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There is some confusion in the terms applied in articles and conversations about Celiac Disease, gluten, gliadin, and food intolerance.  The terms Celiac, gluten, and gliadin each have general and specific definitions, and knowing which one is being used is important for full understanding of articles and research on the subject.  The following Glossary is provided to give some orientation as to how these important terms are used.  A companion essay is available that introduces The Basic Factors of Gluten Sensitivity and Celiac Disease and how these factors cause and contribute to illness.

Another shorter glossary is found on http://www.naspgn.org/sub/celiac_disease.asp.

Gluten

·     Specifically, gluten is the storage protein found in grains of wheat.  But other similar proteins are also called gluten in a general sense and are widely found in grains and in at least one fruit (this fruit happens to be Buckwheat, but Buckwheat is neither a wheat or a grass).

·     In the general sense, glutens are a family of very useful, very cheap, and very tasty proteins.  Because wheat gluten is so useful, cheap, inexpensive, cheap, tasty, and cheap, it can be found added to most packaged or restaurant foods.

·     The “gluten” from each type of glutinous seed is a little bit different and has its own name, but all are loosely called “gluten”.  Likewise, tolerance to these different proteins varies between people.  The point is that some glutens may be safe for some people to eat while others are not.

·     More people have health problems with wheat gluten and very similar glutens in rye and barely than with other types of gluten and more people have health problems with wheat gluten than with any other single staple foodstuff.  Most other glutens are generally well tolerated (but not always).

·     The chemical problem in Celiac Disease and Gluten Intolerance is a specific fragment of wheat gluten, a family of sequences of amino acids called Gliadin.  Very similar fragments that also cause injury are found in rye and barley (also in oats but that is a special case).

  Gliadin  (glī΄-ə-dĭn)  [gly-eh-din]

·     Gliadin is a molecule found on the surface of the Adenovirus (ặd΄-ən-ō-vī΄-rəs), which causes common lung infections.  Gliadin’s job is to dig the virus into and between cell walls. Many humans have the dominant genes needed to made antibodies that bind to gliadin and rapidly stop any Adenovirus infection.  This is a great survival trait for people who live or work indoors in winter with many other humans.

·     Gliadin is also found in large quantities in wheat gluten.  When gliadin in gluten becomes water soluble, it is free to bind to cells.  If the victim can make antibodies to gliadin, the body then treats those cells as a virus infection.

·     Gliadin triggers an immune response when it contacts any of a number of cells in the body of genetically susceptible individuals.  This response damages the surrounding tissue and thereby has the potential to set off many other heath problems throughout the body.

·     Gliadin is classified as a member of a family of sequences called prolamines.  Prolamines in rye and barley glutens are have their own technical names, but they are often just called gliadin because they are chemically similar and have the same toxic reactions (the actually prolamin from rye is secalin, from barley hordein and from oats avenin).

·     Gliadin is very unique among foods in that it contains substantial lengths of poly-glutamine.  Prolamines in other grains associated with milder gluten sensitivity happen to contain shorter lengths of poly-glutamine.

·     Gliadin molecules in gluten are not very water soluble, and so they are not very digestible unless they are subject to such processes as fine grinding, baking, fermentation, and chemical treatment and synthesis. 

·     If the gliadin remains intact within the digestive tract (and it is a particularly stable molecule) it can bind to the intestines, especially if the intestine lining is weak or flawed.  Significant amounts of gliadin eaten can cross the intestine into the blood stream.

·     Since the 1970’s, more chemically treated gliadin is in the diet.  In the 80’s, Americans increased the amount of wheat they ate; having been told it was healthier than meat.  In the 1990’s, additions of “vital gluten” and gluten-based flavors were increased in manufactured foods.  In the 2000’s Kansas State University Grain Science Department (and other places) works to increase gliadin content in wheat and may attempt introduction of gliadin in other grains such as rice.

