Celiac disease

Gluten is a substance that is naturally present in wheat, barley, and rye. Unlike a gluten allergy, intolerance appears slowly and can go unnoticed for many years. In Western countries, between 0.7 and 2% of the population is affected.

An often asymptomatic disease

In its classic form, celiac disease starts around the age of six months, after the introduction of the first cereals into the diet. The classic symptoms are chronic diarrhea, lack of appetite, and apathy. However, most often celiac disease is asymptomatic.

A genetic predisposition at fault?

Celiac disease appears in people who have a genetic predisposition to it. Their immune system produces antibodies in the presence of gluten that attack the wall of the intestine. The result is that digestion is altered and nutrients aren’t absorbed as well. Other factors are involved such as the age at which gluten was introduced and repeated intestinal infections. The gastrointestinal microbiota may also play a triggering or aggravating role, according to a hypothesis that is supported by the existence of dysbiosis in these patients. The gastrointestinal flora contains fewer beneficial bacteria and more potentially pathogenic germs in comparison to healthy subjects. A gluten-free diet reduces this imbalance, but cannot fully correct it.

Diagnosis rests on a clinical examination and the presence of indicative signs, along with the search for specific antibodies in the blood and a biopsy (if necessary). Genetic predisposition has been shown through gene study (HLA typing).

Modifying the microbiota as prevention

The only treatment for celiac disease is to remove gluten from the diet. However, another approach – targeting the dysbiosis – has researchers interested. It consists of modifying the gastrointestinal microbiota to prevent the disease from developing, in cases of increased genetic risk, or to improve forms that are severe or even resist the gluten-free diet.