Prenatal Testosterone and Risk for Disordered Eating During Puberty

描述（由申请人提供）：饮食失调是严重的心理健康问题，对女孩的影响尤为严重。这些疾病导致的大量精神和医学发病率证明了它们的公共卫生重要性和了解其病因的必要性。研究表明，产前睾丸激素可能会使饮食失调（DE）的风险男性化（即降低），并解释患病率的性别差异，但这些影响如何或何时出现仍不清楚。在动物青春期期间和之后，产前睾酮升高会降低对卵巢激素的敏感性。重要的是，卵巢激素与青春期后几种类型的DE有关，因此，睾酮影响DE的一种潜在机制可能是降低青春期对卵巢激素的敏感性。异性双胞胎为检验这一假设提供了一种新的人类设计，因为异性女性双胞胎在子宫内与男性双胞胎一起发育，并且被认为在出生前暴露于更高水平的睾丸激素。该双胞胎设计将用于：1)检查产前睾酮对DE的男性化效应是否在青春期出现；2)确认这些发现不是由于青春期变化的其他因素（如肥胖、情绪、自主困难）或与兄弟一起抚养的混杂影响。参与者（10-15岁）将包括同性男性（N= 270）和女性（N= 350）双胞胎的档案样本和新的样本：1)异性双胞胎（N= 120）；2)与兄弟一起饲养的非双胞胎雌性（N = 60）。为青少年设计的自我报告问卷将用于评估DE、青春期状态、自主困难和情绪。将用生物电阻抗和体重指数来评估肥胖。层次线性模型将用于检查双胞胎类型（异性或同性）和青春期状态（青春期前、青春期早期、青春期中后期）在DE方面的差异。预计异性和同性双胞胎在青春期前的DE水平不会有显著差异，无论双胞胎性别如何。然而，在青春期早期和之后，DE水平与双胞胎类型之间的线性关系预计会出现，同性男性双胞胎预计会显示出最男性化（即最低）的DE水平，其次是异性男性双胞胎，异性女性双胞胎和同性女性双胞胎。此外，这些影响不能用异性双胞胎和同性双胞胎在肥胖、情绪或自主困难方面的差异来解释。最后，异性女性的DE男性化不会因为与兄弟一起长大，因为这些双胞胎的DE水平会低于与兄弟一起长大的非双胞胎女性。公共卫生相关性：研究结果可能需要新的生物学范式来理解DE的出现和饮食失调风险的性别差异。

DESCRIPTION (provided by applicant): Eating disorders are significant mental health problems that disproportionally affect girls. The substantial psychiatric and medical morbidity resulting from these disorders attest to their public health significance and the need to understand their etiology. Research suggests that prenatal testosterone may masculinize (i.e., lower) risk for disordered eating (DE) and account for sex differences in prevalence, yet how or when these effects emerge remains unknown. Elevated prenatal testosterone decreases sensitivity to ovarian hormones during and after puberty in animals. Importantly, ovarian hormones are associated with several types of DE after puberty, thus, one potential mechanism for testosterone's effects on DE may be to decrease sensitivity to ovarian hormones during puberty. Opposite-sex twin pairs provide a novel human design for examining this hypothesis, as opposite-sex female twins develop in utero with a male co-twin and are believed to be exposed to higher levels of testosterone prenatally. This twin design will be used to: 1) examine whether the masculinizing effects of prenatal testosterone on DE emerge during puberty; 2) confirm that these findings are not due to the confounding effects of other factors that change during puberty (e.g., adiposity, mood, autonomy difficulties) or to being reared with a brother. Participants (ages 10-15) will include an archival sample of same-sex male (N= 270) and female (N = 350) twins and new samples of: 1) opposite-sex twins (N = 120); and 2) non-twin females reared with brothers (N = 60). Self-report questionnaires designed for young adolescents will be used to assess DE, pubertal status, autonomy difficulties, and mood. Adiposity will be assessed with bioelectrical impedance and body mass index. Hierarchal Linear Models will be used to examine differences in DE by twin type (opposite-or same-sex) and puberty status (pre-pubertal, early puberty, mid-to-late puberty). It is expected that opposite-sex and same-sex twins will not differ significantly on levels of DE during pre-puberty, regardless of twin sex. However, linear relationships between levels of DE and twin type are expected to emerge during and after early puberty, when same-sex male twins are expected to show the most masculinized (i.e., lowest) levels of DE, followed by opposite-sex male twins, opposite-sex female twins, and same-sex female twins. Moreover, these effects will not be accounted for by differences in adiposity, mood, or autonomy difficulties between opposite-sex and same-sex twins. Finally, masculinization of DE in opposite-sex females will not be due to being raised with a brother, as these twins will have lower levels of DE than non-twin females reared with brother. PUBLIC HEALTH RELEVANCE: Findings could necessitate new biological paradigms for understanding the emergence of DE and sex differences in eating disorder risk.