Inflammatory bowel disease (IBD) has become a 'prototype disease' for chronic auto-inflammatory disorders with a polygenic background and important multifaceted environmental trigger components. The environmental factors contribute both to pathogenesis and disease flares. Thus, IBD is a disease par excellence to study the interactions between host genetics, environmental factors (such as infections or smoking) and 'in-vironmental' factors - for example, our intestinal microbiota. Longitudinal intercurrent events, including the impact of long-term medication on disease progression or stabilization, can exemplarily be studied in this disease group. Whilst alterations in the human genome coding relevant variant protein products have most likely not emerged significantly over the last 50 years, the incidence of Crohn's disease and ulcerative colitis has dramatically increased in Western countries and more recently in the Asia Pacific area. An interesting concept indicates that 'Western lifestyle factors' trigger chronic intestinal inflammation or disease flares in a genetically susceptible host. To understand the disease pathogenesis as well as triggers for flares or determinants of disease courses, we must further investigate potential en(in)vironmental factors. As environmental conditions, in contrast to genetic risk factors, can be influenced, knowledge on those risk factors becomes crucial to modulate disease incidence, disease course or clinical presentation. It is obvious that prevention of environmentally triggered disease flares would be a goal most relevant for IBD patients. An increased prevalence of IBD in urban environment has been documented in Switzerland by the Swiss IBD cohort study. Several studies have attempted to identify such factors; however, only a few have been validated. The best investigated environmental factor identified in IBD cohort analyses is smoking. Other environmental factors that have been associated with clinical presentation or risk of inflammatory flares as well as increased incidence are diet and food additives. The so-called 'hygiene hypothesis' suggests that increased hygiene in childhood associated with reduced exposure to pathogens may leave the mucosal immune system insufficiently trained and thus prone to uncontrolled inflammation. Oral contraceptives and non-steroidal anti-inflammatory drugs are the 2 main classes of frequently taken drugs that have been attributed to have the potential to cause flares of the disease. What is likely to be the connection between the genetic susceptibility and the environmental triggers? There is broad evidence for a critical role of the commensal enteric microbiota as a modulator of immunologic responses relevant during onset and chronification of IBD.