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To the Essay List * To the Main Gluten Page * To the Symptoms List *

“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.” [1]

News reported by Celiac.com: Research into the relationship between

diabetes and gluten intolerance has yeilded “the first successful result in
preventing the autoimmune process characteristic of development of Type 1
Diabetes”! [2] Please see commentary under the Type 1 Diabetes heading
below.

Diabetes is another one of those cases where an understanding of gluten intolerance needs to
cross medical disciplines. Endocrinologists noticed that many of their patients had a common
condition that they called “diabetic diarrhea”. Elsewhere, enterologists notice that too many of
their celiac patients had diabetes. But, diabetic diarrhea couldn’t be Celiac Disease, right?
Diabetes is common and everybody knew Celiac Disease was rare, right?

Some might argue that we know the cause of diabetes, i.e., diabetes is genetic. Ah, but that is
really a pattern or association, not a cause – we don’t yet know how the genes associated with
Type 1 Diabetes relate to the condition. But we do know that the gluten intolerance that
commonly underlies diabetes is also genetic. In this case, we now know the genes. We know
how the genes relate to the gliadin reaction. Now we need to know how the gliadin reaction
relates to the autoimmune attack of the pancreas.

A symptom once called Diabetic Diarrhea has turned out to be mostly Celiac diarrhea; how
much will the symptoms called Diabetic Seizures and Diabetic Neuropathy turn out to be
gluten seizures and gluten neuropathy?

The following paragraphs are notes about what is known about how gluten intolerance is
related to diabetes.

Contents:
Type 1 Diabetes / Insulin Dependent Diabetes Mellitus
Brittleness of Diabetes Control
Hypoglycemia
Type 2 Diabetes
Clippings: Diabetes and Gluten

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Lots of abstracts and links: Type 1 Diabetes, Autoimmune Thyroid Disease and Gluten on
BrainTalkCommunities’ site.

Type 1 Diabetes / Insulin Dependent Diabetes Mellitus

A treatment of diabetes was predicted by studying the association between gluten and
diabetes. Celiac.com reports that excess of a human protein Zonulin present in Celiac Disease
allows gluten and other allergens to pass through the intestines into the body, this process can
trigger allergic and autoimmune reactions. Celiac.com also reports that this knowledge has
produced a drug treatment that prevents the onset of the autoimmune destruction of pancreatic
beta cells and the onset of Type 1 Diabetes in 2/3 of diabetic prone rats. Whether or not this
discovery eventually leads to a more or less safe drug that prevents either T1DM or gluten
intolerance, today this discovery bolsters the idea that people at risk for T1DM are also at
high risk for gluten intolerance and reinforces the application of the Gluten Free Diet for
possible treatment and prevention[3] of certain chronic diseases.

Previously known:

· Type 1 Diabetes results from autoimmune attack on the pancreas.

· Recent experiments suggest that stopping the autoimmune attack on the islet cells in the
pancreas may reduce or reverse some cases of Type 1 Diabetes.

· Type 1 Diabetes is associated with blood antibodies to wheat protein. [4]

· Autoimmune conditions are strongly associated with gliadin sensitivity. (Refer to “The
Basics…”)

· The earlier children develop Type 1 Diabetes, the more likely they develop full-blown
classic Celiac Disease.[5] (Thanks to Celiac.com)

· Studies of infants of Type 1 Diabetic parents demonstrate that feeding gluten to those
infants greatly increases the development of autoimmune attack on the infant pancreas
(by factors of 5 to 7 times greater risk)[6].

· Children with Type 1 Diabetes are 50 times more likely to have classic Celiac
Disease[7].

Click on this text for a collection of abstracts of medical studies on the links between Type
1 Diabetes and Celiac Disease.

See also Clippings: Diabetes and Gluten

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Brittleness of Diabetes Control

The Gluten Free Diet is reported to make diabetes easier to control[8].

