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LSU Historical Dissertations and Theses Graduate School

1989

The Affective Variant Hypothesis: How Is BulimiaNervosa Related to Depression?Rita C. PratherLouisiana State University and Agricultural & Mechanical College

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The affective variant hypothesis: How is bulimia nervosa related to depression?

Prather, Rita C., Ph.D.

The Louisiana State University and Agricultural and Mechanical Col., 1989

UMI300 N. Zeeb Rd.Ann Arbor, MI 48106

The Affective Variant Hypothesis: How isBulimia Nervosa Related to Depression?

A Dissertation

Submitted to the Graduate Faculty of the Louisiana State University

in partial fulfillment of the requirements for the degree of

Doctor of Philosophy

m

The Department of Psychology

byRita C. Prather

B.A.. University of Central Florida, 1983 M.A., Louisiana State University, 1985

December 1989

AcknowledgementsWith infinite thanks I acknowledge my dissertation

committee members, Donald A. Williamson, Ph.D., W.Drew Gouvier, Ph.D., Mary Lou Kelly, Ph.D., Arthur J. Riopelle, Ph.D., and William F. Waters, Ph.D. In addition to participation in this dissertation, each Professor has influenced my professional career in several unique and positive ways.

Special acknowledgement and gratitude goes to Dr. Williamson for serving as chairman of my dissertation committee. I thank him for the time and interest spent on my behalf.

I wish also to thank William G. Johnson, Ph.D., University of Mississippi Medical Center, for aiding in subject recruitment and reviewing this manuscript and making several important suggestions.

Mr. Jeff Baker was instrumental in the completion of this dissertation. He supervised much of the data collection which meant many hours of work and attention to troubleshooting and problem-solving. It is very difficult to communicate the depth of appreciation that goes to Mr. Baker.

This acknowledgement could not be complete without

recognition of Robert E. Prather whose support and participation have always been freely given. His support has been absolutely invaluable throughout my personal and career development.

Table of Contents

Acknowledgements................................. ii-iiiList of Tables........................................ viList of Figures......................................viiAbstract......................................... viii-ixIntroduction........................................ 1-42

Bulimia and Bulimia Nervosa............... 1- 7Major Depression and Dysthymia............7-10Affective Variant Hypothesis.............10-26Comparison of Bulimia Nervosaand Depression.............................26-27Affective Variant Hypothesis:Further Evaluation........................ 27-40

Summary......................................40-42Method..............................................43-52

Research Participants.....................43-45Assessment Instruments................... 46-51Procedure.................................. 51-52

Resul ts.............................................53-63Discussion......................................... 64-79References......................................... 80-103Appendices........................................ 104-162

Appendix A: Demographic Questionnaire..105-107iv.

Appendix B: Diagnostic InterviewBulimia Nervosa............. 108-113

Appendix C: The Bulimia Test............ 114-121Appendix D: Schedule for Affective

Disorders....................122-130Appendix E: Beck Depression Inventory..131-133Appendix F: Center for Epidemiological

Studies Depression Scale ... 134-136 Appendix G: Dysfunctional Attitude

Scale........................ 137-141Appendix H: Pleasant Events Schedule ... 142-150Appendix I: Maudsley Obsessive-Compulsive

Inventory....................151-153Appendix J: State-Trait Anxiety

Inventory....................154-156Appendix K: Informed Consent Form.......157-158Appendix L: DSM-IIIR Diagnostic

Checkl ists...................159-162Bulimia Nervosa....... 160Major Depression...... 161Dysthymia.............. 162

Vita.............................................. 163-169

v.

List of Tables

Table 1. Russell Diagnostic Criteria forBulimia Nervosa............................. 3

Table 2. DSM-III Diagnostic Criteria forBulimia Nervosa............................. 4

Table 3. DSM-IIIR Diagnostic Criteria forBulimia Nervosa............................. 4

Table 4. DSM-IIIR Diagnostic Criteria forMajor Depression............................ 8

Table 5, DSM-IIIR Diagnostic Criteria forDysthymia.....................................11

Table 6. Beck's Cognitive Dysfunctions............. 30Table 7. Group Demographics..........................45Table 8. Tests of Bulimia, Depression,

and their Interaction .....................55Table 9. Summary of Combined Effects................57Table 10. Correlational Analyses..................... 59Table 11 Stepwise Multiple Regression: BULIT.......61Table 12. Stepwise Multiple Regression: BDI......... 61

vi .

List of Figures

Figure 1. Anxiety Model of Bulimia................. 35

vi i .

AbstractBulimia nervosa patients frequently score from

mild to severe on measures of depressive symptoms.This association between bulimia nervosa and depression led some researchers to hypothesize that bulimia nervosa is a variant of the affective disorder of depression. The main purpose of this study was to provide further evaluation of the affective variant hypothesis of bulimia nervosa. It was postulated that bulimia nervosa patients with and without depression would differ from each other and from depressives without eating disorders on specific measures of cognitive, behavioral, and somatic symptoms associated with depression. Secondly, it was hypothesized that the nondepressed and depressed bulimic patients would differ from depressives but not from each other on measures of anxiety and obsessiveness which would lend support to the anxiety model of bulimia nervosa. The results did not support either the affective variant hypothesis or the anxiety model of bulimia nervosa.The depressed bulimia nervosa patients evidenced higher levels of somatic symptoms, cognitive

dysfunction, state anxiety, and obsessiveness than nondepressed bulimics. These two groups were similar in severity only in trait anxiety and anhedonia. The bulimic and nonbulimic depressed patients did not statistically differ on any measure when the bulimic was also clinically depressed. The dually diagnosed patients were more disturbed than either the nondepressed bulimics or the nonbulimic depressed patients. The nonbulimic depressed patients' scores were more severe than the normals' on four of the six significant measures (somatic symptoms, cognitive dysfunction, state anxiety, trait anxiety), the depressed bulimics' more severe on all six, and the nondepressed bulimics' more severe on only three measures (cognitive dysfunction, anhedonia, trait anxiety). While no measure was associated with bulimia nervosa, several measures were highly associated with depression.

The Affective Variant Hypothesis: How is BulimiaNervosa Related to Depression?

IntroductionThis dissertation presents an overview of bulimia

nervosa and depression as well as a review of the research literature addressing the affective variant hypothesis of bulimia nervosa. The affective variant hypothesis explains bulimia nervosa as a variant of affective disorder and not distinct from the disorder of depression. An association between the two disorders has repeatedly been demonstrated, but the nature of the relationship has been unclear. This investigation was undertaken to identify variables that would be useful in defining the relationship between bulimia nervosa and depression.Bulimia and Bulimia Nervosa

Bulimia nervosa first emerged as a subclinical variant of anorexia nervosa and since then has carried various labels as well as different diagnostic criteria. The disorder has been known as dysorexia (Guiora, 1967), bulimarexia (Boskind-Lodahl & White,1978), subclinical anorexia (Crisp, Kalucy, Lacey, &

1

2

Harding, 1977), binge-purge syndrome (World Health Organization, 1978), dietary chaos syndrome (Palmer,1979), bulimia nervosa (Russell, 1979, 1983; American Psychiatric Association, 1987), and bulimia (American Psychiatric Association, 1980).

Since 1979, four sets of diagnostic criteria have been reported most frequently in the research literature. Russell's (1979, 1983) criteria have been utilized in Britain while the American Psychiatric Association Diagnostic and Statistical Manual of Mental Disorders (DSM-III, 1980; DSM-IIIR, 1987) criteria have been preferred in the United States. These sets of diagnostic criteria are listed in Tables 1 through 3.

Three major symptoms have .been found to comprise the bulimic syndrome (Fairburn & Garner, 1986). The primary feature of this eating disorder, regardless of the label, has been episodic, uncontrolled overeating. A second clinical feature is engaging in one or more extreme behaviors designed to control body weight. These weight control behaviors include self-induced vomiting, laxative or diuretic use, fasting or severe dieting, and excessive exercise. A third symptom.

3

Table 1.Russell's Diagnostic Criteria for Bulimia Nervosa

Bulimia nervosa-original criteria (Russell, 1979)1. The patients suffer from powerful, intractable

urges to overeat;2. They seek to avoid the "fattening" effects of

food by inducing vomiting or abusing purgatives;3. They have a morbid fear of becoming fat.

Bulimia nervosa-revised criteria (Russell. 1983)1. Preoccupations with food, irresistible cravings

for food and repeated episodes of overeating;2. Devices aimed at counteracting the "fattening"

effects of food;3. A psychopathology resembling that of classical

anorexia nervosa;4. A previous overt or cryptic episode of anorexia

nervosa.

4

Table 2. DSM-III Diagnostic Criteria for Bulimia

A. Recurrent episodes of binge eating (rapid consumption of a large amount of food in a discrete period of time, usually less than two hours);

B. At least three of the following;1. consumption of high-caloric, easily ingested

food during a binge2. unconspicuous eating during a binge3. termination of such eating episodes by abdominal

pain, sleep, social interruption, or self-induced vomiting

4. repeated attempts to lose weight by severely restrictive diets, self-induced vomiting, or use of cathartics and/or diuretics

C. Awareness that the eating pattern is abnormal and fear of not being able to stop eating voluntarily;

D. Depressed mood and self-deprecating thoughts following eating binges,-

E. The bulimics episodes are not due to anorexia nervosa or any known physical disorder.

American Psychiatric Association (1980)

Table 3. DSM-IIIR Diagnostic Criteria for Bulimia Nervosa

A. Recurrent episodes of binge eating (rapid consumption of a large amount of food in a discrete period of time);

B. A feeling of lack of control over eating behavior during the eating binges;

C. The person regularly engages in either self-induced vomiting, use of laxatives or diuretics, strict dieting or fasting, or vigorous exercise in order to prevent weight gain;

D. A minimum average of two binge eating episodes a week for at least three months;

E. Persistent overconcern with body shape and weight.American Psychiatric Association (1987).

5

preoccupation with body size, has been found to be associated with bulimia nervosa (Fairburn & Garner,1986). These three symptoms are included as diagnostic criteria for bulimia nervosa in the recent revision of DSM-III (DSM-IIIR. American Psychiatric Association, 1987).

DSM-III (American Psychiatric Association, 1980) required both depressed mood and self-deprecating thoughts following binge eating. The revision of DSM-III (American Psychiatric Association, 1987) eliminated this criterion, however. The elimination of this symptom might be due to findings that the mood immediately following binge eating is varied (cf. Mizes, 1985), and when present, the depressive mood is often more pervasive and not limited to the period following binging (Davis, Freeman, & Solyom, 1985; Fairburn & Cooper, 1982; Herzog, 1982, 1984; Johnson & Larson, 1982; Lee, Rush, & Mitchell, 1985; Mitchell, Hatsukami, Eckert, & Pyle, 1985; Williamson, Prather, Upton, Davis, Ruggiero, & VanBuren, 1987). Fairburn and Garner (1986) suggested that the psychopathology associated with bulimia nervosa is less specific than

6

the three main symptoms of binge eating, purging, and preoccupation with body weight and shape. However, they report that anxiety and depression are the most commonly associated symptoms. Others have suggested that depression is not an associated feature of bulimia nervosa but is the central problem (Hudson, Pope, Jonas, Laffer, Hudson, & Melby, 1983). This issue will be discussed in more detail in a subsequent section.

Bulimia is a relatively common disorder, with prevalence rates reported in the literature ranging from 1 to 16 percent (American Psychiatric Association, 1980; Cooper & Fairburn, 1983; Johnson, Lewis, Love, Stuckey, & Lewis, 1983; Mizes, 1985;Pyle, Mitchell, Eckert, Halvorson, Neuman, & Goff, 1983). The large variability in estimates of prevalence is probably due to differences in the diagnostic criteria utilized and whether or not self­induced vomiting was required for a positive diagnosis of bulimia. Although DSM-IIIR criteria are more restrictive than DSM-III, vomiting is still not essential for the diagnosis of bulimia nervosa. A patient may be diagnosed with bulimia nervosa if the

7

patient engages in either fasting, vigorous exercise, uses laxatives or diuretics, or self-induces vomiting to prevent weight gain between binges. Results from prevalence studies requiring the presence of self­induced vomiting suggested an incidence rate of approximately 4 percent (Johnson, Lewis, Love,Stuckey, & Lewis, 1983), while higher rates have been reported in studies not requiring self-induced vomiting.

Onset usually occurs between the ages of 15 to 18 years (Fairburn & Cooper, 1982; Pyle, Mitchell, & Eckert, 1981), however age of onset may range from 13 to 30 years (Russell, 1979). Ninety-five percent of those diagnosed with bulimia have been females.Major Depression and Dysthymia

The diagnosis of major depression is indicated when a designated cluster of symptoms has been present for a period of at least two weeks (American Psychiatric Association, 1987). Refer to Table 4 for complete DSM-IIIR diagnostic criteria. The symptom cluster includes a relatively pervasive and prominent dysphoric mood or decreased interest in usual

8

Table 4. DSM-IIIR Diagnostic Criteria for Major Depression

A. At least five of the following symptoms have been present during the same two-week period and represent a change from previous functioning; at least one of the symptoms is either (1) depressed mood, or (2) loss of interest or pleasure:1. depressed mood most of the day, nearly every

day;2. markedly diminished interest or pleasure in

all, or almost all, activities most of the days, nearly every day;

3. significant weight loss or gain when not dieting or decrease or increase in appetite nearly every day;

4. insomnia or hypersonmia nearly every day;5. psychomotor agitation or retardation nearly

every day;6. fatigue or loss of energy nearly every day;7. feelings of worthlessness or excessive or

inappropriate guilt;8. diminished ability to think or concentrate, or

indecisiveness nearly every day;9. recurrent thoughts of death, recurrent suicidal

ideation without a specific plan, or a suicide attempt or specific plan for committing suicide

American Psychiatric Association (1987).

