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 Dolfi Herscovici, Jr.
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The Surgical
Management of the
Diabetic Foot and Ankle

123
The Surgical Management
of the Diabetic Foot and Ankle
Dolfi Herscovici, Jr.
Editor

The Surgical
Management
of the Diabetic Foot
and Ankle
Editor
Dolfi Herscovici, Jr.
Foot and Ankle/Trauma Service
Tampa General Hospital
Florida Orthopedic Institute
Tampa, FL, USA

ISBN 978-3-319-27621-2 ISBN 978-3-319-27623-6 (eBook)

DOI 10.1007/978-3-319-27623-6

Library of Congress Control Number: 2016935692

© Springer International Publishing Switzerland 2016

This work is subject to copyright. All rights are reserved by the Publisher, whether the whole or
part of the material is concerned, specifically the rights of translation, reprinting, reuse of
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The use of general descriptive names, registered names, trademarks, service marks, etc. in this
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The publisher, the authors and the editors are safe to assume that the advice and information in
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Printed on acid-free paper

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The registered company is Springer International Publishing AG Switzerland
This book is dedicated to all of the healthcare providers
currently taking care of, or will provide care to, the diabetic
patient who presents with a problem to their foot or ankle.
Hopefully, this information will give you more insight for
managing these patients. It is also dedicated to those patients
who have allowed us, as contributing authors, a chance to
learn how to provide better options for the management of
diabetic pathology and injuries, enabling diabetics to continue
down the successful road to recovery. With the completion of
this book, there are a few people I would like to specifically
thank. First, I would like to thank the people who helped
mentor me in the art and science of foot and ankle surgery:
Randall E. Marcus, M.D.; V. James Sammarco, M.D.; and
especially to G. James Sammarco, M.D. Thank you all for
explaining things to me I did not understand and having the
patience to answer all of my questions. Second, I would like to
thank all of the authors for their hard work and patience with
the edits. Thank you all for your contributions. Third, I would
like to thank my four boys—Derek, Jake, Brad, and Troy—for
putting up with me when I sequestered myself in my office
editing the manuscripts and for understanding the demands
that it took to complete this job. Lastly, I would like to thank my
beautiful wife, Lisa, who through good times and bad has
always been my biggest supporter, has played the task of my
sounding board for ideas and suggestions, and has also played
the role as my de facto editor.

Dolfi Herscovici, Jr., DO

Foreword

Diabetes, a disease of the world, is as old as the pyramids themselves. In fact,

the earliest reference to the condition dates from the Ebers Papyrus, 1552
BCE, in which the patient was observed “… to eliminate urine which is too
plentiful.” This simple observation characterized the most obvious symptom
of the disease. In India, a diabetic was noted to pass “honey urine” since the
urine attracted ants and flies, and in the second century BCE the word diabe-
tes, “to go through,” was introduced. Two centuries later, symptoms leading
to early death were recorded. By the fifth century CE in India, young thin
diabetics were observed to die earlier than older heavier ones, and in China,
patients were noted to be prone to infection. In Bagdad, diabetics were found
to have sweet urine, increased appetite, gangrene, and sexual dysfunction.
During the Renaissance, recorded observations became more detailed.
Paracelsus recognized that a white residue remained when diabetic urine was
allowed to evaporate. In the Age of Enlightenment, Crowley observed that
some patients with severe abdominal and pancreatic trauma developed diabe-
tes. Dobson recorded sweetness in both urine and in blood serum, deducing
that diabetes is a systemic disease.
In the nineteenth century science expanded the understanding of diabetes
with many more investigators contributing findings. Chevreal associated the
sugar in urine with glucose. Rollo added the descriptor “mellitus,” meaning
honey, to differentiate it from diabetes insipidus. Bernard created a model for
diabetes in the laboratory, while Petters found acetone in the urine of patients
in diabetic coma. Noyes described diabetic retinopathy. Allen deduced that
diabetics used food inefficiently, noting that type 1 diabetics died early while
those with type 2 survived longer. Following Langerhans’ discovery of spe-
cial pancreatic cells, Laguesse linked them to a substance he called hormone,
Greek meaning “set in motion,” which, in 1909, de Mayer named “insulin.”
Prior to the twentieth century, natural medicines such as digitalis and
opium, and techniques such as purging, special diets, starvation, physical
therapies, and behavior modification, had failed to control the disease. But
with advances in chemistry, extracts and other compounds began to appear.
In Germany, Zuelzer used acomatol, a pancreatic extract, to treat diabetic
coma. Other attempts followed including the early sulfonylureas.
In 1922, Frederick Banting, a Canadian orthopedist turned researcher, and
his student, Charles Best, isolated the hormone insulin. The purified extract
was administered to a severely diabetic 14-year-old boy resulting in a dra-
matic decrease in his blood sugar. When this was presented at a medical

