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Re: Heidi-- a-gliaden and T1 Diabetes

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>Heidi,

>

>If you save your links and whatnot in an organized fashion, could you post a

>compilation of resources connecting wheat to T1 Diabetes? I'd like to provide

>them to my A & P professor. All of it is good, but I have particular interest

>in the possibility of diabetes developing gestationally from a mother's

>consumption of wheat, if any such research has been done.

>

>Thanks!

>Chris

Most of what I've read has to do with rats, and one interesting thing to do with

people.

About 10% of T1 diabetic kids seem to react to gluten (and removing the gluten

causes

them to stop making the antibodies that lead to diabetes) but that doesn't say

what the OTHER 90% are reacting to. Might be casein or something else. But the

studies seem to indicate it is from REALLY EARLY consumption of the allergen,

not in utero. Anyway, here is what I've saved (not too much, I don't save much)

I like this one (about halfway down):

Prior studies have suggested that the presence of organ-specific

autoantibodies in patients with celiac disease is " related to the

presence of a second autoimmune disease. " However, the fact that serum

organ-specific autoantibodies tended to disappear in the current study

when patients were placed on a gluten-free diet supports the position

that these antibodies are at least partly gluten-dependent.

------------------------------------

http://www.lef.org/newsarchive/disease/2002/02/02/23769/99999734-0490-KEYWORD.Mi\

ssing.html

\\

------------------------------------

>

>CELIAC DISEASE

>Organ-Specific Autoantibodies Linked to Dietary Gluten in Celiac Disease

>Patients

>WESTPORT, Sep 07 (Reuters Health) - Patients with celiac disease have

>high levels of diabetes- and thyroid-related autoantibodies that

> " disappear " when the patients are placed on a gluten-free diet.

> The finding confirms the high prevalence of organ-specific

>autoantibodies in patients with celiac disease, and supports the theory

>that these antibodies are gluten-dependent, Dr. Alessandro Ventura, of

>the Universita di Trieste, Italy, and colleagues say in the August issue

>of the Journal of Pediatrics.

> The investigators tested 90 children with celiac disease for serum

>antibodies to islet cells, glutamic acid decarboxylase, insulin, and

>thyroperoxidase. The overall prevalence of diabetes- and thyroid-related

>autoantibodies was 11.1% and 14.4%, respectively.

> Prior studies have suggested that the presence of organ-specific

>autoantibodies in patients with celiac disease is " related to the

>presence of a second autoimmune disease. " However, the fact that serum

>organ-specific autoantibodies tended to disappear in the current study

>when patients were placed on a gluten-free diet supports the position

>that these antibodies are at least partly gluten-dependent.

> " A gluten-free diet started early may prevent the other autoimmune

>diseases frequently associated with celiac disease, " Dr. Ventura and

>colleagues hypothesize. However, further studies will be needed to

>determine the clinical significance of the organ-specific autoantibodies

>in these patients and to confirm this hypothesis.

>J Pediatr 2000;137:263-265.

>

>Information from Shomon:

>

>CELIAC/AUTOIMMUNE THYROID DISEASE CONNECTION: A CURE FOR AUTOIMMUNE

>THYROID PROBLEMS?

>

>The medical journal Digestive Diseases and Sciences has recently reported

>that a significant number of people who have autoimmune thyroid disease

>also have a condition known as celiac disease. Celiac disease causes the

>intestines to react abnormally to a substance called gluten. Gluten is a

>protein found in wheat, rye, barley, oats, spelt, kamut, and other

>related grains. Celiac disease is also sometimes called celiac sprue,

>sprue, or gluten intolerance. If you have celiac disease, your body may

>have difficulty absorbing nutrients from foods, leaving you malnourished,

>or deficient in key nutrients and vitamins. Celiac disease symptoms

>include various intestinal difficulties, recurring abdominal bloating and

>pain, nausea, gas, diarrhea, constipation, and other

>problems. The key news out of this research for thyroid patients is that

>researchers found that organ-specific autoantibodies (i.e., thyroid

>antibodies) can disappear after 3 to 6 months of a gluten-free diet.