Poly-Glutamine

Poly-glutamine (poly-Q) is a chain where the molecule glutamine (Q) is repeated many times within a protein.  This is actually quite rare. Long poly-glutamine chains are really only found in three places:

1)      Normal transcriptional regulation proteins, which are found especially in the central nervous system and which are normally short lived and regulated by Ubiquitin.

2)      Specific protein "mutations" associated with degeneration of the central nervous system.

3)      Gliadin in wheat (Alpha and beta). (Shorter glutamine chains are found in other grain storage proteins.)

Excessive long chain poly-glutamine is associated with neuron toxicity. Toxicity of poly-glutamine is implicated in poly-glutamine diseases, which include Huntington’s Disease and some types of ataxia.  This mechanism provides (hypothetical at this time) means by which gluten triggers, aggravates, or seems to cause degenerative CNS disorders and provides means by which gluten mimics genetic CNS disorders when the genetic disposition is not present.

Celiac

In reference to a person, a Celiac is specifically someone who has Celiac Disease.  Some generally call anyone who has any gliadin sensitivity a “Celiac” because the diet therapy is the same regardless of the symptoms and also because gliadin sensitivity is a required precursor to classic Celiac Disease.  It is a lot easier to refer to a person as being a “Celiac” than as “a gluten intolerant person” or as “a gliadin sensitive person”.

Celiac Disease / Celiac Sprue (also Coeliac)

Just as Celiac Disease has many symptoms, there is also more than one definition of Celiac Disease.  As classically defined, a Celiac only had a chance of correct diagnosis if that person was already wasting away.

Many texts describe Celiac Disease as food intolerance or inability to digest gluten, but this is outdated since we now know about the involvement of the immune system.  The question remains whether Celiac Disease is an allergy to gluten or an autoimmune condition caused by gluten.  Actually, gliadin sensitivity is the common delayed allergy to wheat gluten that usually progresses into one or more autoimmune conditions, of which Celiac Disease is just one of many.

As you study the relationships between gluten and any given disease, it is important to know which definition applies to the research you are reading.  Usually, the Classic Celiac Disease definition is used, and therefore it is likely that such a study has not considered the broader cases of general gluten intolerance.

Classic Celiac Disease / Typical Celiac Disease

In its most traditional, narrow, or specific definition, “Classic” Celiac Disease is a diagnosis of:

1.      antibodies against gluten (allergy) OR the body’s own tissues (autoimmunity), AND

2.      specific microscopic injury to the small intestine, AND

3.      malabsorption possibly with chronic diarrhea (sprue), AND

4.      clinical response to a gluten-free diet, AND

5.      return of symptoms on return of gluten to the diet.

Clearly, this is a very narrow definition of the condition, one that can delay treatment as the full-blown classic symptoms often develop separately and slowly over time.

This classic definition is convenient for researchers and primary care doctors because of its narrowness and historical precedent. The narrow definition is also profitable for drug manufactures as it delays application of a diet therapy to many chronic conditions.  But the narrow definition can be worse than useless to people who suffer from some form of Gluten Intolerance or Gluten_Sensitivity other than Classic Celiac Disease because its use may lead to misdiagnosis. 

Celiac Disease Autoimmunity (CDA)

This new term is an even narrower definition of the condition.  Diagnosis of CDA requires detection of antibodies to Human tissue Transglutaminase (HtTG) in the blood.  The presence HtTG antibodies indicates that a patient’s gluten sensitivity has progressed to an autoimmune condition against the intestines or possibly the brain or other organs containing HtTG.  According to proponents of this test, if you to not have HtTG antibodies in the blood then you do not have Celiac Disease -- for better or worse, such a protocol excludes from treatment any patient whose food sensitivity has not yet progressed to intestinal autoimmunity.

Atypical Celiac Disease

In its most general definition, any illness, condition, or symptom caused by sensitivity to gliadin from gluten could be called Celiac Disease because the basic cause and the diet therapy would be the same in any case.  The term Atypical Celiac Disease applies to many conditions other than malabsorption that can improve or be cured on a gluten free diet.  Such conditions include nerve damage, obesity, and thyroid and skin problems to name a very few.  For a more complete list, please see the annotated list of symptoms and health problems associated with gluten sensitivity.

