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Let me start this off by asking, Of those of you who know you are casein
intolerant as well as gluten intolerant, how many of you have gout in
your family medical history?

I had an eureka moment this weekend, one where everything fell together
for me, and I thought I'd share it with those of you who have expressed
an interest in the dark side of celiac disease, where we have fatigue,
depression, and muscle aches.  I think I've finally found the overlap
where celiac disease and the form of autism that responds to a
gluten-free diet intersect.

A lot of this revolves around an amino acid that a lot of us take
already...glutamine.  Glutamine is the most abundant amino acid found in
the human body.  It's in muscle tissue, blood, brain, and important for
us, it's found in the gut.  Glutamine is different from other amino
acids because it has 2 nitrogen atoms.  One of the things that glutamine
does is clean the body of excess nitrogen wastes. (ammonia and urea.

We celiacs have heard of the tissue transglutaminase test.  I looked up
transglutaminase in Yahoo, and I got an interesting link.  Apparently
transglutaminase is an enzyme that links amino acids glutamine and
lysine. (link:  http://www.esf.org/life/lp/PCL/PCLb.htm )

But let's go back to that glutamine/nitrogen/cleansing thinggie...  This
is what I learned this weekend:  That the most common form of autism is
a metabolic defects in the processing of compounds called purines.
Either too many or too few of the needed enzymes are produced.  Gout is
an example of a purine metabolism disease...hence my question, how many
people who know they are casein intolerant besides myself have a family
member who had gout?

Here's a link to the Purine Metabolism Research page:
http://www2.dgsys.com/~purine/

Here's another link that in great, great detail, explains how the body
uses glutamine to rid itself of excess nitrogen wastes:
http://web.indstate.edu/thcme/mwking/nitrogen-metabolism.html#clinical

I find myself asking now, when I get fibromylagia-like aches. is it a
form of gout?  Gout typically is more common among men - my father had
it - if women show gout, it happens after menopause.

Apparently, menstruating women have lower levels of uric acid to
accumulate.

So how do we improve our health over all?  I'm going to make an educated
guess here...those of us who probably have a purine metabolic defect
would respond to the same kind of diet and supplementation that would be
recommended to a gout patient.  In other words, if you maintain a gluten
free diet, and you still have other issues, like aches and pains and
brain fog (in this case due to ammonia build-up) this might give you a
regimen to try.  If you respond to it, problem solved.

I cribbed these recommendations from:
http://www.wellweb.com/ALTERN/Diseases/gout.htm

Supplements that help gout:

    1.. Flavanoids. Quercetin, in particular. Available in certain
fruits, also supplemental form at health food store;

    2.. Folic acid. Has been shown in studies to help with gout, but
exact amounts not determined. Recommended daily dosage is 10-40 mg.
(This is considered a "pharmacological dose"; supplements of folic acid
come in micrograms.) Important Note: Have a health care practitioner
help you with this;

    3.. Vitamin B complex, with extra pantothenic acid;

    4.. Vitamin C with bioflavanoids -- 3,000 to 5,000 mgs total daily,
in divided doses.


After reading this, I ran out and bought folic acid and pantothenic
acid, and I feel great...for the first time in a long while!  No more
aches and pains....I finally felt ready to take on the holidays.  I'm
not sure what the role of lysine is, though...notice above it
cross-links with glutamine...Most of us use lysine for cold sores, and
it has an viral-suppressant reputation.  I went ahead and supplemented,
along with glutamine.  This works for me, and finally, I understand
why.....

Bec
Erie, PA


Postscript:  This is from the Nitrogen metabolism website...about the
build-up of excess nitrogen waste.

I wonder if this explains the migraines I used to get.....

Neurotoxicity Associated with Ammonia

Earlier it was noted that ammonia was neurotoxic. Marked brain damage is
seen in cases of failure to make urea via the urea cycle or to eliminate
urea through the kidneys. The result of either of these events is a
buildup of circulating levels of ammonium ion. Aside from its effect on
blood pH, ammonia readily traverses the brain blood barrier and in the
brain is converted to glutamate via glutamate dehydrogenase, depleting
the brain of a-ketoglutarate. As the a-ketoglutarate is depleted,
oxaloacetate falls correspondingly, and ultimately TCA cycle activity
comes to a halt. In the absence of aerobic oxidative phosphorylation and
TCA cycle activity, irreparable cell damage and neural cell death ensue.
In addition, the increased glutamate leads to glutamine formation. This
depletes glutamate stores which are needed in neural tissue since
glutamate is both a neurotransmitter and a precursor for the synthesis
of g-aminobutyrate, GABA, another neurotransmitter. Therefore,
reductions in brain glutamate affect energy production as well as
neurotransmission. back to the top