The study determined the following:

These results are much higher than previous studies have found, and they indicate that celiac disease is perhaps the most common genetic disorder in the United States, as well as one of the most poorly diagnosed diseases.

February 10, 2003 edition of Archives of Internal Medicine

Am J Clin Nutr 2002;75:914-921.

Celiac.com 06/06/2002 - Results of a recent study conducted by Anneli Ivarsson and colleagues at Umea University in Sweden suggest that continuing to breast-feed infants while they are being introduced to new foods may reduce their risk of getting celiac disease. Dr. Ivarssons study suggests that the cause of celiac disease may include environmental factors, and not just be limited to genetic factors. Their study evaluated the breast-feeding habits of 627 children with celiac disease and 1,254 healthy children, and specifically looked at their responses to newly introduced foods. The results, published in the May issue of the American Journal of Clinical Nutrition, indicate that dietary patterns of infants may have a strong influence on the bodys immune responses, and certain dietary patterns could lead to lifelong food intolerances. Children under 2 years of age who were still being breast-fed when they were introduced to dietary gluten had a 40% lower incidence of celiac disease.

Another important factor was the overall amount of gluten in an infants diet, and a direct correlation was found between increased gluten consumption and an increased incidence of celiac disease. According to the researchers, the protective effect of breast feeding was even more pronounced in infants who were breast-fed beyond the introduction of gluten. Ultimately the teams findings indicate that breast feeding infants through the period of gluten introduction can significantly lower their risk of getting celiac disease. More research needs to be done to determine if this protective effect will extend over a lifetime.

Gut 2002;50:624-628

Celiac.com 05/02/2002 – Results of the first large population-based twin study of celiac disease were recently published in the April edition of the journal Gut. The study was conducted by Professor L Greco and colleagues at the Università di Napoli Federico II, Dipartimento di Pediatria. The study compared identical twins (genetically identical) to fraternal twins (genetically not identical) who share only the same number of genes as non-twin siblings. This methodology allowed the researchers to determine what role a shared environment plays in the onset of celiac disease in comparison to a genetic role.

The researchers matched the Italian Twin Registry with the membership lists of a patient support group for celiacs. Forty seven twin pairs were found and screened for antiendomysial (EMA) and antihuman-tissue transglutaminase (anti-tTG) antibodies. Identical twins were verified using DNA fingerprinting and fraternal twins were typed for HLA class II DRB1 and DQB1 molecules.

Their results indicate that 38% of the combined twin pairs showed signs of celiac disease, which breaks down to 75% of the identical twin pairs and 11% of the non-identical twin pairs. Additionally, females who had a twin with celiac disease were 30% more likely to develop it themselves, in comparison to an unaffected male twin. Further, the results of the study indicate that environmental factors have little or no effect on the acquisition of celiac disease, and that there is substantial evidence of a very strong genetic component that is only partially related to the HLA region. The researchers suggest that several genes work collectively to cause celiac disease, and a single missing or altered gene is probably not its cause.

Lancet 2001; 358: 356-61

Celiac.com 08/10/2001 - In line with past studies on the mortality rate of people with celiac disease, the results of a new study conducted by Dr. Giovanni Corrao (Cattedra di Statistica Medica, Università di Milano-Bicocca, 20126 Milano, Italy), et. al., indicate that the death rate among people with celiac disease is double that of the normal population. The prospective cohort study examined 1,072 adults who were diagnosed with celiac disease between 1962 and 1994, and their 3,384 first-degree relatives. The mortality rates by 1998 among both groups were compared to that of the normal population.

Their findings show that 53 people in the celiac disease group died compared with the 25.9 deaths that were expected (Standardized Mortality Ratio - SMR). Unlike past studies, however, this one also looked for different patterns of clinical presentation of the disease. For example, the results indicate that within three years of diagnosis there was a significant increase in the mortality rate for those who presented symptoms of malabsorption. This same increase was not seen in those who were originally diagnosed because of minor symptoms, or via an antibody screening. The SMR also increased when there was a delay in diagnosis, and when a gluten-free diet was not followed. Non-Hodgkin lymphoma was the main cause of death, and no excess in mortality rate was seen in the groups first-degree relatives.

