The physiological and environmental elements that contribute to the progressive decline in gamete quality, gonadal function, and fertility across the lifespan in both males and females. These factors encompass genetic predispositions, cumulative oxidative stress damage to ovarian and testicular tissue, and the impact of endocrine-disrupting chemicals on the hypothalamic-pituitary-gonadal (HPG) axis. Managing these factors is essential for extending reproductive vitality.
Origin
This term stems from reproductive endocrinology and toxicology, recognizing that reproductive decline is not solely chronological but is highly sensitive to biological and environmental insults. Research has increasingly focused on the role of cellular damage in diminishing ovarian reserve and spermatogenesis.
Mechanism
A primary mechanism involves mitochondrial dysfunction and increased reactive oxygen species within the oocytes and sperm, compromising DNA integrity and cellular viability. Furthermore, the cumulative exposure to xenobiotics, such as heavy metals and pesticides, can directly impair steroidogenesis and alter the delicate feedback loops between the hypothalamus, pituitary, and gonads. This disruption leads to a reduction in sex steroid production and an increase in gonadotropin release as the body attempts to compensate for failing gonadal function.
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