Premium
Prenatal testosterone of progenitors could be involved in the etiology of both anorexia nervosa and autism spectrum disorders of their offspring
Author(s) -
RomeroMartínez Ángel,
MoyaAlbiol Luis
Publication year - 2014
Publication title -
american journal of human biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.559
H-Index - 81
eISSN - 1520-6300
pISSN - 1042-0533
DOI - 10.1002/ajhb.22597
Subject(s) - offspring , digit ratio , etiology , anorexia nervosa , autism , hum , autism spectrum disorder , psychology , testosterone (patch) , medicine , endocrinology , pregnancy , clinical psychology , physiology , developmental psychology , eating disorders , genetics , biology , art , performance art , art history
Objectives High intrauterine testosterone (T) levels seem to play a role in the development of autism spectrum disorders (ASDs), but their role in anorexia nervosa (AN) is controversial. Parents with masculinized 2D:4D ratios, a marker of the organizational effects of T, may have other relevant biological characteristics, in particular exposing their offspring to high T levels in the prenatal environment. This would increase the likelihood of their offspring developing these disorders. Methods The present study examined whether parents of offspring with AN ( n =34; mean age= 51) and ASD ( n =36; mean age=45) differ from control parents ( n =40; mean age=43) in 2D:4D ratio, as well as by salivary T levels and its relationships. Results Our results revealed that AN and ASD parents (fathers and mothers) have masculinized 2D:4D ratios of the right hand compared to control parents. However, the difference compared to controls was larger in the ASD than the AN group. Furthermore, current salivary T levels were negatively related to the 2D:4D ratio in ASD and AN parents only. Conclusions Our data partially support the view of high prenatal masculinization as a potential intermediate phenotype to the development of these disorders in their offspring. Am. J. Hum. Biol. 26:863–866, 2014. © 2014 Wiley Periodicals, Inc.