{"Affiliation":[{"label":"Affiliation","value":"Arts and Sciences, Irving K. Barber School of (Okanagan)","attrs":{"lang":"en","ns":"http:\/\/vivoweb.org\/ontology\/core#departmentOrSchool","classmap":"vivo:EducationalProcess","property":"vivo:departmentOrSchool"},"iri":"http:\/\/vivoweb.org\/ontology\/core#departmentOrSchool","explain":"VIVO-ISF Ontology V1.6 Property; The department or school name within institution; Not intended to be an institution name."},{"label":"Affiliation","value":"Biology, Department of (Okanagan)","attrs":{"lang":"en","ns":"http:\/\/vivoweb.org\/ontology\/core#departmentOrSchool","classmap":"vivo:EducationalProcess","property":"vivo:departmentOrSchool"},"iri":"http:\/\/vivoweb.org\/ontology\/core#departmentOrSchool","explain":"VIVO-ISF Ontology V1.6 Property; The department or school name within institution; Not intended to be an institution name."}],"AggregatedSourceRepository":[{"label":"Aggregated Source Repository","value":"DSpace","attrs":{"lang":"en","ns":"http:\/\/www.europeana.eu\/schemas\/edm\/dataProvider","classmap":"ore:Aggregation","property":"edm:dataProvider"},"iri":"http:\/\/www.europeana.eu\/schemas\/edm\/dataProvider","explain":"A Europeana Data Model Property; The name or identifier of the organization who contributes data indirectly to an aggregation service (e.g. Europeana)"}],"Citation":[{"label":"Citation","value":"Nutrients 9 (3): 259 (2017)","attrs":{"lang":"en","ns":"https:\/\/open.library.ubc.ca\/terms#identifierCitation","classmap":"oc:PublicationDescription","property":"oc:identifierCitation"},"iri":"https:\/\/open.library.ubc.ca\/terms#identifierCitation","explain":"UBC Open Collections Metadata Components; Local Field; Indicates a bibliographic reference for the resource if it has been previously published."}],"Creator":[{"label":"Creator","value":"Haskey, Natasha","attrs":{"lang":"en","ns":"http:\/\/purl.org\/dc\/terms\/creator","classmap":"dpla:SourceResource","property":"dcterms:creator"},"iri":"http:\/\/purl.org\/dc\/terms\/creator","explain":"A Dublin Core Terms Property; An entity primarily responsible for making the resource.; Examples of a Contributor include a person, an organization, or a service."},{"label":"Creator","value":"Gibson, Deanna L.","attrs":{"lang":"en","ns":"http:\/\/purl.org\/dc\/terms\/creator","classmap":"dpla:SourceResource","property":"dcterms:creator"},"iri":"http:\/\/purl.org\/dc\/terms\/creator","explain":"A Dublin Core Terms Property; An entity primarily responsible for making the resource.; Examples of a Contributor include a person, an organization, or a service."}],"DateAvailable":[{"label":"Date Available","value":"2019-06-03T15:01:48Z","attrs":{"lang":"en","ns":"http:\/\/purl.org\/dc\/terms\/issued","classmap":"edm:WebResource","property":"dcterms:issued"},"iri":"http:\/\/purl.org\/dc\/terms\/issued","explain":"A Dublin Core Terms Property; Date of formal issuance (e.g., publication) of the resource."}],"DateIssued":[{"label":"Date Issued","value":"2017-03-10","attrs":{"lang":"en","ns":"http:\/\/purl.org\/dc\/terms\/issued","classmap":"oc:SourceResource","property":"dcterms:issued"},"iri":"http:\/\/purl.org\/dc\/terms\/issued","explain":"A Dublin Core Terms Property; Date of formal issuance (e.g., publication) of the resource."}],"Description":[{"label":"Description","value":"Diet has been speculated to be a factor in the pathogenesis of inflammatory bowel disease and may be an important factor in managing disease symptoms. Patients manipulate their diet in attempt to control symptoms, often leading to the adoption of inappropriately restrictive diets, which places them at risk for nutritional complications. Health professionals struggle to provide evidence-based nutrition guidance to patients due to an overall lack of uniformity or clarity amongst research studies. Well-designed diet studies are urgently needed to create an enhanced understanding of the role diet plays in the management of inflammatory bowel disease. The aim of this review is to summarize the current data available on dietary management of inflammatory bowel disease and to demonstrate that dietary modulation may be an important consideration in managing disease. By addressing the relevance of diet in inflammatory bowel disease, health professionals are able to better support patients and collaborate with dietitians to improve nutrition therapy.","attrs":{"lang":"en","ns":"http:\/\/purl.org\/dc\/terms\/description","classmap":"dpla:SourceResource","property":"dcterms:description"},"iri":"http:\/\/purl.org\/dc\/terms\/description","explain":"A Dublin Core Terms Property; An account of the resource.; Description may include but is not limited to: an abstract, a table of contents, a graphical representation, or a free-text account of the resource."}],"DigitalResourceOriginalRecord":[{"label":"Digital Resource Original Record","value":"https:\/\/circle.library.ubc.ca\/rest\/handle\/2429\/70464?expand=metadata","attrs":{"lang":"en","ns":"http:\/\/www.europeana.eu\/schemas\/edm\/aggregatedCHO","classmap":"ore:Aggregation","property":"edm:aggregatedCHO"},"iri":"http:\/\/www.europeana.eu\/schemas\/edm\/aggregatedCHO","explain":"A Europeana Data Model Property; The identifier of the source object, e.g. the Mona Lisa itself. This could be a full linked open date URI or an internal identifier"}],"FullText":[{"label":"Full Text","value":"nutrientsReviewAn Examination of Diet for the Maintenance ofRemission in Inflammatory Bowel DiseaseNatasha Haskey and Deanna L. Gibson *Department of Biology, The Irving K. Barber School of Arts and Sciences, University of British Columbia, Room,ASC 368, 3187 University Way, Okanagan campus, Kelowna, BC V1V 1V7, Canada; natasha.haskey@gmail.com* Correspondence: deanna.gibson@ubc.ca; Tel.: +1-250-807-8790Received: 20 January 2017; Accepted: 8 March 2017; Published: 10 March 2017Abstract: Diet has been speculated to be a factor in the pathogenesis of inflammatory bowel diseaseand may be an important factor in managing disease symptoms. Patients manipulate their dietin attempt to control symptoms, often leading to the adoption of inappropriately restrictive diets,which places them at risk for nutritional complications. Health professionals struggle to provideevidence-based nutrition guidance to patients due to an overall lack of uniformity or clarity amongstresearch studies. Well-designed diet studies are urgently needed to create an enhanced understandingof the role diet plays in the management of inflammatory bowel disease. The aim of this review is tosummarize the current data available on dietary management of inflammatory bowel disease andto demonstrate that dietary modulation may be an important consideration in managing disease.By addressing the relevance of diet in inflammatory bowel disease, health professionals are able tobetter support patients and collaborate with dietitians to improve nutrition therapy.Keywords: diet; diet therapy; nutrition; nutrition therapy; inflammatory bowel disease; ulcerativecolitis; Crohn\u2019s disease1. IntroductionInflammatory Bowel Disease (IBD) is a chronic inflammatory condition that includes ulcerativecolitis (UC) and Crohn\u2019s disease (CD). CD is a transmural inflammatory disease of the gastrointestinalmucosa that can affect any component of the gastrointestinal tract including the small and\/or largeintestine, the mouth, esophagus, stomach and anus. UC is non-transmural and primarily involvesonly the colonic mucosa. Patients with IBD experience periods of relapse (active disease) and clinicalremission [1]. Clinical symptoms of IBD are diarrhea and\/or constipation, passage of blood or mucusin the stool and abdominal cramping. In addition, CD patients may also experience bowel obstruction,strictures and abscesses.Medications are the first-line of therapy in the management of IBD. Surgery is generally reservedfor those patients who are intolerant to medications or have refractory disease. The main classesof drugs used in the treatment of IBD include 