Obesity among outpatients with Major Depressive Disorder
Harvard University, Cambridge, Massachusetts, United StatesThe International Journal of Neuropsychopharmacology (Impact Factor: 4.01). 04/2005; 8(1):59-63. DOI: 10.1017/S1461145704004602
Studies focusing on the prevalence of obesity in Major Depressive Disorder (MDD), or the impact of excess body fat on the treatment of MDD are lacking. The aim of the present work is to systematically study obesity in MDD outpatients. A total of 369 MDD outpatients enrolled in an 8-wk trial of 20 mg fluoxetine had height and weight measured at baseline. We then examined: (1) the prevalence of being overweight or obese, (2) the relationship between obesity and a number of demographic and clinical variables, and, (3) the relationship between relative body weight and obesity with clinical response. We found that more than 50% of patients were overweight [body mass index (BMI) > or =2 5 kg/m2], while 20% were obese (BMI > or = 30 kg/m2). Obese patients presented with worse somatic well-being scores than non-obese MDD patients, but they did not differ with respect to depression severity, anxiety, somatic complaints, hopelessness or hostility. Greater relative body weight, but not obesity, predicted non-response. In conclusion, greater relative body weight was found to place MDD outpatients at risk for fluoxetine resistance.
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- "This is consistent with findings that early trauma is also associated with increased risk of general obesity and elevated IAAT in adult life (Thomas et al., 2008). Both cross-sectional (Papakostas et al., 2005; Simon et al., 2001) and longitudinal (Rotella and Mannucci, 2013) studies have shown increased risk for obesity in depressed patients. What has received considerably less attention, however, is the association between obesity and systemic inflammation in depressed patients. "
ABSTRACT: Many people with major depressive disorder (MDD) show evidence of systemic inflammation, including elevations in inflammatory factors, but the cause is unclear. The purpose of this analysis was to determine if obesity might contribute to the pro-inflammatory state in MDD patients. Blood was obtained from 135 MDD patients and 50 controls. Serum was extracted and assayed for interleukin (IL) -1β, IL-2, IL-5, IL-6, IL-8, IL-10, IL-12p70, IL-17, interferon-γ (IFNγ), tumor necrosis factor α (TNFα), C-reactive protein (CRP), leptin, and adiponectin using single- or multi-plex human immunoassay kits. The primary analysis contrasted IL-6, TNFα, and CRP between MDD and control groups with body mass index (BMI) as a covariate. The other analytes were compared in an exploratory fashion. IL-6 (but not TNFα or CRP) showed significant differences between MDD and controls even after covarying for BMI. Obese controls and obese MDD groups were significantly higher in IL-6 than both lean groups, but the two obese groups did not differ from each other. In the exploratory analyses, the IL-2 level showed robust and significant differences between MDD and controls even after covarying for BMI. Both lean and obese MDD were higher than lean and obese controls. Adiponectin levels were also lower in the MDD sample than controls. Prior findings of higher IL-6, and CRP in MDD patients may be explained, at least in part, based on obesity. High IL-2, however, was associated with depression and not obesity. The results have significant implications for the understanding of pathophysiology and, potentially treatment of MDD.Journal of Psychiatric Research 10/2015; 70:91-97. DOI:10.1016/j.jpsychires.2015.09.001 · 3.96 Impact Factor
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- "Body mass index (BMI), a continuous measure of body weight relative to height, was calculated as body weight in kilograms divided by squared height in metres (kg m x2 ). Categorical definitions of underweight (BMI <19), overweight (BMI >25 to 30) and obesity (BMI >30) follow the recommendations of the World Health Organization (WHO, 1998) and the US National Institute of Health Clinical Guidelines on the Identification, Evaluation and Treatment of Overweight and Obesity in Adults (NIH, 1998) and are consistent with previous reports (Khan et al. 2007 ; Kloiber et al. 2007 ; Papakostas et al. 2005 ; Uher et al. 2009c). Depression severity was measured weekly using several rating scales, including the clinician-rated 10-item Montgomery–Asberg Depression Rating Scale (MADRS ; Montgomery & Asberg, 1979), with high inter-rater reliability (Uher et al. 2008). "
ABSTRACT: The risk of weight gain is an important determinant of the acceptability and tolerability of antidepressant medication. To compare changes in body weight during treatment with different antidepressants, body weight and height were measured at baseline and after 6, 8, 12 and 26 wk treatment with escitalopram or nortriptyline in 630 adults with moderate-to-severe unipolar depression participating in GENDEP, a part-randomized open-label study. Weight increased significantly more during treatment with nortriptyline compared to escitalopram. The weight gain commenced during the first 6 wk of nortriptyline treatment, reached on average 1.2 kg at 12 wk (0.44-point BMI increase), and continued throughout the 6-month follow-up period. Participants who were underweight at baseline gained most weight. Participants who were obese at baseline did not gain more weight during treatment. Weight gain occurred irrespective of whether weight loss was a symptom of current depressive episode and was identified as an undesired effect of the antidepressant by most participants who gained weight. There was little weight change during treatment with escitalopram, with an average increase of 0.14 kg (0.05-point BMI increase) over 12 wk of treatment. In conclusion, treatment with the tricyclic antidepressant nortriptyline was associated with moderate weight gain, which cannot be explained as a reversal of symptomatic weight loss and is usually perceived as an undesired adverse effect. While treatment with nortriptyline may be recommended in underweight subjects with typical neurovegetative symptoms, escitalopram is a suitable alternative for subjects at risk of weight gain.The International Journal of Neuropsychopharmacology 04/2011; 14(3):367-75. DOI:10.1017/S1461145710000933 · 4.01 Impact Factor
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- "There is evidence, however, to suggest that depression may, in many cases, precede diabetes and act as a causal factor for weight gain and subsequent development of diabetes.4 Approximately 80% of diabetic patients are overweight or obese, and a complex relationship exists between obesity and depression.5–7 Depression can be a precursor or aggravating factor in the development of obesity, but there is also evidence that obesity may lead to depression.8,9 "
ABSTRACT: Peter HofmannUniversity Clinic of Psychiatry, Graz Medical University, Graz, AustriaAbstract: Depression is twice as frequent in patients with diabetes as in the general population, and has a negative impact on self-care, adherence to treatment, and the general prognosis of diabetes. This underscores the importance of screening all diabetic patients for depression and, if necessary, treating it with an effective antidepressant drug in parallel with standard diabetes treatment. In a recent study, a simple two-question screening tool was used to screen diabetic patients for comorbid depression. The effects of the serotonin and norepinephrine reuptake inhibitor antidepressant, milnacipran, on metabolic parameters and depressive symptoms in 64 diabetic patients with comorbid depression detected by this screen were studied. Patients received milnacipran for 6 months, in addition to standard diabetes treatment with metformin. At the end of the study, 72% of patients had responded to antidepressant treatment (≥50% reduction of baseline Beck Depression Score). The proportion of patients with <8% glycosylated hemoglobin HbA1c (a common indication in diabetes of the need for intensive therapeutic intervention) had decreased significantly from 46.6% at baseline to 6.9%. HbA1c, fasting blood glucose, body mass index, total and low-density lipoprotein cholesterol, and serum triglyceride levels were all significantly decreased in patients with an antidepressant response, but not in patients whose depressive symptoms had not responded to milnacipran.Keywords: depression, diabetes, milnacipran, serotonin, norepinephrine, reuptake inhibitors
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