Below is the abstract of the study:

Celiac.com 09/12/2006 - Symptoms of celiac disease prominently include fat malabsorption. One would expect this to impact levels of essential fatty acids in celiacs. The omega-3 essential fatty acids, especially eicosapentaenoic (EPA) and docosahexaenoic (DHA) acids available in fish oil supplements have been demonstrated to have numerous health benefits. However, there are almost no studies on the effect of celiac disease on essential fatty acid levels. I am currently in the process of writing an article on essential fatty acids that will appear in Open Original Shared Link, so a new study on lipid profiles in celiac disease caught my eye with promise. I was disappointed to find the study only measured cholesterol levels in celiacs, which showed an improvement in the "bad" to "good", LDL to HDL, ratio and an increase in "good" HDL cholesterol in patients on a gluten-free diet. The opportunity to study essential fatty acid levels in celiacs was again missed. However, omega-3 fatty acids have a proven beneficial effect on cholesterol levels, and improved fat absorption of omega-3 fatty acids due to a gluten-free diet may be responsible for the results presented in this new celiac disease lipid profile study.

Below are the abstract of this study and two studies on the effects of omega-3 fatty acids on cholesterol levels:

Am J Med. 2006 Sep;119(9):786-90.
Change in lipid profile in celiac disease: beneficial effect of gluten-free diet.
Brar P, Kwon GY, Holleran S, Bai D, Tall AR, Ramakrishnan R, Green PH.

Am J Cardiol. 2006 Aug 21;98(4 Suppl 1):71-6.
Clinical overview of omacor: a concentrated formulation of omega-3 polyunsaturated Fatty acids.
Bays H.

Am J Clin Nutr. 2000 May;71(5):1085-94.
Purified eicosapentaenoic and docosahexaenoic acids have differential effects on serum lipids and lipoproteins, LDL particle size, glucose, and insulin in mildly hyperlipidemic men.
Mori TA, Burke V, Puddey IB, Watts gluten-free, ONeal DN, Best JD, Beilin LJ.

New Fatty Acid Celiac Disease Study

No sooner do I complain there arent any studies of essential fatty acid levels in celiac disease then, at least, a limited pediatric study of essential fatty acids appears! The results of this study on 7 pediatric patients with active celiac disease, 6 with celiac disease in remission, and 11 controls, show serum levels of fatty acids are similar between celiac disease and control patients, but abnormal fatty acid levels exist in intestinal mucosa tissue of active celiac disease patients. Results suggest an omega-6 fatty acid deficiency, at least in the mucosa. Not too surprising because prostaglandin E2 secretion increases in the intestines of active celiac disease patients, and prostaglandin E2 is produced from omega-6 fatty acids. It should be noted that fatty acid profiles may prove to be different in adult celiac disease patients. Also while omega-6 fatty acids may be deficient, increasing intake of omega-3 fatty acids may help reduce inflammatory processes in celiac disease.

J Pediatr Gastroenterol Nutr. 2006 Sep;43(3):318-323.
Abnormal Fatty Acid Pattern in Intestinal Mucosa of Children with Celiac Disease is Not Reflected in Serum Phospholipids.
Steel DM, Ryd W, Ascher H, Strandvik B.

This also means increased intestinal permeability and associated problems such as liver damage may continue to be a lasting problem in older patients beyond two years on a gluten-free diet. Below is the abstract:

In the commercial supplement product, Glisodin, the properties of gliadin have, in fact, already been used for the last few years to facilitate the delivery of the antioxidant enzyme superoxide dismutase (SOD) protecting it from digestive acids and getting it through the intestinal mucosa, probably taking advantage of the zonulin effect. Aware of celiac disease, the developer of Glisodin tried to use other peptides as a carrier of SOD, but the only gliadin was effective. Unfortunately, this denies celiacs the benefit of using Glisodin to treat oxidative stress.

Abstract of Study:

It does bring up the idea of a gluten-ingesting bacteria link which I proposed in my article, Open Original Shared Link. In that article I proposed that a bacteria capable of transporting and internalizing gluten peptides resistant to breakdown could initiate a T cell immune response to gluten. Antigen presenting cells (dendritic cells) might present gluten peptides internalized by the bacteria along with peptides and chemical signals from the bacteria to T cells. The T cells would not be able to distinguish the gluten peptides from the bacteria peptides and would, therefore, initiate an immune response to gluten peptides as though they were components from pathogenic bacteria. The presence or non-presence of such a bacteria in twins offered an explanation as to why one identical twin could develop celiac disease and not the other.

After 10 years on a gluten-free diet, it is possible that the numbers of such gluten-ingesting bacteria might diminish to a level too few to initiate a gluten immune response, especially if the bacteria largely depend on gluten for nutrition. So, like the twin who does not develop celiac disease, she remains symptom free.

I urged researchers to look for such gluten-ingesting bacteria in my article, and I continue to urge such research. Such bacteria could be found through the use of immunogold electron microscopy. This technique permits gluten peptides to be bound to and labeled with gold particles which show up as distinct opaque spots under the electron microscope. Such spots found within microscopic cross sections of fecal bacteria samples would identify gluten-ingesting bacteria.

