Why do we age at the cellular level?

The answer

Cellular aging is driven by multiple interconnected mechanisms. The Hayflick limit describes how most human cells can divide only about 50 to 70 times before entering senescence, primarily because telomeres (protective DNA caps at chromosome ends) shorten with each division until they reach a critical length that triggers growth arrest. Accumulated DNA damage from reactive oxygen species, environmental mutagens, and replication errors gradually impairs cellular function. Senescent cells that stop dividing secrete inflammatory molecules (the senescence-associated secretory phenotype or SASP) that damage surrounding tissues. Mitochondrial dysfunction reduces energy production and increases oxidative stress. Epigenetic drift (changes in gene regulation without DNA sequence changes) alters gene expression patterns over time. Research into senolytics (drugs that selectively kill senescent cells) and other anti-aging interventions has shown promise in extending healthspan in animal models.