Often when people find out that I eat gluten-free, they ask me if I have celiac disease. I then have to decide if I should I give them the long answer, or the short answer.
The short answer is, “I’m gluten sensitive.”
The long answer is… “Well, I don’t really know, because I took gluten out so long ago, back when doctors believed celiac disease to be extremely rare. No one listened to me when I said the stuff made me sick, so no one ever tested me for celiac disease. If I wanted to get tested today, I would have to eat gluten – a significant amount, for a significant amount of time, in order to get some definitive test results. And there is no way that is going to happen! I will never eat any amount of gluten again. Not knowingly anyway. The extreme discomfort that I feel is just not worth it. But knowing whether or not I have celiac disease, will not change the way that I already eat, anyway, so it doesn’t really matter in the end.” That’s the long answer.
I realize that I find myself almost apologizing for eating gluten-free, since I have never been diagnosed with celiac disease. But I shouldn’t! Gluten sensitivity (GS) is a real and legitimate disorder that finally received official status in February, 2011 . But somehow the media has turned the gluten-free diet into a fad, and has proclaimed that only people with celiac disease have a right to eat gluten-free (see Gluten Sensitivity is NOT a Social Contagion, and Is Gluten Sensitivity All in Your Head? This is simply untrue.
But now that doctors are more aware of celiac disease today than they were a decade ago, I urge you to get all the necessary tests before cutting gluten out of your life, so that you can get as close to a definitive answer as possible about how gluten is affecting you.
So how do you get a diagnosis of celiac disease? First, let’s talk biology. Or microbiology, really. Whenever anyone eats wheat, whether a slice of whole grain bread, or a chocolate cupcake, gluten makes its way to your digestive tract, where enzymes work to break it down (along with all other foods). Gluten is broken down into gliadin and glutenin, both of which can be seen as invaders to the body  (called antigens), with gliadin considered to be the most toxic. When this happens, T-cells (a branch of the body’s military) sends out toxins (called cytokines) to fight these invaders.
But in the case of celiac disease, for some reason, they not only attack the gliadin, they also attack the endomysium (a layer of connective tissue surrounding muscle fiber) and specifically tissue transglutaminase or tTg (also abbreviated as TG2 or TG) found along the intestinal wall (as well as other locations throughout the body). This eventually causes the intestinal villi & microvilli, the finger-like projections on the lining of the intestine that absorb nutrients, to atrophy. But diseased villi cannot absorb nutrients, leading to a whole array of further complications caused by malabsorption issues. This is what makes celiac an autoimmune disease — a disease in which the body attacks itself.
Why do you need to know all this terminology? Because the most definitive test for celiac disease is considered the one that tests for antibodies to endomysium, called the anti-endomysial antibody test or EMA. If you have antibodies to EMA, then you are pretty much guaranteed to have celiac disease (although the absence of EMA doesn’t necessarily mean you don’t have celiac disease ). The second most definitive test is for antibodies to tTG.
In addition to the blood tests, biopsies of the small intestine are taken to determine the extent of damage (if any) that has been done. Dr. Michael Marsh came up with a classification system to describe this damage in 1992 . Where intestinal damage lies on the spectrum is referred to as Marsh 1, 2, 3 or 4 with Marsh 4 being the most severe. Oberhuber and colleagues later subdivided the Marsh 3 and 4 classes into subsets of Marsh 3a, 3b, and 3c, and now this classification is often referred to as the Marsh-Oberhuber system . So you may see a classification of Marsh 3c instead of 4, depending on whether your doctor is using the older or newer version of the classification system.
Intestinal tissue damage can be caused by other conditions aside from celiac disease, which is why the Marsh classification is just one of several criteria used in reaching a diagnosis.
So there are 5 criteria that are assessed in diagnosing celiac disease:
1) Signs or symptoms compatible with celiac disease. These can include: digestive issues such as abdominal pain, bloating, diarrhea and/or constipation; as well as extra-intestinal complaints such as “brain fog,” headaches, fatigue, join and muscle pain, leg or arm numbness, dermatitis, depression and anemia . And so much more.
2) Positive blood tests for antibodies, including anti-gliadin, anti-tTG, and EMA.
3) Presence of genetic markers HLA-DQ2 or DQ-8.
4) Symptoms that resolve after following a gluten-free diet.
5) Intestinal damage typical of celiac disease, i.e. Marsh 2 – 3c.
Most doctors looking for celiac disease, would expect a patient to meet all 5 criteria before being officially diagnosed as a celiac patient.
However, this method for diagnosing celiac disease is not fool-proof. For instance, there are cases of celiac disease that show no symptoms, called the “silent form.” There have also been cases where intestinal damage is found, but antibody tests come back negative. Furthermore, intestinal damage may not always be found, even if it does exist. This can be due to the fact that damage to the intestines is known to be patchy, or the damage may be further down the gastrointestinal tract in an area that an endoscope can’t reach. Finally, in some cases, symptoms don’t always resolve on a gluten-free diet.
