The Methyl group is so important that when a cell is broken down the methyl is saved inside a toxic amino acid called Homocysteine. It is toxic to keep bacteria and parasites away from it during the short trip to the liver where it is unpacked and the methyl gets used up by the various steps of methylation which supply compounds ranging from Tryptophan to SAMe used for DNA methylation and neurotransmitters, hormones and Serotonin.
Steps that can be solved via Supplementation
Homocysteine – unpacking of this amino can be blocked by Mercury. One way to bypass is to supplement with TMG, the readily available methyl will get the body to dump Homocysteine instead of attempting to recycle it. This stage can cause anything from allergies to itching and heart damage if the liver is not able to unpack this amino acid.
Tryptophan – if this step is broken due to Mercury supplementing with both TMG and Tryptophan will work
5-htp - if this step is broken due to Mercury supplementing with both TMG and 5-htp will work
SAMe - if this step is broken due to Mercury supplementing with both TMG and SAMe will work.
SSRI and Benzodiazepines can even block receptors of SAMe, in the case of Benzo for decades after use. One guy who tried to kill himself in his teens with Benzo still needed these receptors unblocked +40 years later…
SSRI and Benzodiazepines
These frqs will be posted soon in this thread, if interested add a thread notification.
What I read here is that methionine is depleted by mercury (note mercury secretions increase with higher methionine levels), this is IMO another link between mercury and neurotic behavior. SAMe, a methionine based product used in Europe instead of Prozac may be a far better way to treat depression. Also supplementing with methionine or better a precursor to it (Trimethlylglycine) which has better absorption potentials.
BTW: This also allows larger Selenium doses since the bottle neck of methionine depletion is eliminated.
From the link in prior post:
Methionine: Methionine levels are a major determinant in the liver's concentration of sulphur-containing compounds, such as glutathione and cysteine. As methionine is the precursor for the manufacture of cysteine in the body, extra supplementation of this critical amino acid should increase available cysteine. Animal studies have shown that methionine protects rats from the toxic effects of lead and mercury. Chelating agents such as DMSA (dimercapto succinic acid) and DMPS (dimercapto-propane sulfonic acid) bind to cysteine for excretion. L-cysteine bound to mercury (L-penicillamine, N-acetyl-L-cysteine, DMSA and glutathione complexed with methylmercury) resembles the L-methionine molecule and can cross the blood brain barrier. L-methionine inhibits the transport of these complexes into the brain. Methionine increases the bioavailability of glutathione. Most of the cysteine required for the resynthesis of glutathione must originate from methionine and not from cysteine generated by the catabolism of glutathione. Patients taking only D-L-methionine increased mercury excretion in the urine by 60% over the excretion rate before taking the methionine. Lead excretion was also increased. The L-form is rapidly metabolized by the liver and does not offer a sustained antioxidant level. Over half of the D-form is slowly metabolized by the same pathways as excess L, and acts identical to L as an antioxidant. The benefit of the D-L form of methionine is the D form provides sustained blood levels allowing he L-form to be converted to other sulfur antioxidants. Babies need 22 mg/Kg body weight of methionine on a daily basis while adults need 10 mg/Kg of body weight daily.