How does heredity affect our weight? Part of the answer seems to be described in set-point theory, which proposes that each person’s body has a certain or “set” weight that it strives to maintain. The body tries to maintain its weight near the set-point by means of a thermostat-like physiological mechanism. When a person’s weight departs from the set-point, the body takes corrective measures, such as by increasing or decreasing metabolism. According to the theory, people whose caloric intake is either drastically reduced or increased for a few months should show rapid corresponding weight changes initially, but the weight should then show slower changes and reach a limit. Studies have found that these predictions are correct and that people quickly return to their original weight when they can eat what they want again But set-point theory is incomplete: it doesn’t explain, for instance, why some people who lose a lot of weight manage to keep it off.
The mechanism controlling the set-point seems to involve the hypothalamus. Research with animals has shown that damage to specific parts of the hypothalamus causes weight to change and eventually level off, suggesting that a new set-point has been established. If the damage is in the lateral region of the hypothalamus, the new set-point is for a lower 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 instance, that after obese people lost weight, they began to produce large amounts of an enzyme that makes it easier to store fat in cells and gain weight. Moreover, the more obese the people were before losing weight, the more of this enzyme they produced. It may be that the loss of fat in cells triggers the hypothalamus to initiate enzyme production to maintain the set-point.
Another way the hypothalamus may affect the process of weight control is by regulating the level of insulin in the person’s blood. Insulin is a hormone that is produced by the pancreas, speeds the conversion of sugar (glucose) to fat, and promotes the storage of fat in adipose tissue. Obese people tend to have high serum levels of insulin, which is called hyperinsulinemia. Elevations in serum insulin levels increase the person’s sensations of hunger, perceived pleasantness of sweet tastes, and food consumption. Taken together, these findings indicate that weight gain results from a biopsychosocial process in which physiological factors interact with psychological and environmental factors
It seems likely that the setting and function of the set-point in regulating a person’s weight depend on the number and size of fat cells in the body. Psychologist Kelly Brownell has suggested that people whose weights are above the set-point may be able to reduce fairly readily until the fat cells reach their lower limit in 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, the diets of individuals during that time in the life span are likely to be very important. Obese children between 2 and 10 years of age have fat cells that are as large as those of adults. As these children gain weight, they do so mainly by adding fat cells. Fat cell size for normal-weight children does not reach adult levels until age 12, and the number of their fat cells does not increase very much between 2 and 10 years of age.