Hello.

Long time lurker, pre and current. Thought you all would find this interesting. For those without the 2 main genes, negative testing or low-end Enterolab numbers (i.e., Fecal Antitissue Transglutaminase IgA 11 Units [Normal Range <10 Units]), perhaps the problem isn't gluten, afterall. Are the un-DQ2/DQ8ers actually allergic to various lectins? Maybe the reactions to these sneaky little proteins tends more towards neurological and/or psychological symptomology?


Philipena

THE LECTIN REPORT

http://www.krispin.com/lectin.html

Historically diagnosis and treatment of Celiac-Sprue related to 'gliadin' (also known as gluten) sensitivity. Gliadin is found in wheat, rye, barley, oats, and foods containing these grains (including beer, grain based alcohols, mayonnaise, grain vinegar, etc). Some Celiacs did not respond to elimination of gluten/gliadin. In 1951 Drs. Sidney V. and Merrill P. Haas published Management of Celiac Disease documenting treatment and cure of celiac and cystic fibrosis of the pancreas with a carbohydrate limiting diet introduced as the 'Specific Carbohydrate Diet'. More information about this diet can be gotten from Breaking the Vicious Cycle E Gottschall, BA, MSc. Kirkton Press Ltd. Baltimore, Ontario, Canada 1998.

In many cases cited in the book, elimination of certain carbohydrates 'cured' diagnosed Celiacs after one year and they were able to return to eating gluten containing foods. In hindsight many of the foods eliminated in this plan are high lectin foods known to be associated with gut and systemic inflammatory reactions. Celiac-Sprue is a genetic disorder treated by elimination of offending foods. The response of some to the specific carbohydrate elimination diet would mean that the patients who responded did not have classical gluten intolerance, Celiac-Sprue, which requires life long elimination of gluten/gliadin. It suggests that other lectins may cause similar symptoms and overlapping diagnostic and treatment difficulties.

If all cases of lectin intolerance were genetically based reversal of intolerance would not be possible. There must therefore be a subgroup of IBS, Crohn's, Celiac, colitis that is related to sensitization to food lectins that can be reversed by avoidance of these lectins and a restoration of gut function including SIgA and other immune protectors. Bacteria, virus, or other conditions, drugs or injurious substances acting directly on the gut wall may cause sensitization.

Tests are available to determine SIgA levels, and gut immune reactions to soy, dairy, wheat and egg. These tests do not cover the entire family of lectins, nor would blood or skin tests necessarily show sub-clinical sensitivity reactions. Most of the conditions associated with sub-clinical lectin intolerance appear to be degenerative, often taking extended periods of time to appear and longer to reach life threatening or painful (such as arthritis) stages. Many lectin related conditions may be considered to be 'autoimmune'.