Diet
General description
Results
References
Gluten-free diet
Exclude wheat, rye, barley
Improvement of symptoms
[14]
Mediterranean diet
Reduce meat
Increase bread, fish, fruits, vegetables and olive oil
Decreased CRP levels after 6 weeks
[15]
Specific carbohydrate diet
Exclude processed meats and all sugars other than monosaccharides
Decreased Crohn’s disease activity (Harvey-Bradshaw Index) at week 12 in 9/10 patients
[16]
FODMAP diet
Exclude many fruits, vegetables and legumes, wheat, rye, milk
Improvement of symptoms
[17]
10.1.2 Lifestyle
10.1.2.1 Smoking
Nowadays, it is unquestionable that smoking negatively affects our health. Smoking is a leading cause of cancer (among others, lung, esophagus, larynx, and colon cancer) and death from cancer worldwide. However, the effect of cigarette smoking in IBD course is surprising. Available data suggest that current smokers are more protected against UC, while at the same time smoking increases the risk of CD in a dose-dependent manner. Moreover, UC activity in smokers is lower when compared to non-smokers. Smoking UC patients have lower flare-up and hospitalization rates, less often need oral steroids, immunomodulators and biologic agents and—what is even more important—have lower colectomy rates compared to non-smokers [18, 19]. Interestingly, primary sclerosing cholangitis is observed almost exclusively in non-smoking patients [20].
In contrary, smokers with CD have a risk of flare-up increased by more than 50 %, an increased need of steroids, immunosuppressants and biologic agents as well as lower quality of life compared to non-smokers [21, 22]. Furthermore, smoking is connected with more frequent intestinal penetrating complications and a higher risk of being operated during disease course [18]. Moreover, the harmful effect of smoking is more marked in women and in patients with ileal disease [23, 24].
Finally, smokers with UC note symptom exacerbation when they quit smoking and symptom relief when they start smoking again [25]. Furthermore, smoking patients with UC who stop smoking experience an increase in disease activity; also, the number of hospital admissions within the first few years following the cessation of smoking is higher [26]. In contrast, patients with CD who quit smoking display similar disease severity to non-smokers and better course than continuing smokers [27].
To conclude, in clinical practice patients with IBD should be encouraged to quit smoking to reduce the risk of lung cancer and cardiovascular disease. However, smokers with UC should be informed that quitting smoking may potentially increase disease activity. Therefore, doctors should intensify treatment in patients with UC who plan to stop smoking.
10.1.2.2 Alcohol Consumption
The role of alcohol in causing or aggravating IBD in still unclear [28]. Usual consumption of alcohol (defined as alcoholic drinks 1–4 days per week) reduces the risk of UC when compared with less frequent use (odds ratio = 0.57, 95 % CI: 0.37–0.86) [29]. In line, light alcoholic drinking has protective effect against development of UC. Nevertheless, this effect disappears when smoking is included [30].
10.1.2.3 Physical Activity
The role of exercise in IBD has not been well studied, while some older epidemiological data suggest that physical activity is associated with a decreased risk of CD [18]. Results from a study, in which the effect of one-hour exercise in a cycle ergometer in six males with ileal CD was evaluated suggest that a moderate-intensity exercise program is probably safe for those patients [31]. In another study Loudon et al. [32] investigated the effects of a three-month low-intensity group walking program in CD patients. Significant improvement in CD activity and IBD Questionnaire were observed. In line, Ng et al. [33] using similar three months program found an improvement in quality of life in CD patients, with no exacerbation of disease symptoms.
Nowadays, the role of physical activity and exercise in the prevention and treatment of bone loss is well established in healthy population [35]. Furthermore, patients with CD in remission have decreased muscle function, which is self-described as a reduced strength and endurance, especially for lower limbs [34]; the may lead in longer term to osteoporosis. Thus, despite the fact that there is no clear evidence that exercise has any effect on IBD itself, some low-intensity training should be implemented to improve muscular mass and to prevent osteoporosis in IBD patients. A study performed by Robinson et al. [36] provides evidence supporting this recommendation, showing that low-intensity exercise in CD patients significantly improves bone mineral density after one year. Moreover, the increases in bone mineral density were correlated with the number of exercise sessions completed [36].
10.1.2.4 Obesity
While previously obesity in IBD has been considered unusual, nowadays its prevalence is increasing in CD, simultaneously with an increased prevalence in the whole population [37]. For example, epidemiological data from Scotland showed a prevalence of 18 % of obesity in CD [38].
