Longevity Articles

Clinical Study Shows That the Right Amount of Eating, Sleeping and Exercising Can Keep Your DNA Young

Clinical Study Shows That the Right Amount of Eating, Sleeping, and Exercising Can Keep Your DNA Young

Aging typically involves a decrease in overall health and an increase in the risk of developing serious chronic diseases. Yet, researchers have struggled to develop interventions that could preserve health in advanced age and extend the lifespan. But, is it possible that we can just eat, sleep, exercise, and relax a bit to age better?

Now, a new clinical study (NCT03472820) recently published in the journal Aging gets at this question and shows that several lifestyle interventions can have a positive effect on biological age (1). In just eight short weeks, Fitzgerald and colleagues show that people partaking in an intervention program that included diet, sleep, exercise, relaxation guidance, and supplemental probiotics tested an average of 1.96 years younger, according to a measure of biological aging. 

This marks the second time that a diet and lifestyle intervention has been proven to reduce biological aging in healthy individuals. “Notably, the shorter timeframe of this study and the scale of potential reduction, while modest in magnitude, may correlate with meaningful socioeconomic benefits, and appears to have the potential to be broadly achievable,” said Fitzgerald and colleagues.

What is Biological Aging and How Can We Measure It?

We often think of aging chronologically, celebrating birthdays every 365 days. But our bodies don’t all age at the same rate and in the same way when measured against this calendar. Biological aging is the process by which our cells and tissues begin to fall apart, leading to a deterioration in our body’s function.

There are several proposed ways to measure biological aging. One such way is based on a process called DNA methylation. This process of modifying DNA is known to protect our genetic material that may become damaged or defective as we get older, preserving the integrity of DNA and allowing for proper gene activity. 

When the methylation process is not functioning properly, gene activity is affected and can lead to significant health consequences. If a site is methylated excessively, tumor suppressor genes may be inhibited and tumor growth may go unchecked, whereas if sites are under-methylated, certain pro-inflammatory compounds like cytokines may be overproduced. Research on aging has found that chronic inflammation is closely related to the aging process (2).

Several million methylation sites have been identified, and tests that map these sites are relatively easy and inexpensive. These patterns of methylation sites have led to the development of methylation-based assessments that can serve as a biochemical marker of an individual’s age. Researchers think that the process of aging is dependent on biological changes like DNA methylation.

Can a Healthy Diet and Exercise Impact Your Biological Age?

Simple dietary changes, such as consuming leaner meats and including fish and plant-based proteins, have been shown to influence biological aging. But, to really slow down the aging process, a more in-depth holistic approach is likely required. Researchers have also speculated that providing the proper methylation components in a consistent diet may provide an adequate supply of the nutrients necessary for our cells to carry out the methylation process properly.

Exercise also has numerous health benefits, and several animal models show that it can extend the lifespan. Human studies show that habitual exercise can help preserve the DNA methylation process. One study found that practicing light exercise was beneficial to the DNA methylation process, but partaking in consistent physical activity may be even more beneficial. A study found that women who regularly exercise have a much younger biological age than women who lead a more sedentary lifestyle (6).

Lifestyle Interventions Affect Biological Age

A Clinical Trial Shows That Lifestyle Interventions Affect Biological Age

In this study, Fitzgerald and colleagues used a special tool called the Horvath DNAmAge clock to assess the “age” of participants’ DNA by measuring the amount of activity at known methylation sites (1). This tool has previously been used to predict all-cause mortality and overall health.

A group of 44 men participated in the trial. These participants took part in an 8-week protocol that would include dietary, supplemental, and lifestyle changes. A series of tests recorded health parameters at the beginning of the 8-week intervention, to be compared against results seen at the end of the study. During this time, participants were provided with a healthy, plant-based diet. The diet was not strictly vegetarian since it included eggs and certain beef products, such as liver. It also included certain foods that are known to promote methylation like berries, rosemary, turmeric, garlic, and green and oolong teas. A special mix of supplements made of organic vegetables and fruits, as well as a probiotic, was also included at mealtimes.

Exercise and stress were also taken into consideration since researchers believe that these factors may play a role in the methylation process. Participants were asked to exercise for 30 minutes at least 5 days per week. Rest was encouraged by asking participants to sleep for at least 7 hours per night. Special breathing techniques and relaxation strategies were also part of the protocol.

After eight weeks, participants in the treatment group scored an average of 3.23 years younger according to their DNAmAge assessment, when compared to the control group. Control group participants scored almost 2 years older after the eight weeks. Metabolic measures improved significantly for the treatment group, and an unhealthy type of fat in the blood called triglycerides were reduced by 25%, compared to the control group.

Results from this intervention demonstrate the potential for reversal of biological age. It also demonstrates that dietary sources and probiotics are an effective method of nutrient repletion for promoting methylation. Although this intervention was effective at reducing biological age, more studies will be needed to further understand this approach and fine-tune it for the reversal of biological aging.

Cautions and Future Directions

One significant limitation of this pilot trial is the relatively small sample size. Confirmation of these results is therefore needed in larger study groups and populations beyond middle-aged men.

Also, it is not yet fully established whether interventions that slow any of the “methylation clocks” necessarily curtail risks of age-related disease. This unknown remains an important area of investigation by researchers working to validate predictors of age-related morbidity and mortality, which would otherwise require very long clinical trials.

The use of an intervention based on multiple factors has advantages, but it also means it is not possible to attribute improved outcomes to any one element of the intervention. The combination of interventions used in this study may yet be improved upon and may be more impactful when further personalized.

Future iterations of the intervention in continued clinical trials will attempt to optimize the program for efficacy, efficiency, scalability, and affordability. An ever-evolving understanding of the personalized application of such dietary and lifestyle interventions will likely lead to refinements to this kind of intervention that may further extend indicators of biological age.


  1. Fitzgerald KN, Hodges R, Hanes D, et al. Aging (Albany NY). 2021;13(7):9419-9432. 
  2. Franceschi C, Garagnani P, Parini P, Giuliani C, Santoro A. Nat Rev Endocrinol. 2018;14(10):576-590. 
  3. Field AE, Robertson NA, Wang T, Havas A, Ideker T, Adams PD.  Mol Cell. 2018;71(6):882-895. 
  4. Quach A, Levine ME, Tanaka T, et al. Aging (Albany NY). 2017;9(2):419-446. 
  5. Ren H, Collins V, Clarke SJ, et al. Evid Based Complement Alternat Med. 2012;2012:841810. 
  6. White AJ, Sandler DP, Bolick SC, Xu Z, Taylor JA, DeRoo LA. Eur J Cancer. 2013;49(9):2199-2206. 

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