Malnutrition is usually considered a medico-social issue only in a few underdeveloped countries and typically characterized by not having enough to eat (undernutrition).

However, individuals in developed countries are also at risk, particularly hospitalized patients. Notably, the definition of malnutrition has expanded to include deficiencies, excesses, or imbalances in an individual’s energy and/or nutrient intake. In this article, we have restricted the definition of malnutrition to deficiencies.

Intestinal failure is the most representative gut condition in which nutritional therapy forms a major component of treatment. It occurs secondary to several inflammatory intestinal conditions such as CD or ischemic bowel disease. The range and type of nutritional therapy required in patients with intestinal failure depend on the extent and location of the diseased intestinal segments mainly in small intestine, which show disruption in absorptive capacity. If clinical presentations of the intestinal failure show a severe condition such as short bowel syndrome, intravenous supplementation for fluid, electrolyte and various nutrients would be a major component of the treatment strategy. Although limited evidence and guidelines are available regarding the optimal timing and methods of implementation and discontinuation of enteral nutrition (EN) or parenteral nutrition (PN), it is usually recommended that reintroduction of EN should be attempted as soon as patients recover from the severe intestinal disease. The insufficient energy not met by EN alone can be fulfilled by PN, which is called supplemental PN.

The multifactorial etiology of undernutrition in intestinal diseases includes lack of nutritional intake secondary to GI symptoms, malabsorption in the diseased segments of the gut, excessive GI losses secondary to diarrhea or fistula, and the influences of medications such as steroid and sulfasalazine [47]. Other less common conditions affecting nutrition include missing teeth, orofacial pain conditions, salivary dysfunction, and oral complications during cancer treatment and certain GI disorders. These conditions are relatively unrelated to intestinal diseases themselves [48].

Malabsorption is a major contributor to underweight in adults with CD during remission [49]. Previous reports in the available literature had described that patients with IBD showed a higher basal metabolic rate than healthy controls, secondary to the action of inflammatory cytokines in the former [50]. However, recent reports have shown that the energy requirements of patients with IBD were similar to those of the healthy population. Adults with IBD may show increased metabolic activity during episodes of severe disease associated with systemic disturbances (fever and tachycardia) compared to remission states; however, resting energy expenditure can be offset by reduction of physical activity. Changes in resting energy expenditure are not significant in mild disease states, even in children [47].

Regardless of the diagnosis, accurate assessment of the patient’s current nutritional status is important to fulfill the energy and protein requirements for optimal nutritional supplementation and to improve the prognosis of the disease. Correcting nutrient deficiencies and malnutrition in hospital and outpatient settings can reduce comorbidities, shorten recovery times, and reduce readmission rates [47,51].

Knowledge regarding the sites and mechanism of absorption of key nutrients is essential to determine the appropriate micronutrients that should be administered to a patient with intestinal disease and to accurately predict deficiency states of micronutrients based on the intestinal segments affected by disease. For example, vitamin B₁₂ absorption occurs exclusively in the terminal ileum; therefore, vitamin B₁₂ supplementation is essential in patients undergoing terminal ileal resection or in those with severe inflammation of the terminal ileum because nutrient absorption is markedly affected in such cases.

Dietary intervention refers to any alteration or treatment in an individual’s diet with a planned goal, which is usually designed to improve the individual’s overall health. The 3 principal models of dietary intervention include supplementation with selected dietary components, exclusion of selected dietary components, or use of dietary formulas to replace a normal diet [52].

Another aspect of dietary intervention is based on the understanding that diet significantly affects gut microbiome with consequent changes in the gut environment, as mentioned earlier. Metabolism of the host’s immune and nonimmune cells, as well as that of the gut microbiome is altered in intestinal inflammation. Thus, the nutrient demands of the host and/or the microbiome may be altered in a setting of GI disease. With regard to selecting treatment strategies, an accurate understanding of the appropriate dietary changes that could restore gut microbial diversity is important for optimal therapeutic dietary intervention.

Extensive research focusing on the effects of diet on the onset and exacerbation of GI disease has triggered interest in the utility of dietary modification as a treatment option. However, to date, few well-designed clinical trials and large-scale, randomized prospective studies have been performed to conclusively establish the optimal diet to treat specific diseases or induce/maintain remission. Meta-analyses reported in the literature have included small-scale studies.

