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The Cochrane Database of Systematic Reviews logoLink to The Cochrane Database of Systematic Reviews
. 2017 Oct 25;2017(10):CD012839. doi: 10.1002/14651858.CD012839

Dietary interventions for induction and maintenance of remission in inflammatory bowel disease

Berkeley N Limketkai 1, Alyssa Parian 2, Ronald L Koretz 3,4, Julie E Nanavati 5, Russel T Shinohara 6, Gerard E Mullin 2,✉
PMCID: PMC6485839

Abstract

This is a protocol for a Cochrane Review (Intervention). The objectives are as follows:

The objective of this systematic review is to evaluate the efficacy and safety of dietary interventions on IBD outcomes.

Background

Description of the condition

Inflammatory bowel disease (IBD), predominantly comprised of Crohn's disease (CD) and ulcerative colitis (UC), is characterized by chronic mucosal inflammation, frequent hospitalizations, adverse health economics, and compromised quality of life. Common symptoms of IBD include abdominal pain, diarrhea, and rectal bleeding. Inflammation in UC is limited to the colonic mucosa. Inflammation in CD is a non‐uniform transmural disease process that can occur anywhere along the alimentary tract and can lead to complications including intestinal strictures, fistulization to surrounding tissues or organs, and abscesses. Other complications that can arise in both CD and UC include intestinal cancer, nutrient malabsorption, malnutrition, and extra‐intestinal manifestations (e.g. arthralgias, dermatologic lesions, uveitis).

The incidence of CD is approximately 20 per 100,000 person‐years in North America and 13 per 100,000 person‐years in Europe (Molodecky 2012). Higher disease incidence and prevalence are seen in North America and Europe compared to lower rates in Asia and the Middle East. Nonetheless, the incidence and prevalence of IBD have more recently been rising in Asia and the Middle East, and individuals from these geographic regions experience an increased risk of developing IBD when immigrating to North America or Europe (Benchimol 2015; Pinsk 2007). This overall increase in IBD among populations not traditionally associated with IBD has been hypothesized to stem from the Westernization of lifestyles and diets (Foster 2013; Ooi 2016). For example, immigrants from Latin American to South Florida develop IBD at a later age; however, first‐generation US‐born Hispanics develop IBD at an age similar to non‐Hispanic whites (Damas 2013). The development of IBD in this generation of immigrants is also occurring sooner than previously documented (Damas 2017).

Factors that contribute to the development of IBD are unclear, although the current paradigm of pathogenesis involves the interaction of disease‐susceptibility genes, inappropriate immune response, gut microbiota, and environmental factors (Abraham 2009). Some potential environmental factors include gastrointestinal infections, antibiotics, tobacco use, and oral contraceptives (Birrenbach 2004; Cornish 2008; Garcia Rodriguez 2006; Gradel 2009; Ungaro 2014). Epidemiologic studies have implicated diet in IBD pathogenesis (Chapman‐Kiddell 2010). Increased intake of refined sugars has been associated with an increased risk of CD in several small cohort studies (Bianchi 1985; Hansen 2011; Jakobsen 2013; Martini 1976; Silkoff 1980). Other studies have associated dietary fiber consumption with a reduced risk of CD (Amre 2007; Persson 1992; Thornton 1979). An analysis of the Nurses' Health Study that included 170,776 adult women, who were prospectively followed over 26 years, revealed that long‐term consumption of dietary fiber was associated with a reduced incidence of CD (Ananthakrishnan 2013). Compared with the lowest quintile of energy‐adjusted cumulative average intake of dietary fiber, intake of the highest quintile (median of 24.3 g/day of dietary fiber) was associated with a 40% reduction in risk of CD. Fiber derived from fruits was significantly associated with a reduced risk of CD, while fiber from vegetables, cereals, and whole grains was not associated with a reduced risk of IBD. A separate analysis of the Nurses’ Health Study revealed that higher intakes of fruits, vegetables, and fish in high school were associated with a 53% lower risk of developing CD with fish having the greatest impact (Ananthakrishnan 2015). Dietary fat may also play a role in CD pathogenesis, although this relationship appears less clear. Some studies have associated an increased fat intake with CD risk (Hou 2011; Reif 1997; Sakamoto 2005). However, an analysis of the large prospective Nurses' Health Study did not find an association between the intake of total fat, saturated fats, unsaturated fats, omega‐6 polyunsaturated fatty acids (PUFAs), or omega‐3 PUFAs and CD risk (Ananthakrishnan 2014). A greater intake of omega‐3 PUFAs and higher ratio of n‐3:n‐6 PUFAs were associated with a lower risk of UC. Furthermore, high long‐term intake of trans‐unsaturated fatty acids was associated with a trend towards an increased incidence of UC. Table 1 summarizes the influence of some dietary components on the risk of IBD.

Table 1.

Dietary Components Can Influence Risk of Inflammatory Bowel Disease

Dietary Component Effect on IBD Risk References
Animal Protein Increased Jantchou 2010
Heme iron, sulfur Increased Ananthakrishnan 2015
Refined sugars Increased Janerot 1983
High trans‐fat Increased Ananthakrishnan 2014
Fiber Decreased Ananthakrishnan 2015
Fruit Decreased Hou 2011
Vegetables Decreased Hou 2011
High omega‐3 fatty acids Decreased Chan 2014
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Adpated from Mullin 2016.

Given its potential effects on disease pathogenesis, dietary intake has similarly been hypothesized to influence disease activity. For instance, exclusive enteral nutrition may be effective for the induction and maintenance of remission in pediatric CD (Akobeng 2007; Critch 2012; Zachos 2007). A high intake of red and processed meat or alcoholic beverages may increase the risk of a UC flare among adults (Jowett 2004). Diet‐derived micronutrients, such as zinc, iron, and vitamin D, may have modifying effects on immunity, barrier function, and oxidative load with a downstream potential to impact the course of CD (Brown 2011; Lih‐Brody 1996; Limketkai 2016). There may be a role of nutritional therapies for the induction and maintenance of remission in IBD, although the potential efficacy may vary according to diet composition, disease type, and age group (pediatric or adult).

Description of the intervention

The intervention is a controlled manipulation of the subject’s oral diet by a deliberate change in the consumption of food (i.e. no formulas or supplements used) for a specified period of time.

