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Celiac Disease: Where We Are and Where We Are Going
Alessio Fasano, MD
New Orleans, Tuesday, May 18, 2004 --
Celiac disease (CD) is an immune-mediated enteropathy triggered by the ingestion of gluten-containing grains (including wheat, rye, and barley) in genetically susceptible individuals. CD is associated with HLA molecules DQ2 (90%-95%) and DQ8 (5%-10%), and in the continued presence of gluten the disease is self-perpetuating. CD is one of the most common lifelong disorders worldwide. This condition can manifest with a previously unsuspected range of clinical presentations. These include the typical malabsorption syndrome (chronic diarrhea, weight loss, bloating) and a spectrum of symptoms potentially affecting any organ or body system. Because CD is often atypical or even silent on clinical grounds, many cases remain undiagnosed and become exposed to the risk of long-term complications, such as osteoporosis, infertility, or cancer. There is also a growing interest in the social dimension of CD, because the burden of illness related to this condition is doubtless higher than previously thought.
Many aspects of CD were discussed during this year's Digestive Disease Week (DDW) meeting that may help pave the way for future breakthroughs concerning the pathogenesis, diagnosis, and, most important, alternative treatment options.
The Genetics
The major component of the genetic predisposition to CD resides in the HLA region of chromosome 6. CD is strongly associated with HLA class II antigens, and approximately 90% of cases show a particular DQ2 alpha/beta heterodimer, with the remaining cases being HLA DQ8-positive. Therefore, the presence of HLA DQ2 and/or DQ8 is considered absolutely essential and their absence essentially rules out CD. The latter already has applications in clinical practice, particularly in those cases in which the diagnosis has not been validated by the currently recommended diagnostic algorithm. However, the HLA alleles explain only part of the genetic susceptibility to CD. In most European and North American populations, the frequency of DQ2 is high (15%-30%), but only a minority of DQ2-positive subjects develop CD. In the absence of strong functional candidate genes, several genome-wide scans in families with affected sib-pairs have been conducted. Although no additional susceptibility loci have been clearly identified thus far, there is some evidence of a genetic risk factor on chromosomes 5q and 11p11.[1]
The Immunopathology
The celiac enteropathy is the result of immune-mediated damage to the small intestinal mucosa. The cascade of pathophysiologic events most likely starts with an alteration in the barrier function and/or increased transcellular passage of gluten through the small intestinal mucosa. In the lamina propria, the tissue transglutaminase (tTG), a ubiquitous enzyme that catalyzes the cross-linking of proteins, deamidates gliadin peptides, strongly increasing their affinity for the HLA molecules located on the membrane of antigen-presenting cells (APC; eg, the macrophages). The HLA molecule forms a "groove" where short peptides (eg, a product of gliadin digestion) can be specifically linked. Among these fragments, the recently described 33-mer seems to be the most intriguing gliadin fragment, given its exceptional resistance to intraluminal as well as surface digestion and its immunodominant motifs particularly suited to bind to T lymphocytes either directly or following manipulation by APC.[2] Ultimately, the interaction between gliadin peptides and HLA molecules activates intestinal T cells. The release of proinflammatory cytokines (eg, interferon-gamma) by activated T cells could determine the damage to the enterocyte, increased proliferation in the intestinal crypts, and, finally, severe damage to the intestinal mucosa architecture.
The Epidemiology
Traditionally, CD was perceived as a rare disorder typical of infancy, with wide incidence fluctuation in space and time, and confined to the European population. Both evolutionary and epidemiologic observations suggested an inverse relationship between CD frequency and the introduction of wheat with agriculture. However, this theory is now challenged by recent epidemiologic studies showing that, beside being frequently found in countries where individuals are mostly of European origin, CD is a common disorder in many areas of the developing world where agriculture started 10,000 years ago.