Some cases of Atypical Celiac Disease might only be diagnosed by diet test or by detection of anti-gliadin anti-bodies anywhere in the body.  Because the gut is not fully involved, antihuman tissue transglutaminase (TTG) and endomysial antibody (EMA) tests may be negative.

All forms of Celiac Disease are also forms of Gluten Intolerance, Gluten Sensitivity, or Gliadin Sensitivity.  Ironically, it turns out that Atypical Celiac Disease is 5 to 10 times more common than “Typical” Celiac Disease!

Silent Celiac Disease / Asymptomatic Celiac Disease

Silent Celiac Disease is the condition where a person has blood test results that show celiac disease and also has injured small intestines, but has no recognized classic or atypical symptoms (or the symptoms may so very mild as to be barely noticeable).

When Celiac Disease is silent, it may develop more classically or atypically at any time later in life.

Latent Celiac Disease

Latent Celiac Disease is the condition where a person has blood test results that show celiac disease but has normal small intestines and no recognized signs of malabsorption or diarrhea.  However, the severity of malabsorption and diarrhea symptoms in Celiac Disease are greatly dependent on diet and medical history and are in some part dependent on the severity of the gliadin sensitivity.  The patient has to be particularly vigilant that a doctor doesn’t consider the blood tests to be false in these cases.

When Celiac Disease is latent, it may develop more classically at any time later in life. The Latent Celiac probably has other immediate health injuries that could benefit from a gluten free diet.

Celiac Sprue

While we are here, the term Celiac Sprue is an older name for Celiac Disease.  Sprue is a condition of chronic diarrhea, emaciation, and anemia, caused by defective absorption of nutrients from the intestinal tract.  Classic Celiac Disease is the most common form of Sprue other than Tropical Sprue, but most cases of Gluten Intolerance would not be characterized as sprue.

Genetic Disorder 

It is interesting that many places refer to gluten intolerance or Celiac Disease as a genetic disorder.  The ability to make antibodies to gliadin is a dominant gene and it is a perfectly good defense against a common virus.  This is a survival trait, not a disorder.  Is not the problem really wheat, which is a genetically manipulated grain that was not quite perfectly adapted for human food?[1]

Antibody

Consider this scene: An infantryman with a laser designator is specifically trained to hunt for and recognize an enemy tank by its characteristic shape.  When the infantryman contacts and recognizes an enemy tank, he shines his laser designator on the tank.  A combat aircraft drops a smart bomb that tracks the laser designation on the tank.

Now, in terms of the immune system, the tank is a germ with a characteristic “shape”, the smart bomb is a Killer T-cell, and the specifically trained infantryman with a laser designator is the antibody.

Antibodies are made so one end is coded to match a specific protein on the surface of a specific germ while the other end is made to trigger a Killer T-cell.  When an antibody contacts a germ that matches its code, it latches onto the germ.  When a Killer T-cell contacts an antibody on a germ, it “blows up” and releases a poison right next to the germ.

The problem is, an antibody will latch to anything that fits its code.  An antibody evolved over 100 million years to fight off an adenovirus infection can’t tell an adenovirus from a matching piece of wheat protein.

By the way, inflammation is often the collateral damage caused by the Killer T-cell “smart bomb”.

Allergy

An allergy is an abnormally high sensitivity to certain substances, such as pollens, foods, or microorganisms.  However, it seems conventional that an allergy is particularly a sensitivity that involves an immune reaction.  Familiar allergies are reactions to things in the air like pollen and mold, and immediate reactions to food where you “swell up and drop dead”.  However, common food allergies are mostly delayed reactions where noticeable symptoms develop over hours or days, even months or years.  It is very difficult to recognize the causes of delayed allergic reactions.

