© Magnific
September 7, 2026
Marianne Waldenfels
How quickly we age depends on more than just our genes. Exercise, diet, stress, and environmental factors can all leave epigenetic marks. What these changes may mean for our health – and what biological age tests can really tell us.
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Two people, the same age, born the same year – and yet biologically years apart. Epigenetics offers one explanation: chemical markings on our DNA that help determine which genes are active and which remain silent.
Unlike the genetic sequence itself, this pattern is not fixed. Diet,exercise, sleep, and environmental exposures can all leave measurable traces on it. That is precisely what makes epigenetics one of the most exciting fields in aging research. But how much influence do we actually have? And could the biological clock perhaps even be turned back?
A person's DNA sequence remains virtually unchanged throughout their lifetime. What does change is which sections of it are read – that is, whichgenes are active. Two mechanisms play an important role here: in DNA methylation, small chemical groups are attached to specific sites on the DNA, where they can influence gene activity.
In histone modification, the proteins around which our DNA is wound are altered – and with them, how accessible certain gene segments are.
Think of it like a book: the text itself stays the same. Epigenetic markings, however, act like margin notes that help determine which chapters get opened and read.
The fact that these markings change over the course of a lifetime is particularly evident in identical twins. Although they share virtually the same DNA sequence, they develop increasingly different epigenetic patterns as they age.
It was precisely these age-dependent changes in DNA methylation that aging researcher Steve Horvath drew on. In 2013, he developed one of the most influential methods in modern aging research: hisepigenetic clock uses 353 DNA methylation sites to predict the age of various human tissues with remarkable accuracy.
This is where epigenetics becomes particularly interesting: some of these markings appear to be reversible. For instance,polyphenols from berries, green tea, or turmeric, as well as omega-3 fatty acids, are being investigated for their influence on epigenetic processes. However, the long-term significance of such effects for health and aging has not yet been fully established.
That exercise can influence gene regulation is demonstrated by a widely citedstudy by Romain Barrès and colleagues. After just a single intense training session, the researchers found changes in DNA methylation in the muscle cells of untrained subjects – including at genes that control energy metabolism and the formation ofmitochondria. Exercise can therefore influence which genes are read in muscle tissue with surprising speed.
Psychological stress can also leave epigenetic traces. A widely notedhuman study by McGowan and colleagues found differences in the methylation of a gene important for the stress response in people who had experienced severe abuse in childhood. However, the tissue samples were examined post-mortem, which means it cannot be conclusively established whether the traumatic experiences actually caused the changes.
In general: it is well established that environment and behavior can be associated with epigenetic changes. However, how large the influence of individual lifestyle factors is, how long such changes persist, and what they mean for long-term health are all still being researched.
Changes in DNA methylation have led researchers to a fascinating idea: if certain patterns shift consistently with age, it should be possible to read from them how a body is aging. Since Horvath's first epigenetic clock, an entire family of such models has emerged.
GrimAge was developed, for example, to better capture age-related health risks and mortality.DunedinPACE takes a different approach: rather than primarily stating a biological age in years, the model aims to capture the pace at which biological aging processes are occurring.
This also explains an initially puzzling phenomenon: someone who takes two different tests can receive two different results. This does not necessarily mean that one of them is wrong. The clocks were developed for different target variables and therefore measure different facets of aging.
Commercial providers have turned biological age into their own market segment. Tests such as TruAge from TruDiagnostic, myDNAge, and the Elysium Index analyze DNA methylation in blood, saliva, or urine samples and claim to determine, among other things, biological age or individual aging pace – at prices that can run into several hundred US dollars.
Not every test that advertises a biological age is an epigenetic test in the strict sense: GlycanAge, for example, examines specific sugar structures on antibodies rather than DNA methylation.
Such results can certainly be interesting. But the seemingly precise age figure should not be mistaken for a conventional medical measurement. Different methods can yield different results, and there is currently no universally accepted clinical consequence that can be automatically derived from a particular "epigenetic age."
Measuring biological age is one thing. Far more interesting is a different question: could the clock one day actually be turned back?
Research does not yet fully understand what epigenetic clocks actually measure. A team from the Leibniz Institute on Aging in Jena has therefore worked with international partners to take a closer look at the DNA methylation changes most strongly associated withaging. At the heart of this work lies a critical question: do epigenetic clocks merely reliably indicate that we are getting older, or do they capture processes that are genuinely involved in driving aging itself?
Even more far-reaching is what is known as partial epigenetic reprogramming. The idea sounds almost like science fiction: age-related changes in a cell would be partially reset, without reverting the cell itself to its original stem cell state. This approach builds on the work of Japanese Nobel laureate Shinya Yamanaka. Today, researchers are experimenting with three factors – OCT4, SOX2, and KLF4, known collectively as OSK – which are intended to reset cells to a younger epigenetic state.
What was long confined to basic research is now being tested in humans for the first time. In 2026, the biotech company Life Biosciences received clearance from the US Food and Drug Administration (FDA) for a Phase I study of the gene therapy ER-100 in diseases of the optic nerve. The first patient was treated in June. This marks the first time that partial epigenetic reprogramming has made the leap into a clinical trial in humans.
The study is primarily designed to show whether the procedure is safe and well tolerated. Whether it can actually reverse age-related changes in humans remains to be seen.
This is precisely where the current fascination withepigenetics lies: it shows that our genome is not a rigid program. Which genes are active, and to what degree, can shift over the course of a lifetime – shaped in part by the conditions under which we live. Whether these processes can one day be deliberately harnessed to influence aging itself remains one of the great open questions in modern aging research.
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