Celiac.com 08/29/2007 - A study that appeared in the August issue of Journal of Clinical Gastroenterology, found that celiac disease and small intestinal bacterial growth both show increased levels of intraepithelial lymphocytes (IELs), especially gammadelta+ IELs. A sharp increase in gammadelta+ IELs has been noted in people with celiac disease, but little is known about the role of this particular class of IELs in other intestinal pathologies.

A team of researchers led by J.M. Remes-Troche set out to assess the levels of IEls, especially of gammadelta+, in the duodenal mucosa biopsies from individuals w/ celiac disease and to compare them with those of patients with small intestinal bacterial overgrowth (SIBO), and irritable bowel syndrome (IBS).

The study team looked at 12 individuals with untreated celiac disease, 8 patients with SIBO, and 10 patients with diarrhea-predominant IBS. All patients were given an upper-endoscopy for mucosal biopsy and jejunal aspirate. Intraepithelial cells were isolated from 2 small bowel biopsies, and labeled with monoclonal antibodies CD103-PE (phycoerythrin), CD3-FITC (fluoresecein isothio-cynate), celiac disease-7R-PE, CD45RO-APC (allophycocyanin), and TcR gammadelta-FITC.

Researchers conducted flow cytometry analysis using a standard FACScan. Total IEL levels and subsequent levels were catalogued as percentages as follows: 16.7 +/- 6% for IBS patients; 25.7 +/- 17% for SIBO patients; and 26 +/- +/- 13% in celiac patients (P=0.2). Patients with SIBO & celiac disease showed significantly higher percentages of gammadelta+ IELs (14.6 +/- 8% and 15.7 +/- 13%) compared to IBS patients (4.1 +/- 2.5%, P<0.05).

The results of the study indicate that gammadelta+ IELs might play a crucial role against intestinal bacterial infections.

Journal of Clinical Gastroenterology. 2007 Aug;41(7):671-676

They looked at data for children genetically at risk for celiac disease, specifically, children who carried HLA-conferred risk of celiac disease who had been monitored frequently since birth. The research team was made up of S. Simell, S. Hoppu, A. Hekkala, T. Simell, M.R. Ståhlberg, M. Viander, H. Yrjänäinen, J. Grönlund, P. Markula, V. Simell, M. Knip, J. Ilonen, H. Hyöty, O. Simell.

The team looked at serum samples from 1,320 children who were genetically at risk for celiac disease. Serum samples taken between 2000 and 2003 were assessed for TGA. Samples testing positive for TGA were evaluated for all five antibodies. Also, all future samples for the given patient were similarly evaluated. Also, positive TGA patients were encouraged to have a duodenal biopsy.

The assessment was completed in August 2004. At that time, the test subjects ranged in age from 1 year to 9.5 years, with a mean age of 4.1 years. In all, 49 children (3.7%) were TGA positive. 26 of these TGA positive children submitted to biopsy. Celiac disease was diagnosed by biopsy in 20 of the 26. Of the 49 children who tested TGA positive, AGA-IgA surfaced at an average age of 2 years (+/- 1.5 over a range of 0.5 to 6.6 years for subjects). Compared to AGA-IgA, TGA, EMA, and ARA all surfaced together about 1 year later (TGA at 3.2 +/- 1.5, 1.0-7.0 yr, P < 0.001).

Key Antibodies Can Vanish Early in Childhood Celiac Disease

Even with ongoing gluten consumption, positive TGA values disappeared in 49%, EMA values disappeared in 49%, ARA values disappeared in 43%, AGA-IgA values disappeared in 41%, and AGA-IgG in 32%.

The research team concluded that there are likely potential triggers for celiac disease that are active before AGA-IgA surfaces, or about 3 months earlier on average than when the TGA-associated antibodies appear.

In a significant number of children, antibodies vanish spontaneously. This indicates that in many cases, conditions allow the regulatory immune phenomena to eliminate incipient celiac disease in genetically at-risk children even when gluten is still significant part of the diet.

Am J Gastroenterol 2007;102:1–10

Celiac.com 06/26/2007 - In a study published recently in the Scandinavian Journal of Gastroenterology, researchers found that celiac patients commonly have high rates of anti-Saccharomyces cerevisiae antibodies (ASCA). A team of researchers recently set out to assess the frequency anti-Saccharomyces cerevisiae antibodies (ASCA) in patients with celiac disease.

