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Diabetes and Celiac Disease - By Kemp Randolph
In 1994 I was diagnosed with celiac disease, which led me to create Celiac.com in 1995. I created this site for a single purpose: To help as many people as possible with celiac disease get diagnosed so they can begin to live happy, healthy gluten-free lives. Celiac.com was the first site on the Internet dedicated solely to celiac disease. In 1998 I foundedÂ The Gluten-Free Mall, Your Special Diet Superstore!, and I am the co-author of the book Cereal Killers, and founder and publisher of Journal of Gluten Sensitivity.View all articles by Scott Adams
Of the many immune related disorders linked with the celiac condition, the best established connection is with Type I diabetes (mellitus). Type I diabetes occurs at a rate of about 0.5% in the general population, but at a rate estimated at 5-10% among celiacs. Normally the diabetes is diagnosed first, both because this form of diabetes tends to strike early in life and its diagnosis is certain. No connection has been found with the more common form of diabetes (mellitus= honey , from the sugar laden urine when uncontrolled), Type II which occurs at a rate of 2-2.5% in the general population.
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.
- 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
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