Page 1, 2
Gluten-Associated Disorders: Beyond the Gluten-Free Diet
Complaints of adverse physiologic reactions to gluten are becoming more common in medical offices. Many health professionals question whether this trend is due to an actual increase in incidence, an improvement in diagnostic methods, or simply a rise in awareness. Which of these is true remains to be clarified by research, but there is no doubt that our tools for identifying food allergies and furthering our understanding of the immune system are rapidly expanding.
With any food-related symptoms or diagnoses, the astute physician would recommend identification and – at least temporary – removal of offending foods from the diet. And while it is essential to determine if gluten is a problematic food protein for patients, we must take further steps in laboratory diagnosis to determine a patient's exact immunological response to gluten in order to develop appropriate treatment plans and prevent further tissue destruction. The importance of identifying celiac disease is paramount, because if left untreated it may contribute to infertility, development of other related autoimmune disorders, and a higher incidence of certain cancers including lymphomas.12
We have yet to fully understand the implications of genetic susceptibility in autoimmune diseases, but it is known that specific HLA haplotypes are also associated with type 1 diabetes mellitus, multiple sclerosis, and Graves' disease.23 Because of the potential for food to be antigenic, the impact of diet and genetics on autoimmune conditions can be pivotal in shifting the immune response. While gluten-free diets can alleviate symptoms, it is important that we continually review the literature and use of diagnostic testing, as this is an evolving discussion and recommendations are sure to change in the future. Researchers continue to discover immunologic and genetic etiologies of gluten-induced symptoms, leading to important branching points in treatment approach. Oral or sublingual immunotherapy, for example, may be a possibility in NCGS or IBS, while in celiac disease this therapy would be contraindicated due to the potential for autoimmune gastrointestinal and systemic sequelae.8 Identifying the exact pathophysiology and category of immune response for each individual can aid not only in determining the necessary length and course of a gluten-free diet, but also in preventing comorbidities and improving autoimmune prognosis.
1. National Institute of Allergy and Infectious Diseases. Guidelines for the Diagnosis and Management of Food Allergy in the United States. December 2010. Available at: http://www.jacionline.org/article/S0091-6749(10)01566-6/fulltext. Published Dec 2010. Accessed September 8, 2013.
2. Sapone A, Bai J, Ciacci C, et al. Spectrum of gluten-related disorders: consensus on new nomenclature and classification. BMC Medicine 2012;10:13.
3. Brostof J, Challacombe S. Food Allergy and Intolerance. New York: Saunders; 2002:127–162.
4. Kazemi-Shirazi L, Gasche C, Natter S, et al. IgA autoreactivity: a feature common to inflammatory bowel and connective tissues diseases. Clin Exp Immunol 2002;128:102–109.
5. Gonzalez-Quintela A, Alende R, Gude F, et al. Serum levels of immunoglobulins (IgG, IgA, IgM) in a general adult population and their relationship with alcohol consumption, smoking and common metabolic abnormalities. Clin Exp Immunol 2007;151:42–50.
6. Sandin A, Björkstén B, Böttcher M, et al. High salivary secretory IgA antibody levels are associated with less late-onset wheezing in IgE-sensitized infants. Pediatr Allergy Immunol. 2011;22:477–481.
7. Rubio-Tapia A, Hill I, Kelly C, et al. American College of Gastroenterology Clinical Guidelines: Diagnosis and Management of Celiac Disease. Am J Gastroenterol. 2013;108:656–676.
8. Mousallem T, Burks A. Immunology in the Clinic Review Series;focus on allergies: immunotherapy for food allergy. Clin Exp Immunol. 2001;167:26–31.
9. Stapel S, Asero R, Ballmer-Weber B, et al. EAACI Task Force. Testing for IgG4 against foods is not recommended as a diagnostic tool: EAAC1 Task Force Report. Allergy. 2008;63(7):793–796.
10. Atkinson W, Sheldon T, Shaath N, et al. Food elimination based on IgG antibodies in irritable bowel syndrome: a randomised controlled trial. Gut. 2004;53:1459–1464.
11. Bellanti J. Immunology IV: Clinical Applications in Health and Disease. Bethesda, MD: I Care Press; 2012:729.
12. Feldman M, Friedman L, Brandt L. Sleisenger and Fordtran's Gastrointestinal and Liver Disease: Pathophysiology, Diagnosis and Management. Philadelphia, PA: Saunders; 2010:1797–1820.
13. Fasano A, Berti I, Gerarduzzi T, et al. Prevalence of celiac disease in at-risk and not-at-risk groups in the United States. Arch Intl Med. 2003;163(3):268–292.
14. Hadjivassiliou M, Sanders D, Grünewald R, et al. Gluten sensitivity: from gut to brain. Lancet Neurol. 2010;9(3):318–330.
15. Bushara K. Neurologic presentation of celiac disease. Gastroenterology. 2005;128(4 Suppl 1):S92–S97.
16. Rheenen P, Van de Vijver E, Fidler V. Faecal calprotectin for screening of patients with suspected inflammatory bowel disease: diagnostic meta-analysis. BMJ. 2010;341:c3369.
17. Burri E, Beglinger C, et al. Fecal calprotectin – a useful tool in the management of inflammatory bowel disease. Swiss Med Wkly. 2012;142:w13557.
18. Dellon E, Gonsalves N, Hirano I. ACG clinical guideline: Evidence based approach to the diagnosis and management of esophageal eosinophilia and eosinophilic esophagitis. Am J Gastroenterol. 2013;108(5):679.
19. Dellon E. Eosinophilic esophagitis: diagnostic tests and criteria. Curr Opin Gastroenterol. 2012;28(4):382–38.
20. Lundin K, Alaedini A. Non-Celiac Gluten Sensitivity. Gastrointest Endoscopy Clin N Am. 2012;22:723–734.
21. Eswaran S, Goel A, Chey W. What role does wheat play in the symptoms of Irritable Bowel Syndrome? Gastroenterol Hepatol. 2013;9(2):85–91.
22. Drossman D. The functional gastrointestinal disorders and the Rome III process. Gastroenterology. 2006;1377–1390.
23. Gough S, Simmonds M. The HLA region and autoimmune disease: associations and mechanisms of action. Curr Genomics. 2007;8(7):453–465.
Bethany Glynn, ND, acquired her doctorate of naturopathic medicine from Bastyr University with specialty training in pediatrics, family health, neuropsychological conditions, autoimmunity, and environmental medicine. She is a licensed primary care physician to families living with autism, anxiety, and ADHD in the Greater Seattle area. She currently runs two active medical websites and hosts community outreach classes, summarizing and sharing the latest in natural health research with fellow practitioners and the public.
Page 1, 2