5-aminosalicylates (5-ASA) (e.g., sulphasalazine, andmesalamine), corticosteroids (e.g., hydrocortisone, prednisone, and prednisolone), immunomodulators(e.g., azathioprine, 6-mercaptopurine, methotrexate and cyclosporine) and biologics (e.g., infliximab,adalimumab, and vedolizumab). Although many patients have a good response to pharmacotherapy,medications can have severe adverse side effects. Drug hypersensitivity, nephrotoxicity, fever, rash,lymphadenopathy, hepatitis, pancreatitis, diarrhea exacerbation, nausea, vomiting, abdominal pain,myalgia and an increased risk for lymphoma with the use of immunomodulators are some of thereported side effects. In addition, medication adherence is a concern, as a recent study reported thatapproximately one quarter of patients with IBD attending at a tertiary care practice did not use theprescribed IBD-specific medications [2]. It is clear the adoption of novel strategies and preventativeNutrients 2017, 9, 259; doi:10.3390\/nu9030259 www.mdpi.com\/journal\/nutrientsNutrients 2017, 9, 259 2 of 20medicine is crucial to the well-being of patients with IBD to avoid complications and side-effectsrelated to both the disease, as well as the treatments.Exclusive enteral nutrition is a nutritional therapy where 100% of a patient\u2019s nutritionalrequirements are met via a liquid nutrition formula and administered orally or through a feeding tube.Exclusive enteral nutrition is provided for 6\u20138 weeks and then an oral diet is gradually reintroduced [3].In children with active CD, exclusive enteral nutrition can be used in place of corticosteroid therapyand has been shown to improve time to relapse [4]. This approach has also been shown to positivelyimpact inflammatory changes, mucosal healing, enhance growth and overall nutritional status inchildren [4]. Outside of Japan, exclusive enteral nutrition is not routinely used as first-line therapy inadults. There is some evidence to support the use of exclusive enteral nutrition as a treatment modalityin a select group of adult patients with CD, specifically those with a new diagnosis of CD, those withileal involvement and those that are motivated to adhere to the exclusive enteral nutrition regimen [5].IBD is associated with nutritional complications during both relapse and clinical remission. Someof the nutritional complications include reduced dietary intake, nutrient malabsorption, macro- ormicronutrient deficiencies, weight loss and osteoporosis [6\u201310]. IBD patients are concerned about foodand diet [11,12] and use various dietary strategies in attempt to control or minimize gastrointestinaldistress [13], as well as improve overall health. Up to 71% of patients with IBD believe diet affectstheir disease symptoms, with 90% of CD patients and 71% of UC patients employing elimination dietswhile in remission [14,15]. Dietary modification can be of concern if patients drastically reduce orcompletely avoid nutritionally important foods\/food groups, as this may place them at increased riskfor developing nutritional deficiencies [16], as well as poorer quality of life. Up to 77.1% of patientswith IBD report avoidance of particular foods [14]. A case-control study found significantly lowermean daily intakes of carbohydrates, monounsaturated fat, fiber, calcium, and vitamins C, D, E, and Kcompared to controls, as a result of the exclusion of dairy products, vegetables and fruit [17].There is a plethora of information on the internet that assert that certain diets improve orexacerbate symptoms, yet few rigorous nutrition studies have examined specific dietary factor(s)as being detrimental or protective against UC or CD. Implementation of diet strategies and approachesinto clinical practice are slow and limited. Common barriers to implementation into practice includeissues relating to knowledge management, such as access to research evidence sources, time toreview evidence-based sources and a lack of skills to appraise and understand research evidence [18].In addition to knowledge management, financial barriers, inappropriate skill mix and problemsworking with and across professional disciplines contribute to the lag in knowledge translation [18].This review attempts to consolidate the existing evidence on diet\/pharmoconutrition and maintenanceof remission in IBD, including studies that evaluate the association between pre-illness intake ofnutrients and food groups and the risk of a subsequent diagnosis of IBD, diet intervention studiesin maintaining remission in IBD, as well as existing guidelines [19\u201321], in light of the most currentlimitations in evidence and practice. Evidence-based dietary recommendations for IBD patients aresummarized in Tables 1 and 2 and Figure 1.Table 1. Evidence-based diet recommendations for the maintenance of remission in IBD.Statement RecommendationEncourage high dietary fiber intake from foods,especially from fruits and vegetables [22\u201325] Strongly Recommend *Avoid n-6 PUFA (safflower oils, corn oils, margarine) andtrans-unsaturated fatty acid consumption [23,24,26,27] Strongly RecommendEncourage consumption of dairy products [28,29] Recommend \u2020 (if tolerated)Limit\/avoid refined carbohydrates, especially sweetenedbeverages and soft drinks [30] RecommendNutrients 2017, 9, 259 3 of 20Table 1. Cont.Statement RecommendationLimit red meat consumption, especially from beef, pork,lamb and processed meats [22,31] RecommendFODMAP Diet [32\u201334] Optional \u2021 (for the management of IBS-overlay)Mediterranean Diet Pattern [35\u201337] OptionalSpecific Carbohydrate Diet [38\u201341]No Recommendation \u03b2Low Residue Diet [42]Semi-vegetarian Diet [43]IgG4-guided Elimination Diet [44]IBD-AID [45]Paleo Diet No RecommendationEvidence graded according to the American Academy of Pediatrics, Steering Committee on Quality Improvementand Management\u2014\u201cClassifying recommendations for clinical practice guidelines\u201d [46]. * Strongly Recommend:The quality of the supporting evidence is excellent, based on well-designed randomized control trials (RCTs) and\/orconsistent evidence from observational studies. Benefit clearly outweighs harm. \u2020 Recommend: The quality ofthe supporting evidence is good, but RCTs and\/or evidence from case-control\/cohort studies has limitations.Anticipated benefits outweigh harm. \u2021 Optional: The quality of evidence is suspect, further well-performedstudies needed. May be of limited advantage, however there is still unclear balance between benefit and harm.\u03b2 No recommendation: There is a lack of or poor evidence. Unclear balance between benefit and harm.Table 2. Evidence-based nutrition recommendations for supplements in the maintenance of remissionin IBD.Statement Type of IBD RecommendationVitamin D (minimum 1200 IU\/day) [47\u201351] BothStrongly Recommend *(aim for levels of serum 25 (OHD)>75 nmol\/LPsyllium (minimum 4 grams\/day) [52,53] UC Recommend \u2020Curcumin (1-gram bid) [54\u201356] UC Optional \u2021Oat bran supplementation (20 grams\/day) [57] UC OptionalGerminated Barley Foodstuff(minimum 20 grams\/day) [58\u201360] UC OptionalWheat bran (1\/2 cup daily) [61] CD OptionalEvidence graded according to the American Academy of Pediatrics, Steering Committee on Quality Improvementand Management\u2014\u201cClassifying recommendations for clinical practice guidelines\u201d [46]. * Strongly Recommend:The quality of the supporting evidence is excellent, based on well-designed randomized control trials (RCTs) and\/orconsistent evidence from observational studies. Benefit clearly outweighs harm. \u2020 Recommend: The quality ofthe supporting evidence is good, but RCTs and\/or evidence from case-control\/cohort studies has limitations.Anticipated benefits outweigh harm. \u2021 Optional: The quality of evidence is suspect, further well-performedstudies needed. May be of limited advantage, however there is still unclear balance between benefit and harm.