Body Mass Index and Response to Antidepressants in Depressed Research Subjects

Oskooilar, Nader; Wilcox, Charles S.; Tong, My-Linh; Grosz, Daniel

doi:10.4088/jcp.09l05226blu

Cited by 38 publications

(21 citation statements)

References 2 publications

(2 reference statements)

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“…Consistent with this, being obese was found to be associated with a risk of developing depression ranging from 1.18 to 5.25 depending on studies and methods of assessment Kasen et al, 2008;Ma and Xiao, 2010;Simon et al, 2008) and to predict recurrence of depressive episodes as well as antidepressant non-response in depressed patients (Kloiber et al, 2007;Nigatu et al, 2015;Oskooilar et al, 2009;Rizvi et al, 2014;Woo et al, 2016). Conversely, and supporting the bidirectional relationship between obesity and depression, the rates of obesity are particularly high in depressed patients, and depression was found to represent a strong predictor of weight gain and obesity, probably owing to effects of antidepressant medications and changes in eating behaviors and lifestyle (Lasserre et al, 2014;Lee et al, 2016;Simon et al, 2008).…”

Section: Fat and Depression: A Vicious Circlementioning

confidence: 61%

Role of Adiposity-Driven Inflammation in Depressive Morbidity

Capuron

Lasselin

Castanon

2016

Neuropsychopharmacol

136

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Depression and metabolic disorders, including overweight and obesity, appear tightly interrelated. The prevalence of these conditions is concurrently growing worldwide, and both depression and overweight/obesity represent substantial risk factors for multiple medical complications. Moreover, there is now multiple evidence for a bidirectional relationship between depression and increased adiposity, with overweight/obesity being associated with an increased prevalence of depression, and in turn, depression augmenting the risk of weight gain and obesity. Although the reasons for this intricate link between depression and increased adiposity remain unclear, converging clinical and preclinical evidence points to a critical role for inflammatory processes and related alterations of brain functions. In support of this notion, increased adiposity leads to a chronic low-grade activation of inflammatory processes, which have been shown elsewhere to have a potent role in the pathophysiology of depression. It is therefore highly possible that adiposity-driven inflammation contributes to the development of depressive disorders and their growing prevalence worldwide. This review will present recent evidence in support of this hypothesis and will discuss the underlying mechanisms and potential therapeutic targets. Altogether, findings presented here should help to better understand the mechanisms linking adiposity to depression and facilitate the identification of new preventive and/or therapeutic strategies.

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Section: Fat and Depression: A Vicious Circlementioning

confidence: 61%

Role of Adiposity-Driven Inflammation in Depressive Morbidity

Capuron

Lasselin

Castanon

2016

Neuropsychopharmacol

136

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“…Moreover, what has become increasingly clear is that none of these disorders, including notably major depression, are fundamentally inflammatory disorders, but rather in each case, there is a subgroup of patients who exhibit evidence of increased inflammation (Raison and Miller, 2011). Factors that have been associated with a greater likelihood of increased inflammation in these patient populations include treatment resistance as well as childhood maltreatment, obesity, increasing age, medical illness, and genetic predisposition (Iosifescu et al, 2003;Miller et al, 2009;Oskooilar et al, 2009;Nanni et al, 2012). Taken together, these data suggest that the various neurobiological pathways and resultant symptoms secondary to inflammation (discussed in detail below) occur across disorders (are transdiagnostic) in subgroups of patients with increased inflammation.…”