In light of these drawbacks, Dr. Alessio Fasano of the Center for Celiac Research has proposed now that only 4 out of the 5 criteria need to be met for a patient to be diagnosed as a celiac . If the first 4 criteria do get met, then the biopsy may be skipped, which takes some burden off the patient. This is helpful especially for children, since the endoscopy is such an an invasive procedure. Hopefully, your doctor is up-to-date on celiac disease research, and knows this. Otherwise, he may be expecting you to meet all 5 of these pillars.
How is Gluten Sensitivity Different?
Many people think that if you don’t have celiac disease, then you have no business being on a gluten-free diet. But this is not true. You might actually have gluten sensitivity (GS), which is a legitimate condition. Experts in gluten-related disorders from around the world, convened in 2011, and declared it so.
While celiac disease is an autoimmune disorder that affects less than 1% of the population, gluten sensitivity is estimated to affect anywhere from 6% to 12% of the general population and possibly much more , , , .
Many of the symptoms of gluten sensitivity are the same as celiac disease, making it difficult to distinguish between the two. So then what’s the difference between celiac disease and gluten sensitivity?
Where the two diseases differ is in the blood tests. Antibodies to gluten are still found in patients with GS, just not antibodies to tTG or EMA , , . Which means that your body is not attacking itself (yet). But you could still be producing antibodies! And if you are, your body is trying to tell you something about gluten!
The two diseases also differ in their extent of gut damage. Gut damage in GS ranges from none to mildly inflamed, i.e. Marsh 0 – 1. This means that some GS patients can have higher than normal T-cells in their intestines (Intraepithelial lymphocytes or IELs to be exact), which again, means your body is fighting something! As Sapone et al. say, this suggests “an intermediate level, yet pathogenically significant, involvement of the adaptive immune system condition .”
Even though there are no actual lesions, Sapone et al. go on to say, that “it does not rule out the intrinsic toxicity of gluten, whose intake, even in non-CD individuals, has been associated with damage to other tissues, organs and systems besides the intestine.” Indeed the most serious examples are of very dangerous brain diseases that can occur because of gluten sensitivity, without correlating damage to the intestine .
Some have also surmised that increased IELs in the absence of gut damage might be considered “latent coeliac disease” and often this scenario is found in relatives of celiac patients . Regardless, raised antibodies and inflammation of any kind are alarm bells that should be listened to, even if it isn’t yet full-blown celiac disease.
Unfortunately, however, there are currently no real laboratory bio-markers that can give a definitive diagnosis of gluten sensitivity. Therefore, it is a disease of exclusion (meaning all others should be ruled out) and somewhat subjective. Its possible your conventional doctor may not even be looking for it (yet). So currently, the best way to find out if you are gluten sensitive is to simply take gluten out of your diet for a few weeks. Then you may challenge yourself by eating gluten again (if you are up for it!) and paying attention to the way your body reacts.
Also, because gluten sensitivity is newly recognized as its own medical condition, we have no historical data on it. So we actually have no idea what happens when gluten sensitivity is left untreated. Could gluten sensitivity be the forerunner of full-blown celiac disease or other autoimmune diseases? We just don’t know at this point in time. But given that you can have antibodies, inflammation, and serious health issues due to gluten, even with no intestinal damage whatsoever, means to me, that you should take gluten sensitivity just as seriously as if you have celiac disease. At least until we have more information.
 Sapone, A.; Bai, J.C.; Ciacci, C.; Dolinsek, J.; Green, P.H.; Hadjivassiliou, M.; Kaukinen, K.; Rostami, K.; Sanders, D.S.; Schumann, M.; et al. Spectrum of gluten-related disorders: Consensus on new nomenclature and classification. BMC Medicine. 2012, 10, 13.
 Howdle, Peter D. Gliadin, glutenin or both? The search for the Holy Grail in coeliac disease. European Journal of Gastroenterology & Hepatology: July 2006. Volume 18, Issue 7. pp 703-706.
 Braly, J. and R. Hoggan. Dangerous Grains. Why Gluten Cereal Grains May Be Hazardous to Your Health. Avery. New York. 2002. p. 70-71.
 Marsh MN. 1992. Gluten, major histocompatibility complex, and the small intestine. A molecular and immunobiologic approach to the spectrum of gluten sensitivity (‘celiac sprue’). Gastroenterology. 1992 Jan;102(1):330-54. Review.
 Corazza, G R, and V Villanacci. “Coeliac Disease.” Journal of Clinical Pathology 58.6 (2005): 573–574. PMC. Web. 10 Feb. 2015.
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 Fasano, A. Gluten Freedom. Wiley. 2014. 320 pp.
 Giacomo Caio, Umberto Volta, Francesco Tovoli and Roberto De Giorgio. Effect of gluten free diet on immune response to gliadin in patients with non-celiac gluten sensitivity. BMC Gastroenterology. 2014, 14:26.
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 Louisville Celiac Sprue Support Group, June 2003. Early Diagnosis Of Gluten Sensitivity: Before the Villi are Gone. https://www.enterolab.com/StaticPages/EarlyDiagnosis.aspx
 Dr. Vikki Petersen, personal communication.
 Catassi, et al. 2013.
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 Hadjivassilou M., Sanders DS, Grunewals RA, Woodroofe N, Boscolo S, Aeschlimann D. Gluten Sensitivity: from gut to brain. Lancet. Neurology. 2010. 9:318-330.
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