How does heredity affect our weight? Part of the answer seems to lie in the fixed-point theory, which proposes that each person’s body has a certain or “set” weight that it strives to maintain. The body tries to keep your weight close to the set point through a physiological mechanism similar to a thermostat. When a person’s weight starts from the set point, the body takes corrective action, such as increasing or decreasing metabolism. According to the theory, people whose caloric intake is drastically reduced or increased for a few months should show corresponding rapid weight changes initially, but then the weight should show slower changes and reach a limit. Studies have found these predictions to be correct and that people quickly return to their original weight when they can eat what they want again. But the set-point theory is incomplete: it doesn’t explain, for example, why some people who lose a lot of weight manage to keep it off.

The mechanism that controls the set point appears to involve the hypothalamus. Animal research has shown that damage to specific parts of the hypothalamus causes weight to change and eventually level off, suggesting that a new benchmark has been set. If the damage is in the lateral region of the hypothalamus, the new set-point is of lesser weight; damage to the ventromedial region leads to obesity. One way the hypothalamus might regulate body weight is by monitoring some aspect of fat cells. One study found, for example, that after obese people lost weight, they began to produce large amounts of an enzyme that facilitates fat storage in cells and weight gain. Also, the more obese people were before losing weight, the more of this enzyme they produced. It may be that the loss of fat in the cells causes the hypothalamus to start producing enzymes to maintain the set point.

Another way that the hypothalamus can affect the process of weight control is by regulating the level of insulin in the person’s blood. Insulin is a hormone produced by the pancreas, it speeds up the conversion of sugar (glucose) into fat and promotes fat storage in adipose tissue. Obese people tend to have elevated serum insulin levels, which is called hyperinsulinemia. Elevations in serum insulin levels increase a person’s feelings of hunger, perceived pleasure from sweet tastes, and food consumption. Taken together, these findings indicate that weight gain is the result of a biopsychosocial process in which physiological factors interact with psychological and environmental factors.

It seems likely that the adjustment and function of the set point in regulating a person’s weight depends on the number and size of fat cells in the body. Psychologist Kelly Brownell has suggested that people whose weight is above the set point can reduce it fairly easily until the fat cells reach their lower limit of size. The body weight at which this level is reached would depend on the number of fat cells in the body. Since the number of fat cells increases mainly in childhood and adolescence, it is likely that people’s diets during this period of life are very important. Obese children between the ages of 2 and 10 have fat cells the same size as adults. As these children gain weight, they do so primarily by adding fat cells. The size of fat cells in normal-weight children does not reach adult levels until age 12, and the number of fat cells does not increase much between 2 and 10 years of age.