Considering disease severity, overweight or obese patients with UC had to undergo colectomy more often than normal weight patients [38]. Interestingly, patients with CD had lower levels of surgery in the obese group compared to the normal-weight group [38]. On the other hand, other studies showed that obese CD patients had shorter time to first surgery [37, 39]. Taken together, it can be suggested that obese patients with IBD may require more aggressive medical therapy with avoidance of corticosteroids and should be encouraged to lower their body weight.
10.2 Intestinal Microflora
The human GI tract is colonized by a wide variety of microorganisms. Interestingly, more than 70 % of all microbes in the human body are in the colon, where they constitute a relatively stable ecosystem. Instantly after birth, oral cavity and gut are settled by an extensive range of microbes, mainly bacteria. Microbial load in the GI tract is not homogenous and ranges from 101 to 103 in the stomach and duodenum, progressing through the ileum in order to achieve a total number of 1011–1012 bacterial cells per gram in the colon [40].
Commonly called human microbiota, it consists of trillions of organisms from over 1000 species [41]. The most abundant species are members of the phyla Bacterioides and Firmicutes. Bacterial diversity changes with age [42]. Apart from Bacterioides and Firmicutes phyla, adult gut ecosystem is colonized by Actinobacteria, Proteobacteria and Verruvomicrobia [43, 44]. It is important to emphasize that—among anaerobic bacteria in the human colon—Bifidobacterium spp and Faecalibacterium spp. can be found. Moreover, oxygen tolerant bacteria, such as Lactobacillus spp. may also appear in the gut, but in low number. The population of aerobic bacteria is fluctuating over time and depends on diet and other environmental factors, such as hygiene, climate, geography and ethnicity [45].
The GI tract microbiota is known to play an important role in the regulation of metabolic functions and maintenance of immune homeostasis. Microbiota is responsible for performing important biochemical reactions for host physiology, including degradation of xenobiotic substances, vitamin biosynthesis, fermentation of indigestible polysaccharides into beneficial short chain fatty acids, immune development and intestinal homeostasis maintenance [46].
Detrimental alterations in microbiota structure and functions causing the loss of ability to maintain homeostasis in GI tract are considered as a dysbiosis. Nowadays, a variety of pathologies are connected with the changes not only in the structure, but also the function of the gut microbiota, thereby suggesting a linkage between dysbiosis and disease etiology [46]. Namely, multiple disorders including type 2 diabetes, allergies, neurological disorders as well as IBD can be associated with dysbiosis [47].
IBD can be described as an immune-mediated disorder that originates from a breakdown of the normal symbiosis between the mucosal immune system and the commensal microbiota. This leads to the development of aberrant reactivity against intraluminal antigens and dysregulation of the innate and adaptive immunity. Consequently, these alterations may be responsible for tissue injury. Several studies have already demonstrated differences between microbiota of IBD patients and healthy individuals [48–53].
Regarding CD patients, lower diversity of microbiota, as compared with healthy individuals, was largely due to lower amounts of Firmicutes, especially Clostridium leptum phylogenetic group. Furthermore, another study reported that samples from small intestine of CD patients were less enriched in the Bacillus genus of Firmicutes and more rich in Proteobacteria [48]. Moreover, lower fecal concentrations of the Bacterioides fragilis group, Clostridium coccoides group, the Atopobium cluster and Clostridium leptum subgroup were observed in CD patients compared to healthy subjects [49].
Faecalibacterium prausnitzii, which is believed to be an important member of the normal gut flora, merits special attention. Research conducted by Sokol et al. [50] demonstrated a decrease in F. prausnitzii in samples from CD patients compared with healthy subjects. This is noteworthy in view of the fact that F. prausnitzii, through bacterial fermentation generate anti-inflammatory products which may act as a source of energy for the epithelial cells of intestine. Furthermore, they are believed to have impact on epithelial barrier integrity and play a role in intestinal immunomodulation [48].
Finally, higher abundance of Enterobacteriaceae has been observed in the intestinal samples of patients with CD. The increase in these bacteria may be due to intestinal inflammation itself, which promotes the growth of this strain of bacteria. Particularly, adherent-invasive E. coli (AIEC) strains were observed in higher abundance in mucosal samples from CD patients compared to healthy individuals [48].
