Family ties point to recessive 'obesity gene.'

Family ties point to recessive 'obesity gene'

An estimated 5 percent of the U.S. population may have inherited a tendency toward obesity, according to a new study examining family weight patterns. The research suggests obesity follows a classic model of recessive inheritance, with some individuals receiving a copy of a so-called obesity gene from each parent. People born with this genetic double whammy who fulfill their fat potential are among the heaviest in the nation and run a high risk of cardiovascular disease, the reserchers say.

Other studies have indicated that obesity has a genetic component (SN: 1/25/86, p.56), but the new work points to the existence of one major obesity gene that can cause excessive weight under the right conditions. Trudy L. Burns of the University of Iowa City described the research this week at the American Heart Association's scientific sessions in New Orleans.

Burns and her collegues studied 277 high school students and 1,303 of their siblings, parents, aunts, uncles and first cousins. The scientists calculated each person's body mass index as a measure of obesity, then used statistical methods to see whether genes appeared to control obesity in the families studied.

The found that family weight patterns fit a model in which one highly influential gene codes for either obesity or slimness, while other genes play lesser roles. In that model, the gene coding for obesity is recessive, manifesting itself when inherited from both parents. While people who inherit two copies of the obesity gene are not condemned to a life of flab, they stand a greater chance of gaining excessive weight than do people who inherit two slimness genes or one slimness gene plus one obesity gene, Burns says. The model predicts that 34 percent of the U.S. population carries both gene types and 61 percent carries two slimness genes.

People with the genetic odds stacked against them can minimize their weight gain by altering environment risk factors such as diet or a sedentary lifestyle, Burns says. Conversely, people genetically predisposed to slimness can become obese if they eat too much or maintain a low activity level. Burns says further studies are needed to clarify the interaction between environmental and genetic factors in the development of obesity.

Compared with their slimmer peers, obese individuals face a host of cardiovascular risk factors, including significantly higher blood pressure and lower levels of high density lipoprotein, the transport molecule that carries cholesterol from the blood to the liver for excretion.

The Iowa researchers have not identified any specific obesity gene, but one candidate is the gene coding for lipoprotein lipase, an enzyme that helps the body store fat. At the same meeting, Todd G. Kirchgessner at the University of California, Los Angeles, presented new findings about the structure and evoluation of the lipoprotein lipase gene. Variation in this gene may cause obesity in some people, he speculates. Kirchgessner and scientists at the Johns Hopkins University in Baltimore plan to study the inheritance of this gene in families with a tendency toward obesity.

In the future, scientists may use genetic information to identify children at high risk of obesity. early identification and intervention may help such people avoid obesity and reduce their risk of developing heart desease, Burns says.