Tena, I think you are stretching here.
SAMe is an enteric coated (hence the "e" of SAM). SAM is naturally made in your body by converting homocysteine to SAM using 3 B vitamins.
B12, folic acid, and B6.
I think younger people "react" negatively to it, because their bodies are making enough of it for them at that time in youth. As we age, this system deteriorates and hence, more may be needed.
SAMe is a methyl donor to your liver, joints/collagen, and neurotransmitters.
It enables the body to repair itself, it simply gives up a methyl group to many many systems. It is NOT a drug like SSRIs and it does not affect receptors
like they do.
They are using SAMe for liver disease in Europe. Some patients can even be taken off of liver transplant lists because of its success. Here in this country studies are still ongoing for that. It is also excellent for those with arthritis, or disc disease.
It is well known that people with Parkinson's have very low, insufficient levels of SAM in the brain.
Here is a really good monograph:
http://www.umm.edu/altmed/articles/s...ine-000324.htm
and this is too:
http://healthlibrary.epnet.com/GetCo...chunkiid=21460
There have been alot of papers on Parkingson's and SAM on PubMed.
This one explains how normal amounts of SAM are useful to PD patients, while high doses may enhance metabolism of Levodopa. Depletion of SAM by levodopa metabolism is thought to cause the depression PD's patients experience.
Quote:
Clin Neuropharmacol. 2005 Nov-Dec;28(6):274-6.Click here to read Links
Levodopa intake increases plasma levels of S-adenosylmethionine in treated patients with Parkinson disease.
Müller T, Fowler B, Kuhn W.
Department of Neurology, St. Josef-Hospital, Ruhr-University of Bochum, Gudrunstrasse 56, 44791 Bochum, Germany. thomas.mueller@ruhr-uni-bochum.de
Metabolism of levodopa via the enzyme catechol-O-methyltransferase requires S-adenosylmethionine (SAM) as a methyl donor. SAM caused Parkinson disease (PD)-like symptoms in rodents. Therefore, SAM could contribute to a decreased efficacy of levodopa in the long term. SAM levels were significantly reduced in levodopa-treated PD patients, but they showed increased enzyme methionine adenosyl transferase (MAT) activity, which induces SAM synthesis from methionine (MET). This may result from a rebound increase of SAM production. The objective of the study was to demonstrate an effect of acute levodopa intake on SAM synthesis in the plasma of treated PD patients. The authors measured SAM, MET, and levodopa plasma concentrations in 13 levodopa-treated PD patients before and after application of 125 mg levodopa/benserazide. Plasma levels of SAM and levodopa significantly increased, but MET concentrations did not significantly decrease. The SAM increase after levodopa intake may exert both a certain antidepressant and cognitive function improving effect. This is often observed in untreated PD patients who receive levodopa for the first time, or in more advanced, fluctuating PD patients, when they turn from the OFF to the ON phase. Because SAM in higher dosages may also counteract the antiparkinsonian efficacy of levodopa according to animal trials, this SAM increase may hypothetically contribute to the onset of wearing-off phenomena and other clinical signs of limited efficacy of levodopa during long-term treatment with levodopa in PD patients.
PMID: 16340382 [PubMed - indexed for MEDLINE]
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