Diagnosing Gluten Intolerance and its Link to Autoimmune Diseases
Food and microbial products are the main stimulants of the immune system and the main external regulator of various metabolic pathways. Accordingly, composition of the consumed food can influence immune responses and inflammatory processes leading to the development of distinct forms of autoimmune diseases.
Gluten (a protein composite found in foods processed from wheat and related grain species, including barley and rye) and related proteins are the most common food components capable of triggering a broad spectrum of inflammatory and autoimmune diseases in predisposed individuals. Human digestive enzymes cannot completely digest gluten in the gastrointestinal tract. As a consequence, consumption of gluten-containing foods results in the formation of large protein fragments stimulating an inflammatory reaction within the intestinal wall. These fragments can penetrate in systemic circulation and trigger immune responses in internal organs distant from the intestine (thyroid gland, salivary glands, brain etc).
60-70% of people with gluten intolerance will develop various rheumatic/metabolic diseases during their lifetime. These diseases can be divided into several groups:
1. Diseases associated with malabsorbtion of various nutrients, minerals and vitamins. Typical examples include:
Osteopenia and osteoporosis
Pseudogout (abnormal calcium deposits in various joints)
Anemia (iron-deficient and pernicious)
2. Autoimmune disease affecting endocrine glands. Typical examples include:
Autoimmune thyroid diseases
Diabetes type 1
3. Major autoimmune diseases. Typical examples include:
Several subtypes of scleroderma
4. Arthritis. Typical examples include:
Several subsets of juvenile rheumatoid arthritis
Chronic inflammation in sacroiliac joints
5. Other rheumatic disease, such as:
Chronic fatigue syndrome
Irritable bowel syndrome
Diagnosing gluten intolerance
Based on genetics and epidemiologic studies, 10 to 35% of the general population is genetically predisposed to gluten intolerance and gluten-associated diseases. Approximately 95%of patients with gluten intolerance have a particular type of HLA DQ alpha and beta chain encoded by two genes, HLA-DQ2 (85-90%), and HLA-DQ8 (5-10%). T lymphocytes invariably recognize gluten peptides that are presented by HLA-DQ2 or DQ8 molecules. This results in the lymphocyte activation and initiation of the inflammatory reaction and autoimmune responses. 35-40% of people carrying HLA DQ2 or DQ8 phenotype will develop gluten intolerance during their lifetime, 3-5% of them will develop celiac disease (a severe form of gluten intolerance associated with anatomical damage of the intestinal lining).
The diagnosis of gluten intolerance is based on genetic testing as well as specific immunologic testing of blood, saliva and feces. Patients with clinical presentations suspicious for celiac disease typically undergo an intestinal or colon biopsy to prove the diagnosis. However, the ultimate diagnosis of gluten intolerance is based on elimination of gluten from the diet for 3-4 months with its subsequent reintroduction focused on reproduction of gluten-driven symptoms.
For patients with gluten-driven autoimmune diseases elimination of gluten and correction of the aforementioned abnormalities may provide major therapeutic benefits comparable and sometimes exceeding those of prescription drugs.