The Response of Epigenetic Clocks to Physical Activity
Epigenetic clocks of various sorts have become quite diverse in recent years, and it is worth noting that more recent clocks do not exhibit the insensitivity to physical fitness that was a characteristic of the earliest clocks. We should assume that any clock will have quirks, even those that do well with exercise. Since the relationships between specific causes and dysfunctions in aging and the specific epigenetic marks used in epigenetic clocks remain almost entirely unknown, a clock cannot be trusted to correctly assess the impact of any specific intervention on aging. The clock has to be calibrated against that intervention. This defeats the whole point of the exercise, which is to find ways to quickly assess the merits of potential novel rejuvenation therapies, without having to run lengthy studies to assess life span and mortality.
Epigenetic clocks include several specific measures such as HorvathAge, HannumAge, SkinBloodAge, LinAge, WeidnerAge, VidalBraloAge, ZhangAge, and PhenoAge. Ageing research increasingly focuses on understanding the biological mechanisms that contribute to ageing and how lifestyle factors, such as physical activity (PA), can influence these processes. The above epigenetic ageing indicators represent different approaches to estimating biological age and have been associated with various health outcomes. Recent studies have highlighted the stronger and more consistent associations between PA and epigenetic aging, especially with GrimAge.
This study investigates the relationship between physical activity (PA) levels and DNA methylation (DNAm)-predicted epigenetic clocks in a U.S. population sample (n = 948, mean age 62, 49% female). The eight above mentioned epigenetic clocks were analyzed, revealing that higher PA levels were significantly associated with younger biological ages across all indicators, with the strongest effects observed for SkinBloodAge and LinAge. Subgroup analyses indicated that these associations were more pronounced among non-Hispanic whites, individuals with a BMI of 25-30, and former smokers, suggesting that the impact of PA varies across different groups. These findings emphasize the role of PA in slowing biological ageing and reducing age-related health risks.
Despite spending half the paper discussing the importance of physical activity they did not explain how they quantified physical activity level. It would have also been informative to stratify the cohort based upon fitness level determined by a battery of tests and compare that to methylation tests.
Epigenetic clocks don't measure or predict remaining life expectancy. So if, (for example)
An epigenetic clock indicates that my biological/functional age is 39 years and my true chronological age - number of years since my birth year- 50 years of age. It does not mean that I will live eleven years longer than average life expectancy for humans of my demographic.
Epigenetic clock must consistently show / indicate every year that my functional age is eleven year younger than my true chronological age.
No one had done experiments / studies long term with epigenetic clocks. It would require many human experimental subjects and waiting for all of them to die - which is expensive and may be regarded UNETHICAL.. …… DEATH WATCH - researchers waiting for you to die - to record date of death and calculate statistics of all deaths of all experimental human subjects.