\u03b2 No recommendation: There is a lack of or poor evidence. Unclear balance between benefit and harm.Nutrients 2017, 9, 259 4 of 20Nutrients\u00a02017,\u00a09,\u00a0259\u00a0 4\u00a0of\u00a020\u00a0 \u00a0Figure\u00a01.\u00a0Summary\u00a0of\u00a0practical\u00a0dietary\u00a0recommendations\u00a0for\u00a0maintenance\u00a0of\u00a0remission\u00a0in\u00a0IBD.\u00a02.\u00a0Literature\u00a0Search\u00a0A\u00a0systematic\u00a0literature\u00a0search\u00a0was\u00a0conducted\u00a0using\u00a0PubMed,\u00a0EMBASE\u00a0and\u00a0Medline\u00a0from\u00a01966\u00a0to\u00a0October\u00a02016\u00a0using\u00a0 the\u00a0medical\u00a0 subject\u00a0heading\u00a0 (MeSH)\u00a0 terms\u00a0\u201cinflammatory\u00a0bowel\u00a0disease\u201d,\u00a0\u201cCrohn\u2019s\u00a0disease\u201d,\u00a0\u201culcerative\u00a0colitis\u201d,\u00a0\u201cnutrition\u201d,\u00a0\u201cnutrition\u00a0therapy\u201d,\u00a0\u201cdiet\u201d\u00a0and\u00a0\u201cdiet\u00a0therapy\u201d.\u00a0Searches\u00a0containing\u00a0relevant\u00a0synonyms\u00a0and\u00a0combinations\u00a0of\u00a0the\u00a0above\u00a0terms\u00a0were\u00a0also\u00a0utilized.\u00a0We\u00a0reviewed\u00a0intervention\u00a0studies,\u00a0systematic\u00a0reviews,\u00a0as\u00a0well\u00a0as\u00a0relevant\u00a0review\u00a0articles\u00a0that\u00a0contained\u00a0practice\u00a0guidelines\u00a0with\u00a0a\u00a0focus\u00a0on\u00a0adults.\u00a0Studies\u00a0covering\u00a0active\u00a0IBD,\u00a0enteral\/parenteral\u00a0nutrition\u00a0and\u00a0IBD\u00a0with\u00a0colectomy\/ostomy\u00a0were\u00a0excluded\u00a0from\u00a0the\u00a0review.\u00a03.\u00a0Diet\u00a0in\u00a0the\u00a0Etiology\u00a0of\u00a0IBD\u00a0IBD\u00a0has\u00a0traditionally\u00a0been\u00a0thought\u00a0of\u00a0as\u00a0a\u00a0disease\u00a0of\u00a0the\u00a0Western\u00a0hemisphere,\u00a0however\u00a0there\u00a0is\u00a0an\u00a0 increasing\u00a0 incidence\u00a0 in\u00a0 Japan,\u00a0Hong\u00a0Kong,\u00a0Korea\u00a0 and\u00a0Eastern\u00a0Europe\u00a0 [62,63].\u00a0Although\u00a0 still\u00a0rarer,\u00a0an\u00a0increasing\u00a0incidence\u00a0of\u00a0IBD\u00a0is\u00a0also\u00a0being\u00a0identified\u00a0in\u00a0South\u00a0Africa,\u00a0South\u00a0America\u00a0and\u00a0Saudi\u00a0Arabia\u00a0[64\u201366].\u00a0The\u00a0dramatic\u00a0rise\u00a0in\u00a0incidence\u00a0of\u00a0IBD,\u00a0particularly\u00a0in\u00a0South\u00a0Asia,\u00a0India\u00a0and\u00a0Japan,\u00a0where\u00a0 traditionally\u00a0 there\u00a0was\u00a0 a\u00a0 low\u00a0 incidence,\u00a0 suggests\u00a0 that\u00a0 environmental\u00a0 factors,\u00a0 such\u00a0 as\u00a0 the\u00a0Western\u00a0diet\u00a0pattern,\u00a0play\u00a0 an\u00a0 important\u00a0 role\u00a0 in\u00a0disease\u00a0pathogenesis\u00a0 [67\u201369].\u00a0This\u00a0hypothesis\u00a0 is\u00a0further\u00a0 confirmed\u00a0 by\u00a0 the\u00a0 increasing\u00a0 incidence\u00a0 of\u00a0 the\u00a0 disease\u00a0 in\u00a0 immigrants\u00a0 to\u00a0 the\u00a0 Western\u00a0hemisphere.\u00a0Migration\u00a0 from\u00a0 a\u00a0 country\u00a0with\u00a0 a\u00a0history\u00a0 of\u00a0 low\u2010incidence\u00a0 to\u00a0 a\u00a0 country\u00a0 of\u00a0 a\u00a0 higher\u00a0incidence\u00a0increases\u00a0the\u00a0risk\u00a0of\u00a0developing\u00a0IBD,\u00a0particularly\u00a0in\u00a0the\u00a0first\u00a0generation\u00a0children\u00a0[70].\u00a0Diet\u00a0composition\u00a0has\u00a0long\u00a0been\u00a0suspected\u00a0to\u00a0contribute\u00a0to\u00a0IBD.\u00a0Thus,\u00a0dietary\u00a0patterns\u00a0and\u00a0nutrients\u00a0are\u00a0important\u00a0environmental\u00a0factors\u00a0to\u00a0consider\u00a0in\u00a0the\u00a0etiology\u00a0of\u00a0IBD\u00a0[22,71].\u00a0Figure 1. Sum ary of practical dietary reco e atio s for aintenance of remission in IBD.2. Literature SearchA systematic literature search was conducted using PubMed, EMBASE and Medline from 1966 toOctober 2016 using the medical subject heading (MeSH) terms \u201cinflammatory bowel disease\u201d, \u201cCrohn\u2019sdisease\u201d, \u201culcerative colitis\u201d, \u201cnutrition\u201d, \u201cnutrition therapy\u201d, \u201cdiet\u201d and \u201cdiet therapy\u201d. Searchescontaining relevant synonyms and combinations of the above terms were also utilized. We reviewedintervention studies, systematic reviews, as well as relevant review articles that contained practiceguidelines ith a focus on adults. Studies covering active IBD, enteral\/parenteral nutrition and IBDwith colectomy\/ostomy were excluded from the review.3. Diet in the Etiology of IBDIBD h traditionally been thought of as a disease of the Western hemisphere, however thereis an increasing incidence i Japan, Hong Ko , Korea and Eastern Europe [62,63]. Although stillrarer, n increasing incidence of IBD s also being identified in South Africa, South Americ andSaudi Arabia [64\u201366]. The dram tic rise in incidence of IBD, particularly in South A ia, India andJapan, where traditionally there was a low incidence, suggests that environmental factors, such asthe Western diet pattern, play an important role in disease pathogenesis [67\u201369]. This hypothesis isfurther confirmed by the increasing incidence of the disease in immigrants to the Western hemisphere.Migration from a country with a history of low-incidence to a country of a higher incidence increasesthe risk of developing IBD, particularly in the first generation children [70]. Diet composition has longbeen suspected to contribute to IBD. Thus, dietary patterns and nutrients are important environmentalfactors to consider in the etiology of IBD [22,71].Nutrients 2017, 9, 259 5 of 203.1. The Western Diet PatternThe diet of today is considerably different from the traditional diet of previous generations,when the prevalence of IBD was considerably lower. The Western diet pattern is dominated byincreased consumption of refined sugar, omega-6 polyunsaturated fats and fast food, combined witha diet deficient in fruit, vegetables, and fiber [72]. Much of today\u2019s food supply has been processed,modified, stored and transported great distances, in contrast to the traditional diet, where food thatwas produced locally was consumed shortly after harvest. This shift to the Western diet pattern ishypothesized to increase pro-inflammatory cytokines, modulate intestinal permeability, and alter theintestinal microbiota promoting a low-grade chronic inflammation in the gut [73]. A diet that containspro-inflammatory foods is an important risk factor in the development of UC. A case-control studycompleted in Iran with newly diagnosed UC patients (n = 62 UC patients, 124 controls) found thatsubjects that had a higher dietary inflammatory index (pro-inflammatory diet) had an increased riskof developing UC (Odds Ratio (OR): 1.55, 95% Confidence Interval (CI): 1.04\u20132.32) [23]. The authorsconcluded that encouraging intake of more anti-inflammatory dietary factors, such as plant-basedfoods rich in fiber and phytochemicals, and reducing intake of pro-inflammatory factors, such asfried or processed foods rich in trans-fatty acids, could be a potential strategy for reducing risk ofUC. This was one of the first studies that has examined dietary inflammatory index as an outcome fordeveloping UC. Several large scale studies have attempted to elucidate the dietary components thatare associated with IBD risk [22,24,26,27]. Overall, this suggests that the Western diet pattern is a riskfactor for IBD.3.2. Carbohydrate Intake as a Risk Factor for IBDA systematic review (n = 19 studies with 2609 IBD subjects) reported a negative associationbetween dietary fiber (OR 0.12, 95% CI: 0.04\u20130.37) and fruit intake (OR: 0.2, 95% CI: 0.1\u20130.9) and CDrisk [22]. Soluble fiber from fruit may have a protective effect on CD [24]. High vegetable intakemay be associated with decreased risk of UC (OR range 0.32\u20130.75) [22]. The European Investigationinto Cancer and Nutrition study (n = 366,351 with 256 incident cases of UC and 117 of CD, and fourmatched controls per case) reported that an increased consumption of sugar and soft drinks with lowvegetable intake was positively associated with UC risk (OR 1.31, 95% CI: 0.85\u20132.02; p = 0.05) [25].Increased consumption of sweets is positively associated