Undiagnosed Celiac Disease is reported to underlie difficult to control cases of

diabetes[9].

"Diabetes is usually diagnosed before celiac disease, and diabetic control is difficult with
repeated episodes of hypoglycemia[…]. Diabetic control improves with institution of a
gluten-free diet, and insulin requirements increase"[10].

Hypoglycemia

“It has been observed that patients with GSE have hypoglycemic episodes and reduced
insulin needs before diagnosis, presumably because of malabsorption.- In a detailed study
of growth parameters, blood glucose control, and dietary intake in a group of children and
adolescents with GSE and type 1 diabetes, Westman et al.-- found no differences between
GSE and non-GSE patients. This population was screened annually for GSE and so were
diagnosed at an asymptomatic point of the illness. In a case-controlled study of the
incidence of hypoglycemia in patients with untreated GSE [Gluten Sensitive Enteropathy =
Celiac Disease], Mohn et al.-- found that there were significantly more episodes of
hypoglycemia in the GSE patients than in controls. Institution of a gluten-free diet reduced
hypoglycemia, but only several months after initiation.”[11]

Hypoglycemia and Celiac Disease are commonly associated. Cravings from malabsorption
typically cause an unsuspecting person to eat too much carbohydrate, especially the
simpler types like sugar, bread, crackers, rice, pasta, and potato chips. Eating habits can
develop that result in the sequence:

1. Excessive blood sugar spikes (without follow-on sugars from more complex
carbohydrates)
2. Excessive insulin release (contributing to insulin resistance)
3. Rapid blood sugar crash: hunger, fatigue, irritability, disorientation, vision problems,
and cravings for more carbohydrate.
4. Eating more carbohydrates.
5. Pleasure from satiation of hunger (which reinforces the cravings)
Repeat…

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Both excessive blood sugar spikes and excessive insulin releases damage the body, the
insulin spikes contributing to Type 2 Diabetes.

The above is also stated a little more thoroughly on www.csaceliacs.org (scroll down to the
heading “Symptoms Associated with IDDM”).

Since hypoglycemia, or hypoglycemic symptoms can result from untreated gluten

intolerance, and since fatigue, depression, and disorientation can result from
hypoglycemia, therefore, one might expect that hypoglycemic symptoms resulting from
untreated gluten intolerance could account for some of the fatigue, depression, and
disorientation normally associated with untreated Celiac Disease.

Type 2 Diabetes

Past studies have not yet indicated a relationship between gluten intolerance and Type 2
Diabetes. However, these studies applied a narrow definition and screening method for
classic Celiac Disease. This definition would have excluded the majority of relatively
milder forms of gliadin sensitivity. Studies should be conducted to determine the
association between fecal anti-gliadin antibodies and Type 2 Diabetes.

Hypothesis: Type 2 Diabetes can be caused by gliadin dependent malabsorption and it is the
form of diabetes that dominates (as opposed to Type 1) when any of the following is the
case:
a) The pancreas-specific antibody co-factor to the gliadin antibody attack is not
present, so autoimmune Type 1 diabetes doesn’t occur.
b) Co-factors for Celiac Disease are absent resulting in milder but still serious forms
of gliadin sensitivity.
c) The infant at risk for Type 1 Diabetes is not fed gliadin in the first few months of
life[12], so that the development of Type 1 Diabetes is delayed, lessened, or avoided
when wheat is introduced later (although some gliadin injury may still occur).

Clippings: Diabetes and Gluten

The followings are clippings of a sample of articles that address the relationship between Diabetes and
Gluten. Bold highlights for emphasis and italicized comments are added by Harold G. Kraus.

Summary: Type I Diabetes is the loss of islet cell function to autoimmune attack! The Gliadin fraction of
Gluten contributes to the autoimmune attack of islet cells in those genetically disposed to type I Diabetes.
From articles such as the following, my thinking is that all people with type I Diabetes should be presumed
gluten intolerant and should investigate that possibility. Gluten in their diet can be interfering with their
insulin therapy as well as causing, aggravating, or contributing to many other degenerative health problems.
Furthermore, children of type I Diabetics should be screened for gluten intolerance to reduce their chances of
developing Diabetes or any other autoimmune condition.

