The introduction of wheat into the global food regiment sparked one of the most influential changes in the human diet known to man. After discovering the staple grain more than 9000 years ago, the human race has integrated wheat into almost every type of diet, regardless of culture or religion (Aziz et al, 2015). The wealth of nutrients contained in wheat, like vitamins B and E cause it to be the key foundation of nourishment in the lives of millions around the world (De Ancos et al, 2002). It is clear that the benefits of this grain are universal; however, in the unfortunate lives of approximately 1% of the world population, the benefits of grain are little to none (Lebwohl et al, 2015). In fact, instead of digesting and processing wheat like the average person, the bodies of this small group of people launch an attack against their intestines, leaving their abdomens swollen and inflamed. This tragic and painful war against the gut is known as Celiac Disease.

Celiac disease is an autoimmune disorder, meaning the immune system, which usually guards our bodies against disease, recognizes normal cells and proteins as foreign (Alessio, 2009). In celiac disease, the main component of wheat, called gluten, is considered foreign to the body after it has been processed into a form called gliadin (Lebwohl et al, 2015). The intestines are sites in our bodies which absorb incoming nutrients into the blood or foreign molecules which are attacked by the immune system. Usually, incoming foreign molecules are broken down at the intestines into non-foreign compounds so they do not illicit an immune response (Sollid et al, 2013). However, gliadin is unique in that it is resistant to the forces of the intestines that break down foreign molecules. In most people, indigestible gliadin is not a problem as the gliadin particles are simply excreted out of the body. However, due to a combination of genetics and a leaky gut, gliadin is absorbed in the intestines of celiac patients and causes painful problems (Alessio, 2009).

The first problem contributing to the unusual absorption of gliadin in the intestines of patients with celiac disease is a leaky gut. Usually, the cells lining the intestines are very compact, meaning big molecules like gliadin cannot pass through. However in celiac patients, due to the fact that they have a molecule in their body called zonulin, their intestines are very permeable to large molecules. As soon as they pass through the intestines, gliadin molecules cause a cascade of autoimmune effects (Alessio, 2009).

In most people, even if gliadin molecules had somehow permeated the intestinal barrier, the immune response would not be very strong. However, in celiac patients, certain genes cause their bodies to be more sensitive to gliadin, creating the detrimental autoimmune attack (Sollid et al, 2013). Genes are molecules that contain the information for all the processes that occur in our bodies. The genes involved in celiac disease, called Human Leukocyte Antigen (HLA) genes, provide the information to create HLA antibodies (Alessio, 2009). In celiac patients, there are two main types of HLA antibodies present, HLA-DQ2 and HLA-DQ8 (Alessio, 2009). In the intestines, specific guard cells of the immune system, called antigen presenting cells, process the incoming gliadin, together with the HLA antibodies. After they process the gliadin with the HLA, the antigen presenting cells present the gliadin-HLA mixture to immune cells in the body known as T-Cells (Alessio, 2009). As soon as T-Cells recognizes the mixture, they send a large signal attracting many more immune cells. Not only does this lead to inflammation, it also leads to the breakdown of the intestines, causing the painful symptoms associated with the disease.

HLA genes are present in 95% of celiac disease cases, however, it is not the sole cause of the disease. Many individuals with these genes do not have celiac disease, so other factors are at play (Alessio, 2009). Scientists have not discovered these possible factors, but have identified possibilities of other genes causing some of the prominent symptoms (Sollid et al, 2013).

As opposed to the small population of people suffering from celiac related gluten sensitivity, approximately 6% of the population claim to experience painful symptoms after ingesting gluten, without having celiac disease. These people have what is known as Non-Celiac Gluten Sensitivity (NCGS) (Aziz et al, 2015). Diagnosis of this sensitivity is usually stated after all possible intestinal diseases have been ruled out, including testing for the presence of HLA antibodies. NCGS does not have a measurable biological characteristic that would prove the presence of the sensitivity, so diagnosis is usually completed on the basis of self-reported symptoms experienced by patients (Lebwohl et al, 2015). However, patients with NCGS are generally more likely to have nutritional deficiencies, a lower body mass index, and other autoimmune disorders (Lebwohl et al, 2015).

