What is celiac disease?
A gluten-free diet is a must for people with celiac disease, which is an autoimmune disorder that can get triggered by gluten. Gluten is a protein that is usually found in foods such as wheat, rye, and barley. When people with celiac disease ingest this protein, damage to the intestinal villi happens, which often lead to malabsorption and malnourishment. It can also cause loss of bone density, infertility, and miscarriage.
Symptoms of Celiac Disease
The symptoms of celiac disease include:
- Abdominal pain
- Loss of bone density
- Bone or joint pain
- Mouth ulcers
- Weight loss
Since this autoimmune disorder slowly progresses, its diagnosis can take years. Very few people are able to get a proper diagnosis. To find out if you have celiac disease, you must be screened first. Serology tests can be done to check for antibodies, which the body produces after ingesting gluten.
The doctor can also recommend an endoscopic biopsy, which is performed by a gastroenterologist. The doctor will collect a tissue sample in the small intestine and further examine it to determine if the damage is consistent with celiac disease. The diagnosis is usually confirmed when there is improvement observed while the patient is on a gluten-free diet.
There are no specific medications that can treat the disorder. The only treatment applicable for celiac disease is a strict gluten-free diet. Individuals with celiac disease have to refrain from eating food items that contain wheat, rye, barley, and other grains.
History of Celiac Disease
The early man’s diet consisted only of fruits, nuts, tubers, and sometimes meat. People long ago were simple hunters and gatherers. Gradually, domestication of plants and animals replaced this way of life. Man started to cultivate plants, and this is when the agricultural revolution began. Some unexpected problems arose during man's change of habit. For more than 2 million years, the human gut had developed into a sophisticated organ, which could develop tolerance towards food antigens. These food antigens were a part of man's diet for thousands of years.
The Neolithic period, in its agricultural revolution, generated whole new food antigens, which were formerly unfamiliar to man. They included protein in cow’s milk, goat’s milk, eggs of birds, and cereals. Some humans were able to adjust and adapt to these food antigens, but some could not, which led to food intolerance.
The Case of Cosa
In the year 2008, a woman's skeleton found in an archeological site in Tuscany, Italy showed the presence of the HLA-DQ2.5 gene along with malnutrition, which are characteristic features of celiac disease damage. Most probably, her poor condition was due to a long-term consumption of gluten. It was called the Case of Cosa, and was regarded as the earliest documented case of celiac disease.
Until 10,000 years ago, wheat, oats, corn, and barley were not introduced into man's diet. With agricultural revolution, these grains became a part of the human staple diet. These grains contained gluten, which could not be tolerated by man, and to some, its long-term consumption led to health issues and even death. Hence, in pre-farming, celiac disease was very common but quite rare in post-agriculture.
Early Description of Celiac Disease
Celiac disease was named and identified after 8,000 years of its onset. Aretaeus of Cappadocia, a Greek physician, wrote about The Coeliac Affection in the 1st century AD, and first described the symptoms of celiac disease. Initially, he called it as koiliakos, which means "pain in the bowels". In 1856, his work was translated from Greek into English by Francis Adams and coined the term "coeliacs".
Early in the 19th century, Dr. Mathew Baillie published his work about chronic diarrhea that causes malnutrition and bloating in adults. That time, he was probably unaware of Aretaeus' work. According to Dr. Baillie's observations, some patients depended almost entirely on rice. He also noticed that the only cure was to change a person's diet. However, his observations back then went unnoticed. He even suggested that farinaceous food intake should be limited. He said that a child who would take Dutch mussels daily would survive the disease wonderfully, but when the season of mussels was over it, there would be a relapse of the disease. Based on his records, improvements were seen in people who consumed a gluten-free diet along with relapses after the reintroduction of gluten in their diet.
Seventy-five years later, an English physician named Samuel Jones Gee got full credit of the modern clinical description of the disease. Dr. Samuel Gee gave a lecture regarding the "celiac affection" to medical students and provided a milestone description of the disease. However, no one could still explain the cause of the disease and nobody knew the damage done to the intestinal mucosa, although some things were already known earlier, such as:
- Presence of celiac disease without diarrhea
- Breastfeeding could protect against the development and severity of celiac disease
- Increased risk of having celiac disease in families, especially in twins
Celiac Disease in the 1920s
Another dietetic treatment came up in the 1920s. It was followed for decades and was considered as the cornerstone of therapy. This therapy was the banana diet. In 1924, Sidney Haas was successfully able to treat eight children who were diagnosed with the disease. When the children had anorexia, he treated it using the banana diet. Similarly, he experimented on the case and found that the children were clinically cured. However, two out of the ten children diagnosed with the disease did not survive. The banana diet became quite popular since it cured and prevented many deaths of children diagnosed with celiac disease. The diet prohibited bread, potatoes, crackers, and cereals. However, in scientific observation, the effectiveness of the banana diet could also be due to the elimination of foods that contained gluten in the children's diet. Haas was very proud that his insight was correct and was very resistant to the viewpoint of others. He believed that carbohydrates were the culprit.
Forty years later, a Dutch pediatrician named Dr. Willem Dicke showed that the main culprit was wheat and not the starch present in foods. However, Hass still insisted and argued that his insight was correct. He debated that the banana diet provided a lasting cure without any relapse.
During the World War II, particularly the time when there were bread shortages in Netherlands, Dicke noticed an improvement in children with the disease. He also observed that when the Allied Planes dropped bread into the Netherlands, the children's health rapidly deteriorated. He further worked on his findings and documented that in celiac disease, it was the gluten from wheat and rye that largely contributed to the disease.
