People born in the 1990s are ageing significantly faster at a cellular level than their counterparts born three decades earlier, according to a study that tracked biological markers in more than 150,000 UK Biobank participants and a separate US cohort of 10,000. The research, published in Nature Medicine by scientists at Washington University School of Medicine in St. Louis, found that the gap between chronological age and biological age—measured through epigenetic clocks, telomere length and blood biomarkers—was markedly wider in younger generations. This accelerated biological ageing was associated with a higher incidence of early-onset cancers, particularly colorectal tumours, for which the risk in the 1990s birth cohort is at least four times that of people born in the 1950s across Australia, Canada, the UK and the US.

The study is the first to establish a statistical link between faster whole-body ageing and the rise in cancer before age 50, though researchers in Germany caution it remains a correlation, not proof of causation. “What one must not forget is that this is a correlational study,” said Ron Jachimowicz, a physician at University Hospital Cologne and group leader at the Max Planck Institute for Biology of Ageing. The findings arrive as global data show a 79% increase in new cancer cases among under-50s since 1990, according to a British Medical Journal analysis. Clinicians in Buenos Aires have separately flagged a rise in HPV-related head and neck cancers in younger men, attributing part of the shift to epigenetic changes driven by lifestyle and environmental exposures.

The biological ageing gap was most pronounced when comparing those born between 1990 and 1999 with those born between 1965 and 1969, and it was already detectable in the 1965–1974 cohort relative to the 1950–1954 group. Researchers suspect that a combination of factors—ultra-processed diets, obesity, sedentary behaviour, alcohol, chronic stress and exposure to pollutants—is driving the acceleration, with genetics accounting for roughly half the variance. A separate 2025 study in Nature on hair greying offered a parallel insight: when melanocyte stem cells in hair follicles sustain DNA damage, they can either be eliminated, causing grey hair, or persist in a damaged state, potentially raising tumour risk. This cellular trade-off illustrates how the body’s ageing machinery can influence cancer susceptibility.

Investigators now aim to move beyond correlation by tracking biological age markers alongside cancer incidence in long-term prospective studies. The next milestone will be the launch of intervention trials that test whether slowing biological ageing—through drugs, dietary changes or other means—can reduce early-onset cancer rates. For now, the findings refocus attention on the whole-body ageing process rather than isolated tumour biology, a shift that researchers in both Europe and the Americas describe as a necessary step toward understanding a trend that has puzzled oncologists for over a decade.