Cancer is strongly associated with age. The longer people live, the more opportunities their cells have to accumulate changes that can contribute to tumor growth. The body's ability to remove or repair damaged cells can also become less effective over time.
Yet age does not tell the whole story. Rates of several cancers—including colorectal, breast, kidney, and uterine cancers—have risen in at least some groups of younger adults. Each newer generation also appears to face a higher risk of certain cancers than the generation before it.
That trend has prompted researchers to investigate a provocative possibility: Could some younger adults be accumulating biological damage earlier, causing their bodies to appear older than expected?
A large observational study led by researchers at Washington University School of Medicine in St. Louis offers an important clue. The researchers found that people in more recent birth cohorts had older biological profiles than earlier-born participants at comparable chronological ages. A larger gap between biological and chronological age was also associated with a higher risk of developing certain cancers before age 55.
The findings, published in Nature Medicine, are intriguing. They do not establish that accelerated biological aging causes cancer, explain every increase in early-onset cancer, or provide a clinical test that can tell an individual when to begin screening.
Key Takeaways
Researchers analyzed 154,169 UK Biobank participants and 10,262 participants in the U.S. All of Us Research Program.
Later-born groups had larger gaps between their biological and chronological ages after the researchers adjusted for age.
In the UK analysis, each one-standard-deviation increase in the main biological age measure was associated with an 8% higher relative risk of an early-onset solid cancer.
Immune-system aging was associated with early-onset lung cancer, while adipose-tissue aging was associated with early-onset colorectal cancer.
The study was observational and measured most participants at one point in time. It found associations; it did not prove that anyone's body was aging faster or that biological aging caused cancer.
The study by itself does not change current cancer-screening recommendations.
First, Are Cancer Rates Really Rising in Younger Adults?
The most accurate answer is that some cancers are rising in some younger age groups, not that every cancer—or cancer overall—is increasing everywhere.
In a 2025 U.S. analysis, National Cancer Institute researchers examined 33 cancer types. Incidence rose for 14 types in at least one age group under 50, while it fell for 19 others. The total incidence of all cancers among younger adults did not rise from 2010 through 2019. Breast, colorectal, kidney, and uterine cancers accounted for most of the additional early-onset cases in that analysis. The NCI's summary of those findings provides useful context for the broader trend.
Across countries and longer time periods, however, researchers have documented substantial increases in several early-onset cancers and strong birth-cohort effects. The new biological-aging study was designed to investigate one possible process that may connect many exposures over a lifetime with those changing cancer patterns.
“Early-onset cancer” does not have one universal cutoff. Many studies use diagnosis before age 50. The Nature Medicine researchers primarily examined solid cancers diagnosed before age 55 and repeated key analyses using a before-50 cutoff, with similar findings.
Biological Age Is Not the Same as the Age on Your Birth Certificate
Chronological age simply measures how many years a person has been alive. Biological age is an estimate of how old the body appears based on measurable patterns in blood, metabolism, proteins, organs, or other physiological systems.
Two people who are both 45 can therefore have different biological profiles. One person's blood markers may resemble the typical pattern seen in someone older, while another person's may appear younger.
For the main analysis, the researchers used PhenoAge. This established algorithm combines chronological age with nine clinical blood measurements, including albumin, creatinine, glucose, C-reactive protein, and several blood-cell markers. It was originally developed to estimate mortality and disease risk—not specifically cancer.
The team also used the Klemera-Doubal Method, or KDM, and a metabolomic score based on age-related patterns in small molecules involved in metabolism. To estimate aging in individual organs and biological systems, the researchers analyzed patterns of proteins circulating in the blood.
These tools do not reveal a literal expiration date for the body or an organ. They summarize a pattern of biomarkers and compare it with a reference population.
How the Researchers Studied Aging and Cancer
The study included two large groups of adults younger than 55 at enrollment.
The work was led by senior author Yin Cao, ScD, a molecular epidemiologist at WashU Medicine, and first author Ruiyi Tian, a doctoral researcher in Cao's laboratory.
The UK Biobank Group
Researchers analyzed 154,169 UK Biobank participants for generational patterns in biological aging. The group was 55% female and 92% White.
For the prospective cancer analysis, 148,317 participants contributed more than 953,000 person-years of follow-up. Their cancer diagnoses were identified through national cancer registries and death records. Average follow-up was 6.4 years.
The researchers accounted for numerous factors that could influence both biological aging and cancer risk, including sex, race, socioeconomic deprivation, education, body mass index, smoking, alcohol, diet, physical activity, diabetes, cardiovascular disease, chronic lung disease, and genetic ancestry. Cancer-specific models also considered relevant family and reproductive history.
The U.S. All of Us Group
The researchers then looked for similar patterns among 10,262 participants in the NIH's All of Us Research Program. This group was more racially and ethnically diverse than the UK cohort.
