Currently, there is a pressing demand to find therapeutic targets for anorexia. This disorder “has the highest mortality rate of any psychiatric disease” and is, therefore, in need of further research. Lack of knowledge and treatment for this disorder can be greatly attributed to the absence of anorexic behavior in animals. It is difficult to study possible treatments on animals that do not mimic the behavior of their human counterparts. Although scientists have found genetic, biological, psychological, and sociocultural aspects that increase vulnerability to anorexia, there has been no evidence of a single, driving factor of the disorder. It is common for anorexic patients to be suffering from multiple psychiatric illnesses at a time, so it is impossible to analyze which elements directly contribute to the disorder.
Recently, a study in the scientific journal Nature examined how the combination and timing of Anorexic risk factors in mice contributes to the susceptibility and severity of the disorder. The study combined factors that are usually associated with higher vulnerability to anorexia: the mice used in the study were adolescent females who were genetically predisposed to anxiety (imposed by the BDNF-Val66Met gene variant), social stress, and caloric restriction. This study tested the hypothesis that the Val66Met allele, a gene known to contribute to the onset of Anorexia, could cause mice to become more sensitive to environmental factors such as stress, ultimately causing the disorder.
The researchers found that the Val66Met allele stimulates anorexic behavior only when environmental factors are imposed during adolescence. “Val66Met genotype promotes anorexic behavior in mice exposed to social isolation stress and CR (caloric restriction) during adolescence, but not when these environmental variables are imposed in adulthood.”
These findings suggest that treatments and therapies for anorexia are probably more realistic than we may have thought. Because this study revealed that role of juvenile stress is critical in provoking anorexia, future therapies should aim to lessen adolescent’s exposure to stress. What makes this discovery even more important is that physicians have the ability to lessen stress in the human brain. “Pharmacological treatments can reverse the impacts of adolescent social stress on the neuroanatomical organization of circuits in the prefrontal cortex.”
While these results move the understanding of anorexia and possible treatments for the disorder forward, further research needs to be done in order to explore the possibility of targeting neurotransmitter activity to treat anorexia. A possible next step is to identify what circuits are responsible for anorexic behavior.
Rose Beatty ‘17
Madra, M., and L. M. Zeltser. “BDNF-Val66Met Variant and Adolescent Stress Interact to Promote Susceptibility to Anorexic Behavior in Mice.” Nature (2016): n. pag. Print.