In the mid-50s came another major breakthrough. In 1954, a physician named John W. Paulley from Ipswich, UK noticed a characteristic abnormality in the lining of the jejunum when taking samples during surgery. His assumption about such abnormalities was confirmed. He also observed that if the patient followed a gluten-free diet, the intestinal lining would return back to normal.
In 1956, a new jejunal biopsy apparatus was described by Dr. Margot Shiner. It was a quick and safe method of performing oral biopsies. She was also able to successfully perform a biopsy of the distal duodenum.
Shortly after this, American Lieutenant Colonel Crosby developed a capsule. The capsule was called as the Crosby capsule and was used to perform biopsies. This instrument has led doctors to associate celiac disease with a particular pattern of damage to the proximal part of the small intestinal mucosa.
In 1958, Cyrus Rubin and his coworkers were able to demonstrate that celiac disease in children and nontropical sprue in adults had the same clinical pathogenic feature.
In the early 1960s, three important elements were discovered:
- A diet containing gluten can trigger celiac disease
- Celiac disease is characterized by mucosal lesions
- Availability of a biopsy instrument
All these discoveries unraveled the mysteries of the pathogenesis of celiac disease. Thus, it was clear that doing a jejunal biopsy was possible for the diagnosis of celiac disease. A biopsy can show identifiable mucosal lesions or villous atrophy. However, since there could be other causes of mucosal lesions, experts urged doctors not to confirm the disease until it was proven that the mucosal lesions were caused by the ingestion of gluten. The following steps were needed to be done:
- Complete clinical remission on a gluten-free diet
- Documentation of lesion normalization
- Reintroduction of gluten into the diet
The criterion was formalized by the experts from the European Society for Pediatric Gastroenterology. They termed it as the "Interlaken criteria". It was a standard diagnostic criterion, which was accepted worldwide.
A few years earlier, an important discovery was made that were overlooked by the Interlaken criteria. It was discovered that the children who had celiac disease had antibodies in their blood due to the consumption of gluten.
In 1960, specialized skin care physicians discovered that patients with dermatitis herpetiformis also had gluten sensitivity. Although the villi of the intestine returned to normal by following a gluten-free diet, doctors still disagreed that the skin lesions could return back to normal after following a gluten-free diet.
In 1964, Berger identified and reported the anti-gliadin antibodies.
Actual autoantibodies in the blood of children with celiac disease called the antireticulins were identified by Seah and others seven years later after Berger’s discovery. However, it took several years to fully understand and appreciate their diagnostic use.
In the 1970s, a gastroenterologist named Anne Ferguson discovered that celiac disease developed due to the response of the immune system to the gluten in the digestive tract. She showed in her published papers that tissues of celiac patients obtained through biopsy reacted to the proteins in wheat, whereas the same biopsied tissue of a control individual did not react to wheat.
During the 1980s, celiac disease was linked to autoimmune disorders such as type 1 diabetes and Down syndrome. It was also observed that celiac disease was changing its pattern and was becoming more of an extraintestinal symptom and less of an intestinal disorder.
In the years 1960-1980, it was unknown as to why gluten could affect the intestinal villi. However, molecular biology, in which the DNA of the individual cells is studied, is now being applied to celiac disease.
In the 1990s, ESPGHAN published a new diagnostic guideline that is still being followed until present. After 1990, celiac disease was found to be associated with a specific gene. It was also accepted as an autoimmune disease. The autoantigen that was missing was found and identified in the enzyme called tissue transglutaminase. It was finally concluded that celiac disease is an autoimmune disease, which could be triggered by gluten and autoantigens.
If you have a family history of celiac disease, then you are at an increased risk of developing the disease. Celiac disease is associated with two genetic markers: HLA-DQ2 and HLA-DQ8 gene. About 95 percent have the gene HLA-DQ2 and remaining 5 percent have the gene HLA-DQ8. These genes can be tested by genetic testing. Although the presence of these genes may mean that there is a risk of developing the disease, it does not necessarily mean that you have the disease.
- 1990 - A blood test was developed to measure the anti-gliadin antibodies in the serum. This was done through an enzyme immunoassay. However, the test did not exclude the need for a biopsy.
- 1992 - The Crosby capsule was replaced by optic fiber endoscopy.
- 1995 - Australian laws adopted the new gluten-free standard. Foods that are labeled as "gluten-free" should not contain detectable gluten. This was basically intended for a gluten-free diet.
- 1996 - Anti-endomysial antibody tests became widely available in Australia.
- 1997 - A screening test for tissue transglutaminase was introduced.
- 2000 - Dr. Alessio Fasano at the University of Maryland discovered a molecule known as zonulin. He believed that this molecule increased the permeability of the intestine and also increased the vulnerability of the body to cause celiac disease.
- 2010 - Nondietary therapies began to develop through clinical testing. A nondietary therapy could possibly reduce the permeability of the intestine.
- 2013 - In the Western population, a correlation was shown between the increased use of glyphosate in agriculture and the growth of celiac disease. This was shown by Anthony Samsel and Stephanie Seneff.
There is an increasing number of celiac disease cases. This condition is prevalent due to many factors such as chemically treated wheat, GMO wheat, modified genes of wheat, Candida infections, and the leaky gut syndrome. All these factors increased the risk of developing celiac disease.