with CD (OR: 2.83, 95% CI: 1.38\u20135.83) and UC(OR: 2.86, 95% CI: 1.24\u20136.57) [30]. Overall, this suggests that while refined and processed carbohydratesand intake of sweetened beverages are risk factors for IBD, complex carbohydrates including fruit,vegetables and fiber should be included in the diet to manage IBD.3.3. Protein Intake as a Risk Factor for IBDA large prospective cohort study (n = 67,581) completed over a 10.5-year period found that highprotein intake, specifically animal protein (meat, not dairy products) was positively associated withan increased risk of IBD [31]. A systematic review (n = 2609 IBD patients; 19 studies) reported anassociation with high total protein intake with the development of UC (OR range 0.2\u20133.7) and CD(OR range 0.45\u20133.34) [22]. High protein intake was associated with a 3.3-fold increased risk of IBD,suggesting a diet high in animal protein is a major risk factor for the development of IBD.3.4. Dairy Intake as Risk Factor for IBDThe European Investigation into Cancer and Nutrition study found that individuals thatconsumed milk had significantly reduced odds of developing CD (OR: 0.30, 95% CI: 0.13\u20130.65),suggesting a protective effect with dairy product consumption [28]. Individual dairy productsconsisted of milk, yogurt, and cheese with varying fat content (e.g., full fat, skimmed, semi-skimmed,and unspecified). This is supported by a case-control study in children (n = 130 CD patients andn = 202 controls) that demonstrated that consumption of dairy products was not associated with CDNutrients 2017, 9, 259 6 of 20(OR: 0.86, 95% CI: 0.42\u20131.76, p = 0.65) [29]. Overall, the consumption of dairy products is not a riskfactor for IBD.3.5. Dietary Fat Intake as a Risk Factor for IBDThere have been conflicting data on the association between dietary fat intake and thedevelopment of IBD, as many of the studies are retrospective and use small sample sizes. However,a very large, long-term, prospective study (n = 170,805) completed over 26 years did not observea significant association with increased risk of developing CD or UC with total dietary fat intake,saturated fatty acids (SFA) and monounsaturated fatty acids (MUFA) [26], which has been wellsupported by other research studies [74\u201376]. A growing body of scientific evidence indicates that theMediterranean diet pattern has been associated with significant improvements in health status [77,78]and decreases in inflammatory markers in humans [79]. The protective effect is hypothesized to bederived from the balance in fats, which includes incorporating MUFA, SFA and fish intake [80]. While afew studies do show that MUFAs are beneficial during colitis, studies on the effects of SFA and PUFAson gut health are controversial.Dietary n-6 PUFA, in particular linoleic acid, have been implicated in the etiology of IBD. Dietaryn-6 PUFAs are essential fatty acids present in high amounts in red meat, cooking oils (safflower andcorn oil) and margarines. A prospective cohort study (n = 203,193) conducted over four years foundthat intake of linoleic acid was associated with an increased risk of UC (OR: 2.49, 95% CI: 1.23 to5.07, p = 0.01) [27]. Further analysis of the European Investigation into Cancer and Nutrition study(n = 260,686) over five years found an increased risk of UC with a higher total PUFA intake (trendacross quartiles OR = 1.19 (95% CI: 0.99\u20131.43) p = 0.07) [74], which was also supported by a systematicreview (n = 2609 patients with IBD) that examined pre-illness intake of nutrients and subsequentdevelopment of UC [22]. A case-control study in CD found that increased total PUFA consumptionwas positively associated with CD risk (OR: 2.31, 95% CI: 1.12\u20134.79) [30].The Nurses\u2019 Health Study cohorts (n = 170,805 women with 269 incident cases of CD and 338incident cases of UC) reported high, long-term intake of trans-unsaturated fatty acids was associatedwith a trend towards an increased incidence of UC (HR 1.34, 95% CI: 0.94\u20131.92) but not CD [26].An increased relative risk of developing IBD has also been associated with frequent intake of fastfoods (fast foods are high in trans-unsaturated fatty acids) [81,82]. The relative risk associated with theconsumption of fast foods at least two times a week was estimated at 3.4 (95% CI: 1.3\u20139.3) for CD and3.9 (95% CI: 1.4\u201310.6) for UC [82]. Frequent fast food intake, defined as more than once a week, wassignificantly associated with a risk of UC (43%, OR: 5.78, 95% CI: 2.38\u201314.03) and CD (27%, OR: 2.84,95% CI: 1.21\u20136.64) [81].It has been speculated that the intake of long-chain n-3 PUFAs (docosapentaenoic acid,eicosapentaenoic acid, docosahexaenoic acid), known as omega-3s, may be of benefit to patientswith IBD. The beneficial effects are believe to be derived from the anti-inflammatory properties of n-3PUFAs; however, clinical and experimental studies have shown conflicting results [83]. Meta-analyseshave failed to show benefit with supplementation with fish oils in the maintenance of remission inCD and UC [84\u201386]. Dietary intake of n-3 PUFAs were inversely associated with risk of UC, whereasno association has been found with CD [26]. The European Investigation into Cancer and Nutritionstudy (n = 203,193) found a negative association with the development of UC with increasing dietaryintake of the n-3 PUFA, specifically docosahexaenoic acid (OR: 0.23, 95% CI: 0.06 to 0.97) [27], andis supported by the European Investigation into Cancer and Nutrition -Norfolk study (n = 26,639)(OR: 0.43, 95% CI: 0.22\u20130.86) [57]. Two case-control studies in CD report that a diet with regularconsumption of fish had a protective effect on the development of CD (OR 0.52, 95% CI: 0.33\u20130.80,p = 0.003) and (OR 0.46, 95% CI: 0.20\u20131.06, p = 0.02) [29,69].The total ratio of n-3 PUFA: n-6 PUFA found in the diet has been hypothesized to be an importantconsideration. One prospective cohort [87] and one case-control study [29] report that a high n-3PUFA:n-6 PUFA ratio in the diet is inversely associated with the risk of IBD. In support of this explanation,Nutrients 2017, 9, 259 7 of 20a dietary intervention trial that focused on increasing the n-3 PUFA: n-6 PUFA ratio was found tobe effective in maintaining disease remission in patients with both UC and CD, through increasingn-3 PUFA intake [88]. Overall, it does not appear that full fat diets should be avoided, however fatincluding diets rich in olive oil, dairy products and fish but not fish oil pills should be consumed whileavoiding large intakes of vegetable oils rich in n-6 PUFA.In summary, several epidemiological studies provide compelling evidence for the role of food inIBD pathogenesis. Furthermore, the rise in incidence of IBD in countries that previously have had avery low incidence suggests that industrialization and adoption of the westernized diet may be a riskfactor in the development of IBD. Reduced consumption of fruits and possibly vegetables, resulting ina reduced overall intake of fiber, with high intake of meats, fast foods and trans-fatty acids appears tobe associated with an overall increase in the risk of developing IBD [71].4. Diet Interventions and IBDDiet interventions have been studied in IBD in attempt to manage active disease or to maintainremission. A number have been shown to be efficacious, however, the precise components that areimportant for each diet are not clearly delineated or often contradict one another. With no goldstandard, nutrition guidance provided at this time by health professionals is based on the \u201cbestavailable evidence\u201d.4.1. Low Residue DietA low-residue diet is often recommended for the management of an acute flare of IBD, especiallyin patients that have intestinal strictures or narrowing. Although the low-residue diet is prescribed forshort-term use, in clinical practice, patients often follow the diet long-term. The primary purpose ofa low residue diet is to reduce the frequency and volume of stools