Perhaps, the best known and risk factor for Crohn’s disease is cigarette smoking which has been associated with a doubling of the risk for CD when compared to those that have never smoked [1]. This risk for CD associated with smoking may linger for several years even after quitting smoking. Additionally, smoking is a risk factor for more aggressive Crohn’s disease [2]. Smokers have higher incidence of surgery and higher rates of disease recurrence postoperatively compared to nonsmokers [1]. The exact mechanism of action of smoking in Crohn’s disease is not clear at this time, and all CD patients should be strongly encouraged to quit smoking.

Current smokers appear to be protected against development of UC, and smoking cessation increases the risk of UC onset, especially within the first year of quitting. This risk may persist for more than 10 years after cessation [3]. The effect of smoking is also seen on the disease course. Active smoking in UC has been shown to be weakly associated with a trend toward lower colectomy rates, and smoking cessation has been associated with an increased need for hospitalization and escalation of medical therapy [3–9]. The mechanism of the effect of smoking on UC onset and disease course is unclear. Overall smoking is not recommended as a therapeutic option for UC given its many deleterious side effects.

While its role in regulating calcium and bone heath is well understood, Vitamin D plays a role in regulating many different aspects of the immune system that we are just starting to understand [10]. Vitamin D metabolism requires exposure to UV light to create the active metabolite, 1,25-dihydroxy D3. There is known to be a north-south gradient when it comes to the incidence of IBD, in that there is a higher risk of IBD in residents of northern latitudes. It has been suggested that reduced ultraviolet light exposure in northern latitudes may cause reduced active vitamin D (1,25-dihydroxy D3 active metabolites) which may then explain the increased IBD incidence in more northern latitudes [11]. For this reason several people have looked at vitamin D levels as a possible factor in the development of IBD. Analysis of the Nurses’ Health Study showed that women with the highest predicted serum levels of vitamin D had a 40 % reduction in the risk of being diagnosed with Crohn’s disease when compared to women with the lowest predicted levels of vitamin D [12]. They were unable to show a correlation between vitamin D and UC in this same study. Additionally, when compared to other CD patients with normal vitamin D levels, Crohn’s patients with low vitamin D levels have a poorer quality of life and tend to have increased disease activity scores [13].

Enteric infections appear to increase the risk of UC onset which is evidenced by the association of Clostridium difficile infection (CDI) with about 40 % of UC flares [14]. CDI is more common in patients with inflammatory bowel disease (IBD) and is associated with increased morbidity and mortality [15]. Interestingly, the common predisposing risk factors for CDI such as recent antibiotic use and exposure to health care appear to be less common in the IBD population [14]. Salmonella or Campylobacter infections have been shown to have a three-time increased risk for IBD onset [16].

Given the higher incidence of IBD in developed countries and that the incidence of IBD appears to be increasing in developing countries, it only seems logical to look at the Western diet as a possible etiology for IBD. This “Western diet” is typically low in fiber and high in animal fats and processed food, and we see it slowly becoming adopted in developing countries where we see the increasing incidence of IBD. While several studies have been inconclusive or conflicting, there does appear to be some correlations with diet and the development of IBD. In particular, a high dietary fiber intake has been shown to reduce the risk of both CD and UC onset, particularly soluble fiber from fruits and vegetables as opposed to insoluble fiber from cereals and bran [17]. High intake of linoleic acid and arachidonic acid has been associated with increased UC risk [18, 19], and dietary n-3 polyunsaturated fatty acid and docosahexaenoic acid intakes were associated with reduced UC risk [20]. There is limited data about the effect of protein intake on UC incidence, and high animal protein intake has been associated with increased risk of CD [21]. Carbohydrates do not seem to influence UC or CD risk. The effect of diet or dietary modifications on IBD needs further evaluation in larger intervention studies.

Treating inflammatory bowel disease with a particular diet is very attractive to physicians and patients alike; unfortunately, there is very little data to guide recommendations in this area. While it has not been extensively studied, a low-residue diet (low insoluble fiber) plays a role in the management of stricturing Crohn’s disease. Although this is not typically a good long-term solution (it can be deficient in some essential vitamins), it can help to alleviate symptoms while awaiting surgery or medical therapy. While several popular exclusion diets have been proposed for treatment of IBD (e.g., gluten-free diet and specific carbohydrate diet), no elimination diet has been found on a prospective basis to be effective in treating IBD. Elemental and enteral feedings have been shown to be effective for treatment of Crohn’s disease, but not ulcerative colitis. Although this may be effective in the short term, patients frequently relapse when resuming a regular diet and the long-term sustainability is often limited by cost and palatability of these diets [22].