The team was made up of Dorsaf Toumi; Amani Manka&IUML;; Ramla Belhadj; Leila Ghedira-Besbes; Moncef Jeddi; and Ibtissem Ghedira. They used ELISA to evaluate blood serum for ASCA, IgG and IgA in 238 patients with celiac disease. The team used 80 non-celiac blood donors as a control group. The 238 study subjects were divided into separate groups as follows: 125 untreated celiac patients; 42 celiac patients following a strict gluten-free diet; and 71 celiac patients who did not follow a gluten-free diet.

Celiac Patients Have Significantly Higher IgG and IgA Antibodies

Compared to the control group, the 125 untreated celiacs showed a markedly higher frequency of ASCA (IgG or IgA). 27.2% for untreated against 3.7% for control (p=10-5). Among the 71 patients who did not follow a gluten-free diet the occurrence of ASCA was significantly higher in adults than in children (60% against 26.1%, p=0.004). In the 238 patient study group as a whole, ASCA was substantially higher in adults than in children. 35.4% adults showed positive results compared to 21.1% children (p=0.01). Of the 238 subjects 19% (p=0.001), both children and adult, were positive for ASCA IgG versus 6.3% (p=0.001) for ASCA IgA.

ASCA IgG More Common Than ASCA IgA

Overall, ASCA IgG was much more common than ASCA IgA. 19% of children and 33% of adults were positive for ASCA IgG compared to 6.3% of children and 12.5% for ASCA IgA. Of the 42 patients who followed a gluten-free diet, all children and 90.5% of adults were negative for ASCA IgG.
Of the 125 patients with untreated celiac, 20% of children were positive (p=0.01), and 34% of adults were positive. Of those 71 patients who did not comply with a gluten-free diet, 60% of adults and 26.1% of children were positive for ASCA.

The results of the study confirm that patients with celiac disease show a high rate of ASCA. There was no statistical difference between celiacs following a gluten-free diet and those without celiac disease.

Scandinavian Journal of Gastroenterology, Volume 42, Issue 7 2007 , pages 821 - 826

Patients Diagnosed in Childhood Might Evolve toward Latency on a Normal Diet

Celiac.com 05/23/2007 - The results of a study recently published in the journal Gut indicate that some people who suffer from celiac disease might not need to remain on a gluten free diet for their entire lives, and that some celiac patients might be able to safely introduce gluten containing foods without suffering a relapse.

Previous Studies Showing Positive Response to Wheat Introduction in Patients with Celiac Disease are Promising, But Incomplete

Several studies have shown that some patients diagnosed with celiac disease in childhood were able to remain on a gluten-containing diet after gluten challenge without suffering a relapse. However, most of these studies included a small number of patients, or followed the patients for only a short period after gluten was reintroduced into their diets.

These previous studies also limited their evaluation largely to assessment of celiac disease serology and histology of duodenal biopsies, and did not attempt to identify what factors might predict the development of tolerance to gluten.

Determining Long-term Response to Gluten Consumption in Celiac Disease Patients

A research team made up of doctors Tamara Matysiak-Budnik (1), Georgia Malamut (1,2), Natacha Patey-Mariaud de Serre (3), Etienne Grosdidier (2), Sylvie Seguier (3), Nicole Brousse (3), Sophie Caillat-Zucman (4), Nadine Cerf-bensussan (1), Jacques Schmitz (5) and Christophe Cellier (1,2), set out to determine whether children diagnosed with celiac disease must follow a gluten free diet for life.

To determine the effects of reintroducing gluten into the diets of celiac patients, the research team set out to monitor the clinical and physical progress of adult celiac patients who had been diagnosed as children, who underwent a gluten challenge, and who were asymptomatic.

The study focused on a specific group of patients, all but two of whom were diagnosed as children and followed until adulthood in the Department of Pediatric Gastroenterology in Necker Hospital and thereafter at the Georges Pompidou European Hospital in Paris; after which, they were entered into a local register of adult celiac patients and were recruited for the study based on two criteria: celiac disease diagnosed in childhood; and adherence to a normal diet.

