GSE
SAMe and other methyl donors
SAMe - And other Methyl Donor Molecules
Study-supported Health benefits of SAMe
Supplementation
Reference:
http://www.ajcn.org/content/76/5/1151S.long#R4
SAMe
for Depression - 40 clinical supporting studies involving
~1400 patients. In 1994 Dr. Giorgio Bressa, a psychiatrist at the University
Cattolica Sacro Cuore in Rome, pooled results from a dozen controlled trials and
found that "the efficacy of SAMe
in treating depressive syndromes... is superior [to] that of placebo and
comparable to that of standard... antidepressants."
Janicak PG, Lipinski JD, Comaty JE, et al. S-Adenosylmethionine: a literature
review and preliminary report. Ala J Med Sci 1988;25:306-13.[Medline]
Friedel HA, Goa KL,
Benfield P. S -Adenosyl-L-methionine: a review of its therapeutic
potential in liver dysfunction and affective disorders in relation to its
physiological role in cell metabolism. Drugs 1989;38:389-416.[Medline]
Bressa GM. S -Adenosyl-L-methionine
(SAMe )
as antidepressant: meta-analysis of clinical studies. Acta Neurol Scand
1994;154:7-14.
Link to several supporting studies for
SAMe with
depression
SAMe
for
pain/inflammation/arthitis
- In a dozen clinical trials
involving more than 22,000 patients, researchers have found SAMe as
effective
as pharmaceutical treatments for pain and inflammation - but unlike the NSAIDs, SAMe shows no
sign of damaging the digestive tract. The Arthitis Foundation medical experts
concur.
- Joint-protective - after
SAMe loses a methyl group to become
homocysteine, it can be broken down to form glutathione, which reaction also
yields sulfate groups, which help generate joint-protective proteoglycans.
SAMe accumulates in the synovial fluid that
lubricates joints. Certain chemicals resulting from
SAMe breakdown can relieve pain and inflammation
SAMe for liver diseases - "The
administration of a stable salt of SAMe , either orally or parenterally, has been
shown to restore normal hepatic function in the presence of various chronic
liver diseases (including alcoholic and non-alcoholic cirrhosis,
estrogen-induced and other forms of cholestasis (bile impairment or blockage),
to prevent or reverse hepatotoxicity due to several drugs and chemicals such as
alcohol, paracetamol (acetaminophen), steroids and lead, and to have
antidepressant properties."
Friedel HA, Goa KL, Benfield P"S-adenosyl-L-methionine. A review of its pharmacological properties and
therapeutic potential in liver dysfunction and affective disorders in relation
to its physiological role in cell metabolism." Drugs 1989 Sep;38(3):389-416.
(ADIS Drug Information Services, Auckland, New Zealand).
-
SAMe has been found to prevent or reverse liver
damage caused by certain drugs, alcohol, and cytokines -
It protects against liver damage caused by MAO inhibitors and anti-convulsants.
- It reverses
hyperbilirubinaemia
- Rat study showed the
beneficial effects of
SAMe on liver disease - Fetal rat liver cells were exposed to ethanol, causing a 40% reduction in
DNA synthesis, a doubling of free radicals, a 30% decrease in cellular
ATP ,
altered mitochondrial function, and cell damage. Pretreatment with
SAMe maintained cell replication, decreased
free radicals and prevented ATP and glutathione depletion.
A
study in Hepatology
Lieber CS. Role of
S-adenosyl-L-methionine in the treatment of liver diseases. J Hepatol
1999;30:1155-9.
Medline
Williams R, Lieber CS. The role of
SAMe in the treatment of liver disease. Drugs 1990;40(suppl):1-2.
Medline
Mato JM, Camara J, Fernandez de Paz J, et al. S -Adenosylmethionine
in alcoholic liver cirrhosis: a randomized, placebo-controlled, double-blind,
multicenter clinical trial. J Hepatol 1999;30:1081-9.
Medline
SAMe
for INSULIN resistance
- SAMe
"improved whole
body
INSULIN
sensitivity, and
prevented body weight gain"- in animal model
of type 2 diabetes mellitus and
INSULIN resistance.
"S-Adenosyl-L-Methionine Increases
Skeletal Muscle Mitochondrial DNA Density and Whole Body Insulin Sensitivity in
OLETF Rats1" .
SAMe for
osteoarthritis
Bradley JD, Flusser D, Katz BP, et
al. A randomized, double blind, placebo controlled trial of intravenous loading
with S -adenosylmethionine (SAM) followed by oral SAM therapy in patients
with knee osteoarthritis. J Rheumatol 1994;21:905-11.[Medline]
Padova C. S -Adenosylmethionine
in the treatment of osteoarthritis: review of the clinical studies. Am J Med
1987;83:60-5.[Medline]
SAMe for
schizophrenia
SAMe
for
demyelination diseases - has a variety of pharmacological
effects in the CNS, especially on monoamine neurotransmitter metabolism and
receptor systems
-
Protects against
neuronal death caused by lack of oxygen (anoxia).
-
Regenerates nerves
and provokes remyelination of nerve fibers
- SAMe
Treatment with
methyl donors (betaine, methionine
and SAMe ) is associated with remyelination in
patients with inborn errors of folate and C-1 (one-carbon)
metabolism
SAMe
for Dementia, Alzheimers
-
Alzheimer's
patients have severely decreased levels of
SAMe
in their brains - a turnaround from an idea that the
brain had too much
SAMe !
Morrison LD, Smith DD
and SJ Kish. 1996.
J Neurochem 67: 1328-1331.
SAMe for CVD
-
Swiss researchers
showed that high homocysteine levels that precede heart disease
Stampfer MJ, Malinow MR, Willett WC, et al. 1992. A prospective study of plasma
homocysteine and risk of myocardial infarction in US physicians. JAMA 268:
877-81
-
Low blood SAMe levels are correlated with the development of CAD
- SAMe deficiency has a deterimental effect on homocysteine metabolism.
SAMe
plays a crucial role preventing the breakdown of MTHFR -The enzyme
methylenetetrahydrofolate reductase (MTHFR) needed to convert folate to its
active form,
5-methyltetrahydrofolate (5-MTHF). This folate form is directly involved in
homocysteine metabolism.
Loehrer MTF, Angst CP, Haefeli WE, Jordan PP, Ritz
R and B Fowler. 1996. Low whole-blood S-adenosylmethionine and correlation
between 5- methyltetrahydrofolate and homocysteine in coronary artery disease.
Arth Throm Vasc Biol 16: 727-733.
- SAMe
also remethylates homocysteine back into methionine
SAMe
for
Cancer
- Scientists suspect that
adequate methylation of DNA can prevent the expression of harmful genes