Why treating aging could be more impactful than treating individual diseases
Aging is the single largest risk factor for most chronic diseases that cause disability and death in older adults, including heart disease, neurodegeneration, diabetes, and cancer [1]. Rather than tackling each disease separately, targeting the underlying aging process could prevent or delay multiple conditions at once. This is because aging itself is driven by a set of interconnected biological hallmarks—such as genomic instability, telomere shortening, mitochondrial dysfunction, and cellular senescence—that are now well-characterized and potentially modifiable [1]. For example, the accumulation of senescent (aged, non-dividing) cells contributes to inflammation and tissue dysfunction across the body; drugs that selectively eliminate these cells are already in clinical trials [1].
What treatments are being developed, and how well do they work?
Current research has identified several promising intervention strategies that target the root causes of biological aging. Caloric restriction and nutritional interventions have been shown to extend lifespan in animal models by improving metabolic health and reducing oxidative damage [1]. More advanced approaches include stem cell therapy to replenish exhausted tissue stem cells, and senolytic drugs that clear senescent cells, which have been shown to improve physical function and reduce frailty in preclinical studies [1]. Additionally, anti-inflammatory and antioxidative treatments aim to dampen the chronic low-grade inflammation that accelerates aging [1]. While these interventions are not yet approved for treating aging itself in humans, they represent a shift from managing symptoms to addressing the underlying biology.
The catch: chronological age is not the same as biological age
A key insight from recent research is that chronological age (how many years you've lived) is a poor predictor of health outcomes compared to biological age (the accumulated damage to your cells and tissues) [5]. For example, in cancer patients, chronological age alone does not reliably predict who will benefit from treatment; instead, measures of biological age like sarcopenia (loss of muscle mass and function) are more accurate indicators of frailty and treatment tolerance [5]. This means that two people of the same chronological age can have very different biological ages, and therefore different risks for age-related diseases and different responses to therapies. The implication is that treatments targeting biological aging should be personalized based on biological markers, not just the number of candles on the birthday cake.
Sources used in this answer
Aging and aging-related diseases: from molecular mechanisms to interventions and treatments
Aging is driven by 12 interconnected hallmarks (e.g., genomic instability, mitochondrial dysfunction, cellular senescence) that are potential therapeutic targets; interventions like caloric restriction, senolytic drugs, and stem cell therapy are being developed to delay aging and age-related diseases.
Should the European Medicines Agency consider ageing a disease?
The European Medicines Agency does not classify aging as a disease, which hinders development of anti-aging drugs; reclassifying it would have moderate positive effects like increased research and better chances of completing vital health projects.
Skin health and biological aging
Biological aging is accelerated by environmental exposures (exposome), and the skin serves as a window to study systemic aging; skin aging shares hallmarks with whole-body aging, offering potential for preventive and therapeutic interventions.
Frailty, aging, and periodontal disease: Basic biologic considerations
Frailty and periodontal disease are common in older adults, share risk factors, and are bidirectionally linked through inflammatory dysregulation; targeting age-related immune changes could improve management of both conditions.
Sarcopenia, biological age and treatment eligibility in patients with cancer.
Chronological age is a poor predictor of treatment outcomes in cancer patients; biological age, measured via sarcopenia (muscle loss), is a more robust predictor, and integrating it into treatment decisions could improve precision oncology.