Celiac.com 08/08/2002 - A recent study conducted by Dr. David B. Dunger (Addenbrookes Hospital in Cambridge) and colleagues found that children with type 1 diabetes and latent celiac disease who were put on a gluten-free diet showed significant improvement in their metabolic control and growth. The study, which was published in the July issue of Diabetes Care, looked at 11 children with type 1 diabetes and who were diagnosed with celiac disease using anti-gliadin and anti-endomysial antibodies and a biopsy for confirmation.

The group with celiac disease had a significantly lower mean BMI standard deviation score (SDS) than that of a control group of 22 age and sex-matched children with diabetes who did not have celiac disease. The mean height SDS and C-peptide levels in the two groups were similar, while the mean HbA-1-c was lower (better) in the group with celiac disease. After one year on a gluten-free diet the group with celiac disease improved its mean BMI score to that of the control group, and its HbA-1-c score went down (improved), while the control groups HbA-1-c score increased (worsened).

The researchers conclude that more studies are needed to support their findings that a gluten-free diet significantly improves glycemic control in children with type 1 diabetes and celiac disease.

Celiac.com 08/08/2002 - Dr. Anette-G. Ziegler, of the Academic Teaching Hospital Muenchen-Schwabing in Munich, Germany, and colleagues looked at seven first-degree relatives of patients who had type 1 diabetes and were under seven years of age and found that their titers of type 1 diabetes-associated autoantibodies did not improve after one year on a gluten-free diet. At the same time the subjects IgG antibody titers to gliadin were reduced. The researchers conclude that even though studies have shown that a gluten-free diet protects against autoimmune diabetes in animal models, it does not appear to do so in humans, although there is research that shows that it can reduce the frequency of type 1 diabetes in patients with celiac disease. According to the researchers, gluten is not the driving antigen for type 1 diabetes-associated islet autoimmunity.

Pediatrics 2002;109:833-838.

Celiac.com 06/06/2002 - The results of a study conducted by Dr. Graziano Barera and colleagues from the Scientific Institute H San Raffaele, Milan, Italy and published in the May issue of Pediatrics indicate that those with type 1 diabetes are 20 times more likely to also have celiac disease. The researchers collected data on 274 consecutive newly diagnosed type 1 diabetes patients with a mean age of 8.28 years. These patients were studied for the following 6 years. At the time of their diagnosis 10 of them (3.6%) already had celiac disease, and over the next 4 years an additional 12 children tested positive for antiendomysial antibodies, and 7 underwent biopsies and were confirmed to have celiac disease. The overall prevalence of biopsy confirmed celiac disease in the group was 6.2%, and most of the cases were asymptomatic and the children showed no obvious signs of the disease. The researchers conclude that greater than 10% of children with newly-diagnosed type 1 diabetes had developed serological markers for celiac disease within the first 6 years of diagnosis, and they recommend that children in this category be screened annually for celiac disease for several years following their type 1 diabetes diagnosis.

J Pediatr Gastroenterol Nutr 2001;33:462-465.

Celiac.com 11/12/2001 - According to a recent report published in the October issue of the Journal of Pediatric Gastroenterology and Nutrition nearly 5% of US children with juvenile diabetes also have celiac disease. Dr. Steven L. Werlin of the Medical College of Wisconsin in Milwaukee and colleagues tested 218 patients with juvenile diabetes and 117 matched control subjects for the IgA endomysial antibody. Patients with positive results were offered a small bowel biopsy. The patients symptoms were assessed via a parent questionnaire.

Results: Seventeen diabetic patients tested positive for the IgA endomysial antibody, while no positive results were found among control subjects. Fourteen of the 17 patients who tested positive underwent a follow-up small bowel biopsy. Villous atrophy was found in 11 of the patients. Two patients had increased intraepithelial lymphocytes without villous atrophy. Interestingly, more than half of the patients with biopsy-proven celiac disease were asymptomatic.

According to Dr. Werlin, the results indicate that there is an association between asymptomatic celiac disease and juvenile diabetes. According to other research the treatment of the celiac disease in these patients will make the management of their diabetes easier. He further states that treating asymptomatic celiac disease will prevent many of its complications, and recommends that children with diabetes mellitus be screened for possible celiac disease with an antibody test and possible follow-up small bowel biopsy.

