title: Prenatal hormone exposure and risk for eating disorders: a comparison of opposite-sex and same-sex twins.
abstract: BACKGROUND
  Although the sex difference in eating disorder prevalence has typically been attributed to psychosocial factors, biological factors may also play a role. Prenatal testosterone exposure is a promising candidate, since it masculinizes behavior in animals and humans via its permanent effects on the central nervous system.
  
  
  OBJECTIVE
  To examine whether in utero testosterone exposure has masculinizing effects on disordered eating (DE) by comparing opposite-sex (OS) and same-sex (SS) twins. Twin type (SS vs OS) is considered a proxy measure of prenatal hormone exposure, since females from OS pairs are exposed to more testosterone in utero than females from SS pairs. A linear trend in mean levels of DE was predicted based on expected prenatal testosterone exposure, with SS female twins exhibiting the highest levels of DE followed by OS female twins, OS male twins, and SS male twins.
  
  
  METHODS
  A twin study comparison of OS vs SS twins.
  
  
  METHODS
  Michigan State University Twin Registry.
  
  
  METHODS
  Participants included 304 SS female twins, 59 OS female twins, 54 OS male twins, and 165 SS male twins.
  
  
  METHODS
  Overall levels of DE were assessed with the Minnesota Eating Behavior Survey.
  
  
  RESULTS
  Confirming hypotheses, DE exhibited significant linear trends, with SS female twins exhibiting the highest levels of DE followed by OS female twins, OS male twins, and SS male twins. This linear trend could not be accounted for by levels of anxiety or socialization effects. Indeed, OS female twins exhibited lower levels of DE compared with an independent sample of undergraduate women (n = 69) who were raised with 1 or more brothers.
  
  
  CONCLUSIONS
  The masculinization of DE in OS female twins is unlikely to be due to socialization effects alone. Biological factors, such as the masculinization of the central nervous system by prenatal testosterone exposure, may also contribute to sex differences in DE prevalence.
authors.affiliation: Department of Psychology, Michigan State University, East Lansing, MI 48824-1116, USA.
authors.forename: Kristen M
authors.initials: KM
authors.lastname: Culbert
authors.forename: S Marc
authors.initials: SM
authors.lastname: Breedlove
authors.forename: S Alexandra
authors.initials: SA
authors.lastname: Burt
authors.forename: Kelly L
authors.initials: KL
authors.lastname: Klump
mesh_terms: D000293:Adolescent; D000328:Adult; D001068:Feeding and Eating Disorders / Q000453:epidemiology* / Q000235:genetics; D005260:Female; D006801:Humans; D008297:Male; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D012307:Risk Factors; D012919:Social Behavior; D013739:Testosterone / Q000502:physiology*; D014429:Twins, Dizygotic; D014430:Twins, Monozygotic
chemical_list: D013739:Testosterone