Plant-Based Diets May Slow Aging

By Irene Yeh 

Emerging evidence shows that plant-based diets, defined as being rich in plant foods and low in animal products, are linked to decreased risk of chronic disease, all-cause mortality, and incidence of cardiovascular disease. Studies have indicated that certain foods (e.g. tea, vegetables, olive oil) and nutrients (e.g. catechin, lycopene, omega-3 fatty acid), which are generally consumed more in plant-based diets, may contribute to slower aging.  

There is limited data on how overall diet patterns affect epigenetic aging, the biological age estimated from DNA methylation markers. Previous studies focused on diet quality or vegan diets showed lower epigenetic aging. However, it is still unknown if diets relatively higher in plant foods and relatively lower in animal products in a non-vegetarian population affect epigenetic aging. It is also unknown if a healthy or unhealthy plant-based diet plays a factor. 

To determine the connection between plant-based diets and epigenetic aging, a team of researchers from the University of Washington evaluated four different plant-based diets indices (PDI) (overall PDI, provegetarian diet, healthy PDI, and unhealthy PDI) and three measures of epigenetic aging (GrimAge2, PhenoAge, and HannumAge). Their study was published last month in Aging-US (DOI: 10.18632/aging.206362).  

Plant-Based 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 having their DNA used, resulting in a sample size of 2,810 participants. For NHANES, participants older than 50 years of age 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 2,056 participants. More than half of the participants in each study were women. Two-thirds of the ARIC participants were Black, and two-thirds NHANES participants were non-white. 

According to the team’s analysis, dietary patterns characterized by higher intake of plant foods and lower intake of animal products were consistently associated with slower aging, as measured by DNA methylation-derived aging biomarkers, especially GrimAge2 and PhenoAge. Greater adherence to healthy plant-based diets was connected to decelerated GrimAge2, although this association was attenuated in sensitivity analyses. Overall intake of healthy plant foods was also linked to slower aging, according to both GrimAge2 and PhenoAge. In mediation analyses, GrimAge2 partially explained the relationship between plant-based diets and reduced risk of all-cause mortality.  

The study confirmed the team’s hypothesis: diets high in plant-based foods, especially those categorized as healthy, may be the key to promoting decelerated biological aging. The authors note that the diets with higher intake of plant-based foods tend to be rich in dietary fiber and antioxidants while being lower in pro-inflammatory components such as saturated fat, resulting in decreased inflammation. Lower inflammation levels 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 inflammation levels. Together, these factors can help decelerate biological aging, as well as limit cellular dysfunction and cell death. 

The researchers said in a press release, “No significant association was observed for unhealthy PDI and any of the DNA methylation-based aging.” In the ARIC Study, participants with greater adherence to unhealthy plant-based diets had higher added sugar intake, but this association was a very small difference (.02 accelerated GrimAge2 per one gram of added sugar). The team recommends further investigation into whether unhealthy plant-based foods influence epigenetic aging in comparison to healthy plant-based foods, as well as assess if added sugars change aging.  

The team also emphasized that the relationship between healthy plant-based diets and GrimAge2 was not consistent across the two study populations. In the ARIC Study, a healthy plant-based diet was not significantly associated with GrimAge2 while in NHANES, it was linked to decelerated GrimAge2. Furthermore, after adjusting blood cell composition, the association lessened. When analyzing food groups, several components of healthy plant foods—whole grains, fruits, and vegetables—were linked to reduced GrimAge2 in NHANES but not in ARIC. These inconsistencies highlight a need for further research to confirm if a healthy plant-based diet is correlated with GrimAge2. 

Limitations and the Different Measurement Systems 

The present study found that plant-based diets were consistently associated with slower aging, specifically when measured by GrimAge2 and PhenoAge. GrimAge2 was also shown to align with previous studies (Healthy Eating Index, Alternative Healthy Eating Index, DASH diet, and the alternate Mediterranean diet), meaning it might be particularly responsive to dietary factors. In contrast, only overall plant-based diets showed an inverse association with HannumAge, which suggests some epigenetic aging metrics may be more sensitive to dietary influences than others. 

The team noted in the same press release that the study consists of observational data and does not establish causality. The data were assessed from a single point of time, which means the study design does not allow causal interference regarding the relationship between plant-based diets and epigenetic aging.  

One limitation of the study is that the timing of dietary assessment and DNA methylation profiling was not aligned for some participants in the ARIC Study. Another limitation is potential error in self-reported data on dietary intake, though the ARIC Study used administered food frequency questionnaires that included standardized portion size estimates, which probably helped with decreased measurement error.  

Though the analyses adjusted for key confounders (e.g. physical activity, alcohol consumption, and smoking), there is still the possibility of residual confounding from unmeasured or imperfectly measured variables. Finally, the three measurements have their own different coverage of cytokine-phosphate-guanine sites, the primary site for DNA methylation in mammals, which may influence the calculation of epigenetic aging measures. These factors must be taken into consideration when evaluating associations with dietary types. However, because GrimAge2 showed the strongest and most consistent relationship between dietary type and aging, the authors recommend using GrimAge2 for assessing anti-aging effects of dietary exposures in future research.