Inverse Association Between BMI and Prefrontal Metabolic Activity in Healthy Adults

National Institute on Drug Abuse, Bethesda, Maryland, USA.
Obesity (Impact Factor: 3.73). 11/2008; 17(1):60-5. DOI: 10.1038/oby.2008.469
Source: PubMed


Obesity has been associated with a higher risk for impaired cognitive function, which most likely reflects associated medical complications (i.e., cerebrovascular pathology). However, there is also evidence that in healthy individuals excess weight may adversely affect cognition (executive function, attention, and memory). Here, we measured regional brain glucose metabolism (using positron emission tomography (PET) and 2-deoxy-2[(18)F]fluoro-D-glucose (FDG)) to assess the relationship between BMI and brain metabolism (marker of brain function) in 21 healthy controls (BMI range 19-37 kg/m(2)) studied during baseline (no stimulation) and during cognitive stimulation (numerical calculations). Statistical parametric mapping (SPM) revealed a significant negative correlation between BMI and metabolic activity in prefrontal cortex (Brodmann areas 8, 9, 10, 11, 44) and cingulate gyrus (Brodmann area 32) but not in other regions. Moreover, baseline metabolism in these prefrontal regions was positively associated with performance on tests of memory (California Verbal Learning Test) and executive function (Stroop Interference and Symbol Digit Modality tests). In contrast, the regional brain changes during cognitive stimulation were not associated with BMI nor with neuropsychological performance. The observed association between higher BMI and lower baseline prefrontal metabolism may underlie the impaired performance reported in healthy obese individuals on some cognitive tests of executive function. On the other hand, the lack of an association between BMI and brain metabolic activation during cognitive stimulation indicates that BMI does not influence brain glucose utilization during cognitive performance. These results further highlight the urgency to institute public health interventions to prevent obesity.

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    • "Positron emission tomography (PET) and functional magnetic resonance imaging (fMRI) research suggests that obesity is associated with alterations in metabolic activity within the brain. Volkow et al. (2009) used PET imaging to examine the relationship between BMI and brain glucose metabolism at baseline (no stimulation) and during cognitive stimulation in 21 healthy controls . Results showed a significant negative relationship between BMI and metabolic activity in the prefrontal cortex and cingulate gyrus at baseline, which in turn predicted test performance on measures of executive function and memory. "
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    ABSTRACT: This review paper will discuss the recent literature examining the relationship between obesity and neurocognitive outcomes, with a particular focus on cognitive changes after bariatric surgery. Obesity is now recognized as an independent risk factor for adverse neurocognitive outcomes, and severely obese persons appear to be at even greater risk. Bariatric surgery is associated with rapid improvements in cognitive function that persist for at least several years, although the mechanisms underlying these improvements are incompletely understood. Assessment of cognitive impairment in bariatric surgery patients is challenging, and improved methods are needed, as poorer performance on neuropsychological tests of memory and executive function leads to poorer clinical weight outcomes. In addition to its clinical importance, further study in this area will provide key insight into obesity-related cognitive dysfunction and clarify the possibility of an obesity paradox for neurological outcomes. Copyright © 2015 John Wiley & Sons, Ltd and Eating Disorders Association. Copyright © 2015 John Wiley & Sons, Ltd and Eating Disorders Association.
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    • "The hypothesis regarding transfer of addiction seems more likely, following even longer periods post-bariatric surgery. While there is evidence for a decreased availability of D2R in obese subjects (Volkow et al., 2009), there is some controversy that argues this is only true for severe obesity (Eisenstein et al., 2013; Kessler, Zald, Ansari, Li & Cowan, 2014). Confounding variables include control cohorts from which other RDS behaviors have not been excluded, the use of BMI as a factor may not be appropriate as a phenotype and mild obesity may not indicate the real disorder. "
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