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OBESITY This term derives from the Latin (obesus, meaning ''to eat up''), and it came into use in English in the early 1600s to mean a condition characterized by excessive bodily fat. Excess body weight is associated with the increased storage of energy in the form of adipose tissue. Standard criteria for obesity are (1) greater than 20 percent above ideal body weight (IDW) for a given height, as determined from actuarial tables, or (2) body mass index (BMI), defined as weight in kilograms divided by height in meters squared (kg m2 = BMI), greater than 27 for men and greater than 25 for women.

Obesity represents the upper end of a body-weight continuum, rather than a qualitatively different state. Obesity can derive from a variety of causes, but a significant genetic contribution has been demonstrated.

Being overweight to a statistically significant above-average degree or having proportionately more body fat than average is believed to be due primarily to genetic factors that influence appetite, metabolism, and activity levels. Most notably, obesity is more prevalent (ten times more likely) in persons whose parents, brothers, or sisters are obese. Studies in identical twins have clearly demonstrated that genetics plays a major role. For example, nonidentical twins raised together were less similar in weight than identical twins raised apart.

Beyond the genetic component, researchers have been examining the role of hormones, most specifi cally leptin, a hormone secreted by fat tissue that affects the brain's appetite control centers. In some studies, mice given injections of leptin lost their appetites and, consequently, lost weight. The human response to leptin varies dramatically, and the relationship between plasma leptin levels and obesity in humans is not yet clear or confirmed. According to one study, mutations in the leptin gene are indeed responsible for obesity in both mice and humans, but these mutations are quite rare outside of the laboratory setting. Another study shows that leptin is a signal to the hypothalamus of peripheral fat deposits, but further studies are being conducted to determine if obese individuals have trouble with leptin access into the brain. Other researchers have found that lean, physically active men have lower levels of leptin than heavier, sedentary men (ages 47 to 83).

Leptin research continues since solid findings could help in the treatment and prevention of obesity and diseases and health problems linked to obesity, such as hypertension, stroke, and type 2 diabetes (diabetes mellitus).

The prevalence of obesity (in this case defined as having body fat in excess of 25% for males or 30% in females) varies remarkably across ethnic groups and cultures, and across age groups. In the United States, obesity is consistently less common among African-American men than among white men across the entire age range; is consistently more common among African-American women than among white women; and tends to be more com mon among women of Eastern European and Italian ancestry than among those of British ancestry. Socioeconomic factors affect the prevalence of obesity, but men and women are affected differently: It is more common among all women in lower socioeconomic groups, but men in lower socioeconomic groups are leaner than average. Overall, approximately 40 million Americans are obese.

Some researchers and clinicians see similarities among certain patterns of overeating and other excessive behaviors such as drinking too much Alcohol, compulsive Gambling, engaging in ''too much'' sexual activity, and even exercising compulsively. Although there may be such similarities, the semantics attached to problems of overeating and OBESITY are formidable.

Not all persons whose weight is above average are obese (they may have excess muscle mass); not all who are obese eat excessively; not all who eat excessively become obese; and some individuals who have clinically recognized disorders centered on eating and body weight, such as BULIMIA, may or may not be obese.

(SEE ALSO: Bulimia Nervosa; Overeating and Other Excessive Behaviors)

BIBLIOGRAPHY

Ball, G. G., & Grinker, J. A. (1981). Overeating and obesity. In: S. J. Mule (Ed.), Behavior in excess. New York: Free Press. Bradley, R. L., et al. (2000). Melanin-concentrating hormone regulates leptin synthesis and secretion in rat adipocytes. Diabetes. Burguera, B. et al. (2000). Obesity is associated with a decreased leptin transport across the blood-brain barrier in rats. Diabetes. COUZIN, J. (1999). Leptin's uncertain promise. U.S.

News & World Report, 8 November. D'ARRIGO, T. (1999). Looking at leptin. Diabetes Forecast, October.

Fruhbeck, G. et al. (2000). Chronobiology of recombinant leptin therapy. The Journal of the American Medical Association, 22 March. Links between hormones and obesity. (2000). The Journal of Physical Education, Recreation, & Dance, May.

Obesity. Clinical Reference Systems, (1999). July.

SURWIT, R. S., et al. (2000). Transient effects of long-term leptin supplementation in the prevention of diet-induced obesity in mice. Diabetes, July.

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