The patients in the study were from 18 to 65 years old, and had been diagnosed with celiac disease in childhood. The research team recorded data in the following categories: biological parameters of malabsorption; bone mineral density; clinical celiac status; gluten intake; HLA genotype; serological markers of celiac disease; as well as histological and immuno-histochemical parameters in duodenal biopsies.

Results Show 20% Long-term Latency in Celiac Patients who Eat Normal Diet

Of those studied, 61 patients had returned to a normal diet, and were asymptomatic. 48 showed various degrees of villous atrophy (silent celiac disease), and 13 had no detectable atrophy (latent celiac disease) on duodenal biopsies. Compared to those with silent celiac disease, patients with latent celiac disease showed markedly less osteopenia/osteoporosis [1/9 (11%) versus 23/33 (70%), p<0.001)], and lower TcR- + intraepithelial T cell counts (38±20 vs. 55±15, p<0.01).

Patients with latent celiac disease had a lower mean age at the time of their first gluten free diet compared to patients with silent celiac disease (14.4±5 vs 40.1±47 months, p<0.05).

Compared to the seven control patients on a long-term gluten free diet, the latent patients did not differ significantly, except for a higher frequency of celiac disease-specific serum antibodies. However, a follow-up found that two of the patients with latent celiac disease had suffered a clinical and histological relapse.

Results showed that of those patients who remained asymptomatic after the reintroduction of gluten, 20% showed long-term latency.

The study concludes that some patients with celiac disease may not need to remain on a life-long gluten free diet, and that some may indeed be able to safely reintroduce gluten into their diets with no adverse effects. However, the latency patients may experience may be transient, and therefore a regular follow-up is necessary. Also, patients with silent celiac disease should remain on a gluten free diet.

Participating hospitals:
(1) INSERM, U793, Faculté de Médecine René Descartes, IFR94, Paris, France.
(2) AP-HP, H&OCIRC;pital Européen Georges Pompidou, Department of Hepato-Gastroenterology,
Paris, France.
(3) AP-HP, H&OCIRC;pital Necker-Enfants Malades, Department of Pathology, Paris, France.
(4) INSERM, Equipe Avenir, Faculté de Médecine René Descartes, Paris, France.
(5) AP-HP, H&OCIRC;pital Necker-Enfants Malades, Department of Pediatric Gastroenterology, Paris, France.

Gut 2006;13(10).

Comments on this Study by Ron Hoggan

Celiac.com 05/08/2007 - One of the strategies for developing alternative therapies for treating celiac disease centers on the identification of antagonist peptides that might inhibit the abnormal immune response caused by gliadin peptides in celiac disease.

A recent study published in the journal Pediatric Research indicates that a peptide that occurs naturally in durum wheat may protect against the effects of celiac disease by acting as an antagonist against gliadin peptides associated with abnormal immune response.

The study was conducted by a team of Italian researchers made up of Drs. Marco Silano, Rita DiBenedetto, Antonello Trecca, Gioachhino Arrabiato, Fabiana Leonardi, Massimo De Vincenzi.

The research team set out to assess the antagonistic effects of 10mer, a decapeptide (sequence QQPQDAVQPF) from the alcohol–soluble protein portion of durum wheat, and to evaluate its prospects for preventing gliadin peptides from activating celiac peripheral blood lymphocytes.

The team extracted peripheral blood mononuclear cells from children with celiac disease who tested DQ2-positive, and from a healthy control group. These samples were then incubated with the peptic-tryptic digest of bread wheat gliadin (GLP) and peptide 62-75 from [alpha]-gliadin, both alone and separately with 10mer.

PBMC proliferation, release of pro-inflammatory Th1 cytokines interferon-[gamma] and tumor necrosis factor-[alpha], release of immuno-regulatory cytokine IL-10, and analysis of CD25 expression as indexes of lymphocytes activation were performed.

Exposure to wheat gliadin peptide and peptide 62-75 from [alpha] gliadin both showed increased activation of lymphocytes. However, the incubation samples with 10mer showed inhibited lymphocyte action.

The study indicates that naturally occurring peptide 10mer in durum wheat may protect against lymphocyte activity in patients with celiac disease, and that further study and evaluation of these findings is warranted.

Pediatric Research. 61(1):67-71, January 2007.