It is interesting to note that the highest frequency of CD in the world has actually been reported among the Saharawi refugees, an inbred population of Berber-Arabic origin. These results raise an interesting question: Why is a disease that is associated with a high rate of morbidity and increased mortality, if left untreated, not segregated out by genetic evolution? The disease has remained one of the most frequent genetically based disorders of humankind. One possible explanation is that gluten, a protein introduced in large quantities in the human diet only after the advent of agriculture, activates "by mistake of evolution" mechanisms of innate immunity that are too important for human survival to be eliminated.
Treatment
One of the most innovative aspects of today's session on CD was discussion of the possible alternatives to the gluten-free diet that can be developed based on the new pathophysiologic findings discussed above. Inhibition of the gliadin-induced increased permeability of the intestinal barrier is a strategy already applied in the setting of type-1 diabetes, a disease that shares a leaky gut pathology with CD.[3] The digestion of the proteolytic-resistant gliadin peptides (33-mer) using bacterial-derived prolyl endopeptidase is another attractive therapeutic strategy. This enzyme has already been used to predigest gliadin with interesting preliminary results in human trials that need to be confirmed on a larger scale.[4] The inhibition of the tTG deamidating activity is another theoretical strategy for treatment; however, the caveat of affecting other important functions of the enzyme, such as wound repair, requires further scrutiny. Finally, the recently reported crystallographic data on gliadin binding on the T-lymphocyte groove offer the possibility to block the receptor using synthetic peptide inhibitors.
Concluding Remarks
CD is a common disorder in children as well as adults. At any age, the spectrum of clinical presentations is wide, and at present, extraintestinal manifestations (eg, anemia or short stature) are more common than the classical malabsorption symptoms. A high degree of awareness among healthcare professionals and a "liberal" use of serologic CD tests (case findings) can help to identify many of the atypical cases. Although the gluten-free diet currently remains the cornerstone of treatment for CD, new perspectives are on the horizon that may help disclose a better future for all individuals affected with this condition.
References
Fasano A. Prevalence and genetics. In: AGA Clinical Symposium -- Celiac Disease Clinical Symposium. Program and abstracts of Digestive Disease Week 2004; May 15-20, 2004; New Orleans, Louisiana. [Sp418]
Sollid LM. Immunology. In: AGA Clinical Symposium -- Celiac Disease Clinical Symposium. Program and abstracts of Digestive Disease Week 2004; May 15-20, 2004; New Orleans, Louisiana. [Sp 419]
Sapone A, Warrs T, Counts D, et al. Inhibition of the zonulin-dependent increased intestinal permeability prevents the onset of type 1 diabetes in BB/Wor rats. Gastroenterology. 2004;126(suppl 2):A-518. [T1820]
Gray GM. Treatment. In: AGA Clinical Symposium -- Celiac Disease Clinical Symposium. Program and abstracts of Digestive Disease Week 2004; May 15-20, 2004; New Orleans, Louisiana. [Sp 419]
Copyright © 2004 Medscape.
http://www.medscape.com/viewarticle/478293
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Gastrointestinal Motility Disturbances in Celiac Disease.
Journal of Clinical Gastroenterology. 38(8):642-645, September 2004.
Tursi, Antonio MD
Abstract:
It is quite frequent to recognize celiac patients who show gastrointestinal motor abnormalities in clinical practice. In fact, in 30 to 60% of patients, physical examination and dyspeptic symptoms (epigastric discomfort, early satiety) suggest a gastrointestinal motility disorder. Consistent data are now available on the presence of a disturbed motility of the esophagus, stomach, small intestine, gallbladder, and colon of untreated celiac patients. Gastrointestinal abnormalities differ in different gastrointestinal districts. In fact, esophageal transit, gastric and gallbladder emptying, and orocecal transit time are delayed, while colonic transit is faster. These findings are related to the complex interactions among reduced absorption of food constituent (in particular, fat), neurologic alteration, and hormonal derangement. Motility disorders of the gut are also a predisposing factor in the development of small intestinal bacterial overgrowth and may contribute both to development of symptoms in some untreated celiacs and to the persistence of symptoms after gluten-free diet in some of them. All these alterations fortunately disappear after gluten-free diet, and patients return to well being status.
