Chapter 21: Obesity, Starvation, and Anorexia of Aging

Adipose tissue exists in distinct forms, including white adipose tissue that stores triglycerides and mobilizes fatty acids for systemic energy use, brown and beige adipose tissues that dissipate energy as heat through nonshivering thermogenesis to maintain metabolic health and prevent weight gain, and dysfunctional expanded adipose tissue that perpetuates systemic inflammation and disease. The chapter establishes how adipokines—including leptin, adiponectin, resistin, and inflammatory cytokines—regulate hunger signals, metabolic rate, insulin sensitivity, vascular function, and immune tolerance, with dysregulation linking obesity to cardiovascular disease, type 2 diabetes, stroke, cancer, sleep-disordered breathing, joint degeneration, and kidney dysfunction. Obesity pathophysiology involves leptin resistance preventing appetite suppression, reduced adiponectin concentrations impairing glucose metabolism, altered gastrointestinal hormone secretion disrupting satiety signaling, lipotoxicity from excess free fatty acids damaging tissues, chronic inflammatory states, and shifts in gut microbial composition. The distinction between visceral obesity characterized by intra-abdominal fat accumulation conferring elevated cardiometabolic risk and peripheral obesity with subcutaneous distribution conferring relatively lower systemic harm is emphasized, alongside emerging phenotypes of normal-weight obesity and metabolically healthy obesity that challenge traditional body mass index classifications. Management strategies progress from behavioral and dietary modification through pharmaceutical interventions to bariatric surgery, which produces sustained weight loss and metabolic improvement. The chapter then addresses starvation's metabolic phases, beginning with hepatic glycogen mobilization and gluconeogenesis maintaining blood glucose, progressing to ketone body utilization and lipolysis during prolonged deprivation, and culminating in proteolysis and severe organ dysfunction. Severe chronic starvation manifests as marasmus from total caloric deficiency, kwashiorkor from selective protein insufficiency, or cachexia from chronic disease and systemic inflammation. Refeeding syndrome represents a critical medical emergency during nutritional restoration when metabolic substrate shifts precipitate electrolyte derangements and cardiac arrhythmias. Finally, anorexia of aging describes the multifactorial appetite decline in older adults stemming from diminished central hunger drive, sensory impairment of taste and smell, medication side effects, persistent inflammatory signaling, advanced chronic illnesses, social disconnection, and reduced functional capacity, ultimately contributing to frailty, protein-energy malnutrition, mitochondrial deterioration, and excess mortality risk.