ArticleLiterature Review

Role of diet in the development of inflammatory bowel disease

Authors:
  • Griffith University, Gold Coast campus, Southport, Australia
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Abstract

The inflammatory bowel diseases (IBDs) are a group of heterogeneous disorders characterized by acute and chronic inflammatory changes in the small or large bowel, or in both. Increasing incidence and prevalence figures for IBD both in the developed and developing world indicate that environmental factors are at least as significant in IBD as genetic susceptibility. Of these, diet and the host microbiota are likely to play important but as yet poorly defined roles. The major constituents of a standard "Western" diet may contribute to, or protect against, intestinal inflammation via several mechanisms. These include the effects of insulin resistance and short-chain fatty acids such as butyrate, modification of intestinal permeability, the antiinflammatory role of polyunsaturated fatty acids, and the effect of sulfur compounds from protein on host microbiota. This detailed review critically assesses the evidence for the role of diet in the development of IBD and examines the evidence for obesity as a contributing factor to IBD pathogenesis. Particular attention is focused on methodological issues including suitability of cases and controls, confounders such as smoking, and total energy expenditure.

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... The increased prevalence of CD in economically developed countries may be linked to lifestyle, particularly the diet primarily followed in these countries [10]. Epidemiological studies have shown that the American diet with a high intake of fats and carbohydrates and a low intake of fiber led to the increased risk of CD development [11]. In addition, dietary antigens along with bacterial antigens are the most common in the intestine, which supports the evidence of the diet's contribution to CD development [11]. ...
... Epidemiological studies have shown that the American diet with a high intake of fats and carbohydrates and a low intake of fiber led to the increased risk of CD development [11]. In addition, dietary antigens along with bacterial antigens are the most common in the intestine, which supports the evidence of the diet's contribution to CD development [11]. Changes in gene expression, modification of gut microbiome composition and effect on the intestine wall permeability can be identified among possible mechanisms of CD development exerted by food antigens [12]. ...
... Changes in gene expression, modification of gut microbiome composition and effect on the intestine wall permeability can be identified among possible mechanisms of CD development exerted by food antigens [12]. Additionally, an unhealthy diet can lead to obesity, which increases the risk of CD [11]. In one study [13], CD patients were found to consume significantly more carbohydrates than those in the control group. ...
Article
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Crohn’s disease remains one of the challenging problems of modern medicine, and the development of new and effective and safer treatments against it is a dynamic field of research. To make such developments possible, it is important to understand the pathologic processes underlying the onset and progression of Crohn’s disease at the molecular and cellular levels. During the recent years, the involvement of mitochondrial dysfunction and associated chronic inflammation in these processes became evident. In this review, we discuss the published works on pathogenetic models of Crohn’s disease. These models make studying the role of mitochondrial dysfunction in the disease pathogenesis possible and advances the development of novel therapies.
... [5][6][7] Specific data linking dietary factors with IBD in human populations have been limited and conflicting. [8][9][10] Most previous studies of diet and IBD For numbered affiliations see end of the article Correspondence to: N Narula neeraj.narula@medportal.ca (or @narulaneeraj on Twitter ORCID 0000-0002-1536-8436) Additional material is published online only. ...
... | BMJ 2021;374:n1554 | the bmj have used retrospective or case-control designs. 9 10 The few prospective studies that have examined dietary risk factors have been limited by small numbers of participants, lack of adjustment for potential confounders, or use of homogenous populations confined to individual countries or specific regions of countries. 6 7 11-15 A recent systematic review synthesised all studies that evaluated dietary intake and risk of IBD. 10 It was evident from the findings that many associations have been examined repeatedly, including the association of different dietary fats, carbohydrates, proteins, fruit, vegetables, fibre, and dairy with IBD. 10 Meats have been assessed as a whole, with some, but not all, studies suggesting an increased odds for the development of IBD with higher meat intake. ...
Article
Background Dietary guidelines recommend limiting red meat intake because it is a major source of medium- and long-chain SFAs and is presumed to increase the risk of cardiovascular disease (CVD). Evidence of an association between unprocessed red meat intake and CVD is inconsistent. Objective The study aimed to assess the association of unprocessed red meat, poultry, and processed meat intake with mortality and major CVD. Methods The Prospective Urban Rural Epidemiology (PURE) Study is a cohort of 134,297 individuals enrolled from 21 low-, middle-, and high-income countries. Food intake was recorded using country-specific validated FFQs. The primary outcomes were total mortality and major CVD. HRs were estimated using multivariable Cox frailty models with random intercepts. Results In the PURE study, during 9.5 y of follow-up, we recorded 7789 deaths and 6976 CVD events. Higher unprocessed red meat intake (≥250 g/wk vs. <50 g/wk) was not significantly associated with total mortality (HR: 0.93; 95% CI: 0.85, 1.02; P-trend = 0.14) or major CVD (HR: 1.01; 95% CI: 0.92, 1.11; P-trend = 0.72). Similarly, no association was observed between poultry intake and health outcomes. Higher intake of processed meat (≥150 g/wk vs. 0 g/wk) was associated with higher risk of total mortality (HR: 1.51; 95% CI: 1.08, 2.10; P-trend = 0.009) and major CVD (HR: 1.46; 95% CI: 1.08, 1.98; P-trend = 0.004). Conclusions In a large multinational prospective study, we did not find significant associations between unprocessed red meat and poultry intake and mortality or major CVD. Conversely, a higher intake of processed meat was associated with a higher risk of mortality and major CVD.
... Epidemiological studies illustrated that the intake of a higher ratio of n − 6 polyunsaturated fatty acids (n − 6 PUFAs) and a lower ratio of n − 3 polyunsaturated fatty acids (n − 3 PUFAs) was associated with an increased risk of developing IBD [12,13]. Researches to date have demonstrated that n − 3 PUFAs may offer a promising approach to improving dysbacteriosis, reducing the likelihood of relapse, and lowering the mortality of colitis [14,15]. ...
... However, fiber intake is controversial. Scientists found that the risk of fiber was >15 g/day, while ornton showed there was no difference between patients and controls [12]. e future study should pay more attention to the amount of fiber and IBD. ...
