Decreased Physical Activity and Abnormal Feeding Regulation as Causes of Obesity

Decreased Physical Activity and Abnormal Feeding Regulation as Causes of Obesity

The causes of obesity are complex. Although genes play an important role in determining food intake and energy metabolism, lifestyle and environmental factors may play the dominant role in many obese people. The rapid increase in the prevalence of obesity in the past 20 to 30 years emphasizes the important role of lifestyle and environmental factors, because genetic changes could not have occurred so rapidly.

Sedentary Lifestyle Is a Major Cause of Obesity. Regular phys-ical activity and physical training are known to increase muscle mass and decrease body fat mass, whereas inadequate physical activity is typically associated with decreased muscle mass and increased adiposity. For example, studies have shown a close association between sedentary behaviors, such as prolonged televi-sion watching, and obesity.

About 25 to 30 per cent of the energy used each day by the average person goes into muscular activity, and in a laborer, as much as 60 to 70 per cent is used in this way. In obese people, increased physical activity usually increases energy expenditure more than food intake, resulting in significant weight loss. Even a single episode of strenuous exercise may increase basal energy expen-diture for several hours after the physical activity is stopped. Because muscular activity is by far the most important means by which energy is expended in the body, increased physical activity is often an effective means of reducing fat stores.

Abnormal Feeding Behavior Is an Important Cause of Obesity.

Although powerful physiologic mechanisms regulate food intake, there are also important environmental and psychological factors that can cause abnormal feeding behavior, excessive energy intake, and obesity.

Environmental, Social, and Psychological Factors Con- tribute to Abnormal Feeding. As discussed previously,the importance of environmental factors is evident from the rapid increase in the prevalence of obesity in most industrialized countries, which has coincided with an abundance of high-energy foods (especially fatty foods) and sedentary lifestyles.

Psychological factors may contribute to obesity in some people. For example, people often gain large amounts of weight during or after stressful situations, such as the death of a parent, a severe illness, or even mental depression. It seems that eating can be a means of releasing tension.

Childhood Overnutrition as a Possible Cause of Obesity.

One factor that may contribute to obesity is the preva-lent idea that healthy eating habits require three meals a day and that each meal must be filling. Many young children are forced into this habit by overly solicitous parents, and the children continue to practice it throughout life.

The rate of formation of new fat cells is especially rapid in the first few years of life, and the greater the rate of fat storage, the greater the number of fat cells. The number of fat cells in obese children is often as much as three times that in normal children. Therefore, it has been suggested that overnutrition of children— especially in infancy and, to a lesser extent, during the later years of childhood—can lead to a lifetime of obesity.

Neurogenic Abnormalities as a Cause of Obesity. We pre-viously pointed out that lesions in the ventromedial nuclei of the hypothalamus cause an animal to eat excessively and become obese. People with hypophysial tumors that encroach on the hypothalamus often develop progressive obesity, demonstrating that obesity in human beings, too, can result from damage to the hypothalamus.

Although hypothalamic damage is almost never found in obese people, it is possible that the functional organization of the hypothalamic or other neurogenic feeding centers in obese individuals is different from that in nonobese persons. Also, there may be abnor-malities of neurotransmitters or receptor mechanisms in the neural pathways of the hypothalamus that control feeding. In support of this theory, an obese person who has reduced to normal weight by strict dietary measures usually develops intense hunger that is demonstrably far greater than that of a normal person. This indicates that the “set-point” of an obese person’s feeding control system is at a much higher level of nutrient storage than that of a nonobese person.

Studies in experimental animals also indicate that when food intake is restricted in obese animals, there are marked neurotransmitter changes in the hypothala-mus that greatly increase hunger and oppose weight loss. Some of these changes include increased formation of orexigenic neurotransmitters such as NPY and decreased formation of anorexic substances such as leptin and a-MSH.

Genetic Factors as a Cause of Obesity. Obesity definitelyruns in families. Yet it has been difficult to determine the precise role of genetics in contributing to obesity, because family members generally share many of the same eating habits and physical activity patterns. Current evidence, however, suggests that 20 to 25 per cent of cases of obesity may be caused by genetic factors.

Genes can contribute to obesity by causing abnor-malities of (1) one or more of the pathways that regu-late the feeding centers and (2) energy expenditure and fat storage. Three of the monogenic (single-gene) causes of obesity are (1) mutations of MCR-4, the most common monogenic form of obesity discovered thus far; (2) congenital leptin deficiency caused by mutations of the leptin gene, which are very rare; and (3) muta-tions of the leptin receptor, also very rare. All thesemonogenic forms of obesity account for only a very small percentage of obesity. It is likely that many gene variations interact with environmental factors to influ-ence the amount and distribution of body fat.