Obesity among outpatients with Major Depressive Disorder

Papakostas, George I.; Petersen, Timothy; Iosifescu, Dan V.; Burns, Alana M.; Nierenberg, Andrew A.; Alpert, Jonathan E.; Rosenbaum, Jerrold F.; Fava, Maurizio

doi:10.1017/s1461145704004602

Cited by 85 publications

(44 citation statements)

References 12 publications

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“…We therefore believe that this Perspective Article will equip practitioners with the essential knowledge base for understanding the rationale for naltrexone therapy and will sharpen their sensitivity to the unmet medical needs of their schizophrenic patients. Lastly, this model may also provide important leads for recognition and treatment of hazardous eating habits in patients with other disorders, including obesity (Wang et al, 2001), SUDs (Kampov-Polevoy et al, 2001), and major depression (Papakostas et al, 2005).…”

Section: Discussionmentioning

confidence: 99%

Food Intake and Reward Mechanisms in Patients with Schizophrenia: Implications for Metabolic Disturbances and Treatment with Second-Generation Antipsychotic Agents

Elman

Borsook

Lukas

2006

Neuropsychopharmacol

131

138

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Obesity is highly prevalent among patients with schizophrenia and is associated with detrimental health consequences. Although excessive consumption of fast food and pharmacotherapy with such second-generation antipsychotic agents (SGAs) as clozapine and olanzapine has been implicated in the schizophrenia/obesity comorbidity, the pathophysiology of this link remains unclear. Here, we propose a mechanism based on brain reward function, a relevant etiologic factor in both schizophrenia and overeating. A comprehensive literature search on neurobiology of schizophrenia and of eating behavior was performed. The collected articles were critically reviewed and relevant data were extracted and summarized within four key areas: (1) energy homeostasis, (2) food reward and hedonics, (3) reward function in schizophrenia, and (4) metabolic effects of the SGAs. A mesolimbic hyperdopaminergic state may render motivational/incentive reward system insensitive to low salience/palatability food. This, together with poor cognitive control from hypofunctional prefrontal cortex and enhanced hedonic impact of food, owing to exaggerated opioidergic drive (clinically manifested as pain insensitivity), may underlie unhealthy eating habits in patients with schizophrenia. Treatment with SGAs purportedly improves dopamine-mediated reward aspects, but at the cost of increased appetite and worsened or at least not improved opiodergic capacity. These effects can further deteriorate eating patterns. Pathophysiological and therapeutic implications of these insights need further validation via prospective clinical trials and neuroimaging studies. INTRODUCTIONObesity has reached pandemic proportions and it is rapidly surpassing smoking as a number one killer in the industrialized world (Sturm, 2002;Skidmore and Yarnell, 2004). Its annual cost to the American society is staggering, and is estimated to be around $117 billion owing to related illnesses and loss of productivity (National Institute of Diabetes and Digestive and Kidney Diseases, 2005).In schizophrenia, obesity is twice as prevalent as in the general public, afflicting over half this patient population (Allison et al, 1999a;Dixon et al, 2000; American Diabetes Association, 2004;Marder et al, 2004;Wirshing, 2004). Besides negative psychosocial impacts (distorted selfesteem and societal stigmatization) and medications noncompliance, schizophrenics appear to be particularly susceptible to the detrimental medical sequelae of obesity such as the 'Metabolic Syndrome', which is a cluster of cardiovascular risk factors, including abdominal adiposity, insulin resistance, impaired, glucose tolerance, dyslipidemia, and hypertension (McKee et al, 1986;Mukherjee et al, 1996;Brown et al, 2000;Haupt and Newcomer, 2002;Ryan and Thakore, 2002;Ryan et al, 2003;Holt et al, 2004;Kohen, 2004;Marder et al, 2004;Lieberman et al, 2005).Excessive body weight gain (BWG) could be attributed to a constellation of endocrine, molecular, genetic, demographic, and lifestyle-related factors. Provided that a common tra...

