Faster Biological Aging Could Explain Rise in Cancer Rates in Younger Adults

Cancer rates in younger adults are rising—could accelerated biological aging be the reason why? 

New research from Washington University School of Medicine in St. Louis indicates that younger generations are aging faster and has linked this accelerated aging with an increased risk of early-onset cancers. 

Cancer as an aging disease 

For most cancers, cellular damage that triggers tumor formation accumulates over time. Older adults are therefore at greater risk because they have had more time for cellular damage to build up.

 

Cancer has traditionally been considered a disease of aging for this reason. However, cancer rates in younger adults are on the rise, with trends indicating that each generation faces a higher risk of early-onset cancer than the generation before. 

  

In Australia, Canada, the UK, and the US, the risk of early-onset colorectal cancer is four times higher in people born in the 1990s compared to people born in the 1960s. 

This has led researchers to question whether there are generation-specific risk factors that are contributing to the rise in early-onset cancers. 

One theory is that accelerated biological aging in younger generations could be causing cancer-linked cellular damage to accumulate faster, resulting in tumors forming sooner. 

Physiological and environmental factors influence aging processes, including chronic inflammation, epigenetic changes, accumulation of genetic damage, and immune dysregulation. These hallmarks of aging are also hallmarks of cancer. 

Systemic aging linked to cancer risk 

In the new study, using data from more than 154,000 young adults in the UK Biobank, the researchers focused on two areas of biological aging: systemic and organ specific. Systemic aging measures the influence of aging on the whole body, whereas organ-specific aging focuses on organs of interest, enabling the researchers to capture the impact of multiple risk factors.  

“Our ultimate goal is to decode how modern environments become biologically embedded to drive cancer risk, transforming prevention from broad recommendations to personalized interventions,” said Dr. Yin Cao, a molecular epidemiologist and an associate professor of surgery and of medicine. “This brings us closer to identifying risk earlier and developing prevention strategies that are tailored to an individual’s biology.”

 

Systemic aging was measured using PhenoAge, the Klemera–Doubal method, and metabolomics-based systemic aging algorithms. 

The researchers found that systemic aging was faster in younger adults—people in more recent birth cohorts had a larger gap between their chronological and biological ages. Compared to the 1950–1954 birth cohort, people born in 1965–1974 had a 23% higher chronological–biological age gap after standardization.  

The larger the gap between chronological and biological age, the greater the risk of early-onset solid cancers, particularly lung, gastrointestinal, and uterine cancers. When participant data were split into three groups based on chronological–biological age gap, those in the highest age gap tertile had a 15% higher risk of early-onset cancer compared to those in the lowest age gap group. 

Furthermore, every standard deviation increase in chronological–biological age gap was associated with an 8% increase in early-onset cancer risk. 

This increase in risk persisted after controlling for inherited genetic cancer risk factors and genetic susceptibility to accelerated aging.  

Organ-specific aging independently contributes to cancer risk 

As aging trajectories may vary from organ to organ, and between organs and the whole body, the researchers also examined whether organ-specific aging influenced cancer risk using proteomics-based organ-specific aging clocks.  

The researchers identified the key organ sites contributing to early-onset cancer risk, finding that immune tissue aging was associated with lung cancer and adipose tissue aging was associated with an increased risk of colorectal cancer.

Identifying people with a higher cancer risk 

The causes of faster biological aging in younger generations are still under investigation, and the mechanisms linking accelerated aging and cancer development are yet to be defined.

 

However, this study indicates that systemic aging could potentially be used to pinpoint people at a greater risk of early-onset cancer. 

“If we can identify younger people with the highest cancer risk when they are still healthy, we can focus on prevention and early-detection strategies for the individuals who will benefit most from early interventions,” Cao said. 

In a comment to the Science Media Centre, Dr. John Riches, a clinical reader in cancer immuno-metabolism at Barts Cancer Institute, who was not involved in the research, said: “This study offers an important new clue as to why we are seeing more cancers diagnosed in younger adults... researchers around the world are trying to understand why rates of some cancers are rising in younger generations, and these findings suggest that accelerated biological aging may be playing a role.” 

“Importantly, this study does not show that faster biological aging directly causes cancer, but it provides a strong basis for further research,” he continued. 

Dr. Jyoti Nangalia, group leader at the Wellcome Sanger Institute, who was also not involved in the research, noted that “measurements of biological age are likely capturing the combined effects of many exposures such as genetics, lifestyle, and environmental factors. We now need further research to understand exactly what these measurements are telling us. Are they capturing processes that directly drive cancer development, or are both these biological changes and cancer being driven by other shared underlying factors?” 

Reference: Tian R, Zong X, Ren D, et al. Biological aging and generational shifts in early-onset cancer risk. Nat Med. 2026. doi: 10.1038/s41591-026-04448-w 

This article is a rework of a press release issued by Washington University School of Medicine in St. Louis. Material has been edited for length and content.