9

activities every day during the worst point of the depression. In addition, at least four of the following eight symptoms must also be present to satisfy diagnostic criteria. These symptoms include (a) appetite disturbance, (b) sleep disturbance, (c) psychomotor retardation or agitation, (d) a decrease in sexual interest and/or interest in usual activities, (e) loss of energy or fatigue, (f) feelings of worthlessness and/or excessive guilt, (g) indecisiveness and concentration difficulties, and (h) persistent suicidal ideation or attempts (DSM-IIIR, American Psychiatric Association, 1987).

Prevalence rates indicate that approximately 18 to 23 percent of females have had a major depressive episode at some time, and this rate is twice as high as that for males (Boyd & Weissman, 1981) . Onset can occur at any age, and occurrence is relatively evenly distributed across adult age groups (American Psychiatric Association, 1980).

Dysthymia is similar to major depression with symptoms differing only in duration and severity (American Psychiatric Association, 1987). The DSM- IIIR diagnostic criteria for dysthymia are listed in

10

Table 5. Dysthymia is essentially a chronic disturbance of mood, and impairment in social and occupational functioning is usually mild to moderate. As in major depression, dysthymia is a common disorder and is identified more frequently in adult females. Onset generally occurs before or during early adult 1 ife.Affective variant hypothesis

As discussed earlier, bulimia nervosa is frequently accompanied by depressive symptoms which are pervasive and sometimes severe (cf. Mizes, 1985; Williamson et al., 1987). Thus, it has been hypothesized that bulimia nervosa is another behavioral manifestation of depression and is not an independent syndrome. In the affective variant hypothesis, bulimia nervosa and depression are viewed as equivalent disorders with the same organic etiology (cf. Hudson, Pope, Jonas, Laffer, Hudson, & Melby,1983) .

Biological or organic formulations of depression are based on three main classes of observations.First, depressive disorders are accompanied by changes

11

Table 5. DSM-IIIR Diagnostic Criteria for Dysthymia

A. Depressed mood most of the day, more days than not for at least two years.

B. Presence, while depressed, of at least two of the following:1. poor appetite or overeating;2. insomnia or hypersomnia;3. low energy or fatigue;4. low self-esteem;5. poor concentration or difficulty making

decisions;6. feelings of hopelessness;

C. During a two-year period of the disturbance, never without the daily depressed mood for more than two months at a time.

American Psychiatric Association (1987).

12

In biological functions such as appetite and sleep, psychomotor activity, and sexual interest; second, depressed patients frequently report a positive history of affective disorder in first degree relatives which may support the theory of genetic transmission; third, biological treatments such as antidepressant medication frequently result in amelioration of depressive signs and symptoms (Carson & Carson, 1984; Davis & Sharma, 1986) although the mechanism of antidepressant action is unclear (Gerner & Bunney, 1986).

The affective variant hypothesis of bulimia nervosa was derived from these same three areas of research. In addition, several studies have suggested a high prevalence of depressive symptoms to be associated with bulimia nervosa. Research addressing the family history of depression in those diagnosed as bulimic, results of biological tests for depression in bulimia, and outcome using antidepressant medications to treat bulimia have led to the theory that bulimia nervosa is a variant of depressive disorder. These three areas of research as well as studies looking at the association of depression and bulimic symptoms

13

will be reviewed.Depressive symptoms in bulimia nervosa. An

association between depression and bulimia nervosa has frequently been reported (Pyle et al., 1981). Some studies have shown that bulimic patients do evidence mood disturbance (cf. Davis, Freeman, &. Solyom, 1985; Fairburn, 1983; Herzog, 1984: Russell, 1979).Although survey studies are methodologically weak, results from these studies suggest that from 17 to 75 percent of subjects who endorsed bulimic behaviors also endorsed symptoms indicative of either current or past depression (Abraham & Beaumont, 1982; Fairburn & Cooper, 1982; Johnson, Stuckey, Lewis, & Schwartz, 1983; Hatsukami, Eckert, Mitchell, &. Pyle, 1984; Herzog, 1982; Johnson, Stuckey, Mitchell, Hatsukami, Eckert, & Pyle, 1985). This wide range in number of subjects endorsing both bulimia and depression exists in part to methods of assessment as well as differences in the criteria used to identify both bulimia and depression. These studies have used unstructured interviews and questionnaires designed for the specific project and the psychometric

14

properties were not reported. Studies in which standardized diagnostic criteria and structured interviews were employed found the lower incidence of depression associated with bulimia (Herzog, 1984; Walsh, Roose, Glassman, Gladis, & Sadik, 1985).Another problem with survey studies is that because investigators were not blind to diagnosis the data were subject to experimenter bias. Hinz and Williamson (1987) pointed out that the incidence rate of current affective disorder in bulimic subjects was lower (24 to 33 percent) when structured interviews and standardized diagnostic criteria were used, and the high incidence rates occurred only when lifetime (past and present depressive episodes) data were included.

A number of studies have used standardized objective measures and included a non-eating disordered control group (Hatsukami, Owen, Pyle, & Mitchell, 1982; Prather & Williamson, 1988; Weiss & Ebert, 1983; Williamson, Kelley, Davis, Ruggiero, & Blouin, 1985; Williamson, Prather, Upton, Ruggiero, Davis & VanBuren, 1987). Without exception depression scores were found to be significantly higher in

15

bulimic groups than the control groups. Williamson et al. (1985) found that 35 to 40 percent of their bulimic subjects obtained clinically significant scores on objective measures of depression (T-score above 70 on the MMPI Depression subscale and/or a Beck Depression Inventory score above 20). Prather and Williamson (1988) replicated this incidence of clinically elevated scores using the MMPI and BDI.In addition, one study documented that more frequent self-induced vomiting was associated with higher scores on measures of depression (Williamson, Prather, Upton, Davis, Ruggiero, & VanBuren, 1987).

An association between bulimia nervosa and depression has been consistently documented in approximately 30 percent of patients with bulimia nervosa. However, causality should not be inferred from this association. Depression has been found to be associated with several disorders. One can entertain other hypotheses which have not been empirically eliminated to explain the asso'ciation between depression and bulimia nervosa. For example, depression could occur due to the lack of control the

16

bulimic individual begins to feel, or depressive symptoms could be a reflection of inadequate nutrition.

Family history of depression. The second area of research used to support the affective variant hypothesis is familial association of depression. The heritability of depression is measured by investigating the incidence of affective disorders occurring in bulimics' relatives. Some researchers have reported a high occurrence of affective disorders among the relatives of bulimia nervosa patients (Hudson, Laffer, & Pope, 1982; Hudson, Pope, Jonas, & Yurgelun-Todd, 1983; Pyle, Mitchell, & Eckert, 1981). The first investigators of the family history of depression in bulimia nervosa reported that approximately 60 percent of bulimics had a positive family history of affective disorder (Hudson, Laffer,& Pope, 1982; Hudson, Pope, Jonas, & Yurgelun-Todd, 1983; Lee, Rush, & Mitchell, 1985). There were several methodological problems with these studies which included small sample size, investigators not blind to diagnosis, and use of patient report of family history of affective disorder when relatives

17

were not available.Controlled studies using investigators blind to

diagnosis have found a much lower occurrence of affective disorder in relatives of individuals diagnosed as bulimic. In fact. Stern, Dixon, Nemzer, Lake, Sansone, Smetzer, Lantz, and Schrier (1984) using a control group, blind diagnosis, and interviews of subjects' mothers found no difference between the frequency of affective disorder in relatives of bulimics and relatives of a control group. There were 368 relatives of bulimics and 384 relatives of control subjects included in the Stern et al. (1984) study. Rates of familial depression have been the highest when using retrospective, self-report methods. To date no studies have been reported investigating the familial association of depression in monozygotic and dizygotic twins who are also bulimic. This information is important as it has been shown that monozygotic twins have a higher concordance rate of affective disorder than do dizygotic twins (Bertelson, Harvald, & Hauge, 1977).

In addition to incidence rates of affective

18

disorder in relatives of bulimia nervosa patients, it would also be relevant to investigate the incidence rates of bulimia nervosa in relatives of affective patients. If bulimia nervosa and affective disorder had the same etiology the relatives of affective disorder patients would be expected to develop bulimia nervosa more frequently than would occur in the general population. In a study described by Strober and Katz (1987) first-degree relatives of patients diagnosed with affective disorders had a low incidence rate of eating disorders. The rates of eating disorders in relatives of depressed, manic, and schizophrenic patients ranged from 0.6 to 1.3 percent which was not significantly different than lifetime expectancy in the general population (Strober & Katz,1987) .

Dexamethasone suppression test of depression. A third group a studies addressing the affective variant hypothesis were designed to investigate the results of a biological test of depression. The dexamethasone suppression test (DST) has been purported to identify depressive patients due to their abnormal or nonsuppression of cortisol following injection of

19

dexamethasone. The dexamethasone suppresses cortisol In nondepressed patients. Results of DST studies have shown similarities in nonsuppression of cortisol between bulimia nervosa and affective disorder patients (Gwirtsman, Roy-Byrne, Yager, & Gerner, 1983; Hudson, Laffer, & Pope, 1982; Hudson et al. , 1983; Lindy &. Walsh, Roose, Gladis, & Glassman, 1985) . Four studies found that a high percentage of bulimic patients evidenced abnormal DST responses, that is, failed to suppress cortisol. Percentages varied from 35 percent (Lindy et al., 1985) to 67 percent (Gwirtsman et al., 1983). The abnormal DST responses in bulimic patients could be a result of other factors such as weight or nutrition abnormalities.

The ability of the DST to identify depressives has been adequately challenged (Birch, 1985; Walsh, Roose, Glassman, Gladis, & Sadik, 1985), and results of the DST are even more questionable for eating disordered individuals. It is known that weight change and nutrition affect the outcome of the DST (Carroll, Feinberg, & Greden, 1981; Fichter, Pirhe, & Holsboer, 1986; Smith, Bledsoe, &. Chetri, 1975; Stahl & Kravitz,

20

1986). Bulimic patients often have frequent weight fluctuations and inconsistent nutritional intake. Gwirtsman et al. (1983) did find that low body weight was related to abnormal DST responses. Lindy et al. (1985) failed to confirm this relationship between body weight and DST response. Other studies (Hudson et al., 1982; Hudson et al., 1983) did not control for weight status.

The DST has also been faulted for not being specific. Other disordered populations such as alcoholics, obsessive-compulsive patients, and patients diagnosed with borderline personality disorder have been found to evidence an abnormal DST response (Hinz & Williamson, 1987).

Antidepressant medications. The final area of research included in the affective variant hypothesis comes from the treatment of bulimic patients with antidepressant medications. It has been reported that bulimia nervosa patients reduced bulimic behaviors when treated with antidepressant medications (Agras & McCann, 1987; Pope & Hudson, 1986). Early uncontrolled reports (Jonas, Pope, &. Hudson, 1983; Mendels, 1983; Moore, 1977; Pope & Hudson, 1982; Rich,

21

1978; Roy-Byrne, Gwirtsman, & Edelstein, 1983; Shader & Greenblat, 1982; Walsh, Stewart, Wright, Harrison, Roose, S. Glassman, 1982) were suggestive that some bulimic patients may improve when treated with antidepressants.

The first controlled study to be reported (Sabine, Yonance, Farrington, Barratt, & Wakeling, 1983) treated 50 bulimic patients with the antidepressant mianserin. They found no differences in bulimic symptoms between placebo and drug conditions. They also reported that no significant improvement occurred in binge eating or self-induced vomiting during pharmacological treatment. In contrast. Pope, Hudson, Jonas, & Yurgelun-Todd (1983) reported a significant difference between placebo and imipramine groups in decreased binge eating behavior. At the end of treatment 35 percent of their patients treated with imipramine were reported to be in remission of bulimic symptoms (Pope et al., 1983). Pope and Hudson (1986) suggested that the differing results between Sabine et al. (1983) and Pope et al. (1983) may have been due to insufficient dosage in Sabine et al. (1983) and/or

22

more severely 111 patients In Pope et a l . (1983). Walsh. Stewart, Roose, Gladis, and Glassman (1984) reported a significant difference between placebo and phenelzine treated bulimic patients in binge eating frequency but no differences for measures of depression. Very few of the original 35 patients were included in the final data analysis (15 patients) so results must be interpreted cautiously. Placebo responders were eliminated during a wash-out phase thus biasing the results in favor of phenelzine.

