Changing trends in the epidemiology of IBD provide an opportunity to examine possible etiological hypotheses. Why did IBD emerge in developed nations in the middle of the 20th century? Why did it emerge initially as ulcerative colitis but now Crohn’s disease has become the predominate form of IBD in developed nations? Why is IBD emerging in recent years in developing nations and why is it that ulcerative colitis is the predominate form in these countries? In this chapter we will explore what is known about environmental issues that impact on disease presentation and where they provide opportunities for therapy. Managing smoking cessation in Crohn’s disease is substantiated by evidence showing that smokers have a worse course of disease than non-smokers or than persons who quit smoking. Introducing nicotine to patients with ulcerative colitis has not brought the positive results anticipated with the widespread observation that smoking cessation was associated with flaring of this disease. Assessing and managing stress in both Crohn’s disease and ulcerative colitis has emerged as an important consideration for clinicians caring for patients with IBD, especially for patients with active disease who may develop maladaptive coping mechanisms. Recent data suggest that stress may antedate flares. It is unknown what may induce changes in the gut flora of patients with IBD compared to controls. There are suggestions that antibiotic use in childhood and specific diets particularly those lower in ω-3 fatty acids may impact on disease presentation and the common mechanism may be through alteration of gut flora. For at-risk families (where there are affected family members) perhaps greater vigilance with antibiotic use in childhood and ensuring diets are higher in ω-3 fatty acids can be considered. In the future there may be approaches to modulate gut flora either with antibiotics targeted against identified noxious microbes or with selective probiotics that can rebalance the gut dysbiosis.

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