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Indirect Effects of Elevated Body Mass Index on Memory Performance Through Altered Cerebral Metabolite Concentrations

Gonzales, Mitzi M. MA; Tarumi, Takashi MA; Eagan, Danielle E. MA; Tanaka, Hirofumi PhD; Vaghasia, Miral BS; Haley, Andreana P. PhD

doi: 10.1097/PSY.0b013e31825ff1de
Special Series on Neuroscience in Health and Disease
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Objective: Elevated body mass index (BMI) at midlife is associated with increased risk of cognitive decline in later life. The goal of the current study was to assess mechanisms of early brain vulnerability by examining if higher BMI at midlife affects current cognitive performance through alterations in cerebral neurochemistry.

Methods: Fifty-five participants, aged 40 to 60 years, underwent neuropsychological testing, health screen, and proton magnetic resonance spectroscopy examining N-acetylaspartate, creatine (Cr), myo-inositol (mI), choline, and glutamate concentrations in occipitoparietal gray matter. Concentrations of N-acetylaspartate, choline, mI, and glutamate were calculated as a ratio over Cr and examined in relation to BMI using multivariate regression analyses. Structural equation modeling was used to determine if BMI had an indirect effect on cognition through cerebral metabolite levels.

Results: Higher BMI was associated with elevations in mI/Cr (F(5,45) = 3.843, p = .006, β = 0.444, p = .002), independent of age, sex, fasting glucose levels, and systolic blood pressure. Moreover, a χ2 difference test of the direct and indirect structural equation models revealed that BMI had an indirect effect on global cognitive performance (Δχ2 = 19.939, df = 2, p < .001). Subsequent follow-up analyses revealed that this effect was specific to memory (Δχ2 = 22.027, df = 2, p < .001).

Conclusions: Higher BMI was associated with elevations in mI/Cr concentrations in the occipitoparietal gray matter and indirectly related to poorer memory performance through mI/Cr levels, potentially implicating plasma hypertonicity and neuroinflammation as mechanisms underlying obesity-related brain vulnerability.

From the Departments of Psychology (M.M.G., D.E.E., M.V., A.P.H.) and Kinesiology and Health Education (T.T., H.T.), The University of Texas at Austin; and University of Texas Imaging Research Center (A.P.H.), Austin, Texas.

Address correspondence and reprint requests to Andreana P. Haley, PhD, Department of Psychology, The University of Texas at Austin, 1 University Station, A8000, Austin, TX 78712. E-mail: haley@psy.utexas.edu

This work was funded in part by grants from the American Heart Association (09BGIA2060722 to A.P.H.), American Federation for Aging Research (8A0024 to A.P.H.), the National Institutes of Health (NS075565 to A.P.H.), and The University of Texas at Austin (to A.P.H.).

A.P.H. is funded by the National Institutes of Health, the American Heart Association, and the American Federation for Aging Research and has received research support from The University of Texas at Austin and National Institute of Nursing Research Center (P30 NR005051). H.T. received research support from the American Heart Association. M.M.G., T.T., D.E.E., and M.V. have no disclosures to report.

The publication of this article in Psychosomatic Medicine will not constitute a conflict of interest with any financial or other relationships for any of the authors.

Received for publication September 29, 2011; revision received March 29, 2012.

Copyright © 2012 by American Psychosomatic Society
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