the study for the case in question. The
external validity of causal claims based on RCTs might be low when we are faced
with marginal cases, or with multi-morbid, chronically sick patients, who rarely
meet the inclusion criteria of an RCT. To what extent does the available evidence
from clinical studies represent these patients? Scientists and philosophers of science
have worried about this issue, when thinking about evidence based decisions and
how they should be made. As we shall see, the inductive inference from ‘it worked
there’ (in the study) to ‘it will work here’ (in my case) is not an easy one, and it is
paved with challenges and pitfalls where the doctor’s expertise and knowledge of
her patient seem to be indispensable ingredients (for a critical discussion of the
external validity of RCTs, see Rothwell 2005, 2006; Cartwright and Hardie 2012).

3.3 Probability as Degree of Belief: Subjective Credence

Say you are evaluating whether to prescribe a painkiller to a 30 year old patient and
want to predict the probability that the patient will get gastrointestinal side effects
from the treatment. Imagine that you have also already prescribed painkillers of the
same class to 100 patients, and of those patients, 30 patients experienced that side
effect. If this is the only information you have on the matter, and you want to make
a prediction about the probability of side effects for your patient, you might think
that such probability is 0.3 or 30%.
Let us assume that after a conversation with your patient, you learn that she suf-
fered from chronic gastritis for a number of years and only got better 5 years ago,
while she still suffers from temporary relapses. With this information at hand, you
might now change your belief on the likelihood of a gastrointestinal effect in the
patient, from 0.3 to >0.3. Another colleague in the same situation, however, might
just have been to an information meeting with the manufacturer of the pain killer
and learned that this particular painkiller acts through a different molecular pathway
than the others in the same class, and does not interfere with gastrointestinal path-
ways. In light of this additional information, your colleague might have a different
opinion than yours, and conclude that the probability of the patient getting a side
effect is not that high after all, and at <0.3 or even less.
We see that, within this philosophical theory, we can have three different esti-
mates of probability for the same patient in the same situation. The estimate will
depend on which relevant facts we are aware of and how important we think these
facts are for this particular patient. This suggests that the estimation of probability
P is not objective or ontological, but subjective and epistemological: it concerns the
information and knowledge that the healthcare professional has available at that
time. The value assigned to P will then be the subjective measure of one’s own
3 Probability for the Clinical Encounter 43

degree of belief that an outcome O will happen, given the available evidence E. In
mathematical language, this can be written in the following way:
P (O|E) (‘the probability P of the outcome O happening, given the evidence E’)
Every time we acquire new information, the evidence E changes and therefore
our degree of belief in the outcome is updated. This might strike us as an intuitive
and straightforward practice, but there are nevertheless some practical and philo-
sophical issues to consider.

3.3.1 Updating Belief

The first issue is a practical one. How exactly should we update our degree of belief in
light of new information? Who is apt to do it? And does ‘subjective measure’ of prob-
ability entail an uncontrolled subjectivism, by which anyone and anything goes?
Certainly not. Proponents of subjective probability postulate that the way in which
new evidence is used to update the degree of belief must follow some common rules.
These are the rules of probability calculus. In other words, two clinicians might calcu-
late a different probability of a certain treatment to work in a specific patient, but this
will only happen because they have access to different information. But the way in
which a piece of evidence updates the belief, should be the same for both clinicians.

Simply put...

Subjective probability (credence) is the degree of belief, or confidence, in a

specific outcome given certain available evidence, as estimated by a suitable
agent. A suitable agent is an agent that uses the rules of probability calculus
in order to update its expectations, and the value of the probability is always
expressed quantitatively.

One way to update beliefs or expectations in light of new evidence is given by the
Bayesian formula. The Bayesian formula for calculating probability includes some
prior probability (or belief), which in light of a new piece of evidence is then
updated into posterior probability (or belief). One necessary assumption of the
Bayesian formula is that we adopt a specific way to calculate probabilities that
depends on the value of another probability. In the clinic, the need for such evalua-
tions is quite common. For instance, we might want to know the probability that a
therapy works well, given the patient’s conditions. This is called ‘conditional prob-
ability’, which intuitively means ‘the probability of an outcome given an interven-
tion’. In probabilistic calculus, however, ‘conditional probability’ has a technical
meaning and is calculated in a specific way. (For more details on the notion of
conditional probability, see Anjum et al. 2018.)
44 E. Rocca

3.3.2 Understanding the Basic Bayesian Formula

Bayesian calculations of probability can be rather complicated, and often they are
made through a computational tool, such as a software. Many of the software avail-
able to the decision makers, not only in medicine and healthcare, but also more
generally in the field of risk assessment, are based on Bayesianism. These software
programs calculate the posterior probability of an outcome, every time new evi-
dence is typed into the software. The disadvantage of making decisions based on
software packages is that the user has to adopt the assumptions of the programmer,
without the possibility of critical consideration. Although the programming of soft-
ware based on Bayesian principles can be complicated, the principle on which the
whole system is based is not difficult to grasp. Let us have a look at it.
The Bayesian formula postulates a way to derive posterior probabilities from the
combination of prior probabilities, new evidence, and the likelihood of the event
that constitutes the new evidence occurring if our prior hypothesis is correct. In its
most basic form, the formula looks like this:
P(Hypothesis│Evidence) = P(Hypothesis) x [P(Evidence│Hypothesis) / P(Evidence)]
First of all, let us explain every term of the formula with an example from
the clinic.
P (Hypothesis) is the prior probability, or the probability of a hypothesis being true
prior to getting to see the new evidence. For instance, P (Hypothesis) could be
the probability of a patient having hypertension. Let us say that the patient is
young and has a healthy lifestyle. The prior probability in this case is low. Note
that the problem of how to assign prior probabilities is an important one, and
Bayesians disagree on the matter. We will come back to this later on.
P (Hypothesis│Evidence) is the posterior probability, or the probability that the
Hypothesis is true given that we get to know the new Evidence. In our example,
this could correspond to the probability that the same patient has hypertension
after she came to consultation complaining about a severe headache
(Evidence = headache).
P (Evidence│Hypothesis) is the likelihood that the new Evidence occurs given that
our Hypothesis is true. In our example, it would be the likelihood that our patient
has a headache given that she has hypertension.
P (Evidence) is the likelihood of the new Evidence happening at all. For instance,
the likelihood of a young healthy person having a severe headache.
Now that we know what the terms mean, let us have a look at what the formula
tells us.
In order to obtain the posterior probability, Bayes is telling us to multiply the
prior probability by the factor [(likelihood of Evidence given Hypothesis)/(likeli-
hood of Evidence at all)]. Why this?
The first observation is that the posterior probability is directly proportional to
the likelihood of evidence happening given that the hypothesis is true. We can
3 Probability for the Clinical Encounter 45

understand this by thinking about our example. The likelihood of a hypertensive

patient having a severe headache is high, therefore the posterior probability (i.e., our
degree of confidence) of the patient having hypertension after knowing that he has
headache, is higher than before knowing it. Let us imagine for a moment that the
patient, instead of complaining about a headache, had complained about lower back
pain. The probability of a hypertensive patient having lower back pain is not par-
ticularly high, therefore the value of posterior probability would not be higher than
the probability prior to knowing that he has back pain.
The second observation is that the posterior probability is inversely proportional
to the probability that the new evidence happens at all. In other words, the lower the
probability of the new evidence, the higher is the updated belief on the hypothesis.
Why? Think again about our example. P (Evidence) corresponds to the probability
that a young healthy patient has severe headaches. This probability is low. Therefore,
if it happens in our patient, it updates consistently the belief that we had in the
hypothesis that he is hypertensive, before knowing the new piece of information.
But let us now imagine that the patient, instead of complaining about a headache,
complains about moderate fatigue. Moderate fatigue is a relatively frequent condi-
tion even in young and healthy people. Therefore, after knowing that the patient is
often tired, our posterior belief in the hypothesis of hypertension is not that much
higher than it was before knowing the new evidence.
We see, then, that the Bayesian formula is intuitive, as long as we bear in mind
that prior and posterior probabilities are not intended as existing entities, but rather
as subjective knowledge, or degrees of belief. Note that, ontologically speaking, it
would not make so much sense to suggest that the probabilities of me having hyper-
tension given that I have a headache somehow depends on the probability of a
generic healthy woman having a headache. (For a dispositionalist discussion of the
Bayesian formula, see Anjum and Mumford 2018, ch. 19 and 21.)
There is, however, something called objective Bayesianism, which might create
some confusion. For our purposes here, it is sufficient to point out that what we said
so far is general enough to apply both to subjective and objective Bayesian infer-
ence. The difference between these two is the strategy one might use to assign prior
probabilities: what is the probability of a young healthy woman having hyperten-
sion, if we just know about her that she is young and otherwise healthy? How should
one assign such probability? Objective Bayesian inference postulates that there
needs to be a rational and agreed way to do this task (e.g. Williamson 2010). For
instance, one could use the incidence of hypertension in the general population of
young and healthy women.

3.3.3 Uncertainty as Lack of Knowledge

One important aspect of interpreting probability as degree of belief is to notice what

it is exactly that generates the uncertainty. Given a certain patient and a certain treat-
ment, why are we uncertain about the outcome? According to this philosophical
46 E. Rocca

understanding of probability, any uncertainty in prediction comes from lack of

knowledge. There are many sources of uncertainty in the clinic. We might lack
information about our patient, her condition or about how the treatment works. We
might base our expectation on clinical studies or lab tests that are flawed. Not least,
we cannot know the complete set of possible outcomes, for instance whether the
treatment might provoke some hitherto unknown side effects in this specific patient.
If all the possible knowledge were available to us, there would be no uncertainty left.
Within the subjective Bayesian notion of probability, uncertainty is treated as an
epistemological matter: a matter of what we can possibly know. In this case, prob-
ability is not understood as an ontological matter. The uncertainty or degree of
belief that we estimate using the subjective Bayesian inference should then not be
understood as something that exists outside of us, in the world. In other terms, given
a certain set of initial conditions (a patient, an illness, a stage of illness, a treatment,
a context of treatment) there would be no inherent uncertainty about the outcome.
The possible outcome is only one: the trouble is that it is impossible to know it for
sure unless we were omniscient beings. This suggests that the credence notion of
probability assumes that causality is a deterministic matter: of all (probability 1) or
nothing (probability 0). Probability itself, then, does not come in degrees.
Probabilistic claims do not, therefore, express something about the causal strength
of an intervention, but about the limits of our knowledge and our confidence in a
particular outcome. We will now look at a third notion of probability that instead
sees probabilities as ontological, dispositional and intrinsic.

3.4 Probabilities as Dispositional and Intrinsic: Propensities

We have seen two possible interpretations of probability: probability as the fre-

quency of outcome in a relevant population, and probability as subjective degree of
belief, or credence. Both these approaches, however, might seem somehow inade-
quate or unsatisfactory for the clinic. Frequentism because it must treat the patient
as a statistical average of their relevant sub-group, and credence because it takes
probabilities to be entirely subjective. Indeed, clinicians are likely to think of the
probability that their patient will recover as ontological: something real, physically
existing in the world, but also to some extent as something that is intrinsic to the
patient. Regardless of whether I have a limited knowledge about a certain condition
and its prognosis, there is an actual, existing probability that the patient will recover.
And this is entirely independent from my own subjective belief. Such physical prob-
ability that the patient will recover is produced by the patient’s own pathophysiolog-
ical and contextual situation and can be called a propensity.
There are many different understandings of propensity in literature. Common to
all these definitions, however, is that propensities refer to the single event. Karl
Popper, one early proponent of the propensity theory of probability, describes pro-
pensities as dispositional properties of singular events (Popper 1959). Propensities,
we might say, are an explanatory understanding of probabilities. The probability of
3 Probability for the Clinical Encounter 47

me falling asleep after an injection of morphine is explained and qualified by the

sedative power of morphine, by my degree of habituation and by other properties of
the whole situation, which in total we can call an overall propensity. A further exam-
ple might help to clarify this idea.
An elderly person affected by influenza, for instance, has a certain probability of
recovery, which is generated by the type of viral infection, the state of the patient’s
immune system, his general health and his context and lifestyle. This set of disposi-
tions of the whole single situation generates a certain propensity of the patient to heal.
Certainly, a clinician might draw insights into this individual case from the previous
experience of similar cases. However, the probability of recovery of this particular
patient is affected only by the physical properties, or dispositions, in place (type of
virus, patient’s immune system, et cetera). Ontologically, this probability is indepen-
dent of the outcomes in other similar cases. Epistemologically, what happens in simi-
lar cases can be an indication for the probability of outcome in the single patient, but
not necessarily. To use a brutal example, if a bus full of patients with a rare condition
crashes on its way to a medical conference, their collective death does not affect the
propensity of the patient who missed the bus to survive the rare condition. On a fre-
quentist account, however, that patient’s probability of survival will have changed with
the bus accident (without it being a good epistemological indicator either, in this case).

Simply put…

The individual propensities of a single patient, treatment or context are given

by its unique combination of dispositions and the dispositions’ degree of ten-
dency toward certain outcomes in that individual case.

3.4.1 Individual Propensities Are Not Always Seen

Through Frequencies

A dispositionalist understanding of causality, as described in Chap. 2, fits best with

a view of probabilities as single propensities. Although propensity interpretations of
probability are less known than frequentism and credence, it has been defended by
philosophers (e.g. Popper 1959, 1990; Mellor 1971; Gillies 2000, 2018) and scien-
tists (e.g. Bohm 1957) since the early 1900s. Propensities seem particularly relevant
in the clinic.
Think about an epileptic child who is about to start a therapy with valproic acid,
a widely used anticonvulsant. What are the probabilities that the patient develops
liver toxicity as an undesired effect of the drug? One possible answer is that the
child will most probably be unhurt, thus with probability close to zero, on the basis
of the outcome for the majority of children. However, this evaluation might be met
as superficial, or unsatisfactory, given that children can be hurt by valproic acid,
sometimes even fatally.
48 E. Rocca

A better clinical approach to the question might be: what are the propensities of
this child to develop liver toxicity from valproic acid? If the child has the particular
physical and contextual onset that makes her sensitive to the drug’s undesired effect,
then the toxic outcome, no matter how rare, will nevertheless be very likely for her.
The frequency of the toxic outcome in other children can in some cases be indica-
tive of the individual propensity to the outcome (for instance, if we consider closely
the properties of the patient in comparison with the properties of the harmed chil-
dren), but is not necessarily so.

3.4.2 Propensities as Qualities

How should propensities be expressed? Can a number between 0 and 1 be estimated

for this purpose, as is generally done in probability theory? Philosophers have dif-
ferent views on this matter, depending on their understanding of propensity. In the
CauseHealth project, however, we favour a singular and qualitative, rather than a
numerical, description of propensities. (For an approach to propensities that is more
compatible with frequentism, see Gillies 2018.)
Propensities, we said, are generated by dispositions. These are intrinsic qualities
of things. But a propensity also depends on the disposition’s magnitude or intensity,
which, although being in some sense quantitative, cannot be directly derived from
statistical frequencies. The presence (or absence) of mutual manifestation partners
for a certain disposition, and the presence (or absence) of possible causal mecha-
nisms which might result in an outcome, affect the propensity of such an outcome
to happen. Evaluating the propensity for an outcome therefore requires describing
and understanding, at least partially, how that certain outcome could or could not
happen. Numbers or scores cannot completely fulfil this purpose, at least not alone,
since what happens statistically at a population level might not reflect what happens
in each individual case.
On average, for instance, a population might seem to have a weak propensity
toward cirrhosis, but this average only represents the sum of all the manifestations
of individual propensities toward cirrhosis. Individual propensities will depend on a
number of dispositions related to age, gender, genetics, lifestyle, diet and medical
history. All of these will be different from one individual to another, so we should
not expect two people to have exactly the same combination of dispositions, or dis-
positions with exactly the same magnitude.

3.4.3 Propensities and Prediction

There is a further important consequence of propensities being generated by dispo-

sitions. We saw in Chap. 2 that dispositions can exist unmanifested. A patient might
carry a certain genetic mutation that disposes toward an allergic reaction from
3 Probability for the Clinical Encounter 49

penicillin, for instance. However, we are likely to remain unaware of such a disposi-
tion until it meets its proper mutual manifestation partner. In other words, it might
be difficult to correctly evaluate the propensity toward this toxic reaction until the
patient uses penicillin. In some cases, we might even get it totally wrong. As a con-
sequence, evaluations of propensity ought to be carried out with some degree of
epistemic humility. That means, there might be dispositions and interactions in this
particular case, which we were not aware of at the moment of evaluation. Any evalu-
ation or prediction must therefore be interpreted with some caution.
Although this attitude is valid for any interpretation of probability, it is especially
important when we think about propensities and dispositions. Accordingly, proba-
bilities as propensities are a matter of qualitative evaluation, theoretical knowledge
and practical expertise, and cannot be generated by an algorithm as a definite num-
ber. Notice that this does not mean that propensities are more fallible than other
ways to calculate probability. Rather, it might just make us more aware of the falli-
bility of prediction.
If we accept the dispositionalist notion of probability, a question remains: how
should clinical inquiry (as well as research) be organised in order to uncover pro-
pensities for the single patient?

3.5 Propensities and the Clinic

A clinician who adopts the propensity approach to probability also adopts a certain
specific approach to clinical inquiry. In this section, we list some of the method-
ological and epistemological implications of the propensity view of probability.
Note that these follow from the particular version of propensities here presented and
dispositionalism presented in Chap. 2, and that other versions of propensity theory
might have other implications.

3.5.1 The Importance of Local Knowledge

The more one knows about the dispositions and interactions in place in the particu-
lar case of interest, the more reliably one can evaluate the propensity toward one
specific outcome in that case. This might sound like nothing particularly new. The
frequentist approach, indeed, also requires us to know as much as possible about the
case of inquiry, so that the most relevant sub-population can be found, and more
reliable statistics performed. So what is particular about the propensity approach?
The difference is in the type of knowledge required. Uncovering propensities
requires knowledge about local processes and interactions, rather than knowledge
of mere values and parameters. Typically, local processes and interactions need to
be observed in their own context and as aspects of a whole, while values and param-
eters can be picked and chosen, and analysed in isolation. Local knowledge of a
50 E. Rocca

patient, ideally, would not be reduced to knowing the value of his biomarkers or
genetic onset, but requires that we have as much knowledge as possible about his
unique context, including history, lifestyle, reactions and interactions.

3.5.2 Person Centered Clinical Analysis

Knowing about the patient’s local context requires, first of all, time. While param-
eters and values can be collected through tests and orthodox clinical enquiry, pro-
cesses and interactions need to be understood through person centered dialogue.
Person centered dialogue is a type of interaction in which the patient is met as a
whole person: her biology, her biography, her history and her narrative are taken as
equally important information for the purpose of the clinical inquiry (see also
Anjum and Rocca, Chap. 4 and Low, Chap. 8, this book).

3.5.3 Focus on Theories of Causal Mechanism

In order to evaluate the propensity of an outcome for a single case, it is necessary to

have an insight into how and why such an outcome might be generated. This requires
a certain degree of general, theoretical knowledge about the process at hand. It is
impossible, for instance, to evaluate the propensity of someone to develop diabetes
without having an idea about the biological mechanisms underlying the onset of the
illness. This requires that the clinician cultivates a high level of theoretical, patho-­
physiological knowledge along with statistical evidence. At the same time, as men-
tioned above, local causal mechanisms are of considerable relevance for the propensity
approach. These include biological symptoms of broad interest that the clinician
might notice in the patient, besides the symptoms of relevance for the targeted exami-
nation. But such local mechanisms also include higher level, socio-­psychological
mechanisms which might influence a patient’s physiological conditions.

3.5.4 Multidisciplinarity and Networking

By adopting the propensity approach to probability, the clinician makes use of a

wide number of scientific and theoretical insights, besides statistical and population
studies. For instance, in order to maximise the propensity for recovery in a depressed
patient, a clinician must be updated about scientific insights on the various causal
mechanisms influencing the onset of depression. But the connection between
research and the clinic is not a one-way street. Since the clinical search for propensi-
ties is focused on local processes and interactions, it potentially becomes a reliable
source of new general scientific hypotheses about the mechanisms of healing and
3 Probability for the Clinical Encounter 51

disease. This is particularly the case with unexpected clinical observations, such as
side effects of drugs. We can illustrate this with an example.
Zolpidem is a hypnotic drug used to treat short-term insomnia. Clinicians
reported a variety of anecdotal undesired and beneficial effects in Zolpidem users:
sleepwalking, sleep-eating and sleep-driving, compulsory behaviours followed by
amnesia, but also speech recovery after stroke, recovery of mobility after brain
injury, and recovery from posttraumatic semi-unconscious state. These insightful
clinical observations resulted in new hypotheses for basic research, for instance
about the mechanism of recovery after brain injury. Notice that these effects are
very rare and sometimes unique, therefore they would not count as particularly rel-
evant evidence for a frequentist.
These considerations highlight that clinicians should ideally work in a multidis-
ciplinary network with researchers, so that information can be easily shared among
diverse experts.

3.5.5 The Potential of Clinical Experience for Advancing

Medical Knowledge

We often think of the perfect medical research and healthcare system as a system
that places patient care as the final aim of a long process. In a way, this is hardly
controversial: patients’ interests must be prioritised over commercial or other eco-
nomic interests, for instance. Research hypotheses, funding, and experimental
designs ought to be developed with a special consideration that they are meant to be
primarily useful for the patient. Important steps are being taken in this direction, and
bioethics has this as a key principle of both healthcare and research.
This conception, however, must be somehow adjusted. There is nothing “final”
about the clinical meeting between practitioner and patient. Quite the contrary: each
of such encounters is potentially the beginning of a new hypothesis, a challenge for
established paradigms, and the springboard for broadening medical knowledge.
This is not difficult to believe if we think about the history of medicine.
Many have already emphasised the value of patient centered medicine and
healthcare for the final purpose of improved clinical decision making, patient care,
and clinical ethics. But few have talked about the fact that a patient centered clinical
approach also has a significant epistemological value: it is the best available oppor-
tunity for advancing causal knowledge in research. Expansion of knowledge does
not happen in a straight line, with the patient at the end of it. It is a continuous circle
of trial and success or failure, where evidence from clinical cases are looping back
to pre-clinical and clinical research. The more attention that is given to the clinical
cases, therefore, the more opportunities we have to improve research (Rocca 2017).
From a practical point of view, what does this entail? First of all, the clinical
interview takes on a crucial role, not only for the patient’s wellbeing, but also for the
whole healthcare community. This important process of gathering clinical evidence
should not be left to individual skills and improvisation (see Hagen, Chap. 10, this
52 E. Rocca

book). Medical schools should teach patient centered models of clinical communi-
cation, and should stress their key value (see Broom, Chap. 14, this book). Second,
clinical evidence should be collected in databases and networked within the broad
medical community (see Copeland, Chap. 6, this book). Third, researchers should
recognise the primary role of patient centered evidence for the corroboration, chal-
lenge, and advance of causal knowledge.

3.5.6 What Does N = 1 Mean, Within

the CauseHealth Project?

We have seen that a propensity approach to probability requires that theoretical

understanding of physiology and of illness is prioritised. Statistical knowledge can
sometimes be a useful tool to gain such knowledge, but it is certainly not the only
type of evidence one needs in order to understand the how and why of medical phe-
nomena. The single patient represents a major part of the causally relevant informa-
tion for understanding the illness and choosing the best treatment. In CauseHealth,
we sometimes summarise this central concept through the slogan “N = 1”, which
has been a source of philosophical debate among healthcare practitioners. We give
a specific meaning to N = 1, which is distinct from the traditional meaning of N = 1
trials in medical research. In the following, physiotherapist Roger Kerry provides a
full explanation of the slogan’s meaning:
“N = 1” is a slogan used to publicise a core purpose of the CauseHealth project. N = 1
refers to a project which is focussed on understanding causally important variables which
may exist at an individual level, but which are not necessarily represented or understood
through scientific inquiry at a population level. There is an assumption that causal variables
are essentially context-sensitive, and as such although population data may by symptomatic
of causal association, they do not constitute causation.

The project seeks to develop existing scientific methods to try and better understand indi-
vidual variations. In this sense, N = 1 has nothing at all to do with acquiescing to “what the
patient wants”, or any other similar fabricated straw-man c­ haracterisations of the notion
which might emerge during discussions about this notion.

In Evidence Based Medicine terms, of course, an N = 1 trial is a randomised controlled trial

involving a single subject with a random allocation of the temporal sequence of interven-
tions. Such a trial has traditionally sat at the very top of evidential hierarchies because it
offers the best scientifically controlled conditions. CauseHealth is sympathetic to such a
methodology, although the clinical notion of N = 1 means much more than just this method.

N = 1 is both an ontological claim, about the causal singularism (this means that causation
is something intrinsic to the person and the situation, and does not have to be repeated in
exactly the same way elsewhere to count as causation) and possibility/plausibility of the
situation that each causal setting is unique.

It is also a methodological claim, arguing against the idea that the individual can best be
captured by searching for the relevant sub-population. Which group should represent Rani?
3 Probability for the Clinical Encounter 53

Women between 40 and 50 years of age? Mixed ethnic background? Norwegians?

Educational status? Etc. Say we find such a group, then why assume that this group is
Rani’s ‘twin population’? There might be all sorts of causally relevant factors that they can-
not represent but that are important in Rani’s individual case. N = 1 is about starting from
the expectation that everyone is different, rather than from the assumption that everyone is
statistically average. This is a fundamentally important scientific shift in how research
should be operationalised and interpreted.

Despite the above, N = 1 thinking is not at all dismissive of population studies, and sees
them as critical tools which are well suited to signalling to where causal activity may well
lie. However, the above limitations of population studies related to individual clinical deci-
sion making are highlighted within the N = 1 notion.

Paradoxically, as we gain more data, experience, and maturity with our population
research programmes, contextual analysis of such data starts to reveal that there is indeed
no “one size fits all” approach to the management of much burdensome disease, for exam-
ple low back pain. Such analyses are exemplars of how N = 1 and population data work
together.

N = 1 is about contextualising the individual human within population data. It moves

beyond a level of thinking which says “here is a patient with low back pain, let me see what
evidence based interventions are available for low back pain”. Rather, it is committed to
understanding the human in front of us and the causally relevant factors which will influ-
ence that person’s return to a desired functional level. Some of those factors will have been
represented in population data, many will not have been.

Roger Kerry, ‘What does CauseHealth mean by N = 1?’, CauseHealth blog ­(https://causeh-
ealthblog.wordpress.com/2017/06/22)

3.6 To Sum Up…

This chapter outlined three different interpretations of the concept of probability and
explained why causal dispositionalism supports an understanding of probability as
propensities, and how this influences clinical decision making and medical investiga-
tions in general. For a final illustration of the difference between the three perspec-
tives presented above, imagine a situation in which we are going to cross a bridge
with a heavy truck, and we want to evaluate the probability that the bridge will endure
the weight of the truck (and consequently the risk of an accident). The frequentist
approach would face this challenge by looking at how often similar bridges collapsed
under the weight of similar trucks. The Bayesian approach would treat the probabil-
ity as a subjective matter that changes depending on the information we have about
the bridge and the truck, and would treat the probability as the value of how certain
we are that an accident will (or will not) happen. The measure of such certainty will
be updated every time we gain a new piece of information. The propensity approach
would describe the probability using the qualities of the bridge, the truck, and the
54 E. Rocca

whole situation, and trying to understand the intrinsic disposition of the bridge to
collapse under a certain weight. Such intrinsicality will be evaluated by investigating
the properties at hand (height, length, solidity, material) and by understanding the
causal and physical processes involved. All these perspectives – frequencies, uncer-
tainty and propensities – offer something that can be useful for expanding our causal
knowledge. The philosophical question is which we take to be basic.

References and Further Readings

Anjum RL, Mumford S (2018) Causation in science and the methods of scientific discovery.
Oxford University Press, Oxford
Anjum RL, Mumford S, Myrstad JA (2018) Conditional probability from an ontological point
of view. In: Anjum RL, Mumford S (eds) What tends to be. The philosophy of dispositional
modality. Routledge, London, pp 101–114
Bohm D (1957) Causality and chance in modern physics. Routledge, London
Cartwright N, Hardie J (2012) Evidence-based policy. A guide to do it better. Oxford University
Press, Oxford
Clarke B, Gillies D, Illari P, Russo F, Williamson J (2013) The evidence that evidence-based medi-
cine omits. Prev Med 57:745–747
Clarke B, Gillies D, Illari P, Russo F, Williamson J (2014) Mechanisms and the evidence hierarchy.
Topoi 33:339–360
Gillies D (2000) Varieties of propensity. Br J Philos Sci 51:807–835
Gillies D (2018) Causation, probability, and medicine. Oxford University Press, Oxford
Mellor DH (1971) The matter of chance. Cambridge University Press, London
Popper K (1959) The propensity interpretation of probability. Br J Philos Sci 10:25–42
Popper K (1990) A world of propensities. Thoemmes, Bristol
Rocca E (2017) Bridging the boundaries between scientists and clinicians. Mechanistic hypotheses
and patient stories in risk assessment of drugs. J Eval Clin Pract 23:114–120
Rothwell PM (2005) External validity of randomised controlled trials: “to whom do the results of
this trial apply?”. Lancet 365:82–93
Rothwell PM (2006) Factors that can affect the external validity of randomised controlled trials.
PLoS Clin Trials. https://doi.org/10.1371/journal.pctr.0010009
Wallmann C, Williamson J (2017) Four approaches to the reference class problem. In: Hofer-­
Szabó G, Wroński L (eds) Making it formally explicit, European studies in philosophy of sci-
ence, vol 6. Springer, Dordrecht
Williamson J (2010) In defence of objective Bayesianism. Oxford University Press, Oxford

Open Access This chapter is licensed under the terms of the Creative Commons Attribution 4.0
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adaptation, distribution and reproduction in any medium or format, as long as you give appropriate
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the copyright holder.
Chapter 4
When a Cause Cannot Be Found

Rani Lill Anjum and Elena Rocca

In Western countries, most persons asking their regular general practitioner for help and
advice share certain common characteristics: they show up repeatedly and over time,
although at varying intervals and for a variety of reasons; they present complex health prob-
lems which may involve acute maladies but often include chronic, somatic and/or psychiat-
ric distress; at the same time, they may seek advice for medically unexplained or undefined
malfunctions, which may be equally if not more problematic and incapacitating than the
supposedly well-defined diseases or disorders…

Experienced GPs are aware of patterns of sickness, both within groups of patients and in
individuals, that seem to point to sources of bad health beyond the medically defined hori-
zon of causality. These patterns are complex and transgress such medical dichotomies as
“somatic” and “mental”. They are specific in the sense that they represent clusters of dis-
eases or malfunctions, which apparently have such common “causes” as inflammation,
infection or invasion (in the sense of tumour growth). This, however, leads to the next level
of relevant questions, those regarding the “cause” or “causes” of a dangerously compro-
mised immune system manifesting in systemic inflammations, repeated infections or mul-
tiple invasive processes. Here, a rapidly growing documentation highlights the medical
significance of context, offering ways of understanding the detrimental impact of lifetime
adversity on health.

Anna Luise Kirkengen, ‘Map versus terrain?’, CauseHealth blog (https://causehealthblog.

wordpress.com/2017/04/18)

4.1 The Clinical Challenge of Medically Unexplained

Symptoms (MUS)

Healthcare professionals are regularly faced with patients who suffer from multiple
conditions at the same time. How exactly these conditions relate is not a straightfor-
ward question and, in some cases, the causes themselves remain a mystery. Patients
who experience what are commonly referred to as medically unexplained

R. L. Anjum (*) · E. Rocca

NMBU Centre for Applied Philosophy of Science, Norwegian University of Life Sciences,
Ås, Norway
e-mail: rani.anjum@nmbu.no; elena.rocca@nmbu.no

© The Author(s) 2020 55

R. L. Anjum et al. (eds.), Rethinking Causality, Complexity and Evidence for the
Unique Patient, https://doi.org/10.1007/978-3-030-41239-5_4
56 R. L. Anjum and E. Rocca

symptoms, or MUS, exhibit a number of symptoms that appear together but do not
seem to have a single, common biomedical cause.
The increase in medically unexplained symptoms represents an emerging prob-
lem in European and other industrialised countries. ‘Medically unexplained’ refers
to the lack of explanatory pathology. Researchers have not been able to find a com-
mon set of causes, a definite psyche-soma division, or even clear-cut classifications
for these symptoms. The problem with these conditions not being explained gener-
ally means that the biological causes of the symptoms are unknown. Some of the
causal factors involved might be known, but the underlying mechanisms are not
understood. In general, no adequate psychological or organic pathology can be
found, and medical examination is unsuccessful in giving a diagnosis to the symp-
toms (Eriksen et al. 2013a). Each patient seems to have a unique combination of
symptoms and a unique expression of the condition, and medical uniqueness appears
to be the rule rather than the exception. A problem with this is that evidence from
population studies are of limited use for these patients.
That no causal explanation is found for a condition is not a rare or unfamiliar
phenomenon. MUS have been estimated to account for up to 45% of all general
practice consultations, and a study from secondary care suggests that after 3 months,
half of the patients received no clear diagnosis (Chew-Graham et al. 2017). It is dif-
ficult to give a precise number, however, since there is no general agreement over
what counts as a MUS. Some examples are chronic fatigue syndrome, irritable
bowel syndrome, low back pain, multiple chemical sensitivity, general anxiety dis-
order, tension-type headache, post-traumatic stress disorder and fibromyalgia. Some
other conditions lack a commonly accepted diagnosis, or even a clear definition, yet
they seem to be increasingly common, in some cases almost mass phenomena.
Another example of a medically unexplained condition is burnout, which indicates
a pathological condition somehow connected with severe stress and work overload.
Psychotherapist Karin Mohn Engebretsen has dedicated her doctoral research to the
analysis of burnout as a challenge for the current scientific paradigm. She writes:
As a Gestalt psychotherapist, I have seen an increasing number of individuals over the last
fifteen years that experience themselves as burned out. This fact has triggered my interest
to explore the phenomenon further. Burnout is a medically unexplained syndrome (MUS).
As with other MUS, there is a tendency to assume a narrow perspective to focus on prob-
lems related to psyche or soma as pathologies located exclusively within the patient.
Research has mainly looked for clear-cut one-to-one relations between cause and effect.
These relationships are however difficult to find in complex syndromes.

Burnout might instead be seen as a reaction to complex causes and a broad contextual setup,
but unfortunately, such point of view has only been marginal. Consequently, medical pro-
fessionals are faced with comprehensive challenges due to factors such as lack of a causal
explanation, lack of diagnostic descriptions and lack of a treatment or medical
interventions.

Karin Mohn Engebretsen, ‘Are we satisfied with treating the mere symptoms of medically
unexplained syndromes?’, CauseHealth blog (https://causehealthblog.wordpress.
com/2017/03/27/are-we-satisfied-with-treating-the-mere-symptoms-of-medically-
unexplained-syndromes/)
4 When a Cause Cannot Be Found 57

As pointed out by Engebretsen, healthcare professionals who deal with a person

experiencing burnout will face some deep theoretical and methodological issues
(Engebretsen 2018; Engebretsen and Bjorbækmo 2019). For instance, is a response
to stress overload to be considered a medical condition? Should it be seen as one of
the symptoms, or one of the causes? How to distinguish burnout from other well-­
defined pathologies with similar symptoms, such as depression? And, even more
problematically: how to act when no clear-cut causality can be found, given that
curing a disease means to counteract its causes?
The problem of understanding MUS could be interpreted as an empirical matter,
to be solved by doing more of the same. On this view, more observation data, RCTs,
symptom measurements and classification could ultimately lead to a clearer under-
standing of these conditions. Given the dispositionalist framework of CauseHealth,
however, we see MUS as a symptom of some deeper problems in current medical
thinking (Eriksen et al. 2013b). Specifically, the problem of MUS seems to point to
a philosophical challenge, namely: how to understand causality in cases of com-
plexity, individual variation and uniqueness.
The challenge of dealing with MUS, even conceptually, played a central role in
the CauseHealth project. We started from the idea that the problem of MUS is a
practical challenge for medicine, but one that has a philosophical source. MUS are
troubling and chronic conditions that are often depicted as outliers: atypical ill-
nesses where standard causal explanation fails. From the dispositionalist perspec-
tive, however, every patient is to be considered, in one way or another, an outlier.
Recall that dispositionalism is a singularist theory of causality (see Anjum, Chap. 2,
this book). Since causality happens in the single case, we need to be armed with
strategies to look for it in the single patient, while at the same time making use of
general medical and other theoretical knowledge. The problem of dealing with
MUS, then, is rooted in a deep conceptual challenge of the current paradigm.
Finding a way to deal with these conditions epistemologically was therefore seen as
the key to getting a better grasp of medicine as a whole. If we understand the prob-
lem of MUS, we thought, we will better understand the problem of investigating
causes of health and illness generally.
In this chapter, we take a closer look at the challenge that causal uniqueness
represents, not only for the healthcare professional having to deal with MUS and
other complex conditions, but also for the whole medical paradigm. We make a
‘philosophical diagnosis’ of the problems of dealing with causal uniqueness in the
clinical encounter: they come from a positivist, or Humean, understanding of cau-
sality. We then explain how an ontological turn toward a dispositionalist starting
point should help us deal better with the challenging features of MUS: causal com-
plexity, heterogeneity and medical uniqueness. From a dispositionalist perspective,
we will argue, these features should not be seen as problems for causality, but
instead as typical for it, and therefore as opportunities to understand causality better.
58 R. L. Anjum and E. Rocca

4.2 The Problem of Uniqueness

While in medicine and healthcare the default assumption is that all patients are dif-
ferent, causation itself is sought as something that is robust throughout different
contexts. This leaves us, in effect, to search for same cause and same effect:
–– Same symptoms, same diagnosis (diagnostics)
–– Same diagnosis, same intervention (standardised treatment)
–– Same intervention, same effect (tested though RCTs)
Although individual variations are acknowledged, they are nevertheless not the
focus when trying to establish causality. Instead, variations can be used to form
more fine-grained classifications or sub-groups, where one again looks at what is
the same. In other words, uniqueness is considered an obstacle when one tries to
establish causality scientifically.
This contrasts with the dispositionalist framework. No two individuals will have
exactly the same combination of causal dispositions or propensities. Even if there
are some dispositions that we share, such as gender, age or medical condition, so
many other dispositions will be different from one individual to another. Grouping
patients into more relevant sub-groups will plausibly tend to give a more appropri-
ate average than broader and unspecific sub-groups. We know, however, that not all
pregnant women in their thirties or all men over 60 with hypertension are identical
in all their dispositions – or even sufficiently identical. Which of these dispositions
are taking part in the single causal process that we are investigating? This is a ques-
tion that cannot plausibly be answered with certainty. We will therefore never be
sure of whether or how precisely a sub-population represents the dispositions in
place in the individual process. A frequentist approach, we have said, will either
have to overlook this knowledge gap or try to further specify the relevant sub-group
(see Rocca, Chap. 3, this book). Eventually, however, one might end up with a sub-­
group with only one member: the N = 1 group consisting of the single patient. Still,
the problem remains how to establish, predict and explain causality for a patient for
whom no suitable, or suitable enough, sub-population can be found.
This is one reason why MUS represent a methodological challenge for medicine
and healthcare. In the current paradigm, the best way to establish causality is by
showing that the same cause makes a difference toward the same effect in suffi-
ciently similar contexts. To make this clear, think back to the principle of ran-
domised controlled studies (RCTs), as explained above in Sect. 3.2. We saw here
that RCTs are considered to be the best way to establish causality within the current
paradigm of evidence based medicine and practice, and they are designed to test for
a type of homogeneity: common causes and common effects. This means that even
though there is plenty of individual variation within the clinical study, these varia-
tions are not what the RCT is designed to study or establish. On the contrary, such
individual variations are supposed to be shielded off through randomisation, so that
4 When a Cause Cannot Be Found 59

test group and control group are overall very similar. With RCTs, we look for the
overall effect of an intervention in the test group, compared with the overall effect
in the control group. The intervention is then the same, and the effect tested is
the same.
RCTs thus target same cause (intervention), same effect (outcome). This is com-
pletely in line with Hume’s regularity theory of causality (Hume 1739), but it
doesn’t acknowledge the dispositionalist perspective that causes as dispositions are
intrinsic properties: they tend to manifest, but not always. They tend to make a sta-
tistical difference, but not always. They tend to produce one effect, but not always
the same (Anjum and Mumford 2018, see also Anjum, Chap. 2, this book). RCTs
are great tools to detect manifestations that make a difference at population level,
but they are not useful for studying dispositions that remain mostly unmanifested,
and which tend to manifest themselves in single and causally unique cases. We see,
then, that the problem of MUS is not an isolated one, but one that has its roots in the
Humean influence on medical thinking about causality that can be summarised in
the following three points:
1. A and B are observed repeatedly (empiricist criterion: causality must be detected
empirically)
2. Whenever A, B, under some normal or ideal conditions (regularity criterion:
same cause, same effect)
3. B happens because of A (monocausality criterion: one cause, one effect)
4. If not B, then not A (falsification criterion: a difference in effect must mean that
there is a difference in the cause).
For A to be the cause of B, these conditions must be met, according to the
Humean notion of causality. Medically unexplained symptoms, however, typically
fail to meet one or several of these criteria, which is why we cannot say that a medi-
cal cause has been found.
Let us show this by considering the case of unspecific lower back pain. Qualitative
studies show that in the clinical dialogue, patients usually associate this condition
with an episode such as bending or lifting. Patients mention that they felt sudden
pain during a certain activity, and that they have been in pain ever since (Jeffrey and
Foster 2012). There is, in the clinical encounter, a deep intuition of a causal link
between a certain accident, or event, and the condition. However, this cannot be
epidemiologically confirmed. There is much literature on unspecific lower back
pain, but no systematic association has been shown with mechanical factors (lifting,
standing, walking, postures, bending, twisting, carrying, and manual handling) nor
with activity levels, obesity, smoking, mood, or genetic factors (see Eriksen et al.
2013b for a review of the epidemiological evidence). None of these causal factors
seem to fulfil the Humean criteria of regularity, repeatability and falsification.
Epidemiologically, and according to Humean criteria, therefore, there is no clear
cause of unspecific lower back pain, despite decades of research. And yet, single
60 R. L. Anjum and E. Rocca

patients tend to be able to indicate a cause, at least as they experience it. This and
similar cases of medically unexplained conditions represent a challenge for any
attempt at standardisation or universal approach to cure and healthcare.

4.2.1 The Patient Context: What Was There Before

From a healthcare perspective, one does not expect that the same cause will give the
same effect in different individuals. Individual responses depend on what else was
there already, as part of the patient’s own context. A person who is at a vulnerable
stage in life might be more disposed to an infection than a person who is at a more
robust stage, for instance. This is, one can say, elementary clinical knowledge. Still,
this real-life complexity becomes a problem for causal understanding when we try
to analyse it using the Humean criteria. Dispositionalism instead acknowledges
complexity and context-sensitivity as basic features of causality.
We can represent the different impact of one causal disposition in different
patients with the vector model of causality (Mumford and Anjum 2011), where each
vector represents one causal disposition in place, and the line T represents the
threshold for the manifestation of an effect, as explained in Chap. 2. In the vulner-
able patient (Fig. 4.1), the situation is much closer to the threshold of illness than in
the robust case (Fig. 4.2). This means that even a minor burden on health can have
a major impact, because it pushes the situation over a threshold. This is a well-­
known phenomenon. We often speak of the straw that broke the camel’s back, which
was simply the final straw adding to the already heavy burden. A cause might then
be simply what tips the situation over the threshold, which seems far too insignifi-
cant if we ignore what was already there before it.
Let us say that the two patients get affected by influenza, and after that only one
of them develops a chronic burnout syndrome, while the other recovers normally.

Fig. 4.1 A vulnerable T

situation, where R is close
to the threshold for illness

F G

R
4 When a Cause Cannot Be Found 61

Fig. 4.2 A robust T

situation, where R is far
from the threshold
for illness

F G

From a Humean point of view, this does not tell us much about the causal role of the
influenza for the onset of burnout. Instead, we would need to check whether there
are other patients as similar as possible to the patient who develops burnout symp-
toms after getting influenza (same cause – same effect, all else being equal).
From a dispositionalist perspective, however, looking further into cases of indi-
vidual variation and context-sensitivity represents a chance for understanding
something about the underlying causal story. When the same cause gives different
effects in two different contexts, we might learn something new. Clearly, to do that,
it does not help to focus on the single cause or the single effect. Instead, one should
try to understand what was already there in the two different contexts, disposing
toward or away from health and illness. This type of reasoning needs to be qualita-
tive and explanatory, in order to be fruitful. By trying to understand all the causal
dispositions in place, and the way they interact with each other, we build a causal
explanation – a hypothesis – for how and why things went the way they did.
Note that the causal explanation, or causal mechanism, although being based on
empirical evidence, is not itself something we can observe directly. This is why
Hume’s empiricist approach does not include causal theories or explanations but
sticks to what can be observed and counted. On the contrary, the search for evidence
of a plausible causal explanation (which dispositions are present, how they interact
and manifest) is at the core of the dispositional approach. It is also crucial for any
scientific theory, including in medicine and healthcare.
Humean and empiricist influence have been strong, not only in research, but also
in the clinic. There tends to be the expectation, at least in the implementation of some
health policy and clinical guidelines, that patients with the same diagnosis should
respond similarly to the same treatment. Personalised medicine and system medicine
have been rising trends and can be seen as attempts toward a more dispositionalist
approach: aiming to fit the treatment to the patient’s own dispositions. However,
these approaches are mainly focussed on genetic or molecular dispositions and have
less focus on psycho-social or ecological complexity (Vogt et al. 2014). This will be
discussed in Chap. 5 when we look at the biomedical model of medicine.
62 R. L. Anjum and E. Rocca

Allowing the features of uniqueness and complexity to guide the clinical encoun-
ter, we should focus less on what is the same and more on what is different and
unique for this particular patient, also for causal matters.

Simply put…

Humeanism refers to David Hume’s regularity theory of causality, which

emphasises features such as empiricism, observable features (data), mono-­
causality, repetition and same cause – same effect. Probabilities are under-
stood as generated statistically (frequentism).

4.2.2 Qualitative and Quantitative Approaches

to Causal Inquiry

What exactly do we mean by a qualitative analysis? And how should such analysis
help us look for causal explanations? How does this approach contrast with quanti-
tative analysis and the search for same cause – same effect? In our philosophical
framework, we have a particular take on what should count as qualitative and quan-
titative approaches to causal inquiry. Qualitative approaches will be concerned with
the investigation of many types of information in few tokens, and with how these
relate, and under which conditions. In contrast, quantitative methods will look for
few types of information that are in common for many tokens (see also Anjum and
Mumford 2018: 106). Notice that from the dispositionalist perspective, qualitative
research can advance causal understanding and theory, and is not limited to the
purposes of meaning and lived experience (see Sect. 4.4). Qualitative research, in
our definition, encompasses scientific enquiry of a phenomenon, as long as such
enquiry aims to understand a causal process, while quantitative research aims to
identify the numerical relationship between variables. A qualitative approach, in our
understanding, might involve numerical values, but is always process-oriented,
aims to generate theoretical understanding, it is adapted to the most relevant context
of application of the research, and it happens in-situ, often in a participatory way.
An example might help illustrate this distinction.
For example, a recent large study compared the whole-genome sequences of participants
with food allergy to peanuts, egg or milk with non-allergic participants (in total almost
3.000 individuals were included)[…] The results showed statistically significant DNA
modifications in specific loci of the genome, indicating that these loci are probably part of
the genetic component of the food allergy. Other information about the participants were
age, sex, ancestry (European or non-European), results of food allergy tests, and presence
of other allergy-related disease. While such a horizontal analysis has big statistical power,
it relies on the preliminary selection of a limited amount of variables to compare. The selec-
tion is informed by existing knowledge and working hypothesis (in the case of this study,
that allergies have a genetic component). Additionally, it is dictated by practical consider-
ations since these studies include a large amount of participants. While results are statisti-
4 When a Cause Cannot Be Found 63

cally robust, their contribution is limited to a small part of the picture. In fact, genetic
predisposition is only one of many actors for the onset of a condition.

Let us imagine using a larger filter to evaluate which contextual variables to include in the
analysis. We might then consider a complete range of clinical factors, blood levels, present
and former state of health, dietary habits, lifestyle, polypharmacy, psychological health,
addictions, traumas, including as much information as possible about the unique context
that was exposed to the allergen. This would necessarily restrict the comparison to a limited
number n of patients […].

The experiment would then be a qualitative, rather than quantitative, analysis. It would have
a different aim: the aim of identifying not a single element that is frequently involved, but
enough elements to suggest a pattern, or offer an explanation that is valid in this specific
instance. Such explanation might fall outside the boundaries of existing knowledge and
suggest an advance in the overall understanding of causal mechanisms. Finding out whether
these hypotheses are generalizable and to which extent, belongs to a subsequent stage of
research. (Rocca 2017: 117)

Simply put…

In our framework we propose that qualitative approaches to causal inquiry

collect many types of information in few tokens and look for a theoretical
understanding of how these relate causally in a particular context. Quantitative
approaches, instead, look for few types of information in many tokens, and
aim to identify numerical correlations among them.

4.2.3 Dispositional Take On Perfect Regularity: Is It Causality

or Something Else Entirely?

A dispositionalist denies that causality is something that produces perfect regularity

between cause and effect. Instead, causality is understood as tendencies, where the
cause A only tends or disposes toward the effect B. So even if A is present, B can
still be counteracted by adding an interferer I (Mumford and Anjum 2011). All of
medicine is premised on this idea. Even if one has not yet been able to find a treat-
ment, the expectation is still that if one can understand the causal mechanisms of the
disease, it should be possible to counteract or interfere with the causal process in
one way or another.
This has a surprising consequence. If there were to be a perfect correlation of A
and B, where no changes in context could influence the situation in any way, a dis-
positionalist should become suspicious. Is this a case of causality after all? Or could
it be a case of classification or identity? For instance, all humans are mortal. And
although scientists are still working on ways to counteract and delay death, one
could still argue that any immortal being could not be human. So even if there were
64 R. L. Anjum and E. Rocca

a human-like immortal species in the future, we might say it’s not the same as
a human.
Now take a medical case. It is said that Down syndrome is a genetic disorder
caused by the presence of all or part of a third copy of chromosome 21. But is this
the right way to phrase it? As long as a person has the extra chromosome, they will
be diagnosed with Down syndrome. If Down syndrome is then defined as the condi-
tion of having the third copy of chromosome 21, then, of course, there will be a
perfect regularity between A and B. But the reason why we have the situation that
whenever A then B, is that A is defined as B. In that case, A = B. This does not mean
that there is no causality going on here. The causal relationship would then be
between the extra chromosome and the expression of the condition, which vary in
degree from individual to individual. The symptoms of Down syndrome are then
caused by the extra chromosome, and will be manifested in different ways in differ-
ent individuals. Whether someone has the syndrome will correlate perfectly with
whether they have the extra chromosome, without any individual variations. This
suggests that it is an identity relation, not a causal one.
Perfect regularities, on the dispositionalist perspective, could be produced by
other types of truths than causal ones, such as classification (all humans are mam-
mals), stipulation (all electrons are negatively charged), identity (bachelors are
unmarried men) or essence (humans are mortal). In contrast to these types of claims
that have the categorical form ‘All As are Bs’, causal claims are about what happens
under certain conditions. A causal claim is therefore a hypothetical or conditional
matter: ‘If we do x to y, would z follow?’. To say that ‘All As are Bs’ is to make a
statement about how to categorise A and B with respect to one another. In contrast,
when we ask whether A is a cause of B, we want to know whether and to what
degree A is able to bring about B or at least contribute to the production of B.
Note, however, that if A is indeed a cause of B, a dispositionalist should not
expect that all instances of A will actually and successfully produce B. Causes, as
dispositions, are irreducibly tendential. There is never more than a tendency of A to
produce B. As discussed in Chap. 2, a dispositional tendency can be stronger or
weaker. Someone can be more or less vulnerable, more or less violent and more or
less allergic to peanuts, for instance. We also saw that dispositional tendencies give
rise to individual propensities, rather than statistical frequencies (see Rocca, Chap.
3, this book). The degree of tendency does not determine how often a disposition
will manifest, but only how strong the intrinsic disposition is in this individual situ-
ation. For instance, if we want to know how fertile someone is, one should do a
sperm count rather than counting the number of offspring. The higher the sperm
count, the stronger the disposition of fertility. It does not follow from the strong
fertility that one will eventually have a lot of children. It also does not mean that
other people with the same sperm count will have many children.
We see, then, that a dispositionalist should not expect perfect regularity of cause
and effect. Instead, a dispositionalist should be sceptical if there is a perfect correla-
tion that is insensitive to contextual change. Could it be a case of identity, classifica-
tion or essence instead? Or have we already stipulated some ideal conditions or
idealised model under which the cause would always produce the effect? Either
4 When a Cause Cannot Be Found 65

way, we cannot expect that causality will manifest itself in perfect correlation in a
real-life situation such as what we encounter in the clinic. The only way we can
expect that the same cause will always produce the same effect, is by stipulating
some average, normal or ideal patient with average, normal or ideal responses. In
the clinic, however, such encounters are rare.

