1. In this prospective cohort study, a healthier diet in midlife did not affect the risk of developing dementia compared to unhealthier diets.
2. Patients who would go on to develop dementia were more likely to have unhealthier diets in later life.
Evidence Rating Level: 2 (Good)
Study Rundown: Dementia is an irreversible cause of cognitive decline that occurs during aging, and the lack of effective treatments to reverse or slow the progression of dementia necessitate better preventative strategies. Diet has been shown to impact other chronic diseases, and it is unclear if healthier diets during midlife may slow or prevent dementia pathogenesis. In this prospective cohort study over a median of nearly 25 years, there was no association between a healthier diet in midlife and dementia risk compared to unhealthier diets. Patients who would go on to develop dementia had less healthy diets in the later years before dementia diagnosis, suggesting a decrease in diet quality in the pre-clinical period of cognitive decline.
Though this study provides compelling evidence, given its rigor of design and over two decades of follow-up, the study is limited to non-causal associations between diet and dementia. In addition, it is unclear if certain subpopulations, such as those with midlife co-morbidities including heart disease and diabetes, would have decreased dementia risk with healthier diets.
In-Depth [prospective cohort]: Out of 10,308 civil servants in London, UK from the study start in 1985 to 1988, 8225 were assessed in 1991to 1993 and 5544 in 1997 to 1999. Study follow-up ended in 2017. Dietary intake was assessed with a Food Frequency Questionnaire (FFQ) in 1991 to 1993, 1997 to 1999, and 2002 to 2004 and was used to compile the Alternative Healthy Eating Index (AHEI), a metric of overall diet quality. Participants at the most extreme ends of the calorie intake spectrum (>3500 or <500 kcal women; >4200 kcal or <800 men) were excluded. There was no significant effects of age or sex on analyses (p = 0.17), and so these subgroups were not analyzed separately. There were no significant differences in the incidence of dementia between the top and bottom AHEI tertile recorded in 1991 to 1993, 1997 to 1999, or 2002 to 2004 (p > 0.05). In 1991 to 1993, the absolute difference in dementia incidence between the top and bottom AHEI tertiles was 0.04 per 1000 person-years (CI95 -0.42 to 0.51); 0.14 in 1997 to 1999 (CI95 -0.58 to 0.85); -0.73 in 2002 to 2004 (CI95 -1.67 to 0.22). For dietary exposures in 2002 to 2004, a higher AHEI score was associated with a lower incidence of dementia when controlling for age, sex, race, total energy intake, sociodemographic, and behavioral factors (adjusted hazard ratio per 1 SD increment 0.86; CI95 0.75 to 0.99). Those with dementia had reduced AHEI scores during the last 10 years of follow-up compared to those without (between group mean difference -1.26; CI95 -2.49 to -0.04). The mean decline in cognitive z-score over the 18-year follow-up period was -0.74 (CI95 -0.73 to -0.76) and was not associated with AHEI score (p = 0.23) or western diet (p = 0.62). A higher AHEI in 1997 to 1999 was associated with greater cognitive decline in 2015 to 2016 (difference in cognitive function per 1 SD -0.03; CI95 -0.01 to -0.05).
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