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  • Jefferson Adams
    Jefferson Adams
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    Higher Risk of Non-alcoholic Fatty Liver Disease After Celiac Diagnosis

    Caption: Slide showing non-alcoholic fatty liver disease. Photo: Wikimedia Commons--Nephron

    Celiac.com 06/29/2015 - Non-alcoholic fatty liver disease is a common cause of chronic liver disease. There's good data showing that celiac disease changes intestinal permeability, and that treatment with a gluten-free diet often causes weight gain, but so far there is scant documentation of non-alcoholic fatty liver disease in patients with celiac disease.

    A team of researchers recently set out to assess increased risk of non-alcoholic fatty liver disease following diagnosis of celiac disease. The research team include Norelle R. Reilly, Benjamin Lebwohl, Rolf Hultcrantz, Peter H.R. Green, and Jonas F. Ludvigsson. They are affiliated with the Department Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden, and the Department of Pediatrics at Örebro University Hospital, Örebro University in Örebro, Sweden.

    The team assessed the for risk of non-alcoholic fatty liver disease diagnosed from 1997 to 2009 in 26,816 individuals with celiac disease to 130,051 matched reference individuals.

    The team excluded patients with any liver disease prior to celiac disease. They also excluded individuals with a lifetime diagnosis of alcohol-related disorder to minimize misclassification of non-alcoholic fatty liver disease. They used Cox regression estimated hazard ratios for non-alcoholic fatty liver disease.

    Their results showed that over 246,559 person-years of follow-up, 53 individuals with celiac disease had a diagnosis of non-alcoholic fatty liver disease (21/100,000 person-years).

    In comparison, in the reference group showed 85 individuals diagnosed with non-alcoholic fatty liver disease during 1,488,413 person-years (6/100,000 person-years).

    This corresponded to a hazard ratio of 2.8 in the celiac group (95% CI), with the highest risk estimates of 4.6 seen in children (95% CI).

    The risk increase in the first year after celiac disease diagnosis was 13.3 (95% CI), but remained significantly elevated at 2.5 even beyond 15 years after celiac diagnosis of celiac disease (95% CI).

    Individuals with celiac disease do have an increased risk of non-alcoholic fatty liver disease compared to the general population.

    Excess risks were highest in the first year after celiac disease diagnosis, but continued at least 15 years after celiac diagnosis. This much more comprehensive study provides much clearer and convincing data than any of the previous studies, and will likely serve as a baseline that clinicians have been lacking to this point.

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    Guest Thelma King Thiel

    Posted

    Diet is critical in dealing with Celiac disease and fatty liver disease as well. Promoting liver health is essential in controlling both diseases. I would like to share an approach that we have found successful in helping motivate both adults and children to address the issue of fatty liver disease, obesity and other liver related illnesses in their own lives.

     

    Extensive evaluation of liver health education programs have shown that individuals who understand HOW liver damage occurs and the detrimental impact it can have on innumerable life sustaining body functions, are motivated to make informed healthful decisions about their food and lifestyle choices. Providing simple messages they can relate to about the important role the liver plays in maintaining hundreds of body functions and sustaining life itself. . . is the key to empowering them to act on what they have learned.

     

    The following information is NEW to most Americans:

     

    The liver has zillions of liver cells serving as the body's micro-chips, converting food into hundreds of essential body functions including producing energy, immune factors, digestive juices (bile), clotting factors, excretion of toxins (alcohol, drugs, pollutants), control of cholesterol and hundreds more. Liver cells are the employees in your personal chemical refinery.

     

    WITHOUT WARNING excess sugar, fats, alcohol and drugs ingested can kill liver cells turning them into scar tissue called cirrhosis. Continued assault over months and years resulting in too many dead cells and too few healthy liver cells causes the liver to slow down and eventually shut down. When your liver shuts down-- so do you.

    Early warning signs of liver trouble can be fatigue, a fat belly and derriere, and possibly flu- like symptoms. Assess your own risks! Look in the mirror - A waistline over 35 inches for women and 40 inches for men may indicate a fatty liver.

    Making healthy food and lifestyle choices and daily exercise will help keep liver cells healthy and your body in good shape. Ask your healthcare provider to check the status of your liver.

    It could save your life.