Article
Full-text available
Inflammatory bowel disease (IBD), most commonly known as Crohn’s disease (CD) and ulcerative disease (UC), is a chronic and relapsing intestinal disease which cannot be cured completely. The prevalence of IBD in Europe and in North America has increased over the past 20 years. As most IBD patients are young at onset, their quality of life (QOL) can be influenced to varying degrees. Thus, current treatment goals are typically focused on preventing complications, including maintaining clinical remission and improving the QOL. Adjuvant therapies have been widely concerned as an effective treatment in alleviating IBD symptoms, including dietary intervention, traditional Chinese medicine, smoking, alcohol, and physical activities. This review focuses on different ancillary therapies for IBD treatments, in particular the mechanism of reducing inflammation based on the actual data from research studies. Moreover, comparing the latest data, this review also presented potential future prospect for adjuvant therapies.
... IBD includes Crohn's disease (CD) and ulcerative colitis (UC). The altered response of the immune system leads to the inflammation of the gastrointestinal tract clinically defined by relapsing and remitting episodes [4,5]. The inflammatory process is characterized by a long-term overproduction of pro-inflammatory factors and an enhanced intestinal permeability [6]. ...
... The etiology of the IBD is not still completely understood [9,10]. Many studies have indicated that the genetic predisposition, diet, the environment, the intestinal microbial flora, and the immune responses are involved in the pathogenesis of IBD [4,5,11,12]. ...
Preprint
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Inflammatory bowel disease (IBD) is a chronic disease mediated by the immune system and characterized by the inflammation of the gastrointestinal tract. This study is to understand how the use of parenteral nutrition (PN) can affect the adult population diagnosed with IBD. We conducted a systematic review, meta-analysis and a meta-regression. On the different databases, (MEDLINE, Scopus, Cochrane, LILACS, CINAHL, WOS) we found 119 registers, the accuracy was 16% (19 registers); After a Full-text review, only 15 research studies were selected for qualitative synthesis and 10 for Meta-analysis and Meta-regression. The variables used were Crohn’s Disease Activity Index (CDAI), albumin, body weight (BW) and post-operative complications (COM). PN has shown to have efficacy for the treatment of IBD and is compatible with other medicines. The CDAI and albumin improve although the effect of PN are greater after a while. However, the effect on the albumin could be less than the observed value in the meta-analysis, due to a possible publication bias. The BW does not change after intervention. COM utilizing PN has been observed, although the proportion is low.
... Several dietary risk factors are associated with CD, including high sugar, fat, and protein content. Insufficient amounts of vegetables or fruits in the diet and consumption of fast food are also risk factors [71]. ...
... The compositions of these two intestinal bacteria have been shown to be disrupted in patients with CD [23]. With a Westernized diet, the intestine is continuously exposed to a considerable number of antigens, which may irritate the mucosal immune system, suppress the intestinal microbiota, and influence the progression of CD [71]. Total parenteral nutrition has proven to be an efficacious therapy for CD, as it gives the bowel a chance to rest [24]. ...
Article
Full-text available
Purpose To review role of environmental factors in the pathogenesis of Crohn’s disease. Methods We systematically reviewed trials and systematic reviews using PubMed and Web of science databases. Here, we review the current information on the causative factors and mechanisms of CD, including smoking, exercise, diet, animal protein, breastfeeding, history of childhood infection and vaccination, oral contraceptives, and antibiotics of CD. We also highlight important knowledge gaps that need to be filled in order to advance the field of CD research. Results Epidemiological studies have indicated the significance of environmental factors in the disease behavior and outcome of Crohn’s disease (CD). There are a few recognized environmental factors, such as cigarette smoking, exercise, dietary habits, and breastfeeding, which are associated with the pathogenesis of CD. These factors are hypothesized to change the epithelial barrier function, which disturbs both the innate and adaptive immune systems and the intestinal flora. However, the effect of several risk factors, such as appendectomy and pharmaceutical use, differs across several studies, indicating the need for more rigorous research. Furthermore, few studies have examined effective interventions based on environmental factors that can improve disease outcomes. Recent studies have indicated that the pathogenesis of CD is related to environmental and genetic factors. Conclusion We review the current information on the causative factors and mechanisms of CD, including smoking, exercise, diet, animal protein, breastfeeding, history of childhood infection and vaccination, oral contraceptives, and antibiotics of CD. However, further studies are needed to understand knowledge gaps in the field of CD.
... IBD includes Crohn's disease (CD) and ulcerative colitis (UC). The altered response of the immune system leads to the inflammation of the gastrointestinal tract clinically defined by relapsing and remitting episodes [4,5]. The inflammatory process is characterized by a long-term overproduction of pro-inflammatory factors and an enhanced intestinal permeability [6]. ...
... The etiology of the IBD is not still Nutrients 2019, 11, 2865 2 of 20 completely understood [9,10]. Many studies have indicated that the genetic predisposition, diet, the environment, the intestinal microbial flora, and the immune responses are involved in the pathogenesis of IBD [4,5,11,12]. ...
Article
Full-text available
Inflammatory bowel disease (IBD) is a chronic disease mediated by the immune system and characterized by the inflammation of the gastrointestinal tract. This study is to understand how the use of parenteral nutrition (PN) can affect the adult population diagnosed with IBD. We conducted a systematic review, meta-analysis, and meta-regression. From the different databases (MEDLINE, Scopus, Cochrane, LILACS, CINAHL, WOS), we found 119 registers with an accuracy of 16% (19 registers). After a full-text review, only 15 research studies were selected for qualitative synthesis and 10 for meta-analysis and meta-regression. The variables used were Crohn’s Disease Activity Index (CDAI), albumin, body weight (BW), and postoperative complications (COM). PN has shown to have efficacy for the treatment of IBD and is compatible with other medicines. The CDAI and albumin improve, although the effect of PN is greater after a while. However, the effect on the albumin could be less than the observed value in the meta-analysis due to possible publication bias. The BW does not change after intervention. COM utilizing PN has been observed, although the proportion is low. More studies specifically referring to ulcerative colitis (UC) and Crohn’s disease (CD) are needed to develop more concrete clinical results.
... CD is, however, not a genetic disease as many studies observed discordances in monozygotic twins [8][9][10], indicating the involvement of other factors in its etiology. Talking in regards with the environmental factors, smoking has been identified as a risk factor for the development of CD, and consumption of Western diet (low-fiber diet enriched in total fat and sugar) and dietary emulsifiers (present in processed foods) are together associated with a higher susceptibility to develop CD [11][12][13][14]. The role of microbial composition of the intestinal microbiota has also been largely studied for its implication in the etiology of CD. ...
