BACKGROUND: Autism spectrum disorder (ASD) is a neurodevelopmental condition associated with sleep disturbances that may result from abnormalities in melatonin production. The correlations of melatonin levels with the severity of sleep disorder and/or severity of ASD were reported. OBJECTIVES: To evaluate urinary levels of the melatonin metabolite, 6-sulphatoxymelatonin (aMT6s), in children with ASD, and their associations with sleep abnormalities and behavioural impairments. METHODS: Study involved 77 children with ASD and 84 controls aged 2.5-15.5 years. Sleep disorders were assessed by Children's Sleep Habits Questionnaire. Morning and afternoon levels of aMT6s were determined by radioimmunoassay method. Urinary creatinine levels were assessed by an enzymatic method. RESULTS: The urinary aMT6s/creatinine values indicate that the night-time melatonin levels are signifi cantly lower in ASD than in controls, but there are no signifi cant differences in the daytime levels. In the ASD group, on average, a 6.8-fold difference between night-time and daytime values of urinary aMT6s/creatinine was found, whereas for the controls a 12.5-fold difference was observed, indicating a lower night-time increase in melatonin levels. In ASD group, the difference in night-time-daytime aMT6s/creatinine value correlated with some types of sleep problems, but not with the severity of ASD. CONCLUSION: The results indicate that in ASD there are differences in the patterns of melatonin secretion that may be associated with sleep impairment (Tab. 4, Fig. 2, Ref. 28).
sis of autism and fetal testosterone levels were positively correlated with autistic traits in general population. [1][2][3][4] In addition, females with conditions of abnormal prenatal exposure to testosterone and its sex steroid precursors, such as congenital adrenal hyperplasia and polycystic ovary syndrome, were found to have higher rate of autistic traits as well as their children were of higher risk of developing autism. 5,6 However, the exact mechanism by which these hormones influence the manifestation of autistic traits remains undiscovered. Another model explaining higher prevalence of ASD in males is a female protective model which suggests that multiple genetic factors contribute to the development of ASD and that higher threshold of genetic liability is required in females compared to males. 7 Zhang et al. 8 demonstrated genetic evidence of sex differences in ASD confirming female protective model, employing investigation of de novo mutations, common variants of ASD candidate genes and their co-expression in male and female brains. Genetic architecture of ASD involves rare and de novo variants that were identified in studies using whole genome or exome sequencing technologies as well as low-risk com-
The second to fourth digit ratio (2D:4D) is according to previous studies a likely biomarker for prenatal testosterone exposure and its effect on the human brain. It was found to be linked to autism spectrum disorders (ASD). Recently, 2D:4D raised a lot of questions with regard to its stability and autism‐related behaviors. Here, we present a cross‐sectional study of 2D:4D in boys (N = 91, mean age 7.63) and adults (N = 36 mean age 22.8) with ASD as well as neurotypical students, 506 participants in total. Digit ratio was assessed by taking measurements from digital scans, compared between groups and correlated with the autism quotient. Significant differences were found in the digit ratio of children and adults. Both girls and boys had 2D:4D ratio lower than women and men, both on the right (p = 0.000 in females, p = 0.000 in males) and left hand (p = 0.018 in females, p = 0.011 in males). No significant differences were found in digit ratios between neurotypical subjects and those with ASD nor was there a relationship with the reported autistic traits, which leads us to question the reliability of 2D:4D and its relation to ASD.
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