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Here is a simply written explanation of why the GFCF diet may help autistic children. The theory is that many if not all autistic children  have a damaged intestine/gut. The damage may be there from birth but more likely comes from some immunological  injury like a bad reaction to an immunization.  (keep in mind this is mostly theory). Autistic children seem to have weaker immune systems, and a lot seem to have digestive problems. This "leaky gut" allows some food proteins to pass through into the bloodstream only partially digested, particularly the gluten from wheat/oats/rye/barley, and the casein from milk and other dairy products. These partially digested proteins form peptides which have an opiate-like affect (opioids is another term for them). They can bind to the receptors and cause harmful effects in the brain  just like a regular opiate. Opiates can either cause or magnify autistic symptoms. The opiates are a type of narcotic.  There are receptors in the brain that they bind with to reduce pain and induce pleasure, but they also have harmful side effects. An example of an opiate is morphine or heroin. Until it can be figured out how to heal the "leaky guts", many parents are putting their children on the gluten free/casein free diets .  By Barbara Byers  The following has been [Contributed by Lisa Esmond with permission given for website inclusion] By Alan Friedman, Ph.D. Johnson & Johnson Researcher This is a more complicated, yet more thorough explanation of the diet, written by a doctor.  It also explores the relationship of the diet with the work being done currently by Johnson and Johnson:   There are some very interesting developments in autism research which are not yet published but have been presented in several meetings. Alan Friedman, Ph.D., is a chemist who works for the Ortho Clinical Diagnostics division of Johnson & Johnson. He was interested in the opioid theory of autism - first proposed by Panksepp, confirmed by Reichelt and Shattock - which held that children with autism had many abnormal peptides (small pieces of partially broken down proteins) in their urine, including casomorphine and gliadomorphin. This is where the rationale for the gluten-free, casein-free diet came from. Many children with autism (some but not all) do not seem to break gluten and casein down completely, but rather keep their metabolites casomorphine and gliadomorphin intact which then get into the bloodstream (and therefore into the urine).   Presumably this is because they have a leaky gut since normal people do not have significant amounts of these molecules in their circulation or urine. Many other abnormal protein fragments were found in the urine of these children, but the significance was not clear since the earlier researchers did not have very high tech equipment available.  Alan Friedman was able to use the multimillion dollar technology of Johnson & Johnson to look into this area further. First of all he confirmed that some of the autistic children studied had casomorphine and gliadomorphin unless they were on the diet. More importantly, he also found what looks like 2 other morphine-related compounds, dermorphin and deltorphin II, in the urine of these children.   Dermorphin and deltorphin are compounds which until now had only been found in the skin secretions of poison-dart frogs in South America. Scientists had studied these frogs since they were known for their hallucinogenic properties -- natives used the secretion subcutaneously to have hallucinogenic experiences and used them to tip darts to "stun" targets. These compounds turned out to be more than 1 million times more potent than morphine and were widely studied in the 1980s and early 90s since they were very different from the known morphine peptides. They bind to a different kind of receptor than morphine or human endogenous opioids like the endorphins.   Of great interest is the fact that it appears that these compounds are only found on the skin of these frogs when they are in the wild, but not when raised in captivity outside of their natural environment. Therefore, it is possible that they might be the products of a bacteria or fungus on the skin.  (If autistic children are also manufacturing this substance, this may explain why some children benefit so dramatically from antifungal treatment).  So if autistic children have deltorphin and dermorphin in their urine, which have never been found in humans until now, it is possible that it is coming from a bacteria (or possibly a fungus) in their gut.   The reason that it is clear that they are of "non-human" origin is that they contain a form of amino acid not found in mammals - a "D" amino acid instead of "L". D is for "dexter" or right and means that the amino acid is twisted to the right while all human amino acids are twisted to the left or "levo" amino acids.  Why do autistic children have these compounds circulating  when "normal" people do not? One possibility involves an enzyme in the small intestines called DPP-IV (dipeptydyl peptidase four) which seems to be responsible for breaking down morphine-related peptides in the gut and also plays a role in the immune system, especially in turning on T-cells.   The absence of this enzyme might be responsible for the non-breakdown of these opiate peptides. Some children might be missing this enzyme (maybe the autistic-from-birth subset) while there are other children who might make the enzyme but have an inhibitor which makes the DDP-IV ineffective (the group that regresses?). Rats who are missing this gut enzyme exhibit very abnormal behavior and die when fed gluten.   It is quite possible that the "bug" producing the dermorphin and deltorphin is something that everybody has in their gut. Perhaps a “leaky gut” is what causes them to be released into the bloodstream. Or perhaps these kids are unable to handle it because of lack of normal DPP-IV function.  If the theory is true, there might be a 3-pronged approach to dealing with this problem. No one knows what the "bad bug" in the gut is at this point, but it certainly is possible that an antibacterial or antifungal might be able to knock down the amount (but we don't know which one). Somehow replacing DDP-IV or blocking the inhibitor might enable these children to break these abnormal morphine peptides rather than having them circulate. Blocking the opioid receptors in the brain so that whatever does get into the circulation wouldn't have CNS effects would be the other part.   Deltorphin and dermorphin bind to different opioid receptors than morphine, which is why naltrexone is only slightly effective in children with autism. There are some possible candidates for this, but none currently available (because there never has been a need for them).  When you look at what dermorphin and deltorphin do when they have been injected into animals, they interfere with memory, attention (can't filter out the "background" from the important stuff), behavior (causing hyperactivity as well as stereotypic activity), temperature control (lowers basal body temperature), and cause abnormal EEGs. Opioids which bind to the same receptors as dermorphin also play a role in auditory processing (although I can't find anywhere that these compounds have specifically been looked at for this). Sound familiar?   