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  • About Me

    Jefferson Adams earned his B.A. and M.F.A. at Arizona State University, and has authored more than 2,000 articles on celiac disease. His coursework includes studies in biology, anatomy, medicine, and science. He previously served as Health News Examiner for Examiner.com, and provided health and medical content for Sharecare.com. Jefferson has spoken about celiac disease to the media, including an appearance on the KQED radio show Forum, and is the editor of the book "Cereal Killers" by Scott Adams and Ron Hoggan, Ed.D.

  • Related Articles

    Scott Adams
    Gastroenterology 2002;122:881-888.
    Celiac.com 05/02/2002 - In the April issue of Gastroenterology Dr. Pekka Collin of the University of Tampere, Finland, and colleagues describe four patients with severe liver disease who were also found to have celiac disease. One of the patients had congenital liver fibrosis, one had massive hepatic steatosis, and two had progressive hepatitis without apparent origin. Three of the four were considered for liver transplantation. In each case a gluten-free diet reversed heptic dysfunction.
    The reasearchers then studied the prevalence of celiac disease in 185 adults who had already undergone liver transplantation. Eight of them (4.3%) tested positive for celiac disease, and it had already been detected in six of the eight prior to transplantation. Only one the the diagnosed patients followed a strict gluten-free diet. Of these eight patients, three had primary biliary cirrhosis, one had autoimmune hepatitis, one had primary sclerosing cholangitis, and one had congenital liver fibrosis. Additionally, one of the patients had autoimmune hepatitis and one had secondary sclerosing cholangitis.
    The researchers also noted that not all of patients with both liver and celiac disease showed symptoms of celiac disease, which suggests that the liver disease may not be caused by malabsorption. Dr. Collin suggests that it could be a "gluten-dependent immunologically induced extraintestinal manifestation of celiac disease."
    The researchers conclude that some cases of serious liver disease may result from unrecognized celiac disease, and patients with severe liver disease should also be evaluated for celiac disease. Further, dietary treatment in patients with both celiac and liver diseases may prevent progression to hepatic failure, even in cases in which liver transplantation is considered.

    Scott Adams
    Author: Hagander B; Berg NO; Brandt L; Nord en A; Sj olund K; Stenstam M.
    Source: Lancet, 1977 Aug 6, 2:8032, 270-2.
    In an attempt to determine the frequency of liver injury in adult coeliac disease (A.C.D.) the case records of 74 consecutive patients were examined. In 13 cases histological sections of the liver were available and in 5 of these there were signs of reactive hepatitis. Histological signs of distinct hepatic injury with cirrhosis and/or chronic active hepatitis were found in 7 other patients. In 5 of these serum-IgA was normal, whereas 16 out of 20 control patients with liver cirrhosis not associated with A.C.D. had raised serum-IgA. Serum-aspartate-aminotransferase and serum-alanine-aminotransferase were determined in 53 patients; 29 had raised concentrations. In 19 patients serum-aminotransferases were repeatedly determined before and during the dietary regimen and there was a significant reduction in enzyme concentrations during treatment. The median concentration of serum-alkaline-phosphatase was also reduced during treatment but not significantly. The histological evidence of liver injury in 16% and the abnormal liver-function tests in 39% of the patients indicate that hepatic injury is common in A.C.D. Since liver-function tests or liver biopsy specimens were available for only about two-thirds of the patients, liver damage in A.C.D. may be more common than indicated by these results. The effect of a gluten-free diet on aminotransferase concentrations indicates that the liver injury may be reversible and suggests that in some A.C.D. patients, progressive liver damage may be prevented by suitable treatment. Since A.C.D. is not always recognized, the diagnosis should be considered in patients with liver disease of unknown aetiology.

    Roy Jamron
    Celiac.com 05/31/2006 - I previously discussed how liver abnormalities are highly prevalent in celiac disease. Why damage to the liver occurs is unknown, and gluten toxicity and increased intestinal permeability have been proposed as factors. The following free full text article appearing in the current issue of Gastroenterology may shed light on why liver damage occurs in celiacs.
    Toll-like receptors (TLRs) reside on the surface of many cells which participate in the immune system. TLRs sense molecules present in pathogens but not the host, and when the immune system senses these molecules, chemicals are released which set off inflammatory and anti-pathogen responses. One class of molecules recognized by TLRs and common to most pathogenic bacteria is lipopolysaccharides (LPS).
    Gluten increases intestinal permeability in celiacs. The disruption of the intestinal barrier permits endotoxins, such as LPS, from gut bacteria to reach the portal vein of the liver triggering a TLR response from immune cells in the liver. Proinflammatory mediators are released cascading into the release of more chemicals leading to inflammation and liver damage. This may be the cause of liver damage in celiacs. Gluten itself could also trigger a liver immune response. Kupffer cells in the liver are capable of antigen presentation to T cells, along with liver dendritic cells, and could initiate a T cell response to gluten within the liver.
    The following article is somewhat technical, but discusses the role of various liver cells involved in the immune process and how intestinal permeability and TLRs contribute to liver injury. The article is a good read and provides valuable information about the liver I have not seen elsewhere.
    Gastroenterology Volume 130, Issue 6, Pages 1886-1900 (May 2006)
    Toll-Like Receptor Signaling in the Liver
    Robert F. Schwabe, Ekihiro Seki, David A. Brenner
    Free Full Text:
    http://www.gastrojournal.org/article/PIIS0016508506000655/fulltext