vii
viii Foreword

conference, there was a standing ovation. An avalanche of research soon fol-

lowed with the rapid manufacturing of many different forms of insulin, thus
saving the lives of millions. This discovery of insulin had propelled research
into virtually all areas of medicine and surgery.
Better control of the disease, however, led to other problems, due to longer
survival and a more active lifestyle of diabetics. Peripheral neuropathy,
peripheral vascular and cardiac disease, and kidney and eye disease became
more common. Neuroarthropathy of the weight-bearing extremities also
increased in incidence. For example, a diabetic woman, while climbing stairs,
would be surprised to see her foot begin to swell without pain, turn red, and
then would be alarmed to watch her foot collapse within a few days. Her doc-
tor would diagnose a “simple fracture” and treat it in “the standard manner.”
The deformity would then progress into “the worst arthritis you have ever
seen.” Closed or open treatment, using the current “acceptable standard of
care,” would result in nonunion or malunion with subsequent foot ulcers and
osteomyelitis leading to possible amputation.
When Jean Martin Charcot described neuropathic deformity, he associated
it with late-stage syphilis, but these patients were not syphilitic. Early case
reports of diabetic Charcot foot and ankle neuroarthropathy now began to
appear in medical literature more frequently. Treatment with nonsurgical
modalities such as rest, limited weight-bearing, bracing, and modified foot-
wear were standard. Surgical treatment generally consisted of soft tissue
debridement and limb amputation.
In the 1950s Paul Brand, at the Carville National Leprosarium, began
using total contact casting to off-weight neuropathic foot ulcers in patients
with Hanson’s disease. This soon became a modality also for treating diabetic
foot ulcers. Total contact casting could help prevent or at least control col-
lapse of an asensory foot or ankle. But it was not a panacea. In the 1980s,
surgical treatment expanded beyond exostectomy, Achilles tenotomy,
arthrodesis, and amputation to include reconstruction, as a means of limb
salvage. Orthopedic researchers along with vascular surgeons became part of
a broad group of diabetic specialists who contributed to reducing the need for
major amputation. The introduction of external fixation as a part of the tech-
nique in controlling deep infection, reducing deformity, and maintaining limb
viability has been remarkable. Likewise staged surgery, intramedullary rods,
and locking screw-plate fixation are now in the orthopedic surgeon’s arma-
mentarium for salvaging severe foot and ankle collapse. Allografts, bone
growth stimulators, bone growth hormone, bone substitutes, and wound suc-
tion devices are also used to fill bony gaps and promote wound healing.
The disease of diabetes has been a focus of physicians and surgeons for
millennia. This book presents current information on diagnosis, treatment,
and prevention of the foot and ankle orthopedic complications related to the
disease. Advances in research will continue to improve our understanding of
this common ailment. The experts offer the special knowledge and skills
developed over recent decades here as a guide to orthopedic surgeons as they
seek to improve care for their patients.