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Clipping from http://allallergy.net/abstracts/index.cfm?ShowMonth=March2003#15801

A protein from wheat (Triticum aestivum), a wheat storage globulin, Glb1, linked to islet
damage in diabetics.

The development of autoimmune type 1 diabetes involves complex interactions among several genes
and environmental agents. Human patients with type 1 diabetes show an unusually high frequency of
wheat gluten-sensitive enteropathy; T-cell response to wheat proteins is increased in some patients,
and high concentrations of wheat antibodies in blood have been reported.

In this study, antibodies to Glb1 protein were found in serum from diabetic patients but not in matched
controls, which raises the possibility that in some individuals, type 1 diabetes may be induced by
wheat proteins. Also, it provides a first candidate wheat protein that is not only antigenic in diabetic
rats and human patients but is also closely linked with the autoimmune attack in the pancreas.

“A type 1 diabetes-related protein from wheat (Triticum aestivum). cDNA clone of a wheat storage
globulin, Glb1, linked to islet damage.”
MacFarlane AJ, Burghardt KM, Kelly J, Simell T, Simell O, Altosaar I, Scott FW.
J Biol Chem 2003;278(1):54-63

Clipping from http://www.nutramed.com/celiac/celiac_mechanisms.htm

Celiac Disease: Immune Mechanisms Stephen Gislason MD
...
Diabetes, thyroid disease, purpura, anemia, rheumatoid arthritis, sacroileitis, sarcoidosis,
vasculitis, lung disease, myositis, eye inflammation, encephalopathy and cerebellar atrophy and
schizophrenia are all linked to gluten intolerance. These associations suggest a tendency to
immune hypersensitivity diseases and a possible role for food antigens in causing systemic
autoimmune disease. The prevalence of celiac disease among children with diabetes (IDDM)
[Insulin Dependent Diabetes Mellitus] is 50 times more likely than chance. IgA deficiency is 10
times more common in celiac patients than in the general population. ...

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Clipping from http://www.mipharm.com/pharm_prof/Celiac%20Disease%20article.pdf

Celiac Disease: The Great Mimic

...
Celiac disease is associated with a side range of autoimmune (attack by one’s immune system against
oneself) diseases including insulin-dependent diabetes, dermatitis herpetiformis, autoimmune thyroid
disease, autoimmune hepatitis, primary biliary cirrhosis, atrophic gastritis, gluten-related ataxia and
connective tissue diseases. This has been explained by the sharing of certain common genetic factors.
It has been recently discovered that the prevalence of autoimmune disorders in celiac disease is
related to the duration of exposure to gluten. The longer the exposure to gluten, the greater the
risk of autoimmunity developing in other organ systems. Also, it is apparent that those who had
been challenged with gluten for diagnostic purposes had an increased risk for the developing of
autoimmune disorders. This data adds weight to the argument for the development of screening
programs to ensure diagnosis as early as possible and also casts doubt on the practice of gluten
challenge to confirm the diagnosis of CD.1
· Celiac disease has a strong association with insulin-dependent diabetes. The estimated
prevalence of celiac disease was found to be 6 to 8 percent in these diabetics [25% or higher
in more recent studies – HGK], suggesting that screening is justified in patients with newly
diagnosed insulin dependent diabetes. Finding and treating these diabetics with CD
dramatically improves insulin therapy in these often-brittle patients.
· Neurological abnormalities were formerly thought to be sequel to the gut disease, but is now
recognized that they may not only precede celiac disease but can also be its only
manifestation. It is thought that in celiac disease the target organ for gluten sensitivity is the
cerebellum or peripheral nerves, a situation analogous to that of the skin in dermatitis
herpetiformis. Patients with gluten-related ataxia had antigliadin IgG of IgA antibodies. These
patients had HLA genotypes known to be associated with gluten-sensitive enteropathy.
Duodenal biopsies showed changes compatible with celiac disease in less than 50 percent of
patients and 60 percent of patients had no GI symptoms. Antigliadin antibody testing is
essential in the assessment of idiopathic ataxias [the fecal test is the most sensitive- HGK].
Endomyseal antibodies are not as reliable because they may be positive only in those with gut
involvement, missing those without the small bowel lesion. Both the ataxia and the neuropathy
in these patients may be reversible with adherence to a gluten-free diet.