and reduce the risk for intestinalobstruction [89]. In the literature, there have been discrepancies as to the actual composition oflow-fiber and\/or low-residue diets. A low-residue diet requires the elimination of whole grains,legumes and all fruits and vegetables (except for bananas and skinless potatoes), dairy and fibrousmeats [89]. This is not the same as a low-fiber diet which excludes only insoluble fiber. A prospectivestudy in subjects with active CD (n = 70) that compared a low-residue diet to an unrestricted dietfound no differences in outcome including symptoms, need for hospitalization, need for surgery, newcomplications, nutritional status, or postoperative recurrence [42]. Due to lack of evidence, thereappears to be no reason to restrict residue from the diet, however anecdotally CD patients withobstructive symptoms and strictures report improvement in symptoms when following a diet reducedin fiber (total daily fiber intake < 10 g) [89,90].Research is still in its infancy, however there is growing evidence for an association between IBDand an alteration in the gut microbiota. The Westernized diet, characterized by increased consumptionof PUFA, animal protein, and sugar as well as decreased consumption of fiber has been implicated asfactor contributing to dysbiosis [91\u201393]. A small pilot study in CD (n = 6), reported a marked decreasein microbial diversity with a low-residue diet [94]. This is concerning considering that low diversity ofthe microbiota has been linked to a variety of chronic diseases [95]. Furthermore, improvements ininflammatory markers have not been demonstrated with a low-residue diet in CD [96]. More research isrequired; however, a low-residue diet could potentially have negative consequences on IBD, thereforeprolonged avoidance of fiber is discouraged [90].4.2. Semi-Vegetarian DietA prospective trial conducted in Japan in hospitalized subjects with CD (n = 22) examined theeffect of a semi-vegetarian diet on maintaining remission [43]. The diet was lacto-ovo vegetarian, inwhich eggs and milk were allowed with small portions of meat offered once every two weeks andfish weekly. Remission rate achieved with the semi-vegetarian diet was 100% after one year and92% after two years. A semi-vegetarian diet showed significant prevention of relapse compared to thatNutrients 2017, 9, 259 8 of 20of individuals following an omnivorous diet (p = 0.003 log rank test). Based on these observations,the semi-vegetarian diet may be a highly effective way to maintain remission CD. While this study ispromising, large, randomized control studies are required to validate the efficacy of this type of dietfor IBD patients.4.3. FODMAPs DietThe low Fermentable Oligosaccharide, Disaccharide, Monosaccharide, and Polyol diet(FODMAPs) consists of eliminating foods high in fermentable but poorly absorbed carbohydratesand polyols for six to eight weeks [97]. FODMAPs comprise fructose, lactose, fructo- and galacto-oligosaccharides (fructans and galactans), and polyols (sorbitol, mannitol, xylitol and maltitol) [97].Common food sources of foods containing FODMAPS are as follows: (1) fructans: onion,garlic and wheat; (2) fructose: fruits and fruit products, honey, and foods with added high-fructosesweeteners; (3) lactose: mainly dairy products; (4) oligosaccharides: legumes, nuts, seeds, some grains;and (5) polyols: fruits and vegetables, and sugar-free products. After symptom resolution, patientsare guided by a dietitian on how to gradually reintroduce foods high in fermentable carbohydrates todetermine individual tolerance to specific FODMAPs.Fair evidence supports the effectiveness of a low-FODMAP diet for the symptom management ofirritable bowel syndrome (IBS), especially a reduction in abdominal bloating, pain, and diarrhea [98,99].IBS-like symptoms are common in IBD and have been reported in 57% of patients with CD, and 33%of patients with UC [100], therefore a low-FODMAP diet has been proposed for the managementof patients with IBD with IBS-overlay. There have been three retrospective studies evaluating thelow-FODMAP diet in IBD [32\u201334]. A retrospective study of 72 IBD patients who received dietaryintervention focusing on low-FODMAP diet, reported one in two patients reported a significantimprovement in abdominal symptoms, abdominal pain, bloating, wind and diarrhea (p < 0.02 forall symptoms) [32]. Second, a case-note review of electronic medical records of 88 IBD patientswith functional gut symptoms who received low-FODMAP diet advice found a significant reductionin symptoms of any severity (mild, moderate, or severe) for abdominal pain (p < 0.001), bloating(p < 0.001), flatulence (p = 0.041), belching (p = 0.001), incomplete evacuation (p = 0.012), nausea(p = 0.011), and heartburn (p =0.035) [33]. Improvements in stool consistency and frequency wereobserved, including an increase in \u201cnormal\u201d stool form (p = 0.002) and \u201cnormal\u201d stool frequency(p < 0.001) [33]. A retrospective, cross-sectional study (n = 49) was conducted to investigate long-termadherence and effect on disease course in IBD patients treated with the low-FODMAP diet [34].Forty-three percent of the IBD patients reported full efficacy (p = 0.08) with greatest improvementsseen in abdominal pain (63%) and bloating (83%) while on the low-FODMAP diet. The proportion ofpatients having normal stools increased by 66% in the IBD group (p < 0.001). Twenty-four percent ofIBD patients became asymptomatic while following the diet. In summary, while there have been noprospective intervention trials completed in IBD, retrospective data suggests that a low FODMAP dietmay be a strategy to manage concurrent functional gut symptoms in this population.4.4. Exclusion DietsEnteral feeding is often used as an adjunctive therapy for maintenance of remission in CD,particularly in Japan. In a randomized control trial, subjects were provided half of the nutritionrequirements by an elemental formula (taken orally (n = 21) or by nasogastric tube (n = 5)), with theremaining 50% of the nutrition requirements met by consuming an unrestricted diet [101]. The relapserates in the half elemental diet group were significantly lower (34.6% vs. 64.0%; multivariate hazardratio 0.40 (95% CI: 0.16\u20130.98)) than the control group after a mean follow-up of 11.9 months. A follow-upreport on this study stated that the elemental diet as a maintenance therapy for CD contributed tokeeping subjects in a clinically stable state, without affecting their quality of life, nor leading toadditional medical expenses [102].Nutrients 2017, 9, 259 9 of 20Exclusion diets can be unpalatable and difficult to follow, therefore in a double blind, randomizedcontrol trial, the efficacy of a IgG4-guided exclusion diet in subjects with CD was evaluated [44].The objective of the study was to identify which components of the diet are most important to avoiddue to the induction of IgG4, an antibody produced in response to chronic exposure to an antigenicstimulus like a food antigen. It is hypothesized that dietary protein antigens might perpetuateinflammation in CD as a result of previous sensitization. IgG4 titers were tested against 16 commonfood types. Subjects in the treatment group removed the four food types with the highest antibodytiter for four weeks, whereas controls removed the four food types with the lowest antibody titer.The researchers found significant improvements in quality of life, measured by the short inflammatorybowel disease questionnaire (3.05 (0.01\u20136.11) p < 0.05) and disease activity scores, measured by CrohnsDisease Activity Index (41 (10.4\u201371.5) p = 0.009). Forty-one percent of subjects receiving the treatmentexperienced an improvement in Crohns Disease Activity Index score of >100, whereas 16% of controlsexperienced an improvement. The exclusion of milk, pork, beef and egg was most strongly associatedwith improvement. This study was underpowered, however, it did demonstrate clinical improvementand this novel