Reading Time: 2 minutes

Crohn’s and Ulcerative colitis are understood to have a number of genetic related risks, but increasingly scientists are having to accept that our double helix does not predict our health risks except in a few single gene diseases such as cystic fibrosis, the haemoglobinopathies. In fact the enormous endeavours and resources spent pursuing this elucidation have produced surprisingly modest practical benefits.

Even when dozens of genes have been linked to a trait, both the individual and cumulative effects are surprisingly small and nowhere near enough to explain earlier estimates of heritability.[1]

The recent discovery by a New Zealand group that there are a number of childhood factors associated with the development of Inflammatory Bowel Disease, further supports the concept that environment – in this case during childhood plays an important role in modulating the risk for developing these conditions. The rising incidence of these diseases over the last 50 years also supports the role of environment, as genes take many hundreds of years to change.[2]

Reading Time: 5 minutes

IBD’s are characterised by wasting and chronic intestinal inflammation induced by many different cytokine-mediated pathways. It is clearly recognised that medical and surgical interventions do not cure Crohn’s disease because relapse is the rule after remission.

Until a few years ago, IBD was classified into Th1-dependent, that is, Crohn’s disease, and Th2-dependent, that is, ulcerative colitis, phenotypes. However, in recent years, it has been shown that new T-cell subclasses, that is, Th17 and regulatory T cells (TR), exist independently of Th1 and Th2 and that they play a central role in modulating IBD.

Reading Time: < 1 minute

Ulcerative colitis (UC) is a chronic relapsing inflammatory disease of the colon with extraintestinal manifestations. UC is associated with increased risk of developing colorectal cancer and increased mortality. Pathogenesis of UC is postulated to be linked to a defect in the microbial population of the colonic mucosa. Patients with UC requiring surgery tend to have