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Relationship Between Obesity and Depression: Characteristics and Treatment Outcomes With Antidepressant Medication

Toups, Marisa S.P. MD; Myers, Alyson K. MD; Wisniewski, Stephen R. PhD; Kurian, Benji MD, MPH; Morris, David W. PhD; Rush, Augustus John MD; Fava, Maurizio MD; Trivedi, Madhukar H. MD

doi: 10.1097/PSY.0000000000000000
Original Articles

Objective Obesity and major depressive disorder often co-occur. However, differences between obese and normal-weight depressed patients and the moderating effect of obesity on antidepressant treatment outcome are not well studied.

Methods Adults (n = 662) with major depressive disorder in the Combining Medications to Enhance Depression Outcomes study were randomized to treatment with escitalopram plus placebo, bupropion plus escitalopram, or venlafaxine plus mirtazapine for a 12-week primary treatment phase and 16-week follow-up. Body mass index (BMI) was calculated at baseline and categorized according to World Health Organization criteria: normal or low weight (NW), overweight, Obese I and Obese II+. A repeated-effects model, unadjusted and adjusted for baseline variables, assessed outcomes.

Results Obesity was common (46.2%), only 25.5% were NW. Higher BMI was associated with greater medical illness (p < .001), social phobia (p = .003), and bulimia (p = .026). Lower BMI was associated with more frequent post-traumatic stress disorder (p = .002) and drug abuse (p < .001). Treatment outcomes did not differ including Week 12 remission rates (NW 36%, overweight 40%, Obese I 43%, Obese II+ 37%; p = .69). Lower BMI was associated with more frequent (p = .024 [unadjusted] and .053 [adjusted]) and more severe (p = .008 [unadjusted] and .053 [adjusted]) adverse effects.

Conclusions BMI was related to clinical presentation and prevalence of comorbidities, but not antidepressant outcomes. Lower BMI classes had more psychiatric comorbidities, potentially obscuring the relationship between BMI and antidepressant effects.

Trial Registration identifier: NCT00590863

Supplemental digital content is available in the text.

From the Departments of Psychiatry (M.S.P.T., A.K.M., B.K., D.W.M., M.H.T.), and Endocrinology (A.K.M.), University of Texas Southwestern Medical Center, Dallas Texas; Epidemiology Data Center (S.R.W.), University of Pittsburgh, Pittsburgh, Pennsylvania; Duke-National University of Singapore (A.J.R.), Office of Clinical Sciences, Singapore, Singapore; and Massachusetts General Hospital (M.F.), Boston, Massachusetts.

Address correspondence and reprint requests to Madhukar H. Trivedi, MD, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd, Dallas, TX 75390-9119. E-mail:

Supplemental digital content is available for this article. Direct URL citations appear in the printed text and are provided in the HTML and PDF versions of this article on the journal’s Web site (

Received for publication January 22, 2013; revision received July 26, 2013.

Copyright © 2013 by American Psychosomatic Society
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