Treatment protocol

A Functional Medicine Approach to the Treatment

of Inflammatory Bowel Disease
By Leo Galland, MD, and Helen Lafferty, MB, MRCPI

Introduction

The gastrointestinal tract is essentially an external space enclosed

within the body, an internalized interface between the human host and
the outside world that is in constant contact with potential nutrients
as well as a vast array of drugs, microbes, toxins, and other foreign
antigens. Disruptions of immune regulatory processes in the gastrointestinal tract have profound effects on inflammatory processes
and responses throughout the body, including a role in the initiation
and continuation of many seemingly disparate signs and symptoms,
syndromes, and diseases that clinicians encounter on a daily basis.
While it is easy to imagine that immune dysregulation initiated at
the level of the gastrointestinal tract results in dysfunction and disease
in the tract itself, the far-reaching effects of inflammation in the gut
may be less easily appreciated. A high degree of awareness of the
connection between gut immune dysregulation, uncontrolled inflammation, and systemic pathology is necessary when treating patients
with chronic inflammatory conditions of the gastrointestinal tract
such as inflammatory bowel disease (IBD). Following is the Functional
Medicine definition of antecedents, triggers, and mediators, which can
help make this connection more salient and thereby assist in the diagnosis and treatment of this condition.

Antecedents, Triggers And Mediators

The first step in applying functional medicine to clinical practice in

the treatment of inflammatory bowel disease is recognizing that what
appears to be an illness is really a state of disharmony resulting from
the interplay of antecedents, triggers, and mediators.
Antecedents are any factors, genetic or acquired, that predispose
to illness (from the perspective of prevention, they are risk factors).
A precipitating event is a critical antecedent that closely precedes the
development of chronic illness. A salient characteristic of antecedents
and precipitating events is that they precede the development of clinical disease but are essential to its formation.
Triggers are entities or events that provoke an illness or the emergence or exacerbations of symptoms. Common triggers include physical or psychic trauma, microbes, drugs, allergens, foods (or even the
act of eating or drinking), environmental toxins, temperature changes,
stressful life events, adverse social interactions, and powerful memories. For chronic illnesses, multiple interacting triggers are often
continually present, which leads to illness exacerbation.
The gastrointestinal tract, with its load of microbes and food components, is an important source of triggers for patients with inflammatory bowel disease. Understanding the role of gut microbes may be
complicated by difficulty in ascertaining whether they act as triggers,
as precipitating events, or both. For example:
Amebic infection may produce an acute or chronic colitis that
resolves with treatment. In such a case, acquisition of the infec-

tion is the precipitating event, and the amebic organism itself is

the discrete trigger.
Amebic infection may also provoke an exacerbation of chronic
ulcerative colitis; following its treatment, the exacerbation
resolves and the patient returns to his/her usual state of colitis.
The amebic infection was one among many other putative triggers for colitis.
In another case, amebic infection may precede the development
of ulcerative colitis, making it an antecedent, but treatment
of amebiasis does not cure the patients colitis. The intestinal
boundary between the intestinal contents and the lamina propria,
rich in immune active cells, may be disrupted by the infection,
providing a permeable barrier. In such a case, amebiasis leaves
behind an environment ripe for potential triggers that may result
in exacerbation. Triggers such as colonic auto-antigens can maintain disease activity.
Triggers do not cause disease in and of themselves; all triggers exert
their effects through the activation of host-derived mediators.
Mediators are intermediaries that contribute to the manifestations of disease. Mediators vary in form and substance; they may be
biochemical (like prostanoids and cytokines), ionic (like hydrogen
ions), social (like reinforcement for staying ill), psychological (like fear),
or cultural (like beliefs about the nature of illness). Common mediators of illness include hormones, neurotransmitters, neuropeptides,
free radicals, fear of pain or loss, poor self-esteem, low perceived selfefficacy, learned helplessness, lack of relevant health information, and
social isolation. The most striking characteristic of all mediators is their
lack of disease specificity. Each mediator can be implicated in many
different and apparently unrelated diseases, and every disease involves
multiple mediators in its formation.
There are four salient aspects of mediators that are crucial for clinical practice:
Mediators are not only agents of illness they are agents of
health. They are intrinsic components of regulatory systems that
subserve homeostasis. Any therapeutic strategy based solely
upon mediator suppression will produce undesirable effects that
result from the disruption of regulatory systems.
All illness involves multiple interlocking, reinforcing mediators,
both biochemical and psychosocial.
The ebb and flow of mediator activation can be strongly influenced by the common components of life, including circadian
and ultradian rhythms, physical activity and exercise, thoughts,
hormones, and diet.
Gut-derived mediators may have systemic effects. Patients with
inflammatory bowel disease, for example, are at great risk for
osteoporosis. Part of this risk is attributable to malabsorption,
weight loss, or the effects of glucocorticoid therapy. A large

