Introduction: Prevalence of obesity in Autism Spectrum Disorder (ASD) has been reported to be higher than in the general population. Determining prevalence may help increase awareness of obesity in ASD and potentially lead to initiatives to reduce obesity. In order to understand obesity in ASD children, common risk factors were assessed including physical activity, feeding problems and sleep disturbances. Methods: This is a cross-sectional study performed at the Child Development Center at Universiti Kebangsaan Malaysia Medical Center on 151 ASD children aged 2–18 years. Anthropometric and demographic information were obtained and parents completed three questionnaires; Children Sleep Habits Questionnaire (CSHQ), Physical Activity for Older Children Questionnaire (PAQ-C) and Brief Autism Mealtime Behavior Questionnaire (BAMBI). Results: For ASD children in our sample, the prevalence of overweight (BMI ≥85th to <95th percentiles) was 11.3% and the prevalence of obesity (BMI ≥95th percentile) was 21.9%. The overweight/obese ASD children's median age was higher at 8.5 years (IQR 5.81–10.13) compared to the normal/underweight group of 6.33 years (IQR 4.75–7.7) with a p -value of 0.001. The two groups also differed significantly for maternal BMI and paternal age. The median maternal BMI in the overweight/obese group was 26.05 (IQR 23.35–32.25), statistically significantly higher ( p = 0.003) than in the non-overweight/obese group, 24.7 (IQR 21–27.9). The median paternal age of 40 years (IQR 37–44) was statistically significantly higher ( p = 0.039) in the overweight/obese group, compared to the median paternal age in the non-overweight/obese group of 38 (IQR 35–42). The male overweight/obese children had median PAQ-C score of 2.44 (IQR 2.00–3.00) vs. 2.89 (IQR 2.35–3.53) in the counterpart group with a p -value of 0.01. Using the multiple linear regression stepwise method, three predictors associated with BMI percentiles reached a statistical level of significance; PAQ-C score in males ( p < 0.001), the BAMBI domains of Food Refusal ( p = 0.001) and Limited Variety of Food ( p = 0.001). Conclusions: The prevalence of obesity and overweight is high among Malaysian ASD children and adolescents. Older child age, high maternal BMI, older paternal age, low physical activity, low likelihood of food refusal and high likelihood of food selectivity were found to be risk factors for high BMI in these children.
Autism spectrum disorder (ASD) is a neurodevelopmental condition of the central nervous system (CNS) that presents with severe communication problems, impairment of social interactions, and stereotypic behaviours. Emerging studies indicate possible associations between viral infections and neurodegenerative and neurobehavioural conditions including autism. Viral infection during critical periods of early in utero neurodevelopment may lead to increased risk of autism in the offspring. This review is aimed at highlighting the association between viral infections, including viruses similar to COVID-19, and the aetiology of autism. A literature search was conducted using Pubmed, Ovid/Medline, and Google Scholar database. Relevant search terms included “rubella and autism”, “cytomegalovirus and autism”, “influenza virus and autism”, “Zika virus and autism”, “COVID-19 and autism”. Based on the search terms, a total of 141 articles were obtained and studies on infants or children with congenital or perinatal viral infection and autistic behaviour were evaluated. The possible mechanisms by which viral infections could lead to autism include direct teratogenic effects and indirect effects of inflammation or maternal immune activation on the developing brain. Brain imaging studies have shown that the ensuing immune response from these viral infections could lead to disruption of the development of brain regions and structures. Hence, long-term follow up is necessary for infants whose mothers report an inflammatory event due to viral infection at any time during pregnancy to monitor for signs of autism. Research into the role of viral infection in the development of ASD may be one avenue of improving ASD outcomes in the future. Early screening and diagnosis to detect, and maybe even prevent ASD are essential to reduce the burden of this condition.
Objective: This study was conducted to determine the gross and fine motor profiles of children with autism spectrum disorder compared to typically developing children. Additionally, we also assessed if the motor delay was more pronounced with increasing age.Method: This was a retrospective study involving children aged 12–60 months of age comparing motor development in children with autism spectrum disorder with typically developing children. Their developmental profile was assessed using Schedule of Growing Skills II. Descriptive statistics was used to analyse the developmental profile between the groups.Results: ASD children had significant gross motor (6.7%) and fine motor delay (38.5%) compared to typically developing children, who did not show any delay. The motor delay in ASD children was more prominent in older children.Conclusion: It is important to assess motor development in ASD children as there is significant motor delay in these children compared to typically developing children, and the delay becomes more prominent with age. Early detection of motor delay could allow provision of early intervention services to optimize developmental outcomes.
Autism spectrum disorder (ASD) is a heterogeneous, behaviorally defined, neurodevelopmental disorder that has been modeled as a brain-based disease. The behavioral and cognitive features of ASD are associated with pervasive atypicalities in the central nervous system (CNS). To date, the exact mechanisms underlying the pathophysiology of ASD still remain unknown and there is currently no cure or effective treatment for this disorder. Many publications implicated the association of ASD with inflammation, immune dysregulation, neurotransmission dysfunction, mitochondrial impairment and cell signaling dysregulation. This review attempts to highlight evidence of the major pathophysiology of ASD including abnormalities in the brain structure and function, neuroglial activation and neuroinflammation, glutamatergic neurotransmission, mitochondrial dysfunction and mechanistic target of rapamycin (mTOR) signaling pathway dysregulation. Molecular and cellular factors that contributed to the pathogenesis of ASD and how they may affect the development and function of CNS are compiled in this review. However, findings of published studies have been complicated by the fact that autism is a very heterogeneous disorder; hence, we addressed the limitations that led to discrepancies in the reported findings. This review emphasizes the need for future studies to control study variables such as sample size, gender, age range and intelligence quotient (IQ), all of which that could affect the study measurements. Neuroinflammation or immune dysregulation, microglial activation, genetically linked neurotransmission, mitochondrial dysfunctions and mTOR signaling pathway could be the primary targets for treating and preventing ASD. Further research is required to better understand the molecular causes and how they may contribute to the pathophysiology of ASD.
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