Eine interessante Studie beleuchtet die Auswirkungen verschiedener Hormone und ihrer Stände auf das Verhalten:
Abnormal sex hormone levels in utero have been associated with child behavioral problems, but it is unclear if normal variation in prenatal sex hormones is associated with subsequent behavior in childhood. We assessed maternal sex hormones, including serum estrone (E1), estradiol (E2), estriol (E3), free testosterone (FT), and total testosterone (TT), during early pregnancy (gestational week 6–21 (mean = 11.1)) and evaluated child behavior at ages 4–5 using the Behavioral Assessment System for Children (BASC-2) and Social Responsiveness Scale (SRS-2) in 404 mother/child pairs (211 girls, 193 boys) within The Infant Development and Environment Study, a multi-site pregnancy cohort study. Associations between hormones and composite scores were evaluated using multiple linear regressions in both sexes combined, and separate models assessed effect modification by sex with the addition of interaction terms. A 10-fold increase in maternal FT or TT was associated in both sexes with a 4.3-point (95 % CI: 0.5, 8.2) or 4.4-point (0.8, 8.0) higher BASC-2 internalizing composite T score, respectively. In addition, a 10-fold increase in FT or TT was associated with a 3.8-point (0.04, 7.5) or 4.0-point (0.5, 7.5) higher behavioral symptoms index composite score. In models evaluating effect modification by sex, a 10-fold increase in E1 was associated with a 4.3-point (1.2, 7.4) decrease in adaptive skills composite score in girls only (interaction p = 0.04). We observed associations between testosterone and internalizing behaviors and behavioral symptoms index in both sexes, as well as a female-specific association between E1 and adaptive skills. Sex hormones during pregnancy may play a key role in influencing later-life behavior, and additional studies should further examine different periods of susceptibility to hormonal signals.
Bereits die Einführung in das Thema bietet einiges an interessanten Studien:
Sex hormones play an important role in regulating the development of sex-differentiated brain structures and sex-specific reproductive behaviors (Cohen-Bendahan et al., 2005; Auyeung et al., 2013; Martel, 2013). Their role in child behavioral problems and psychiatric disorders is suggested by sex differences in the prevalence of these disorders, with some disorders found to be more common in males (e.g., autism spectrum disorder (ASD) and attention deficit hyperactivity disorder (ADHD)) (Werling and Geschwind, 2013; Arnett et al., 2015) and others more common in females (e.g., anxiety disorders) (Eaton et al., 2012; Altemus et al., 2014). Given that sex hormone levels remain low until puberty (Sisk and Zehr, 2005), pre-pubescent behavioral effects of sex hormones are likely programmed during fetal development (Miranda and Sousa, 2018). A key period for this programming is likely in early pregnancy, which is thought to be a critical period for neurological sex differentiation as this is when male fetal testosterone surges, driving subsequent masculinization of brain structures and gender-stereotyped behavior (Hines et al., 2002; McCarthy, 2016).
Prenatal sex hormone associations with child pathologic behavior have primarily been evaluated in the context of androgens (Gore et al., 2014), with several studies observing associations between second trimester amniotic fluid testosterone and a variety of problematic behaviors, including attention problems in boys (Korner et al., 2019) and autistic traits in both sexes (Auyeung et al., 2012). Studies of disorders of sex development such as congenital adrenal hyperplasia (CAH), a disorder that results in abnormally high androgen concentrations in utero and throughout life, have observed higher scores for assessments of later-life autism-like behaviors (Knickmeyer et al., 2006) or increased incidences of anxiety and depression-related disorders and substance abuse in later life in both males and females with CAH (Falhammar et al., 2014; Engberg et al., 2015). Maternal hyperandrogenic endocrinopathies such as polycystic ovarian syndrome (PCOS) have also been associated with neurobehavioral outcomes in children lacking CAH or any other salient endocrine disorders, including higher odds of ASD, ADHD, and their comorbidity in children (Kosidou et al., 2017; Cherskov et al., 2018; Cesta et al., 2019). Another study evaluating behavioral assessments in the context of maternal PCOS and directly measured amniotic testosterone levels found that increased autism-like behaviors and lower empathetic behaviors were associated with higher testosterone in both boys and girls and with maternal PCOS in girls (Palomba et al., 2012). In contrast to these findings related to hyperandrogenism, boys with reproductive disorders associated with lower prenatal testosterone levels, such as hypospadias and cryptorchidism, have also been shown to have higher odds for ASD (Rotem et al., 2018).
Compared with androgens, fewer studies have examined the relationship between prenatal estrogens and child behavior problems. Although estrogen levels have been associated with inhibition and related internalizing features, most of these studies focus on activational effects in adolescence, when sex differences in internalizing disorders tend to emerge (Martel, 2013). In the adult brain, estrogens are considered neuroprotective, in part due to neuronal trophic and antiapoptotic effects (Kajta and Beyer, 2003). Increased ASD risk was observed in association with decreases in maternal serum E3 sampled between gestational weeks 15–20, which coincides with the protective effect of E3 observed for birth outcomes like pre-term birth (Windham et al., 2016). By contrast, a recent pilot study observed the opposite, with greater maternal serum E2 in gestational weeks 15–18 associated with an increased ASD risk in offspring (Bilder et al., 2019). Though an earlier study of second trimester amniotic E2 found no association with autistic traits in toddlers (Auyeung et al., 2012), a more recent maleonly study of second trimester amniotic estrogens found increased risk of ASD associated with E1, E2, E3, and progesterone but not testosterone; however, those models did not adjust for covariates (BaronCohen et al., 2019). Beyond direct estrogen measures, recent studies of fetal single nucleotide polymorphisms (SNPs) in sex hormone receptors have yielded mixed results and some evidence of effect modification by sex (Miodovnik et al., 2012).
Auch diese Studie belegt damit wieder, dass Hormone, gerade solche im Mutterleib, einen ganz erheblichen Einfluss haben.