Conclusion: Prompt diagnosis and dietary treatment will decrease the mortality rate of people with celiac disease. More studies are needed regarding asymptomatic people with celiac disease and their risk of intestinal lymphoma.

Nature Immunology 2, 353 - 360 (April 2001)

Celiac.com 04/12/2001 - According to an article published in the April issue of Nature Immunology, Dr. Marc Rothenberg and colleagues at the Childrens Hospital Medical Center in Cincinnati, Ohio performed a series of experiments on mice which led them to the conclusion that white blood cells called eosinophils could be the cause of many food allergies and gastrointestinal inflammation. The researchers believe that the eosinophil cells, which are present throughout the body, mistakenly identify food proteins as germs in individuals with food allergies. When the intestinal lining of an allergic person is exposed to an allergen, a substance called eotaxin is released by the cells lining the intestine, which causes the eosinophil cells and other immune cells to attack them and release powerful proteins that destroy the surrounding tissues and cause eosinophilic inflammation.

The results of this study are unique because this is the first time eosinophils cells have been implicated in causing allergies, even though scientists have known for some time that they were present in great numbers at the sites of inflammation caused by reactions to food. The implication of this study is the possible development of drugs that stop this reaction from occurring, and thus prevent digestive inflammation and destruction that occurs when people with food allergies eat foods to which they are allergic. These results put scientists one step further in understanding how and why the digestive system is attacked in certain individuals, and a possible means of one day controlling the process.

Zonulin is a human protein that acts like a traffic conductor for the bodys tissues by opening spaces between cells, and allowing certain proteins to pass through, while keeping out toxins and bacteria. People with celiac disease have higher levels of zonulin, which apparently allows gluten to pass through the cells in their intestines, which triggers an autoimmune response in their bodies. Until now, researchers could never understand how a big protein like gluten could pass through the immune system. According to author Alessio Fasano, M.D., people with celiac have an increased level of zonulin, which opens the junctions between the cells. In essence, the gateways are stuck open, allowing gluten and other allergens to pass. Further: I believe that zonulin plays a critical role in the modulation of our immune system...(f)or some reason, the zonulin levels go out of whack, and that leads to autoimmune disease. Ultimately these finding may help doctors understand the causes of other, more severe autoimmune disorders.

Eff Clin Pract 2002 May-Jun;5(3):105-13
Mustalahti K, Lohiniemi S, Collin P, Vuolteenaho N, Laippala P, Maki M.
Department of Pediatrics, Tampere University Hospital, Finland.

CONTEXT: Since the advent of serologic testing for celiac disease, most persons who receive a diagnosis of celiac disease have few or no symptoms. Although pathologic changes of celiac disease resolve on a gluten-free diet, how a gluten-free diet affects the quality of life for patients with screen-detected celiac disease is unclear.

OBJECTIVE: To evaluate the effect of a gluten-free diet on the quality of life of patients with screen-detected celiac disease.

DESIGN: Prospective study of patients before and 1 year after initiating a gluten-free diet.

PARTICIPANTS: 19 patients with screen-detected celiac disease (found by serologically testing first-degree relatives of celiac patients) and 21 consecutive patients with symptom-detected disease. In all cases, celiac diagnosis was confirmed by finding villous atrophy and crypt hyperplasia on small-bowel biopsy.

INTERVENTION: Gluten-free diet (explained during a single physician visit). MAIN OUTCOME

MEASURES: Gastrointestinal Symptoms Rating Scale (GSRS), in which scores range from 0 to 6 (higher scores represent worse symptoms); and quality of life measured with the Psychological General Well-Being Questionnaire (PGWB). Scores range from 22 to 132 (higher scores mean greater well-being).

