{"id":{"repo_id":"unsw","oai_identifier":"oai:unsworks.library.unsw.edu.au:1959.4/105603"},"canonical_url":"https://search.dev.ndltd.org/etd/unsw/oai:unsworks.library.unsw.edu.au:1959.4/105603","repository":{"repo_id":"unsw","name":"University of New South Wales","base_url":"https://unsworks.unsw.edu.au/oai/provider"},"display":{"title":"Exploring the spectrum: The heterogeneity of autism and associations with gastrointestinal inflammation","abstract":"Autism is a neurodevelopmental condition that is highly heterogeneous in terms of pathophysiology and clinical presentations. While the aetiology is unknown, higher rates of gastrointestinal (GI) issues in autism may be mediated by the gut-brain axis with dysregulated inflammation affecting the nervous system and GI homeostasis. GI inflammation is understudied and there is limited examination of intersections with the heterogeneity of autism. This thesis bridged this gap by investigating diet, systemic, and GI inflammation, individually and in combination, through a meta-analysis and analysis of linked clinical data and biological samples from the Australian Autism Biobank (AAB). As diet can impact GI dysfunction, the diets of autistic children, siblings, and unrelated controls from the AAB were first examined in Chapter 2. This study, published in Autism Research, revealed nuanced relationships with diet shaped by familial influences, autistic traits, sensory processing and age. Associations between GI inflammation and autism were explored in Chapters 3 and 4. Chapter 3, published in Molecular Autism, is a systematic review and meta-analysis of faecal markers of GI inflammation, which found no group differences in studies of calprotectin and lactoferrin. This synthesis was however limited by methodological concerns and highlighted the need for large community-based studies of GI inflammation including non-autistic siblings and representative controls. This gap is addressed in Chapter 4 through a study of faecal calprotectin independently and in relation to dietary and clinical findings from Chapter 2. Elevated calprotectin was found in a subset of autistic children relative to controls but not siblings. GI inflammation may be independent of core autistic traits as no associations were found between autistic traits, behavioural dysfunction and elevated calprotectin. In Chapter 5, plasma cytokines were used to examine links between GI and systemic inflammation. Cytokines were comparable in siblings and autistic children, but some differences were found relative to controls. No cytokines were associated with the elevated calprotectin identified in Chapter 4. This thesis underscores the complex interplay of autistic traits, diet and inflammation and suggests the presence of heterogeneity in markers of systemic and GI inflammation within the autistic population. This work has implications for research and clinical practice as it highlights the need for a systems approach and deep phenotyping in autism research.","abstract_html":"Autism is a neurodevelopmental condition that is highly heterogeneous in terms of pathophysiology and clinical presentations. While the aetiology is unknown, higher rates of gastrointestinal (GI) issues in autism may be mediated by the gut-brain axis with dysregulated inflammation affecting the nervous system and GI homeostasis. GI inflammation is understudied and there is limited examination of intersections with the heterogeneity of autism. This thesis bridged this gap by investigating diet, systemic, and GI inflammation, individually and in combination, through a meta-analysis and analysis of linked clinical data and biological samples from the Australian Autism Biobank (AAB). As diet can impact GI dysfunction, the diets of autistic children, siblings, and unrelated controls from the AAB were first examined in Chapter 2. This study, published in Autism Research, revealed nuanced relationships with diet shaped by familial influences, autistic traits, sensory processing and age. Associations between GI inflammation and autism were explored in Chapters 3 and 4. Chapter 3, published in Molecular Autism, is a systematic review and meta-analysis of faecal markers of GI inflammation, which found no group differences in studies of calprotectin and lactoferrin. This synthesis was however limited by methodological concerns and highlighted the need for large community-based studies of GI inflammation including non-autistic siblings and representative controls. This gap is addressed in Chapter 4 through a study of faecal calprotectin independently and in relation to dietary and clinical findings from Chapter 2. Elevated calprotectin was found in a subset of autistic children relative to controls but not