Abstract P2100: Longitudinal association between MIND diet adherence, inflammatory mechanism, and cognitive health

Introduction: Evidence is limited on the cognitive benefits of the Mediterranean-DASH Intervention for Neurodegenerative Delay(MIND) diet and biological mechanism for middle-age adults. We examined the longitudinal association of MIND diet with cognitive change over time and whether the association was mediated by reduced inflammation.
Hypothesis: A higher MIND diet score, indicating better adherence to the dietary pattern, was associated with slower cognitive decline, and inflammation—measured by circulating inflammatory biomarkers—mediated the association.
Methods: This study included data from 3,515 participants of the 2013 Health Care and Nutrition Survey (HCNS), a subsample of the Health and Retirement Study, who were over 50 years of age, were without probable dementia at the baseline in 2012, and had self-reported cognitive measures between 2012 and 2020, MIND diet score, and key demographics. Inflammatory biomarkers included C-reactive protein (CRP), tumor necrosis factor receptor (TNFR1), and Insulin-like growth factor 1 (IGF-1). Change in cognition were estimated using linear mixed effects models. All models were adjusted for age, sex, race/ethnicity, educational attainment, household income, and presence of APOE e4 allele.
Results: Over half of the respondents were aged 65 years and older (51.7%) and female (54.7%). At baseline, compared to the low tertile, higher adherence to MIND diet was associated with better cognitive score [middle tertile: β(SE)=0.41(0.12); high tertile: β(SE)=0.66 (0.16), p<0.001], lower levels of CRP (p<0.001) and TNFR1 (p<0.001), and higher level of IGF1 (p<0.001); higher TNFR1 was associated with worse cognitive scores [β(SE)=-0.038(.17), p<0.029]. TNFR1 mediated 16.02% of the total effect of the MIND diet on cognitive function (indirect β = 0.11, 95% CI [0.08, 0.15]). During the 8-year follow-up, participants in the higher tertile of MIND diet had a slower rate of cognitive decline over time compared to those in the low tertile [low: β(SE)=-0.24(0.023); middle: β(SE)=-0.19(0.023); high: β(SE)=-0.11 (0.028)], p<0.001. The association between MIND diet and cognitive change was attenuated—7.90% for the high tertile—after including TNFR1.
Conclusions: Following a healthy MIND dietary pattern at middle-age can help slow down cognitive decline, which occurs at least partially through mitigating the TNFR1-related inflammation pathway.