DNA damage reduction is a key physiological and therapeutic goal focused on minimizing the incidence of mutations, strand breaks, and other molecular lesions within the cell’s genetic material. This reduction is vital for maintaining genomic stability, preventing cellular senescence, and significantly decelerating the biological aging process across all organ systems. Clinical strategies target both the prevention of initial damage from free radicals and the enhancement of endogenous DNA repair mechanisms within the nucleus.
Origin
This concept is rooted in molecular biology and the “damage theory” of aging, which posits that the progressive accumulation of molecular errors, including damage to the DNA helix, is a primary driver of age-related decline. The term gained prominence in longevity medicine as a measurable, fundamental biomarker of healthspan and biological age. It underscores the central and indispensable role of genetic integrity in systemic function and cellular replication.
Mechanism
Damage reduction is achieved through several integrated pathways, including the effective neutralization of reactive oxygen species (ROS) via powerful antioxidant enzymes like superoxide dismutase, thereby preventing oxidative stress-induced damage. Cells also possess sophisticated, energy-intensive DNA repair mechanisms, such as Nucleotide Excision Repair and Base Excision Repair, whose efficiency is often supported by specific micronutrients and metabolic cofactors. Optimizing the hormonal milieu, particularly with balanced sex steroids, can indirectly support these critical repair pathways and improve overall genomic maintenance.
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