Whatever the initial event in the pathogenesis of the celiac lesions may be, we know for certain at this time that gastrointestinal disturbances play an important role in the genesis of gastrointestinal symptoms in celiac disease and that surveillance for celiac disease in patients complaining of dysmotility-like dyspeptic symptoms should be increased.
(C) 2004 Lippincott Williams & Wilkins, Inc.
http://www.mdlinx.com/GILinx/thearts.cfm?artid=1041735&specid=13&ok=yes
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Relief for coeliac patients
An easy-to-use tool for the detection of gluten in foods will be developed in an EU-funded project designed to help people with coeliac disease avoid problem foods.
Gluten, which causes the symptoms of the disease, is common in many foodstuffs, even if the product itself is not a cereal product, and due to its increasing use as a food additive its presence in many products is not immediately obvious.
Scientists in the project will use new knowledge on the development of reliable and easy to handle test systems for the detection of gluten in food products.
Coeliac disease affects approximately 1million Europeans. The intolerance to gluten causes damage to the small intestine mucosa which is reversible with avoidance of dietary gluten. The damaged mucosa disturbs the absorption of water and nutrients. This can cause malnutrition, which can be severe, especially for small children and adolescents. Coeliac disease is different from allergy: some people with wheat allergies are not gluten intolerant and can eat rye and barley. According to present knowledge, oats can be consumed by coeliac patients.
The symptoms of coeliac disease can vary with each individual and they do not always involve the digestive system. They can range from no symptoms at all, to severe ones, such as gas, bloating, diarrhoea, abdominal pain, irritability, muscle cramps or fatigue. Because of the broad range of symptoms that coeliac disease presents, it can be difficult to diagnose.
http://www.nutraingredients.com/news/ng.asp?id=37123
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Babies at Celiac Disease Risk Should Wait for Wheat
Timing of first gluten in diet could help ward off the illness, study suggests.
By Serena Gordon
HealthDay Reporter
WEDNESDAY, May 18 (HealthDay News) -- New parents with a family history of either celiac disease or type 1 diabetes should be very careful about when they introduce wheat into their baby's diet, a new study suggests.
Researchers found that if wheat was introduced before 3 months of age or after 7 months, the risk of developing celiac disease was increased compared to babies who had their first taste of wheat when they were between 4 and 6 months old.
"Children fed wheat, barley or rye cereals in the first three months had a fivefold increased risk [for developing celiac disease] compared to children who didn't have those cereals until they were 4 to 6 months old," said study co-author Jill Norris, head of the section of epidemiology and community health at the University of Colorado at Denver and Health Sciences Center.
"Children who had cereals after 6 months had a small increase -- about a twofold increased risk," Norris said.
Norris and her colleagues published their findings in the May 18 issue of the Journal of the American Medical Association.
Celiac disease is an autoimmune disorder that causes the body to perceive gluten, a protein substance found in wheat, rye and barley, as harmful. As a result, the small intestine becomes damaged from the immune system's ongoing assault on gluten. Eventually, the small intestine becomes so damaged it can no longer process nutrients from other foods, and serious nutritional deficits can occur.
The disease is inherited and researchers have identified several genes associated with celiac disease autoimmunity. Not everyone with the gene defects, however, develops celiac disease.
All of the children in the study had known genetic defects that put them at greater risk of developing the disease, and Norris was quick to point out that because all of the children in her study were at increased risk to begin with, these findings do not apply to the general population of newborns.
Another important issue this study wasn't able to address is whether the early -- or late -- introduction of gluten into the diet contributed to the development of celiac disease, or simply accelerated the appearance of the illness, Norris said.
