Obesity is a chronic, multifactorial disease characterized by excess body fat that harms health. It arises from a complex interaction of genetics, biology, behavior, and environment rather than simple overeating or lack of willpower.

Body weight is regulated by a homeostatic system centered in the hypothalamus. Hormones such as leptin, insulin, ghrelin, GLP-1 and others signal energy stores and food intake to the brain. In obesity, this system becomes dysregulated: leptin resistance and altered reward pathways in the brain weaken satiety signals and enhance food motivation, particularly for highly processed, energy dense foods.

Genetic variation contributes significantly to susceptibility. Rare single gene mutations in pathways like leptin and the melanocortin 4 receptor can cause severe early onset obesity. More commonly, many small effect genetic variants combine with environmental factors to raise risk in modern obesogenic settings.

Adipose tissue itself is metabolically active. In obesity it becomes inflamed and dysfunctional, releasing cytokines and altering lipid and glucose metabolism. This promotes insulin resistance, type 2 diabetes, fatty liver disease, cardiovascular disease, some cancers and sleep apnea. Visceral fat around internal organs is especially harmful.

Environmental drivers include abundant cheap ultra processed foods, large portion sizes, sedentary work, car dependent lifestyles, stress, sleep disruption and exposure to endocrine disrupting chemicals. Early life factors such as maternal obesity, gestational diabetes, and rapid infant growth can program long term obesity risk.

Effective management typically requires a combination of dietary change, increased physical activity, psychological support, medications that target appetite and metabolism, and in some cases bariatric surgery. Prevention efforts must also address social and environmental conditions that favor weight gain.