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Obesity Nutrition - Additional risks

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Obesity refers to the presence of excess total body fat (i.e., increased adipose tissue, or increased adiposity). Obesity is assessed by many different methods, and its exact definition varies widely. The so-called gold standard for the measurement of adiposity (degree of fatness) is underwater weighing, in which a subject is placed in a tank of water with only the head above the water line. The amount of space displaced by the subject*apos;s body (i.e., the rise in the water level) indicates the body*apos;s volume; that number is then compared to the subject*apos;s total weight (obtained on a balance scale), which determines the percentage of fat in the body. In 2002, the most accurate method for measuring total body fat, as well as body composition, was dual-energy X-ray absorptiometry, or DEXA. This instrument used in DEXA scans the entire body and, based on differences in the density of different tissues, calculates the bone mass, the lean tissue mass, and the fat mass. Percent body Figure 1 Prevalence of overweight and obese adults adults by sex and age, 1997. SOURCE: Centers for Disease Control/National Center for Health Statistics, National Health Interview Survey, 1997 fat is the amount of fat tissue relative to the total body weight.

As people age, body composition changes very gradually, with both total body weight and amount of body fat increasing into the fifties and sixties (see Figure 1). In later years, body weight usually stabilizes or declines slightly, while body composition changes to produce a greater percentage of body fat.

The most commonly used method for assessing degree of obesity is the Body Mass Index (BMI). The BMI is calculated from the height and weight. It was developed using metric numbers and is based on the following equation:

BMI = weight (in kilograms) divided by height (in meters squared)

In order to calculate the body mass index using pounds and inches, use the following formula to get BMI:

  • Step 1: Multiply weight in pounds by 705
  • Step 2: Divide the answer by height (in inches)
  • Step 3: Take that answer, and divide in again by height (in inches)

Table 1 shows a break down of body mass index by weight and height.

BMI is not a perfect measurement of the degree of fatness. For example, body builders can increase their weight without increasing their fat level. Similarly, elderly persons can have reduced muscle mass, which means that, for a given weight or BMI, they show a higher percentage of fat. Nevertheless, for the vast majority of persons, the BMI is a good indicator of obesity.

The National Institutes of Health (National Heart, Lung, and Blood Institute) has developed "Clinical Guidelines on the Identification, Evaluation, and Treatment of Overweight and Obesity in Adults." These guidelines define two major levels of excess body weight: overweight, which is a body mass index number of 25 to 29.9; and obese, which is a body mass index number of 30 or greater. Further, the institute's guidelines are in accordance with the standards created by the World Health Organization, which allow for several degrees of obesity ranging from moderate to severe, all within the obese category. These degrees are shown in Table 2. With each increase in body mass index, there is an increase in the risk of comorbidities (obesity related diseases). As noted above, BMI tends to increase from early adulthood to late middle age, and this increase is primarily due to an increase in fat accumulation (Wolf and Colditz). In addition to this natural Table 1 Body Mass Index—BMI (kg/m2) SOURCE: Author change in body weight with aging, increased body weight in general is associated with higher rates of mortality (see Figure 2).

There is controversy about the contribution of body fat to mortality in the elderly. Some studies indicate that link between increased body fat and the increased risk of death is limited to people in the age range of twenty to sixty. Around age sixty, those studies say, the contribution of body fat to an increased risk of death decreases until it is negligible. Nevertheless, obesity has been identified as the second leading cause of preventable death in the United States (McGinnis and Foege).

Causes of obesity. For most individuals, the underlying cause of obesity is unknown. Strong evidence suggests that the degree of obesity is, in part, hereditary, the result of genes transmitted from the mother and the father. Estimates as to how large a role heredity and genes plays in obesity range from 30 to 70 percent. The remaining factors that contribute to obesity are thought to be environmental and behavioral factors, such as the ready availability of high calorie foods and the reduced levels of physical activity required on the job and in day-to-day activities.