... The gut environment can also be impacted by the diet, especially in people living in developed countries having a Western lifestyle. Western diet, enriched in total fat, animal proteins, n-6 polyunsaturated fatty acids, and refined sugars, have been associated with a high risk to develop CD [12][13][14]. The object of several studies was to better catch the impacts of a HF/HS diet on the intestinal microenvironment composition and on AIEC infection. ...
Article
Full-text available
Besides genetic polymorphisms and environmental factors, the intestinal microbiota is an important factor in the etiology of Crohn’s disease (CD). Among microbiota alterations, a particular pathotype of Escherichia coli involved in the pathogenesis of CD abnormally colonizes the intestinal mucosa of patients: the adherent-invasive Escherichia coli (AIEC) pathobiont bacteria, which have the abilities to adhere to and to invade intestinal epithelial cells (IECs), as well as to survive and replicate within macrophages. AIEC have been the subject of many studies in recent years to unveil some genes linked to AIEC virulence and to understand the impact of AIEC infection on the gut and consequently their involvement in CD. In this review, we describe the lifestyle of AIEC bacteria within the intestine, from the interaction with intestinal epithelial and immune cells with an emphasis on environmental and genetic factors favoring their implantation, to their lifestyle in the intestinal lumen. Finally, we discuss AIEC-targeting strategies such as the use of FimH antagonists, bacteriophages, or antibiotics, which could constitute therapeutic options to prevent and limit AIEC colonization in CD patients.
... [5][6][7] Specific data linking dietary factors with IBD in human populations have been limited and conflicting. [8][9][10] Most previous studies of diet and IBD For numbered affiliations see end of the article Correspondence to: N Narula neeraj.narula@medportal.ca (or @narulaneeraj on Twitter ORCID 0000-0002-1536-8436) Additional material is published online only. ...
... | BMJ 2021;374:n1554 | the bmj have used retrospective or case-control designs. 9 10 The few prospective studies that have examined dietary risk factors have been limited by small numbers of participants, lack of adjustment for potential confounders, or use of homogenous populations confined to individual countries or specific regions of countries. 6 7 11-15 A recent systematic review synthesised all studies that evaluated dietary intake and risk of IBD. 10 It was evident from the findings that many associations have been examined repeatedly, including the association of different dietary fats, carbohydrates, proteins, fruit, vegetables, fibre, and dairy with IBD. 10 Meats have been assessed as a whole, with some, but not all, studies suggesting an increased odds for the development of IBD with higher meat intake. ...
Article
Full-text available
Objective To evaluate the relation between intake of ultra-processed food and risk of inflammatory bowel disease (IBD). Design Prospective cohort study. Setting 21 low, middle, and high income countries across seven geographical regions (Europe and North America, South America, Africa, Middle East, south Asia, South East Asia, and China). Participants 116 087 adults aged 35-70 years with at least one cycle of follow-up and complete baseline food frequency questionnaire (FFQ) data (country specific validated FFQs were used to document baseline dietary intake). Participants were followed prospectively at least every three years. Main outcome measures The main outcome was development of IBD, including Crohn’s disease or ulcerative colitis. Associations between ultra-processed food intake and risk of IBD were assessed using Cox proportional hazard multivariable models. Results are presented as hazard ratios with 95% confidence intervals. Results Participants were enrolled in the study between 2003 and 2016. During the median follow-up of 9.7 years (interquartile range 8.9-11.2 years), 467 participants developed incident IBD (90 with Crohn’s disease and 377 with ulcerative colitis). After adjustment for potential confounding factors, higher intake of ultra-processed food was associated with a higher risk of incident IBD (hazard ratio 1.82, 95% confidence interval 1.22 to 2.72 for ≥5 servings/day and 1.67, 1.18 to 2.37 for 1-4 servings/day compared with <1 serving/day, P=0.006 for trend). Different subgroups of ultra-processed food, including soft drinks, refined sweetened foods, salty snacks, and processed meat, each were associated with higher hazard ratios for IBD. Results were consistent for Crohn’s disease and ulcerative colitis with low heterogeneity. Intakes of white meat, red meat, dairy, starch, and fruit, vegetables, and legumes were not associated with incident IBD. Conclusions Higher intake of ultra-processed food was positively associated with risk of IBD. Further studies are needed to identify the contributory factors within ultra-processed foods. Study registration ClinicalTrials.gov NCT03225586 .
... In contrast, diets enriched in fiber, indoles and vitamins implement beneficial effects on intestinal homeostasis by increasing microbial variety and inducing a regulatory environment. (14,15), and WTD has been associated with higher incidence of IBDs (16). Moreover, high intake of calories derived from processed meat, butter and fried products, all components of WTD, have been described to instantly alter the composition of the intestinal microbiota, a phenomenon called dysbiosis, toward a lower Bacteroidetes to Firmicutes ratio (17)(18)(19). ...
Article
Full-text available
Dietary habits have a profound impact on intestinal homeostasis and in general on human health. In Western countries, high intake of calories derived from fried products, butter and processed meat is favored over dietary regimens rich in fruits and vegetables. This type of diet is usually referred to as Western-type diet (WTD) and it has been associated with several metabolic and chronic inflammatory conditions of the gastrointestinal tract. In this review, we describe how WTD promotes intestinal and extra-intestinal inflammation and alters mucosal immunity acting on CD4⁺ T cells in a microbiota-dependent or –independent fashion, ultimately leading to higher susceptibility to infectious and autoimmune diseases. Moreover, summarizing recent findings, we propose how dietary supplementation with fiber and vitamins could be used as a tool to modulate CD4⁺ T cell phenotype and function, ameliorating inflammation and restoring mucosal homeostasis.
... Several mechanisms prove that diet could influence the occurrence of IBD, which includes a change in the gut microbiota, direct dietary antigens, and altered the permeability of the gastro intestine [123]. [125]. ...
Article
Full-text available
Dietary proteins exert a wide range of nutritional and biological functions. Apart from their nutritional roles as the source of amino acids for protein synthesis, they take part mainly in the regulation of food intake, blood pressure, bone metabolism, glucose and lipid metabolism, and immune functions. The interaction of dietary proteins with the gastrointestinal (GI) tract plays a chief role in determining the physiological properties of proteins. The enzymes protease and peptidase hydrolyze dietary protein to generate dipeptides, tripeptides, and amino acids in the lumen of the gastrointestinal tract. These products digested from dietary proteins are utilized in the small intestine by microbes. Moreover, the microbes also convert the macro and micronutrients from the diet into an enormous number of compounds that may have either beneficial or adverse effects on human health. The present review discusses the various impacts caused by both dietary plant and animal protein sources on microbiota in the GI tract.Keywords: Animal protein; Plant protein; Dietary proteins; Gut microbiota; Human health.
