Your Frequently Asked Questions Answered
Our antibody tests range numerically from a positive value of 10 to as high as 500 Units. The average positive value is about 45 Units. The “units” are based on the amount of antibody detected in the assay which is reflected by more color developing as the result of a color-generating chemical reaction. Thus, the more antibody present, the higher the units of positivity. However, the amount of antibody present is not a measure of clinical severity, but rather, the amount of antibody being produced by the plasma cells in the intestine in response to gluten at that site. A positive value of any degree means your immune system is reacting to dietary gluten in the way the immune system reacts to an infection. With an infection, this immune reaction ultimately kills and clears the infectious organism. But with gluten, the reaction continues as long as it is eaten. Thus, the only way to halt this immune reaction is to remove all gluten from the diet. This is true whether your positive test is 10 units, 500 units, or anything in between.
As mentioned above, the numeric value of antibody is not necessarily a measure of severity of how your body is reacting to gluten, or the resultant damage of the reaction. This is because the main perpetrator of the immune response to gluten is not antibody but T lymphocytes (T cells) producing tissue-damaging chemicals called cytokines and chemokines. How much antibody is produced at the stimulus of T cells differs in different people. Furthermore, some people simply do not or cannot make alot of intestinal IgA antibody even though gluten may be stimulating a severe T cell-mediated immune response. Unlike antibody levels, the numeric value of malabsorption test results are an indicator of severity of intestinal damage (see below).
This question is more “wishful thinking” resulting from the mind trying to turn a positive test into what might want to be called “low positive” or even the equivalent of negative. However from our experience, a positive antigliadin antibody of any degree is like a positive pregnancy test. When a pregnancy test is positive, you are not a little pregnant, you are pregnant. The same is true for gluten sensitivity.
There are several reasons why an antigliadin antibody test can be positive despite being on a gluten free diet. The most obvious reason is that there may be hidden gluten in the diet. Gluten is ubiquitous, and if a person does not prepare 100% of their own food, one can not guarantee no gluten intake. Hidden gluten in unsuspected sources or contaminating otherwise gluten-free foods is also possible. But more often, the values are indeed on the lower end of positive, and previous values may have been higher still. So in fact the “elevated value” in fact may represent a marked improvement over previous antibody levels. Sometimes, however, people are so immune suppressed from damage to the intestine and malnutrition that a gluten free diet actually can make the antibody values go up for a time, a reflection of enhanced immune function and response.
All clinical laboratory tests must define a normal range that best distinguishes those with disease from those without. Depending on what range is used to define normal will determine how many people with disease will fall into the normal range, and conversely, how many people without disease will fall into the abnormal range. Our determined cut off for normal of 10 Units was derived after years of comparing antibody levels with gene and malabsorptive test results, as well as clinical histories before and after treatment with a gluten free diet. Although our stool test is multitudes more sensitive in picking up gluten sensitivity than blood tests, no single diagnostic test can rule out gluten sensitivity with 100% certainty (we estimate our antibody test misses about 1 in 500, about equal to the frequency of IgA deficiency in the general population). Thus, while it is very unlikely that a person with an antigliadin antibody level in the normal range has active gluten sensitivity, anyone with symptoms of gluten sensitivity and/or having an autoimmune disease, especially if accompanied by an antibody level just below the cut off, or with a gluten sensitive gene and/or intestinal malabsorption, should consider a 6-12 month trial of a gluten free diet, looking for improvement in symptoms, autoimmune disease severity, and/or intestinal malabsorption. It is only in this population that a gluten free diet should be considered a “trial”; all other people must consider gluten-free diet for positive tests definite and permanent therapy.
