No effects of siblings and twin testosterone transfer on autistic traits.
No effects of siblings and twin testosterone transfer on autistic traits.
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DOI：
10.1002/jcv2.12069
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发表时间：
2022-03
期刊：
影响因子：
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通讯作者：
van Bergen, Elsje
中科院分区：
文献类型：
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作者：
de Wit, Melanie M;Begeer, Sander;Nivard, Michel G;van Bergen, Elsje
双胞胎和非双胞胎兄弟姐妹可能会影响产前和产后的自闭症特征。双胞胎睾酮转移假说认为，有双胞胎兄弟的女孩比有双胞胎姐妹的女孩在产前暴露于更高水平的睾酮，增加睾酮暴露使神经发育男性化并增加自闭症特征。出生后，兄弟姐妹可能会提供榜样行为，这可能会减少自闭症特征。我们在7714对双卵双胞胎中研究了双胞胎和非双胞胎兄弟姐妹对母亲和老师报告的自闭症特征的产前和产后影响。我们研究了先证者子女和兄弟姐妹的性别效应。我们拟合了回归模型（分别针对男孩和女孩），其中双胞胎的性别以及每个性别的年长和/或年幼兄弟姐妹作为预测因素。有双胞胎兄弟的女孩的母亲报告的自闭症特征略低于有双胞胎姐妹的女孩（β =-0.08，p = 0.001，科恩d =-0.13）。这种差异在教师报告的自闭症特征中没有重复（β = 0.01，p = 0.734）。男孩的（母亲和老师报告的）自闭症特征与他们的孪生兄弟的性别无关（ps> 0.50）。如果女孩有一个哥哥，教师报告的自闭症特征略高（β = 0.07，p = 0.013，Cohen's d = 0.12）。除了这个小的影响，我们发现非双胞胎兄弟姐妹对女孩或男孩的自闭症特征没有影响（ps>.18）。我们没有发现有双胞胎兄弟的女孩比有双胞胎姐妹的女孩的自闭症特征增加。这一发现有助于否定双胞胎睾酮转移假说的文献。此外，我们几乎没有发现产前和产后兄弟姐妹影响的证据。我们的研究结果与ASD的高遗传性和缺乏共享环境影响一致。利用一个大的双胞胎样本（N = 7700），我们没有发现与双胞胎女孩相比，双胞胎男孩女孩的自闭症特征增加。我们的研究结果否定了双胞胎之间的睾丸激素产前转移和/或产前睾丸激素暴露增加儿童自闭症特征的假设。此外，儿童的自闭症特征似乎不会受到与非双胞胎兄弟姐妹一起长大的影响。
Having twin and non‐twin siblings might influence autistic traits both prenatally and postnatally. The twin testosterone transfer hypothesis suggests that girls with a twin brother are exposed to higher levels of prenatal testosterone than girls with a twin sister, and that increased testosterone exposure masculinizes neural development and increases autistic traits. Postnatally, siblings may provide example behaviour, which could reduce autistic traits. We studied pre‐ and postnatal influences of twin and non‐twin siblings on mother and teacher‐reported autistic traits in 7714 dizygotic twins. We examined the effect of sex of the proband child and of the siblings. We fitted regression models (for boys and girls separately) with sex of co‐twin and having older and/or younger siblings of each sex as predictors. Girls' mother‐reported autistic traits were slightly lower for those with a twin brother than those with a twin sister (β = −.08, p = .001, Cohen's d = −.13). This difference was not replicated in teacher‐reported autistic traits (β = .01, p = .734). Boys' (mother and teacher‐reported) autistic traits were not related to the sex of their co‐twin (ps > 0.50). Teacher‐reported autistic traits were slightly higher if girls had an older brother (β = .07, p = .013, Cohen's d = .12). Other than this small effect, we found no effect of non‐twin siblings on autistic traits in either girls or boys (ps > .18). We did not find increased autistic traits in girls with a twin brother compared to girls with a twin sister. This finding contributes to a body of literature that rejects the twin testosterone transfer hypothesis. In addition, we found little evidence for pre‐ and postnatal sibling influences. Our findings align with high heritability and absence of shared‐environmental influences in ASD. Leveraging a large twin sample (N∼7700), we did not find increased autistic traits in girls with a boy twin compared to girls with a girl twin. Our findings reject the hypothesis that testosterone is transferred prenatally between twins and/or that prenatal testosterone exposure increases children's autistic traits. In addition, children's autistic traits did not seem to be influenced by growing up with non‐twin siblings.