approach to dietary management of IBD does warrant further investigation.4.5. Novel Anti-Inflammatory Diet TherapiesWhile the exact etiology of IBD remains unclear, increasing evidence suggests that thegastrointestinal microbiome plays a critical role in disease pathogenesis [103,104]. Manipulation of thegastrointestinal microbiome through diet interventions, in attempt to reduce systemic inflammation, isincreasingly recommended as adjuncts to ongoing medical therapy. The Anti-Inflammatory Diet(IBD-AID) is a nutritional approach designed to address nutrient adequacy, malabsorption andsymptoms [45]. IBD-AID restricts the intake of particular carbohydrates (lactose, refined and processedcomplex carbohydrates), includes the ingestion of pre- and probiotic foods, and modifies dietaryfatty acid intake specifically decreasing the total fat, saturated fats, the elimination of hydrogenatedoils, and encouraging the increased intake of foods rich in n-3 PUFA. A retrospective case seriesusing IBD-AID found that subjects who attempted the diet (n = 40), 60% reported reduced symptoms,including reduced stool frequency (patient self-report). A small subset of the subjects (n = 7) was ableto discontinue at least one of their IBD medications. An intervention trial with a rigorous study designthat examines both biomarkers of inflammation, as well as histological changes is needed to furtherassess efficacy.4.6. Fiber SupplementsThe benefits of fiber in IBD are more commonly seen for the use of supplements rather than dietinterventions and for the management of UC and CD [105]. Although the evidence is still not clear,interventions with fiber have the potential to relieve symptoms and\/or to maintain disease remissionin IBD patients. The type of fiber may be an important consideration.4.6.1. Oat BranA controlled intervention study adding 60 grams\/day of oat bran (equivalent to 20 grams oatfiber\/day) to the diet of subjects (n = 22) with quiescent UC reported no signs or symptoms of colitisrelapse after 12 weeks [57]. A subgroup of subjects noted a decrease in abdominal pain, reflux anddiarrhea (p < 0.05). The greatest impact of the oat bran intervention was seen on the fecal short chainfatty acid (SCFA) concentrations found in the stool. Fifteen subjects demonstrated a 36% increase in fecalbutyrate concentrations within four weeks (p < 0.01) of intervention which was maintained throughoutthe 12-week intervention. This finding is important as increasing evidence suggests SCFAs play anessential role in maintaining the health of colonic mucosa as butyrate is the main energy substratefor colonocytes [106]. Butyrate also plays an important role in the prevention and treatment of distalUC [107]. Supplementation with oat bran in this population warrants further investigation with a largersample size, over a longer-term to determine the overall benefit as a maintenance therapy for UC.Nutrients 2017, 9, 259 10 of 204.6.2. Wheat BranA randomized control trial completed in CD (n = 7) where subjects were instructed to consume ahigh fiber diet, including consumption of whole wheat bran cereal (1\/2 cup daily) and restrict refinedcarbohydrates, reported improved health-related quality of life as measured by the InflammatoryBowel Disease Questionnaire (p = 0.028) [61]. Significant improvements were seen in the clinical diseaseactivity scores, as measured by partial Harvey-Bradshaw index (p = 0.008). This was a feasibility studywith a very small sample size (n = 4 receiving intervention) that did not include subjects receivingbiologic therapies. A much larger sample size, over a longer term, including subjects receiving avariety of medications, is needed to verify the results of this study.4.6.3. PsylliumA randomized control trial in subjects with UC in remission (n = 105) comparing psyllium fiber(10 g bid) versus mesalamine (500 mg tid) versus psyllium fiber plus mesalamine (10 g bid + 500 mgtid) reported continued remission at 12 months and slightly lower relapse rates in the mesalamine pluspsyllium fiber group [52]. Probability of continued remission was similar between all three groups(Mantel-Cox test, p = 0.67; intent-to-treat analysis). Hallert et al. (1991) conducted a randomizedcontrol trial with UC in remission over four months (n = 29) found psyllium (7 g\/day testa ispaghula)to be superior to placebo in relieving gastrointestinal symptoms (p < 0.001), especially for diarrhea andconstipation [53]. Although the dosage of psyllium needs to be elucidated, weak evidence suggeststhat psyllium fiber may be efficacious in maintaining remission in UC.4.6.4. Germinated Barley FoodstuffGerminated barley foodstuff is an insoluble dietary fiber made by milling and sieving brewer\u2019sspent grain [108]. Germinated barley foodstuff has prebiotic properties, containing glutamine-richprotein and hemicellulose-rich fiber which has been shown to reduce clinical activity and prolongremission in UC [58\u201360]. An open-label trial with 41 patients (21 controls, 20 germinated barleyfoodstuff intervention) with UC in remission received 30 grams (three times daily) of germinatedbarley foodstuff in addition to conventional medication for two months [59]. A statistically significantreduction in mean CRP was seen in the germinated barley foodstuff intervention group (p = 0.017),as well as a significant reduction in abdominal pain and cramping (p = 0.017). A similar designedstudy found that 20 grams of germinated barley foodstuff (n = 41) reduced levels of TNF-\u03b1, IL-6 andIL-8, with significant reductions in IL-6 (p = 0.034) and IL-8 (p = 0.013) [60]. Length of remission hasalso been prolonged with long-term administration (12 months) of 20 grams of germinated barleyfoodstuff [58]. Germinated barley foodstuff appears to be a safe and effective maintenance therapy toprolong remission in patients with UC.4.7. Role of Fat in the DietSystematic reviews of the efficacy of n-3 PUFA supplementation in maintaining remission in IBDhave shown no clear evidence of their efficacy [84,85,109]. However, it may be the type of fatty acidsconsumed in the diet that are important in maintaining remission. Uchiyama et al. implemented adiet therapy in IBD subjects (n = 230) that involved the use of an \u201cn-3 PUFA food exchange table\u201d(n-3 PUFA diet plan)) to achieve a dietary n-3\/n-6 ratio of [almost equal to]1 [88]. In this regimen,to achieve an n-3\/n-6 ratio of ~1, the n-6 PUFA intake was restricted to 50% of the mean intake, andthe n-3 PUFA intake was increased. The subjects were prohibited from consuming the main sourcesof dietary n-6 PUFA, i.e., vegetable oil; seasonings such as margarine, dressings, and mayonnaise;food cooked in vegetable oil; and snacks. In a subset of subjects, the mean n-3\/n-6 ratio significantlyincreased after intervention. The mean n-3\/n-6 ratios in the remission were significantly higher thanrelapse groups (0.65 \u00b1 0.28 and 0.53 \u00b1 0.18, p < 0.001) and increase in the n-3\/n-6 ratio was seen in theNutrients 2017, 9, 259 11 of 20erythrocyte membrane of IBD subjects. This study concluded that n-3\/n-6 ratio may influence diseaseactivity in IBD subjects.The Mediterranean diet pattern may have a protective effect on IBD, as the incidence of IBD in thesouth of Europe is lower than in northern Europe [110]. The Mediterranean diet pattern is a diet that ishigh in fiber-rich plant-based foods (e.g., cereals, fruits, vegetables, legumes, nuts, seeds and olives),with olive oil as the principle source of added fat, along with high to moderate intakes of fish andseafood, moderate consumption of eggs, poultry, dairy products (cheese and yogurt), wine and lowconsumption of red meat [111]. A growing body of scientific evidence indicates that the Mediterraneandiet pattern has been associated with significant improvements in health status and [77,78] decreasesin inflammatory markers [79]. The protective effect is hypothesized to be derived from the balance inthe omega-6\/omega-3 ratio of the Mediterranean diet