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A new investigation indicates that the process of biological aging might be advancing somewhat more rapidly in younger demographics when contrasted with older ones. This phenomenon could potentially be linked to an increased risk of cancer.(Image credit: Maciej Toporowicz, NYC via Getty Images)
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Younger demographics may be experiencing aging at a quicker pace than their forebears, and this may be connected to an increase in cancers diagnosed at an earlier age, according to a recent study.
Recent upticks in the incidence of certain cancers among individuals under 50, including breast, colorectal, kidney, and uterine cancers, have been noted. One 2023 paper suggests that diagnoses of these early-onset cancers saw a global increase of 25% between 1990 and 2019, and researchers are still endeavoring to ascertain the reasons behind this trend.
“The trend of increased cancers at younger ages is very real, and it is not simply because of more efficient diagnosis, or diagnosis at earlier stages,” stated Dr. Jyoti Nangalia, a hematologist and cancer researcher at the Wellcome Sanger Institute in the U.K., who was not involved in the recent research. “It is possible that we are being exposed to new cancer-causing risks or that [our] defences to them are somehow altered,” she informed Live Science via email.
The new research, published on June 22 in the journal Nature Medicine, posits that younger generations might exhibit a wider “discrepancy” between their chronological ages and their biological ages — a metric assessing the rate at which the body’s tissues and systems are aging — compared to older generations. The larger gap observed in younger adults appears to be associated with an elevated risk of developing cancer prematurely.
While the new study cannot definitively establish that accelerated biological aging leads to early-onset cancer, it offers novel insights for scientists working to decipher the potential drivers of this concerning pattern.
“This is really proof-of-concept,” remarked Yin Cao, a co-author of the study and a molecular and clinical epidemiologist at the Washington University School of Medicine and Siteman Cancer Center, speaking to Live Science.
Concerning trends lurking in dense data
Chronological age is straightforward: It represents the number of years elapsed since an individual’s birth. “Biological age,” however, can fluctuate significantly among individuals. This encompassing term refers to a spectrum of measurements, including markers present in DNA and the bloodstream. These are often quantified using “aging clocks,” which aim to ascertain if an individual’s body is functioning at an age considerably beyond their chronological age.
Researchers have increasingly employed these summary measures in an effort to comprehend why certain individuals are more susceptible to age-related ailments than others. To investigate whether a connection might exist between biological age and the surge in early-onset cancers, the new study examined data from over 150,000 adults within the UK Biobank, an extensive, long-term initiative that has been monitoring the health of approximately half a million U.K. residents since the mid-2000s.
The participants contributed blood samples, many of which had already been analyzed for markers used in tracking biological aging. The study authors inputted these findings into PhenoAge, a statistical model designed to estimate an individual’s “age gap” at a specific chronological age. Essentially, this model can compare profiles of two 40-year-olds — one born in 1950 and the other in 1965 — and determine if their blood markers suggest they are of the same biological age.
“The traditional approach is really focusing on individual risk factors” for cancer, such as a history of obesity or a high intake of ultraprocessed foods, Cao explained. “We are testing whether we can leverage these large biobanks and potentially find some biological imprint as a potential reflection of many exposures that can be linked with cancer risk,” she added.
The analysis uncovered a troubling pattern: UK Biobank participants born between 1965 and 1974 exhibited a greater age gap than those born between 1950 and 1954, when assessed at identical chronological ages. According to PhenoAge’s metrics, the younger cohort displayed systemic aging levels approximately 0.23 standard deviations higher than the older cohort — a subtle shift towards biology that appeared older.
The researchers applied this methodology to approximately 10,000 participants in the U.S. National Institutes of Health’s All of Us Research Program, another substantial biobank. In this group, they observed a more pronounced trend: Individuals born between 1990 and 1999 showed age gaps about 0.92 standard deviations higher than those born between 1965 and 1969.
Another blood-based aging assessment tool, known as the Klemera-Doubal method, yielded broadly comparable patterns to PhenoAge, although with slightly less pronounced results, the investigation found.
Breast cancer is among the types experiencing a rise in incidence among adults under 50.
(Image credit: kali9 via Getty Images)Real trend or data mirage?
Within the UK Biobank cohort, the researchers observed that participants with larger age discrepancies were more prone to developing early-onset solid tumors, which are cancerous growths appearing in tissues, as opposed to “liquid” cancers found in bodily fluids. This association was most pronounced for lung, gastrointestinal, and uterine cancers. This conclusion was drawn from the patients’ medical histories.
When participants were categorized into three groups based on their biological ages, those in the highest group faced an approximate 15% elevated risk of early-onset solid cancer compared to those in the lowest group.
To delve further, the authors employed a distinct model that estimates biological aging at the organ and system level, utilizing protein patterns in the blood. In nearly 20,000 UK Biobank participants, they identified markers indicative of an “older-than-expected” immune system that were associated with a heightened risk of early-onset lung cancer. Similarly, markers suggesting that adipose tissue was older than anticipated correlated with an increased risk of early-onset colorectal cancer.
Does this imply that younger generations are aging more rapidly, thereby causing the increase in cancers? Perhaps, but it’s also possible that not — the study’s findings are subject to important qualifications.
The observed patterns necessitate confirmation across different datasets and populations, Cao pointed out. Biological aging assessments, including PhenoAge, are also relatively novel, and their full implications are not yet completely understood. While they demonstrably capture aspects of health and risk at a population level, at an individual level, various biological age tests can yield divergent results for the same person. This raises questions about the precise meaning of any single score concerning individual health.
It’s conceivable that the distinctions uncovered by PhenoAge between younger and older individuals are related to the test’s original calibration, Stephen Burgess, a professor of biostatistics at the University of Cambridge who was not involved in the research, suggested to Live Science via email. To ascertain if this is the case, a more in-depth examination of PhenoAge score calculations would be required to determine if this might have influenced its assessment of the UK Biobank and All of Us cohorts, he stated.
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Cao further noted that while PhenoAge scores have been linked to mortality risk across various adult groups, the test “requires further validations” when applied to assessing cancer risk.
As is typical with any observational study utilizing extensive databases, establishing a definitive cause-and-effect relationship presents challenges, Nangalia added.
“The main issue for this paper is one of correlation versus causality,” she commented. “Either way, it is useful — with the first, as a potential way of tracking population health and cancer risk, and with the second, as insights into cancer-causing mechanisms.”
Cao expressed hope that her team’s methodology will serve as an additional valuable instrument in understanding why an increasing number of young individuals are developing cancer. “Hopefully this is just a starting point,” Cao concluded.
