Gluten-free, casein-free diet

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A gluten-free casein-free diet (or GFCF diet) eliminates intake of the naturally-occurring proteins gluten (found naturally in wheat, barley, and rye) and casein (found in milk). The Autism Research Institute and other advocacy groups recommend the diet as a treatment for autism and related disorders. Studies supporting these claims have had significant flaws, so the data are inadequate to guide treatment recommendations.[1]

Background and theory

In the 1960s, Dohan speculated that the low incidence of schizophrenia in certain South Pacific Island societies was a result of a diet low in wheat- and milk- based foods.[2] Dohan proposed genetic defect as a probable etiology for schizophrenia, wherein individuals were incapable of completely metabolizing gluten and casein. The consequence of incomplete metabolism is excess peptide levels in the gastrointestinal tract, which Dohan hypothesizes are responsible for schizophrenic behaviors.

The possible relationship between gluten, casein, and autism was first articulated by Karl Ludvig Reichelt, M.D. in 1991.[3] Based on studies showing correlation between autism and increased urinary peptide levels, Reichelt hypothesized that some of these peptides may have an opiate effect. Further work determined opioid peptides such as casomorphines[4] (from casein) and gluten exorphines and gliadorphin (from gluten) as possible suspects, due to their chemical similarity to opiates. Reichelt hypothesizes that long term exposure to these opiate peptides may have effects on brain maturation and contribute to social awkwardness and isolation. On this basis, Reichelt and others have proposed a gluten-free casein-free diet to minimize the buildup of opiate peptides and promote typical development of brain function.

Reichelt's hypothesis is not generally regarded as a definitive etiology for autism, nor is the GFCF diet advocated as a "cure".[5]

Effectiveness of the GFCF diet

Reports on the effectiveness of the GFCF diet come overwhelmingly from testimonials of individual parents or teachers. Reported results range from no discernible effect to claims of complete recovery following implementation of a gluten-free casein-free regimen.[6] There have been insufficient adequately designed, large-scale controlled studies and clinical trials to state whether the GFCF diet is effective.[7] A small single-blind study has documented fewer autistic behaviors in children fed a gluten-free, casein-free diet but noted no change cognitive skills, linguistic ability or motor ability.[8] This study has been criticized for its small sample size, single-blind design which may have skewed results on the basis of a "parent placebo effect".[1]

A 2006 double-blind short-term study found no significant differences in behavior between children on a gluten-free, casein-free diet and those on regular diets.[6] A long term double-blind clinical trial sponsored by the National Institute of Mental Health is scheduled for completion in April 2008; preliminary results are not yet available.

Practical implementation

The implementation of a GFCF diet involves removing all sources of gluten and casein from the child's diet. Gluten is found in all products containing wheat, rye, and barley and may sometimes contaminate oats grown nearby or processed on the same equipment as gluten-containing cereals.[citation needed] Because a gluten-free diet is a well-established treatment for other disorders, such as celiac disease and dermatitis herpetiformis, there are many gluten-free breads, pastas, and snacks available commercially. Gluten-free cookbooks have been available for decades. Casein is found in dairy products such as milk or cheese, but is also present in smaller amounts in many substitute dairy products such as vegetarian cheese substitutes, which use casein to provide texture. On a separate note, whey is a different milk protein from casein and can be included in this diet.

While testimonials vary, a significant fraction report symptoms similar to withdrawal in the early stages of GFCF diet implementation. Positive testimonials also vary in the time required to see improvements in autistic behaviors; some reports claim an immediate reduction in such behaviors while others take up to a year or more to achieve noticeable results. These observations are the result of parent and teacher reporting and have not been substantiated in terms of formal diagnostic criteria or quantitative behavioral assessments.[citation needed]

Other indications

Those suffering from celiac disease and/or dermatitis herpetiformis are instructed to avoid all forms of gluten, though their metabolic disorders are apparently distinct from the autism-related metabolic disorder hypothesized by GFCF proponents.[citation needed]

See also


  1. 1.0 1.1 Christison GW, Ivany K (2006). "Elimination diets in autism spectrum disorders: any wheat amidst the chaff?". J Dev Behav Pediatr. 27 (2 Suppl 2): S162–71. PMID 16685183.
  2. Dohan, F.C. (1966) Cereals and Schizophrenia, data and hypothesis Acta Physiologica Scandinavica, 42, 125-132.
  3. Reichelt KL, Knivsberg A-M, Lind G, Nødland M. Probable etiology and possible treatment of childhood autism. Brain Dysfunct 1991; 4: 308-19
  4. Sun, Z. and Cade, J.R. (1999) A peptide found in schizophrenia and autism causes behavioral changes in rats. Autism, 3(1), 85-95.
  5. White, John F. (2003) "Intestinal Pathology in Autism" Experimental Biology and Medicine, 228, pp. 639-649.
  6. 6.0 6.1 Elder JH, Shankar M, Shuster J, Theriaque D, Burns S, Sherrill L (2006). "The gluten-free, casein-free diet in autism: results of a preliminary double blind clinical trial". J Autism Dev Disord. 36 (3): 413–20. doi:10.1007/s10803-006-0079-0. PMID 16555138.
  7. Millward, C. (2007). "Gluten- and casein-free diets for autistic spectrum disorder". Cochrane Database of Systematic Reviews. 3. doi:10.1002/14651858.CD003498. Retrieved 2007-07-23. Unknown parameter |coauthors= ignored (help)
  8. Knivsberg, A.M. (2002). "A randomised, controlled study of dietary intervention in autistic syndromes". Nutritional Neuroscience. 5 (4): 251–261. PMID 12168688. Unknown parameter |coauthors= ignored (help); |access-date= requires |url= (help)

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