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part of the risk, however, is a direct result of inflammation.

Gut-derived inflammatory mediators, especially interleukin-1,
stimulate osteoclasts (thereby increasing the rate of bone loss)
and inhibit osteoblasts (thereby decreasing the rate of new
bone formation).
Understanding the unique antecedents, triggers, and mediators that
underlie inflammatory bowel disease in each patient permits therapy to
be targeted to the needs of the individual.

Inflammatory Bowel Disease

Antecedents
Several antecedents of inflammatory bowel disease have been identified.
Positive family history is the largest independent risk factor1; for firstdegree relatives of Crohns disease patients, the lifetime risk of developing
inflammatory bowel disease is 5.2% for non-Jews and 7.8% for Jews, and
for relatives of ulcerative colitis patients, the risk is 1.6% for non-Jews and
5.2% for Jews.2 The absence of simple Mendelian inheritance, however,
suggests that multiple gene translational products contribute to the risk,3
and several susceptibility regions on different chromosomes were found
by genome-wide scans.1, 3 Defects in genes affecting the innate immune
system, epithelial barrier function, and the adaptive immune system
have been implicated in inflammatory bowel disease:4
Mutations in environmental sensors and their signaling pathways
(such as nucleotide-binding oligomerization domain receptors
like NOD2, also known as CARD15) may affect the function of
the innate immune system; NOD2/CARD15 mutations appear
to account for 10% to 15% of Crohns disease cases.1 The functional consequence of these mutations appears to be a loss of
physiological tolerance to commensal bacteria,5 although it has
also been suggested that these mutations are implicated in the
increased gastrointestinal permeability seen in patients with
Crohns disease and their relatives.6, 7
Mutations in genes coding for transporters such as organic cationic
transporter (OCT)1 and OCT28 may affect gut permeability.4
Mutations in genes involved in adaptive immunity, such as HLA
and TNF- genes,9, 10 as well as genes encoding cytokines and
cytokine receptors (such as the IL23R gene11), may cause an imbalance between regulatory and effector cell immune responses.4
Gastrointestinal infection is another well-described antecedent
of inflammatory bowel disease. Patients presenting with their first
episode of inflammatory bowel disease have often traveled abroad,
had an episode of gastrointestinal infection, or taken antibiotics.12 In
a study of risk factors for development of inflammatory bowel disease,
twins with either ulcerative colitis or Crohns disease reported prior
recurrent gastrointestinal infections more often than their healthy
co-twins; hospitalizations for gastrointestinal infection were also more
common, and age at onset of disease was earlier in those who had
reported gastrointestinal infection than those who did not.13
Because dietary antigens are, next to microbial antigens, the most
common luminal antigens, it is not surprising that dietary factors may
be important disease antecedents. No consensus has emerged, however,
regarding the role of dietary patterns as antecedents of inflammatory
bowel disease.1, 14, 15 Though interpreting studies of dietary factors is
difficult (most are small and retrospective, involve long-term dietary
recall, and often investigate post-illness diets16), there is at least suggestive evidence of the following:
Increased refined sugar intake and high overall carbohydrate
intake may precede the development of Crohns disease.17, 18
Increased consumption of chemically modified fats (such as
those found in margarine) may be involved in the etiology of
ulcerative colitis.19
High consumption of fast food (typically high in fat that may have
been chemically modified) is an antecedent of both ulcerative
colitis and Crohns disease.20