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Section: Discussionmentioning

confidence: 99%

Food Intake and Reward Mechanisms in Patients with Schizophrenia: Implications for Metabolic Disturbances and Treatment with Second-Generation Antipsychotic Agents

Elman

Borsook

Lukas

2006

Neuropsychopharmacol

131

138

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“…Body weight alone has been shown to have an effect on response to antidepressants. A study of 384 outpatients reported that lighter patients responded preferentially to the SSRI fluoxetine (Papakostas et al, 2005) and a further study investigating response to a number of antidepressants supported these findings (Kloiber et al, 2007).…”

Section: Physiological Differencesmentioning

confidence: 95%

Gender differences in antidepressant drug response

Keers

Aitchison

2010

International Review of Psychiatry

142

101

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Epidemiological studies suggest there are considerable differences in the prevalence and presentation of depression in men and women. Women are more than twice as likely to be diagnosed with depression and may also report more atypical and anxiety symptoms than men. Men and women also differ in the metabolism and distribution of antidepressants and the presence of oestrogen in women of childbearing age may interfere with the mechanism of action of a number of antidepressants. These differences have led many researchers to question whether antidepressants are equally effective and tolerated in men and women. While some reports suggest that selective serotonin re-uptake inhibitors (SSRIs) are more effective and result in fewer adverse drug reactions in women than tricyclic antidepressants (TCAs), gender differences in antidepressant response remains a controversial topic. The potential effects of antidepressant exposure in utero and in breast milk further complicate treatment options for antenatal and postnatal depression. While some research suggests the SSRI paroxetine is teratogenic, further carefully designed naturalistic studies are required to fully evaluate these effects. Finally, response to antidepressants and the occurrence of adverse drug reactions is marked by inter-individual variability which may be in part due to genetic differences. Future studies should therefore consider genotypes of the mother, foetus and infant in antidepressant response.

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“…Studies on antidepressant therapies have found that higher body weight, but not obesity, was associated with a poorer response to fluoxetine (Papakostas et al, 2005), a higher body mass index (BMI) and obesity predicted poorer response to nortripitlyine but had no influence on the response to escitalopram (Uher et al, 2009), and individuals with higher BMI experienced a slower clinical response to general antidepressant treatment (Kloiber et al, 2007). Khan et al (2007) also found that depressed, obese men experienced little or no therapeutic benefit from antidepressant treatment.…”

Section: What Effect Does Obesity Have On Treatment Outcomes?mentioning

confidence: 99%

Obesity and psychiatric disorders: Commonalities in dysregulated biological pathways and their implications for treatment

Lopresti

Drummond

2013

Progress in Neuro-Psychopharmacology and Biological Psychiatry

189

126

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Rates of obesity are higher than normal across a range of psychiatric disorders, including major depressive disorder, bipolar disorder, schizophrenia and anxiety disorders. While the problem of obesity is generally acknowledged in mental health research and treatment, an understanding of their bi-directional relationship is still developing. In this review the association between obesity and psychiatric disorders is summarised, with a specific emphasis on similarities in their disturbed biological pathways; namely neurotransmitter imbalances, hypothalamus-pituitary-adrenal axis disturbances, dysregulated inflammatory pathways, increased oxidative and nitrosative stress, mitochondrial disturbances, and neuroprogression. The applicability and effectiveness of weight-loss interventions in psychiatric populations is reviewed along with their potential efficacy in ameliorating disturbed biological pathways, particularly those mediating inflammation and oxidative stress. It is proposed that weight loss may not only be an effective intervention to enhance physical health but may also improve mental health outcomes and slow the rate of neuroprogressive disturbances in psychiatric disorders. Areas of future research to help expand our understanding of the relationship between obesity and psychiatric disorders are also outlined.

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Obesity among outpatients with Major Depressive Disorder

Cited by 85 publications

References 12 publications

Food Intake and Reward Mechanisms in Patients with Schizophrenia: Implications for Metabolic Disturbances and Treatment with Second-Generation Antipsychotic Agents

Food Intake and Reward Mechanisms in Patients with Schizophrenia: Implications for Metabolic Disturbances and Treatment with Second-Generation Antipsychotic Agents

Gender differences in antidepressant drug response

Obesity and psychiatric disorders: Commonalities in dysregulated biological pathways and their implications for treatment

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