Obesity Epidemiology and Etiology

Epidemiology

It is estimated that 34% of adults in the United States are obese. The prevalence increases with age up to age 50, at which point it falls sharply in accordance with the increased mortality rate. Obesity is more common in women, particularly after age 50, because of the higher mortality rate among obese men after that age. Obesity is also more common among minorities and low-income populations. It has been estimated that about 25% of children and 20% of adolescents are significantly overweight.

Family studies of obesity show that 40% of adolescents studied at age 15 who had one obese parent were obese, whereas 80% of those with two obese parents were obese. This compares to only a 10% incidence of obesity among adolescents whose parents are of normal weight. Studies of monozygotic and dizygotic twins suggest genetic factors, but environmental influences are also present. Adoption studies have shown conflicting evidence for genetic transmission. Evidence for the heritability of somatotypes is stronger than for obesity. This fact may be significant in that even a moderate degree of ectomorphic body habitus may protect against the development of obesity.

Etiology
Although there is great variability in weight among humans, individuals show remarkable consistency over time. Humans who agree to increase or decrease their weights for experimental purposes generally return to their starting weights when allowed to eat freely. Such observations have led to the theory that there is a biological set point for body weight in humans. This is supported by animal studies in which lesions of the ventromedial hypothalamus cause hypo- and hyperphagia, respectively. To the extent that the "set point theory" is applicable to humans, many obese individuals may be dieting in opposition to biological factors that make dieting far more difficult for them than for other people.

Weight gain can occur as a result of an increase in either the number or the size of fat cells. The fat cells of adults with juvenile-onset obesity may be about the same size as those of normal-weight persons, but there may be up to five times as many. Persons with adult-onset obesity may have a normal number of larger-than-normal fat cells. In studies in which fat cell number and size were determined, individuals tended to stop losing weight when fat cell size returned to normal. Since fat cells once formed do not disappear, fat cell number may determine the lower limit of weight for persons who by dieting have worked to reduce cell size to normal. There are two periods of cellular proliferation in normal-weight children: birth to 2 years of age and 10-14 years of age. In obese children, the period may extend well past 2 years of age, with consequent hypercellularity of fat tissue early in life. Although this may be partly under genetic control, the cellular theory of obesity thus has important implications regarding nutritional practices and weight regulation for children.