Inert, inorganic, nonnutritive microparticles such as food additives and caking agentsfeatures of the modern urban diet
may combine with gastrointestinal luminal components such as
bacterial wall lipopolysaccharides to become antigenic and either
initiate disease or trigger disease exacerbations.21
A recent study demonstrated an inverse association between dietary
intake of vegetables, fruits, fish, fiber, and omega-3 fatty acids and
the subsequent development of Crohns disease inchildren.22
Formula feeding (or, more specifically, short duration of breastfeeding or the absence of breast-feeding) may be an antecedent of
inflammatory bowel disease. Breast-feeding may protect against enteric
infections during infancy, aid with early development of a competent
gastrointestinal immune system, or delay exposure to foreign antigens
such as cows milk. Several studies have found that people who develop
inflammatory bowel disease are less likely to have been breast-fed than
controls.16, 23 Intolerance to cows milk has also been implicated as an
antecedent of disease, although the data are somewhat conflicting.16,24
In one study, patients with a history of milk allergy during infancy
who subsequently developed ulcerative colitis did so at an earlier age
than those without a history of milk allergy,24 and at least one reviewer
suggests that allergy to milk proteins still remains a possible cause of
dairy sensitivity or milk intolerance in a small percentage of [inflammatory bowel disease] patients.16
Several studies have demonstrated an association between allergic
symptoms, asthma, rhinitis, and the subsequent development of inflammatory bowel disease, particularly ulcerative colitis.25-27 The connection
between these diseases may relate to what has been termed the hygiene
hypothesis, which states that excessive cleanliness in the environment of
newborns and toddlers limits exposure to common antigens and predisposes the immune system to a state of persistent inflammation.
Abnormal gut permeability is a feature of established inflammatory
bowel disease,6, 28 but there is evidence to suggest that this abnormality
precedes the development of frank disease. Studies have demonstrated
that relatives of patients with inflammatory bowel disease demonstrate increased permeability (possibly, as discussed above, genetically
influenced), suggesting that increased permeability is an antecedent
of disease.6, 28 Although there are very few studies following relatives
to assess for subsequent development of inflammatory bowel disease,
Irvine and Marshall showed that, in a woman tested because of a family
history of Crohns disease, hyperpermeability preceded the development of frank disease.29
Deficiency of vitamin D, a vitamin now widely recognized as a
regulator of the immune system, may also be an antecedent of inflammatory bowel disease.30 The incidence of inflammatory bowel disease is
higher at northern latitudes, and both symptomatic onset and relapses
occur more commonly in autumn and winter months, when levels of
sunlight are low.30 Further evidence that hypovitaminosis D may be an
antecedent comes from animal studies showing that the active form of
vitamin D inhibits the development of inflammatory bowel disease and
that the absence of the vitamin D receptor is associated with activation
of the innate immune system and the development of colitis.31
Other factors thought to be antecedents of inflammatory bowel
disease include the use of oral contraceptives or hormone replacement
therapy,32, 33 perinatal passive smoke exposure,34 childhood smoke exposure (passive or active),35 smoking (for Crohns disease),36 prematurity
(but not mode of delivery),37 appendectomy (for Crohns disease),38 and
treatment of acne with isotretinoin.39, 40

Triggers

Environmental triggers such as pollution and exposure to industrialized chemicals can exacerbate this condition. Infectious agents are
also well-described triggers of inflammatory bowel disease exacerbations. Indeed, in one study, enteric infections were responsible for 10%
of disease flares.41