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Clipping from From http://www.gutdoc.org/Celiac.htm

...
Sprue is a condition that is frequently overlooked or misdiagnosed.
Sprue frequently occurs as a latent condition and is found in about 25% of diabetics [may be
higher with application of the more sensitive fecal test- HGK]. This is a genetic disorder that is
inherited, common in Ireland and north-western Europe. It is rare among Asians, people of Jewish
heritage, and African Americans. Sprue occurs in about 4 to 5% of the population; latent sprue
(hidden gluten allergy) may be as frequent as 10%. It is frequently associated with blood group O and
occasionally in type A blood.
Problems due to sprue actually occur at the level of the cell. Research has found that sugar residues
(lectins) on the cell surface selectively bind the microscopic particles of wheat that are toxic (gliadin
fractions). This explains why extremely tiny amounts of wheat or gluten can set off this condition.
Avoiding sprue symptoms means far more than just avoiding bread, or even wheat. It means not eating
any prepared or processed food to which wheat or gluten has been added. It is important to keep a
strict diet because a number of more serious illnesses can occur as the result of an untreated sprue
condition.
...
ASSOCIATED DISEASES
There are a large number of associated conditions. Of these, the most common is Type I Diabetes.
Neurological conditions that can also result from the malnutrition of sprue include peripheral
neuropathy, abnormal demyelinization of the spinal cord, and night blindness. In rare cases,
encephalopathy can occur – a toxic brain syndrome due to sprue and B vitamin deficiency which can
lead to coma, because insufficient nutrient absorption is taking place. Other serious complications that
can occur in rare cases include increased incidence of lymphatic cancer. Incidents of hypocalcemia
have also been reported (tetany), as well as increased incidence of fractures and collapsed vertebrae.
...

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Clipping from http://content.health.msn.com/content/article/74/89328.htm?printing=true

Cereal May Trigger Type 1 Diabetes
Introducing Gluten Products Too Early or Too Late May Increase Risk [long term gluten
consumption or avoidance is not assessed, how long were the children monitored, 1, 2, 5, 25 years?
HGK]
By Salynn Boyles Reviewed By Brunilda Nazario, MD on Tuesday, September 30, 2003 WebMD
Medical News
Sept. 30, 2003 -- Introducing cereal into the diet too early or too late may trigger type 1 diabetes in
children who are genetically predisposed to get the disease.
In two separate but similar studies, high-risk infants fed cereal products during the first three months
of life were up to five times more likely than other high-risk babies to develop antibodies thought to
cause type 1 diabetes. Neither study found early introduction of cow's milk to be linked to diabetes
risk, however.
...
The two new studies, reported in the Oct. 1 issue of The Journal of the American Medical
Association, included roughly 2,800 infants genetically predisposed to develop type 1 diabetes. The
children were followed from birth and parents were questioned periodically about the foods the
children ate.
Researchers conducting the study found that children at risk for type 1 diabetes who were exposed to
cereals before the age of 3 months were at increased risk for developing the antibodies that lead to the
development of type 1 diabetes, as were children introduced to cereals after the age of 7 months. The
risk was roughly four times higher in high-risk infants fed cereal early and five times higher in the
infants fed late. The study found no association between type 1 diabetes and cow's milk.
...
The second newly reported study involved 1,610 German children at high risk for type 1 diabetes who
were followed from birth to age 8. Researchers examined whether exposures to breast milk, cow's
milk, solid foods, and gluten-containing foods such as cereals were associated with an increase in
diabetes risk.
They found that babies fed cereal or other gluten-containing foods before the age of 3 months were
five times as likely to develop the antibodies that lead to type 1 diabetes as children exposed to dietary
gluten at 3 months or older. Early introduction of cow's milk was not found to increase risk.
....
In an editorial accompanying the studies, diabetes researcher's Mark Atkinson, PhD, and Edwin Gale,
MD, urged clinicians and parents to use caution when interpreting the findings.
"It is clear that (these studies) do not present sufficient evidence to suggest that 'infant cereal causes
diabetes,' and hopefully will not be misinterpreted as such by parents and the public," they wrote.
...
SOURCES: The Journal of the American Medical Association, Oct. 1, 2003. Ezio Bonifacio, PhD,
Scientific Institute San Raffaele, Milan, Italy. Jill M. Norris, MPH, PhD, department of preventive
medicine and biometrics, University of Colorado Health Sciences Center, Denver. Mark Atkinson,
PhD, department of pathology, Center for Immunology and Transplantation, University of Florida,
Gainesville.