Only a few people can trace their obesity to a precise gene defect. For example, in 1994 a gene was identified in rats and in mice which, when mutated or defective, caused them to become very obese (Zhang et al.). This gene, dubbed the ob (obese) gene, governs the production of a protein called leptin. Leptin is made by the adipose tissue and is released into the circulation system, where it is transported to other tissues containing the receptor for this protein, which is called the leptin receptor. Defects in either the leptin or the leptin receptor can result in obesity, but this form of obesity is very rare. Defects in a number of specific other genes can result in obesity in rodents, and scientists have identified the human counterparts to those genes. Nevertheless, all of the known gene mutations added together account for fewer than 100 cases of obesity in humans. In addition, there are a number of very rare genetic syndromes that are characterized by obesity, including, for example, Prader-Willie Syndrome and Pickwickian Syndrome. Even when those syndromes are factored in, less than one percent of obese persons have a known genetic cause of their obesity.

Some scientists believe that most of the genetic contribution to obesity is conveyed by the interactions of many different genes on many different chromosomes, each contributing in some small way to obesity. Genes interact with each other and with the environment, thus further Figure 2 BMI and Age-Related Mortality SOURCE: Adapted from Waaler, H. T. Acta Med Scand. 679 (supplement) (1984): 1–56. complicating the medical community's ability to identify the exact causes of obesity, and as noted, the degree of obesity often naturally increases with age from the thirties to the sixties, further complicating the assessment of causes of obesity.

In addition to increasing the risk of death, obesity carries with it many other physiological changes that contribute to reduced health or increased morbidity (illness) (Bray and James). Obese persons have a higher likelihood of developing type 2 diabetes and cardiovascular disease. They also have a greater incidence of gallstones, joint disorders, certain cancers, and sleep apnea. In addition, obese persons frequently suffer from discrimination due to their body weight. Recent studies of the very obese in which significant weight loss was achieved and sustained using various gastrointestinal (stomach and intestinal) surgical procedures showed a great reduction in the illnesses listed above after obesity was reduced (Sjostrom et al.). Also, in nonhuman primates, the long term restraint of calories, adjusted to maintain a health body weight and to prevent the development of obesity, has been shown to prevent (or greatly delay) the development of the adult onset of Type 2 diabetes, which is the type most often associated with obesity (Hansen and Bodkin). In 2001, evidence suggested that the life long restraint of caloric intake sufficient enough to prevent the development of obesity also would postpone the average age of death and possibly extend overall life span (Hansen). The mechanisms underlying this improved morbidity and mortality through obesity prevention and calorie restraint are not yet known.

BARBARA C. HANSEN

BIBLIOGRAPHY

BRAY, G.; BOUCHARD, C.; and JAMES, W. P. T. Handbook of Obesity. New York: M. Dekker, 1998.

HANSEN, B.C. "Prevention of Obesity." In The Management of Eating Disorders and Obesity. Edited by D. J. Goldstein. Totowa, N.J.: Humana Press, 1999. Pages 347–357.

HANSEN, B. C., and BODKIN, N. L. "Primary Prevention of Diabetes Mellitus By Prevention of Obesity in Monkeys." Diabetes 42 (1993): 1809–1814.

Table 2

MCGINNIS, J. M., and FOEGE, W. H. "Actual Causes of Death in the United States." Journal of the American Medical Association 270, no. 18 (1993): 2207–2212.

National Institute of Health–NHLBI. "Clinical Guidelines on the Identification, Evaluation, and Treatment of Overweight and Obesity in Adults." In Eds. Washington, D.C., Government Printing Office, 1998.

SJOSTROM, C. D.; LISSNER, L.; and SJOSTROM. L. "Long-term Effects of Weight Loss on Hypertension and Diabetes: The S.O.S. Intervention Study." International Journal of Obesity 22 supp. 3 (1998): S78.

WOLF, M., and COLDITZ, G. A. "Social and Economic Effects of Body Weight in the United States." American Journal of Clinical Nutrition 63 (1996): 466S–469S.

World Health Organization. "Obesity: Preventing and Managing the Global Epidemic." In Eds. Geneva: World Health Organization, 1998. Page. 276.

ZHANG, Y.; PROECA, R.; MAFFEI, M.; BARONE, M,; LEOPOLD, L.; and FRIEDMAN, J. M. "Positional Cloning of the Mouse Obese Gene and its Human Homologue." Nature 372 (1994): 425–432.

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