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 Clostridium difficile is associated with exacerbations, particularly in patients with ulcerative colitis (Crohns disease patients
are more likely to have been treated with metronidazole, which
may eradicate C. difficile). The incidence of C. difficile infection
in inflammatory bowel disease patients has increased in recent
years; most of the infections are acquired outside the hospital,
and many of them are not acquired secondary to antibiotic treatment. C. difficile infection negatively impacts clinical outcome in
inflammatory bowel disease patients because the associated diarrhea is often thought to represent a noninfectious disease flare
and is thus not appropriately treated.42, 43
Mycobacterium avium subspecies paratuberculosis has also been
found in Crohns disease patients and may be responsible for
triggering disease flares. In some patients, it may set the stage
for the exacerbation (in this case, it would be an antecedent and
then a trigger). Paratuberculosis was cultured from the blood of
patients with Crohns disease,44 and paratuberculosis DNA was
found in tissue samples45, 46; its presence in both inflamed and
normal tissue led the authors of one study to speculate that the
infection may be systemic, thereby serving as an antecedent.45 In
another study, antibodies against paratuberculosis were found in
Crohns disease patients, and the antibody titers correlated with
the presence of penetrating or stricture-type disease.47 Recently
it has been suggested that cross-reactivity between paratuberculosis and human intestinal proteins may explain the association
between mycobacterial infection and Crohns disease.48
Certain strains of Escherichia coli may also trigger disease flares or
serve as a disruptor of the system antecedent to the flare. Invasive
adherent strains of E. coli were found in gut tissue from patients
with inflammatory bowel disease, in particular patients with
Crohns disease.49-52 In one study, the isolated E. coli strains were
shown in vitro to be associated with proinflammatory cytokine
expression and decreases in epithelial barrier function.50 And in
a study of E. coli in an animal model of inflammatory ileitis, the
bacteria induced toll-like receptor sensing and subsequent activation of the innate immune system.53
Cytomegalovirus has been found in both blood and intestinal
tissue of patients with inflammatory bowel disease54 and has been
detected frequently in patients experiencing acute exacerbations
of colitis,55 thus acting as a trigger.
Yersinia enterocolitica has also been associated with the development of inflammatory bowel disease,56acting as both an antecedent and trigger.
It has recently been hypothesized that infection with a pathogenic variant of Blastocystis, which may have been transmitted
from the Middle East following its emergence there in the 1980s,
may trigger the development of inflammatory bowel disease.57
Other infectious agents that have been found in association
with disease exacerbations include Campylobacter, Entamoeba
histolytica, Salmonella, Plesiomonas shigelloides, and Strongyloides stercoralis.41
Small bowel bacterial overgrowth may also be a trigger of flares in
Crohns disease.58, 59 In a study of Crohns disease patients, up to 20% of
patients (and up to 30% of patients with previous surgeries) were found
to have small bowel bacterial overgrowth; treatment of the overgrowth
resulted in an improvement in bloating, stool consistency, and pain.60
It is likely that certain antigens in food are responsible for triggering disease exacerbations in at least a subset of Crohns disease
patients. Yeast antigens are widespread components of food and have
been implicated in such exacerbations. Antibodies against Saccharomyces cerevisiae were found in up to 70% of patients with Crohns
disease, suggesting a loss of tolerance to this dietary antigen.61, 62 The
presence of such antibodies is associated with more severe disease,
and higher titers have been associated with more rapid development