How the intervention might work

The mechanisms that drive the benefits or harms of diets in IBD are unclear, although studies on dietary macronutrients may provide some insight. For instance, omega‐6 PUFAs are pro‐inflammatory mediators, while omega‐3 PUFAs, medium‐chain oils, and a family of diverse plant‐derived flavonoids (e.g., phytonutrients) have anti‐inflammatory properties (Kono 2010; Papada 2014). Dietary fiber can be converted by intestinal bacteria to short‐chain fatty acids, which have anti‐inflammatory properties (Galvez 2005). In IBD mouse models, high‐fat diets promote further intestinal inflammation by disrupting gut barrier function and the resident microbiome (Devkota 2012; Gruber 2013; van der Logt 2013). Similarly, one of the theories underlying the efficacy of exclusive enteral nutrition or elimination diets for induction of remission in IBD relates to an avoidance of dietary triggers. These pro‐ or anti‐inflammatory nutrients are thus suspected to confer respective pro‐ or anti‐inflammatory properties of diets. Others have hypothesized that IBD patients may possess individualized food sensitivities and disease activity could improve with the personalized exclusion of foods that provoke symptoms or cause abnormal increases in food‐specific IgG antibodies (Bentz 2010; Gunasekeera 2016; Rajendran 2011), although food‐specific IgG antibodies have not been found to correlate with gastrointestinal symptom severity (Zuo 2007). The elimination of foods that are high in short‐chain carbohydrates (i.e. FODMAP: Fermentable Oligo‐, Di‐, Monosaccharides, And Polyols) may improve CD symptoms through several possible mechanisms including reduction of gaseous byproducts of bacterial fermentation, gaseous distention, osmotic diarrhea, and shifts in the gut microbiome (Gearry 2009; Gibson 2015; Halmos 2015; Halmos 2016; Prince 2016; See Figure 1).

Figure 1.

Figure 1

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Source: Mullin 2016.

Why it is important to do this review

Patients and clinicians have long sought guidance on the dietary management of IBD. A prospective evaluation of 400 consecutive IBD patients at a tertiary‐care center reported that approximately half felt that diet could be the initiating factor in their disease and the majority cited food provocation of IBD symptoms (57%) and disease flares (60%) (Limdi 2016). Several 'brand' diets (e.g. Specific Carbohydrate Diet, gluten‐free diet, Anti‐Inflammatory Diet, Gut and Psychology Diet) are promoted on the Internet by healthcare practitioners and even non‐licensed individuals, often without supporting evidence. These diet programs restrict, exclude, or promote the intake of differing food types to achieve purported improvements in IBD symptoms. Several clinical trials and observational cohort studies have studied the effects of diverse diets on clinical endpoints in IBD. Nonetheless, the individual studies are often limited by small sample sizes and inconsistent findings. Despite several opinion papers and reviews on the issue of dietary management of IBD, there is still no consensus or clear guidance in the literature on optimal dietary therapies for induction or maintenance of remission in IBD. A systematic review is lacking and could potentially benefit both clinicians and patients to guide dietary management of IBD based on the best available evidence.

Objectives

The objective of this systematic review is to evaluate the efficacy and safety of dietary interventions on IBD outcomes.

Methods

Criteria for considering studies for this review

Types of studies

Randomized controlled trials (RCTs) and non‐randomized observational studies will be considered for inclusion.

Types of participants

The study populations of the included trials will include adults or children with established IBD (CD, UC). For studies that only report on IBD, we will contact the authors to request a breakdown of results for participants with CD and UC. Trials conducted in all settings (e.g. single‐center, multi‐center) with any established method used to confirm disease diagnosis will be included. Trials (RCT, NRS) will not be included unless stratified results for IBD (and type) only are provided.

Types of interventions

The controlled interventions of interest include all defined oral diets that are compared to a different or unrestricted oral diet. Studies that exclusively focus on enteral nutrition, oral nutrient supplementation, medical foods, probiotics, and parenteral nutrition will be excluded.

Types of outcome measures

Primary outcomes

Primary outcomes will include induction and maintenance of remission as defined by the included studies.

  1. Induction of remission involves the therapeutic reduction of intestinal symptoms below a clinical threshold as measured by; CD and UC symptom scores including the Pediatric Crohn’s Disease Activity Index (PCDAI), the Crohn’s Disease Activity Index (CDAI), the Harvey‐Bradshaw Index (HBI), the Mayo score, modified Mayo score or Colitis Activity Index (CAI).

  2. Maintenance of remission involves the continual abatement of symptoms over time attributable to a therapeutic modality (in this case, diet). Maintenance of remission will be assessed based on available fixed time intervals (e.g. six months, one year) and as variable time contributions (e.g. person‐years). A clinical relapse is defined as the transition from a state of clinical remission to active disease, based on symptom scores (i.e. PCDAI, CDAI, HBI, Mayo score, or CAI).

Although symptom scores are validated indices routinely used to assess disease activity in IBD clinical trials, a potential limitation is their inability to differentiate between IBD or irritable bowel syndrome (IBS)‐associated mediators of non‐specific gastrointestinal symptoms.

Secondary outcomes

Secondary outcomes (when available) will include the following:

  1. Clinical improvement as defined by the included studies;

  2. Corticosteroid‐free remission;

  3. Surrogate biomarkers of inflammation (i.e., erythrocyte sedimentation rate [ESR] and C‐reactive protein [CRP]), fecal biomarkers (i.e., calprotectin);

  4. Endoscopic endpoints of improvement and remission;

  5. Histologic endpoints of improvement and remission;

  6. Health‐related quality of life as measured by the Inflammatory Bowel Disease Questionnaire (IBDQ), Short Inflammatory Bowel Disease Questionnaire (SIBDQ), or related surveys;

  7. Hospitalizations;

  8. Need for surgery;

  9. Progression of disease from a state of inflammation‐only disease to stricturing/obstructing to penetrating/fistulizing disease;

  10. Escalation of therapy including the need to add or modify pharmacologic therapy due to lack of efficacy at inducing or maintaining remission after enrolment in the trial;

  11. Adverse events;

  12. Withdrawal due to adverse events; and

  13. Serious adverse events.

Search methods for identification of studies

Electronic searches

We will conduct a comprehensive and systematic search to identify RCTs and non‐randomised studies (i.e. cohort or case‐control) from inception to date using the following databases:

  • CENTRAL;

  • Cochrane IBD Group Specialized Trials Register;

  • EMBASE (Wiley);

  • MEDLINE (PubMed); and

  • Web of Science.

We will search databases using controlled vocabulary and keywords (details in appendices). No restrictions will be placed on publication dates (after 1966) or language. Note that the searches are designed to include interventional and observational studies on adults and children but exclude those using oral nutrition supplements (enteral nutrition drinks, tube feeds), medical foods, probiotics, parenteral nutrition or a combination of these modalities. We report the detailed search strategies in Appendix 1.