Celiac.com 05/08/2007 - For people with celiac disease, accurate and comprehensive information on maintaining a healthy, high-level quality of life can be difficult to find. Research is particularly sketchy with respect to factors that have a negative impact on health and quality of life for adults with celiac disease.

Factors that have a negative impact on health and quality of life are often modifiable through changes in diet, or adjustments in treatment. Thus researchers are motivated to identify which celiac patient groups are at risk of being impacted in a negative way, and to determine which adjustments might bring positive results.

In an effort to refine treatment approaches and improve the lives of patients with celiac disease, clinical researchers in Gastroenterology have become increasingly interested in health-related quality of life issues as primary or secondary endpoints in their studies.

A recent study published online in Medscape Today suggests that, in addition to physical and mental co-morbidities, a failure to sustain a gluten-free diet and disappointment with doctor-patient communication are also important factors associated with health-related quality of life concerns in people with celiac disease.

Motivated by inconsistencies in available data, a team of German researchers made up of Drs. W. Häuser, A. Stallmach, W. F. Caspary, and J. Stein, set out to evaluate the various predictors for reduced health-related quality of life in adult patients with celiac disease.

Using logistic regression analysis, the researchers catalogued responses to medical and socio-demographic questionnaires by 1000 adult celiac disease patients who were members of the German Coeliac Society.

The subjects responded to the following three survey questionnaires, which were administered by post:
1) the Short-Form Health Survey (SF-36); 2) the Celiac Disease Questionnaire; 3) the Hospital Anxiety and Depression Scale.

The results showed that physical co-morbidities (ß = -0.41; OR = 0.66, P < 0.001) and mental disorder (ß = 0.88; OR = 2.4, P = 0.03) were associated with a reduced physical summary score of the SF-36 Scale.

Mental disorder (ß = 2.5; OR = 11.9, P < 0.001), physical co-morbidities (ß = -0.26; OR = 0.77, P = 0.004) and younger age at diagnosis (ß = -0.10; OR = 0.91, P = 0.05) predicted a reduced mental summary score of the SF-36 Scale.

Mental disorder (ß = 0.90; OR = 2.5, P = 0.03), non-compliance with gluten-free diet (ß = 0.44; OR = 1.6, P = 0.009), active medical co-morbidities (ß = -0.28; OR = 0.76, P = 0.007) and dissatisfaction with doctor–patient communication (ß = 0.55; OR = 1.7, P = 0.03) were associated with reduced Celiac Disease Questionnaire scores.

In adult patients with celiac disease, the following factors were associated with reduced health-related quality of life: female gender, younger age at diagnosis, newly diagnosed patients, latency of diagnosis, failure to follow a gluten-free diet, anxiety and somatic and psychiatric co-morbidity.

Until this study, attempts to measure health status in patients with celiac disease relied on generic health-related quality of life methods, rather than validated, disease specific instruments, and thus the relative predictive value of these variables had not been fully assessed.

Aliment Pharmacol Ther. 2007;25(5):569-578.

Celiac.com 04/23/2007 - A study published in a recent issue of the journal Gut suggests that wheat gliadin might trigger pathological development in mucosal cells that are already abnormal, but otherwise tolerated, within the intestinal tracts of individuals with celiac disease.

Researchers at the Universita degli Studi di Napoli Federico II in Naples, Italy, led by Dr. Salvatore Auricchio looked at the effects of gliadin peptides on various cell lines and celiac mucosal cells in culture.

More specifically, the study evaluated the effects of gliadin and affiliated toxic peptides such as A-gliadin P31-43 on endocytosis, cell proliferation, apoptosis, cytoskeleton rearrangements, and activation of epidermal growth factor receptor (EGFR).

The researchers report that gliadin peptides induce EGF-like effects across a wide range of cell types. Actin rearrangements and cell proliferation are examples of these effects. Also, they state that gliadin peptides act not as ligands of the EGF receptor, but that they actually inhibit EGFR endocytosis.

According to the research team, these observations of gliadin-induced delay of EGFR endocytosis, along with S-phase entry of epithelial intestinal cells, clearly indicate that EGFR plays a role in celiac disease. Dr. Auricchio proffers that a genetic factor in celiacs may bring about deregulated activity in the endocytotic pathway that is compensated in the absence of gliadin.