Gluten-induced intestinal damage is fully reversible provided gluten-free dietary treatment is strict and permanent. However, the length of time to full healing and disappearance of malabsorption depends on the severity and disease duration at onset of treatment. Hence, children and those with more mild disease at onset of treatment will resolve malabsorption quicker, usually within 6-12 months. Some adults with severe disease, or those who do not quickly grasp or employ strictness to their gluten-free diet, may have continued nutrient malabsorption for longer periods. If intestinal malabsorption persists beyond 18-24 months, dietary and clinical re-evaluation should be undertaken. Unlike antibody levels, our malabsorption test is a measure of disease severity in the intestine. Values from 300 to 600 malabsorption units represent mild malabsorption; 600-1000 moderate; 1000-1500 severe; and greater than 1500 very severe malabsorption (and possibly indicating a combination of gluten-induced intestinal damage and insufficient pancreatic enzyme secretion).
So that you do not get it, or damage of any other organ. Prevention is the key to lasting health. Once disease sets in, it is much harder and takes more healing energy to reverse than it does to prevent it. An ounce of preventive health eradicates a ton of disease. Do not wait for villous atrophy, osteoporosis, autoimmune disease, or even symptoms to treat gluten sensitivity; prevent it all!
The immune reaction to gluten is gluten sensitivity. Testing for the presence of an antibody produced against gluten is the diagnostic hallmark of gluten sensitivity (for years in the blood, and now more sensitively detected in stool with our testing). Although the immune reaction to gluten, i.e., gluten sensitivity, is the cause of the villous atrophy of celiac sprue, having these antibodies in stool, or even malabsorption, does not necessarily mean you will have detectable villous atrophy in an intestinal biopsy. But why does it matter, since it is known that a person can have every last complication from gluten sensitivity and never have villous atrophy? In other words, one can have gluten sensitivity damaging the intestine on a sub-microscopic level destroying function, or damaging other organs/tissues without having celiac sprue. Thus, there is no reason to expose yourself to the risks, invasive nature, and expense of an intestinal biopsy. This idea is not new. Some have said this for years with respect to positive antiendomysial antibodies. Now we extend this ideology to our stool testing; if you have the immune reaction, and especially if you have detectable malabsorption, symptoms, and/or immune disease, what is there to wait for to go gluten-free? And if you have none of these consequences, why wait for them to appear? Be thankful you do not, and go gluten-free.
Clearly most immune-related damage in the intestine heals with a gluten-free diet. Now it appears from early research of this question that many if not all autoimmune diseases such as autoimmune thyroid disease, psoriasis, alopecia, arthritis, lupus, hepatitis, diabetes, among others, and autism improve with a gluten-free diet. Because the immune reactions to cow’s milk proteins also are immune and autoimmune stimulating, new research is focusing on the benefits of what has come to be called a gluten-free/casein-free diet, which likely is more beneficial in this regard than a gluten-free diet alone (see below). The less immune-stimulating the diet, the less fuel on which the immune fire has to burn. Other immune-stimulating foods include other grains, legumes (including soy), dietary yeast, and especially for arthritic patients, nightshades (tomatoes, potatoes, egg plant, and hot red peppers).
