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Appetite-Regulating Hormones and Eating Behaviors in Children with Autism Spectrum Disorder

  • Author / Creator
    Dhaliwal, Khushmol K.
  • Autism Spectrum Disorder (ASD) is a complex neurodevelopmental disorder that involves deficits in social, behavioral, and communicative domains. As an increasing number of children are diagnosed with ASD, within Canada and globally, there has also been increased findings of higher rates of overweight and obesity among this population. Excessive weight gain is of concern due to the social, physical, and psychological impacts of obesity and its secondary associated disorders. Particularly for individuals with ASD and families, this can lead to an added burden placed onto this already vulnerable population. In order to improve the effectiveness of treatments and curb the development of overweight and obesity in ASD, a more comprehensive understanding of some of the underlying mechanisms such as possible hormonal factors and feeding behaviors is needed. Therefore, the overall objective of this research was to (1) assess the risk factors for unhealthy weight gain and obesity that have been implicated in ASD, (2) examine hormones involved in regulation of appetite and energy balance (leptin, ghrelin, GLP-1, PYY, insulin) and how they may differ based on weight status among children with ASD, and (3) to explore differences in mealtime feeding behaviors among groups of varying weight status with ASD.
    In chapter 2, risk factors for unhealthy weight gain and obesity were explored among children with ASD. We discussed the role of selective feeding behaviors, which are often related to sensory challenges and specific behavioral phenotypes, such as restricted and repetitive behaviors. We also discussed the research on physical activity opportunities and sedentary behaviors among this population. Parents also often report more barriers to physical exercise due to the social nature of many activities. Furthermore, we discussed the role of genetics and specific genes that have been implicated in both ASD and obesity development. In addition, many children with ASD often present with secondary comorbidities (e.g., depression), and medications to manage these symptoms can further impact weight status. We also discussed emerging factors, which we defined as factors independently associated with increased risk for both obesity and ASD, that have not yet been studied as risk factors for unhealthy weight gain and obesity among children with ASD. The latter included the gut microbiota, endocrine influences, and maternal metabolic disorders.
    Chapter 3 summarizes the findings of a cross-sectional study comprised of 21 children with ASD between the ages of 5 to 12 years old. Of the recruited children, 15 were of normal weight (NW) status and 6 children were of overweight or obese (OWOB) weight status. Information through anthropometric measurements, blood samples, and questionnaires was collected. The major findings of this study included that under fasting conditions, the group with OWOB weight status was found to have higher leptin concentrations (p=0.018). We also found there were higher reported feeding challenges among the OWOB group (p=0.045).
    The major findings of this thesis are that a combination of behavioral, lifestyle, and physiological components contribute to overweight and obesity among children with ASD. This research highlights that behavioral and hormonal factors may also contribute to accelerated weight gain among children with ASD, and there is a need for further research to clarify the interplay among these factors in order to better define potential targets for prevention and intervention strategies.

  • Subjects / Keywords
  • Graduation date
    Fall 2020
  • Type of Item
    Thesis
  • Degree
    Master of Science
  • DOI
    https://doi.org/10.7939/r3-fgx8-ef42
  • License
    Permission is hereby granted to the University of Alberta Libraries to reproduce single copies of this thesis and to lend or sell such copies for private, scholarly or scientific research purposes only. Where the thesis is converted to, or otherwise made available in digital form, the University of Alberta will advise potential users of the thesis of these terms. The author reserves all other publication and other rights in association with the copyright in the thesis and, except as herein before provided, neither the thesis nor any substantial portion thereof may be printed or otherwise reproduced in any material form whatsoever without the author's prior written permission.