The study concludes that wheat gliadin slows receptor deactivation of Epidermal Growth Factor. This may explain how wheat gliadin and related cereal prolamines trigger rapid increase in cell growth and associated disease activity in people with celiac disease.

Gut 2007;56:480-488.

Celiac.com 04/23/2007 - A recent study published in the American Journal of Gastroenterology suggests that individuals afflicted with celiac disease in childhood suffer long-term mortality rates that are three times higher than those of the general population

The study set out to determine the most common celiac symptoms faced by clinicians, and to determine how effective an active case-finding strategy might be in raising the levels of diagnosis.

Researchers led by Dr. Masoud Solaymani-Dodaran of Queens Medical Centre, Nottingham, UK, compared differences in long-term mortality in celiac patients diagnosed as children or adults against long-term mortality rates for the general population.

The results showed that standardized mortality ratios for celiac patients more than 5 years after childhood diagnosis were 3.32, while ratios for those diagnosed as adults were 1.38.

Deaths from accidents, suicide, and violence, malignancies, and cerebrovascular diseases largely accounted for the elevated mortality risk among celiacs diagnosed as children. For those diagnosed as adults, excess mortality rates were largely due to malignant neoplasms.

Researchers said that nature of, and the increase in, mortality rates suffered by children with celiac was both largely unexpected, and surprising, when compared to those of adults.

Noting that celiacs diagnosed as adults faced only a "reassuringly small increase" in long-term mortality rates; rates that are approximately half of those of patients with Crohn's disease, for example.

They contrasted the adult rates to the markedly higher mortality rates faced by celiacs diagnosed as children, which, they said was "difficult to attribute directly to the disease itself."

They concluded that even though the increased risk of mortality for faced by celiacs diagnosed as children was small overall, the excess of deaths from accidents, suicides, and violence, were, nonetheless, a "cause for concern."

American Journal of Gastroenterology. April, 2007; 102:864-870

Stephen Sundlof, director of the FDAs Center for Veterinary Medicine, stated that: The association between the melamine in the kidneys and urine of cats that died and the melamine in the food they consumed is undeniable," though he stopped short of placing blame for the animal deaths conclusively on the melamine-tainted wheat gluten.

Sundlof did go on to say that melamine, in any amount, is not permitted in pet foods sold in the U.S.

Wheat Gluten is Not Part of Your Pet's Natural Diet

These stories invite a deeper consideration about the role that non-tainted wheat gluten may play in chronic illness and degenerative diseases in our beloved cats and dogs.

The simple truth is that cats and dogs are, by nature, primarily meat eaters. Dogs are historically scavengers, whose natural diets, according to a recent study by biologists Ray and Lorna Coppinger, consisted of "bones, pieces of carcass, rotten greens and fruit, fish guts, discarded seeds and grains, animal guts and heads, some discarded human food and wastes"³. In the wild, a dogs diet included only the smallest amounts of grains, while cats are almost totally carnivorous, and subsist in the wild on a diet made up almost exclusively of small rodents. The natural diets of both cats and dogs provide large amounts of animal protein and fats, water, and little in the way of carbohydrates.

Dogs and Cats Should Avoid Grains and Carbohydrates

Most veterinary textbooks agree that both cats and dogs need almost no carbohydrates, yet the so called recommended diet of dry pet foods, which is a major component of most pets diets, contradicts both their natural diets and the veterinary literature. Many of these dry pet foods are high in carbohydrates, low in animal protein and fats, and contain almost no water.

This fact is largely ignored by major pet food producers, which is also noted in the book Canine and Feline Nutrition, which states that "the nutrient content of most commercial foods includes carbohydrates"⁴.

Many pet owners who feed canned, moist food to their cats and dogs do so believing that they are providing much-needed meat and moisture to their animals. This is largely true, but what is also true, as came to light in the recent spate of illnesses and deaths from tainted wet formula pet foods, is that wheat gluten is a significant ingredient in such foods.

The problem is that the digestive systems of dogs and cats have not evolved to digest plant proteins like gluten—they are designed to digest animal protein, and gluten is not the same—and feeding these animals foods that contain gluten can result in many of the same problems that afflict their human counterparts who are sensitive to gluten.