... Chronic intestinal pathologies, where a correlation between symptomatology, disease activity and eating habits has been observed, can be both inflammatory and dysfunctional, particularly in common diseases such as irritable bowel syndrome (IBS) [4], inflammatory bowel disease (IBD) [5], chronic constipation [6] and functional dyspepsia [7]. Another example, although less frequent, can be given by an organic pathology of unknown etiology such as eosinophilic esophagitis (EoE), where new dietary approaches seem very promising for future therapies [8]. ...
Article
Full-text available
Diet and nutrition are known to play key roles in many chronic gastrointestinal diseases, regarding both pathogenesis and therapeutic possibilities. A strong correlation between symptomatology, disease activity and eating habits has been observed in many common diseases, both organic and functional, such as inflammatory bowel disease and irritable bowel syndrome. New different dietary approaches have been evaluated in order improve patients' symptoms, modulating the type of sugars ingested, the daily amount of fats or the kind of metabolites produced in gut. Even if many clinical studies have been conducted to fully understand the impact of nutrition on the progression of disease, more studies are needed to test the most promising approaches for different diseases, in order to define useful guidelines for patients.
... The results obtained from Cr(D-phe) 3 treated acetic acid-induced colitis are in correlation with previous reports of its capability to inhibit the TNF-α, IL-6 and oxidative stress in high glucose-exposed and also in H 2 O 2 treated cultured monocytes. 11 Accumulating reports suggests that consumption of refined sugar and fat may be responsible for the development of UC. 28 As mentioned earlier chromium is an essential trace element required for the normal metabolic process of carbohydrate, lipid, and protein in humans. Some foods, particularly those containing high simple sugars levels, reduce the absorption of chromium. ...
Article
Full-text available
Chromium-D-phenylalanine [Cr(D-phe)] is known to be anti-diabetic, anti-inflammatory and antioxidant complex. Our preliminary work reveals the beneficial effect of Cr(D-phe) in indomethacin-induced enterocolitis. The present work was intended to explore the effect of Cr(D-phe) in acetic acid-induced ulcerative colitis in rats. Further, molecular docking simulation experiments were performed. Colitis was induced through intra-rectal instillation of acetic acid (3% v/v) and the effectiveness of Cr(D-phe)(30, 60 and 90 μg/kg) and sulphasalazine was measured using clinical, macroscopic, biochemical, contractility and histopathological studies. In addition, drug likeliness, molecular docking and dynamic studies of Cr(D-phe) and sulphasalazine with NF-kappa B (1NFK) were carried out. Pretreatment of different doses of Cr(D-phe)showed significant reduction (P<0.01; P<0.001) in clinical, macroscopic score, oxidative stress and elevated biochemical parameters. Protective nature of Cr(D-phe)was further confirmed by histopathological examination and colonic contractility studies. In silico studies reveals that Cr(D-phe)exhibited better docking score (-14.121) compared to sulphasalazine (-5.654). Dug likeliness studies showed that Cr(D-phe)passes lipinski’s rule and exhibited better bioavailability properties with negligible hepatotoxicity compared to standard. Molecular dynamic studies reveal that Cr(D-phe)showed better stability compared to standard compound, while interacting with 1NFK for 10 ns. The observed beneficial activity of Cr(D-phe)could be due to its anti-oxidative and anti-inflammation by preventing NF-kB activity.
... L'alimentation joue un rôle important dans notre santé qui va bien au-delà de l'aspect nutritif. En plus de l'impact sur la composition du microbiote intestinal [140], nos changements d'habitudes alimentaires ont été mis en cause dans la recrudescence de maladies telles que l'obésité [21], le diabète de type 2 [141], les maladies cardiovasculaires [142] ainsi que les maladies inflammatoires chroniques de l'intestin [9,72,143]. Hormi les effets de l'aliment proprement dit, les micro-51 organismes associés aux produits fermentés pourraient avoir un effet sur la santé. ...
Thesis
Le travail décrit dans cette thèse a commencé avec la découverte d effets anti-inflammatoires chez certaines souches de L. delbrueckii. Il avait été montré que l effet anti-inflammatoire est souche-dépendant, et implique l action de protéines exposées à la surface de la bactérie. Dans le but d identifier l effecteur bactérien à l origine de l effet immuno-modulateur, 8 souches de L. delbrueckii ont été sélectionnées. Deux de ces souches sont à fort effet anti-inflammatoires, et les 6 restantes sont à effet faible ou intermédiaire. Pour l identification des protéines potentiellement responsables pour l effet anti-inflammatoire, des études de génomique et transcriptomique comparatives des 8 souches de L.delbrueckii ont été entreprises, ainsi qu une étude comparative du protéome de surface bactérienne.La première partie de cette thèse décrit les résultats de finition du génome d une des deux souches hautement anti-inflammatoires. Cette étape a révélé que la partie manquante de la séquence génomique était principalement composée de séquences répétées de type séquences d insertions (IS), dont le nombre s avère particulièrement élevé.La deuxième partie de la thèse décrit une étape de valorisation des données génomiques à travers une étude comparative entre souches de la ssp. lactis et souches de la ssp. bulgaricus. Cette étude révèle que les deux ssp. de L. delbrueckii évoluent en adaptation au milieu lait. Toutefois, la ssp. bulgaricus semble avoir atteint un stade d adaptation plus avancé que celui de la ssp. lactis. L adaptation des deux ssp. à leur environnement se fait principalement par un phénomène de perte spontanée de gènes devenus superflus.Une étude plus avancée de la structure génomique des deux ssp. révèle deux nouveaux aspects des différences de structure génomique. Tout d abord, au sein du core génome des deux sous-espèces, les évènements d échange génétique et recombinaison ont contribué plus à la diversité au sein de la ssp. lactis qu à la diversité chez la ssp. bulgaricus. Ensuite, une structure inversée répétée de grande taille, rarement observée dans les génomes bactériens, s avère caractéristique de la ssp. bulgaricus. La troisième partie de thèse décrit les trois approches comparatives menées dans le but d identifier les protéines bactériennes à l origine de l effet anti-inflammatoire. Au bout de ces études, nous avons sélectionné 56 gènes candidats, dont 41 ont été clonés dans un système d expression hétérologue. Pour l instant, 17 clones d expression ont été testés in vitro pour leur potentiel immuno-modulateur. Les résultats préliminaires ont permis l identification d une protéine à effet anti-inflammatoire.