The cancer-risk analysis included 8,935 U.S. participants. Follow-up averaged 2.4 years, during which researchers identified 104 early-onset solid cancers. That smaller number of cases makes the U.S. result useful but less precise than the main UK analysis.
Systemic and Organ-Specific Aging
The team studied aging at two levels:
Systemic aging estimated the biological-aging profile of the body as a whole.
Organ-specific aging used blood-protein patterns to estimate aging across individual organs and systems, including immune and adipose tissue.
The organ-specific analysis involved a smaller subset of 19,874 UK participants and was exploratory.
Younger Birth Cohorts Had Older Biological Profiles
The generational pattern appeared in both countries.
Among UK participants, people born from 1965 through 1974 had a PhenoAge-defined age gap 0.23 standard deviations higher than those born from 1950 through 1954 after chronological age was taken into account.
The difference was larger in the U.S. data. Participants born from 1990 through 1999 had an age-gap score 0.92 standard deviations higher than participants born from 1965 through 1969.
Put simply, later-born participants tended to show older biological profiles when compared with earlier-born participants of comparable chronological ages.
That is not quite the same as watching individuals age faster. Most participants had their biomarkers measured at one point, so the study compared different birth cohorts rather than following each person's rate of biological change over many years.
The study does not prove that younger generations are biologically aging faster, that an older biological profile causes cancer, or that a commercial “biological age” result can predict who will develop cancer. Those conclusions require repeated measurements, external validation, and clinical trials or other evidence designed to test causality and medical usefulness.
A Larger Age Gap Was Linked to Early-Onset Cancer
The researchers next examined whether an older biological profile was associated with cancer diagnosed before age 55.
In the UK cohort, each one-standard-deviation increase in the PhenoAge-defined age gap was associated with an 8% higher relative risk of an early-onset solid cancer. Participants in the highest third of systemic aging had a 15% higher relative risk than those in the lowest third.
The strongest site-specific associations involved:
Lung cancer: 57% higher relative risk per standard-deviation increase in the age gap
Gastrointestinal cancers: 17% higher relative risk
Uterine cancer: 31% higher relative risk
These are relative comparisons from statistical models, not an individual's absolute chance of developing cancer. Early-onset cancers remain uncommon, and the study did not provide a simple personal-risk conversion for these percentages.
In the smaller U.S. cancer analysis, each standard-deviation increase in the PhenoAge-defined age gap was associated with a 22% higher relative risk of an early-onset solid cancer. The confidence interval was wider, however, and only 104 cancers occurred during the relatively short follow-up.
The relationships also persisted in sensitivity analyses that considered telomere length and inherited susceptibility to aging or certain cancers. That suggests the age-gap measure may capture information beyond those inherited factors, although it cannot eliminate every alternative explanation.
Different Biological Systems Were Linked to Different Cancers
Aging did not appear to affect every organ system in the same way.
In the exploratory protein analysis, a one-standard-deviation increase in immune-system aging was associated with an 89% higher relative risk of early-onset lung cancer. More advanced adipose, or fat-tissue, aging was associated with a 60% higher relative risk of early-onset colorectal cancer.
Those associations remained after the researchers also accounted for systemic aging. The results may point researchers toward more specific biological pathways, such as chronic inflammation, immune remodeling, metabolism, and communication between fat tissue and the gut.
They should not yet be used to assess an individual's lung or colorectal cancer risk. The organ-specific models were exploratory, involved a smaller group, and require independent validation.
Not Every Biological-Age Measure Produced the Same Result
One detail deserves more attention than it is likely to receive in headlines: the overall early-onset cancer association was strongest for PhenoAge.
The KDM age-gap measure showed a smaller overall association that was not statistically significant. The metabolomic measure also showed a modest overall association that did not reach statistical significance. KDM produced stronger associations with lung and gastrointestinal cancers, while the metabolomic measure produced stronger associations with lung and uterine cancers.
That does not erase the main finding. It shows that “biological age” is not one universally agreed number. Different clocks measure different aspects of health, and results can change depending on the method used.
“This brings us closer to identifying risk earlier,” Cao said in WashU Medicine's research announcement. Whether these measurements can improve real-world prevention will require additional studies.
Why Might Biological Aging Be Connected to Cancer?
Cancer develops through changes that allow abnormal cells to survive, divide, and spread. Chronological aging creates more time for DNA damage and other cellular changes to accumulate, but the surrounding biological environment also matters.