G. James Sammarco
Foreword ix

References
Jacek Z, Shrestha A, et al. Chapter 1: The main events in the history of diabetes. In:
Poretsky L, editors. Principles of diabetes mellitus. 2nd ed. New York: Springer; 2009.
Charcot J-M, Fere C. Affections osseuses et articulaires du pied chez les tabétiques (Pied
tabétique). Archives de Neurologie. 1883;6:305–319 [in French].
Preface

All progress has resulted from people who took unpopular positions.
Adlai Stevenson (1954)

According to the National Center for Health Statistics, in 1900 the life
expectancy in the United States approached 47 years. Of the ten most com-
mon causes leading to death in 1900, six were due to infectious diseases with
strokes, accidents, cancer, and senility contributing to the final four reasons
that someone died. By 1949, the life expectancy had increased to 68 years,
and diabetes mellitus was identified as the tenth most common cause leading
to death. By 2013, the life expectancy increased to almost 79 years with dia-
betes then listed as the seventh most common cause leading to someone’s
death. This indicates that diabetes is certainly a disease of the late twentieth
and early twenty-first centuries. In fact, a report from the World Health
Organization recognizes diabetes as a growing epidemic affecting almost
350 million people worldwide. What does this mean to us, as physicians who
treat and manage diseases of the musculoskeletal system? It means that
because people are living longer, we can expect to see more patients present
with chronic conditions or injuries that are specifically caused or affected by
their diabetes.
Foot and ankle problems produce serious long-term complications, and
any anatomical abnormality can progress to an ulceration, infection, or gan-
grene. These problems are often caused by a combination of such factors as
peripheral neuropathy, vascular disease, immobile joints, an impaired ability
to heal or fight infections, poor management of their diabetes, or outright
denial of their medical problems. That these problems are costly to manage is
implied because these patients often require lengthy and expensive hospital-
izations, which may lead to an amputation.
When a diabetic patient presents with a significant foot or ankle problem,
there are still many physicians who continue to offer only conservative care
or amputation as option. In fact, this approach has not significantly changed
over the last 30–40 years, even though it can ultimately lead to a poor out-
come. There are a few reasons for this. First, the literature is replete with
studies discussing higher rates and more significant complications in diabet-
ics than in the control population. Second, most treating physicians rarely see
these patients and thus have little experience in managing these problems.
Third, there may be a significant hesitancy in offering a surgery, which can

xi
xii Preface

lead to a bad outcome and potential medicolegal issues. Fourth, physicians

often fail to understand that the patients’ associated comorbidities need to be
preoperatively assessed and managed in order to avoid greater problems.
Lastly, for a lot of surgeons their surgical approach that is used to manage a
diabetic patient is similar to techniques used to care for a nondiabetic patient,
often leading to failure of fixation and producing higher rates of morbidity
and mortality. Given these reasons, it is understandable that physicians are
tentative about managing these patients surgically.
This text has been put together to act as a reference guide, with up-to-date
chapter references for the problems associated with the diabetic foot and
ankle. It is also intended to function as a primer with the most current con-
cepts of epidemiology, pathophysiology, workups needed, and treatments
available for the diabetic who presents with abnormalities or injuries to their
foot and ankle. In addition, a glossary has been provided so that the reader
can understand some of the terms used throughout the text. A major strength
of this book is that authors who were solicited are recognized as leading
authorities when it comes to managing problems of the foot and ankle. This
has been demonstrated in some of the treatment chapters with the authors
providing their preferred step-by-step approach for the management of some
of the more commonly encountered foot and ankle problems. By providing a
better understanding of diabetes, and offering improved techniques for man-
aging these patients, we should be able to demonstrate improved outcomes.
This can produce happier patients and families, lower hospital usage, and
decreased overall medical expenses, and it may also allow patients to main-
tain more active lifestyles and potentially return them into the workforce. As
we advance through this century, it is hoped that the information provided in
this text will help all healthcare professionals tasked with caring for the dia-
betic patient who presents with problems to their foot and ankle.