In studies assessing blood plasma levels to insure a therapeutic medication dose was reached treatment outcome results have been inconsistent. Three studies to date have been reported (Agras, Dorian, Kirkley, Arnow, & Bachman, 1987; Hughes, Wells, Cunningham, & Ilstrup, 1986; Mitchell & Groat, 1984). One study (Hughes et al., 1986) reported significant differences between placebo and desipramine treated bulimic patients in improved binge eating frequency and one depression measure. Agras et al. (1987) found imipramine to be superior over placebo in reducing bulimic symptoms, however depression was not significantly improved. Mitchell and Groat (1984)

23

comparing amitriptyline to placebo found no differences between placebo and drug groups on any bulimic symptoms. They did report significant improvement in the drug group on one measure of depression (Hamilton Depression Scale) but not on another (Zung Depression Scale).

Due to the inconsistent treatment outcome in these studies treating bulimic patients with antidepressant medications one cannot conclude that bulimia nervosa is a variant of affective disorder with the same organic etiology. The fact that some antidepressants were found to be effective in reducing binge eating frequency in some patients does not mean that bulimia is an affective disorder. One must consider the fallacy of inferring causality from treatment results. The mechanism of antidepressant treatment effects is unclear. These medications have been used in treating disorders that have not been considered affective variants (Hinz & Williamson, 1987). As Walsh et al., (1985) stated, imipramine has been used to treat cardiac arrhythmias even though cardiac disorders are not a variant of affective disorder. It is

24

inappropriate to assume the circular logic that two or more disorders are the same because the same intervention is effective across the disorders. More importantly, when comparing the outcome of treatment studies, treatment of bulimia with antidepressant medications has been no more effective than cognitive-behavioral treatments. Typically, a 30 to 40 percent abstinent rate is reported in studies incorporating either treatment modality (Agras, 1987; Kirkley, Schneider, Agras, & Bachman, 1985).

Summary of research evidence. In summary, it has been documented that bulimia nervosa has been frequently accompanied by depression. Depression is known to be associated with many chronic psychological and physical disorders, e.g., agoraphobia (Munjack & Moss, 1981), alcoholism (Cadoret & Winokur, 1974), chronic pain (Keefe, 1982). The depressive symptoms associated with bulimia nervosa may also be due to the chronic, cyclic pattern of this eating disorder. As noted by Klerman (1980) pathological depression may exist as a separate syndrome or in association with another disorder.

Studies investigating family history of

25

depression, the dexamethasone suppression test for depression, and treatment of bulimia nervosa with antidepressant medications have not provided conclusive evidence that bulimia nervosa is a variant of affective disorder. It has been established that there is an association between depression and bulimia nervosa in some patients, however, these studies are incapable of determining the etiology of bulimia nervosa. A review of the research literature related to the affective variant hypothesis conducted by Swift, Andrews, and Barklage (1986) summized that although there may be some type of relationship between eating disorders and affective disorder, the nature of the relationship is unclear. In a more recent review Hinz and Williamson (1987) concluded that although some research has supported the affective variant hypothesis of bulimia the propositions which follow from this hypothesis have not been conclusively supported. They suggested further research directly comparing bulimics and depressives using measures related to depression as well as measures related to bulimia (Hinz &

26

Williamson, 1987).Comparison of bulimia nervosa and depression.

Prior to this study only one study has directly compared the symptoms of patients diagnosed with bulimia nervosa against patients diagnosed with major depression (Cooper & Fairburn, 1986). Both bulimia nervosa and major depression groups were assessed using the Present State Examination (Wing, Cooper, & Sartorius, 1974) and the Montgomery and Asberg Depression Rating Scale (Montgomery & Asberg, 1979). Bulimia nervosa patients were diagnosed using criteria from Russell (1979). A diagnosis of depression was based on the Research Diagnostic Criteria (Spitzer, Endicott, & Robins, 1978). The affective variant hypothesis was evaluated by comparing the presence of depressive symptoms in the two clinical groups.Bulimia nervosa patients were found to evidence more anxiety, obsessional ideas, and pessimistic thought. These same subjects were found to endorse less simple depression, apparent sadness, sleep disturbance, and suicidal thought than the major depression patients. The authors concluded that there were different symptom patterns evident for the two patient groups

27

and that depressive symptoms are likely to be secondary to bulimia nervosa (Cooper & Fairburn,1986). They did not compare bulimia nervosa with a dual diagnosis of major depression to bulimia nervosa without major depression. If the affective variant hypothesis is valid bulimia nervosa patients with and without clinical depression should not differ on a variety of measures of psychopathology. Whereas, if depression is secondary to bulimia nervosa, then only those bulimics who are also depressed should evidence psychopathology similar to a depressed sample. Affective variant hypothesis: Further evaluation.

Bulimia nervosa subjects and major depression subjects consistently achieve similar scores on general measures of depressive symptomatology, but research does not support the hypothesis that these two disorders are necessarily derived from the same etiology (Hinz & Williamson, 1987; Swift, Andrews, & Barklage, 1986). Cooper and Fairburn (1986) further questioned the hypothesis by finding that bulimia nervosa and depressive patients have different symptom patterns.

28

The important question then becomes, are depressed bulimia nervosa patients different from nondepressed bulimia nervosa patients? What variables besides specific eating behaviors might define the relationship between bulimia nervosa and depression? Researchers frequently evaluate depression on three dimensions which include cognitive, behavioral, and somatic symptoms. Perhaps bulimic and depressed individuals differ on one or more of these specific dimensions of depression even though they do not differ on general measures of depression.

Cognitive Dimension. Cognitive theories of depression (Beck 1967, 1976) postulate that depressives experience negative cognitions that distort their view of the self, world, and future. Depressive symptoms are seen as a direct result of this negative cognitive set. In cognitive theory of depression it has been proposed that individuals learn, through early experiences, cognitive styles (or schemata) that function to screen, categorize, and evaluate stimuli (Beck, 1974). These schemata result in self-concepts and personal expectations that are global, rigid, and negative (Hollon & Beck, 1979).

29

Several systematic cognitive distortions may result from these schemata (Beck, 1967). The most common of these errors in logic are explained in Table 6. The relationship of the biased cognitive style to depression has been widely researched and supported. Hammen, Krantz, and Cochran (1981) found that perceptions of globality (belief that the event would affect other aspects of the person's life) and low controllability were predictive of depression onset. This finding has been replicated in other investigations (cf. Golin, Sweeney, & Shaeffer, 1981). Because the presence of a negative cognitive style has been adequately linked to the onset of depression, it is plausible that measures of dysfunctional cognitions would not discriminate between bulimia nervosa and depression subjects if the affective variant hypothesis was correct. The questions of interest were, (a) do bulimics and depressives have similar cognitive dysfunction and (b) do depressed bulimics differ from nondepressed bulimics on measures of cognitive dysfunction?

Behavioral Dimension. In behavioral theories of

30

Table 6.Common Cognitive Errors

1. Arbitrary inference: drawing a conclusion in the absence of evidence or when the evidence is contrary to the conclusion.

2. Selective abstraction: focusing on a negative detail in a situation and conceptualizing the entire experience on the basis of this negative fragment.

3. Overgeneralization: drawing a general rule or conclusion on the basis of one isolated incident and appling the concept indiscriminately to both related and unrelated situations.

4. Magnification and minimization: overestimating the significance or magnitude of undesirable events and underestimating the significance or magnitude of desirable events.

5. Personalization: relating external events to oneself without evidence.

6. All-or-none thinking: thinking in absolute black or white, all-or-none terms.

Beck (1967)

31

depression it has been postulated that depression is a consequence of reduced response-contingent positive reinforcement (Lewinsohn, 1974). Reinforcement, in this context, refers to the quality of one's interactions with one's environment. Productive, social behavior of depressed persons does not result in sufficient positive reinforcement to maintain the behavior. This low rate of pleasurable activity provides little or no rewarding interactions with the environment and is assumed to lead to dysphoric feelings that lead to further reduction in responses that might be positively reinforcing. A positive correlation between positive mood and frequency of participation in pleasant activities has been documented by Lewinsohn and Graf (1973) and Lewinsohn and Libet (1972). The average rate of participation in pleasurable activities as well as the subjective enjoyability of potentially reinforcing events were both lower in depressed subjects relative to psychiatric and normal control subjects (Lewinsohn & MacPhillamy, 1974; MacPhillamy & Lewinsohn, 1974). Again, the question to be answered was, would the interaction between depression and bulimia nervosa

32

result in more severe scores indicating less participation in and enjoyabi1ity of activities?

Somatic Dimension. Endogenous depression or depression with an organic etiology is well known to be accompanied by physical or somatic signs which have been described as vegetative. These somatic signs include appetite disturbance, sleep disturbance, psychomotor disturbance, and fatigue or loss of energy. The presence of these somatic features in depressed patients has been used to support the biological theory of affective disorders. Cooper and Fairburn (1986) reported a significant difference between bulimics and depressives in sleep disturbance. Other somatic signs were either not significant or not reported.

Bulimics have been found to endorse test items reflecting somatic distress arising from concerns about bodily dysfunction (Williamson et al., 1985). Bulimics achieved higher scores than normals did on the Somatization subscale of the Symptom Checklist 90-Revised. The Somatization subscale measures complaints focused on cardiovascular.

33

gastrointestinal, respiratory systems, and other signs with strong autonomic mediation (Derogatis, 1977).The signs and symptoms included on this subscale are reported to be somatic equivalents of anxiety (Derogatis, 1977). Available reports concerning somatic symptoms suggest that bulimic individuals may experience anxiety symptoms, but the presence of vegetative signs associated with depression in bulimic individuals is unclear. Knowing whether vegetative signs differ between bulimics with and without a diagnosis of depression would be useful in evaluating the affective variant hypothesis of bulimia nervosa, especially since this hypothesis was based on a biological theory.

Obsessions-compulsions. As noted by Lehmann (1985), an association between depression and compulsive and obsessional features has long been recognized. This relationship, however, has been reported to be a complex one since not all depressed patients develop obsessive-compulsive problems nor do all obsessive-compulsive patients develop depressive complaints (Sturgis, 1984). Co-occurrence rates have been reported to range from 20 to 45 percent

34

(Gittleson, 1966; Kringlen, 1965; Rachman & Hodgson,1980). Cooper and Fairburn (1986) found that only 2.5 percent of the depressed subjects evidenced obsessional ideas and ruminations. It appears that obsessive-compulsive patients may also evidence symptoms of depression but few depressive show obsess ive-compu1s ive symptoms.

The anxiety model of bulimia, incorporated obsessive-compulsive components as a central feature of bulimia nervosa (Rosen & Leitenberg, 1982).Anxiety and fear of weight gain are reported to follow binge eating. As can be seen in Figure 1, purgative behavior reduces this anxiety and fear thus negatively reinforcing purging (Williamson, Prather, Goreczny, Davis, & McKenzie, 1989). The DSM-IIIR (American Psychiatric Association, 1987) diagnostic criteria for obsessive-compulsive disorder follow a similar pattern. Ruminative obsessions result in anxiety and distress; engaging in compulsive behavior is said to aid the patient in avoiding or escaping anxiety and obsessive thoughts (DSM-IIIR, 1987).

Several studies have consistently demonstrated

Depression-

& Low Self-E steem

\/

// Biological

/ Deprivation/ &I Hunger

I \\\\s/

ObsessiveCompulsive

Habits

Distorted Body Image

tInterpersonal

& Family Problems/\

Anxiety&Worry

concerningWeight

Gain

Anxiety \ Reduction \

Purge \

\

\ \

Eliminationof

Energyand

Nutrients

Stress aiSubstance

Abuse

36

that bulimic individuals who purge evidence obsessive-compulsive characteristics (Cooper & Fairburn, 1986; Hatsukami, Owen, Pyle, & Mitchell, 1982; Prather & Williamson, 1988; Scott & Baroffio, 1986; Williamson, Kelley, Davis, Ruggiero, & Blouin, 1985). Cooper and Fairburn (1986) found that 80 percent of their bulimic sample endorsed items on the Present State Examination indicative of obsessional ideas and ruminations. Obsessional ideas and ruminations contributed most to the discrimination of bulimia nervosa subjects from depressives (Cooper & Fairburn, 1986). Williamson et al. (1985) reported that bulimics differed significantly from a normal control group on the MMPI clinical scale number seven (Psychasthenia) which is associated with obsessive thinking and anxiety. Prather and Williamson (1988) found that 62 percent of bulimia nervosa subjects obtained clinically elevated scores (T-score equal to or greater than 70) on MMPI scale seven or Psychasthenia.

In summary, although obsessive-compulsive patients may also evidence symptoms of depression few depressives show obsessive-compulsive symptoms. In

37

comparison, several studies have documented that bulimia nervosa subjects experience obsessive- compulsive characteristics. From these data, it could be expected that bulimic patients but not depressives would frequently endorse obsessive-compulsive symptoms.

Anxiety. Anxiety symptoms may accompany depressive disorders although anxiety disorders are less commonly accompanied by depression (Lehmann,1983). A 58 percent incidence rate of anxiety symptoms in a group of depressed patients was reported by Leckman, Weissman, Merikangas, Pauls, and Prusoff (1983). They also concluded that depressed patients feeling anxiety symptoms had early onset and severe depression (Leckman et al., 1983). Cooper and Fairburn (1986) found that within their depressed group 60 percent endorsed general anxiety while 37.5 percent endorsed situational anxiety.