Celiac disease is the most common disease for which dietary modification remains the main treatment. However, celiac disease is a chronic immune-mediated enteropathy triggered by dietary gluten, which serves as an antigen. Thus, it differs from the previously mentioned condition that involves complex interactions with the gut environment including microbiome. Currently, strict adherence to a gluten-free diet (GFD) is the only recommended treatment, which however is not useful in all patients. GFD has been shown to promote mucosal healing, reduce serum levels of celiac antibodies, improve nutritional deficiencies and bone health, and increase body fat [53].

The efficacy of medical treatment is variable and the underlying pathophysiology remains largely unclear in patients with IBS, and the role of dietary interventions in patients with IBS is being widely investigated. FODMAP is an acronym for fermentable oligosaccharides, disaccharides, monosaccharides and polyols, which constitute poorly absorbed and rapidly fermented carbohydrates that are osmotically active and increase the small intestinal luminal water content, as well as intraluminal hydrogen and methane content secondary to colonic bacterial fermentation. Thus, FODMAPs can cause functional bowel symptoms including diarrhea, gas, abdominal pain, and flatulence in susceptible individuals [54]. Several studies have shown that a low-FODMAP diet alleviates IBS symptoms. The adequate symptom relief was observed in 68% to 76% of patients with IBS who maintained the low-FODMAP diet over 4 to 8 weeks [55-58]. However, the following concerns warrant consideration in this regard: (1) An interesting paradox observed in such cases is that a low-FODMAP diet markedly reduces the luminal concentration of Bifidobacteria in the gut. It is well known that gut dysbiosis observed in patients with IBS is characterized by a reduction in Bifidobacteria species, which might be associated with an unfavorable symptom profile. However, some FODMAPs function as prebiotics (e.g., fructo- and galacto-oligosaccharides) and presumably produce beneficial effects on the GI microbiome. A study has shown that short-term FODMAP restriction correlated with reduced numbers of luminal Bifidobacterium spp. and Faecalibacterium prausnitzii [54,56,59]. (2) Long-term dietary restrictions can precipitate nutritional deficiencies because FODMAPs are constituents of a lot of food items. Therefore, a few researchers recommend a strategy comprising short-term FODMAP restriction for symptom control, followed by reintroduction of FODMAPs using food challenges to personal tolerance and finally, avoidance of only high FODMAP foods that trigger symptoms [14]. A recent study showed that long-term FODMAP restriction was a nutritionally adequate and acceptable strategy in >50% of the patients receiving dietary intervention [60].

Studies have shown that FODMAPs could cause functional GI symptoms even in patients with IBD [14,61,62].

Soluble fiber absorbs water and turns to gel during digestion and appears to improve IBS symptoms. Insoluble fiber increases stool volume, and soluble fiber is digested by colonic microbiome to form SCFAs, which nourish the colonic mucosal cells, improve mucus production, and may decrease inflammation at the cellular level. Although bran was not shown to be beneficial, there is no evidence to indicate any harmful effect associated with its use. A few studies have investigated the role of bran; however, most results are speculative and based on uncontrolled data [63,64].

Dietary intervention, which aims to limit potential nutritional hazards, is an important treatment option in patients with IBD to induce and extend disease remission [14]. Exclusive enteral nutrition (EEN) is an active nutritional intervention that serves as primary induction therapy for active pediatric CD. EEN is the most extensively researched dietary intervention for induction of remission in mild-to-moderate pediatric and adult CD [65]. EEN was reported to induce clinical remission in approximately 80% of pediatric patients [66]; however, the efficacy of EEN in adults is unclear because few studies have been performed in adults and these were of poor quality. The therapeutic effect of EEN is attributed to bowel rest, anti-inflammatory action, restoration of the epithelial barrier, favorable changes in the gut microbiome, and importantly, the exclusion of specific dietary components [67,68]. Several researchers have reported that EEN decreased pro-inflammatory and increased anti-inflammatory molecules such as transforming growth factor β [69,70]. A mouse model of CD showed that EEN maintained normal gut barrier function and integrity with resolution of inflammation [71]. To date, EEN-induced changes in gut microbiome remain inconclusive. Several studies have reported that EEN causes an extensive reduction in bacterial diversity, changes community-level metabolic functions and, at least initially, may increase microbial dysbiosis. With regard to taxonomic shifts, reportedly, EEN reduces the abundance of Firmicutes (including Faecalibacterium), Bacteroides/Prevotella, and Proteobacteriaceae and increases the abundance of Bacteroidetes [72-74]. A metagenomic study reported that EEN increased genes that play a major role in cell growth and renewal and possibly in tissue healing, in spite of the similar change of microbiota with the previous unfavorable changes [72]. Mechanisms of action of EEN warrant further research to gain a deeper understanding of the complex interplay between epigenetic, immunological, and microbiological changes.

