From creams and serums promising to erase wrinkles, to billionaires like Bryan Johnson pouring fortunes into reversing the clock, the anti-aging industry has exploded into a global obsession. Valued at billions, this market is fuelled by humanity’s deepest fear: the inevitability of ageing and death.
But are we approaching the science of ageing in the right way?
Researchers have uncovered a surprising connection between random genetic mutations and epigenetic changes that could reshape how we understand ageing.
Why We Age: Two Theories Collide
For years, scientists debated two theories:
- Somatic Mutation Theory: DNA mutations, or tiny errors in our genetic code, build up over time and drive ageing.
- Epigenetic Clock Theory: Epigenetic modifications, which alter gene expression without changing the DNA sequence, accumulate and influence ageing. Unlike DNA mutations, these are reversible.
The research, published in the journal Nature Aging, describe a novel link between these two explanations. New findings suggest these are intricately linked. A single mutation could cause a ripple effect of epigenetic changes across the genome, beyond the site of mutation.
The researchers analysed data from over 9,300 patients catalogued in the Cancer Genome Atlas and the Pan-Cancer Analysis of Whole Genomes. By comparing genetic mutations to epigenetic modifications, they found that random mutations were predictably correlated with changes in DNA methylation (a type of epigenetic modification).
Using this relationship, the researchers were able to make similar predictions of age using either mutations or epigenetic changes.
Implications for Anti-Ageing Science
The findings call into question existing anti-ageing approaches, such as therapies aimed at reversing the epigenetic clock. If mutations are the primary drivers, therapies targeting the symptoms – like epigenetic modifications – may not be enough.
“Major research institutions and companies are betting on turning back the epigenetic clock as a strategy to reverse the effects of ageing, but our research suggests that this may only be treating a symptom of ageing, not the underlying cause.” Dr Trey Ideker, one of the study authors shared.
Reversing ageing may be harder than we think, as it shifts the view from a programmed process to one driven by random, cumulative changes. Anti-ageing therapies that slow the epigenetic clock might only delay the inevitable, without addressing the root cause.
A New Perspective In Ageing and Anti-Ageing
If ageing is truly random, can we ever beat it? Could we eventually develop therapies that protect against mutations or enhance our resilience to them?
These questions lead to exciting, albeit speculative, possibilities: targeted DNA repair systems, advanced gene editing, or entirely new ways to manage the cascade of epigenetic changes? Advanced gene-editing tools, such as CRISPR, have already shown potential in tackling specific genes in age-related diseases like Alzheimer’s to reduce disease risk.
Still, the path forward is steep. DNA mutations occur unpredictably, and tackling them requires a level of precision we are only beginning to understand.
While the road to anti-ageing therapies may be more complex than imagined, these findings provide a foundation for rethinking what it means to age – and how we might intervene.