Food Intolerance

Food intolerance is sensitivity to a specific food or set of foods.  But there are several different forms of sensitivity.  Glucose intolerance is the weakened ability of cells to absorb glucose (also known as Type 2 Diabetes).  Lactose intolerance is the inability to digest lactose.  The immune system reacting to a specific protein in a food is a delayed allergy, but is still a form of food intolerance.

Gluten Intolerance

Most technically, gluten intolerance is sensitivity to gluten.

A problem is that some out-of-date publications say that Gluten Intolerance or Celiac Disease is food intolerance, not an allergy (probably because the author was not yet familiar with the role of the immune system in Gluten Intolerance).  But other publications say that Celiac Disease is an allergy, not food intolerance.

Gluten intolerance is an allergy.  But whereas most recognized allergies involve fast IgE type antibody reactions, Gluten intolerance involve slower IgA and IgG type antibody reactions.  But the general symptoms of this reaction are such that that the localized IgA and IgG gluten allergy reaction in the gut look a lot like a digestion problem. 

In fact, gluten intolerance does cause other food intolerances, such as to lactose (milk sugar), but also to many other starches, proteins, and fats, because gluten intolerance damages the body’s ability to digest food.

There has been a tendency to describe Gluten Intolerance as the inability to digest wheat gluten.  A Celiac can probably digest gliadin just as well as anybody (i.e., poorly), at least until the immune reaction damages the gut and then the Celiac has more trouble digesting a lot of things.  When a person drinks milk he can’t digest, bacteria go crazy on the undigested milk sugar and make gas and toxins.  This condition is commonly recognized as lactose intolerance.  But when a Celiac eats gliadin, he likely also has trouble digesting milk because of the injuries caused by the reactions to gliadin, so it might just look like the Celiac has a digestive problem rather than an immune problem.

Gluten Sensitivity / Gliadin Sensitivity

From http://bmj.bmjjournals.com/cgi/content/full/318/7200/1710

“Marsh's "modern" definition of gluten sensitivity is to be recommended: "a state of heightened immunological responsiveness to ingested gluten in genetically susceptible individuals."10 Such responsiveness may find expression in organs other than the gut. Gastroenterologists, dermatologists, neurologists, and other physicians need to be aware of these developments if the diagnosis and treatment of the diverse manifestations of gluten sensitivity are to be advanced. The aetiology [study of causes or origins] of such diverse manifestations presents the next challenge.”

The reaction to gluten is brought about by a person’s ability to make anti-gliadin antibodies.  If a person has anti-gliadin antibodies in the body, then that person is gluten and gliadin sensitive, and that person’s immune system will kill any tissue that is contacted by gliadin.  Sometimes, anti-gliadin antibodies can be detected in the blood, and this has been part of the conventional diagnosis for Celiac Disease.  The problem is, blood testing for anti-gliadin antibodies in the blood has proven unreliable[2].  However, it has recently been demonstrated that it is much more reliable to test for anti-gliadin antibodies in the stool than in the blood[3].

Autoimmune Condition

In an autoimmune condition, the immune system treats some part of the body just as if that part is some sort of infection or cancer.  (It may well be that most Autoimmune Conditions are actually reactions against remains of damaged tissue or some other chemical associated with tissue repair rather than reactions against healthy tissue.)

Endomysial

Anything relating to, or affecting the endomysium is called endomysial. The endomysium is the fine connective tissue sheath surrounding a muscle fiber and also nerve fibers.  Autoimmune reaction to the endomysium is associated with Classic Celiac Disease.  The presence of antibodies to the endomysium could cause an autoimmune attack to muscles and nerves.  This would also weaken the defenses of nerves against other toxins.

Transglutaminase

Tissue transglutaminase is a very important enzyme that helps repair damaged tissue.  Elevated levels of tissue transglutaminase occur where there is tissue damage or inflammation.  Concentration of tissue transglutaminase also normally occurs in the brain. Autoimmune reaction to tissue transglutaminase is associated with Classic Celiac Disease.  The presence of antibodies to tissue transglutaminase could cause an autoimmune attack at any wound or site of inflammations, slowing healing and perpetuating chronic inflammation.  Concentration of tissue transglutaminase also normally occurs in the brain, so autoimmunity to tissue transglutaminase could trigger immune attack in the brain.

