Celiac Disease and Liver Disorders

[mle_ii]

Well, take a look here:

Celiac Disease and Liver Disorders
http://www.celiac.com/articles/21501/1/ ... Page1.html

I knew that the liver was somehow involved. What and the thing in this article that got me the most was mention of "hypertransaminasemia", which basically means elevated liver enzymes (ALT and AST for example). They're not clear about the tie in, but it was rather interesting that just this year I started to get mildly elevated liver enzymes, last test they came down. Wonder how it's related. My guess would be that it might be related to the bacterial overgrowth, makes me wonder what might have happend during this time if I was consuming gluten, might this have triggered Celiac Disease?

Even more so I think that the liver is somehow tied in with MC/CC/LC. Especially with the numbers here with liver/gallbladder issues. My guess is that there are a few here with pancreas issues as well due to it's location near the liver/gallbladder.

Mike

[mle_ii]

What is interesting is that, on a limited search of Pub Med, it appears that bacteria, specifically lipopolysaccharides, play a role in liver injury and thus elevated liver enzymes. So it wouldn't be too far to think that bacterial overgrowth of the small intestine could play a role in this liver injury, gut permeability would play a role as well. Gut permability can be increased by bacterial overgrowth as well as, what we've found in various studies, with gluten.

Mike

[mle_ii]

To further add on to this. Part of the damage is caused by increased oxidation by the LPS (lipopolysaccharides) oxidation of various materials, which would lead to oxidation of glutathione (an antioxident produced by the body) and melatonin (also an antioxident produced by the body) helps reduce the oxidation of glutathione.

Might this explain the elevated melatonin found in my saliva.
Might this explain the decreased glutathione and antioxident levels found in my blood lymphocytes.
Might this also explain the elevated liver enzymes.
I also wonder if it was the oxidation of fat that might have brought about the xanthomas on my eyelid.

More food for thought, eh? :)

Thanks
Mike

[mle_ii]

Things thus far that help block or reduce this damage:
Melatonin
Curcumin
Tea polyphenols
Liposomal N-acetylcysteine
Glycyrrhizin (part of Licorice Root)
HDL (the good fat found in our blood)

[mle_ii]

Wow, and doing a search like "(lipopolysaccharide or Endotoxin) mercury" in pubmed seems to indicate that mercury multiplies the damage done by lipopolysaccharides. Interesting.

Mike

[harvest_table]

Interesting Mike, thanks for the info.

Also noteworthy, may be the production of "autoantibody antitissue transglutaminase"

Another clinical setting in which patients have been identified to have an elevated relative risk of celiac sprue is that of elevated hepatic transaminase levels in blood. Although it has been observed for many years that as many as 40% of patients with celiac sprue have elevated liver enzymes at the time of diagnosis, it has been noted only recently that almost 10% of patients presenting to physicians with elevated serum liver transaminase levels of unknown etiology have celiac sprue, and many more may have gluten sensitivity of milder degrees. Indeed, celiac sprue, which has been epidemiologically linked to certain autoimmune liver diseases, has recently been identified to be associated with production of the specific autoantibody antitissue transglutaminase.

While it is possible that immunologic gluten sensitivity and inflammatory damage of the small intestine as a primary event may secondarily cause liver inflammation, evidenced by normalization of elevated serum transaminase levels and resolution of nonspecific hepatic histopathologic inflammation after removal of gluten from the diet in celiac sprue patients so-affected, it is also possible that certain hepatic inflammatory diseases trigger immunologic gluten intolerance and autoimmune attack on the intestine in genetically predisposed individuals. One common hepatic disease, viral hepatitis C, in particular has been identified to lead to secondary autoimmune processes in other parts of the body; infection with the hepatitis C virus has been associated with development of antinuclear antibodies, mixed cryoglobulinemia, and lichen planus of the skin. Additionally, the cell-mediated inflammatory response of a patient with hepatitis C has been linked to T cells restricted to HLA-DQ2, an allele commonly associated with gluten sensitivity. Through testing, Applicant has shown that 1.2% of patients with hepatitis C have celiac sprue compared to 0% in liver control patients. Therefore, hepatitis C is a trigger for the autoimmune reactions that are pathogenic to celiac sprue.