4.3 An Important Lesson from Medically Unexplained

Symptoms (MUS)

We saw that medically unexplained symptoms remain a challenge for the healthcare
profession because of some problematic features: causal complexity, heterogeneity
and medical uniqueness. If this is a problem for establishing causality, then we got
a much bigger problem than MUS. In most health conditions, there is at least some
complexity of causes, some individual variation and some unique factors. This is the
case for cancer, heart disease, obesity, Alzheimer’s, hypertension, diabetes, stress-­
related symptoms and many other conditions. Although these conditions are not
medically unexplained, because there is some common pathology, they are still
complex disorders with multiple causes.
All conditions that are caused by a combination of genetic, environmental and
lifestyle factors, will have many unknown causes and many causes that are unique
to that patient (Craig et al. 2008). And since each patient has a unique combination
of biological, social and psychological factors, complex diseases are very likely to
be heterogeneous (Hellhammer & Hellhammer 2008). From the dispositionalist
perspective, therefore, there is a lot more in common between medically unex-
plained and medically explained conditions than what is normally assumed. What
can we learn from this?
First of all, this means that our understanding of illness cannot rely solely on
single or few physical, or biomedical, homogeneous causes. When a common phys-
ical cause of illness is found, such as the bacterium helicobacter pylori (HP) for
peptic ulcer, it can quickly become the main focus of medical attention while other
causes gain the status of ‘background conditions’. This is the case with lifestyle fac-
tors such as stress and diet, for instance, which were thought to cause ulcer before
the discovery of HP, and have been since decades at the periphery of the therapeutic
focus (de Boer and Tytgat 2000). Looking at this case in more detail, however, it has
been estimated that at least half the world’s population is infected by the HP bacte-
rium, but most of those infected never develop an ulcer (Go 2002). We see then that
although one causal factor might be the necessary condition for the development of
a pathology, whether such pathology is triggered, how it is expressed, when, and to
what degree, will be influenced by a plethora of other causal factors. When disposi-
tionalism emphasises causal complexity, it means that a mono-causal focus on a
common physical cause will necessarily mean that we miss out on some of the
causal story, if not most of it (Copeland 2017). This is why CauseHealth proposes
66 R. L. Anjum and E. Rocca

that the challenging features of MUS should be treated as the norm, rather than be
dismissed as marginal and atypical. All illness is complex, and many of the causal
factors will be unique to the individual case.
This has a practical consequence, not only for research, but also for the clinical
encounter. It means that by understanding the complexity and uniqueness of the
patient’s situation, one will find a number of factors that might be influencing their
condition positively or negatively. And although the known biomedical factor (such
as the HP bacterium) leaves little wiggle-room other than the standard medical
interventions, many of those other influences (lifestyle, diet, stress) are usually
important to target too, and might be even easier to counteract. Being aware of these
other dispositions that are causally relevant for the health condition, and under-
standing how exactly they influence the experience of health and illness, can then
empower both patient and clinician. The patient might get a better understanding of
what caused their condition, but that is not all. The patient might also be able to
influence and work with some of these dispositions, thus getting a better sense of
control and agency with respect to their own health (see Price, Chap. 7, this book).

4.3.1 We Need Many Methods to Establish Causality

Searching for and establishing causes in the dispositionalist framework is not some-
thing that can be done using only one single method, such as RCTs (Rocca and
Anjum 2020a). In CauseHealth, we have argued that causal enquiry requires a plu-
rality of methods, each of which picks out one or more symptoms of causality (for
details, see Anjum and Mumford 2018). In an open letter to BMJ Evidence Based
Medicine, co-signed by 42 clinicians and philosophers from international and inter-
disciplinary research networks working specifically on causality in medicine, we
urged that EBM approaches widen their notion of causal evidence:
The rapid dominance of evidence based medicine has sparked a philosophical debate con-
cerning the concept of evidence. We urge that evidence based medicine, if it is to be prac-
tised in accordance with its own mandate, should also acknowledge the importance of
understanding causal mechanisms… Our research has developed out of a conviction that
philosophical analysis ought to have a direct impact on the practice of medicine. In particu-
lar, if we are to understand what is meant by ‘evidence’, what is the ‘best available evi-
dence’ and how to apply it in the context of medicine, we need to tackle the problem of
causality head on… In practice, this means understanding the context in which evidence is
obtained, as well as how the evidence might be interpreted and applied when making practi-
cal clinical decisions… It also means being explicit about what kind of causal knowledge
can be gained through various research methods. The possibility that mechanistic and other
types of evidence can be used to add value or initiate a causal claim should not be ignored.
(Anjum et al. 2018: 6)

How exactly would this work if we assume a dispositionalist understanding of

causality?
In dispositionalist terms, if we want to establish a causal link between A and B,
this corresponds to establishing whether A has intrinsic dispositions that, in
4 When a Cause Cannot Be Found 67

combination with other dispositions, can eventually produce B. Different methods

will have some strengths and some limitations for the purpose of finding such intrin-
sic dispositions. For instance, RCTs are good for picking out which factors make a
difference, or raise the probability of an effect, on population level. But positive
results from RCTs do not guarantee that this difference-making or probability-rais-
ing happened because of some intrinsic disposition in the test group, since that would
require a further theoretical explanation. RCTs are also less suitable for testing the
contextual complexity of mutual manifestation partners, since the focus is on one or
few particular interventions (for which there can be a control or comparison) and one
or few outcomes. Other methods could be more suitable than RCTs when we are
searching for dispositions or manifestations that are too rare to show up in statistical
approaches. In this case, retrospective case-control studies allow us to study outlier
cases or very rare conditions. However, since these studies are designed to find com-
mon dispositions for the same outcome across different contexts, any non-­common
dispositions contributing to the outcome in the individual cases will not be targeted.
These are just two examples, but all scientific methods will similarly be designed
to test some specific symptoms of causality, while other symptoms will fall outside
the scope of the test. The problem is if we think that one method should be a perfect
test for picking out causality. Such a perfect test might require that we operation-
alise causality. This means that we simply identify the phenomenon of causality
with the method we use to test it. Examples of operationalization can be to identify
temperature with the measure shown on the thermometer, depression with a series
of specific behaviours, or cancer with a positive screening. In the case of causality,
operationalisation might correspond to saying that causality is nothing more than
the statistical difference of effect between experimental group and control group, as
detected for instance by a positive RCT.
Operationalisation of causality would be a perfectly acceptable strategy for a
strict empiricist, since they would reject any ontological reality that cannot be
observed. Indeed, Hume already stated which observable features would be neces-
sary and sufficient for calling something causality: constant conjunction, temporal
priority and contingency. From a dispositionalist perspective, however, there would
be no one perfect test of causality that could empirically pick out all its features. A
cause will tend to make a difference, but there is no perfect overlap between
difference-­making and causality. A cause will also tend to produce some regularity,
but again there is no perfect overlap (Anjum and Mumford 2018).
Embracing the idea of methodological pluralism – that we need more than one
method to establish causality – we will now look at another method for obtaining
more qualitatively rich causal information, namely patient narratives. We make a
case for the epistemological importance of obtaining detailed information from the
patient herself when searching for causal explanations of illness. As a methodology,
rich patient information allows the detection of relevant dispositions that are
uniquely combined in this individual patient (biomedical, biographical, lifestyle,
and life situation), and that could be relevant for their condition or the treatment.
This type of knowledge should therefore not be ignored if we understand causality
in a dispositionalist sense.
68 R. L. Anjum and E. Rocca

4.4 Patient Narratives as a Way Forward

We have said that the clinical encounter can contribute to improving the causal
understanding of health and illness, in the dispositionalist sense. We saw that, in
order to evaluate individual propensities, one needs to learn as much as possible
about the dispositions and interactions in place in the particular case of interest (see
Rocca, Chap. 3, this book). In the case of healthcare, this means learning more
about the patient and their context. From the dispositionalist perspective, therefore,
the clinical encounter has a pivotal role to play for advancing our understanding of
the causal story behind illness and suffering. Notice that we do not talk only about
the clinical examination, which is just a part of the encounter. In the examination,
the clinician collects biological and medical information, while in the encounter she
meets the patient as a person with a unique biography, context and story. Osteopath
Stephen Tyreman argues that a whole person centred approach is crucial for under-
standing illness and symptoms.
What do symptoms tell us about the person rather than their disease? Symptoms are key
elements in a person’s narrative about illness in general and their illness in particular. We
want to know what symptoms mean, what they tell us (in a narrative sense) about what has
happened and what the future will be like. As much as indicating a particular biological
problem, symptoms reflect how we live—the smoker’s cough, the athlete’s muscle ache, the
workaholic’s tiredness, the sedentary person’s breathlessness, and so on. Are these indica-
tors of actual or potential disease or is disease a possible emergent outcome of such behav-
iour? Many symptoms we accept as normal and healthy—the discomfort of pregnancy and
childbirth or the stiffness after a day’s physical activity, for example. In other words, do
symptoms tell us more about a person’s living before they tell us about disease?

Stephen Tyreman, ‘More on symptoms’, CauseHealth blog https://causehealthblog.word-

press.com/2017/04/03/more-on-symptoms/

How exactly can the clinical encounter contribute to improving causal knowledge of
the dispositions in place? The way modern medicine is generally practiced does not
seem to leave much space for understanding the full complexity of the causal situa-
tion of patients. In the last century, for instance, the objectivity of doctors’ reports
was emphasised. Physicians have to ‘translate’ patient reports and accounts of their
condition into a standard medical language. This is not in itself a limitation. The
problem is when such standard medical language is seen as the only information of
significance, while the information that is excluded, about the patient’s version and
interpretation of their condition, is considered irrelevant for the purpose of diagno-
sis and treatment (for an example of this, see Kirkengen, Chap. 15, this book).
There is an alternative to this orthodox practice that is more in line with the dis-
positionalist framework. This is to use patient narratives as an essential part of the
evidence available (Greenhalgh and Hurwitz 1998). We see this in a recent develop-
ment in medical humanities, called narrative medicine, although it would not gener-
ally be considered as causal evidence. Instead, patient narratives are often dismissed
as causally irrelevant because of their anecdotal nature, a story from a single unique
4 When a Cause Cannot Be Found 69

patient. In CauseHealth we have promoted the importance of qualitatively rich

information about the dispositions provided by the local context (the patient), based
on causal singularism (medical uniqueness), context-sensitivity (heterogeneity) and
genuine causal complexity (holism and emergence) (Rocca and Anjum 2020b). The
main idea that we here want to emphasise is that the subjective and embodied expe-
rience as told by the patient, traditionally seen as a possible obstacle to the objective
medical diagnosis, is in fact a powerful tool for exactly that purpose. Patients, in
their narrations, choose to include some information and to omit some other. A nar-
ration also gives meaning to the medical events, and such meanings will most prob-
ably vary depending on the narrator. Crucially, there is a reason for such
interpretations and this reason is not possible to capture in the standard medi-
cal story.
We can illustrate this point with an example from the treatment of morbid obesity.
Guidelines recommendations for this condition are based on knowledge about the
biological mechanisms underlying normal and irregular food intake and appetite.
Recommended treatments consist in lifestyle modification programs, pharmacother-
apy and bariatric surgery. Depending on the single patient and her standard medical
story, physicians can choose the treatment that is thought to be best suited for the
patient. Although all these interventions could result in some modest to good improve-
ment, there is a systemic tendency toward re-gain of weight in the vast majority of the
patients, provoking frustration in both clinicians and patients (Karmali et al. 2013).
What might happen if the standard medical story is accompanied by a thorough
analysis of patient narratives? One answer comes from general practitioner Kai
Brynjar Hagen. He has been working for many years as a senior consultant at a
Norwegian regional centre for morbid obesity. His job is to assess the patients
before bariatric surgery, which is the last step in the therapy of obesity. The assess-
ment included interview sessions with patients. During these sessions, Hagen col-
lected the stories of their embodied, lived illness experience. He came to the
hypothesis that what practitioners treat at the moment (energy homeostasis imbal-
ance, food intake, lifestyle) are in the majority of cases only the symptoms or the
condition, and not what he understands as the real or core cause of obesity. By tak-
ing the time to listen to his patients, asking them about their childhood, whether
they enjoyed school, how their family life is and how they feel about their life in
general, he observed that many of his patients had experienced some sort of emo-
tional traumas that affected, triggered or worsened their eating disorder. His worry
is that if these biographical aspects are ignored and obesity is treated as a purely
biomedical condition, to be solved by eating less, one will fail to target the true
cause of the problem (see Hagen, Chap. 10, this book). This could also explain why
the current treatments for obesity in many cases fail and why there is a tendency
toward suicide among patients who have undergone bariatric surgery (Lagerros
et al. 2017; Neovius et al. 2018; Castaneda et al. 2019).
When overlooking important causes of obesity, such as the dispositions of trauma
that manifest themselves in an eating disorder, one fails to target the source of the
problem or even the core cause. If a person is obese but used to be anorexic or
bulimic, then the solution to overeating is not to go on a diet. That might trigger a
70 R. L. Anjum and E. Rocca

relapse into the other extreme, of undereating. This shows the importance of under-
standing the whole causal story of complex conditions, of which obesity is just one
example. But these causes cannot be identified without taking the narrative of each
single patient as an essential part of the available causal evidence.

4.5 Using Patient Narratives

Patient narratives can be different things and we will here mention three examples.
They are all from the clinical encounter but represent slightly different approaches
(see also Solomon 2015).

4.5.1 Narrative as a Tool for Causality Assessment

When a new drug is introduced on the market, it must be monitored for risk and
safety purposes. In this process, patient narratives about possible side effects of
medications are collected systematically and used as the basis for causality assess-
ment and hypothesis generation. Some of these narratives come from the patients
directly and into global databases such as VigiBase. Other narratives come from
clinicians or from pharmacists, but in those cases, the narrative is interpreted and
reported by someone other than the patient. Behind every case report, there is a
patient narrative that is typically richer in detail and more personal than what is
reported. If one is interested in causal complexity, individual variation and medical
uniqueness, the patient narrative should be a better source of information than the
case report, if the narrative contains more biographical, personal and contextual
information. Rebecca Chandler, medical doctor at the Uppsala Monitoring
Centre, writes:
Professionals working in drug safety also need patient stories. At its very essence, an indi-
vidual case safety report is a patient story of an adverse experience after using a medicine.
Often in pharmacovigilance we focus on numbers and statistics. We discuss Information
Component values, proportional reporting ratios, completeness and VigiRank scores.
Signal detection using spontaneously reported adverse event data is a hypothesis-­generating
exercise, a clinical science which is based upon individual reports of suspicions of causality
between a medicinal product and an adverse event.

It is logical therefore that clinical stories contained in adverse event reports, complete with
details and context, are integral to the development of hypotheses of drug safety concerns.
Certain details within the patient story are integral to the building of hypotheses of causal-
ity, such as past medical history, concomitant medications, time to onset of symptoms.
Other details, if provided, allow us to understand the impact of the event upon the patient’s
life, their ability – or inability – to manage the adverse event, and even how the patient was
treated within the healthcare system.
4 When a Cause Cannot Be Found 71

Pharmacovigilance is more than the identification of causal associations between drugs and
new adverse events. It is about creating a culture of awareness of drug safety, and using
patient stories to contribute to an evidence base that can be used by physicians and patients
to make wise therapeutic decisions. (Chandler 2017: 23)

4.5.2 Narrative as a Tool for Understanding the Causal Story

Many clinicians who are interested in patient narratives are motivated by a philo-
sophical commitment to phenomenology. Ontologically, phenomenology is a ver-
sion of holism or wholism, and there are a number of overlapping ideas with
dispositionalism. Phenomenology has been emphasised and practiced as a method-
ology by many of the CauseHealth clinicians, including Stephen Tyreman, Anna
Luise Kirkengen (Chap. 15, this book), Brian Broom (Chap. 14, this book) and
Karin Mohn Engebretsen (Chap. 11, this book). Depending on the version of phe-
nomenology, the narrative should come solely or primarily from the patient, and it
should remain as uninterpreted as possible by the clinician. As a clinical methodol-
ogy, phenomenology emphasises the subjective experiences of health and illness,
and also meaning, interpretation, values, existential questions and embodiment. In
the case of chronic medically unexplained conditions, phenomenological approaches
will have a broader focus suited for uncovering complexity and uniqueness. One
example is presented by general practitioner Anna Luise Kirkengen:
For many years, Katherine Kaplan had been in specialist care due to a long sequence of
diseases deemed as separate, different in origin and, consequently, requesting different
types of approach. She had been frequently hospitalised with a variety of serious health
problems since her late teens. She had encountered physicians in many medical specialties
due to what was diagnosed as different diseases in various organ systems. She had been
delayed in her studies due to these frequent periods of sickness and was, when finally reach-
ing her graduation, completely incapacitated by chronic states of bad health which could
not be responded to with specific treatments any more. Years of medical investment on
specialist level were terminated with a referral to a General Practitioner.

In order to understand this disabling process, an analysis of the prevailing concepts of the
human body, of diseases, and of medical causality needs to be performed.

When contrasting the “case” depicted above with a biographical account grounded in the
“story”, a different picture emerges. Katherine Kaplan, the third child of a highly educated
and resourceful couple, had been maltreated by both her parents but mostly by her elder
brother from early childhood through adolescence and while she was a student of medicine
at a Norwegian university. Her parents, defining their abusive acts as deserved punishment,
had never realised that their daughter suffered grave and frequent maltreatment by the
hands of their son. The on-going threat, embodied as toxic stress in Katherine, increasingly
compromised her health preserving systems to the point of breakdown by the time of her
graduation.

Anna Luise Kirkengen, ‘What if…’, CauseHealth blog ­(https://causehealthblog.wordpress.

com/2017/10/17)
72 R. L. Anjum and E. Rocca

4.5.3 Narrative as a Collaborative Tool in Healthcare

A third type of narrative is the collaborative or co-written story, developed in the

dialogue between the patient and the clinician. Here the clinician takes a more active
role in bringing out, analysing and emphasising different parts of the patient’s nar-
rative. In this process, the narrative might change from the individual perspectives
of the patient and of the clinician toward a commonly constructed narrative (Low
2017, see also Low, Chap. 8 and Price, Chap. 7, this book). For example, a patient
might not think much of how an experience affected their condition, while the clini-
cian might think it is highly relevant. The opposite might also happen. The clinician
might not initially understand why the patient mentions something that seems tan-
gential to the medical issue, but then discover from the conversation that this was
crucial. In this case, the patient’s own narrative becomes re-written as a result of the
clinical interaction. This can be an important therapeutic tool, but it is also a tool for
uncovering the causal complexity of how the person became ill and what affects the
condition in positive and negative ways. The physician then offers the patient some
tools to analyse her own subjective experience.
So why is the notion of story in medicine so foreign to clinicians? Typically we (the clini-
cians) want the medical truth rather than the human truth (we need both). Medical truth is
largely about science, measurement, labelling (diagnosis), and standard ways of treating.
These perspectives give us enormous benefits. But in our narrow desire to essentialise,
master, know medically, deploy, and instrumentalise, we frequently fail to get close to the
patient’s unique and individual story, and thus we lose a crucial dimension of the person
that may be helping make them sick and keep them sick. If we make it safe for patients to
tell their stories, many will do so. We need both the medical perspectives and the stories.

Brian Broom, from the mindbody website: https://wholeperson.healthcare

4.6 To Sum Up…

This chapter offered a philosophical diagnosis of the challenges that medicine is

facing, regarding medically unexplained symptoms and complex illnesses. We pro-
posed that a crucial problem comes from applying a Humean regularity theory of
causality, in which a cause is understood as something that always provokes the
same effect under ideal conditions, to the clinical reality, where no ideal condition,
or average patient, can ever be found. A dispositionalist understanding of causality
proposes instead to start from the particular and unique situation of the single case
in order to understand causality. The medical evidence, including causally relevant
evidence, must then be generated from the single patient. This includes not only the
patient’s medical data, but also the patient’s condition, narrative and perspective.
This is fundamental in order to generate causal hypotheses about the complex situ-
ation and all the dispositions that influence the medical condition. Ultimately, evi-
dence from the clinical encounter could assist the design of experiments both in the
4 When a Cause Cannot Be Found 73

lab and in the clinics. When possible, one should also use insights from statistical
population studies to make decisions about single patients. The best approach to
causality, we argue, is to use a plurality of methodologies. We have also explained
how, when starting from a dispositional theory of causality, heterogeneity, unex-
pected results and outlier cases actually represent an epistemological advantage,
instead of an obstacle, for the causal enquiry.

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Chapter 5
Complexity, Reductionism
and the Biomedical Model

Elena Rocca and Rani Lill Anjum

5.1 The Biomedical Model of Illness

Up until the nineteenth century, illness, health and recovery were mysterious mat-
ters. Infections, cancer and disease in general were understood as some sort of
invading curses, leaving little space for rational treatment. It was only with advances
in biological knowledge, such as the development of cell theory, the germ theory of
disease and bacteriology, that definite explanations of illness, suffering and death
could be formulated. The work of influential scientists and physicians, such as
Rudolf Virchow, who is sometimes considered the father of modern pathophysiol-
ogy, had a revolutionary impact on medical thinking. Virchow introduced the idea
that every pathology arises from a damaged cell, which paved the way for the work
of Robert Koch and Louis Pasteur, as well as for the development of the first theo-
ries of the onset of cancer from a malfunction of host cells. By identifying the origin
of disease with a malfunction at the simplest structural and functional level of
organisms, the cell, this new paradigm allowed us to conceive of new ways to target
the causes of disease, for instance by pharmaceutical interventions.
There is little doubt that the discovery of antibiotics and other drugs changed the
course of human history. The consequences of these revolutionary developments,
however, go beyond the practical outcomes. There was also a deep change at the
cultural and conceptual levels, namely in the way illness and health were under-
stood. The biomedical model of illness became the dominant paradigm until the end
of the twentieth century.

E. Rocca (*) · R. L. Anjum

NMBU Centre for Applied Philosophy of Science, Norwegian University of Life Sciences,
Ås, Norway
e-mail: elena.rocca@nmbu.no; rani.anjum@nmbu.no

© The Author(s) 2020 75

R. L. Anjum et al. (eds.), Rethinking Causality, Complexity and Evidence for the
Unique Patient, https://doi.org/10.1007/978-3-030-41239-5_5
76 E. Rocca and R. L. Anjum

5.1.1 Reductionism in Medicine and Science

Within the biomedical model, an illness is always explained with one or more physi-
cal malfunctions at a lower level of organisation. For instance, an infection is
explained with the invasion of parasites, a metabolic disorder with a genetic muta-
tion, a psychiatric disorder with an imbalance of neurotransmitters, a speech impair-
ment or a physical disability with neuronal damage and so on. In philosophy, the
idea that a complex phenomenon is best understood by analysing its physical parts
in isolation, is called reductionism or even physicalism.
There are many versions of reductionism (for an overview, see Dupré 1993, part
II). The version that we are concerned with here is ontological reductionism.
According to this view, the world is thought to only have one causally potent level,
namely the physical one. Any non-physical phenomenon would then be nothing but
the effect of lower-level causes. This idea of reductionism can be seen in the standard
hierarchy of the sciences, where physics is the fundament. Above physics is chemis-
try, then bio-chemistry, biology, psychology and finally on top, social sciences.
Typical for this hierarchy is that for each higher level, more complexity is intro-
duced. Societies consist of people with individual minds and brains, consisting of
cells and tissues, which consist of genes, which again consist of molecules and
atoms. Ontological reductionism is thus depicting the different levels of existence in
a part-whole relationship, where all higher-level phenomena are composed of the
levels below (Figs. 5.1 and 5.2).
Medicine might then be placed between biology and psychology, where the com-
plexity of the human mind is treated separately from the body. This distinction is
manifested in the way healthcare services are divided into treatment of the psyche
(psychotherapy) and treatment of the soma (medicine). A dualist would say that
psyche and soma are separate, but equally real, while a reductionist would try to
explain psyche as a result of somatic causal processes, such as biochemical

Social
sciences

Psychology

Biology

Bio-chemistry

Chemistry

Physics

Fig. 5.1 The hierarchy of science

5 Complexity, Reductionism and the Biomedical Model 77

Fig. 5.2 A Venn diagram

illustrating a reductionist Atoms,
ontology of wholes electrons
and parts
Molecules

Cells, tissues,
organs

Minds,
cognitions

Social
relations

interactions. Psychopharmaceuticals, for instance, target psychiatric phenomena as

biochemical processes gone wrong. But this is only one way in which reductionism
is manifested in the field of medicine.
Another case of reductionism is medicalisation, which is the tendency to treat
existential issues and life events as medical ones, and then exclusively as biomedical
problems. Instead of feeling shy, one might have social anxiety, for instance, and
instead of grieving the loss of a family member, one might be depressed. In some
extreme cases, healthy human responses to inhumane life conditions, such as severe
childhood trauma or sexual abuse, are defined as psychiatric disorders and
approached primarily from a biological perspective (Kirkengen and Thornquist
2013). Once a problem is characterised as a biomedical problem, one will naturally
start to search for a biomedical solution to it. As we shall see, this is one of the rea-
sons why the biomedical model has been criticised for being reductionist, and for
ignoring important aspects of what it is to be a healthy human being (Getz et al. 2011).

Simply put…

Reductionism is the philosophical idea that all higher-level (e.g. social, men-
tal or medical) phenomena and processes can in principle be explained at a
lower level (e.g. biology, chemistry, physics). Ontological reductionism states
that all processes and events must ultimately be the result of physical causes.

The biomedical model brings about some specific ways to understand health,
illness and disease. First, illness is always reducible to a physical, biological dis-
ease. It concerns purely the physical body, which is seen as analysable into separate
78 E. Rocca and R. L. Anjum

parts. This is a mechanistic view of biology, in which parts are not changed by the
context, and therefore can be studied in isolation, as one would do with a car engine,
for instance. The mechanistic view, together with the dualism that separates body
from mind, are deeply set in the Western culture, mostly because of the influential
work of René Descartes (1641).
Another idea introduced with the biomedical model is a specific understanding
of ‘health’, which is seen merely as the absence of physical signs of disease. As a
result, curing a disease is exclusively a task for medical professionals and medical
technology, while the patient is only a receiver of such cures. The biomedical model
has an intuitive appeal for many types of conditions, such as bacterial infections.
But for a long time this view was taken as generally valid for medical science. Also,
the biomedical approach acquired a normative connotation. This means that the
orthodox medical thinking has been to consider the most ‘scientific’ medical inter-
vention to be the one based on the biomedical model. This frame of mind, as we will
see, has been widely criticised in the last few decades. Nevertheless, the biomedical
model is so influential and deep-seated that it has survived and is still the prevailing
view in medicine.
For example, although Attention Deficit Hyperactivity Disorder (ADHD) is
diagnosed in children as an alteration of their behaviour, mainstream medicine
explains the condition as a neurobiological disorder (cf. DeVreese et al. 2010). As a
consequence, the main therapy for ADHD is pharmacological psycho-stimulation,
although the precise biological mechanism of such intervention is at the moment
unclear. A public health study revealed that children born late in the year were more
likely to receive an ADHD diagnosis than those born earlier in the year (Karlstad
et al. 2017), suggesting that lack of school maturity in the younger children might
be an important causal factor. If so, the symptoms interpreted as an intrinsic neuro-
biological disorder, ADHD, might actually be the effect of social and contextual
factors.

5.1.2 Critical Reflections Concerning the Biomedical Model

The limitation of the biomedical model has been highlighted by many, already since
the 1950s. The main criticism is that illness is a condition of the whole person, and
treating the patient’s bodily parts in separation might alleviate some symptoms
without solving the source of the problem. This became increasingly evident with
the epidemics of chronic illnesses and metabolic disorders due to an unhealthy life-
style in Western society, such as diabetes, obesity and cardiovascular disease.
Medicalisation without a thorough intervention at the social and psychological level
has not been successful in solving these conditions (see for instance Hagen,
Chap. 10, this book).
Another criticism of the biomedical model is that it objectifies the patient and
reduces them to a passive target of therapy, rather than seen as an active (and the
most crucial) actor in healing. As Stephen Tyreman noted, ‘patient’ is the opposite
5 Complexity, Reductionism and the Biomedical Model 79

of ‘agent’, and a loss of agency is experienced as illness (Tyreman 2017: 277). This
suggestion of a lack of agency is why many person centred practitioners insist on
avoiding the term ‘patient’ and prefer ‘person’ instead. This also signals a holist
view where the person is a subject and not primarily seen as an object of illness (the
damaged knee, the hurting back, the malignant tumour), as they are within a reduc-
tionist view. Finally, the biomedical model fails to account for all the conditions
under which a patient is in fact ill, but without presenting any physical or biological
sign of dysfunction. Such is the case for the medically unexplained symptoms or
syndromes that we discussed in Chap. 4. These are also referred to as medically
unexplained physical symptoms (MUPS).
Modern medicine, therefore, is faced with a contradiction by which scientific
advances and medical technology offer the best opportunities ever, but at the same
time an increasing number of patients are over-medicalised, over-diagnosed,
become chronically ill, do not find a place in the health system, or feel that they are
not met as whole persons in the healthcare system. The biomedical model seems to
have played a central role in this development.
In the CauseHealth project (described in Chap. 1), we have seen that people who
experience medically unexplained symptoms often become victims of the biomedi-
cal model. Since burnout was not generally accepted as a medical diagnosis until the
WHO declared it a diagnosis in 2019, individuals with burnout face the societal
stigma of being thought of as not ‘really ill, but just lazy’ (Engebretsen and
Bjorbækmo 2019). However, the lack of a biomedical cause also results in a finan-
cial burden for patients without a diagnosis, since one might then not qualify for
economic compensation in case of long-term sick-leave (Engebretsen 2018). One
obvious solution for helping this patient group is to find a symptom or diagnosis that
is already recognised by the healthcare system. While this might solve some prob-
lems, it might also create some new ones. Psychotherapist and researcher on burn-
out, Karin Mohn Engebretsen, has seen how the biomedical model motivates the
choice of treatment of people suffering from burnout.
A matter of debate is whether burnout should be considered a distinct medical diagnosis or
a form of depression. Recent research has suggested that public health policies should focus
on and medically treat one of the core symptoms, which is asserted to be depression. The
preferred medication is selective serotonin reuptake inhibitors (SSRI). A problem, however,
is that these patients, referred to me by their general practitioners, often complain about
worsened symptoms that might be a side effect of the medication they are on.

Although burnout and depression have similar symptoms, my experience is that there may
be substantial differences on the underlying psychological process. I experience the patients
grieving a loss quite differently from patients being ill due to an overwhelming life situa-
tion. Treating the symptom without any idea of the underlying process in this case might
provoke serious trouble. For instance, as some research pointed out, SSRI can lower corti-
sol levels and therefore worsen the symptoms in stress-induced conditions, possibly through
interfering with hypothalamic-pituitary-adrenal axis functioning. Therefore if burnout, as
we can reasonably suppose, is a stress-induced syndrome, SSRI can hurt much more than
they can help.
80 E. Rocca and R. L. Anjum

To increase the knowledge of burnout as a phenomenon, complementary research methods

are required. Person centred healthcare and the Biomedical Model represent two central
methodological perspectives that constitute the main camps in contemporary medical and
social science. They depict two extremely different ways of studying social phenomena and
as such, they may complement each other. Instead of limiting the medical model to specific
biological factors, I argue that it is necessary to include the entire human being within a
contextual setting to be able to understand the underlying mechanisms. So to improve the
healthcare system related to medically unexplained symptoms it is due time to open up for
a philosophical reflection on what research questions we need to answer and choose the
methodology that will provide these answers.

Karin Mohn Engebretsen, ‘Are we satisfied with treating the mere symptoms of medically
unexplained syndromes?’, CauseHealth blog (https://causehealthblog.wordpress.
com/2017/03/27/are-we-satisfied-with-treating-the-mere-symptoms-of-medically-
unexplained-syndromes/)

By translating burnout into depression (seen as a biochemical imbalance in the

brain), one effectively reduces a complex psychosocial phenomenon to one of its
medically accepted symptoms. The serious problem arises when burnout is then
treated medically, as if it was actually caused by depression.

5.2 The Bio-psychosocial Model of Illness

In the second half of last century, George Engel (1977) proposed a new model to
understand health and illness: the bio-psychosocial model. Engel thought that a
whole new way of thinking about human conditions was needed. In particular, he
found it necessary to acknowledge that not all illnesses are detectable by biological
measurements. The bio-psychosocial model embraces all the scientific advances
underlying modern medicine, while also highlighting that many conditions cannot
be explained by detecting changes at the cellular or molecular level.
For instance, infants who do not receive care and attention from adults might not
develop correctly, although all the other physical needs are met. Similarly, patterns
of recovery after heart surgery in children are dependent on relationship and com-
munication with family, and even vary depending on whether or not patients have
animal companions (Ellis 2012). In these cases, although there are changes at the
cellular and molecular level, such changes do not provide a causal explanation for
the developmental disruption. Instead, the changes at the lower level of biological
organisation are caused by higher level phenomena: in these cases, by social inter-
action. It is by intervening at this higher level that one can really influence the
course of development and recovery.
The bio-psychosocial model aims to introduce to medical and healthcare practice
the concept of downward causality, or top-down causality. This is the concept by
which causality travels from the higher to the lower level of organisation. In other
words, the whole can sometimes cause a change in its parts. Consequently, it is not
possible to understand the causal story by analysing the parts in isolation.
5 Complexity, Reductionism and the Biomedical Model 81

Simply put…

Bottom up causality means that the direction of causality goes from causes at
a lower level or organisation to effects at a relatively higher level of organisa-
tion, while top down causality goes from causes at a higher level of organisa-
tion to effects at a lower level of organisation.

Example: a headache can be caused by hormonal fluctuations (bottom up) or

by financial worries in times of economic recession (top down).

There are frequent examples of this in medicine: cases in which the social and
psychological well-being of the patient influence her physical state are well known
to every clinician. Resilience and motivation of the patient, for instance, are often
seen as important ingredients for a medical intervention to yield the desired result.
This is why, according to Engel and many others in the last decades, a biomedical
model, based on the exclusive treatment of physical constituent parts, cannot pro-
vide the correct concept of human suffering and healing, and consequently cannot
guarantee effective healthcare. Rather, medicine needs to be informed by a more
complete understanding of health and illness, which better depicts the reality of
human conditions (Loughlin et al. 2018).
Since its original formulation, the bio-psychosocial model had a considerable
influence in medical practice, research and education (Farre and Rapley 2017).
However, it has also been the object of controversies and criticism. One problem
with this model is that it is vague in the formulation of a method for collecting the
relevant biopsychosocial information (ibid.). As an amendment to this, some schol-
ars proposed the phenomenological model, the necessity of understanding the
patient and the use of narratives as a clinical tool (Greenhalgh and Hurwitz 1998).
We already discussed the value of these tools for the causal enquiry in Chap. 4.
Another criticism is that the bio-psychosocial model is very difficult to put into
practice in the current medical community. In the context of today’s extremely spe-
cialised medical education, which practitioner is trained to catch all three levels in
depth? The most realistic picture is the one in which different professionals care
about different levels: the physician about the biological, the psychologist about the
psychological, and the social caretaker about the social. We see, then, that rather
than achieving a truly integrated analysis like the one originally proposed by Engel,
the whole person is again separated into different levels of complexity, and such
levels are likely to be analysed and treated in isolation from each other
(Kirkengen 2018).
82 E. Rocca and R. L. Anjum

5.2.1 Bottom Up and Top Down Causality in Medical

Research: Two Views on Cancer Aetiology

We already mentioned how there can be top down or bottom up explanations of

causality. The choice of direction will necessarily affect how we think of causality
in medicine. Bottom-up explanations typically look for medical causes at the physi-
cal level, while top-down explanations will emphasise higher level causes of illness,
which might include contextual, psychosocial or ecological dispositions.
Let us look at a concrete example of these competing views from the field of
cancer research. There are two competing theories about the onset of cancer. The
first, the somatic mutation theory (SMT), is based on bottom up causality, in so far
as it identifies molecular entities as the initiating causes of cancer. An early version
of this theory was first stated in Weineberg’s 1998 book One Renegade Cell, where
the author proposes that cancer is originated by a single genetically mutated cell.
This extreme form of genetic reductionism was reformulated when knowledge
about the complexity of cancer was still developing. Today, the SMT theory postu-
lates that there are several types of mutations that can result in cancer, and such
mutations are always altering the communication between one cell and its environ-
ment. For instance, a carcinogenic cell loses the ability to react to anti-growth sig-
nals from the environment. Still, this view is based on bottom up causality, because
it identifies some causes at molecular level which modify higher organisation levels,
such as the tissue.
A competing view is the tissue organisation field theory (TOFT), formulated in
1999 by Sonnenschein and Soto in the book Society of Cells. Causality here works
in a top down process: from the tissue to the cell. According to the theory, it is the
disrupted tissue that provokes a change of environment and consequently a change
in the cell phenotype, from regular to carcinogenic. Cancer, then, would be a devel-
opmental illness, because it would derive from a failure in tissue development. Cells
would change their phenotype because of a change in their environment (the tissue),
and not primarily because of a change in their components (genes, for instance).
Lately, scientific insights on the epigenetic regulation of the cell phenotype are
used to understand cancer. For instance, the relapse after cancer pharmacological
therapy is not necessarily due to the presence of a randomly mutated cell since
before the therapy. This very Darwinian interpretation, where the mutated cell is
passively selected, has been questioned (Pisco and Huan 2015). Instead, cancer
cells might change their phenotype independently from a genetic mutation, and as
epigenetic adaptation to the environment. If this theory is correct, it would highlight
that carcinogenic cells adapt actively to changes in the environment.
These different views have profound consequences for the way cancer is under-
stood, but also for how it should be treated. A bottom up view of causality is thus
one of the ontological assumptions that tacitly influence medicine both theoretically
and practically.
5 Complexity, Reductionism and the Biomedical Model 83

5.3 The CauseHealth Approach: Change Must Start

from Ontology

Although the bio-psychosocial model is a step in the right direction, we said, health-
care needs to move beyond it. The model starts with the quest for a more holistic
view of health and illness that does not reduce human conditions to merely the sum
of their constituent parts. Still it ends up with the fragmentation of the biological,
psychological and social dimensions. Is it possible to reach a genuine integration
among these three dimensions of humanity, and if so, how?
In the philosophical framework so far presented (see Chaps. 1, 2, 3, and 4), we
promote a view by which any genuine change in the practice and the norms of sci-
ence must start from the revision of the underlying concepts motivating such prac-
tice and norms. The way we think about complexity, causality and probability, for
instance, is going to affect what we consider to be the best method to study them.
Scientists and practitioners often lament the shortcomings of a certain methodology
and try to improve it. However, if this improvement does not start from an update of
the most fundamental basic assumptions about the reality to be investigated, the
methodological improvements will not be very radical.
In other words, a genuine change in scientific and clinical approaches must start
from the most fundamental level to the practical one (Fig. 5.3).
Norms of science are here understood as the norms for the ‘correct, systematic
acquisition of empirical knowledge’ (Anjum and Mumford 2018). Note that the
norms we refer to in this context are restricted to epistemology: norms about how
researchers and practitioners should best collect and process empirical knowledge.
These norms differ from the ethical norms, such as for instance autonomy, justice
and equality. The reason why we highlight the relevance of epistemological norms
of science in this context, is that any practice that falls outside of an established
norm of science is likely to be considered unscientific and met with scepticism. We
see then that, in order to change practice, one must first make a more radical change

PRACTICE

METHODS

NORMS OF SCIENCE

ONTOLOGY

Fig. 5.3 A change in methods and practice must start from a change in ontology
84 E. Rocca and R. L. Anjum

in the norms of science that motivates this practice. Norms of science, in turn,
depend on basic ontological assumptions about concepts such as causality, com-
plexity and probability.
Ontology concerns basic implicit assumptions and such assumptions are always
present in any type of science, including in medical practice. In the paper
‘Philosophical bias is the one bias that science cannot avoid’ (Andersen et al. 2019),
we argue that such basic implicit assumptions are a necessary prerequisite for any
practice informed by science, and for science itself. However, in times of what
Thomas Kuhn (1962) calls ‘normal science’, there is little talk about such assump-
tions, which remain tacitly and commonly accepted. It is only in times of paradig-
matic changes that scientists and practitioners start to talk about ontological basic
assumptions and critically discuss them.
One example of such discussion at the ontological level is the criticism of the
reductionist and dualistic view of human biology, and the call for a renewal in which
human conditions are conceptualised as complex and emergent phenomena. But
even if such critical discussion has been ongoing for many decades, we think that
there is still conceptual and fundamental work to do to inform a genuine change in
clinical practice. A foundational change in ontology ought to lead to a change in
norms and practices, and it should also challenge the way medicine and healthcare
is organised, managed and financed. If no such change is seen, it might be because
our concepts only sound new, but their meaning is defined within the old ontology.
For instance, there is general agreement about the complexity and multi-causality of
pathogenesis of most illnesses, but there is no general agreement about what it
means to say that causality is ‘complex’. We will now show how a discussion of this
concept can be useful for healthcare and for the clinical encounter.

5.4 What Is Causal Complexity and How Should It

Be Investigated?

We have already discussed causal complexity (see Anjum, Chap. 2 and Anjum and
Rocca, Chap. 4, this book). But we have not said much about what we mean by such
complexity. Does it simply mean that there are multiple causes? This seems to be
what the term ‘multifactorial’ indicates. We will now present two philosophical
views on complexity. Depending on which of these views one assumes, different
norms, methods and practices will follow.
A common way to think about a complex whole is to see it as the sum of many
parts, connected by intertwined causal interactions. For instance, the human genome
can be seen as a complex whole in the sense that it is constituted by a large number of
functional units, the genes, which are linked by an intricate net of causal interactions.
One gene can cause or prevent the expression of many other genes, and can in turn be
regulated by a number of different others. In order to understand the causal role of
single genes within the genome, scientists then isolate the gene from the genome one
5 Complexity, Reductionism and the Biomedical Model 85

by one and study their sequence and their function in different contexts. This practice
of isolating one causal factor from its normal complexity is a dominant epistemologi-
cal norm in science when studying causality. What does this tell us? First of all, it tells
us something about how we think of causality, as something that is best established by
looking at the behaviour of a single factor in isolation from contextual interferences.
Secondly, it reveals something about how we understand complexity.

5.4.1 Mereological Composition

We can illustrate this first view of a ‘complex whole’ with a simple example.
Imagine a construction made with Lego bricks. Depending on the shape of the
brick, each brick can bind to one or more of the other bricks. Together the bricks can
combine to form different wholes, such as a castle or a ship. But crucially the indi-
vidual bricks do no change from taking place in the different constructions. The
bricks maintain their original properties throughout. We will call this view of com-
plexity, in which a whole does not induce a change in its parts, mereological
composition.
Mereological composition is an ontological thesis about how parts relate to
wholes and to the other parts within that whole. Crucially, the parts are thought to
maintain their properties and identity when combined with other parts to form the
whole. Mereological composition might also entail the view that wholes can be
decomposed into their parts. This is for instance how a car works. One can put the
parts together to make the car and then one can take it apart. The parts of the car will
be the same before the composition and after the decomposition. How does this
relate to healthcare and the clinical encounter?

Simply put…

Mereological composition here means that the whole is the sum of its parts
and that, throughout the process of composition and decomposition, the parts
remain unchanged within the whole.

Example: a car engine is produced by the mereological composition of

its parts.

A criticism of the biomedical model has been that it sees a person in the same
way – as a whole that is best understood by studying and treating its individual parts
in separation: the liver, the heart, the lungs, and so on. The bio-psychosocial model
might end up with a similar assumption if we have to study the biological, psycho-
logical and social causes separately and then add up the results. This is not primarily
86 E. Rocca and R. L. Anjum

a shortcoming of the bio-psychosocial model, but of the scientific methodology of

isolating and separating each causal factor and studying them independently of their
natural context. This scientific approach comes from the ontological assumption of
mereological composition.
A genuine whole-ist should not accept a compositional view of complexity, even
if the complexity consists in biological, psychological and social parts. What does
this mean for the clinical encounter? Is the orthodox scientific approach, based on a
mereological idea of complexity, the only feasible option? What is the role of bio-
medical knowledge in the wholistic clinical encounter? Immunologist and psycho-
therapist Brian Broom has explored this question in depth during his career. He writes:
So, does this mean that the whole person-oriented biomedical clinician should, in addition
to the normative clinical requirements of his discipline, somehow become a skilled psycho-
therapist, psychologist, social worker, spiritual advisor or whatever, and be required to per-
form elaborate, expert, systematised assessments normative within each of those disciplines?
This is nonsensical and impossible. Nobody can attend to all of this.

The usual solution is of course the multidisciplinary team. But many of these are pass-the-­
parcel scenarios where each discipline functions narrowly according to the pattern ordained
by the modern biomedical model as expressed in each individual discipline. In sum it usu-
ally manifests as an additive framework of highly expert clinicians, patients seen from
multiple narrow perspectives, a dualistic concept of disease, and a lack of attention to the
highly nuanced individual personal life experiences and subjectivity factors or stories that
contribute to the development and perpetuation of disease.

Apart from that critique, I actually value multidisciplinary teams, but believe that each of
the practitioners in the team need to be functioning in a whole person way. This is possible
whatever one’s discipline. By adopting a whole person approach each clinician can do a
great deal to enhance healing without feeling overwhelmed.

Brian Broom, ‘Imagination and its Companions’, CauseHealth blog (https://causehealth-

blog.wordpress.com/2017/07/03)

According to Broom, multi-disciplinary teams of clinicians, where each clinician

adopts a ‘whole person approach’, is the way forward to enhance healing. The ques-
tion then becomes: how should clinicians successfully and genuinely embrace the
whole person approach? This cannot be done without revising perhaps the most
foundational premise of medical research and practice: the way we understand
complexity.

5.4.2 Genuine Complexity and Emergence

There is another way to understand complexity than as mereological composition.

This is what we will call ‘genuine complexity’. On this view, complex wholes con-
sist in parts that interact with each other in a way that also influences and alters the
parts themselves in the process. As parts of a whole, the parts are no longer clearly
separated in a way that they can easily decompose and compose into new wholes,
5 Complexity, Reductionism and the Biomedical Model 87

with their identity intact. Instead, the interaction of the parts within that whole is
what will give the identity to each part. Outside the context of the whole, the parts
would not be that particular part with those particular causal powers or dispositional
properties. Their causal role is given by their place and interaction as part of that
particular whole. The molecule of DNA, for instance, has a specific causal power
because it is part of a whole cell, and of a whole organism. DNA extracted from the
cell has no causal power, and degrades in a short time.
Recall the concept of a mutual manifestation partner (see Anjum, Chap. 2, this
book): the same causal disposition in a different context, or whole, manifests differ-
ently because it interacts with different manifestation partners. If this is the case, as
dispositionalism assumes, then a complex whole can never be completely under-
stood by observing its parts in isolation. On this view, the interaction among the
constituent parts and the whole is as important for the causal inquiry as the parts
themselves. This is also because the result of such interactions cannot be seen as
mere composition. Instead, the whole is the result of a continuous and complex
process where the parts that interact lose their prior identity along the way. The
whole is therefore more than the sum of its parts, or even something else entirely.
We can say that the whole is an emergent phenomenon. From the perspective of
dispositionalism, ontological emergence is the view that the whole has new proper-
ties and new causal powers as a result of the causal interactions of its parts, where
the change also happens in the parts during this process (for more details on dispo-
sitionalist emergence, see Anjum and Mumford 2017). A simple example of this
could be water, which has a number of causal powers that are not found in its atomic
components. Water is thus the result of a process of change that happens when the
atoms interact to form the molecule.

Simply put…

Emergence happens when there are new properties and causal powers of
wholes in virtue of causal interactions among their parts. The whole is then
more, or something else, than the sum of its parts.

Example: sodium chloride is composed by sodium and chlorine, yet its prop-
erties are completely different from the properties of its components.

This way of thinking about complexity is more common in the discipline of ecol-
ogy, where the interaction between a species (the part) and an ecosystem (the whole)
changes both. A beaver, for instance, modifies its surroundings by building a dam.
But at the same time, the surroundings modify the beaver by natural selection. For
this reason, ecology studies the interactions between species and ecosystems, and
would not be interested in studying a species in captivity, isolated from its natural
context.
88 E. Rocca and R. L. Anjum

Can the ecological perspective add something to healthcare and to the clinical
encounter? We think so. Up until now the biomedical model has been dominant in
medicine, but with a limited understanding of biology, taken from molecular biol-
ogy, biochemistry and physiology. Although this knowledge is necessary for clini-
cal work, we urge that it not sufficient for it. Dispositionalism suggests that medicine
would benefit from an ecological turn. Such a turn toward an ecological perspective
in medicine would place much more emphasis on understanding human biology as
genuinely interactive, and on investigating how biological processes are integrated
with human context and lived experience. In the words of osteopath Stephen
Tyreman:
Understanding what person-centred means is much more complex and multi-factorial than
I once assumed. It is not merely a question of considering a person’s individual needs and
concerns and putting them first. It is recognising that human beings face up to the challenge
of illness, pain and disability differently from how we might understand and seek to correct
a fault in a car, say. (Tyreman 2018: 2)

5.4.3 Practice Is Motivated by Ontological Bias

We have presented two views on complexity: mereological composition and genu-

ine complexity or emergence. Mereological composition was illustrated by the
Lego bricks, where the parts combine to compose different wholes, but without any
change to the parts themselves. Genuine complexity was the holist alternative,
where the whole is an emergent existence in which the parts interact and change
each other. The whole then has properties that are different from the composition of
the properties of its parts. How does our ontological assumption about complexity
affect scientific and medical practice? We can show this by applying the two philo-
sophical perspectives to human pathogenesis.
Consider an autoimmune disease that might have biological causes (e.g. genetic
predisposition) as well as psychosocial causes (e.g. lifestyle or emotional stress).
Under the assumption that complexity is compositional mereology, the intertwining
of different types of causes would represent a challenge to understanding causality.
This is why fragmentation of different causal contributions, and their evaluation in
isolation, is a well-established norm for scientific inquiry into causality. Genetic
predisposition, for instance, might be tested by genotyping of patient groups, or by
looking at the susceptibility of a lab animal strain with the genetic mutation(s) we
want to test. The causal role of emotional stress might then be investigated through
case studies, cohort studies, or other types of clinical studies. In the end, the results
from different studies can be added together to give us the causally complex result.
This way of thinking about the scientific approach in medical research also influ-
ences medical practice, when dealing with complex medical conditions. Current
medical practice aims to combine biological causes with psychosocial causes of
illness. But also here complexity seems to be understood and handled according to
the biomedical orthodoxy.
5 Complexity, Reductionism and the Biomedical Model 89

ONTOLOGICAL BIAS
Complexity is mereological composition of changeless parts.
⇓
NORM
The investigation into causal complexity starts with separation and isolation of each component.
⇓
PRACTICE
Fragmentation of causes into separate biological, psychological and social spheres is the starting-
point for medical inquiry into complex conditions.

The introduction of person centered healthcare was partly motivated by the anti-­
dualist and anti-reductionist view that health and illness must be understood as
belonging to the person, not to one or more bodily part. From this perspective, the
mereological composition view is a simplification of the human condition. Such
simplification might at times be useful in some contexts, but it can be dangerous,
too. In the words of Marie Lindquist, director of the WHO collaborating Uppsala
Monitoring Centre for International Drug Monitoring:
Our ability to quickly categorise things around us is a basic instinct, a survival mechanism,
and it was essential in a time when the ability to quickly identify danger was a matter of life
or death. By classifying and grouping things, we make a complex reality more manageable.
The problem is if we categorise in a way that is confining and excluding, and reduces reality
too much – a simplistic reductionist approach easily leads to stereotyping, which can be
anything from irritating to seriously damaging. (Lindquist 2018: 2)

Dispositionalism replaces mereological composition with emergence, which we

take to be a type of genuine complexity. Genuine complexity is a result, not only of
the composition of different parts, but also of their mutual interactions. For instance,
the outcome of organ transplantation depends on how well the new organ interacts
with the rest of the body. By focusing on such causal interactions, we also need to
replace the epistemic norm for how to deal with causal complexity, scientifically
and in medical practice.

ONTOLOGICAL BIAS
Complexity is genuine and emergent.
⇓
NORM
The investigation of causal complexity starts with observing the whole, and the interaction of
different elements as parts of that whole.
⇓
PRACTICE
Whole person centred practice and patient narratives are the starting-point for medical inquiry into
complex conditions.

We see, then, that it makes a difference both to scientific norms and practices how
we understand complexity, ontologically. Ontology thus influences the norms and
practices that define a scientific discipline. By questioning the philosophical biases of
our methods and practices, one can also challenge what counts as scientific practice.
90 E. Rocca and R. L. Anjum

5.5 We Need an Ecological Turn in Medicine and Healthcare

We have argued that, once we acknowledge a phenomenon as genuinely complex,

we also need to make some epistemological commitments for how to study that
phenomenon scientifically. The most important is the fact that, if we aim to under-
stand (and heal) living beings, we need to start by understanding complex interac-
tions. This is not to deny the obvious: we all consist of parts (a liver, a heart, a brain,
and so on), and there is much general and indispensable knowledge to gain about
organs, tissues and cells by observing their behaviour in experimental and isolated
contexts. The tricky part comes when we need to make use of such knowledge for
the treatment of the whole person. In that case, it is necessary to keep in mind that
although whole persons consist of parts, the identity of such parts is defined by their
interactions: not only their interactions with the rest of the body, but also with the
person’s context, her history and her lived experience.
Not many would disagree with this, we think, when asked to reflect upon it.
Denying it would be like comparing the human body to a machine, in which single
parts interact without ever changing as a result of such interaction. This would entail
that human life could be disassembled into its parts, and then re-created by re-­
assembling them. An absurdity, we might say. Yet, current practice and thinking in
the medical profession tend to drift toward the mereological, or mechanical, simpli-
fication of human biology. Talking about a ‘heart condition’, ‘irritable bowel’ or
‘skin disease’ has a practical function, but in the long run it does make us think of
illness as belonging primarily to a part of the body. As a consequence of this, we
might come to think of illness as something that is curable by treating that part
alone. In the clinical reality this becomes highly problematic. Here, co- and multi-­
morbidity are the rule rather than the exception, and most if not all medical condi-
tions are at least partly caused by contextual factors. Patients with complex
conditions will then have to be treated by different specialists for different health
complaints, and the full picture is often lost.
While co- and multi-morbidity is the norm in medicine, clinical guidelines are for individ-
ual illnesses. The ‘guidelines mentality’ often results in a situation that has been referred to
as silo medicine… where each diagnosis has its own expert groups, patient organisations,
industry sponsors and clinical guidelines. Diseases are then treated as wholes (“disease
holism”), while patients are treated as composed of parts (“patient compositionality”).
(Anjum 2016: 423)

What do we need, then, in more practical terms? How can we move toward an eco-
logical turn in medical care: that is, one that understands health and illness by start-
ing from interactions both with the physical and with the psycho-social? One
important step is suggested by Getz et al. (2011) in their paper ‘The human biol-
ogy – saturated with experience’. Here they argue that the medical profession must
acknowledge lived experience, meaning, and interpretation as not just ‘side infor-
mation’ about the patient and her preferences, but as actually and physically influ-
encing human biology.
5 Complexity, Reductionism and the Biomedical Model 91

Long-term overtaxation of the physiological adaptability of human beings may lead to

health impairment. This phenomenon, called «allostatic overload»…, is a consequence of
physiological «wear and tear» due to strong and/or persistent threats to an individual’s
existence or integrity (the word encompasses both mental and physical aspects). The human
body’s reaction to stressors, which in our culture can be classified as physical (e.g. under-
nourishment, overfeeding, malnutrition, pollution, lack of sleep, lack of exercise, infec-
tions, noise) prove to converge at the same biological «level» as stressors we would classify
as psychosocial (e.g. a life characterised by threats, neglect, abuse, poverty or overwhelm-
ing caregiving burdens): Both categories of stress can contribute over time to the develop-
ment of autonomic dysfunction, changes in the immune system, chronic low-grade
inflammation, endocrine disruptions and accelerated cell aging, measured as telomere
shortening… (Getz et al. 2011: 684)

Accordingly, if we understand human biology from an ecological perspective, we

cannot treat health or illness solely as the results of internal physiological or bio-
chemical processes. Instead we should look for internal as well as external and
contextual causes that might influence a person’s health in a positive or negative
way. For health, all levels of nature are united within one single patient: physiologi-
cal, biological, psychological and social. All these levels affect and are affected by
health and illness. Ecologically, we should also expect that these different influ-
ences will interact in nonlinear ways, and that what happens in one context cannot
automatically be transferred to another context. Consequently, human biology can-
not be understood without including, and even starting from, the higher level of
complexity, in a top-down way.
From this ecological perspective, we might ask how efficient it is for medicine to
be organised into separate specialisms, each with their own clinical guidelines (see
Copeland, Chap. 6, this book for a more detailed discussion of guidelines).

