Stress and Aging describes the profound, bidirectional relationship where chronic physiological and psychological stress accelerates the biological aging process, leading to premature senescence and an increased risk of age-related disease. The impact is systemic, affecting telomere length, DNA repair mechanisms, and the delicate balance of the neuroendocrine system. Persistent exposure to stressors increases the allostatic load, essentially causing the body’s regulatory systems to wear out faster due to continuous compensatory effort. Managing this stress-aging axis is a central pillar of preventative medicine and longevity science, requiring a comprehensive, multi-system approach.
Origin
This concept is a synthesis of decades of research in psychoneuroimmunology, endocrinology, and cellular biology, notably linked to the concept of allostatic load developed in stress research. The clinical observation that chronic stress correlates with shorter telomeres provided a tangible, molecular link between stress exposure and cellular aging. It is a critical area of study in understanding the environmental and behavioral determinants of healthspan and lifespan.
Mechanism
Chronic stress activates the hypothalamic-pituitary-adrenal (HPA) axis, leading to sustained high levels of glucocorticoids, primarily cortisol. This hypercortisolemia disrupts metabolic homeostasis, suppresses immune function, and promotes chronic low-grade inflammation, a recognized hallmark of aging. Furthermore, chronic stress accelerates telomere shortening through increased oxidative stress and impaired DNA repair, limiting the replicative capacity of somatic cells. This persistent state of imbalance drives cellular senescence and contributes directly to the decline in organ reserve associated with advanced age.
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