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Dissertation
Presented to
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In Partial Fulfillment
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of the Requirements for the Degree
Doctor o f Philosophy
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by
David J. Kutz
May 1999
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UMI Number: 9943603
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UMI
300 North Zeeb Road
Ann Arbor, MI 48103
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SCHOOL OF HEALTH PROFESSIONS
THESIS APPROVAL
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has been examined and is acceptable in both scholarship and literary quality.
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COMMITTEE M E M B E R S’ SIGNATURES
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O CHAIRPERSON
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THESIS.APP
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Abstract
Commonly, an individual with Type 2 diabetes will produce insulin, but it is ineffective
in controlling blood glucose levels within the normal range. Epidemiological studies
have indicated that Type 2 diabetes affects approximately 5 million people in the United
States alone.
compel the patient to make life-long behavioral changes. These include following strict
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dietary and exercise regimens, as well as checking one’s blood glucose levels and taking
insulin. Through extensive research, it has been determined that many patients do not
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follow their prescribed treatment plans. Previous studies have alluded to varying
psychosocial factors in explaining why certain individuals adhere more to their doctors’
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recommendations than others.
The current study examined the role that a number o f psychosocial variables may
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have played in affecting adherence behaviors in two populations o f patients with Type 2
relationship (PPR), coping style, social support, psychological distress, perceived stress,
and SES.
interpersonal aspects o f their medical care they were receiving in their endocrinology
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was discovered that when patients were less likely to utilize avoidance as a means by
which to cope with their illness, they tended to adhere more to prescribed treatment
regimens. It was also indicated that general satisfaction with medical care, as well as the
perceived level of social support the patients felt they obtained, contributed to adherence
practices.
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Dedication
I would like to dedicate this paper to my parents, Alan and Nancy Kutz. Without
their help, love, and support, I would have never been able to complete this task.
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Acknowledgments
I would first like to thank the endocrinology clinics that offered their help and
patient populations. These include Dr. Hasinski’s clinic at MCP Hahnemann Hospital,
and Dr. Pendergrass’ clinic at the Tulane University Medical Center. Furthermore, I
Dr. Julie Landel. Throughout our entire working relationship, she has always extended a
helping hand and pointed me in the right direction. Finally, I would like to thank all of
my friends and family for their understanding and support as I made it through the
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vi
Table o f Contents
I. Introduction to Diabetes 3
V. Method 60
VI. Results 72
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IX. Discussion 83
X.
XI.
Main Analyses
Supplementary Analyses
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XII. Clinical Considerations 97
XIII. Limitations 99
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List of Tables
Table 2: Descriptive Statistics for the Psychosocial Scales and Metabolic Control
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List o f Figures
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NOTE TO USERS
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UMI
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Type 2 Diabetes 3
working model that conceptualizes the roles that certain psychosocial variables may play
in affecting adherence behaviors and health outcomes in patients with Type 2 diabetes
presented first. Following this, a description of the present study is outlined, and the
results of the data are presented and explained. Finally, clinical considerations,
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limitations, and conclusions associated with the present research endeavor are illustrated.
