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This essay is a brief description of condition of gluten sensitivity and intolerance as an interconnected sum of its parts, a description that might not have been possible before the year 2000. It is intended as a general introduction to the complex biochemistry of gluten intolerance and as a companion to the Annotated List of Symptoms and Health Problems.
In the simplest sense, Gluten Sensitivity is what happens when a person’s immune system reacts to a specific protein in wheat as if it were a virus. This reaction basically results in two big problems; first, the small intestine is injured so most of the digestive tract doesn’t work right, second, the immune system becomes very aggressive and can begin attacking organs through out the body. Much focus in the past has been on Celiac Disease. But with the discovery of the role of gliadin, it is now known that Celiac Disease is just a part of a larger picture.
Gliadin
Gliadin is a molecule that makes up a large part of the protein in wheat. The same gliadin molecule is found on the surface of the adenovirus, a common cause of lung infections. Other grains have similar molecules, some so similar that they cause the same reaction (barley and rye).
The Gliadin Reaction
The gliadin reaction is a type of allergy somewhat milder than the anaphylactic allergies most people think they know about. But because it is milder, many more people suffer without knowing what is wrong.
As wheat protein (gluten) is digested, some of the gliadin becomes water-soluble, and is able to come in contact with human tissue. If the gluten was subject to processing, such as flour grinding, cooking, bleaching, fermentation, or hydrolysis (acid treatment), much more gliadin becomes water-soluble.
The gliadin molecule readily sticks to certain tissue. The first tissue it generally contacts is the upper small intestine, but gliadin easily crosses into the blood stream and can stick to many places thorough out the body. This attachment happens whether or not a person's body can make anti-gliadin antibodies.
If a person's body can make anti-gliadin antibodies, then the body will mistake healthy tissue for a virus. In this case, the immune system will kill the cells that have the gliadin attached as well as some neighboring cells. This causes inflammation in the areas where the gliadin was attached.
Antibodies may also attach to gliadin molecules flowing in the blood. The resulting antibody-gliadin “clumps” can collect in capillaries. This effect is recognized in the case of Dermatitis Herpetiformis and may be involved in many other conditions.
Enteritis
The immune attack against gliadin molecules attached to the lining of the small intestine causes Gluten Sensitive Enteritis. Eventually, this enteritis can develop into an autoimmune attack against the small intestine as well, possibly indicated by anti-endomysial antibodies in the blood. This enteritis results in:
- Malabsorption caused by the injured small intestine no longer being able to absorb enough nutrients.
- Malabsorption caused by the injured small intestine no longer being able to produce enough digestive enzymes.
- Ulceration or microscopic perforation of the small intestine causing a Leaky Gut.
- A weakening of the mucus defenses, which permits more direct exposure to other toxins as well as infections.
Malabsorption
Malabsorption results in deficiencies in vitamins and minerals, as well as vital sugars and fatty acids needed for proper function of organs and body systems. Malabsorption causes deficiencies even if all nutrients are plentiful in the diet. These deficiencies caused by gluten can be for very few nutrients and affect few organs or very many nutrients and affect the whole body. In effect, someone who is malabsorbing is very slowly starving to death, and maybe only a piece at a time.
Nutrients that are eaten but not absorbed have to go somewhere. As they remain in the intestine, they oxidize and form acids and other toxins. These toxins further inflame and damage the small and large intestines.
These unabsorbed nutrients also provide greatly excessive food supplies for infectious bacteria and yeasts in the gut. This causes excessive bacteria and yeast growth that results in more toxins and infections in the intestines and nearby organs. Malabsorption also forms chronic gas and causes chronic diarrhea or constipation.
By causing combinations of overuse, toxicity, and deficiencies, malabsorption greatly stresses the pancreas, gall bladder, liver and spleen resulting in disease and cancers in those organs.
Autoimmunity
Autoimmune diseases are strongly associated with wheat gluten -- Celiac Disease is just one of many such autoimmune diseases. Roughly 10%-30% of general autoimmune patients are also classic Celiacs. As much as a third of autoimmune patients have anti-gliadin antibodies detected in their blood. 4 out of 5 autoimmune patients have anti-gliadin antibodies detected in their stool.
One hypothesis for the association between autoimmune diseases and gluten intolerance is that the continuous presence offending proteins, an infection that never goes away, causes the immune system to become over sensitive and over aggressive. The spectrum of symptoms of untreated gluten intolerance is similar to the spectrum of symptoms associated with cancers and transplanted organ rejection.
Another hypothesis: In a normal immune reaction, the main cells destroyed would be virus and bacteria. But if a never ending continuously damages the body's own tissue, then the body has to deal with the damage cell tissue that remains. This damaged "self" tissue may well be the actual target of the organ specific antibodies associated with autoimmune diseases, rather than the undamaged "self" tissue of healthy organs.
Inflammation and Anti-Oxidant Deficiencies
Ironically, a gluten sensitive person needs more anti-oxidants at the same time that person is getting less anti-oxidants from food, a double whammy. As discussed above, a gluten sensitive person is subject to both autoimmune attack and malabsorption to one degree or another. Both autoimmune attack and malabsorption cause inflammation damage to tissue. Inflammation damage to tissue consumes anti-oxidants for control, removal and healing of the damage. So, even though a gluten sensitive person may eat plenty of anti-oxidants, and may take anti-oxidant supplements, that person could still be deficient because of the combined effects of increased need and decrease absorption.
Deficiencies in anti-oxidant vitamins A, E, C, as well as anti-oxidant minerals like zinc and selenium are widely linked to number of heath problems from infections to heart disease and cancer. So one would expect the gluten sensitive person would be more susceptible to the sorts of problems associated with deficiencies in anti-oxidants.
Leaky Gut
Normal, healthy intestines only permit smaller molecules to cross into the body. These smaller molecules are small fragments of digested proteins called amines, simple sugars digested out of complex sugars and starches, and short fatty acids, which are small pieces of digested fats.
Because of its particular physical and chemical properties, gliadin is a large molecule that can actually cross the intestine into the blood on its own (this the very reason the adenovirus uses gliadin.) But in general, healthy intestine walls block most large molecules. MSG manufactures are quick to point out that MSG is too large of a molecule to get across a (healthy) intestine, so there is no way MSG can cause, say, headaches (“in healthy people” they whisper).
The damage from the inflammation, toxins, and infections caused by
malabsorption as well as immune reaction cause microscopic holes and even
ulcers. A perforated or “leaky” gut permits larger molecules to enter the
blood. Naturally many of these foreign
molecules can interfere with body chemistry and organ function. For example, foreign MSG can
interfere with normal nerve communication and is a neurotoxin in high
concentrations. In general, large foreign
protein fragments in the blood and organs can trigger immune reactions all over
the body.
A very technical discussion of much of the above information may
be found in the 2004 review article, “Advances
in celiac disease”.
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