Dietary intervention may also play a role in the prevention of diverticulitis, a common condition observed in clinical practice. It was previously presumed that nuts and food items with small seeds could lodge in the diverticula and cause inflammation. However, there is lack of scientific evidence to prove the role of nuts and seeds in the causation of diverticulitis flares. Data suggests that a high-fiber diet that includes insoluble fiber, such as wheat bran or fiber-based cereals reduces symptomatic disease or hospitalization for diverticular disease [75-77]. Dietary fiber benefits patients with diverticular disease via the following mechanisms of action: (1) It increases stool bulk and decreases colonic pressures and stool transit time; (2) A high-fiber diet affects the composition and metabolism of gut microbiome and via the diet-gut microbiome interaction, it increases the production of SCFAs, which are essential for the maintenance of colonic epithelial integrity and may also reduce systemic inflammation; (3) An inverse correlation is observed between dietary fiber intake and obesity [41,78,79]. In contrast, red meat intake, which might promote chronic low-grade inflammation, is reportedly strongly associated with symptomatic diverticular disease [80,81].

A recent large cohort study reported that a “prudent diet” decreased and a Western diet increased the risk of diverticulitis. Alcohol or caffeine intake was not significantly associated with diverticular disease. Moreover, more recent or current dietary intake showed a stronger association than chronic or previous intake [41]. The term “prudent diet” was introduced to describe the cholesterol-controlled diet in the Anti-Coronary Program of the New York City Department of Health since 1957 [82]. The “prudent diet” is one that is rich in fruits, vegetables, whole grains, legumes, poultry, and fish [83].

An analysis of the role of diet in diverticular disease must be based on the understanding that dietary patterns are closely associated with lifestyle and cultural behavior. For example, it is observed that men consuming the “prudent diet” usually tend to be more physically active and are less likely to be smokers or consume alcohol. In cases of incidental diverticulitis, non-dietary risk factors, such as genetics, obesity, physical activity, and NSAID use may be closely associated with the development of the disease [83].

The micronutrient and polyphenol content of diet should also be considered because these constituents affect microbial ecology, including its composition and metabolic activities.

Probiotics and prebiotics are natural dietary components that improve the intestinal environment and are recently being used as biotherapeutic agents for microbial-based therapy, comparable to fecal microbiota transplantation. Various probiotics are commonly used to prevent dysbiosis in patients undergoing prolonged antibiotic or immunosuppressive therapies. The mechanisms of action of probiotics are dependent on microbial strains.

With regard to immunological functions, probiotic strains produce growth factors that strengthen the gut epithelium/gut barrier and antimicrobial substances such as SCFAs, bacteriocins, hydroperoxides, bile acids, and lactic acid, which destroy pathogens [84]. Moreover, probiotics activate host immune responses via release of cellular components from the strains and improve macrophage and lymphocyte activity [85].

With regard to non-immunological function, probiotics/prebiotics improve digestion and absorption, compete with potential pathogens for nutrients and intestinal adhesion sites, modulate pH alterations, and promote agglutination of pathogens and sequestration of metabolic toxins [86,87]. These agents are also known to inhibit apoptosis and participate in mucin synthesis and tissue repair, thereby enhancing the protective function of the gut barrier [88].

However, probiotics or prebiotics have shown limited efficacy in microbial modulation of active GI disease [87,89]. Additionally, lack of standard therapeutic regimens, small-sized study samples, and poor disease characterization are limitations of the clinical and experimental studies that have investigated the efficacy of probiotics/prebiotics. Thus, their role remains inconclusive in this context. Nonetheless, probiotics are shown to be potentially useful in the management of IBS, diverticulitis (with some success), and IBD, in addition to a few other conditions [59,90].

Akkermansia muciniphila, an intestinal symbiont that plays a key role in mucin degradation, is recently gaining increasing attention as a promising probiotic secondary to its ability to improve host metabolic functions and immune responses. A few animal studies have reported that the ingestion of live A. muciniphila counteracts the metabolic disturbances caused by a high-fat diet including fat-mass gain, metabolic endotoxemia, adipose tissue inflammation, and insulin resistance and aids in restoration of normal mucus layer thickness by reducing endotoxemia. A. muciniphila could serve as a novel potential therapeutic agent in various GI diseases including colitis (particularly IBD), colon cancer, and other microbiota-related diseases. Preliminary data from human studies suggest that oral administration of A. muciniphila is safe; however, further studies are required to verify the effectiveness and safety of this agent [91-93].