<<Disclaimer: Verify this information before applying it to your situation.>>

Liver abnormalities have been found in a high percentage of celiacs when 
first diagnosed, around 42% according to some studies.  Gluten toxicity 
and increased intestinal permeability have both been suspected as a cause 
of liver abnormalities.  Serious liver disorders, including cirrhosis, 
have been found in association with a number of celiac disease cases which 
appear to resolve upon treatment and maintaining a gluten-free diet.  It 
is not clear whether some damage to the liver may remain long term even 
after maintaining a gluten-free diet.  Below is an interesting study of 
the effects of induced liver cirrhosis on the intestinal mucosa which 
results in oxidative stress and an alteration of intestinal permeability, 
intestinal bacteria makeup, and bacterial overgrowth.  Hence not only does 
damage to the intestine in response to gluten often result in bacterial 
overgrowth, but damage to the liver by gluten may also contribute to 
bacterial overgrowth and mucosal alterations.  

Damage to the liver caused by celiac disease may also have other 
consequences, as the liver plays many important roles including storage 
and production of important compounds and proteins and the removal of fat 
soluble toxic substances.  As we are increasingly exposed to endocrine 
disrupting xenobiotic environmental chemicals and toxic substances, a 
dysfunctional liver's inability to remove fat soluble toxic substances may 
leave celiacs more susceptable to adverse effects from these chemicals 
which can accumulate in adipose (fatty) tissue.  In the Winter 2006 issue 
of Scott Adams Celiac.com Newsletter, I discuss in detail, in "Unraveling 
Fibromyalgia", how a dysfunctional liver and fat soluble toxic substances 
accumulating in innervated and vascularlized adipose tissue in the 
vicinity of joints may be the cause of fibromyalgia.  Bacterial overgrowth 
has also been found in association with fibromyalgia.  But clearly, lesser 
degrees of fatigue, muscle and joint pain, thyroid disorders, and other 
symptoms could also result from liver dysfunction caused by celiac 
disease.  The inability of the liver to remove xenobiotic chemicals may 
also increase the risk of breast and other cancers.

Some Links of Interest:

Environmental Influences on Women's Health 
How to Avoid Endocrine Disrupting Compounds
by Marianne Marchese, ND
http://www.townsendletter.com/July2004/womenhealth0704.htm

Xenoestrogens and Breast Cancer:
Nowhere to Run
By Luita D. Spangler
http://www.fwhc.org/health/xeno.htm

Uncertainties for Endocrine Disrupters: Our View on Progress 
George P. Daston, Jon C. Cook and Robert J. Kavlock 
http://toxsci.oxfordjournals.org/cgi/content/full/74/2/245

Statement from the Work Session on 
Environmental Endocrine-Disrupting Chemicals: Neural, Endocrine and 
Behavioral Effects
http://www.pmac.net/erice.htm

Our Stolen Future
Widespread Pollutants with Endocrine-disrupting Effects
http://www.ourstolenfuture.org/Basics/chemlist.htm

Endocrine Disruptor Knowledge Base 
http://edkb.fda.gov/

----------
Hepatology. 2006 Mar 23;43(4):837-846 
 
Intestinal mucosal alterations in rats with carbon tetrachloride-induced 
cirrhosis: Changes in glycosylation and luminal bacteria.

Natarajan SK, Ramamoorthy P, Thomas S, Basivireddy J, Kang G, Ramachandran 
A, Pulimood AB, Balasubramanian KA.

The Wellcome Trust Research Laboratory, Department of Gastrointestinal 
Sciences, Christian Medical College, Vellore, India.

Spontaneous bacterial peritonitis is a major cause of mortality after 
liver cirrhosis. Altered permeability of the mucosa and deficiencies in 
host immune defenses through bacterial translocation from the intestine 
due to intestinal bacterial overgrowth have been implicated in the 
development of this complication. Molecular mechanisms underlying the 
process are not well known. In order to understand mechanisms involved in 
translocation of bacteria, this study explored the role of oxidative 
stress in mediating changes in intestinal mucosal glycosylation and 
luminal bacterial content during cirrhosis. CCl(4)-induced cirrhosis in 
rats led to prolonged oxidative stress in the intestine, accompanied by 
increased sugar content of both intestinal brush border and surfactant 
layers. This was accompanied by changes in bacterial flora in the gut, 
which showed increased hydrophobicity and adherence to the mucosa. 
Inhibition of xanthine oxidase using sodium tungstate or antioxidant 
supplementation using vitamin E reversed the oxidative stress, changes in 
brush border membrane sugar content, and bacterial adherence. In 
conclusion, oxidative stress in the intestine during cirrhosis alters 
mucosal glycosylation, accompanied by an increased hydrophobicity of 
luminal bacteria, enabling increased bacterial adherence onto epithelial 
cells. This might facilitate translocation across the mucosa, resulting in 
complications such as spontaneous bacterial peritonitis. (HEPATOLOGY 
2006;43:837-846.).

PMID: 16557555 [PubMed - as supplied by publisher] 

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