High levels of anxiety have been reported in bulimic samples (Cooper & Fairburn, 1986; Fairburn & Cooper, 1982; Pyle, Mitchell, & Eckert, 1981; Williamson et al., 1985). Some researchers have

38

proposed that the cycle of binging and self-induced vomiting may be directly linked to anxiety (Leitenberg, Gross, Peterson, Janis, & Rosen, 1984; Rosen & Leitenberg, 1982). Others have associated anxiety with the anticipated lack of control experienced by bulimics (Palmer, 1979; Rau & Green, 1975). Cooper and Fairburn (1986) reported that 48.6 percent of bulimia nervosa subjects endorsed generalized anxiety items and 71.4 percent endorsed situational anxiety items on the Present State Examination. Williamson et a l . (1985) reported significantly more severe scores for bulimic subjects than normal controls on the anxiety scale of the Symptom Checklist 90-Revised. Using behavioral observation procedures Rosen and Leitenberg (1982) and Leitenberg et al. (1984) found that bulimics reported increased subjective anxiety following eating a large test meal which they were kept from purging. Several studies utilizing psychophysiological recording have reported increased heart rate in bulimics after eating (Janata, Klonoff, & Ginsberg, 1985; Leitenberg et a l ., 1984; Jarrell, Johnson, & Williamson, 1986;Williamson, Goreczny, Davis, Ruggiero, & McKenzie,

39

1988). Two studies also reported a reduction heart rate immediately following purging a test meal (Janata et a l ., 1985; Jarrell et al. , 1986). In a controlled study by Williamson et al. (1988) bulimics responded to eating with an immediate increase in heart rate, whereas the heart rate of normals decreased after eating. Thus, studies using subjective, behavioral, and psychophysiological measures consistently support the role of anxiety in bulimia nervosa. This anxiety is clearly associated with eating but may also be more generalized.

Current research has suggested that bulimic subjects experience more situational anxiety, while depressed subjects report more generalized anxiety.The unanswered question was, how do bulimics with depression differ on situational and general anxiety symptoms from bulimics without depression and depressive patients without bulimia nervosa?

In summary, no past study of the affective variant hypothesis has controlled for depression in bulimia nervosa. It is unknown how bulimics with depression differ from bulimics without depression. In addition.

40

it is not known how these two eating disordered groups differ in cognitive style, behavioral style, or somatic signs from depressives or normal subjects. Comparison of research on bulimia nervosa and research on depression suggests that bulimia nervosa subjects may exhibit more obsessive and situational anxiety characteristics than do both depressives and normals and more general anxiety than normals.Summary

Bulimia nervosa is frequently accompanied by depressive symptoms which are often pervasive and severe. This association has led some researchers to hypothesize that bulimia nervosa is a variant of affective disorders. The only study comparing bulimics to depressives found that bulimics reported a different pattern of symptoms than the depressive patients (Cooper & Fairburn, 1986). The bulimic sample was found' to be more anxious and obsessive and less depressed than were the depressives.

The purpose of this study was to further examine the affective variant hypothesis expanding upon the findings of Cooper and Fairburn (1986) using specific measures of depression, anxiety, and obsessions-

41

compulsions. The main goal was to compare bulimia nervosa patients with and without depression, depression patients without eating disorders, and normal control subjects on cognitive, behavioral, and somatic variables. These patients were compared on cognitive dysfunction, behavioral activity and anhedonia, somatic signs of depression, general and situational anxiety, and obsessive-compulsive symptoms in an attempt to identify variables other than eating and purging behaviors that could define the relationship between bulimia nervosa and depression.

Two main questions were addressed. First, would there be an interaction effect of bulimia nervosa and depression? Would bulimics with depression be more disturbed than nondepressed bulimia nervosa patients as reflected by scores on specific measures of different dimensions of depression? If the affective variant hypothesis was valid then these patients should not be disparate. It was hypothesized that bulimia nervosa patients without depression would be less disturbed than bulimia nervosa patients with depression who would be more disturbed than depressed

42

patients on cognitive, somatic, and behavioral aspects of depression.

Second, would there be a main effect of bulimia nervosa, main effect of depression, and/or an interaction effect of bulimia nervosa and depression on the measures of anxiety and obsessiveness? The second hypothesis proposed in this study was that there would be a main effect of bulimia nervosa but no main effect of depression or interaction effect of bulimia nervosa and depression. Nondepressed and depressed bulimics were predicted to endorse more anxiety and obsessiveness than depressives but not differ from each other. If the anxiety model of bulimia nervosa, which is analogous to an anxiety model of obsessive-compulsive disorder, was cogent bulimia nervosa patients with and without depression would not differ from each other on measures of anxiety and obsessive-compulsiveness.

MethodResearch Participants

Clinical subjects were recruited from patients presenting for evaluation and treatment during the 1987-88 year at three fee-for-services outpatient clinics and two inpatient hospitals. These treatment centers served both student and nonstudent patients. Normal subjects were recruited through publicity from undergraduate psychology classes and from the community.

Included in the clinical sample were seventeen patients diagnosed with bulimia nervosa without depression, 18 patients diagnosed with bulimia nervosa and depression, and seventeen patients diagnosed with depression without eating disorders using DSM-IIIRcriteria for bulimia nervosa, major depression, and dysthymia. The bulimia nervosa with depression group was comprised of 15 patients with major depression and three patients with dysthymia. The depression without eating disorders group included 11 patients with major depression and six patients with dysthymia. The normal control group consisted of 20 subjects who reported no depression or eating disorder problems.

The 72 subjects were all Caucasian. Using

43

44

Kruskal-Wal1 is nonparametric test of homogeneity ofdemographic variables, it was determined that the fourgroups were from the same population. Chi squareanalysis confirmed the groups were comparable indistribution of gender and marital status (see Table7). The distribution of educational status was also

2similar across groups, "X (.05, 3) = 0.59, p > .05). Analysis of variance (ANOVA) verified the similarity of groups on the variables of age, height, and weight. Comparing the clinical groups there were no differences in either distribution of outpatient and inpatient or medication status across the groups. Comparing the depression groups there were no significant differences in distribution of major depression or dysthymia. To ensure that the clinical groups did not differ in severity of either depression or bulimia nervosa they were compared on the respective scores on the BDI and BULIT. The depressed bulimics and the noneating disordered depressed subjects did not differ on the BDI. The nondepressed bulimics were more depressed than the normals, however. The nondepressed and depressed bulimics did not differ on the BULIT. Complete demographic statistics can be reviewed in Table 7.

45

Table 7. Group Demographics

Variables Group Means F £BN(Y) BN (Y) BN(N) BN(N)D (N) D (Y) D (Y) D (N)

Age 21.7 26.4 29.2 23.2 2.75 NSHeight 65.3 64.8 66.3 65.8 0.66 NSWeight 134.4 141.4 143. 1 143.7 0.33 NS

a b b cBDI 10.0 31 . 9 27.8 3.0 75.29 <.0001

a a b bBULIT 116.6 125.7 56.9 49.5 128.61 < .0001

Group Distributions Chi-Sq. d

n n n nGenderMale 2 1 3 2 1.38 NSFema1e 15 17 14 18

MaritalMarried 3 7 8 4 4.81 NSSingle 14 11 9 16

OutpatientYes 16 14 14 NA 1.23 NSNO 1 4 3 NA

MedicationYes 2 8 7 NA 3.28 NSNO 15 10 10 NA

DepressionMajor Dep. NA 15 11 NA 2.27 NSDysthymia NA 3 6 NA

BN(Y)=BulImia Nervosa, BN(N)=No Bulimia Nervosa,D(Y)=Depression, D(N)=No Depression.

Groups with different superscripts are significant at £ < .05.

46

Assessment InstrumentsDemographic data was collected from each subject

using a questionnaire developed from the first two pages of the Diagnostic Survey of Eating Disorders (Johnson, 1985). Race, age, gender, height, weight, marital and educational status information was reported on the Demographic Questionnaire (see Appendix A ) .

The Diagnostic Interview for Bulimia Nervosa (DIBN), developed from Johnson’s (1985) Diagnostic Survey of Eating Disorders, was used as a structured interview to elicit information following the DSM-IIIR criteria for a diagnosis of bulimia nervosa. Areas of information covered during this interview were weight history, weight and body shape concerns, dieting behavior, binge eating behavior, feelings of control while binging, purging behaviors, and exercise habits (see Appendix B ) .

The Bulimia Test (BULIT) designed by Smith and Thelen (1984) is a 32-item questionnaire which assesses abnormal eating attitudes and behaviors associated with bulimia (see Appendix C). Temporal stability was reported as r = .54, p<.0001. Smith and Thelen (1984) recommended using the research cut-off

47

score of 102 to reduce false positives, but that a score above 88 warrants clinical attention. Scores obtained on the BULIT were used for inclusion/exclusion criteria in this study. Normal control subjects had to score below 88 to be included while clinical subjects meeting the DSM-IIIR diagnostic criteria for bulimia nervosa had to also receive a score of 102 or above to be included.

The Schedule for Affective Disorders and Schizophrenia (SADS) developed by Endicott and Spitzer (1978) provide distinctive guidelines for interviewing patients to establish the presence of depressive symptoms and signs. Also available is a subtype of the SADS (see Appendix D) using questions that elicit information concerning signs and symptoms of major depression and dysthymia according to DSM-IIIR criteria (Leber, Beckham, &. Danker-Brown, 1985) . The SADS depression Scale has been demonstrated to have high inter-rater reliability (r = .95 or higher) and high internal consistency (r = .95 or higher). Concurrent validity for a diagnosis of depression has also been demonstrated (Endicott & Spitzer, 1978).The SADS, DSM-III Subtype, was used to determine the diagnosis of major depression or dysthymia.

48

Scores obtained on the Beck Depression Inventory (BDI) were used as an inclusion/exclusion criterion for subjects diagnosed as depressed. Depressed subjects had to obtain a score of 20 or above to remain in the study. Normal control subjects had to score below 11 on the BDI. The BDI is a standardized 21-item self-report questionnaire or interview measure which taps cognitive symptoms, somatic signs, and behavioral signs associated with clinical depression (see Appendix E). A score of 20 or above has been recommended for research inclusion (Beck, 1978; Beck, Ward, Mendelson, Mock, &. Erbaugh, 1961). A score above 10 has been considered clinically significant (Beck, 1978). Test-retest reliability has been reported to range from r = .69 to .90 (Gallagher,Nies, & Thompson, 1982; Strober, Green, & Carlson.1981). Numerous studies of concurrent validity have demonstrated the BDI to have moderate to good validity (Shaw, Vallis, & McCabe, 1985).

The Center for Epidemiological Studies Depression Scale (CES-D) developed by Radioff (1977) is a self- report measure designed to provide an index of the number and frequency of depressive signs and symptoms (Orme, Reis, & Herz, 1986). The CES-D can be reviewed

49

in Appendix F. The CES-D has been found to have good internal consistency across diverse population subgroups as well as good test-retest stability (Aneshensel, Clark, & Frerichs, 1983; Fava, 1983; Radloff, 1977; Roberts, 1980; Ross & Mirowsky, 1984). The CES-D differentiates between those in treatment and those not in treatment for depression (Orme et al., 1986). Factor analysis of the CES-D resulted in four subscales related to depression, (a) depressed affect, (b) positive affect, (c) somatic signs, and (d) interpersonal difficulty (Radloff, 1977). The Somatic subscale (CESD-SC) was used to measure whether differences existed in somatic signs of depression among the four groups.

The Dysfunctional Attitude Scale (DAS) was developed by Weissman and Beck (1978) to assess cognitive dysfunction centering around general irrational themes in thinking and negative thoughts (see Appendix G). The DAS has been shown to have good internal consistency (Weissman, 1979) and stability over time (Hamilton & Abramson, 1983; O'Hara, Rehm, & Campbell, 1982; Riskind, Beck, &. Smucker, 1983). Construct validity was demonstrated by use of the DAS with both clinical and nonclinical populations (Eaves

50

& Rush, 1984; Hamilton & Abramson, 1983). Concurrent validity has been demonstrated in several studies (Dobson & Breiter, 1983; Riskind et al., 1983;Weissman & Beck, 1978). Differences in cognitive dysfunction among the groups were assessed using DAS.

MacPhillamy and Lewinsohn (1972) designed the Pleasant Events Schedule (PES) to assess self-reported frequency and enjoyment of engaging in common positive, reinforcing activities (see Appendix H ) . It was their contention that depressed individuals engage in fewer activities and experience less pleasure from activities. The psychometric properties of the PES reported by MacPhillamy and Lewinsohn (1972, 1974,1982) were quite good. Test-retest reliability ranged from .69 to .88 for one-month test-retest. Validity studies reported satisfactory concurrent and predictive validity, and several studies also demonstrated construct validity showing significant correlations between mood and engagement in pleasant events (Hammen & Krantz, 1985). The PES was used to compare groups on both frequency (PES-F) and pleasantness (PES-P) of activities.

The State-Trait Anxiety Inventory (STAI) consists of two twenty-item self-report scales (see Appendix I)

51

which assess general anxiety proneness (trait anxiety) and current tension and apprehension or state anxiety (Spielberger, Gorsuch, & Lushene, 1970). Adequate validity has been demonstrated as has satisfactory reliability (Spielberger. 1983). The STAI scores were included to compare situational (STAI-S) and general (STAI-T) anxiety symptoms across groups.

