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Crohn's Disease

What Causes Crohn’s Disease?

Researchers have not yet identified the cause of Crohn’s disease, so it is described as an “idiopathic” disease. It is known that inflammation is part of the body’s immune response, and an immune response is usually triggered by something. But to date no specific “trigger” has been found to cause the inflammatory response seen in Crohn’s disease.

There is some evidence that Crohn’s disease has a genetic component. While there is no simple correlation from parent(s) to offspring, the disease tends to “run” in families. As many as 20 to 25 percent of patients with Crohn’s disease have a relative with CD or ulcerative colitis. There is also a higher incidence among certain ethnic groups.

In addition, some possible environmental factors have been linked to initial episodes or relapses. Crohn’s disease appears to be a disease that primarily affects those living in Western, industrialized societies. Whether this is due to some condition of the environment in which people live or their diet has not been determined.

The Role Of Heredity

Physicians classify Crohn’s disease as one of the “familial” or “complex” genetic diseases, as opposed to a “simple” genetic disease. In simple genetic diseases, such as sickle cell disease or cystic fibrosis, a person who inherits a copy of the defective gene from each parent is certain to get the disease.

In Crohn’s disease, this is not the case. In fact, 75 to 80 percent of people with Crohn’s disease have no relative with either Crohn’s disease or ulcerative colitis. But because there are fewer than 500,000 Americans with Crohn’s disease, the level of multiple incidence in families (20 to 25 percent of Crohn’s patients) means that the risk of being diagnosed with the disease is statistically somewhat higher in individuals who have a family member with either Crohn’s disease or ulcerative colitis.

Other evidence that suggests a genetic basis for Crohn’s disease is the fact that populations who have intermarried closely within their communities for many generations, such as Eastern European Jews, have a higher incidence of inflammatory bowel disease than do other groups.

Weakened Immune Response

In the healthy intestine, certain types of bacteria (enteric microflora) are present and necessary. In fact, between one billion and one trillion normal intestinal bacteria exist in every gram of intestinal content. These “normal” bacteria contribute to the process of digestion and keep abnormal bacteria, which can enter the GI tract in food, water, etc., from surviving and causing illness.

If abnormal bacteria do survive and multiply, the body recognizes them as invading organisms, or “antigens.” To a certain extent, these antigens are ignored in the GI tract – the immune system has a certain level of tolerance for them.

But immunologic evidence shows that in the intestines of those with inflammatory bowel disease, some of this tolerance for bacteria is lost. The TH1 cells, which are responsible for activating the immune response against invading organisms, do their job. But the TH2 cells, which are responsible for deactivating the immunologic response after invading organisms are destroyed, fail to perform theirs.

The result is an inflammatory overreaction, resulting in pain, fever, and, sometimes, tissue damage.

Some evidence also suggests that flare-ups of Crohn’s disease or ulcerative colitis are a heightened response to seasonal allergies, upper-respiratory infections, or other transient illnesses.

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