Better diet quality linked to longer lifespan

A higher quality of diet appears to decelerate epigenetic age acceleration, which partially explains the beneficial effect of diet on prolonged lifespans, according to a study. This effect seems to be more noticeable for those with a smoking history.

“A mediation analysis further demonstrated that DNA methylation may partly explain the beneficial relation between a healthy diet and all-cause mortality, particularly in individuals who have a history of smoking,” the researchers said.

Data from 1,995 participants (mean age 67 years, 55 percent women) of the Framingham Heart Study Offspring Cohort were analysed. The researchers also examined cross-sectional associations between the Dietary Approaches to Stop Hypertension (DASH) score and three whole-blood DNA methylation‒derived epigenetic age acceleration measures­—Dunedin Pace of Aging Methylation (DunedinPoAm), GrimAge acceleration (GrimAA), and PhenoAge acceleration (PhenoAA).

Finally, a mediation analysis was performed to determine the mediating role of epigenetic age acceleration on all-cause mortality and DASH.

A significant association was observed between a higher DASH score and lower levels of DunedinPoAm (β, −0.05; SE, 0.02; p=0.007), GrimAA (β, −0.09; SE, 0.02; p<0.001), and PhenoAA (β, −0.07; SE, 0.02; p=0.001). [Am J Clin Nutr 2022;115:163-170]

All epigenetic measures mediated the association between DASH score and all-cause mortality (DunedinPoAm: mean proportion [MP], 22.1 percent; p_mediation=0.04; GrimAA: MP, 45.1 percent; p_mediation=0.001; PhenoAA: MP, 22.9 percent; p_mediation=0.03).

An interaction was also noted between DASH score and smoking status with respect to epigenetic ageing markers, in which the association between DASH score and epigenetic ageing markers appeared more robust in “ever smokers” (former and current smokers) than “never smokers.” Mediation proportions were 31.3 percent, 46.8 percent, and 10.3 percent for DunedinPoAm, GrimAA, and PhenoAA, respectively in ever smokers; no significant mediation was seen in never smokers.

“This favourable relation between higher diet quality scores and epigenetic age deceleration may be related to reductions in oxidative and inflammatory stress,” the researchers said. “It was demonstrated that epigenetic age acceleration relates to inflammatory biomarkers and postprandial lipid levels in White individuals.” [Nutr Metab Cardiovasc Dis 2014;24:929-939; Clin Epigenetics 2018;10:56]

Additionally, the three measures of epigenetic ageing acceleration were found to be related to the consumption of nuts and legumes, which can be linked to decreases in oxidative and inflammatory processes prohibited by bioactive compounds such as mono- and polyunsaturated fatty acids, phenolic compounds, tocopherols, and carotenoids. [Circ Genom Precis Med 2020;13:e002766]

“Previous studies have shown that the epigenetic ageing markers used by the present study have stronger predictive abilities for the time to chronic diseases and death compared to the first-generation epigenetic ageing markers,” the researchers said. [Aging 2019;11:303-327]

The current study also showed that whole blood‒derived DNA methylation-based epigenetic ageing markers are useful for gauging the effects of diet on health in observational studies and may be applied to intervention studies. [Genes Nutr 2017;12:24]

“Further studies are warranted to validate our findings, including studies with larger sample sizes, studies with racially and ethnically diverse populations, and studies investigating the causal role of dietary factors on epigenetic regulations,” the researchers said.