siblings. GI inflammation may be independent of core autistic traits as no associations were found between autistic traits, behavioural dysfunction and elevated calprotectin. In Chapter 5, plasma cytokines were used to examine links between GI and systemic inflammation. Cytokines were comparable in siblings and autistic children, but some differences were found relative to controls. No cytokines were associated with the elevated calprotectin identified in Chapter 4. This thesis underscores the complex interplay of autistic traits, diet and inflammation and suggests the presence of heterogeneity in markers of systemic and GI inflammation within the autistic population. This work has implications for research and clinical practice as it highlights the need for a systems approach and deep phenotyping in autism research.","abstract_has_math":false,"creators":["Mathew, Nisha"],"institution":"UNSW, Sydney","degree_name":null,"degree_level":null,"degree_discipline":null,"degree_department":null,"school":null,"contributors":[],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2025,"date_issued":"2025","date_published":"2025","updated_at":"2026-07-24T05:32:40Z","subjects":["Autism","Autism spectrum disorder","Gastrointestinal inflammation","Systemic inflammation","Cytokines","Diet","anzsrc-for: 3213 Paediatrics","anzsrc-for: 321302 Infant and child health","anzsrc-for: 321301 Adolescent health"],"languages":["en"],"rights":["open access","CC BY 4.0","free_to_read"],"rights_urls":["https://purl.org/coar/access_right/c_abf2","https://creativecommons.org/licenses/by/4.0/"],"identifier_entries":[{"key":"dc:identifier","label":"Identifier","values":["https://doi.org/10.26190/unsworks/31488"],"render_values":[{"text":"https://doi.org/10.26190/unsworks/31488","href":"https://doi.org/10.26190/unsworks/31488","code":true}]}]},"links":{"outbound_url":"http://hdl.handle.net/1959.4/105603","outbound_label":"Handle","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:creator","label":"Author","values":["Mathew, Nisha"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date","label":"Dc Date","values":["2025"]},{"key":"dc:publisher","label":"Institution","values":["UNSW, Sydney"]},{"key":"dc:type","label":"Dc Type","values":["doctoral thesis","http://purl.org/coar/resource_type/c_db06"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["Autism","Autism spectrum disorder","Gastrointestinal inflammation","Systemic inflammation","Cytokines","Diet","anzsrc-for: 3213 Paediatrics","anzsrc-for: 321302 Infant and child health","anzsrc-for: 321301 Adolescent health"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language","label":"Dc Language","values":["en"]},{"key":"dc:rights","label":"Dc Rights","values":["open access","https://purl.org/coar/access_right/c_abf2","CC BY 4.0","https://creativecommons.org/licenses/by/4.0/","free_to_read"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["http://hdl.handle.net/1959.4/105603","https://unsworks.unsw.edu.au/bitstreams/4b1ec8bd-a223-4c00-8291-64ee31660f12/download","https://doi.org/10.26190/unsworks/31488"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description","label":"Description","values":["Autism is a neurodevelopmental condition that is highly heterogeneous in terms of pathophysiology and clinical presentations. While the aetiology is unknown, higher rates of gastrointestinal (GI) issues in autism may be mediated by the gut-brain axis with dysregulated inflammation affecting the nervous system and GI homeostasis. GI inflammation is understudied and there is limited examination of intersections with the heterogeneity of autism. This thesis bridged this gap by investigating diet, systemic, and GI inflammation, individually and in combination, through a meta-analysis and analysis of linked clinical data and biological samples from the Australian Autism Biobank (AAB). As diet can impact GI dysfunction, the diets of autistic children, siblings, and unrelated controls from the AAB were first examined in Chapter 2. This study, published in Autism Research, revealed nuanced relationships with diet shaped by familial influences, autistic traits, sensory processing and age. Associations between GI inflammation and autism were explored in Chapters 3 and 4. Chapter 3, published in Molecular Autism, is a systematic review and meta-analysis of faecal markers of GI inflammation, which found no group differences in studies of calprotectin and lactoferrin. This synthesis was however limited by methodological concerns and highlighted the need for large community-based studies of GI inflammation including non-autistic siblings and representative controls. This gap is addressed in Chapter 4 through a study of faecal calprotectin independently