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A MODEL OF ADHERENCE IN TYPE 2 DIABETES MELLITUS
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THE ROLE OF PSYCHOSOCIAL FACTORS

Dissertation

Presented to

The Faculty o f the School o f Health Professions

MCP Hahnemann University

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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

Department o f Clinical and Health Psychology

May 1999

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UMI Number: 9943603

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UMI Microform 9943603


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SCHOOL OF HEALTH PROFESSIONS

THESIS APPROVAL

This is to certify that the thesis presented to us by T V ^aA K u ~ f 7 , ______________

on the day o f ,n xu_______ . 19 ° f \ . in partial fulfillment o f the

requirements fo r the degree o f PIa.T>._______ in the 0 1 Lr\\ 1 JnfA ogy Program

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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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x o ~ C ~^2° < T N j€-----
O CHAIRPERSON
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ORIGINAL FORM: F irst Page of Thesis


XCOPY: S tudent’s File

THESIS.APP

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Abstract

Type 2 diabetes is identified by insulin resistance and beta cell dysfunction.

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.

The treatment o f Type 2 diabetes involves a number o f factors that invariably

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

diabetes mellitus. The studies’ psychosocial variables included the patient-practitioner

relationship (PPR), coping style, social support, psychological distress, perceived stress,

and SES.

Ultimately, it was discovered that when individuals were satisfied with

interpersonal aspects o f their medical care they were receiving in their endocrinology

clinics, they were more likely to adhere to treatment recommendations. Furthermore, it

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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

would like to acknowledge all of the guidance provided to me by my research mentor,

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

arduous process o f completing my dissertation.

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vi

Table o f Contents

I. Introduction to Diabetes 3

n. Psychosocial Factors Related to Adherence 34

m. Rationale for Present Study 52

IV. Working Model 55

V. Method 60

VI. Results 72

VII. Main Analyses 76

VIII. Supplementary Analyses 80

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IX. Discussion 83

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XI.
Main Analyses

Supplementary Analyses
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XII. Clinical Considerations 97

XIII. Limitations 99

XIV. Conclusions 103


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XV. References 106

XVI. Tables 117

XVII. Figures 120

XVIII. Appendix 123

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List of Tables

T ab let: Sample Characteristics

Table 2: Descriptive Statistics for the Psychosocial Scales and Metabolic Control

Table 3: Correlational Matrix

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List o f Figures

Figure 1: Hypothesized Path Model

Figure 2: Path Model

Figure 3: Correlation o f Adherence and Metabolic Control

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Type 2 Diabetes 3

A Model o f Adherence in Type 2 Diabetes Mellitus:

The Role o f Psychosocial Factors

The present paper addresses the formulation, results, and conclusions of a

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

mellitus. A literature review indicating relevant clinical and theoretical issues is

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

problems o f glucose metabolism. In an individual without diabetes, glucose metabolism


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is predominantly controlled by a feedback system that monitors concentrations o f blood

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,

there is a problem within this system regarding insulin production or utilization.

Therefore, people with diabetes often have abnormally elevated levels o f glucose in their

bloodstream. The accumulation of glucose in the blood stream is referred to as

hyperglycemia. The hyperglycemic condition can be caused by a number o f different

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

(Cox, Gonder-Frederick, & Saunders, 1991).

Diagnosis and Classification

Diagnosis. Diagnostic criteria for diabetes mellitus and impaired glucose

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,

but less than 126 mg/dl (ECDCDM, 1998).


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Classification. There are numerous classifications o f diabetes, all with the

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

distinguish the closely related disorders.

Type 1 diabetes is characterized by a destruction of pancreatic beta cells and thus

an inability to produce an adequate amount of insulin. As a result, individuals with Type

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Type 2 Diabetes 5

1 diabetes must administer daily injections o f insulin to survive (Cox et al., 1991). The

most common etiological explanation for Type 1 diabetes is that it is caused by a

combination o f genetic and autoimmunological processes (Cox & Gonder-Frederick,

1992). An individual who may be genetically predisposed towards diabetes may

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

than insufficient insulin production (ECDCDM, 1998). Commonly, an individual will


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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

contributor to insulin resistance (Cox & Gonder-Frederick, 1992).

Unlike Type 1 diabetes, which is often diagnosed in childhood, Type 2 diabetes is

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

Furthermore, Type 2 diabetes is more often diagnosed in nonwhite populations (Raskin et

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).

Pathogenesis o f Type 2 Diabetes

Type 2 diabetes is known as a heterogeneous disease that is characterized by

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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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versa (Raskin et al., 1994).

Impaired Insulin Secretion. In non-diabetic persons, there are two phases o f

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

following phase o f insulin secretion that represents newly synthesized insulin. In

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

have increased, normal, or decreased plasma insulin responses (Cambell, Mandarino,

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Gerich, 1988).

There are a number of physiological consequences to impaired insulin secretion.


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When insulin release is initially inhibited, the portal vein insulin concentration remains

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

lead to excessive hyperglycemia. In addition, glucose uptake by surrounding tissues


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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

to normal, it is at the expense o f late hyperglycemia and hyperinsulinemia. Furthermore,

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

and diabetes develop (Raskin et al., 1994).

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Type 2 Diabetes 8

Insulin Resistance. Insulin resistance is an early defect. It is common in

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

(Moller & Flier, 1991).


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Binding abnormalities (defects in the first stage o f insulin action) refer to a

reduction in insulin binding. This is followed by a reduction in insulin action. Such an


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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

hyperinsulinemic, and a decrease in binding may be secondary to these conditions

(DeFronzo & Bonadonna, 1992).

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

significant fasting hyperglycemia. These defects involve a decrease in glucose transport

and other intracellular processes involved in glucose metabolism; notably insulin-

stimulated glycogen synthesis (DeFronzo & Bonadonna, 1992).

As it has been mentioned, it is unclear whether impaired insulin secretion or

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

(Raskin et al., 1994).

Pathogenetic Sequences Leading to Type 2 Diabetes. Although it is still difficult

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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).

As it has been briefly discussed, the insulin secretory response to glucose is

delayed or diminished in almost all patients with Type 2 diabetes. This impaired insulin

secretory response leads to an inadequate suppression o f hepatic glucose production and

a decrease in the uptake o f glucose by peripheral tissues during the time immediately

following the ingestion o f glucose. The resulting hyperglycemia provides a continuous

stimulus to insulin secretion, and this will eventually return plasma glucose

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Type 2 Diabetes 10

concentrations to normal. However, while fasting euglycemia is maintained, increased

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

insulin resistance (Campbell et al., 1988).

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

impairment in insulin secretion, or (3) a yet to be understood metabolic disturbance

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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

elevated glucose utilization is also impaired (DeFronzo & Bonadonna, 1992).

Complications o f Type 2 Diabetes

Although Type 2 diabetes has been referred to as a “milder” form o f diabetes

when compared to Type 1, patients with Type 2 diabetes can be affected by the same

spectrum o f diabetes-specific complications as persons with Type 1 diabetes.

Furthermore, because Type 2 often occurs in an older population than Type 1, it is

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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

responsibility on our health care system (Raskin et al., 1994).

Major Chronic Complications. Studies have found accelerated macrovascular

disease, namely atherosclerosis involving the coronary, cerebrovascular, and peripheral

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

disease (Raskin et al., 1994).


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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

common long-term complication o f diabetes (Cox et al., 1991).

There are three types of diabetic retinopathy: nonproliferative, preproliferative,

and proliferative. Nonproliferative diabetic retinopathy (NPDR) occurs in most patients

who have long-term Type 2 diabetes. In its earliest phase, NPDR is characterized by

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