Between 1994 and 2004, Norris and her colleagues identified 1,560 newborns from the Denver area at increased risk of celiac disease, either because they carried a genetic mutation associated with celiac disease or had a first-degree relative with type 1 diabetes. The genetic defects associated with celiac disease are the same as those for type 1 diabetes, so a family history of type 1 diabetes is also a risk factor for celiac disease, Norris explained.
The investigators tracked health outcomes in each of the babies for an average of five years, interviewing parents, checking each child's blood for signs of celiac disease, and monitoring the youngsters' diets.
Fifty-one children developed celiac disease during the study, the researchers report. Children fed products containing gluten before they were 3 months old faced more than a fivefold increase in risk for the illness, while children first fed gluten products during their seventh month or later were at a slightly less than twofold increased risk of the disease, compared to babies fed gluten between 4 and 6 months.
Norris said the researchers weren't able to learn exactly why early and late wheat introduction was associated with the development of celiac disease, but she suspects that young babies' digestive systems are too immature to process gluten, a complex protein. This may cause some gluten to cross into the bloodstream, where the immune system would start to attack it.
And, in the case of those introduced to wheat later, Norris said they may simply be getting exposed to more gluten at once because older babies take in much larger amounts of food per meal than newborns.
While calling the trial a "welcome study, and the first to suggest that timing [of first wheat ingestion] may be a risk factor," Dr. Richard Farrell, an assistant professor of medicine at Harvard Medical School, said these findings must also be interpreted with caution.
"Only three infants actually exposed to gluten before four months developed celiac disease," noted Farrell, who wrote an accompanying editorial in the same issue of the journal. He said a much larger study needs to be done to corroborate the findings.
"As the editorial author said, this study leaves 'too many questions' unanswered," added Angela Kurtz, a pediatric nutritionist from New York University Medical Center.
Kurtz said previous research has shown a protective effect from breast milk, and she pointed out that this study did not address the potential effects breast-feeding might have on the development of celiac disease.
She recommends breast-feeding children exclusively until they reach 6 months of age. Then, when babies start eating solid food, Kurtz recommends starting with rice cereals, or fruits or vegetables.
"Hold off on wheat, rye and barley, and when you do introduce them, only give small amounts once a day," she said.
Both Norris and Farrell said the results of this study are far too preliminary to recommend any changes to the current feeding guidelines, which suggest beginning solid foods at 4 to 6 months of age.
More information
To learn more about celiac disease, visit the Celiac Disease Foundation.
SOURCES: Jill Norris, Ph.D., M.P.H., professor and head, epidemiology and community health, University of Colorado at Denver and Health Sciences Center, Denver; Richard Farrell, M.D., assistant professor, medicine, division of gasteroenterology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston; Angela Kurtz, M.S., R.D., pediatric nutritionist, New York University Medical Center, New York City; May 18, 2005, Journal of the American Medical Association
http://www.principalhealthnews.com/article/hscoutn/104095771
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Non-Toxic Wheat May Be an Answer to Celiac Disease
NEW YORK (Reuters Health) Oct 14 - It may be possible to produce varieties of wheat that can be safely consumed by patients with celiac disease, according to Dutch researchers.
"Our work," lead investigator Dr. Liesbeth Spaenij-Dekking told Reuters Health "indicates that not all wheat varieties appear to be equally harmful for patients. This suggests that through breeding programs new varieties may be generated that will be acceptable for consumption by celiac disease patients. Moreover, such varieties may be used to prevent disease in individuals at risk."
In the September issue of Gastroenterology, Dr. Spaenij-Dekking of Leiden University Medical Center and colleagues note that it unknown whether all wheat types are of equivalent toxicity for patients with celiac disease.
To investigate, the researchers examined wheat gluten protein information contained in public databases. The aim was to find varieties low in the T-cell stimulatory sequences that prompt celiac disease.