5.5.1 Whole Person Healthcare in Practice

Immunologist and psychotherapist Brian Broom started a multidisciplinary centre

in New Zealand in 1987 to offer what he calls whole person healthcare. The idea is
to understand health and illness in a way that genuinely overcomes both reduction-
ism and dualism, emphasising the link between life experiences and physical ill-
ness. The main goal is that patients, once they feel met as a whole and not as the sum
of biological parts, will start to explore their own illness in a whole-istic way, in
light of their lived experience. Broom and his team use patient stories, together with
the medical perspective, as an essential tool to understand and treat chronic illness.
This is how he describes his practice.
Asking for a story may seem a simple matter but the implications are hugely important.
And, in listening to a story, imagination is important… An example: A clinician asks a
patient for her ‘story’, about what happened in her life when her symptoms started many
years ago when she was 18 years old. This question is actually asked because the clinician
assumes to some degree that the patient is a unitive whole, and that the patient’s life experi-
ence (at 18) may be very relevant, and that opening this up may help the person get well in
some way. Simply asking the question rests on really serious foundations. For me it entails
92 E. Rocca and R. L. Anjum

the conviction that mind and body co-emerge together from the beginning of life, and
therefore it is natural to imagine the story being part of the illness. It follows that there may
be therapeutic potential in knowing the story. This is the paradigm of whole person care.
The paradigm allows the clinician to imagine ‘something’ important in the story around age
18, and to ask the simple question.

Brian Broom, ‘Imagination and its Companions’, CauseHealth blog (https://causehealth-

blog.wordpress.com/2017/07/03)

Since biological conditions are part of meaningful humans, they are also meaning-
ful. Broom talks about ‘meaning-full disease’, and his books collect many astonish-
ing examples of the identity between mind and body, which he calls ‘mindbody’.
The whole person website offers numerous resources, including a tool called ‘ill-
ness explorer’, in a version for patients and one for practitioners. This tool is meant
to guide the understanding of the disease as meaningful, and of meaning as embod-
ied (https://wholeperson.healthcare). In Chap. 14 of this book, Brian Broom gives a
detailed historical account and description of his practice.

5.6 To Sum Up…

We have seen that the biomedical model of illness relies on a dualistic and reduc-
tionist view of the human condition. Although intuitive and attractive for medical
research and especially for some types of pathologies, this perspective has neverthe-
less been criticised for almost a century. The problem is that the biomedical model
fails to see illness as a matter of the whole person, in that it overlooks the impor-
tance of social, lifestyle and psychological factors in the onset of complex and
chronic disorders. Despite decades of criticism of the biomedical model, the current
state of the art suggests that it is still predominant in medicine. Proposed alternative
views, such as the bio-psychosocial model, still convey a fragmented perspective on
human biology, and consequently a fragmented medical care. To face this problem,
we propose a re-discussion of the foundational concept of complexity. While this
concept is widely used, its meaning and interpretation usually remain implicit.
Although complexity and emergence have become important words in medicine
and clinics, we think that there is not enough reflection on what they really mean.
In this chapter, we have shown that a mereological view of complexity, in which
complexity is seen as composition of multiple parts, motivates an investigation that
starts from the separation of causal factors, and their investigation in isolation. In
contrast, we propose what we call ‘genuine complexity’, in which the parts of a
whole not only compose and interact, but also change each other through such inter-
action. This, however, requires that we start an investigation from the higher level of
complexity: by observing the whole. At such a level, indeed, it is possible to focus
5 Complexity, Reductionism and the Biomedical Model 93

on interactions between context, lived experience and physical body parts. Several
clinicians, globally, are pushing for a change in this direction. An ecological shift in
medicine, we argued, will be not only necessary, but also unavoidable, if we
acknowledge that human biology is genuinely complex and we truly reflect on the
meaning and implications of this.

References and Further Readings

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bias that science cannot avoid. elife. https://doi.org/10.7554/eLife.44929
Anjum RL (2016) Evidence-based or person-centered. An ontological debate. Eur J Pers Cent
Healthc 4:421–429
Anjum RL, Mumford S (2017) Emergence and demergence. In: Paoletti M, Orilia F (eds)
Philosophical and scientific perspectives on downward causation. Routledge, London,
pp 92–109
Anjum RL, Mumford S (2018) Causation in science and the methods of scientific discovery.
Oxford University Press, Oxford
De Vreese L, Weber W, Van Bouwel J (2010) Explanatory pluralism in the medical sciences: the-
ory and practice. Theor Med Bioeth 31:371–390
Descartes R (1641) Meditations on first philosophy. In: Cottingham J, Stoothhoff R, Murdoch D
(eds) The philosophical writings of Descartes, vol 2. Cambridge University Press, Cambridge
Dupré J (1993) The disorder of things. Metaphysical foundations of the disunity of science.
Harvard University Press, Cambridge
Ellis GFR (2012) Top-down causation and emergence: some comments on mechanism. Interface
Focus 2:126–140
Engebretsen KM (2018) Suffering without a medical diagnosis. A critical view on the biomedical
attitudes towards persons suffering from burnout and the implications for medical care. J Eval
Clin Pract 24:1150–1157
Engebretsen KM, Bjorbækmo WS (2019) Naked in the eyes of the public: a phenomenological
study of the lived experience of suffering from burnout while waiting for recognition to be ill.
J Eval Clin Pract. https://doi.org/10.1111/jep.13244
Engel GL (1977) The need for a new medical model: a challenge for biomedicine. Science
196:129–136
Farre A, Rapley T (2017) The new old (and old new) medical model: four decades navigating
the biomedical and psychosocial understanding of health and illness. Healthcare. https://doi.
org/10.3390/healthcare5040088
Getz L, Kirkengen AL, Ulvestad E (2011) The human biology-saturated with experience. Tidsskr
Nor Laegeforen 131:683–687
Greenhalgh T, Hurwitz B (eds) (1998) Narrative based medicine. Dialogue and discourse in clini-
cal practice. BMJ Books, London
Karlstad Ø, Furu K, Stoltenberg C et al (2017) ADHD treatment and diagnosis in relation to chil-
dren’s birth month: Nationwide cohort study from Norway. Scand J Public Health 45:343–349
Kirkengen AL (2018) From wholes to fragments to wholes—what gets lost in translation? J Eval
Clin Pract 24:1145–1149
Kirkengen AL, Thornquist E (2013) When diagnosis makes us blind. Tidsskr Nor Legeforen
133:1466–1468
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Lindquist M (2018) Director’s message. Uppsala Rep 78:2
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Clin Pract 24:919–929
94 E. Rocca and R. L. Anjum

Pisco AO, Huan S (2015) Non-genetic cancer cell plasticity and therapy-induced stemness in
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Standen C (eds) Textbook of osteopathic medicine. Elsevier, Munich, pp 277–283
Tyreman S (2018) A personal reflection on person-centred care and the role of stories in healthcare.
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Chapter 6
The Guidelines Challenge

Samantha Copeland

6.1 The Tension Within

6.1.1 Evidence Based Medicine and the Rise of Guidelines

Part of the reason behind the popularity of evidence-based medicine, or EBM, in the
last few decades has been its promise to standardise care. When Guyatt et al. (1992)
introduced the concept and practice of EBM in medical education, it was in direct
response to the ‘old ways’ of medicine. As they depict it, medicine was a profession
where well-known doctors were looked to as the authorities about healthcare: exper-
tise came from experience, and was demonstrated by the admiration of one’s peers.
Standards of care could vary widely from hospital to hospital, and new evidence
about what practices and interventions worked best was rarely taken up by institu-
tions (Guyatt et al. 1992). The appeal to the ‘best evidence’ as the driver of the stan-
dard of care meant that everyone could have access to the reasons behind why things
were done in a certain way; such reasons ought to be objectively good reasons, rather
than merely authoritative. Patients could expect the same quality of care from every
practitioner, and doctors would know the best thing to do for their patients.
For many reasons, this ideal was hard to realise in the world. First, because indi-
vidual doctors could not possibly be expected to study all the available evidence for
any given intervention, and so assessments of what is the best evidence and the
recommended strategy for care had to be centralized. Organizations like Cochrane

In this chapter, we look at guidelines as an example of a medical institution and practice that would
be affected by a shift in ontology from the current biomedical models toward a dispositional model
of causality.

S. Copeland (*)
Ethics and Philosophy of Technology Section, Delft University of Technology,
Delft, The Netherlands
e-mail: s.m.copeland@tudelft.nl

© The Author(s) 2020 95

R. L. Anjum et al. (eds.), Rethinking Causality, Complexity and Evidence for the
Unique Patient, https://doi.org/10.1007/978-3-030-41239-5_6
96 S. Copeland

gained in authority, becoming the sources of ‘systematic reviews’ that did this work
on behalf of practitioners. Second, because standardizing care takes more than
everyone having access to the best evidence about which practices are optimal. It
takes governance, and the organization of institutions with many levels of care and
expertise, with different needs and different jobs. Furthermore, medical institutions,
in many nations, are public institutions. Consequently, their governance is the con-
cern of national governments, too, and standards must be set for ethical and political
reasons. As a result of these and other influences, healthcare guidelines became a
resource for governments, medical institutions, and practitioners alike. They are a
means for standardizing care, they are meant to communicate which practices and
decisions the best evidence says is optimal, and they are both a guide to uncertain
practitioners and the means to inform patients of their options.

6.1.2 Guidelines in Practice

However, given what has been said in this book so far, it seems there must be a
conflict between standardizing care, as guidelines seek to do, and using the best
available evidence to provide optimal care for the individual patient, as practitioners
who use guidelines seek to do. That is, the possibilities offered by dispositional
causality for understanding health, disease, and the effectiveness (or not) of medical
interventions, point to a tension in the goals of guidelines, under the EBM interpre-
tation of what they can and should do.
This tension is found at a larger scale as well. That is, governments take a public
health approach to medicine, and for that purpose, statistics are indeed ideal.
Clinicians on the ground in medical care, however, find themselves dealing with
individual patients in unique situations. There is not always a box to tick to describe
their patient, or what they have done to care for them, on the standard forms they are
required to fill out. Insofar as EBM encourages the standardization of care and the
quantification of medical evidence, it caters to the public management approach to
healthcare that is currently frustrating many healthcare practitioners.
In this chapter, we take a look at this tension, and give some ideas about how we
can use the philosophical tools introduced so far to resolve it. Specifically, we focus
on how this tension has manifested itself in the debate about healthcare guidelines.
Healthcare guidelines in one sense exemplify the standardization of medical care.
They present a predetermined list of options, they identify and plan a treatment
course for a patient according to the category that fits them best, and they are gener-
ated by interdisciplinary committees using the best available evidence. However,
they are simultaneously an honest attempt to provide guidance to the practicing,
individual clinician, who hasn’t the time to delve into all the relevant evidence her-
self, and must rely on others to assemble the best available evidence into a format
she can use in her daily, busy practice. Thus, the guideline can be both a hegemonic
force, representing consensus and conformity, and also a helpful aide when a clini-
cian is truly in need of information and guidance—they are meant to be both rule
6 The Guidelines Challenge 97

and resource. This dual role creates tension in the clinical encounter because follow-
ing the rule is not always the best thing to do in a particular situation, and so in many
cases what the clinician needs is a resource that is not at all a rule. Guidelines, then,
to truly aide the clinician, must be something other than rules.
These tensions can be truly problematic, when clinicians are asked or are other-
wise inclined to believe it is better to follow guidelines even when their expert judg-
ment would suggest a different path.
What singular question could be more pressing for clinicians today: how do we prepare the
way for the return of the person in contemporary healthcare amidst rife healthcare com-
modification and the mechanical one-size-fits-all approach that is EBM? …In clinics and
hospitals the world-over, the narrative, the personal and the biographical person is often
found bullied and threatened by this hegemony that is contemporary EBM; healthcare is
de-personalised.
Chris Worsfold, ‘Learn to stop worrying and love evidence based medicine’, CauseHealth
blog https://causehealthblog.wordpress.com/2016/02/07

6.2 Guidelines and Tramlines

A point that was frequently brought up in discussions during CauseHealth events

was the worry that guidelines were often regarded as rules to be followed, rather
than as guidance about what care options are available and appropriate. This phe-
nomenon is captured by the frequently used phrase ‘Guidelines not tramlines’—
rather than a set track, the following of which is not a choice but rather given,
guidelines ought to offer choices to clinicians and patients. The tendency to treat
guidelines as though they were tramlines is, as suggested above, part and parcel of
the public management approach to medicine, and presents clinicians with a con-
flict of interest: do they risk reprimand and even litigation, if they follow their expert
clinical judgment to act in a way not advised by the guideline? Osteopath Stephen
Tyreman thought this was a problem in health care, and promoted Values Based
Practice (VBP) as a remedy:
VBP is being given further support by the recent Montgomery judgement [UK] in which
‘doing the right thing’ for a patient is not just following the guidelines or taking account of
risks as a percentage, but taking into account ‘what matters’ to the patient, what his/her
values are. This involves a different kind of decision-making and can’t be achieved by read-
ing out all the risks, or ticking a box that says we’ve told the patient the implications of the
procedure being recommended. It involves asking how this treatment might impact on the
patient’s life and what matters to them. This requires a proper dialogue. What the regulators
realise they are up against in supporting this is that practitioners will not be able to follow a
safe procedure—an algorithm or guideline—that will guarantee they do the right thing;
they must make a judgment weighing up a range of fact and value-based criteria, which of
course is what David Sackett originally intended EBM to be (e.g. Sackett et al. 1996). The
response from some practitioners is to say, ‘we haven’t got time to do all this deep and
meaningful discussion stuff, just tell me what the right thing to do is.’ Or, ‘what if I make
the wrong decision? I don’t want to get into trouble.’
Stephen Tyreman, ‘Standards for regulation’, CauseHealth blog https://causehealthblog.
wordpress.com/2016/12/15/standards-for-regulation/
98 S. Copeland

6.2.1 Guidelines and Evidence Based Policy

One of the issues is the content of guidelines themselves. When designed, for
instance, to effect changes in the management of healthcare, guidelines indeed pres-
ent as rules to be followed. Unless everyone follows such guidelines, the changes
won’t happen. For example, there may be a guideline about how much time to spend
with a patient on average. Or, there may be specific guidelines about what steps to
take with patients who have certain diagnoses—which tests ought to be done, which
specialists engaged, or even how long a session of cognitive behavioural therapy is
allowed. When such guidelines are tied to billing processes in the healthcare sys-
tem, they can become constraints on what is possible for clinicians to do or to offer
their patients, rather than guidance about what might help. One could argue, how-
ever, that guidelines that focus on management issues really ought to be treated as
tramlines, since they require maximum compliance in order to be effective. As an
example, expensive experimental therapies should not be used up on patients who
cannot clearly benefit from them, for instance because they are in a terminal phase
of life. It is hard to think of a good reason to deviate from this managerial guideline.
But in the example above, where the length of a cognitive therapy session is man-
dated rather than suggested, management-focused guidelines seem to cross over
into the territory of the clinical encounter.
Another example of this was given at the Guidelines Challenge Cause Health
conference by speaker Hálfdán Pétursson (Pétursson et al. 2009; for a review of
talks at that conference, see Anjum et al. 2018). He discussed the problems encoun-
tered by general practitioners (GPs) who are trying to follow the guidelines for
preventing cardiovascular disease in Norway. If the guidelines are followed as writ-
ten, it would require more hours of work than the entire GP workforce in the country
could put in, just for the one task of preventing cardiovascular disease in those who
are deemed at risk. As this example shows, not all aspects of healthcare are manage-
able through rules, and sometimes implementing the best evidence in an ideal way
is simply impractical.
Further, when we bring what has been said so far in this book into play in this
discussion of the problem of guidelines, we can see that there are also ontological
and epistemological reasons behind the problematic but common view that guide-
lines present tramline-type rules rather than mere guidance. We explore these rea-
sons in the next two sections, as well as how the philosophical framework of
dispositionalism might offer a resolution to these guidelines-related challenges.

6.3 The Ontology of Guidelines

The ontology of guidelines can mean two different things. It can mean the nature of
a guideline itself—its function, its form, and what goes into developing it—or it
could point to the ontological assumptions that shape guidelines as they are
6 The Guidelines Challenge 99

developed and used. It is the position of CauseHealth that these two meanings of
ontology are intertwined. How we think guidelines ought to be used reflects, and in
turn is reflected in, what we think guidelines are about, and why we think they can
be effective.
One might say that healthcare guidelines exemplify a utilitarian approach, for
instance. Utilitarians like Jeremy Bentham argue that the best (moral, correct) action
is the one that will result in the greatest utility (pleasure, or happiness) for the great-
est number of people overall. So, a frequentist utilitarian would argue that guide-
lines should be designed as rules to follow that, overall and if everyone follows
them, are most likely to lead to the best possible outcome for the highest number of
people. This works well at a population level: consider, for instance, the importance
of ‘herd immunity’ as a reason for making a vaccination mandatory for all healthy
members of a population. But this, as we have seen, is not the same as obtaining the
best outcome for a particular person at a particular time, which is generally the goal
in the clinical encounter.

Simply put…

Utilitarianism is a form of consequentialism, the ethical framework that assesses

moral action according to its impact on others. That is, we need to consider the
consequences of the action, to know if it is the right one, when compared with
the consequences of other possible actions. Bentham popularized the idea of
‘utility’ as a way of measuring and comparing the impact of possible actions—
actions with greater utility caused more pleasure and less pain overall.

The nature of guidelines is just what we discussed in the last section: are guide-
lines rules to be followed, or are they collections of good advice and a presentation
of relevant options to a clinician and her patient? In order not to treat guidance for
the clinical encounter as a managerial rule, we have said that it is important to avoid
seeing guidelines as tramlines. But more than this, it is also important to conceive
of the function, form, and creation of a guideline in the right way, so that they are
developed and used correctly and effectively. The difficulty is in resolving the ten-
sion between the need for flexibility, to allow for the particularities of the clinical
encounter to influence decisions about care, and the need for standardization of
access for all patients to quality care.

6.3.1 Logically Speaking, Guidelines Cannot Be Rules

Anjum and Mumford have written on the nature of guidelines (2017), arguing that
guidelines must, logically speaking, be mere guidance rather than hard rules. Even
if a guideline is effective as a rule, it still doesn’t help the clinician decide what to
100 S. Copeland

do in the individual case. That is, the clinician must, in each case, still weigh up
whether the guideline offers the best path or options for treatment for the particular
patient in care. Thus, the guideline cannot be designed as a rule that can be univer-
sally followed, given a diagnosis or situation; because its relevance can be ques-
tioned in reflection upon the particularities of an individual patient, the guideline
itself offers a choice, rather than a rule. For instance, in Chap. 4 of this book, Anjum
and Rocca describe the case of guidelines for morbid obesity. While current guide-
lines do offer choices to the clinician, all of those choices rely on biological concep-
tions of obesity only. When practitioners encounter a case of morbid obesity that
seems to be caused by trauma instead, then they must choose to go outside the
guidelines. Kai Brynjer Hagen (see Chap. 10, this book) suggests that the best avail-
able evidence in such cases is not captured in guidelines, but rather in the patients’
narratives themselves. In cases like these, a clinician must himself evaluate what the
best evidence is, in choosing whether to follow the guideline at all.
That is, the complexity of a patient’s situation seems to call for a unique approach
to their treatment, rather than the application of a general rule. Thus, the ontology
of the patient requires that guidelines be treated as advisory rather than regulatory,
as a resource rather than a rule. This then calls into question the idea of guidelines
as being rule-utilitarian—there will be no ‘rule’ that benefits more than the singular
patient to whom it will absolutely apply (presuming such a patient does in fact exist,
which is up for debate if guidelines are written for statistically ‘average’ patients,
for instance, see Anjum, Chap. 2, this book). Even when a guideline represents the
treatment paths that tend to work, they will not always present the best thing to do
in a particular case. For this, judgement is needed, and familiarity with the patient
himself.

Simply put…

Rule-utilitarianism suggests that we can find a rule that, if everyone follows

it, will provide the most utility for the most people, overall. Act-utilitarianism
suggests, in contrast, that each individual decision about whether to take a
moral action must weigh up the potential consequences and utility of that
particular action.

Therefore, rather than rule-utilitarianism, we might accept that act-utilitarianism

is the correct way to understand the nature of guidelines: act-utilitarianism allows
one to consider the consequences for overall utility of a specific act or decision,
rather than of a generally applied rule (for a full review of this argument, see Anjum
and Mumford 2017). However, note that this moves the source of the guideline’s
utility from the guideline itself to the decision about whether to use the guideline: it
is not about the nature of guidelines anymore, if we follow this line of reasoning, but
about the nature of the clinician’s decision in that particular case. Consequently, it
is not guidelines but the clinician who would be utilitarian in nature, after all.
6 The Guidelines Challenge 101

There is thus an ontological reason for not seeing guidelines as tramlines, even if
we do consider them to be utilitarian in nature. We cannot think of guidelines, onto-
logically, as utilitarian rules that represent (from a public health perspective) the
best treatment options for the greatest number of people. In order to bring the most
utility to the most people, rather, each case must be considered individually, before
it can be decided whether the rule should apply. So the rule is not utilitarian on its
own. Rather, it is the act of using or not using the rule that could be utilitarian, if
making that decision for that patient also brings about the most possible utility over-
all. It seems, then, that the best action to take will be the action that brings about the
best consequences for that particular patient. Even when we look at it in terms of the
most utility for the most patients over all, this will happen only when each individ-
ual patient is given the best possible care for that patient specifically (a singularist
approach) rather than when all patients who fit into a generalized category are all
given the same care (a frequentist approach). But how do we make guidelines spe-
cific enough to give the best care to each individual patient, when patients can differ
greatly in practice? Before addressing this problem, we will explore the practical
reasons for making guidelines more specific than general.

6.3.2 What Does This Mean for Guidelines in Practice?

There are practical reasons for not seeing guidelines as tramlines as well; practitio-
ners have good reasons for resisting the imposition of guidelines as rules for their
practice. As we saw above, pressure to follow guidelines, and the presumption that
they capture the best available evidence, means that practitioners may fear repercus-
sions for not treating them as rules. But, as we see in the obesity case, guidelines do
not always capture the best available evidence in relation to the particular patient at
hand. So, when we take dispositional causality and person centered medicine as our
paradigms for medical science and care, we can see there is a serious conflict
between creating a rule to follow in the clinical encounter and using the best evi-
dence available to decide on a course of care. It is simply not possible for a guide-
line to do both.
Indeed, one of the best known explorations of this problem has been written up
by Gabbay and le May (2004), in their introduction to the idea of seeing guidelines
as ‘mindlines’ instead of tramlines. Gabbay and le May show that guidelines play a
complementary role to other practices for healthcare practitioners, including refer-
ring to other known authorities in their professional networks. That is, guidelines act
as additional sources of evidence about best practices, weighed up in relation to
practices they already rely upon in deciding what the best available treatment
options for their patients are. Practitioners use their own judgment to decide when
and if they will incorporate the advice given in guidelines into their practice and
decisions. So guidelines are not treated as rules to follow in practice; thus, it does
not make sense to develop them or to try to enforce them as such rules.
102 S. Copeland

The best evidence available is going to include evidence related to the particu-
larities of a situation—to the dispositions of the particular patient, and to the spe-
cific context of that patient as a person. But this kind of evidence cannot support the
formulation of a rule that should be followed beyond this particular case. Once we
understand that tramlines simply cannot do the work that guidelines are supposed to
do, any conception of guidelines that insists they be followed as rules is wrongly
conceived.

6.4 The Epistemology of Guidelines

Guidelines are meant to represent the best options for care in a given situation, given
the best evidence available. But this recalls the problem of how we can know which
of the available evidence is, in fact, the best. Guidelines developers regularly strug-
gle with this problem. Many of them have adopted a system called ‘GRADE’ing the
evidence; the principles of the GRADE (the Grading of Recommendations
Assessment, Development and Evaluation) working group can be followed in order
to rank evidence from best to least, in respect to how reliable it is for grounding
guidelines. The claim is that this methodology offers greater flexibility than the
original hierarchies of evidence developed by EBM proponents, because it incorpo-
rates a wider scope of evidence and then evaluates that evidence via a greater num-
ber of parameters. Whereas the hierarchies relied upon the methods by which
evidence was generated to rank one kind of evidence higher or lower than another,
GRADE methodology takes into consideration perceptions about the reliability of
specific research results, sometimes allowing, for example, evidence that was gen-
erated by a low-level method on the EBM hierarchy to be ranked higher, and vice
versa. For example, if an observational study reported a large enough effect, confi-
dence in its results would be strong enough to rank it alongside an RCT; or, if there
were a risk of bias in the way an RCT had been conducted, for instance if not
enough women had been included as participants in a drug study, then its results
would be ranked with lower confidence, especially in respect to women. However,
even this more flexible way of ranking evidence still limits itself to considering the
best available evidence to come from organised, clinical trials. This leaves out, for
example, mechanistic evidence, which many believe to be of highest importance for
determining causality, and patient narratives, key to understanding causality in the
single case (see Anjum and Rocca, Chap. 4, this book).
A second epistemological concern in the development and use of guidelines is
how to integrate this wider scope of evidence into a single or set of decision-making
options for clinicians and patients. Different kinds of evidence require different
kinds of expertise and even different kinds of reasoning to be employed in their
evaluation. This is the task taken up in recent years, for instance, by the GIN
6 The Guidelines Challenge 103

(Guidelines International Network) AID (Appraising and Including Different)

Knowledge working group (Wieringa et al. 2018). One way of tackling this is to
engage a diverse group of experts in the developing of guidelines, who are able to
evaluate a wider scope of evidence through their joint efforts (Zuiderent-Jerak et al.
2012). A second way is to improve upon the transparency of guidelines, including
details about the way in which decisions were made by developers as well as the end
results of their deliberations.

6.4.1 Transparency and the Tension Between Flexibility

and Standardization

Transparency, that is, is one of the ways that more flexibility is being built into
guidelines by developers. When developers are able to be transparent about the
choices they have made—for instance, about the reasons for why they made the
decisions they did about which evidence was best, and how that evidence translates
into the best practices they describe in the guideline—then clinicians have better
tools for deciding whether they ought to follow the guideline itself. A clinician
might, for instance, disagree with the reasons behind the choices that developers
have made, insofar as that clinician would not have made the same choices either
generally speaking or in respect to the particular patient at hand.
Of course, there are limits to how much transparency is useful. Too much trans-
parency could mean that guidelines offer no better guidance than the evidence itself
to clinicians and patients, who must first decide whether they agree with the experts
in order to make use of their guidelines. An effective guideline is developed by
experts who can be trusted to evaluate the evidence on the behalf of others who lack
either the expertise or the time at the moment when decisions must be made to do
that evaluating work themselves. Again, this follows the observations of Gabbay
and le May (2004), that practitioners are more likely to accept new evidence when
it is promoted as good evidence by trusted colleagues and authorities in the field.
The ontological concerns raised in the previous chapters and section come into
play here, as well. Knowing what evidence is best, and knowing what treatment
options it is evidence for, requires an ontological judgment about evidence—we
have to first have an idea of what good evidence really is, to tell if the evidence we
have is also good. Thus, any process by which experts come together to evaluate
evidence starts from their assumptions about what makes good evidence. In devel-
oping a guideline, it can be supposed that the best evidence available is also the best
evidence for the purpose of developing a guideline. If we further see guidelines as
rules to be followed, and a good outcome as achieving the best results most often for
the most people, then we are evaluating evidence in terms of its quality as a support
for a rule. As we say above, this backs us into an uncomfortable corner, in the thick
of the tension between flexibility and standardization.
104 S. Copeland

6.4.2 When Should the Particular Be Engaged?

The epistemological factor that needs to be highlighted here is the point at which
nuance and particularities become relevant for whether a guideline will be useful.
This point, I argue now, is whenever decisions must be made about what are the best
available healthcare options for the particular patient at hand. For these decisions,
evidence about the patient’s condition and evidence about what treatment options
are best must come together. Guidelines are meant to offer guidance on how to do
this. Often, this point of convergence is assumed to be the point of diagnosis. But,
as previous chapters have shown, there is much more to determining which treat-
ments are best than diagnosing the patient. Further, in many cases, no accepted
diagnosis fits (see Anjum and Rocca, Chap. 4, this book). And, diagnosis should not
present a point when the clinician has to decide which guideline to follow, or
whether to follow one at all. Guidelines should be ever-present tools for the clini-
cian, no matter the diagnosis, leading them through the resources available in a way
that really helps. So the particularities should be an inherent part of guidelines, act-
ing for the clinician as starting points from which to begin a search, for example.
Additionally, guidance is needed from the moment the clinical encounter begins
because, from the very beginning of the encounter, a clinician is observing new and
varied evidence about her patient’s health, and thus needs correlating knowledge
about what treatment options might be available and best. Thus, guidelines ought to
offer guidance not only after a diagnosis has been settled upon, but from the moment
the clinical encounter begins.
And finally, we consider flexibility to be important in respect not only to how
guidelines can be used, but also in how they might be formed. The clinical encounter,
that is, should be seen as a resource for gathering further evidence, not only about the
individual patient but also about the effectiveness of the guideline itself or the useful-
ness of the evidence available in respect to that patient and that clinical encounter.
New knowledge is gathered at the site of care, and guidelines should not be imposed in
a way that constrains such knowledge production, but rather can play a role in enabling
it. For instance, as Rocca (2017) recommends, building bridges that enable evidence
from the clinical encounter to be taken up by scientific researchers may be the best
way to gather mechanistic evidence, which must be observed in the singular case and
reported along with its qualitative context. Further, unexpected discoveries frequently
occur within the context of the clinical encounter (such as unusual responses to drugs,
whether adverse or beneficial), and processes for developing and using guidelines
ought to not only allow for this to happen, but also be prepared to learn from serendip-
ity—fortunate, though unexpected discoveries—when it happens (Rocca et al. 2019).
Guidelines, in the right form, could build such bridges and enable serendipity.
All of this means that attempts to build in those particularities and nuance by
developing any single guideline that will work as a linear and certain pathway
through the steps of treatment are misdirected. No matter how wide the scope of
evidence, or diverse the expertise and reasoning employed, guidelines developers
cannot hope to capture all details that may be needed by a decision-making team of
clinician and patient in the clinical encounter. Therefore, it cannot be the function of
6 The Guidelines Challenge 105

guidelines to offer a complete set of evaluations and options. Rather, as suggested

in Chap. 3, local knowledge, patient narratives and a variety of evidence are needed
to determine the propensities that are relevant in this clinical situation (Rocca, Chap.
3, this book). That is, the epistemic role of guidelines cannot be to provide all the
knowledge that will be needed in this context (i.e., all the material that will be
needed to make the best possible decisions about care).
Let’s return again to the idea of Gabbay and le May (2004), that ‘mindlines’ are
created through the tacit and ubiquitous interactions between colleagues and experts
within the practice of healthcare, in contrast to guidelines being imposed from outside
and accepted as new rules to follow in and of themselves. Guidelines, in their depic-
tion, are useful insofar as they are trusted sources of new evidence. To be trusted
sources, they need to be trusted by trustworthy colleagues, for instance; similarly, if
they are developed by trustworthy experts, it is the expertise and not the evidence that
will be followed by practitioners. So any guideline will have to be transparent, at least,
about who made the decisions when creating it, what their claims to expertise in the
interpretation and application of such evidence are, and why they made the decisions
they made. It is these decisions, then, that are the true content of a guideline (the guid-
ance they offer), and not the actual treatment paths that are recommended. This gives
us one way of understanding how guidelines can be formed and transmitted in a useful
way—as collections of expert advice, rather than as a simplified rule or set of options.
Consider one of the biggest challenges for guidelines developers—the preva-
lence of comorbidity among healthcare patients. As we have discussed (see Rocca
and Anjum, Chap. 5, this book), the tendency is to divide the medical body (both the
body of the patient and the body of medicine’s institutions) into disparate parts. But
the reality is that many patients present with multiple conditions, which interact in
ways that single-disease guidelines may fail to capture.
A related challenge is how to deal with the wealth of potentially relevant particu-
larities, and how does one identify patterns (that is, decide what counts as evidence)
in a unique situation? Guidelines must not only allow for intersection, but also for
the flexibility that is needed in the face of the variety between patients and the fact
that each patient will also change over time. They need to provide the means for
telling a causal story about that patient, one that includes emerging causal relations
and genuine complexity (see Rocca and Anjum, Chap. 5, this book).
So guidelines must be broad enough in scope to be useful before diagnosis as well
as after, and they must be flexible enough to be adaptable to a changing and unique
situation. The epistemic role of guidelines, then, is to offer a navigable network of
connections between observable evidence in the clinical encounter and generaliz-
able evidence obtained via the results of medical research, as well as information
about what treatment options are actually available and likely to be beneficial. That
is, rather than a flowchart of pathways to take in a certain direction once the starting
point is decided upon, a guideline could present more like a web of data and infor-
mation that can be searched in any direction and that would highlight interconnec-
tions between possible pathways. These pathways ought to come in the form of
expert advice on how to integrate the best available evidence into practices that are
already in play. Rather than an imposition of a new rule upon practice, then,
106 S. Copeland

guidelines would act as a resource for ways to improve upon existing practice, allow-
ing for variation between practices and for the best available evidence to change
practice from the bottom up, rather than the top down. This is just one way to imag-
ine how guidelines might work, if we start from a dispositionalist perspective.
To suggest that guidelines should work bottom up, should trace the interaction
between expertise and the best available evidence in a way that is both transparent
and helpful to practitioners, and should allow for variations within practice and
between institutions, however, seems to bring us back to the original problem iden-
tified by the proponents of EBM—that is, how do we standardize best practices in
healthcare without also linking best practices to authority figures instead of to the
evidence? We have argued that the solution is not to create guidelines in a way that
makes them rules to follow, or as inflexible as tramlines. In the next section, we
explore further how dispositionalism allows us to imagine a middle way, by linking
best evidence directly to the individual, and promoting singularism over frequentist
or utilitarian approaches to the standardization of best practices.

6.5 Guidelines in the Dispositionalist Way

In moral philosophy, the idea that right and wrong can be defined by a system of rules has
been challenged. If nothing else, it’s obvious that two rules could easily come into conflict
and one of them has to be sacrificed. Telling the truth is good but not necessarily if a killer
asks for the whereabouts of any intended victim. There could be circumstances in which it is
right to lie. In response, Dancy [2004] proposed a theory of moral particularism, a view in
which each situation has to be understood as complex and requiring its own moral assess-
ment, which could well be unique and unrepeatable. I would favour coupling this with a
strongly dispositional version of virtue ethics. Telling the truth tends to be right but not neces-
sarily so. Assessing the whole complex of circumstances might weigh in favour of lying.
Now I think the issue of how to understand and use a guideline clearly relates to this discus-
sion. We could interpret a guideline in a dispositional way rather than as an absolute rule. A
particular intervention may tend to relieve a particular symptom but in many contexts it
need not be the right intervention to prescribe. If this is right, I think it would be to the
benefit of all stakeholders—clinicians, guideline bodies, regulatory authorities, and
patients—to understand dispositionalism and particularism. This could be a challenge when
rule-based laws and codes of ethics are easy to grasp, but there is a potential benefit to be
gained from pushing ahead for a conceptual change.
Stephen Mumford, ‘The Notion of Guidelines’, CauseHealth blog
https://causehealthblog.wordpress.com/2016/12/08/the-notion-of-guideline/

6.5.1 So, What Should We Do with Guidelines?

We wrote earlier about the fact that we cannot know about a causal relationship until
after it has been observed (see Anjum, Chap. 2, this book). However, even after we
have seen the same cause and same effect occur together repeatedly, this does not
6 The Guidelines Challenge 107

mean that the causal relationship did not, in that first instance, actually exist. That
is, our epistemological state does not determine the ontological case. In the case of
guidelines, it seems we are trying to use what we know, epistemically speaking, to
say something about what must be true, ontologically speaking. When we set a
guideline, we pass a judgment about what treatment options are best, given our
evaluation of the evidence available. This judgment is not just a guess, it came about
via rational deliberation among experts. However, the best evidence available, as
has been shown in previous chapters, still cannot tell us what will actually happen,
in a particular case, given the specificity of the mutual manifestation partners
involved. In most cases, the best available evidence can only give us a probability
range of an outcome occurring; epistemically speaking, probability is often the best
knowledge we can have. Thus, guidelines are still useful, even if they cannot pre-
scribe exactly what the best decision will be.
But dispositionalism gives us something further to work with than this. It is true
that we cannot use our knowledge to determine exactly what will happen when a
particular patient embarks on a particular treatment path. However, as I mentioned
in the last section, the clinical encounter itself provides considerable observable
evidence about the particularities and nuance needed in deciding what options pre-
sented in a guideline to follow. What is important is that guidelines be written in
such a way that the general medical knowledge we have already can be met effec-
tively by the knowledge gained during the clinical encounter itself. What the clini-
cian might know to be true about a situation gives her new tools for evaluating the
relevance of a guideline for her patient.
What might a guideline look like, then, if we take up the conclusions drawn in
this book? Above, we said that they ought to offer a navigable network of connec-
tions between observable evidence in the clinical encounter and generalizable evi-
dence obtained via the results of medical research, as well as information about
what treatment options are actually available and likely to be beneficial. Mumford,
in the quotation above, adds the concerns of particularism and virtue to be consid-
ered by those who develop and use guidelines (see also Anjum and Mumford 2017).
Add to this what I have brought up in this section, that guidelines provide only half
of what is needed for their own effectiveness in the clinical encounter—it is up to
the clinician to make observations and the patient to contribute further evidence in
order for them to work successfully with the guideline to make decisions. Taking all
this together, it could be argued that guidelines are most effective as tools for use in
the clinical encounter when they are transparent and accessible in a way that allows
patients and clinicians to question the guideline itself where necessary, and to easily
draw connections between their particular situation and the more generalizable
advice given by the guideline.
In order to be fully dispositional, however, guidelines also need to provide more
information about what kinds of mechanisms might be in play, and what kinds of
dispositions are likely to affect the treatment path’s effectiveness, if chosen. This
will require not only a transparent process, but an iterative process, that takes up
new evidence gained in clinical encounters and makes it accessible to future users
of those guidelines. As in pharmacovigilance, patient reports can play a key role
108 S. Copeland

here (Rocca et al. 2019). With the increasing use of data mining techniques and
electronic records, paired with clinician and patient narratives when helpful, such
information is already taken up in guideline development—it could, perhaps, more
prominently shape the way guidelines work, so that using guidelines also means
actively engaging with them on a regular basis. The experts whose advice will be
accepted by practitioners, as we have seen, comes not only from guidelines develop-
ers, but also from colleagues and leaders in the field who have put them into practice
and reflected upon their impact. So the development of guidelines (especially if we
take them seriously as ‘mindlines’) does not stop at their implementation, but rather
needs to be continued afterward by taking up and disseminating the ways in which
individual practitioners have been able to use them in practice. In addition, this kind
of new evidence can communicate details about what kinds of patients the guide-
lines have worked best for, and the contexts in which they have so worked.
In addition, guidelines could offer advice on how to interpret different kinds of
evidence that will arise in the clinical encounter, such as what kinds of things to note
within a patient narrative that may be clues to relevant dispositions, or other symp-
toms not immediately evident from a patient’s physiology but which may affect
treatment options. In this way, guidelines could do more than offer a dispositionalist
clinician the right guide to assessing and treating a patient, they could promote a
dispositionalist approach to care. Rather than seeing guidelines as presenting ready-­
made options for a suitably assessed patient, then, guidelines would provide sugges-
tions for how to assess the situation and how to take various psychological and
social factors into account when making decisions with patients about their care.
Many of them, indeed, are already taking this task on.
Such an approach may seem complicated, but only if we hold on to the utilitarian
ideal of finding guidelines that maximise the utility of medical care over a popula-
tion. Once we have taken a dispositionalist turn, toward the particular patient and
the integration of a plurality of evidence types in order to focus on mutual manifes-
tation potentials, then it makes no sense to spend our time developing such rules, if
they are not also useful. Rather, it would be more natural to create guidelines that
work more like networks and databases, giving access to a constantly updating base
of evidence and resulting advice, and highlighting the fact that evidence collection
is a continuous process, not ending at the point of diagnosis and treatment choice.
Finally, we at CauseHealth recommend taking an ecological turn in medicine
(see Rocca and Anjum, Chap. 5, this book). Guidelines could be part of such a
major change in focus, away from specialist focus on different parts or systems of
the body, and toward integration with extra-physiological factors. Just as recogniz-
ing mutual manifestations, complexity and causal singularism also means that we
cannot best study a causal relation in isolation, we cannot expect to fully treat the
so-caused condition in a patient by isolating it from its context and environment (see
Price, Chap.7, and Low, Chap. 8, this book). Similarly, it is unlikely that a single
6 The Guidelines Challenge 109

guideline or set will fully treat that condition without also engaging the interacting
factors. Consequently, and importantly, guidelines need to express an acceptance
that many clinical decisions will be made in a state of uncertainty. We are unlikely
to know, even with the best evidence available, whether a treatment plan will work
in the predicted way, because it is unlikely that we will have full knowledge of all
the mechanisms, dispositions and, thus, causal relations that may interact with that
treatment in producing its effect in that particular patient. The ecological account,
that is, takes seriously the complexity of the kinds of interactions that influence an
individual’s health. Once we take the ecological nature of health and healthcare into
account, then, we see that the design of guidelines must also be a holistic process,
seeing guidelines as sets of intersecting advice and increasing awareness of possible
interactions—guidelines must be living resources, embodying both the uncertainty
and the expertise of the clinicians and patients who use them.

6.6 To Sum Up…

One of the key problems in medicine today, as the clinicians we have had the plea-
sure to work with have told us, is how to handle guidelines. Public management
approaches to medicine tend to promote guidelines as rules to follow, and clinicians
often feel pressure to follow a guideline even when their judgment cautions them to
do otherwise. This ‘tramline’ approach to guidelines, we have shown, is philosophi-
cally as well as practically problematic. Especially when we take dispositions as the
ontology of the causal relations that guidelines want to key in on—the best way to
cause a recovery, or to counteract the causes of a condition—we see that guidelines
cannot and ought not be treated as rules to be followed.
If this is taken seriously, then the development of guidelines must be more than
the collective effort of diverse experts on a particular category of disease or sub-­
group of patients. Rather, guidelines must give clinicians the tools to assess the
potential for mutual manifestations between the patient and the treatment options.
They must allow clinicians to be flexible with the treatment plan, making changes
as the treatment progresses and new evidence arises. And finally, their development
does not end with the creation of a rule, but rather continues with the collection of
that new evidence, taken back up into the guidelines to provide a continuously
improving resource for each new clinical encounter. These features are needed for
guidelines to be useful resources for clinicians, and we have used dispositionalism
to ground them in the very nature of causation. This chapter, then, has presented one
way in which the ontological assumptions we hold about medicine directly affect
how our medical institutions work.
110 S. Copeland

References and Further Readings

Anjum RL, Mumford S (2017) A philosophical argument against evidence-based policy. J Eval
Clin Pract 23:1045–1050
Anjum RL, Copeland S, Kerry R, Rocca E (2018) The guidelines challenge—philosophy, practice,
policy. J Eval Clin Pract 24:1120–1126
Dancy J (2004) Ethics without principles. Oxford University Press, Oxford
Gabbay J, le May A (2004) Evidence based guidelines or collectively constructed “mindlines?”
Ethnographic study of knowledge management in primary care. BMJ 329:1–5
Guyatt G, Cairns JA, Churchill D et al (1992) Evidence-based medicine. A new approach to teach-
ing the practice of medicine. JAMA 268:2420–2425
Petursson H, Getz L, Sirudsson JA, Hetlevik I (2009) Current European guidelines for manage-
ment of arterial hypertension: are they adequate for use in primary care? Modelling study base
on the Norwegian HUNT 2 population. BMC Fam Pract 10:70
Rocca E (2017) Bridging the boundaries between scientists and clinicians. Mechanistic hypotheses
and patient stories in risk assessment of drugs. J Eval Clin Pract 23:114–120
Rocca E, Copeland S, Edwards IR (2019) Pharmacovigilance as scientific discovery: an argument
for trans-disciplinarity. Drug Saf 42:1115–1124
Sackett DO, Rosenberg WM, Gray JAM, Haynes RB, Richardson WS (1996) Evidence based
medicine: what it is and what it isn’t. BMJ 312:71–72
Wieringa S, Dreesens D, on behalf of the AID Knowledge Working Group of the Guidelines
International Network et al (2018) Different knowledge, different styles of reasoning: a chal-
lenge for guideline development. BMJ EBM 23:87–91
Zuiderent-Jerak T, Forland F, Macbeth F (2012) Guidelines should reflect all knowledge, not just
clinical trials. BMJ 345:36702

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the copyright holder.
 Part II
Application to the Clinic
Chapter 7
The Complexity of Persistent Pain –
A Patient’s Perspective

Christine Price

7.1 Introduction

For several years I thought my persistent pain story started at the time I experienced
a manual handling injury, but now I know it didn’t, it started the day I was born. I
thought the pain was simply explained by the physical ‘damage’ in my back, but it
isn’t, persistent pain is much more complex. Before my injury, like everyone else, I
experienced pain periodically, for example when I fell over, when I sprained my
ankle or when I burnt myself on a hot pan. I assumed that pain meant I had physi-
cally ‘hurt’ a part of myself and that when it ‘healed’ the pain would stop. I didn’t
put much thought into what pain was or what it was affected by. I didn’t need to.
Following my injury, I travelled a long journey of discovery, learning about the
complexities of persistent pain and considering carefully how I could use that learn-
ing to better manage my pain. This is an account of that journey.

7.2 The Injury I Haven’t Recovered From

My severe pain started on a Saturday morning in July 2008. I’d spent the previous
2 weeks helping to clear out a large Victorian house ready for some improvements.
I had been doing a lot of heavy manual handling. I was told later by clinicians that
it was this intensive manual handling over a short time period that likely led to my
resultant back difficulties.
Shortly after breakfast, my husband and I headed off to a local beauty spot. On
the journey out, I could feel my right leg starting to hurt. It was annoying, but noth-
ing too bad, and not enough to stop us going. However, by the time we arrived home

C. Price (*)
Bournemouth, England, UK
e-mail: christine@cprice.me.uk

© The Author(s) 2020 113

R. L. Anjum et al. (eds.), Rethinking Causality, Complexity and Evidence for the
Unique Patient, https://doi.org/10.1007/978-3-030-41239-5_7
114 C. Price

for lunch I was in a great deal of pain. By early afternoon I was experiencing severe
pain in both my back and my leg, and I could barely walk. The pain had progressed
quickly. The severe pain continued the next day, and my husband called out a gen-
eral practitioner. Armed with strong painkillers I assumed that things would settle,
however Monday morning saw no improvement, and if anything, the pain was
worse. I was totally unable to walk, even as far as the bathroom. I phoned 101 for
advice, and they called out an ambulance. I was taken by the ambulance to hospital.
My L5-S1 lumbar disc had herniated and it was compressing my S1 nerve root. I
was experiencing excruciating back pain and neuropathic pain. I was started on a
range of strong painkillers, including morphine.
After 5 days in hospital I was discharged home. For several weeks I struggled to
walk more than a few paces and I struggled to sit down or stand. Despite the power-
ful medication I was still in intense pain. September came around and I was deter-
mined to go back to my job as a teacher for the beginning of term. I was lucky, my
headteacher was extremely supportive and allowed me to work flexibly.

7.3 Being Treated Within a Narrow View of Pain

I struggled on for many months. I was given epidural injections, very powerful pain
medication, and some physiotherapy. Eighteen months after my injury I had back
surgery, but unfortunately by then my S1 nerve root had been permanently damaged
and surgery did little to relieve my pain. Following advice from a clinician I left the
physical demands of teaching and January 2010 saw me start a new part-time self-­
employed life, which eased my pain situation considerably. I have never looked back.
I was given further injections, further medication and further physiotherapy.
Eventually I was told there was little more that could be done for me apart from
implanting a spinal cord stimulator. I was duly put on the spinal cord stimulator
pathway.
For the first few years most of my discussions with the various clinicians revolved
around medications, injections and surgery. I knew no different, and certainly was
not adequately equipped to challenge this or move my care into something more.
My pain management skills were minimal and centred mainly on managing medica-
tions. I was experiencing daily debilitating pain. The ‘medical’ interventions were
not helping me sufficiently. Most of the physiotherapy I received had limited suc-
cess for me. Although I was being given some basic advice during physiotherapy
sessions, I didn’t really understand why my body was constantly in pain, what the
triggers for my pain were, and what the realistic likely outcomes were for me. I
simply didn’t understand persistent pain or how I could better manage my pain. I
didn’t know how to move my pain situation further forward, despite my best endeav-
ours to do so. I was struggling day to day.
7 The Complexity of Persistent Pain – A Patient’s Perspective 115

7.4 Starting to Learn About the Complexity of Pain

Around 4 years after my injury I was fortunate to receive an episode of care under-
taken by Advanced Scope Physiotherapist Matthew Low. It was through this that I
started my journey towards understanding persistent pain and how better to
manage it.
Matt’s approach was entirely different to previous physiotherapists. He focussed
on improving my functional abilities and minimising my maladaptive compensation
methods, which other physiotherapists had not done. He also started to teach me to
understand persistent pain, and in particular my persistent pain, and how to manage
it better. Matt demonstrated a genuine interest in both my pain story and me as a
person. He used sensitive non-judgemental questioning, and carefully prompted me
when needed in order to better understand my narrative. Through the sessions he got
to know me as an individual and I felt valued. I felt an equal partner in my care, and
I trusted him. I felt I was able to disclose anything about my pain, including the
irrational fears and emotions it was causing me to experience.
Matt recognised that my understanding of pain, in particular my pain, was pretty
low. He combined verbal, pictorial and physical explanations with suggestions for
reading outside of the physiotherapy sessions in order to improve my basic under-
standing of pain. He skilfully revisited and extended my understanding throughout
the episode of care. I entered this episode of care thinking that persistent pain was
basically unidimensional (i.e. there was something physically wrong with my back
at that moment in time and it was therefore responding with pain). Matt explained
that persistent pain is much more complex and affected by many different things,
including what I do during the day and my emotions. This learning was hugely
important for me. It opened the door to me understanding what in simple terms
might be feeding into my pain, and even more importantly what I could try and do
to self-manage my pain. I left that episode of physiotherapy care with a much better
understanding of the complexity of pain, and with much better pain manage-
ment skills.
Following this episode of care, I took a personal decision to stop all medications,
and to rely purely on pain management techniques. I withdrew from the spinal cord
stimulator pathway. Armed with my new understanding of persistent pain I worked
on minimising my stress levels, remaining positive, boosting my resilience and
making adaptations to my personal life, work and home. This helped to minimise
and manage my pain and I was able to live a much richer, more pain-free and more
fulfilled life.
This approach to pain management worked well for several years but when my
personal circumstances changed, partly through a change in my self-employment,
my pain began to be more problematic for me. I felt I needed some more profes-
sional input and so I asked to be re-referred to Matt. Despite the intervening years,
Matt and I were able to pick up almost where we left off. The strong therapeutic
alliance we had built up together remained.
116 C. Price

Since my first episode of care Matt had become an NHS Consultant

Physiotherapist, and a key member of CauseHealth. Pain science had moved for-
ward, and predictive processing had become a key focus for research. Whilst Matt’s
knowledge and skills had further improved, mine had taken a turn for the worse. I
remained fully on board with the basic idea that persistent pain is complex and
involves more than just the pathology that I presented with. However, during these
intervening years I had heard and read various bits and pieces about back condi-
tions, sciatica and pain, which had just served to confuse my understanding of pain,
and in particular my pain. During this second episode of care, as well as working on
the physical difficulties I was presenting with, Matt patiently took me through the
basics of understanding pain once more. He also introduced me to causality, dispo-
sitionalism and predictive processing (see Low, Chap. 8, this book).

