Inflammatory bowel diseases (IBDs) are chronic, progressive, immune-mediated diseases of the intestinal tract [1] characterized by a progressing or relapsing and remitting disease course [2]. They are associated with significant morbidity, disability, and risk of complications [1] such as abdominal abscesses, fistulae, strictures and subsequent bowel obstruction, and an increased risk of gastrointestinal (GI) cancer [2]. To date, the etiology of these diseases is still not clear [3,^[3]4]; nevertheless, it is known that there are genetic ^{[4][5][6][7][8][9][10][11][12][13][14][15][16]}[5,6,7,8,9,10,11,12,13,14,15,16,17], host-related ^{[17][18][19][20][21]}[18,19,20,21,22] and environmental ^[15][18][22][16,19,23] factors that contribute to the development of gut inflammation and IBD (Table 1).

The main subtypes of IBDs are Crohn’s disease (CD) and ulcerative colitis (UC) ^[3][4]. CD inflammation affects the whole intestine but the most common sites are in the small and large intestine (especially in the ileum) and perianal region and are classified as “L1: ileal-type”, “L2: colonic-type”, “L3: ileocolonic-type” and “L4: isolated upper disease” ^[19][20]. UC, on the other hand, is classified as: E1 ulcerative proctitis, when the site of the disease is limited to the rectum; E2 distal UC, when it is limited to a portion of the colorectal distal to the splenic flexure; and E3 extensive UC or pancolitis, when it extends from proximal to the splenic flexure ^[23][24]. The severity of IBD is classified as “remission”, “mild”, “moderate”, or “severe” based on clinical symptoms, signs, and blood tests ^[23][24]. Signs and symptoms of CD and UC are presented in Table 2.

For IBD, there are both pharmacological and non-pharmacological options to manage symptoms. Current drug treatments for IBD are aminosalicylates (5-ASA) that can be used in combination with steroids to induce and maintain remission ^[27][28][28,29]. If CD is mild to moderate, mesalamine is the first-line therapy while sulfasalazine is most effective at maintaining remission in UC ^[27][29][28,30]. The mainstay treatments of IBDs are hydrocortisone and prednisolone with glucocorticoid properties ^[27][28]. The preferred steroid is prednisolone, administered orally ^[27][28] (0.75–1 mg/kg of body weight) ^[4][5] and can be used in the short term to alleviate symptoms of moderate and severe CD ^[27][28]. Moreover, with a low dose of steroids, azathioprine may be introduced ^[27][28]; in fact, immune suppressants have been adapted for the treatment of IBD. Thiopurines (azathioprine, 6-mercaptopurine and methotrexate) are beneficial in 50 to 70% of patients ^[27][28] but are generally reserved for patients who are steroid resistant or steroid dependent ^[27][30][28,31]. Anti-TNF monotherapy is effective in maintaining remission ^[27][28], especially in patients with moderate–severe UC who have inadequate response or intolerance to conventional therapy ^[27][28][28,29].