Hodgson and Rachman (1977) developed the Mauds 1ev Obsessive-Compulsive Inventory (MOCI) to assess both general and specific obsessive-compulsive symptoms (see Appendix J ) . The MOCI yields an overall obsessive-compulsive score plus five subscores of checking, cleaning, slowness, doubting­conscientiousness, and ruminations. The MOCI total score has been found to have adequate reliability and validity, and two of the subscales (checking and cleaning) have been validated (Rachman & Hodgson,1980). The MOCI total score was used to compare groups on obsessive—compulsivness.Procedure

All subjects were given an informed consent form to read and sign before participating in this study (Appendix K ) . All patients and control subjects were informed that they could decline participation at any

52

point without penalty.Subjects were interviewed for diagnostic purposes

using the structured interview for diagnosing bulimia nervosa (DIBN) and diagnosing depression (SADS).Height and weight was measured for all subjects and the Demographic Questionnaire, BDI, and BULIT were administered. A diagnosis of bulimia nervosa with or without depression and depression without eating disorders was made during staffing supervised by licensed psychologists with extensive experience in both eating disorders and depressive disorders. Subjects meeting all inclusion criteria then completed a battery of instruments which included the DAS, PES- F, PES-P, CESD-SC, STAI-S, STAI-T, and MOCI.

Normal control subjects were interviewed and administered the BDI and BULIT. To qualify the control subjects had to score below 88 on the BULIT and below 10 on the BDI. Those subjects not endorsing either bulimia nervosa or depressive signs and symptoms during the interview or on the BDI and BULIT were then measured for height and weight and administered the Demographic Questionnaire, DAS, PES- F, PES-P, CESD-SC, STAI-S, STAI-T, and MOCI.

Results

Group Comparisons

A 2 X 2 between—subjects multivariate analysis ofvariance (MANOVA) was calculated on the sevendependent variables: PES-F, PES-P, STAI-S, STAI-T,MOCI, CESD-SC, and DAS. Independent variables werebulimia nervosa (yes and no) and depression (yes andno). Results of the multivariate test for homogeneityof variance-covariance revealed statistically similarvariance-covariance matrices. Box's M = 12.83, p >.05.Total number of subjects included was 72. The MANOVAwas followed by 2 X 2 factorial analyses of variance(ANOVA), and significant ANOVAs were subjected to theScheffe' post hoc comparison test. The strength ofeach effect was tested using canonical correlationalanalyses (r ). To further describe these patients,

cANOVAs of group effects was also conducted. Summaries of the results are presented in Table 8 and Table 9.

Using Wilks' criterion, the 2 X 2 MANOVA resulted in significant main effects for both bulimia [F(7,62)= 8.25, p. < .0001] and depression (F(7,62) = 22.80, p < .0001]. There was a significant main effect of bulimia nervosa on all measures except the PES-F and CESD-SC. The results reflected a relatively strong

53

54

association between bulimia nervoea and the combineddependent variables, r - .69.

cThe main effect for depression, [F(7,62) = 22.80,

p < .0001], resulted in a significant effect on fiveof the seven measures. The association was quitesubstantial between depression and the dependentvariables, r = . 85. There was no main effect of

cdepression on the PES-F or PES-P. The summary of maineffects is presented in Table 8.

There was a significant interaction betweenbulimia nervosa and depression [F(7,62) = 3.07, jo< .01] on two dependent variables (see Table 8). TheSTAI-T and PES-P were found to be high for all threeclinical groups. These two measures were low only inthe nondepressed subjects that were also not bulimic.The addition of depression to bulimia had asignificant effect on scores obtained by the clinicalpatients on the STAI-T and PES-P. The associationbetween the interaction of the independent variablesand the dependent variables was moderate, r = .51.

cAnalyses of variance (ANOVAs) investigating the

combined effects of bulimia nervosa and depression yielded significant group effects for six of the seven variables. Only PES-F was not significant. A

55

Table 8. TESTS OF BULIMIA, DEPRESSION, AND THEIR INTERACTION

IV DV1

UnivariateF P

Buiimla CESD-SC 0.50 NSSTAI-T 34.08 .0001STAI-S 4.60 .0360DAS 22.55 .0001MOCI 5.78 .0190PES-P 6. 16 .0260PES-F 0.39 NS

Depression CESD-SC 116.56 .0001STAI-T 49.58 .0001STAI-S 74.92 .0001DAS 36.83 .0001MOCI 19.80 .0001PES-P 3.52 NSPES-F 3.57 NS

Buiimla by

Depression CESD-SC 0. 18 NSSTAI-T 15.75 .0001STAI-S 2.33 NSDAS 2.12 NSMOCI 0.10 NSPES-P 4.15 .0460PES-F 2.18 NS

1Degrees of freedom for all ANOVAswas (1,68) .

56

complete summary of these analyses Is presented in Table 9. The Scheffe post hoc test revealed that four measures (CESD-SC, STAI-S, DAS, and MOCI) distinguished between the two bulimia nervosa groups (depressed and nondepressed). The depressed bulimics obtained more severe scores than did the nondepressed bulimics suggesting that the former is more obsessive, more situationally anxious, experiencing more somatic signs of depression and cognitive dysfunction. Two measures differentiated the nondepressed bulimics and the depressed group. The depressed patients (without bulimia nervosa) received higher scores on the CESD-SC and STAI-S. The nondepressed bulimic patients endorsed more symptoms than the normals on three measures including the STAI-T, DAS, and PES-P. The depressed bulimia nervosa and depressed groups did not differ statistically on any dependent variable. The depressed bulimics scored higher than the normals on all six of the significant measures, while the depressed group scored higher than the normals on four of the six measures (CESD-SC, STAI-S, STAI-T, and DAS). These results suggest that the depressed bulimia nervosa patients were the most disturbed group.

57

Table 9. Summary of Combined Effects of Bulimia1

Nervosa and Depression

Group Means and Standard Deviations 3 4

BN BN+D D NC FMeasure

CES-D,SCa

2.9(2.4)

b9.1(2.7)

b8.9(3.3)

a2.2(1.6)

39.6 <.0001

STAI-Ta

65.8(5.4)

a72.2(6.9)

a68.3(8.3)

b45. 1 (12.5)

35.7 < .0001

STAI-Sa

53.4(8.2)

b69.8(7.5)

b68.3(9.4)

a44.9(12.6)

28.3 <.0001

DASa

140.4(24.3)

b170.6(25.8)

a,149 .1 (27.5)

b c 99.8 (31.9)

21.9 < .0001

PES-Pa

330 .4 (74.0)

a333.6(99.1)

a , b b 338.1 414.2 (99.3) (50.3)

4.6 < .005

PES-F 233.4(56.3)

227.7(73.0)

209.8(65.6)

256 .8 (37.8)

2.0 NS

MOCIa

8.7(4.1)

b14.3(6.6)

a.11.1 (5.3)

b a 6.3 (3.5)

9.0 <.0001

1 MANOVA F(21.179)=9.26, pC.OOOl.2 Standard Deviations are presented in parentheses.

Means with different superscripts differ significantly (g < .05).

3 BN=Bulimia Nervosa, BN+D=Bulimia Nervosa with Depression, D=Depression, NC=Normal Control.

4 Degrees of freedom for all ANOVAs was (3,68).

58

Correlational and Multiple Regression Analyses.The results of the 2 X 2 Factorial MANOVA yielded

strong main effects for both bulimia nervosa and depression, however, the interaction effect suggested that the combination of the independent variables had only an additive rather than a multiplicative effect on the dependent variables across the clinical subjects. Correlational analyses were computed among the seven variables and the BDI and BULIT to determine patterns of association among the seven measures of secondary psychopathology and measures of primary psychopathology of depression or bulimia nervosa (see Table 10). Stepwise multiple regression analyses were used to determine the variables most highly associated with either depression or bulimia nervosa (see Table 11 and Table 12). Both correlational and stepwise multiple regression analyses were computed on bulimia nervosa subjects alone, depressed subjects alone, and total sample. These analyses were done to assess the association between level of severity of bulimia nervosa and depression and the measures of secondary psychopatho1ogy.

Bulimia nervosa. Correlational analysis including only bulimic subjects (both depressed and

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Table 10. Correlational Analyses

Psychopatho1ogy Primary Secondary

BULIT

Groups

BDI

Buiimic Depressed All(n-35) (n-35) (n-72)

STAI-T NS NS .53*DAS NS NS .48*BDI NS NS .34*STAI-S NS NS .31*CESD-SC NS NS NSMOCI NS NS NSPES-P NS NS NSPES-F NS NS NSCESD-SC .75* NS .77*STAI-S .77* NS .75*DAS .58* .41* .65*STAI-T .51* NS .64*MOCI .46* NS .51*BULIT NS NS .34*PES-P NS NS .31*PES-F NS NS NS

NS = No significant correlation.* Correlations listed differ significantly at £ <.01.

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nondepressed) resulted in no significant associations between the BULIT and the seven dependent variables. There were several significant positive correlations between the BDI and secondary measures. The STAI-S, CESD-SC, DAS, STAI-T, and MOCI scores were significantly correlated with the BDI scores within the bulimic group (see Table 10).

Stepwise multiple regression analysis wasunsuccessful in producing any secondary measure thatwas significant in prediction of the primarypsychopathology (BULIT) in the bulimic groups (seeTable 11). Stepwise multiple regression analysispredicting BDI score for only the bulimic subjectsfound only two variables contributed significantly toprediction of the BDI score (see Table 12). TheSTAI-S and CESD-SC were significantly correlated withthe BDI scores and accounted for a large proportion of

2the variance (R = .69).

Depression. Correlational analysis including only the depressed subjects resulted in no significant correlations between the primary psychopathology of bulimia nervosa (BULIT) and the secondary variables. One significant correlation between the primary psychopathology of depression (BDI) and the DAS was

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Table 11. Stepwise Multiple Regression Analyses for BULIT

GroupsVariables in Equation Beta

2R p

Buiimic (n-35)

None

Depressed(n-35)

None

All(n-72)

STAI-T 0.53 .28 <.0001

Table 12. Stepwise Multiple Regression Analyses for BDI

Variables2

Groups in Equation Beta R pBulimic STAI-S 0.49(n-35) CESD-SC 0.43

.69 <.01Depressed DAS 0.34 .12 <.05(n-35)

All CESD-SC 0.48(n-72) STAI-S 0.44

.70 <.0001

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found.Stepwise multiple regression analysis correlating

BDI score for the depressed groups found one variableto be significantly correlated with level ofdepression. The DAS was found to be correlated with

2the BDI (R = .12). Stepwise multiple regressionanalysis found no associations between the BULIT andsecondary variables within the depressed subjects.

Total sample. There were several significantcorrelations between the BULIT and BDI and thesecondary variables when all subjects were included.The BULIT was found to correlate with the STAI-T, DASBDI, and STAI-S. Stepwise multiple regressionanalysis, however, showed the STAI-T to be the onlymeasure of secondary psychopathology to be associated

2with BULIT scores (R = .28). The BDI was found tocorrelate with all of the other measures except PES-FStepwise multiple regression analysis found the CESD-SC and STAI-S to account for the most variance in BDI

2scores (R = .57).

Finally, there was no significant correlation between the BULIT and the BDI within either the bulimia nervosa or the depression subjects. When the normal control subjects were included a significant

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correlation between these two measures of primary psychopathology was found.

DiscussionIt has been hypothesized that bulimia nervosa is a

form of affective disorder and that the two disorders share a common etiology (cf. Hudson et al. 1983). Although the research has not supported the hypothesis of common etiology, the fact remains that bulimia nervosa patients frequently report depressive signs and symptoms (cf. Mizes, 1985). Cooper and Fairburn(1986), however, found depressive symptoms in bulimia nervosa patients to be nonspecific and different than the symptom pattern of depressed patients (Cooper & Fairburn, 1986). In addition to finding differing patterns of depression between the bulimia nervosa and the depressed group. Cooper and Fairburn (1986) also found that bulimia nervosa patients evidenced higher levels of situational anxiety and obsessiveness, while depressives were more generally anxious. Their findings suggested a difference between bulimia nervosa and depression. However, it was not known how many of the bulimia nervosa patients also met criteria for depression. The question unanswered was how nondepressed and depressed bulimia nervosa patients compared to depressed patients on measures of depression, anxiety, and obsessiveness.

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65

This study was designed to address that question by testing the affects of bulimia nervosa and depression on various dimensions of depression, anxiety, and obsessive-compulsive characteristics. Dimensions of depression included in this investigation were somatic complaints, cognitive style, and behavioral style. Specific measures of state and trait anxiety and obsessive-compulsiveness were included.

The first hypothesis addressed the affective variant hypothesis. In this study it was proposed that bulimics without depression would be healthier than both depressed bulimics and non-eating-disordered depressives on various dimensions of depression. The second hypothesis supporting the anxiety model of bulimia nervosa stated that there would be a main effect of bulimia nervosa but no interaction effect of bulimia nervosa and depression on the anxiety measures. Nondepressed and depressed bulimics were predicted to not differ from each other but to achieve more severe scores than depressives on measures of anxiety.