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Clipping from http://www.curezone.com/art/read.asp?ID=38&db=6&C0=108

...
Of particular interest is the implication for autoimmune diseases. Lectins stimulate class II HLA
antigens on cells that do not normally display them, such as pancreatic islet and thyroid cells.9 The
islet cell determinant to which cytotoxic autoantibodies bind in insulin dependent diabetes
mellitus is the disaccharide N-acetyl lactosamine,10 which must bind tomato lectin if present and
probably also the lectins of wheat, potato, and peanuts. This would result in islet cells expressing
both class II HLA antigens and foreign antigen together a sitting duck for autoimmune attack.
Certain foods (wheat, soya) are indeed diabetogenic in genetically susceptible mice.11 Insulin
dependent diabetes therefore is another potential lectin disease and could possibly be prevented by
prophylactic oligosaccharides.
...

The islet cell ... must bind tomato lectin if present and probably also the lectins of wheat, potato,
and peanuts. ... a sitting duck for autoimmune attack

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Clipping from: http://www.blackwell-synergy.com/rd.asp?issn=1464-5491&vol=18&page=169

Diabetic Medicine
Volume 18 Issue 3 Page 169 - March 2001
doi:10.1046/j.1464-5491.2001.00498.x

Coeliac disease and Type 1 diabetes mellitus - the case for screening
G. K. T. Holmes

SUMMARY

Aim: To review the relationship between coeliac disease and Type 1 diabetes mellitus with emphasis
on prevalence of coeliac disease, presentation and implications for screening.

Methods: Papers collected over many years by the author have been included in the review and a
literature search employing Medline was undertaken to August 2000. Search words used were coeliac
disease and diabetes mellitus.

Results: Twenty papers exploring the prevalence of coeliac disease by serological screening of Type 1
diabetes in children, eight in adults and two including both groups were found. An additional 48
papers are included and relate to serological screening tests for coeliac disease, expressions and
complications of coeliac disease, the value of GFD and the genetics of the two conditions. Unless
formal screening studies are undertaken coeliac disease will not be diagnosed because patients are
asymptomatic, have atypical symptoms or even in those with symptoms the diagnosis is overlooked.
Based on small bowel biopsy, diagnosis the prevalence of coeliac disease in Type 1 diabetes in
children is 1:6 to 1:103 and in adults 1:16 to 1:76. [Prevalence would be much higher on a
serological or fecal basis.] Patients may improve following the start of a gluten-free diet (GFD) in
terms of symptoms, growth in children, serum antibody levels, haematological and biochemical
indices, morphology of the small intestinal mucosa and control of diabetes.