The team found that ancient grass-like wheat varieties had less gluten, but subsequent breeding led not only to an increase in yield, but an increase in gluten and potential toxicity.
Eventually the researchers assayed samples of 16 wheat varieties, only 2 of which are commercially available, and found that there were considerable differences in the levels of T-cell- stimulatory epitopes.
Thus they conclude that through breeding and screening, "varieties may be identified with a reduced or even absent toxicity profile for celiac disease patients."
In an accompanying editorial, Dr. Marco Londei and colleagues at University College London characterize the study as providing important information, but among caveats, point out that the commercially viability of growing "less toxic" wheat varieties is open to question.
Gastroenterology 2005;129:797-806,1111-1113.
http://www.medscape.com/viewarticle/514562?src=mp
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Predictors of Clinical Response to Gluten-Free Diet in Patients Diagnosed With Diarrhea-Predominant Irritable Bowel Syndrome
Ulrich Wahnschaffe, , , Jörg–Dieter Schulzke‡, Martin Zeitz‡ and Reiner Ullrich‡
‡Medical Clinic I (Gastroenterology/Infectious diseases/Rheumatology), Charité-Universitätsmedizin Berlin, Campus Benjamin Franklin, Berlin, Germany
Medical Clinic A, Department of Gastroenterology, Endocrinology and Nutritrion, University Hospital Ernst Moritz Arndt Universität Greifswald, Greifswald, Germany
Refers to: Exam 2: Predictors of Clinical Response to Gluten-Free Diet in Patients Diagnosed With Diarrhea-Dominant Irritable Bowel Syndrome
Clinical Gastroenterology and Hepatology, Volume 5, Issue 7, July 2007, Page 769
U. Wahnschaffe
Background & Aims: Gluten sensitivity might cause abdominal symptoms in the absence of villous atrophy. We examined the prevalence of celiac disease–associated serum antibodies in diarrhea-dominant irritable bowel syndrome (d-IBS) patients and their efficacy in combination with HLA-DQ2 expression to predict the response to gluten-free diet.
Methods: HLA-DQA1*0501/DQB1*0201 expression and celiac disease–associated IgA and IgG serum antibodies against gliadin and tissue-transglutaminase were measured in 145 patients with d-IBS, 74 patients with untreated and treated celiac disease, and 57 patients with active IBD. Follow-up antibody levels, stool frequency, and gastrointestinal symptom scores were determined in 41 d-IBS patients (26 women, 15 men; median age, 46 years, range, 30–67 years) who participated in a nonrandomized evaluation of 6 months of gluten-free diet.
Results: Increased celiac disease–associated serum IgG, but not IgA, was found in the majority of patients with treated (55%) as in most patients with untreated celiac disease (97%). In d-IBS patients, celiac disease–associated serum IgG antibodies (37%) and HLA-DQ2 expression (39%) were more frequent than in IBD patients (18% and 23%, respectively). After 6 months of gluten-free diet, stool frequency and gastrointestinal symptom score returned to normal values in 60% of d-IBS patients who were positive and in 12% who were negative for HLA-DQ2 and celiac disease–associated serum IgG; both parameters combined yielded positive and negative predictive values of 56% (95% confidence interval, 30%–80%) and 88% (69%–97%), respectively.
Conclusions: Celiac disease–associated serum IgG and HLA-DQ2 expression can identify likely responders to gluten-free diet in d-IBS patients.
Clinical Gastroenterology and Hepatology
Volume 5, Issue 7, July 2007, Pages 844-850
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Dig Liver Dis. 2007 Sep;39(9):824-8.
Effect of gluten-free diet and co-morbidity of irritable bowel syndrome-type symptoms on health-related quality of life in adult coeliac patients.
Usai P, Manca R, Cuomo R, Lai MA, Boi MF.
Gastroenterology Unit, University of Cagliari, S.S. 554 Bivio per Sestu, 09042 Monserrato (CA), Italy.