A treatment which can prevent inflammation remains a cornerstone for IBD management and the diet also plays a pivotal role in the prevention of inflammatory bowel disease risk development ^[31][32][32,33]. The spread of the Western diet, rich in fats, protein, simple sugars and low in fruit and vegetables, represents a possible cause for the increase in IBD ^[33][34]. Indeed, diet affects intestinal inflammation through mechanisms such as the ability to present antigens and the alteration of the balance of prostaglandins (involved in the inflammatory pattern) and microbiota ^[34][35][35,36]. In particular, numerous studies have underlined the increased incidence of IBD due to excessive consumption of sugars or sugar-sweetened beverages ^[18][36][19,37], proteins (especially from red meat) ^[37][38], animal fats and linoleic acid. In fact, red meat consumption has been suggested to have a pro-inflammatory effect. This may be due to the cooking method and the concurrent presence of saturated fats that establish deleterious effects ^[18][19]. A high consumption of total fatty acids, polyunsaturated fatty acids (PUFAs), especially omega 6 fatty acids, increases the risk of developing both UC and CD ^[22][23]. The recent literature also shows that nutrition could influence the development of IBD ^[38][39] but actually few dietary recommendations exist. The American Journal of Gastroenterology published the American College of Gastroenterology (ACG) Practice Guidelines for CD and UC, which suggest eating frequent small meals or snacks every 3–4 h, drinking enough fluids to avoid dehydration, eating food with added probiotics and prebiotics and using multivitamins ^[39][40]. During remission, patients can include whole grains and a variety of fruits and vegetables in their daily eating plan; however, when there are symptoms, it is recommended to consume low-fiber foods ^[39][40]. Foods recommended for IBD are: low-fat and lactose-free milk and dairy products, lean and white meat, fish or eggs, grains with less than 2 g of fiber per serving, low-fiber vegetables and fruits (i.e., lettuce, strained vegetable juice, fruit juice without pulp, ripe banana or melons), less than eight teaspoons/day of oils and to drink water or beverages without caffeine ^[39][40]. The effect of alcohol in IBD is still controversial: some studies document positive effects of alcohol consumption in the development of UC ^[40][41][41,42] but this effect seems to be nullified if alcohol consumption is associated with cigarette smoking ^[42][43].

In the literature, since 1978, there has been considerable interest in dietary fibers as a therapeutic option in IBD but its role is unclear, with conflicting findings ^[43][63].

In the case of IBD, it is suggested that a diet rich in fibers, vitamin D and adequate consumption of citrus fruits has a protective role ^[38][39]. In fact, high consumption of fiber and fruit is associated with a 73–80% decreased risk of CD, while a high intake of vegetables reduces the risk of UC ^[22][23].

It is important to underline that patients with stricturing Crohn’s disease should be careful to their intake of dietary fiber and fibrous foods for symptomatic management of strictures and may need supplementation with enteral or parenteral nutritional requirements ^[44][64].

Although Anantakrishnan et al. observed that the consumption of at least 24.3 g of fiber per day (particularly fruit-derived fiber) reduces the risk of developing Crohn’s disease by 40% but not UC ^[45][65], in the literature, there are some conflicting evidence on the use of high-fiber foods in IBD. To date, it is clear that they are not recommended during flare-ups or during active disease states, fistulas or strictures ^[39][40]. In fact, in CD, a low-fiber diet should be used for a short period, and it is indicated only in certain conditions, such as acute relapses (with diarrhea and cramps), intestinal stenosis, bacterial proliferation of the small intestine and after some type of surgery ^[39][40]. In 2020, Day et al., in a systematic review, analyzed different study designs to determine the correct amount of dietary fiber in individuals with IBD ^[46][66]. They compared the adequacy of fiber intakes with that of a control group or compared to national dietary guidelines, and examined factors associated with fiber consumption ^[47][67]. They concluded that individuals with IBD are used to consuming less fiber than healthy populations and that fiber intakes are inadequate compared to national fiber guidelines ^[46][66].

