Obesity can be defined as an excess of body fat. A surrogate marker for body fat content is the body mass index (BMI), which is calculated as:

In clinical terms, a BMI between 25 and 29.9 kg/m2 is called overweight, and a BMI greater than 30 kg/m2 is called obese. BMI is not a direct estimate of adiposity and does not take into account the fact that some individuals have a high BMI due to a large muscle mass. A better way to define obesity is to actually measure the percentage of total body fat. Obesity is usually defined as 25 per cent or greater total body fat in men and 35 per cent or greater in women. Although percentage of body fat can be estimated with various methods, such as measuring skin-fold thickness, bioelectrical impedance, or underwater weighing, these methods are rarely used in clinical practice, where BMI is commonly used to assess obesity.

The prevalence of obesity in children and adults in the United States and in many other industrialized countries is rapidly increasing, rising by more than 30 per cent over the past decade. Approximately 64 per cent of adults in the United States are overweight, and nearly 33 per cent of adults are obese.

Obesity Results from Greater Energy Intake than Energy Expenditure. When greater quantities of energy (in the form of food) enter the body than are expended, the body weight increases, and most of the excess energy is stored as fat. Therefore, excessive adiposity (obesity) is caused by energy intake in excess of energy output. For each 9.3 Calories of excess energy that enter the body, approximately 1 gram of fat is stored.

Fat is stored mainly in adipocytes in subcutaneous tissue and in the intraperitoneal cavity, although the liver and other tissues of the body often accumulate significant amounts of lipids in obese persons. The metabolic processes involved in fat storage were discussed in Chapter 68.

It was previously believed that the number of adipocytes could increase substantially only during infancy and childhood and that excess energy intake in children led to hyperplastic obesity, associated with increased numbers of adipocytes and only small increases in adipocyte size. In contrast, obesity developing in adults was thought to increase only adipocyte size, resulting in hypertrophic obesity. Recent studies, however, have shown that new adipocytes can differentiate from fibroblast-like preadipocytes at any period of life and that the development of obesity in adults is accompanied by increased numbers, as well as increased size, of adipocytes. An extremely obese person may have as many as four times as many adipocytes, each containing twice as much lipid, as a lean person.

Once a person has become obese and a stable weight is obtained, energy intake once again equals energy output. For a person to lose weight, energy intake must be less than energy expenditure.

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 physical 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 television 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 expenditure 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 Contribute 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 prevalent 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 previously 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 abnormalities 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 hypothalamus 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 definitely runs 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 abnormalities of (1) one or more of the pathways that regulate 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) mutations of the leptin receptor, also very rare. All these monogenic forms of obesity account for only a very small percentage of obesity. It is likely that many gene variations interact with environmental factors to influence the amount and distribution of body fat.

Treatment of Obesity

Treatment of obesity depends on decreasing energy input below energy expenditure and creating a sustained negative energy balance until the desired weight loss is achieved. In other words, this means either reducing energy intake or increasing energy expenditure. The current National Institutes of Health (NIH) guidelines recommend a decrease in caloric intake of 500 kilo-calories per day for overweight and moderately obese persons (BMI greater than 25 but less than 35 kg/m2) to achieve a weight loss of approximately 1 pound each week. A more aggressive energy deficit of 500 to 1000 kilocalories per day is recommended for persons with BMIs greater than 35 kg/m2. Typically, such an energy deficit, if it can be achieved and sustained, will cause a weight loss of about 1 to 2 pounds per week, or about a 10 per cent weight loss after 6 months. For most people attempting to lose weight, increasing physical activity is also an important component of successful long-term weight loss.

To decrease energy intake, most reducing diets are designed to contain large quantities of "bulk," which is generally made up of non-nutritive cellulose substances. This bulk distends the stomach and thereby partially appeases hunger. In most lower animals, such a procedure simply makes the animal increase its food intake even more, but human beings can often fool themselves because their food intake is sometimes controlled as much by habit as by hunger. As pointed out later in connection with starvation, it is important to prevent vitamin deficiencies during the dieting period.

Various drugs for decreasing the degree of hunger have been used in the treatment of obesity. The most widely used drugs are amphetamines (or amphetamine derivatives), which directly inhibit the feeding centers in the brain. One drug for treating obesity is sibu-tramine, a sympathomimetic that reduces food intake and increases energy expenditure. The danger in using these drugs is that they simultaneously overexcite the central nervous system, making the person nervous and elevating the blood pressure. Also, a person soon adapts to the drug, so that weight reduction is usually no greater than 5 to 10 per cent.

Another group of drugs works by altering lipid metabolism. For example, orlistat, a lipase inhibitor, reduces the intestinal digestion of fat. This causes a portion of the ingested fat to be lost in the feces and therefore reduces energy absorption. However, fecal fat loss may cause unpleasant gastrointestinal side effects, as well as loss of fat-soluble vitamins in the feces.

Significant weight loss can be achieved in many obese persons with increased physical activity. The more exercise one gets, the greater the daily energy expenditure and the more rapidly the obesity disappears. Therefore, forced exercise is often an essential part of treatment. The current clinical guidelines for the treatment of obesity recommend that the first step be lifestyle modifications that include increased physical activity combined with a reduction in caloric intake. For morbidly obese patients with BMIs greater than 40, or for patients with BMIs greater than 35 and conditions such as hypertension or type II diabetes that predispose them to other serious diseases, various surgical procedures can be used to decrease the fat mass of the body or to decrease the amount of food that can be eaten at each meal.

Two of the most common surgical procedures used in the United States to treat morbid obesity are gastric bypass surgery and gastric banding surgery. Gastric bypass surgery involves construction of a small pouch in the proximal part of the stomach that is then connected to the jejunum with a section of small bowel of varying lengths; the pouch is separated from the remaining part of the stomach with staples. Gastric banding surgery involves placing an adjustable band around the stomach near its upper end; this also creates a small stomach pouch that restricts the amount of food that can be eaten at each meal. Although these surgical procedures generally produce substantial weight loss in obese patients, they are major operations, and their long-term effects on overall health and mortality are still uncertain.

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