Celiac disease (CD) is a digestive disease that damages the small intestine and interferes with absorption of nutrients from food. People who have celiac disease cannot tolerate a protein called gluten (or a gluten fraction called gliadin), which is found in wheat, rye, barley, and possibly oats. When people with celiac disease eat foods containing gluten, their immune system responds by damaging the small intestine. Specifically, tiny fingerlike protrusions, called villi, on the lining of the small intestine are lost. Nutrients from food are absorbed into the bloodstream through these villi. Without villi, a person becomes malnourished – regardless of the quantity of food eaten.
There is increasing evidence that most people with gluten sensitivity have latent CD with such mild manifestations in the digestive tract that the diagnosis is never made. An allergy or intolerance to specific grains, such as wheat, may be due to a gluten sensitivity, but may occur for other reasons as well.
CD is considered an autoimmune disorder because the body’s own immune system causes the damage. Also classified as a disease of nutrient malabsorption, celiac disease is also known as celiac sprue, nontropical sprue and gluten-sensitive enteropathy. Approximately 0.5% of Americans have symptoms brought on by this condition.
While the gastrointestinal tract is the primary target organ, systemic disease is an important consequence of gluten ingestion in many patients. Latent disease may manifest itself as irritable bowel syndrome with iron deficiency anemia, but little or no diarrhea. There is increasing evidence that most people with gluten/gliadin sensitivity have latent celiac disease with such a mild manifestation that the diagnosis is never made. The undamaged part of their small intestine is able to absorb enough nutrients to prevent symptoms. However, people without symptoms are still at risk for the complications of celiac disease.
CD runs in families. Sometimes the disease is triggered by surgery, pregnancy, childbirth, viral infection or severe emotional stress. CD affects people differently; some develop symptoms as children, others as adults. One factor thought to play a role in when and how celiac appears is whether and how long a person was breastfed – the longer one was breastfed, the later and more atypical the symptoms appear. Other factors include the age at which one began eating foods containing gluten and how much gluten has been eaten.
Symptoms may or may not occur in the digestive system. For example, one person might have diarrhea and abdominal pain, while another person has irritability, depression or a rash.
To diagnose CD, physicians test blood to measure levels of antibodies to gluten. These antibodies are antigliadin, anti-endomysium and antireticulin. If the tests and symptoms suggest celiac disease, the physician may remove a tiny piece of tissue from the small intestine to check for damage to the villi. Gluten sensitivity should not be self-diagnosed, since other medical problems could be the cause of similar symptoms. A gluten-free diet should not be followed until you have been seen by your doctor. Tests for CD cannot produce a proper diagnosis if a person is not currently reacting to gluten in their diet. Once a diagnosis is made and a person responds to the gluten-free diet, the physician will know for certain that the diagnosis of celiac disease is correct.
Screening for CD involves testing asymptomatic people for the antibodies to gluten/gliadin. Because celiac disease is hereditary, family members – particularly first-degree relatives – of people who have been diagnosed may need to be tested for the disease. About 10% of an affected person’s first-degree relatives (parents, siblings, or children) will also have the disease. The longer a person goes undiagnosed and untreated, the greater the chance of developing malnutrition and other complications.
James Braly and Ron Hoggan, have published a book, Dangerous Grains, claiming that what was thought to be a relatively rare condition may be more widespread than was previously thought. They claim that gluten sensitivity (GS) is at the root of a proportion of cases of cancer, auto-immune disorders, neurological and psychiatric conditions and liver disease. The implication is that the heavily wheat-based western diet – bread, cereals, pastries, pasta – is actually making millions of people ill.
Both authors claim great personal benefits from avoiding gluten. “After eliminating gluten grains,” writes Hoggan, “I realized how uncomfortable and chronically ill I had been for most of my life.”
Dr. Harold Hin, a GP from Banbury in Oxfordshire, England carried out a blood test on the first 1,000 patients who came to his surgery complaining of symptoms that might indicate CD, such as anemia or being “tired all the time”. Thirty proved positive and a diagnosis of CD was confirmed by a biopsy. This was a rate 30 times more than expected.
The test for anti-gliadin antibodies is known as AGA and people who test positive to AGA often have no sign of gut damage.
Worldwide, CD ‘out of the intestine’ is 15 times more frequent than CD ‘in the intestine’. Braly estimates that between 10% and 15% of the US and Canadian populations have anti-gliadin antibodies, putting them at risk of conditions as varied as psoriasis, multiple sclerosis, jaundice, IBS and eczema. The authors claim considerable clinical success in treating patients with conditions such as Addison’s disease, lupus, rheumatoid arthritis and ulcerative colitis with a gluten-free diet.
If you suffer from any of the following, the possibility that you are GS may be worth investigating. Upper respiratory tract problems such as sinusitis, “allergies”, “glue ear”, symptoms related to malabsorption of nutrients such as anemia and fatigue, osteoporosis, insomnia, diarrhea, constipation, bloating and distention, spastic colon, diverticulitis, bursitis, certain forms of epilepsy, behavioral difficulties, ME and ADD.
It has been discovered that a relatively short fragment of the gluten protein is exceptionally toxic to CD patients. This gluten fragment is unusually resistant to breakdown by digestive enzymes in the intestine, where it remains intact to have a destructive effect on the intestinal lining. There is a a bacterial enzyme that can rapidly degrade this and other related toxic fragments from gluten, but it will not likely be available to patients in the near future.
(Reuters Health) By Janice Neumann 11/26/2014 – A classical set of celiac disease symptoms no longer reflects the profile of most newly-diagnosed patients, according to a new study from Italy.
Instead, doctors need to take other symptoms into account and consider the possibility of celiac disease, even when patients don’t fit the old image of the condition, researchers say.
“It’s been a gradual phenomenon since the 1970s that fewer people are presenting with the classical diarrhea and more with non-classical or silent presentation, both in adults and children,” said Dr. Peter Green, who wasn’t involved in the study.
“We don’t actually know why one person has diarrhea and another presents with abdominal pain or osteoporosis,” said Green, director of the Celiac Disease Center at Columbia University in New York.
Dr. Umberto Volta and his coauthors write in the journal BMC Gastroenterology that just 15 years ago, celiac disease was still thought of mainly as a rare pediatric food intolerance, whose most common signs were diarrhea and intestinal damage that was diagnosed through a biopsy.
The disease is now known to be an autoimmune disorder, caused by an inability to tolerate the gluten protein in wheat, barley and rye.
Eating gluten typically causes inflammation of the intestinal lining in people with celiac disease and makes it hard to absorb nutrients.”