and in relation to dietary and clinical findings from Chapter 2. Elevated calprotectin was found in a subset of autistic children relative to controls but not siblings. GI inflammation may be independent of core autistic traits as no associations were found between autistic traits, behavioural dysfunction and elevated calprotectin. In Chapter 5, plasma cytokines were used to examine links between GI and systemic inflammation. Cytokines were comparable in siblings and autistic children, but some differences were found relative to controls. No cytokines were associated with the elevated calprotectin identified in Chapter 4. This thesis underscores the complex interplay of autistic traits, diet and inflammation and suggests the presence of heterogeneity in markers of systemic and GI inflammation within the autistic population. This work has implications for research and clinical practice as it highlights the need for a systems approach and deep phenotyping in autism research."]},{"key":"dc:format","label":"Dc Format","values":["application/pdf"]},{"key":"dc:title","label":"Title","values":["Exploring the spectrum: The heterogeneity of autism and associations with gastrointestinal inflammation"]}]}],"canonical_facts":{"dc:creator":["Mathew, Nisha"],"dc:date":["2025"],"dc:description":["Autism is a neurodevelopmental condition that is highly heterogeneous in terms of pathophysiology and clinical presentations. While the aetiology is unknown, higher rates of gastrointestinal (GI) issues in autism may be mediated by the gut-brain axis with dysregulated inflammation affecting the nervous system and GI homeostasis. GI inflammation is understudied and there is limited examination of intersections with the heterogeneity of autism. This thesis bridged this gap by investigating diet, systemic, and GI inflammation, individually and in combination, through a meta-analysis and analysis of linked clinical data and biological samples from the Australian Autism Biobank (AAB). As diet can impact GI dysfunction, the diets of autistic children, siblings, and unrelated controls from the AAB were first examined in Chapter 2. This study, published in Autism Research, revealed nuanced relationships with diet shaped by familial influences, autistic traits, sensory processing and age. Associations between GI inflammation and autism were explored in Chapters 3 and 4. Chapter 3, published in Molecular Autism, is a systematic review and meta-analysis of faecal markers of GI inflammation, which found no group differences in studies of calprotectin and lactoferrin. This synthesis was however limited by methodological concerns and highlighted the need for large community-based studies of GI inflammation including non-autistic siblings and representative controls. This gap is addressed in Chapter 4 through a study of faecal calprotectin independently and in relation to dietary and clinical findings from Chapter 2. Elevated calprotectin was found in a subset of autistic children relative to controls but not siblings. GI inflammation may be independent of core autistic traits as no associations were found between autistic traits, behavioural dysfunction and elevated calprotectin. In Chapter 5, plasma cytokines were used to examine links between GI and systemic inflammation. Cytokines were comparable in siblings and autistic children, but some differences were found relative to controls. No cytokines were associated with the elevated calprotectin identified in Chapter 4. This thesis underscores the complex interplay of autistic traits, diet and inflammation and suggests the presence of heterogeneity in markers of systemic and GI inflammation within the autistic population. This work has implications for research and clinical practice as it highlights the need for a systems approach and deep phenotyping in autism research."],"dc:format":["application/pdf"],"dc:identifier":["http://hdl.handle.net/1959.4/105603","https://unsworks.unsw.edu.au/bitstreams/4b1ec8bd-a223-4c00-8291-64ee31660f12/download","https://doi.org/10.26190/unsworks/31488"],"dc:language":["en"],"dc:publisher":["UNSW, Sydney"],"dc:rights":["open access","https://purl.org/coar/access_right/c_abf2","CC BY 4.0","https://creativecommons.org/licenses/by/4.0/","free_to_read"],"dc:subject":["Autism","Autism spectrum disorder","Gastrointestinal inflammation","Systemic inflammation","Cytokines","Diet","anzsrc-for: 3213 Paediatrics","anzsrc-for: 321302 Infant and child health","anzsrc-for: 321301 Adolescent health"],"dc:title":["Exploring the spectrum: The heterogeneity of autism and associations with gastrointestinal inflammation"],"dc:type":["doctoral thesis","http://purl.org/coar/resource_type/c_db06"]},"updated_at":"2026-07-24T05:32:40Z"}