Temple Terrace, FL, USA Dolfi Herscovici, Jr.

Acknowledgments

When I accepted the offer from Springer to put this book together, I knew that
it would be a difficult project. Given the contributions from many authors,
I knew that there were certain technical aspects that I needed to finish this
project. With his input and skills, I would like to acknowledge my son Derek
M. Herscovici for his assistance in helping me prepare and organize this text.
Thanks for all your technical expertise downloading and formatting all of the
incoming information sent to me and making sure that I had everything I
needed to complete this book.

xiii
Contents

1 Introduction, Demographics, and Epidemiology

of Diabetes...................................................................................... 1
Erin A. Baker and Paul T. Fortin
2 Pathophysiology of Diabetes and Charcot
Neuroarthropathy ......................................................................... 9
Sandeep P. Soin, Joshua G. Hunter, and Stephen L. Kates
3 Evaluation and Management of Vascular Disease
in the Diabetic Patient .................................................................. 19
Erin Green and Brad Johnson
4 Classification of Diabetic Foot Disease........................................ 29
Ross Taylor
5 Nonoperative Care and Footwear for the Diabetic
Foot and Ankle Patient ................................................................. 51
David E. Karges
6 The Diagnosis and Treatment of Diabetic
Foot Infections ............................................................................... 67
Michael S. Pinzur
7 Management of Acute Hindfoot Fractures
in Diabetics .................................................................................... 85
Stefan Rammelt
8 Management of Acute Diabetic Fractures of the Ankle ............ 103
Dolfi Herscovici, Jr. and Julia M. Scaduto
9 Plate Fixation Techniques for Midfoot
and Forefoot Charcot Arthropathy ............................................. 117
Eric W. Tan and Lew C. Schon
10 Treatment of Charcot Midfoot Deformity
by Arthrodesis Using Long Axial Screws ................................... 133
V. James Sammarco
11 Management of the Charcot Ankle ............................................. 143
John S. Early

xv
xvi Contents

12 Exostectomy for Charcot Arthropathy ....................................... 155

Steven Anthony and Gregory Pomeroy
13 Use of External Fixation for the Management
of the Diabetic Foot and Ankle .................................................... 165
Bradley M. Lamm and Dror Paley

Appendix ................................................................................................ 181

Glossary ................................................................................................. 183

Index ....................................................................................................... 187

Contributors

Steven Anthony, DO Advanced Orthopedic Center, Port Charlotte, FL, USA

Erin A. Baker, MS Department of Orthopaedic Research, William Beaumont
Hospital - Royal Oak, Royal Oak, MI, USA
John S. Early, MD Clinical Professor Orthopedic Surgery, University of
Texas Southwestern Medical Center, Texas Orthopaedic Associates LLP,
Dallas, TX, USA
Paul T. Fortin, MD Foot and Ankle Service, Department of Orthopaedic
Surgery, William Beaumont Hospital - Royal Oak, Royal Oak, MI, USA
Erin Green, MD Division of Vascular Surgery, University of South Florida,
Tampa, FL, USA
Dolfi Herscovici, Jr., DO Foot and Ankle/Trauma Service, Tampa General
Hospital, Florida Orthopaedic Institute, Tampa, FL, USA
Joshua G. Hunter, MD Department of Orthopaedic Surgery and
Rehabilitation, University of Rochester Medical Center and 2 Virginia
Commonwealth University, Rochester, VA, USA
Brad Johnson, MD Division of Vascular Surgery, University of South
Florida, Tampa, FL, USA
David E. Karges, DO Department of Orthopaedic Surgery, Saint Louis
University, Saint Louis, MO, USA
Stephen L. Kates, MD Department of Orthopaedic Surgery and Rehabilitation,
University of Rochester Medical Center and 2 Virginia Commonwealth
University, Rochester, VA, USA
Bradley M. Lamm, DPM, FACFAS International Center for Limb
Lengthening, Rubin Institute for Advanced Orthopedics, Baltimore, MD, USA
Dror Paley, MD, FRCSC Paley Advanced Limb Lengthening Institute,
St. Mary’s Hospital, West Palm Beach, FL, USA
Michael S. Pinzur, MD Department of Orthopaedic Surgery, Loyola
University Health System, Maywood, IL, USA
Gregory Pomeroy, MD Orthopaedic Foot & Ankle, Mercy Hospital,
Portland, ME, USA