Searching other resources

We will search reference lists from included articles and any existing relevant reviews. We will also scan proceedings from Digestive Disease Week (2005 to date), Advances in Inflammatory Bowel Disease (2005 to date), Clinical Nutrition Week (2005 to date), European Crohn's and Colitis Organisation (2005 to date), and United European Gastroenterology Week (2005 to date). We will also search ongoing trials registered in ClinicalTrials.gov and the WHO International Clinical Trials Registry Platform portal.

Data collection and analysis

Selection of studies

The stages of article selection include the following: (i) title screening; (ii) abstract screening; and (iii) full‐text review. Two authors (BNL and GEM) will independently review each article at each stage of selection. Included and excluded studies will be recorded.

  1. Title screening will involve selection of articles that report studies with even a minor possibility of inclusion. Articles that are clearly unrelated will be excluded. Adjudication will not occur at the title screening stage and studies that are ambiguous will be included by default.

  2. Abstract screening will involve selection of articles that report studies with a reasonable possibility of inclusion. Differences in assessment for inclusion will be resolved by discussion between the two independent investigators. Adjudication will not occur at the abstract screening state and studies that are ambiguous will be included by default.

  3. Full‐text review will involve selection of articles based on careful examination of the full report. Differences in assessment for inclusion will be resolved by discussion between the two independent investigators. Adjudication will be performed as needed by a third author (AP).

Data extraction and management

Two authors (BNL and GEM) will independently perform data extraction from each included study. Any discrepancies will be resolved by discussion between the two independent investigators. Adjudication will be performed as needed by a third author (AP). Extracted data will include the study design, population characteristics, intervention, comparator, duration of interventions and follow‐up, outcomes, timing, setting, the method of handling missing data, funding source, and potential conflicts of interest.

Assessment of risk of bias in included studies

Two authors (BNL and GEM) will independently assess the study quality of each included RCT using the Cochrane risk of bias tool. Adjudication will be performed as needed by a third author (AP). Domains of interest include random sequence generation, allocation concealment, blinding of participants and personnel, blinding of outcome assessment, completeness of outcome data, selective reporting, and other potential sources of bias (e.g. baseline imbalance). Each domain will be assessed as having a low, moderate, high, or unclear risk of bias. Based on the aggregate assessment of these items, study quality will be rated as good (low risk of bias), fair, or poor (high or unclear risk of bias). Each domain will follow standard definitions used for Cochrane systematic reviews (Higgins 2011).

We will consider trials which were classified as having a low risk of bias for sequence generation, allocation concealment, blinding of participants and personnel, blinding of outcome assessment, completeness of outcome data, and selective reporting as low bias‐risk trials. All other trials will be considered to be at high risk of bias. We will tabulate the risk of bias in the 'Risk of bias' table as part of the 'Table of characteristics of included studies'. We also illustrate the risk of bias of each trial using the 'Risk of bias summary' and cross‐tabulate all the judgement of risk on a 'Risk of bias graph'.

We will assess the risk of bias in observational studies using the Newcastle‐Ottawa Scale (NOS) for assessing the quality of non‐randomized studies in meta‐analyses (Wells 2017).

The overall strength of evidence supporting the primary outcome and selected secondary outcomes will be assessed using the GRADE (Grades of Recommendation, Assessment, Development, and Evaluation) criteria (Guyatt 2008; Schünemann 2011). Evidence from RCTs starts as high quality and evidence from observational studies starts as low quality. The quality of the evidence can be downgraded due to risk of bias, indirect evidence, inconsistency (unexplained heterogeneity), imprecision; and publication bias. GRADE also allows for the potential of rating up the overall quality of evidence from methodologically sound observational studies (Guyatt 2011). For example, evidence could be rated up if high quality observational studies show a two‐ to five‐fold reduction or increase in risk (Guyatt 2011). Taking all of these factors into account, we will rate the overall quality of evidence as follows:

  1. High. We are very confident that the true effect lies close to that of the estimate of the effect;

  2. Moderate. We are moderately confident in the effect estimate. The true effect is likely to be close to the estimate of the effect, but there is a possibility that it is substantially different;

  3. Low. Our confidence in the effect estimate is limited. The true effect may be substantially different from the estimate of the effect; or

  4. Very low. We have very little confidence in the effect estimate. The true effect is likely to be substantially different from the estimate of effect.

Measures of treatment effect

For binary outcomes, we will calculate the odds ratio (OR) with corresponding 95% CI. For nominal or ordinal outcomes, we will calculate the OR with corresponding 95% for each category relative to a reference category. For continuous outcomes, we will calculate the mean difference (MD) and corresponding 95% CI.

Unit of analysis issues

The unit of analysis will be each diet intervention for each individual participant for all study designs, including cross‐over studies and studies with multiple interventions. We will include cross‐over trials if data are available from the first phase of the study (i.e. before cross‐over occurred). For studies where events may recur (e.g. clinical relapses, adverse events), we will calculate the proportion of patients who experienced at least one event, individual events will not be counted separately. The studies are otherwise not anticipated to have repeated observations of outcomes or multiple treatment events. Ecologic studies that do not include individual‐level intervention and analyses will be excluded.

Dealing with missing data

We will collect information on how each trial handled missing data. When a study does not report all primary outcomes of interest, the original investigators will be contacted to request missing data. If the original investigators do not provide the data, this will be noted in the systematic review. For studies with missing dichotomous data, a separate intention‐to‐treat analysis will be performed where participants with missing data will be assumed to have been treatment failures. For studies with missing continuous data, separate analyses will be performed, including the (i) use of available cases and (ii) imputation with the last observation carried forward. Where possible, multiple imputation would be applied to missing data.

Assessment of heterogeneity

Heterogeneity will first be assessed qualitatively considering the study populations (e.g. adults, children, age, sex, race), research setting, methods of dietary interventions, duration of interventions, and definitions and thresholds for remission. For studies that have qualitative homogeneity, statistical heterogeneity will be assessed using the Chi2 test (P value < 0.10 will be considered statistically significant heterogeneity). The degree of heterogeneity across studies will be estimated using the I2 statistic. An I2 of 25% or less will be considered low heterogeneity, 26 to 50% will be considered moderate heterogeneity, and 50% and greater will be considered substantial heterogeneity. We will only report on summary effect estimates from meta‐analyses of groups of studies with clinical, methodologic, and statistical homogeneity (i.e. I2 < 50%). Additionally, we will visually inspect the forest plots and perform a sensitivity analysis excluding any obvious outliers.

