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Re: Deplin: Dosage too high? bulldog2

Posted by Larry Hoover on September 28, 2008, at 13:38:17

In reply to Re: Deplin: Dosage too high?, posted by bulldog2 on September 14, 2008, at 16:18:41

I didn't realize what this thread was talking about....I found it while looking up something else.

Bulldog, you said (in two posts):

> I believe that deplin works by converting > homocysteine to sam-e. Would it not be cheaper > to just purchase sam-e and play around with > the dosage?

> Here is a chart from the deplin site that > shows it's mechanism of action.


The way they've shown the mechanism is simplified, and the simplification may be misleading. The enzyme involved in the L-methylfolate mediated conversion of homocysteine to methionine is called (not surprisingly) 5-methyltetrahydrofolate-homocysteine methyltransferase, or MTR. Although the methyl group that ends up being added to homocysteine to yield methionine arises from L-methylfolate (e.g. Deplin), the actual donor is methyl-cobalamin, or methylated vitamin B12. The B12 acts as a shuttle between the L-methylfolate and the homocysteine.

If there is a shortage of L-methylfolate, vitamin B12 can be methylated by another methyl donor, called SAMe. Yes, SAMe can be consumed in the formation of its own precursor. Obviously, that is not an efficient or effective cycle.

There is, however, another enzyme which can facilitate the conversion of homocysteine to methionine, and it's called betaine-homocysteine methyltransferase. Betaine is also known as trimethylglycine. This mechanism does not involve a B12 shuttle, as TMG is the direct methyl donor.

Now, to consider the supplementation of SAMe, it really helps to consider the whole methionine-SAMe-homocysteine cycle. Let's assume we start with dietary methionine. An enzyme adds adenosine to the sulphur atom of methionine (the location being designated by the letter S), yielding S-adenosyl-methionine (SAMe). The sulphur atom is also attached to a methyl group, and the adenosine makes the sulphur atom more stable, so it can more readily lose (donate) the methyl group. Once it has done so, the molecule becomes S-adenosyl-homocysteine. The adenosine group is removed by another enzyme (and recycled), yielding homocysteine.

Because methionine is a rather uncommon amino acid in protein-containing foods, and the body requires a stable supply, there are mechanisms to recycle homocysteine back to methionine. Problems arise when those mechanisms fail (e.g. via enzyme defect; deficiency of B12, L-methylfolate, or betaine; defect in L-methylfolate synthesis), both because of possible decrease in availability of SAMe, but also because homocysteine is a cardiovascular irritant, implicated in atherosclerosis. Depressives are more likely than healthy people to have cardiovascular disease, possibly because both may be associated with an underlying homocysteine recycling defect.

If that recycling problem isn't remediated, supplemental SAMe will simply exacerbate the homocysteine problem. SAMe may have short-term benefits, but I am concerned about long-term harm. Far better, IMHO, to enhance natural SAMe synthesis via enhancing homocysteine to methionine turnover, via supplemental L-methylfolate or betaine/TMG.





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