Toxic Effects of Wheat Gluten and Other Proteins in Pets...and Humans

According to veterinarian John B. Symes (Dogtor J), gluten and other proteins that are added to dog and cat foods are causing many of the same diseases that they cause in their human counterparts. Dogs and cats that have suffered and died from consuming tainted pet food belie the fact that even untainted gluten can cause many of these same problems and more. In human celiacs and gluten-sensitive individuals, untainted gluten can induce both chronic and acute kidney failure. This form of kidney failure is typically called an IgA nephropathy, in which antibodies and immune complexes formed against gluten are deposited in the kidneys, which leads to damage and ultimately failure. Again, this can be chronic leading to persistent blood (microscopic) and protein in the urine or it can be acute.

Dr. Symes claims that it is a startling but well-established fact that the lectins of gluten (wheat, barley, rye) dairy products (e.g. casein, lactalbumin) soy, and corn are all capable of inducing serious health issues in those humans who are sensitive to them. He takes this belief even further and states that such foods are actually not healthy for anyone—neither pets nor humans and they just happen to be more harmful to some individuals than others. According to him anyone who consumes or feeds these foods to their pets on a daily basis will encounter resulting health problems—it is only of matter of time.

Dr. Symes believes that the onset of a lectin-related disorder—whether it be rheumatoid arthritis, type-one diabetes, lupus, etc.—is usually preceded by another event such as viral or bacterial infection. Vaccines can act as triggers as well. The result of such secondary events is a sudden influx and attachment of these inflammatory proteins to various cells in the body, ushering in what we often refer to as autoimmune disorders. That term implies an immune system that has gone haywire, attacking the body for no reason. According to him, our immune systems, along with those of our pets, never make that kind of mistake. These conditions happen for certain reasons, and these food proteins are often the cause.

All one needs to do, according to Dr. Symes, is to study celiac disease to see how all of this works and appreciate the health implications that accompany this extremely common condition. That a similar condition does occur in dogs and cats has become painfully obvious during the past seven years that he has been studying the issue. Dr. Symes states: "The Irish Setter is a breed known to suffer from gluten intolerance, but it is clear that gluten is affecting many other breeds of dogs and cats. And why wouldnt it? It is affecting humans and we have had millennia to adapt to eating wheat. Our pets have only been eating wheat-based pet foods for about 20 years now."

According to Dr. Symes it does not matter whether they ever tell us that tainted wheat gluten caused kidney failure, or that it be proven responsible in these pet deaths. The fact is that wheat gluten, tainted or not, can, and does cause and/or contribute to these conditions. Thus, according to Dr. Symes, gluten should never end up in pet foods.

To illustrate his theory Dr. Symes points out that the average American dog lives 12 years—13 for cats, when their wild counterparts, eating a natural diet, can live to be nearly thirty and t forty years respectively. For the cause, we need look no further than what we put in their bowls. A European study shows that pets fed with table scraps lived an average of three years longer than those fed commercial diets alone. Why? The answer, at least in part, is that highly processed foods cannot possibly contain all of the essential nutrients found in fresh meats, fruits and vegetables.

Reasons for Your Pets to Avoid Gluten

For all of the reasons stated, its probably a good practice to keep wheat gluten and carbohydrates away from you pet in favor of a "natural" diet rich in animal protein and fats and low in (or free of) carbohydrates. As specialty foods can be expensive, a list of readily available pet foods that are free of wheat gluten is provided below.

Avoid senior, light and diet foods, as they contain increased fiber and carbohydrates and reduced protein and fat, compared to adult maintenance diets. This is the opposite of what they really need, and this food has no scientific foundation. Older and overweight pets usually respond well to increased protein and fats gained through a diet rich in meat, not grains.
Another benefit of this approach is that many dogs on the dangerous non-steroidal and steroid drugs so commonly prescribed for dogs may see marked improvements in their conditions and, in fact, may no longer need such drugs, which tend to shorten dogs lives. Many owners who feed their pets fewer grains see less inflammation.

