Problems with Certain Foods

Posted on November 12th, 2012

“I continue to see patients with multiple problems with certain foods. We see the rare patients with celiac disease in which antibodies to gliadin (AGA) co-exist with antibodies to tissue transglutaminase (TTG-IgA). These patients won’t be able to eat gluten ever. They aren’t suffering from mold illness.

Others will have AGA antibodies but no TTG-IgA, invariably in association with low MSH, high TGF beta-1 and low levels of the mucosal T regulatory cells (see Josefowicz S and co-authors, Nature 2012 482: 395-400. Extrathymically generated regulatory T cells controls mucosal TH2 inflammation) called induced T reg cells. These are demonstrated in blood as CD4+CD25++ (the two pluses are referred to as “double bright”). We have measured these cells since Quest Baltimore set up a panel for use of participating docs December 2010. The people with this immune regulatory defect must stay away from gluten and correct their mold illness. Such a dietary restriction usually takes about three months in kids and a bit longer in adults to fix.

In August 2012, Quest Baltimore set up a more precise panel (run at their Chantilly labs) for me that allows me to separate T reg cells as thymus derived or induced. We now know that the thymically-derived T reg cells, called CD4+CD25++127lo/- cells, are the ones that control tissue-based autoimmune and inflammatory elements. These cells usually are low in mold illness and if combined with low levels of double bright T regs give mucosal problems and systemic problems.

Underlying these new insights into abnormalities in T reg cells is the role of TH 17 immunity, in which plasma TGF beta-1 is a major marker. When we have the combo of high TGF beta-1 and low T regs what is happening is that the helpful, good guy T regs are being directed into tissue by TGF beta-1 where the wonderfully helpful T regs are converted (plasticized) into pathogenic T cells that make more TGF beta-1 (OH NO!) which sends more T regs to their death in tissue. Get used to hearing TH 17/T reg imbalance: it is the new jargon word in modern immunology. We are now seeing countless references to TH17/T reg imbalance in assessment of inflammatory illness from acute coronary syndrome to cirrhosis. No where can we show such abnormalities better than in mold illness.

I had a Mom contact the office, desperately seeking help for her nearly three year old child with a severe problem with foods, called Food Protein Induced Enterocolitis (FPIEC). The child is intolerant of soy and dairy, as well as just about everything else. Mom can only eat a few foods herself or consumption of her breast milk, essentially the sole source of nutrition for this tiny baby, will cause the child to develop profound vomiting and GI distress, acidosis and near death. I have no data base on such kids. Frankly, neither does anyone else.

Mom is worried about inflammation causing the FPIEC as the home is moldy as can be. I told her that if we could show TH17/T reg imbalance then there would be a basis to treat the child in an effort to lower TGF beta-1, thereby raising T regs (these are the inducible T regs). Moreover, treatment would likely be accompanied by a rise in thymus-derived T reg cells. This effort is getting started.

We have a developing database of changes from untreated to treated of mold illness, and with relapse and re-treatment as well. TGF beta-1 is a giant in assessment of this approach. Our data sets on controls are getting large; our VIP treated patients are showing a return to normal of both double bright (we knew that) and thymus-derived T regs cells (we didn’t know that).
This correction of low T regs is another mechanism of benefit of its use. The point of sharing this heart-wrenching case is that the advances seen in the immunology of mold illness are going to have application to countless areas of medicine.”

-Ritchie Shoemaker, MD

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