Assessment of reporting biases

The total number of registered trials that could qualify for inclusion if published will be compared against the number of peer‐reviewed publications. Study contacts for registered trials without a peer‐reviewed publication will be contacted to assess reasons for the absence of publication. If 10 of more studies are included in the meta‐analysis, a funnel plot will be used to assess for potential publication bias.

Data synthesis

This systematic review will qualitatively report on the included study characteristics and outcomes. We will conduct a meta‐analysis of studies where at least two studies with similar interventions, participants and reported outcomes are present (to be determined by consensus). Analyses will be performed separately according to disease type (CD or UC), population (adult or pediatric), and type of diet. For dichotomous outcomes, we will calculate the pooled RR and corresponding 95% CI. For continuous outcomes, we will calculate the pooled MD and corresponding 95% CI. Studies will be pooled using a random‐effects model.

Subgroup analysis and investigation of heterogeneity

We will qualitatively evaluate the usage patterns of concurrent IBD‐specific therapies (e.g., antibiotics, aminosalicylates, immunomodulators, biologics) in the study populations. Where possible, subgroup analyses will be performed based on therapy classes.

Sensitivity analysis

We will conduct sensitivity analyses that exclude studies with high risk of bias.

Acknowledgements

None.

Appendices

Appendix 1. Medline Search Strategy

Search Strategy for MEDLINE (PubMed) (1966‐Present)

#1 Search ("Inflammatory Bowel Diseases"[mh] OR "Ileitis"[mh] OR "colitis"[mh])

#2 Search ("inflammatory bowel disease"[tw] OR "inflammatory bowel diseases"[tw] OR "ibd"[tw] OR "crohn"[tw] OR "crohn's"[tw] OR "crohns"[tw] OR “terminal ileitis”[tw] OR "enteritis regionalis"[tw] OR "Regional enteritis"[tw] OR "regional enterocolitis"[tw] OR "Ileitis"[tw] OR "colitis"[tw] OR proctit*[tw] OR proctocolit*[tw] OR colitide*[tw] OR “ulcerative colorectitis”[tw])

#3 Search (#1 OR #2)

#4 Search ("Diet"[mh:noexp] OR "Diet Therapy"[mh:noexp] OR "oligosaccharides"[mh] OR "dietary fiber"[mh] OR "Diet, Carbohydrate Loading"[mh] OR "Diet Fads"[mh] OR "Diet, Carbohydrate‐Restricted"[mh] OR "Diet, Fat‐Restricted"[mh] OR "Diet, Gluten‐Free"[mh] OR "Diet, High‐Fat"[mh] OR "Diet, Mediterranean"[mh] OR "Diet, Paleolithic"[mh] OR "Diet, Protein‐Restricted"[mh] OR "Diet, Sodium‐Restricted"[mh] OR "Diet, Vegetarian"[mh] OR "Diet, Macrobiotic"[mh] OR "Diet, Vegan"[mh] OR "Diet, Western"[mh] OR "Healthy Diet"[mh] OR "Ketogenic Diet"[mh] OR "Psyllium"[mh])

#5 Search (diet[tw] OR "diets"[tw] OR "dietary"[tw] OR "oligosaccharides"[tw] OR "oligofructose"[tw] OR "raw food"[tw] OR fermented[tw] OR "Whole 30"[tw] OR "atkins"[tw] OR "south beach"[tw] OR "makers diet"[tw] OR "maker's diet"[tw] OR fodmap[tw] OR fodmaps[tw] OR fructooligosaccharide*[tw] OR polyols[tw] OR monosaccharide*[tw] OR gluten[tw] OR "fish diet"[tw] OR "fatty acid"[tw] OR "fatty acids"[tw] OR omega‐3[tw] OR omega‐3s[tw] OR omega‐6[tw] OR omega‐6s[tw] OR elimination[tw] OR microparticle[tw] OR "red meat"[tw] OR sugar[tw] OR sugars[tw] OR dairy[tw] OR fiber[tw] OR fibre[tw] low‐residue[tw] OR "low residue"[tw] OR fruit[tw] OR fruits[tw] OR vegetable[tw] OR vegetables[tw] OR “olive oil”[tw] OR "olive oils"[tw] OR “Protein diet”[tw] OR “protein diets”[tw] OR “Protein restricted”[tw] OR “Protein‐restricted”[tw] OR “Protein‐free”[tw] OR “Protein free”[tw] OR carbohydrate[tw] OR carbo[tw] OR "fad diet"[tw] OR "fad diets"[tw] OR "high fat"[tw] OR "high fats"[tw] OR mediterranean[tw] OR paleolithic[tw] OR paleo[tw] OR sodium[tw] OR vegetarian[tw] OR vegan[tw] OR macrobiotic[tw] OR ketogenic[tw] OR “antinflammatory diet”[tw] OR “anti‐inflammatory diet”[tw] OR “IBD AID”[tw] OR “IBD‐AID”[tw] OR dissacharide*[tw] OR lactose[tw] OR sucrose[tw] OR fructose[tw] OR “exclusion diet”[tw] OR “exclusion diets”[tw] OR SCD[tw] OR solbitol[tw] OR xylitol[tw] OR bran[tw] OR brans[tw] OR psyllium[tw] OR Metamucil[tw] OR plantaglucide[tw] OR “ispaghule gum”[tw] OR “plantago seed”[tw] OR ispaghula[tw] OR isogel[tw] OR reguval[tw])

#6 Search (#4 OR #5)

#7 Search (#3 AND #6)

Search Strategy for EMBASE (Wiley) (1980 – present)

#1 'inflammatory bowel disease'/exp OR 'colitis'/exp OR 'ileitis'/exp

#2 ('inflammatory bowel disease':ti,ab OR 'inflammatory bowel diseases':ti,ab OR ibd:ti,ab OR crohn:ti,ab OR crohns:ti,ab OR 'terminal ileitis':ti,ab OR 'enteritis regionalis':ti,ab OR 'regional enteritis':ti,ab OR 'regional enterocolitis':ti,ab OR Ileitis:ti,ab OR colitis:ti,ab OR proctitis:ti,ab OR proctit*:ti,ab OR proctocolit*:ti,ab OR colitide*:ti,ab OR 'ulcerative colorectitis':ti,ab)