RESULTS: At baseline, patients with symptom-detected celiac disease had poorer quality of life and more gastrointestinal symptoms than those with screen-detected celiac disease. Reported compliance with the gluten-free diet was good. All mucosal lesions of the small bowel had resolved at the follow-up biopsy. After 1 year of following the diet, quality of life for patients with screen-detected disease significantly improved (mean PGWB score increased from 108 to 114; P

CONCLUSIONS: Gluten-free diet was associated with improved quality of life for patients with symptom-detected celiac disease and patients with screen-detected celiac disease. Concerns about the burden of a gluten-free diet, at least over the short term, may be unfounded.

PMID: 12088289

Oberhuber G, Schwarzenhofer M, Vogelsang H
Dig Dis 1999 Nov- Dec;16(6):341-4

Department of Clinical Pathology, University of Vienna, Vienna, Austria. The in vitro challenge of duodenal mucosa with gliadin is a useful model to reproduce the immunological features of celiac disease (celiac disease) and allows the study of early pathogenetic events in this disease. With this model it was shown that antigens such as ICAM-1 and HLA-DR are upregulated as early as 1-2 h after gliadin challenge in patients with celiac disease. After 24 h the lamina propria contained CD4+ T cells expressing the IL-2 receptor alpha-chain, which is a sign of activation. Intraepithelial lymphocytes increased in number and showed proliferative activity. After in vitro stimulation with gliadin, endomysial antibodies were found in the supernatant of the cultured mucosa from patients with celiac disease following a gluten-free diet. This supported the notion that endomysial antibodies are at least in part produced locally. The model was also successfully used to identify toxic constituents of gliadin. Presently, organ culture is not commonly used for diagnostic purposes.

Troncone R, Greco L, Mayer M, Mazzarella G, et. al.
Gastroenterology, 1996; 111: 318-324

The final paragraph says:

In conclusion, our data show that approximately half of the siblings of patients with celiac disease show signs of sensitization to gluten as they mount an inflammatory local response to rectal gluten challenge. The genetic background and the clinical meaning of such gluten sensitivity need to be established. Further studies, particularly at the jejunal level, are necessary before deciding if any action is to be taken in this subset of first-degree relatives.

Troncone R, Greco L, Mayer M, Mazzarella G, et. al.
Gastroenterology, 1996; 111: 318-324

The final paragraph says:

In conclusion, our data show that approximately half of the siblings of patients with celiac disease show signs of sensitization to gluten as they mount an inflammatory local response to rectal gluten challenge. The genetic background and the clinical meaning of such gluten sensitivity need to be established. Further studies, particularly at the jejunal level, are necessary before deciding if any action is to be taken in this subset of first-degree relatives.

This paper is a critical appraisal of current theories on the mechanisms of toxicity of wheat and other cereals in celiac disease and some related enteropathies. The peptidase deficiency, primary immune defect, and gluten-lectin theories on celiac disease are examined and critically discussed on the basis of the relevant data available in 88 references. Special attention has been paid in this review to the nature of the cereal components triggering the appearance of toxic symptoms and signs in celiac disease as well as to underlying action mechanisms. The gluten-lectin theory is the one best able to explain celiac disease. It also explains some secondary intolerance that may occur in temporarily predisposed individuals as a consequence to viral hepatitis and intestinal infections, as well as the occurrence of intestinal lesions in healthy subjects that are administered very high amounts of gluten.

Paul V, Henkerr J, Todt H, Eysold R.
Z.Klin.Med., 1985; 40: 707-709.

In this study 90 EEGs were performed on 58 celiac children. Researchers concluded that abnormal brain waves resulted from the ingestion of gluten by celiac children. They also concluded that a gluten challenge should not be given before a child reaches the age of 6 years old, and the challenge should not last longer than 5 months. The researchers main concern seems to be the risk of permanent brain damage that they believe could be caused in a celiac child who eats gluten for a prolonged period of time.