In Type I diabetes, the insulin producing cells of the pancreas are destroyed by the immune system, perhaps in overreaction to some kind of infection (The incidence of Type I is highest in the winter.) Normally, insulin is released into the blood for distribution to nearly all cells in the body so glucose can be burned for energy. There are indirect connections with protein and fat metabolism as well which give rise to some of the poisons that build up in the absence of insulin. For glucose, cells have an insulin receptor on the surface: once insulin is bound there, glucose can enter and hence be metabolized.

At diagnosis, the Type I presents itself with a better defined form of malnourishment than celiac disease: hyperglycemia (high blood sugar), weight loss, excessive thirst, excessive urination laden with (un-metabolized) sugar and protein, a fruity smell to the breath and little or no insulin in the blood. Treatment consists of 1-3 subcutaneous injections of insulin a day and control of carbohydrate intake.

The recommended diet for diabetes, long before it was recommended for everyone, consisted of less fat and protein and more carbohydrate. Complex carbohydrates (less quickly metabolized) were recommended to cut down the peak in blood glucose that occurs about two hours after eating. It was, and is, a perfect Jane Brody diet - lots of fresh fruit and vegetables, hence with lots of fiber. The restriction on sugar is indirect: only the total carbohydrates must be controlled. So, if you have some sugar, you must eliminate something else (less carbohydrates probably), and have to put up with less on the plate.

Control of Type I is certainly more of a nuisance than celiac disease, but also one with much better information readily available. Food labels are nearly adequate for controlling carbohydrate intake; the risks of the various long term complications versus average blood glucose are well known; relatively inexpensive, reliable home monitoring of blood glucose is possible to even out the daily peaks and valleys; a longer term blood test reliably measures average blood glucose for sufficient monitoring of longer term risks.

Like celiac disease, Type I diabetes is more common in those of northern European extraction. Like celiac disease, it is highly linked to the so-called HLA markers of the immune system (those marking white blood cells). Celiacs are likely to be positive for both HLA-B8 and HLA-DR3; Type Is are most linked to HLA-B8 and either HLA-DR3 or HLA-DR4. An English study several months ago found that multiple genes were linked to Type I reflecting the fact that parents of a Type I are often diabetes free (the interpretation being that genes were required from both sides). The recent request for celiac siblings for a study of genetic typing intends to duplicate the study which looked for celiac genes.

Reference:

• Gluten Intolerance Group of North America newsletter, V. 13, Issue 2, 1987; New York Times, Sept. 13, 1994, genetics study by Dr. John Todd at Oxford

This article was posted to the Celiac Listserv by Ashton Embry at: Open Original Shared Link in January, 1998:

I became interested in the concept of a Paleolithic Diet in a circuitous way which began with the diagnosis of my oldest son with multiple sclerosis two and a half years ago. I hit the med library soon after I was told that there was no known cause and no effective treatment for MS. My goal was to determine the most likely cause and to then devise a therapy which countered this cause. After reading hundreds of papers and countless more abstracts I reached the conclusion that the main cause of MS is dietary and that dairy, gluten and saturated fat were the three main offending foods. I have summarized this analysis in an essay which is at

The evidence I used to reach my interpretation was a combination of epidemiology, theory (molecular mimicry) and anecdotal data. After the essay was on the web I was contacted by Loren Cordain who pointed out that the foods implicated in MS were recently introduced to the human diet from a genetic point of view and he gave me the references to Boyd Eatons classic papers on Paleolithic Nutrition. From my geological background this concept seemed eminently reasonable so now I had an excellent unifying concept to go along with all the other data. One shortcoming of the evidence was that it was all circumstantial. There was no smoking gun evidence, that is, empirical evidence which demonstrates beyond a reasonable doubt that food proteins really do cause cell-mediated, organ-specific autoimmunity.

As a dutiful civil servant, I made one of my required pilgrimages to Ottawa last week to participate in various mind-numbing meetings. I had a free afternoon so I went out to the Nutrition Research Division of Health Canada where I had the good fortune to meet with Dr Fraser Scott. Dr. Scott has been studying the effect of diet on the development of Type 1 Diabetes in BBdp rats for 20 years. He and co-workers have demonstrated conclusively that Type 1 diabetes can be generated by proteins derived from wheat, soy and milk. So now I had found the smoking gun. Food proteins can indeed induce cell-mediated autoimmunity and not surprisingly the foods which supply the pathogenic proteins are those added to the human diet during the Neolithic. I believe Dr. Scotts work is of great significance for understanding the cause of autoimmune disease and strongly supports Eatons suggestion the diet of our ancestors is the best defense against the diseases of civilization.