7.5 Learning About Causality and Dispositionalism

Before I could evaluate whether the concepts of causality and dispositionalism would
be able to help my understanding, and management, of my persistent pain, I needed
to first explore and understand them. In order to aid, and test out, my understanding
of causality and dispositionalism, I created the following smallholding analogy.
The analogy is based on a smallholding commune, with individual commune
members working together to benefit the whole. It considers how the individual
members’ dominant traits, or dispositions, dynamically vary, interact and affect the
commune, sometimes resulting in a healthy commune and sometimes in an
unhealthy, or unwell, commune. The way the smallholding commune works in
terms of having a number of dispositions dynamically varying and interacting with
one another, resulting in a healthy or unhealthy outcome, compares well to that of
an individual person. Every individual person has a unique range and combination
of traits, or dispositions, that dynamically vary, interact, and act as causal factors in
the health of that person.

7.6 A Smallholding Analogy

Nine young friends decide to club together to buy a smallholding in a beautiful part
of Dorset. Everyone will help grow food on the land, care for their animals and look
after the smallholding. The aim is to have a vibrant, happy, hardworking, outward
looking commune with enough food on the table, and maybe even some to sell.
Each of the friends has one particularly strong trait, or disposition:
Carl – catastrophising
Henry – hypervigilance
Amy – anxiety
7 The Complexity of Persistent Pain – A Patient’s Perspective 117

Debra – depression
Sue – sleep difficulties
Patricia – positivity
Rebecca – resilience
Tammy has experienced trauma
Danny has low blood pressure.
Some of these dispositions may have been present from birth, e.g. anxiety, whilst
others may have been affected by their upbringing, e.g. resilience. Some disposi-
tions may be related to their physical body, such as low blood pressure.
Each friend’s strong traits, or dispositions, vary in intensity over time, often
depending on interactions with one another and what else is going on in life for
them, including their physical health. Some friends have a stronger individual influ-
ence on the rest of the group than others, for example Debra is a strong influence,
whilst Rebecca has a much lower influence.
Each hour, each day, each week and each month is different in the commune. One
day might include Amy being highly anxious, Debra’s depression being minimal,
Tammy being troubled with memories of her trauma and Rebecca’s resilience being
high. On other days there will be a different mix of the friends’ dispositional levels.
The following vector diagram (see also Anjum, Chap. 2, this book) illustrates the
friends’ levels of dispositions at a good time (Fig. 7.1). The dispositions represented
by vectors to the left of the centre line are ‘negative’ and likely to cause the friend’s
difficulty, whilst those to the right are ‘positive’.

Debra (depression)

Amy (anxiety)

Tammy (trauma)

Sally (sciatica)

Sue (sleep difficulties) Patricia (positivity)

Danny (low blood pressure) Rebecca (resilience)

Strong influence
Medium influence
Lower influence

Fig. 7.1 Dispositions on a good day

118 C. Price

Debra (depression)

Amy (anxiety)

Tammy (trauma)

Tammy (PTSD)

Henry (hypervigilance) Patricia (positivity)

Carl (catastrophising)

Sue (sleep difficulties)

Strong influence Danny (low blood pressure) Rebecca (resilience)

Medium influence
Lower influence

Fig. 7.2 Dispositions on a difficult day

The length of the vectors is an indication of the level of each disposition at that
time. The colour of the vectors indicates the strength of their influence. The vector
diagram above illustrates the friends’ levels of disposition at a more difficult time
(Fig. 7.2).
In such a close community, the friends will inevitably have an impact on each
other. For example, when Tammy becomes overwhelmed by memories of her
trauma and discusses them with Amy, then Amy may find her anxiety becomes
worse. Sue may not have had any sleep difficulties for some time but as she listens
to Tammy’s stories, her tendency, or disposition, to sleep difficulties may become
triggered. Patricia’s positivity may have a beneficial effect on all the friends. It could
also happen that when Tammy and Amy get together the effect of Amy’s anxiety on
Tammy may mean that Tammy develops a new, second disposition of PTSD (Post
Traumatic Stress Disorder). This new disposition of PTSD has ‘emerged’ from the
dispositions of anxiety and trauma.
As well as changes within, and between, the friends themselves, there are other
factors affecting the friends. Some of the factors are environmental, for example
whether the heating is working or not or whether there is a storm outside. Some may
be financial. A bill for repairs to the roof may have come in or some money may
have been left to the friends in a will. Some may be social. One of the friend’s fam-
ily may be causing difficulties or the neighbours may be upset by their barking dogs.
Some may be biological. Some of the friends may have become unwell with a virus.
7 The Complexity of Persistent Pain – A Patient’s Perspective 119

All these factors will affect the friends differently. For example, Amy may become
anxious over financial concerns and Sue may find it difficult to sleep when there is
a storm outside. At such times Rebecca’s resilience may reduce.
When everyone is at their best, the heating works, the weather is good, the friends
have enough money, their families are supportive, they have no extra physical ail-
ments and they are working well together the ‘health’ of the commune is good. The
commune is ‘healthy’, and the friends are happy and contented. At this point the
group of friends could be considered to have developed a new disposition, that of
being a community of mutual support. This mutually supportive community may
well provide positive benefits to its members. For example, Carl may benefit from
the support of the commune and cease to be hypervigilant in that environment. If
Carl moved out of the commune then he may be able to maintain this benefit, for at
least a period of time. However, if he then moved into a more dysfunctional com-
munity, then this hypervigilance would likely return.
Life isn’t always good for the commune, though. As the friends vary, including
for example Amy becoming more anxious, Catherine catastrophising and Debra’s
depression becoming more prominent, then things might start to get a little harder
for them. The commune becomes less ‘healthy’, although outwardly it may still
appear to be fine, the friends may still be reasonably content, and the commune may
still be functioning.
Unfortunately, at some point in time the commune may cross a ‘threshold’ and
become ‘unhealthy’ or ‘sick’. It is impossible to predict what combination of the
friends’ levels of dispositions might cause this to happen. The threshold could be
crossed due to a combination of Amy experiencing high levels of anxiety, Sue hav-
ing substantial difficulties sleeping, Debra suffering moderate levels of depression
and Rebecca’s resilience being unusually low. However, it could be crossed due to
a completely different combination. No one friend in isolation is likely to cause the
threshold to be crossed, it is the novel mix of their levels of dispositions at that
moment in time that causes this.
It may be that the commune oscillates around the threshold, being ‘healthy’ at
times, and being ‘unhealthy’ and struggling at other times. I find it useful to repre-
sent the interactions of the dispositions as a circular vector diagram. The diagram in
Fig. 7.3, based on the vector diagram above for a good day (Fig. 7.1), represents the
‘health’ of the commune on that good day. Each oval is a representation of the
strength and level of each friend’s disposition. Dispositions within the circle are
negative, whilst those outside the circle are positive. The dotted circle is a represen-
tation of a dynamic ‘threshold’ which shows the commune’s ‘capacity’ for health.
The higher the level of positive dispositions, the bigger the ‘capacity’ of the com-
mune to be healthy.
The diagram in Fig. 7.4 is based on the vector diagram for a difficult day (Fig. 7.2)
and represents the health of the commune on that particular difficult day. We see that
the representation of the dispositions crosses the capacity ‘threshold’, which is now
smaller than it was on a good day.
As the commune becomes ‘unhealthy’ or ‘sick’ it starts to struggle. Everything
becomes harder and some of the friends’ individual traits may worsen. This serves
120 C. Price

Fig. 7.3 A dynamic threshold for health

Fig. 7.4 Threshold on a difficult day

to maintain the unhealthy situation, maybe even making it worse. The circle, or
threshold, is smaller this time, in line with the levels of the positive dispositions
being smaller, and so the ‘capacity’ of the commune to be healthy is reduced.
Once the commune has crossed over the threshold and become ‘unhealthy’ or
‘sick’ then it can be difficult to improve the situation and get it back over the thresh-
old to become a healthy commune once more. There is unlikely to be a quick ‘fix’.
There is unlikely to be a single ‘cause’ that can be addressed in isolation in order to
fix the problem. For example, just a clinician supporting Debra to improve her
depression may not have enough of an impact on the overall complicated mix of the
7 The Complexity of Persistent Pain – A Patient’s Perspective 121

friends’ dispositional levels and therefore the commune. It may also not be effective
without addressing, for example, the commune’s financial difficulties at the
same time.
Improving just one friend’s dispositional level is unlikely to improve the mix
enough to bring the commune back over the threshold. Attention needs to be paid to
the multiple factors, or causes, including both the friends’ dispositional levels and
the external factors, such as finances, social relationships etc. that impact on them.
Professional input could be helpful in addressing the variety of factors. For exam-
ple, support in resolving financial difficulties, support with depression or support
with any medical conditions such as low blood pressure. Advice could be given to
help support the commune self-manage their situation more effectively. As well as
trying to reduce the levels of the more negative dispositions, such as Debra’s depres-
sion and Amy’s anxiety, then boosting the more positive dispositions could help the
group. For example, boosting Patricia’s positivity might help ‘lift’ the group.
Supporting all the friends, in a variety of different ways, will give the best chance
for the group to rise back above the threshold and become a healthy, happy, produc-
tive commune once more.

7.7 The Analogy Explained

We all have a unique set of traits, or dispositions. An individual’s dominant traits, or

dispositions, might be, for example, anxiety, hypervigilance, catastrophising,
depression, sleep difficulties, positivity and resilience. That individual may also
have experienced trauma and have low blood pressure. These dispositions will vary
and interact, as they did in the commune.
In the same way these dispositions were affected in the smallholding commune by
external factors, such as unexpected bills or social problems, they will be affected
within an individual. For example, an impending court case might cause an individual’s
anxiety levels to rise, or a break up with a partner might cause depressive levels to rise.
Sometimes, a specific mix of the relative strengths, weaknesses and interplay of
these dispositions may cause that individual to cross a ‘threshold’, which is unique
to that individual, and they may become unwell. The individual’s unique genetic
makeup, existing health and health dispositions will be factors in the presentation of
their illness. For example, at any one time, one individual may be pre-disposed to
suffering Chronic Fatigue Syndrome, whilst another may be pre-disposed to suffer-
ing a chronic pain condition, or generalised anxiety disorder or maybe shingles.
This doesn’t of course mean that individuals who are happy, stress free and who
have few outside pressures do not become unwell. One of their dispositions, or
causal factors, may be physical, for example in my case I have a damaged S1 nerve
root. This factor may be very dominant, either in short bursts, or for extensive peri-
ods, so causing the individual to cross a threshold, in my case of pain, for either a
short or long period of time. Although this factor may be dominant, all the factors
still vary and interact together, giving a varying experience of pain and wellness.
122 C. Price

In terms of recovery, or improvement, in the same way that the causal factors
associated with the smallholding commune becoming unhealthy are complex, so it
is with the individual. Trying to address one factor alone is unlikely to improve an
individual’s situation enough to allow them to cross back over the threshold and
return to good, or better, health. A wide-ranging approach is needed. This might
include the need for mental health support, GP support, counselling, peer group
support and social support.
Crossing back over that threshold and returning to good, or better, health is not
always easy. Perhaps the most important first step for that individual is to under-
stand that there are many causal factors involved, which dynamically vary and inter-
act with each other. These causal factors ideally need to be supported and addressed
together.

7.8 Combining Causality, Dispositionalism

and Predictive Processing

I currently mainly suffer from neuropathic pain, caused by ‘damage’, and ongoing
irritation, to my S1 nerve root. I wanted to know how the nerve signals being gener-
ated from this nerve root, often spuriously, might be processed in me as pain and so,
with Matt’s help, I sought to understand the predictive processing model of pain.
Fundamentally the predictive processing model of pain considers peripheral sensi-
tisation, and looks at how anxiety, emotion, expectation and attention may change
and impact pain. With the help of Matt, I was able to combine the basic concepts of
causality, dispositionalism and predictive processing to come up with a simple
understanding of MY pain that works well for me.

7.9 A Simple Understanding of My Pain

I have in my mind/body a ‘model’ (predictive model) which informs me as to

whether to give an experience of pain or not, in a variety of circumstances, based on
presenting factors. When a part of my body, in this case my damaged S1 nerve root
(which may be being irritated by, for example, position, load or temperature), emits
an ‘impulse’, then my predictive model considers this factor, along with other fac-
tors, to evaluate whether to give an experience of pain or not. These factors include
my current novel mix of the levels of my traits.
I have a number of personal traits, or dispositions, which vary over time. For
example, I have a tendency, or disposition, towards anxiety and poor sleep. I am
naturally positive and have high resilience. I experience interaction between these
dispositions. For example, my sleep is likely to be worse when I am anxious, and
my resilience is likely to be reduced when I am sleep deprived. Some of these
7 The Complexity of Persistent Pain – A Patient’s Perspective 123

dispositions have a stronger influence than others on my presentation, for example

anxiety and poor sleep have a greater impact on me than positivity. I am also affected
by external factors. For example, my anxiety will increase if I experience work
place bullying or an unexpected household bill, and my positivity will increase
whilst experiencing success. I have an ever-changing novel mix of the levels of my
dispositions. At a ‘good time’, my anxiety might be low, my positivity high and I
might have had good sleep. At a ‘bad time’, my anxiety may be high, my resilience
low and my sleep poor.
My predictive model ‘knows’ what combination of dispositional levels and other
factors, including the impulse from my S1 nerve root, are likely to be ‘ok’ and don’t
need a response of pain. If the combination of factors at a moment in time, including
the ‘impulse’ from my S1 nerve root (which is likely for me to be a dominant fac-
tor), matches the predictive model of being ‘ok’, then no action is taken, and no pain
emerges. If not, then pain emerges to alert me to do something to stop the irritation
on the S1 nerve root continuing. Changes in the novel mix of my dispositional lev-
els, and my S1 nerve root impulse, may, or may not, be sufficient to change whether
I experience pain or not.
My experiences inform my predictive model. These experiences might result in
the predictive model being changed. In order to improve my pain situation, then I
would need to work on optimising my personal factors, e.g. anxiety, sleep, resil-
ience and positivity, my physical factors, e.g. S1 nerve root irritation and also exter-
nal factors, e.g. temperature, finances and work conditions. This is because my
predictive model takes the combination of these factors into account when deciding
whether to give me a pain experience following an impulse from my S1 nerve root.
Improving one factor only is unlikely to bring about sufficient change.

7.10 How Has Understanding Pain in This Way Helped Me?

Understanding pain has been hugely important to me in terms of my learning to

manage my pain situation and lead as full and fulfilled a life as possible. Having a
narrative in my head about what is likely affecting my pain and what is happening
with my body, which I can fully identify with, is very important to me. It provides
me with the confidence to try different things, cope when I am experiencing a flare
of symptoms, work out different ways of doing things in order not to ‘wind up’ my
condition and generally live well despite living in pain.
Although important, on its own this understanding isn’t enough to successfully
manage my pain condition on a day to day basis. I need to use this understanding to
seek ways to manage and improve my condition and continue to live as well as
possible.
In overall terms I view my pain management situation as needing to reduce the
physical irritants on my S1 nerve root, and to optimise my personal, social, health
and emotional factors. I also need to consider, and hopefully address, any negative
thoughts, beliefs and past experiences which might be acting as factors in my pain
124 C. Price

Fig. 7.5 Mind map illustrating the complexity of my pain

experience. As part of this I need to recognise, and hopefully improve, any negative
dispositions I have, such as anxiety, and build on my positive dispositions, such as
my resilience and having a naturally positive outlook.
I created a mind map (Fig. 7.5) to highlight the areas I need to attend to if I want
to live as pain free a life as possible.
The mind map is complex, reflecting the complexity of pain. There are some S1
nerve root specific elements, for example using soft cushions when sitting, keeping
my right leg warm etc. There are also elements that are more general, for example
good sleep hygiene, enjoying good friendships and reducing anxiety.
It is hard to address all these factors at the same time when trying to improve
pain, and it is hard to work out whether the measures you are taking are having a
positive impact on your pain, or not. In order to provide a focus for improvement,
and to track my improvement, I decided to use the idea of vector diagrams. The vec-
tor diagram in Fig. 7.6 shows factors I identified as being the main contributors and
improvers to my pain experience in January 2018. The length of the vector gives an
indication of the ‘size’ of the factor, as I saw it at the time. The red vector at the bot-
tom gives an overall indication of the ‘size’ of all the pain contributors combined,
and the green vector at the bottom an overall indication of the ‘size’ of all the pain
improvers combined. The aim is to decrease the pain contributors and increase the
pain improvers as much as possible.
The diagram in Fig. 7.7 shows how I rated the same factors in August 2018.
Notice that there are some elements I have been able to change, but some that have
stayed static. More work to do!
Using vector diagrams works well for me. They give me an instant visual indica-
tor of the problems I have chosen to work on, and I can see visually whether I am
making progress with those elements or not, and how much progress.
In my experience clinicians put more emphasis on negative pain factors, the pain
contributors, but I think it is helpful to put an equal emphasis on positive factors, the
pain improvers. When you are in pain it is far too easy to focus on the negative. I
find putting an equal focus on positives really helps to take control of my pain situ-
ation and move it forward.
7 The Complexity of Persistent Pain – A Patient’s Perspective 125

Fig. 7.6 The main contributors and improvers of my pain in January

Fig. 7.7 The main contributors and improvers of my pain in August

7.11 The Complexity of Persistent Pain

During the first few years following my manual handling injury I was treated pre-
dominantly, if not solely, within a ‘medical’ model. I had no understanding that
persistent pain was complex, and looked only to physiological factors, medications
and surgical interventions. I struggled badly with the pain I was experiencing and
had few pain management skills.
126 C. Price

Following interventions by physiotherapist Matthew Low I was introduced to an

understanding that persistent pain is inherently complex. Through my understand-
ing of causality, dispositionalism and the predictive processing model of pain, and
with Matt’s help, I have been able to come to a much better understanding of pain,
and in particular my pain. Understanding that persistent pain is inherently complex
has enabled me to develop my pain management skills, focussing them on a wide
variety of causal factors.
Good understanding and good pain management has enabled me to lead a much
richer, more pain free and more fulfilled life.

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Chapter 8
Above and Beyond Statistical Evidence.
Why Stories Matter for Clinical Decisions
and Shared Decision Making

Matthew Low

8.1 Musculoskeletal Disability

Musculoskeletal (MSK) disability has an enormous effect on the quality of life of

millions of people worldwide. In the UK alone:
• One in four, or around 9.6 million UK adults, many of working age, are affected
by MSK disability.
• 30% of GP consultations in England are MSK related (Department of
Health 2006).
• 10.8 million working days are lost per year due to MSK conditions. A large num-
ber of co-morbidities, including diabetes, depression and obesity are associated
with MSK conditions (Arthritis Research UK 2013).
• In 2013, more than 25% of all surgical interventions in the National Health
Service are MSK related and this is set to rise over the following 10 years
(Arthritis Research UK 2013).
• In 2012, £4.76 billion of National Health Service spending each year is on MSK
conditions (Department of Health 2012)
I work as a Physiotherapist in the UK, helping people with MSK disability.
Patients are often referred to me because they have not improved with previous
treatment. I receive requests from diverse other healthcare professionals such as
Orthopaedic Surgeons, Rheumatologists, General Practitioners, Geriatricians,
Neurologists, Psychologists as well as other Physiotherapists and Occupational
Therapists. MSK conditions can be treated in a number of ways, using diverse treat-
ment approaches, in varying sequences and concentrating on different aspects of a
presentation. Some conditions may improve by focussing on lifestyle factors, others
by addressing physical or psychological factors.

M. Low (*)
The Royal Bournemouth and Christchurch Foundation NHS Trust, Christchurch, Dorset, UK
e-mail: Matthew.Low@rbch.nhs.uk

© The Author(s) 2020 127

R. L. Anjum et al. (eds.), Rethinking Causality, Complexity and Evidence for the
Unique Patient, https://doi.org/10.1007/978-3-030-41239-5_8
128 M. Low

Even these categories of influencing factors may be misnomers, due to the inter-­
relations among them. Exercise, for example, may be described as a physical inter-
vention, but has clear psychological effects and requires confidence and motivation
to perform. Exercise also exists within a social situation, environment and circum-
stance. Physiotherapists are privileged in that they, within an accepted social con-
text, have permission to touch, hold and physically assist people through movement
in both assessment and treatment. This is a tacit form of communication as well as
a method of therapeutic interaction and may assist with the re-education of move-
ment, perhaps by building confidence or trust in one’s body through physical reas-
surance. It is for these reasons that Physiotherapists and other Physical Therapists
commonly see people with MSK conditions.
The field of MSK has always interested me; like a detective, who would try to
investigate and scrutinise all the evidence to catch the criminal, an MSK practitioner
needs to unpack the complexity of a person and their symptoms to get to the heart
of the matter. When first learning about being an MSK practitioner, it seemed to me
that if you knew all of the research data, or had all the knowledge of the pathology,
the rest would just fit into place. Very quickly, however, I found out that this is not
the case. There are many skills and types of knowledge—particularly about peo-
ple—that are required. It is not all about knowing the numbers.
The majority of the patients I see present with their main symptom being pain. Pain
has been described by some in practice and research in an objective and impersonal
way, such as on a scale between 0 and 10. This may suit quantitative research designs
but in no way shape or form does this describe how pain affects a person. Every person
has individual hopes, thoughts, feelings, aspirations, abilities, relationships and biog-
raphies. The idea of trying to assign a numeric value to these very individual and per-
sonal aspects of life seems to me to be both counter intuitive and destructive. In fact, it
is an unreasonable expectation that one could examine each aspect independently
without regard to the whole person—they play a role not only in a person’s life, but in
relation to how they experience their pain. I always focus on a person’s pain experience.
A person’s pain experience usually has a significant impact on what a person can
or cannot do. They lose their agency, which is a person’s ability to participate in the
everyday things that they want to do, such as the normal activities of daily living,
but also in things that are meaningful to them, such as family activities, sporting
activities and so on.
The patients I tend to see also suffer with persistent pain. By that I mean that the
pain has lasted longer than would normally be expected—it has not resolved within
an expected time frame. Most patients attend their appointments with me without
providing a specific history of injury or trauma, and I can see that their symptoms
have gradually worsened over a period of time, often without a clear reason. Some
of the problems with pain are that it manifests in a very individual and personal way,
it affects relationships, and it changes depending on the situation and circumstances
of the environment that a person lives in. Pain is inherently context dependent. By
that I mean, amongst a number of things, that a person’s history and current situa-
tion can change the experience of pain. For instance, if a person is running away
from a potentially life threatening situation, they may not feel their ankle break
8 Above and Beyond Statistical Evidence. Why Stories Matter for Clinical Decisions… 129

when they twist it, but after experiencing something like that, they might at another
time feel severe pain when gently rolling their ankle as they walk over uneven ground.
The non-specific nature of persistent pain presents a number of challenges, particu-
larly if one assumes a biomedical perspective. A biomedical viewpoint is a traditional
and very successful form of medicine that assumes a linear interaction between cause(s)
and effect(s). An example of this would be identifying a bacterium that causes a disease
(such as tuberculosis) and treating it by using antibiotics (medications that affect a
bacterium’s cell wall or change its genetic makeup) that then eradicates the bacterium
and consequently the disease, and thus the symptoms are cured. In MSK conditions,
however, the cause(s) are usually multi-dimensional and are inter-connected with other
causes, which interact in ways that are not predictable. For example, in low back pain,
a person may suffer with severe symptoms of pain and disability and the tests (such as
x-ray, magnetic resonance imaging and blood tests) are unable to identify a specific
cause and the diagnosis is therefore typically labelled as non-specific low back pain.
The research literature suggests that the majority of cases of low back pain in
primary care are non-specific (Koes et al. 2006). There are people who present with
specific causes of back pain, sometimes serious, but their symptoms are usually
very atypical in that they affect a person’s systemic health, leading to weight loss,
malaise, fever, or night pain with sweats, none of which are in keeping with an MSK
disorder. These presentations are rare and the medical literature suggests that they
constitute 1–2% of cases (Koes et al. 2006). Therefore, in addition to the challenges
presented by non-specific back pain, such as a lack of an easily identifiable causal
relationship to focus on treatment, even those with specific diagnoses present with
the challenge of having a distinct and personal symptom profile.
In order to make sound and clinically reasonable decisions for the treatment of
MSK disorders, a practitioner needs to take these challenges into account. Therefore,
a coherent strategy based upon the judicious collection of pertinent information and
evidence that is centred on the patient is of paramount importance. Understanding
the clinically relevant and biographical context is needed to begin to unpack the
clinical picture and the only valid source for this evidence comes from the clinicians
and patients themselves. However, many healthcare scientists and practitioners may
not trust the information provided about a condition or treatment from a clinician or
patient as it may present a number of confounding factors, including bias, based on
personal experience or anecdotal information. Such untrustworthy information may
cloud judgement and lead an optimal therapeutic strategy astray. To overcome this,
a movement of evidence based medicine (EBM), or evidence based healthcare
(EBHC), came about in the early 1990’s.

8.2 Evidence Based Healthcare: The Heart Is in the Right

Place, But…

EBM is explicitly cautious about justifications for treatments that are not grounded
in ‘trustworthy evidence’. The EBM and EBHC framework states that degrees of
trustworthiness can be described in a hierarchy of evidence, in which research
130 M. Low

evidence generated by controlled trials is valued higher than the evidence generated
by uncontrolled trials. In short, the EBHC movement acknowledges “the role of all
empirical observations”, however, “it contends that controlled clinical observations
provide more trustworthy evidence than do uncontrolled observations, biological
experiments, or individual clinician’s experiences” (Djulbegovic and Guyatt 2017).
This is due to the three main principles that EBM is based upon, according to
Djulbegovic and Guyatt (2017). Firstly, “not all evidence is created equal, and… the
practice of medicine should be based on the best available evidence.” Essentially,
those observations drawn from any uncontrolled methodology such as clinical
expertise are ranked as the lowest form of evidence, due to risk of bias, and ran-
domised controlled trials (RCT) are ranked as the highest form of evidence.
Secondly, EBM represents “the philosophical view that the pursuit of truth is best
accomplished by evaluating the totality of the evidence, and not selecting evidence
that favours a particular claim.” Consider that co-morbidities are usually excluded
from high quality research trials and therefore are not reflective of the reality of
clinical practice. That is, for a study population, a treatment may seem to have been
‘effective’ for a particular condition, but in practice, for the same treatment the pres-
ence of co-morbidities may cause harm. Paradoxically, it is the judgement of the
clinician that is required to evaluate and synthesise the totality of the available evi-
dence within the context of the individual patient and their environment, including
taking into account various co-morbidities that exist in the clinical setting. Yet it is
this clinical judgement that is felt to be untrustworthy in the first place.
Efforts are made to reconcile the paradox in the third and last principle: “Evidence
is, however, necessary but not sufficient for effective decision making, which has to
address the consequences of importance to the decision maker within the given
environment and context. Thus, the third epistemological principle of EBM is that
clinical decision making requires consideration of patients’ values and preferences.”
But, this appears to ‘bolt on’ patient preferences to the end of the aforementioned
principles and then offer no insight on how to gather the complexity of evidence
together in a person centred way.
One of the natures of ‘truth’ that the EBM/EBHC movement implicitly suggests,
is that statistics, given the ‘objective’ status of statistical methods, have a higher
‘truth’ value than other sources of evidence, such as subjective or inter-subjective
accounts (e.g. through the sharing of language, experience and understanding)
(Øberg et al. 2015). The analyses of studies are often communicated to patients in an
absolute or deterministic way, usually in the form of data such as the statistical sig-
nificance of a finding, the size of a treatment effect, the confidence interval, or the
probability of outcome. This assumes a specific philosophical view of what causality
is, namely a Humean view of causality (see Anjum, Chap. 2, and Anjum and Rocca,
Chap. 4, this book). On the one hand, the clinician may feel confident that the infor-
mation is ‘factually correct’, but on the other hand the clinician is assuming that the
information that they are providing to the patient recognises all eventualities and all
contexts. However, in reality they are giving information based on a ‘closed world’
where many factors have been controlled for: a world distinctly separate from that of
the open, complex and context sensitive world that the patient actually exists within.
8 Above and Beyond Statistical Evidence. Why Stories Matter for Clinical Decisions… 131

I am not suggesting that epidemiological data or carefully controlled RCT’s are

not helpful, in fact they can be seen as the best available way to understand an aver-
age treatment effect on an average person from a clinical trial. This could act as a
baseline measure of how effective a treatment may be, but RCT’s need to be seen in
full light of the limitations that they have, rather than being put up on a pedestal
where they are interpreted as the facts of the matter that determine clinical deci-
sion making.

8.3 Therapeutic Alliance: A Dispositional View

EBM/EBHC has been described as a map that creates guidelines for treatment or
intervention. As has been shown above, however, EBM/EBHC may serve as a map
but it does not describe the terrain. The treatment effects of a person who has such
individuality, with a complex, sensitive and biographically inscribed biology, sim-
ply cannot be reduced to a sequence of recurring events that are seen to occur time
and time again. In other words, the Humean view of causality will not do. A dispo-
sitional view of causality, however, has the ability to change the perspective of both
the clinician and the patient, moving them toward a much clearer perspective that
embraces such complexity.
To recap from Part I of this book, causes are dispositions or ‘powers’ that may
tend toward an effect rather than necessitate one. They can operate amongst other
dispositions and may lie unmanifested but still be present—they may, for example,
still be acting in a way that creates a stable situation, but in such a way that no
observable effect is seen. In addition, they interact in non-linear ways and depend-
ing on context. This, in my mind, makes absolute sense and accounts for the appar-
ent discrepancies of observed events, but also forms a distinctive and clinically
relevant framework for helping people (Low 2017).
Rather than assessing a person, establishing a diagnosis and then looking to the
research evidence to inform us how to treat a patient with their preferences, our atten-
tion should be particularly drawn towards the person’s story. A person’s story is a
phenomenological account that far supersedes that of a descriptive and categorical
diagnosis with regards to how to frame and personalise a treatment or management
approach. A categorical diagnosis may provide clinical options for treatment but they
are often shaped within broad guidelines. An example of this would be ‘education,
exercise and weight loss’ for the management of hip osteoarthritis. A person’s story
establishes a unique biography that sets up the clinical context by opening a window
of insight into a person’s biology. For example, a person’s challenging childhood
may shed light on their behaviour towards comfort eating and the complex relation-
ships they may have towards those who may be able to support them. What then lies
beneath the statistical data is a person who has hopes, fears, relationship and lifestyle
considerations, as well as a rich number of historical events that have influenced them.
The understanding of a person’s story can elicit copious amounts of causal ele-
ments that are essential, not only for the clinician but for the patient, in understanding
132 M. Low

and coming to terms with their pain experience. These causal elements, or disposi-
tions, can be inferred through the creation of a co-constructed narrative. Both the
patient and the clinician bring their understanding together within a space where they
each attempt to make sense of the situation. This sense-making is inter-­subjective;
the clinician is interpreting and coming to terms with what the patient is explaining,
demonstrating and exploring while in exactly the same way, the patient is trying to
make sense of the clinician’s thoughts, feelings and perspectives. I believe that recog-
nising that this sense-making process, that is bi-directional between therapist and
patient, is essential to building a strong, therapeutic alliance. There is emerging
research evidence to support the idea that having a strong therapeutic alliance
improves pain outcomes in patients with persistent pain. Factors such as trust, open
communication, using a whole person approach, tailoring an individualised plan and
the ability to work through challenges in the patient-­clinician relationship have all
been identified as enhancing this alliance (Kinney et al. 2018; Bunzli et al. 2016).
Often, in graduate and postgraduate training, a clinician is asked to divide a clini-
cal consultation into subjective and objective phenomena. The ‘subjective’ informa-
tion is the information that the patient gives to the clinician, including their story
and the ‘objective’ information is the clinician’s observations, measurements and
judgements. This way of understanding ‘subjective’ and ‘objective’ phenomena
undermines the patient as it assumes that the clinician’s observations and judgement
are objective whilst the thoughts, beliefs and perspectives of the patient are ‘subjec-
tive’ and therefore questionable. It is therefore paradoxical that clinicians who claim
that they are ‘evidence based’ appear to pay only lip service to the idea that ‘patient
preferences’ are on an equal footing with clinical research and clinician judgement
when making clinical decisions.
Indeed, a careful physical examination that takes into account the context of the
story is essential in gaining trust with the patient. The sensitivity, order and coher-
ence of the physical examination unveil more than positive or negative tests that
fulfil diagnostic criteria. The examination may reveal the distress, the inability to
cope and painful memories of living with pain. This clinical information that pro-
vides clinical context is essential in formulating a person centred management plan.
One way to bring this together is by using a mind map where a person’s story, physi-
cal examination findings, clinical investigations and judgements of the clinician
form this co-constructed narrative. This bringing together of the normative and the
narrative (Launer 2018) seems to me to be far more humanising than the division of
a person into constituent parts: biological, psychological and social elements that
are further separated into subjective and objective data findings.
I use a mind map, where all the relevant information from the patient is collected,
honoured and placed in a timeline. This allows the patient to make sense of all the
available information in one place. The patient has explicit permission to give feed-
back and change any aspect of the mind map if they feel that it does not capture their
reality and the situation. The mind map is personal to the patient, so it is important
that the patient has the autonomy to change the mind map to reflect their experience.
Following the co-construction of the mind map, a vector model can be made, con-
veying the complexity of interaction between causal elements (see Price, Chap. 7,
8 Above and Beyond Statistical Evidence. Why Stories Matter for Clinical Decisions… 133

this book). It is the use of the vector model that allows a patient to see that the vari-
ability and context-dependent nature of their pain experience could be better under-
stood (Low 2017, 2018). Causal elements may be non-linear, interactive, contextual
and time sensitive. Understanding this can help a patient look beyond the false
understanding of their pain being caused by single elements that stack up or aggre-
gate. Assumptions that causal relationships are linear can, for example, result in
surprise when pain is experienced even when patients purposely choose not to do
activities or tasks felt to increase their pain.
Instead of using statistical data to determine the prognosis and management of a
patient, a dispositional view allows and even encourages the context sensitive use of
propensities that have been carefully considered in light of the individuality of the
patient. Instead of only describing the probability based upon a research population,
the individuality of the patient is also considered within the context of how that
person relates to the research population.
The use of terms such as ‘propensity’ or ‘tendency’ avoids the deterministic
qualities, like inevitability, that can come with MSK diagnoses such as osteoarthritis
(OA). Although the incidence of OA increases as we get older, it manifests with a
significant amount of variation in different people with different experiences.
Socially, it is believed that the presence of osteoarthritis always causes pain and dis-
ability, but this is not the case. People believe that a diagnosis of osteoarthritis will
mean that their joint will erode, crumble or fall apart (Barker et al. 2009) leading to
unnecessary fear, anxiety and loss of activity and agency. This self-fulfilling cycle
perpetuates or leads to more pain and disability. However, osteoarthritis is a com-
plex process that is affected by multiple systems including the immune, endocrine,
and neuromusculoskeletal systems. Amongst these systems, the experience of pain
is modulated by multiple social, psychological and biographical factors, some of
which can be tempered, altered and positively changed. Reductions in pain and
improvement in function is possible and the manifestation of pain and progressive
disability is most certainly not inevitable. Using a mind map and vector model of a
person’s individual situation can make a difference and turn the tide.
The phrase, “treat the person, not the scan”, commonly used in medicine, cannot be
stated enough as one person may have significant OA changes seen via imaging and
present with joint stiffness but no pain, whereas another person with very mild OA
changes may present with disabling and distressing pain. This is true across an entire
spectrum of MSK diagnoses, including the most commonly found conditions such as
low back pain, fibromyalgia and neck pain. Often, MSK diagnoses do not exist in iso-
lation. Mind-body dualism, what the philosopher René Descartes is known for, under-
pins biomedicine and is reflected within the objectivity of EBM/EBHC in the way that
distinct quantitative physical and psychological measurements are used to draw causal
inferences without considering the interaction and non-linearity of causal elements that
exist within a complex situation such as the lived experience of a person. A disposi-
tional perspective, in contrast, can ground a non-judgemental viewpoint of a person’s
lived experience through the use of a mind map and a vector model of powers. Aspects
of the clinical picture can be displayed to convey the complex nature of a situation but
still allow space to develop a management strategy that a person can understand, accept
and initiate.
134 M. Low

8.4 Bringing the Totality of Evidence Together

When implementing a person centred clinical reasoning perspective, how should

one proceed? There are many different perspectives on this; my personal approach
is to centre the process on the patient. Their story, viewpoint, narrative and situation
are central and of the utmost importance as they provide the vital context of the
therapeutic encounter. The evidence drawn from clinical research is then applied
within the context of the patient, and with sound judgement the clinician then evalu-
ates the applicability of the research to the patient, at this time. Then, both the
patient and the clinician bring together the narrative and normative information
alongside the clinical research in order to create a truly shared perspective on treat-
ment and management using the mind map and vector model.
All interventions in healthcare aim to improve a patient’s healthcare need, situa-
tion or circumstance and they carry a form of risk that may delay progress or
adversely affect the outcome. In MSK disorders, the most common risk to a patient
in a physical therapy clinic is the potential to worsen a patient’s pain experience.
Therefore, careful discussions of the potential risks and benefits of any future action
should be made prior to the implementation of treatment. The use of the mind map
and vector model makes this process easier and better understood, allowing treat-
ment recommendations to be made in a coherent fashion. The added benefit of
doing this allows the clinician to provide options if symptoms adversely change and
offer potential reasons why this may happen. For example, a patient with persistent
non-specific back pain may present with fear of bending their back, as they may
believe that their symptoms are indicative of the spine being damaged. The reason
for the patient’s fear may relate to their previous experience of bending to lift an
object in the past, for example, or by well-meaning family, friends or healthcare
practitioners telling the patient that the pain when bending is harming their spine.
The treatment option that may be the most appropriate for this situation is a graded
exposure form of treatment whereby the patient starts to understand how their fears
relate to their pain and are encouraged to participate in the activities that they fear
in a graduated way. It is important to understand why the patient is fearful and this
can be explored narratively and by performing behavioural experiments or safe ver-
sions of the feared activity. This creates an opportunity to understand the cause and
relationship of fear to the current situation and is made explicit by using the mind
map. The mind map can help explain a vicious cycle of fear, avoidance of activity
and deconditioning that is perpetuating and maintaining the pain experience. The
treatment option of graded exposure may increase the patient’s symptoms, so a
strategy of the patient being comfortable with the treatment and having options of
what to do if their symptoms increase is therefore important.
The details of this are highly context dependent and cannot be demonstrated
through statistical data, nor can the clinical adjustments and variations that allow a
patient to stay in control of their symptoms. Self-efficacy or the sense of a person’s
ability to feel in control of their circumstances or situation is, amongst a number of
factors, important for health outcomes (Holden 1992; Keedy et al. 2014). Using the
8 Above and Beyond Statistical Evidence. Why Stories Matter for Clinical Decisions… 135

mind map and vector model are useful tools to convey the totality of evidence in
describing the patient’s story, their context, the clinical research evidence, the social
situation, the risks and benefits of treatment options as well as opportunities to tailor
a personalised management plan for the patient.
I have previously written on related cases, of a person with medically unex-
plained neck, thoracic and shoulder pain (Low 2017), and of a person with persis-
tent and recurrent low back pain (Low 2018), which more fully explain this
approach. The former describes a little more of a philosophical account whereas the
latter describes a clinical account in greater detail.
In summary, understanding the clinical research that is epitomised traditionally
through statistical data does not help the clinical encounter. If anything, there is a
greater risk of alienating and depersonalising the lived experience of the patient.
Respecting the patient, rather than the statistics, at the centre of the evidence brings
with it key aspects of a therapeutic alliance, characterised by connectedness
(Babatunde et al. 2017). This connectedness, established through the creation of a
co-constructed shared narrative, improves the therapeutic alliance, adherence to
treatment from the patient (Babatunde et al. 2017) and personal job satisfaction for
the clinician. Although biomedicine has brought about huge successes in the eradi-
cation of diseases in the past, it no longer is appropriate for the devastating impact
of MSK related disorders. This may be because of biomedicine’s focus on a cure of
a disease based upon the implicit belief of monocausality (single cause, single
effect), linear causal relationships found amongst statistical frequencies and the lack
of acknowledgement of context. In fact, the maintenance of biomedical causal
beliefs in regards to pain has been found to be a barrier in the recovery of patients
with low back pain (Bunzli et al. 2016). This may be because these patients are still
looking for ‘the’ cure or the scan that will identify ‘the’ cause which will lead to the
correct treatment and cure. This often feeds a self-fulfilling cycle of negative emo-
tion, despondency, frustration and anger that also adds to the pain experience.
The mutual understanding and respect of the patient creates the cornerstone of
positive change and the opportunity for restoring wellbeing. The patient’s context,
not the statistical average, guideline or diagnostic classification, is the key to
improving the challenges that patients with MSK conditions have. As clinicians we
are, after all, here to help people through the difficult challenges of life and, in my
mind at least, there is no better purpose in life than to help others. I mentioned ear-
lier that being a physical therapist is like being a detective, but it is really much more
than that. Physical therapists are coaches, mentors, and care providers, but most
importantly, they are relatable humans who can provide the structure and therapeu-
tic environment for people to recover, heal and grow. Getting to the heart of the
matter is more than statistical observations and analysis of average treatment effect
sizes; it is the embodiment of human understanding, genuine curiousness, purpose-
ful support and thoughtful guidance towards the emancipatory experience of agency
and the fulfilment of our patient’s goals. It is our patient’s stories that ought to be
honoured, respected and understood as the centrepiece for clinical decision making,
with population data, clinical research, policy and guidelines used to support, rather
than to dictate person centred care.
136 M. Low

References and Further Readings

Babatunde F, MacDermid J, MacIntyre N (2017) Characteristics of therapeutic alliance in muscu-

loskeletal physiotherapy and occupational therapy practice: a scoping review of the literature.
BMC Health Serv Res 17:375
Barker K, Reid M, Minns Lowe J (2009) Divided by a common language? A qualitative study
exploring the use of language by health professionals treating back pain. BMC Musculoskelet
Disord 123:1–10
Bunzli S, McEvoy S, Dankaerts W, O'Sullivan P, O'Sullivan K (2016) Patient perspectives on par-
ticipation in cognitive functional therapy for chronic low back pain. Phys Ther 96:1397–1407
Djulbegovic B, Guyatt GH (2017) Progress in evidence-based medicine: a quarter century on.
Lancet 390:415–423
Holden G (1992) The relationship of self-efficacy appraisals to subsequent health related out-
comes. Soc Work Health Care 16:53–93
Keedy NH, Keffala VJ, Altmaier EM, Chen JJ (2014) Health locus of control and self-efficacy
predict back pain rehabilitation outcomes. Iowa Orthop J 34:158–165
Kinney M, Seider J, Floyd A, Beaty K, Coughlin K, Dyal M, Clewley D (2018) The impact of
therapeutic alliance in physical therapy for chronic musculoskeletal pain: a systematic review
of the literature. Physiother Theory Pract 28:1–13
Koes BW, van Tulder MW, Thomas S (2006) Diagnosis and treatment of low back pain. BMJ
332:1430–1434
Launer J (2018) Narrative based practice in health and social care: conversations inviting change.
Routledge, London
Low M (2017) A novel clinical framework: the use of dispositions in clinical practice. A person
centred approach. J Eval Clin Pract 23:1062–1070
Low M (2018) Managing complexity in musculoskeletal conditions: reflections from a physio-
therapist. In Touch 164:22–28
NHS England. https://www.england.nhs.uk/ourwork/ltc-op-eolc/ltc-eolc/our-work-on-long-
term-conditions/si-areas/musculoskeletal/, https://www.england.nhs.uk/ourwork/ltc-op-eolc/
ltc-eolc/resources-for-long-term-conditions/
Øberg G, Normann B, Gallagher S (2015) Embodied-enactive clinical reasoning in physical ther-
apy. Physiother Theory Pract 21:244–252

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Chapter 9
Causality and Dispositionality in Medical
Practice

Ivor Ralph Edwards

9.1 Some Background

I am a clinically qualified general consultant physician in general medicine and

clinical pharmacology in the UK, with over 20 years of clinical experience. I have
held professorial chairs in both subjects, in Zimbabwe and New Zealand respec-
tively. In New Zealand I was also Director of the National Toxicology Group and
had 10 years of experience in drug regulation and pharmacovigilance as Medical
Assessor for the New Zealand Medicines Adverse Reaction Committee and the
Medicines Assessment Advisory Committee. I also had similar responsibilities to
the New Zealand Toxic Substances Board for the registration of other chemicals and
for advice on chemical safety. I was appointed Chairman of the Advisory Committee
to the World Health Organisation (WHO) Programme for International Drug
Monitoring whilst in New Zealand. Following the above, for the last 25 years I was
the founding Director of the Uppsala Monitoring Centre, which is responsible for
the technical support to all WHO supported drug safety monitoring programmes
worldwide. In that role, I was the first to develop data mining in pharmacovigilance
and risk-benefit analysis. I have written over 350 scientific papers and, whilst I am
now retired, I am still actively involved in teaching and projects. In all this work, the
challenge of determining causality in individual patients has been paramount.
A very important issue I investigated many years ago were reports of blindness
in 7 patients from around Germany, reported as possibly being due to omeprazole,
a drug used to treat peptic ulcer. It was a very wide selling drug and the pharmaceu-
tical company was particularly concerned: because of the very high sales, chance
associations with blindness were possible, but it was odd that the reports were all
from Germany, and besides, they were from intensive care units around Germany.
The first issue that I found was that a trial use of the drug (unknown to both the

I. R. Edwards (*)
Uppsala Monitoring Center for International Drug Monitoring, Uppsala, Sweden

© The Author(s) 2020 137

R. L. Anjum et al. (eds.), Rethinking Causality, Complexity and Evidence for the
Unique Patient, https://doi.org/10.1007/978-3-030-41239-5_9
138 I. R. Edwards

pharma company and regulators) was being conducted on the prevention of peptic
‘stress’ ulcers in patients in intensive care. Then I found that about half the seven
patients had taken methanol overdoses, a well-known cause for blindness. The other
three were diagnosed as ischaemic optic neuropathy, which is a complication of life
threatening trauma or other illness affecting the eye circulation by hypotension,
which was the case for these other patients. Since literally millions of patients from
around the world had used the drug without reporting blindness, and there was no
known toxicological or pharmacological reason for blindness, I thought the other
possible causes were most likely, in spite of the one unusual feature about these
cases: they were receiving omeprazole intravenously and not by the far more com-
mon oral route. About 20 years further on I find that in huge longitudinal patient
databases of over a million exposures it is suggested that blindness occurs in a few
patients on omeprazole, who are predominantly female, over 60 and have hyperten-
sion: but this is another group in which blindness could be due to other causes.
Am I wrong to think that when I can see a more likely cause with a known
mechanistic explanation – toxic methanol, prolonged and profound hypotension –
that those are more likely the causes? And the damage from hypertension and other
changes to eyesight in an aging population is at least as likely an explanation. But
why especially women? There is clearly some uncertainty about my causal diagno-
ses here.

9.2 Considering Causality

Always we need the best information possible; we need to be transparent in our rea-
soning; we need to follow up and we must be open to new evidence. Clinical medi-
cine uses multiple ways of accomplishing its ends, which are the diagnosis, treatment,
amelioration or cure and, if possible, prevention of any dis-ease causing problems in
an individual. At the heart of clinical medicine is an empathy with the patient in
understanding what ails them in as deep and broad a way as possible. To do this, a
practitioner uses, or a coordinated group of practitioners use science, art, learning
and experience, and indeed whatever wisdom they can effectively bring to bear on a
problem. A practicing clinician is not a scientist per se, but rather uses science.
Diagnosis is an essential first step. Some illnesses are easy to recognise, but even
with those, there are competing possible diagnoses. Illnesses are shape-changing
masquerades. Only a careful case history and examination of the patient will give us
a useful picture of a range of clinical conditions for further consideration using
observations and tests. A diagnostic assessment usually produces a list of possible
causes to explain the patient’s clinical signs and symptoms and their chronology,
and that can be listed in order of probability in any given patient and in their particu-
lar context. The key challenge is what might be the cause of this patient’s clinical
state, but it is not only the various disease states (medically recognised clinical ill-
nesses rather than their phenomenological consequences) that need to be consid-
ered, but also how that individual patient will react to a given dis-ease entity
9 Causality and Dispositionality in Medical Practice 139

(dis-ease being the symptoms, signs, anxieties and any other personal consequences
that are concerning them). A diagnosis must take into account not only context
(environmental and familial) and the various disease attributes but also those pro-
clivities of the patient in how they respond to dis-ease challenges.
A classic triad of questions is useful:
Can a disease ever cause this clinical state?
Has it done so in other humans?
Is it responsible for the clinical picture in this particular patient?
The essence of these questions is to understand the phenomenology of the dis-­
ease and then to consider causality. Some would argue that consideration of the
broader phenomenological aspects (their dis-ease) – the overall impact of disease –
has little or no place in determining its cause. But this is to disregard the ways in
which the patient’s personal background and context may influence the ways in
which they present the features of their dis-ease to the clinician, and in turn how the
clinician interprets those features into different categories (physical, social, psycho-
logical, spiritual etc.) and then cares for and manages them. Variations in diseases
themselves and their presentations in patients may alone lead to considerable mis-
conceptions, for example about the severity and nature of pain, or indeed the
description and localisation of any symptoms within their bodies.
Commonly, we make diagnoses. We look for the cause of an illness, or at least
for an explanation of the physical signs and symptoms the patient presents. We are
limited in interpreting those pieces of clinical information by what we have remem-
bered about disease entities and the ways in which humans respond to them. We are,
however, able to use many other information sources to aid our thinking, although
it will take time, experience and imagination to find all the relevant material. We
may have an easy task with a clearly recognisable pattern we commonly see in our
daily experience, but if we find that there are dis-ease components in the pattern
(due to individual dispositions) we do not recognise, this leads to confusions.
Consider a patient whose family history is one of close members having had coro-
nary artery disease. If that patient should have chest pain, she will naturally first
think that her chest pain is due to heart disease and indeed may be more likely to
describe her pain as having anginal qualities, perhaps ignoring the exact position of
the pain in her chest. In turn, the patient’s context is ever changing and needs to be
considered while making a diagnosis and subsequently during their treatment. It is
at this point that the dispositions of the disease should be considered as being modi-
fied by those dispositions of the patient.
Sometimes the patterns are complex and responding to their intricacy can be very
demanding. Patients are not just carriers of disease entities, they have their own
dispositions which react to disease differently and also to the same disease at differ-
ent times and in other situations. Dispositionality, as a way of probing the phenom-
enon of a person’s dis-ease seems to be a useful way of analysing a clinical situation.
In respect to the example just given, we now know that women with coronary artery
disease present a different spectrum of symptoms compared to men.
140 I. R. Edwards

I and some colleagues were concerned by the roll out of WHO’s ‘3 by 5’

Programme in 2003, which aimed to provide AIDS treatment to 3 million people in
Africa by 2005. It was a laudable and ambitious programme, but we were concerned
about the little attention to monitoring possibilities for effectiveness and safety of
the known toxic treatments. I attended a meeting in South Africa soon after the
launch and there were several reports of deaths from lactic acidosis, a result of mito-
chondrial damage. It was noted that those early South African cases were all women.
The drugs concerned were part of the ‘highly active antiretroviral regime’. Stavudine
and didanosine were the main suspected drugs that had been noted to cause this
problem, which was rarely seen in the US and Europe, where it was usually only
symptomatic and reversible. Now we know that around 80–90% of cases of lactic
acidosis occur in women (in Africa) and that their mortality is as high as 50%. The
early experience of these drugs in the western world was largely in men, and an
early paper (Brinkman 2001) promoted the idea that there was small incidence with
no serious clinical significance. We therefore knew of the potential problem from
before the WHO roll out, but epidemiology in males suggested a small risk.
More recent reviews (e.g. Trang et al. 2015) explain more about the mechanisms.
But there is more: it is obese African women with a high body mass index that are
particularly at risk. Why? Also unknown is whether there is a possible genetic cause
in African women. Are there other dispositional reasons why these patients are so
badly affected? Are there contextual problems, such as poor availability of lactic
acid screening for early symptomatic patients, that makes the mortality so high?
Suppose the clinician elicits a full case history (and this supposes no time con-
straint) and does a complete relevant physical examination. Each of the findings may
be a disposition of a disease entity, or of the patient reacting to their situation, or may
indeed be a general disposition of that patient. For example, does one patient always
look pale and possibly anaemic, or perhaps another may have so called ‘white coat
hypertension’ (raised blood pressure whenever it is measured in a hospital environ-
ment)? We may be faced with a patient that is garrulous and often chatters inconse-
quentially. I once had such a patient with a large open, varicose ulcer on the leg, and
a mild fever. Her son accompanying her was a senior clinician himself, who apolo-
gised saying, “She’s always chatty like this.” I accepted this, but decided to admit her
since she needed both analgesia and antibiotics: it was also late in the evening. The
following day she had a very high fever, was very drowsy and had a falling blood
pressure. This was a septicaemia with delirium and the knowledge of such a possibil-
ity should have alerted me to investigate more thoroughly whether infection was
starting to cause a delirium. I was swayed by my colleague’s reassurances with near
disastrous consequences. She had a perilous passage through intensive care with a
severe septic shock. Embarrassingly both mother and son were grateful to me.
In the past and now also in the present, many seek a single cause for an effect. It
seems, however, much more useful to think of possible causes and to understand
their mechanisms, and so consider a range of probabilities of causality based on the
situation for a particular patient. A sore throat is likely to be infectious if a person
has been enclosed in a crowded space during a winter epidemic but one would be
more likely to consider a drug cause (e.g. the much rarer agranulocytosis) than if the
9 Causality and Dispositionality in Medical Practice 141

sore throat occurred de novo while the patient was convalescing alone and already
taking an antibiotic.
This clinical consideration of patients demands a broader view, deeper thinking
and longer timeframes than most epidemiological studies or clinical trials allow in
providing evidence useful in clinical practice. Clinical trials tend to focus on a sim-
ple connection between cause and effect – the likelihood of drug X being strongly
associated with effect Y for a statistically significant proportion of those who take
it, compared with controls. But a strong association is not proof of causality on its
own, it remains a strong probability only. Nor is probability proof of a cause: it is
essential to couple cause with effect by understanding the various ways in which
attributes (or dispositions) of the disease, of the patient, and of the treatment and the
context of the patient all interplay. Moreover, perfect, linear, causal relationships are
rare in medicine, and the strength and variation of a disposition are as important as
the fact of its mere presence or absence.
Causality will also become ever more important as we attempt to make the best
use of genetic mechanisms behind the ways our bodies function. The new genera-
tion of gene therapies and other such ‘personalized’ treatments are more targeted to
specific basic biomic functions in the body, which result in our dispositions and
their strengths of expression. So, a proper, dispositional grasp of causality is a vital
tool in helping healthcare professionals reach the best judgements, especially when
time, resources and reliable information are in short supply. A keen understanding
of all the factors underlying a clinical problem is the path to efficient use of
resources, rather than the use of an overly simplistic but rigid ‘guideline’; guidelines
should reflect nuances of variation rather than simply dictating a pathway to a single
algorithmic ‘truth’. It is therefore better to consider a causal explanation of how a
patient’s symptoms and signs might appear as they do rather than to concentrate on
the ideal of a single direct cause and effect. That is, to consider that the whole phe-
nomenon of dis-ease includes the propensities of other dispositions to have an addi-
tive, augmenting effect as well as possible secondary effects.
Consider for instance a hypertensive patient, treated with beta-blockers, who
dies from anaphylaxis after a bee sting or another allergen such as penicillin. The
beta-blocker may well have contributed to the causal mechanism underlying the
fatal event, by reducing the cardiovascular response to the severe hypotension
caused by the acute allergic response. Similarly, the known sedative effects of a beta
blocker may add to those of a benzodiazepine in a patient with a high blood pressure
thought to be due to anxiety, with the result in a secondary effect of a fall with inju-
ries. There would be a degree of speculation in such situations about what was in
fact causative. Such speculations would probably not prove practically useful in the
acute situation but they may give some chance of avoiding similar occurrences in
the second case, and accumulating experiences of this kind might point towards a
way to allow avoidance of important problems for patients in the future.
An elderly relative, taking warfarin anticoagulant after a series of minor strokes,
developed heart failure and was treated with a frusemide, a diuretic commonly used to
remove excess water from the body. He improved and his ankle swelling from the
heart failure reduced. Some days later, he had a rash and painful ulcers on his lower
142 I. R. Edwards

legs and feet. The nursing home staff said they thought it was bed sores since he had
been sitting and lying most of the time. I was sceptical because the ulcers were on the
front of the feet and legs, not the right place at all. A dermatologist was consulted who
suggested that the rash was a vasculitis, and I was able to suggest that frusemide was
the cause, and the diuretic was changed. It was all too late; for he found the pain from
the vasculitic ulcers so bad he needed morphine which made him sleepy and his
breathing was also suppressed. He developed pneumonia and died peacefully from
two adverse reactions to his treatments: the frusemide caused vasculitis, which caused
pain, which caused morphine, which caused respiratory depression, which caused
bronchopneumonia, which caused death. This kind of complex chain is quite common
in medicine and illustrates why a causal explanation is valuable for understanding.

