MY RESEARCH ARCHIVES

Genetics of Food Intolerances


This is the most amazing piece of writing I have found to date on Auto Immune Diseases….. Fully agree with everything stated….. a man thinking well before his time 🙂

Professor Ayers has a blogspot called coolinginflammation and I would recommend anyone with Alopecia to read up on his blogs.

http://coolinginflammation.blogspot.co.uk

Genetics of Food Intolerances

Food intolerance is based on missing bacteria in the the gut rather than inadequacy of human enzymes, e.g. lactase, or altered immune system.
I make the extreme statement that food intolerance is not genetic, to emphasize that the vast majority of intolerance can be cured by changing the bacterial composition of the gut’s microbiological community, the gut flora, rather than attempting to accommodate a permanent deficiency.  The two common “intolerances” that are offered by my readers to invalidate my sweeping statement are lactose and gluten (celiac) intolerance.
Lactose Intolerance is Not Due to Inadequate Lactase Everybody has the same gene for lactase, but some people have altered upstream control elements and continue to express lactase in their intestinal cells after infancy, whereas others don’t.  The racial pattern of adult lactase expression is an interesting note on human evolution, but is irrelevant with respect to an individual’s ability to tolerate the lactose sugar in dairy products.
Lactose is the major sugar present in milk and the ability of the intestines to utilize lactose directly like glucose is a selective advantage for human evolution.  Absent that ability, lactose would just pass through the gut without impact.  However, bacteria in the colon also have lactose digesting enzymes.  These bacteria produce hydrogen and methane gases, and these products in turn can feed other bacteria.  If all of the products are consumed, then the lactose has been treated as a soluble fiber and the result is more gut bacteria and a happy gut.  If some of the bacteria are missing, then the lactose acts as a laxative, e.g. lactulose, and the bowels are not so happy.
All that is needed to cure lactose intolerance, as in all food intolerances, is to provide the gut bacteria that are missing to fully metabolize the offending sugars or polysaccharides.  Just continuing to eat dairy without also eating or introducing new species of bacteria into your gut, will just provide more symptoms, but eating yogurt still containing live probiotic bacteria that have the enzymes to ferment lactose, will lead to a rapid cure.  (See reference below.)  As the fermenting bacteria grow in the gut, they transfer their genes to gut bacteria in the biofilms lining the gut and these new species of bacteria keep the lactose out of trouble.
The point is that having a food intolerance means that the aggregate of all of the genes in all of your gut microorganisms is lacking the genes/enzymes needed to completely digest a food component.  In the case of lactose intolerance, the missing genes are present in typical probiotics, bacteria that grow on milk/lactose.
Celiac is not a Typical Food Intolerance Celiac is a complex interaction between major toxic proteins in wheat (gliadin), detox gut enzyme (tissue transglutaminase, tTg) and antibodies.  Gliadin is a wheat protein adapted to attack the intestines of herbivores.  Herbivores, such as insects and humans, can in turn protect themselves from gliadin and other polyglutamine proteins with the enzyme transglutaminase.  tTg binds to glutamines in gliadin and converts them to glutamic acids.  Unfortunately, while the gliadin is bound to the tTg, inflammation can predispose the gut to present these proteins to the immune system for processing to trigger antibody production.  This is the start of the autoimmune disease.
The major histocompatibility antigens (MHAs) code for the proteins that display fragments of proteins on cell surfaces for antigen presentation and immune response.  There is a lot of MHA variation and evolutionary adaptation.  Some MHAs favor antibody production to gliadin and tTg.  This just shows that celiac and grain/gluten intolerance is not a typical food intolerance, which will be remedied by simply altering gut bacteria, even though establishing gut bacteria that metabolize gliadin or that reduce autoimmunity, may be part of the cure.
Enhancing Gut Flora is Part of the Cure for all Autoimmune Diseases There are rare food allergies, even though the majority are misdiagnosed intolerances.  The production of antibodies to food antigens is a symptom of the breakdown in communication between the gut immune system and gut flora.  Particular species of bacteria are responsible for the development of both the aggressive and suppressive components of the immune system, which occurs in the lining of the gut.  Loss of the suppressive cells, Tregs, can result from unhealthy diets and exposure to antibiotics, and results in autoimmune disease, in which the aggressive immune system is out of control and attacks self antigens.
Symptoms of all autoimmune diseases can be improved by reestablishing normal control of the aggressive part of the immune system via healthy gut flora.  Clostridium species of bacteria normally induce healthy development of the suppressive immune system and these types of bacteria are common in soil clinging to fresh vegetables prior to extensive washing.  Which of the bacteria that are eaten become established in the gut flora is unpredictable, because the bacteria interact with each other, food and cells lining the gut.  The only safe and simple procedure currently available is the fecal transplant.  Some experimental fecal transplants are facilitated by the use of encapsulated freeze-dried gut flora.  There is great resistance to this simple, safe, cheap approach from the medical industry.
Reference: Almeida CC, Lorena SL, Pavan CR, Akasaka HM, Mesquita MA.  2012.  Beneficial Effects of Long-Term Consumption of a Probiotic Combination of Lactobacillus casei Shirota and Bifidobacterium breve Yakult May Persist After Suspension of Therapy in Lactose-Intolerant Patients.  Nutr Clin Pract., 27(2):247-51.

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