Top 10 Pet Foods that are Free of Gluten and Other Potentially Harmful Proteins

The following pet foods are recommended by John B. Symes, D.M.V., and according to him, none are ideal, but each is gluten-free, wheat-free, barley-free, dairy-free and soy-free and can produce miraculous results in treating chronic diseases that are now found in many pets:

• IVD/Royal Canin - L.I.D.s (potato-based diets)
• Nutro Natural Choice Lamb and Rice
• NaturalLife Lambaderm
• Canidae and Felidae- Dog and cat foods
• Dick Van Patten Natural Balance Duck and Potato, Venison and Brown Rice, and Sweet Potato and Fish Formulas
• Solid Gold Barking at the Moon
• Natura California Naturals
• Canine Caviar Lamb & Pearl Millet and Chicken & Pearl Millet formulas
• Eagle Pack Holistic Select®Duck Meal & Oatmeal and Lamb Meal & Rice Formulas
• Eukanuba Response KO and FP

Resources:

• Your Whole Pet - Bigger than you think: The story behind the pet food recall (http://www.sfgate.com/cgi-bin/article.cgi?f=/g/a/2007/04/03/petscol.DTL&feed=rss.news)
• Coppinger, Ray and Lorna, Dogs: A Startling New Understanding of Canine Origin, Behavior & Evolution, Scribner, 2001. 59 -- 78.
• Case: Cary, and Hirakawa, Canine and Feline Nutrition, Mosby, 1995. 93.
• Morris, Mark, Lewis, Lone and Hand, Michael, Small Animal Clinical Nutrition III, Mark Morris Associates, 1990. 1-11.
• Burger, I., Ed. The Waltham Book of Companion Animal Nutrition, Pergamon 1995. 26-27: 10.
• Symes, D.M.V., Dr. John B. (Dogtor J) www.dogtorj.net

Celiac.com 03/26/2007 - According to a recent Norwegian research report, the adverse immune response to gluten may be tied to a specific set of dendrite cells in the small intestine.

A team led by Dr. Melinda Raki set out to compare the antigen-presenting cells in the small intestine of patients with celiac disease versus those from normal individuals.

The study used multiple duodenal biopsy specimens from 14 patients with untreated celiac disease, 6 with treated celiac disease and 4 controls.

Antigen presenting cells are so termed because they present gluten to the T-cells, which then contribute to the inflammation that damages the villi in the intestinal lining of those with celiac disease.

Researcher found that in the normal duodenal mucosa, about 20% of the HLA-DQ2 molecules associated with celiac disease were Cd11c+ dendritic cells. These dendritic cells accrued in the celiac lesions of the untreated celiac subjects.

When these CD11c+ cells were removed from the biopsy samples, they provoked an adverse gluten reaction in the T-cells.

The study indicates that a greater knowledge of antigen-presenting cells will yield a more complete understanding of the dynamics of celiac disease, the means by which inflammation occurs, and the means by which it can be controlled or avoided altogether.

Gastroenterology 2006;131:428-438.

The study was motivated by the following two hypotheses:

• Celiac patients with Helicobacter pylori might present different clinicopathological profiles from those celiacs without H.pylori.
• Celiac patients with Helicobacter pylori might show different histopathological responses to a gluten-free diet than those celiacs without H.pylori.

The research team compared the duodenal and gastric biopsies of 80 adults who had histologically and serologically confirmed celiac disease. The biopsies were taken both before and after patients had adhered to a gluten-free diet for 12 to 18 months.

The team classified and scored gastritis using the Updated Sydney System. They classified duodenal biopsies using both the Marsh-Oberhuber and a simplified classification developed by the team.

Three test subjects who were positive for Helicobacter pylori, and 12 who were negative (a total of 15 test subjects), presented with lymphocytic gastritis.

Overall, a greater proportion of Helicobacter pylori-negative patients had severe villous atrophy (p

Regardless of their initial Helicobacter pylori status, all subjects showed marked improvement of duodenal aspects following a gluten-free diet (p

With the exception of the intraepithelial lymphocytes (IEL), which returned to normal in two Helicobacter pylori-positive patients, and in ten Helicobacter pylori-positive patients, gastric variables remained unchanged.

The study concludes that Helicobacter pylori gastritis is not related to the clinical features of celiac disease, and that a gluten-free diet is equally effective for both groups.

The study also notes that the inflammatory and structural changes to the mucosal architecture that are associated with celiac disease might eclipse some of the signs of lymphocytosis induced by Helicobacter pylori gastric infection.