#3 #1 OR #2

#4 ('diet'/de OR 'diet therapy'/exp OR 'oligosaccharide'/exp OR 'dietary fiber'/exp OR 'carbohydrate loading diet'/exp OR 'low carbohydrate diet'/exp OR 'low fat diet'/exp OR 'gluten free diet'/exp OR 'lipid diet'/exp OR 'Mediterranean diet'/exp OR 'paleolithic diet'/exp OR 'protein restriction'/exp OR 'sodium restriction'/exp OR 'vegetarian diet'/exp OR 'macrobiotic diet'/exp OR 'vegan diet'/exp OR 'Western diet'/exp OR 'healthy diet'/exp OR 'ketogenic diet'/exp OR 'ispagula'/exp)

#5 (diet:ti,ab OR diets:ti,ab OR dietary:ti,ab OR oligosaccharides:ti,ab OR oligofructose:ti,ab OR ‘raw food’:ti,ab OR fermented:ti,ab OR ‘Whole 30’:ti,ab OR atkins:ti,ab OR ‘south beach’:ti,ab OR ‘makers diet’:ti,ab OR fodmap:ti,ab OR fodmaps:ti,ab OR fructooligosaccharide*:ti,ab OR polyols:ti,ab OR monosaccharide*:ti,ab OR gluten:ti,ab OR ‘fish diet’:ti,ab OR ‘fatty acid’:ti,ab OR ‘fatty acids’:ti,ab OR omega‐3:ti,ab OR omega‐3s:ti,ab OR omega‐6:ti,ab OR omega‐6s:ti,ab OR elimination:ti,ab OR microparticle:ti,ab OR ‘red meat’:ti,ab OR sugar:ti,ab OR sugars:ti,ab OR dairy:ti,ab OR fiber:ti,ab OR fibre:ti,ab low‐residue:ti,ab OR ‘low residue’:ti,ab OR fruit:ti,ab OR fruits:ti,ab OR vegetable:ti,ab OR vegetables:ti,ab OR ‘olive oil’:ti,ab OR ‘olive oils’:ti,ab OR ‘Protein diet’:ti,ab OR ‘protein diets’:ti,ab OR ‘Protein restricted’:ti,ab OR ‘Protein‐restricted’:ti,ab OR ‘Protein‐free’:ti,ab OR ‘Protein free’:ti,ab OR carbohydrate:ti,ab OR carbo:ti,ab OR ‘fad diet’:ti,ab OR ‘fad diets’:ti,ab OR ‘high fat’:ti,ab OR ‘high fats’:ti,ab OR mediterranean:ti,ab OR paleolithic:ti,ab OR paleo:ti,ab OR sodium:ti,ab OR vegetarian:ti,ab OR vegan:ti,ab OR macrobiotic:ti,ab OR ketogenic:ti,ab OR ‘antinflammatory diet’:ti,ab OR ‘anti‐inflammatory diet’:ti,ab OR ‘IBD AID’:ti,ab OR ‘IBD‐AID’:ti,ab OR dissacharide*:ti,ab OR lactose:ti,ab OR sucrose:ti,ab OR fructose:ti,ab OR ‘exclusion diet’:ti,ab OR ‘exclusion diets’:ti,ab OR SCD:ti,ab OR solbitol:ti,ab OR xylitol:ti,ab OR ‘bran’:ti,ab OR ‘brans’:ti,ab OR psyllium:ti,ab OR Metamucil:ti,ab OR plantaglucide:ti,ab OR ‘ispaghule gum’:ti,ab OR ‘plantago seed’:ti,ab OR ispaghula:ti,ab OR isogel:ti,ab OR reguval:ti,ab)

#6 #4 OR #5

#7 #3 AND #6

Search Strategy for Web of Science (1900 – present)

#1 TS=("inflammatory bowel disease" OR "inflammatory bowel diseases" OR "ibd" OR "crohn" OR "crohn's" OR "crohns" OR “terminal ileitis” OR "enteritis regionalis" OR "Regional enteritis" OR "regional enterocolitis" OR "Ileitis" OR "colitis" OR proctit* OR proctocolit* OR colitide* OR “ulcerative colorectitis”)

#2 TS=(diet OR "diets" OR "dietary" OR "oligosaccharides" OR "oligofructose" OR "raw food" OR fermented OR "Whole 30" OR "atkins" OR "south beach" OR "makers diet" OR "maker's diet" OR fodmap OR fodmaps OR fructooligosaccharide* OR polyols OR monosaccharide* OR gluten OR "fish diet" OR "fatty acid" OR "fatty acids" OR omega‐3 OR omega‐3s OR omega‐6 OR omega‐6s OR elimination OR microparticle OR "red meat" OR sugar OR sugars OR dairy OR fiber OR fibre OR low‐residue OR "low residue" OR fruit OR fruits OR vegetable OR vegetables OR “olive oil” OR "olive oils" OR “Protein diet” OR “protein diets” OR “Protein restricted” OR “Protein‐restricted” OR “Protein‐free” OR “Protein free” OR carbohydrate OR carbo OR "fad diet" OR "fad diets" OR "high fat" OR "high fats" OR Mediterranean OR Paleolithic OR paleo OR sodium OR vegetarian OR vegan OR macrobiotic OR ketogenic OR “antinflammatory diet” OR “anti‐inflammatory diet” OR “IBD AID” OR “IBD‐AID” OR dissacharide* OR lactose OR sucrose OR fructose OR “exclusion diet” OR “exclusion diets” OR SCD OR solbitol OR xylitol OR bran OR brans OR psyllium OR Metamucil OR plantaglucide OR “ispaghule gum” OR “plantago seed” OR ispaghula OR isogel OR reguval)

#3 #1 AND #2

Search Strategy for CENTRAL (Cochrane Library)

#1 MeSH descriptor: [Inflammatory Bowel Diseases] explode all trees

#2 MeSH descriptor: [Ileitis] explode all trees

#3 MeSH descriptor: [Colitis] explode all trees

#4 ("inflammatory bowel disease" or "inflammatory bowel diseases" or "ibd" or "crohn" or "crohn's" or "crohns" or "terminal ileitis" or "enteritis regionalis" or "Regional enteritis" or "regional enterocolitis" or "Ileitis" or "colitis" or proctit* or proctocolit* or colitide* or "ulcerative colorectitis"):ti,ab,kw