of complications.61 The exact antigen responsible for the development

of these antibodies is unknown, but a recent study suggests Candida
albicans as a candidate.63 In a small study, rectal exposure to yeast and
citrus antigens produced increased rectal blood flow and submucosal
edema in Crohns disease patients compared to controls.64
In ulcerative colitis, the role of food as a trigger is uncertain. In one
study, high intake of meat (particularly red meat and processed meat)
and protein was associated with an increased risk of exacerbation in
ulcerative colitis patients; high sulfur and sulfate intake was also associated with relapse, and the authors postulated that the sulfur content
of high-protein foods and processed foods may influence their ability
to trigger exacerbations.65 In a study in which patients avoided specific
foods that they believed triggered symptoms, higher rates of remission were seen at two years than in controls.66 An observational study,
however, failed to show an association between patients avoidance of
foods and the risk of relapse.67
Nonsteroidal anti-inflammatory drugs (NSAIDs) have been
associated with exacerbations of inflammatory bowel disease (both
ulcerative colitis and Crohns disease) in several studies,68-71 although
this is not the case in all studies.72, 73 Attempts to discover whether the
selective COX-2 inhibitors are less likely to cause exacerbations73, 74 are
less relevant in light of the withdrawal of some of these agents from the
market. Although relapses are not uniformly associated with NSAID
use, there is enough evidence for one reviewer to suggest that NSAIDs
may precipitate a relapse in some patients with inflammatory bowel
disease75 and for another to suggest that in patients with inflammatory
bowel disease, NSAIDs should be avoided, when possible.76
Stress has long been known to be associated with relapses of inflammatory bowel disease,77-79 although study of this trigger is difficult
since it requires teasing out the exact contribution of stressful events,
the baseline personality, patient perceptions of events as stressful,
and other coincident factors affecting disease activity.78 Stresses that
appear to influence the disease course include those associated with
the disease itself, chronic daily life stresses, and acutely stressful events.
Depression (which was found to occur at rates triple that of the general
population in 2 recent large surveys of patients with inflammatory
bowel disease80) was noted to exert a negative influence on the course
of inflammatory bowel disease and should be considered a predisposing factor for disease relapse.81

Mediators

T cells are important mediators in inflammatory bowel disease, but

Crohns disease and ulcerative colitis appear to have different immune
pathways and inflammatory mediators.3, 82 In Crohns disease, the
mucosa is dominated by CD4+ lymphocytes with a T-helper-1 (Th1)
phenotype; the differentiation into Th1 cells is mediated through interleukin-23.1 These activated T cells produce and release proinflammatory cytokines such as interleukin-2, -12, and -18 and IFN-, which
stimulate macrophages to release interleukin-1, interleukin-6, and
TNF-.1, 3, 82 In contrast, in ulcerative colitis, the mucosa is dominated
by atypical T-helper-2 (Th2) cells, characterized by the production of
transforming growth factor-beta (TGF-) as well as interleukin-5 and
interleukin-13 and possibly interluekin-4 and interleukin-8.3, 82, 83
Examples of mediators of inflammation also may include:
Leukotriene B4, a potent neutrophil attractor84
Interleukin-6, which facilitates resistance of T cells to apoptosis85
Substance P, which is secreted by macrophages, eosinophils,
lymphocytes, and dendritic cells86
Insulin-like growth factors87
Activation of immune cell populations is eventually accompanied
by the production of a wide variety of nonspecific mediators of inflammation, including growth factors, prostaglandins, leukotrienes, and
reactive oxygen species such as nitric oxide, which enhance inflammation and tissue destruction.3

