Over the past decades, significant progress has been made in understanding the factors that determine the state of the female reproductive system. Alongside endocrine, genetic, and infectious causes, increasing attention has been given to disturbances in sleep-wake rhythms, climate change, and psychoemotional stress. These factors often remain unnoticed, yet they may trigger a cascade of pathological processes — from menstrual irregularities to decreased ovarian reserve and the development of premature ovarian insufficiency (POI). At the molecular level, stress exposure is accompanied by suppression of the antioxidant defense system, mitochondrial dysfunction, and alterations in intracellular signaling pathways. Melatonin acts as a major endogenous protective factor with potent antioxidant and antiapoptotic properties. Prolonged exposure to stressors activates the hypothalamic-pituitary-adrenal (HPA) axis, thereby suppressing the hypothalamic—pituitary—ovarian (HPO) axis, leading to a reduction in ovarian reserve and deterioration in oocyte quality. Clinical and experimental data confirm the high sensitivity of the female reproductive system to stress. Psychoemotional, circadian, climatic, metabolic, and oxidative stressors are considered potential triggering mechanisms for premature ovarian insufficiency. This review analyzes key stress biomarkers that reflect both physiological and molecular changes as well as neuropsychological characteristics. Effective diagnosis and prevention of stress-associated disorders are possible only through an interdisciplinary approach that aligns with modern trends in personalized medicine and aims to preserve women’s reproductive health.
Adamyan et al. (Sun,) studied this question.