Objectives This study aimed to investigate the associations of parental SA recorded within 3 years before childbirth and parental SA recorded during pregnancy with the odds of autism in offspring. Methods We conducted a nationwide nested case-control study using Taiwan’s 2006–2015 national birth cohort linked to multigenerational health records from 2003 to 2017. The study included 14,961 children with autism and 59,844 controls individually matched by birth year and sex. Conditional logistic regression with inverse probability of treatment weighting (IPTW) was used to estimate adjusted odds ratios (aORs) and 95% confidence intervals (CIs). Results Paternal SA recorded within 3 years before childbirth was associated with higher odds of offspring autism in the IPTW model (aOR of 2.208, 95% CI = 1.542–3.163). SA recorded during pregnancy was also associated with higher odds of offspring autism, with an aOR of 2.055 (95% CI = 1.021–4.136) for maternal SA and 1.653 (95% CI = 1.311–2.084) for paternal SA. Conclusion Paternal SA recorded within 3 years before childbirth and parental SA recorded during pregnancy were associated with higher odds of autism in offspring. Further studies are needed to clarify the underlying mechanisms.
Virtual reality (VR) exercise is a promising modality for supporting physical activity and mental health in autistic young adults. However, simulator sickness (nausea, dizziness, and disorientation arising from VR-induced sensory conflict) is a practical barrier whose predictors in autistic populations are poorly understood. Resting heart rate variability (HRV) indexes autonomic flexibility that may support adaptation to sensory conflict. This proof-of-principle study examined whether baseline HRV predicted simulator sickness across a 4-week VR boxing intervention. Six exercise completers (M age = 23.0 years; 5 male, 1 female) provided baseline HRV recordings (Polar H10; primary index ln-RMSSD) and completed the Simulator Sickness Questionnaire (SSQ) after Sessions 1, 4, and 8. Lower baseline ln-RMSSD was associated with higher SSQ scores at Session 4 (r = −.84, p = .036; ρ = −.78, p = .072) and with symptom persistence (post hoc mean of Sessions 4 and 8; r = −.91, p = .011; ρ = −1.00, p = .003). At Session 1, the association was evident in rank order only (ρ = −.88, p = .033; r = −.65, p = .159). Excluding one participant with extreme first-session symptoms weakened the Session 1 rank-order association but not that for persistence (ρ = −1.00, p = .017). Higher-HRV participants reported only sweating and fatigue, whereas lower-HRV participants reported persisting or emerging sickness symptoms; group-level habituation was not evident. These preliminary findings suggest resting HRV may index the persistence of VR sickness in autistic adults, warranting replication in larger, pre-registered studies.
Autism spectrum disorder (ASD) is a complex neurodevelopmental disorder arising from the interplay between genetic susceptibility and environmental factors. Much focus has been given to the known environmental contaminants, but the effects of emerging contaminants including micro- and nanoplastics (MNPs) on the pathogenesis of ASD have not been adequately explored. Given their widespread environmental distribution, ability to cross biological barriers, persistence in tissues, and potential neurodevelopmental toxicity, MNPs have emerged as a major public health concern. This review aims to comprehensively examine the potential mechanistic links between MNP exposure and ASD. The available evidence suggests that MNPs trigger generation of ROS, mitochondrial dysfunction, chronic neuroinflammation and disruption of several important neurodevelopmental signaling pathways, such as PI3K/Akt/mTOR, Wnt/β-catenin and AGE–RAGE signaling. In addition, disruption of gut-brain axis may contribute to MNP neurodevelopmental abnormalities through gut microbiota dysbiosis, intestinal barrier dysfunction and aberrant immune activation. MNPs may also serve as carriers for persistent organic pollutants (POPs), endocrine disrupting chemicals (EDCs) and heavy metals, which may act synergistically to enhance the neurotoxic effects of these contaminants through a ‘Trojan horse’ mechanism. These molecular and cellular activities may be interdependent and lead to defects in synaptic plasticity, neurotransmission and neuronal development, potentially contributing to ASD-like behaviour. This review provides an integrated mechanistic perspective and identifies research priorities for environmental risk assessment and the development of preventive strategies.
Background Although individuals with autism experience elevated rates of victimization, evidence concerning their experiences at specific stages of legal processes remains fragmented. This scoping review mapped the available evidence on victimization, legal-process experiences, barriers, supports, and research gaps. Method Web of Science, Google Scholar, and the Anadolu University Library discovery service (inc. Scopus and PubMed) searches were conducted between February and 5 March 2026 for peer-reviewed sources published from 1 January 2016–5 March 2026. Eligible quantitative, qualitative, and mixed-methods primary studies and reviews were charted. The results were summarized using descriptive numerical analysis and inductive basic qualitative content analysis. Sixteen sources were included: 12 primary research reports and four reviews. Results The findings clustered into five categories: victimization patterns, prevalence, and risk factors; communication and procedural barriers in police, forensic interview, and court processes; difficulties in recognizing, disclosing, and reporting abuse; need for expert support, staff training, and interdisciplinary collaboration; and structural gaps in the legal system and accessible justice. Across studies, victimization was associated not only with elevated exposure to violence, but also with communication mismatches, limited accommodations, diagnostic overshadowing, credibility bias, and low professional preparedness. Three defendant- or custody-focused sources were retained as contextual evidence concerning systemic preparedness and structural accessibility; they were not interpreted as direct evidence of victim experiences. Conclusions The evidence indicates recurring communication, professional-knowledge, and accessibility barriers, but the literature is heterogeneous and relies heavily on adult, professional, caregiver, mixed-role, and contextual evidence. Victim-focused research evaluating accommodations and support practices, particularly for children and adolescents, remains limited.
Purpose This retrospective study assessed the potential developmental and demographic risk factors influencing the occurrence of Traumatic dental injuries (TDI) in children with autism spectrum disorder (ASD). Method This study conducted a retrospective chart review of children aged 3–15 years with ASD who received care over an eight-year period at a major pediatric dental hospital in Atlantic Canada. Relevant demographic and clinical information were extracted, and statistical analyses were used to examine the relationship between risks of TDI and demographic and clinical factors. Results A total of 441 patients with ASD were included. No statistically significant associations were found between TDI and variables including sex, ASD severity, global developmental delay, gross motor delay, or seizure history. However, a trend toward increased rate of TDI was observed among children with concurrent attention-deficit-hyperactivity disorder (ADHD). Conclusion These findings suggest that commonly considered clinical and demographic factors may not independently predict TDI risk in children with ASD. Further research is needed to investigate the association between comorbid ADHD and the risk of TDI in children with ASD.