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There are also several secondary mediators of morbidity in inflammatory bowel disease patients, including nutritional deficiencies, systemic
effects of inflammation, iatrogenic factors, and psychosocial factors.
Nutritional deficiencies are common in inflammatory bowel disease
patients and may be due to inadequate dietary intake, malabsorption,
or chronic disease activity. In a recent study, patients with inflammatory bowel disease were found to have deficiencies in levels of vitamin
E (63%), vitamin D (36%), vitamin A (26%), calcium (23%), folate (19%),
iron (13%), vitamin C (11%), hemoglobin (40%), ferritin (39.2%), vitamin
B6 (29%), carotene (23.4%), vitamin B12 (18.4%), vitamin D (17.6%),
albumin (17.6%), and zinc (15.2%).88 The authors noted that these deficiencies may be present even in patients who appear well nourished.
In another study, serum concentrations of several nutrients (beta-carotene, magnesium, selenium, and zinc) were significantly lower in ulcerative colitis patients compared with controls, and serum vitamin B12
concentrations were significantly lower in Crohns disease patients.89
Key consequences of these nutritional deficiencies include:
A lack of certain vitamins, notably B12 and folate, are associated with hyperhomocysteinemia. Homocysteine is believed to
promote inflammatory processes through its effects on oxidative
stress, endoplasmic reticulum stress, and host-microbial interactions, and levels of homocysteine were shown to correlate with
disease activity in ulcerative colitis.90
Zinc deficiencies may also be particularly significant. Zinc was
shown to regulate gut permeability in animal models of colitis,91
and zinc supplementation was shown to decrease permeability in
patients with quiescent Crohns disease.92
Magnesium deficiency may lead to cramps, bone pain, fatigue,
depression, delirium, and urolithiasis.93, 94
Anemia (which, according to a recent review,95 occurs in
anywhere between 8.8% and 73.7% of patients with inflammatory
bowel disease) decreases patient well-being and overall quality of
life and is associated with increased hospitalizations.95 In inflammatory bowel disease, anemia has several causes, including bone
marrow suppression and deficiencies of vitamins and iron. Irondeficiency anemia occurs in up to one-third of patients96 and
clearly negatively impacts quality of life.
Systemic effects of inflammation that mediate morbidity include
oxidative stress, osteoporosis, muscle wasting, hypogonadism, and
depression. Reactive oxygen species are produced in abnormally
high quantities in patients with inflammatory bowel disease, and it is
suggested that they act to mediate (or even possibly trigger) gut inflammation. Reactive oxygen species can increase gut permeability and
damage colonic epithelium, thus contributing to the disease process.97
Osteoporosis occurs in up to 30% of patients with inflammatory
bowel disease98; causative factors include malnutrition, immobilization,
and steroid use.98-100 Osteoporosis may predispose to the development
of fractures, and the prevalence of vertebral fractures in patients with
severely reduced bone density can be up to 22%.101 The gastrointestinal
inflammatory process itself also contributes to bone loss; proinflammatory cytokines produced in inflammatory bowel disease, such as
interleukin-1 and TNF-, displace the balance of bone formation and
resorption toward resorption.98
Muscle wasting is also a feature of inflammatory bowel disease102,
103
and clearly contributes to morbidity. Muscle wasting appears to be
a systemic effect of gut inflammation, mediated by oxidative stress that
is transmitted to remote organs (in this case, muscle) via proinflammatory cytokines such as interleukin-1, interleukin-6, TNF-, and IFN-.104
Cytokines activate peripheral leukocytes that invade tissue and produce
excess oxidants; the oxidants, in turn, may directly damage muscle tissue
or may turn on catabolic signals such as reactive oxygen species.104 Proinflammatory cytokines also were shown to suppress the expression and
function of the local anabolic growth factor insulin-like growth factor1.105 In addition, the immobility that may be a feature of inflammatory

bowel disease can also act on muscle to induce atrophy; atrophy due to
immobility or inactivity is strongly linked to oxidative stress.104
Hypogonadism is another systemic effect of inflammation seen in
several chronic diseases. It can be associated with decreased energy,
decreased concentration, decreased memory, depression, and a loss of
well-being, as well as the obvious decrease in sexual function; it can also
lead to loss of muscle and bone.106 Hypogonadism that occurs secondary
to inflammation may be mediated through TNF-, interleukin-1, and
interleukin-6, which act directly to suppress testicular function and
possibly also suppress the hypothalamic-pituitary-gonadal axis.106
Depression is a common feature of inflammatory bowel disease.80
While depression may be a psychological response to the presence of
chronic disease (and may indeed induce disease exacerbation), there
is increasing evidence to suggest that inflammatory processes mediate
depression; thus, the inflammatory processes in inflammatory bowel
disease may be at least in part responsible for the associated depression. The relationship between immune, autonomic, neuroendocrine,
and central neurotransmitter processes is multidirectional.107 Just as
psychological factors may affect immunity, inflammatory mediators (in
particular interleukin-1, interleukin-6, and TNF-) may affect neuroendocrine and neurotransmitter processes, influencing the susceptibility
to affective disorders.107
In addition to these systemic effects of inflammation, certain iatrogenic factors also mediate morbidity in inflammatory bowel disease.
Folic acid deficiency is associated with the use of the 5-aminosalicylic
acid-based compound sulfasalazine, a common treatment which interferes with folate transport108 (although we must add a note of caution
about folate supplementation following the recent report suggesting
that it may be associated with carcinogenesis109). Methotrexate,
another common treatment, is also a folate antagonist.110 Side effects
of other drugs used in the treatment of inflammatory bowel disease are
discussed in chapter 3. For example, corticosteroids have several welldocumented side effects, including metabolic, dermatologic, ocular,
neuropsychiatric, and immunologic disturbances.111
Psychosocial factors also mediate morbidity in inflammatory
bowel disease. Patients were shown to have lower quality of life, as well
as a lower sense of well-being and mastery, decreased social support,
and increased levels of distress and anxiety about their health.112 The
depression that so frequently accompanies the disease was shown to
negatively affect response to treatment.113 Personality traits such as
poor tolerance of frustration and perfectionistic body ideal also were
shown to negatively affect psychosocial adjustment after surgery.114
Social and emotional aspects of the quality of life in inflammatory
bowel disease patients have been show to be influenced by the level
of social support received.115 Unemployment and sick leave are more
common in inflammatory bowel disease patients and impact negatively
on quality of life.116

