[Research] Wheat an Diabetes Link

[RobinN]

We know that food -- specifically too much of it and the resulting weight gain -- causes type 2 diabetes. But could what we eat be a cause of type 1 diabetes? Perhaps, says a new study that has linked wheat consumption to development of type 1 diabetes in young people (generally age 40 and younger), in a finding that has surprised many doctors and scientists. This is research that Daily Health News contributing editor, Andrew L. Rubman, ND, says is "quite amazing and hugely important."

Unlike the more common type 2, type 1 diabetes is a progressive autoimmune disorder that people develop early in life. Some cases have clear genetic roots, but scientists have believed that environmental factors could also play a role -- including, possibly, something in the diet. This small study from the University of Ottawa demonstrates that one factor may be wheat consumption.

WHEAT AND DIABETES LINK

The study included 42 men and women, mostly young adults, with type 1 diabetes and a control group of 22 similar young people who did not have diabetes or any other known autoimmune disease. Researchers wanted to see how the immune systems in those with diabetes would respond to wheat.

What they learned: Twenty of the 42 diabetes patients were "high responders" to wheat, which was demonstrated by heightened immune system activity. According to the researchers, this response was found at a "significantly higher" rate than in the control group. Also, nearly all patients in this group carried a gene known to increase risk of diabetes.

WHEAT AND WHAT ELSE?

Wheat cannot be said to actually have caused the onset of diabetes in these patients, Dr. Rubman said, but the study does make a case that wheat consumption (specifically gluten found in wheat, rye and barley) could play a role in turning the genetic diabetes switch to "on" for those who carry the risk gene. Other factors may be involved too, he noted, while affirming that this study provides an early seed of knowledge that may someday help people avoid diabetes onset, or at the very least reduce the distress it causes. While there is more to learn, it is a healthy habit for all, especially children, to limit wheat consumption, rotating it with assorted other grains in order to minimize its impact on the body.

Dr. Rubman says that gluten avoidance might prove useful for people who already have type 1 diabetes because it may reduce the impact of the disease. If you have this type of diabetes, try a gluten-free diet for four to six months to see if symptom severity and blood sugar control improve. If the answer is yes, Dr. Rubman advises staying gluten-free for life.

Source(s):

Andrew L. Rubman, ND, medical director, Southbury Clinic for Traditional Medicines, Southbury, Connecticut. www.SouthburyClinic.com.

Daily Health News

[Cint]

My Type 1 diabetes was brought on as an adult by a medication, but read on.......

Diet, Gut, and Type 1 Diabetes: Role of Wheat-Derived Peptides?

by Mikael Knip

The role of the gut and gut-associated lymphoid tissue in the development of type 1 diabetes has come into the research focus over the last 20 years. Accumulated evidence suggests that the gut is involved in the pathogenesis of this immune-mediated disease, and there seem to be several mechanisms by which such an effect may be mediated (1). Decreased microbial diversity in the gut, increased intestinal permeability, local inflammation in the gastrointestinal tract, and abnormal mucosal immune responses all may contribute to the appearance of β-cell autoimmunity and further progression to overt type 1 diabetes. The intestinal mucosa comprises the largest surface area in the body, and the gut-associated lymphoid tissue represents the most extensive immune organ. The gut plays accordingly a crucial role in the interaction between the host and the environment. Given that type 1 diabetes is the unfortunate consequence of the combined effects of the individual genetic setup and exogenous and host-related factors, it is not surprising that the gut might be involved in the process leading to clinical disease.

In this issue of Diabetes, Mojibian et al. (2) report that approximately half of the patients with type 1 diabetes, whom they studied, had a proliferative T-cell response to dietary wheat polypeptides and that the cytokine profile of the response was predominantly proinflammatory. A positive T-cell response to wheat polypeptides was associated with the HLA DR4-DQ8 haplotype but surprisingly not with the HLA DR3-DQ2 haplotype, which confers strong susceptibility to celiac disease. The investigators interpret their observations as reflecting a diabetes-related inflammatory state in the gut immune system associated with defective oral tolerance and a possible gut barrier dysfunction (Fig. 1). Accordingly, these observations add to the accumulating concept that the gut is an active player in the diabetes disease process.

Proposed pathway for a wheat-induced intestinal inflammation in patients with type 1 diabetes. Wheat polypeptides pass through the apical junction system from the gut lumen to the mucosa and are presented to T-cells by dendritic cells (DCs) in an HLA DR-restricted manner. The activated T-cells stimulate T-helper type 1 (Th1) cells to produce γ-interferon (INF-γ) and tumor necrosis factor (TNF), Th2 cells to secrete IL-4, and Th17 cells to secrete IL-17A. This cytokine cascade results in local inflammation.

The findings of Mojibian et al. also raise a series of questions. Are the observed T-cell responses to wheat polypeptides present in subjects with preclinical type 1 diabetes? The mean duration of clinical diabetes was 11.2 years in the 42 patients included in the present study. Accordingly, one cannot exclude the possibility that the observed T-cell responses to wheat polypeptides may reflect hyperglycemia-induced changes in the intestinal barrier function. No data were provided on glycemic control in the patients studied nor any comparison on the metabolic control between the patients with a positive T-cell response and those lacking such a response. It would be important to assess T-cell responses to wheat polypeptides in subjects with preclinical type 1 diabetes in order to exclude the possibility that the responses are secondary to the disease condition.

Another issue is why T-cell responses to wheat polypeptides could be seen in only approximately half of the patients. Would that indicate that the other half have developed clinical type 1 diabetes without any intestinal involvement? It is intriguing that other studies focusing on various aspects of the gastrointestinal system have also reported abnormalities in ∼20–50% of the patients analyzed. Westerholm-Ormio et al. (3) found enhanced expression of HLA-DR and -DP, intracellular adhesion molecule-1, α4β7-integrin, interleukin (IL)-4, IL-1α, and γ-interferon in small intestinal biopsy samples from ∼20–30% of children with type 1 diabetes, and they interpreted these findings as signs of intestinal inflammation. Auricchio et al. (4) observed higher density of intraepithelial CD3+ and of γ/δ T-cells and lamina propria CD25+ T-cells reflecting the activation of intestinal immunity in ∼50% of the patients with type 1 diabetes. Sapone et al. (5) measured elevated serum levels of zonulin, implicated as one of the tight junction proteins, in 42% of patients affected by type 1 diabetes. Taken together, these observations imply that only a proportion of patients with type 1 diabetes do have signs of intestinal inflammation and increased permeability.

Although additional work is needed to verify that the observed phenomena are primary and present already in subjects with preclinical type 1 diabetes, these observations add to the growing evidence that dietary components may be involved in the disease process resulting in clinical type 1 diabetes by intestinal pathways. These may include effects on gut microbiota, intestinal permeability, and gut immune function as recently discussed by Vaarala et al.

© 2009 by the American Diabetes Association.