What if your body were a different age from the one on your identity card?
We all have a chronological age, calculated from our date of birth. Yet scientists now know that there is another measure of time: biological age. This reflects the actual state of our cells, tissues and organs. Some 60-year-olds may have a biological profile comparable to that of a 45-year-old, while others age more quickly.
In recent years, epigenetics has emerged as one of the most promising tools for measuring biological age. A major study published in 2026 even offers new evidence that epigenetic changes are not merely markers of ageing: they could be one of its direct causes.
Epigenetics: the conductor of our genes
Contrary to a common misconception, our DNA is not a fixed programme. Genes can be activated, slowed down or put on standby according to the body’s needs.
Epigenetics encompasses the mechanisms that alter gene expression without changing the underlying sequence. Among them, the methylation of DNA is one of the most studied. It involves adding small chemical groups to certain regions of DNA, thereby influencing gene activity.
With age, these epigenetic marks gradually change in remarkably predictable patterns. This observation led researchers to develop the well-known epigenetic clocks, which can estimate an individual’s biological age from a simple biological sample.
Epigenetic clocks: a new way to measure ageing
Epigenetic clocks analyse thousands of methylation sites across the genome. Using sophisticated algorithms, they can estimate a person’s biological age with great precision.
Until recently, however, a fundamental question remained unanswered: are epigenetic changes simply witnesses to ageing, or do they actively contribute to the process?
A study published in July 2026 offers part of the answer
On 15 July 2026, Springer Nature highlighted an article entitled "Increased DNA methylation linked to aging phenotypes in a progeria syndrome", discussing a major discovery in ageing research.
The article draws on a study published in Nature Genetics on an extremely rare genetic disorder: Heyn-Sproul-Jackson syndrome, a form of accelerated ageing.
The researchers identified a mutation in these patients in the gene DNMT3A, an enzyme essential to controlling DNA methylation. This mutation causes an abnormal increase in methylation across many regions of the genome.
More surprisingly still, the methylation profiles observed in these patients closely resemble those seen during natural ageing. Affected individuals also show several characteristics usually associated with older age: altered stem cells, bone disorders, metabolic abnormalities and dysfunction in certain tissues.
When stem cells age prematurely
One of the study’s most important contributions concerns the role of stem cells.
The researchers showed that excessive methylation disrupts the normal functioning of these cells, which are essential for tissue renewal. Their ability to produce new cells declines, gradually leading to a loss of the repair and regeneration functions normally seen in a young organism.
In other words, the study suggests that excessive epigenetic modification can reproduce some fundamental mechanisms of ageing. Researchers therefore have a much stronger basis for considering epigenetics a causal contributor to biological ageing.
When stem cells age prematurely
These results strengthen the credibility of the epigenetic clocks currently used in biomedical research.
If methylation signatures truly reflect mechanisms involved in ageing, measuring them could become a valuable indicator for:
- assessing an individual’s overall health;
- detecting accelerated ageing before symptoms appear;
- personalising prevention strategies;
- monitoring the effectiveness of nutritional or therapeutic interventions;
- developing approaches to longevity medicine.
The aim is no longer simply to know our chronological age, but to understand how quickly our bodies are actually ageing.
When stem cells age prematurely
This prospect is particularly exciting. In the future, an epigenetic analysis could help a physician identify people at increased risk of developing certain age-related diseases at an early stage.
Researchers are also considering therapies that could target abnormal epigenetic mechanisms to restore more youthful cellular function. Although these applications remain largely experimental, the results published in 2026 represent an important step towards this future medicine.
Conclusion
The study highlighted in July 2026 marks a turning point in our understanding of ageing. By showing that an abnormal increase in DNA methylation can cause features resembling accelerated ageing, it strengthens the idea that epigenetics is not merely a witness to the passage of time: it could be one of its drivers.
For medical research, this discovery opens considerable possibilities. Epigenetic clocks could soon become essential tools for assessing biological age, preventing certain age-related conditions and perhaps, one day, slowing the ageing process itself.
Sources:
Increased DNA methylation linked to aging phenotypes in a progeria syndrome, Nature Structural & Molecular Biology, 15 July 2026.
A progeria syndrome links DNA hypermethylation to age-related pathology, Nature Genetics, June 2026.
Springer Nature — "Epigenetics" thematic collection, July 2026.
Data associated with the study of Heyn-Sproul-Jackson syndrome and DNA hypermethylation.