@article{Nor2019,
title = {Prevalence of overweight and obesity among children and adolescents with autism spectrum disorder and associated risk factors},
author = {N K Nor and A H Ghozali and J Ismail},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-85064414280&doi=10.3389%2ffped.2019.00038&partnerID=40&md5=4bb61b1df043a4adf79618e223d77f26},
doi = {10.3389/fped.2019.00038},
issn = {22962360},
year = {2019},
date = {2019-01-01},
journal = {Frontiers in Pediatrics},
volume = {7},
number = {FEB},
publisher = {Frontiers Media S.A.},
abstract = {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. © 2019 Kamal Nor, Ghozali and Ismail.},
note = {cited By 5},
keywords = {Adolescent, Adult, Article, Autism, Body Mass, Brief Autism Mealtime Beahavior Questionnaire, Child Development, Childhood Obesity, Children, Children Sleep Habits Questionnaire, Controlled Study, Cross-Sectional Study, Feeding Difficulty, Female, Food Refusal, Human, Major Clinical Study, Malaysian, Male, Mother, Paternal Age, Physical Activity, Physical Activity for Older Children Questionnaire, Prevalence, Questionnaires, Risk Factor, Sleep Disorder, Underweight},
pubstate = {published},
tppubtype = {article}
}

@article{Cheah2012451,
title = {Neurodevelopmental and neuropsychiatric behaviour defects arise from 14-3-3ζ deficiency},
author = {P -S Cheah and H S Ramshaw and P Q Thomas and K Toyo-Oka and X Xu and S Martin and P Coyle and M A Guthridge and F Stomski and M Van Den Buuse and A Wynshaw-Boris and A F Lopez and Q P Schwarz},
url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-84859007028&doi=10.1038%2fmp.2011.158&partnerID=40&md5=7f507fef31a192a10b3cde7bf69b5442},
doi = {10.1038/mp.2011.158},
issn = {13594184},
year = {2012},
date = {2012-01-01},
journal = {Molecular Psychiatry},
volume = {17},
number = {4},
pages = {451-466},
abstract = {Complex neuropsychiatric disorders are believed to arise from multiple synergistic deficiencies within connected biological networks controlling neuronal migration, axonal pathfinding and synapse formation. Here, we show that deletion of 14-3-3ζ causes neurodevelopmental anomalies similar to those seen in neuropsychiatric disorders such as schizophrenia, autism spectrum disorder and bipolar disorder. 14-3-3ζ-Deficient mice displayed striking behavioural and cognitive deficiencies including a reduced capacity to learn and remember, hyperactivity and disrupted sensorimotor gating. These deficits are accompanied by subtle developmental abnormalities of the hippocampus that are underpinned by aberrant neuronal migration. Significantly, 14-3-3ζ- deficient mice exhibited abnormal mossy fibre navigation and glutamatergic synapse formation. The molecular basis of these defects involves the schizophrenia risk factor, DISC1, which interacts isoform specifically with 14-3-3ζ. Our data provide the first evidence of a direct role for 14-3-3ζ deficiency in the aetiology of neurodevelopmental disorders and identifies 14-3-3ζ as a central risk factor in the schizophrenia protein interaction network. © 2012 Macmillan Publishers Limited All rights reserved.},
note = {cited By 58},
keywords = {14-3-3 Proteins, Animal Experiment, Animal Model, Animal Tissue, Animals, Article, Autism, Behaviour Disorder, Bipolar Disorder, Brain, Cell Movement, Cells, Cognitive Defect, Controlled Study, Cultured, Disease Models, Disrupted in Schizophrenia 1 Protein, Embryo, Female, Gene, Gene Deletion, Genetic Predisposition to Disease, Glutamic Acid, Hippocampal Mossy Fiber, Hippocampus, Human, Hyperactivity, Inbred C57BL, Isoprotein, Knockout, Learning, Male, Maze Learning, Memory, Mice, Motor Activity, Mouse, Neurogenesis, Neuronal Migration Disorder, Neurons, Neuropsychiatry, Nonhuman, Priority Journal, Protein 14-3-3, Protein 14-3-3 Zeta, Protein Deficiency, Protein Interaction, Recognition, Risk Factor, Schizophrenia, Sensory Gating, Synapse, Unclassified Drug},
pubstate = {published},
tppubtype = {article}
}