Abstract
The debate about whether obesity should be called a disease continues. From a clinical perspective, it meets the criteria needed to call it a disease. It has an etiology—an imbalance between energy intake and expenditure. It has a pathogenesis in the feedback systems involving leptin, neurochemicals in the brain, and the neural and endocrine messages that respond to the intake of food. The pathology of obesity lies in its enlarged fat cells, and the pathophysiology lies in the changes in the secretion of products from these enlarged fat cells, including cytokines, procoagulants, inflammatory peptides, and angiotensinogen. These secretory products of fat cells and the increased mass of fat are responsible for the associated metabolic diseases, such as diabetes, hypertension, heart disease, sleep apnea, and some sorts of cancer. Treatments consist of techniques to alter the balance between energy intake and energy expenditure. This constellation of factors leads to the conclusion that obesity should be called a disease.