Obesity and Bipolar Disorder
By Roger S. McIntyre, MD, FRCPC |
January 26, 2012
Dr McIntyre is associate professor of psychiatry and pharmacology at the University of Toronto and head of the Mood Disorders Psychopharmacology Unit at the University Health Network, Toronto, Canada. Dr McIntyre is involved in multiple research endeavors, which primarily aim to characterize the association between mood disorders and medical comorbidity. This research involves elucidating metabolic adverse events associated with the use of psychotropic medications, the impact of medical comorbidity on the course of mood disorders, and the effect of glucose homeostasis on neurocognition.
Answer: All of the above.
Bipolar disorder (BD) has been highly associated with disparate cognitive deficits, including attention, psychomotor performance, executive function, verbal fluency, learning, memory, and global neurocognitive functioning.1-4 The pertinacity of cognitive deficits in BD is underscored by reports that document an association between cognitive deficits and psychosocial functioning, workforce performance, and interpersonal adjustment.5-7
Emerging evidence also indicate that obesity is associated with reduced cognitive function in otherwise healthy individuals.8-15 The association between anthropometrics and cognitive deficits is detectable in individuals without obesity-associated comorbidities (eg, type 2 diabetes mellitus, hypertension) known to independently affect brain function.13,15.16 Most cognitive domains are reported to be adversely affected by excess weight with replicated abnormalities in measures of learning, memory, and executive function.9
It has been amply documented that individuals with BD are differentially associated with overweight/obesity and abdominal obesity and excess weight adversely effects illness presentation, course, and outcome. Available evidence is beginning to suggest that excess weight is negatively associated with cognitive function in BD.17
It is well established that impairments in executive function are apparent in mixed populations of individuals with BD as well as obese individuals without psychiatric disorders.3,4,9,12,13,18-22 It could be hypothesized that obesity and BD are associated with common CNS structural and/or functional changes in brain regions that subserve cognitive functioning. For example, frontal cortical regions that mediate executive function are hypometabolic in depressed individuals; similarly, overweight/obese individuals manifest reduced metabolic activity, as well as atrophy, in several cortical and subcortical structures.21,23,24
Moreover, the interrelationship between obesity and mood disorders may be due to a pathophysiological nexus that includes abnormalities in hypothalamus-pituitary-adrenal axis function, inflammatory and metabolic systems, disruption of brain circuitry, all of which are potential mediators of cognitive function.9,20,25,26 Further structural and functional investigations, as well as the establishment of mechanisms that mediate cognitive deficits in obesity and BD, are required before a firm conclusion can be drawn.
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