#5 #1 or #2 or #3 or #4

#6 MeSH descriptor: [Diet] explode all trees

#7 MeSH descriptor: [Diet Therapy] this term only

#8 MeSH descriptor: [Diet Therapy] explode all trees

#9 MeSH descriptor: [Diet] this term only

#10 MeSH descriptor: [Diet Therapy] this term only

#11 MeSH descriptor: [Oligosaccharides] explode all trees

#12 MeSH descriptor: [Dietary Fiber] explode all trees

#13 MeSH descriptor: [Diet, Carbohydrate‐Restricted] explode all trees

#14 MeSH descriptor: [Diet Fads] explode all trees

#15 MeSH descriptor: [Diet, Fat‐Restricted] explode all trees

#16 MeSH descriptor: [Diet, Gluten‐Free] explode all trees

#17 MeSH descriptor: [Diet, High‐Fat] explode all trees

#18 MeSH descriptor: [Diet, Mediterranean] explode all trees

#19 MeSH descriptor: [Diet, Paleolithic] explode all trees

#20 MeSH descriptor: [Diet, Protein‐Restricted] explode all trees

#21 MeSH descriptor: [Diet, Sodium‐Restricted] explode all trees

#22 MeSH descriptor: [Diet, Vegetarian] explode all trees

#23 MeSH descriptor: [Diet, Macrobiotic] explode all trees

#24 MeSH descriptor: [Diet, Macrobiotic] explode all trees

#25 MeSH descriptor: [Diet, Vegan] explode all trees

#26 MeSH descriptor: [Diet, Western] explode all trees

#27 MeSH descriptor: [Ketogenic Diet] explode all trees

#28 MeSH descriptor: [Psyllium] explode all trees

#29 #6 or #7 or #8 or #9 or #10 or #11 or #12 or #13 or #14 or #15 or #16 or #17 or #18 or #19 or #20 or #21 or #23 or #24 or #25 or #26 or #27 or #28

#30 #5 and #29.

Contributions of authors

The protocol was drafted by BNL, AMP, RLK, JEN, RS, GEM.

Sources of support

Internal sources

  • None, Other.

External sources

  • None, Other.

Declarations of interest

All investigators report no conflict of interest.