... By the global shifting to WD habits, most of the population of industrialized and developing countries has converted their dietary lifestyles to the massive consumption of high-fat, high-sucrose, and ultra-processed food items. Undeniably, WD is on the defendant bench for the possible causal link between large consumption and the overall incidence of obesity, colorectal cancer and chronic inflammatory conditions affecting the intestine such as Crohn's Disease (CD) and ulcerative colitis, which are part of the so-called IBDs [160][161][162][163]. WD is very rich in saturated fats, refined grains, sucrose, corn-derived fructose, proteins from high processed red meats, salt, alcohol, sweetened and carbonated beverages [164,165], and its consumption is associated with dysbiosis and derangement of microbial composition [166] (Figure 1). ...
Article
Full-text available
The gut-brain axis is a multimodal communication system along which immune, metabolic, autonomic, endocrine and enteric nervous signals can shape host physiology and determine liability, development and progression of a vast number of human diseases. Here, we broadly discussed the current knowledge about the either beneficial or deleterious impact of dietary fatty acids on microbiota-brain communication (MBC), and the multiple mechanisms by which different types of lipids can modify gut microbial ecosystem and contribute to the pathophysiology of major neuropsychiatric diseases (NPDs), such as schizophrenia (SCZ), depression and autism spectrum disorders (ASD).
... 1 Although the whole pathogenesis of IBD is not well understood, diet seems to be one of the key determinants of IBD. 2 Several studies have focused on the association between food intakes or dietary behavior and disease risk. Meat might expose consumers to a higher risk of IBD, whereas higher consumption of fruits and vegetables has been associated with a lower risk. ...
Article
Background The incidence of inflammatory bowel diseases (IBDs) tended to increase for several decades. Diet is suspected to be a major determinant of the occurrence of these diseases. This prospective study aimed to assess the associations among occurrence of IBD, dietary patterns, and ultra-processed food in the French NutriNet-Santé cohort. Methods Participants of the NutriNet-Santé cohort who completed at least three 24-hour dietary records were included. Incident IBD cases were identified from 3 questionnaires and confirmed by phone or email interview. Major dietary patterns (DPs) were computed using a principal component analysis (PCA) based on 29 food groups’ consumption, whereas proportions of ultra-processed foods (UPFs) were obtained using the NOVA classification. Multivariable Poisson models were performed to evaluate associations among DP quintiles, UPF proportion (UPFp) in the diet, and incident IBD. Results A total of 105,832 participants were included, contributing 238,924 person-years in a mean follow-up of 2.3 ± 2.2 years. Among them, 75 participants reported an incident IBD. Three major DPs were retained: “healthy,” “traditional,” and “western.” No significant association was found for DPs and UPFp after adjustments for covariates. Conclusions In this study, neither DPs nor UPF proportion in the diet were significantly associated with the risk of incident IBD after adjustments for covariates. Further studies are needed to investigate the long-term association between diet and IBD.
... Over the past several decades, increased incidence rates of diseases associated with chronic inflammation, including inflammatory bowel disease (IBD), diabetes, and asthma have been observed in countries experiencing industrial and urban growth (1)(2)(3). While the causes of this incidence surge are still highly debated in biology and medicine communities, there is increasing epidemiological evidence that the rise of chronic inflammatory diseases (CIDs) can be attributed to nutritional changes (4)(5)(6)(7). A dietary basis for CIDs is further supported by the fact that they frequently involve physiological changes in the gastrointestinal tract including alterations in gut microbiota composition and metabolism (8)(9)(10)(11). ...
Article
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The molecular foundation of chronic inflammatory diseases (CIDs) can differ markedly between individuals. As our understanding of the biochemical mechanisms underlying individual disease manifestations and progressions expands, new strategies to adjust treatments to the patient's characteristics will continue to profoundly transform clinical practice. Nutrition has long been recognized as an important determinant of inflammatory disease phenotypes and treatment response. Yet empirical work demonstrating the therapeutic effectiveness of patient-tailored nutrition remains scarce. This is mainly due to the challenges presented by long-term effects of nutrition, variations in inter-individual gastrointestinal microbiota, the multiplicity of human metabolic pathways potentially affected by food ingredients, nutrition behavior, and the complexity of food composition. Historically, these challenges have been addressed in both human studies and experimental model laboratory studies primarily by using individual nutrition data collection in tandem with large-scale biomolecular data acquisition (e.g. genomics, metabolomics, etc.). This review highlights recent findings in the field of precision nutrition and their potential implications for the development of personalized treatment strategies for CIDs. It emphasizes the importance of computational approaches to integrate nutritional information into multi-omics data analysis and to predict which molecular mechanisms may explain how nutrients intersect with disease pathways. We conclude that recent findings point towards the unexhausted potential of nutrition as part of personalized medicine in chronic inflammation.
... La plupart des études épidémiologiques concernant le rôle de l'alimentation dans les MICIs se sont concentrées sur les macronutriments (Chapman-Kiddell et al., 2010;Hou et al., 2011). Une consommation élevée de fibres, en particulier de fibres provenant de fruits et de légumes, serait associée à une réduction significative du risque de MC (Amre et al., 2007;Ananthakrishnan et al., 2013). ...
