April 6,2001 The Associated Press
- Researchers have found that one form of a gene involved in controlling appetite is more frequent among anorexics, a discovery that suggests disruptions of the brain's system for governing food intake contribute to eating disorders.
This is the first time an anorexia-related gene has been identified, though researchers have known for several years that a person's chances of developing an eating disorder depend partly on genetics.
The study by researchers from Germany and the Netherlands found that 11 percent of anorexics had a variant form of the gene for agouti-related protein, a chemical messenger that stimulates appetite. In contrast, only 4.5 percent of subjects without anorexia had the variant form.
The study compared 145 anorexia patients and 244 people without the disorder, and concluded that having the mutation more than doubles a person's chance of developing anorexia.
The finding suggests that a drug mimicking agouti-related protein might help some anorexics regain their appetites.
The study was published in the May issue of Molecular Psychiatry.
It is certainly not the only gene involved in the disease. Researchers believe that many genes work together with environmental factors to cause eating disorders.
"It may contribute to explaining why a small proportion of people get eating disorders," said Walter Kaye, a psychiatrist at the University of Pittsburgh. "But it's not going to explain everybody."
Anorexia affects about 1 percent of teen-age girls in the United States, and sometimes occurs in boys as well. It causes an obsession with dieting and thinness so powerful that it sometimes proves fatal.
The effect of the genetic variation is not yet known, but it is thought to cause a slight change in the shape of the appetite-stimulating agouti-related protein. Such a change could reduce the protein's effectiveness and consequently the brain's ability to stimulate eating during times of hunger, the researchers said.
Copyright 2001 The Associated Press. All rights reserved.