A recent study posted to medRxiv* preprint server tested whether healthy diets slowed biological aging and, thus, dementia.
Study: Diet, pace of biological aging, and risk of dementia in the Framingham Heart Study. Image Credit: RossHelen/Shutterstock.com
*Important notice: medRxiv publishes preliminary scientific reports that are not peer-reviewed and, therefore, should not be regarded as conclusive, guide clinical practice/health-related behavior, or treated as established information.
Background
People eating healthy diets have a lower risk of developing dementia, but the underlying biological mechanisms are poorly understood.
Biological processes associated with healthier diets and lower risk of dementia include the reversal of hallmarks of aging, such as metabolic regulation and lower oxidative stress and inflammation.
The findings from animal models and observational studies in humans linking healthy diets with lifespan and health span suggest that the likely mechanism involves slowing biological aging processes. Biological aging occurs due to the accumulation of molecular changes undermining the resilience and functioning of tissues and organs, leading to disease/death.
Research advances have yielded new biological aging measures, such as epigenetic clocks. These clocks are algorithms combining information from hundreds of methylation marks on leucocytes' DNA to estimate the pace/progress in biological aging.
Substantial evidence suggests that epigenetic clocks, such as DunedinPACE, PhenoAge, and GrimAge, are biomarkers for predicting health span and lifespan.
About the study
In the present study, researchers tested whether people eating healthier diets had a slower pace of aging in the Framingham heart study that followed three generations of individuals. They analyzed data from the offspring cohort that commenced in 1971, involving the second generation of participants who were since followed up every four to seven years.
At follow-up visits, participants underwent blood sampling, physical examination, and neurocognitive testing. They also completed questionnaires related to their lifestyles. The team obtained DNA methylation (DNAm) profiles from the database of genotypes and phenotypes.
DunedinPACE was computed for the DNAm dataset. A semi-quantitative food frequency questionnaire was administered at each follow-up to obtain dietary information.
The team computed the dietary guideline adherence index (DGAI) scores to assess compliance with the dietary guidelines for Americans for data from the fifth, seventh, and eighth follow-up assessments during 1991-95, 1998-2001, and 2005-08, respectively. The DGAI score comprised sub-scores on healthy choices and energy-specific food intake.
Subjects were flagged for additional assessment if 1) they (or their family) reported subjective cognitive impairment, 2) they were referred by the physician/investigator, or 3) their mini-mental state examination scores were lower than education-based cut-offs. These flagged subjects underwent additional neuropsychologic and neurologic examinations.
A committee reviewed possible cases of cognitive decline to determine dementia and the onset date. The eighth follow-up visit served as the baseline in the present study.
Participants were followed up until 2018 for outcomes (dementia or death). The independent effects of DunedinPACE and DGAI scores on dementia or all-cause mortality were assessed.
Findings
The offspring cohort comprised 2,798 participants. After exclusions, the final sample included 1,525 individuals aged 69.7, on average. The average DGAI score was 61.5 on a 100-point scale.
Individuals with greater adherence to dietary guidelines were older, married, less likely to be smokers, and had higher education and physical activity but lower body mass index (BMI). During the follow-up, dementia was diagnosed in 129 subjects, and 432 deaths occurred.
Individuals with a faster pace of aging were at an increased risk of dementia at baseline. By contrast, participants with healthier diets over past decades had a slower pace of aging and lower dementia risk at baseline.
The faster baseline pace of aging also increased the risk of all-cause mortality. By contrast, a healthy diet alleviated the risk of mortality. DunedinPACE mediated 15% and 39% of the effects of DGAI scores on dementia and mortality, respectively.
The associations did not differ by sex or apolipoprotein E ε4 status. However, the association between diet and aging was stronger among ever-smokers than never-smokers.
Finally, the researchers used the Mediterranean diet score as an alternative measure and repeated the analysis; they found that 15% and 46% of the associations of Mediterranean diet scores with dementia and mortality, respectively, were mediated by DunedinPACE.
Conclusions
In summary, the findings reveal that eating healthier diets was associated with lower dementia and mortality risks; this effect was partly mediated by the slower pace of aging, as measured by DunedinPACE.
The study's limitations include the self-reported nature of dietary data, which is subject to recall bias.
Moreover, the data could not distinguish the processes wherein diet improves organ health, leading to slower aging. The sample predominately included White individuals, limiting the generalizability of the results.
Overall, monitoring the pace of aging could inform dementia prevention; future studies are required to corroborate these findings in diverse populations.
*Important notice: medRxiv publishes preliminary scientific reports that are not peer-reviewed and, therefore, should not be regarded as conclusive, guide clinical practice/health-related behavior, or treated as established information.
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