Introduction to Diabetes
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“Diabetes” is a term used to describe a number of different disorders that reflect
glucose (BG), and allows beta cells o f the pancreas to produce and release the hormone
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insulin to metabolize glucose if levels of BG become too high. In persons with diabetes,
Therefore, people with diabetes often have abnormally elevated levels o f glucose in their
variables. Among them are: insufficient insulin, insulin resistance, excess food intake,
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Type 2 Diabetes 4
fever or infection, stress or emotional changes, and other factors that are not yet known
tolerance can be found in a report published in Diabetes Care (The Expert Committee on
the Diagnosis and Classification o f Diabetes Mellitus; ECDCDM, 1998). The report
states that for a diagnosis o f diabetes mellitus, a patient must have one o f the following:
(1) a casual plasma glucose level o f 200 mg/dl or greater plus classic signs and symptoms
o f diabetes mellitus including polydypsia, polyuria, polyphagia, and weight loss, (2) a
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fasting plasma glucose level o f 126 mg/dl or greater, or (3) a two-hour plasma glucose
level greater than or equal to 200 mg/dl. (The 2-hour sample and at least one other
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between 0 and 2 hours after the 75-gram anhydrous glucose dose should be 200 mg/dl or
greater.) For a diagnosis o f impaired glucose tolerance, the committee stated that a
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patient must present a fasting plasma glucose level greater than or equal to 110 mg/dl,
common etiological determinant o f glucose intolerance. However, there are two major
types o f diabetes: Type 1 and Type 2 (ECDCDM, 1998). Although Type 2 diabetes will
be the focus on the present study, a background of Type 1 diabetes will be given to
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Type 2 Diabetes 5
1 diabetes must administer daily injections o f insulin to survive (Cox et al., 1991). The
encounter a stressful situation, such as a viral infection, and this may trigger an
autoimmunological reaction that destroys pancreatic beta cells (Raskin, Beebe, Davidson,
Nathan, Rizza, & Sherwin, 1994). Although Type 1 diabetes can occur at any age, it is
most often diagnosed during childhood or adolescence, between the ages o f 5-6 and 10-
12. Approximately 500,000-600,000 persons in the United States suffer from Type 1
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diabetes (Cox et al., 1991), and it is most evident in Caucasian populations (Raskin et al.,
1994).
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Type 2 diabetes is identified by insulin resistance and beta cell dysfunction, rather
produce insulin, but it is ineffective in controlling BG levels within the normal range
(Johnson, 1992). Most patients with Type 2 diabetes are obese (approximately 80%), or
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have a history o f obesity at the time o f diagnosis. However, nonobese individuals may
also develop Type 2 diabetes, particularly the elderly. It is believed that obesity is a main
usually diagnosed after the age o f 30 (Raskin et al., 1994). Type 2 diabetes is also
considered to be 7-10 times more prevalent than Type 1 diabetes (Polonsky, 1994).
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Type 2 Diabetes 6
al., 1994).
Persons with Type 2 diabetes may not present the classic symptoms o f Type 1
diabetes, such as polydipsia, polyuria, polyphagia, and weight loss. In addition, Type 2
patients are not likely to develop other complications often seen with patients with Type
1 diabetes, such as ketoacidosis, except during periods o f traumatic stress (Raskin et al.,
1994).
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“diminished tissue (liver and muscle) sensitivity to insulin and impaired beta cell
function.” (Rifkin et al., 1984). Although research has debated whether it is impaired
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insulin secretion or impaired insulin action that is the initial marker in the pathogenesis
of Type 2 diabetes, it is clear that both insulin secretion and insulin action become
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significantly impaired in persons who have had the disorder for a long time. Currently,
studies have found that defects in insulin secretion can lead to insulin resistance and vice
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insulin release. There is an early phase that occurs within the first 10 minutes after
glucose ingestion which represents the release o f insulin stored within the beta cell, and a
individuals with diminished glucose tolerance and fasting plasma glucose levels o f less
than 115 mg/dl, the plasma insulin response after oral or intravenous glucose
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Type 2 Diabetes 7
administration can be either normal or, more often, elevated. However, if the fasting
plasma glucose concentration surpasses 115 mg/dl in a person with impaired glucose
tolerance, the early phase o f insulin secretion is lost or becomes significantly impaired,
and the later phase remains normal or, more often is increased (Rifkin et al., 1984).
Essentially, the plasma insulin response to glucose is often inversely correlated with the
degree of fasting hyperglycemia. So that patients with Type 2 diabetes with moderate to
severe hyperglycemia (>180-200 mg/dl) will tend to have all phases o f insulin secretion
impaired, and those with intermediate fasting plasma glucose levels (120-180 mg/dl) may
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Gerich, 1988).
low and hepatic glucose production is not suppressed. Ancillary output o f glucose by the
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liver, in addition to glucose entering circulation through the gastrointestinal tract, can
tends not to be adequate for the level of glucose and insulin concentrations. Early in the
development o f diabetes, this leads to increased secretion o f insulin during the hours
following the ingestion o f glucose. Although the plasma glucose level eventually returns
as the beta-cell secretion defect worsens with prolonged marked fasting hyperglycemia,
the later phase o f insulin secretion is diminished. As this occurs, fasting hyperglycemia
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Type 2 Diabetes 8
individuals with impaired glucose tolerance, and fundamentally resides in all Type 2
diabetes patients who have fasting plasma glucose levels greater than or equal to 140
mg/dl. Insulin resistance has been found to be positively correlated with elevations in
fasting plasma glucose concentrations. Therefore, those with greater glucose intolerance
become more insulin resistant than those who are less glucose intolerant (Moller & Flier,
1991).
