Alzheimer disease pathology can be found in the brains of older persons without dementia or mild cognitive impairment and is related to subtle changes in episodic memory.
Mild cognitive impairment is associated with an increased risk of death and incident AD, and a greater rate of decline in selected cognitive abilities.
Background
In a previous study, higher concordance to the MIND diet, a hybrid Mediterranean-DASH diet, was associated with slower cognitive decline. In this study we related these three dietary patterns to incident Alzheimer’s disease.
Methods
We investigated the diet-AD relations in a prospective study of 923 participants, ages 58 to 98 years, followed on average 4.5 years. Diet was assessed by a semi-quantitative food frequency questionnaire.
Results
In adjusted proportional hazards models, the second (HR=0.65, 95% CI 0.44, 0.98) and highest tertiles (HR=0.47, 95% CI 0.26, 0.76) of MIND diet scores had lower rates of AD versus tertile 1 whereas only the third tertiles of the DASH (HR=0.61, 95% CI 0.38, 0.97) and Mediterranean (HR=0.46, 95% CI 0.26, 0.79) diets were associated with lower AD rates.
Conclusion
High adherence to all three diets may reduce AD risk. Moderate adherence to the MIND diet may also decrease AD risk.
Background
The Mediterranean and DASH diets have been shown to slow cognitive decline, however, neither diet is specific to the nutrition literature on dementia prevention.
Methods
We devised the MIND diet score that specifically captures dietary components shown to be neuroprotective and related it to change in cognition over an average 4.7 years among 960 participants of the Memory and Aging Project.
Results
In adjusted mixed models, the MIND score was positively associated with slower decline in global cognitive score (β=0.0092; p<.0001) and with each of 5 cognitive domains. The difference in decline rates for being in the top tertile of MIND diet scores versus the lowest was equivalent to being 7.5 years younger in age.
Conclusion
The study findings suggest that the MIND diet substantially slows cognitive decline with age. Replication of these findings in a dietary intervention trial would be required to verify its relevance to brain health.
The exclusion of sex and gender has impeded faster advancement in the detection, treatment, and care of AD across the clinical spectrum. Greater attention to these differences will improve outcomes for both sexes.
GROWING BODY OF EVIDENCE suggests that oxidative processes may be involved in the etiology of Alzheimer disease (AD). 1 Accumulated damage to lipid membranes and DNA by oxygen free radicals and reactive oxygen species is thought to disrupt normal cell functioning and lead to neuronal death. 2 Antioxidant nutrients, including vitamin E, vitamin C, and beta carotene, are among the body's natural defense mechanisms against oxidative stress. The antioxidant nutrients have been shown through animal and laboratory studies of brain tissue to decrease lipid peroxidation 3-11 and the oxidation of proteins, 12,13 inhibit the production of reactive oxygen species, 6,14,15 prevent mitochondrial dysfunction 12,16 and DNA fragmentation, 6,17 and reduce neurotoxicity, 18,19 apoptosis, 15,19-21 and neuronal death. 18,22 Few studies have examined the relation between dietary intake of antioxidant nutrients and the development of AD. Two prospective studies 23,24 that reported on the association of vitamin E and vitamin C supplement use and AD yielded conflicting results, but both had limited power to test the hypothesis, and neither had dietary information. We report on the association between incident AD and intake of antioxidant nutrients from foods and supplements in a large community study, the Chicago Health and Aging Project (CHAP).
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