Abstract of Study:

Arch Dis Child 2006;91:39-43.

Celiac.com 12/08/2005 – Researchers in the United Kingdom conducted a systematic review and meta-analysis of 15 studies published between 1966 and 2004 that evaluated the association between breast-feeding and celiac disease. Their review covered more than 4,000 children and found that breast-feeding may offer protection against the development of celiac disease, especially if it is prolonged and covers the period when gluten is introduced. It was unclear, however, whether breast-feeding merely delays the onset of symptoms, or actually offers permanent protection against the disease, and more long-term prospective cohort studies will be necessary to make such a determination.

Nat Genet. 2005 Nov 13

Celiac.com 11/29/2005 - The following is an abstract of a study by Dutch researchers which demonstrates a new level of understanding with regard to the role that specific genes play in the cause of celiac disease. These findings may eventually lead to a treatment that lies beyond the gluten-free diet:

Dig Liver Dis. 2005 Sep 29;
Dickey W, McMillan SA.
Department of Gastroenterology, Altnagelvin Hospital, Londonderry BT47 6SB, Northern Ireland, UK.

Celiac.com 10/11/2005 - BACKGROUND.: Serological testing, using IgA class endomysial and tissue transglutaminase antibodies has high sensitivity and specificity for celiac disease and allows case finding by clinicians other than gastroenterologists. We reviewed new celiac patients seen over a 9-year period to determine how the availability of serology, particularly to primary care physicians, has changed rates and sources of diagnosis.

METHODS.: Files of patients attending a specialist celiac clinic who were diagnosed from 1996 through 2004 were reviewed. Patients with villous atrophy consistent with gluten sensitive enteropathy (Marsh III) on duodenal biopsy were selected. Data analyzed included clinical characteristics, endomysial and tissue transglutaminase antibodies status and source of request for serology.

RESULTS.: Over the study period 347 new celiac patients, comprising adults and children aged 10 years and over, were identified, of whom 163 (47%) were identified by serological testing in primary care, 152 (44%) at the hospital gastroenterology department and 32 (9%) by other physicians in secondary care. Over three consecutive 3-year periods, the percentage of patients identified in primary care rose from 28% through 47% to 60%, with a rise in total numbers diagnosed from 93 through 118 to 136. There was no change in patient clinical characteristics over the study period. Though tissue transglutaminase antibodies were less sensitive than endomysial antibodies, combined testing obtained a sensitivity of over 90%. Patients identified in primary care were significantly younger and more likely to present with diarrhea as a primary symptom.

CONCLUSION.: Currently over half of our celiac patients are identified by serological testing in primary care, which has resulted in an overall rise in diagnosis rates. Primary care practitioners have an important role in the diagnosis of celiac disease, particularly of patients who present with non-gastrointestinal symptoms. The contribution of specialists other than gastroenterologists in secondary care is disappointing and may improve with directed education.

Celiac.com 10/11/2005 - Arcadia Biosciences, an agricultural biotechnology company focused on products that benefit the environment and human health, today announced that it has received a Small Business Technology Transfer Program (STTR) grant from the National Institutes of Health in partnership with Washington State University (WSU) to research novel lines of wheat with reduced celiac disease-causing proteins. The grant will be split equally between Arcadia and its academic collaborator at WSU, Dr. Diter von Wettstein, the R.A. Nilan Distinguished Professor in the Department of Crop and Soil Science.

Nearly 1 percent of American people and 4 percent of European people are estimated to suffer from celiac disease, or gluten intolerance. This genetic disorder can create symptoms that range from chronic diarrhea to malnutrition. Studies also indicate that celiac disease sufferers who continue to eat gluten are between 40 and 100 times more likely to develop gastrointestinal cancer than non-celiac disease sufferers. The only known treatment for celiac disease is adherence to a gluten-free diet, which includes complete abstinence from wheat, rye, barley, and their derivatives.

"New diagnostic tests continue to identify people who suffer from celiac disease and who need to make extreme dietary adjustments," said Eric Rey, president of Arcadia Biosciences. "This grant is the first step in our effort to identify and develop wheat varieties that can significantly expand the dietary options for people on gluten-free diets. Our goal is to help enable people who suffer from celiac disease to enjoy wheat-based products, like bread and cookies, and not experience an adverse reaction."

Working with Dr. von Wettstein and his colleagues at WSU, Arcadia will use its proprietary TILLING® technology to identify wheat plants in which harmful gluten proteins are minimized.

Arcadias current product pipeline includes six technologies that either protect the environment or improve human health. The company expects to launch its first product, GLA-enriched safflower oil, to the nutritional supplement market in 2008. Other technologies include higher-yielding plants that use less nitrogen fertilizer, salt-tolerant plants, and fresh produce with high levels of antioxidants such as lycopene. These products are being developed using both genetic engineering and advanced breeding technologies.