Thesis
Les maladies inflammatoires chroniques de l’intestin (MICI), qui comprennent les deux principales formes, la maladie de Crohn (MC) et la rectocolite hémorragique (RCH), sont caractérisées par une inflammation chronique et récurrente de la muqueuse intestinale, ayant un impact considérable sur la qualité de vie. À l'heure actuelle, la prise en charge thérapeutique de la MC n'est pas curative et un tiers des patients ne réagissent pas aux traitements biologiques et aux immunosuppresseurs. Par conséquent, de nouvelles stratégies pour traiter cette maladie sont fortement attendues. La dérégulation de l'interaction entre d'une part les facteurs génétiques et le système immunitaire de l'hôte, et d'autre part le microbiote intestinal et les facteurs environnementaux, est impliquée dans le développement des MICI. Cette perturbation entraîne effectivement une augmentation de la perméabilité intestinale et une inflammation persistante. Restaurer le microbiote «dysbiotique» et les fonctions intestinales altérées représentent donc une thérapeutique alternative intéressante. De ce fait, les probiotiques sont une option intéressante et ont été utilisés avec succès chez des patients souffrant de pouchite et de RCH. Cependant, leur effet protecteur est clairement souche-dépendant et plusieurs souches probiotiques bien connues n’ont pu conduire à un résultat clinique probant, en particulier chez les patients souffrant de MC. Le décryptage des mécanismes moléculaires sera donc la clé pour permettre une recommandation efficace des probiotiques dans le traitement ou la prévention des MICI. La sélection de souches basée sur des critères de sélection bien définis et en utilisant des modèles bien maitrisés est indispensable à ce processus. L'objectif principal de cette thèse était de sélectionner des lactobacilles et des bifidobactéries parmi une collection de souches françaises et libanaises, capables de présenter des propriétés protectrices contre les MICI, en se concentrant sur leurs capacités immuno-régulatrices et leurs capacités à renforcer la barrière épithéliale. Des approches in vitro ont été utilisées pour sélectionner des souches ayant une activité anti-inflammatoire et également capables d'améliorer la fonction de la barrière intestinale. Cinq souches ont été identifiées présentant des caractéristiques différentes, mais avec un potentiel thérapeutique élevé. Deux souches se sont révélées hautement protectrices dans deux modèles différents de colite aiguë et de colite de bas grade. Nos résultats ont confirmé en outre l'hypothèse selon laquelle la capacité des souches à atténuer l'inflammation est en partie due à l'amélioration de la barrière intestinale et à la restauration des protéines de jonction serrés.Un nombre croissant d’études génétiques ont prouvé que l’autophagie peut affecter plusieurs aspects de la réponse immunitaire des muqueuses, notamment via l’élimination de bactéries intracellulaires, la sécrétion de peptides antimicrobiens, la production de cytokines pro-inflammatoires et la présentation des antigènes. Par conséquent, l'autophagie peut être considérée comme un mécanisme de régulation clé impliqué dans la physiopathologie de la MC. Nous avons donc évalué la capacité des souches à activer cette voie et montré que les souches sélectionnées étaient en effet capables d’induire une activation de l’autophagie dans des cellules dendritiques murines. Nous avons démontré in vitro que le blocage de l'autophagie pouvait diminuer la capacité des souches à induire la sécrétion d'IL-10, cytokine anti-inflammatoire et, inversement, à exacerber la sécrétion d'IL-1β, cytokine pro-inflammatoire. Nous avons pu confirmer, à l'aide d'un modèle murin de colite, que la capacité protectrice d’une souche impliquait la machinerie autophagique, et nous avons pu mettre en évidence le rôle des cellules dendritiques dans ce processus [...]
... The incidence of gastro-intestinal disorders like CD and UC has been increasing [29][30][31][32]. This has often been related to the current Western diet, which has changed substantially in the past seven decades [33][34][35][36][37][38][39]. This is because of changes in food production and technology, which provides easy access of urban based populations to cheap ultra-processed foods and foods high in refined grains, oil and sugar [40]. ...
Article
Full-text available
This review discusses the personalised dietary approach with respect to inflammatory bowel disease (IBD). It identifies gene–nutrient interactions associated with the nutritional deficiencies that people with IBD commonly experience, and the role of the Western diet in influencing these. It also discusses food intolerances and how particular genotypes can affect these. It is well established that with respect to food there is no “one size fits all” diet for those with IBD. Gene–nutrient interactions may help explain this variability in response to food that is associated with IBD. Nutrigenomic research, which examines the effects of food and its constituents on gene expression, shows that—like a number of pharmaceutical products—food can have beneficial effects or have adverse (side) effects depending on a person’s genotype. Pharmacogenetic research is identifying gene variants with adverse reactions to drugs, and this is modifying clinical practice and allowing individualised treatment. Nutrigenomic research could enable individualised treatment in persons with IBD and enable more accurate tailoring of food intake, to avoid exacerbating malnutrition and to counter some of the adverse effects of the Western diet. It may also help to establish the dietary pattern that is most protective against IBD.
... Key words: Crohn's disease, microbiota, dysbiosis, Escherichia coli, adhesive-invasive Escherichia coli. в сочетании с низким количеством пищевых волокон), а также антибиотикотерапия [24][25][26]. ...
... In addition to genetic variations between ethnic populations, it is now well established that the incidence increases with a westernised lifestyle and diet (158)(159)(160). Smoking confers protection against UC, with patients having milder disease, reduced need for medication and hospital admission (161). ...
Conference Paper
Ulcerative colitis is a relapsing and remitting inflammatory bowel disease involving the large bowel. The current hypothesis on the pathogenesis of UC is that an abnormal innate immune response in genetically susceptible individuals, combined with environmental factors, result in excessive activation of the adaptive immune system within lamina propria. The role of abnormal barrier function is widely accepted. Using transcriptomic analysis of punch biopsies of patients with quiescent UC, CLDN8 was identified as grossly downregulated in the intestine. In this thesis, loss of Cldn8, a tight junction (TJ) molecule, was shown to result in reduced susceptibility of mice to DSS-induced colitis. Cldn8 knock out (Cldn98-KO) mice, had smaller increase in intestinal permeability to 3H-mannitol, reduced neutrophils and macrophages in inflammatory cell infiltrate in lamina propria during the early phase of inflammation. The inner layer of mucous is sterile in naïve Cldn8-KO and WT mice, and remains sterile after the animals have been exposed to DSS-water for 12 hours. Transcriptomic analysis between Cldn8-KO and WT mice did not reveal any significant differences between the two groups at different time points. After correction for multiple-testing, no differentially-expressed genes remained. These results suggest that downregulation of CLDN8 in patients with UC is a physiologic response by the intestine to increase local defences against luminal pathogens.
... First, mesenteric fat increases inflammatory biomarkers, which might be integral to the inflammatory cascade involved in CD [39]. Second, excess macronutrient intake can heighten systematic oxidative stress [40,41]. The study by Aljada et al. [40], showed that feeding people a large meal portion resulted in the induction of nuclear factor kappa beta (NFkB) activity (lasted for about 4-5 h after a meal), indicating that prolonged overeating might lead to chronic oxidative stress. ...
