Association of Obesity With Cognitive Decline in Black and White Americans

Abstract

Background and objectives: There are disparities in the prevalence of obesity by race, and the relationship between obesity and cognitive decline is unclear. The objective of this study was to determine whether obesity is independently associated with cognitive decline and whether the association between obesity and cognitive decline differs in Black and White adults. We hypothesized that obesity is associated with greater cognitive decline compared with normal weight and that the effect of obesity on cognitive decline is more pronounced in Black adults compared with their White counterparts.

Methods: We pooled data from 28,867 participants free of stroke and dementia (mean, SD: age 61 [10.7] years at the first cognitive assessment, 55% female, 24% Black, and 29% obese) from 6 cohorts. The primary outcome was the annual change in global cognition. We performed linear mixed-effects models with and without time-varying cumulative mean systolic blood pressure (SBP) and fasting plasma glucose (FPG). Global cognition was set to a t-score metric (mean 50, SD 10) at a participant's first cognitive assessment; a 1-point difference represents a 0.1 SD difference in global cognition across the 6 cohorts. The median follow-up was 6.5 years (25th percentile, 75th percentile: 5.03, 20.15).

Results: Obese participants had lower baseline global cognition than normal-weight participants (difference in intercepts, -0.36 [95% CI, -0.46 to -0.17]; p < 0.001). This difference in baseline global cognition was attenuated but was borderline significant after accounting for SBP and FPG (adjusted differences in intercepts, -0.19 [95% CI, -0.39 to 0.002]; p = 0.05). There was no difference in the rate of decline in global cognition between obese and normal-weight participants (difference in slope, 0.009 points/year [95% CI, -0.009 to 0.03]; p = 0.32). After accounting for SBP and FPG, obese participants had a slower decline in global cognition (adjusted difference in slope, 0.03 points/year slower [95% CI, 0.01 to 0.05]; p < 0.001). There was no evidence that race modified the association between body mass index and global cognitive decline (p = 0.34).

Discussion: These results suggest that obesity is associated with lower initial cognitive scores and may potentially attenuate declines in cognition after accounting for BP and FPG.

Figure 1. Derivation of the Cohort

Categories for missing data on covariates are not mutually exclusive. Missing data include body mass index (n = 40), glucose (n = 351), waist circumference (n = 118), smoking (n = 8), physical activity (n = 50), LDL cholesterol (n = 350), education (n = 189), antihypertensive medication (n = 26), history of atrial fibrillation (n = 1), and history of myocardial infarction (n = 1). BP = blood pressure; LDL = low-density lipoprotein.

Figure 2. Predicted Global Cognitive Trajectory by BMI Category

Participant-specific (conditional) predicted values of cognition were calculated for a 60-year-old Black participant (female vs male) with the following values of all covariates at or before the first cognitive assessment: NOMAS cohort, eighth grade or lower education, nonsmoking, LDL cholesterol (123.8 mg/dL) and glucose (95.7 mg/dL) that increases by 0.1 mg/dL each year, no history of atrial fibrillation, no hypertension treatment, and a baseline SBP of 150 mm Hg that increases by 1 mm each year. Random effects were set to zero. Linear mixed-effects models included time since the first cognitive assessment and baseline values measured before or at the time of the first cognitive assessment of body mass index (BMI; normal, overweight, and obese), age, race, sex, cohort study, education, current cigarette smoking, waist circumference (WC), physical activity, LDL cholesterol, time-dependent cumulative mean systolic blood pressure (SBP) and fasting plasma glucose (FPG), use of antihypertensive medication, history of atrial fibrillation, age × time, sex × time, BMI × time, and race × time. LDL = low-density lipoprotein.