Abstract | Summary | Original Article

Gluten- and Casein-free Diets in Autistic Spectrum Disorders

Beth A. McConnell, Ph.D.

Dietary restrictions for treatment of ASDs have received heightened exposure in the internet age. The gluten-free, casein-free diet has been reported to reduce the behavioural symptoms of autism, but this is a hotly debated topic among experts. Currently, there is limited support for the use of specialized diets in ASD.

Gluten and casein are two common types of protein found in barley, rye, wheat, and milk, which, if not completely digested, can become opioid peptides. Strict diets that avoid gluten or casein, can, in theory, reduce the opioid peptides that reach the brain.

The idea that dietary restrictions might help autistic symptoms is based on the excess opioid peptide theory of autism¹. In this theory, autistic symptoms are thought to be due to opioid peptides entering the blood stream from the gut and reaching the brain. Once in the brain, the opioid peptides mimic the natural painkillers that our body produces. Too much opioid may have an undesired effect in the brain and contribute to autistic-like symptoms.

The excess opioid peptide theory of autism is controversial because of the problems in measuring opioid peptides. Most research measures opioids in the urine expecting that higher opioid concentrations in the urine reflect higher concentrations in the blood. Some researchers have shown higher urine opioid levels in children with ASDs than normal children, whereas others have not^2-4. One reason for this inconsistency is that actually measuring urine opioids is quite difficult4. Given that the entire theory is based on higher opioid levels, the lack of consistent evidence supporting higher levels of opioids in children with ASD raises doubts about its validity.

Why may children with ASDs have excess opioid peptides? There are two theories about what drives the buildup of opioids in children with ASDs. One theory is that some children with ASD may have an enzyme deficiency⁵. Enzymes help digest the food we eat and some are responsible for breaking down peptides into smaller pieces. If an enzyme is missing or works sluggishly, then peptides may not be degraded into its smaller components, leading to a buildup of undigested peptides. A second theory is that some children with ASD might have a "leaky gut"⁶. Normally, the lining of the gut acts like a fish net – keeping the larger fish inside while letting the smaller fish swim (and be absorbed). A leaky gut means that the net is too porous and some food, such as opioid peptides, are being absorbed before they have a chance to be digested. These two events may either act alone or in concert to cause an excess in opioid peptides.

Interestingly, it has been suggested that enzyme deficiencies and "leaky gut" also contribute to an increased prevalence of gastrointestinal (GI) symptoms in children with ASDs. However, the most recent study looking at the prevalence of GI symptomatology in ASDs found the rate of symptoms in children with ASDs to be comparable to that of typically developing children⁷.

A recent randomized controlled trial of dietary interventions found that children with ASD placed on a gluten- and casein-free diet showed developmental improvements following one year of treatment⁸. The issue of compliance (i.e., sticking to the strict diet) was not addressed, although dieticians were available to parents whose children were on the diet. Another problem with the study was that the parents knew that their child was on the diet. This can cause problems when parents are expected to report improvements. The investigators unfortunately did not measure urinary peptide levels while the children were on the diet, so there was no way to know if the improvements were associated with changes in peptide levels. This is important since previous research has shown that a gluten-free diet does not lead to significant reductions in peptide levels. Although this study has its limitations (e.g., small sample of children, no measurement of peptide levels), it does represent the first randomized controlled trial of dietary interventions in ASDs and highlights many of the challenges in doing this type of research. (See Dietary Interventions in Autism)

Enzyme-based therapies are also emerging as treatments for ASDs⁹. Rather than eliminating gluten and casein from the diet, enzyme-based therapies ensure that gluten and casein are properly digested. This type of intervention is appealing because it is easier than a restrictive diet – which is difficult with picky eaters. There is no available evidence to support enzyme therapies in autism yet.

In summary, gluten- and casein-free diets are novel therapies for ASD that may improve development if maintained for at least one year. The theory backing the therapy remains unproven and controversial. Parents contemplating starting their child on a restrictive diet should first contact their doctor to discuss the available evidence and to ensure that the child's nutritional requirements will be met. Recent research suggests that restricted diets may exacerbate the essential amino acid deficiencies identified in children in ASDs¹⁰. Fortunately, larger scale studies are currently underway on the topic of restricted diets and may provide more specific information about the type of child that might benefit from these interventions.

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2. Seims, AR., & Reichelt, KL. (1995). An enzyme brain barrier theory of psychiatric pathogenesis. Medical Hypotheses, 45, 498-502.
3. Shattock, P., Kennedy, A., Rowell, F., Berney, TP. (1990). Role of neuropeptides in autism and their relationships with classical neurotransmitters. Brain Dysfunction, 3, 328-345.
4. Hunter, LC., O'Hare, A., Herron, WJ., Fisher, LA., Jones, GE. (2003). Opioid peptides and dipeptidyl peptidase in autism. Developmental Medicine and Child Neurology, 45, 121-128.
5. Reichelt, KL., Knivsberg, A-M, Lind, G, Nodland, M. (1991). Probable aetiology and possible treatment of childhood autism. Brain Dysfunction, 4, 308-319.
6. D'Eufemia, P., Celli, M., Finocchiaro, R., Pacifico, L., Viozzi, L., Zaccagnini, M., Cardi, E., and Giardinin, O. (1996). Abnormal intestinal permeability in children with autism, Acta Paediatrica, 85, 1076-1079.
7. Black, CB., Kaye, JA., and Jick, H. (2002). Relation of childhood gastrointestinal disorders to autism: nested case-control study using data from the UK General Practice Research Database. British Medical Journal, 325, 419-421.
8. Knivsberg, AM., Reichelt, KL., Hoien, T., and Nodland, M. (2002). A randomized controlled study of dietary interventions in autistic syndromes. Nutritional Neuroscience, 5, 251-261.
9. Brudnak, MA., Rimland, B., Kerry, RE., Dailey, M., Taylor, R., Stayton, B., Waickman, F., Waickman, M., Pangborn, J., and Buchholz, I. (2002). Enzyme-based therapy for autism spectrum disorders – Is it worth another look? Medical Hypotheses, 58, 422-428.
10. Arnold, GL., Hyman, SL., Mooney, RA., and Kirby, RS. (2003). Plasma amino acid profiles in children with autism: Potential risk of nutritional deficiencies. Journal of Autism and Developmental Disorders, 33, 449-454.

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