Some causal logic Implication

Necessary cause
If D happens then E will happen, if D does not
D E
happen E will never happen
E D necessary cause or condition
Sufficient cause
If either D or Z happens, E will happen
D E
sufficient cause or condition
Z E
Contributary cause
D E If D happens , E may happen, but only with z
contributary cause or condition
Z

Secondary/remote cause If D happens Z may happen & then E happens

D Z E secondary cause

Most clinical healthcare practitioners would like to practice medicine with a detailed
and empathetic diagnostic work-up including some of the considerations above, but
also most of us know that time constraints do not allow for every patient to have a full
assessment. In very many instances, such an approach is unnecessary and even coun-
ter-productive: emergency situations and the treatment of acute common diseases with
generally good outcomes are examples. It is nevertheless wrong to consider one
instance of contact with a patient in isolation as adequate. One meeting with a patient
allows a preliminary assessment of immediately important dispositional factors. A
patient meeting with her family medical practitioner for the first time for years may be
asking for a symptomatic remedy for a persistent cold and cough and then mention a
heavy period as an aside. The same patient may refuse an examination on the grounds
that she is embarrassed because she is currently bleeding. Treating the symptoms of a
cold without making an arrangement to properly pursue the vaginal bleeding would be
a mistake indeed. It is very helpful to have continuity of care where a single clinician
knows a family’s background, and would be alert to behaviour that was unusual.
There are some instances where treatments are routinely commenced with a
complete assessment of how an individual patient differs from the norm, followed
9 Causality and Dispositionality in Medical Practice 143

by a carefully-balanced choice of medication bearing in mind the variability of the

cause(s) and additionally keeping a close eye on how things turn out in the long
term. The way of using antiretrovirals for HIV/AIDS is an obvious example. AIDS
is a chronic disease which has various phases and states of ill-health (dis-ease),
some induced by the changes, sometimes progression, of the disease process and
sometimes due to treatments. Because the immune system is negatively affected, it
also leaves the body open to various kinds of infections and different kinds of neo-
plasia. Patients change over time, as do their diseases and treatments, not only
because of some disease processes but also because of aging. These patients and all
people need careful monitoring in all aspects of their lives. Diseases and their man-
agement are all unique phenomena. But this sort of premium care is still unusual
since it can only be delivered through healthcare systems with extensive personnel
and technical resources linked to stable and well-organised health services.
For all patients, however, it seems best to consider why a particular clinical effect
happens, what can be done about it, and how best to take action. This points to the
need for a far more nuanced and holistic approach, which acknowledges that the
way a treatment acts on an individual depends on their constituent dispositions
towards different disease effects. It is about who those individuals are, where they
are, their circumstances, history, what they eat and any other conditions or sub-
stances that affect their body systems. In aging societies, those older people are
likely to suffer more illnesses, live with more chronic conditions and take more
drugs to counteract them. This has profound implications for understanding causal
relationships between dispositions. Successful management of a patient is best
achieved by getting detailed information from, and on, an individual’s dispositions,
then matching it to the known characteristics (dispositions) of the treatment and
then following up the patient to ensure that an optimal result has been gained.
Traditionally, medicines that demonstrate a high probability of achieving the
desired outcome in controlled conditions are considered safe to market, prescribe
and use. But in the real world, we know that even the best drugs typically only work
as desired around 70% of the time. Variables driven by misdiagnosis, treatment
variables such as dosage and compliance play out alongside environmental, genetic
and individual factors to reduce the actual effectiveness, so therapeutics can only be
improved by exploring risk and benefit probabilities and carefully monitoring out-
comes, particularly of new treatments.

9.3 Diagnosis and Decisions

Causality in individual clinical decision situations is much too important to be left

to chance or limited to the broad-brush norms defined by epidemiology. And we
shouldn’t let the cost or difficulty of pursuing the ideal deter us from doing what’s
right and good. Patients need and deserve nothing less.
Establishing a working diagnosis is the first major goal. The first focus of a clini-
cian will be on the characteristic dispositions of the possible disease entities,
144 I. R. Edwards

arraying them in order of likelihood (differential diagnosis). This should also take
account of the patient’s context (environment) and the ways in which the human
body tends to respond to the disease to produce symptoms. There are likely to be
uncertainties due to gaps in information, or to variation in the strength or likelihood
of features (dispositions) of the disease or of the dispositions of the patient such as
response to pain or blood loss or immunity. What is the most likely causal link that
explains the patient’s symptoms and signs – qualitatively as well as quantitatively?
What important data is missing and must necessarily be found before one can decide
on a plan of action? What are the key dispositions we can use to follow the progress
of the patient and the disease entity? For example, a microbiological identification
and presence of bacteria in different body tissues or excreta usually enables us to
decide on the dispositions of the likely causative organisms. We might, however,
need to act without knowing the precise nature of the infection. But we can start
treatment before the microbiological tests are done, then we must follow up the
effect on the patient carefully, which includes measuring the temperature and heart
rate of the patient and any other key dispositional responses (‘vital signs’) that may
change, as well as measuring the success or otherwise of the patient’s response to
the infection. We also see that therapy and management have dispositions as well:
the chemical structure, pharmacology and toxicology of any medicinal product have
their dispositions, good and bad. They too interact with those of the patient and
disease entity. Management may include other therapies than drugs such as chest
physiotherapy to expel unwanted secretions in acute bronchitis or pneumonia.
A proper, dispositional grasp of causality is a tool to help clinicians reach the
best judgements, especially when time, resources and reliable information are in
short supply. Dispositional thinking is a dynamic way of sifting evidence about both
disease and patient.
Many clinicians will think that talking about dispositions adds nothing to the
way they already do their work, and indeed that dispositionality brings confusions.
Many clinicians also feel that they have enough experience and intuition to pick up
nuances of both patients and disease behaviour that are outside the norm – and many
can. The stress, however, of work, of time pressure, of limited resources, can lead to
mistakes being made. Thinking dispositionally can provide a way of double check-
ing what we do and highlighting uncertainties that are inherent in diagnosis and
management decisions in medicine.
Thinking about the dispositions of both patient and disease leads both to com-
pleteness and clarity in management. For example, the patient may be an aging
alcoholic (dispositions to check might be liver and kidney function etc.) and the
drug might be toxic at higher dose levels (so considering how it is metabolised and
excreted might lead to a lower starting dose). Recognising these factors might also
lead to the necessity of following up the patient after a given time to check on the
patient’s progress, perhaps with appropriate tests. Other less obvious considerations
may follow from these more obvious ones, such as checking the patient’s memory
(any early dementia), their eating habits (if the drug should be taken with food) or
their daily habits (if the drug is a diuretic they should be informed about the likely
time of the diuresis, and plan to be near toilet facilities during that time).
9 Causality and Dispositionality in Medical Practice 145

9.4 Overview of Important Dispositional Insights in

Clinical Care

1. Personal attitudes toward the patient can influence one’s assessment and actions.
This is an underused but key matter and a useful test of one own overall disposi-
tion in relation to the patient.
–– Do I like this patient? Do I find that the patient smells? Are they condescend-
ing and impolite? Or engaging and lively?
–– There are many more sophisticated possibilities and eliciting them will allow
a critical view of factors that need to be considered and allowed for in the
patient interaction.
2. What are the clinical dis-ease symptoms and signs in this patient?
–– Does the patient look ill or in pain? Are they afraid? Are they embarrassed?
Impatient? Are they hesitant or in any way unclear in their responses?
–– These are dispositional features that must be taken into account in the interac-
tion with the patient as well as being of diagnostic import.
3. Checking the clinical findings about diseases against prior clinical knowledge:
what is key, what is missing, and what is unusual?
–– Assumptions dependant on scholarly descriptions of diseases and on experi-
ence can be limited in scope and misleading. A conscious check on the dispo-
sitions presented by the patient can help avoid premature assumptions.
(i) As the patient’s story unfolds and physical signs are elicited, the clinician
will be alerted to a range of diagnostic possibilities to check against known
features of diseases. Missing data must be considered carefully with each
potential diagnosis. The variation in power of disease features needs to be
considered against the array of responses possible given the dispositions of
the patient. Consider an easily understood example from my own experi-
ences of investigating pain. The type of pain is tricky, as it can be challeng-
ing to determine across cultures. In Zimbabwe what many would say is a
‘stabbing pain’ is described as ‘pricking’, thus raising questions about how
severe a pain is. Even when the site of a pain is described, it may confuse a
clinical appraisal because of the anatomy of the nervous system where a
nerve branches, and disease affecting one branch is felt in an area inner-
vated by another (referred pain). This may cause confusions in dental
pathology, for example.
(ii) The patterns of symptoms and signs elicited may overlap for a number of
diseases. The immune responses to infections, to cancers and to other inva-
sions by entities recognised as foreign to the human body can provide
examples of this kind of confusing situation. Spontaneous abortions may be
due to the mother’s body recognising the fetus as a foreign invader, for
example. Infections produce a change in the immune system that result in
146 I. R. Edwards

normal body tissues being seen as foreign, in autoimmune disease (although

this may be triggered in other ways, too).
(iii) Consideration of the interplay between various dispositions of the disease
and its unwilling host, leads us to analyses of powers of diseases, their
modes of expression and their actions. In turn this gives us ideas about use-
ful laboratory tests and further monitoring of the patient’s situation includ-
ing the kinds of treatments that might be useful.
Considering dispositions also leads to considerations about what other evidence
might be available to understand the disease and treatments and particularly in
understanding cause and effect relationships.
4. Specific help can be obtained from the Bradford Hill proposals (Hill 1965) as
well as DoTs (Aronson and Ferner 2003) and EIDOS guidelines (Ferner and
Aronson 2010).
5. It is useful to think about dispositions in considering the value of evidence
available from other sources, and particularly statistical associations. The
choices of keywords in searches are usefully specified using dispositions, for
example.
–– Decisions in managing patients such as choosing a medication are critically
determined by choosing the correct medicinal product to be active against
the disease, but not to do harm to the particular patient, who may be sensitive
and consequently harmed by one product and not another.
–– The weighing of effectiveness against risks makes any such decision chal-
lenging. A dispositional approach to an individual’s possible idiosyncrasies
and much more dispositional information on the effectiveness - risk profiles
of medicines as they are used in routine clinical practice, as opposed to con-
trolled studies, is needed.
6. Interactions between dispositions is important where multiple diseases might or
do coexist in patients, or when multiple therapies are in use.
–– Whilst commonly found in older patients, there is an increasing propensity
for multiple disease/ treatment situations to develop as more medical disease
situations are recognised.
7. Causal explanations, including possible interactions between dispositions, are
of considerable value clinically even if speculative: the speculations are
enhanced with other similar occurrences and by prior scientific or clinical evi-
dence of the powers of those dispositions. Any instances of interactions and
unusual outcomes should be reported in detail and be made available for others
to share.
8. Many individual and rare medical situations fall outside the norms usually con-
sidered in controlled clinical trials and even controlled observational studies.
Thinking about variations in the disease and patient dispositions possible
through theoretical and practical knowledge of mechanisms is important.
9 Causality and Dispositionality in Medical Practice 147

–– Rare disease presentations and unusual adverse reactions may not occur
often in relation to an individual disease or medication, but the totality of
such examples over the whole of healthcare is huge. Adverse drug reactions
were the 5th most frequent cause of death in the US and similar findings
have been seen in several other countries.
9. As we learn more about genomics and biomics, the links to the incidence and
powers of dispositions will be very important in diagnosis and therapeutic
decisions.
–– Linking statements 6 and 7 emphasises the value of individual case reports
with full descriptive detail to allow medicine to progress.
10. Causal explanation needs to be more widely practised to allow us to understand
better how the propensities of different dispositions of disease, patient and
treatment interact for better or worse outcomes.
–– Rejecting the inclusion of subjects with identifiable potentially confounding
propensities is a two-edged sword: it allows for clarity in identifying a pos-
sible statistical association but removes the potential for multivariate
analysis.
–– Statistical association and particularly non-association should always be tem-
pered by what we know about the possible mechanisms by which a proposed
cause could produce an effect, plus any other dispositional evidence demon-
strating why a particular instance of cause and effect might be rare or unique.

9.5 Conclusion

Humans share many attributes but there are many examples of unusual (‘orphan’)
diseases as well as rare adverse reactions to therapies. These situations need dispo-
sitional thinking and not only epidemiological, normative approaches. Having had
the privilege of being a clinician as well as working in a scientific setting experi-
menting with drugs and chemicals, I can conclude that medicine is not a science but
the application of described knowledge or knowledge acquired by experience.
Medicine is its own discipline in which the essential skills are:
1. For the clinician to match the dispositions of the patient in front of them with all
their acquired knowledge of others who have similar dispositions, to find the
closest binary match and to understand the probable constitutions of their patient.
2. The clinician must understand the dispositional weaknesses of their particular
disease(s) and so, choose a treatment that has the maximum benefit for the
patient with the least harm.
3. All of this must be undertaken with a specific aim of treatment that is in agree-
ment with the patient and takes account of the patient’s social context using an
empathetic and holistic (phenomenological) approach.
148 I. R. Edwards

4. Clinicians also have responsibility to ensure that all their reasoning from diagno-
sis and clinical management works in real-life clinical practice. They must pass
on to others their knowledge, particularly when outcomes are unexpected.
5. The responsible clinician should also try to identify why the unexpected outcome
occurred, so adding to global knowledge.
It is clear that the above six points are most difficult to attain, but the vision
should remain.

References and Further Readings

Aronson JK, Ferner RE (2003) Joining the DoTS: new approach to classifying adverse drug reac-
tions. BMJ 327:1222–1225
Brinkman K (2001) Management of hyperlactatemia: no need for routine lactate measurements.
AIDS 15:795–797
Ferner RE, Aronson JK (2010) EIDOS: a mechanistic classification of adverse drug effects. Drug
Saf 33:15–23
Hill AB (1965) The environment and disease: association or causation? Proc R Soc Med
58:295–300
Trang AQ, Xu LHR, Moea OW (2015) Drug-induced metabolic acidosis. F1000 Faculty Rev.
https://doi.org/10.12688/f1000research.7006.1. PMCID: PMC4754009, PMID: 26918138

Open Access This chapter is licensed under the terms of the Creative Commons Attribution 4.0
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adaptation, distribution and reproduction in any medium or format, as long as you give appropriate
credit to the original author(s) and the source, provide a link to the Creative Commons license and
indicate if changes were made.
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Commons license, unless indicated otherwise in a credit line to the material. If material is not
included in the chapter’s Creative Commons license and your intended use is not permitted by
statutory regulation or exceeds the permitted use, you will need to obtain permission directly from
the copyright holder.
Chapter 10
Lessons on Causality from Clinical
Encounters with Severely Obese Patients

Kai Brynjar Hagen

10.1 Introduction

This contribution is about how I came to value and implement the search for a genu-
inely causal diagnosis in a specific group of patients, the severely obese. When I
started to work as a senior consultant at the Regional Centre for Morbid Obesity at
Bodø Hospital (RSSO), my background in General Practice (GP) was unusual for
the position. The RSSO is a specialist hospital centre assigned to endocrinology
within internal medicine, and closely cooperating with surgery. I soon became dis-
tressed in my professional role. It seemed to me that the healthcare system in which
I was supposed to play my part provided only rather shallow symptomatic diagnosis
and therapy. I felt like (one of) “[…] those who are troubled by the disparity between
the formal biomedical diagnoses we learned so proudly and the actual human prob-
lems that patients bring to us in our offices” (Felitti 2003: 84).
The reason for my distress was that I had decided not to mimic the specialty of
endocrinology, but to stick to my GP-approach, conceptualised as whole person
care (WPC). This concept has recently been reviewed and described as follows: “a
multidimensional, integrated approach; the importance of the therapeutic relation-
ship; acknowledging doctors’ humanity; recognising patients’ individual person-
hood; viewing health as more than absence of disease; and employing a range of
treatment modalities” (Thomas et al. 2018: 1). The study suggests that “GPs under-
stand WPC to be an approach that considers multiple dimensions of the patient and
their context, including biological, psychological, social and possibly spiritual and
ecological factors, and addresses these in an integrated fashion that keeps sight of
the whole” (Thomas et al. 2018: 8).
I encountered several discrepancies between my whole person approach and the
specialist hospital setting. First, the specialist routine was to look at one part of the

K. B. Hagen (*)
Regional Centre for Morbid Obesity, Bodø, Norway
e-mail: kai.brynjar.hagen@bodo.kommune.no

© The Author(s) 2020 149

R. L. Anjum et al. (eds.), Rethinking Causality, Complexity and Evidence for the
Unique Patient, https://doi.org/10.1007/978-3-030-41239-5_10
150 K. B. Hagen

patient at a time, not the whole person. Second, the obesity centre’s approach relied
heavily on traditional biomedical practice, reflected in authoritative guidelines for
clinical endocrinology and focusing on the somatic comorbidities of obesity (cf.
Garvey et al. 2016). There was thus little room for attention to life story and psycho-
social conditions. Third, I found that throughout the health system, negative atti-
tudes toward obese people were widespread, assigning them low status and low
priority, just as American psychiatrist Hilde Bruch noted almost 80 years ago:
“Overeating is looked upon as a moral weakness and self-indulgence. Even physi-
cians may express a sarcastic attitude” (Bruch 1948: 84). Stigmatisation of obese
people is paramount, considerably affecting the quality of their care (Phelan et al.
2015; Williams and Annandale 2018).
Were negative attitudes the reason why obese patients with eating disorders were
declined from getting help at the Regional Centre for Eating Disorders? Obesity
was not listed as a diagnosis in line with anorexia nervosa, and would not be funded
as much (less income for the hospital). Consequently, a large group of patients, the
obese ones – many of them with a type of background similar to that of their thin
counterparts – were simply excluded from this part of the psychiatric department.
Referral to trauma treatment was also in many cases declined. The reason that was
given was that the patients did not have symptoms of severe psychiatric disease. No,
they were not mentally ill, but they had an unbearable feeling of emotional pain
inflicted on them. In the manuals of psychiatry diagnosis, there seemed to be no slot
for obese patients with emotional pain.
My impression was that healthcare professionals assumed the obese patients to
“carry some heavy luggage”. These assumptions, however, were neither investi-
gated in depth nor given relevance in the person’s records. The healthcare system
seemed ignorant of the significance of a causal diagnosis in cases of severe obesity
and indifferent towards scientific evidence indicating a potential for improvement
when considering the impact of lifetime adversity on health.
Luckily, at RSSO, I am part of a competent interdisciplinary team, including
specialist nurses, colleague doctors and a clinical nutritionist as well as surgeons,
who have been open to my suggestions to increase the focus on psychosocial factors
and adverse life events. In this collaborative environment we have increasingly
turned away from a purely biomedical perspective and toward a whole person view
on the patients. Discussions within this team have since provided valuable new per-
spectives on diagnosis, therapy and follow up. We soon realised that the framework
for the clinical encounter was one of the things that we could quite easily change. I
will here describe the approach with which we are now trying to get closer to causal
diagnosis for patients with severe obesity at our centre RSSO, and briefly present
three cases from my work there.
10 Lessons on Causality from Clinical Encounters with Severely Obese Patients 151

10.2 A Framework for the Clinical Encounter

If one is truly to succeed in leading a person to a specific place, one must first and foremost
take care to find him where he is and begin there. This is the secret in the entire art of help-
ing. Søren Kierkegaard, 1880
(Kierkegaard et al. 1998)

10.2.1 The Person in the Role of the Patient – What Are

the Goals of Healthcare?

The role of the patient implies a specific status, framed by legislation, informed by
rules and norms, and endowed with rights and duties for the healthcare system as
well as for the patient. Every person has unique reasons for entering the role of the
patient – which is not always an easy decision. Typically, the outcome of medical
intervention depends on the clarification of the reasons for seeking help.
In general practice, learning to identify the patient’s goals is mandatory.
Consultants seeing patients with obesity in a hospital setting face a similar chal-
lenge. Relevant information for understanding the patient’s goals might be found in
the referral letter. In addition, patients are asked to fill in a form including questions
concerning their goals, and how RSSO might help. Reviewing these goals is impor-
tant at all stages of the further process: at the preparatory seminar, at the clinical
encounter and during the follow-up period. Perceptions might change – patients’ as
well as doctors’ – allowing for new perspectives, knowledge and emotional
maturing.
Examples of goals may be:
–– stopping further weight gain
–– losing weight, sometimes specified in kilos or percentage, in some cases aiming
at a “normal” Body Mass Index (BMI)
–– reducing comorbidities like sleep apnoea, diabetes, hypertension or joint pain
–– facilitating improved social participation and avoiding stigmatisation
–– improving physical function like hiking in the mountains
–– meeting the requirements for a specific job
–– enhancing the general quality of life
–– being able to spend time with grandchildren.
The patient’s expectation of help from RSSO, initially simply being bariatric
surgery, may become more differentiated during the course of the consultation pro-
cess. Analogously, the clinical team’s understanding of a patient might improve,
enabling them to offer more well-targeted help.
152 K. B. Hagen

10.2.2 A Group Seminar Before the Clinical Encounter:

Setting the Stage

Information about the patient is initially collected from the referral letter and the
form. Further preparations for the clinical encounter are made a couple of weeks in
advance at a group seminar for 12 patients. At this seminar, members of the clinical
team inform about the medical examination, treatment options, the diagnostic
approach and therapeutic strategies. They also provide an update on the available
knowledge, stress the necessity of avoiding conflicting objectives, and give the
patients the opportunity to discuss with them. During the seminar, the patients and
the team members become more familiar with each other’s attitudes and priorities.
The information the team conveys at the preparatory meeting includes the fol-
lowing points:
• Everyday physical activity on a sustainable level is recommendable, but physical
training normally cannot compensate for too high energy intake.
• Nutrition issues are discussed, especially the discrepancy between cognitive
knowledge and actual practice, which means that emotions often play a major
part in determining eating behaviour. A better mental condition may make it
easier to practice nutritional knowledge.
• The significance of bio-rhythms is outlined, especially the fact that regular circa-
dian rhythm and meal rhythm is physiologically preferable.
• The emerging scientific understanding of the microbiota functions is mentioned,
and also the epigenetic principles.
• We acknowledge that people with obesity might be exposed to different sorts of
bullying and violations of their integrity, which makes active self-defence strate-
gies important.
• Harmful stress is probably one of the most important causal factors for becoming
obese, linked to a variety of adverse life events. Adverse events can lead to men-
tal and physiological overactivation and painful feelings, which to some extent
can be relieved by overeating, called emotional eating. Understanding these
mechanisms should replace moralisation. I give an example from my own expe-
rience of stressful situations during night duties: chocolate with marzipan makes
me more relaxed. A brief stress-relief very much needed at the time, this effect
would not be achieved with a green salad. A stressful situation for a couple of
hours is one thing, chronic never-ending stress is something quite different—per-
haps I would have to ‘take’ chocolate continuously for relief? That might be one
possible mechanism for the onset of overweight. A number of other possible
coping mechanisms are known, for instance drug abuse, self harming and
anorexia. In my opinion, the emotional pain caused by traumatic stress is not a
mental illness, rather a normal reaction to an abnormal strain.
We present the patients with our goal: the dialogue between patient and doctor is
successful if it brings an insight that neither of them could have achieved alone. The
dialogue aims at a deeper understanding of the patient’s life history and the current
10 Lessons on Causality from Clinical Encounters with Severely Obese Patients 153

situation to enhance the validity of the diagnosis, and thus pave the way for effective
therapy. Patients are encouraged to be prepared for a rather thorough and compre-
hensive review of their life history, but of course only as far as it feels natural; no
one will be subjected to pressure. We will ask certain questions, such as, for exam-
ple: Which life events could have contributed to the onset of undesirable weight
gain? How is the current situation maintained? In some cases, one single identifi-
able cause leads to a person becoming overweight; other cases are unclear and com-
plicated. We underline the importance of a whole person view, the uniqueness of
every individual and the complexity of causal factors, rendering comparisons
between patients invalid. We explain that the weight graph will be plotted on a time-
line to look for possible correlations with life events.

10.2.3 The Consultant’s Understanding in Advance

of the Clinical Encounter

In advance of the clinical encounter, I take a few minutes to review the available
information about the patient, filling data in the template for the medical record.
This template includes not only biomedical data, but also an extended part for the
life story, especially psychosocial conditions, as well as data for the weight graph.
Sources of information are the referral letter, the patient’s preceding, written
answers in a form, and results from blood tests or other supplementary tests.
Sometimes I also make notes concerning my impressions during the group seminar.
I reflect upon what the patient’s everyday life may be like, where he or she actu-
ally is. In a meta perspective, as a kind of self observation, I try to be conscious of
my own position, my background, experience, personality, current situation and
communicative ability, since all this will influence the dialogue, the dynamic inter-
action, and consequently also the picture of the patient’s life. Hypothetically,
another doctor in my place would probably have come to slightly different conclu-
sions. In some cases patients came to me for follow-up, and it became quite clear
that the description of the patient’s life story did look quite different in my view
compared to the written record from the original examination. An example of this
might be the patient who, after bariatric surgery some years ago and initial weight
loss, came to me as he now had the same weight as the maximum weight pre-­
surgery. In my view, this was because his traumatic life story had not been addressed,
understood and taken into account. As healthcare professionals, we all have differ-
ent colored glasses through which we see the patient. These aspects of clinical com-
munication have not been part of my training from medical school, but evolved
through the years of clinical practice, and heavily inspired by dispositionalism.
Young doctors have had training in patient-doctor communication, but it seems to
me that the aspect of being part of the causal profile of the patient has not been
addressed.
154 K. B. Hagen

10.2.4 The Clinical Encounter

At the start of the clinical encounter, I ask whether the patient feels comfortable,
which is a way to pay respect to her or his current situation, and also to find a good
starting point for the dialogue. I regularly ask: “Did you sleep well last night? How
was your journey?” In some aircrafts on regional flights, severely obese people are
denied access because the seats are too narrow. In addition, the winter in Northern
Norway can make any journey challenging. I also used to ask: “Does it feel stressful
for you to come here?” Often, the patients express mixed feelings, being happy for
being admitted to the clinic, but feeling uncomfortable about addressing their obe-
sity. The patient may recently have been ill or injured, or is worried about children
back home, among other things.
I go on to inform the patient about my way of working: that I have a template
with the topical themes, that I will type part of what is said as we go along so that
correct expression can be preserved, that we will review blood analysis results and
medication, that we will carry out a brief somatic examination, and that together, we
will assess further follow-up options.
I ask the patient about allergies, surgery, pregnancies/births, diseases, known risk
factors, heredity, social situation (family, education, work, social participation),
natural functions (circadian rhythm, sleep duration/quality, urination, stools, men-
struation), physical activity, dental status (does he or she suffer from odontofobia?),
use of tobacco and alcohol. Sexual function is not routinely addressed, unless the
patient takes the initiative.

10.2.5 As a Child, Did You Feel Safe at Home?

The main focus of the clinical encounter, however, is the life story. I usually ask the
patient: “As a child, did you feel safe at home?” This is one of the themes that can
open the discussion for stories of violence, drug abuse, parental mental illness,
incest, traumatic loss of a person close to them, and so on. I became aware that there
are many forms of violence. As Norwegian writer Yngve Hammerlin – a man with
severe childhood violence experiences – has pointed out, violence is often not ade-
quately understood by doctors. From the point of view of those who have experi-
enced violence, the professional’s response can thus signal desperate simplification
and reductionism. Hammerlin suggests that the attitudes of healthcare professionals
need to reflect a deeper understanding of the many types and consequences of vio-
lence (Hammerlin 2014). The wounds of an unsafe childhood are also described by
Swedish authors, Josefsson and Linge (2011).
I explicitly ask about social participation with children of the same age, as well
as physical activities, well-being at school and how school subjects were managed.
At this point, there are often heart-breaking stories about bullying during many
years at school, and of social isolation. From early childhood, via pre-school,
10 Lessons on Causality from Clinical Encounters with Severely Obese Patients 155

adolescence, elementary school, high school, and into young adulthood, many fac-
ets form a picture of the person’s development, of adverse and supportive events, of
weaknesses and strengths, all in a whole person view. Relations to family members,
partners or spouse, as well as certain social relations, are important determinants for
life quality. Some patients find themselves in a marriage with a psychopathic per-
son, only, after divorce, to be persecuted by the same person. Also, predators abus-
ing children sexually are very seldom brought to justice, based on what patients tell
me. Some report that their childhood predator still lives in the local community, and
there is always a risk of accidentally meeting him, which provokes stress and fear.
We try to compare variations of the weight graph with changes in the psychoso-
cial situation. Sometimes there seems to be a causal relation between adverse events,
or stressful periods, and weight gain. Other forms of emotional regulation like self-­
harming, drug abuse or anorexia life style can have occurred in certain periods of
life. A minority of the patients have had psychiatric therapy, which, however, rarely
seems to have addressed adverse life events. Psychiatric healthcare is comprehen-
sive and includes a large variety of diagnostic and therapeutic methods. It seems to
me that it has been a widespread perception that trauma in the patient’s history
should not be mentioned, due to an estimated risk of re-traumatising, whereas other
institutions practice methods with basic trauma understanding. One example of the
latter is the Viken Senter in Northern Norway (www.vikensenter.no).
During the clinical encounter it sometimes feels like the dialogue exists as an
independent unit, giving insight neither patient nor doctor could have acquired on
their own, based on communication with mutual respect and engagement, and
equally shared contributions.
Before ending the consultation, test results are carefully explained, medication is
considered, somatic screening is done, we summarise and make a plan for further
follow-up.

10.2.6 The Consultant’s and Patient’s Understanding After

the Clinical Encounter

The patient’s nutrition is thoroughly evaluated by the clinical nutritionist or a spe-

cialist nurse, either before or after the clinical encounter. In case bariatric surgery is
an aim or an option, the surgeon will also see the patient. Later on, when the reports
on nutrition and surgery assessment are complete, I summarise the conclusions in
the record which is sent to the local hospital and the patient’s GP, electronically
available for the patient, and sometimes also sent as a referral to a rehabilitation
centre or a psychiatric ward where basic understanding of adverse life events is
practiced. The clinical team might discuss the case.
After 2 days in the clinic, patients have a normal follow-up period of 6 months
during which they are supposed to have a phone consultation with one of the spe-
cialist nurses or the clinical nutritionist every 2 weeks, with the goal of modifying
156 K. B. Hagen

lifestyle to lose weight, often discussing psychosocial conditions. In some cases,

additional consultations at the clinic are necessary. Further treatment can be more
conservative or supported by bariatric surgery. The post-surgery programme has
been extended to 5 years.
A locally based coordinated team can be beneficial during a comprehensive fol-
low-­up, involving the patient, the GP, and other professionals according to the needs
of the individual patient. If needed, RSSO can take part in a meeting with the local
coordinating team by phone or by video/Skype.
The post-encounter period gives a deeper understanding of the individual patient
as well as the causal factors involved. Symptomatic diagnosis and therapy might be
useful for a limited period of time, but our ambition is always the causal diagnosis
and therapy.
In order to demonstrate how this intention might be achieved, three vignettes will
be presented. The clinical encounter can be enriched and provide new insights in
light of biographical information focusing on relational and social issues during the
actual patient’s lifetime from childhood through adolescence to the present state.
The three anonymised persons whose stories unfold in the following have consented
to the publication of their accounts in this book.

10.3 Case Stories

10.3.1 Olav Olsen, a Severely Obese Man

When enrolled and examined at the RSSO, Olav Olsen, 45 years old, weighs 123 kg,
his Body Mass Index (BMI) is 40.6 kg/m2 and the waist circumference is 132 cm.
He relates that his maximum weight has been 126 kg, and that various attempts to
reduce weight have always been succeeded by weight gain.
Olav has been diagnosed with gastrointestinal reflux, oesophagitis, high blood
pressure, sleep apnoea, type II diabetes (insulin-regulated), bronchial asthma since
childhood, Mb. Bechterew since age 21, osteopenia, allergy and eczema.
Additionally, liver enzymes and blood glucose measures are above the upper norm,
and he suffers from generalised muscular pain. Cognitive psychotherapy has
recently ameliorated his previously incapacitating social anxiety. He uses on regular
basis a wide range of medications. With regard to possible heredity, type II diabetes
and coronary heart disease (father) in addition to asthma and hypertension (both
parents) should be mentioned.
Olav is single, has received a disability pension since age 31 and lives with his
parents in a rural area. Meals are typically prepared by his mother and characterised
by being irregular and high in carbohydrates. He himself describes his eating habits
as “always eating too much and never having a feeling of satiety”.
Olav relates that his childhood home was a safe place until he was 9 years old.
From then on and until age 15 years, he was sexually abused by some uncles and
10 Lessons on Causality from Clinical Encounters with Severely Obese Patients 157

cousins. However, he started being overweight already as a pre-schooler, and physi-

cal activities with his peers gradually decreased until he was in 6th grade. He was
not exposed to bullying at school and learned the school subjects reasonably well
until the age of 12, when he became anxious and concentration problems arose.
14 years old, he was so afraid of speaking up in class that he often hid in the lavatory
to avoid such exposures. At 16 he had become clearly obese (91 kg). He did not
enter secondary school due to significant anxiety.
When 24 years old, Olav’s GP referred him to an outpatient psychiatric clinic
where he received considerable help, and by age 27 he felt ready to report his sexual
abusers to the police. Six of his uncles and cousins were taken into custody. The
legal process lasted for 4 years, but without a criminal charge due to insufficient
evidence. Olav received, however, criminal injuries compensation. Olav’s case was
reported in all media, which caused him considerable distress. He rapidly gained
weight during these years, and at age 28 his weight was 103 kg.
In accordance with this highly informative and detailed first encounter, the fol-
lowing measures concerning Olav’s medical demands and further treatment were
proposed: an interdisciplinary follow-up including psychosocial support, improved
co-morbidity disease management, assistance for lifestyle changes via frequent
telephone conversations and, having implemented lifestyle changes leading to 10%
weight loss, possibly bariatric surgery.

10.3.2 Alma Almas, a Severely Obese Woman

Alma is 26 years old when she comes to the clinical encounter. Her weight is
127,5 kg, her BMI 41.6 kg/m2, and her waist circumference 129 cm. Vitamin D
deficiency is found by the blood tests. Alma has been diagnosed with polycystic
ovary syndrome, a condition resulting in multifocal pains and bleeding related to the
menstrual cycle. She reports that her father is obese as well, and that he has been
diagnosed with diabetes.
Alma drinks only minimal amounts of alcoholic beverages and doesn’t smoke
but uses snuff (nicotine). She has lived with her boyfriend for the last 3 years but has
no children. Her level of daily activity is high: housework and dog-walking for
45 min twice a day and exercising 75 min three times a week at a fitness centre. She
has worked as an assistant caretaker for mentally impaired patients since she was
21 years old. Except for the previous year, she has worked at night, resulting in
frequent change of her circadian rhythm, causing stress and insomnia, leading to the
use of sleeping pills.
Alma reports a lack of care during childhood. Her mother had been raped as a
child and has been suffering from fibromyalgia as an adult. Her 2 years younger
sister had craved much of her parent’s attention due to sleeping problems until age
three, and as a result of this they were often exhausted. Alma’s family, living in a
rural area, had poor economic resources, implying, among other things, impaired
158 K. B. Hagen

nutrition for all family members. Her father, working in a grocery store, would bring
home expired food for free. Sweets were locked up.
The onset of Alma being overweight came when she was 8 years old. Although
being one of only five pupils in her school class, her dyslexia was undiagnosed until
she was 11 years old. As she had exercise-induced asthma (also undiagnosed for a
long time), her ability to participate in physical activities was limited. Her social life
as a child was poor, partly because of her habit to withdraw from the others and
preference for being by herself.
Alma recalls that she at age 13, when spending her holidays at her paternal
grandmother’s, experienced a severe food restriction, leaving her constantly hungry
for 4 weeks. This was a relational trauma because of the pressure she was exposed
to, as well as a sort of somatic trauma related to starving. Later she learned that her
grandmother had previously been hospitalised due to anorexia. When reporting this
experience, Alma is visibly emotional.
She is almost amnestic for the time from age 13 to 18 years of age. She assumes
that she must have suffered from severe depression. During these years she con-
sumed large quantities of sweets and gained weight continuously. When 18 years
old, she left home to attend a college in a larger town while also working part-time
in a grocery shop. One year later, she experienced severe symptoms of burnout and
could neither work nor study for 1 year. Frequent psychotherapeutic consultations
over 6 months were helpful.
At 19 she had a break-up with her then boyfriend. At 22 she was assaulted on her
way home from work by one of the mentally impaired patients; he had a knife, but
she managed to escape.
Alma was informed about different treatment options, and has had a quite normal
follow-up at the RSSO, consisting of mainly telephone consultations with the spe-
cialist nurse and no specific psychiatric therapy.

10.3.3 Ebba Eskil, a Severely Obese and Depressed Woman

At the time of medical examination at the RSSO, Ebba is 46 years old. Her weight
is 106 kg, her BMI is 39 kg/m2, her waist circumference is 131 cm. She has been
diagnosed with type II diabetes at age 27, and her blood glucose is not well regu-
lated. In addition, tests indicate vitamin D deficiency. She suffers from sleep apnoea
and was treated with a positive airway pressure ventilator; continuous positive air-
way pressure (the positive air pressure made by a fan reaches the throat and keeps
the airways open through the night). Furthermore, she has chronic lower back pain,
neuropathic pain in both legs, oesophagitis and frozen shoulder. She was diagnosed
with depression at age 42 and takes antidepressants. Her diet is high in carbohydrate
and fat, with emotional eating and sometimes losing control. Previously a cleaner,
she had been unable to work the last 4 years due to myalgia, diabetes and obsessive-­
compulsive disorder (OCD), and is receiving disability benefits.
10 Lessons on Causality from Clinical Encounters with Severely Obese Patients 159

She had surgery for an extrauterine pregnancy at age 25, gave birth to her first
child at age 27 (vaginally), and to her second and third child by means of Caesarean
sections at age 29 and 35 years. She lives together with her husband and three ado-
lescent children.
As a child, she always felt unsafe at home. Her parents often had terrifying con-
flicts. Her father once cut a picture on the wall to pieces with a knife. She had one
older and one younger sister; the children normally had to find food without help
from either parent. Her relationship with her mother was especially difficult. The
mother worked as a cleaner and forced her daughter to assist her at work, thereby
isolating her socially from girls her own age. Her mother was addicted to gambling,
frequently losing money. Her parents did not contribute to activities for children and
parents at school. In addition, her dyslexia made for a difficult time at school. In the
end, she had to take responsibility for her parents, being deprived of her own
childhood.
Until she was 15–16 years of age, her body weight was normal. At 16, she moved
out from home into a dorm. She rapidly gained weight, reaching a maximum of
126 kg. Due to increasing OCD symptoms she was referred to an outpatient psychi-
atric department.
A plan for care and follow-up was made, with focus on mental health support,
improving nutrition and diabetes management, eventually bariatric surgery.

10.4 Where Do We Go from Here?

Her hair reminds me of a warm safe place

Where as a child I’d hide
And pray for the thunder
And the rain
To quietly pass me by
Lyrics from “Sweet Child o’ Mine” (Guns N′ Roses)

For me, the clinical encounters have been a most valuable source of knowledge. In
the dialogues with the patients, new insights have been opened concerning the
causal factors for obesity. It has been a truly educational journey into the unique
history of each individual.
As a child, did you feel safe? From January 2013 to July 2019, this question has
been answered in 755 clinical encounters. The answers have revealed crucial
adverse life events, each one unique, outrageous and challenging. The keywords are
trauma, loss of a related person, sexual assault, deprivation of care and safety, expo-
sure to violence and bullying. It seems especially harmful to be treated badly by
one’s mother. One patient told me that her mother said she wanted just three chil-
dren, but this daughter was her fourth child, and she was treated accordingly.
I have come to reflect on some uncomfortable questions. How many people have
been exposed to severe trauma or other adverse life events in childhood? In how
many cases has trauma been succeeded by the onset of overweight, then bullying,
160 K. B. Hagen

social withdrawal, increasing weight and emerging comorbidities? How many other
sequelae of trauma are prevalent?
Beyond the individuals, the clinical encounters have also provoked fundamental
questions concerning health, disease and healthcare. How much injustice has been
committed? How many people have known but not interfered? How many obese
people have been economically exploited by the providers of the countless, aggres-
sively promoted slimming products, symptomatic treatments and dubious surgery?
What is the total amount of damage to the individual and to society? Are the national
healthcare systems meeting obese persons in an adequate way?
Where do we go from here? In the next sections, I briefly outline the scientific
evidence and make some suggestions for changes in clinical practice.

10.4.1 “What the Hell Is Going on Here?”

Yes, ‘n’ how many times can a man turn his head
Pretending he just doesn’t see?
Lyrics from ‘Blowin’ in the Wind’ (Bob Dylan)

Scientific evidence has at least since 1940 pointed to the importance of life stories
for health and deepened our understanding of this causal relationship – although
apparently without much impact on healthcare systems or clinical practice yet. Here
are some episodes from medical science to illustrate the evidence.
In 1940, psychiatrist Hilde Bruch quoted Lichtwitz (1923) as observing rapidly
developing obesity in women who had been under severe mental stress during and
after the 1914–1918 war. However, it seems that this observation was not taken into
the internal medical discussions on causality in the 1920’s, when quite a lot of medi-
cal research was done on the causal factors of obesity. Life history was ignored,
while biochemical and pathophysiological evidence known at the time seem to be
thoroughly investigated in search for causality. Focus was on metabolic, endocrino-
logic and biochemical conditions. A salient conclusion was that obesity is not pos-
sible without malfunction of the central metabolic regulation (Bernhardt 1929).1
On the basis of her own work, Bruch described a home environment that did not
offer adequate emotional security, and where food had gained an exaggerated
importance; charged with a high emotional value, it represented love, security and
satisfaction. The child may opt for the pleasures of food if it does not get the
pleasure of love from its parents (Bruch and Touraine 1940). In 1949, psychiatrist

1
This might be the roots of endocrinology being the branch of medicine responsible for obesity
during the last century, as established in guidelines. The diagnosis of severe obesity in a traditional
biomedical sense does not focus on life story, psychosocial conditions or adverse life events; how-
ever, somatic comorbidities are highlighted. An example of this is the authoritative American
Association of Clinical Endocrinologists and American College of Endocrinology Comprehensive
Clinical Practice Guidelines for Medical care of Patients with Obesity (Garvey et al. 2016).
10 Lessons on Causality from Clinical Encounters with Severely Obese Patients 161

H. J. Shorvon and GP John S. Richardson at St Thomas’ Hospital in Cambridge,

UK, described some important clinical observations:
The investigation first arose when it was observed that some obese patients who failed to
respond satisfactorily to the usual methods of treatment dated their obesity and also some
psychoneurotic symptoms to a specific incident that might well have inflicted psychological
trauma. We found that too little attention had been paid to the emotional factors in the first
instance, and the patients had been treated on an organic basis for long periods. We do not
claim that the treatment pursued with this group is primarily aimed at reducing weight, but
we have used it to alleviate the associated mental distress and have found that patients often
show a parallel reduction of weight and become more amenable to accepted methods of
treatment of obesity. (Shorvon and Richardson 1949: 951)

In the 1980s, Vincent J. Felitti, an internist who founded the Department of

Preventive Medicine at Kaiser Permanente in San Diego, made similar observa-
tions. He witnessed a paradoxical tendency for patients who had successfully lost
weight in his ward to not participate in the follow-ups. He ended up asking himself:
“What the hell is going on here?” (Kirkengen 2019). Felitti decided to ask these
patients about their background, and he found that each of them had experienced
considerable adversity (ibid.). In the “Adverse Childhood Experiences Study”
(ACE-Study) Felitti and his colleagues later found a dose-response relationship
between childhood trauma and obesity, as well as a range of other diseases (Felitti
et al. 1998). More recently, a relationship in line with the ACE-Study was found in
a Norwegian setting (Tomasdottir et al. 2015). A significant relationship between
exposure to violence in adolescence and being overweight has also been demon-
strated (Stensland et al. 2015). The relationship has been confirmed in recent meta-­
analyses (Danese and Tan 2014; Wang et al. 2015; Hemmingsson et al. 2014). A
chronological relationship between adverse life events and the onset of obesity has
been shown in a study by Lynch et al. (2018).
It is fairly well-established that emotional eating can be caused by trauma,
depression and post-traumatic stress disorder (PTSD) (Talbot et al. 2013). The
observations of the role of mental stress in Litchwitz (1923), and Bernhardt’s (1929)
focus on changes in brain physiology, both point to modern scientific theories of
allostatic overload as a possible mechanism for the connection between trauma and
obesity. Allostasis is “the process by which a state of internal, physiological equilib-
rium is maintained by an organism in response to actual or perceived environmental
and psychological stressors.”2 Allostatic load involves psychological, neurological,
endocrinological and immunological processes to cope with mental or physical
challenges. Overload might result in dysregulation, and possibly disease
(McEwen 2012).
Back at the RSSO, I asked myself why this scientific evidence has not been
implemented in clinical practice. Why has accumulated knowledge from seven or
eight decades not yet been acknowledged in healthcare? Even the modern, authori-
tative medical resource UpToDate does not mention very much about psychological

2
Merriam-Webster online dictionary, entry on “allostasis”. https://www.merriam-webster.com/
dictionary/allostasis [accessed 9 June 2019].
162 K. B. Hagen

causes apart from winter depression (Perreault 2019). Typically, aetiology is out-
lined, both in childhood and adulthood, practically without any reference to psycho-
social conditions.

10.4.2 Is This How the System Works?

I want you to panic.

Greta Thunberg, environmental activist

What lies under the surface of symptoms? What is under the surface of healthcare
systems? Are our healthcare systems built on shallow interpretations of symptoms,
failing to understand and respect the true causes of disease? Can this unpleasant
question generally, or only partially, be answered with “yes”? In that case, a funda-
mental change of concepts would be urgent, a new paradigm needed. I will now
present my subjective impression of some parts of healthcare, based on decades of
clinical experience in a Norwegian setting.
Experiences that exceed a person’s coping capacity result in some kind of dam-
age to health because they provoke harmful stress, emotional pain and pathophysi-
ological consequences. Furthermore, they affect the whole person as well as her or
his interactions within ecosystems he or she is involved in, including epigenetic
effects.
Every living creature will try to get rid of, regulate or at least soften any form of
unpleasant, harmful condition or imbalance. Overeating is only one of many possi-
ble ways to achieve relief. We still don’t know why certain coping strategies are
chosen instead of other alternatives, such as self-harming, drug abuse, and so on.
These desperate measures, meant for regulation, can result in a variety of symp-
toms, some obvious, some hidden and complex.
The obvious symptoms are easily picked up in the healthcare system, interpreted
according to rigid professional guidelines and traditions, then categorised in
algorithm-­based diagnostic systems. One example is the Diagnostic and Statistical
Manual of Mental Disorders (DSM), an American concept generally adopted by
Western countries. The DSM is overwhelmingly comprehensive, barely leaving any
human being without a diagnosis, and it is widely used as a basis for drug manufac-
turing, financing within healthcare systems, for building up specific departments in
healthcare systems and, what is worst: for putting persons into stigmatising catego-
ries, often randomly, as their symptoms may fit into many different diagnoses. As a
person, you are defined in the light of your diagnosis, and you can be stuck in that
narrow prison cell for a long time, deprived of empowerment, deprived of unfolding
on your own terms, forced into the world of white coat guidelines.
Generally, it is hard to get rid of a diagnosis once established, regardless of how
wrong it might have been. In some aspects, the symptomatic diagnosis is useful, but
not as a replacement for the causal diagnosis. A patient with a broken leg who has
symptoms like pain and not being able to walk is grateful for symptomatic therapy
10 Lessons on Causality from Clinical Encounters with Severely Obese Patients 163

with analgesic drugs and a wheelchair, but in the long run he will be even more
grateful for causal therapy: orthopaedic surgery. Persons with obesity are generally
denied such causal diagnosis, and consequently, deprived of causal therapy. The
utterly shallow diagnoses keep people chained in a position with impaired quality of
life, exploited financially by a number of agencies, including health “care”. Causality
means not only considering the top of the iceberg, not being stuck in superficial
symptoms, but to rather take a look beneath the surface, approaching a deeper
understanding.
For the last 80 years or more, the importance of a person’s life story has been
documented. This is where the roots of poor health may often be found, which is a
basic premise for cure and enhanced quality of life. Let the patient’s life story
always be part of the clinical encounter.
We should panic for
• all the people with traumas not receiving adequate help
• the amount of avoidable childhood trauma that our communities fail to prevent
• the healthcare resources being wasted on ineffective or harmful treatment
• the fact that valid knowledge is not implemented in clinical practice
• the fact that our civilisation still stigmatises a large part of the population, meet-
ing them with sarcasm, ruining their self-esteem.

