Eating Behavior in Menopausal Women: From Molecular to Clinical Aspects—What Changes?

The menopausal transition represents a critical period in women’s lives characterized by profound hormonal, metabolic, and behavioral changes. Estrogen deficiency during menopause triggers complex alterations in eating behavior through multiple molecular mechanisms involving hypothalamic neuropeptide systems, neurotransmitter pathways, and peripheral hormonal signals. This narrative review examines the molecular basis of eating behavior changes in menopausal women, integrating evidence from basic science and clinical research. At the molecular level, declining estradiol disrupts the hypothalamic regulation of appetite through estrogen receptors ERα and ERβ, leading to dysregulation of key neuropeptides including neuropeptide Y (NPY), agouti-related peptide (AgRP), and proopiomelanocortin (POMC). Peripheral signals such as leptin, ghrelin, and insulin show altered secretion and sensitivity patterns. Clinically, postmenopausal women experience increased appetite, heightened food reward sensitivity, carbohydrate cravings, and elevated risk of binge eating behaviors. These changes contribute to weight gain averaging 2–3 kg during the menopausal transition, with preferential visceral fat accumulation increasing metabolic syndrome risk. Body composition shifts include 44% increases in visceral adiposity and concurrent sarcopenia. Emerging evidence highlights the role of gut microbiota alterations in mediating metabolic dysfunction. Therapeutic strategies including hormone replacement therapy, targeted nutritional interventions, and lifestyle modifications show promise in mitigating these changes. Understanding the molecular-to-clinical continuum of eating behavior changes in menopause is essential for developing evidence-based preventive and therapeutic approaches to improve metabolic health and quality of life in postmenopausal women.