Inflammatory bowel disease affects hundreds of thousands of people around the world each year. It is, according to conventional medicine, incurable and its cause is unknown (BMJ, August 6, 1994). The number of reported cases is increasing worldwide each year (Canada Health Rep, 1990; 71: 343-59), especially among children.

Generally speaking, IBD is thought to be autoimmune in nature, causing the immune system to attack and inflame the body's own tissues. For diagnostic purposes, doctors divide IBD into two separate categories: Crohn's disease and ulcerative colitis (UC). Crohn's involves all the layers of the bowel but can affect any part of the gastrointestinal tract from the mouth to the anus, while ulcerative colitis affects only the colon/rectum.

While Crohn's and ulcerative colitis are usually categorized as two separate diseases (BMJ, 1994; 309: 355), there is also an argument that they are better described as two examples of the same process, which merely affects different areas in the intestine to a differing degree. No single test is sufficient to diagnose either disease, and sufferers are often put through an endless round of endoscopic, radiological, histologic assessments, laboratory testing and bowel studies in order to come up with a definitive diagnosis (Postgrad Med J, 1995; 112: 46-8; and 54: 57-8). In 10-15 per cent of patients it is almost impossible to differentiate between the two diseases.

Each type may have different causes (Gastroenterol Clin North Am, 1995; 71: 475-507), making the selection of appropriate treatment difficult. Diagnosis can also be made difficult by the fact that both diseases mimic several other infections of the intestines, as well as other conditions (see box below).

While the death rate from IBD is dropping, the risk is still greater than that of the general population (Gastroenterol, 1996; 110: 1339-45). In a retrospective study of death certificates in Rochester, New York from January 1973 to December 1989, Crohn's was the direct cause of death in 25 per cent of cases and in 6 per cent of cases of UC (AM J Gastroenterol, 1995; 90: 927-32).

But what makes someone suceptible to IBD in the first place? Certainly there is a genetic link which is stronger among sufferers of Crohn's. If someone in your family is a sufferer, you are anywhere from 3.5 to 10 times more likely than the general population to contract the disease yourself (Acta Chir Scand Suppl 1990; 559 (Crohn's Disease-EP/GE): 1-42; N Eng J Med, 1991; 324: 84-8).

The use of non-steroidal anti-inflammatory drugs (NSAIDs) is another possible explanation. Research in Jersey showed that in 38 per cent of new cases of inflammatory bowel disease, the disease developed while the patient was taking NSAIDs (Lancet October 8, 1994).

Viral and bacterial links with IBD have also been explored at length, particularly in relation to Crohn's (Ann Med, 1993; 25: 557-61). Studies have shown that the human herpesvirus 6 (HHV 6), Epstein-Barr virus and cytomegalovirus seem to play a much greater role in the development of UC (J Med Viriol, 1992; 38: 183-90). But the weight of research into bacterial causes centres around Crohn's disease and the presence of Mycobacterium paratuberculosis.

This bacterium is known to cause chronic enteritis in many animals and may also be responsible for the disease in humans, especially in those with inherited or acquired susceptibility. Its presence is more common in those with Crohn's than with ulcerative colitis.