Summary

For any individual patient with inflammatory bowel disease, multiple

antecedents, triggers, and mediators interact to produce dysfunction.
The Functional Medicine Matrix Model helps us move away from
a model of disease-centered care and toward a collaborative model
of patient-centered care. Using this model, healthcare practitioners
can assess these multiple interacting components for each patient
and strive to restore function and balance by manipulation of each
patients particular antecedents, triggers, and mediators of inflammatory bowel disease.
Editors Note: This article is excerpted from the monograph
Gastrointestinal Dysregulation: Connections to Chronic Disease by
Leo Galland, MD, with Helen Lafferty, published by the Institute for
Functional Medicine (IFM). IFM is a non-profit 501(c)3 organization

Institute of Functional Medicine 2009 Natural Medicine Journal 1(2), October 2009 | Page 4

dedicated to advancing the assessment and treatment of chronic

disease through promotion of personalized medicine with a focus on
science-based nutritional and lifestyle interventions. For more information about the Gastrointestinal Dysregulation monograph, or to
find out more about IFM, visit www.functionalmedicine.org.

About the Authors

Leo Galland, MD, received the Linus Pauling Award from The Institute of Functional Medicine in 2000 for creating some of the basic principles underlying functional medicine. A board-certified internist, he
has been applying nutritional therapies for the prevention and treatment of chronic disease for the past 30 years, and he is well known
for his work on the relationship between intestinal health and systemic
health. Dr. Galland received his education at Harvard University and
the New York University School of Medicine, and he trained in internal
medicine at Bellevue Hospital Center. He has held faculty positions
at New York University, Rockefeller University, the Albert Einstein
College of Medicine, the State University of New York at Stony Brook,
and the University of Connecticut. Dr. Galland is a Fellow of the American College of Physicians and the American College of Nutrition and
an Honorary Professor of the International College of Nutrition. He is
the author of several dozen scientific articles and textbook chapters, as
well as three books, The Fat Resistance Diet, Power Healing, and Superimmunity for Kids. In addition to his clinical practice in New York City,
Dr. Galland is Director of The Foundation for Integrated Medicine
(www.mdheal.org), a nonprofit educational organization, and the president of Applied Nutrition, Inc. (www.nutritionworkshop.com), which
has created software for analyzing the interactions between drugs, diet,
and dietary supplements.
Helen Lafferty, MB, MRCPI, was raised in Ireland, where she received
her medical degree from University College Dublin in 1980. Following
an internship, residency, and several years of medical practice in Ireland,
she came to the United States, where she completed a clinical fellowship in nephrology in Providence, Rhode Island, and undertook several
years of laboratory research in the Brigham and Womens Hospital/
Harvard Medical School in Boston, Massachusetts. Following a career
break to raise her three children, Dr. Lafferty is currently employed as
a freelance medical writer and editor.

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