    Jefferson Adams
    Celiac.com 09/16/2008 - A team of researchers recently set out to examine the connection between celiac disease and primary biliary cirrhosis, primary sclerosing cholangitis and autoimmune hepatitis.
    The research team was made up of Alberto Rubio-Tapia, Ahmad S. Abdulkarim, Patricia K. Krause, S. Breanndan Moore, Joseph A. Murray, and Russell H. Wiesner.
    The team measured the rates of occurrence for tissue transglutaminase antibodies (tTGAs) and endomysial antibodies (EMAs) in end-stage autoimmune liver disease (ESALD). They then correlated autoantibodies and the human leucocyte antigen (HLA) haplotype. Finally, they assessed the effect of liver transplantation on antibody kinetics.
    The team tested tTGA levels on blood samples from 488 prior to transplant. 310 of these had ESALD, and 178 had non-autoimmune disease. The team tested positive samples for EMAs, and retested at 6-12 and =24 months after transplant. They then correlated their results with the HLA type of the recipient.
    The results showed that 3% of ESALD patients showed evidence of celiac disease compared to 0.6% of those with non-autoimmune disease.  This represents a five-fold greater risk for those with ESALD. The prevalence of tTGAs was 14.2 for ESALD patients compared to 5.4% for those with non-autoimmune disease (P = 0.0001). The prevalence of EMAs was 4.3 for ESALD patients compared to 0.78% for those with non-autoimmune disease (P = 0.01)—significantly higher for those with HLA-DQ2 or HLA-DQ8 haplotypes.
    After transplant, tTGAs and EMAs normalized in 94% and 100%, respectively, without gluten elimination. Also, three out of five patients with classical symptoms of celiac disease improved. The research team found two cases of intestinal lymphoma in two cases that showed no clinical signs of celiac disease.
    Patients with ESALD, particularly those with HLA-DQ2 or HLA-DQ8 gene haplotypes, showed greater occurrances of celiac disease-associated antibodies. Following liver transplants, both tTGA and EMA levels decreased without gluten withdrawal.
    The team also concluded that symptoms of celiac disease might be improved through immune suppression, but those improvements may not prevent the disease from progressing to intestinal lymphoma.
    The study doesn’t tell what effect, if any, early detection and treatment of celiac disease might have on rates of ESALD. It would be helpful to know if celiac disease contributes to liver disease, if liver disease contributes to celiac disease, or if some third connection links the two. Until then, we’ll just have to keep a tight eye on developments concerning celiac disease and liver disease.
    Liver Int. 2008; 28(4): 467-476.


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    Thank you so much for replying I really appreciate it 💗
    I have a theory about my lipomas. I have just recently been diagnosed with hashimotos which is an auto immune disorder. Apparently having one auto immune disorder puts you at greater risk for other immune disorders. I believe cancerous tumors come from the immune system trying to contain and fight the cancer. And my theory is that lipomas come from the immune system targeting fat cells thinking they are bad invaders so they get contained just as a malignant tumor would. I have several lipomas on my lower arms and thighs. I have just been put on a gluten free diet by my doctor for my hashimotos as well as having to take selenium, probiotics and L glutamine daily. Anyways, I believe lipomas are just another auto immune disorder that just might also be fixed by diet and fixing gut issues since the immune system is tightly connected to gut health. Just my two cents.
    Again Primal Kitchen is canola free, they use Avocado Oil in all their mayo, dressings, sauces. I would suggest them for Mayo, Salad Dressings, Sauces, and Condiments. They are grain free also with Paleo Diet base (diet of our ancestors)
    https://thrivemarket.com/brand/primal-kitchen
    https://www.primalkitchen.com/collections
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