New York: A combination of genetic and environmental risk factors may trigger the compulsive restriction of food intake seen in patients with anorexia, a new study in mice has found.
The findings may help to identify new prevention and treatment strategies for the eating disorder in humans, researchers from Columbia University in the US said.
Scientists have long suspected that a combination of genetic, biological, psychological, and sociocultural variables raise the risk of anorexia.
In the new study, researchers described a new mouse model featuring a combination of genetic and environmental risk factors that can trigger the compulsive restriction of food intake seen in patients with anorexia nervosa.
"We think that for the first time, we have a mouse model of anorexia that closely resembles the conditions leading up to the disease in humans," said Lori Zeltser from Columbia University.
"And this model not only shows us the most important factors that contribute to the onset of anorexia, it is also helping us to identify signalling pathways in the brain that ultimately drive this potentially fatal eating disorder," Zeltser said.
Anorexia has a mortality rate of 8 to 15 per cent, the highest of any psychiatric disease. There is no cure for it. For the new mouse model, researchers exposed adolescent mice with at least one copy of a variant of the BDNF gene, which has been associated with anorexia and anxiety in mice and humans, to social stress and caloric restriction.
"One driver of anorexia in humans is peer pressure, specifically, the desire to be thin. People assumed that you could not replicate that in a mouse," said Zeltser.
"We decided to take peer pressure out of the equation and focus on social stress, which can be accomplished by housing mice alone, instead of in groups," she said.
The mice were then placed on a calorie-restricted diet, which usually precedes the development of anorexia in adolescent humans and may act as a trigger for eating disorders.
The impact of dieting was simulated by reducing the mice's caloric intake by 20 to 30 per cent - roughly equivalent to the caloric reduction of a typical human dieter.
Researchers found that adolescent mice with the gene variant, when exposed to both social isolation stress and caloric restriction, were much more likely than controls to avoid eating.
Changes in feeding behaviour did not occur when the environmental variables were imposed during adulthood. When researchers subjected adolescent mice with the gene mutation to either social stress or caloric restriction, but not both, the animals exhibited little change in feeding behaviour.
The study was published in the journal Translational Psychiatry.