Johnson & Johnson would like to have a diagnostic test available in the future to look for a marker for autism and is currently involved with clinical trials. Possibly these compounds would provide that marker, but they are not limiting markers to include these, since for a marker to be valuable it must have high sensitivity and specificity, and J&J would like to provide both (i.e. they don't want a child to slip through the cracks).   Dietary Interventions in the Treatment of Autism Spectrum Disorders: Historical Perspectives Paul Shattock; Autism Research unit, School of Sciences, University of Sunderland,Sunderland. SR2 7EE England http://osiris.sunderland.ac.uk/autism/index.html "Well, why did you decide to remove milk from your son’s diet?" I asked. "I just decided that he was worse when he drank milk - I could see it from his food diary." the young mother replied. This conversation took place yesterday but it is one of dozens of similar ones I have had over the years. Parents, especially mothers, are primed, by instinct, to notice such things whereas  orthodox  researchers are trained to eradicate any form of instinctive element from their studies. Which group is the better in terms of science? These mothers have made an observation. (These foods make their children worse in some way.) They have formed a hypothesis. (Something in the foods is causing these problems.) They have designed an experiment to test the hypothesis. (Take the food out of the diet; see what happens; put it back in and see what happens.) and they have told others about their work. This would seem to constitute perfect science.  Many of us parents of children with autism have seen the curtain come down in the eyes of our beloved sons and daughters. We have seen our children slip away from us and have instinctively felt that these changes could be the consequence of some toxic event. Yet our views have attracted no support from funded research programs which have been dominated by genetic and psychologically based studies which, to a greater or lesser extent, evoke a "So what?" response from parents. That we have progressed at all is testimony to the steadfastness maintained by those many parents and pitifully few professionals who have believed the evidence of their own eyes and experience and ignored the prevailing dogma and fear of innovation which characterizes much of what masquerades as research. Rather that address the real problems faced by severely handicapped people, these funded agencies have sought the plaudits of their own peers and funding bodies. It was in the mid and late 60s that Dohan started suggesting that the ingestion of wheat be a causative factor in schizophrenia. Admittedly his evidence was more circumstantial than anything else but his observations were sound and his conclusions, probably, valid. In the early 70s peptides with morphine like activity were found as normal physiological products in human beings. On account of their activity, these compounds were called "endogenous morphines" or "endorphins". The best known of these is probably beta- endorphin which attracted much activity and research interest in the late 70s. It was in 1979 that Jaak Panksepp published his paper which first drew attention to the similarities between the symptoms of autism and the effects of beta-endorphin in humans (and animals). Although Jaak is a world renowned authority on animal behaviors it was a fortunate coincidence that led him to work with people studying autism and this led to his observations. On a personal level, it was reading this paper that riveted my attention to this approach. So many of the things I saw in my son could be explained in terms of an "opioid excess" theory. Jaak’s contribution was hugely important and, since that time, his interest and enthusiasm has never faltered. Jaak established a trust fund "The Lost Children" to assist research in this area. He did this in memory of his beautiful 16 year old daughter who was killed in a driving accident involving a drunken driver. In the early 80s another of our heroes, Dr. Karl  Reichelt, began publishing his series of papers which contained elements from these two threads. His papers remain seminal but were very controversial for a number of reasons. As previously stated, Dohan’s work had not endeared him to the medical establishment and he and his work had attracted criticism. Reichelt’s first paper, which included evidence supportive of Dohan’s hypotheses was published on the very day that Dohan died. It is said that Dohan had a copy of this paper on his deathbed. I hope that it is true and that he died in the knowledge that his revolutionary ideas would be vindicated. Reichelt extended the hypotheses from schizophrenia into the realm of autism. He demonstrated differences in the urinary peptide content in people with autism when compared to normal controls. His method, molecular sieving, was theoretically elegant but technically rather tricky. The three teams around the world, including ourselves, who attempted replication all failed. Reichelt described two basic types of pattern. One of these corresponded with those children where the onset of the symptoms was very early (milk is taken more or less from birth) and those in which the onset is later (wheat/gluten only enters the diet later in life). I remember a "vigorous debate" at an international conference back in 1986. We reported negative results from our replication attempt and felt that his methodology was flawed. In spite of his nickname, "Tiny" Reichelt is a giant of a man and he appeared even larger in his famous bright red shirt. He suggested, from his seat in the audience, that our technical abilities were less than adequate. I recall that "buckets" and "kitchen sinks" were mentioned and the discussion provided a memorable highlight of the conference. The BBC phoned me, a couple of days later, for information about this argument but I persuaded them that this incident was usual and was no more than the normal cut and thrust of academic debate. It was only Tiny’s transparent honesty and obvious integrity which encouraged us to continue with our (failed) studies. However, we had begun to lose confidence in his method and so switched to a more modern High Performance Liquid Chromatographic (HPLC) based method. It was soon after this that the "flaw" in the Reichelt method became apparent. One of the reagents he was using in Norway was, unknown to Reichelt, heavily contaminated with other substances. Once we became aware of this we were able to obtain results similar to those he had obtained but we decided against using his older, more cumbersome, method. It was at about this time that Robert Cade, the inventor of "Gatorade" began utilizing Reichelt’s method and to obtain meaningful results. The whole incident is worthy of note for two reasons. Firstly, since no-one had been able to replicate his work in the early days, the whole concept fell into doubt and disrepute and these rumblings still continue in many academic circles. The other factor is that Reichelt’s studies only worked because of the heavy contamination of one of his solvents. Had the solvent been pure, no positive results whatsoever would have been achieved and the whole concept stillborn. In the late 80s the Norwegians, under the guidance of Anne-Marie Knivsberg, published the first studies of the effectiveness