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Updated: Aug 14, 2026

Assessing Activity-based Anorexia in Mice
Published on: May 14, 2018
Preliminary evidence that gonadal hormones organize and activate disordered eating
Kelly L Klump1, Kyle L Gobrogge, Patrick S Perkins
1Department of Psychology, Michigan State University, East Lansing, MI 48824-1116, USA. klump@msu.edu
Objective:
Eating disorders are more common in females than in males. Gender differences may be due to organizational (i.e. prenatal) and activational (i.e. post-natal) gonadal hormone effects that influence sex differences in behavior. This preliminary set of studies examined these effects by investigating relationships between eating disorder symptoms, prenatal testosterone exposure, and adult levels of estrogen in women.
Method:
We examined organizational associations by investigating relationships between disordered eating and finger-length ratios, which are known to be somatic markers of prenatal testosterone exposure. Participants included 113 adult female twins drawn from the community. Disordered eating was assessed with the total score from the Minnesota Eating Behavior Survey (MEBS). Finger lengths were hand scored using a ruler and photocopies of both hands. We also investigated activational influences by examining associations between circulating levels of estradiol and disordered eating symptoms. Two independent samples of adult females (n's = 24 and 25) drawn from the community were used for this study. Disordered eating was again assessed with the MEBS total score, while saliva samples were used for assessing estradiol.
Results:
Positive associations were found between disordered eating and both finger-length ratios and circulating estradiol levels.
Conclusions:
Findings suggest that lower levels of prenatal testosterone exposure and higher adult levels of estradiol are associated with increased eating disorder symptoms. We hypothesize that the relatively low level of testosterone before birth in females permits their brains to respond to estrogens at puberty, when the hormones activate the genes contributing to disordered eating in vulnerable girls.
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