With children on the autistic spectrum methylation is a big BIG factor and most of what we do for our boy revolves around methylation in his biomed program.
There is just so much info out there. What would you like to have in particular and i can post, dont want to post everthing but here is a brief rundown.
For methylation we use things like gluthione, large amounts of vitamin c a day, methylcobalamin (see www.drneubrander.com).
If your child is autistic, you can get methylation tested via a number of tests or if you have a good practitioner, he or she can look at the overall picture of your child via organic acids, and bloods and will be able to see if your child is lacking in this structure.
A good panel (though expensive) is the premier autism panel through IWDL.
You can also get supplements and testing for free via the caudwell trust.
I wish we had more talk about this on mumsnet. the UK is so far behind the U.S. in these matters, particularly via the NHS doctors. They just dont want to know. Yet, the peer reviewed research is plentiful as are the doctors who are informed about this, all over the world.
METHYLATION THEORY AND AUTISM
Methylation Theory of Autism
Methylation is an important metabolic process, possibly defective in autism, and pertaining to the control of histamine excess, protection of DNA, promotion of serotonin production, and other brain functions. A number of experiments have suggested a relationship between methyl group metabolism and the exocrine secretion of the pancreas 32.
These included nutritional studies which showed that ethionine, the ethyl analog of methionine which inhibits cellular methylation reactions, is a specific pancreatic toxin. Other studies indicated that protein carboxymethylation might be involved. Capdevila, et al. 32 showed that in vivo ethionine inhibits amylase secretion from freshly isolated rat pancreatic acini, while in vitro ethionine inhibits amylase secretion from the AR42J pancreatic cell line.
S-Adenosylhomocysteine (SAH) is an inhibitor of all methyltransferase reactions involving S-adenosylmethionine (SAMe). Treatments that elevate cellular levels of SAH such as inhibition of S-adenosylhomocysteine hydrolase and the in vitro addition of adenosine and homocysteine result in the inhibition of amylase secretion in both isolated pancreatic acini and AR42J cells. Measurement of SAMe and SAH levels in AR42J cells shows that inhibition of secretion is more closely related to elevation of SAH levels than to a decrease in the SAMe/SAH ratio.
Small G-proteins are carboxymethylated on the C-terminal byprenylcysteine, and inhibitors of membrane-associated prenylcysteine methyltransferase, N-acetylfarnesylcysteine, N-acetylgeranylgeranylcysteine, and farnesylthioacetic acid (FTA), block secretion in AR42J cells. N-Acetylgeranylcysteine is not an inhibitor of the methyltransferase and does not inhibit amylase secretion. FTA inhibits membrane-associated prenylcysteine methyltransferase from AR42J cells.
These results suggest that a methylation event is needed for pancreatic exocrine secretion which may be the reversible methylation of a G-protein involved in signal transduction or membrane trafficking. One theory of action of secretin revolves around restoration of normal methylation in the pancreas, and thereby normalizing pancreatic exocrine secretion. Pancreatic exocrine secretion is blocked by inhibitors of methylation.
www.healing-arts.org/children/autism-overview.htm#Methylation
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