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Non Celiac Disease

From Celiac Disease to general distaste, gluten-free diets are on the rise and it may seem to some that the appearance and prevalence of gluten-sensitivity is a modern phenomenon, cashing in on a Western trend without a real scientific base. It may surprise the cautious reader to discover that Celiac Disease is in fact one of the most common long-term diseases worldwide with a history likely dating back to at least the first and second centuries. This begs the question: what is celiac disease?

Where does it come from, and how is it treated? What about non-celiac gluten sensitivity? Celiac Disease While the word “celiac” derives from the Ancient Greek word “koilia” meaning belly, the disease predominantly targets the small intestine. Celiac Disease (CD) is an autoimmune disease triggered by the presence of gluten in the body. Autoimmune diseases refer to diseases where the body natural defense system—the immune response—unnecessarily attacks naturally-occurring and non-harmful substances in the body.

Gluten is a kind of storage protein that we ingest when we eat foods like wheat, barley and rye; it is not entirely digestible by the intestine, so components of the protein are leftover in the intestine after digestion, one leftover substance within gluten is a substance known as “gliadin. ” These gliadin molecules are what trigger the immune response in a body with CD. Celiac Disease causes gliadin to interact with two different systems within the immune response: the innate system and the adaptive system.

The innate immune system refers is the “immediate action” part of the immune response—where the body identifies a threat from a predetermined set of possibilities and defend against it without targeting any specific microbes. In patients with CD, the innate response is triggered when gliadin molecules damage the epithelial, or “outer layer,” cells of the small intestine. This releases a protein called interleukin-15, which is used to help regulate the immune response, from where it was resting.

The inadvertent release of these proteins jolts them into action, and so they do their job and call for a kind of white blood cell known as a lymphocyte. These lymphocytes then begin to kill cells in the intestinal lining called enterocytes resulting in inflammation in the small intestine, and the breakdown of the epithelial cell layer. As this is occurring, the adaptive response also recognises gliadin molecules underneath the surface layer in the lamina propria.

The adaptive immune response generally works over a longer period of time than the innate response, often taking days to manifest where the innate response takes hours. It works by producing hundreds of thousands of unique immune receptors when can recognise any infectious antigens that enter the body, waiting until one of the receptors identifies a microbe and then targeting it directly to destroy it. CD patients have a gliadin-specific receptor, a CD4+ T-cell, which identify gliadin fragments in the intestine and then call for the production of cytokines cells.

Unfortunately, these cells cause tissue damage and a trigger a secondary response that results in the production of antibodies which aid in the inflammatory response created the innate system. The tissue damage caused by the adaptive system damages the finger-like villi that line the intestine to absorb nutrients from digested food, and causes small glands called crypts to enlarge and reproduce more cells in a response known as hyperplasia. Ultimately, in trying to destroy gliadin, the body of a person with CD ends up doing greater harm to itself.

All of these reactions, from both the innate and adaptive immune system, contribute to the many symptoms and risks associated with Celiac disease. As mentioned above, CD triggers an inflammatory response in the small intestine. Inflammation occurs naturally when your body is trying to defend against an pathogen—your body spots a microbe and induces a strong reaction that brings blood to the infected area, resulting in swelling, redness, and heat. However long-term this response can be negative for your body as it damages not only the infected cells but also your own cells.

In extreme cases, inflammation gone awry leads to septic shock, which can kill you. With CD, if the patient has continuous interactions with gluten, the frequent inflammatory response damages the epithelial cells of the small intestines and affects the rate of nutrient absorption within the body. Constant inflammation can cause the patient to feel abdominal pain and swelling. The disruption of nutrient absorption can result in diarrhea, indigestion, bad smelling stool, and emancipation. However, these are merely the most typical symptoms of CD.

They are obviously indicative of CD because in order to frequently experience them, the intestine has to have been severely damaged. People with CD are at higher risk for cancer, especially Hodgkin’s Lymphoma and small intestine adenocarcinoma—a kind of glandular cancer. There are also a mass of atypical symptoms that result from the localised malabsorption of nutrients by the intestines of those with CD. If the body is misses certain nutrients during digestion, it can result in things like seizures, epilepsy, anemia, chronic fatigue, or osteoporosis which are not as easily associated with CD.

Even short stature can be indicative of CD! It is because of these broad and atypical symptoms that many people with CD live undiagnosed. History and Diagnosis Celiac Disease is thought to affect around 1% of the population worldwide due to a combination of genetic and environmental factors. While traditionally it was associated mostly with European cultures—as a rare disease, thanks to ever-improving diagnosis techniques CD has proven to be prevalent worldwide though largely undiagnosed, especially in developing countries.

