2016: This hypothesis was wrong about the morphology switching. Eventually I looked at the list of gluten sensitive infections and some were not dimorphic. All the linked infections were known to cross the intestinal barrier: e.coli, sutterella, t.gondii.....which lead to a split in the hypothesis. Gluten and casein were not required to build up to autoimmunity but could inflame the situation. See the newer posts.
Celiac disease
I just recently found this ancient article which seems to support the notion that e.coli is involved with Celiac disease.
http://www.ncbi.nlm.nih.gov/pubmed/1107934
When I started researching only Celiac disease was gluten triggered. Then when my son was born I read in a Parents magazine how an autisic child appeared to be gluten and casein sensitive and that removal of these proteins reversed his condition. I started to wonder if Autism was autoimmune like Celiac disease.
I researched online and discovered that schizophrenia too had been associated with gluten and casein...so i had 3 very different diseases with a strange overlap.
Then my daughter developed eczema. We have no family eczema. The neighbors' kids had eczema. I felt sort of crazy telling the doctors that I believed she caught this because we didn't have this allergy. I noticed the eczema waxed and waned with milk and egg. I started to think that what ever this infection was it was changing with milk or egg.
Then on a fluke I read an article on organic weed killers which made me consider gluten as a switch on an infection like what I was seeing on with the eczema.
Corn gluten halts crab grass seeds from forming roots. When you look up the original Ohio state research you discover the original experiment was about a parasitic grass mold. Seems that not only did grass seed not sprout roots but the mold failed to be thrive and be parasitic on the golf-course grass they were protecting.
My thoughts: gluten prevents root growth and mold hyphals are like roots! Gluten was stopping a morphology switch. The fungus could not exist as a mold and had to become a yeast. suddenly i thought of beer yeast...running out of sugar and changing morphology and falling to the bottom of the glass..realizing that lots of fungal infections must do this.
So my first focus was that these autoimmune diseases must be fungal induced. Made sense...I had studied type 1 diabetes and some were associated with candida.
I found an Italian paper where gluten induced antibodies in celiac patients. I realized because I had done diabetes research that celiac disease if they, pateints, didn't have gluten they were protected from type 1 diabetes. Perhaps the immune system only sees one morphology and reacts to and produces antibodies to it? Gluten and casein were causing a peek-a-boo effect.
I started looking for infections in Celiac disease. I could not find fungal infections. The only correlation I could find was a history of bladder infections in a lot of the patients. I looked at the e.coli that was involved in bladder infections. Unlike most e.coli which causes food poisoning the bladder infection form was dimorphic! That e.coli had 2 morphologies a rod and a thread like form. The enzyme controlling it was called LON meaning long. This enzyme was already known to be casein controlled. Even more exciting, the e.coli was shown to change morphology with hydrocase (which contains casein).
If gluten is so similar.....does it act on LON too? Does E.coli change morphologies even faster with gluten? It would help explain celiac disease if it were true.
This is where we are and what needs to be tested by someone out there.
E.coli fits the celiac disease puzzle well because it can explain the over lap of celiac and autoimmune liver disease and type 1 diabetes. E.coli makes bilirubin when it breaks down red blood cells which...our liver makes bilirubin. E.coli makes insulin-related material that the bioassay for insulin reacts with.
The last step in my theory has to do with what pushes the immune system from a state of high antibodies to autoimmune attack: viruses.
Viruses must cause cross-targeting. For Celiac disease any virus that would infect the intestine...for liver disease hepatits...for the pancreas the flu virus infects it.
This is just a hypothesis. This is not proven but something to consider, to test.....it makes logical sense.
2016 update: gluten sensitivity does not have to do with dimorphic switching rather appears when an infection that can tear through the intestinal barrier is there. Gluten then crosses and ramps up the immune system. Gluten and celiac occur when autoimmune cross-targeting occurs at the intestine ontop of the infections making a hole. Please see newer posts.
Can anyone see or understand what I saying?
Hopeful,
Angela Biggs
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