1. Curtin C, Anderson SE, Must A, Bandini L. {{The prevalence of obesity in children with autism: a secondary data analysis using nationally representative data from the National Survey of Children’s Health}}. {BMC Pediatr} (Feb 23);10(1):11.
ABSTRACT: BACKGROUND: The prevalence of childhood obesity has increased dramatically in the last two decades and numerous efforts to understand, intervene on, and prevent this significant threat to children’s health are underway for many segments of the pediatric population. Understanding the prevalence of obesity in populations of children with developmental disorders is an important undertaking, as the factors that give rise to obesity may not be the same as for typically developing children, and because prevention and treatment efforts may need to be tailored to meet their needs and the needs of their families. The goal of the current study was to estimate the prevalence of obesity in children and adolescents with autism. METHODS: This study was a secondary data analysis of cross-sectional nationally representative data collected by telephone interview of parents/guardians on 85,272 children ages 3-17 from the 2003-2004 National Survey of Children’s Health (NSCH). Autism was determined by response to the question, « Has a doctor or health professional ever told you that your child has autism? » Children and adolescents were classified as obese according to CDC guidelines for body mass index (BMI) for age and sex. RESULTS: The prevalence of obesity in children with autism was 30.4% compared to 23.6% of children without autism (p=.075). The unadjusted odds of obesity in children with autism was 1.42 (95% confidence interval (CI): 1.00, 2.02, p=.052) compared to children without autism. CONCLUSIONS: Based on US nationally representative data, children with autism have a prevalence of obesity at least as high as children overall. These findings suggest that additional research is warranted to understand better the factors that influence the development of obesity in this population of children.
2. Ezugha H, Goldenthal M, Valencia I, Anderson CE, Legido A, Marks H. {{5q14.3 Deletion Manifesting as Mitochondrial Disease and Autism: Case Report}}. {J Child Neurol} (Feb 22)
Mitochondrial disorders are usually associated with defects of 1 or more of the 5 complexes (I to V) of the electron transport chain, or respiratory chain. Complex I and IV are the 2 most frequent abnormalities of the electron transport chain in humans. The authors report the case of a 12-year-old boy with dysmorphic facies, mental retardation, autism, epilepsy, and leg weakness. Buccal swab electron transport chain analysis revealed severe decrease in complex IV and mild reduction in complex I activity levels. Chromosomal microarray studies, using array-based comparative genomic hybridization, revealed a 1-Mb deletion in the 5q14.3 region. This case illustrates that this deletion can be associated with complex I and IV deficits, hence manifesting as a mitochondrial disease. It could be hypothesized that genes that either encode or regulate the expression and/or assembly of complex IV or I subunits are located within the deleted region of 5q14.3.
3. Kawaguchi H, Murakami B, Kawai M. {{Behavioral Characteristics of Children with High Functioning Pervasive Developmental Disorders during a Game}}. {J Epidemiol} (Feb 23)
Background: To evaluate children’s sociability through their behavior, we compared the motion features of children with high functioning pervasive developmental disorders (HFPDD) and typical development (TD) during a game. We selected ‘Jenga’ as the game because this is an interactive game played by two people.Methods: We observed the behavior of 7 children with HFPDD and 10 children with TD. An optical motion capture system was used to follow the movement of 3-dimensional position markers attached to caps worn by the players.Results: The range of head motion of the children with HFPDD was narrower than that of the control group, especially in the X-axis direction (perpendicular to the line connecting the two players). In each game, we calculated the range of motion in the X-axis of each child and divided that figure by the matched adult player’s range. The average ratios of children with HFPDD and TD were 0.64 and 0.89 (number of games are 61 and 18), and the difference of these two ratios is significant (P < 0.001).Conclusions: This ratio has sensitivity to identify HFPDD children and could be useful in their child care.
4. Sivaswamy L, Kumar A, Rajan D, Behen M, Muzik O, Chugani D, Chugani H. {{A Diffusion Tensor Imaging Study of the Cerebellar Pathways in Children With Autism Spectrum Disorder}}. {J Child Neurol} (Feb 22)
Children with autistic spectrum disorder are known to have histopathological abnormalities in the cerebellum. Diffusion tensor imaging has been utilized to study abnormalities in connectivity and microintegrity in brains of such children. A region of interest approach was adopted to study cerebellar outflow and inflow pathways in 27 children (24 males; mean age, 5.0 years) with autism, and comparison was made with 16 normally developing controls. An increase in the mean diffusivity of bilateral superior cerebellar peduncles in those with autistic spectrum disorder was noted, as was a reversal of the asymmetry pattern in fractional anisotropy of the middle cerebellar peduncle and the inferior cerebellar peduncle in the autistic spectrum disorder group, compared with controls. This study reiterates the underconnectivity between the cerebellum and neocortex, using diffusion tensor imaging.
5. Yochum CL, Bhattacharya P, Patti L, Mirochnitchenko O, Wagner GC. {{Animal Model of Autism Using GSTM1 Knockout Mice and Early Post-Natal Sodium Valproate Treatment}}. {Behav Brain Res} (Feb 20)
Autism is a heterogeneous, behaviorally-defined developmental disorder with unknown etiology but thought to be the result of environmental insult acting upon the developing brain of a genetically-susceptible individual. Approximately 30% of individuals with autism have normal development up to the age of about 30 months after which they experience behavioral regression and lose previously acquired motor, cognitive and social skills. Early post-natal toxicant administration to mice has been used to model autistic regression. To test the hypothesis that genetically-altered mice might be more sensitive to toxicant exposure early in life, mice with a deletion of glutathione-S-transferaseM1 (GSTM1; a gene associated with increased risk of autism that codes for an enzyme involved in the management of toxicant-induced oxidative stress) and wild-type controls were exposed to valproic acid (VPA; a toxicant known to cause autism-like behavioral deficits that, in part, are mediated through oxidative stress) on post-natal day 14. VPA treatment caused significant increases in apoptosis in granule cells of the hippocampus and cerebellum. There was a genotype by treatment by sex interaction with wild-type females exhibiting significantly fewer apoptotic cells in these regions compared to all other groups. VPA treatment also resulted in long-lasting deficits in social behaviors and significant alterations in brain chemistry. VPA-treated GSTM1 knockout animals performed significantly fewer crawl-under behaviors compared to saline-treated knockout animals as well as wild-type controls receiving either treatment. Collectively, these studies indicate that VPA-treatment causes cerebellar and hippocampal apoptosis and that having the wild-type GSTM1 genotype may confer protection against VPA-induced neuronal death in female mice.
