Some people eat more than they need or exercise less than they should to maintain their body weight, and they get fat. Some eat less or exercise more, and they get thin. Amazingly, many people eat exactly what they need and stay at the same weight year after year. A single extra pat of butter each day would make them gain 5 pounds in a year, but if these people overeat by that much on one day, they apparently undereat by the same amount the next day. How do they do this, and (in contrast) why do some people fail to maintain their weight? In general, most experts believe that obesity is associated with both inside-the-body causes and environmental factors.19
GENETICS The theory that a hereditary, inside-the-body factor for obesity may exist is supported by the existence of animal strains that are genetically fat. Such animals tend to be fat in any environment; that is, they are fat regardless of the kind or variety of food that is available. In humans, studies have shown that identical twins—whether raised together or apart—tend to have similar weight-gain patterns. Also, twins raised by adoptive parents tend to have body shapes similar to those of their biological parents. Not all studies confirm this, however.20 Moreover, pairs of twins purposefully overfed in clinical experiments tend to respond similarly to the extra calories. Some sets of twins gain considerable weight when fed a certain number of calories, whereas other pairs put on relatively few pounds even on the same diet.21
Set-point theory theory that the body tends to maintain a certain weight by adjusting hunger, appetite, and food energy intake on the one hand and metabolism (energy output) on the other so that a person's conscious efforts to alter weight may be foiled.
Set-Point Theory One popular inside-the-body theory is the so-called set-point theory. Noting that many people who lose weight on reducing diets subsequently return to their original weight, some researchers have suggested that the body “wants” to maintain a certain amount of fat and regulates eating behaviors and hormonal actions to defend its “set point.” The theory implies that science should search inside obese people to find the causes of their problems—perhaps in their hunger-regulating mechanisms.
Fat cell theory states that during the growing years, fat cells respond to overfeeding by producing additional fat cells; the number of fat cells eventually becomes relatively fixed, and overfeeding from this point on causes the body to enlarge existing fat cells.
Lipoprotein lipase (LPL) an enzyme located on the surfaces of fat cells that enables the cell to convert blood triglycerides into fatty acids and glycerol to be pulled into the cell for reassembly and storage as body fat.
External cue theory the theory that some people eat in response to such external factors as the presence of food or the time of day rather than to such internal factors as hunger.
Leptin Researchers have identified a gene—named ob (for obese)—that appears to produce a hormone called leptin, after the Greek word for “slender.” When it is released from fat cells, leptin seems to tell the body to stop eating.22 Researchers report that as body fat stores increase, blood leptin also increases. The brain responds by decreasing appetite and increasing energy expenditure. Likewise, when body fat stores decrease, blood leptin decreases, and the brain responds by stimulating appetite and decreasing energy expenditure. Mice who have a defective form of the gene fail to produce leptin and can weigh as much as three times more than normal mice. Overweight people, too, may have a defective form of this gene (or may be unresponsive to leptin).23 More research is needed to clarify this mechanism.
Fat Cell Theory Some overweight infants become overweight adults, but most grow out of their obesity in childhood. An overweight child, however, is more likely to remain overweight into adulthood.24 Some researchers propose the fat cell theory, which holds that childhood obesity is persistent because early overfeeding (during the growing years) may cause fat cells to increase abnormally in number. According to this theory, a person’s number of fat cells is relatively fixed by the time he or she reaches adulthood; after that, a gain or loss of weight either increases or diminishes the size of the fat cells. Unfortunately, persons with greater numbers of fat cells are less likely to lose weight successfully. Some researchers suggest that the body triggers hunger signals when the fat stored in these cells begins to decrease. Because fat cells increase in number during childhood, prevention of obesity is critical during the growing years.
Additionally, fat cells of obese people contain higher levels of the enzyme lipoprotein lipase (LPL), which determines the rate at which adipose cells store fat. The larger the fat cell (and the greater the number of fat cells), the more LPL and the more easily the body can pull triglycerides into fat cells for storage. Unfortunately, LPL activity rises further with weight loss, enhancing the body’s ability to regain the lost weight.25 A question still to be answered is whether some people develop obesity because their fat cells contain an abnormal amount of LPL from birth.
ENVIRONMENT Environmental factors linked with obesity suggest that people overeat or underexercise because they are pushed to do so by factors in their surroundings: foremost among them, the availability of a multitude of delectable foods and a lack of opportunity for vigorous physical activity.