Conclusion Coeliac disease commonly occurs in Type 1 diabetes. It is recommended that screening
for coeliac disease should be part of the routine investigation and offered to all patients because of the
high prevalence and the potential benefits of treatment with a GFD. This includes control of
symptoms, stabilization of diabetes and prevention of complications associated with coeliac disease.
The cost per patient diagnosed with coeliac disease from the existing population with Type 1 diabetes
would be £860 and for those newly arising £950.

Clipping from: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&

list_uids=10925978&dopt=Abstract

Am J Gastroenterol. 2000 Jul;95(7):1742-8. Related Articles, Links

Importance of gluten in the induction of endocrine autoantibodies and organ dysfunction in adolescent
celiac patients.

Toscano V, Conti FG, Anastasi E, Mariani P, Tiberti C, Poggi M, Montuori M, Monti S, Laureti S,
Cipolletta E, Gemme G, Caiola S, Di Mario U, Bonamico M.

II Endocrinologia, Dipartimento di Fisiopatologia Medica, and Istituto di Clinica Pediatrica, Universita

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La Sapienza, Roma, Italy.

OBJECTIVE: It is well known that a high number of celiac patients may develop autoantibodies
against endocrine glands, but it has not yet been clarified if this increased autoimmune response and
the impaired organ function that can develop may be related to the presence or absence of gluten in
the diet. The aim of the present study was to evaluate the effect of gluten on the autoimmunity and
function of the endocrine glands in adolescent celiac patients. METHODS: To clarify this aspect we
investigated 44 patients (28 females), aged 11-20 yr (15.21+/-2.7 yr): 25 (mean age, 15.1+/-2.2 yr) on
a gluten-free diet (treated patients) and 19 (mean age 15.4+/-2.9 yr) with a diet containing gluten
(untreated patients). Forty adolescent subjects, aged 14-19 yr (mean age, 14.9+/-2.7 yr), of whom 20
were females, were studied as controls. Antibodies against the thyroid, adrenal, and pancreas were
evaluated. Thyroid-stimulating hormone FT3, FT4, T3, T4, dehydroepiandrosterone sulphate, 17-OH
progesterone, and cortisol, analyzed basally and 60 min after intravenous ACTH stimulation, were
assayed to evaluate thyroid and adrenal function. The fasting glycemia level was used to evaluate the
endocrine pancreas function. An ultrasonogram of the thyroid gland was performed on all patients.
HLA class II typing for DR3 and DQB1 was performed in 32 of 44 patients. RESULTS: Seven of 44
(15.9%) patients were positive for antibodies against peroxidase. Six of 44 (13.6%) were positive for
antibodies against thyreoglobulin and four of them also showed positive antibodies against peroxidase.
Therefore, in nine of 44 at least one antibody directed against thyroid tissue was positive. Seven of 44
(15.9%) were positive for antibodies against islet cell, one of 44 (2.3%) positive for antibodies against
glutamic acid decarboxilase, one of 44 (2.3%) positive for antibodies against insulin, and none for
antibodies against islet cell- 512bdc. In 15 of 44 (34%) at least one antibody against an endocrine
tissue was positive. The genotype DR3 was found in 21 of 32 (65.6%) celiac patients (10 in the
untreated and 11 in the treated group, respectively) and the genotype DQB1*02 (DQ2) was found in
30 of 32 (93.8%) patients (16 in the treated and 14 in the untreated group, respectively). DHA-S
values were significantly lower in the untreated (30.5+/-28.5 microg/dl) than in the treated group
(61.3+/-59.4 microg/dl, p < 0.05), and both showing significantly (p < 0.01) lower levels with respect
to the controls (161+/-52 microg/dl). One patient showed diabetes, another one clinical
hypothyroidism (thyroid-stimulating hormone > 6), and two patients showed preclinical
hypothyroidism. Interestingly, at least one antibody was positive in 10 of 19 untreated patients
(52.6%) but only in five of 25 treated patients (20%), with a significantly different distribution (p <
0.001) between the two groups and without differences in the HLA genotype. The ultrasonographic
evaluation of the thyroid resulted in a pathological score in six patients of the 44 examined (13.6%),
suggesting the presence of thyropathy. CONCLUSIONS: The main results of this study are the high
incidence of thyroid and pancreatic antibodies, and the possible role of gluten in the induction of the
antibodies as well as, in few cases, the consequent organ dysfunction.