>Don't rush right out and start on a gluten-free diet, however. You should

>have a blood test while eating your *regular* diet, and if you are

>positive, THEN go on the gluten-free diet to confirm the test results and

>diagnosis. For the percentage of people with autoimmune hypothyroidism

>who have celiac disease, diagnosis and a gluten-free diet may represent a

>permanent cure for their hypothyroidism. A detailed article, along with

>references and more information on celiac disease and the gluten-free

>diet, is located in an article at my website.

>

>http://thyroid.about.com/library/weekly/aa040700a.htm

>

>In persons with celiac disease, ingestion of gluten increases prolactin

>production. Scand J Gastroenterol Suppl 1998;228:122-9

>

>Coeliac disease: always something to discover.

>Varkonyi A, Boda M, Endreffy E, Nemeth I, Timar E

>Dept. of Paediatrics, Albert Szent-Gyorgyi Medical University, Szeged,

>Hungary.

>

>The authors present more than 20 years' experience with coeliac disease,

>with a summary of their published studies. Hair shaft characteristics

>were determined by scanning electron microscopy. Hair diameter was

>significantly lower and cuticular erosion scores higher in those who were

>not on gluten-free diets as compared to controls, showing a tendency

>towards normal values following start of gluten-free diets.

>Proton-induced X-ray emission showed significantly lower zinc content of

>the hair shaft in the group with acute coeliac disease and after a

>short-term diet, which approached the normal range only after a year-long

>diet. The serum prolactin levels in healthy controls and in coeliac

>patients on the diet were within normal limits, whereas in children with

>coeliac disease taking gluten in their meals, a significant

>hyperprolactinaemia was found. The erythrocyte glutathione content of

>coeliac children was elevated, and the glutathione disulfide level was

>significantly decreased, as compared to values in normal controls. The

>erythrocyte glutathione disulfide level and glutathione

>disulfide/erythrocyte glutathione ratio in coeliac children also differed

>from those in children with iron deficiency. With genotyping, the

>DQB1*0201/2 (p < 0.00001) and DR3 (p < 0.00001), DR7 (p < 0.01) alleles

>showed significant positive association with the disease.

>CELIAC DISEASE AND VITAMIN D

From the Nutrition Almanac (4th Ed. pg. 83): " Celiac disease is

>indirectly related to a vitamin D deficiency resulting from structural

>damage and unabsorbed fats and calcium salts and vitamin D that are

>flushed out in the stool. "

> Organ-Specific Autoantibodies Linked to Dietary Gluten in Celiac

Disease

>Patients

>WESTPORT, Sep 07, 2000 (Reuters Health) - Patients with celiac disease

>have high levels of diabetes- and thyroid-related autoantibodies that

> " disappear " when the patients are placed on a gluten-free diet.

> The finding confirms the high prevalence of organ-specific

>autoantibodies in patients with celiac disease, and supports the theory

>that these antibodies are gluten-dependent, Dr. Alessandro Ventura, of

>the Universita di Trieste, Italy, and colleagues say in the August issue

>of the Journal of Pediatrics.

> The investigators tested 90 children with celiac disease for serum

>antibodies to islet cells, glutamic acid decarboxylase, insulin, and

>thyroperoxidase. The overall prevalence of diabetes- and thyroid-related

>autoantibodies was 11.1% and 14.4%, respectively.

> Prior studies have suggested that the presence of organ-specific

>autoantibodies in patients with celiac disease is " related to the

>presence of a second autoimmune disease. " However, the fact that serum

>organ-specific autoantibodies tended to disappear in the current study

>when patients were placed on a gluten-free diet supports the position

>that these antibodies are at least partly gluten-dependent.

