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"Persons who are naturally fat are apt to die earlier than those who are slender." Hippocrates (circa 460 bce) was not a man of few words. His many comments have stood the test of time. This quotation is hoary with age, having been written 2500 years ago, and should remind us that fatness is not a new medical concern. What is new is the realization that obesity is a worldwide phenomenon and the consequence of genetic susceptibility, too readily available high-energy foods, and greatly decreased physical activity: a morbid triad [57].

Obesity, unlike AIDS, not only is not on our list of leading causes of death; it is not even in the vicinity of the list. Obesity requires our attention and concern because of its deadly contribution to heart disease, at the top of the charts; to cancer, our second leading cause; to diabetes, the seventh; to hypertension, the fifteenth; to sleep-breathing disorders; and osteoarthritis of large and small joints, and we know, as did Hippocrates, that obesity is inversely related to longevity [57].

Obesity can no longer be regarded as a cosmetic problem, but must be seen as a new pandemic that threatens worldwide well-being. What is obesity? For an answer, dictionaries are to no avail as they speak only of excess weight. Obesity goes beyond excess weight, which raises a second question: How fat is too fat? For Peter Paul Rubens (1577-1640), the great Flemish painter, there was no "too fat." Rubens was the master of rotund femininity. As shown in Figure 1.10 , the fatter, the healthier, the more beautiful. But that was then. Today, obesity is our number 1 malnutrition problem, and a major contributor to numerous deaths. It has replaced under nutrition and infectious disease as the most significant contribution to poor health [58].

For adults, overweight is defined in terms of body mass index (BMI) and calculated as weight in kilograms [2.2 lb (pounds)], divided by the square of

height in meters, is 25 (55 lb over the ideal weight), and obesity entails a BMI of 30, while extreme obesity is BMI 40 or higher. (To calculate your BMI, multiply your weight in pounds by 700, then divide by your height in inches, and repeat that a second time.) Using these numbers, the prevalence of obesity among adults in the United States is understood to be approximately 30.5% of the total population. For children 2-5 years old, it is approximately 10%, and for those 12-19, it is approximately 22% [59]. Paradoxically, these numbers have markedly increased over the past 30 years, during a time of unimaginable preoccupation with diet(s) and weight control. We Americans spent $46 billion on weight loss products and services in 2004. Unfortunately it is now seen that dieting is either ineffective or counterproductive. Those overweight or obese children must not be given short shrift—not taken lightly. The consequences can be enormous. As noted earlier, type 2 diabetes, closely linked to excess weight, is being diagnosed in such high numbers that it can no longer be referred to as "adult-onset diabetes." But that is not the worst of it. In the recent eye-opening report on obesity, Dr. David Ludwig, Director of the Obesity Program at Children 's Hospital, Boston, revealed a threat thus far unmentioned. He warned that the current obesity epidemic has had little public impact, "but when these youngsters start developing heart attacks, stroke, kidney failure, amputations, blindness and ultimately death at younger and younger ages, that will have a huge effect on life expectancy." This is not something we want to look forward to. Obesity appears to be the result of multiple causes: genetic, environmental, and psychosocial factors acting syn-ergistically with energy intake and expenditure. Obesity is consistently found in single-gene disorders such as Prader-Willi syndrome (PWS), with its upper body obesity (due to uncontrolled appetite), short stature, mental retardation, hypotonia, and hypogonadism. As for an environmental component, "predictions about possible interactions between genes and the environment are difficult because there may be a delay in an individual's exposure to an 'obesogenic' environment, and/or alteration in life style related to living circumstances and uncertainty about the precise timing of the onset of weight gain" [58]. Not so uncertain is the energy intake/expenditure component. Pima Indians of the American Southwest, with a common genetic heritage to Pimas in Mexico, are an average 50 lb or more heavier than those in Mexico. A similar trend is seen with Nigerians living in the United States, who are obese compared to Nigerians in Africa; the former are also twice as likely to exhibit hypertension [58]. Migrants coming into a new culture pick up the habits of the majority culture and soon reflect their medical problems.

As noted earlier, obesity is a significant public health problem given its substantial contribution to morbidity and mortality, but the health risk could be significantly reduced even with modest weight loss. The peptide hormone leptin, which appears to hold the key to weight loss or gain, is produced by adipose tissue, and a decrease in body fat decreases the amount leptin, which triggers food intake; the reverse is also true. More leptin, less food intake. Clearly, leptin and the brain are in this together. When the system works properly, there is maintenance of weight within a narrow range [60]. This raises yet another question. Why are some of us obese and others not? Although not yet fully crystalized, it appears that obese individuals are leptin-resistant. How to modulate this is a high-priority research activity. Furthermore, clarification of the mechanisms and pathways that control food intake and energy home-ostasis are of central and crucial importance, and its neurological and hormonal complexity do not suggest a short timeline. However, the enormous cost to human health attributable to obesity is the engine that will drive basic research, leading ultimately to successful medical treatment, and that includes genetic repair, if need be.

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