Gene tests for gluten sensitivity, and other immune reactions are HLA (human leukocyte antigen), specifically HLA-DQ, and even more specifically, HLA-DQB1. The nomenclature for reporting HLA gene results has evolved over the last two decades as technology has advanced. Even though the latest technology (and the one we employ at EnteroLab for gene testing) involves sophisticated molecular analysis of the DNA itself, the commonly used terminology for these genes in the celiac literature (lay and medical) reflects past, less specific, blood cell-based (serologic) antigenic methodology. Thus, we report this older “serologic” type (represented by the numbers 1-4, e.g., DQ1, DQ2, DQ3, or DQ4), in addition to the integeric subtypes of these oldest integeric types (DQ5 or DQ6 as subtypes of DQ1; and DQ7, DQ8, and DQ9 as subtypes of DQ3). The molecular nomenclature employs 4 or more integers accounting together for a molecular allele indicated by the formula 0yxx, where y is 2 for DQ2, 3 for any subtype of DQ3, 4 for DQ4, 5 for DQ5, or 6 for DQ6. The x’s (which commonly are indicated by 2 more numbers but can be subtyped further with more sophisticated DNA employed methods) are other numbers indicating the more specific sub-subtypes of DQ2, DQ3 (beyond 7, 8, and 9), DQ4, DQ5, and DQ6. It should be noted that although the older serologic nomenclature is less specific in the sense of defining fewer different types, in some ways it is the best expression of these genes because it is the protein structure on the cells (as determined by the serologic typing) that determines the gene’s biologic action such that genes with the same serologic type function biologically almost identically. Thus, HLA-DQ3 subtype 8 (one of the main celiac genes) acts almost identically in the body as HLA-DQ3 subtype 7, 9, or other DQ3 sub-subtypes. Having said all this, it should be reiterated that gluten sensitivity underlies the development of celiac sprue. In this regard, it seems that in having DQ2 or DQ3 subtype 8 (or simply DQ8) are the two main HLA-DQ genes that account for the villous atrophy accompanying gluten sensitivity (in America, 90% of celiacs have DQ2 [a more Northern European Caucasian gene], and 9% have DQ8 [a more southern European/Mediterranean Caucasian gene], with only 1% or less usually having DQ1 or DQ3). However, it seems for gluten sensitivity to result in celiac sprue (i.e., result in villous atrophy of small intestine), it requires at least 2 other genes also. Thus, not everyone with DQ2 or DQ8 get the villous atrophy of celiac disease. However, my hypothesis is that everyone with these genes will present gluten to the immune system for reaction, i.e., will be gluten sensitive. My and other published research has shown that DQ1 and DQ3 also predispose to gluten sensitivity, and certain gluten-related diseases (microscopic colitis for DQ1,3 in my research and gluten ataxia for DQ1 by another researcher). And according to my more recent research, when DQ1,1 or DQ3,3 are present together, the reactions are even stronger than having one of these genes alone (like DQ2,2, DQ2,8, or DQ8,8 can portend a more severe form of celiac disease).
Everyone has two copies (or alleles as they are called scientifically) of every gene in the body; one from mother and one from father. The only way to know if a parent definitely has a gluten sensitive or celiac gene without testing them directly, is if a child has two such genes (having received one from mother and one from father). If only one gluten sensitive or celiac allele is present in a child, there is no way to know if it came from mom or dad. One gene is enough, however, to get clinically significant gluten sensitivity or celiac disease, and from published research, two copies yields an even stronger reaction and hence, potentially more severe gluten-related complications.
Because everyone has two copies (alleles) of every gene, but a parent only gives one of these genes to each of their offspring (distributed randomly between a parent’s two alleles), even if a child does not have a gluten sensitive or celiac gene, one or both parents could have one of these predisposing genes as their other allele. Hence, a person without a predisposing gene could still have parents or siblings with these genes. To be sure, each family individual must be tested to know. (The only certainty with respect to genetic testing is that if a person is found to have two predisposing genes, then every one of his/her children and both parents will have at least one copy of these genes, which is enough to get clinically significant gluten sensitivity or even celiac disease.) Because a child gets one allele from each of their parents, even though a particular person does not have a gluten sensitive gene, their children have a good chance of getting one from the other parent since these genes are very common (see next paragraph).
DQ2 is present in 31% of the general American population. DQ8 (without DQ2) is present in another 12%. Thus, the main celiac genes are present in 43% of Americans. Include DQ1 (without DQ2 or DQ8), which is present in another 38%, yields the fact that at least 81% of America is genetically predisposed to gluten sensitivity. (Of those with at least one DQ1 allele, 46% have DQ1,7, 42% have DQ1,1, 11% have DQ1,4, and 1% have DQ1,9.) Of the remaining 19%, most have DQ7,7 (an allele almost identical in structure to DQ2,2, the most celiac-predisposing of genetic combinations) which in our laboratory experience is associated with strikingly high antigliadin antibody titers in many such people. Thus, it is really only those with DQ4,4 that have never been shown to have a genetic predisposition to gluten sensitivity, and this gene combination is very rare in America (but not necessarily as rare in Sub-Saharan Africa or Asia where the majority of the inhabitants are not only racially different from Caucasians, but they rarely eat gluten-containing grains, and hence, gluten-induced disease is rare). Thus, based on these data, almost all Americans, especially those descending from Europe (including Mexico and other Latin states because of the Spanish influence), the Middle East, the Near East (including India), and Russia, are genetically predisposed to gluten sensitivity. (That is why we are here doing what we do!) But be aware that if a person of any race has a gluten sensitive gene, and eats gluten, they can become gluten sensitive.