Therefore, according to the present invention, hepatitis C and other hepatic diseases are indicators which may be used to identify and diagnose gluten sensitivity and other immunologic food sensitivities. Further, the use of a diagnosis of hepatitis C or other hepatic disease, as an indicator for gluten sensitivity or other immunologic food sensitivities, may be coupled with the stool testing methods described below as another aspect of the invention, to further enhance the accuracy of immunologic food sensitivity diagnosis.

http://64.233.167.104/search?q=cache:pd ... cd=8&gl=us

Tissue transglutaminase (abbreviated as TG2 or tTG) is an enzyme (EC 2.3.2.13) of the transglutaminase family. Like other transglutaminases, it crosslinks proteins between an ε-amino grop of a lysine residue and a γ-carboxamide group of glutamine residue, creating an inter- or intramolecular bond that is highly resistant to proteolysis (protein degradation). It is particularly notable for being the autoantigen in coeliac disease, but is also known to play a role in apoptosis, cellular differentiation and matrix stabilisation.[1]

http://en.wikipedia.org/wiki/Tissue_transglutaminase

More food for thought!

Love,
Joanna

[mle_ii]

Thanks for the info Joanna!

[grannyh]

Although my overall cholesterol levels have been high for years.. my good cholesterol is unusually high.. wonder if this will prevent damage?? One can only hope so:)

[Becky]

Last night, I had a pretty good work out. When I was done, I noticed the strangest perspiration smell...the closest thing I could compare it to was ammonia. For kicks, I googled "perspiration that smells like ammonia". Amazing! - there were links to articles that correlated that type of smell to liver and/or kidney problems. I had the serum test for Celiac this week. Seems like so many of these "things" are tied together....interesting!

[tex]

Could that smell have been the odor of acteone? If you are on a low carb diet, and working out, you may have been burning fat instead of carbs, and if this happens at too fast a rate, the liver may be bombarded with too many fatty acids, and incomplete fat metabolism by the liver can occur. When that happens, there will be an increase in ketone bodies, that are released into the system, and at a certain level, the classic symptom of acetone odor on the breath will occur.

I believe this is commonly referred to as ketosis, and it's usually accompanied by a sort of metallic taste in the mouth. A couple of years ago, I tried a trial where I cut out all significant amounts of carbs, and it took only a couple of days before I noticed a strong presence of this effect. Eating protein only seemed to make it worse, but it went away within a few minutes, after I ate a couple of GF cookies, (made with rice flour).

Diabetes mellitus can also cause the odor of acetone on the breath.

Tex

[mle_ii]

Wow, and doing a search like "(lipopolysaccharide or Endotoxin) mercury" in pubmed seems to indicate that mercury multiplies the damage done by lipopolysaccharides. Interesting.

Mike

Wow, and take a look here:

Dihydrolipoic acid inhibits skin tumor promotion through anti-inflammation and anti-oxidation.
http://www.ncbi.nlm.nih.gov/sites/entre ... h=17403519

Alpha Lipoic Acid (ALA) is a precursor to DHLA, and DHLA seems to be of benefit in limiting the damage done by lipopolysaccarides (bacteria). What is very strange and to come full circle is that ALA is something I plan to take to help chelate mercury. ALA is converted by the body into DHLA, DHLA which contains two thoils (sulfer groups) are able to grab onto metals that normally hook themselves to sulfer containing things (such as the cells in our bodies). Mercury is one such thing that hooks itself to parts of the body. Normal chelators do not reach accross the brain barrier or into cells, but ALA does.

And as the following study indicates and Andy Cutler says in his book, taking ALA the wrong way can do more harm than good. According to him taking ALA while you still have amalgams will move the mercury to the brain rather than out of the brain. You're body burden most be low enough for this to work. He says 3 months is what he recommends before using ALA. And it must be in small doses every 3 or 4 hours due to it's half life in the body.

The role of thiols, dithiols, nutritional factors and interacting ligands in the toxicology of mercury.
http://www.ncbi.nlm.nih.gov/sites/entre ... h=17408840

You can learn more here:
http://health.groups.yahoo.com/group/fr ... chelation/

Thanks,
Mike

[mle_ii]

Ok, this just keeps getting more and more interesting.

From this page it appears that ALA is synthesized from Octanoic acid (or more better know as Caprylic acid).
http://lpi.oregonstate.edu/infocenter/o ... metabolism

http://en.wikipedia.org/wiki/Octanoic_acid

And what are some sources of Caprylic acid? Coconut and breast milk. Might this be one of the many reasons why breast feeding is so beneficial to babies? Also I seem to remember some folks here using Caprylic acid to treat candidia.

Finally I do see some studies showing that ALA has uses in treating diabeties, especially the neural aspects of the disease. And has also been useful in treating alzhemers disease. Might ALA be beneficial to those with Celiac disease as well? Perhaps even Inflamitory diseases, IBS.

Mike