BACKGROUND: Both coeliac disease and irritable bowel syndrome show impaired health-related quality of life, however, the impact of irritable bowel syndrome-type symptoms on health-related quality of life in coeliac disease is unclear.
AIM: To evaluate the effect of gluten-free diet adherence and irritable bowel syndrome-type symptoms co-morbidity on health-related quality of life in adult coeliac disease patients.
PATIENTS AND METHODS: A total of 1130 adults were enrolled in the study comprising 1001 controls from the general population and 129 diagnosed coeliac disease patients from the University Clinic in Cagliari. Irritable bowel syndrome-type symptoms and health-related quality of life were assessed using the Rome II and the SF-36 questionnaires, respectively.
RESULTS: Irritable bowel syndrome-type symptoms prevalence in controls was 10.1% (102/1001) and 55% (71/129) in the coeliac disease patients. Irritable bowel syndrome-type symptom controls and coeliac disease patients both presented significantly lower health-related quality of life (p<or=0.05) compared to healthy controls. Strict diet coeliac disease patients, compared to partial diet patients, showed significantly (p<or=0.05) better scores in all domains, except physical functioning, physical-role and bodily pain. The lowest scores were found in partial diet coeliac disease patients with irritable bowel syndrome-type symptoms.
CONCLUSIONS: The present results confirm the burden of irritable bowel syndrome-type symptoms and coeliac disease on health-related quality of life. Moreover, these data show that health-related quality of life in coeliac disease is impaired by poor compliance and by co-morbidity with irritable bowel syndrome-type symptoms.
PMID: 17644056 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov/pubmed/17644056?ordinalpos=18&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum
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Study confirms increase in wheat gluten disorder
Blood samples from '50s show it isn't just improved diagnosis, and researchers wonder if diet is a factor.
By JOSEPHINE MARCOTTY, Star Tribune
A Minnesota study using frozen blood samples taken from Air Force recruits 50 years ago has found that intolerance of wheat gluten, a debilitating digestive condition, is four times more common today than it was in the 1950s.
The findings contradict the prevailing belief that a sharp increase in diagnoses of wheat gluten intolerance has come about because of greater awareness and detection, and raises questions about whether dramatic changes in the American diet have played a role.
"It's become much more common," said Dr. Joseph Murray, the Mayo Clinic gastroenterologist who led the study. No one knows why, he said, but one reason might be rapid changes in eating habits and food processing over the last half century.
"Fifty years is way too fast for human genetics to have changed," Murray said. "Which tells us it has to be a pervasive environmental influence."
Researchers at the Mayo Clinic and the University of Minnesota who conducted the study also found that the recruits who had the undiagnosed digestive disorder, called celiac disease, also had a four-fold increase in the risk of death.
Today an estimated one of 100 people suffer from the inherited disorder, though most of the time people don't know they have it.
The disease occurs in people whose bodies cannot digest gluten, a protein found in wheat, rye and barley. The undigested protein triggers the body's immune system to attack the lining of the small intestine, causing diarrhea, nausea and abdominal pain. Though people live with it for many years, over time it destroys the lining of the small intestine, leading to an inability to absorb nutrients such as iron and calcium. That, in turn, causes serious problems, including anemia, osteoporosis and even infertility.
The only treatment is a gluten-free diet -- no wheat, rye or barley.
Murray said he initiated the study to find out whether the disease is on the rise, and whether it had long-term health consequences if undiagnosed and untreated.
He turned to medical archaeology to find the answers - a treasure-trove of blood samples taken from recruits at the Warren Air Force base in Cheyenne, Wyo., between 1948 and 1954. At the time, strep infections were raging among the recruits, mostly young men on their way to fight in the Korean war. Doctors there drew the samples as part of a study that proved treating the infections with antibiotics would prevent rheumatic fever, a serious heart ailment that can follow strep throat.