Section: Foundations For the Hypothesis That The Immune System Plays mentioning

confidence: 99%

Therapeutic Implications of Brain–Immune Interactions: Treatment in Translation

Miller

Haroon

Felger

2016

Neuropsychopharmacol

118

124

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A wealth of data has been amassed that details a complex, yet accessible, series of pathways by which the immune system, notably inflammation, can influence the brain and behavior. These data have opened the window to a diverse array of novel targets whose potential efficacy is tied to specific neurotransmitters and neurocircuits as well as specific behaviors. What is clear is that the impact of inflammation on the brain cuts across psychiatric disorders and engages dopaminergic and glutamatergic pathways that regulate motivation and motor activity as well as the sensitivity to threat. Given the ability to identify patient populations with increased inflammation, the precision of interventions can be further tuned, in conjunction with the ability to establish target engagement in the brain through the use of multiple neuroimaging strategies. After a brief overview of the mechanisms by which inflammation affects the brain and behavior, this review examines the extant literature on the efficacy of anti-inflammatory treatments, while forging guidelines for future intelligent clinical trial design. An examination of the most promising therapeutic strategies is also provided, along with some of the most exciting clinical trials that are currently being planned or underway.

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“…The degree of antidepressant response observed with NB32 in this population is notable because the presence of obesity in individuals with MDD is associated with greater treatment resistance to the usual antidepressant therapies,9–13 an overall tendency to higher recurrence rates,15 and higher levels of depression chronicity 14. Interestingly, we observed a correlation between improvement in depression symptom severity and weight change at week 24.…”

Section: Discussionmentioning

confidence: 55%

“…Obesity has been reported to predict poor antidepressant response in depression,9–13 more chronic episodes,14 and a higher risk of recurrence in patients with bipolar I disorder 15…”

mentioning

confidence: 99%

Naltrexone/Bupropion Combination Therapy in Overweight or Obese Patients With Major Depressive Disorder

McElroy¹,

Guerdjikova²,

Kim³

et al. 2013

Prim. Care Companion CNS Disord.

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Objective: To evaluate the effect of 32-mg/d naltrexone sustained release and 360-mg/d bupropion sustained release (NB32) in overweight and obese patients with major depressive disorder (MDD).Method: Twenty-five female patients with a DSM-IV diagnosis of MDD, an Inventory of Depressive Symptomatology—Self-Report score > 26, and a body mass index ≥ 27 and ≤ 43 kg/m2 received up to 24 weeks of open-label treatment with NB32 with dietary and behavioral counseling (data collection: March 2008–July 2009). The primary endpoint was change from baseline in the Montgomery-Asberg Depression Rating Scale (MADRS) total score at 12 weeks; secondary endpoints included MADRS total score at week 24, change in weight, and Clinical Global Impressions–Improvement scale responder status (CGI-I score ≤ 2) at weeks 12 and 24 (modified intent-to-treat [mITT]: patients with ≥ 1 postbaseline MADRS total score on study drug; N = 23).Results: MADRS scores showed significant reductions at weeks 12 and 24 (mITT–last observation carried forward [LOCF]: –13.1 ± 7.1 and –15.3 ± 8.1, respectively, P < .001 vs baseline for all). Mean ± SD weight loss was –4.0% ± 4.6% (mITT-LOCF) and –6.1% ± 4.7% (observed cases) at week 12 and –5.3% ± 6.5% (mITT-LOCF) and –9.2% ± 6.2% (observed cases) at week 24 (P < .001 vs baseline for all). By week 24, 95% of patients (mITT-LOCF) were responders (CGI-I score ≤ 2) and 70% were in remission (CGI-I score = 1). The safety/tolerability profile of NB32 was consistent with its individual components; the most common adverse events were nausea, constipation, headache, and insomnia, with no serious adverse events attributed to NB32.Conclusion: Twenty-four weeks of open-label NB32 therapy with dietary and behavioral counseling was associated with improvement in depressive symptoms and reduced body weight in overweight/obese women with MDD.Trial Registration: ClinicalTrials.gov Identifier: NCT00624858

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Body Mass Index and Response to Antidepressants in Depressed Research Subjects

Cited by 38 publications

References 2 publications

Role of Adiposity-Driven Inflammation in Depressive Morbidity

Role of Adiposity-Driven Inflammation in Depressive Morbidity

Therapeutic Implications of Brain–Immune Interactions: Treatment in Translation

Naltrexone/Bupropion Combination Therapy in Overweight or Obese Patients With Major Depressive Disorder

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