Celiac.com 09/27/2005 - What does a positive endomysial antibody (EmA) test mean if the biopsy does not show villous atrophy? The authors studied 35 patients where this was the case. In the authors practice, these patients account for 10% of all EmA positives.

Firstly, the lack of villous atrophy did not necessarily mean a normal biopsy: 14 patients had excess inflammatory cells (lymphocytes) consistent with a mild abnormality of gluten sensitivity.

Secondly, many of these patients had typical celiac features: twelve had a family history of celiac, five had dermatitis herpetiformis and thirteen had osteopenia or osteoporosis on DEXA scan.

After discussion, 27 patients opted to take a gluten-free diet from the first biopsy: 26 of these had clinical improvement. Seven of eight patients who persisted with a normal diet developed villous atrophy on follow-up biopsies.

The authors conclude that a positive EmA result indicates gluten sensitivity even if biopsies do not show villous atrophy. While a biopsy remains important as a baseline reference, these patients should be offered a gluten-free diet to allow clinical improvement and prevent the development of villous atrophy. There may be no such thing as a "false positive" EmA, although the authors emphasise that the same conclusion cannot yet be applied to tissue transglutaminase antibody results.

Celiac.com 09/14/2005 - Researchers have long thought that the resistance of gliadin prolamines to digestive enzymes is a primary contributor to celiac disease—which leads to the intestinal permeability and inflammation in those who are at risk. Taking prolyl-endopeptidase enzymes (PEP) orally has been proposed and explored as a possible treatment for celiac disease (including extensive research done at Open Original Shared Link). In an effort to determine the feasibility of such a treatment, researchers in France conducted both in vitro (outside a living organism) and ex vivo—using biopsy specimens of active celiac disease patients—studies on the effects of PEP on gliadin peptides.

For the in vitro studies the researchers used radio-reverse-phase high-performance liquid chromatography and mass spectrometry to analyze the degradation by PEP of 3H-labeled gliadin peptides 56-88 (33-mer). In the ex vivo studies the researchers added PEP and 3H-peptides together onto the mucosal side of duodenal biopsy specimens that were mounted in Using chambers, and the peptide transport and digestion were analyzed using radio-reverse-phase high-performance liquid chromatography.

The results indicate that in both in vitro and ex vivo studies the gliadin peptides were only partly degraded by 20 mu/ml of PEP. This concentration of PEP decreased the quantity of intact gliadin peptides (31-49 and 56-88) that crossed the intestinal biopsy specimens, but did not prevent the intestinal passage of toxic or immunostimulatory metabolites—for this the researchers determined that PEP concentrations of at least 500 mu/ml for at least 3 hours was required to achieve full detoxification of gliadin peptides, and thus prevent intestinal transport of active fragments—unfortunately this finding virtually eliminates PEP as a possible treatment option for those with celiac disease.

The researchers conclude optimistically, however: "After prolonged exposure to high concentrations of PEP, the amount of immunostimulatory gliadin peptides reaching the local immune system in celiac patients is decreased. These results provide a basis to establish whether such conditions are achievable in vivo (in living organisms)."

Celiac.com 07/28/2005 - In an effort to determine whether gluten exposure in those with celiac disease can cause additional autoimmune diseases, Finnish researchers evaluated the frequency of autoimmune disorders in 703 adults and children with celiac disease, and compared them with 299 controls (normal duodenal histology). For each person in the study the researchers assessed the effect of age at the end of follow-up, age at diagnosis; actual gluten exposure time; and the gender and diagnostic delay time. They then determined autoimmune disease incidence figures that were expressed as a dependent variable via logistic regression analysis (per 10,000 person-years).

The researchers found that the celiac disease group had a significantly higher prevalence of additional autoimmune diseases that was not affected by exposure to gluten.

Additional Comments on this Study by Roy Jamron:

Autoimmune disease has a high prevalence in celiacs. The following study concludes that the duration of gluten exposure in celiacs is not a significant factor in the risk of developing autoimmune disease. One diagnosed late in life with celiac disease does not appear to be at greater risk for developing autoimmune disease. This seems counter-intuitive, but there may be a good explanation for this result.

Studies in the UK and Italy have demonstrated that the prevalence of celiac disease in young children is essentially the same as in adults, meaning celiac disease begins in infancy. Infancy is the critical time period for the development of the immune system. Gluten exposure and the onset of celiac disease symptoms early in life, therefore, have a much greater and more important impact on the immune system and its development than exposure to gluten later in life. Malabsorption during infancy and early childhood can also adversely affect the crucial function of the thymus, T cell production, and T cell repertoire. So the stage is set early in life rather than later for increased risk of autoimmune disease. The timing of gluten exposure in life seems to be more critical to autoimmune disease risk rather than the overall lifetime duration of gluten exposure. It is, therefore, extremely important to diagnose celiac disease and initiate a gluten-free diet as soon as possible during infancy and young childhood to lower the risk of autoimmune disease later in life.