New

References

Additional references

  1. Abraham C, Cho JH. Inflammatory bowel disease. New England Journal of Medicine 2009;361:2066‐78. [DOI] [PMC free article] [PubMed] [Google Scholar]
  2. Akobeng AK, Thomas AG. Enteral nutrition for maintenance of remission in Crohn's disease. Cochrane Database of Systematic Reviews 2007, Issue 3. [DOI: 10.1002/14651858.CD005984.pub2] [DOI] [PubMed] [Google Scholar]
  3. Amre DK, D'Souza S, Morgan K, Seidman G, Lambrette P, Grimard G, et al. Imbalances in dietary consumption of fatty acids, vegetables, and fruits are associated with risk for Crohn's disease in children. American Journal of Gastroenterology 2007;102:2016‐25. [DOI] [PubMed] [Google Scholar]
  4. Ananthakrishnan AN, Khalili H, Konijeti GG, Higuchi LM, Silva P, Korzenik JR, et al. A prospective study of long‐term intake of dietary fiber and risk of Crohn's disease and ulcerative colitis. Gastroenterology 2013;145:970‐7. [DOI] [PMC free article] [PubMed] [Google Scholar]
  5. Ananthakrishnan AN, Khalili H, Konijeti GG, Higuchi LM, Silva P, Fuchs CS, et al. Long‐term intake of dietary fat and risk of ulcerative colitis and Crohn's disease. Gut 2014;63:776‐84. [DOI] [PMC free article] [PubMed] [Google Scholar]
  6. Ananthakrishnan AN, Khalili H, Song M, Higuchi LM, Richter JM, Nimptsch K, et al. High School Diet and Risk of Crohn's Disease and Ulcerative Colitis. Inflammatory Bowel Diseases 2015;21:2311‐9. [DOI] [PMC free article] [PubMed] [Google Scholar]
  7. Benchimol EI, Mack DR, Guttmann A, Nguyen GC, To T, Mojaverian N, et al. Inflammatory bowel disease in immigrants to Canada and their children: a population‐based cohort study. American Journal of Gastroenterology 2015;110:553‐63. [DOI] [PubMed] [Google Scholar]
  8. Bentz S, Hausmann M, Piberger H, Kellermeier S, Paul S, Held L, et al. Clinical relevance of IgG antibodies against food antigens in Crohn's disease: a double‐blind cross‐over diet intervention study. Digestion 2010;81:252‐64. [DOI] [PubMed] [Google Scholar]
  9. Bianchi Porro G, Panza E. Smoking, sugar, and inflammatory bowel disease. British Medical Journal (Clinical Research Edition) 1985;291:971‐2. [DOI] [PMC free article] [PubMed] [Google Scholar]
  10. Birrenbach T, Böcker U. Inflammatory bowel disease and smoking: a review of epidemiology, pathophysiology, and therapeutic implications. Inflammatory Bowel Diseases 2004;10:848‐59. [DOI] [PubMed] [Google Scholar]
  11. Brown AC, Rampertab SD, Mullin GE. Existing dietary guidelines for Crohn's disease and ulcerative colitis. Expert Review of Gastroenterology and Hepatology 2011;5:411‐25. [DOI] [PubMed] [Google Scholar]
  12. Chan SS, Luben R, Olsen A, Tjonneland A, Kaaks R, Lindgren S, et al. Association between high dietary intake of the n‐3 polyunsaturated fatty acid docosahexaenoic acid and reduced risk of Crohn's disease. Alimentary Pharmacology and Therapeutics 2014;39(8):834‐42. [DOI] [PMC free article] [PubMed] [Google Scholar]
  13. Chapman‐Kiddell CA, Davies PS, Gillen L, Radford‐Smith GL. Role of diet in the development of inflammatory bowel disease. Inflammatory Bowel Diseases 2010;16:137‐51. [DOI] [PubMed] [Google Scholar]
  14. Cornish JA, Tan E, Simillis C, Clark SK, Teare J, Tekkis PP. The risk of oral contraceptives in the etiology of inflammatory bowel disease: a meta‐analysis. American Journal of Gastroenterology 2008;103:2394‐400. [DOI] [PubMed] [Google Scholar]
  15. Critch J, Day AS, Otley A, King‐Moore C, Teitelbaum JE, Shashidhar H, et al. Use of enteral nutrition for the control of intestinal inflammation in pediatric Crohn disease. Journal of Pediatric Gastroenterology and Nutrition 2012;54:298‐305. [DOI] [PubMed] [Google Scholar]
  16. Damas OM, Jahann DA, Reznik R, McCauley JL, Tamariz L, Deshpande AR, et al. Phenotypic manifestations of Inflammatory Bowel Disease differ between Hispanics and non‐Hispanic whites: results of a large cohort study. American Journal of Gastroenterology 2013;108(2):231‐9. [DOI] [PubMed] [Google Scholar]
  17. Damas OM, Avalos DJ, Palacio AM, Gomez L, Quintero MA, Deshpande AR, et al. Inflammatory bowel disease is presenting sooner after immigration in more recent US immigrants from Cuba. Alimentary Pharmacology and Therapeutics 2017;46(3):303‐9. [DOI] [PMC free article] [PubMed] [Google Scholar]
  18. Devkota S, Wang Y, Musch MW, Leone V, Fehlner‐Peach H, Nadimpalli A, et al. Dietary‐fat‐induced taurocholic acid promotes pathobiont expansion and colitis in Il10‐/‐ mice. Nature 2012;487:104‐8. [DOI] [PMC free article] [PubMed] [Google Scholar]
  19. Foster A, Jacobson K. Changing incidence of inflammatory bowel disease: environmental influences and lessons learnt from the South Asian population. Frontiers in Pediatrics 2013;1:34. [DOI] [PMC free article] [PubMed] [Google Scholar]
  20. Galvez J, Rodríguez‐Cabezas ME, Zarzuelo A. Effects of dietary fiber on inflammatory bowel disease. Molecular Nutrition and Food Research 2005;49:601‐8. [DOI] [PubMed] [Google Scholar]
  21. García Rodríguez LA, Ruigómez A, Panés J. Acute gastroenteritis is followed by an increased risk of inflammatory bowel disease. Gastroenterology 2006;130:1588‐94. [DOI] [PubMed] [Google Scholar]
  22. Gearry RB, Irving PM, Barrett JS, Nathan DM, Shepherd SJ, Gibson PR. Reduction of dietary poorly absorbed short‐chain carbohydrates (FODMAPs) improves abdominal symptoms in patients with inflammatory bowel disease‐a pilot study. Journal of Crohn's and Colitis 2009;3:8‐14. [DOI] [PubMed] [Google Scholar]
  23. Gibson PR, Varney J, Malakar S, Muir JG. Food components and irritable bowel syndrome. Gastroenterology 2015;148:1158‐74. [DOI] [PubMed] [Google Scholar]
  24. Gradel KO, Nielsen HL, Schønheyder HC, Ejlertsen T, Kristensen B, Nielsen H. Increased short‐ and long‐term risk of inflammatory bowel disease after salmonella or campylobacter gastroenteritis. Gastroenterology 2009;137:495‐501. [DOI] [PubMed] [Google Scholar]
  25. Gruber L, Kisling S, Lichti P, Martin FP, May S, Klingenspor M, et al. High fat diet accelerates pathogenesis of murine Crohn's disease‐like ileitis independently of obesity. PLoS One 2013;8:e71661. [DOI] [PMC free article] [PubMed] [Google Scholar]
  26. Gunasekeera V, Mendall MA, Chan D, Kumar D. Treatment of Crohn's Disease with an IgG4‐Guided Exclusion Diet: A Randomized Controlled Trial. Digestive Diseases and Sciences 2016;61:1148‐57. [DOI] [PubMed] [Google Scholar]
  27. Guyatt GH, Oxman AD, Vist GE, Kunz R, Falck‐Ytter Y, Alonso‐Coello P, et al. GRADE: an emerging consensus on rating quality of evidence and strength of recommendations. BMJ 2008;336(7650):924‐6. [DOI] [PMC free article] [PubMed] [Google Scholar]
  28. Guyatt GH, Oxman AD, Sultan S, Glasziou P, Akl EA, Alonso‐Coello P, et al. GRADE guidelines: 9. Rating up the quality of evidence. Journal of Clinical Epidemiology 2011;64(12):1311‐6. [DOI] [PubMed] [Google Scholar]
  29. Halmos EP, Christophersen CT, Bird AR, Shepherd SJ, Gibson PR, Muir JG. Diets that differ in their FODMAP content alter the colonic luminal microenvironment. Gut 2015;64:93‐100. [DOI] [PubMed] [Google Scholar]
  30. Halmos EP, Christophersen CT, Bird AR, Shepherd SJ, Muir JG, Gibson PR. Consistent prebiotic effect on gut microbiota with altered FODMAP intake in patients with Crohn's disease: a randomised, controlled cross‐over trial of well‐defined diets. Clinical and Translational Gastroenterology 2016;7:e164. [DOI] [PMC free article] [PubMed] [Google Scholar]