xvii
xviii Contributors

Stefan Rammelt, MD, PhD University Center of Orthopaedics and

Traumatology, Technische Universität Dresden, Dresden, Germany
V. James Sammarco, MD Reconstructive Orthopaedics and Sports Medicine,
Cincinnati, OH, USA
Julia M. Scaduto, ARNP Foot and Ankle/Trauma Service, Tampa General
Hospital, Florida Orthopaedic Institute, Tampa, FL, USA
Lew C. Schon, MD Department of Orthopaedic Surgery, MedStar Union
Memorial Hospital, Baltimore, MD, USA
Sandeep P. Soin, MD Department of Orthopaedic Surgery and Rehabilitation,
University of Rochester Medical Center and 2 Virginia Commonwealth
University, Richmond, VA, USA
Eric W. Tan, MD Department of Orthopaedic Surgery, MedStar Union
Memorial Hospital, Baltimore, MD, USA
Ross Taylor, MD, MBA Danville Regional Medical Center, LifePoint
Health, Danville, VA, USA
 Introduction, Demographics,
and Epidemiology of Diabetes 1
Erin A. Baker and Paul T. Fortin

factor in mortality, with the condition recorded

Introduction on 234,051 death certificates in the United States
in 2010 [1].
Diabetes mellitus (DM, diabetes) is a condition The most common classifications of diabetes
caused by an inability of the insulin produced by mellitus are polygenic forms Type I (T1DM) and
the pancreas to adequately transfer glucose into Type II (T2DM). Type I is characterized by an
cells via transporter recruitment. Depending on absence of insulin production, due to autoim-
insulin secretion or lack thereof, the resultant mune destruction of pancreatic beta cells, and
transporter recruitment may be amplified or may be immune-mediated or idiopathic. Type II
reversed, leading to uncontrolled hyperglycemia. is an acquired condition in which the pancreas
The condition increases the risk of developing either becomes insulin deficient or sufficient
other comorbidities and complications, including insulin is produced but cannot be effectively
hypertension, cardiovascular disease, cerebro- used, termed insulin resistance. More than 90 %
vascular accident (CVA), skin infections and dis- of all diabetes diagnoses are of T2DM [2]. A sub-
eases, nephropathy, retinopathy and other ocular set of T2DM diabetes is gestational diabetes
diseases, mental health status changes (e.g., (GDM), which may present during the second or
depression, anxiety), neuropathy, and lower-limb third trimesters of pregnancy and often persists
compromise [1]. Diabetes is also implicated as after pregnancy.
the seventh leading cause and a contributing In 2012, the American Diabetes Association
(ADA) estimated economic costs of diabetes
including hospital or emergency care, clinic vis-
its, and medication, to approach $245 billion. This
E.A. Baker, M.S.
is an increase of $71 million (41 %) over a five-
Department of Orthopaedic Research, William
Beaumont Hospital - Royal Oak, 3811 West Thirteen year period, in the United States and $548 billion
Mile Road, Ste 404, Royal Oak, MI, USA globally [3–5]. Additionally, indirect costs, due to
e-mail: erin.baker@beaumont.org decreased productivity, disability, and premature
P.T. Fortin, M.D. (*) mortality, were estimated at $69 billion in the
Foot and Ankle Service, Department of Orthopaedic United States. The National Diabetes Statistic
Surgery, William Beaumont Hospital - Royal Oak,
Report (NDSR) concluded that medical expenses
3535 West Thirteen Mile Road, Ste 744,
Royal Oak, MI, USA of diabetic patients are 2.3 times more than
e-mail: pfortin@comcast.net expenses of nondiabetic patients [4].

