<<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]
* * *
*Support summarization of posts, reply to the SENDER not the CELIAC List*
Archives are at: Http://Listserv.icors.org/SCRIPTS/WA-ICORS.EXE?LIST=CELIAC
|