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Behavior and Psychology

Body mass index and cognitive function: the potential for reverse causation

International Journal of Obesity volume 39, pages 1383–1389 (2015)Cite this article

Subjects

Abstract

Objective:

Higher late life body mass index (BMI) is unrelated to or even predicts lower risk of dementia in late life, a phenomenon that may be explained by reverse causation due to weight loss during preclinical phases of dementia. We aim to investigate the association of baseline BMI and changes in BMI with dementia in a large prospective cohort, and to examine whether weight loss predicts cognitive function.

Methods:

Using a national cohort of adults average age 58 years at baseline in 1994 (n=7029), we investigated the associations between baseline BMI in 1994 and memory scores from 2000 to 2010. We also examined the association of BMI change from 1994 to 1998 with memory scores from 2000 to 2010. Last, to investigate reverse causation, we examined whether memory scores in 1996 predicted BMI trajectories from 2000 to 2010.

Results:

Baseline overweight predicted better memory scores 6 to 16 years later (β=0.012, 95% confidence interval (CI)=0.001; 0.023). Decline in BMI predicted lower memory scores over the subsequent 12 years (β=−0.026, 95% CI= −0.041; −0.011). Lower memory scores at mean age 60 years in 1996 predicted faster annual rate of BMI decline during follow-up (β=−0.158 kg m−2 per year, 95% CI= −0.223; −0.094).

Conclusion:

Consistent with reverse causation, greater decline in BMI over the first 4 years of the study was associated with lower memory scores over the next decade and lower memory scores was associated with a decline in BMI. These findings suggest that preclinical dementia predicts weight loss for people as early as their late 50s.

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Acknowledgements

The Health and Retirement Study (HRS) is sponsored by the National Institute on Aging (NIA U01AG009740) and is conducted by the University of Michigan. MMG was funded by the American Heart Association (10SDG2640243) and National Institute of Health (R21AG034385). CKS was funded by CAPES (2285/13-4). PG was funded by the National Heart, Lung, and Blood Institute at NIH (NIH 1F31HL112613); the American Heart Association (10SDG2640243), and the Yerby Postdoctoral Fellowship Program. HRS is sponsored by the National Institute on Aging (NIA U01AG009740) and is conducted by the University of Michigan. CKS was funded by CAPES (2285/13-4). PG was funded by the National Heart, Lung, and Blood Institute at NIH (NIH 1F31HL112613); the American Heart Association (10SDG2640243), and the Yerby Postdoctoral Fellowship Program. ERM reports no disclosures. MMG was funded by the American Heart Association (10SDG2640243) and National Institute of Health (R21AG034385).

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Authors and Affiliations

  1. Department of Social and Behavioral Sciences, Harvard School of Public Health, Boston, MA, USA

    C K Suemoto, P Gilsanz & M M Glymour

  2. Discipline of Geriatrics, University of Sao Paulo Medical School, Sao Paulo, SP, Brazil

    C K Suemoto

  3. Department of Epidemiology and Biostatistics, University of California San Francisco, San Francisco, CA, USA

    E R Mayeda & M M Glymour

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Correspondence to C K Suemoto.

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Suemoto, C., Gilsanz, P., Mayeda, E. et al. Body mass index and cognitive function: the potential for reverse causation. Int J Obes 39, 1383–1389 (2015). https://doi.org/10.1038/ijo.2015.83

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