Abstract

Introduction: Evidence shows that individual variation of body weight over time may have a role in explaining cognitive decline later in life independent from obesity status. Yet, the effect of long-term variability from childhood on midlife cognitive function (CF), as well as race differences remains unclear. This study examines this association among Black and White middle-aged individuals from a community cohort in Bogalusa, Louisiana. Methods: A total of 1,268 participants (59.5% women, 34.4% Black) from the Bogalusa Heart Study who had > 4 BMI measurements from childhood (mean age: 9.5 ± 3.5), and complete neuropsychological (NP) tests assessment to evaluate CF at midlife (48.2 ± 5.2) were studied. CF was measured with a global cognitive score (GCS). Long-term BMI variability was computed as standard deviation (SD), coefficient of variation (CV), deviation from age-predicted values (DEV), and residual SD (RSD). Regression models were used to evaluate the associations between BMI variability and GCS. Covariates included age, sex, race, cardiovascular risk factors, depression, class II obesity (BMI ≥ 35kg/m 2 ) at midlife, alcohol use, education and employment status. Race, sex and BMI variability interactions were evaluated. Results: Overall, higher DEV and RSD [Beta (SE): -0.30 (0.10); p = 0.003, and – 0.17 (0.08); p = 0.025, respectively] was associated with lower GCS. Interactions between SD, CV, DEV, and RSD with race were significant, but not with sex. Stratified analyses of the relationship between BMI variability measures and GCS showed the following result among White participants [DEV Beta (SE): -0.25 (0.10); p = 0.01] and Black participants [DEV Beta (SE): -0.03 (0.13); p = 0.81], respectively. Conclusion: We identified diverse associations between BMI variability from childhood and cognitive function in midlife. Although Black participants appear more resilient to the influence of BMI variability on CF in midlife, further studies are needed to identify the nature of this complex phenomenon and its potential to contribute to vascular causes of cognitive decline and dementia.

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