Children with Autism Spectrum Disorder (ASD) are at an increased risk for sleep disturbances, and studies indicate that between 50 and 80% of children with ASD experience sleep problems. These problems increase parental stress and adversely affect family quality of life. Studies have also suggested that sleep disturbances may increase behavioral problems in this clinical population. Although understanding the causes of sleep disorders in ASD is a clinical priority, the causal relationship between these two conditions remains unclear. Given the complex nature of ASD, the etiology of sleep problems in this clinical population is probably multi-factorial. In this overview, we discuss in detail three possible etiological explanations of sleep problems in ASD that can all contribute to the high rate of these symptoms in ASD. Specifically, we examine how neurobiological alterations, genetic mutations, and disrupted sleep architecture can cause sleep problems in individuals with ASD. We also discuss how sleep problems may be a direct result of core symptoms of ASD. Finally, a detailed examination of the relationship between sleep problems and associated clinical features and psychiatric comorbidities in individuals with ASD is described.

Background: Recent studies have examined the association between autism spectrum disorder and schizophrenia spectrum disorders, describing a number of cognitive features common to both conditions (e.g., weak central coherence, difficulties in set-shifting, impairment in theory of mind). Several studies have reported high levels of autistic symptoms in population with schizophrenia spectrum disorders. Our study systematically reviews and quantitatively synthetizes the current evidence on the presence of autistic symptoms in individuals with schizophrenia spectrum disorders. Methods: A comprehensive literature search of the PubMed/MEDLINE, Cochrane Library, CINHAL, and Embase databases was performed from the date of their inceptions until March 2018. The primary outcome measure was the Autism Spectrum Quotient (AQ). As secondary outcome measures, we analyzed the AQ subscales. Data were extracted and analyzed by using a conservative model and expressed by standardized mean difference (SMD). Results: Thirteen studies comprising a total of 1,958 individuals were included in the analysis. Results showed that individuals with schizophrenia spectrum disorders have higher levels of autistic symptoms compared to healthy controls [SMD: 1.39, 95% confidence interval (CI): 1.11 to 1.68] and lower levels of autistic symptoms compared to individuals with autism (SMD: −1.27, 95% CI: −1.77 to −0.76). Conclusions: Current findings support that individuals with schizophrenia spectrum disorders have higher autistic symptoms than healthy controls. Therefore, further studies are needed in order to shed light on the association between these two conditions.

: Vitamin D is a neurosteroid hormone crucially involved in neurodevelopment. Neural cell proliferation, neurotransmission, oxydative stress and immune function, represent the main mechanisms mediated by vitamin D in the Central Nervous System. Therefore, its deficiency during pregnancy and early childhood may significantly impact on a developing brain, leading to possible adverse neuropsychological outcomes including Autism Spectrum Disorder (ASD). Significant vitamin D deficiency is described within children affected by ASD and in pregnant mothers whose offspring will later develop ASD, suggesting a possible role of the hormone as a contributing risk factor in the etiopathogenesis of ASD. We reviewed the actual literature on the potential contributing role of prenatal and early postnatal vitamin D deficiency in ASD etiopathogenesis, at both genetic and environmental level, and the possible effect of vitamin D supplementation in autistic children. Conflicting but promising results emerged on the topic. Further Randomized Controlled Trials studies carried out during pregnancy and early infancy are necessary for better understanding the possible contribution of vitamin D deficiency in the etiopathogenesis of autism and the potential efficacy of the hormone supplementation on the improvement of ASD core symptoms.

Children with autism spectrum disorder (ASD) and their families have represented a fragile population on which the extreme circumstances of the COVID-19 outbreak may have doubly impaired. Interruption of therapeutical interventions delivered in-person and routine disruption constituted some of the main challenges they had to face. This study investigated the impact of the COVID-19 lockdown on adaptive functioning, behavioral problems, and repetitive behaviors of children with ASD. In a sample of 85 Italian ASD children (mean age 7 years old; 68 males, 17 females), through a comparison with a baseline evaluation performed during the months preceding COVID-19, we evaluated whether after the compulsory home confinement any improvement or worsening was reported by parents of ASD individuals using standardized instruments (Adaptive Behavior Assessment System (Second Edition), Achenbach Child Behavior Checklist, Repetitive Behavior Scale-Revised). No significant worsening in the adaptive functioning, problematic, and repetitive behaviors emerged after the compulsory home confinement. Within the schooler children, clinical stability was found in reference to both adaptive skills and behavioral aspects, whereas within preschoolers, a significant improvement in adaptive skills emerged and was related to the subsistence of web-delivered intervention, parental work continuance, and online support during the lockdown.

Autism diagnosis is moving from the identification of common inherited genetic variants to a systems biology approach. The aims of the study were to explore metabolic perturbations in autism, to investigate whether the severity of autism core symptoms may be associated with specific metabolic signatures; and to examine whether the urine metabolome discriminates severe from mild-to-moderate restricted, repetitive, and stereotyped behaviors. We enrolled 57 children aged 2–11 years; thirty-one with idiopathic autism and twenty-six neurotypical (NT), matched for age and ethnicity. The urine metabolome was investigated by gas chromatography-mass spectrometry (GC-MS). The urinary metabolome of autistic children was largely distinguishable from that of NT children; food selectivity induced further significant metabolic differences. Severe autism spectrum disorder core deficits were marked by high levels of metabolites resulting from diet, gut dysbiosis, oxidative stress, tryptophan metabolism, mitochondrial dysfunction. The hierarchical clustering algorithm generated two metabolic clusters in autistic children: 85–90% of children with mild-to-moderate abnormal behaviors fell in cluster II. Our results open up new perspectives for the more general understanding of the correlation between the clinical phenotype of autistic children and their urine metabolome. Adipic acid, palmitic acid, and 3-(3-hydroxyphenyl)-3-hydroxypropanoic acid can be proposed as candidate biomarkers of autism severity.