10.5 Outlook

Starting work in the traditional biomedical environment in hospital, I felt the same
as expressed by Shorvon and Richardson (1949: 951), “that too little attention had
been paid to the emotional factors in the first instance, and the patients had been
treated on an organic basis for long periods.” This situation may have been caused
by the medical funding system that rewards quantity but ignores quality of care.
Reasons for this situation may also include the view on causality on which our
medical system is based. This view – characterised by lack of attention to the indi-
vidual and to the interacting factors in the individual’s life – also suits business
interests too well and contributes to diagnostic and therapeutic restraints. The pres-
ent volume makes a wonderful contribution to addressing this societal problem.
When, at RSSO, we decided to give much more attention to each patient’s life
story, setting aside sufficient time for the dialogue, this was a sign of respect, a
courtesy to the patients – and I also hoped to create room for new insights and
causal diagnosis. The responses from the patients have been positive. They have
appreciated being given more time, being listened to, having an opportunity to get
rid of shame and to develop deeper insight into how their condition and life story
might be interwoven. Many have expressed thankfulness and have been willing to
contribute to research. This suits my feeling that we do in fact generate insights in
the dialogues.
164 K. B. Hagen

I have thus decided to try to contribute to research on the severely obese patients
from Northern Norway.3 On 18 October 2018, Martine B Aaseng (patient), profes-
sor Linn Getz and the chief executive officer of the Health Administration for
Northern Norway (Helse Nord RHF), Lars Vorland, gave an interview on Norwegian
television. Getz said that knowledge about the importance of life history is now so
well founded that it is time it gets implemented into clinical practice. Vorland
responded quite honestly that he had not been aware of this.4
As my profession is medical practice, not research, the apparent deficits in diagno-
sis and treatment of the severely obese were what alerted me to the failure of a system
that I had become a part of. But my encounters with researchers Anna Luise Kirkengen,
Linn Getz and Rani Lill Anjum helped give me a sound theoretical platform that
matches my clinical experience. Four decades after medical school, their work
undoubtedly renewed and expanded the basic platform on which my clinical practice
is built. This has also had a major impact on my work as GP and at the Norwegian
Work and Welfare Authority. It feels right, in every aspect of clinical medicine, to
acknowledge patients’ life stories as essential parts of the causal diagnosis that medi-
cine should always strive to achieve. In the clear light of dispositionalism, elaborated
in this book, it is now time for changing the game, for a new paradigm in medicine to
be accepted and implemented in care, in order to give patients the help they deserve.5

References and Further Readings

Bernhardt H (1929) Kapitel I: Zum Problem der Fettleibigkeit. In: Czerny A (ed) Ergebnisse der
Inneren Medizin und Kinderheilkunde. Springer, Berlin, pp 1–55
Brewerton TD (2017) Food addiction as a proxy for eating disorder and obesity severity, trauma
history, PTSD symptoms, and comorbidity. Eat Weight Disord 22:241–247
Bruch H (1948) Psychological aspects of obesity. J Urban Health 24:73–86
Bruch H, Touraine G (1940) Obesity in childhood; family frame of these children. Psychosom
Med 2:141
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Chapter 11
Reflections on the Clinician’s Role
in the Clinical Encounter

Karin Mohn Engebretsen

11.1 Introduction

Several years ago, I decided to examine the philosophical and cultural roots of my
therapeutic activities. I was aware of how different ontological perspectives – and in
turn methodological choices related to the epistemological question “how do we
know” – could affect the therapeutic encounter. There might be some hundred dif-
ferent approaches to psychotherapy but the crucial division between the psycho-
therapies is not between the “schools” but mainly between what I will refer to as the
positivist and the post-positivist or constructivist paradigms. Those years ago, I
lacked a clear orientation and became aware that I was vacillating between different
methods. I also thought I was able to work without the intention of healing my cli-
ents if I just stayed with what was happening in the process. When I realised that, in
reality, I did actually have an intention of healing, I decided to explore to see what
philosophical theories I might be working from. During this process I wondered
about the nature of my underlying motivations for the ontological and epistemologi-
cal choices I had made in my search for answers to the fundamental questions that
are either implicitly or explicitly contained in the way I practice gestalt psycho-
therapy. Today, psychological theory has become more of a philosophical world-­
view to me, or a way of thinking and perceiving—more than a taught theory about
psychological interventions. In reviewing the path I have followed, I have over time
come to know several different traditions in psychotherapeutic practice and, conse-
quently, my opinions about important therapeutic concepts have changed, becoming
both extended and refined.
With my desire to heal, came a tendency to see myself as being able to know
what was best for my clients. This attitude, I suppose, is still prominent in many
clinical encounters. For instance, Cognitive Behavioural Therapy (CBT) is the

K. M. Engebretsen (*)
Department of Medicine, University of Oslo, Oslo, Norway
e-mail: kme@interdevelop.no

© The Author(s) 2020 167

R. L. Anjum et al. (eds.), Rethinking Causality, Complexity and Evidence for the
Unique Patient, https://doi.org/10.1007/978-3-030-41239-5_11
168 K. M. Engebretsen

“preferred” methodology seen from a political/governmental point of view. This

preference is due to how it fits into the norms, methods and practices of evidence
based medicine and the positivist (Humean empiricist) paradigm. Institutionalised
norms, methods and practices certainly influence our attitudes when working clini-
cally, and inherent values affect patients in clinical practice and medical care.
Although I here use my own experience as a gestalt psychotherapist, I think much
of what I say will apply to any encounter where there is a power imbalance as is the
case between patients and clinicians. I start from a client-centred approach building
on Rogers’ (1962) “non-directive” therapy. In this perspective a healthcare system
should acknowledge the client as an integrative whole, where the medical issues
must be understood not only on the physiological level, but also within a biographi-
cal, social and cultural context.
It is equally important to acknowledge the clinician as a person, with everything
that he or she brings to the clinical encounter in terms of values, expectations, per-
spectives and interpretations. How does the clinician influence the encounter with
the patient, in positive or negative ways? And how important is it to be aware of
one’s own role in the clinical encounter?

11.2 Reflections on How Values Affect Clinical Encounters

Historically, gestalt psychotherapy has rejected diagnosis as being depersonalising

and anti-therapeutic. This can be seen as a reaction to the dualistic biomedical
model, which seems to isolate the issue of psychological suffering as pathological.
The DSM (Diagnostic and Statistical Manual of Mental Disorders) is a psychiatric
diagnosing tool (American Psychiatric Association 2000) where the diagnostic cri-
teria are, for the most part, based on manifest descriptive psychopathology rather
than inferences or criteria from presumed causality or aetiology. The organisational
framework by which disorders are grouped into similar clusters are based on shared
pathophysiology, genetics, disease risk, and other findings from neuroscience and
clinical experience. Being descriptive, it is compatible with how gestalt psycho-
therapists diagnose clients. In a gestalt perspective, however, psychological suffer-
ing is not seen as psychopathology but rather as a creative adjustment to threatening
life-experiences and thus, it is based on observations of phenomenology. This
includes a focus on body and mind processes, the clients’ well-being, character
structure and level of emotional development, but also attention to the strength of
the therapeutic relationship and stage of treatment. This means that gestalt theory
takes into account the total contextual field of the clinical encounter, and thus takes
a holistic, non-reductionist and non-dualistic view. As such, the two diagnostic tools
differ radically as the DSM does not fully take into consideration the person within
his or her context.
When it comes to the diagnostic practices within medicine, I often experience
that clients who are referred to me by their general practitioner (GP) are diagnosed
with depression. When no physical biomarker is found, the patients’ symptoms
11 Reflections on the Clinician’s Role in the Clinical Encounter 169

seem to be attributed to psychopathology and the patients’ subjective health com-

plaints are often conveniently reduced to a diagnosis of depression, which may of
course be one of their symptoms. This is also often the case for persons who suffer
from fatigue and pain related symptoms. The biomedical model and evidence based
medicine (EBM) are rooted in the positivist paradigm. Within this paradigm, knowl-
edge is achieved exclusively by what is directly observable and objectively measur-
able, and little space is left for reflections about subjective factors and underlying
mechanisms (Kerry et al. 2012). Being diagnosed as depressed often upsets these
clients and they often openly disagree with their GP. The result of such disagree-
ment can result in a lack of trust and worsening of the experienced symptoms.
In clinical interactions, the patient can be addressed as an object, or as a person.
Consider the often-used metaphor, that the biomedical model construes the human
being as a complex machine. In this machine, dysfunctions might be caused by
internal or external harmful factors and the machine is unable to re-establish well-­
functioning on its own. On this view the person has lost his or her agency and
becomes the passive victim of the diseased part subjected to external repair-work.
In contrast, gestalt theory sees the human being as an agent who is in constant
interaction with his or her environment, aware of phenomena such as the experience
of bodily sensations in response to internal and external interacting factors. Patients
are to be recognised as subjects in their own right with their own habitual prefer-
ences of behaviour. A clinician cannot truly know what is best for the patient –
therefore, it is necessary to give up the desire to be appreciated as some kind of a
healer. If not, the patient becomes a means to an end in the clinical process.
According to Buber (1965), human interactions can be characterised by a meeting
of subjects or a ‘‘thingification’’ of the other. The subject “I”, can be seen as part of
an I – Thou attitude or the “I” of an I – it attitude. In Buber’s terminology “Thou”
means “you”. Therefore, addressing the client in an I – Thou attitude is a central
perspective in relational gestalt psychotherapy and any other person centred prac-
tices. Accordingly, I will address two pertinent questions. The first one is: how
important is the clinicians’ role within the clinical encounter?
Gestalt psychotherapy is rooted in an existential-phenomenological world-view.
In this world-view, all events are a function of the relationships between multiple
interacting forces where no event occurs in isolation (Yontef 1993). If we apply this
view to the clinical encounter, any therapeutic process is a function of the relation-
ship between the interacting therapist, client and their common field as a whole.
Thus, the field is co-constructed as an integral part of the therapist/client experience,
which will have an impact on the possibilities for different outcomes of the process.
This means that we can no longer speak of individual growth as “self-­development” –
in fact it is “self/other development”. Additionally, growth of the entire individual/
contextual field is only possible if the field has the capacity to adequately support its
members. Similarly, in medical practice, any medical treatment might be seen as a
function of the relationship between the interacting doctor, patient and the field as a
whole, which might be the case in person centred medicine.
In person centred care, the focus is mainly on the patient: how the treatment
influences the particular individual, and how the patient responds to the treatment.
170 K. M. Engebretsen

First of all, I will highlight the word ‘treatment’. How can we understand this term?
When you are treating somebody, it is easy to imagine the doctor as providing the
patient with something that might be what he or she needs. When the dialogic
encounter is understood from a dispositionalist perspective, however, the focus
must be on all the participants who are present. As such, the dialogic encounter can
be seen as an emergent phenomenon where the client and the therapist are mutual
manifestation partners for the outcome of the therapeutic process (see Anjum, Chap.
2, this book). Thus, the dialogic encounter is not simply uncovering the client’s
experience of her situation, but can be seen as a genuinely interactive process where
both the client and the therapist bring themselves in as human beings and thereby
influence the encounter reciprocally.
Gestalt psychotherapy is based on the meeting between the therapist and the cli-
ent as the central healing mode. This means a healing through meeting in reciprocal
humanness. In this view it is important to acknowledge the clinician as a person,
with everything that he or she brings to the clinical encounter. The development and
growth of any healthy self in the field requires a field that includes other healthy
selves. We are all inter-dependent and the quality of my life will influence the qual-
ity of my environment. Therefore, a relational approach requires careful and consis-
tent observation of all the data in the field including my own processes, values and
beliefs as a therapist. This leads us to the second question: how might the clinician
influence the encounter in positive or negative ways?
In my experience, it is “easy” to handle therapeutic processes individualistically
and react as if my existence is separate from my environment – especially when my
own self-process is jeopardised. In such cases, how might the encounter be affected?
Being part of the therapeutic process, I am not only engaged as a supportive
ground, but as a co-participant as well. When “acting” as a tool in the therapy pro-
cess, the therapist might be drawn into phenomena such as transference and coun-
tertransference (Rycroft 1979). These two notions can be understood as the process
by which feelings, behaviours or attitudes of clients and therapists that belong in the
past, are transferred to the therapy participants in real time. Transference is our
unconscious activity that is shaped by normal preverbal perceptions of self and
other, which organise our subjective universe (London 1985). Client and therapist
actively co-create the shared perceptual field of the therapeutic relationship.
Therefore, from a dialogic perspective, the client’s processes of transferring cannot
be interpreted as emanating from the client in isolation, but must be seen as emerg-
ing as part of an inter-subjective relational system (Hycner 1991). Countertransference
refers to the therapist’s feeling towards the client, in response to the projected
transference.
When the therapist is unconsciously drawn into transference processes, the out-
come of the therapeutic relationship might in best case be ruptured and in worst case
be quite the opposite of therapeutic. In my experience, relating objectively to phe-
nomenological data constitutes a major challenge, even for well-trained psycho-
therapists. Therefore, I see supervision as crucial when working dialogically. I have
experienced meeting clients who are sensitive to what they experience as personal
critique. Their emotional reaction might be due to shame proneness. Some of these
11 Reflections on the Clinician’s Role in the Clinical Encounter 171

clients seem to have been severely shamed by previous therapists, before seeing me.
The presentation of the work I did with one of my clients later in this text shows how
easily this can happen, and also reminds us of the importance of being consciously
aware of the therapeutic process. The attentive attitude requires humility and explic-
itly promotes respect and appreciation of differences.
I am aware of how contextual conditions often change the way I work. With cli-
ents who are more psychotic, I work more analytically – just being there, holding
the boundaries, not intervening, challenging or contacting. With healthier clients, I
work more dialogically. These choices mirror the clients’ level of emotional devel-
opment and character structure as well as the strength of the therapeutic alliance. I
am also aware that there might be a difference between theory and practice – how
my values might change in practice. In one-to-one settings I am gentle and soft; in
groups I am often more robust and challenging. The danger of not taking differences
between people seriously enough is constant. In my experience, it is exactly the art
of relational psychotherapy to bring the differences into awareness. And in the dia-
logical encounter differences related to values or attitudes are to be appreciated –
not diluted or combatted.
In what follows I present a snapshot of the psychotherapy I enact. By presenting
the work I did with Marie over several months, I will illustrate how my work embod-
ies the theory. This illustration shows how the phenomenology I enact fits into the
dispositionalist paradigm. I start with a presentation of how I experienced the initial
meetings with Marie and my reflections on what she might need. Then I describe
parts of the work we did together.

11.3 The Work I Did with Marie

11.3.1 Presentation of the Client

Marie1 was a 45 year old married woman with two grown up children. Her husband
was a chief executive officer in a large multinational company and travelled a lot.
Due to this she spent most of her time on her own. Until recently Marie was a man-
ager in a small company, but lost her job last winter. This made her feel lonely and
lost. She told me about her happy childhood; her mum and dad and her sister who
was 3 years younger, whom she adored. The family spent a lot of time together,
either alone or with friends. Both her parents were dead, her father died when she
was 20, her mother 2 years ago. After the death of her mother, she did not have
much contact with her sister, although they lived in the same part of the town.
Before she began seeing me, she had been ill for a month. Her referral to me was
via her GP, who had diagnosed her as depressed. Her reason for wanting therapy

1
‘Marie’ is a fictive name. Some details have been altered for the purpose of de-identification
according to ethical and legal standards and written consent to use her story has been obtained.
172 K. M. Engebretsen

was that she needed some help to fix her life. She presented with issues of anxiety
and panic attacks, feeling isolated from others, especially her husband. Her GP
wanted to give her antidepressants, but she refused because she did not see herself
as depressed. We agreed to work for a 6 week assessment period to determine
whether we were able to work together or not and to review our work after that on
an open ended contract.
The first time I saw Marie, I was struck by her attractiveness; she was tall, slen-
der, and well dressed, with a determined stride. Her long dark hair framed her deep
blue eyes. Her voice was rich, and sensual. With the pitch of her head forward, her
eyes were often cast downward and seldom met mine. Sometimes, when she did
look in my direction, she glared. This look of camouflaged contempt made me feel
tense. Marie’s facial expressions were endless. She commented on everything with
a wince, as if every feeling that passed through her body was expressed only by the
muscles of her face. When she became anxious in the session, this tendency was
especially evident.
My initial reaction to Marie was curiosity and I felt warm and concerned towards
her. I experienced her as being extremely bright, demonstrated by the way she pre-
sented herself and her use of vocabulary. Marie’s connection to her mother changed
at the age of three, when her sister was born, and she was sent to her mother’s sister
for some weeks. Afterwards she became dad’s girl. When telling me about her
father’s death, she teared up, but seemed to be unable to relate to the emotional situ-
ation that she obviously experienced. She turned away from me, silently sitting
there for a while – then she laughed. I often experience such reactions, which I see
as a normal human ability that allows us to put off dealing with emotions until we
feel able to address it. When she laughed, I was aware of feeling irritated and when
reflecting on why, I became aware of one of my personal assumptions that I might
have acquired without full awareness of its purpose: “It’s silly to laugh”. She
described her relationship with her mother as ambivalent, never knowing where she
was in relation to her. Marie told me that her mother must have been depressed – she
could be silent and withdrawn for days, not addressing anybody. I was struck by
how some aspects of her history paralleled my own. I also felt adored by my father
and abandoned by my mother, which alerted me to the possibility of transference/
countertransference processes. And, I was aware that I could easily be drawn into
over-identifying with her. I knew at this early stage that I would need to discuss our
relationship with my supervisor to be able to bracket off my own emotional baggage.

11.3.2 Presenting Problems

Marie came to therapy with difficulties especially in her relationship with her hus-
band. The slightest misunderstanding between herself and others left her with feel-
ings of abandonment and deep loss. Whenever she spoke about an emotion such as
her fear of being abandoned, she would immediately discount it with statements
such as, “But I know that’s crazy, because I should not feel that way!” In this regard
11 Reflections on the Clinician’s Role in the Clinical Encounter 173

she was extremely critical of the vulnerable aspects of herself. She was also highly
critical of others, an aspect of herself which she joked about by stating that it was
due to her superiority complex.

11.3.3 Diagnosis

From a gestalt perspective I think it is fruitful to understand Marie’s process histori-

cally as a “creative” adaptation to her life situation. This adaptation can be seen as
the relationship between Marie and her environment, in which she takes responsi-
bility for creating conditions to take care of her own well-being. Thus, I see diagno-
sis as a descriptive statement that articulates what I notice in the present, which
informs me of how I might be able to help my client.
Gestalt psychotherapy embraces Merleau-Ponty’s holistic view of the human
being, conceptualised as existing in continuing interplay in the “organism-­
environment field” (1945/1962). The organism-environment field can be understood
as a systematic web of relationships, which consists of a totality of mutually influ-
encing forces that together form a unified interactive whole. Out of this intersubjec-
tive field, “figures” emerge. The configuration of a figure against a ground displays
the meaning, and meaning is achieved only through relations in the field. Thus, the
relationship between the ground of the field and the figures that emerge is what
gives meaning to the whole. To perceive and be aware of an emerging figure is the
act of contact.
The idea of “unfinished business” is a core notion in the gestalt approach to
explain how the act of contact might be interrupted. This notion refers to a tendency
of the organism to complete any situation that is experienced as unfinished (Perls
et al. 1951). For example, when Marie was not able to get her needs met, some spe-
cific contact episodes emerged between us at the contact boundary (Clarkson 1989).
I became aware of some aspects of her behaviour, which stood out from the context
like figures against a ground. These figures became interesting as a source of further
exploration when I observed them as a pattern over time and across situations.
Contact boundary disturbances do not refer to psychopathology, but to a disruption
in the clear awareness and organismic flow between self and other, which can be
either healthy or pathological. Very early on in the encounter with Marie, I became
aware of the transference that was taking place between us. I reflected on whom I
might represent to Marie – when I felt warm towards her, I would be her father, and
when I felt irritated and critical, I would be her mother. So, when I was feeling irri-
tated and critical towards her, she might have been unaware of conveying her feel-
ings by giving me as the therapist an experience of how she feels, rather than by
articulating. Thus, there was a possibility that I could end up behaving towards
Marie like her mother did.
After this brief presentation of my initial contact with Marie, I now turn to the
therapeutic process and present some of these interruptions to contact, and how I
work dialogically.
174 K. M. Engebretsen

11.3.4 The I-Thou Process

To illustrate how I worked with my client, I will list four discernible phases in the
“I-Thou” perspective (Buber 1965). These phases are (1) “Exploring self; an it – it
attitude”, (2) “Becoming aware of the therapist’s presence; an I – it attitude”, (3)
“Struggling with abandonment depression; an I – Thou attitude”, and (4) “Moments
of mutual satisfaction; a Thou – Thou attitude”. These four phases show how Marie’s
and also my own ability to integrate personality aspects that previously were not
fully “owned” resulted in an emergent phenomenon, that is, the therapeutic outcome.
Phase 1: Exploring Self; an It – It Attitude. When Marie entered therapy she
talked about herself and objectified both herself and me as a therapist and asked,
“how can you fix me?”. Marie rapidly established an “idealising” transference
towards me, which can be understood as Marie’s unconscious recognition of some
of her mother’s traits in me, and then started acting out how she previously idealised
her mother. When I became aware of the idealising transference she projected onto
me, and the immediate impact it had, I realised how flattered I felt. I was able to see
that I was not fully present to her as another person. However, the loving attitude I
felt towards her, and the mirroring I did during this phase, was an authentic desire
to nurture and “mother” her.
My main goal for this phase (6 weeks of therapy) was to build a therapeutic alli-
ance. I focused primarily on building a trusting relationship, and therefore I was
initially and primarily concerned with “confirming” her (Buber 1965). By confirm-
ing in this context, I mean accepting not only what Marie is aware of, but also
aspects of her existence that are denied, e.g. confirmation of the person in her fullest
potential. I started to practise “inclusion” (Buber 1965) with her. By this I mean
closely listening to both verbal and nonverbal communication, carefully giving her
phenomenological feedback to raise her awareness of herself. In this situation I
address her as a “person” – not as an “object”. Intuitively I felt she was very sensi-
tive to anything I did that she could interpret as being a rejection. However, instead
of telling me directly when she felt ignored or insulted by me, she would get a cer-
tain withdrawn and contemptuous look on her face that I came to recognise. When
I addressed this phenomenologically, she would comment back to me with a wince,
obviously feeling misunderstood and attacked. She was not interested at this point
in insight about herself, because she was convinced that all insight would simply
lead to criticism. I was imagining that her self-esteem was very fragile and instead
of exposing her insecure self, she presented a “false”, defensive self to me. This
imagining must be distinguished from empathy, which leaves out one’s own side as
a therapist. To be able to practice inclusion the therapist needs to be able, as much
as is humanly possible, to attempt to experience what the client is experiencing,
feeling, thinking or knowing from her side of the dialogue, as well as meeting her
authentically and honestly as part of practicing inclusion with her.
Phase 2: Becoming Aware of Therapist’s Presence; an I – It Attitude. Previous
sessions had taught me that experiments had triggered resistance and would be seen
as criticism of Marie’s behaviour. For example, Marie suddenly stopped talking in
11 Reflections on the Clinician’s Role in the Clinical Encounter 175

terms of herself and switched from saying “I” to saying “we” without any apparent
awareness. Instead of saying: “why don’t you try an experiment and say ‘I’ instead?”
I would rather say: “I was wondering if what you were talking about suddenly felt
too painful to continue talking of in terms of yourself?” This response made it easier
for Marie to explore her painful feelings and helped her to stay in contact with me,
and increased her self-awareness without triggering unbearable anxiety.
Marie had introjected her mother’s self-image and idealised her mother in order
to maintain any sense of having an ordered, loving family. An “introject” may be
seen as accepted personal habits acquired without full awareness of their meaning
and purpose (Perls et al. 1951/1998). When she described what she was aware of
when she attempted to make contact with her husband, she became more aware of
her “impasse”. Here, the impasse can be understood as how Marie acted out the
experience of seeing herself as a dis-empowered object (Newirth 1995). She imag-
ined that her husband was much too busy to want contact with her, and the conversa-
tion just stopped. This experience left her frustrated, lonely and longing for
connection. I asked her to describe her experience of longing, which she experi-
enced as a vulnerable and lonely feeling in her stomach. She added that she feared
rejection and quickly stated that her mother had never accepted her husband – and
he was not worth connecting to anyway. I encouraged her to stay with this feeling
of criticism, and we explored further the frustration that emerged in her. When she
was able to disclose more of her feelings of insecurity and low self-esteem, she was
able to ask for more support. At this point, she was able to take in the support I
offered her when raising her awareness of how her attempts to deal with her vulner-
ability by being critical towards herself only left her feeling more frustrated and
distressed. Gradually she became able to honour herself.
During this phase I experienced that she started to sense her feelings of anger,
being aware of her need to express herself, to mobilise her energy, and finally to
vent her feelings towards her mum.
Phase 3: Struggling with Abandonment Depression; an I – Thou Attitude. Once
this trusting and accepting relationship was established, the next phase began, where
some of Marie’s problems related to interactions with others were further explored.
There were more moments in which I – Thou encounters occurred, than there were
moments in which I – it encounters occurred. As Marie started to see me as a person
I became more important to her. This was when the therapeutic relationship was
challenged.

11.3.5 Key Episode 1

Marie started to project the anger outwards, which she had previously controlled,
and became very critical towards me. When I heard her stating: “no one can be
relied upon”, I was aware that this was similar to one of my own introjects and I
recognised the wounds from feeling rejected by my mother. It was therefore impor-
tant for me to “bracket off” my own emotional reactions in order to be available to
176 K. M. Engebretsen

explore and to fully understand how Marie made meaning out of this statement. In
this context “bracket off” means that I held some of my own concerns in abeyance
in favour of attending to what was going on when interacting with Marie. I tried to
meet her honestly and authentically. I did, however, feel wiped out by her and knew
that this was something I would have to explore in supervision. Initially, I was able
to stay in contact with her, but I was aware of feeling induced to behaving towards
her like my mother did towards me. And because of the sensed similarity between
Marie’s mother and my own, I was particularly vulnerable to this induction.
When she started to reveal her dependent, needy side I was aware of feeling irri-
tated and angry with her. I had, in a sense, fulfilled what she expected – being
rejected was what she really feared. She exhibited the anger she previously had
controlled and talked to me with sarcasm and contempt, when the narcissistic and
maternal “supplies” she was seeking from me were withheld. I thought in that
moment and subsequently that Marie had benefited from my firm, withholding pos-
ture and that I had managed to resist her seductiveness. I was however left feeling
uncomfortable about how harsh I had been and continued to be over the next two
sessions. I sensed that Marie was withdrawing. We both had reached an impasse. I
struggled a lot and felt dreadful until I had discussed what had happened and worked
through the process with my supervisor.
Phase 4: Moments of Mutual Satisfaction; a Thou – Thou Attitude. In this last
phase Marie was able to practice inclusion with me, which means that she was able
to stay in the present moment, meeting me honestly and authentically. This hap-
pened after I decided to disclose the pain I had felt and explained to Marie what I
thought had happened in the process.

11.3.6 Key Episode 2

I was able to disclose my humanness to her and say I was sorry for the mistake I had
made after being able to non-defensively own parts of my own history and been able
to heal old wounds. When doing so, the contact between us was paradoxically re-­
established. I felt I was risking a lot, but in this moment of Thou – Thou mutuality,
being authentically present, I felt grace and deep satisfaction. By authentically dis-
closing myself as who I am, something changed.
Over the course of this work, Marie started to see herself differently. There has
been a shift in her attitude towards herself. Instead of seeing herself as the bad part
of the mother-daughter relationship, she has started to see that it was not all her
fault. In this process, she has started to grieve for the mother who was not there for
her. Marie reported that the panic attacks had not occurred since Key Episode 2. She
is now able to feel more satisfaction in her life, and her relationship with her hus-
band has deepened.
11 Reflections on the Clinician’s Role in the Clinical Encounter 177

11.4 Reflections

I see philosophy as the way I hypothesise about everything in my life and the
essence of how I work as a psychotherapist and researcher. Philosophy also helps
deconstruct being social; “how do I connect with what is?”. This fundamental ques-
tion is an inquiry into what collective experience is possible. On the contrary, to
treat knowledge as intellectual, prescribed and something we are taught, is to forget
its social and interpretative nature. Thus, this question is of concern to all of us, and
not so much in terms of “I”, more so in relation to “we”.
In this short text I have reflected on the clinicians’ role and how we as clinicians
might influence the outcome of the encounter. I am intrigued by the relationship
between the therapist and the client, as well as the relationship between the client/
therapist and “significant others” in the clients’ lives. This relational aspect is the
concrete basis for how I work clinically. The ontological stance we take, either con-
sciously or unconsciously, will influence our norms and methods and, in turn, the
way we practice. I hope that this text will stimulate further reflection and discussion
on the clinicians’ role in the clinical encounter.

References and Further Readings

American Psychiatric Association (2000) Diagnostic and statistical manual of mental disorders,
4th edn. APA, Washington, DC
Buber M (1965) The knowledge of man. Harper & Row, New York
Clarkson P (1989) Gestalt counselling in action. SAGE Publications, London
Hycner R (1991) Between person and person: toward a dialogical psychotherapy. The Gestalt
Journal Press, Gouldsboro
Kerry R, Eriksen TE, Li SAN, Mumford S, Anjum RL (2012) Causation and evidence-based prac-
tice: an ontological view. J Eval Clin Pract 18:1006–1012
London N (1985) An appraisal of self psychology. Int J Psychoanal 61:237–248
Merleau-Ponty M (1945/1962) Phenomenology of perception. Routledge, London/New York
Newirth J (1995) Impasses in the psychoanalytic relationship. Sess: Psychother Pract 1(1):73–80
Perls F, Hefferline RF, Goodman P (1951/1998) Gestalt therapy, excitement and growth in the
human personality. The Gestalt Journal Press, Gouldsboro
Rogers CR (1962) On becoming a person. A therapist’s view of psychotherapy. Houghton Mifflin,
New York
Rycroft C (1972/1979) A critical dictionary of psychoanalysis. Penguin Books, Hammersworth
Yontef G (1993) Awareness, dialogue and process: essays on gestalt therapy. The Gestalt Journal
Press, Highland
178 K. M. Engebretsen

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adaptation, distribution and reproduction in any medium or format, as long as you give appropriate
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Commons license, unless indicated otherwise in a credit line to the material. If material is not
included in the chapter’s Creative Commons license and your intended use is not permitted by
statutory regulation or exceeds the permitted use, you will need to obtain permission directly from
the copyright holder.
Chapter 12
The Relevance of Dispositionalism
for Psychotherapy and Psychotherapy
Research

Tobias Gustum Lindstad

12.1 Introductory Preface

Being educated as a clinical psychologist, I am grateful for having had the opportu-
nity to work with unforgettable patients and colleagues. Yet, having worked within
both secondary and primary mental health care services for the last 16 years, some-
thing has persistently felt wrong with my working conditions. Having shaken off
my worry that this feeling is a symptom of something being wrong with me, I have
become convinced that a significant part of the problem is the scientific paradigm of
psychology, which does not only set the conditions for psychotherapy research, but
also for clinical perspectives of relevance for any health professional working in
mental health care.
Through the history of psychology, psychologists have sought to legitimize their
discipline as a science by differentiating it from the humanities. However, as such,
they have unfortunately put more faith in the processing of computers working
inductively on accumulations of empirical data, than to their natural abilities to
scrutinize their assertions via thorough reflection and in critical dialogue. One par-
ticularly detrimental aspect of this paradigm has been the predominant presumption
that statistically supported empirical experiments in the form of randomized con-
trolled trials (RCTs) are needed for clarifying the causal effects of psychotherapy.
However, this idea is not so scientific as it is bad philosophy. Not only does it imply
questionable conceptions of causality, but it also neglects many natural characteris-
tics of being a person.
Moreover, it does not help much that results of RCTs have been used as a bureau-
cratic remote control by governmental health authorities wanting to assure the qual-
ity of health services from the outside (that is, without taking part in the process of
providing the service). On the contrary, this has made clinicians walk around on

T. G. Lindstad (*)
Independent researcher and Clinical Psychologist in Private Practice, Åros, Asker, Norway

© The Author(s) 2020 179

R. L. Anjum et al. (eds.), Rethinking Causality, Complexity and Evidence for the
Unique Patient, https://doi.org/10.1007/978-3-030-41239-5_12
180 T. G. Lindstad

their tiptoes needlessly worrying about whether they conform sufficiently to stan-
dardized procedures thought to have had results on an average level. This runs the
risk of dehumanizing mental health care services by not taking sufficiently into
account the context-bound complexities of clinical encounters and by being an
obstacle for a sufficient focus on the unique needs of individual patients.
Accordingly, though this book promotes an account of causality relevant for all
health sciences and professions, the focus of this chapter is on how dispositionalism
may improve upon the foundations of clinical psychology, psychotherapy research
and mental health care services. This is important not only for psychologists, but for
all clinicians providing psychotherapy or related services (nurses, physiotherapists,
psychiatrists, physicians, social workers etc). Not only will the recent advancements
of dispositionalism (see Anjum, Chap. 2, this book) provide resources for a refresh-
ingly new foundation for psychological science and psychotherapy research, but
also for more humane mental health care services.

12.2 Misleading Statement on Evidence Based

Psychological Practice

Philosophers have often considered it a virtue to be informed by psychology.

Psychologists, however, though they may admit philosophical inspiration, have
only rarely declared philosophy as relevant for improving psychological science
and practice. Accordingly, the widely acknowledged statement on evidence based
psychological practice provided by the American Psychological Association (APA
2006: 273–4) puts a one-sided emphasis on empirical research and neglects the
relevance of philosophical reflection. As such it simply upholds that statistically
supported empirical experiments in form of RCTs are the standard for drawing
causal inferences about the effects of psychotherapy. However, as the APA-statement
is a significant supplier of terms for evidence based mental healthcare services in
general, this emphasis of the statement is beset with difficulties. Not only is the
prevailing presumption that RCTs is the standard for clarifying causal relations part
of a questionable Medical Model of psychotherapy (not to be confused with the
biomedical model discussed in Chap. 5 of this book), but it also hinges on dubious
conceptions of causality inherited from Hume and is therefore not something one
should take uncritically for granted (see Anjum, Chap. 2, this book).
To be fair, to some extent the APA-statement also seems to have relevantly recti-
fied the medical model. Not only does it provide a broader definition of evidence
based psychological practice as the integration of the best available research evi-
dence with clinical expertise in the context of patient characteristics, but it also
approves of multiple types of empirical research evidence, not only RCTs. However,
though these are important steps in the right direction, the understanding of evi-
dence based mental health care must be broadened so as to include philosophical
and theoretical reflection, and moreover, and accordingly, the predominant idea that
12 The Relevance of Dispositionalism for Psychotherapy and Psychotherapy Research 181

RCTs are the best way of drawing causal inferences for the single patient must be
abandoned.
Notice, that though my call for change is critical, it does not have destructive
aims. Rather, it is part of a constructive counter-reaction that seeks to liberate the
health sciences from the detrimental impacts of Humean conceptions of causality
and to pave the way for more apt alternatives. Fortunately, the Humean regularity
view, along with its descendent counterfactual and difference-making accounts, are
not the only accounts of causality available. As such, the recent philosophical
advancements of dispositionalism (e.g. Mumford and Anjum 2011; Anjum and
Mumford 2018a) do not only provide relevant resources for bringing psychology
out of its dead ends, but they may also breathe new life into pertinent alternatives
that have been unheeded. What is at stake is nothing less than the understanding of
what relevant psychotherapeutic competency is, how it may develop, and how the
quality of mental health care services may be assured.

12.3 Questioning the Medical Model

Despite attempts to overthrow its predominance (Wampold and Imel 2015; Duncan
et al. 2010) the Medical model still thrives as the following tripartite set of
presumptions:
(i) RCTs are the best way to clarify causal effects.
(ii) Evidence based psychotherapy depends upon the clarification of causal effects
of specific treatment interventions and methods (often derived from specific
psychotherapy-models) on specific disorders categorized according to specific
symptoms frequently observed together.
(iii) The implementation of such empirically supported treatment methods (so-­
called ESTs) is what evidence based psychotherapy should amount to (cf.
Chambless and Hollon 1998).
As medical research and practice are more varied than what these claims amount
to, the Medical model could perhaps be better called “the Pill Model”. This fits the
idea in question that psychotherapy should be studied and understood in the same
way as drugs. Though this model has never been generally accepted, the idea it
represents has been very much alive among influential scholars. E.g. Kennair et al.
(2002: 9) have claimed that “the major conclusion after years of research into the
effects of psychotherapy is that certain interventions work for specific disorders”,
and that though “there are variations between humans, … there also is a relatively
uniform human nature [which] means that interventions that work on large groups
of humans will probably work for random individuals”. Accordingly, proponents of
the Medical model have not only argued that psychological treatments require the-
ories of causal relations and mechanisms of change, but they have also miscon-
strued psychotherapy as the systematic use of psychological knowledge in such a
way that it leads to expected change with statistical probability. Accordingly,
182 T. G. Lindstad

pyschotherapist1
Statistically probable Specific symptoms person1
difference maker: of specific disorder
pyschotherapist2
person2
Specific interventions of
pyschotherapist3 specific treatments derived person3
... from specific treatment ...
pyschotherapistn models and perspectives personn

Fig. 12.1 The Medical model

Fig. 12.1 illustrates how the predominant Medical model portrays any psychothera-
pist as complying with one or more empirically supported treatments which pur-
portedly makes a statistically probable difference on specific symptoms of a
specific disorder that are allegedly shared by various patients.

12.4 The Challenge from Dodo-Birds and Meaning-Makers

As mentioned, however, the Medical model has not remained unchallenged, and
roughly put, seminal critiques have come from two partly overlapping groups of
scholars; to keep them apart I will henceforth call them the Dodo-birds and the
Meanings-makers. The Dodo-birds have long argued that “psychotherapy does not
work in the same way as medicine” (Duncan et al. 2010: 28), and that RCT-research
has “failed to find a scintilla of evidence that any specific ingredient is necessary for
therapeutic change” (ibid. 33). Moreover, they have claimed that the empirical
research originally conducted in accordance with the Medical model actually pro-
duces evidence that supports an alternative contextual model on which the method-
ological and technical aspects of therapy processes cannot be studied as isolated
from the relational context in which they are part (Wampold and Imel 2015). Thus,
rather than continuing the search for the one and only miracle cure, the Dodo-birds
have emphasized the so-called Dodo-bird-verdict first uttered by the fabulous dodo-­
bird in Lewis Carroll’s tale of Alice in Wonderland: “Everybody has won, and
everyone must have prizes”. Accordingly, the Dodo-birds have claimed that there
are no evidential statistical differences between treatment models and have stressed
the importance of common factors purportedly transcending any specific treatment
method, such as client-, therapist- and alliance factors, as well as factors external to
the therapy, and that psychotherapy processes must be “evidence based one client at
a time” (Duncan et al. 2010: 39–40).
Several Meaning-makers have agreed with these conclusions. However, their
arguments have also cut more deeply by pointing out that the research-design of
RCTs ignores fundamental aspects of human beings, such as responsiveness and
irreversible uniqueness (e.g. Stiles 2009; Smedslund 2009). So far, so good.
However, often inspired by phenomenology or Wittgenstein, the Meaning-makers
12 The Relevance of Dispositionalism for Psychotherapy and Psychotherapy Research 183

have taken the even more radical step of rejecting any psychological relevance of
causal explanation as they think the notions of causality and human meaning-­
making belong to different explanatory domains (Brinkmann 2011; Harré 2002;
Smedslund 2012a). I principally agree with both groups of critics. However, I also
argue that they have not taken the bull by its horns, and that acknowledging the
relevance of dispositionalism will provide the relevant improvement on their argu-
ments. What is wrong is not to emphasize causation, but rather the Humean ideas
about causality that nourish the Medical model.

12.5 The Philosophical Bias of the Medical Model

Whenever one emphasizes some research methods rather than others, one takes for
granted that the phenomena one wants to study may have properties that make one’s
choice appropriate. As such presumptions might be wrong, it ought to be considered
a scientific virtue to make one’s presumptions about what one studies available for
scrutiny. As such, the abovementioned claim of Kennair et al. (2002: 9) admirably
illustrates that the critics of the Medical model have not been attacking a strawman.
The claim of Kennair et al. that “there … is a relatively uniform human nature
[which] means that interventions that work on large groups of humans will probably
work for random individuals” does not only rest on ill-founded Humean presump-
tions about causality, but it also errs seriously on behalf of human nature.
However, as argued by several Meaning-makers (e.g. Smedslund 2009; Stiles,
2009), physiological research is not needed to demonstrate the relevant variability.
There is more to human beings than mere measurable existence: Unless we are in a
coma, we are compulsively meaning-making persons for whom something exists,
and once something has been experienced, this is irreversibly so. As we also
unavoidably attach meanings to the world from never identical contexts, the com-
plete sets of our experiences become inevitably unique. And moreover, we are con-
tinuously susceptible to change by attaching new meanings to our experiences.
Thus, the ways we make sense of things are bound to evolve in unique ways within
unique contexts. Hence, though this does not prevent similar experiences, we cannot
take for granted that persons will react in the same or similar ways to the same event
or similar events.
Most textbooks on psychological research methods have acknowledged that per-
sons have characteristics that make them difficult to experiment with. Nevertheless,
apparently because it is held that these difficulties can be circumvented via statis-
tics, the view still prevails that RCTs are the best way to uncover causal relation-
ships (e.g. Hollon 2006). Thus, regular causal effects are standardly not sought for
on an individual level, but rather on an average level (APA 2006). By randomly
assigning a high number of persons to groups subjected to different conditions – for
instance, offering some persons psychotherapy while others not – and estimating
subsequent statistically significant differences between the average scores of the
groups, one may conclude that the differences have been caused by the
184 T. G. Lindstad

psychotherapy. The viability of this conclusion depends on the two groups being
similar in all other relevant respects, and it is held that this is taken care of by the
randomization procedure. However, though characteristics that are possible for peo-
ple to share (e.g. height) may spread evenly in large-sized random groups, unique
characteristics (e.g. memories) cannot. Thus, as no randomization procedure can
prevent unique experiences (e.g. memories) from being influential, we cannot take
for granted that groups are relevantly similar without having thoroughly considered
the unique experiences of the individuals involved. Also, simply increasing the
number of persons in the hope that the statistical law of large numbers will apply
will not help, as increasing the number of unique aspects does not necessarily make
the groups any more similar, but would rather increase the numbers of influential
factors that ought to be taken into account for understanding why the results occur.
In other words, if we do not get a sufficiently thick understanding of the unique
experiences of the individuals involved, information about aspects that inevitably
influence the results are missed (Smedslund 2009; Stiles 2009). Hence, RCTs risk
throwing the baby out with the bathwater. RCTs can only tell us that psychotherapy
has had such and such results on a mean level, but neither why these results occurred,
nor how and whether similar results are attainable now or in the future.

12.6 Dodo-Birds Must Take the Bull by Its Horns

Unfortunately, the above critique of the Medical model has been largely unheeded.
Admittedly, the APA-statement does offer related rectifications by providing the
somewhat broader definition of evidence based psychological practice mentioned
above, as well as by approving of other empirical research designs than RCTs, such
as the process-outcome studies often emphasized by the Dodo-birds (Orlinsky
et al. 2004). However, by upholding RCT’s as the standard for drawing causal
inferences about the effects of psychotherapy and even declaring that barriers to
this kind of research should be identified and addressed (APA 2006: 274), the state-
ment uncritically makes the same ontological commitment to a regularity view of
causality as do proponents of the Medical model. As such, rather than explicitly
acknowledging the contextual model as an apt meta-understanding to replace the
Medical model, the APA-statement does not only contribute to maintain the flawed
idea that replicated RCTs are the best research design that we have, but at worst it
inspires proponents of the Medical model to uphold the contextual model as just
another specific form of treatment that must be evaluated by RCTs (e.g. Crits-
Christoph et al. 2014).
However, if the prevailing emphasis on RCTs relies upon a faulty understanding
of causality, the argument of the Dodo-birds that evidence from RCTs does not sup-
port the Medical model does not cut deep enough, as it has not explained why this
is so. That is, pointing out that the statistical evidence indicates that the presump-
tion of the Medical model that specific treatments work for specific disorders is
wrong, does not explain why it is wrong. However, as the arguments of the
12 The Relevance of Dispositionalism for Psychotherapy and Psychotherapy Research 185

Dodo-birds wave in the relevant direction, it is to be hoped that they are also prone
to open their eyes and take the bull by its horns. Indeed, the reason Duncan et al.
(2010: 36) are right that “clients are not dependent variables on which independent
variables operate [but] agentive beings who are effective forces in the complex of
causal events”, is that the Humean conception of causality is wrong and disposi-
tionalism right.

12.7 Meaning-Makers Must Target the Right Enemy

Where the Dodo-birds have not yet taken the bull by its horns, the Meaning makers
have overshot their target. If there was no alternative to the prevailing Humean con-
ceptions of causality, the Meaning-makers would have been right to deem causal
explanation as relevant only for the natural sciences while inapt for psychology
(Smedslund 2012a; Harré 2002; Brinkmann 2011). However, as alternative accounts
of causality do exist, their rejection of the relevance of causal explanation amounts
to no less than overkill.
It should be noticed, however, that this rejection stands in a long tradition of
scholars inspired by Dilthey’s distinction between explaining via causal covering
laws (Erklärung) and understanding agents’ points of view (Verstehen) (Harré
1999; Smedslund 2009). This distinction is indeed relevant, as the very point of
RCTs – to compare the outcome of therapy with no therapy – is clearly related to
the so-called covering law model, at least in Hempel’s version inspired by Hume.
According to this model, scientific explanations should reveal the regular anteced-
ent conditions without which something would not happen by appealing to empiri-
cal correlations of one type of event (outcome) with another type of event cited as
its cause (intervention). However, that this kind of explanation by referring to
empirical correlations (covering laws) is inadequate for understanding human
meaning-making, entails neither that meaning-making and causality belong to
mutually exclusive explanatory domains (cf. Smedslund 2012a; Harré 2002;
Brinkmann 2011) nor that it is required to think about human action in ways that go
beyond models of causality (Valsiner 2014). Thus, though Valsiner is right that
sticking to search for linear causality has led psychology to ignore the possibility of
alternative accounts of causality, Valsiner and Brinkmann (2016) are wrong that any
human sign-regulatory system is a catalysed, rather than a causal system (my ital-
ics). Rather, in line with Valsiner’s (2017) more recent statement, talk about causal-
ity must take a new form, and as such, the recent advancements of dispositionalism
(Mumford and Anjum 2011; Anjum and Mumford 2018a) seem related to Valsiner’s
suggestions to emphasize catalytic conditions and mutually beneficial relations
rather than relations between independent and dependent variables.
To sum up: both Dodo-birds and Meaning-makers have compellingly argued
against the second and the third presumption of the Medical model described in
Sect. 12.2, but to no avail. However, as an apt dispositionalist alternative to
Humeanism exists, also the first presumption of the Medical model must be
186 T. G. Lindstad

abandoned: Not only is it wrong that evidence based psychotherapy is equal to

empirically supported treatments, and senseless that specific kinds of outcomes
must be repeatedly found to follow from specific kinds of interventions, but more
fundamentally, it is also wrong that RCT’s are always needed for drawing causal
conclusions.

12.8 Humeanism Must Be Replaced by Dispositionalism

The recent advancements of dispositionalism relate to the resurgent philosophical

interest in understanding the relevance of dispositional properties for causality (e.g.
Groff and Greco 2013). As such properties are also often called causal powers, dis-
positionalism has often been presented as influenced by Rom Harré’s seminal
efforts (with Madden 1975) to replace the Humean regularity theory of causality
with an account that revivifies the notion of causal powers. However, though Harré’s
contributions to discursive psychology (e.g. with Gillett 1994) are relatively well
known to psychologists, his contributions to the philosophy of causality have been
largely unheeded. Probably, this is not so much because Harré (2002) was reluctant
about the relevance of causal explanation for psychology, but because psychologists
are rarely encouraged to be philosophically informed. Yet, the relevance of causal
powers has long been discussed in relation to the social sciences (Groff 2008), and
with the recent advancements of dispositionalism their pertinence for medicine
(Anjum 2016) have been demonstrated. However, pace Harré, these advancements
are no less relevant for psychology. The problem is not that psychologists have
wanted to discover causal relations, but that their Humean conceptions have been
misleading.
A growing number of philosophers now regard the long prevailing Humean regu-
larity theory as no more than a standard against which to contrast and develop more
refined accounts. Though the extent to which Hume himself really held the view is
controversial, there is no doubt that he put both it and the related counterfactual
difference-making account on the table. On the first view, causal relations (infa-
mously exemplified by colliding billiard balls) consist in no more than that events
of one kind can be observed as regularly conjoining or following events of another
kind. On the latter view, causes are events without which their effects would not
happen. However, on both views, causal relations are neither governed by any
necessities nor by any dispositional properties, or if they were, we could simply not
know. Notice, that as these Humean conceptions imply that causal links must either
be demonstrated by statistical evidence of correlation and/or by comparing the aver-
age outcome of exposure by stimuli with the average outcome of no exposure, they
fit with the Medical model’s emphasis on RCTs like a glove. Probably, the Medical
model’s predominance is also due to the continued influence of Hempel’s covering
law model, in which scientific explanations should reveal the regular antecedent
conditions, as well as the empirically observed general laws, without which some-
thing would not happen (Groff 2011).
12 The Relevance of Dispositionalism for Psychotherapy and Psychotherapy Research 187

However, as pointed out by prominent advocates of dispositionalism, scientific

observations of regularities that cannot be prevented by any means hardly exist
(Mumford and Anjum 2011). Probably, this is why the number of citations of gen-
eral laws in the scientific psychological literature have decreased (Teigen 2002).
Yet, the predominant scientific paradigm of psychology still emphasizes research
methods developed for the empirical discovery of regular causal relations and sta-
tistical differences. However, in line with dispositionalism it should be noted that
methodological questions of how to discover causal links should not be confused
with ontological questions of what causality is (Anjum and Mumford 2018b). Thus,
though differences between group averages may indicate that relevant causal rela-
tions exist, causality is not in itself a statistical phenomenon. Without further argu-
ment we therefore cannot take for granted that causal effects is something that ought
to be clarified by demonstrating statistical differences via RCTs. Moreover, RCTs
are not necessarily the best way to clarify causal relations as they can only provide
sparse information about what the relevant causal connections consist in, how they
may come about, and how similar effects might be attainable in the future.
Notice that this argument is related to the arguments made by many Meaning-­
makers that the results of RCTs cannot tell us why any psychotherapy process has
had this or that effect, nor how. However, though dispositionalists would whole-
heartedly agree with the Meaning-makers that the relevant information cannot be
gained by trying to establish knowledge of causal covering laws (Erklärung), pace
the Meaning-makers, dispositionalism implies emphasizing an alternative account
of causal explanation rather than to deny its relevance. Thus, though the Meaning-­
makers have put apposite emphasis on understanding agents’ unique points of view
(Verstehen), causality is not the enemy. Rather than to construe Verstehen as about
non-causal phenomena, understanding what something means for someone is more
often than not to get to know about their causally powerful dispositional properties.
In line with a Humean perspective, both the Medical model and APA’s statement
on evidence based psychological practice treat causal effects as something that must
be clarified by RCTs. At best, this understanding is incomplete. For one thing, it
ignores that there can be regular succession of events that are not causally related,
and moreover, we must account for the possibility of causal processes that happen
only once (the kind of result an RCT would purposely elide). To deal with these
features, dispositionalism revives a realist view of causality, in which causal rela-
tions rest upon the powers of dispositional properties to produce changes. And on
the view developed by Mumford and Anjum (2011), causal relations are constituted
by properties that only dispose towards other properties as their effects. Causes may
thus only tend towards their effects, and these effects might never be manifested in
any observable regularity (Anjum and Mumford 2018a).
Thus, contra the Humean conceptions, isolating variables in the hope of measur-
ing regular relations between them is no royal road to know about causal relations.
Not only do we need more thorough inquiries that explain how and why causal
effects emerge, but knowledge about relevant causal links and mechanisms can even
be gained without having recorded any correlations, for instance, when the possible
interplay between dispositional properties can be understood before any causal
188 T. G. Lindstad

changes emerge. Statistical evidence is thus not needed if we already understand the
mechanisms involved, and causal claims are best supported by theory that explains
how and why causal effects are brought about (Anjum and Mumford 2018a, b). Nor
is statistical evidence needed if we can come to understand how and why causal
effects may emerge by reflecting on the possible interplay between the dispositional
properties of persons and their surroundings. Importantly, these advancements of
causal dispositionalism do not only bring support to the arguments of both Dodo-­
birds and Meaning-makers, but as such they demonstrate the relevance of disposi-
tionalism both for psychotherapy research and psychotherapy.

