Obesity
New Approaches to Obesity
A new concept is emerging that obesity represents a defect in appetite regulation by hormones the body makes, which are supposed to turn off eating, when a person has taken a meal. By this theory, the control of the appetite center is physiologically defective, and the obesity represents a physical problem, rather than a defect in personal discipline. New information suggests that the hormonal signals are different for men versus women. When a woman goes into menopause, the usual signals that turn off her appetite lose their effectiveness, unless she takes estrogen replacement.
At long last, new, and physiologically rational drugs are starting to come out to help with obesity. The prospect of these drugs is associated with a new concept of obesity and possible therapies. For the most part, lay people and health professionals alike have considered obesity a defect of personal discipline and control. By this view, the heavy person becomes obese, because he or she does not exert proper personal control over food selection and exercise. However, a new concept is emerging. This says that obesity represents a defect in appetite regulation by hormones the body makes, which are supposed to turn off eating, when a person has taken a meal. By this theory, the control of the appetite center is physiologically defective, and the obesity represents a physical problem, rather than a defect in personal discipline.
There is a growing body of information about hormones, which regulate the appetite. This base of information suggests that various hormones are secreted with eating. In normal or thin subjects, the amount of hormones produced is directly related to the amount of food ingested. These hormones are supposed to suppress the appetite. Thus, the more food eaten, the more hormones released, and the more the appetite is decreased.
A number of hormones have been identified, which may act in this system. The group includes a gut hormone, called GLP1, a hormone from the pancreas called amylin, and a hormone made by fat cells, known as leptin. All three hormones reduce the appetite in various experimental models, in both humans and animals.
Heavy people may have defects in the secretion or action of these hormones. The secretion of GLP1 and amylin may be inadequate. Leptin secretion is actually increased in heavy people; however, its ability to penetrate the brain and affect the appetite center may be decreased.
New approaches to treatment of obesity with existing drugs and new drug development both offer optimism about more successful treatment of obesity in the future. There may be less negative judgment about patients in this area of therapy
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