Has anyone read the Chez research on L-Carnosine? Has anyone tried it with their child? I have a 3 year old with ASD who is in ABA. This is the first quality study I have ever read on alternatice treatment. If anyone has tried it I would really appreciate feedback. ThanksHi Hasmig
I think I found that study as I was answering this
Link to pubmed article
I also found these two pages while googling around
L-Carnosine page 1
L-Carnosine page 2
hasmig, here is a helpful website of parents who are doing biomedical treatment with their autistic children. If you do a search there, you might find what you are looking for.
While I've been busy preparing my half of the new DAN! Consensus Report (2002 Edition), lots of Internet talk about the peptide carnosine has evidently occurred. While I have no desire or intention to engage those who are enamored with this latest magic bullet for autism, I do find itappropriate to point out some of the concerns and pitfalls of carnosine use in autism.
Carnosine is a dipeptide composed of the amino acids histidine and beta-alanine. It seems that it gets dragged out of the closet every decade for some use or other. In the 1970s it was muscular dystrophy. In thediet, it comes from incomplete digestive proteolysis of beef, pork, tuna and salmon - as you can see in the amino acid analyses on the urine of autistics and other patients with maldigestion. Carnosine is elevated in the urine of 20 to 40% of autistics. In the 1980s, Bernie Rimland and I discussed thisfinding and considered it to be another facet of the maldigestion and peptideexcess per the findings of Karl Reichelt, et al.
In body tissues, carnosine is split into histidine and beta-alanine. Beta-alanine can be a real troublemaker, and I'll get to that shortly. Histidine is the Dr. Jekyll and Mr. Hyde part. Histidine becomes FIGlu and FIGlu pushes the formation of 5-formiminotetrahydrofolate. This is good, even though it often raises FIGlu levels in the urine and blood of autistics. It's good because: (a) it helps remove a potential folate trap, and (b) itleads to two forms of folate that are required for purine and purine nucleotide synthesis. One of these forms, 10-formyltetrahydrofolate, comes in just after the adenylosuccinase step and helps "pull" the process along at adocumented sticking point for some forms of autism.
However, histidine and carnosine are powerful carriers of copper. They transport copper from the intestinal milieu into the portal blood and from there to organs and tissues in the body. And don't think you can displace copper with zinc once the copper is on histidine - you cannot. The equilibrium constannt for copper II chelated to histidine is 18.3; for zinc it is 6.7 to 12.9, depending on chelate structure (Ref. Chaberek and Martell, Organic Sequestering Agents, John Wiley & Sons, p.549). Because these are exponential relationships, the real difference in the constants is 10 tothe 5th up to 10 to the 11th. Only glutathione, cysteine and thionein can intercept this carnosine-copper transport, but that's one of the big problems in autism, isn't it? These sulfur players have gone AWOL, and copper is excessive at the expense of zinc. Dr. Bill Walsh has made excellent presentations on this. You might think that carnosine plus zinc will act to put zinc in and take copper out. With these equilibrium constants and with the natural copper content of food, that's very unlikely. You need a million or more zinc atoms for each copper atom to be competitive in this game!
Histidine/carnosine-copper wisdom has graduated into medical textbooks. We're not talking about research papers; we're talking what you should and shouldn't do per medical texts. Copper homeostasis with histidine and histidine-albumin complexes are well discussed by David Danks, Chapter 58 of Stanbury et al, The Metabolic Basis of Inherited Disease, 5th Ed, p.1252-1254. For carnosine, the publicity is a bit worse. Carnosine is a threat to worsened Wilson's disease because it and its sister anserine are such good importers of copper to body tissues. Ref: Scriver CR and TLPerry, Chapt 26 in Scriver et al eds, The Metabolic Basis of Inherited Disease6th ed McGraw-Hill (1989) 765.
Now, let's go to the really bad guy here, beta-alanine. To be concise: beta-alanine blocks renal conservation of taurine and causeshypertaurinuria - loss of taurine in the urine. This, in tuurn, causes urinary loss of magnesium, which worsens sulfotransferase activity as well as lots ofother necessary enzymatic processes. If you give carnosine, you lose taurine and magnesium. There are lots of references, but you can start with Dr.Charles Scriver's work referenced above, because all of this biochemistry (carnosine, beta-alanine, taurine, etc.) is closely related.
Did you know that, years ago, Monsanto had a R&D project to replace Aspartame with a beta-alanine dipeptide, because of patent expiration? Chemical and Engineering News published a notice, and the project was canned shortly thereafter. I'd like to think that it was because chemists, including me, wrote them letters about beta-alanine. The public can be grateful that product never made it into circulation.
Oh, I forgot to tell you why FIGlu sometimes goes up in autism. A bunch of credit on this goes to Dr. Sid Baker who observed it. Give folate andFIGlu goes up, not down, in some autistics. After some quick library work Ifound that the FIGlu -to-formiminoTHF enzyme requires pyridoxal 5-phosphate.This needs more study, a lot more, but with Dr. Tapan Audhya's finding of very slow P5P formation in autistics, it fits.
In summary, giving carnosine to the average autistic will at first cause perceived improvement - probably due to the FIGlu-push effect. After some weeks, taurine loss, copper accumulation, magnesium loss, etc. can, unfortunately, reverse the trend and may leave you with a worsenedcondition to deal with.
Jon B. Pangborn, Ph.D. Fellow, American Institute of Chemists