WEIGHT MANAGEMENT: HUNGER, APPETITE, AND SATIETY AS RISK FACTORS FOR OBESITY

Theories abound concerning the mechanisms that regulate food intake. Some sources indicate that the hypothalamus (the part of the brain that regulates appetite) closely monitors levels of certain nutrients in the blood. When these levels begin to fall, the brain signals us to eat. In the obese person, it is possible that the monitoring system does not work properly and that the cues to eat are more frequent and intense than they are in people of normal weight.

Other sources indicate that thin people may send more effective messages to the hypothalamus. This concept, known as adaptive thermogenesis, states that thin people can often consume large amounts of food without gaining weight because the appetite center of their brains speeds up metabolic activity to compensate for the increased consumption. Older studies have indicated the possibility that specialized types of fat cells, called brown fat cells, may send signals to the brain, which controls the thermogenesis response.

The hypothesis that food tastes better to obese people thus causing them to eat more has largely been refuted. Scientists do distinguish, however, between hunger, an inborn physiological response to nutritional needs, and appetite, a learned response to food that is tied to an emotional or psychological craving for food often unrelated to nutritional need. Obese people may be more likely than thin people to satisfy their appetite and eat for reasons other than nutrition.

In some instances, the problem with overconsumption may be more related to satiety than to appetite or hunger. People generally feel satiated, or full, when they have satisfied their nutritional needs and their stomach signals “no more”. For undetermined reasons, obese people may not feel full until much later than thin people. The leptin and GLP-1 studies seem to add credence to this theory.

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