Royal Prince Alfred Hospital Royal Prince Alfred Hospital
Allergy Unit

Student research

Can urinary peptides explain the pathophysiology of Autistic Spectrum Disorder (ASD)?

Ann Chee (Angie) Low
Master of Nutrition and Dietetics, The University of Sydney
Supervisors: Velencia Soutter, Robert Loblay, Anne Swain, Zia Ahmad
October 2005

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Introduction: Evidence is growing that the ‘opioid excess’ theory may have a role in the origins of autism. This theory suggests that peptides, derived from gluten and casein, produces excessive opioid activity in the brain and can cause autistic behaviour. Research has reported abnormal levels of peptides in the urine of persons with autism.  Diets to exclude these opioids, commonly gluten and casein free diet, has appeared to improve symptoms in some but not all autistic individuals.

Aim: To validate the ‘Opioid Excess’ Theory.

Method:  24 hour urine & 4-day food records specimens were collected from 2 cohorts of 20 children (ASD & non-ASD) aged between 3 and 10 years. Urines were analysed to detect the presence of seven peptides: Gluten exorphin A4, Gluten exorphin A5, Gluten exorphin B5, Beta-casomorphin (bovine), Dermorphin, Deltorphin II and Indolyl-acrylolglycine (IAG) in both groups.

Results: It was not possible to differentiate ASD and non-ASD group based on the urine profiles of the UV chromatogram. There were no peptides specific to autism as the excretion pattern in ASD group was no different from the control group. There were no significant differences found between presence of IAG in urine of the ASD and non-ASD group.

Conclusion: The present study demonstrated that it is not possible to ascertain that the ‘Opioid excess theory’ exist in children with ASD due to the small sample size involved in this study. However, some preliminary findings indicate that it is not possible to identify peptides specific to autism. All individuals excrete peptides in their urines and the excretory pattern is extremely individual. It is not possible to adapt chromatographic methods to be a diagnostic tool for ASD or form a basis for recommending therapeutic intervention with dietary modification. It is also not possible to ascertain whether IAG could be potential biomarker for ASD. Further research is required to identify the effect of dietary intervention. An increase in the number of participants would assist by enhancing these findings through providing a more conclusive outcome.