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Mediterranean Diet, Alzheimer Disease, and Vascular Mediation
Nikolaos Scarmeas, MD;
Yaakov Stern, PhD;
Richard Mayeux, MD;
Jose A. Luchsinger, MD
Arch Neurol. 2006;63:1709-1717. Published online October 9, 2006 (doi:10.1001/archneur.63.12.noc60109).
Objectives To examine the association between the Mediterranean diet (MeDi) and Alzheimer disease (AD) in a different AD population and to investigate possible mediation by vascular pathways.
Design, Setting, Patients, and Main Outcome Measures A case-control study nested within a community-based cohort in New York, NY. Adherence to the MeDi (0- to 9-point scale with higher scores indicating higher adherence) was the main predictor of AD status (194 patients with AD vs 1790 nondemented subjects) in logistic regression models that were adjusted for cohort, age, sex, ethnicity, education, apolipoprotein E genotype, caloric intake, smoking, medical comorbidity index, and body mass index (calculated as weight in kilograms divided by height in meters squared). We investigated whether there was attenuation of the association between MeDi and AD when vascular variables (stroke, diabetes mellitus, hypertension, heart disease, lipid levels) were simultaneously introduced in the models (which would constitute evidence of mediation).
Results Higher adherence to the MeDi was associated with lower risk for AD (odds ratio, 0.76; 95% confidence interval, 0.67-0.87; P<.001). Compared with subjects in the lowest MeDi tertile, subjects in the middle MeDi tertile had an odds ratio of 0.47 (95% confidence interval, 0.29-0.76) and those at the highest tertile an odds ratio of 0.32 (95% confidence interval, 0.17-0.59) for AD (P for trend <.001). Introduction of the vascular variables in the model did not change the magnitude of the association.
Conclusions We note once more that higher adherence to the MeDi is associated with a reduced risk for AD. The association does not seem to be mediated by vascular comorbidity. This could be the result of either other biological mechanisms (oxidative or inflammatory) being implicated or measurement error of the vascular variables.
Author Affiliations: Taub Institute for Research on Alzheimer's Disease and the Aging Brain (Drs Scarmeas, Stern, Mayeux, and Luchsinger); Gertrude H. Sergievsky Center (Drs Scarmeas, Stern, and Mayeux); and Departments of Neurology (Drs Scarmeas, Stern, and Mayeux) and Medicine (Dr Luchsinger), Columbia University, New York, NY.
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