pattern (35% total fat: 15% MUFA (mainly fromolive oil), 13% SFA, and 6% PUFA [80]. The mechanisms of how MUFA might be beneficial in colitis areunknown, although adherence to the Mediterranean diet pattern has been shown to beneficially affectthe gut microbiome and gut metabolites (metabolome) [35]. A recent case-control study (n = 264 IBDsubjects and 203 controls) found that low adherence to the Mediterranean diet pattern was a significantrisk factor in the development of pediatric UC (OR: 2.3; 1.2\u20134.5) [36]. An intervention study examiningthe impact of the Mediterranean diet pattern in CD (n = 8) demonstrated a trend for reduction ininflammatory biomarkers (p = 0.39) and a tendency for \u201cnormalization\u201d of the gut microbiota [37].The challenge of this study was the lack of statistically significant results and the small sample size.Although a clearer understanding of the role of the Mediterranean Diet Pattern and its impact on IBDis needed, the Mediterranean Diet Pattern may offer a promising approach to reducing markers ofinflammation and normalizing the microbiota, but this will need to be confirmed in future clinical trials.4.8. Popular Diet Plans with PatientsThe Specific Carbohydrate Diet\u2122 is one of the most popular diets in the lay literature used bypatients with IBD. Unfortunately, there is a lack of evidence-based published data on this diet. To date,the evidence for this diet is based on retrospective surveys and case reports. Based on the book\u201cBreaking the Viscous Cycle\u201d, the diet is a strict grain free, sugar-free and complex carbohydrate freediet regimen [112]. An Internet survey (n = 451) that examined the IBD patient\u2019s perceptions of theSpecific Carbohydrate Diet\u2122, reported that symptoms decreased (abdominal pain, diarrhea, and bloodin stool) [38]. Forty-two percent of patients believed the diet helped them achieve remission. A smallerinternet survey (n = 51) of patients that had used the Specific Carbohydrate Diet\u2122 for managementof IBD reported 84% improved on the diet with 75% reporting improved symptoms [113]. Fifty-fourpercent reported that they maintained remission through use of the Specific Carbohydrate Diet\u2122. In acase-series report (n = 50), thirty-three subjects (66%) noted complete symptom resolution at a meanof 9.9 months (range 1 to 60 months) after starting the Specific Carbohydrate Diet\u2122 [41]. Patients\u2019self-report of the effectiveness of the Specific Carbohydrate Diet\u2122 was rated as a mean of 91.3%effective in controlling acute flare symptoms (range = 30% to 100%) and a mean of 92.1% effectiveat maintaining remission (range = 53% to 100%). There are two retrospective studies conducted inpediatric subjects that have examined the outcomes of the Specific Carbohydrate Diet\u2122 on clinicaloutcomes and laboratory parameters in IBD [39,40]. Twenty six patients with IBD (n = 20 withCD, 6 with UC) plus 10 controls were analyzed [39]. A comparative analysis of the subjects on theSpecific Carbohydrate Diet\u2122 versus controls, revealed significant improvement in Pediatric Crohn\u2019sDisease Activity Index, CRP, and fecal calprotectin over time for both groups (p = 0.03, 0.03 and 0.03,respectively). Successful maintenance of remission with the Specific Carbohydrate Diet\u2122 allowedsome subjects to discontinue medications and maintain disease control on the Specific CarbohydrateDiet\u2122 alone. A small retrospective chart review (n = 11) where pediatric patients followed the SpecificCarbohydrate Diet\u2122 for one year found significant improvements in hematocrit, albumin and ESR(p = 0.006, 0.002, 0.002, respectively) [40]. Ten children had improvements in weight percentile andnine children had increases in height percentile while following a strict Specific Carbohydrate Diet\u2122.Nutrients 2017, 9, 259 12 of 20Rigorous prospective, RCTs in pediatrics and adults are needed to determine the merits of this diet formanagement of IBD.The Paleo Diet is another popular diet amongst patients with IBD. It recommends avoidanceof processed food, refined sugars, legumes, dairy, grains and cereals, and instead it advocates forgrass-fed meat, wild fish, fruit, vegetables, nuts and \u201chealthy\u201d saturated fat [114]. While it makessense that a diet that promotes avoidance of refined and extra sugars and processed energy dense foodwould have health effects, there are no clinical trials that have examined the efficacy of this diet forIBD. Randomized controlled studies are required to determine whether the Paleo diet has beneficialeffects over other diet advice.5. Pharmaconutrition5.1. Curcumin (Turmeric)Curcumin is the active ingredient found in turmeric, a common Indian spice. Turmeric iscommonly used in Ayurvedic medicine for managing a variety of inflammatory diseases. The yellowpigment (curcumin) present in turmeric has been shown to exhibit numerous anti-inflammatoryproperties [115]. Curcumin is mainly administered orally in the form of capsules filled with itspowder. A randomized controlled trial of 82 subjects with UC demonstrated that curcumin at a doseof 2 g\/day (1 g\/day following breakfast and 1 g\/day following supper), when added to standardtherapy, significantly reduced relapse rates [54]. Two subjects relapsed during 6 months of therapywith concurrent curcumin therapy (4.65%), whereas 8 of 39 subjects (20.51%) in the placebo grouprelapsed (p = 0.040). Clinical Activity Index and Endoscopic Activity Indices in the curcumin groupsignificantly improved at six months in subjects with UC in remission (Clinical Activity Index: p = 0.038and Endoscopic Activity Indices: p = 0.0001). A systematic review [55] and one Cochrane review [56]conclude that curcumin may be an effective and safe therapy for maintaining remission in UC for upto six months when provided with standard therapy (sulfasalazine and mesalamine). More extensive,well-controlled clinical trials are needed to confirm the benefits of curcumin, at present it appears to bea safe, low cost option for maintenance of remission in UC when added to standard medical therapy.5.2. ProbioticsThe use of probiotics in the maintenance of remission in IBD has been investigated in severalclinical trials, however results are inconsistent. The clinical studies have significant heterogeneity,including a variety of different genera, species, strains and doses of probiotics that have beenexamined, which makes it difficult to draw firm conclusions about efficacy. A meta-analysis ofthe probiotic strain Escherichia coli Nissle 1917 in maintenance of remission in UC found that E.coliNissle 1917 maintained remission as well as standard therapy with mesalazine (OR = 1.07, 95% CI:0.70\u20131.64) [116]. Similarly, another meta-analysis showed that probiotics could prevent relapse ofUC as effectively as mesalazine (n = 638; 316 probiotic group, 322 mesalazine group; RR = 1.0, 95%CI: 0.79\u20131.26) [117]. The strains shown to be effective were E. coli Nissle 1917, E. coli (serotypeO6:K5:H1), Lactobacillus GG and Probio-Tec AB-25 (L.s acidophilus La-5 and Bifidobacterium animalissubsp. lactis BB-1). Shen et al., (2013) also found that probiotics were comparable to 5-ASA inmaintaining therapy in UC (p = 0.69, RR = 0.96) [118]. In contrast, a Cochrane collaboration foundno difference between probiotics and mesalazine for maintenance of remission in UC (3 studies;555 patients: OR 1.33; 95% CI: 0.94\u20131.90) [119]. Supplementation with probiotics in the maintenance ofremission in CD is also unfavorable. Two meta-analyses found that the probiotic strains Lactobacillus GGand Lactobacillus johnsonii LA1 could not prevent relapse in CD (RR = 1.18, 95% CI: 0.81\u20131.70) [118,120]and concluded that probiotics had no significant benefit in CD with probiotic supplementation (p = 0.71,RR = 1.09) [120]. The probiotic strain Lactobacillus GG was shown to have significantly benefit in favorof relapse versus the placebo (RR 1.68, 95% CI: 1.07 to 2.64) [118]. Future studies examining