Anti-obesity medication or weight loss medications are pharmacological agents that reduce or control weight. These medications alter one of the fundamental processes of the human body, weight regulation, by altering either appetite, or absorption of calories. The main treatment modalities for overweight and individuals with obesity remain dieting (healthy diet and caloric restriction) and physical exercise. In the United States, orlistat (Xenical) and semaglutide (Wegovy) are approved by the FDA for long-term use. Because of potential side effects, and limited evidence of small benefits in weight reduction for children and adolescents with obesity, it is recommended that anti-obesity medications only be prescribed for obesity where it is hoped that the benefits of the treatment outweigh its risks. In the United States, the Food and Drug Administration advocates that people with either a body-mass index of at least 30, or a body-mass index of at least 27 with at least one weight-related comorbidity, represent a patient population with sufficiently high baseline health risks to justify the use of anti-obesity medication. Mechanisms of action Anti-obesity medications may operate through one or more of the following mechanisms: Catecholamine releasing agents such as amphetamine, phentermine, and related substituted amphetamines (e.g., bupropion) which act as appetite suppressants are the main tools used for the treatment of obesity. GLP-1 analogues such as tirzepatide, semaglutide, and liraglutide slow gastric emptying and also have neurologically-driven effects on appetite. History The first described attempts at producing weight loss are those of Soranus of Ephesus, a Greek physician, in the second century AD. He prescribed elixirs of laxatives and purgatives, as well as heat, massage, and exercise. This remained the mainstay of treatment for well over a thousand years. It was not until the 1920s and 1930s that new treatments began to appear. Based on its effectiveness for hypothyroidism, thyroid hormone became a popular treatment for obesity in euthyroid people. It had a modest effect but produced the symptoms of hyperthyroidism as a side effect, such as palpitations and difficulty sleeping. 2,4-Dinitrophenol (DNP) was introduced in 1933; this worked by uncoupling the biological process of oxidative phosphorylation in mitochondria, causing them to produce heat instead of ATP. The most significant side effect was a sensation of warmth, frequently with sweating. Overdose, although rare, led to a rise in body temperature and, ultimately, fatal hyperthermia. By the end of 1938 DNP had fallen out of use because the FDA had become