Researchers are investigating several processes that could connect an older biological profile with cancer at a younger age:
chronic inflammation
metabolic dysfunction and insulin signaling
weakening or remodeling of immune responses
accumulated genetic and epigenetic changes
changes in the tissue environment surrounding cells
interactions among adipose tissue, the gut, and the microbiome
Environmental, lifestyle, and social conditions may influence several of these pathways at once. Obesity and metabolic disease beginning earlier in life, poorer diet quality, sedentary time, disrupted sleep, air pollution, and other chemical or social exposures are among the possibilities researchers are studying.
The new study did not identify which exposures created the observed age gaps. It also did not show that changing one habit would reverse the score or prevent cancer.
What the Study Cannot Tell Us
Several limitations are important:
It was observational. The researchers found patterns; they did not assign exposures or prove cause and effect.
Most aging measurements came from one point in time. The study compared cohorts but generally did not measure each person's speed of aging over many years.
Residual confounding is possible. Statistical adjustment cannot capture every exposure, medical condition, or behavior.
The UK cohort had limited diversity. Ninety-two percent of participants in the primary group were White, which may limit generalizability.
The U.S. follow-up was short. Only 104 early-onset cancers occurred in the All of Us analysis, limiting cancer-specific validation.
The aging clocks differed. The two alternative systemic clocks did not show statistically significant associations with early-onset cancer overall.
The organ findings were exploratory. The organ-aging models need confirmation in independent and more diverse populations.
Reverse causation cannot be completely excluded. An undiagnosed cancer or precancerous process might affect blood markers before diagnosis, although the researchers excluded cancers diagnosed within six months of baseline and ran additional sensitivity analyses.
What Does This Mean for You Right Now?
The study is more useful as a direction for research than as a new medical instruction for individuals.
Keep Up With Evidence-Based Screening
Do not start, stop, or delay cancer screening based on a biological-age score. Screening recommendations depend on age, sex, anatomy, smoking history, family history, genetic risk, and previous test results.
The CDC's cancer-screening overview covers breast, cervical, colorectal, and lung screening. People at higher risk may need a different schedule, so discuss your personal and family history with a qualified healthcare professional.
Do Not Dismiss Persistent Changes Because You Feel “Too Young”
Screening is for people without symptoms. A new lump, unexplained bleeding, a persistent change in bowel habits, an unexplained weight change, or another symptom that does not resolve deserves medical attention at any age. Most such symptoms are not cancer, but age alone should not be used to dismiss them.
Focus on Established Ways to Lower Risk
Avoiding tobacco, limiting alcohol, staying physically active, maintaining a health-supporting weight when possible, using sun protection, receiving recommended HPV and hepatitis B vaccines, and following screening guidance are supported by much stronger evidence than trying to “hack” a biological-age result.
These steps cannot remove every cancer risk, and cancer is never a personal failure. Genetics, environmental exposures, infections, healthcare access, chance, and many other factors also matter.
Before paying for a direct-to-consumer biological-age test, ask three questions: Has this exact test been validated in people like me? Does the result reliably predict a clinical outcome? Would it change care under an evidence-based guideline? For now, the study's research measures are not a substitute for a clinician's risk assessment or recommended screening.
Frequently Asked Questions
Does an older biological age mean I will develop cancer?
No. The study found a statistical association at the group level. It cannot determine whether one person will develop cancer, and an age-gap score is not a diagnosis.
Can a routine blood test calculate my cancer risk from biological age?
Not in a clinically established way. Some of the underlying biomarkers are commonly measured, but the algorithms in this study remain research tools. They are not currently recommended as stand-alone cancer-screening or risk-prediction tests.
Should people under 50 begin screening earlier because of this study?
Not solely because of these findings. Follow current screening recommendations and ask a clinician whether your family history, inherited risk, smoking history, symptoms, or previous findings justify a different schedule.
Can diet or exercise reverse biological aging and prevent early-onset cancer?
The study did not test an intervention, so it cannot answer that question. Healthy behaviors can lower the risk of several cancers and chronic diseases, but no single diet, supplement, workout, or anti-aging product can guarantee cancer prevention.
Why did the researchers use age 55 when early-onset cancer often means under 50?
The researchers said excess risk seen in younger birth cohorts can continue into ages 50 through 54, and the broader cutoff gave them more cases to analyze across cancer sites. They also repeated key analyses using diagnosis before age 50 and reported similar findings.
The Bottom Line
The study adds a compelling piece to the early-onset cancer puzzle. In two large UK and U.S. cohorts, people born more recently tended to have older biological profiles, and a larger biological age gap was associated with a higher relative risk of certain cancers before age 55.
It does not show that faster aging is solely—or definitively—to blame for rising cancer rates. It also does not turn biological age into a ready-to-use screening test.
The most reasonable takeaway is not to fear your birth year or chase an anti-aging score. Keep up with recommended screening, share your family history with your healthcare team, seek care for persistent symptoms, and watch this area of research as scientists test whether biological-age measures can eventually improve prevention and early detection.