Some people seem to have inherited or learned a way of resisting external stimuli to eat, but others have not. In a classic experiment with “cafeteria rats,” ordinary rats who were fed regular rat chow maintained normal weight (for rats), but when those very same rats were offered free access to a wide variety of tempting, rich, highly palatable foods, they greatly overate and became obese. Similarly, one study found a positive correlation between overfatness and a diet offering a wide variety of snacks and sweets.26 This is the basis of the external cue theory, which posits that, at least in some people, the internal regulatory systems are easily overridden by environmental influences. Does this mean obesity is hereditary, environmental, or both?
It seems likely that both hereditary and environmental factors influence obesity in human beings. The tendency to obesity is probably inherited, but the environment is probably influential in the sense that it can prevent or permit the development of obesity when the potential is there.
A CLOSER LOOK AT EATING BEHAVIOR In human beings, learning plays an important role. Although we have genetically inborn instincts, things learned during early childhood experiences combined with our current environments may conflict with
These instincts. Thus, the hunger drive is programmed by heredity, but appetite is influenced by learned responses that may cause us to ignore or over-respond to our hunger. Another way to say this is to say that hunger is physiological, whereas appetite is psychological, and the two don’t always coincide. We have all experienced appetite without hunger: “I’m not hungry, but I’d love to have some.” We also often experience the reverse: “I know I’m hungry, but I don’t feel like eating.”
The ways people respond to hunger and appetite determine whether they eat too much, too little, or just enough to maintain their weight. A third factor, satiety, which signals that it is time to stop eating, also affects our eating patterns and weight issues.
In human physiology, research is beginning to find possible answers to what regulates eating behavior. The stomach’s nerves perceive stretching, and you stop eating when your stomach feels stretched full. Blood glucose level is also thought to be involved. You get hungry when your blood glucose level falls—or perhaps when your liver glycogen is beginning to be exhausted. Blood lipids, and possibly amino acids and other molecules, also play a role. When you eat, you secrete hormones to regulate digestive activity; these hormones may also convey the message to the brain that it is time to start or stop eating.48
Where in the brain are these messages received (whatever they are)? One brain area stands out as a regulator for food behavior: the hypothalamus. The hypothalamus communicates with the hormone system and the nervous system. It integrates many signals received from the rest of the body, including information about the blood’s temperature, sodium content, and glucose content. We know it is important in regulating eating because damage to the hypothalamus produces derangements in eating behavior and body weight. In some cases it can cause severe weight loss, and in others it can cause extreme overeating. In the person with a normal hypothalamus, however, appropriate eating behavior seems to be a response to a whole host of signals rather than a response to a single signal arriving at some one location in the hypothalamus. Somehow these many inputs become integrated into a final common path: the act of eating.
A person who eats inappropriately may have established a habitual behavior pattern that inappropriately links certain stimuli to the act of eating. The study of behavior offers insight into the causes of overeating by viewing it as a conditioned response. Sometimes eating behavior is initiated by the wrong triggers. For example, a crying child with a skinned knee who is offered a lollipop may learn to associate food with comfort and inappropriately feel the need for food when experiencing emotional pain later in life.
Eating behavior, then, may be a response not only to hunger or appetite but also to complex human sensations such as yearning, craving, addiction, or compulsion. Often, eating is used to relieve boredom or to ward off depression. Some people respond to anxiety—or, in fact, to any kind of arousal—by eating. Significantly, however, when these people are able to name their aroused condition, they often gain a feeling that they have some control over it and are not as likely to overeat.
Stress may also directly promote the accumulation of body fat. The stress hormones favor the breakdown of energy stores (glycogen and fat) into glucose and fatty acids, which can be used to fuel the human “fight or flight” response. If a person doesn’t use the fuel in physical exertion, however, the body cannot turn these fragments back into glycogen. Thus, its only alternative is to convert them to fat. Each time glucose is pulled out of storage in response to stress and then transformed into fat, the lowered glucose level or exhausted glycogen will signal hunger, and the person will eat again soon after.
Stress eating may appear in different patterns. Some people eat excessively at night, whereas others binge during emotional crises. Some people react oppositely and reject food when stressed. We do not know why these behaviors occur, but research continues.
The many possible causes of obesity mentioned so far all relate to the input side of the energy equation. What about output? Probably the most important contributor to the obesity problem in our country is underactivity.27 Some obese people eat less than lean people, but due to extraordinary inactivity, they still manage to store surplus calories. Some people move more efficiently than others, too. Two people of the same age, height, and weight might use different amounts of calories walking five miles because of the different ways in which they move their muscles.
No two people are alike, either physically or psychologically, and the causes of obesity are no doubt as varied as the obese people themselves. Many causes may contribute to the problem in a single person. Given this complexity, it is obvious that there is no panacea. The top priority should be prevention, but where prevention has failed, the treatment of obesity must involve a simultaneous attack on many fronts.28