In several recent threads, arguments about
food, symptoms, and pathology have been unnecessarily muddled. Definitions matter. Science matters.
Maybe not for, "holy crap, how do I get this blood to stop so I can get my life back?", but it does matter for identifying the exact underlying pathology, and for teasing out symptom uptick from IBD flare.
In a recent thread I mentioned that biopsy likely could not tell cell damage from chronic inflammation due to hypersensitivity to certain foods from similar damage due to chronic inflammation because of autoimmune response. Just like patterns of inflammation can often distinguish UC from CD, I suspect pattern could also be the differential for IBD vs hypersensitivity. (I have not found literature directly on this point.)
Besides visual patterns, genetic profiles could likely help with diagnosis - but they are expensive and seldom done. Of the 168 and counting gene-loci associated with IBD, some are UC specific, some CD specific, some both. The genetic profile could help decide if it was UC or CD based on whether there were more UC genes or CD genes, or that there were not UC genes ... etc. It would never be definitive because none of these genes are necessary and sufficient for IBD. These are gene-diagnosis associations that show up across individuals, and any one individual may not have the association on a particular gene. That's how population average effects work.
Living things have antigens. Antigens are usually peptides, polysaccharides or lipids. We eat living things and we get infested by living things, so there are many foreign antigens. Our immune system detects and forms antibodies to attack foreign antigens. We are living so we have antigens. Our immune system does not attack our native antigens. In autoimmune disease our immune system also forms antibodies to attack some of our native antigens (autoantigens). Which autoantigens get attacked, where the attack occurs, and the type of immune response (and tissue damages) involved determines the type of autoimmune disease.
Here is a chart showing disease and type of damage, although it does not have IBD:
/www.ncbi.nlm.nih.gov/books/NBK27155/figure/A1907/?report=objectonlyThe point here is that in addition to symptoms, cell deformation biopsies, visual patterns of inflammation, and abundance of known gene polymorphisms, it would also be theoretically possible test for antibodies to self-antigens to diagnose autoimmune. BUT - it is expensive and you have to know what human antigens to test for antibodies. Not all of the antigens associated with IBD are even known, although some have been found.
Here is an interesting article about
the antigen FAM84A, which a very significant number of UC patients have antibodies to.
/www.ncbi.nlm.nih.gov/pubmed/21560193 said...
Antibodies to FAM84A were significantly more prevalent in IBD patients (20%) than in gastrointestinal-diseased controls (5%) (P = 0.0004) and healthy controls (0%) (P < 0.0001). Anti-FAM84A antibodies were found in 18% of UC patients and in 22% of CD patients. CONCLUSIONS: We identified FAM84A as a novel autoantigen in IBD.
For most people if you have UC symptoms, there is visual inflammation, the biopsies show cell deformation consistent with chronic inflammation, and infectious causes are screened out, you get diagnosed with IBD.
Sometimes they do not even do a good job testing for infectious sources. Sometimes Celiac is also ruled out. Very seldom is hypersensitivity to a number of foods tested, although maybe it would be good practice. Each test is expensive, and there are always false positives/negatives, so diagnosis remains an art.
Someone could also have both food hypersensitivites and IDB. Having antibodies to certain food antigens and to self-antigens would mean you had BOTH. One quite likely causes the other.
So, food can affect symptoms because it affects the microbes in our guts and the dry bulk of our stool. Food could also cause inflammation/bleeding if there is a hypersensitivity involved. The inflammation/bleeding could trigger IBD if it is already present. BUT - these hypersensitivities are fairly individual, so a some people could find food does not manage their IBD inflammation.
For the most part it is the same drugs to treat inflammation. People with IBD and people with hypersensitivities and IBD benefit from these medications. People who had only hypersensitivity (and have been misdiagnosed as having IBD for reasons discussed above) would benefit from eliminating these foods even if they did not take anti-inflammatory meds.
In my opinion, this is why some people diagnosed with IBD find food is almost totally related to their disease, and why many people find no one food helps/hurts them. By the time you also figure in how the food interacts with the gut microbes and how the gut microbes interact with the immune system - well you get all kinds of variations where it would take some sophisticated analyses to say what exactly was going on with any one individual - and also we would need to discover more of the self-antigens involved.
- It does not need to be an either/or fight with food.
- Most everybody is likely accurately diagnosed by symptoms, scope, and biopsy
- There could be some folks here with both IBD and hypersensitivities
- There might even be someone here that if given genetic tests and specific antibody tests who would no longer have an IDB diagnosis (or at least change to IBD, type unknown).
I hope this helps somewhat quiet down the "great food debates".
Post Edited (DBwithUC) : 3/13/2017 4:02:08 PM (GMT-6)