Ok, this is getting more and more interesting. A quick search on PubMed did confirm that taurine actually protects against hyperammonia, so it does look like Yasko is wrong.
I emailed Susan Owens, who gave me permission to repost her post (from the yahoo group "Trying Low Oxalates").
One of the members was asking about Yasko's advice re b6, ammonia, sulfur, etc. Here's Susan's reply:
When Yasko came out with this advice I cut and pasted it and sent it to
scientists whose life work has been this area (which is definitely NOT the case
with Dr. Yasko who just began to dabble with this area after going to two autism
conferences...look at her CV).
Scientists from this field keep telling me there is NO EVIDENCE for what she
claims happens with the increased ammonia. One of my worries about this is she
is testing urine ammonia, which can mean something completely different.
One scientist I wrote said in response to Yasko's text:
"In the case of reduced activity of cystathionase,
this does not induce the enzyme even though there is excess
cystathionine. I can see that the long term possibility if cystathionine is not
rapidly excreted, as appears to be the case, is that you would get more cysteine
and ammonia. However, the urea cycle is normally very active so this shouldn't
be a problem while there is any liver function at all.
As for the cysteine, in man ( as opposed to Martha Stipanuk's rats, which are
quite different) the conversion of cysteine to taurine is very low. We get
nearly all of our taurine from the diet.
Your [her] case history may have reduced activity of cystathionine synthase, not
a super-active variant, as this would give an accumulation of homocysteine and
then higher methionine levels. If this is the case, apparently extra
pyridoxine/vitamin B6 often helps.
I can't see why she does not recommend sulfate donors as nothing happens to
sulfate apart from reduction by gut bacteria (if autistic children have sulfate
-reducing bacteria and I have never seen this proved, although they do exist in
large numbers in ulcerative colitis). "
Another scientist said:
"Yes and I don't understand the basis for her assumptions. There is a common
68bp insertion at position 844 in the CBS gene that is associated with lower
homocysteine (modest increase in CBS activity) and has been most extensively
characterized and studied. Much less common is the C699T she refers to. I can
find no references to a 10 fold increase in activity with this SNP or for that
matter much at all on the functional characterization of that SNP. I frankly
doubt that there is a 10-fold increase activity with this SNP and would ask for
this reference."
{sco note:
every scientist I wrote said this same thing, and when I asked for
Yasko's references from some of her "disciples", they sent back an article about
a ten-fold increase in activity that wasn't about this SNP at all, and I don't
even think it was about CBS!]
back to the scientist:
" My understanding of regulation of cysteine metabolism in the paper she
references is that when cysteine is high, there is a diversion to taurine
synthesis but when it is low (as we see in most autistic children) the Km favors
glutathione synthesis. We rarely see an increase in cystathionine which would be
expected if CBS activity is high...A low protein diet would limit methionine
which I would think would not be indicated for our kids.
I have seen her slides
on the connection between MTHFR 1298AC and BH4 and they are simply wrong - MTHFR
does NOT reverse under physiologic conditions. "Spurious" logic could be applied
to her assumptions."
Paula, what I keep seeing on these OATs is evidence that
CBS is upregulated
because of oxidative stress (as Dick Deth has talked about and researches), and
that upregulation is appropriate because if glutathione is depleted, the whole
story starts to be over! Trying to make glutathione, B6 is being depleted and it
is also needed for the step under CBS, which is clearly happening because
2-hydroxybutyrate is elevating. The glycolic acid is the evidence that B6 is
depleted.
Reducing sulfur sources would only make this whole scenario worse, and do more
to deprive methylation because once the switch is turned to make gluatathione,
you stop doing so much recycling of methionine, and this ends up a sulfur drain
on the body that may only be resolved when adequate B6 allows this pathway to
succeed in making glutathione!
Dr. Yasko also seemed very unfamiliar with the source of ammonia in URINE being
related to the kidney's regulation of the body's pH. When I went to a nephrology
conference in the last few years, I was amused to hear them say, it is a serious
problem if the kidney's are not generating ammonia. The kidneys contain a cycle
called the gammaglutamyl cycle, and this is used to recycle glutathione and
regenerate cysteine that can be imported to cells. If plasma cysteine is low, it
may most often reflect a kidney issue!
But this cycle is invoked, and the enzyme GGT shifts when because of acidosis,
it needs to start creating ammonia in the kidney to get rid of excess protons.
There are lots of discussions of this on sulfurstories. So
raised urine ammonia
is generally ADAPTIVE and the question should be, is the body in acidosis?
Yasko's model just leaves out a lot, and according to everyone I've asked whose
career has been in the areas she "teaches" she just has a lot of this chemistry
wrong. If you don't see the same thing taught in the literature, there is a
reason it is not there! "In the mouth of many witnesses let every matter be
confirmed."
That's Owen's explanation/understanding of the situation. It is confusing to sort all this out! Not sure who's right, but it seems like these other scientists at least have papers published to back up their claims, while Yasko does not. Again, it would be great if Rich sees this so he can explain it further.