Menopause is the permanent cessation of menstruation following ovarian follicular depletion, diagnosed retrospectively after 12 months of amenorrhea. It represents a pivotal biological transition with far-reaching endocrine and systemic consequences. The menopausal transition, typically spanning several years, is marked by progressive depletion of ovarian follicles, diminished inhibin B, and compensatory elevations in follicle-stimulating hormone (FSH) and luteinizing hormone (LH). Estradiol concentrations fluctuate initially but ultimately decline sharply around the final menstrual period, accompanied by falling progesterone levels due to anovulation. Anti-Müllerian hormone, reflecting ovarian reserve, also declines and may assist in predicting menopausal timing. These hormonal perturbations underlie the clinical manifestations of menopause. Vasomotor symptoms, notably hot flashes and night sweats, result from hypothalamic thermoregulatory instability secondary to estrogen withdrawal. Estrogen deficiency further contributes to accelerated bone resorption, increasing the risk of postmenopausal osteoporosis and fragility fractures. Urogenital atrophy manifests as vaginal dryness, dyspareunia, urinary symptoms, and heightened infection risk, while adverse metabolic changes—including dyslipidemia, central adiposity, and endothelial dysfunction—contribute to the heightened cardiovascular risk observed after menopause. Understanding the endocrinological basis of menopause is essential to guide evidence-based strategies for optimizing midlife and long-term women’s health.