Scientists have proposed a new model suggesting that chronic illnesses linked to aging, including cancer and arthritis, may develop through two distinct but connected phases over a lifetime. Researchers from University College London and Queen Mary University of London detailed this two-stage process in a review published inAging-US, offering a different perspective on the strong connection between aging and disease.
The review, authored by David Gems and Alexander Carver from University College London, and Yuan Zhao from Queen Mary University of London, integrates evolutionary biology with modern biomedical research. Their work aims to explain how initial damage in the body can contribute to conditions such as cancer, arthritis, and various infections years later.
The first stage, according to the researchers, begins early in life. During this period, the body encounters various disruptions like infections, physical injuries, or genetic mutations. While the body often repairs or contains much of this damage, some of it may persist in a hidden state, not fully removed. This early damage sets the stage for later problems.
The second stage unfolds later in life. Normal genetic activity starts to change in ways that no longer benefit the body. These late-life biological shifts can weaken the body's capacity to keep earlier damage under control. Consequently, previously contained issues may gradually escalate into full-blown diseases.
Early Damage, Later Disease
This process helps clarify why many illnesses predominantly affect older adults, even if their origins trace back much earlier. The review emphasizes aging as a multifactorial process, driven by numerous interacting biological factors rather than a single cause. The proposed model suggests that the interplay of earlier damage and later-life genetic changes plays a significant role in age-related diseases.
Dormant viruses, for instance, can remain inactive for years, only to reactivate when the immune system weakens with age, leading to conditions such as shingles. Similarly, injuries sustained in youth might eventually contribute to osteoarthritis as aging tissues lose resilience. Inherited genetic mutations can also lie silent for decades before increasing the risk of diseases like cancer or fibrosis later in life.
Evolutionary Theories and Future Strategies
The second stage unfolds later in life.
The researchers indicate their model builds on long-standing evolutionary theories of aging. One influential idea posits that natural selection weakens later in life, permitting harmful biological processes to emerge with age because they have less impact on reproduction and survival earlier on. Studies involving the roundwormCaenorhabditis elegans also referenced in the review, showed that early mechanical damage in the worms eventually led to fatal infections in old age. Similar patterns, the scientists suggest, may occur in humans.
The review presents aging as a process shaped by multiple interacting causes that develop over time. By dividing aging into two primary stages—early-life damage and later-life genetic activity—the researchers believe their framework could guide future strategies aimed at preventing disease and promoting healthier aging. Reducing damage earlier in life or targeting harmful late-life biological changes could help lower the risk of chronic disease in older adults, according to the findings.
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