Written by Erin Yeh
Emerging evidence suggests that vegetarian diets, which are defined as high in plant foods and low in animal products, are associated with a lower risk of chronic disease, all-cause mortality, and the incidence of cardiovascular disease. Studies have indicated that certain foods (such as tea, vegetables, and olive oil) and nutrients (such as catechins, lycopene, and omega-3 fatty acids), which are consumed more in vegetarian diets, may contribute to slowing aging.
There is limited data on how overall dietary patterns influence epigenetic aging, which is biological age estimated through DNA methylation markers. Previous studies focusing on diet quality or plant-based diets have shown a reduction in epigenetic aging. However, it is still unknown whether diets relatively higher in plant foods and relatively lower in animal products in non-vegetarian populations influence epigenetic aging. It is also unknown whether a healthy or unhealthy vegetarian diet plays a role.
To determine the relationship between plant-based diets and epigenetic aging, a team of researchers from the University of Washington evaluated four different plant-based diet indices (PDI) (Total PDI, Plant-Based Diet, Healthy PDI, and Unhealthy PDI) and three measures of epigenetic aging (GrimAge2, PhenoAge, and HannumAge). Their study was published last month in Aging-United States (DOI: 10.18632/aging.206362).
Vegetarian diets and inflammation
The team used data from the Atherosclerosis Risk in Communities (ARIC) study and the National Health and Nutrition Examination Survey (NHANES). In the ARIC study, participants were selected for DNA methylation if they consented to the use of their DNA, resulting in a sample size of 2,810 participants. For NHANES, participants older than 50 years with available biospecimens were eligible for DNA methylation assessment. Applying similar exclusion criteria from the ARIC study and excluding participants older than 85 years, the sample size was a total of 2056 participants. More than half of the participants in each study were women. Two-thirds of ARIC participants were black, and two-thirds of NHANES participants were non-white.
According to the team’s analysis, dietary patterns characterized by increased intake of plant foods and low intake of animal products were consistently associated with slower aging, as measured by biomarkers of aging derived from DNA methylation, particularly GrimAge2 and PhenoAge. Greater adherence to healthy plant-based diets was associated with slower GrimAge2, although this association was attenuated in sensitivity analyses. Eating healthy plant foods in general has also been linked to slower aging, according to both GrimAge2 and PhenoAge. In mediation analyses, GrimAge2 partially explained the association between vegetarian diets and lower risk of all-cause mortality.
The study confirmed the team’s hypothesis: Diets high in plant foods, especially those classified as healthy, may be the key to promoting a slowing of biological aging. Researchers note that diets containing higher amounts of plant foods tend to be richer in dietary fiber and antioxidants while lower in pro-inflammatory components such as saturated fat, leading to lower inflammation. Lower levels of inflammation can prevent harmful changes in DNA methylation patterns. Furthermore, people who follow plant-based diets have lower body fat and healthier lipid profiles, which are associated with lower levels of inflammation. Combined, these factors can help slow biological aging, as well as reduce cellular dysfunction and cell death.
The researchers said In a press release“No significant association was observed between unhealthy PDI and any DNA methylation-based aging.” In the ARIC study, participants with greater adherence to unhealthy plant-based diets had a higher intake of added sugar, but this association was a very small difference (0.02 GrimAge2 acceleration per 1 gram of added sugar). The team recommends further investigation into whether unhealthy plant foods influence epigenetic aging compared to healthy plant foods, as well as evaluating whether added sugars alter aging.
The team also stressed that the relationship between healthy plant-based diets and GrimAge2 was not consistent between the two study groups. In the ARIC study, a healthy plant-based diet was not significantly associated with GrimAge2 while in NHANES, it was associated with slowed GrimAge2. Furthermore, after blood cell composition was modified, the binding decreased. When analyzing food groups, several components of healthy plant foods—whole grains, fruits, and vegetables—were associated with lower GrimAge2 in NHANES but not in ARIC. These discrepancies highlight the need for further research to confirm whether a healthy, plant-based diet is associated with GrimAge2.
Various limitations and measurement systems
The current study found that plant-based diets were consistently associated with slower aging, especially when measured by GrimAge2 and PhenoAge. GrimAge2 has also been shown to be consistent with previous studies (Healthy Eating Index, Alternative Healthy Eating Index, DASH Diet, and Alternative Mediterranean Diet), meaning it may be particularly responsive to dietary factors. In contrast, only inclusive plant-based diets showed an inverse association with HannumAge, suggesting that some measures of epigenetic aging may be more sensitive to dietary influences than others.
The team noted In the same press release The study consists of observational data and does not prove causality. Data were evaluated from a single time point, meaning that the study design does not allow for causal interference regarding the relationship between plant-based diets and epigenetic aging.
One study limitation is that the timing of dietary assessment and DNA methylation profiling was not consistent for some ARIC study participants. Another limitation is potential error in self-reported data on dietary intake, although the ARIC study used administered food frequency questionnaires that included standardized estimates of portion size, which may have helped reduce measurement error.
Although analyzes were adjusted for key confounders (eg, physical activity, alcohol consumption, smoking), there remains the potential for residual confounding from unmeasured or incompletely measured variables. Finally, the three measures have different coverage of cytokine, phosphate, and guanine sites, the major site of DNA methylation in mammals, which may influence the calculation of measures of epigenetic aging. These factors should be taken into account when evaluating associations with food species. However, because GrimAge2 showed the strongest and most consistent relationship between dietary type and aging, the authors recommend using GrimAge2 to evaluate the anti-aging effects of dietary exposure in future research.
