Mood disorders and medical illnessDepression and obesity
Introduction
Obesity is a very common disorder: 65% of Americans are considered overweight or obese (Flegal et al 2002). There is thus a strong probability that they will occur together with major depression, for which the prevalence has been estimated at 10% (Kessler et al 1994). However little is known about the relationship between the two disorders and there has been little systematic research on the topic. They have been studied as two largely independent disorders and investigators in the two fields have had little contact. For years it has been assumed that any relationship of obesity to depression in the general population is largely coincidental.
Part of the problem in associating depression and obesity is derived from the many differences between treatment-seeking obese persons and nontreatment-seeking obese persons (community samples) (Fitzgibbon et al 1993). Despite uncertainty regarding the relationship in community studies, relationships between obesity and psychopathology have been found among obese persons seeking treatment. This report will explore the nature of this relationship, making use of the framework provided by the moderator/mediator distinction. This distinction, first utilized in the social psychological literature by Baron and Kenny (1986), is attracting increasing attention in treatment studies in psychiatry (Kraemer et al 2002). Moderators specify for whom and under what conditions agents exert their effects; mediators identify why and how they exert their effects. Moderators always precede what they moderate, which, in turn, precedes the outcome; mediators always come between what they mediate and the outcome. In this review, moderators are defined as variables on which the obesity-depression covariation is conditional, whereas mediators bridge the causal relationship between obesity and depression.
The critical role of theory in distinguishing those variables that are moderators as opposed to mediators cannot be overstated. Variables that are conceptualized as moderators in one researcher's framework may be conceptualized as mediators in another researcher's framework. Perhaps the one exception to this note is DNA and genetic polymorphisms, which would almost naturally seem to function as moderators rather than mediators. Even here, however, the picture is not entirely clear as the process of gene transcription can be influenced by environmental conditions (Plomin and Crabbe 2000). Hence, the putative moderators and mediators listed in this domain—as in any other—are not written in stone. Arguably no single study can “resolve” such issues, in contrast to the cumulative database gleaned from multiple studies that replicate findings. The ultimate value of adopting a moderator/mediator framework, compared to not adopting such a framework, can be evaluated by the knowledge base and clinical innovations stimulated by such a framework.
The present review article is, by necessity, a brief one in light of the existing data. There are numerous inconsistencies in the literature which, according to Friedman and Brownell (1995), stem in large part from considerable study heterogeneity. The moderators and mediators illustrated herein are not presented with definitive certainty but rather as putative pathways to be tested in subsequent research. The ultimate identification of “true” moderators and mediators is of utmost clinical importance. Identifying moderators such as gender, ethnicity, or age would pinpoint those obese individuals among whom depression is more likely to occur and who may be the most appropriate candidates for psychiatric treatment. Similarly, identification of “true” mediators (whether they be they physiologic and behavioral) would lead to better pharmacological and lifestyle interventions as causal pathways are delineated.
Section snippets
Moderators and mediators
A list of potential moderators and mediators is shown in Table 1.
Treatment of obese patients with depression
There is a fascinating relationship between the treatment of depression in the presence of obesity, and vice versa. Treatment of obesity often leads to a decrease in depression. The most striking such example is the dramatic improvement in mood that accompanies the large weight losses achieved by gastric bypass surgery Waters et al., 1991, Dymek et al., 2001. In the case of modest weight loss, the reduction in depression tends also to be modest (Gladis et al 1998).
In contrast to the favorable
Recommendations for future research
We suggest that future studies invoke a moderator/mediator framework for better understanding the relationship between obesity and depression. We have reviewed some putative variables in this report, although the limited data currently available suggests that these should be interpreted cautiously and used as illustrators to stimulate future research. In addition, many other substantive issues related to obesity/depression covariation deserve attention. For example, an understanding of social
Acknowledgements
Aspects of this work were presented at the conference, “The Diagnosis and Treatment of Mood Disorders in the Medically Ill,” November 12–13, 2002 in Washington, DC. The conference was sponsored by the Depression and Bipolar Support Alliance through unrestricted educational grants provided by Abbott Laboratories, Bristol-Myers Squibb Company, Cyberonics, Inc., Eli Lilly and Company, Forest Laboratories, Inc., GlaxoSmithKline, Janssen Pharmaceutica Products, Organon Inc., Pfizer Inc, and Wyeth
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