The process of insulin resistance can be best explained by first examining the
basic action o f insulin in nondiabetic persons at a cellular level. This occurs in two
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phases. Initially, insulin binds to a specific receptor located on the surface of a cell.
Then, this interaction begins a series of intracellular sequences which result in enhanced
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glucose transport and stimulation o f a number o f intracellular enzymatic pathways
occurrence can be found in patients with mutations in the insulin gene or insulin receptor
gene. However, such abnormalities account for less than 1% of the those with Type 2
diabetes. This may be because most o f those with Type 2 diabetes are obese and
Postbinding abnormalities, which occur after the insulin has bound to the cell, are
fundamentally responsible for insulin resistance in those with Type 2 diabetes and
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Type 2 Diabetes 9
impaired insulin action explains the pathogenesis for Type 2 diabetes. Therefore, it
should be noted that by the time Type 2 diabetes is diagnosed in a specific individual, it
is often difficult to determine the primary etiological process for that particular patient
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to determine if impaired insulin action or defects in insulin secretion occur first in
individuals with Type 2 diabetes, current trends in research have pointed to abnormalities
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in insulin secretion as being a more common etiological starting point for this disease.
Recent studies have described a dual process by which impaired insulin secretion leads to
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the development o f insulin resistance, while defects in glucose uptake by peripheral
tissues may secondarily result in beta-cell failure (Raskin et al., 1994; Rifkin et al.,
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1984).
delayed or diminished in almost all patients with Type 2 diabetes. This impaired insulin
a decrease in the uptake o f glucose by peripheral tissues during the time immediately
stimulus to insulin secretion, and this will eventually return plasma glucose
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Type 2 Diabetes 10
plasma insulin concentrations result from this process. This is important because insulin
is involved in the regulation o f its own receptor. So, when chronic hyperinsulinemia
exists, a downregulation in the number o f insulin receptors may occur. This may lead to
An insulin secretory abnormality may result from several factors: (1) the natural
history o f the beta-cell defect (which may be genetically determined), (2) persistent
hyperglycemia, which may have deleterious effects on the beta-cell and can cause
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(Rifkin et al., 1984).
Taken together, the etiological process o f Type 2 diabetes may be viewed in the
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following manner: Both early and late phases o f insulin secretion become impaired,
while insulin resistance is also often seen in peripheral tissues (i.e. muscle). In addition,
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postbinding abnormalities tend to be responsible for diminished insulin action. These
patients tend to have elevated hepatic glucose production both prior to, and after, food
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consumption. Finally, the ability o f insulin to suppress hepatic glucose output and
when compared to Type 1, patients with Type 2 diabetes can be affected by the same
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Type 2 Diabetes 11
accompanied by a higher rate o f premature cardiac and cerebral and peripheral vascular
disease than Type 1 and nondiabetic populations. In addition, because Type 2 diabetes
makes up approximately 90% o f the cases o f diabetes in the United States, these
complications afflict a large number o f people (over 13 million), and place an immense
vessels, to be responsible for approximately 80% o f the mortality in adults with diabetes.
Hence, macrovascular disease presents the most serious threat to the health o f diabetes
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patients (Raskin et al., 1994). Furthermore, these disorders tend to occur at an earlier age
and at a greater frequency in diabetic patients than in the general population. In fact,
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Type 2 diabetes is viewed as an independent risk factor for macrovascular disease (Cox
etal., 1991). In addition, many common coexistent conditions seen in diabetic patients,
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such as hypertension, dyslipidemia, and obesity, are also risk factors for macrovascular
Diabetes also targets other areas of the body; including the eyes, kidneys, feet,
blood vessels, and nervous system. Retinopathy, a degenerative disorder that affects
blood vessels in the retina and can cause visual impairment and blindness, is the most
who have long-term Type 2 diabetes. In its earliest phase, NPDR is characterized by
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