© Springer International Publishing Switzerland 2016 1

D. Herscovici, Jr. (ed.), The Surgical Management of the Diabetic Foot and Ankle,
DOI 10.1007/978-3-319-27623-6_1
2 E.A. Baker and P.T. Fortin

Table 1.1 Incidence (per 1000 people in age cohort) of

newly diagnosed diabetes cases
Demographics
1980 2011 (most
When categorizing countries into seven geo- Age (first recent 31-year
cohort year) year) average Range (year)
graphic regions (i.e., Africa, Middle East/North
18–44 1.7 3.3 2.5 1.4
Africa, South East Asia, South/Central America, (1985)–4.3
Western Pacific, Europe, North America/ (2008, 2009)
Caribbean), the International Diabetes Federation 45–64 5.2 11.9 8.9 4.6
(IDF) estimated that the highest rates of preva- (1991)–14.3
(2008)
lence of DM will be in Africa (93 %), the Middle
65–79 6.9 15.4 10.2 5.1
East/North Africa (85 %) and South East Asia
(1989)–15.4
(64 %) by the year 2035 [5]. The IDF report has (2011)
also defined the international cost of diabetes as
11 % of total healthcare expenses (i.e., expenses
by health systems and patients), as approximat- lence of diagnosed and undiagnosed diabetes
ing $612 billion. This expenditure is expected to approached 11.8 million, or 25.9 % for that age
increase to about $627 billion by 2035 [5]. demographic [10].
An increased risk of DM has been linked to
numerous demographic factors, including age,
sex, race/ethnicity, socioeconomic/employment Sex
status, and environment/location. Although these
factors have been reported to increase the risk of The CDC also discussed the incidence of DM
developing DM, it may be difficult to explain sorted by patient sex. In the female population,
how their interactions lead to DM since at times the incidence of newly diagnosed cases ranged
no specific cause and effect may be found. between 2.8 (1988) and 5.9 (2011), with a 31-year
average of 3.9 cases (per 1000 females per year).
The male population showed similar data, with
Age the incidence of new cases ranging between 2.6
(1981) and 7.0 (2010) (per 1000 males per year)
The risk of developing DM appears to increase as with a 31-year average of 4.1 cases [6]. This indi-
patients get older. The Centers for Disease cates that since 1988 there appears to be an
Control (CDC) has reported the incidence of DM overall increase in the development of DM in
(per 1000 people) between 1980 and 2011 in the both sexes.
United States (Table 1.1). For patients 18–44
years of age it reported a peak of 4.3 cases (per
1000 people) in 2008 and 2009 (tied). Within this Race/Ethnicity
age group there were 23,525 new cases of DM,
18,436 diagnosed as T1DM and 5089 as T2DM, In the United States, the rate of diabetes diagno-
in patients under 20 years of age. By 2014, the ses were found to be the greatest in the adult
NDSR estimated 208,000 cases of DM had been American Indian and Native Alaskan popula-
diagnosed in Americans under 20 years of age, or tions, with an incidence of 15.9 % (per 1000) in
about 0.25 % of that age cohort. The 45–64 age 2014. For other races, the reported rates of dia-
cohort showed a peak of 14.3 newly diagnosed betes diagnoses were 13.2 % for non-Hispanic
cases (per 1000) in 2008, while patients 65–79 blacks, 12.8 % for Hispanics, 9.0 % for Asian
years of age had a peak incidence of 15.4 cases in Americans, and 7.6 % in non-Hispanic whites.
2011 with a 31-year average of 10.2 cases per Within this subgroup of the Asian American
1000 people. In addition, it also reported that in population, the largest rates of diagnoses were
patients greater than 65 years of age, the preva- identified in Asian Indians (13.0 %) and Filipinos
1 Introduction, Demographics, and Epidemiology of Diabetes 3

