Posted by Larry Hoover on October 21, 2002, at 16:38:12
In reply to Mysterious SAM-e, posted by Latinlover on October 21, 2002, at 13:36:58
> What is it about SAM-e that there is so little information about it? Why is it so secret?
> I asked my Dr. last week about the possibility of using that famous SAM-e and, guess what? First time he ever heard about it!
> So any information about it from this forum will be very thanked. I am specially concerned about (in this order) sexual side effects, if it works, sleeping effects, eating effects, hair loss, bone or other organ damages, other deseases.First, methionine is an amino acid, a constituent of protein. It's a little special because it has a sulphur atom in its structure. When there's an adenosine molecule bonded to that sulphur, it's called S-adenosyl-methionine, or SAMe. And in that form, SAMe is one of the body's premier methyl-donors. Some B-vitamins are methyl-donors. Methylation reactions are of fundamental importance to 100's of different bodily processes, including DNA transcription, and neurotransmitter production. SAMe is part of the machinery of neurotransmitter production.
A general shortage of methyl donors, or SAMe in particular, could well underlie many of the symptoms of depression: decreases in cognitive power, poor memory, low energy, decline in mood. It also contributes to heart disease, inflammatory reactions, and many other stress-related disorders. Stress depletes methyl donors.
SAMe is part of a recycling loop. In depressed people, that often stalls part way around, after SAMe is used up, but before its raw materials are replenished. That point is the chemical known as homocysteine. It needs to get a methyl group back to turn it into methionine again.
There are two normal processes for accomplishing that, but the dominant one requires folate and methylcobalamin (the activated form of B-12). That's one of the reasons why doctors tell depressed people to take their vitamins. You need some every day.
There's another process that involves a transfer of a methyl group from another amino acid known as betaine, and also as trimethylglycine. There is an inducible enzyme that converts homocysteine into methionine whenever betaine is in the diet.
If you take SAMe, you will indeed increase the availability of this essential biochemical, but you will do nothing about the buildup of homocysteine. In fact you will make that problem worse.
One gram a day of betaine costs a whole lot less than an equivalent of SAMe, but kills two birds with one stone. It provides the raw materials needed for your liver to make more SAMe, while reducing the levels of the artery-toxic homocysteine. You must take B-vitamins, zinc, and selenium, as well.
Full text of the following at: http://jnnp.bmjjournals.com/cgi/content/full/69/2/228
J Neurol Neurosurg Psychiatry. 2001 Mar;70(3):419.
Homocysteine, folate, methylation, and monoamine metabolism in depression.
Bottiglieri T, Laundy M, Crellin R, Toone BK, Carney MW, Reynolds EH.
Department of Neurology, King's College Hospital, London, UK.
OBJECTIVES: Previous studies suggest that folate deficiency may occur in up
to one third of patients with severe depression, and that treatment with the
vitamin may enhance recovery of the mental state. There are, however,
difficulties in interpreting serum and red cell folate assays in some
patients, and it has been suggested that total plasma homocysteine is a more
sensitive measure of functional folate (and vitamin B12) deficiency. Other
studies suggest a link between folate deficiency and impaired metabolism of
serotonin, dopamine, and noradrenaline (norepinephrine), which have been
implicated in mood disorders. A study of homocysteine, folate, and monoamine
metabolism has, therefore, been undertaken in patients with severe
depression. METHODS: In 46 inpatients with severe DSM III depression, blood
counts, serum and red cell folate, serum vitamin B12, total plasma
homocysteine, and, in 28 patients, CSF folate, S-adenosylmethionine, and the
monoamine neurotransmitter metabolites 5HIAA, HVA, and MHPG were examined.
Two control groups comprised 18 healthy volunteers and 20 patients with
neurological disorders, the second group undergoing CSF examination for
diagnostic purposes. RESULTS: Twenty four depressed patients (52%) had
raised total plasma homocysteine. Depressed patients with raised total
plasma homocysteine had significant lowering of serum, red cell, and CSF
folate, CSF S-adenosylmethionine and all three CSF monoamine metabolites.
Total plasma homocysteine was significantly negatively correlated with red
cell folate in depressed patients, but not controls. CONCLUSIONS: Utilising
total plasma homocysteine as a sensitive measure of functional folate
deficiency, a biological subgroup of depression with folate deficiency,
impaired methylation, and monoamine neurotransmitter metabolism has been
identified. Detection of this subgroup, which will not be achieved by
routine blood counts, is important in view of the potential benefit of
vitamin replacement.
poster:Larry Hoover
thread:124527
URL: http://www.dr-bob.org/babble/20021019/msgs/124555.html