<<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