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*Percent overweight was determined by comparing each man's actual weight with a standard recommended weight for his height.

Source: After A. J. Standard, T.T. Foch, and Z. Hrubec, A twin study of human obesity, Journal of the American Medical Association 256(1986):52.

The degree of environmental similarity between monozy-gotic twins and dizygotic twins is assumed to be the same. This assumption may not always be correct, particularly for human behaviors. Because they look alike, identical twins may be treated more similarly by parents, teachers, and peers than are nonidentical twins. Evidence of this similar treatment is seen in the past tendency of parents to dress identical twins alike. In spite of this potential complication, twin studies have played a pivotal role in the study of human genetics.

Twin Studies and Obesity

To illustrate the use of twins in genetic research, let's consider a genetic study of obesity. Obesity is a serious public-health problem. About 50% of adults in affluent societies are overweight and from 15% to 25% are obese. Obesity increases the risk of a number of medical conditions, including diabetes, gallbladder disease, high blood pressure, some cancers, and heart disease. Obesity is clearly familial: when both parents are obese, 80% of their children will also become obese; when both parents are not overweight, only 15% of their children will eventually become obese. The familial nature of obesity could result from genes that influence body weight; alternatively, it could be entirely environmental, resulting from the fact that family members usually have similar diets and exercise habits.

A number of genetic studies have examined twins in an effort to untangle the genetic and environmental contributions to obesity. The largest twin study of obesity was conducted on more than 4000 pairs of twins taken from the National Academy of Sciences National Research Council twin registry. This registry is a database of almost 16,000 male twin pairs, born between 1917 and 1927, who served in the U.S. armed forces during World War II or the Korean War. Albert Stunkard and his colleagues obtained weight and height for each of the twins from medical records compiled at the time of their induction into the armed forces. Equivalent data were again collected in 1967, when the men were 40 to 50 years old. The researchers then computed how overweight each man was at induction and at middle age in 1967. Concordance values for monozygotic and dizygotic twins were then computed for several weight categories (Table 6.3).

In each weight category, monozygotic twins had significantly higher concordance than did dizygotic twins at induction and in middle age 25 years later. The researchers concluded that, among the group being studied, body weight appeared to be strongly influenced by genetic factors. Using statistics that are beyond the scope of this discussion, the researchers further concluded that genetics accounted for 77% of variation in body weight at induction and 84% at middle age in 1967. (Because a characteristic such as body weight changes in a lifetime, the effects of genes on the characteristic may vary with age.)

*Percent overweight was determined by comparing each man's actual weight with a standard recommended weight for his height.

Source: After A. J. Standard, T.T. Foch, and Z. Hrubec, A twin study of human obesity, Journal of the American Medical Association 256(1986):52.

This study shows that genes influence variation in body weight, yet genes alone do not cause obesity. In less affluent societies, obesity is rare, and no one can become overweight unless caloric intake exceeds energy expenditure. One does not inherit obesity; rather, one inherits a predisposition toward a particular body weight; geneticists say that some people are genetically more at risk for obesity than others.

How genes affect the risk of obesity is not yet completely understood. In 1994, scientists at Rockefeller University isolated a gene that causes an inherited form of obesity in mice ( FIGURE 6.13). This gene encodes a protein called leptin, named after the Greek word for "thin." Leptin is produced by fat tissue and decreases appetite by affecting

I 6.13 Obesity in some mice is due to a defect in the gene that encodes the protein leptin. Obese mouse on the left compared with normal-sized mouse on the right. (Remi Banali/Liason.)

the hypothalamus, a part of the brain. A decrease in body fat leads to decreased leptin, which stimulates appetite; an increase in body fat leads to increased levels of leptin, which reduces appetite. Obese mice possess two mutated copies of the leptin gene and produce no functional leptin; giving leptin to these mice promotes weight loss.

The discovery of the leptin gene raised hopes that obesity in humans might be influenced by defects in the same gene and that the administration of leptin might be an effective treatment for obesity. Unfortunately, most overweight people are not deficient in leptin. Most, in fact, have elevated levels of leptin and appear to be somewhat resistant to its effects. Only a few rare cases of human obesity have been linked to genetic defects in leptin. The results of further studies have revealed that the genetic and hormonal control of body weight is quite complex; several other genes have been identified that also cause obesity in mice, and the molecular underpinnings of weight control are still being elucidated.


Higher concordance in monozygotic twins compared with that in dizygotic twins indicates that genetic factors play a role in determining individual differences of a characteristic. Low concordance in monozygotic twins indicates that environmental factors play a significant role in the characteristic.

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