Unveiling the Link Between Accelerated Aging and Cancer Risk in Younger Adults

As scientists delve into the factors behind the surge in certain cancers among younger adults, they have stumbled upon a compelling lead: a correlation with accelerated biological aging.

Conventionally, aging has been identified as a primary risk factor for various types of cancer, signifying that as individuals age, their likelihood of cancer diagnosis increases. However, contemporary insights suggest that age encompasses more than just the passing years marked by birthday celebrations. It encompasses the cumulative effects of lifestyle, stress, and genetic predispositions on the body, collectively referred to as one’s biological age.

Dr. Yin Cao, an associate professor of surgery at the Washington University School of Medicine in St. Louis and lead author of the recent study, underscores the evolving landscape of cancer incidence. While cancer has long been recognized as a disease associated with aging, its prevalence is now extending to younger demographics. This shift prompts the exploration of whether the well-established concept of biological aging can be applied to the younger generation, presenting a novel frontier in research. Dr. Cao presented these findings at the American Association of Cancer Research’s annual conference in San Diego.

Dr. Cao and her research team conducted a comprehensive analysis of medical records from 148,724 individuals aged 37 to 54, drawn from the UK Biobank database. Focusing on nine blood-based markers associated with biological aging, they sought to identify potential correlations:

  • Albumin: A liver-produced protein that diminishes with age.
  • Creatinine: A blood waste product indicative of kidney function, with lower levels linked to enhanced longevity.
  • Glucose: Blood sugar levels tend to remain elevated for longer periods after meals as individuals age.
  • C-reactive protein: Liver-produced in response to inflammation, higher levels are associated with accelerated aging.
  • Lymphocyte percent: Concentration of white blood cells linked to immune function, which typically declines with age.
  • Mean cell volume: Reflects the average size of red blood cells, which increases with age.
  • Red cell distribution width: Measures the variation in red blood cell size, which tends to rise with age.
  • Alkaline phosphatase: An enzyme primarily produced by the liver and bones, levels of which typically increase with age.
  • White blood cell counts: Elevated counts in the upper end of the normal range may signify greater aging.

Utilizing an algorithm known as PhenoAge, the researchers calculated each participant’s biological age by integrating these nine markers. By comparing individuals’ biological ages with their chronological ages, they identified instances of accelerated aging.

Furthermore, the researchers cross-referenced cancer registries to ascertain the prevalence of early-onset cancers, defined as those emerging before the age of 55. Their analysis revealed nearly 3,200 such cancer diagnoses.

Of note, individuals born in 1965 or later exhibited a 17% higher likelihood of accelerated aging compared to those born between 1950 and 1954, shedding light on potential trends in biological aging and cancer susceptibility among different birth cohorts.

Upon meticulous data adjustments to mitigate potential biases, researchers uncovered a significant association between accelerated aging and heightened cancer risk. Notably, the strongest correlations were observed with lung, stomach, intestinal, and uterine cancers.

In comparison to individuals exhibiting minimal signs of accelerated aging in the biobank cohort, those with the highest scores faced substantial risks. Specifically, they were twice as likely to develop early-onset lung cancer, over 60% more susceptible to gastrointestinal tumors, and had an over 80% elevated risk of uterine cancer.

While the study wasn’t explicitly designed to delve into the underlying reasons for the pronounced link between accelerated aging and these particular cancer types, Ruiyi Tian, the lead researcher, speculated on potential explanations.

Tian posited that the lungs might be particularly susceptible to aging due to their limited regenerative capacity. Additionally, she suggested that stomach and intestinal cancers could be influenced by age-related inflammation, which tends to escalate with advancing years.

Dr. Yin Cao, one of the study’s authors, emphasized the robustness of the findings stemming from a large cohort. However, she acknowledged certain study limitations. For instance, the absence of longitudinal follow-up and reliance on a single blood test render the risk assessment a mere snapshot rather than a dynamic trajectory, which ideally necessitates repeated sampling over time.

To enhance the reliability and applicability of such findings, Cao underscored the imperative of validating associations across diverse population cohorts, particularly in elucidating the role of social factors tied to racial disparities.

Dr. Anne Blaes, an expert in biological aging’s impact on cancer survivors, lauded the study’s implications, envisioning a paradigm shift in identifying individuals at heightened cancer risk, especially among young adults lacking familial predispositions or discernible risk factors.

Blaes highlighted the potential for tailored interventions targeting lifestyle modifications such as nutrition, exercise, and sleep to mitigate accelerated aging-associated risks. Furthermore, she emphasized ongoing research into senolytics, medications aimed at eliminating damaged and aging cells, which hold promise in attenuating accelerated aging.

While the precise beneficiaries of such interventions remain uncertain, assessments of accelerated aging like PhenoAge may serve as invaluable tools in guiding personalized treatment strategies in the future.

Blaes characterized the research as groundbreaking, laying the groundwork for potential therapeutic avenues to address accelerated aging and its ramifications in cancer susceptibility.