Unlike celiac disease, non-celiac gluten sensitivity does not have any significant biological characteristic that would prove the existence of the sensitivity, causing many scientists to be skeptical about the validity of the disease (Cameron, 2016). Several scientists have published studies proving that other factors besides gluten cause NCGS symptoms experienced by these patients. One of the main studies against NCGS was published in 2013 in Australia claiming that Fermentable-Oligosaccharide-Disaccharide-Monosaccharide-And-Polyols (FODMAPs) are the cause of the NCGS symptoms (Gibson et al, 2013). These molecules are small sugars found in a wide variety of grain-based products. FODMAP sensitivity could easily be confused with gluten sensitivity by both the average patient and doctor, since FODMAP sensitivity does not have any biological characteristic indicating its presence. (Cameron, 2016). In the Australian study, researchers removed both gluten and FODMAPs from participant’s diets then reintroduced gluten back into their food. Only 8% of people reacted specifically to the gluten, indicating most patients were sensitive to the FODMAPs in their food and not to the gluten (Gibson et al, 2013).

Several scientists as well as the general public used this study as proof that non-celiac gluten sensitivity does not exist. The explanation for those who experience NCGS was that they were under a “placebo effect: some people may feel better on a gluten-free diet simply because they expect to” due to forces like the media (Cameron, 2016). However, as convincing as the study seems, the Australian study did not directly prove that NCGS do not exist, rather, they just provided an explanation for the symptoms of a small group of individuals. In order to extend upon this research, several scientists have continued to test for the presence of gluten sensitivity, and contrary to popular belief, several have found concrete evidence that NCGS sufferers are indeed suffering due to the presence of gluten, not secondary components like FODMAPs. For example, a new randomized double blind trial in 2016, completed in Iran, recently designed a study testing the gluten sensitivity of people with NCGS to determine if the benefits of their gluten free diets were due to other reasons besides gluten (Shahbazkhani et al, 2016). The results had proven that 84% of participants had severe reactions that were specific to gluten alone, completely contradicting the Australian study and leaving several questions unanswered. For example, what is the prevalence of those with this type of gluten sensitivity? Recent findings prove that it may be much greater than what is generally believed by the public, as many forms of non-celiac gluten sensitivity are starting to appear in the form of non-intestinal symptoms (Kresser, 2015).

With the prevalence of non-celiac gluten sensitivity rising, the popularity of gluten free diets has sky rocketed in the past 10 years (Emine, 2017). Because of the negativity associated with gluten in those suffering from celiac disease and NCGS, many companies and bloggers have taken advantage of the situation and began to promote gluten free products to the general public. This 9-billion-dollar market produces advertisements in the media that contain statements about losing weight and greater energy levels. According to The Guardian, "the health halo surrounding the gluten-free category continues to drive general consumer interest" even though most report not completely understanding what is in their gluten-free foods (Emine, 2017). After a thorough analysis of hundreds of gluten free products, it is clear that eating gluten free foods has no apparent health benefits for those that are not suffering from celiac disease or NCGS.

In fact, in most cases, gluten free products are less healthy than their gluten containing counterparts. Because gluten is a key element in the texture and taste of many foods, several companies add preservatives, sugars, and excess fats to their gluten-free products so that the foods remain palatable to the public (Kremer, 2015). To put this into perspective, a normal cookie contains around 70-100 calories, but a gluten-free cookie can contain as much as 290 calories due to excess sugar and fat (Kremer, 2015).

To conclude, it is clear that celiac disease and non-celiac gluten sensitivity are debilitating diseases that require important lifestyle changes. Because there are not any physical signals visible in NCGS, there is a general lack of support among the scientific community for this disease. However, NCGS remains on the rise with millions of people without celiac disease or NCGS adopting a gluten-free diet for the perceived health benefits promoted by the media and food companies. The accessibility of gluten free foods makes life easier for those suffering from celiac disease, but in general, society does not need to worry about gluten containing products. So remember, keep calm and eat some bread.