probioticsin the maintenance of remission in IBD need to focus on the effects of different probiotic strains andNutrients 2017, 9, 259 13 of 20different dosages, together with the homogeneous patient populations to determine which patients aremost likely to benefit from probiotic treatment.5.3. Vitamin DVitamin D deficiency is common in IBD patients with a frequency ranging from 16% to 95% [121].One study reports that patients with UC had more than double the odds of vitamin D deficiencywhen compared with normal controls (OR = 2.28; 95% CI: 1.18\u20134.41; I = 41%; p = 0.01) [47]. There isalso evidence to suggest that vitamin D deficiency may influence the severity of inflammation inIBD [48\u201350]. A cross-sectional study revealed that subjects with active disease had more frequentlow vitamin D levels (80% vs. 50.4%, p = 0.005) when compared to subjects in remission [49].A large prospectively collected cohort of 230 subjects demonstrated an inverse association betweenserum 25(OH)D concentrations and mucosal inflammation, as assessed by the Mayo endoscopyscore (p = 0.01), disease activity as indicated by the total Mayo score (p = 0.001), and histologicactivity (p = 0.02) in subjects with UC [48]. Serum 25(OH)D concentrations have been found to beinversely correlated with fecal calprotectin (r = \u22120.207, p = 0.030), particularly among CD subjects inclinical remission (r = \u22120.242, p = 0.022) [50]. Furthermore, a large cohort of over 3200 IBD patientsdemonstrated that low plasma 25(OH)D level (<50 nmol\/L) was independently associated with anincreased risk of subsequent surgery (OR: 1.76; 95% CI: 1.24\u20132.51) and hospitalization (OR: 2.07; 95% CI:1.59\u20132.68) in CD with similar results found in UC [51]. A study that followed IBD patients for fiveyears (n = 965) found that patients with low mean vitamin D levels (<50 nmol\/L) had worse pain,disease activity scores, health care utilization and quality of life (p < 0.05) compared with subjects withnormal mean vitamin D levels (>75 nmol\/mL) [122]. A large-multi-institutional cohort of IBD patientsfound that patients with vitamin D deficiency (<50 nmol\/L) had an increased risk of cancer (OR: 1.82;95% CI: 1.25\u20132.65) compared to those patients that had sufficient levels [123].Given that vitamin D status appears to be an independent risk factor for potential poorer outcomesin IBD, supplementation of vitamin D in this population is judicious. Patients with CD who weredeficient in vitamin D (<75 nmol\/L) and normalized their 25(OH)D had a reduced likelihood ofsurgery (OR: 0.56; 95% CI: 0.32\u20130.98) compared with those who remained deficient [51]. A prospectivestudy in UC (n = 70) demonstrated that low vitamin D levels (<88 nmol\/L) increased the risk ofclinical relapse over 12 months, as well as was associated with increased presence of endoscopicinflammation (OR: 1.29; 95% CI: 1.07\u20131.85; p < 0.01) or histologic inflammation (OR: 1.46; 95% CI:1.13\u20131.88; p = 0.005) [124]. The optimal concentration for patients with IBD remains unknown, buttargeting serum 25(OH)D concentrations above 75 nmol\/L appears safe and may have benefits for IBDdisease activity, improving bone health, preventing colo-rectal cancer, and alleviating depression [125].Daily doses of 1800\u201310,000 IU of vitamin D3 (cholecalciferol) are probably necessary, depending onthe baseline vitamin D serum concentration, ileal involvement in CD and body mass index [125]. In aclinical trial by Jorgensen et al. (2010) (n = 108), in CD, oral vitamin D3 treatment with 1200 IU dailyincreased serum 25(OH)D from mean 69 nmol\/L to mean 96 nmol\/L after three months of treatment(p < 0.001) [126].6. Challenges in Creating Evidence-Based GuidelinesAlthough there are diet intervention trials that show promise in maintaining remission, theirefficacy remains in question. The short duration of the interventions (less than 12 weeks), the lackof a proper control group in some instances, and the small sample sizes (less than 20 individuals)make it very challenging for clinicians to draw firm conclusions from existing data. There is an overalllack of objective clinical and endoscopic disease markers. For example, many studies are completedretrospectively and they rely on patient questionnaires regarding disease symptoms, such as pain andstool frequency. Well-designed clinical trials in IBD are urgently required to define the precise role ofeach of these diets in the prevention or management of IBD. Up until now, the role of diet in IBD ishighly undermined by lay and anecdotal reports without sufficient scientific proof.Nutrients 2017, 9, 259 14 of 20High quality diet intervention studies for the treatment of IBD need to include the following:(1) quantification of baseline intake of the habitual diet; (2) monitoring of diet adherence through foodrecalls; (3) large prospective, control trials over a longer-term; (4) use of a control diet to determinethe specificity of observed effects to the intervention; (5) use of a variety of endpoints (symptoms,quality of life, clinical biomarkers, endoscopic indices, diet and fecal assessment) to monitor responseto diet interventions; and (6) consider the use of IBD animal models (e.g., gnotobiotic mouse model) todiscover the mechanisms of pathogenesis.As research in this field moves forward, a personalized approach to nutrition for individualsor for subsets of patients may be the next frontier. A personalized approach may not only be usefulfor primary prevention of IBD but also treating disease. We must be mindful that a generalized diettreatment for all patients may not work. Certainly, we are seeing emerging research to suggest thatmicrobiota-targeted approaches have demonstrated some promise for managing chronic disease [127].7. ConclusionsAs our knowledge of the associations between a disrupted intestinal microbiota (dysbiosis) andchronic inflammatory diseases expands, the influence of diet becomes increasingly important. Clearly,diet and nutrition are of major interest for patients with IBD. Patients use a variety of diet strategies inattempt to manage underlying disease, as well as to provide relief from symptoms. Diet plays a keyrole in IBD pathogenesis, and there is a growing appreciation that the interaction between diet andmicrobes in a susceptible person contributes significantly to the onset of disease [128]. Several linesof evidence point to aspects of the typical Western diet that may promote the development of IBD.A low-residue diet is frequently recommended for IBD by health professionals [19] to reduce symptomsmay be adding further insult. A diet that lacks dietary fiber may accelerate dysbiosis in IBD [94,95].Pre-illness studies in IBD and intervention trials provide convincing evidence that a plant-baseddiet, with increased consumption of fruit\/vegetables and less red meat intake could be suggested topatients with IBD in remission. Several of the diets\/supplements discussed in this review appear tohold promise for in the maintenance of remission in IBD, especially when provided in addition tostandard medical therapy.Acknowledgments: Grant funding from the Canadian Foundation for Dietetic Research to NH and DLG supportthis work. 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Dolan, K.T.; Chang, E.B. Diet, gut microbes, and the pathogenesis of inflammatory bowel diseases. Mol. Nutr.Food Res. 2016. [CrossRef] [PubMed]\u00a9 2017 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open accessarticle distributed under the terms and conditions of the Creative Commons Attribution(CC BY) license (http:\/\/creativecommons.org\/licenses\/by\/4.0\/).","attrs":{"lang":"en","ns":"http:\/\/www.w3.org\/2009\/08\/skos-reference\/skos.html#note","classmap":"oc:AnnotationContainer"},"iri":"http:\/\/www.w3.org\/2009\/08\/skos-reference\/skos.html#note","explain":"Simple Knowledge Organisation System; Notes are used to provide information relating to SKOS concepts. 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