The study also further documents the pathogenic connections between celiac disease and lymphocytic gastritis.

Am J Gastroenterol. 2006;101(8):1880-1885.

Celiac.com 10/30/2006 - Two recent scientific publications have now shown that a rotavirus protein may be linked to celiac disease through a molecular mimicry mechanism and that the risk of developing celiac disease appears to increase in children in relation to the number of rotavirus infections. What does this mean? Does rotavirus cause celiac disease?

Research has not yet determined the exact role of rotavirus in celiac disease. Researchers found, in active celiac disease, a subset of anti-tTG IgA antibodies recognize the rotavirus protein, VP-7. This means, in celiacs, that the immune system appears to respond to the rotavirus protein the same as it would to a gluten peptide. Hence, a rotavirus infection might, in part, look just like a large dose of ingested gluten in individuals predisposed to celiac disease.

In the study, children genetically susceptible to celiac disease seemed to develop celiac disease in greater numbers after experiencing rotavirus infections than did those children who did not have rotavirus infections. Note that children NOT experiencing a rotavirus infection STILL developed celiac disease. Hence, some OTHER mechanism must be the actual CAUSE of celiac disease, NOT rotavirus. The fact is, the study does NOT show whether the children having rotavirus infections would have eventually developed celiac disease if they were NOT infected with rotavirus (and no study would be able to do so.) The study followed the children from infancy. The study needs to follow the children for many more years to see if the risk rates of children developing celiac disease who experience or do not experience rotavirus infections eventually match. This would eliminate rotavirus as a significant risk factor.

Think of it this way. If instead of experiencing rotavirus infection, some children were fed large quantities of gluten and some children were fed small amounts of gluten, wouldnt it be expected that children fed MORE gluten would be more likely to develop celiac disease SOONER than the children receiving LESS gluten? Now, due to molecular mimicry, think of a rotavirus infection as being a large daily feeding of gluten. Hence, children experiencing rotavirus infections would be more likely to develop celiac disease SOONER than those children who are uninfected. Eventually, ALL children who would have developed celiac disease, sooner or later, would develop the disease.

A Open Original Shared Link. Now a new study of rotavirus antibodies in 1,931 children carrying HLA alleles for celiac disease in the Denver metropolitan area seems to show that the risk of developing celiac disease increases as the frequency of rotavirus infection increases. The study followed children from infancy, taking blood samples at 9, 15, and 24 months and annually, thereafter. 54 children developed celiac disease at a median age of 4.4 years. The study found "Frequent rotavirus infections predicted a higher risk of celiac disease autoimmunity (compared with zero infections, rate ratio 1.94, 95% confidence interval [CI] 0.39-9.56, for one infection and rate ratio 3.76, 95% CI 0.76-18.7, for 2 or more infections, rate ratio for trend per increase in number of infections = 1.94, 95% CI 1.04-3.61, p= 0.037)."

Could rotavirus infection as an adult trigger celiac disease? Not likely. Though symptoms and diagnosis of celiac disease may come late in life, it has been shown celiac disease begins in early childhood. The prevalence of celiac disease in studies of children is the same as the prevalence of celiac disease in adults and does not increase with age.

New Study:
Am J Gastroenterol. 2006 Oct;101(10):2333-40.
Rotavirus infection frequency and risk of celiac disease autoimmunity in early childhood: a longitudinal study.
Stene LC, Honeyman MC, Hoffenberg EJ, Haas JE, Sokol RJ, Emery L, Taki I, Norris JM, Erlich HA, Eisenbarth
GS, Rewers M.
Barbara Davis Center for Childhood Diabetes, University of Colorado School of Medicine, Aurora, Colorado.

Previous study:
PLoS Medicine Volume 3, Issue 9, SEPTEMBER 2006
In Celiac Disease, a Subset of Autoantibodies against Transglutaminase Binds Toll-Like Receptor 4 and Induces Activation of Monocytes
Giovanna Zanoni, Riccardo Navone, Claudio Lunardi, Giuseppe Tridente, Caterina Bason, Simona Sivori, Ruggero Beri, Marzia Dolcino, Enrico Valletta, Roberto Corrocher, Antonio Puccetti