One of the doctors in that study took some of the samples with him when he moved to the Cleveland Clinic in Ohio. When he decided to retire two decades ago, he asked Dr. Edward Kaplan, a strep specialist at the University of Minnesota, to become their guardian. The vials were transported in frozen-pizza delivery trucks to Minneapolis, where they reside today.
"Nobody has anything like it," said Kaplan. "There are other collections, but none go back this far."
In 2000 they were used to help resolve an intense debate among researchers over whether hepatitis C infection meant certain death, or whether many people could live with it for years.
Murray used a similar design for the study on celiac disease, published today in the journal Gastroenterology. He tested more than 9,133 samples for the antibodies that proved the recruits had celiac disease; 43, or about one out of 652, had the disease. He then tested blood samples from groups of men from Olmsted County, more than 12,000 in all. In an older group of men, one in 121 tested positive, and in the younger group one in 106 tested positive, an increase of four to four-and-a-half times.
His findings raise questions about why the number of people with the disease has grown so fast. But rates of other immune diseases have also increased a lot. One theory is that modern, clean living, which has resulted in fewer infections, parasites and microbes in our bodies, causes the immune system to turn on healthy tissue instead. Or it might be the modern diet, Murray said.
"The types of food we eat now are different," he said.
http://www.startribune.com/lifestyle/health/49558522.html?elr=KArks:DCiUo3PD:3D_V_qD3L:c7cQKUiD3aPc:_Yyc:aUU
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Review
Am J Gastroenterol 2009; 104:1587–1594;
doi:10.1038/ajg.2009.188;
Between Celiac Disease and Irritable Bowel Syndrome: The "No Man's Land" of Gluten Sensitivity
Elena F Verdu MD, PhD1, David Armstrong MA, MB, BChir1 and Joseph A Murray MD2
1. 1Farncombe Family Digestive Health Research Institute, Department of Medicine, McMaster University, Hamilton, Canada
2. 2Division of Gastroenterology, Mayo Clinic, Rochester, Minnesota, USA
Correspondence: Joseph A. Murray, MD, Division of Gastroenterology and Hepatology, McMaster University, Mayo Clinic, 200 First Street SW, Rochester, Minnesota 55905, Hamilton, Canada.
The repertoire of gastrointestinal (GI) symptoms is finite; however, the etiologies and mechanisms underlying symptom generation and perception are diverse and, in many cases, unknown. This review examines the clinical and experimental evidence exploring the putative relationship between gluten sensitivity (GS) and the generation of GI symptoms. It explores the hypothesis that, in a proportion of patients, GS causes functional bowel disorder (FBD)-like symptoms. We propose a model for investigating and understanding the induction of GI symptoms and dysfunction by gluten in FBD and organic disease. We hypothesize that, even in the absence of fully developed celiac disease, gluten can induce symptoms similar to FBD. We discuss the hypothesis that GS and post-infectious irritable bowel syndrome (IBS) provide two triggers that can explain at least part of the spectrum that constitutes IBS, further advancing an understanding of the role of mucosal responses to luminal factors in FBDs. We propose that the animal model of GS in human leukocyte antigen (HLA)-DQ8 mice allows investigation of mucosal pathophysiological changes that occur before the onset of full-blown inflammation in a GS host. A better understanding of how gluten can cause symptoms in sensitive individuals will illuminate the interaction between host genotype, diet, and intestinal microbiota in generating one of the most common GI conditions.
http://www.nature.com/ajg/journal/v104/n6/abs/ajg2009188a.html
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Oats may boost nutritional profile of gluten-free diets
By Stephen Daniells, 08-Jan-2010
Adding oats to a gluten-free diet may enhance the nutritional values of the diets, particularly for vitamins and minerals, as well as increasing antioxidant levels, say two studies from Scandinavia.
Kilned or unkilned oats were found to increase levels of vitamin B1, magnesium and zinc during six months of an oat-enriched gluten-free diet, according to results published in the European Journal of Clinical Nutrition.
