#HealthyLifeMatters: "Obesity", A Gbobal Epidemic

Obesity is clinically defined as a weight more than 20% above the recommended norm for one’s age, sex, and height. In the United States, about 30% of the population is obese and another 35% is overweight; there has lately been an alarming increase in the number of children who are morbidly obese by the age of 10. You can judge whether you are overweight or obese by calculating your body mass index (BMI).

If W is your weight in kilograms and H is your height in meters, BMI = W/H2 or, if using weight in pounds and height in inches, BMI = 703W/H2. A BMI of 20 to 25kg/m² is considered to be optimal for most people. A BMI over 27kg/m² is considered overweight, and above 30 kg/m2 is considered obese.
Excess weight shortens life expectancy and increases a person’s risk of atherosclerosis, hypertension, diabetes mellitus, joint pain and degeneration, kidney stones, and gallstones; cancer of the breast, uterus, and liver in women; and cancer of the colon, rectum, and prostate in men. Excess thoracic fat impairs breathing and results in increased blood carbon dioxide, sleepiness, and reduced vitality. Obesity is also a significant impediment to some surgeries. Heredity plays as much role in obesity as in height, and even more than in many other disorders generally acknowledged to be hereditary. However, a predisposition to obesity is often greatly worsened by overfeeding in infancy and childhood. Consumption of excess calories in childhood causes adipocytes to increase in size and number. In adulthood, adipocytes do not multiply except in some extreme weight gains; their number remains constant while weight gains and losses result from changes in cell size (cellular hypertrophy).

As so many dieters learn, it is very difficult to substantially reduce one’s adult weight. Most diets are unsuccessful over the long run as dieters lose and regain the same weight over and over. From an evolutionary standpoint, this is not surprising. The body’s appetite- and weight-regulating mechanisms have evolved more to limit weight loss than weight gain, for a scarcity of food was surely a more common problem than a food surplus for our prehistoric ancestors. Were it not for the mechanisms that thwart weight loss, our ancestors might not have made it through the lean eons and we might not be here; but now that we are surrounded with a glut of tempting food, these survival mechanisms have become mechanisms of pathology. Understandably, pharmaceutical companies are keenly interested in developing effective weight-control drugs. There could be an enormous profit, for example, in a drug that inhibits ghrelin signaling or enhances or mimics leptin or melanocortin signaling. Such efforts have so far met with little success, but clearly a prerequisite to drug development is a better understanding of appetite-regulating peptides and their receptors.
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