12.9 Implications for Psychotherapy Research

Of the many relevant implications of dispositionalism for psychotherapy research

only five will be delved into here. That is, (i) methodological pluralism and (ii)
causal singularism, and the related potentials for (iii) advancing theoretical reflec-
tion, (iv) avoiding pseudo-empirical research and advancing the (v) theoretical inte-
gration of psychotherapy perspectives. These interrelated aspects are picked out
both because they have profound potential for changing the field of psychotherapy
research for the better and because they are relevant for the implications of disposi-
tionalism for psychotherapy discussed in the next section.
As mentioned, the statement of APA (2006) approves of a multitude of evidential
resources, but from a dispositionalist perspective it is still too narrow. By upholding
RCT’s as the standard for drawing conclusions about the effect of psychotherapy
one treats causal relations as something that must be discovered through RCTs.
However, questions of how to clarify causal relations must not be conflated with
ontological questions of what causality is. Thus, though RCTs can indicate the pos-
sibility of relevant causal links by demonstrating difference making and regularity
on an average level, there are also other, and often better, ways to get in touch with
causality. For instance, by understanding what was experienced by someone; say,
when we wonder why a child suddenly got anxious when playing with his dad, and
get to know that playing with toy-soldiers with his dad suddenly made the child
remember that his dad could not only act unpredictably, but also just as aggressively
as the toy-soldiers. Accordingly, we must emphasize methodological pluralism
which is also related to causal singularism: Causality is manifested in concrete
particular instances because of the dispositional properties involved (Anjum and
Mumford 2018b). Whether a child becomes anxious when experiencing a parent as
unpredictable, depends upon the properties of the child, the parent, and their sur-
roundings, not on whether a statistically significant number of children experienc-
ing their parents as unpredictable become anxious when together with their parents.
This brings us to the third implication of dispositionalism: Singularism means
not only that the priority traditionally given to quantitative research rather than qual-
itative research is untenable, but also that we should emphasize the primacy of
causal theory over statistical data. Thus, methodological pluralism does not only
12 The Relevance of Dispositionalism for Psychotherapy and Psychotherapy Research 189

mean that there are many ways to get in touch with causality, but also that psycholo-
gists must put more emphasis on theoretical reflection. Agreeing with APA (2006:
274) that one should recognize the strengths and limitations of evidence from dif-
ferent types of research, we should notice that where Hume’s covering law model
suggests collecting more and more data of the same type from repeated instances,
dispositionalism encourages us to collect more data about singular instances. What
matters is that we can understand the causal processes involved in actual singular
cases. What happens elsewhere and at different times is not only ontologically irrel-
evant but may also be epistemologically extraneous. Not only do we need more
thorough inquiries that explain how and why causal effects emerge here and now,
but we can also clarify possible interplay between dispositional properties before
any causal changes have emerged (Anjum and Mumford 2018b).
This leads us to the fourth implication of dispositionalism, that is, the potential
for avoiding pseudo-empirical research. The notion of pseudo-empiricism, acknowl-
edged by most Meaning-makers (e.g. Brinkmann 2011; Valsiner 2012; Harré and
Moghaddam 2012), that we should not mindlessly put assertions to empirical test if
they can be evaluated by other means, was first introduced by Smedslund (1995).
Notice, however, that acknowledging the relevance of this notion does not mean that
we ought to follow Smedslund’s arguments all the way towards concluding that
psychology cannot be an empirical science. On the contrary, not only is it probably
more coherent to think of theoretical reflection as comprising kinds of inquiries in
which experience plays a significant role (cf. Casullo and Thurow 2013), but in line
with methodological pluralism, RCTs and other kinds of empirical research do have
their areas of application. Thus, acknowledging the relevance of avoiding pseudo-­
empirical research only means that an emphasis on empirical research must not
exclude the relevance of theoretical reflection and that the relevance of advancing
theories of causal tendencies is often more relevant than statistical data.
For instance, collecting more empirical data to test the hypothesis that people
tend to attempt to do what they think they are able to do when they also want it, or
whether people tend to get anxious when together with unpredictable people, will
be pseudo-empirical. Thus, if we already have relevant and sufficient amount of
information about the relevant dispositional properties, we can know this by reflect-
ing on the possible interplay between them without further empirical inquiry. For
instance, if we know that someone (say, Caesar) has come to think that he is vulner-
able, and if we also know that he thinks that someone else (Brutus) may come to do
something (stab with a knife) that might kill or hurt him, and he also thinks that he
cannot know whether this may be done at a time when he is able to prevent it, then
we know that he is disposed to become anxious when together with Brutus.
Moreover, we can also know by reflecting on possible preventing circumstances,
that these are only tendencies. For instance, though Brutus thinks that he is able to
stab Caesar and wants it, he might not attempt to do it because he thinks that Caesar’s
guards may be able to protect Caesar, and Caesar may feel safe with Brutus when
his guards are around. Similarly, there are no unpreventable laws to be found that
children having unpredictable parents will become anxious when together with their
parents. They may feel safe in context of their grandparents, by believing they are
190 T. G. Lindstad

stronger and/or more competent than their parents, etc. Nevertheless, knowing
about such tendencies is practically relevant, and we should avoid being unpredict-
able with regards to potentially harmful actions if we want to become worthy of
anyone’s trust, our children included.
Though these examples may sound trivial, the point itself is not. Though it is a
matter of controversy how much psychological research has been pseudo-empirical,
a growing number of psychologists have recognized the relevance of the notion.
Indeed, the point does not only extend to many psychological theories, many of
which are clinically relevant, but also to psychotherapy research. A striking example
is the aforementioned Dodo-bird-claim that the great mass of empirical data actu-
ally produces evidence that falsifies the Medical model. There is nothing wrong
with this conclusion, except that it is pseudo-empirical. In other words, that the
practical relevance of psychotherapy perspectives must be tested on an average level
by RCTs – as if psychotherapy was some kind of context-transcending pill with
regular and replicable effects working independently of the unique properties of the
persons involved – is simply nonsense. This is adeptly demonstrated by the above-
mentioned Meaning-maker-argument that RCTs cannot ever pay due respect to the
fact that existing persons are someone for whom something exists: As none of us
will ever make sense of things from the exact same perspective as any other, and no
experience can ever be undone, and moreover, that we are continuously open for
change by attaching new meanings to things, implies that we cannot take for granted
that persons will react in the same or similar ways to neither the same nor similar
events. Hence, there is no other option than to qualify our services one psychother-
apy process at a time.
This also brings us to the fourth potential of dispositionalism for psychotherapy
research mentioned above. Alas, the prevailing emphasis on RCTs has thrown a
plethora of psychotherapy perspectives, models and theories1 into pointless rivalry,
needlessly competing for the best results on an average level. This has been at the
expense of theoretical work to clarify the extent to which these perspectives may be
integrated. However, the idea of psychotherapy perspectives as consisting of com-
peting empirical hypotheses of regular causal relations between isolated variables is
misleading, and the many various perspectives, models and theories are better char-
acterized as compatible and/or overlapping attempts to put possible relations
between the clinically relevant dispositional properties of persons into words. This
also makes it relevant to consider the extent to which the perspectives can and ought
to be theoretically integrated. The further upshot is that such integrative work will

1
A far from complete list would include Narrative Therapy, Cognitive Behavioural Therapy,
Schema Therapy, Meta-cognitive Therapy, Acceptance and Commitment therapy, Emotion-
focused Therapy, Gestalt Therapy, Client- and Person Centred Therapy (not to be confused with
person-centred medicine), Compassion-focused Therapy, Existential- and Humanistic Therapy,
Mindfulness, Rational Emotive Therapy, as well as various psychoanalytically oriented and psy-
chodynamic perspectives such as Intensive Short Term Psychodynamic Therapy, Self-Psychology,
Mentalization Based Therapy, Object Relations Therapy, Traditional Psychoanalysis, Relational
Psychodynamic Therapy, and many more.
12 The Relevance of Dispositionalism for Psychotherapy and Psychotherapy Research 191

highlight the relevance of a capacity that is not only pivotal for psychological
research, but also vital for any psychotherapy process: To study and take part in the
ever-evolving unique and vastly complex contexts of psychotherapy processes
requires that we take advantage of our capacity for thorough theoretical reflection,
so as to critically calibrate our knowledge of possible and impossible relations
between the dispositional properties that persons may have.
Notice that philosophers sometimes speak of dispositional properties by using
the shorter term “dispositions”. However, to avoid confusion it should be noticed
that psychologists have often used the latter term in another sense, that is, to refer to
character traits by which one can purportedly predict behaviour by referring to the
frequency of past behaviour. For instance, one may think of one’s father as danger-
ous now or in the future simply because he has often done hurtful things in the past.
By contrast, dispositionalism emphasizes a notion of dispositions (causal powers)
as constituted by intrinsic properties, or propensities (see Rocca, Chap. 3, this
book). Thus, whether a father is dangerous or trustworthy here and now, depends
upon his properties here and now not on how often he has had these properties
before. For instance, whether he comes to do something that hurts his child or not
does not depend upon whether he has been violent in the past, but on whether he
actually cares for and understands his child, on whether he currently has the relevant
amount of self-control, on whether he is currently able to act autonomously, etc.
Accordingly, developing relevant clinical competency depends not so much on
being able to attribute statistically based character traits, as on being able to cali-
brate one’s notions of possible and impossible relations between the dispositional
properties that persons may have in various singular cases here and now.

12.10 Implications for Psychotherapy

Thus, where the Humean commitments of the Medical model lead to a narrow
emphasis on empirical research and a one-sided compliance to empirically sup-
ported treatments, dispositionalism implies pluralism with respect to both research
methodology and practice. In significant respects, this pluralist stance of disposi-
tionalism is related to the proposals of a so-called bricoleur-model of psychotherapy
(Smedslund 2012b). On this view, practitioners should not let an emphasis on spe-
cific pre-construed models and interventions stand in the way for focusing on the
needs of the unique patient, but should rather be prepared to use whatever is at hand
that might contribute to solve the problems encountered.
Alas, the need for emphasizing a practice where one strives to meet persons as
openly and unprejudiced as possible so as to ensure a sufficiently flexible adjust-
ment to the unique case, is not only different from the Medical model, but it has
been disregarded by governmental authorities aiming to ensure the quality of the
therapy process from the outside. The implementation of the so-called “Quick
Psychological Health Services” in Norway (Norwegian: Rask psykisk helsehjelp)
inspired by the “Improving Access to Psychological Therapies Programme” in
192 T. G. Lindstad

England, may serve to illustrate this. The primary aim of this programme, to provide
people with free, low threshold, professional aid when suffering from depression
and anxiety, is impeccable and I’m proud to have contributed to fulfilling this aim
for 5 years. However, the programme has also suffered from one great mistake dic-
tated by the dogmas of the Medical model, that is, it has exclusively emphasized
cognitive behavioural therapy (CBT). Presumably, this is because it has been main-
tained that it has been demonstrated by RCTs that CBT is effective for relieving
depression and anxiety. In line with the Medical model this understanding accounts
for CBT as an empirically supported treatment, that is, a kind of “miracle drug”
comprising statistically proven effective specific interventions. However, though the
principles of the CBT-models undoubtedly contribute to understanding psychologi-
cal phenomena in ways that may be practically relevant, this picture is seriously
flawed. First, CBT is not the only perspective providing relevant assertions, neither
for low threshold services, nor for dealing with depression in general. Second, it
may not always be the most relevant one, and third, if it is relevant, it may be so in
combination with other perspectives.
However, though cognitive-behavioural-therapists have often been eager to pro-
mote CBT as an empirically supported treatment they have also often described
matters as being more complicated than as construed by the Medical model. Rather
than picturing persons attending psychotherapy as patients who passively receive
some kind of miracle drug, one has not only emphasized the relevance of establish-
ing a trusting relationship, but also of motivating clients to contribute as active
agents towards reaching their goals. However, how various dispositional properties
of patients, therapists and their surroundings may combine and intertwine towards
establishing a trusting relationship are not described by CBT-models, but more
extensively by other psychotherapy-perspectives (e.g. various psychoanalytically
oriented and psychodynamic perspectives). Also, though one actively encourages
patients to take active part in the process, this is normally done by “socializing the
patients” towards proceeding within the frame of specific CBT-models, and this
way of proceeding puts us right back into the linear scheme of the Medical model;
as if all patients always suffer in ways to be treated by the same treatment procedures.
Yet, that one size does not fit all, is also well known among cognitive-­behavioural
therapists. E.g. it has been recognized that it is not always sufficient to deal with the
content of cognitions triggered in specific situations to counteract various prob-
lems. For instance, realizing that your first thought that someone did not like you
actually was wrong – and that it was more likely that the reason this person avoided
you was that he was shy – may not be enough to overcome social anxiety. Rather,
or additionally, more fundamental and context-transcending assertions (often
called schemas) may have to be dealt with. For instance, being convinced that no
one will ever really like you if you fail at something, and thus, that you have to
make sure not to fail in any kind of situation. To take such more fundamental asser-
tions into account so-called Schema-focused models of psychotherapy was con-
strued by integrating aspects from CBT and psychodynamic perspectives. More
recently, the fact that it is not always sufficient, sometimes not necessary, and per-
haps not even desirable, to alter the content of cognitions has been incorporated
12 The Relevance of Dispositionalism for Psychotherapy and Psychotherapy Research 193

into the therapy-models. For instance, we may not want to change our minds about
it being both true and sad that someone we love is no longer alive. Thus, one has
acknowledged the relevance of working with how to deal with having thoughts
without altering their content by integrating Mindfulness exercises, for instance,
practicing on recognizing one’s thoughts as a natural and harmless aspects of the
fluctuating moment, or by bringing in the principles of Meta-cognitive therapy, for
instance, by recognizing that scary thoughts about something are actually not dan-
gerous in themselves.
From the perspective of dispositionalism, this picture could not only easily, but
also ought to, be expanded by aspects of further therapy models and perspectives
not traditionally thought of as part of the cognitive paradigm. For instance, one may
take into account the aspect emphasized by models of Emotion-focused therapies
that simply work on how to think differently without making sure that this actually
creates emotional change, may not be sufficient, or one may aptly integrate aspects
traditionally emphasized by various psychodynamic perspectives such as Object-­
relations therapy and Self-psychology. For instance, validating the experiences of
patients (making their thoughts understandable without necessarily agreeing with
their content) so as to foster self-esteem by the recognition of the value and intelli-
gibility of being who they are (this may have been prevented by inhospitable cir-
cumstances when growing up, insensitive or violent parents and/or by bullying at
school). Or one may inquire into whether inhospitable growing up conditions have
made persons prone to satisfying other people’s needs rather than their own, per-
haps even to the extent of having become unable to recognize their own real wants
and needs, eventually leading to depression or anger. Such inquiries may have the
aim of providing the patients with the relevant understanding of themselves both to
prevent feeling ashamed about one’s suffering and to foster opportunities for explor-
ing how to flourish in one’s life on one’s own premises.
However, as aptly pointed out by Wampold (2019) there is a risk that the idea of
integrating various approaches will be taken to be a specific approach in its own
right, so that one simply adds to the expanding number of specific therapies that
purportedly must be evaluated by RCTs. Fortunately, dispositionalism offers a via-
ble solution to overcome this risk. Thus, the aim of clarifying the extent to which
various perspectives are overlapping or may be fruitfully combined is not to con-
struct yet another empirically supported treatment, but to get a hold on how the vari-
ous perspectives describe possible causal links between the possible dispositions of
persons that might be relevant in possible singular and unique cases. The aim of
integration is not to construct yet another miracle drug suitable for all, but to widen
one’s scope, so as to be more flexible and able to deal with the immensely complex
ways in which the various dispositional properties of unique persons may interact
both with each other and the properties of the surroundings. As such, theoretical
integration is no aim in itself, but may serve the more general bricoleurious aim of
being prepared to use whatever is at hand that might contribute to solve the prob-
lems encountered. Thus, this overall aim does not only include taking various psy-
chotherapy perspectives into account, but also perspectives and ideas suggested by
professionals primarily working with other kinds of services than psychotherapy,
194 T. G. Lindstad

such as social workers and physiotherapists, as well as anything else that might be
beneficial. For instance, making a phone call to a social worker to get help solving
financial problems, may be no less relieving than psychotherapy. Or by taking into
account how moods may change by altering body-posture, helping patients to rec-
ognize that though their traumatic experiences may have made them more prone to
strain their muscles (e.g., as part of being angry or terrified), become restless or
agitated (e.g. as part of being worried or more alert) or collapsed (e.g. as part of
being depressed or shameful) as part of a bodily defence against perceived threat,
their inborn ability to create a more balanced and harmonious posture is not
destroyed.
Thus, where the Medical model portrays clinical competency as the ability to
use psychological knowledge in such a way that it leads to statistically probable
change, dispositionalism emphasises our abilities to critically calibrate our knowl-
edge of the vast amount of possible and impossible relations between the disposi-
tional properties that persons may have in various circumstances. In other words,
though we should not deny ourselves the possibility of looking to RCTs for inspira-
tion, making it obligatory to look to this kind of research for evidence runs the risk
of distracting focus away from what matters, which is to deal with the properties
and processes involved in actual singular cases. Just as one does not necessarily get
wiser simply from having had more experience, we cannot know whether relying
on RCTs conducted elsewhere and with other patients at another time is relevant
here and now. Accordingly, just as clinical competency cannot be assured through
inductions from the unavoidably limited and biased experience of individual thera-
pists, neither can it be built on inductive generalisations from accumulations of
empirical data from RCTs or other correlational studies alone. Rather, the clinical
competency relevant for psychotherapy has to do with having gained the relevant
degrees of interpretational freedom for dealing with possible tendencies. The extent
to which humans really differ from other animals with respect to the capability for
building such competency might be discussed. What is clear however, is that human
beings are normally able to recognize more opportunities, say, with a nut than eat-
ing it raw (e.g. baking a cake). Similarly, we not only can but should be more flex-
ible than simply complying with empirically supported treatments. By working to
clarify the possible and impossible relations between the dispositional properties
that persons may have in various contexts, one might not only get a reflective over-
view of various possibilities that may be actualized in concrete situations, but one
might also gain relevant resources for avoiding overgeneralizations and avoiding
jumping to unwarranted conclusions. Thus, clarifying possible links between the
dispositions of persons may not only strengthen an apposite sensitivity for more
possibilities than one’s immediate first impressions, but it might also provide
resources for understanding and dealing with actualized feelings, thoughts and
behaviour.
12 The Relevance of Dispositionalism for Psychotherapy and Psychotherapy Research 195

12.11 As Statistics Don’t Get It, Try Getting

the Vectors Right

To the extent that the above discussions are up to something, dispositionalism does
not only improve earlier critique of the Medical model, but may as such also have
profound consequences for psychotherapy research and mental healthcare services.
Dispositionalism provides an account of causality that implies pluralism with
respect to both research methododology and practice, all toward the aim of dealing
sufficiently with the complex interplay between the unique properties of persons,
their circumstances, and clinical practitioners. This can be illustrated by the vector
model suggested by Mumford and Anjum (2011) and introduced in Chap. 2 in
this book.
Thus, where the Medical model portrays all psychotherapists as complying with
the same empirically supported treatments purportedly making a statistically prob-
able difference on specific symptoms of specific disorders purportedly shared by
various patients (see Fig. 12.1 above), the vector model (see Figs. 12.2 and 12.3)
provides a way to emphasize and clarify aspects of a vastly more complex reality
consisting of both catalysing and preventing dispositional properties of patients,
therapists, and their circumstances.
The broken line T on top in the picture represents a threshold that has to be met
for the experience of improvement and/or wellbeing to occur for some patient P,
while the broken line at the bottom of the picture represents some threshold condi-
tion for the experience of suffering or of having some kind of problem. The horizon-
tal lines P and S represent some points in time where the various properties of the
patient and various conditions of his/her current situation, respectively, push and

Fig. 12.2 The vector model part 1: patient and his/her situational circumstances
196 T. G. Lindstad

Fig. 12.3 The vector model part 1: patient, situational circumstances and psychotherapist

pull towards the thresholds for experiencing wellbeing or suffering. The arrows
pointing upwards from the horizontal line P represent the properties of the patient
that dispose towards wellbeing, while the arrows pointing downwards represent the
properties of the patient that dispose towards suffering. The thicker arrow R repre-
sents the overall result of all the vector-dispositions; alas, at this point in time, cross-
ing the line for suffering to emerge. Hopefully, however, there are some potentials
for helping the patient. First, there are already some dispositions still pointing
upwards, and if it could be possible either to strengthen these or to add some vectors
pointing in the upwards direction, the overall resultant vector R might turn in the
other direction, and hopefully dispose as far as reaching not only improvement, but
also well-being. Alternatively, or additionally, the vectors pointing downwards
could be removed or at least weakened, so as to bring the overall result less in the
direction of suffering and more in the direction of wellbeing. However, at this point
in time, the properties of the patient and his/her surroundings leave the patient stuck
in suffering.
Say, however, that one of the properties of the situation involves a friend who
encourages the patient to consult a psychotherapist, and even better, one of the prop-
erties of the patient is that he/she thinks of the friend as trustworthy. Fig. 12.3 illus-
trates what could ideally have happened if the patient and the psychotherapist met.
Now that the psychotherapist has become part of the complex situation, the horizon-
tal line PT represents the period in the patient’s life when consulting the therapist,
and the arrows pointing upwards from PT represent properties of the psychothera-
pist that dispose towards the wellbeing of the patient. The arrows pointing down-
wards, however, represent the properties of the psychotherapist that dispose towards
worsening the suffering of the patient. For instance, the therapist may be prone to
misunderstand, or act in ways that the patient experiences as too challenging.
12 The Relevance of Dispositionalism for Psychotherapy and Psychotherapy Research 197

Fortunately, however, though there are arrows pointing downwards, the downward
arrow in the far right of the figure is rather weak compared to the other vectors, and
moreover, the vectors pointing upwards represent properties of the therapist that
dispose towards helping the patient. For instance, the therapist cares for the patient,
dares to call a social worker for relevant financial advice or aid, knows about the
various ways that actions, thoughts, and emotions may relate to various experiences,
does not let statistical considerations take focus away from the actual patient, has
sufficient amount of self-control, and so on.
Moreover, the other arrow pointing downwards from PT is dotted, which repre-
sents that the therapist has had the ability to prevent some property of him- or
herself from contributing negatively to the therapy process, for instance, his dis-
agreement with the patient’s political views, being hungry, or prone to think about
his/her own family-problems. Notice also, that during the therapy process captured
by Fig. 12.3, the number of patient- and situation- vectors pointing upwards has
increased compared to Fig. 12.2, and although this could possibly have happened
independently of the psychotherapy process, it might also be the result of, or per-
haps even dependent upon, the therapy-process. Moreover, one of the vectors
pointing downwards from P, as well as one from S, are now dotted. Again, this
represents that they are removed from the complete set of properties relevant for
the mental health of the patient. For instance, in line with the examples described
in the former section, some financial problems may be gone, weakened or pre-
vented by making contact with a helpful social worker. Or the patient has become
able to recognize that he/she has tended to take more care of others than him/her-
self, and has additionally managed to forgive him/herself for this by having worked
with the therapist to understand these actions as having had an understandable
rationale. Moreover, this may have contributed to release potential for working
towards being able to act more autonomously, flexibly and in tune with one’s own
desires. Thus, the overall result R is now different from in Fig. 12.2, pointing
upwards.
There is clearly much more work to do in order to clarify the implications of
dispositionalism for psychotherapy research and mental health care. However, the
take-home message so far is that nothing (except from ethical concerns) should stop
us from doing whatever it takes to find out about and to deal with the relevant dis-
positional properties involved. Statistics may help to indicate the existence of rele-
vant causes in larger groups and on an average level. And if we are lucky, these
causal tendencies are relevantly similar to what happens when encountering unique
individuals here and now. However, beyond that, statistics don’t help us much.
Thus, we are rather in need of thicker explanations, a deeper understanding of the
properties and experiences of persons and their contexts that dispose towards well-
being and suffering. If statistics don’t get it, try getting the vectors right.
198 T. G. Lindstad

References and Further Readings

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Anjum RL, Mumford S (2018b) Causation in science and the methods of scientific discovery.
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Chapter 13
Causal Dispositionalism and Evidence
Based Healthcare

Roger Kerry

13.1 Complexity in Practice

When I was a young Junior Physiotherapist, a department I worked for was chosen
as a centre to collect data for one of the first multi-centred low back pain trials in the
UK. My job was to identify any of my low back pain patients to see if they could be
included in the trial. I was keen to be involved, as I was very curious about what
might work for people with low back pain. People with low back pain typically
struggle to respond well to many interventions, hence the global epidemic status of
non-specific low back pain. I was surprised (naively) that the trial criteria excluded
people with co-morbidities, poor general health status, and repeated previous treat-
ments – this would be most of my patients. When I had the chance to discuss this
with the visiting trial co-investigator, he explained that they were trying to get the
conditions of the trial as controlled as possible so that they could get a “good, clear
view” of what worked for people with low back pain. The identification of causal
associations between two variables is of course the scientific ideal. The removal and
control of possible confounders is a hallmark of high-quality health research. Yet
this is not what my patients looked like. What was the impact of their co-­morbidities?
How did their general health affect their painful experience? What were the biologi-
cal and psychological consequences of repeated previous treatment? It was clear
that the trial conditions were not representative of the complex and context-sensitive
clinical shop-floor.
My interest in the CauseHealth project stems primarily from questions raised on
the shop-floor of clinical healthcare – and specifically physiotherapy. As a clinician,
teacher, and researcher in physiotherapy, there has been one question in particular,
which I first began thinking about many years ago during the emergence of evidence
based healthcare in the early 1990s when I was training as a physiotherapist.

R. Kerry (*)
Faculty of Medicine and Health Sciences, University of Nottingham, Nottingham, UK
e-mail: Roger.kerry@nottingham.ac.uk

© The Author(s) 2020 201

R. L. Anjum et al. (eds.), Rethinking Causality, Complexity and Evidence for the
Unique Patient, https://doi.org/10.1007/978-3-030-41239-5_13
202 R. Kerry

Is the sort of causation we establish in population research studies the same sort of
causation we are seeking with an individual patient?
Witnessing contradictory results on the shop-floor – for example, a patient not
responding to a strongly ‘evidence based’ intervention – is not uncommon and can
easily be passed off by considering that person as a “non-responder”. However, is
this always the case? Or is there something about the individual context which is not
readily represented in population studies? If so, what are the fundamental assump-
tions about causation in both clinical practice and scientific, systematic research?
With all this in mind, my philosophical interest in causation began, and my relation-
ship with CauseHealth was soon cemented.
Causation lies at the heart of healthcare. This is clearly manifest in aspects of
healthcare such as causes of disease, but of course it is also the core focus of research
methods which try to establish the therapeutic effectiveness of health interventions:
what causes someone to get better. Such research methods represent a central fea-
ture of the practice framework of evidence based healthcare (EBHC) – that is the
proposal that all healthcare practice and decision making should be based on the
best available evidence. This evidence is multi-factorial and can in principle emerge
from a number of sources, such as systematic clinical research, laboratory research,
clinical observations, experience, and so on. The most recent formal iterations of
EBHC stems from literature regarding evidence based medicine in the early 1990s
(Guyatt 1991; Guyatt et al. 1992; Sackett et al. 1996). This literature sets out spe-
cific and detailed structures by which different evidential sources are given different
priorities and is still explicitly reflected in the most contemporary re-workings of
EBHC, for example the GRADE framework (Mercuri and Baigrie 2018; Guyatt
et al. 2011). Philosophically, this is a critical feature of EBHC, as it allows us to
understand some fundamental assumptions on which clinical decision making is
based. If certain evidential sources are given priority over others, we have an insight
into the epistemological and ontological groundings of what we do as healthcare
professionals, in both practice and research.
In this chapter I therefore summarise an early and central idea from the
CauseHealth project, which served to motivate much of the direction of thought and
research within the project. That idea was that the way in which EBHC prioritises
its evidential sources demonstrates that the underpinning causal theory of health-
care is essentially Humean (Kerry et al. 2012). To problematise this, we sought to
consider what the limitations of practicing healthcare were if a strict Humean notion
of causation was assumed. In doing so, it became clear that perhaps what the evi-
dential structuring of EBHC meant by causation was not necessarily the sort of
causation which is at play in real-life, complex healthcare decision making. As
such, we offered an alternative causal theory, based on dispositionalism. This theory
could better account for both the scientific processes (methods) used to establish
data from populations, and the context-sensitive, complex mass of information wit-
nessed in individual clinical encounters. Where Hume saw causes as nothing more
than regularly occurring events with certain temporal and spatial relationships,
while Hume’s opponents argue that, in addition, causes necessitate their effect, we
13 Causal Dispositionalism and Evidence Based Healthcare 203

take causes as real features of the world which interact with each other and have
only a tendency to manifest in an effect (Kerry et al. 2012). Dispositionalism, I will
argue, offers a more real-world account of causation.

13.2 Evidential Hierarchies Expose Causal Theory

During my formative years as a physiotherapist, I was schooled in the ways of best

practice and the limitations created by our human biases. I would often be the first
to dismiss any enthusiasm which other ‘lesser’ colleagues might experience when
patients responded well to our interventions: for example, a patient claiming they
had a huge reduction in pain after some hands-on therapy. My responses would
always be along the lines of “you don’t know that it was the treatment that made the
difference”, or “there is no RCT-level evidence to support that”, and “you have to be
aware of your own perception biases”, and so on.
But what if that patient had been a subject as part of a trial? What if the trial
protocol was just the same as what had happened in clinic that day? The improve-
ment seen would then be recorded and added to data from other similar subjects,
and then compared to data from subjects who had a different intervention, or what-
ever. That response would then be considered positive and causally associated to the
intervention. But this causal claim would not be made on what had been observed
that day, but rather what had happened to other subjects.
This counterfactual reasoning is again part of the essence of our research struc-
tures. However, dispositionalism would suggest that the causal process was always
a real feature of what happened in that individual case. Can the clinician be their
own scientific data collector, ensuring critical analysis, reflection, and a systematic
approach to patient care, and in doing so observe real causation? A dispositionalists
account of causation would permit this. The reaction from EBHC is that you cannot
make generalised claims from such individual observations. We would agree.
Dispositionalism takes all causal cases as context-sensitive, so what works in one
context is not what would work in another one.
I will now demonstrate how a Humean notion of causation can be read from
evidential hierarchies. I explain some of the problems with this and present four key
desideratum to highlight how the dispositionalist alternative can address the short-­
falls of Hume’s approach to causation.
If we take the inaugural papers of Guyatt, Sackett et al. (as above) as the onset of
the contemporary working of evidence based healthcare (originally referred to as
evidence based medicine), the structuring of evidential sources is clear. Essentially,
research methods with a low risk of bias for confounding are given evidential prior-
ity. Randomised controlled trials (RCTs) are considered a gold standard method as
they are able to control for both known and unknown confounding variables. In
doing so they, ideally, isolate the hypothesised causal variables from other possible
causes and observe the effect in repeated conditions (large samples, repeated stud-
ies, etc.). The data from such trials is then sought, to be synthesised and presented
204 R. Kerry

in systematic reviews, which sit at the top of accepted evidential hierarchies.

Methods with increasing risk of bias are progressively de-emphasised down the
hierarchy. This is in line with what La Caze (2008) refers to as a categorical reading
of evidential hierarchies. High quality RCTs and low risk observational studies thus
provide confidence in causal claims, whereas de-emphasised sources do not. This
structuring is honourable and adheres to fundamental principles of science. It also
gives a direct indication of the causal assumptions which healthcare works on.
Consideration of the characteristic differences between ‘causal methods’ (RCTs
etc.) and ‘non-causal methods’ (case studies, mechanistic studies, experience, etc.)
provides a starting point here. What defines these causal methods is the fact that
they first systematically observe the relationship between two events (say, A and B)
multiple times whilst controlling for possible confounding, and then, facilitated by
statistical modelling based on a frequentist idea of probability (see Rocca, ch. 3, this
book), make a judgment on whether causation exists, i.e. whether the intervention
(A) causes a desired health improvement (B). The difference between RCTs and
observational studies is that the observations within RCTs are then compared to
observations in another group which does not include the variable of interest (i.e.
A). The de-emphasised methods and evidential sources do not possess these features.
With these characteristics in mind, it is now possible to analyse these processes
a little further in order to draw out what ontological background these methods, and
the associated causal claims, operate on.
Even with a superficial reading, it is clear to see a Humean essence to the causal
ontology: Hume allowed that causation could be wholly represented in fact by
adherence to three criteria; temporal priority, contiguity, and constant conjunction:
… we may define a cause to be an object, followed by another, and where all the objects
similar to the first are followed by objects similar to the second. (Hume 1748 EUH 7.1.60)

Further,
Every object like the cause, produces always some object like the effect. Beyond these three
circumstances of contiguity, priority, and constant conjunction, I can discover nothing in
the cause. (Hume 1740: A 9)

So, the cause always precedes the effect (A precedes B in time), the effect is
consistently close to the cause (A and B are spatiotemporally contiguous), and the
association is repeatedly and constantly observed (events like A are invariably fol-
lowed by events like B). We can thus claim causation in a Humean sense (A causes
B). This is a regularities view of causation, which is typically Humean and satisfies
many tenets of conventional scientific principles.
This analysis can now take a short step further if RCTs are considered separately.
If we assume that the characteristic difference between RCTs and observational
studies is in essence the presence of a comparative group (current treatment, con-
trol, placebo), then there is a further aspect of the causal theory which can be con-
sidered in a Humean sense. This is the impact of counterfactual dependency, and
also identifying the truthmaker of causation.
13 Causal Dispositionalism and Evidence Based Healthcare 205

Recruitment

Randomisation

Allocation Allocation

Intervention A Not Intervention - A

Outcome B Outcome B
(x) (y)

Fig. 13.1 Randomised controlled trial methodology

The randomisation and allocation processes create the counterfactual conditions by which B(x) –
B(y) would, under a counterfactual account of causation, constitute a causal claim. However, cau-
sation is happening in each group, irrespective of the other group.

The fundamental set-up of RCTs is represented in Fig. 13.1. This illustrates a

typical, simple comparative study. The left-hand group is the intervention group
(A). The right hand is the counterfactual (¬A), which is the control in which not-­
A. In the intervention group a level of outcome is observed, B(x). In the counterfac-
tual control group, outcome B(y) is obtained. The Randomisation and Allocation
stages provide the strict counterfactual conditions. If the truthmaker was the coun-
terfactual, then causation is B(x) – B(y). This satisfies that A➔B. Without y, and
therefore without the control ¬A, there could be no claim to causation.
So, a comparative group can be thought of as a counterfactual condition. This is
a condition wherein the variable of interest (the therapeutic intervention under
investigation) does not exist but where as much as possible otherwise remains the
206 R. Kerry

same. Neo-Humean philosophers refer to this as the closest possible world (Lewis
1973). In RCTs, the counterfactual acts as the truthmaker to causation. Here’s how:
let’s say that in Group 1 (intervention), 62% of all participants achieved a positive
outcome. If this were an observational, uncontrolled study, all we could say is that
there is some sort of correlation, to the magnitude of 62%, between the variable A
and variable B. We would not be confident in drawing causal claims from that
because other variables (confounders) could in fact be the cause of B. So, another
group is set up which does not include A (the counterfactual), and if there was a
similar response rate, we might logically say that the cause of the 62% positive
responses was not because of A. Alternatively, if there was a much lower response
rate in the counterfactual group, for instance 30%, we might (using statistical meth-
ods) say that the difference is sufficiently significant such that we are confident that
A was the cause of B, because not half as many participants in Group 2 achieved a
positive response to the intervention.
In either of these scenarios, the element of the methodological make-up which
gave us confidence in inferring causation from Group 1 was not in fact what hap-
pened in Group 1, but rather what happened in Group 2, the counterfactual. It wasn’t
until we observed the response rate in the counterfactual group that we were confi-
dent to read causation into what happened in Group 1; thus Group 2, the counterfac-
tual, is taken as the real truthmaker of causation. This is in line with the Humean
conception of causation, which also has this counterfactual element:
Or in other words where, if the first object had not been, the second never had existed.
(Hume 1748 EUH 7.1.60)

We now have two distinctly Humean aspects of causation identified within the
hierarchies of evidence for EBHC: a regularities view, and counterfactual
dependency.
To complete the Humean picture, note that because causation is drawn from
regularly occurring patterns of events and/or counterfactual conditions, any allusion
to an actual substance or matter of causation is absent. That is, the processes or
mechanisms of how and why A causes B is missing, or at least considered unneces-
sary on this causal account. Indeed, Hume said as much:
Every object like the cause, produces always some object like the effect. Beyond these three
circumstances of contiguity, priority, and constant conjunction, I can discover nothing in
the cause. (Hume 1740: A 9)

and,
The impulse of one billiard-ball is attended with motion in the second. This is the whole
that appears to the outward senses. The mind feels no sentiment or inward impression from
this succession of objects: consequently, there is not, in any single, particular instance of
cause and effect, any thing [sic] which can suggest the idea of power or necessary connex-
ion [emphasis added] (Hume 1748 EUH 7.1.50)

In summary, Hume considered causation to be nothing more than observed regu-

larity, supported by observations of the effect not happening in the absence of the
cause and irrespective of there being some explanatory mechanism for the events.
13 Causal Dispositionalism and Evidence Based Healthcare 207

This account visibly underpins the desired evidential hierarchies supported by

EBHC. We see this as problematic for a discipline which is characterised by com-
plexity and context-sensitivity, as person centred healthcare might be (Miles and
Mezzich 2011, 2012).

13.3 A Dispositionalist Response

I will now outline a dispositionalist’s response to the emergent problems of a

Humean account of causation. I will do this in a framework of four desideratum
which have been developed from existing commentary on how a causal account for
healthcare should look. In order for a causal account for healthcare to be valid,
it should:
1. explain the causal role of content from particular research methods;
2. motivate a viable epistemology;
3. account for causal processes in individual level clinical decision making;
4. help understand and assess additional premises and assumptions needed to
bridge the inferential gap between population level evidence and clinical
decisions.
These can now be taken in turn, with brief attention to the limitations of
Humeanism, and an alternative dispositionalist response.

13.3.1 Explain the Causal Role of Content from Particular

Research Methods

For the clinician, this simply means that a research theory which we draw causal
claims from (i.e. “does exercise work?”) should be able to satisfactorily explain how
and why the data from particular methods relates to such claims. Our examples
throughout this chapter have been about data from RCTs, and we have seen that the
statistical outcomes of RCTs tell us something about the differences between
groups, but they do not meaningfully give us an insight into the real causal explana-
tions of that difference. We suggest that a dispositionalist reading of scientific data
better explains how it relates to causation.
A traditional Humean account of causation offers some explanation as to how
causal claims are developed from research methods relying on statistical data and
comparisons of these. Humeans are able to discuss causal claims in terms of either
frequencies of occurrence of events, or the degree of differences between two fre-
quencies, or both. Proponents of the Humean account are satisfied that this suffi-
ciently explains the causal role of research content, specifically highlighting that
this avoids unnecessary matters of ontology. The dispositionalist response is
208 R. Kerry

straightforward: the content that is being referred to here is not of causation, but of
something else. The essence of causation has not been reached, and as such any
explanation related to causation cannot be given. The truthmaker of causation within
Humean accounts is too far removed from where causation itself is most likely to
be found.
What dispositionalism offers is a view that sees causation within the core of the
content itself: the properties involved in the causal process. Changes are seen within
groups, and these changes occur as a result of the interactions of multiple disposi-
tions tending towards and away from effects. Whereas Humeans consider single
causes by proxy of frequently occurring observed events, dispositionalists see vari-
ous causal factors that may or may not manifest in an effect. The causal role of these
events for dispositionalism is the notion of how they manifest and how they may
tend towards and away from anticipated thresholds. Dispositionalists are unsatisfied
with causal explanations that relate to frequentist interpretations of probability, as
probability should be thought of in relation to the propensities held by causal factors
(see Rocca, ch. 2, this book). (For those who are interested, Donald Gillies (2017)
provides a useful primer on the different interpretations of probability on health-
care.) The response here has allowed some appreciation of the way causal content
from research methods might be thought of in relation to different ideas about
causation.

13.3.2 Motivate a Viable Epistemology

Epistemology basically means ‘theory of knowledge’ and allows us to judge on

what grounds our beliefs and opinions are made. So when we say “exercise works
for low back pain”, we can satisfactorily answer how we know this. In healthcare,
we want our beliefs and opinions to be as close to the ‘truth’ as possible. Therefore,
any underpinning theory for research and practice must be able provide and encour-
age an epistemology which any logical, scientifically-minded practitioner could be
comfortable with using to justify their beliefs and opinions. We see that there are
limitations to a Humean-motivated epistemology which dispositionalism can
respond to.
The motivation for a viable and pluralistic epistemology comes from the dispo-
sitionalists’ commitment to an ontology of the reality of causes, and the understand-
ing that those causes are the most basic and fundamental features of the world.
Although others have spoken about multiple methods, (for example, Williamson
2007 and Howick’s views on mechanisms in Howick et al. 2013), they struggle to
conclude with a convincing epistemology due to their Humean commitments.
Framed by epistemological matters, these attempts have been instances of identify-
ing the problems of a traditional monistic account, but trying to resolve these with
either pluralistic accounts, or epistemologically driven theories. This is unsatisfac-
tory on two counts: one that there is confusion and conflict between competing
13 Causal Dispositionalism and Evidence Based Healthcare 209

theories of causation; and two that in refusing to commit to an ontology of causa-

tion, it is not even possible to identify what the methods are searching for.
A theory of dispositions has clearly defined what causation is, and is confident
that a methodological pluralistic framework, whereby all methods point to the same
thing, offers a satisfactory account of its causal epistemology. A common element
in the dispositionalist response across these two desiderata has been the primacy of
causation in a dispositions account. Causes are assumed as fundamental and real
features of the world with dispositions.
That causes are primitive and real has allowed commentary on both how causal
content of methods can be explained, and how a viable epistemology can be moti-
vated. Humeans struggle with explaining causal content because they admit to cau-
sation being nothing more than accidental regularity, represented through a
frequentist interpretation of probability. Dispositionalists on the other hand take
causes as real entities and so can describe and explain precisely their content. As
causes can only ever tend towards an effect, dispositionalism does not have to rep-
resent causes through frequencies. Rather, a probabilistic theory based on individual
propensities offers deeper explanation of the causal content.
Dispositionalism is confident that its visible ontology prepares the ground well
for talking about and accounting for a reconceptualised causal epistemology. Its
reference to methods such as RCTs being symptomatic rather than constitutive of
causation facilitates a methodological pluralist stance whereby information from
multiple methods and sources may reveal parts of the causal process. These sources
can include indicators of causation such as mechanistic science and patient narra-
tives. Dispositionalists do not need to worry about the reconciliation of multiple
theories of causation, because causes are only one thing.

13.3.3 Account for Causal Processes in Individual Level

Clinical Decision Making

This is the key issue in science and practice – the problem of induction: how do
claims made at a population level relate to individual clinical decision making? Do
the outcomes of an RCT relate directly to your patient in front of you? And if so,
how do you account for and explain that relationship? A satisfactory theory of cau-
sation and research must be able to do just that.
As physiotherapists, we have guidelines which recommend (based on RCT level
evidence) that exercise should be considered as an effective intervention for people
with lower back pain (LBP) (NICE 2016). This is encouraging on many levels, as
there can be many possible co-benefits to exercising, such as improved general fit-
ness and cardio-vascular health. However, a particular patient may have a disposi-
tional make-up which either inhibits them from doing exercise (desire, time,
capacity, co-pathologies, etc.), or indeed which tend to make the pain worse during
exercise (fear, anxiety, previous experience with exercise, inappropriate
210 R. Kerry

loading, etc.). Thus, the person with low back pain is not seen as a discrete and
independent variable onto which ‘exercise’ can be put on to. Rather, this person
becomes part of a causal process within which the many dispositional traits of both
themselves and the undertaking of exercise can be sculpted together to work towards
a therapeutically beneficial response to exercise, such as addressing anxieties and
fears, coaching on appropriate loading, developing capacity, and so on.
Dispositionalism is a singularist view (Mumford and Anjum 2011: 71–2), and
takes particular causal claims and singular instances to be where causation lies (see
Anjum, ch. 2, this book). However, the dispositionalist ontology moves quickly
beyond a world of discrete events. The relata for causal relations are not discrete
events or facts – for example, event C (exercise) and event E (improvement LBP) –
but the powers and properties of things – for example, the disposition of exercise
and the disposition of a patient with LBP.
At the same time, however, dispositionalism sees general claims as having a role
to play in a theory of causation, especially when particular circumstances are not yet
known. General claims allow us to be “armed for future actions” (Mumford 2009:
14). However, the truth of any general causal claim is substantiated by the properties
or dispositions of such claims, and not associations of discrete events and the statis-
tical facts that relate to such. The particular instance, however, that is able to stand
separate from a general claim, allows further insight into what causation is.
If causal relata are the properties of things, then immediately there is a glimpse
of the essence of what causation might be. Causation is now something primitive.
That is, it is not something that can be analytically reduced to something else, such
as non-causal facts about (repeated) observed associations between events, a
difference-­maker or a raised statistical probability. Particular instances provide a
notion that the modality of a dispositionalist account is neither one of contingency
(that is, the probability or possibility of an effect happening), nor of necessity (that
the effect will (or will not) happen). What dispositions can say about a particular
instance is that there is a modality of tendency that is unique – a sui generis (Anjum
and Mumford 2018). A cause is something that tends towards its effect in a way that
cannot be reduced to accidental regularity or necessity.

13.3.4 Help Understand and Assess Additional Premises

and Assumptions Needed to Bridge the Inferential Gap
Between Population Level Evidence
and Clinical Decisions

This point continues to work on the challenge of the “inferential gap”. The tradi-
tional Humean theory of EBHC can only take things so far and bases its assump-
tions to cross the gap between general and particular claims on the quality of the
research method and frequentist probability. Both are problematic assumptions
which are abstract to the world of clinical practice.
13 Causal Dispositionalism and Evidence Based Healthcare 211

Causes are clearly not to be understood as factors that have exactly the same
effect in every context in which they appear. Causes that have been identified
through RCTs, carried out to perfectly acceptable standards, and clearly suggestive
of a certain prediction and clinical intervention, could nevertheless fail to produce
their expected effect. When one looks to the ontological matters of causation, one
sees that this further consideration, concerning context and composition, can be
highly significant. Adding together a combination of drugs, for instance, each of
which has been found to have a safe and positive effect in RCTs, could still possibly
produce a ‘cocktail effect’ that is unsafe. Again, this explains why causal inferences
are fallible. They are based on an assumption of a finite number of operating factors.
An unknown factor could effectively be an additive interferer, for some expected
effect. Worse still, it might be a factor that composes nonlinearly with the presence
of the other factors to produce an antipathetic effect.
The predictive value of such dispositional reasoning might, however, be ques-
tioned by those schooled in (probabilistic) deductive necessity – at least robust
methods might have some predictive utility within a traditional account, it might be
claimed. However, dispositionalism is not relativism and prediction is a feature of
dispositionalism. It is not that dispositionalism denies deductivism, although it does
judge it to be “over-ambitious” (Mumford and Anjum 2011: 140). The difference is
subtle but clear: whereas the traditionalist would say ‘if A, then necessarily B (to a
degree of probability)’, the dispositionalist would say ‘if A, then B is disposed or
tends to happen’.
The Humean response is simply to assert that if prioritised methods are con-
ducted correctly – without experimental error – then predictions should be forth-
coming that are simple, exact and unfailing. We know this to be false. Any account
of causal inferences has to respect the obvious datum that predictions are fallible
and defeasible. Dispositionalism offers an explanation of prediction and inference
within a fallibilist framework in which dispositions tend to produce their effects but
might not always do so.

13.4 Conclusion

We often use interventions with our patients which are based on the best of evidence,
yet still see no positive response. The Humean might see this as a normal artefact of
frequentist reasoning – on average the intervention works, bad luck in this case. The
dispositionalist, however, sees it as an example whereby there are insufficient addi-
tive causal factors, or too many subtractive factors than desired and so a therapeutic
threshold is not reached. The “intervention” is just one possible causal factor, and its
success relies on its manifestation with other causal partners. This is what is charac-
teristic about complex and context-sensitive clinical practice. Neither the interven-
tion nor the patient has ‘failed’, rather, there has not been the anticipated mutual
manifestation of variables in this case. Multi-dimensional clinical reasoning frame-
works, such as Mitchell et al. (2017), are exemplars of a dispositionalist theory at
play. The constantly evolving understanding of how aspects of a person’s biological,
212 R. Kerry

psychological, social dimension of their life and experience may dispose them
towards either an improvement, or a worsening of their health status.
In this chapter, we have learnt something about the relationship between EBHC
and causation, and also between theory and methods. Less-than-perfect correlations
can indicate something causal occurring, but are by no means irrefutable evidence
of some consistent or generalisable causal trend, however strong the correlation.
Prioritised research methods can indicate causal processes. However, the causal
work is being done within each group and thus it is the groups themselves, not the
regularities or counterfactuals, which act as the truthmakers. Robust population
studies may be very good at displaying symptoms of causation, but they are not
constitutive of causation.
The greatest causal work can be seen in single instance cases. This is where the
real nature of causation is witnessed. The interaction between causal agents, sub-
tractive and additive dispositions tending towards and away from an effect, causal
powers being passed from one partner to another. For the dispositionalist, the
essence of causation becomes apparent. In a dispositionalist ontology, scientific
research should focus on the interaction of causal partners and not be dominated
singularly by the pursuit for statistical invariance in large groups. For the clinician,
the relationship between research findings and individual clinical decisions becomes
clearer.
Despite those who reject the utility of anything other than epistemological analy-
ses, an ontological review allows the notion of EBHC to be re-evaluated from bot-
tom-­up. One of the foundational intentions of this chapter was to work towards a
philosophical underpinning of EBHC that would better support what already hap-
pens in clinical practice. This bottom-up approach relates well to clinical practice.
Least of all because a dispositionalist account of causation takes the individual
patient and the therapeutic interaction, along with all that is known about the pro-
cess of disease and interventions, as its starting point for an account of causation.
The ontological locus of dispositionalism allows the theory to escape commit-
ments to – and therefore shortcomings of – proxy truthmakers, universal laws,
causal necessity, probabilistic inference, and restrictive logical forms. A causal
theory based on causal dispositionalism is well positioned to account for the prob-
lems represented by the claims of EBHC, and furthermore provides an appealing
commentary on a causal epistemological framework. For the shop-floor clinician, a
dispositional ontology for causation far better facilitates a person-centred, evidence-­
informed clinical reasoning approach to best healthcare practice. If this were the
only legacy of the CauseHealth project, then it has been a worthy venture.
13 Causal Dispositionalism and Evidence Based Healthcare 213

References and Further Readings

Anjum RL, Mumford S (2018) What tends to be; the philosophy of dispositional modality.
Routledge, London
Gillies D (2017) Frequency and propensity: the interpretation of probability in causal models for
medicine. In: Solomon M, Simon JR, Kincaid H (eds) The Routledge companion of philosophy
of medicine. Routledge, London, pp 71–81
Guyatt G (1991) Evidence-based medicine. ACP J Club 114. https://doi.org/10.7326/
ACPJC-1991-114-2-A16
Guyatt G, Cairns JA, Churchill D et al (1992) Evidence-based medicine. A new approach to teach-
ing the practice of medicine. JAMA 268:2420–2425
Guyatt G, Oxman AD, Akl EA, Kunz R et al (2011) GRADE guidelines: 1. introduction-GRADE
evidence profiles and summary of findings tables. J Clin Epidemiol 64:383–394
Howick J, Glasziou P, Aronson JK (2013) Problems with using mechanisms to solve the problem
of extrapolation. Theor Med Bioeth 34:275–291
Hume D (1740) Abstract of a treatise of human nature. In: Millican P (ed) An enquiry concerning
human understanding. Oxford University Press, Oxford, pp 133–145
Hume D (1748) An enquiry concerning human understanding. Oxford University Press, Oxford
Kerry R, Eriksen TE, Lie SAN, Mumford SD, Anjum RL (2012) Causation and evidence-based
practice: an ontological review. J Eval Clin Pract 18:1006–1012
La Caze A (2008) Evidence-based medicine can’t be…. Soc Epistemol 22:353–370
Lewis D (1973) Counterfactuals. Oxford University Press, Oxford
Mercuri M, Baigrie BS (2018) What confidence should we have in GRADE? J Eval Clin Pract
24:1240–1246
Miles A, Mezzich JE (2011) Person-centred medicine: advancing methods, promoting implemen-
tation. Int J Pers Cent Med 1:423–428
Miles A, Mezzich JE (2012) The care of the patient and the soul of the clinic: person-centered
medicine as an emergent model of clinical practice. Int J Pers Cent Med 1:207–222
Mitchell T, Beales D, Slater H, O’Sullivan P (eds) (2017) Multi-dimensional clinical reasoning
framework. Curtin University Press, Curtin. https://www.musculoskeletalframework.net/
Mumford SD (2009) Causal powers and capacities. In: Beebee H, Hitchcock C, Menzies P (eds)
The Oxford handbook of causation. Oxford University Press, Oxford
Mumford S, Anjum RL (2011) Getting causes from powers. Oxford University Press, Oxford
NICE (2016) Low back pain and sciatica in over 16s: Assessment and management. Nice
Guideline [ng59]
Sackett DL, Rosenberg WMC, Gray JAM, Haynes RB, Richardson WS (1996) Evidence based
medicine: what it is and what it isn’t – it’s about integrating individual clinical expertise and
the best external evidence. Brit Med J 312:71–72
Williamson J (2007) Causal pluralism versus epistemic causality. Philos Mag 77:69–96

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the copyright holder.
Chapter 14
The Practice of Whole Person-Centred
Healthcare

Brian Broom

In the spirit of being whole person centred I will start with a story (some details are
changed or not included to ensure confidentiality):

14.1 A Woman with Skin Disease

Recently I was consulted by a woman with a 35 year history of a disfiguring skin

condition complicated by a crippling arthritis. She had sought help from many prac-
titioners, orthodox and unorthodox. Despite much medical treatment it remained
out of control. She admitted quite spontaneously that she had moved quickly from
one promising healing modality to another. She asked for help from me because she
had read in a magazine that I looked at the ‘whole person’. The unaddressed story
that unfolded in our meeting began in her family of origin. She was conspicuously
clever. In contrast, her sisters were more oriented to traditional domestic roles. Her
father could appreciate the sisters’ practical skills but could not validate her inclina-
tions and academic achievements. As a young adult she spread her wings and trav-
elled widely. Again in contrast, her sisters were all mothers by the age of 21. In her
late twenties she married and conceived. The comment in the wider family was “Oh
my God, she is going to have a baby!” The sense of inadequacy and self-doubt was
steadily accumulating. The birth of her baby was a disaster: a very prolonged deliv-
ery in a remote setting, a genuine risk of both baby and mother dying, the baby with
the cord tight around its neck and snatched away after delivery for resuscitation, the
baby not held for two days and ensuing poor bonding, and a crushing sense of pow-
erlessness and loneliness. She struggled with the child for years and while he was
still an infant the father left the marriage for one of her friends. She blamed herself,
her inadequacy, for this. The skin condition began and has continued ever since. She

B. Broom (*)
Auckland University of Technology, Auckland, New Zealand

© The Author(s) 2020 215

R. L. Anjum et al. (eds.), Rethinking Causality, Complexity and Evidence for the
Unique Patient, https://doi.org/10.1007/978-3-030-41239-5_14
216 B. Broom

noted that it got much worse after another of her children suddenly died of unknown
cause. Another child has developed a different serious inflammatory disorder. One
way and another she blames all this on her inadequacy. There were some hints of
very early sexual abuse. Notably, she described herself as struggling with something
“ugly and dark” within her.
The question of course is why would I bother to take out such a history in a per-
son with a serious medical condition? My reactive response is simply this: why not?
A more considered answer is that the story seems really powerful and that from a
unitive, nondualistic, whole person-centred perspective, in which mind and body
are not separated in the ways we have traditionally accepted in medicine and culture
generally, it is very likely these story factors are playing a significant role in her
suffering and disease.