According to scientists led by Tarja Kemppainen from the University of Kuopio in Finland, gluten-free diets have been shown to be deficient in nutrients in some of the patients. Results from their new study indicate that 100 grams of oats a day may increased intakes of various nutrients in adult celiac patients in remission.
The gluten-free market is growing rapidly. According to a recent report from Packaged Facts, the market has grown at an average annual rate of 28 per cent since 2004, when it was valued at $580m, to reach $1.56bn last year. Packaged Facts estimates that sales will be worth $2.6bn by 2012.
The market researcher said it expected to see a much wider range of gluten-free products on shelves by 2012, and said that this will be driven by companies reformulating existing products for gluten-free acceptability, as well as by releasing new ones.
Care with oats
It should be noted that, although oats do not actually contain gluten there is some concern over their presence in foods since they are commonly contaminated during processing with gluten from wheat, rye or barley, according to Coeliac UK.
Study details
Kemppainen and co-workers recruited 13 men and 18 women with celiac disease in remission and assigned them to receive a gluten-free diet with kilned or unkilned oats. At the end of the study, addition of kilned oats to the diet increased intake of vitamin B1 and magnesium, while the unkilned oats increased intakes of magnesium and zinc, said the researchers.
Antioxidant boost
The results were supported by another study from Scandinavia. Writing in the e-SPEN, the European e-Journal of Clinical Nutrition and Metabolism, Astrid Lovik and her co-workers from Oslo University Hospital report that gluten-free oats allowed people on gluten-free diets to achieve their recommended daily intakes of fibre, as well as increasing levels of the antioxidant bilirubin in coeliac disease patients.
"So far there are no documented clear nutritional advantages of oats in gluten-free diet, except for increased dietary fibre intake," wrote Lovik. "Results from our pilot study of nineteen patients and supportive evidence from a large cohort of patients, suggest increased levels of bilirubin after oats intake.
"To confirm this finding, controlled and randomised studies in oats consuming and oats non-consuming coeliac disease patients have to be performed," they concluded.
The researchers gave 19 people with coeliac disease 50 grams per day of gluten-free rolled oats for 12 weeks. At the end of the study, the gluten levels of only three people were outside of the proposed safe levels. Bilirubin levels were significantly higher following oat consumption.
In a separate experiment with 136 coeliacs and 141 healthy controls in the general population, the researchers noted that bilirubin blood levels were higher amongst oat consumers..
"In healthy subjects, lower serum bilirubin levels are associated with endothelial dysfunction and increased carotid intima-media thickness, while moderately increased serum bilirubin levels are connected to reduced risk for atherosclerosis," wrote the researchers. "Whether serum bilirubin in oats consuming coeliac disease patients is an independent and inversely related predictor of atherosclerosis has yet to be studied," they added.
Source: European Journal of Clinical Nutrition
2010, Volume 64, Pages 62-67, doi:10.1038/ejcn.2009.113
"Nutrient intakes during diets including unkilned and large amounts of oats in celiac disease"
Authors: T.A. Kemppainen, M.T. Heikkinen, M.K. Ristikankare, V-M. Kosma, R.J. Julkunen
e-SPEN, the European e-Journal of Clinical Nutrition and Metabolism
Pages e315-e320
"Oats in a strictly gluten-free diet is associated with decreased gluten intake and increased serum bilirubin"
Authors: A. Lovik, A.U. Gjoen, L. Morkrid, V. Guttormsen, T. Ueland, K.E.A. Lundin
http://www.foodnavigator.com/Science-Nutrition/Oats-may-boost-nutritional-profile-of-gluten-free-diets
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Heather is the Administrator of the IBS Message Boards. She is the author of Eating for IBS and The First Year: IBS, and the CEO of Heather's Tummy Care. Join her IBS Newsletter. Meet Heather on Facebook!
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