> " A gluten-free diet started early may prevent the other autoimmune

>diseases frequently associated with celiac disease, " Dr. Ventura and

>colleagues hypothesize. However, further studies will be needed to

>determine the clinical significance of the organ-specific autoantibodies

>in these patients and to confirm this hypothesis.

>J Pediatr 2000;137:263-265.

>------------------------

There is an interesting article published the Oct 1st issue of Journal of

the American Medical Association regarding the introduction of cereal to

infants. Their focus is diabetes but there has been discussion of the same

issue related to CD.

The full text is of the article is available free at:

Timing of Initial Cereal Exposure in Infancy and Risk of Islet Autoimmunity

Jill M. Norris, Barriga, anna Klingensmith,

Hoffman, S. Eisenbarth, Henry A. Erlich, and n Rewers

JAMA 2003;290 1713-1720

http://jama.ama-assn.org/cgi/content/abstract/290/13/1713?etoc

-----------------------------

There was an interesting piece this morning on The Early Show about the

timing of the introduction of cereals and the development of type I

diabetes in at-risk children. Hannah Storm inteviewed Dr. Senay who

reported on the new paper in JAMA that is available free

at: http://jama.ama-assn.org/cgi/content/full/290/13/1713. A story and

the video can be viewed at:

http://www.cbsnews.com/stories/2003/09/30/earlyshow/contributors/emilysenay/main\

575958.shtml

-------------------------------

This is from Pediatrics, Vol. 109, No. 5, 5/02, " Diabetes and CD are both

autoimmune disorders, sharing the same high-risk HLA DQ2 genotype. One

third of type 1 diabetes patients with the CD-associated HLA DQ2 genotype

tested serologically positive for CD compared with <2% of patients lacking

DQ2. Other autoimmune diseases associated with CD and type 1 diabetes

include autoimmune thyroiditis, pernicious anemia, Sjogren syndrome,

's disease, alopecia areata, and rheumatoid arthritis. The reasons

for these associations may be that CD and these other disorders share a

similar autoimmune pathogenic mechanism, or that the same gene is

responsible for a proportion of these disorders. It is possible that

chronic lymphocyte stimulation in the intestine in CD could result in an

increase in autoantibody production and therefore stimulate the development

of other autoimmune disorders. Older, untreated CD patients have a higher

prevalence of autoantibodies that younger patients, suggesting that duration

of gluten exposure increases the risk of developing autoantibodies. In some

individuals with rehematoid arthritis and pericarditis, the conditions

disappeared when the patients followed gluten-free diets. Although type 1

diabetes is occasionally identified in previously diagnosed individuals with

CD, in most cases CD antibodies are present at the time of or after

diagnosis of type 1 diabetes. Diabetic autoantibodies generally precede the

onset of clinical diabetes by an average of 3 years. .... There is ,

however, no evidence that treating CD with a gluten-free diet prevents type

1 diabetes. "

The following quote is from the Journal of Pediatrics and Child Health, Vol.

37, Issue 3, Page 218, 6/01:

" Approximately 40% of the genetic susceptibility in Caucasians is explained

by the high risk alleles HLA DR3-DQ2 and HLA DR4-DQ8. The HLA DR2 locus

confers dominant protection. One of these susceptibility alleles HLA DR3-DQ2

(A1*501, B1*0201) has interesting associations. It is associated with type

1 diabetes in congenital rubella, coeliac disease and selective IgA

deficiency; the latter two conditions show high antibodies to cows milk

protein. It has also been associated with higher levels of antibodies to GAD

in at-risk subjects for type 1 diabetes and with increased immunity to cows

milk protein in diabetic patients and controls. It seems possible that this

haplotype and/or other haplotypes predispose an individual to sensitization

to dietary and viral antigens and thereby increase the risk of autoimmune

disease. It is also possible that an alteration in gut mucosal immune

function in genetically susceptible individuals, the gut mucosa being the

major immunoregulatory barrier in the infant, underlies an effect of dietary

or viral proteins on islet autoimmunity in early life. "

-----------------------------

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