A recently published investigation has shed light on a significant correlation between the pace of biological aging at a molecular level and the propensity for developing colorectal cancer, particularly among women who have completed menopause. This comprehensive analysis suggests that certain individual biological indicators, rather than just chronological age, are critical in determining disease vulnerability. It further proposes that specific dietary habits and hormonal influences can either mitigate or exacerbate this risk, offering new avenues for preventative health strategies.
The study, featured in Volume 17, Issue 7 of Aging on July 7, 2025, titled \"Epigenetic age and accelerated aging phenotypes: a tumor biomarker for predicting colorectal cancer,\" was spearheaded by Su Yon Jung and her team at the University of California, Los Angeles. Their groundbreaking work centered on understanding how variations in biological aging, specifically epigenetic aging, influence an individual’s susceptibility to colorectal cancer. This form of cancer represents a major health concern globally, particularly impacting individuals over the age of 50. The core premise of the research revolved around the concept that biological aging, driven by chemical alterations to DNA, can progress at different rates among individuals of the same chronological age, thereby affecting their cellular and tissue health.
Researchers tapped into the extensive Women's Health Initiative Database for Genotypes and Phenotypes (WHI-dbGaP), a valuable resource containing genetic and health data from postmenopausal white women aged 50 to 79. To assess biological age, they employed three recognized 'epigenetic clocks'—Horvath’s, Hannum’s, and Levine’s—to analyze blood samples. These samples were collected up to 17 years prior to any colorectal cancer diagnosis, allowing for a long-term perspective on risk assessment. The 'epigenetic clocks' meticulously track DNA methylation patterns, providing an estimation of an individual's molecular aging rate. A key finding emerged: women exhibiting a biological age higher than their chronological age displayed a notably increased likelihood of developing colorectal cancer.
A compelling aspect of the research involved examining the influence of daily habits on mitigating this elevated risk. The study revealed that women who maintained a diet rich in fruits and vegetables did not experience an increased risk of colorectal cancer, even if their epigenetic clocks indicated accelerated aging. Conversely, women with both a lower intake of fruits and vegetables and signs of accelerated biological aging faced a significantly higher risk, up to 20 times greater, of developing the disease. This observation underscores the critical role that a nutritious diet can play in counteracting the biological pathways associated with accelerated aging and reducing cancer risk.
Another notable discovery pertained to the impact of surgical menopause. Women who underwent the removal of both ovaries before naturally reaching menopause were found to exhibit an elevated epigenetic age. When this factor combined with accelerated aging, it led to a heightened probability of developing colorectal cancer. This particular insight emphasizes the complex interplay between hormonal factors, reproductive health, and their collective influence on the aging process and an individual’s predisposition to various diseases.
The findings derived from this investigation were rigorously cross-validated using several independent datasets, lending robust support to the idea that epigenetic aging markers, detectable in blood samples, could serve as early indicators for colorectal cancer risk. Such markers hold immense promise for guiding future strategies aimed at early detection and prevention within aging demographics. However, the study’s authors stress the importance of conducting additional large-scale replication studies to further solidify these results and translate them into clinical practice.
This study significantly advances our comprehension of the intricate relationship between epigenetic aging and cancer development. It reinforces the notion that lifestyle choices can exert a powerful influence over disease risk, even in individuals experiencing more rapid cellular aging. The implications of these findings are profound, suggesting that personalized interventions based on biological age and tailored lifestyle modifications could become crucial components of future cancer prevention efforts.