  31. Hansen TS, Jess T, Vind I, Elkjaer M, Nielsen MF, Gamborg M, et al. Environmental factors in inflammatory bowel disease: a case‐control study based on a Danish inception cohort. Journal of Crohn's and Colitis 2011;5:577‐84. [DOI] [PubMed] [Google Scholar]
  32. Higgins JP, Green S. Cochrane Handbook for Systematic Reviews of Interventions Version 5.1.0 (updated March 2011). The Cochrane Collaboration, 2011. [Google Scholar]
  33. Hou JK, Abraham B, El‐Serag H. Dietary intake and risk of developing inflammatory bowel disease: a systematic review of the literature. American Journal of Gastroenterology 2011;106:563‐73. [DOI] [PubMed] [Google Scholar]
  34. Jakobsen C, Paerregaard A, Munkholm P, Wewer V. Environmental factors and risk of developing paediatric inflammatory bowel disease ‐‐ a population based study 2007‐2009. Journal of Crohn's and Colitis 2013;7:79‐88. [DOI] [PubMed] [Google Scholar]
  35. Jarnerot G, Jarnmark I, Nilsson K. Consumption of refined sugar by patients with Crohn’s disease, ulcerative colitis, or irritable bowel syndrome. Scandinavian Journal of Gastroenterology 1983;18(8):999‐1002. [DOI] [PubMed] [Google Scholar]
  36. Jantchou P, Morois S, Clavel‐Chapelon F, Boutron‐Ruault MC, Carbonnel F. Animal protein intake and risk of Inflammatory Bowel Disease: the E3N prospective study. American Journal of Gastroenterology 2010;105(10):2195‐201. [DOI] [PubMed] [Google Scholar]
  37. Jowett SL, Seal CJ, Pearce MS, Phillips E, Gregory W, Barton JR, et al. Influence of dietary factors on the clinical course of ulcerative colitis: a prospective cohort study. Gut 2004;53(10):1479‐84.. [DOI] [PMC free article] [PubMed] [Google Scholar]
  38. Kono H, Fujii H, Ogiku M, Tsuchiya M, Ishii K, Hara M. Enteral diets enriched with medium‐chain triglycerides and N‐3 fatty acids prevent chemically induced experimental colitis in rats. Translational Research 2010;156:282‐91. [DOI] [PubMed] [Google Scholar]
  39. Lih‐Brody L, Powell SR, Collier KP, Reddy GM, Cerchia R, Kahn E, et al. Increased oxidative stress and decreased antioxidant defenses in mucosa of inflammatory bowel disease. Digestive Diseases and Sciences 1996;41:2078‐86. [DOI] [PubMed] [Google Scholar]
  40. Limdi JK, Aggarwal D, McLaughlin JT. Dietary Practices and Beliefs in Patients with Inflammatory Bowel Disease. Inflammatory Bowel Diseases 2016;22:164‐70. [DOI] [PubMed] [Google Scholar]
  41. Limketkai BN, Bechtold ML, Nguyen DL. Vitamin D and the pathogenesis of Inflammatory Bowel Disease. Current Gastroenterology Reports 2016;18:52. [DOI] [PubMed] [Google Scholar]
  42. Martini GA, Brandes JW. Increased consumption of refined carbohydrates in patients with Crohn's disease. Klinische Wochenschrift 1976;54:367‐71. [DOI] [PubMed] [Google Scholar]
  43. Molodecky NA, Soon IS, Rabi DM, Ghali WA, Ferris M, Chernoff G, et al. Increasing incidence and prevalence of the inflammatory bowel diseases with time, based on systematic review. Gastroenterology 2012;142:46‐54. [DOI] [PubMed] [Google Scholar]
  44. Mullin GE. Role of diet in Inflammatory Bowel Disease. Presented at: Digestive Disease Week; May 2016; San Diego, CA.
  45. Ooi CJ, Makharia GK, Hilmi I, Gibson PR, Fock KM, Ahuja V, et al. Asia Pacific consensus statements on Crohn's disease. Part 1: definition, diagnosis, and epidemiology. Journal of Gastroenterology and Hepatology 2016;31:45‐55. [DOI] [PubMed] [Google Scholar]
  46. Papada E, Kaliora AC, Gioxari A, Papalois A, Forbes A. Anti‐inflammatory effect of elemental diets with different fat composition in experimental colitis. British Journal of Nutrition 2014;111:1213‐20. [DOI] [PubMed] [Google Scholar]
  47. Persson PG, Ahlbom A, Hellers G. Diet and inflammatory bowel disease: a case‐control study. Epidemiology 1992;3:47‐52. [DOI] [PubMed] [Google Scholar]
  48. Pinsk V, Lemberg D A, Grewal K, Barker C C, Schreiber R A, Jacobson K. Inflammatory bowel disease in the South Asian pediatric population of British Columbia. American Journal of Gastroenterology 2007;102:1077‐83. [DOI] [PubMed] [Google Scholar]
  49. Prince AC, Myers CE, Joyce T, Irving P, Lomer M, Whelan K. Fermentable carbohydrate restriction (low FODMAP diet) in clinical practice improves functional gastrointestinal symptoms in patients with Inflammatory Bowel Disease. Inflammatory Bowel Diseases 2016;22:1129‐36. [DOI] [PubMed] [Google Scholar]
  50. Rajendran N, Kumar D. Food‐specific IgG4‐guided exclusion diets improve symptoms in Crohn's disease: a pilot study. Colorectal Disease 2011;13:1009‐13. [DOI] [PubMed] [Google Scholar]
  51. Reif S, Klein I, Lubin F, Farbstein M, Hallak A, Gilat T. Pre‐illness dietary factors in inflammatory bowel disease. Gut 1997;40:754‐60. [DOI] [PMC free article] [PubMed] [Google Scholar]
  52. Sakamoto N, Kono S, Wakai K, Fukuda Y, Satomi M, Shimoyama T, et al. Dietary risk factors for inflammatory bowel disease: a multicenter case‐control study in Japan. Inflammatory Bowel Diseases 2005;11:154‐63. [DOI] [PubMed] [Google Scholar]
  53. Schünemann HJ, Oxman AD, Vist GE, Higgins JPT, Deeks JJ, Glasziou P, et al. Chapter 12: Interpreting results and drawing conclusions. In: Higgins JPT, Green S editor(s). Cochrane Handbook for Systematic Reviews of Interventions Version 5.1.0 (updated March 2011). The Cochrane Collaboration, 2011. Available from www.cochrane‐handbook.org. [Google Scholar]
  54. Silkoff K, Hallak A, Yegena L, Rozen P, Mayberry JF, Rhodes J, et al. Consumption of refined carbohydrate by patients with Crohn's disease in Tel‐Aviv‐Yafo. Postgraduate Medical Journal 1980;56:842‐6. [DOI] [PMC free article] [PubMed] [Google Scholar]
  55. Thornton JR, Emmett PM, Heaton KW. Diet and Crohn's disease: characteristics of the pre‐illness diet. British Medical Journal 1979;2:762‐4. [DOI] [PMC free article] [PubMed] [Google Scholar]
  56. Ungaro R, Bernstein CN, Gearry R, Hviid A, Kolho KL, Kronman MP, et al. Antibiotics associated with increased risk of new‐onset Crohn's disease but not ulcerative colitis: a meta‐analysis. American Journal of Gastroenterology 2014;109:1728‐38. [DOI] [PubMed] [Google Scholar]
  57. Logt EM, Blokzijl T, Meer R, Faber KN, Dijkstra G. Westernized high‐fat diet accelerates weight loss in dextran sulfate sodium‐induced colitis in mice, which is further aggravated by supplementation of heme. Journal of Nutritional Biochemistry 2013;24:1159‐65. [DOI] [PubMed] [Google Scholar]
  58. Wells GA, Shea B, O'Connell D, Peterson J, Welch V, Losos M, et al. The Newcastle‐Ottawa Scale (NOS) for assessing the quality of non randomised studies in meta‐analyses. www.ohri.ca/programs/clinical_epidemiology/oxford.asp (accessed 28 August 2017).
  59. Zachos M, Tondeur M, Griffiths AM. Enteral nutritional therapy for induction of remission in Crohn's disease. Cochrane Database of Systematic Reviews 2007, Issue 1. [DOI: 10.1002/14651858.CD000542.pub2] [DOI] [PubMed] [Google Scholar]
  60. Zuo XL, Li YQ, Li WJ, Guo YT, Lu XF, Li JM, et al. Alterations of food antigen‐specific serum immunoglobulins G and E antibodies in patients with irritable bowel syndrome and functional dyspepsia. Clinical and Experimental Allergy 2007;37(6):823‐30. [DOI] [PubMed] [Google Scholar]

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