Article
Full-text available
Purpose Fish consumption and dietary intake of n-3 polyunsaturated acids (PUFAs) may be associated with inflammatory bowel disease (IBD). We aimed to conduct a systematic review and summarize published articles on the association between fish consumption and dietary intake of n-3 PUFAs with the risk of IBD. Methods PubMed, Scopus, and Web of Science databases were used to conduct a comprehensive search and identify eligible literature published prior to January 2019. Fixed-effects model or random-effects models (DerSimonian–Laird method) were applied to pool the effect sizes. Cochrane Q test was used to trace the potential source of heterogeneity across studies. Results 12 studies (5 prospective and 7 case–control) were included in the systematic review, which ten of them were eligible for inclusion in the meta-analysis. Studies were included a total sample size of 282610 participants which 2002 of them were cases of IBD [1061 Crohn’s disease (CD) and 937 ulcerative colitis (UC)]. A negative association was found between fish consumption and the incidence of CD (pooled effect size: 0.54, 95%CI: 0.31–0.96, P = 0.03). There was no relationship between total dietary n-3 PUFAs intake and IBD (pooled effect size: 1.17, 95%CI: 0.80–1.72, P = 0.41). A significant inverse association was observed between dietary long-chain n-3 PUFAs and the risk of UC (pooled effect size: 0.75, 95%CI: 0.57–0.98, P = 0.03). Moreover, no association was found between α-Linolenic acid (ALA) and IBD (pooled effect size: 1.17, 95%CI: 0.63–2.17, P = 0.62). Conclusions Findings showed a negative association between fish consumption and the risk of CD. Moreover, there was a significant inverse association between dietary long-chain n-3 PUFAs and the risk of UC.
... Foods high in saturated fat or "Western" diets have been associated with a variety of autoimmune and chronic inflammatory disease including IBD and COPD (142,153,154). A "Western" diet can influence the composition of the intestinal microbiota, promote intestinal barrier permeability, and enhance inflammation (155)(156)(157). ...
Article
Full-text available
Inflammatory bowel disease (IBD) and chronic obstructive pulmonary disease (COPD) are chronic inflammatory diseases of the gastrointestinal and respiratory tracts, respectively. These mucosal tissues bear commonalities in embryology, structure and physiology. Inherent similarities in immune responses at the two sites, as well as overlapping environmental risk factors, help to explain the increase in prevalence of IBD amongst COPD patients. Over the past decade, a tremendous amount of research has been conducted to define the microbiological makeup of the intestine, known as the intestinal microbiota, and determine its contribution to health and disease. Intestinal microbial dysbiosis is now known to be associated with IBD where it impacts upon intestinal epithelial barrier integrity and leads to augmented immune responses and the perpetuation of chronic inflammation. While much less is known about the lung microbiota, like the intestine, it has its own distinct, diverse microflora, with dysbiosis being reported in respiratory disease settings such as COPD. Recent research has begun to delineate the interaction or crosstalk between the lung and the intestine and how this may influence, or be influenced by, the microbiota. It is now known that microbial products and metabolites can be transferred from the intestine to the lung via the bloodstream, providing a mechanism for communication. While recent studies indicate that intestinal microbiota can influence respiratory health, intestinal dysbiosis in COPD has not yet been described although it is anticipated since factors that lead to dysbiosis are similarly associated with COPD. This review will focus on the gut-lung axis in the context of IBD and COPD, highlighting the role of environmental and genetic factors and the impact of microbial dysbiosis on chronic inflammation in the intestinal tract and lung.
... The modern diet, rich in processed foods, sugar, and fat, contains much less Mn than traditional diets (44 decrease in Mn consumption was reported in Korea and China due to industrialization and Westernization of lifestyle (44). In addition, the Western diet with its high content of fat and sugar confers risk for the development of IBD due to dysbiosis and increased intestinal permeability (46)(47)(48). Additive effects of environmental modification can enhance genetic vulnerability, leading to intestinal inflammation. While Slc39a8 A391T mice do not exhibit severe spontaneous colitis at baseline, it is possible that A391T-induced barrier dysfunction in humans could be exacerbated by diet-induced dysbiosis, leading to chronic inflammatory conditions. ...
Article
Full-text available
Common genetic variants interact with environmental factors to impact risk of heritable diseases. A notable example of this is a single-nucleotide variant in the Solute Carrier Family 39 Member 8 (SLC39A8) gene encoding the missense variant A391T, which is associated with a variety of traits ranging from Parkinson's disease and neuropsychiatric disease to cardiovascular and metabolic diseases and Crohn's disease. The remarkable extent of pleiotropy exhibited by SLC39A8 A391T raises key questions regarding how a single coding variant can contribute to this diversity of clinical outcomes and what is the mechanistic basis for this pleiotropy. Here, we generate a murine model for the Slc39a8 A391T allele and demonstrate that these mice exhibit Mn deficiency in the colon associated with impaired intestinal barrier function and epithelial glycocalyx disruption. Consequently, Slc39a8 A391T mice exhibit increased sensitivity to epithelial injury and pathological inflammation in the colon. Taken together, our results link a genetic variant with a dietary trace element to shed light on a tissue-specific mechanism of disease risk based on impaired intestinal barrier integrity.
... Diet involvement plays an important role in the pathogenesis and management of UC both in pediatric and adult patients 6,7 . The typical Western diet (high sugar intake with low intake of vegetables) may contribute to the development of UC 8 , because intestinal inflammation can be influenced in several pathways, including affecting the intestinal permeability, altering the gut microbiome, and dietary constituents acting as food antigens 9 . As for the role of diet in the management of UC, enteral nutrition, which is supplemented with colostrum, probiotics, and transforming growth factor-β, produces limited treatment responses in UC patients 10 . ...
Article
Full-text available
Accumulating evidence has shown many similarities and differences of gene profiles and pathways between pediatric and adult ulcerative colitis (UC) patients. In this study, we aimed to investigate the shared genes and pathways in intestinal tissues of pediatric and adult UC. Differentially expressed genes (DEGs) between pediatric and adult UC were identified via bioinformatic analysis of Gene Expression Omnibus datasets GSE87473 and GSE126124. Gene Ontology and pathway enrichment were used to analyze overlapped and distinguished DEGs. Gene Set Variation Analysis (GSVA) was utilized for contrast consistency. Mice colitis models were induced by dextran sulfate sodium (DSS) and Citrobacter rodentium. 2616 DEGs were screened out in intestinal tissues of adult UC compared with those of adult healthy controls, and 1195 DEGs in pediatrics. Same pathways between pediatric and adult UC were enriched using overlapped DEGs, mainly related to immune responses and metabolic processes, including butyrate metabolism, which was also identified by GSVA analysis. Of note, butyrate metabolism was the exclusive down-regulated pathway enriched by these two analyses, indicating that butyrate metabolism is one of the key pathways associated with both pediatric and adult UC. In addition, butyrate suppressed DSS-induced and Citrobacter rodentium-induced intestinal inflammation in mice. Therefore, the study revealed that butyrate metabolism was critical in both pediatric and adult UC. And butyrate suppressed colitis in mice, which provided a theoretical basis for the potential treatment of butyrate for UC patients.
