Royal Prince Alfred Hospital Royal Prince Alfred Hospital
Allergy Unit

Student research


Is there evidence to support the hypothesis that there is a “leaky gut”
in Autistic Spectrum Disorder (ASD)?

by
Rebecca Elias
Master of Science (Nutrition and Dietetics), University of Wollongong
Supervisors: Velencia Soutter, Anne Swain, Robert Loblay
November 2004

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Abstract

Introduction: ASD encompasses a number of developmental disorders and for children with ASD normal development is hampered by a triad of marker characteristics including impaired social interaction, communication and imaginative skills. The role of diet in ASD has been in question since abnormalities in urinary peptide excretion were first investigated in the early 1980's. These peptides, derived from the insufficient breakdown of dietary proteins gluten and casein, are hypothesised to enter the blood through a “leaky gut” and cross the blood brain barrier to act on opioid receptors causing neurological abnormalities seen in ASD. Consequently dietary intervention in the form of a gluten and casein free diet is used in the management of ASD with clinical improvements reported. However, absence of these dietary proteins cannot be conclusively said to be the cause of these improvements, as removing these foods from the diet is also likely to result in an altered intake of other food chemicals.

Aim: To determine whether children with ASD have a “leaky gut”.

Method: Questionnaires, 4 day food records and 24 hour urine specimens were collected from sub populations of children with and without ASD, aged between 3 and 10 years. The 4 day food record was kept over the time the urine was collected, in order to validate dietary intake with excretion, of particular interest being the opioid peptides. Questionnaires were also used to examine issues such as behaviour and food related symptoms potentially related to food intolerance.

Results: Data was analysed from 44 participants. No significant correlations were established between gluten intake and gluten excretion and also casein intake and casein excretion for the ASD and non-ASD groups. From an intolerance point of view, no correlations could be made with behaviour and intakes of gluten, casein, salicylates and amines for ASD subjects. However a relationship was observed for the non-ASD group, where increasing intakes of total casein, amines and salicylates were associated with increasing incidence of bowel problems.

Conclusion: It is not possible to ascertain whether an opioid peptide effect or “leaky gut” exists in this population, as in general, everyone excretes peptides and the excretory pattern is extremely individual. A relationship between gluten and casein in the diet and the excretion of peptides could not be found. It is essential that other potential gut mechanisms be investigated to determine whether they are related to peptide excretion. Food intolerance issues also need to be explored further to truly establish whether ASD children are sensitive to food chemicals and whether clinical improvements reported can be attributed to reducing the load of these chemicals.