References:

• The best reference for Scotts work is: Scott, FW, 1996, Food-induced Type 1 Diabetes in the BB Rat. Diabetes/Metabolism Reviews, v.12, p. 341-359.
• This paper summarizes all his results up to 1996 and contains references to all his earlier work.

The following was written by Joseph A. Murray, MD. (Open Original Shared Link) of the Mayo Clinic Rochester, MN, who is a gastroenterologist who specializes in treating Celiac disease:

Subject: diabetes and celiac disease, gastroparesis

There is a definite incidence of celiac disease in type one diabetes in Caucasians at least. Anywhere from of 3.3% to 10 % of people with type one diabetes will have or develop celiac disease. Any form of diabetes can lead to gastroparesis, usually after many years of diabetes. The symptoms can be similar in many ways, bloating after meals, abdominal pain. Diarrhea is not usually caused by the gastroparesis itself (diabetic diarrhea may occur as part of the nerve damage caused by the long-standing diabetes). I have several patients who have diabetes, gastroparesis and celiac disease. Certainly identifying the celiac disease often makes a big difference to the symptoms.

Mdki M, Hupponen T; Holm K, Hallstrom O, _Gut_ 1995; Feb 3692) pgs. 239-42

In a study of 238 children and adolescents with insulin dependent diabetes mellitus (IDDM), serum IgA reticulin antibody tests were performed once a year. During the initial testing, within one year of the onset of IDDM, 5 children (2%) were positive. During follow up, 11 of the antibody-negative children (5%) became positive; of these 9 were shown to have silent celiac disease by jejunal biopsies. This study suggests that repeated serological screening and biopsies should be considered to detect late developing, clinically silent celiac disease among patients with IDDM.

Author: Rensch MJ; Merenich JA; Lieberman M; Long BD; Davis DR; McNally PR.
Address: Fitzsimons Army Medical Center, Aurora, Colorado, USA.
Source: Ann Intern Med, 124: 6, 1996 Mar 15, 564-7

OBJECTIVE: To determine the prevalence of celiac disease in a cohort of patients with insulin-dependent diabetes mellitus and to describe the clinical characteristics of patients with coexistent disease.

DESIGN: Prospective cohort study.

SETTING: U.S. Army medical center.

PATIENTS: 47 patients with insulin-dependent diabetes mellitus.

MEASUREMENTS: Antiendomysial antibody testing was used to screen for celiac disease. The diagnosis of celiac disease required histologic evidence of villous atrophy and crypt hyperplasia and a positive antiendomysial antibody test result. In patients identified as having coexistent disease, complete blood counts, multiphasic biochemical testing, D-xylose absorption testing, and bone mineral density estimates were done.

RESULTS: 3 of 47 patients with insulin-dependent diabetes mellitus (6.4%; 95% CI, 1.4% to 17.5%) had positive antiendomysial antibody test results and small-bowel biopsy specimens consistent with celiac disease. The 95% CI lies entirely above the estimated prevalence of celiac disease expected in the general U.S. population, which ranges from 0.02% to 0.1%. Mean bone mineral densities were 0.8 and 1.1 SD below age-, ethnicity-, and sex-matched controls in each of the 2 antiendomysial antibody-positive patients tested. Small bowel absorption was abnormal in 1 of the 2 patients tested by D-xylose. Anemia and hypoalbuminemia were not detected in any of the patients with coexistent disease. Only 1 of the 3 patients had symptoms of diarrhea. All patients were at or above their ideal body weights.

CONCLUSIONS: Celiac disease appears to be more common among patients with insulin-dependent diabetes mellitus than in the general U.S. population (p less than 0.001). Two of the three patients with coexistent disease in this study had sub-clinical or latent celiac disease.

Clin Immunol. 2004 Apr;111(1):108-18

According to German researchers, delaying the introduction of wheat and barley proteins could reduce the incidence of diabetes. The scientists looked at mice on diets that were modified according to protein source, and specifically looked at mice pups from female non-obese diabetic mice. Mice on lifelong wheat-free and barley-free diets (their protein source was poultry) had significantly reduced levels of diabetes (45% by age 32 weeks vs. 88% in control mice), and when they did develop diabetes, its onset was delayed. Interestingly the development of diabetes in these mice was not fully restored after adding wheat and barley proteins to their diets (58%). Further, insulin autoantibodies and insulitis scores were both reduced in the wheat and barley-free mice, and their intra-pancreatic IL-4 mRNA levels were increased. The researchers conclude: "These data support a link between dietary wheat and barley proteins and the development of autoimmune diabetes."