How does heredity affect our weight? Part of the answer seems to be outlined in set point theory, which proposes that each person’s body has a certain or “fixed” weight that they strive to maintain. The body tries to keep its weight close to the set point by means of a physiological mechanism similar to a thermostat. When a person’s weight deviates 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 rapid corresponding weight changes initially, but the weight should 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 get back to eating what they want. But the set point theory is incomplete: It does not explain, for example, why some people lose much the weight manages not to regain it.
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 shift and eventually stabilize, 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 controlling some aspect of the 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 weight management process is by regulating the level of insulin in the person’s blood. Insulin is a hormone produced by the pancreas, accelerates the conversion of sugar (glucose) into fat and promotes the storage of fat in adipose tissue. Obese people tend to have elevated serum insulin levels, which is called hyperinsulinemia. Elevations in serum insulin levels increase the person’s feeling of hunger, the perception of liking sweet tastes, and the consumption of food. 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 fit 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 fairly easily until fat cells reach their lower limit in size. The body weight at which this level is reached will 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 as large as those of 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 the age of 12, and the number of fat cells does not increase much between the ages of 2 and 10.