Results suggested both bulimia nervosa and depression have strong main effects, but the

66

interaction of the two does not appear to have more than an additive affect upon the secondary psychopathology measured in this study. Depression was more clearly associated with these measures than was bulimia nervosa. Level of depression was highly associated with dysfunctional cognitions, somatic complaints, state anxiety, trait anxiety, and obsessiveness. Level of bulimia nervosa was not associated with any secondary measure.

Hypothesis One. The results of this investigation argue against the affective variant hypothesis. The proposition that depressed and nondepressed bulimia nervosa and depressed patients would be similar was not supported. The depressed bulimia patients were more disturbed than the nondepressed bulimics. In addition, there was no main effect of bulimia nervosa on somatic signs and frequency of activity, and there was no main effect of depression on either frequency of activity or pleasure rating of activities. Even though nondepressed bulimics did not evidence the somatic signs of depression they were not completely free from symptoms associated with depression (anhedonia and cognitive dysfunction). It should be kept in mind that the nondepressed bulimic subjects

67

did score higher than the normals on the BDI. It may be that even a very mild level of depression may affect the scores on these two variables, although there was no influence on somatic signs.

Cooper and Fairburn (1986) reported more pessimistic thinking in bulimia nervosa patients than depressed patients. In this study, although cognitive dysfunction occurred in both depressed and nondepressed bulimics, the dysfunction was associated only with depression. The dysfunction of the depressed bulimic was significantly more severe than nondepressed bulimics. Cooper and Fairburn (1986) found that their depressed group endorsed more somatic signs of depression than did the bulimics. The current study confirmed and expanded upon that finding; somatic complaints were associated only with depression and not bulimia nervosa.

Results related to hypothesis one have relevant assessment implications. Although incidence reports of affective disorder in bulimia nervosa have averaged around 50 percent (Lee, Rush, & Mitchell, 1985), Katz(1987) has questioned whether depression may be missed in the remaining bulimia nervosa patients. The findings in this study argue against that explanation.

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Bulimia nervosa patients not diagnosed with affective disorder were different from both the depressed bulimia nervosa and the depressed patients. The bulimia nervosa group was generally less disturbed than either the depressed bulimia nervosa group or the depressed group.

In contrast to Katz's (1987) questioning whether a diagnosis of depression is being overlooked, Altshuler and Weiner (1985) questioned whether those bulimia nervosa patients diagnosed with affective disorder actually had a depressive disorder. These authors stated that core sign and symptom of somatic difficulties and anhedonia are typically not present in "depressed" bulimia nervosa patients. Because the depressed bulimics in this study achieved a score similar to depressives on the somatic scale of the CES-D suggests the presence of these somatic difficulties. Anhedonia measured by the PES-P was similar across both bulimic groups and the depressed group indicating that not only is anhedonia a problem for depressed bulimics but also for nondepressed bulimics. More research investigating the relationship between bulimia and anhedonia is needed.

Hypothesis Two. The second proposition of this

69

investigation stated there would be a main effect of bulimia nervosa on the anxiety measures. That is, the nondepressed bulimics and depressed bulimics would not differ from each other but differ from depressives on anxiety and obsessive-compulsive variables. Following from the anxiety model of bulimia nervosa, bulimic patients were believed to be more anxious and obsessive than depressives. This hypothesis was not supported. There was a main effect of bulimia nervosa on these measures, however there was also a main effect of depression. The interaction effect suggested that the addition of depression to bulimia did not statistically affect the scores of bulimics on any of the anxiety measures beyond that achieved by depression alone. Trait anxiety was similar across the clinical patients and was low only in the normal subjects. Nondepressed bulimics shared only trait anxiety with depressed bulimics, and the depressed bulimics did not differ from the depressives on any of the measures. The results of this study differ from Cooper and Fairburn’s (1986) findings. Those authors found bulimics to be more obsessive and situationally anxious than depressives. The current study found that only depression correlated with state anxiety and

70

obsessiveness.Researchers have consistently confirmed the

presence of anxiety and obsessiveness resulting from food and weight related situations in bulimic patients (Barrios & Pennebaker, 1982; Cooper & Fairburn, 1986; Janata et al., 1985; Leitenberg et al., 1984; Jarrell et al., 1986; Rosen & Leitenberg, 1982; Williamson et al., 1988). Investigations of nonfood and nonweight anxiety and obsessiveness have been less convincing. Johnson, Stuckey, Lewis, and Schwartz (1983) found that bulimics did not differ from normals on anxiety and obsessive-compulsive subscales of the Hopkins’ Symptom Checklist. Others have found that bulimics scored higher than normals on the Psychasthenia scale (Scale 7) of the MMPI (Prather &. Williamson, 1988; Scott & Barrofio, 1986; Williamson et al., 1985). Cooper and Fairburn (1986) measured obsessiveness and anxiety as either situational or general. They found situational anxiety and obsessiveness but not general anxiety in bulimics. None of these studies controlled for depression status. The current study found trait anxiety in bulimics regardless of depression while state anxiety and obsessiveness were problematic only in depressed bulimics.

71

Although there has been consistent empirical support for the anxiety model in relationship to eating disorder signs and symptoms, the results from this study suggest that the model may not generalize to nonfood areas. Noneating related anxiety and obsessiveness appear to be related to depression.

A recent study (Burrows, Ribordy, & Johnson, 1989) found that bulimic individuals were accurate when defining their emotional states. Thus, we have confidence that our patients were able to discriminate and apply the dimensions measured in this investigation. Burrows et a l . (1989) also found that bulimic patients were deficient in coping with their emotions and this deficiency was related to depression. The results of the present study combined with Burrows et a l . (1989) and other research suggestthat depression may seriously affect the secondary psychopathology as well as reduce coping abilities of bulimia nervosa patients.

It appears that bulimia nervosa has less association with secondary psychopathology than does depression. The two bulimic groups shared similarities in symptoms of general anxiety and anhedonia. Anhedonia and general anxiety were the

72

only measures that were Independent of clinical depression status in bulimia nervosa patients suggesting that the dual diagnosis of depression with bulimia nervosa had no affect on these two symptoms for the nondepressed bulimia nervosa patients.Although nondepressed bulimics evidenced moderate cognitive dysfunction, the depressed bulimics' dysfunction was significantly more severe.

Differences in signs and symptoms across these groups argue against the hypothesis of a unitary affective or anxiety disorder underlying bulimia nervosa. Instead, these data suggest that nondepressed bulimia nervosa patients experience some of the same problems reported by depressed or anxiety patients, (i.e., trait anxiety, anhedonia, and cognitive dysfunction). They did not, however, report other problems common to depression or anxiety, (i.e., somatic complaints, state anxiety, obsessiveness).

Treatment implications. The combined results from both hypothesis one and hypothesis two may help explain some of the current inconsistencies in the bulimia nervosa treatment outcome research. The literature is inconclusive concerning the effectiveness of frequently used treatment components.

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The debate includes three basic treatment modalities which include (1) antidepressant medication (cf. Hudson, Pope, & Jonas (1986), (2) exposure with response prevention (cf. Wilson, Rossiter, Kleifeld, &. Lindholm, 1986), and (3) cognitive-behavioral (cf. Agras, Schneider, Arnow, Raeburn, & Telch, 1989). Although studies vary in their outcomes, reports of patients remaining abstinent from purging activity at six-month follow-up range from 20 to 60 percent. The most frequent abstinent rate reported has been around 40 percent (Freeman, Barry, Dunkeld-Turnbul1, & Henderson, 1988; Kirkley et a l ., 1985; Pope et al., 1983; White & Boskind-White, 1981). When comparing treatment outcome of E/RP, cognitive-behavioral, and antidepressants it is uncertain which program has been most effective.

What is not clear from any of the treatment outcome studies are the patient characteristics associated with improvement following interventions using different treatment components. From the results of this study it could be postulated that the depression status of the patient could have affected the outcome of treatment studies.

The results of the current study suggest that

74

there may be a subgroup of bulimia nervosa patients that are clinically depressed and might benefit from antidepressant medications plus E/RP and cognitive- behavioral treatment that is both specific to eating/weight related problem areas and noneating/nonweight problem areas. In this study, bulimia nervosa patients with depression were clearly different from patients that were not depressed. Failure to address these differences in treatment could help explain the high relapse rate (approximately 60 to 70 percent) in bulimia nervosa patients.

Research has suggested that depressed patients continue to improve following therapy, while bulimia nervosa patients tend to relapse. Keller, Herzog, Lavori, Bridges, Ott, and Klerman (1986) reported a 35 percent recovery rate at six months for bulimic patients compared to 64 percent at six months for depressed patients. The probability of full recovery from unipolar depression has been reported to range from 42 percent at three months to 79 percent at two years (Keller, 1985). Of particular interest is that out of the 60 percent of bulimic patients also classified with depression only one patient had

75

recovered from both disorders at six months follow-up (Keller et al., 1986). This low recovery rate may be explained by the results of this study. The dual diagnosed patients in this study were found to be more disturbed than nondepressed bulimics. It may not only be useful to design more comprehensive treatment of the depressed bulimia nervosa patient, but also to design interventions of longer duration to overcome both bulimia nervosa and depression.Future Directions

Since this was the first study to compare nondepressed and depressed bulimia nervosa patients, these findings need to be replicated and extended.

Differences in the symptom profiles of bulimia nervosa patients in this study and the symptom profiles presented by Cooper and Fairburn (1986) could be explained by hypotheses independent of the presence or absence of depression in bulimia nervosa. First, different methods were used; the former authors used a structured interview format to establish the presence/absence and severity of symptoms. Secondly, since different measures were used, it is possible that variations of similar dimensions rather than the same dimensions (e.g., pessimistic thought versus

76

dysfunctional cognitions) were actually measured. Lastly, duration of the disorder was not controlled in either study. Perhaps depressed bulimia nervosa patients develop depression due to the chronic, cyclic nature of the eating disorder. Directionality is also an issue. These patients could also develop depression due to the situational anxiety and obsessiveness they experience or develop situational anxiety and obsessiveness due to the depression they experience.

These data suggest that research continue to address the development of depression in bulimia nervosa as well as treatment for bulimia nervosa patients with and without clinical depression. Unanswered questions are whether (a) treating situational anxiety, obsessions, and cognitive dysfunction associated with and independent of eating situations in the depressed bulimia nervosa patients and (b) treating both eating and noneating related general anxiety in all bulimia nervosa patients will increase the improvement rate.

Another area for further investigation is cognitive dysfunction. There has been an abundance of clinical observation and anecdotal information

77

suggesting that bulimics suffer from maladaptive cognitions. The presence of dysfunctional cognitions related to eating disorder symptoms in bulimia nervosa patients has been supported (Scanlon, Ollendick, & Bayer, 1986), however, more general cognitive dysfunction in bulimia has yet to be empirically validated. In a recent review of cognitions and bulimia ReynaMcGlone and Ollendick (1989) suggested several questions that need to be addressed: (1) dobulimics evidence cognitive errors, (2) if yes, to what extent, (3) are they exclusive to weight related concerns (4) if not, what are the other areas, and (5) are they distinguishable from depressives and normals?

The results from this study help answer some of those questions. First, bulimics obtained scores on the DAS indicative of clinical levels of cognitive dysfunction. Second, dysfunction appears to be mild to moderate unless the bulimic is also clinically depressed. The third and fourth questions asked by ReynaMcGlone and Ollendick (1989) can only be partially addressed by these results. Although the cognitive dysfunctions do not appear to be only related to weight concerns, it is unclear whether the depressed bulimics were experiencing different

78

dysfunctions, more dysfunctions at similar severity levels, or similar dysfunctions at higher severity levels. Lastly, scores on the DAS suggest that bulimics are distinguishable from normal subjects but not from depressed patients. It is evident from these results that further research into the cognitive dysfunction of the bulimia nervosa population is needed to clarify the relationship between bulimia, depression, and cognitive dysfunction.Summary

The data from this study support previous research arguing against the affective variant hypothesis. Nondepressed and depressed bulimia nervosa patients achieved different symptom profiles. The results of this study also expanded upon the anxiety model. Nondepressed bulimics and depressed bulimics also reported different anxiety symptom profiles. In addition to different profiles on both depression and anxiety measures, bulimics who were clinically depressed were more disturbed than bulimics who were not diagnosed with depressive disorder. Depression clearly was the important variable affecting the dependent measures. There were several correlations between depression and secondary psychopathology but

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no correlation between bulimia nervosa and secondary psychopatho1ogy.

These results call for further research investigating the development of depression in bulimia nervosa. Another important area needing further research is the cognitive dysfunction associated with bulimia nervosa. It is also suggested that research investigating treatment outcome report the relationship between outcome and the depression status of the bulimia nervosa patient. It may be that choices of treatment for bulimia nervosa patients are dependent upon whether they are also clinically depressed. Standard treatments for eating disordered patients may be acceptable for the nondepressed bulimic, however, the depressed bulimic may require the addition of other treatment components and longer treatment duration.

