A combination of genetic and environmental risk factors can trigger eating disorders in humans, finds a study conducted in mice, which can lead to prevention and treatment strategies for the fatal disorder.
‘People with anorexia nervosa view themselves as being overweight, even when they are underweight.’
The findings showed that apart from genetic risks, social stress like isolation and dieting as a result of peer pressure, which is specifically, the desire to be thin could trigger anorexia in adolescents.
"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 lead researcher Lori Zeltser, associate professor at Columbia University Medical Centre (CUMC) in US.
Adolescent mice with the gene variant -- associated with anorexia and anxiety in mice and humans -- when exposed to both social isolation stress and caloric restriction, were much more likely to avoid eating.
Changes in feeding behaviour did not occur when the environmental variables were imposed during adulthood. Further, when adolescent mice were subjected to either social stress or caloric restriction, but not both, the animals exhibited little change in feeding behaviour.
"Our findings show that having the at-risk genotype alone is not sufficient to cause anorexia-like behaviour, but it confers susceptibility to social stress and dieting, especially during adolescence," Zeltser explained in the paper published online in the journal Translational Psychiatry
People with anorexia view themselves as being overweight, even when they are underweight. Also, they are relentlessly obsessed about eating, food and weight control. For the study, the team exposed adolescent mice with at least one copy of a variant of the BDNF gene -- associated with anorexia and anxiety in mice and humans -- to social stress and caloric restriction.
The mice were then placed on a calorie-restricted diet, which usually precedes the development of anorexia in adolescent humans. The results revealed that it acted as an onset for eating disorders.