(11.3 %). A study of six Asian ethnic groups patients. PON1 and PON2 belong to a multigene
residing in California showed a higher preva- family related to oxidative activities on chromo-
lence of T2DM in second-generation Asian some 7 [13]. Therefore, for many ethnic groups
Chinese and Filipino men, and in first-generation with this genetic susceptibility, decreasing the
Asian Filipino women and Korean women, com- prevalence of diabetes relies almost exclusively
pared to a Caucasian/White cohort [7]. In the on lifestyle modification.
Hispanic subgroup population, Puerto Ricans
(14.8 %) and Mexican Americans (13.9 %) were
identified as having the greatest rates of diabetes Socioeconomic/Employment Status
diagnoses [1].
The large differences, in prevalence of diabetes Socioeconomic status has also been shown to
between various racial/ethnic groups, highlight correlate with the risk of developing diabetes. In
environmental and genetic risk factors [8, 9]. regions with depressed economic development,
Patterns of increased prevalence of diabetes have the prevalence of T2DM is elevated in the upper
been established for ethnic groups migrating from classes; however, in regions with increased
rural/agricultural environments to urban or wealth, the rates of T2DM are increased 2–4
Westernized settings; however, any geographic times in groups with low socioeconomic status
location adjustment, not necessarily from rural to and may be exacerbated by healthcare access and
urban, has also shown an increase in prevalence quality, that are dependent on payment [2, 14,
[9]. For instance, second- and third-generation 15]. In the United States, Everson et al. discussed
Japanese Americans, whose ancestors migrated to an inverse relationship for diagnoses of T2DM
the Seattle, Washington area, demonstrated when comparing a patient’s education level,
increased rates of diabetes (16–20 %) compared occupation, and income [13–15]. There also
to the native Japanese population (4–5 %) for both appeared to be a higher prevalence of diabetes
sexes [10, 11]. Genetically, the Japanese popula- with the poverty income ratio (i.e., annual income
tion has shown a propensity for beta cell dysfunc- divided by federal poverty line) and low socio-
tion, specifically Fujimoto et al. defined an economic status. Evaluating education in this
association between the −30 beta cell GCK gene same study, Everson at al. also reported that the
promoter, beta cell dysfunction, and abnormal prevalence of diabetes was almost three times
glucose tolerance as well as other gene variants greater in adults with less than 9 years of educa-
related to beta cell dysfunction. Combining envi- tion than adults with at least a high school
ronmental factors, such as increased caloric diet diploma [16–18]. These social determinants
and decreased physical activity leading to obesity, (e.g., education, employment security, housing,
in this genetically vulnerable population may ulti- access to nutritious food) also relate to the devel-
mately lead to increased rates of diabetes, espe- opment and progression of diabetes through the
cially if these modifiable disease influencers are pathways of psychological, physiological, and
unchecked [11]. behavioral responses (e.g., chronic stress, devel-
Other ethnic groups have also shown a similar opment of mental health conditions). After diabe-
genetic susceptibility to diabetes, including tes diagnosis, health disparity and disease
Mexican Americans, Latinos, African Americans, progression may persist due to financial burden,
American Indians, and Pacific Islanders [8]. insufficient access to quality healthcare and other
Epigenetic- and gene-based research has associ- resources to manage the disease, as well as
ated the rs10811661 T allele to T2DM in both employment- and education-limiting effects [15].
Asian and European ethnicity groups [12]. These disparities are illustrated by the high rates
Additionally, a study of eastern Asian Indian of uncontrolled diabetes (HbA1C ≥ 9 %), 48.7 %
T2DM patients and controls found a significant and 27.3 %, in patients insured with Medicaid
relationship between the haplotype of two risk and Medicare, respectively [19, 20]. Additionally,
alleles of two genes, PON1 and PON2, in T2DM socioeconomic status may overlap with genetically
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