cotherapy have resulted in improved outcomes. However, the etio-pathogenesis of both Crohn's disease (CD) and ulcerative colitis (UC) remains poorly defined. Risk alleles determined by genome-wide association studies have been shown to only modestly increase the risk of IBD.3 Given that the recent exponential rise of IBD over the last century parallels industrialisation, significant association with specific environmental risk factors appears more likely.
2In the current study, Hammer et al. determined the IBD incidence of first-, second-and third-generation Faroese immigrants in Denmark relative to the risk in the local Danish population using linked population databases. 4 The Stan- that low-risk migrants over subsequent generations adopt the risk of the country to which they migrated. Consistent with the findings of the present study, our group also demonstrated an increased risk of IBD in migrants from a high incidence region, UK, to Canterbury, New Zealand where IBD incidence had previously been low. Interestingly, a significant adjusted association was seen for UC [1.4 (95% CI: 1.14-2.01)] but not for CD [1.38 (95% CI: 0.92-2.05)].
7These observations highlight the importance of environmental exposures occurring early in life. A range of early life exposures have been shown to be associated with the subsequent development of IBD including having been breastfed, the early use of antibiotics and a range of markers of increased hygiene. However, some of these risk factors, such as the presence of a hot water tap in the home were only found to be associated with subsequent development of IBD in early studies.8 As such potential risk factors became ubiquitous, the ability to show their importance reduced.To determine the specific environmental factors that may lead to IBD, it is likely that researchers will need to characterise not just the environmental variables but also its timing of exposures to both cases and controls.9 Furthermore, the interaction of environmental factors with specific genotypes is also likely to identify genes that may only be important in IBD risk in the presence of specific environmental exposures. 10 In short, large cohorts of well genotyped, phenotyped and environmental exposure described cases and controls are likely to be needed to explore the role of the environment in the etio-pathogenesis of IBD.ACKNOWLEDGEMENT