Epigenetic clocks are a topic of considerable interest in the research community. They are perhaps the most promising of the present techniques for assessing biological age, the closest to becoming a useful biomarker of aging. Epigenetic clocks are weighted algorithmic combinations of the DNA methylation status of various sites on the genome, reflecting changes that are very similar for everyone, and which map to age with a margin of error of a few years.

These changes are likely reactions to the growing damage and dysfunction of aging – and since everyone ages for the same underlying reasons, it makes sense for some of the changes that take place in cellular processes to be much the same for everyone. The initial epigenetic clocks are now being joined by many others, as there are any number of ways in which to create a viable combination of epigenetic marks that reflects aging.

The interesting aspect of an epigenetic age measure is the degree to which it is higher or lower than chronological age for a given individual. Acceleration of epigenetic age, a higher epigenetic age than chronological age, is quite robustly correlated with incidence of many age-related conditions, as well as with mortality risk. If aging is damage, then more damage has the expected outcome. Today’s research materials, looking into lung function and epigenetic age, are illustrative of the numerous other correlational studies published in recent years.

The development of biomarkers of aging is an important topic. A low-cost way to quickly and rigorously measure the damage and dysfunction of age would greatly speed up research and development of rpotential rejuvenation therapies. At present, the only rigorous test of an approach to slow or reverse aging (versus treating a specific age-related condition) is a life span study. That is out of the question for human trials, and even in mice running a life span study is an expensive, slow proposition.

As a result, researchers are beginning to use epigenetic age assessments in their studies of aging. Unfortunately, these tools are not yet finalized. Because it is unclear as to what exactly causes the characteristic epigenetic changes of age, it is unknown as to how an epigenetic clock will react to any given new class of ejuvenation therapy. The outcome of an assessment isn’t yet actionable, whatever the result. The clocks will have to be calibrated and verified alongside rejuvenation therapies as they are developed – the results cannot yet be taken at face value.

Association of adult lung function with accelerated biological aging