high homocysteine = low glutathione

[Guest guest]

Rich Please respond to this statement:

The second pathway to lower homocysteine involves converting it into

cysteine (an very important amino acid), which then through a cascade

of chemistry becomes glutathione.

http://www.y2khealthanddetox.com/truthchol.html

[Guest guest]

Hi, Colorbleu.

Yes, this is correct. The methionine (or methylation) cycle is

coupled to the transsulfuration pathway. Homocysteine (in the

methionine cycle) can either be converted back to methionine,

closing the cycle, by means of vitamin B12 together with folic acid

or by means of trimethylglycine (betaine), or it can be converted to

cysteine (in the transsulfuration pathway), by means of vitamin B6,

and from there can either go into making glutathione or can proceed

to taurine or to sulfate. The sulfur in the original homocysteine

is excreted from the body either as taurine or as sulfate. The

amounts that go in each direction are controlled by various

parameters. In people who have a genetic defect involving MTHFR,

the pathway from homocysteine to methionine is inhibited. In people

who have mercury toxicity, both the methionine cycle and the pathway

to glutathione can be inhibited. Some people also have the pathway

to sulfate inhibited at the enzyme sulfite oxidase, sometimes

because of a molybdenum deficiency. This causes them to be

sensitive to essentially all foods or supplements containing sulfur,

because sulfite builds up and produces symptoms.

Rich

> Rich Please respond to this statement:

>

> The second pathway to lower homocysteine involves converting it

into

> cysteine (an very important amino acid), which then through a

cascade

> of chemistry becomes glutathione.

>

>

> http://www.y2khealthanddetox.com/truthchol.html

[Guest guest]

Nelly,

I think there must be quite a few labs characterizing the MTHFR

genetic polymorphisms now, because it is turning out to be important

in several disorders. One of them in the U.S. is the Great Smokies

Diagnostic Lab, as part of their Genovations testing. Check

http://www.gsdl.com

Another lab in the U.S. is the ARUP lab in Salt Lake City, Utah.

The url is http://www.aruplab.com/guides/ug/tests/0055655.jsp

There must be a lab in Paris that does these characterizations as

well.

Rich

> In people who have a genetic defect involving MTHFR,

> the pathway from homocysteine to methionine is inhibited. In

people

> who have mercury toxicity, both the methionine cycle and the

pathway

> to glutathione can be inhibited. Some people also have the

pathway

> to sulfate inhibited at the enzyme sulfite oxidase, sometimes

> because of a molybdenum deficiency. This causes them to be

> sensitive to essentially all foods or supplements containing

sulfur,

> because sulfite builds up and produces symptoms.

>

> Rich,

>

> How can we determine whether we have these genetic defects?

>

> Nelly

[Guest guest]

Hi, Colorbleu.

Yes, that's the treatment. An alternative is to take

trimethylglycine (also called betaine, but not the same as the

betaine HCl used for low stomach acid correction). Trimethylglycine

promotes a parallel pathway for completing the methionine cycle.

One could also use both these approaches at the same time.

Rich

> > >  In people who have a genetic defect involving MTHFR,

> > > the pathway from homocysteine to methionine is inhibited.  In

> > people

> > > who have mercury toxicity, both the methionine cycle and the

> > pathway

> > > to glutathione can be inhibited.  Some people also have the

> > pathway

> > > to sulfate inhibited at the enzyme sulfite oxidase, sometimes

> > > because of a molybdenum deficiency.  This causes them to be

> > > sensitive to essentially all foods or supplements containing

> > sulfur,

> > > because sulfite builds up and produces symptoms.

> > >

> > > Rich,

> > >

> > > How can we determine whether we have these genetic defects?

> > >

> > > Nelly

> >

> >

> >

> >

> >

> >

> >