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APPENDICES A through L

Assessment Measures

104

Appendix A Demographic Questionnaire

106

I d e n t i f y i n g a n d D e m o g r a p h i c I n f o r m a t i o n

Sea M « l( O female (_J

A|« ____Race (C hech o ne )

W hite a o i « k O o i i m (S p e c ify ) G

M a ilta l S latua (C hech one )

P ic ie n H y In l i n t m a r r ia g e

D iv o rc e d a n d p « K n i l f t e m e r r le d

D iv o rc e d 01 te p a ra ic d a n d n o t p r c t c n t l y re m a r r ie d

W idow ed and f t f i r n l l f f fo ra r r le d

W id o w e d a n d n o t p t e t e n t ly r e m a r r ie d

M ( * t i m a u le d

W hat I t yo u r p ic K n t p i im n jr t o l c ! (C h e c k o n e )

W i( « e a rn e r LJ l l v u i c w i l c LI) S ty d c r r l LI) •

l l i g h c t t O c c u p a t io n a l le v e l a t t a in e d

Higher eaecu llve . p to p t ic lo t o f la rge c o n c e rn .

M a jo r p ro fe r iin n a l

D u jin e ii manager o f Ii« ;c c o n c e rn .p to p fie lo t o f

m edium tile d b u iln c it .Ic ttc t p t b l t t i io n i l

A d m i f l l i l i i lU f p c ttu n n e l. o w n e r o f i t t t a l l In d e p e n d e n t

b u i in c t t . m ln o f p to fe i t iu n a l . o w n e r o f la rge fa in t

C le rica l or t a l ( t « u i l « , te c h n ic ia n , o w n c t o f l i t t le

b u i in c t t .o w n e r o l m e d ium t i r e d fa tn t

S h ille d m anua l e m p loye e , o w n c t o f em a il b u t ln c i t

M ach ine o p e ra to r, tc m ltk l l lc d e m p lo y e e , te n a n t

fa im c t who o » n t l i t t le e q u ip m e n t

U n th ll lc d e m p loye e , th a rc to p p c i

Doe I n o t a pp ly (N e *e t w o rk e d In p a id e m p lo y m e n t)

D u e t n o t a pp ly (N o ip o u a c |

In fo rm a tio n n o t available

aaaaaa

O th e r ( S p e c i f y ) U

C h e c k o n e f o r e a ch p e r m oStir r.u.«. Muttxi S|t|l»Ka a a □a a □ a□ a □ □□ □ □ □□ a □ a□ □ □ a□ o □ oa a a □a a a a□ □ □ □

107

C u i ic r t f l iW n | a < «angcn«cn l ( C h e c k o t ic )

W ith P a te n ts o t

1k * tm o«SIu k J i p u lm t t i l w ill* F i l tn d

f « * * i j * * ( t t ( |< H l i i * * l r i ( U l i i t n * l i i | i w i l l * to ie « ill«e t| K t i o n , in c lu d in g t p u u w , I m y l t l e o d . e tc . )

A lo n e

l l i g h e i t le v e l o f e d u c a t io n

C o m p le te d p m l - | i i < J u i ( ( n a m in g

S o m e p o t l - g i a d u a te n a m in g

C o m p le te d c o l le g e , e c c e iv e d l o u i y e a r

a c a d e m ic d e g tc c

A t te n d e d c o l le g e . I m l d id n ’ t te c e iv e

f o u i y e n a c a d e m ic d e g tc c

C o m p le te d h ig h s c h o o l ; m a y ha ve

a t te n d e d o t c o m p le te d l u d c s c h o o l a t o t l i e t n a n -a c a d e m ic S ta in in g te e p ii t tn g h ig h s c h o o l c o m p le t io n

A t te n d e d h ig h i c l io o t

C o m p le te d p a m n u i s c h o o l ( f l t h g ia d e I

A t te n d e d g ia m m a t scI m m i I

H o s c h o o lin g

( k t e t n o t a p p ly ( H o sj*«Mttc|I n f o im a t t o n n o t a v a ila b le ( S p e c i f y w h y )

aua

C h e c k o n e f o t e a c h p e i i o o

S e lf f a t h e r M o lh c t S p o u ie

a a □ □

a a a □

□ □ a a□ □ □ □

a a a a□ o □ □a a a aa a □ □a □ a aa a ID C)a □ □ □

108

Appendix BDiagnostic Interview for Bulimia Nervosa

109

DIAGNOSTIC INTERVIEW FOR BULIMIA NERVOSA

Have you ever been an a diet?

Yes __ No____

At what age did you begin to restrict your food intake due to concern over your body size?

_______years old

Over the last year how often have you begun a diet?

_______number of times

Have you ever had a episode of eating a large amount of food in a short period of time <an eating binge)?

Yes No____

How old were you when you binged for the first time?

_______years old

How characteristic are the following of your binge eating?

Nevei— Rare! y~Someti rues-Of ten—A1 ways

Consuming a large amount of food N R

Eating very rapidly N R

Feeling out of control N R

Feel ,down or annoyed afterward N R

Get uncontrollable urges to eatuntil physically ill N R

Binge eat in private N R

Within the last three months, what has been your average number of binge episodes per week?

_______Number of binges/week

Have you ever vomi ted or spit out food after eating in order to avoid weight gain?

Y e s No____

How old were you when you induced vomiting for the first time?

_Years old

S 0 A

S 0 A

S 0 A

S □ A

S 0 A

S 0 A

110

10- ‘Have you ever used laxatives or diuretics to control your weight or“get rid of faod”?

Yes No____

11. How aid were you when you first tool: 1 a.'jat i ves/di uret i cs for weight control 7

_______Years old

12- During the entire last month, what is the average frequency that youhave engaged in the following bnhavi or u to control weight?

Dinge eating:

Never-- 1 /Month — > 1 /Month — 1 / Wee!: — > 1 / Week — 1 / Day — > 1 / Day

Self-induced vomiting:

Never 1/Month — >1/Month — 1/Week — > I/Week — I/Day— >1/Day

Laxative use:

Never 1/Month— >1/Month — 1/Week — >1/Week — 1/Day— >1/Day

Use of diet pills:

Never-- 1/Month — >1/Month — 1/Week — >1/Week— 1/Day— >1/Day

Use of enemas:

Never I/Month — > I/Month— 1/Week — >1/Week — 1/Day— >1/Day

Exere i se:

Never 1 /Month — > 1 /Month — 1 / Week — >1 / Week — 1 / Day— > 1 / Day

Fasti ng:

Never— 1/Month— >1/Month— 1/Week— > I/Week— 1/Day— >1/Day

13. How many minutes a day do you currently exercise (including going on walks, riding bicycle, etc.)?

Minutes

Ill

14. Weight History

Current weight______________________________ ______ lbs.

Current height______________________________ _____ finches

Desired weight______________________________ ______ lbs.

Adult Years

Highest adult weight since age 1G_____________ lbs. at__age______

Lowest adult weight since age 1G________ ______ lbs. at__ago______

Mow long did you remain at your lowest adult weight?

_______days __ ___m o n t h s _______years

Adolescent years

Highest weight between ages 12— 1G ______ lbs. at age_______

Lowest weight between ages 12— 18________ _______lbs- at age______

15. Childhood

Mow did you perceive your weight as a child between ages 6— 12

years old?

Very thin— Somewhat thin— Normal— Somewhat overwt.— Very overwt.

16. At your current weight do you feel that you are:

Very thin— Somewhat thin— Normal — Somewhat overwt- — Very overwt-

17. Mow much does a two pound weight gain affect your feelings about

yourself7

Ex tremel y— Very much— Noderat el y— SI i ght 1 y— Not at all

How much does a two pound weight igss affect your feelings about

yourself7

Extremely— Very much— Moderately— Slightly— Not at all

112

10- How much does a five pound weight gai_n affect your feelings about

yourselfV

Extremely— Very much— Moderately— Slightly— Not at all

How much does a five pound weight l.gss affect your feelings about

yourself?

E>: tremel y— Very much— Moder a tel y— SI i gh 11 y— Not at all

17. Has there ever been a time when your feelings about yourself or your

social life have changed substantial1y as a result of losinq weight?

Yes______ No_______

If the answer is yes — Please tell me about it.

20- ! !c‘»* cftr" do you «•' vnur^pl f *?

More than daily Daily More than weekly____

Weekly Monthly Less than monthly____

21. How dissatisfied are you with the way your body is pcop.ortioned?

Extremely dissatisfied— Very dissatisfied— Moderately dissatisfied

Slightly dissatisfied— Not at all dissatisfied

22. How often do you think about your body shape?

A 1 ways— Of ten— Sometimes— Rarely— Never

Haw do you feel about the di f

Face:

Strongly positive— Moderately

Maderately negative— Strongly

Arms:

Strongly positive— Moderately

Moderately negati ve— Strongly

Shouldersl

Strongly positive— Moderately

Moderately negati ve— Strongly

Breast:

Strongly positive— Moderately

Moderately negative— Strongly

Stomach:

Strongly pcsi ti ve— Moderately

Moderately negati ve— Strong1y

Buttocks:

Strongly positive--Moderately

Moderately negati ve— Strongly

Thighs:

Strongly positive— Moderately

Moderately negative— Strongly

Haw often do you measure your

More than daily Daily__

Weekly Monthly Le;

ferent areas of your body

pos i ti ve—“Neutral

negat ive

posi tive— Neutral

negat i ve

posi tive— Neutral

negati ve

posi tive— Neutral

negat i ve

posi ti ve— Neutral

negati ve

posi ti ve— Neutral

negative

posi ti ve— Neutral

negati ve

body size?

More than weekly____

;s than monthly____

11<

Appendix C The Bulimia Test (BULIT)

PLEASE NOTE:

Copyrighted materials in this document have not been filmed at the request of the author. They are available for consultation, however, in the author's university library.

These consist of pages:

115-121123-130132-133135-136138-141143-150152-153

122

Appendix D Schedule for Affective Disorders

131

Appendix E The Beck Depression Inventory (BDI)

134

Appendix F Center for Epidemiological Studies

Depression Scale

137

Appendix G Dysfunctional Attitude Scale

Appendix H Pleasant Events Schedule

Appendix IMauds ley Obsessive-Compulsive Inventory

Appendix J State-Trait Anxietv Inventory

SELF-EVALUATION Q U E S T IO N N A IR EDeveloped by Charles D. Spiclbcrgcr

«M COlUtKM«lioa *»MhK. L . G o fsu ch . K. L ushcnc. P . R . Vagg, a n d G . A . Jaco b s

S T A I Form V-l

N am e - —______ D ale_______A g e _____________Sex: M _____ F _____

D IR E C T IO N S: A num ber o f statem ents which people have used todescribe themselves are given below. Read each statem ent and thenb lacken in (he appropria te circle to the right o f the statem ent to iudi- ^ ^cate how you feel right now , that is, at (his moment. There are no right ^o r w rong answ ers. Do not spend to o m uch tim e o n any one statementb u t give the answer which seems to describe your present feelings best. '<

1. I feel calm ................................................................................................................ ,,t

2 . I feel se cu re ........................................................................................................... {"

S. I ;iiii ten se ............................................................................................................... f' )

4 . ( feel s tra in e d .........................................................................................................

5. I l e d a* ease ........................................................................................................... 0*

(>. I feel upse t ............................................................................................................. r,)

7 . I am p resen tly w o rry in g o v e r |x>ssihle m isfo rtu n e s ........................... u>

8 . I feel satisfied ........................................................................................................ :o

*1. I feel frig h te n e d .................................................................................................. <’*

It). 1 feel c o m fo rtab le ................................................................................................

11. 1 feel se lf-con fiden t ............................................................................................. fo

12. I feel n erv o u s .........................................................................................................

l ‘J. I a m ji t te ry ...............................................................................................................