It is also necessary to mention the role of fermentable carbohydrates, or FODMAPs (oligosaccharides, disaccharides, monosaccharides and fermentable polyols), in IBD. FODMAPs have an osmotic and fermentative action because they recall water and gas in the intestinal lumen being partially or completely indigestible ^[48][68]. A low-FODMAP diet is usually suggested in the case of Irritable Bowel Syndrome (IBS) that is characterized by symptoms such as abdominal pain, meteorism, bloating, diarrhea or constipation ^[49][50][69,70]. Approximately one-third of IBD patients complain of IBS-like intestinal symptoms in the absence of actual gastrointestinal inflammation, thus usually an overlap of symptoms has been recognized ^[51][71]. There are several studies that evaluate the association between IBD and consumption of FODMAPs. In a randomized controlled trial (RCT), improvements in gastrointestinal symptoms were observed in patients in remission or with mild–moderate disease and coexisting IBS-like symptoms after following a low-FODMAP diet for approximately 6 weeks ^[52][72]. Results showed a significant reduction in symptoms in the Low-FODMAP diet group compared to the No Diet group (p = 0.02) ^[52][72]. A further study evaluated the effect of FODMAP consumption in quiescent IBD patients allocated to a series of 3-day fermentable carbohydrate challenges in a random order (fructan: 12 g/die; galacto-oligosaccharides: GOS, 6 g/die; sorbitol: 6 g/die; and glucose placebo: 12 g/die), each separated by a washout period ^[53][73]. At the end of the researchtudy, the authors observed that fewer patients reported adequate relief of functional gastrointestinal symptoms (62.1%) compared to glucose (89.7%) (p = 0.033), and that fructans, but not GOS or sorbitol, exacerbated gastrointestinal functional symptoms ^[54][74]. However, it is necessary to carry out further studies to evaluate the effect of different types and doses of FODMAP in patients with IBD ^[53][73].

To date, the daily amount of dietary fiber is suggested by the EFSA, The American Heart Association Eating Plan and the Academy of Nutrition and Dietetics ^[55][56][57][59,60,61] but there is no tolerable upper limit for total fiber intake; thus, eating more fibers can cause uncomfortable side effects ^[58][75], such as constipation, intestinal blockage, bloating or diarrhea ^[59][60][61][76,77,78]. Inadequate hydration and reduced physical activity combined with high fiber consumption can induce constipation; fiber is not fully digested or excreted from the body, generating intestinal blockages. In this case, intestinal bacteria ferment these undigested fibers ^[62][79], producing gas ^[63][80] and leading to symptoms such as bloating and flatulence. One strategy to minimize intestinal gas production is to consume fibers gradually and not suddenly. On the other hand, excessive consumption of fibers, especially insoluble ones, can also lead to diarrhea ^[58][64][75,81].

Moreover, high fiber consumption can reduce the rate of gastrointestinal micronutrient absorption, especially calcium and iron ^[65][82]. This is due to the chemical and physical characteristics of fiber such as fermentation, bulking capacity, binding capacity, viscosity and gel formation, water retention capacity and solubility ^[66][83] and also to the presence of some compounds such as phytates, oxalates, and tannins ^[67][84]. This is a big issue for IBD patients, who are already malnourished for gastro-intestinal malabsorption, and are further destabilized.

IBD patients report intolerance to some types of fibers because they lack fermentative microbe activities compared to individuals with normal microbial fermentative activity ^[67][84]. The absence of these microbes makes the fibers indigestible and therefore intact; this fibers interact with host cell receptors and promote intestinal inflammation ^[67][84].

The study by Armstrong et al. investigated the role of unfermented β-fibers in fueling inflammation in IBD patients ^[68][85]. β-Fructans (inulin and oligofructose/FOS) are β-(2 → 1)-linked fructose oligo- and polysaccharides. They are abundant in plant sources such as chicory root, agave and artichokes, while less abundant in banana, wheat, onion and garlic ^[69][86].

In some IBD patients, β-fructan fibers have shown potential negative impacts. Indeed, dietary β-fructans induce inflammation through activation of TLR2 and NLRP332 pathways ^[70][87] and promote the production of reactive oxygen species (ROS) interacting with carbohydrate receptors (GLP-1R) ^[71][72][88,89].

Although inulin could present positive effects on inflammation, there are several studies that have shown that it exacerbates the severity of colitis in an IL10-/- and DSS model of colitis ^[73][90] and facilitates the progression of hepatocellular carcinoma in mice ^[74][91].

Moreover, it has been seen that the consumption of unfermented FOS could also induce the production of pro-inflammatory cytokines in peripheral blood mononuclear cells (PBMCs) and in THP-1 macrophages, and this was seen in biopsies from IBD patients ^[75][76][92,93].