The reduction of bacterial diversity and richness was also observed in UC patients. It included changes in abundance of Firmicutes, especially Clostridium leptum clusters, Fecalibacterium prausnitzii, Clostridium coccoides, Roseburia, Ruminococcus, Enterococcus and Lactobacillus [51]. Moreover, increased Proteobacteria populations, such as Eschericia sp., Helicobacter sp. and Campylobacter sp. were also reported [51]. Similarly to CD patients, AIEC has been observed in UC patients and implicated in the pathogenesis of UC [52]. Interestingly, AIEC were isolated from stools and rectal biopsies of UC patients during relapses and remissions.
It is worth mentioning that Campylobacter sp. is significantly more frequently detected in UC patients compared to controls [51]. These findings suggest that in UC patients specific immunological defect appears, which results in an inability to eliminate Campylobacter spp. Fusobacterium varium is another species of commensal bacteria increased in inflamed mucosa of UC patients. F. varium is believed to be responsible for production of high concentrations of butyric acid, which causes intestinal lesions in mice similar to those observed in human UC patients [53]. In contrast, many reports have demonstrated a decrease in Faecalibacterium prausnitzii in UC patients. Other studies showed that patients with UC had lower numbers of Butyricicoccus bacteria in their stools as well as lower abundance of Roseburia hominis. These three bacteria belong to Clostridium leptum group within the Firmicutes family and are known to produce butyrate [51].
It is indisputable that microbiota dysbiosis increases pathogenic and pro-inflammatory bacteria and decreases beneficial and anti-inflammatory bacteria. Genetic susceptibility of IBD patients leads to defective mucosal barrier function, which promotes invasion of pathogenic bacteria causing ulcerations and inflammation of the mucosa. Subsequent studies focused on the linkage between microbiota and the mucosal immune system are essential to understand the pathogenesis of IBD.
10.3 Psychological Aspects and Treatment
10.3.1 Introduction
Crohn’s disease and ulcerative colitis are chronic disorders characterized by the presence of unpleasant symptoms from the GI tract impairing everyday functioning. IBD is often accompanied by harmful extraintestinal manifestations, with unpredictable course resulting in a significant reduction in the quality of life (QOL). The QOL is lower in women and CD patients than in men and UC patients, respectively. Higher levels of depression and anxiety are observed in CD compared to UC patients. Furthermore, in CD patients QOL was associated with disease activity; lower QOL was observed in relapse in comparison to patients with remission. Interestingly, patients after biological therapy with infliximab who achieved remission had higher quality of life than patients who did not received remission. In turn, in the UC patients the quality of life was connected with the extension of colon inflammation. Generally, patients after surgery presented lower QOL compared to patients treated pharmacologically.
Inflammatory bowel disease affects mainly young people, at the life phase when they obtain proper education and experience. Interestingly, research have suggested that patients with IBD have higher level of education comparing to healthy individuals. In contrast, patients with IBD have higher risk of not finishing higher school. Currently, it seems that besides difficulties with attendance in class patients with IBD achieve comparable level of education to healthy individuals. Furthermore, process of education among patients with IBD may be extended. Summarizing, IBD itself, as well as accompanying symptoms may affect future plans of patients and the type of obtained education.
10.3.2 Psychological Symptoms in IBD
There is growing evidence that psychological factors play a role in the pathophysiology and the course of IBD. Presence of stressful events, as well as perception of stress is believed to contribute—along with other factors such as the use of NSAIDs or infections—to triggering flares of IBD [54]. Family stress was the most commonly reported. Patients with IBD also report stress accompanied with work, school and finances to be responsible for exacerbations of IBD.
The levels of depression and anxiety in patients with IBD are reported to be higher versus general population, but lower than in patients with functional bowel disorders [55]. Depressive disorder appears to affect more commonly older people and individuals with previous history of a psychiatric disorder. Moreover, females may have a higher risk of disease activity and relapses than men [56]. It has been suggested that depression, anxiety and impaired quality of life may exhibit negative influence on the course of IBD. Moreover, patients with IBD take more medications, such as antidepressants and anxiolytics than the healthy populations. Use of antidepressants to treat depression in IBD patients was found to be associated with decrease in relapse rates and steroid use [55].
Both depression and anxiety precede UC significantly more often, whereas no such relationship was seen in CD [55]. The association with UC is strongest when depression and anxiety are diagnosed in the same year as UC. Nevertheless, the origin of depression and anxiety in IBD patients remains not completely explained. It is suggested that depression and anxiety are consequences of IBD symptoms, such as frequent stools, abdominal pain and bloating.
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