14. I feel indecisive .................................................................................................... l*)

lf>. I a m re lax ed ........................................................................................................... W

1(3. I feel c o n te n t ......................................................................................................... (0

17. I a m w o rried ........................................................................................................ ^

18. I feel co n fu sed ...................................................................................................... ti)

I ‘J . I l e d Mcatly ........................................................................................................... 10

20. I l e d p l e a s a n t ............................................................................................. ........... <!>

0 C onsulting Psychologists Press577 College A venue, Palo A lto, C alifornia 94506

156

SELF-EVALUATION Q U E ST IO N N A IR ESTAI Form V-l

N a m e D ale

DIRECTIONS: A nuirtber o f statements wtiich people Itave used (odescribe (lictttsclves are given below. Read each statement and llien _ /.Mark... ... .1,, .1.. _r V. >yblacken in ilie appropriate circle to the right o f the statement to in- ^ d ica te how you generally feel. There are no right o r wrong answers. Do n o t spend to o much time o n any one statement but give the answer w hich seems to describe how you generally feel. V 7 % . * ''•

2 1 . 1 feel p l e a s a n t ......................................................................................................... © CO t i t ©

2 2 . I feel nerv o u s a n d r e s t l e s s ................................................ ........................ © (!> t i t ©215. 1 feel satisfied w ith m y s e l f .............................................................................. © d) 0) ©

2 1 . 1 w ish 1 cou ld l>c as h a p p y as o th e rs seem to l>e .................................... © d> "V ©

© (*» ti) ©

2(». I fee! re sted .................................................................................................. .. . © l i i 0 } ©

© <i> t i ) ' ©

2 8 . 1 feel th a t d iflicu h ies a re p iling u p so th a t 1 can n o t overcom e th em © i i f ti) ©

2 0 . I w o rry m o im it h o v e r so m e th in g that really do esn 't m a tte r ............ © i i ; t i t ©

0) (i> ( i t ©

© q> ti t ©

© ti* ©

© d» ti t ©

!M. 1 m ak e decisions e a s i l y .................................................................................... © f i t ti) ©

© ( i l ti* ©

i. 1 an* < n ii tc « it ......................................... . . . . © <i> t i t ©

*5 /. S o m e im im |M irtau( th o u g h t ru n s th ro u g h my m im l a n d Ix ithers m e © <■* ti? ©

!5tt. 1 ta k e d isap]>ohtiiuciiis m i keenly th a t 1 can 't p u l th em o u t o f my

m in d ................................ © l i t t i t ©

Ii*i. i a m a steatiy ............................................................ ............................ © w ti) ©

•10. 1 ge l in a sta te o l ten s io n o r tu rm oil as 1 th in k o v e r m y recen t co n cern s

© ti* (y ©

Appendix K Informed Consent Form

158

Psychological Scn’iccs Center Department of Psychology

L o u i s i a n a S t a t e U n i v e r s i t y AM>AG«Ku.iuiiAi.AM>Mt<.iiANK.Ai.coutc(B A T O N R O U C E • L O U I S I A N A • 7 0 8 0 1 -5 5 0 1

CONSENT FORM FOR BATING PISOROERS RESEARCH

I > _____________________________________ , vo lu n ta rily conAent to pantic ipa tzin -the. Eating Oi&ondens ReAeanch pnognam din.zcX.exl by Donald A. Williamion, Ph.D.. Thi& nzAeanch involvzh both nanmaX and eaXJLnq diAondenzd ind iv idualA . Thenz(onz, pnoviAion o£ my con ten t dozA n o t im ply th a t I havz pnoblemA nela ted to eating.By my A ignatunz, 1 agaze to p a n tic ip a tz in th e neAzanch axtXi.viti.zA indicated below and to allow data pznXaining to mz to bz nepontzd in Acholanly pabticationA, Acholanly meeting a , on in educational pnognami nela tzd to th e Eating PiAondzru Kz&zanck pnojzxtl. The a c l iv i t iz A which I agnzz to p an tic ipa tz one thoAZ checked below:

1. C lin ica l imXenviewA2. Height a n d Weight m zaAunem ent I . Pbychological t z A t i n q

A l l o 6 m y q u zA tio n A h a v z b e e n anA w zned a n d I u n d zh A ta n d t h a t I may w ith d n a w

oa. t h e n zA z a n c h p-to/ecX w i t h o u t p e n a l t y .

iUgnatunz Date

Sngnatunz of, Wi tn z A A

159

Appendix L DSM-IIIR Diagnostic Checklists:

Bulimia Nervosa Major Depression

Dvsthvmia

PLEASE NOTE:

Copyrighted materials in this document have not been filmed at the request of the author. They are available for consultation, however, in the author's university library.

These consist of pages:

160-162

UMI

VITA

Name: RITA C. PRATHER

ACADEMIC HISTORY1989 Ph.D. Louisiana State University

Baton Rouge, Louisiana Major: Clinical PsychologySpecialty Area: Behavioral MedicineMinor: Behavioral NeurologyDissertation title:

The Affective Variant Hypothesis: How is Bulimia Nervosa Related to Depression?

1987-88 Internship:University of Mississippi Medical Center Department of Psychiatry & Human Behavior Jackson, Mississippi

1985 M.A. Louisiana State UniversityBaton Rouge, Louisiana Major: Clinical PsychologyThesis title:

Differential Diagnosis of Eating Disorders: Purgers, Bingers, Obese,and Norma 1s .

1983 B.A. University of Central FloridaOrlando, Florida Major-. Psychology Honors: Summa Cum Laude

HONORS1986 Outstanding Young Women of America1983 Summa Cum Laude, University of Central Florida1983 Who's Who Among Students in American Universities1982 PHI KAPPA PHI National Honor Society1981 PSI CHI National Honor Society1981 DELTA TAU KAPPA International Honor Society1981 OMICRON DELTA KAPPA National Honor Society

163

164TEACHING ACTIVITIES1988-1989 Assistant Professor. Appointed to Graduate

faculty September, 1988 Texas A & M University Department of Psychology

1987-1988 Teaching Instructor.University of Mississippi Medical Center Department of Psychiatry & Human Behavior

1986-1987 Instructor. Appointed to faculty August,1986 .Department of Psychology Louisiana State University

1983-1984 Teaching Assistant.Department of Psychology Louisiana State University

RESEARCH ACTIVITIES1987-1988 Research Associate

Eating Disorders UnitUniversity of Mississippi Medical Center

Research Associate UMC Headache ClinicUniversity of Mississippi Medical Center

Research AssociateBehavioral CardiologyVeterans Administration Medical Center Jackson, MS

1983-1987 Research AssociateEating Disorders Clinic Psychological Services Center Louisiana State University

CLINICAL EXPERIENCE1987-1988 Psychology Resident.

University of Mississippi Medical Center Department of Psychiatry & Human Behavior Jackson, MS

1651983-1987 Clinical Psychology Trainee.

Eating Disorders Clinic Psychological Services Center Louisiana State University, Baton Rouge, Supervisor: D. A. Williamson, Ph.D.

1985-1986 Psychological Consultant.Center on Problem EatingBaton Rouge General Medical CenterBaton Rouge, LA

1985-1987 Clinical Psychology Trainee.Neuropsychological Clinic Psychological Services Center Louisiana State Univesity Supervisor: Wm. D. Gouvier, Ph.D.

1985-1986 Clinical Psychology Trainee.Adult Services Clinic Psychological Services Center Louisiana State University Supervisor: Wm. D. Gouvier, Ph.D.

1984-1985 Clinical Psychology Trainee.Child Services Clinic Psychological Services Center Louisiana State University Supervisor: June Tuma, Ph.D.

LA

ADMINISTRATIVE/SERVICE ACTIVITIES1988-1989

1984-1985

1984-1985

1981-1983

Texas A & M UniversityClinical Search Committee Library Committee TAMU MENTORS Program In Search of a Speaker Program

Graduate Assistant.Psychological Services Center Louisiana State University Supervisor: Donald A. Williamson, Ph.D.

Graduate Student Representative Clinical Training Committee Department of Psychology Louisiana State University

Peer AdvisorDepartment of Psychology University of Central Florida Orlando, FL

1661981-1982 Charter President

PSI CHI National Honor Society University of Central Florida

OTHER PROFESSIONAL ACTIVITIES1988 Eating disorders and psychopathology.

Presented at University of Mississippi Medical Center Psychiatry Grand Rounds February 19.

1988 Body Image: Impossible dreams andunrealistic means. Presented at the University of Mississippi Medical Center Community Education meeting March 17.

1988 Overview of Eating Disorders. Presented atthe Mississippi State University annual Women's Week March 29.

PROFESSIONAL MEMBERSHIPS1981-Present 1986-Present1988-Present1982-Present1984-Present1985-Present

AssociationAssoc iation

American Psychological Division 12,American Psychological Division 38,American Psychological Association Association for Advancement of Behavior TherapySoutheastern Psychological Association The Society of Behavioral Medicine

GRANTSCoauthor with D. B. Penzien, Ph.D.

Behavioral versus pharmacological treatment of recurrent migraine headache.

Funded 1/88 by Clinical Research Center, University of Mississippi Medical Center. $2500.00Coauthor with D. B. Penzien, Ph.D.

Menstrual versus non-menstrual migraineurs: Fluctuationsof reproductive hormones and physical symptoms across the menstrual cycle.

Funded 1/88 by Clinical Research Center, University of Mississippi Medical Center. $3000.00

167PUBLICATIONSWilliamson, D. A., Prather, R. C., & Blouin, D. C. (in

press). Differential diagnosis of bulimia nervosa, binge-eaters, obese, and normal subjects using behavioral assessment procedures.Behavioral Assessment.

Williamson, D. A., Prather, R. C., Bennett, S. M., Davis,C. J., Watkins, P. C., & Grenier,C. E. (1989). An uncontrolled evaluation of inpatient and outpatient cognitive-behavior therapy for bulimia nervosa.Behavior Modification. 13, 340-360.

Williamson, D. A., Prather, R. C., Goreczny, A. J., Davis, C. J., & McKenzie, S. J. (1989). Psychopathology of bulimia. In W. G. Johnson (Ed.) Advances in Eating Disorders. (2nd. Ed.) Greenwich, Conn: JAIPress.

Prather, R. C. (1988). Sexual dysfunction of diabeticfemales: A review. Archives of Sexual Behavior. 17(3), 277-284.

Prather, R. C., &. Williamson, D. A. (1988).Psychopathology associated with bulimia, binge eating, and obesity. Internationa 1 Journal of Eating Disorders, 7, 177-184.

Williamson, D. A., Davis, C. J., & Prather, R. C. (1988). Assessment of health related disorders. In M. Hersen & A. S. Bel lack (Eds.) Behavioral Assessment: A practicalhandbook (3rd. Ed.). New York: Pergamon Press.

Williamson, D. A., Prather, R. C., Kelley, M. L., & Hefer, R. (1988). Eating Disorders. In J. L. Matson (Ed.) Treating Childhood and Adolescent Psychopathology. New York: Plenum.

Williamson, D. A., Prather, R. C., Upton, L., Davis, C. J., Ruggiero, L., &. VanBuren, D. (1987). Severity of bulimia: Relationship with depression and otherpsychopathology. International Journal of Eating Disorders. 6. 39-47.

Williamson, D. A., Kelley, M. L., Cavell, T. A., & Prather, R. C. (1987). Eating and eliminating disorders. In C. L. Frame &. J . L. Matson (Eds.) Handbook of Assessment in Child Psychopathology: Applied issues indifferential diagnosis and treatment evaluation. NewYork: Plenum.

168PRESENTATIONS AND SYMPOSIAPenzien, D. B., Johnson, C. A., Carpenter, D., Prather, R.

C. et al (March, 1989). Home-based behavioral treatment vs. propranolol for recurrent migraine: Preliminary findings. Society of Behavioral Medicine,San Francisco.

Krug, L. M . , Johnson, C. A., Penzien, D. B., Meeks, G. R., Prather, R. C. et al (March, 1989). Fluctuation of hormones and physical symptoms across menstrual cycles of miqraineurs. Society of Behavioral Medicine, San Francisco.

Payne, T. J., Johnson, C. A., Penzien, D. B., Parisi, S., Beckham, J. C., Prather, R. C. et al (March, 1989). Cluster analysis of functional capacity, somatic, and psychological symptoms in cardiac outpatients. Society of Behavioral Medicine, San Francisco.

Payne, T. J., Penzien, D. B., Porzelius, J., Eldridge, G., Parisi, S., Johnson, C. A., Beckham, J. C., Prather, R. C., &. Rodriguez, G. (March, 1989). The relationship between smoking and chest pain symptoms in an outpatient cardiac population. Society of Behavioral Medicine, San Francisco.

Prather, R. C., & Williamson, D. A. (November, 1987).Do obese requesting weight loss treatment differ from obese not seeking treatment? Paper presented at the annual meeting of the Association for Advancement of Behavior Therapy, Boston.

Williamson, D. A., Prather, R. C., McKenzie, S. J., &.Davis, C. J. (November, 1986). Inpatient versus outpatient treatment of bulimia. J. Scott Mizes (Chair), The cognitive behavioral treatment of bulimia: A comparison of different treatment approachesand prediction of treatment efficacy. Symposium conducted at the annual meeting of the Association for Advancement of Behavior Therapy, Chicago.

Upton, L. R., Williamson, D. A., Klug, F., Davis, C. J., & Prather, R. C. (November, 1986). Exercise habits in an eating disorder population. Paper presented at the annual meeting of the Association for Advancement of Behavior Therapy, Chicago.

169Prather, R. C., Upton, L., Williamson, D. A., Davis, C. J.,

Ruggiero, L., & VanBuren, D. (November, 1985).Bulimia, depression, and general psycho 1 opatho 1 ocrv.Paper presented at the annual meeting of the Association for Advancement of Behavior Therapy, Houston.

Prather, R. C., McKenzie, S., Upton, L., & Williamson, D.A. (November, 1985). A four-component behavioral treatment for bulimics who puree. Paper presented at the annual meeting of the Association for Advancement of Behavior Therapy, Houston.

Prather, R. C., & Phillips, P. A. (April, 1983).Pretraininq and muscle relaxation while playing video games. Paper presented at the annual meeting of the Florida Academy of Science, Melbourne, FL.

Prather, R. C. (December, 1982). The importance ofthorough assessment as demonstrated in the elimination of insomnia: A case study. Paper presented at theannual meeting of the Florida Association of Behavioral Analysis, Tampa, FL.

Zegman, M . , Baker, B., & Prather, R. C. (November, 1982). Assessing adherence to program and nonprogram behaviors for weight reduction. Paper presesnted at the annual meeting of the Association for Advancement of Behavior Therapy, Los Angeles.

DOCTORAL EXAMINATION AND DISSERTATION REPORT

Candidate: Rita C. Prather

Major Field: Psychology

Title of Dissertation: The Affective Variant Hypothesis: How Is BulimiaNervosa Related to Depression?

Approved:

Major Professor and Chairman

Dean of the Graduate^ggftppT

EXAMINING^XOMMITTEE:

Date of Examination:

Sept. 26, 1989-