Malnourishment

Malnourishment is the problem where some nutrition is missing in the diet, which results in health problems from nutritional deficiencies.

Malabsorption

Malabsorption is the problem where the nutrition is present in the diet, but it is not being absorbed.  This is a bigger problem than simple malnutrition!  Sure, you get deficiency problems, but you also get problems caused by undigested food decaying and fermenting in your gut for days (imagine alcohols, acids, and much worse forming in your gut).

In malabsorption, a some types of fats, starches, sugars, or proteins can’t be absorbed completely.  They can’t be absorbed because of inflammation or loss of tissues that normally absorb certain nutrients or produce the enzymes needed to break down certain nutrients.  This brings about several problems:

First, there are the same nutritional deficiencies that happen with malnutrition.

Second, the patient or doctor might not suspect a deficiency because the nutrients are known to be in the diet, resulting in a missed diagnosis.

Third, and this a very important feature of malabsorption, food not absorbed remains in the intestinal flow where it can become rancid and acidic or become rich food for excessive bacteria and yeast.  Fermentation of unabsorbed food produces excess gas.  Rancid food chemicals and bacterial toxins irritate the intestine and surrounding organs.  Inflamed intestines increase that body's requirements for antioxidant vitamins and further reduce the intestine's ability for absorb nutrients.  A doctor not trained to recognize malabsorption may not recognize it in this case.

Specific malabsorption may be diagnosed as specific food intolerances, but the real culprit is the gliadin that causes secondary intolerances.  The doctor that was taught that gluten intolerance is rare would not consider investigation of the underlying problem.

Forth, general or specific food cravings may be initiated by the malabsorption, possibly resulting in overeating and all attendant complications of obesity. The doctor might recommend diet and exercise weight reduction rather than an investigation of the cause of the weight gain.

 

Hydrolyzed Plant Protein

Hydrolyzed Vegetable Protein

A Hydrolyzed Vegetable protein is a protein obtained from various foods (like soybeans, corn or wheat) and broken down into amino acids by a chemical process called acid hydrolysis. Hydrolyzed plant or vegetable protein is used as a flavor enhancer in numerous processed foods like soups, chilis, sauces, stews and some meat products like frankfurters. The whole point of these additives is to spoof the nervous system into thinking that the processed food is high in protein on a habit-forming manner.  Some hydrolyzed vegetable proteins act directly on nerves and some like MSG actually kill nerves in high quantities.

Normally, the body’s digestion does its own job of breaking proteins down into water-soluble amines, which the body then absorbs and recombines into new proteins.   Eating Hydrolyzed Proteins presents some foreign proteins to the body in a whole water-soluble form that the body is not generally prepared to manage.  If these foreign proteins enter the body, say, over an intestine perforated by the gliadin reaction, then these foreign proteins can interfere with body chemistry in many ways.

Furthermore, when Hydrolyzed Vegetable Protein is made from wheat (sometimes without notification to the consumer), this converts the gliadin into its most toxic water-soluble form.

 

 

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[1]Cereal Grains: Humanity’s Double-Edged Sword”, Loren Cordain, Simopoulos AP (ed): Evolutionary Aspects of Nutrition and Health, Series: World Review of Nutrition and Dietetics, Basel, Karger, 1999, vol 84, pp 19–73.

[2]False Negative Serological Results Increase with Less Severe Villous Atrophy

Digestive Disease and Science, 2004 Apr;49(4):546-50. (Found on Celiac.com)

[3]Early Diagnosis Of Gluten Sensitivity: Before the Villi are Gone Transcript of a talk given by Kenneth Fine, M.D. to the Greater Louisville Celiac Sprue Support Group, June 2003.