14.2 A Professional Evolution

In 1982, in mid-life, I abandoned a flourishing academic clinical immunology

career, at the Christchurch School of Medicine, to train in psychiatry. I was respond-
ing to an increasing sensitivity to fragmentation. I had been reared within a Christian
spirituality largely unaffected by science and modern thought and scholarship. I had
trained to high levels in internal medicine which largely ignored subjective experi-
ence. And I was yet to discover a psychiatry and psychotherapy largely ignoring the
body. I felt that this systemic fragmentation was a fundamental cultural problem,
but had little ability to articulate it, let alone convert it into clinical practice.
Thus began a journey specifically undertaken to explore relations between medi-
cal practice and patients as whole persons. I had the impulse but no real concept of
what it meant and certainly no idea where I was heading. I was not popular. My
highly esteemed mentor, senior colleague, and head of the department of medicine,
Professor Don Beaven, gave a simple and direct response to this change in direction:
“You are an idealist!” and of course he was right. Other colleagues and peers seemed
to feel I was betraying an unwritten professional code. The forces maintaining nor-
mative cultural structures in medicine are very powerful.
Already having expertise in the body (or at least, diseases of the body), my first
move was to embrace the ‘mind’. Entering psychiatry allowed me to begin this pro-
cess, to maintain my medical functioning, and to earn a sufficient living to sustain
my growing family. The four years in psychiatry taught me many interesting and
useful things, but I found that as a medical discipline it was pretty much just as
deeply embedded in physico-materialist and dualistic assumptions as my previous
internal medicine framework. This was not what I wanted. I was seeking to under-
stand persons and the potential for integration of all dimensions of personhood in
our understanding and treatment of illness and disease.
Psychiatry does have an interest in those physical illness presentations known as
psychosomatic conditions, but had long vacated interest or professional
14 The Practice of Whole Person-Centred Healthcare 217

responsibility for mind factors in all the other physical conditions, the ‘real’ (sic)
physical diseases. Indeed, mostly, it was felt that the apparently non-psychosomatic
conditions had nothing to do with mind or subjectivity.
Psychotherapy, on the other hand, held more promise, and so I veered away from
psychiatry. New ‘worlds’ of thinking opened up cumulatively over many years,
about the mind or the subjectivity of persons as patients. The most influential
emphases were psychodynamic theory, infant development, stages of life concepts,
family and systems theory, trauma concepts, object relations theory, interpersonal
psychotherapies, self psychology, learning theory, narrative theory, and conscious-
ness studies. These worlds had been entirely invisible to me previously as a clinical
immunologist. They remain invisible to the vast majority of medical clinicians
working in practice in the Western world. The point I make here is that there is a vast
panorama of the subjectivity of persons excluded from the ordinary arenas of medi-
cal care.
Psychiatry was not a suitable base for further exploration. I initiated a multidis-
ciplinary Centre (Arahura Centre, Christchurch, New Zealand) committed to the
integration of high standard medical practice, psychotherapy, and spiritual values.
All of the staff and trainees came from diverse Christian backgrounds and felt simi-
lar if not identical aspirations for integration. With two colleagues I mentored this
unusual journey of integration. Over the next ten years what developed was a multi-­
dimensional, multi-factorial, multi-causal, and multi-methodological approach
towards disease (vide infra).
Personally, I began a psychotherapy practice and re-ignited my role as a clinical
immunologist. There was nothing particularly intentional or inspired about that
decision—it just seemed a sensible way to continue my life as a clinician. But, to
my surprise, startling and jolting things emerged. Before entering psychiatry I had
enacted my clinical life largely by perceiving physical diagnoses and diseases. Now,
as both a physician and as a psychotherapist, working with individual patients pre-
senting with a wide range of physical conditions, I was still making diagnoses and
treating diseases but also hearing ‘stories’ in the same clinical time/space. And I
started to see connections between diseases and stories in many cases. Thus began
my work with ‘Medicine and Story’ (Broom 2000).

14.3 Somatic Metaphors

What was more disturbing was that these stories suggested that some of the physical
conditions I was treating were actually symbolic. I have written extensively about
these (2, 3). I called these instances somatic metaphors (Broom 2002). There were
sexually abused patients with oral and genital conditions. A patient with a facial
rash keeping a ‘brave face’ on a partner’s depressive condition and unable to talk
about it. A patient with years of crippling mouth ulceration resolved when she
218 B. Broom

finally talked to her daughter about leaving the Catholic Church. My books relate a
myriad of such examples, in both relatively minor and also very severe and serious
physical disorders, most of which could not be confined and dismissed as psychoso-
matic, in the old sense of the term. More than that, the stories couldn’t be simply
dismissed as retrospective, narrative constructions or interpretations. The stories
appeared to be triggers of the disease. Many were very chronic and had failed to
respond to biomedical therapies, but got better when these meanings were ascer-
tained and worked with.
This was very challenging. Initially a major issue was scientific plausibility. How
can very specific meanings get expressed in the body, emerging as a symbolic dis-
order? The dualistic model we are trained in treats the mind (with its meaning-­
making) separately from the body, in which meaning has no place or role in the
aetiology and pathogenesis of disease. In the end, I had to toss this model away and
start to think of persons as wholes. The dualistic model itself becomes the implau-
sible construction of reality. Thankfully, in recent years this is becoming more
mainstream, at least in wider culture, though it hasn’t dawned significantly on medi-
cal practice.

14.4 Whole Persons in the Clinic

While I found all of this both exciting and difficult conceptually, the next important
issue was how to talk to patients about mind and body connections. What I found
was that if I was skilful and did not psychiatrise these connections, patients were by
and large cautiously open to a multi-causal view of disease that included ‘story’, or
subjectivity in general.
Instinctively most people know we are ‘wholes’, it is just common sense.
Nevertheless, one reason why we may express our life struggles in physical illness
is that we may be unable, for one reason or another, to find a better way to represent,
express, and work through certain difficult or painful emotions and issues. But I
gradually learned to educate, to warmly ‘hold’ people through their uncertainties,
and to enquire in such a way and at a pace which enabled trust and safety to flourish.
Thus, skills were needed, beyond the algorithmic protocols of normative medical
interrogation. A majority of patients love being treated as persons with stories, as
opposed to just being diagnostic challenges and objects. We clinicians need to make
room for these stories, and, contrary to what most clinicians assume, this does not
need to be principally about time cost. Curiously, it is much more about generosity,
safety, empathy, and simple information and education about mind and body con-
nections (see www.wholeperson.healthcare for an expanded review of appropriate
listening skills). But until clinicians accept that human subjectivity or stories play a
role in disease development none of this is going to be prioritised.
14 The Practice of Whole Person-Centred Healthcare 219

14.5 Reactions from Colleagues

Another issue was how to communicate with my colleagues. Patients were referred
to me as an immunologist for immunological assessment. I wrote report letters back
to my colleagues which certainly offered that, but also, where relevant (and almost
universally), the review was wrapped in or permeated by a story.
I was anxious about this initially. How would I be seen? Would referrals dry up?
My practice flourished. Many family practitioners welcomed these more fulsome
reports. The odd one was dismissive (usually reported by a patient). Many carried
on as before, impressed by but seemingly unaffected by my educative reports.
Increasingly doctors sent me their problematic patients—the people who did not
respond to standard biomedical care. I became known as a doctor who could hold
complexity. Some doctors embraced the approach and trained with me.
But I learned early that despite even overwhelming evidence of mind and body
connectedness most clinicians want to stay with what they know and do, with their
dualistic biomedical model, even if this is not in the best interests of their patients.
As an example of this, there are a host of scientific psycho-neuroimmunological
articles suggesting an impact on the immune system of psychological factors, stress
or abuse. And yet again and again I have attended huge immunology conferences
where there is clearly no interest in or evidence of any impact of this work.
This problem of the neglect of the role of the mind or subjectivity factors is both
multifactorial and formidable. The issues include: vested interest based on training,
time and income flow; the dominance of the biomedical model; default behaviours
and skills that militate against listening; lack of psychological understanding on the
part of clinicians; relational inadequacy; inability to cope with patients’ emotions;
financial, institutional, cultural and systemic structures that avoid human experi-
ence; the valuing of quantitative over qualitative evidence; and the difficulties of
dealing with data that is not easily ‘measured’.

14.6 Dualist Psychotherapy

But we pressed on. The numbers coming to me increased and I found myself need-
ing psychotherapists to help me. I would assess the patients and refer them on to
excellent community psychotherapists. A new phenomenon appeared.
Psychotherapists are good with ‘stories’ but they often, by default, exclude the
‘body’ from their clinical working space. This would happen even if I sent a patient
specifically for ‘mindbody’ psychotherapy for a physical condition like urticaria,
eczema, asthma, irritable bowel syndrome, migraine and much more. I also discov-
ered that the patients would not do as well as I had expected. On review, I found
220 B. Broom

these patients told me that they might introduce their physical symptoms in the ses-
sion with the therapist, who then would typically ask if the patient had talked to the
family doctor about it again. That is, essentially, the therapist was saying to the
person, ‘take your body to the doctor, it is not my job.’ Psychotherapists are cer-
tainly conceptually more open to the mindbody connections, but in practice are as
dualistic as doctors. So I established supervision groups for psychotherapists, and
from that time only ever referred my patients to the eight therapists I had in mind-
body supervision. The therapists themselves needed holding in a whole person-­
centred framework. The outcomes were much better.
The point is of course that all of us in our specialised clinical work are dualists
to some degree. Professionalism and scopes of practice serve to keep us in our con-
ceptual silos. Again and again I find myself reiterating the two bulwarks of whole
person healthcare work. We need to have a non-dualistic view of persons and dis-
ease, and we need to have the skills to comfortably allow mind and body to be
together in our clinical workspace with patients, and to listen and respond. We now
have many clinicians who can do this. They do not need to be dually trained (Broom
2013), as I am in both medicine and psychotherapy. It helps greatly if different dis-
ciplines are in close contact, supporting (for example) the doctor towards stories and
psychotherapists towards bodies.

14.7 Publications

Time went by, and eventually in 1997 I published my first book, Somatic Illness and
the Patient’s Other Story (Broom 1997), essentially to tell the story of physical illness
as related to the predisposing, precipitating and perpetuating ‘story’ factors of causal-
ity, especially focusing on those diseases generally regarded as physical, but also
those considered as psychosomatic. The principles of non-dual, unitive, whole person
practice apply of course to all illnesses. The book provides many examples of the
observed clinical phenomenology, and lays out in detail the skills necessary to provide
treatments that actively integrate normative biomedical principles with story factors.
In 2007 I published a second book, Meaning-Full disease. How Personal
Experience and Meanings Cause and Maintain Physical Illness (Broom 2007), sys-
tematically addressing and arguing a theoretical basis for seeing persons as wholes,
understanding diseases as being expressions of wholes (that is, multifactorial, mul-
tidimensional and multicausal), and the benefits of treating them as wholes. In that
book I drew on many resources and concepts that can contribute to such discussions.
Once we escape the grip of strict scientism we can find help from many disciplines,
such as philosophy, modern physics, complexity theory, cultural and trans-cultural
studies, the arguments for and results of qualitative research, and much more.
But clearly the biopsychosocial model (BPSM), psychosomatic studies and
insights, and psychoneuroimmunology (PNI) deserve brief further mention here. I
have gained a lot from these perspectives, but I diverge from them in one crucial
respect. All are permeated with a fundamental dualism or physicalist reductionism
or both.
14 The Practice of Whole Person-Centred Healthcare 221

My view is that George Engel, the originator of the biopsychosocial model, was
not particularly dualistic, but the vast majority since who have espoused the model
are indeed so. I really tire of hearing clinicians claiming to believe in the biopsycho-
social model, but essentially happily ignoring the role of psychosocial elements in
the supposedly ‘real’ physical diseases.
For its part, the psychosomatic tradition keeps mind-oriented clinicians focussed
on a small group of disorders that cannot be easily explained by biomedicine—as if
subjectivity is really only relevant in this small grouping of disorders, which cannot
be explained by the biomedical model. This is rampant dualism.
Psychoneuroimmunology presents a different story again. It is as if we can only
accept a role for story if we can find a linear mechanism acceptable to the biomedi-
cal model. Therefore it is fundamentally body-focussed and reductive.
One might also think that narrative medicine and narrative therapies have a lot in
common with my story approach. Essentially they arose out of the 20th Century
post-modern ethos and cross-cultural studies. The narrative focus is important.
Essentially it is about what sense people make of their illness. This is important but
it is a sub-section of story-gathering. Story in the narrative sense is essentially post-­
hoc: that is, the physical disease arises because of purely physical factors and then
is interpreted after the event in one way or another, according to one’s belief sys-
tems and cultural influences. Our work goes beyond that to understanding the role
of story in ‘causing’ disease.

14.8 Human Infant Development

Let us consider a human infant in its earliest phase of development. What kind of
concept do we have of that infant’s evolving dimensions of physicality (bodily
development, growth, movement, coordination etc) and subjectivity (capacity for
experience, perceiving, relating, thinking etc). Surely it is without question that
these capacities emerge and evolve from the beginning, together. The subjectivity
dimension is not some adjunct, latter-day appendage, a kind of discretionary item.
The dimensions we call body and mind co-emerge, and are inextricably integrated.
I and two colleagues have addressed this in a paper titled Symbolic illness and
‘mindbody’ co-emergence. A challenge for psychoneuroimmunology (Broom
et al. 2012).
If mind and body are not inherently separate, why would we assume that, in
disease, body is important but mind is not? The reasons given for this depend a little
on one’s background, but include the sharp ‘turn’ to dualism attributed to the French
Catholic mathematician/philosopher, Descartes, or the inherent dualism of language-­
making, or the primacy given to concrete measurable dimensions of reality, or the
fears we have of revealing the harsh and vulnerable aspects of our personal experi-
ence, or the determined ‘disenchantment’ of the world during the last few centuries
in the name of demystification, positivism, and mastery. Most likely all these have
played a role.
222 B. Broom

But our whole person-centred phenomenology of disease suggests strongly that

we must engage in a unitive view of persons as wholes, and treat diseases within
that conceptual framework.

14.9 
Mindbody Healthcare

Back to what that meant in practice for me. I worked at the Arahura Centre from
1987 until 2007. In the later years I initiated (2005) a multi-disciplinary Masters and
Diploma Post-Graduate Program in MindBody Healthcare at the Auckland
University of Technology, specifically aimed at experienced clinicians of all kinds
(for accounts by the clinicians themselves see Broom 2013). I had long felt that
what we must do was encourage clinicians to expand their practices to include a
story element. I had done many well-received workshops and seminars, nationally
and internationally, but became aware that for most people it was too hard to make
the changes needed. Once clinicians accepted and embraced the concept of persons
as wholes, they typically became much more aware of what they were not doing.
Some wanted to apply it to everyone and soon became overwhelmed. Many did not
have good listening capacities, did not know how to invite patients to reveal difficult
things, were uncomfortable with emotions, feared running overtime, and simply
didn’t have a language for these kinds of conversations. Some had habits that they
either couldn’t or did not want to break. Some would try, and then run into trouble
based on these issues. So we devised a program which got established at the
University.
The multi-disciplinary side worked out very well. It meant everyone had to see
the generic principles of conceptual understanding of wholes, multifactoriality and
multidimensionality, and also see that the skills of listening to story were the same
whatever discipline we were in. What was different was how this worked out in dif-
ferent disciplinary settings.
Commonly we saw a lot of personal confusion and incoherence developing for
more than 50 percent of the students in the first few months as they started to trans-
form their behaviours and practices. There are typical issues. How do I start a story
conversation without alienating the patient? What do I do now that the story has
come out? Learning not to jump to fixing things was a major hurdle for the body
clinicians (doctors, physiotherapists). Understanding that most stories are about
what and what has not happened in relationships was hard for some to appreciate.
Some would jump at a meaning like a clinician would jump at the result of a CT
scan, and then find the patient pulling away. Being person-centred rather than ‘my
expertise’-centred was a harsh lesson for some. Discovering that collaborative rec-
ognition, between clinician and patient, of just the fact of a connection between the
presenting illness and the story might be in itself enough to settle an illness was an
amazing experience for others. Wanting it to be that way every time was a salutary
lesson for others, whose desire for mastery transcended their capacity for tolerating
complexity.
14 The Practice of Whole Person-Centred Healthcare 223

We have trained some 70–80 clinicians in this way.

In the earlier years I commuted to Auckland to teach this program but in 2008 I
shifted there to live. I continued the AUT program, and was invited to take up a posi-
tion as an Immunologist at Auckland City Hospital. It was then 26 years since I had
initiated and led the Immunology department at Christchurch Hospital. I wondered
how I would fit, given all the developments in my thinking and practice over the
years. It was nice to be back in an old familiar environment. I was determined not to
badger people into my way of thinking, and more or less succeeded in that.
Throughout my time there I continued to practice from a whole person perspective.
This was respected and valued. It has always been important to me to be an excel-
lent physician in a normative sense, and being amongst biomedically-informed col-
leagues helped me keep up that aspect of my functioning. For years now, we have
had two to four Masters level students from the Department of Psychotherapy at
AUT University on placement in the Immunology Department working with
Immunology patients and supervised by myself and a very experienced MindBody
Psychotherapist from AUT.

14.10 I Was Conflicted

But I often felt heavy after my days at the hospital, constantly aware of patients who
were struggling because of inadequate purely biomedical approaches, or suffering
unnecessary side effects of treatments, and who could have been helped by a whole
person approach. I was conflicted. I am very fond of, and greatly enjoyed the com-
pany of my colleagues, but at times I became impatient and frustrated that they
could/would not open themselves a bit wider for their patients. There was a genuine
respect for what I was doing, they wanted me there, but generally they hesitated to
do it themselves. Some things did change in the department. Most of the clinicians
professed to be affected by the whole person approach, and there was a reduction in
useless and pointless testing for many patients. But it didn’t go far enough for me.
Perhaps it was the idealist in me, wanting a more major re-orientation. One of my
colleagues has an enthusiastic and competent grasp of the approach. And we have
14 specialist doctors from throughout the hospital who meet monthly to talk about
and learn the approach.
We are truly faced with a conundrum. There is certainly a hunger for something
different, more whole person-oriented, but there is a powerful inertia in the health-
care system.
There is one thing more for this chapter. What is the cause of improvement in
illness and disease when the whole person-centred approach is used? As stated at
the outset, a major stimulus for me as a clinician was the phenomenology of sym-
bolic disease. Thus a focus on meaning and stories of meaning-full disease became
my initial doorway into the ‘whole person’. But I have resisted a reduction of all
224 B. Broom

disease to meaning. Opening things up by going through the doorway of meaning

mobilises many other elements, including the importance of relationship in healing.
The skills involved in listening to stories are mainly relational skills. Genuine
interest, willingness to tolerate uncertainty, waiting to see what emerges rather than
relying on prior knowing, warmth and empathy, and much more. Certainly not all
patients had symbolic disorders. Most stories we dealt with were crucially about
relational disturbance.
This leads to another issue. Clinicians, by virtue of their training, are very sus-
ceptible to learning a methodology that is based in searching for a story, or the story,
like searching for a diagnosis or a pathogen. But once such a search is initiated they
are confronted with what it means to be in a healing relationship with the patient in
a much more intimate way.
Out of all of this, I came to suspect that much of what we were doing could be
conceptualised roughly as follows. Meaning is important, and it is a physician’s
focus in opening up the field, in which it is accepted by the clinician and patient that
mind and body are connected and need to be addressed in the proper treatment of a
physical condition. Physician interest in the patient’s meanings or story triggers in
the patient a sense of being understood. Sufficient trust and safety can lead to the
patient revealing painful and important material, and with support be nudged into
resolving some long-standing issues, usually of trauma or disturbance in relation-
ship. It might be enough just to name these, or a longer process of mindbody psy-
chotherapy might be needed. At every point physical and non-physical factors are
held to be potentially contributory.
All this might be the physician’s interpretation of what is happening. But what
do the patients say?

14.11 Being Looked at or Being Seen?

Galia Barhava-Monteith, a mature woman who had recovered from the serious dis-
order Churg-Strauss Vasculitis whilst undergoing both normative chemotherapy and
a whole person-centred approach, recently completed a PhD (AUT University 2018)
exploring this question, titled: “The difference between being looked at and being
seen”: An in-depth consideration of experiencing the Whole Person Therapeutic
Approach for chronic illness”. There are many important things to ponder on in this
thesis. It is noteworthy that, in contrast to the perspective of whole person-centred
clinicians as to what is important in disease treatment, few of the patients undergo-
ing such treatment refer to the importance of specific meanings or symbolism in
their stories of recovery.
It will suffice to use Dr Barhava-Monteith’s own words:
I have come to see that the taken-for-granted practices of WPTA (Whole Person Treatment
Approach) clinicians, or the how of their practice, is the thing itself. I now comprehend how
the therapeutically beneficial aspects of WPTA, and any other encounter between two peo-
ple where one’s role is to enable the other to get better, are dependent on the capacity of the
14 The Practice of Whole Person-Centred Healthcare 225

healer to see the person they are trying to heal. The technical knowledge of course must be
there, but it is only the starting point. I came to conceive that this experience of being seen
is the feeling that someone else is truly seeing the whole of you. Risking hyperbole, I argue
that this is a profoundly existential experience, as mostly we spend our lives with people
who only look at aspects of us. Who look at our professional background, or at our symp-
toms, or look at our childhood trauma. From apprehending that the experience of being seen
is somehow important, I now comprehend that it is an existentially humanising and healing
experience that unfortunately too few people experience. My doctoral research has con-
firmed to me that being introduced to non-dualistic concepts as they pertain to health and
wellness in the context of this relationship can be transformative, in that patients come to
reconceptualise their identity with respect to their illness so that they, like me, can experi-
ence freedom and hope. However, I now grasp that to introduce radical new ways of think-
ing about one’s self is something that should be treated with utmost care and reverence.
Introducing such notions may destabilise the very core of one’s personhood. Now I see that
anyone who is involved in activities that are concerned with changing the way another
person thinks and behaves, has to earn the right to do so. And the ways by which we earn
that right is through being careful and mindful of our words, our actions and our capacity to
recognise the personhood of another, and of being experienced as doing so. In a sentence,
my conclusion at the end of my doctoral journey, is that it is through the how, not the what
where profound experiences and changes occur… In concluding this doctoral thesis, I do
think that making explicit the ontological dualistic assumptions underpinning much of the
teaching of modern medicine is important. However, I now think that we need to consider
shifting the almost exclusive focus on content or the what of clinical sciences, to include, as
equal, the how, the ways of acting and being. My reflection in concluding this thesis is that
clinicians who work to embody these humanising practices, are likely through doing and
experiencing, to shift their own preconceptions about the dualistic nature of health and ill-
ness. (Barhava-Monteith: 230)

I finish as I began. In considering causality in illness and disease, our work draws
attention to the fact that we, as patients, are persons, but more than that, persons-in-­
relationship. Any therapy that reduces us to a more limited view of persons, such as
objects to be technologically manipulated, is going to have serious limitations, if not
in many cases profoundly inadequate.

References and Further Readings1

Barhava-Monteith G (2018) The difference between being looked at and being seen: an in-depth
consideration of experiencing the Whole Person Therapeutic Approach for chronic illness.
Dissertation, Auckland University of Technology
Broom BC (1997) Somatic illness and the patient’s other story. A practical integrative mind/body
approach to disease for doctors and psychotherapists. Free Association Books, London
Broom BC (2000) Medicine and story: a novel clinical panorama arising from a unitary mind/body
approach to physical illness. Adv Mind Body Med 16:161–207
Broom BC (2002) Somatic metaphor: a clinical phenomenon pointing to a new model of disease,
personhood, and physical reality. Adv Mind Body Med 18:16–29

1
For clinicians and others wanting ready access to a range of resources in Whole Person-Centred
Healthcare there is a wealth of material at https://wholeperson.healthcare
226 B. Broom

Broom BC (2007) Meaning-full disease: How personal experience and meanings initiate and
maintain physical illness. Karnac Books, London
Broom BC (2013) Transforming clinical practice using a mindbody approach. A radical integra-
tion. Karnac Books, London
Broom BC, Booth RJ, Schubert C (2012) Symbolic illness and ‘mindbody’ co-emergence. A chal-
lenge for psychoneuroimmunology. Explore 8:16–25

Open Access This chapter is licensed under the terms of the Creative Commons Attribution 4.0
International License (http://creativecommons.org/licenses/by/4.0/), which permits use, sharing,
adaptation, distribution and reproduction in any medium or format, as long as you give appropriate
credit to the original author(s) and the source, provide a link to the Creative Commons license and
indicate if changes were made.
The images or other third party material in this chapter are included in the chapter’s Creative
Commons license, unless indicated otherwise in a credit line to the material. If material is not
included in the chapter’s Creative Commons license and your intended use is not permitted by
statutory regulation or exceeds the permitted use, you will need to obtain permission directly from
the copyright holder.
Chapter 15
A Broken Child – A Diseased Woman

Anna Luise Kirkengen

We are such stuff

as life is made of –
and our lived body
tells its tale.

15.1 Cecily Cramer

Now in her mid-forties, Cecily Cramer1 is a well-educated, married mother of three

children under 17-years of age. My initial contact with her came at the suggestion
of her therapists, psychologist Aina, and psychomotor physiotherapist Sanne, both
of whom are highly experienced, trauma-oriented professionals.
In our correspondence prior to our first meeting, Cecily authorised me to access
the medical records from both of her recent university hospital psychiatric ward
admissions, as well as the notes from her out-patient clinical care following the
second of these. Cecily also gave me her consent to read the notes from her sessions
with Aina and Sanne. Lastly, she allowed me to see the detailed results of an x-ray
examination that the university hospital’s radiology department had carried out, req-
uisitioned by the hospital’s oncology department.
As Cecily and I discussed this documentation in depth during our conversations,
I became convinced that her complex sickness history would remain incomprehen-
sible, both to those treating her and to Cecily herself, were her painful life history
not taken into account. In fact, her current symptoms could only be decoded once
their trajectory had been traced back to when they first emerged: at that point, they

1
Cecily Cramer (pseudonym) has contributed to the present form of her history and consented to
its publication.

A. L. Kirkengen (*)
Department of Public Health and Nursing, Norwegian University of Science and Technology
(NTNU), Trondheim, Norway
e-mail: anlui-k@online.no

© The Author(s) 2020 227

R. L. Anjum et al. (eds.), Rethinking Causality, Complexity and Evidence for the
Unique Patient, https://doi.org/10.1007/978-3-030-41239-5_15
228 A. L. Kirkengen

were the sole survival strategies available to her. They did aid her, initially, in her
struggle to protect herself. Over time, however, her continuing to rely on those same
strategies became a dangerous habit, one that depleted her vitality and literally put
her life in jeopardy.
When Cecily recognised the pattern and its impact, she realised that she both
wanted to, and could, seek help to break free of it. Her 4-year cooperation with Aina
and Sanne enabled her to do just that, and, in the process, regain her self-respect,
increase her confidence, improve her health, and help her find the strength to go on,
both with her personal life and with her profession.

15.2 Crisis Onset

At 20 years of age, Cecily was diagnosed with a rare, aggressive cancer requiring
intensive treatment, including surgery, medication and follow-up. After some years,
she was pronounced free of cancer. She married, worked full-time as a specialist
nurse, took part in competitive sports, and gave birth, each time with complications,
to three healthy children who all developed well. Then, her cancer recurred. Again
she went through a difficult course of treatment, and again was declared cancer-free.
Toward the end of the long sick leave that followed her treatment, the new leader of
her department at work, whom she had never met, began urging her to return to her
demanding position, full-time. Cecily feared she would lose her job if she refused.
Although she did not feel ready, particularly with three small children at home,
Cecily “obeyed” and went back to work. She even agreed to work shifts during
Christmas.
By January, she was feeling suicidal. She felt overwhelmed by hopelessness, suf-
fered from frequent nightmares, anxiety, insomnia and an inability to concentrate.
Desperate and scared, she was admitted to the psychiatric ward.

15.3 Two In-Patient Psychiatric Hospital Ward Admissions

Records from her first admission read as follows:

Woman with known depression, admitted by her GP due to increasing depressive
symptoms. Allergic to penicillin and a possible adverse reaction to another drug.
Predispositions: alcoholic father, cousin with personality disorder.
No one, however, asked Cecily: How were you affected by your father’s alcohol-
ism? How would you describe your parents? How did they treat you? What do
you know about your cousin’s condition?
Records:
Somatic: surgery and treatment for kidney cancer, 21-years old.
15 A Broken Child – A Diseased Woman 229

No one, however, asked her: How did that serious disease, and the long-term treat-
ment for it, affect you and your life, especially considering how young you were?
Records:
Patient denies having a substance abuse problem.
No one, however, asked her: Have you ever been abused or maltreated?
Records:
Psychological: Prior depression 2 years ago treated pharmaceutically; consider-
able side effects from the first meds. Second meds, ineffective.
No one, however, asked her: What would you say is the main reason you feel hope-
less and down?
Records:
Patient felt she needed to return to full-time work shortly after treatment for recur-
ring cancer because she was afraid of being fired.
No one, however, asked her: Did you feel pressured, or forced, as if someone had
control over you? If so, might that have reminded you of something that hap-
pened to you earlier?
Records:
In addition, patient has started to see a psychologist, which has opened up old prob-
lems (among these are childhood incest) that the patient, as she puts it, “has
trouble coming to grips with”.
No one, however, tells her: Nobody ever experiences abuse without being deeply
marked by it. No one asks her: What do know about how these early experiences
of being abused have affected you and your life – and what do you remember
about whoever abused you?
Records:
The patient reports that she has lost her appetite, doesn’t sleep properly, doesn’t
want to get up in the morning, that her memory fails her, that she can’t concen-
trate and suffers at night from anxiety and nightmares.
No one, however, suggests: Your ailments seem to be part of a pattern, perhaps con-
nected to having been under too much stress for too long a time. No one inquires:
Do you see any relationship between these problems and experiences from your
childhood?
Records:
The patient says that she wants to commit suicide, sees it as her last way out, but
hesitates out of concern for her husband and her three children.
No one, however, asks: Why can’t you, or why don’t you want to, go on with
your life?
230 A. L. Kirkengen

Records:
The patient confirms that she has had such periods of depression throughout her
entire life.
No one, however, asks: Might your feelings of powerlessness and exhaustion have
something to do with what was done to you when you were a child? Was there
anyone who protected you?
Records:
The patient appears to be suffering, but there is no indication of hallucinations or
psychosis. Conclusion: known depression, increasingly aggravated by work-
place problems; suicidal ideation. Treatment plan: mood stabilising followed by
further treatment.
Addition to the records made by Cecily’s ward psychiatrist the following day:
She describes a personality structure characterised by not wanting to speak out or
object. She has been eager to do her best, which has probably contributed to her
load becoming heavier than necessary. She is sad, prone to weeping, feels hope-
less and her thinking is chaotic. Her depressive symptoms range from moderate
to high. Her personality does seem to predispose her to depression, although
current external stressors have also contributed.
Here, she is assigned a diagnosis while, simultaneously, being defined as its ori-
gin – her predisposing “personality”. No one seems to have been listening to her
when she spoke of having an alcoholic father, or of a childhood marked by incest,
as well as other problems – all of which she says she is struggling even to grasp.
Psychiatry seems totally deaf to this alarming and highly relevant information.
Addition to the records made by the psychiatrist in charge of Cecily’s case,
one week later:
The short-term aim for treatment is for her to become calm and stabilised. The long-­
term aim for treatment is to discharge her in an improved condition.
Nothing in this plan would indicate any intention of seeking to understand the
patient, or of offering to help her come to grips with her basic problems. The record
does mention, though, that Cecily’s medication is to be increased to eight psychoac-
tive drugs.
Addition to the records made by the psychiatrist after 10 days of in-patient
treatment:
The patient still shows depressive symptoms. She finds it difficult to participate in
planned activities. Her thoughts are in turmoil, constantly circling around the
past; in today’s conversation we try again to talk about it being natural to think
of the past when depressed, so that it soon fills all the space. Therefore, we
ought to try to concentrate on the actual here-and-now and work with the
depressive elements, in addition to acquiring tools to think more positively.
[Emphasis added.]
15 A Broken Child – A Diseased Woman 231

The psychiatrist uses the plural: “…we try…we ought”. This we, however, does
not include the patient. By using this we, the physician nullifies the patient’s stated
need to come to grips with what disturbs her thoughts: her past. He shows no inter-
est in this past, nor any intention to inquire into it. He has defined the problem as
“here-and-now” with no relationship to “there-and-then”.
Four weeks into Cecily’s hospitalisation, she meets with psychologist Aina for
the first time. Only now is she invited to recount memories of her traumatic child-
hood and of her inability to comprehend her own emotions. She tells Aina about her
younger, multi-handicapped brother for whom she felt responsible because he was
so vulnerable, describing herself as “defenceless”. She shares that she does feel safe
on the ward but misses her children. She admits that, even after 20 years of mar-
riage, she still keeps secrets from her husband, and she reveals to Aina that she
starved herself as a teenager because she wanted to die.
Cecily meets with Aina six times before being discharged. Aina summarises in
her notes that Cecily has been traumatised, unseen, neglected, and under exception-
ally high stress for a prolonged period. Nonetheless, she avoids making any demands
on the people around her.
Addition to the records made by Cecily’s psychiatrist the day before she is
discharged:
The patient is very concerned about whether to talk with somebody about how she
was earlier in life regarding all the stress she has been under. We discuss that it
is certainly important that everything be dealt with, whenever she is ready. As
things are now, however, we must take one thing at a time. Her depression needs
to be the focus, and for her to feel calmer and not burden herself with too many
stress factors.
The psychiatrist does admit that it would be important, eventually, to discuss the
past, although he does not explain why. For him, the disorder itself, depression,
represents a greater threat to the patient than does the source of the disorder. Thus,
he separates the disorder from its origins, which he terms “stress factors”, without
having made any attempt to learn what those might be.
Upon discharge, Cecily is prescribed seven psychoactive medications. The
physician recommends a prolonged sick leave before a gradual return to work. She
is promised out-patient clinic follow-ups to begin immediately, but none is ever
offered to her. Despite it being clear that Cecily is on extended sick leave, her
employer continues to urge her, insistently, to come back to work.
Six weeks after being discharged, Cecily is readmitted to the same psychiatric
ward, in even worse condition than at her first admission. Again, she states that she
cannot bear entreaties, demands and threats from someone who has power over her.
Again and again, she speaks of how terribly her boss has treated her, of how she has
been abandoned by her employer and by the healthcare system that “forgot about”
her after her recent discharge.
This time, Cecily meets psychologist Aina after only five days, but they manage
to have just two meetings during Cecily’s 18 days of hospitalisation. She is told to
232 A. L. Kirkengen

continue taking four medications for depression, one for restlessness, two different
analgesics to be taken as needed, one drug for nausea and one sleeping pill.

15.4 Follow-Up Care

Without explanation, Cecily is referred to the out-patient clinic for those with per-
sonality disorders for her follow-up care rather than, as had been planned earlier, the
clinic for people suffering from mood disorders and depression. She is immediately
offered an appointment with Aina, however, and from then on, the two meet and talk
on a regular basis.
When asked how Cecily felt being on the ward, she responds:
The ward nurses and the team in charge of my treatment were told not to talk to me about
my past but to keep the focus on my depression symptoms. I felt ignored. Wrong. Put in a
box for depressed women. The conversations were only about what they thought was impor-
tant and about giving me psychological education. Everything was about what I myself
could do to overcome my need for isolation and loneliness. But this was exactly what I’d
been trying to do on my own, before being admitted. The only advantage to being on the
ward was that I didn’t commit suicide. And I met Aina, and she had the courage and strength
to object to “pre-packaged treatment” and take me under her wing.

With Aina, Cecily begins to share information about her life that she had not
shared before, including, after a few meetings, about her fear of her father. The
details that psychologist Aina is enabled to glimpse about what Cecily had been
subjected to as a child, convince her to suggest that they involve psychomotor phys-
iotherapist Sanne in the treatment process. Cecily agrees. Sanne examines Cecily’s
body, her posture, musculature and her patterns of pain and tension. A dual thera-
peutic process then begins, with sessions twice a week. As often as possible, Cecily’s
meetings with the two therapists are scheduled to take place on the same day, some-
times with all three working together.
The issues and specific findings that are uncovered are nowhere to be found in
Cecily’s extensive records, neither within the somatic documentation – the volumi-
nous files from oncology, surgery and radiology – nor in her psychiatric in-patient
records.
Four months into this treatment regimen, Cecily attends her routine post-cancer
check-up at the hospital’s department of radiology. She confides some details about
her childhood to the radiologist. This prompts him, at his own initiative and without
any official requisition, to take x-rays of her entire body. What they reveal is horrify-
ing: they document a literally broken child. There are x-ray images of 32 fractures –
on Cecily’s forearms, legs, hands, fingers, toes, face/jaw and thorax – the majority
dating from ages 6 to 14. Only the seven fractures that had probably been sustained
when Cecily was an adult, the results of sports injuries or a bicycle accident, bear
traces of having been treated medically in any appropriate way. The broken child,
however, had not received adequate help.
15 A Broken Child – A Diseased Woman 233

What then did Cecily gradually piece together about her childhood and
adolescence?
My alcoholic father was unemployed. So my mother held down two jobs and was out of the
house from early morning to late at night, every day, all week. My father stayed home,
drinking – and playing cards with his brother and some friends a few times a week. I used
to clean up when they’d finished so my mother wouldn’t come home to a mess. I also took
care of my very handicapped younger brother. Every morning before I went to school I’d get
him into his wheelchair and to the bus stop, where they picked him up and drove him to the
institution where he stayed all day.
Afternoons were the worst, when the men were around our kitchen table. That’s when I
was physically maltreated and sexually abused by all of those more-or-less drunk, repulsive
men. They cursed me and beat me. They strong-armed me and pushed and threatened and
raped me, vaginally, anally, orally. I was locked in the cellar or tied to a narrow shelf. My
brother and I were often starving because my father and his friends ate whatever was in the
refrigerator. I had no money to buy food because my father spent whatever was in the house
on liquor. I was bullied at school because my clothes were old and worn out. I never brought
a proper lunch to school, my hygiene was poor, and I was never taken to a doctor. I couldn’t
always prevent my brother from being beaten and maltreated as well. I learned to hide my
pain, even when these men broke my bones raping or beating me. The worst of them was my
uncle. My father never molested me sexually, but in all other ways.

15.5 Reflections

15.5.1 Recently Acquired Knowledge

The medical context is changing. The history of Cecily Cramer’s life and illnesses
represents a case-in-point of knowledge that has not simply been accumulating dur-
ing the last three decades, but also converging, within a broad field of research
domains. In 1998, the first findings of the Adverse Childhood Experience Study
were published in the American Journal of Preventive Medicine (Felitti et al. 1998).
These documented that childhood hardships, differentiated into ten types, were
shown to correlate to adult sickness, in a dose-response relationship; that is, the
more hardships experienced during childhood, the higher the risk of becoming ill in
later years (Felitti and Anda 2010).
Since then, many similarly designed studies have supported these findings,
worldwide. There is now no doubt that childhood adversities resembling Cecily’s in
type and duration are harmful to a person’s current and future health and well-being
(Shonkoff et al. 2009). The wide spectrum of detrimental effects reaches into every
specialty within somatic and psychiatric medicine, as well as impacting the social
sectors charged with tackling alcohol and drug abuse, the law enforcement sector,
the family welfare agencies that confront divorces, broken homes, partner violence,
occupational issues, disabilities. In other words: the economic consequences of
child maltreatment and abuse impact a wide range of societal systems and their
budgets, constituting a burden that would be heavy for any society to bear (Knudsen
et al. 2006).
234 A. L. Kirkengen

Once the fact that childhood adversity is related to adulthood sickness had been
documented, the question then arose as to how. How are experiences of strain trans-
formed into pathophysiological processes? An interdisciplinary field of research
currently termed neuroscience has been developing steadily, step-by-step. It has
helped provide a foundation for hypothesising models that might explain the inher-
ent logic of how those processes occur. The neuro-endocrinologists at Rockefeller
University, New York, have made a huge contribution: they developed the now
widely accepted concept of allostasis, a term meaning, “stability through change”
(McEwen 1998). The concept of allostasis aids in exploring the flexibility of human
physiology, how it may adapt to extreme challenges and maintain viability during
long-term strain and hardship. Deriving from allostasis is the concept of allostatic
overload, referring to what happens when stressful conditions must be endured over
excessively long periods of time, with all the energy-providing systems in the body
paying the price. When allostatic overload has exhausted the body’s flexibility and
adaptability, the most central, systemic regulators may break down (Danese and
McEwen 2012). Such a “multisystem-dysregulation” is characteristic of complex
sickness, although that is still conceptualised and termed “multi-morbidity” (Wiley
et al. 2016; Tomasdottir et al. 2015).
The long-term, overwhelming strain of allostatic overload has been shown to
take a toll on the immune system and on the hormonal and central nervous systems
as well. This means that the regulation of glucose, lipids, minerals, blood pressure,
heartbeat, muscular tension, rest, sleep, respiration and digestion are all adversely
affected. These systemic disturbances, or overloads, contribute to an array of seri-
ous and chronic conditions, such as cardiovascular, respiratory, and liver diseases,
as well as type 2 diabetes. They also affect tumour development and the frequency
of infections by suppressing the immune system at the cellular level, both those
features that are innate and those the system acquires. Simultaneously, the hormonal
aspect of the immune system, the inflammatory system, is in a state of constant
hyperactivity, engendering systemic inflammatory diseases, among them the so-­
called autoimmune diseases (Dube et al. 2009; Song et al. 2018). In addition, recent
studies indicate a relationship between Post-Traumatic Stress Disorder (PTSD) and
neurodegenerative diseases such as Alzheimer’s and Parkinson’s.

15.5.2 Updating the Concept of Causality

The knowledge that health professionals have now acquired regarding the poten-
tially adverse impact of certain types of lifetime experience on human health obli-
gates them to re-examine the traditional medical understanding of causality.
15 A Broken Child – A Diseased Woman 235

For a proper diagnosis to be determined and an adequate treatment offered, the

cause of a health problem must be identified correctly; it must not be conflated with
aspects and effects of phenomena that are contextual. To paraphrase how a group of
scientists at Harvard Medical School put it recently: Whenever the effect of lifetime
adversity on the brain is mistakenly labelled as the “cause” of a psychiatric disease,
what results is biased knowledge (Teicher and Samson 2016; Teicher et al. 2016;
Ohashi et al. 2017). Moreover, such “knowledge” masks the actual sources of a
variety of types of morbidity and mortality, ones that are apparently intrinsic to the
structures of our societies (Farmer et al. 2006; Jones 2000). Treatment based on
such mistakes misleads the medical gaze towards diseased individuals and groups,
and away from the pathogenic conditions that they live with and in. However unin-
tentionally, medicine thus becomes complicit in obscuring abuses of power and all
kinds of societal injustice. Must such consequences remain unexplored within med-
icine because they are defined as lying outside the mandate of the profession?

References and Further Readings

Danese A, McEwen BS (2012) Adverse childhood experiences, allostasis, allostatic load, and age-­
related disease. A review. Physiol Behav 106:29–39
Dube SR, Fairweather D, Pearson WS, Felitti VJ, Anda RF, Croft JB (2009) Cumulative childhood
stress and autoimmune disease in adults. Psychosom Med 71:243–250
Farmer P, Nizeye B, Stulac S, Keshavjee S (2006) Structural violence and clinical medicine. PLoS
Med. https://doi.org/10.1371/journal.pmed.0030449
Felitti VJ, Anda RF (2010) The relationship of adverse childhood experiences to adult health,
well-being, social function, and health care. In: Lanius R, Vermetten E, Pain C (eds) The effects
of early life trauma on health and disease: the hidden epidemic. Cambridge University Press,
Cambridge
Felitti VJ, Anda RF, Nordenberg D, Williamson DF, Spitz AM, Edvards V, Koss MP, Marks JS
(1998) Relationship of childhood abuse and household dysfunction to many of the leading
causes of death in adults. Am J Prev Med 14:245–258
Jones CP (2000) Levels of racism: a theoretical framework and a gardener’s tale. Am J Public
Health 90:1212–1215
Knudsen EI, Heckman JJ, Cameron JL, Shonkoff JP (2006) Economic, neurobiological, and
behavioural perspectives on building America’s future workforce. PNAS 103:10155–10162
McEwen BS (1998) Protective and damaging effects of stress mediators. N Engl J Med 338:171–179
Ohashi K, Anderson CM, Bolger EA, Khan A, McGreenery CE, Teicher MH (2017) Childhood
maltreatment is associated with alteration in global network fiber-tract architecture indepen-
dent of history of depression and anxiety. NeuroImage 150:50–59
Shonkoff JP, Boyce WT, McEwen BS (2009) Neuroscience, molecular biology, and the childhood
roots of health disparities. Building a new framework for health promotion and disease preven-
tion. J Am Med Assoc 301:2252–2259
Song H, Fang F, Tomasson G, Arnberg FK, Mataix-Cols D, de la Cruz LF, Almquist C, Fall K,
Valdimarsdottir UA (2018) Associations of stress-related disorders with subsequent autoim-
mune disease. J Am Med Assoc 319:2388–2400
236 A. L. Kirkengen

Teicher MH, Samson JA (2016) Annual research review: Enduring neurobiological effects of
childhood abuse and neglect. J Child Psychol Psychiatry 57:241–266
Teicher MH, Samson JA, Anderson CM, Ohashi K (2016) The effects of childhood maltreatment
on brain structure, function and connectivity. Nat Rev Neurosci 17:652–666
Tomasdottir MO, Sigurdsson JA, Petursson H, Kirkengen AL, Krokstad S, McEwen B, Hetlevik
I, Getz L (2015) Self-reported childhood difficulties, adult multimorbidity and allostatic load.
A cross-sectional analysis of the Norwegian HUNT study. PLoS One. https://doi.org/10.1371/
journal.pone.0130591
Wiley JF, Gruenewald TL, Karlamangla AS, Seeman TE (2016) Modeling multisystem physi-
ological dysregulation. Psychosom Med. https://doi.org/10.1097/PSY.000000000000288

Open Access This chapter is licensed under the terms of the Creative Commons Attribution 4.0
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adaptation, distribution and reproduction in any medium or format, as long as you give appropriate
credit to the original author(s) and the source, provide a link to the Creative Commons license and
indicate if changes were made.
The images or other third party material in this chapter are included in the chapter’s Creative
Commons license, unless indicated otherwise in a credit line to the material. If material is not
included in the chapter’s Creative Commons license and your intended use is not permitted by
statutory regulation or exceeds the permitted use, you will need to obtain permission directly from
the copyright holder.
Chapter 16
Conclusion: CauseHealth
Recommendations for Making Causal
Evidence Clinically Relevant and Informed

Rani Lill Anjum, Samantha Copeland, and Elena Rocca

We have presented an overview of the philosophical framework of CauseHealth and

shown how it relates to the clinical encounter. By giving some examples of how the
abstract philosophical ideas (Part I) can be implemented into clinical practice (Part
II), we hope to have shown how ontological and other foundational considerations
are relevant for healthcare professionals. We also hope to have demonstrated that a
change toward a genuinely person centred practice cannot happen without a corre-
sponding change in the ontology, norms and methods underlying that practice.
Finally, we hope to have empowered and inspired healthcare practitioners to get
involved in debates about the foundation of medicine and healthcare and how
implicit philosophical assumptions shape and define their profession.

16.1 Practical Recommendations for Change

From the philosophical perspective presented in the first part of this book, taken
together with the clinical application of this in the second part, it should now be
clear that we must change the way we approach causal evidence of health and ill-
ness conceptually, methodologically and practically. This has some practical conse-
quences for the clinical encounter, as discussed throughout the book. We now offer
some specific CauseHealth recommendations for making causal evidence more

R. L. Anjum (*) · E. Rocca

NMBU Centre for Applied Philosophy of Science, Norwegian University of Life Sciences,
Ås, Norway
e-mail: rani.anjum@nmbu.no; elena.rocca@nmbu.no
S. Copeland
Ethics and Philosophy of Technology Section, Delft University of Technology,
Delft, The Netherlands
e-mail: s.m.copeland@tudelft.nl

© The Author(s) 2020 237

R. L. Anjum et al. (eds.), Rethinking Causality, Complexity and Evidence for the
Unique Patient, https://doi.org/10.1007/978-3-030-41239-5_16
238 R. L. Anjum et al.

clinically relevant and better informed by the clinical encounter. The recommenda-
tions follow from an overall consideration of the previous chapters, both the philo-
sophical framework and its clinical implications.
Assume medical uniqueness, because there is no normal, standard or statistically
average patient.
Individual dispositions and propensities are given by intrinsic properties and
their interactions within a unique context. What will happen in such a unique con-
text with a unique set of dispositions can therefore not be derived directly from what
happens in similar contexts, for instance in a population of similar individuals.
Assuming causal complexity, context-sensitivity and causal singularism, each
causal process will be unique, including a unique combination of dispositions. This
unique combination of dispositions come from the patient and their total situation.
The idea of an average patient is therefore a statistical artefact: in the clinical reality,
the standard or average patient does not exist.
Treatment should be adapted rather than standardised, because no two patients are
causally equal.
Since causality is intrinsic and unique to a specific context, it follows that an
equivalent intervention in two different patients might amount to different medical
treatments. Decisions on treatment ought therefore to be tailored to the individual
rather than derived from statistical evidence alone. The default expectation is that
treatment cannot be standardised, but must instead be adapted to the patient in their
specific context, with their unique set of dispositions, aims and preferences at that
particular stage of their illness or recovery process. This also means that clinical
knowledge and judgement is vital for making decisions about how to proceed with
the individual seeking care.
Value qualitative approaches, because causal evidence is much more than evidence
from RCTs.
There is no perfect method for establishing causality in the dispositionalist sense;
i.e., that the effect was a result of intrinsic dispositions interacting. Instead, we need a
plurality of methods and multiple types of evidence. This means that the meaning of
‘evidence’ needs to be expanded, and not be restricted to evidence from experiments
and controlled setups. Qualitative approaches based on clinical dialogue and observa-
tion have a huge potential for understanding which causal elements and mechanisms
are in place in the individual case. Indeed, qualitative approaches can contribute to
study complex causal interactions between multiple factors from biology, social con-
text, medical history, genetics and lifestyle. Causal evidence must also include evi-
dence from the specific patient who is supposed to benefit from the intervention.
Consider mechanistic and theoretical knowledge, because we need to understand
hows and whys.
If the healthcare practitioner is to make rational clinical choices for their patients,
it is important to consider the plausible causal mechanisms underlying statistical
16 Conclusion: CauseHealth Recommendations for Making Causal Evidence… 239

evidence. This means that, for the purpose of the single case, theoretical knowledge
about how and why different causes interact to produce the effect must be given
epistemic priority over how often an intervention is followed by the effect in a stud-
ied population. We must seek to understand causal mechanisms and not be satisfied
with evidence from correlation data and comparisons of these. Indeed, knowing
what happens to other patients is most useful for clinical decisions for the single
patient when we also know why it happened and which dispositional properties
were causally relevant for the outcome.
Accept clinical uncertainty, because precise quantitative estimates do not reflect
reality.
Causal knowledge and evidence will never be complete, so clinical uncertainty is
ineliminable. Any causal process can be interfered with by introducing additional
dispositions, and all real-life situations are open systems with an unlimited number
of causally relevant factors or dispositions. The lack of certain predictions thus
reflects the reality of the clinic. Any prediction made with precise numeric estimates
can only come from assuming an idealised model in a deterministic and closed sys-
tem, using an algorithm to calculate the probability of an outcome. Such predictions
might seem certain, but no such certainty can be transferred to practice. Dispositions
and propensities do not generate clearly quantifiable predictions, but rather point to
qualitative and contextual considerations.
Consider individual propensities, because they affect the risk and safety of treatment.
To understand how an intervention works and which contextual factors might
influence the outcome is crucial for assessing potential benefits and harms that the
intervention might have for different individuals. This must also include a consider-
ation of long-term effects. For this, we need to consider not only the dispositions of
the intervention, but also the unique, individual propensities of the person receiving
care and the causally relevant dispositions represented by their life situation. Risk
and safety must be considered on the individual level instead of something that can
be directly derived from frequencies in populations. Specific care must be taken to
pick up on the patient’s vulnerability to the intervention.
Know your patient, because most of the causally relevant evidence will come
from there.
Causal evidence comes not only from clinical studies and medical research, but
also from the patient context. Their biography, genetics, medical history, lifestyle,
diet and life situation will represent most of the causally relevant information
needed to understand and make predictions in this case. The more we know about
the patient, the better we understand their condition and the more causal evidence
we have for making good and safe clinical decisions.
240 R. L. Anjum et al.

Study unexpected outcomes, because there is much to be learned from outliers and
marginal cases.
Theoretical knowledge of complex causal interactions cannot easily be gained
from controlled experiments alone, where single factors are studied in isolation
from background conditions. Only in the single patient will this causal complexity
be observed. In marginal and outlier cases, where unexpected or rare outcomes
occur, we might be able to observe hitherto unknown causal interactions in a unique
combination. Such outlier cases should be studied in detail, since they are an oppor-
tunity to learn more about causal mechanisms from rare interactions and contextual
interferers.
Clinical evidence should inform research, because that is where causal complexity
is observed.
Since the clinical encounter offers us a chance to investigate causal mechanisms
in their full real-life complexity, the medical community should make the most out
of this opportunity. For instance, when the clinical inquiry is done in a whole person
centred way, those results can feed back to basic and clinical research with new
causal hypotheses. Information will thus flow from the clinic to research and not
only from research to the clinic.
Listen to the story, because ‘medically unexplained’ does not equal ‘no causal
explanation’.
That a condition is medically unexplained does not necessarily mean that no
causal explanation for the symptoms can be given in the individual case. Sometimes,
‘medically unexplained’ means simply that none of the causes suspected by the
patient or clinician can be backed up by statistical evidence. Although observed
repetition would have been a good reason to accept it as a medical cause, causal
singularism suggests that no such repetition is required for it to count as a cause,
ontologically speaking. The patient’s story is a vital source of causal insight into the
unique complexity of their condition.
Rebel, because medicine and healthcare must move beyond positivist scien-
tific ideals.
What counts as ‘scientific’ is too narrowly defined within the current medical
paradigm, with emphasis on quantitative data and comparisons of these. Alternatives
to these positivist ideals should be welcomed. For instance, clinical reasoning
should take into account patient narratives and embodied lived experiences as key
sources for investigating causes and effects in the single case. Dispositionalism calls
for a radical change in medicine and healthcare, away from reductionism, standardi-
sation, fragmentation and medicalisation, and toward an ecological, phenomeno-
logical, whole-ist and genuinely person centred approach.
16 Conclusion: CauseHealth Recommendations for Making Causal Evidence… 241

16.2 Toward a New Paradigm

We are not questioning the idea that medicine and healthcare should be evidence
based. On the contrary, we want to challenge the definition of ‘evidence’, and spe-
cifically of ‘causal evidence’. From a dispositionalist perspective, what counts as
causal evidence is much broader than what is suggested by the current framework.
We wish therefore to see the rise of a new paradigm, in which healthcare decisions
are not seen as ‘evidence based’ until they include all the causally relevant evi-
dence. This means that we need to consider, not only evidence from general knowl-
edge and research on populations, but crucially also qualitative and phenomenological
evidence from the particular encounter with the patient. Downgrading the latter as
‘less scientific’, ‘less reliable’, ‘anecdotal’ or ‘secondary’, implies an unspoken
commitment to a very specific philosophical bias about causation, as we have seen.
When translated into clinical practice, those philosophical biases carry an inherent
risk of delivering a poorer, de-humanised, fragmented and at times counter-­
productive healthcare, as the testimonies in this book so powerfully warn.

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