The ratio between diagnosed and undiagnosed CD is thought to be as larger as 1:7. But, how did we get here? What is the history of CD and how did it develop as our knowledge of medicine and disease grew? Perhaps a little whimsically, the beginning of Celiac Disease starts with the advent of agriculture during the Neolithic era and the subsequent adaption of wheat, barley, and rye to our diet. Wheat quickly became popular and to this day remains the most produced crop worldwide.

Despite this, people spread faster than gluten-related crops; wheat and barley consumption was dominant 10, 000 years ago in what is now the Middle-East, but did not spread Northwest to areas like Britain until approximately 2000 BCE. Evolutionary theory, would predict that if CD is determined genetically—which it is—then the Middle-East and other areas, which have consumed gluten for the longest time, should have largely eliminated the gene associated with CD. This is not the case though; in fact, Middle-Eastern countries have an ever higher prevalence of the CD-determining gene than Northern Europe does.

This unexpected distribution is thought to be a result of one of two factors: that the gene that causes CD also protected against tooth decay and so survived regardless of the effects of CD, or that CD is the lingering remains of a function that protected the body from a consequence of switching to a wheat-based diet. However, that understanding of the history of Celiac Disease is not based on historical record, and instead comes from an analysis of CD today and an understanding of how gene preservation occurs.

The records of CD do not go back nearly as far: the earliest surviving description of the disease—or one like it—was written down by famed Greek physician Aretaeus of Cappadocia, also credited for naming it. He describes a disease characterised by enduring diarrhea that results in “atrophy of the body” and called it “koiliakos. ” This record dates back to the first century CE, but the next notable contribution to the study of CD comes in 1887 from British man Samuel Dee who attributes the cause of the disease with choice in diet.

Even still, the association of CD with gluten only occurred when a Dutch pediatrician named Willem-Karel Dicke noticed a correlation between the CD-related child mortality rate and the prevalence of bread in their diets. Today, CD is diagnosed through serologic testing—which analyses blood serum and in the case of CD, screens for IgA class antibodies. Antibodies are produced by the adaptive immune system as a response to and defense against antigens, which are unique structures found on pathogens in the body.

IgA class antibodies are found mainly in bodily secretions such as breast milk, mucus, and saliva and serve to help neutralization pathogens without causing cell damage or inflammation. Patients with CD are more likely to have a deficiency of IgA endomysial antibodies—endomysial refers to a specific kind of autoantibody relevant to CD diagnosis. This style of diagnosis has helped to reveal the unexpected prevalence of CD where historical examination failed.

There are both genetic and environmental factors that have to interact in order for Celiac Disease to develop. 0-40% of the population has at least one of the two alleles—HLA-DQ2 and HLA-DQ8—associated with CD in their DNA, but only 1% of the population develops it. Every person with CD has one of these alleles present, but environmental factors such as the age that they are exposed to gluten, and whether they acquire a gastrointestinal infection. Some researchers such that it is a “triad” of factors that contribute to the development of CD: that the presence of gluten in the intestine, genetic predisposition, and greater gut permeability that cause CD.

Treatment and Non-Celiac Gluten Sensitivity An underlying theme in Celiac Disease, from its manifestation to its history to its diagnosis, is its relation to gluten. Gluten is the driving force behind CD and since the discovery of their correlation, the simplest solution has remained the main treatment: eliminate gluten from the diet. As of yet, there is not a widespread treatment therapy other than avoidance—no drug has made it past trials while several are in development.

While in the past it was difficult to avoid gluten to its prevalence in day-to-day foods, in recent years the “gluten-free diet” has been popularized and become trendy—the idea of “gluten sensitivity” is used to explain away a medley of symptoms that are supposedly “cured” with gluten-free diets. With no relation between this new-found gluten sensitivity and CD, the term coined in these cases is Non-Celiac Gluten Sensitivity (NCGS). In popular culture, NCGS is considered to be a modern invention of the past few years, but the first recorded cases of it date back to the mid-1970s.

Unlike an allergy or CD, gluten sensitivity does not trigger an immune response. Still, in a study looking at individuals who claim to have a gluten-sensitivity, it was shown that some 30% did have negative gastrointestinal responses to wheat. The main affected group with gluten sensitivity is young or middle aged women where CD affects anyone at any age. Gluten-sensitive people also tend to suffer from other gastrointestinal problems, such as Irritable Bowel Syndrome, allergies, or lactose intolerance.

NCGS is highly controversial today as it unclear whether the sensitivity reported is actually one of gluten or whether it is caused by other poorly-digestible products we eat, such as FODMAPs, or perhaps a reaction to natural pesticides found in wheat, such as ATIs or wheat-germ agglutinin. Experiments to determine this has thus far been either biased or inconclusive. Still, it can be concluded that there is some merit to the idea of NCGS, while it is not as clearly established as CD. Only further study will tell us whether gluten is the cause.

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