If you tested your DNA with a personal genomics service like 23andMe, AncestryDNA, FamilyTreeDNA, MyHeritage or another testing company, you can learn more about your risk factors for hundreds of diseases. By clicking the button above ⬆️, you can upload your raw DNA data file and receive a personalized 250-page health report with research links that is the most comprehensive.
Celiac disease (CD) is a chronic condition marked by an intolerance to gluten, primarily affecting the small intestine in individuals with a genetic predisposition. It typically resolves upon excluding gluten from the diet. CD entails nutrient malabsorption due to inflammatory damage to the small intestine's mucosa triggered by consuming wheat gluten or similar proteins found in rye, barley, and triticale (a wheat-rye hybrid).
The clinical presentation of CD varies based on factors such as age of onset, gender (with a female-to-male ratio of 2:1), severity of mucosal damage, and dietary patterns. Symptoms can range from typical gastrointestinal issues to atypical signs or even no symptoms at all.
The risk of celiac disease (or gluten intolerance) can be predicted by genetic testing for the HLA-DQ2 and HLA-DQ8 markers.
The TenDNA health DNA report analyzes single nucleotide polymorphisms related to Celiac disease. While this report isn't a diagnostic test, it holds negative predictive value, suggesting Celiac disease is improbable when the predisposing alleles are absent. A positive result suggests some genetic predisposition to Celiac, though overall likelihood remains low.
Upload your raw DNA data to receive your personalized Celiac Report completely free of charge.
Follow the link of the selected polymorphism to read a brief description of how the selected polymorphism affects Gluten and celiac disease and see a list of existing studies.
SNP polymorphisms related to the topic Gluten and celiac disease:
rs2858331 | Together with the rs4988889 gene breakage, it is a diagnostic criterion for celiac disease. |
rs4988889 | Together with the rs2858331 gene breakage, it is a diagnostic criterion for celiac disease. |
rs2187668 | Risk of autoimmune diseases (lupus, gluten disease). |
rs45450798 | Polymorphisms affecting the disease process in type 1 diabetes and celiac disease. |
rs6441961 | Increased risk of gluten disease. |
rs2395182 | HLA DQ2.2 genes play an important role in many autoimmune diseases such as celiac disease, type 1 diabetes, rheumatoid arthritis, multiple sclerosis, psoriasis and others. |
rs7775228 | HLA DQ2.2 genes play an important role in many autoimmune diseases such as celiac disease, type 1 diabetes, rheumatoid arthritis, multiple sclerosis, psoriasis and others. |
rs4713586 | HLA DQ2.2 genes play an important role in many autoimmune diseases such as celiac disease, type 1 diabetes, rheumatoid arthritis, multiple sclerosis, psoriasis and others. |
rs2816316 | Genetic variant risk for type 1 diabetes and gluten disease. |
rs9851967 | Genetic risk of celiac disease associated with immune response. |
rs1464510 | Common genetic variant in type 1 diabetes and celiac disease. |
rs1738074 | Common genetic variant in type 1 diabetes and celiac disease. |
rs13119723 | Combined with the rs6822844 breakage, the study showed the strongest association with celiac disease among Caucasian patients. |
rs6822844 | Combined with the rs13119723 breakage, the study showed the strongest association with celiac disease among Caucasian patients. |
rs3184504 | A variant of celiac disease genetic risk associated with immune response. Also carrier associated type 1 diabetes. |
rs231775 | |
Li Dali, a National Foundation for Outstanding Youth Fund recipient, is a researcher at the School of Life Sciences in East China Normal University. He earned his PhD in genetics from Hunan Normal University in 2007 and conducted collaborative research at Texas A&M University during his doctoral studies. Li Dali and his team have optimized and innovated gene editing technology, leading to the establishment of a world-class system for constructing gene editing disease models.