Research showing a high association of antibodies to cow’s milk proteins in people who react similarly to gluten has been around for over 40 years. More recent research has now confirmed that these reactions to cow’s milk proteins (mainly casein but also lactalbumin, lactoglobulin, and bovine serum albumin) are indeed epidemiologically related to autoimmune diseases such as diabetes, psoriasis, eczema, and asthma, among others. While formal studies of dairy-free diets, either alone or in combination with gluten-free, have not yet been conducted on a wide scale, the idea of a gluten-free/casein-free diet is not new, having been employed for decades by many health practitioners. From my objective assessment of this field, and my personal experience with my own dietary elimination for health, I recommend complete avoidance of all dairy products in anyone found to be immunologically sensitive to cow’s milk protein by our tests, and anyone with an established autoimmune or chronic immune disease. I predict future research will support this recommendation. Do not bury your head in the sand waiting for such studies. Do your own study and go gluten-free/dairy-free.
The main difference between the milk of cow’s versus that of these smaller animals is the percent protein content, being smaller in the smaller animals (because the newborns do not have to grow as large as fast as calves grow to become cows; human milk is even lower in protein relative to these animals). Thus, to consume products made from goats or sheep is really to consume less of the protein. I believe this is why these alternative milk products tend to be less antigenic than cow’s milk protein. Another potential reason is that goat’s and sheep milk are consumed infrequently, and hence established immune reactions are rare at the time they are introduced to replace cow’s milk. However, less antigenic is not “not antigenic.” They are still foreign proteins to the human body capable of, and often, stimulating immune reactions in the intestine and body. It is like this from my perspective: mammals (mammary animals) are supposed to suckle and drink their mother’s milk until weaning, when the conversion to their natural food source commences and ultimately replaces the milk completely. The replacement is so complete that the genes breaking down milk sugar lactose are down regulated to become absent because they are not to be needed since milk is no longer to be consumed. This is what we call lactose intolerance but is, in fact, the natural evolution of the gut mucosa. There really is no explanation in natural terms that can justify an adult mammal consuming milk beyond the age of weaning, much less the milk of another mammal. It is done (obviously), but it is not natural (and seemingly not healthy).
The immune system considers Saccharomyces cerevisiae foreign causing a reaction that may damage the intestine and other tissues of the body, and/or possibly lead to the development of or indicate the presence of Crohn’s Disease.
The main abnormality of testing to be followed up with a repeat test is an abnormally high malabsorption test. If this is not followed to normality, chronic malabsorption may lead to nutrient, vitamin and mineral loss from the body, causing osteoporosis, osteomalacia, calcium oxalate kidney stones, and other complications of chronic malabsorption. The best interval for this follow up is one year. If moderate to severe malabsorption persists despite a strict gluten-free diet, other causes, including inflammatory bowel disease (especially Crohn’s disease which is more common in gluten sensitive people likely because of the associated immune reactivity to Saccharomyces cerevisiae, dietary yeast) and deficient excretion of pancreatic enzymes, should be considered. Follow up of an abnormal antigliadin antibody also can be done at 1-2 year intervals as a guide to dietary compliance, but remember that in the first year or two, the levels rarely go to normal, and sometimes, because of enhanced immune function, may rise for a time before ultimately trending down. There is no need to repeat a gluten sensitivity gene test.