Dental enamel defects and coeliac disease -- VENTURA and ...

Celiac Disease Statistics

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Hit Counter

[1] “Organ-Specific Autoantibodies Linked to Dietary Gluten in Celiac Disease Patients”, Dr. Ventura, Universita of Trieste, Italy,
Journal of Pediatrics, August 2000; 137,263-265, (review of this article on www.ithyroid.com
[2] “Celiac Disease Research Leads To Successful Treatment Successful Treatment of Type I Diabetes Using Zonulin Antagonist”,
Reported on Celiac.com
[3] “Duration of exposure to gluten and risk for autoimmune disorders in patients with celiac disease.” SIGEP Study Group for
Autoimmune Disorders in Celiac Disease., Ventura A, Magazzu G, Greco L., Department of Pediatrics, University of Trieste, IRCCS
Burlo-Garofolo, Trieste, Italy. ventura@burlo.trieste.it Gastroenterology. 1999 Aug;117(2):297-303.
[4] “A type 1 diabetes-related protein from wheat (Triticum aestivum). cDNA clone of a wheat storage globulin, Glb1, linked to islet
damage.”, MacFarlane AJ, Burghardt KM, Kelly J, Simell T, Simell O, Altosaar I, Scott FW., Ottawa Health Research Institute,
Ottawa, Ontario K1H 8L6, Canada., J Biol Chem. 2003 Jan 3;278(1):54-63. Epub 2002 Oct 29.
[5] “Younger age at onset and sex predict celiac disease in children and adolescents with type 1 diabetes: an Italian multicenter
study”, Cerutti F, Bruno G, Chiarelli F, Lorini R, Meschi F, Sacchetti C; Diabetes Study Group of the Italian Society of Pediatric
Endocrinology and Diabetology., Universita di Torino, Piazza Polonia 94, I-10126 Turin, Italy. franco.cerutti@unito.it, Diabetes
Care. 2004 Jun;27(6):1294-8.
[6] “Cereal May Trigger Type 1 Diabetes”, Salynn Boyles Reviewed By Brunilda Nazario, MD on Tuesday, September 30, 2003
WebMD Medical News
[7] “Celiac Disease: Immune Mechanisms” Stephen Gislason, MD.
[8] “A longitudinal study of the effects of a gluten-free diet on glycemic control and weight gain in subjects with type 1 diabetes and
celiac disease - Clinical Care/Education/Nutrition”, Rakesh Amin, Nuala Murphy, Julie Edge, Marion L. Ahmed, Carlo L.
Acerini, David B. Dunger, Diabetes Care, July, 2002.”
[9] “Prevalence and clinical correlates of immune markers for celiac disease in adult subjects with Type 1 diabetes.” M Buysschaert,
J.A. Decerf, M. P. A. Nermans, Endocrine Division, UCL St Luc, Brussels, Belgium.
[10] “Celiac disease in older people”, Tai V, Crowe M, O'Keefe S., Department of Geriatric Medicine, St Vincent's Hospital,
Dublin, Ireland. J Am Geriatr Soc. 2000 Dec;48(12):1690-6.
[11] “Type 1 Diabetes and Celiac Disease: Overview and Medical Nutrition Therapy ”, Sarah Jane Schwarzenberg, MD and Carol
Brunzell, RD, CDE
[12] Salynn Boyles.

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