The consumption of red meat, due to its high content of saturated fat and cooking method, has been linked to an higher risk of colon cancer and inflammation [22]. Red meat is metabolized by intestinal bacteria with production of branched-chain amino acids and toxic elements like hydrogen sulfide, nitrous compounds, amines, and ammonia that induce DNA damage of eucaryotic cells and promote colon inflammation in murine models [23,24]. Notably, large epidemiological data confirmed the association between high consumption of red meat and risk of IBD development, in particular UC [25], where it was found to affect also the relapse risk [26].

Sugars are part of everyone’s diet. The modern diets are rich in sugar; chocolate, cookies, cakes, ice creams, fruit punches, energy drinks, soft drinks, iced tea, and lemonade contribute to the “pandemic” of obesity, diabetes, and steatosis that plagues the western world [27]. Sucrose, a disaccharide composed of monosaccharides fructose and glucose, is the most common sugar found in processed foods. Many studies have linked high sugar intake with IBD incidence [28,29,30,31].

The pathogenic mechanism that links high sugar intake with the onset of IBD is not fully elucidated. A possible explanation is a reduction of intestinal mucus [32]. A sugar-rich diet favors the increase of Akkermansia muciniphila, a mucolytic bacterium. The mucus layer separates luminal bacteria from intestinal epithelium: A thinner mucus layer allows bacteria to come in contact with the epithelial cells, eliciting an inflammatory response. In addition, this type of diet increases the percentage of pro-inflammatory Sutterellaceae and Marinilabiliaceae, which induce bowel inflammation [33], and reduce bacteria with anti-inflammatory properties like Lachnospiraceae and Lactobacillaceae, able to produce the short-chain fatty acid (SCFA) butyrate, the main anergy source of enterocytes [34].

In contrast to eastern and African diets, the western diet is low in fiber. Butyrate-producing bacteria, like those belonging to Bacteroidetes and Firmicutes phylum, exert their anti-inflammatory activity metabolizing dietary fibers: A low-fiber diet leads to reduced production of butyrate, which acts as a negative regulator of pro-inflammatory pathways and enhances the intestinal barrier function [35]; this, in turn, increased the risk of IBD onset [36]. When substrate is scarce, intestinal bacteria use the intestinal mucus as a nutrient, which leads to inflammation through close contact between bacteria and the epithelial layer [37]. Long-term intake of fibers from fruit has been shown to be protective against the development of CD, but not of UC [38,39,40,41,42].

The benefit of fibers in IBD remission is uncertain. Brotherton et al. [43] found that a low fiber consumption in CD during remission is associated with a higher risk of clinical relapse, but in the case of stricturing CD, the consumption of dietary fibers could precipitate obstruction.

A diet rich in nuts and dried fruits, due to their high content of omega-3 fatty acids, fibers, and antioxidants, has been shown to decrease the cardiometabolic and inflammatory risk; the beneficial effects on health include reduced risk of cancer, diabetes, neurological diseases [44]. A diet rich in walnuts protects mice from dextran sulfate sodium (DSS)-induced colitis [45]. The mechanism of action seems to be a decrease of macrophages activation, reduction in the production of pro-inflammatory cytokines like IL-6, IL-8, IL-1α, tumor necrosis factor (TNF), and an increase of anti-inflammatory cytokine IL-10.

The health benefits of vitamin D are pleiotropic and include bone health, modulation of the immune system, antimicrobial protection, and mucosal integrity [46]. Deficiency of vitamin D is common in patients affected by IBD, in particular CD, due to malabsorption, and is worsened by reduced sunlight exposure and steroid treatment [47].

The positive effects of vitamin D are related to the improvement of epithelial barrier function [48] T-cells development, production of anti-inflammatory cytokines, and modulation on both innate and adaptive immunity [49], but even to antimicrobial peptides secretion [50]. In in vivo experiments, inadequate dietary intake of vitamin D promotes colitis development [51]. One possible explanation for this observation is that vitamin D deficiency produces intestinal dysbiosis, with a reduction of bacteria with anti-inflammatory properties (e.g., Firmicutes) and an increase in pathobiontic bacteria (e.g., Bacteroides and Proteobacteria) [52]. Moreover, even clinical observations have frequently found a link between low levels of vitamin D and a more aggressive course of IBD [53,54,55].

The western diet contains large amounts of emulsifiers, widely used in processed food to improve food appearance, texture, and palatability due to their intrinsic properties. Emulsifiers affect the gut microbiota, disrupt the mucosal barrier, and promote inflammation; in mice models, they induce metabolic syndrome, colitis, and translocation of Escherichia coli [56,57].