Special reviewComorbidity of bipolar and eating disorders: distinct or related disorders with shared dysregulations?
Introduction
It is well documented that bipolar disorder co-occurs with substance use and anxiety disorders (Boyd et al., 1984, Kessler et al., 1997, McElroy et al., 2001), and that eating disorders co-occur with depressive, substance use, and anxiety disorders (Halmi et al., 1991, Braun et al., 1994, Garfinkel et al., 1995, Bulik et al., 2004b). The co-occurrence of bipolar disorder and eating disorders, however, has received extremely little empirical attention (Shisslak et al., 1991, Mury et al., 1995).
To enhance understanding of the relationship between bipolar disorder and eating disorders, we evaluated studies of eating disorders (anorexia nervosa [AN], bulimia nervosa [BN], and binge eating disorder [BED]) in persons with bipolar disorder, and studies of bipolar disorder (types I and II and other “soft spectrum” forms) in persons with eating disorders. We also compared bipolar and eating disorders regarding phenomenology, course, family history, biology, and treatment response.
In undertaking this review, we used the strategy of examining both narrow (syndromal) and broad (spectrum) diagnostic criteria to define both groups of disorders. We did so for several reasons. First, for both bipolar disorder and eating disorders, when compared to those without these disorders, persons with subsyndromal symptoms have been shown to be more similar to those with syndromal disorders with respect to distress, comorbidity, and treatment utilization (Shisslak et al., 1995, Angst, 1998, Crow et al., 2002, Judd and Akiskal, 2003). Second, although important qualitative differences exist among the individual disorders within each diagnostic category, considerable phenomenologic, course, and family history data support their inclusion in their respective broad diagnostic categories (Akiskal and Mallya, 1987, Akiskal, 2002, Akiskal, 2003, Fairburn and Harrison, 2003, Keel et al., 2004). Third, the most severe forms of both conditions – e.g., mania in bipolar disorder and AN in the eating disorders – are each relatively uncommon disorders; by contrast, when viewed as a spectrum of related disorders, both bipolar and eating disorders emerge as prevalent conditions (see Table 1). In brief, we believe the strategy we adopted is more likely to reveal relatively little known relationships between the two spectrum groups of disorders.
Section snippets
Epidemiology
Of the four studies on the co-occurrence of bipolar disorder and eating disorders in community samples, some have focused on syndromal, and others on subthreshold disorders. These studies are reviewed in their order of sophistication with respect to the definition of subthreshold cases.
The Fogarty et al. (1994) study, which evaluated 3258 community residents aged 18 years from Edmonton, Canada with the Diagnostic Interview Schedule (DIS), did not study subthreshold cases. There was no overlap
Eating and weight dysregulation as symptoms of bipolar disorder
Core features of eating disorders include severe disturbances in eating behavior and weight (Dingemans et al., 2002, Fairburn and Harrison, 2003). For AN, such disturbances include severe food restriction with or without binge eating, and inappropriate compensatory behaviors, while weight, by definition, is decreased. For BN, these disturbances are binge eating and inappropriate compensatory behaviors; weight is usually normal or increased. For BED, binging and a general tendency to overeat
Course
Bipolar and eating disorders show similarities in onset and course. Both disorders often begin in adolescence or early adulthood, and both may be episodic or chronic (Goodwin and Jamison, 1990, Keel and Mitchell, 1997, Steinhausen, 2002, Fairburn and Harrison, 2003). The course of eating disorders may be phasic or cyclic, like that of bipolar disorder. Fairburn and Harrison (2003) have discussed how eating disorder patients tend to “migrate” among the diagnostic categories. For example, about
Family history of mood and eating disorders
Controlled family interview studies (in which first-degree relatives are directly assessed for psychopathology) have consistently found elevated rates of both bipolar and unipolar depressive disorders in the first-degree relatives of probands with bipolar disorder (Goodwin and Jamison, 1990, Kelsoe, 2003). Such studies have also consistently found elevated rates of both eating and unipolar depressive disorders in the first-degree relatives of probands with AN and/or BN (Lilenfeld et al., 1998,
Biology
A series of studies comparing levels of various hormones, neurotransmitters, neurotransmitter metabolites, and neuropeptides in the cerebrospinal fluid (CSF) of patients with bipolar disorder, women with AN, patients with major depression, and normal controls was conducted in 1981. No differences were found between manic patients, AN patients, and normal controls in CSF levels of GABA (Gerner and Hare, 1981), beta-endorphin immunoreactivity (Gerner and Sharp, 1982), bombesin-like
Lithium
The antimanic, antidepressant, and long-term prophylactic mood-stabilizing effects of lithium in bipolar disorder, including suicide prevention, have been well documented (Baldessarini et al., 2003, Keck and McElroy, 2004).
In the only placebo-controlled trial of lithium in AN, the 8 patients receiving lithium showed greater weight gain after 3 and 4 weeks of treatment than the 8 patients receiving placebo (Gross et al., 1981). Lithium-treated patients also showed significantly more improvement
Theoretical models
The epidemiologic and clinical comorbidity data reviewed in this paper indicate that bipolar disorder and eating disorders do in fact co-occur. Although the degree and nature of this co-occurrence is not fully understood, it could be explained by at least three hypothetical conceptual models. In the first model, bipolar and eating disorders are pathophysiologically distinct entities which overlap by chance, but with significant frequency, because both are common disorders when their full
Clinical implications
Comorbid eating disorders may contribute to some of the obesity seen in bipolar patients (McElroy et al., 2002), and conversely, comorbid bipolarity may contribute to some of the treatment-resistance seen among eating disorder patients (Simpson et al., 1992). Therefore, clinicians should assess for all syndromal and subsyndromal eating disorders in patients presenting with bipolar disorder, and conversely, for bipolar spectrum disorders in patients presenting with eating disorders.
Potential
Conflict of Interest Statements
Dr. McElroy is a consultant to, or member of the scientific advisory boards of: Abbott Laboratories, Bristol-Myers Squibb, GlaxoSmithKline, Janssen Pharmaceutica, Eli Lilly and Company, Novartis, Ortho-McNeil, and Wyeth-Ayerst. Dr. McElroy is a principal or co-investigator on research studies sponsored by Forrest Labs, Esai, Eli Lilly, Ortho-McNeil, Pfizer, Sanofi-Synthelabo, Astra Zeneca, and Bristol-Myers Squibb.
Dr. Keck is a consultant to, or member of the scientific advisory boards of:
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