... Inflammatory bowel diseases (IBD) are chronic relapsing diseases of unknown origin affecting the gastrointestinal tract [1]. Diet is one of the key factors in their pathogenesis and outcome, since it could have a pro-inflammatory effect [2]. Notably, the incidence of IBD worldwide has significantly increased in the last decades [3,4], and it could be related to differences in lifestyle, including the adoption of a western diet, characterized by high amounts of proteins and saturated fats, in concomitance with low amounts of vegetables, fibers, and fruits [5]. ...
Article
Full-text available
Nutrition has an important impact on inflammatory bowel diseases (IBD). In particular, several studies have addressed its role in their pathogenesis, showing how the incidence of IBD significantly increased in recent years. Meanwhile, nutrition should be considered a component of the treatment of the disease, both as a therapy itself, and especially in the perspective of correcting the various nutritional deficiencies shown by these patients. In this perspective, nutritional suggestions are very important even in the most severe forms of IBD, requiring hospitalization or surgical treatment. Although current knowledge about nutrition in IBD is increasing over time, nutritional suggestions are often underestimated by clinicians. This narrative review is an update summary of current knowledge on nutritional suggestions in IBD, in order to address the impact of nutrition on pathogenesis, micro- and macro-nutrients deficiencies (especially in the case of sarcopenia and obesity), as well as in hospitalized patients.
... [8] Diets have emerged as an important and actionable modifier of IBD pathogenesis and activity. [9][10][11][12][13] Dietary patterns are consistently associated with pro-or anti-inflammatory features of gut bacteria. [14] However, whether specific food can lead to microbiome changes that influence gut inflammatory responses remains largely unknown. ...
Article
Scope We tested the hypothesis that dietary pomegranate extract (PomX) supplementation attenuates colitis in a Western diet fed IL-10 deficient (IL10-/-) murine model. Methods and Results 4 week old male IL-10-/- mice were randomly assigned to a high fat high sucrose (HFHS) diet or a HFHS diet supplemented with 0.25% PomX for 8 weeks. PomX supplementation led to significantly lower histological score for colitis (2.6±0.5 versus 3.9 ± 1.0), lower spleen weight (0.11±0.01 versus 0.15±0.02), and lower circulating IL6 levels (15.8±2.2 versus 29.5±5.5) compared with HFHS fed controls. RNAseq analysis of colonic tissues showed 483 downregulated and 263 upregulated genes with PomX supplementation, which were mainly associated with inflammatory responses, defenses, and neutrophil degranulation. In addition, PomX treatment affected the cecal microbiome with increased alpha diversity, altered microbial composition, and increased levels of the tryptophan-related microbial metabolite indole propionate. Conclusion Our data demonstrated that dietary PomX supplementation ameliorated colitis and lowered inflammatory markers in HFHS fed IL10-/- mice. These data support the anti-inflammatory effects of dietary PomX supplementation for IBD and a potential mediating role of gut microbiome, suggesting the need for future clinical studies to explore the use of PomX dietary supplementation in IBD patients. This article is protected by copyright. All rights reserved
... 12 Dietary antigens and their interaction with the gut microbiome are thought to play significant roles as potential environmental factors, although a causal relationship between diet and IBD development has not been established. 13 In particular, Westernization of diet has been implicated in IBD development, with the highest incidence and prevalence of disease in North America and Europe. 14 Vangay and colleagues demonstrated that migration from a non-Western to a Western country can cause pronounced shifts in the individual microbiome and that microbial diversity decreases with each generation of residence. ...
Article
Inflammatory bowel disease (IBD) consists of chronic, relapsing-remitting autoimmune diseases of the gastrointestinal (GI) tract with an increasing global disease burden. Pathogenetic mechanisms are not well understood, but current hypotheses involve the role of environmental factors, including dietary antigens, in immune dysregulation and proinflammatory shifts in microbial composition (gut dysbiosis) in genetically susceptible individuals. Increased metabolic demand and malabsorption secondary to systemic inflammation, coupled with significant GI symptoms that lead to reduced oral food intake, may leave patients with IBD vulnerable to developing malnutrition. The use of diet as therapy for potential induction or maintenance of remission in IBD has risen to prominence in the past several decades, especially as patients explore diet as a means to improve their symptoms and overall quality of life. However, these nutritional therapies remain underutilized by many gastroenterologists, and randomized controlled trials (RCTs) for most popular diets are lacking. Moreover, formal and consistent assessments of the nutritional status of patients with IBD in the inpatient and outpatient settings are often overlooked. To address these gaps, this article aims to discuss the progress of diet therapy and considerations for optimizing nutrition in patients with IBD, as well as summarize current RCTs evaluating efficacy for the most popular diets in IBD therapy.
... Although microbiota can be as simple as parasites that cling to nutrition from human host or "friendly" bacteria that colonize the gut to assist fermentation, the Westernized lifestyle has made harboring these "good" bacteria in the intestine more difficult. This lifestyle refers to inappropriate use of antibiotics [15], cesarean section [16], artificial milk [17], improved hygiene [18], high-fat and low-fiber diet [19], and stress [20], which all can cause dysbiosis. In particular, dietary fiber is an important nutrient for these probiotic bacteria [21], and the lack of dietary fiber intake in modern society is considered the primary cause of dysbiosis in the gut. ...
Article
Full-text available
The number of patients with inflammatory bowel disease is rapidly increasing in developed countries. The main cause of this increase is thought not to be genetic, but secondary to rapidly modernized environmental change. Changes in the environment have been detrimental to enteric probiotics useful for fermentation, inducing an increase in pathobionts that survive by means other than fermentation. This dysregulated microbiota composition, the so-called dysbiosis, is believed to have increased the incidence of inflammatory bowel disease. Bacteriotherapy, a treatment that prophylactically and therapeutically corrects the composition of disturbed intestinal microbiota, is a promising recent development. In fact, fecal microbiome transplantation for recurrent Clostridioides difficile infection in 2013 was a significant contribution for bacteriotherapy. In this paper, we comprehensively review bacteriotherapy in an easy-to-understand format.
... While inflammation in UC is characteristically described to involve both the colonic mucosal surface [Ordás et al., 2012] and the oral mucosa (in the form of aphthous stomatitis) [Dotson et al., 2010;Ordás et al., 2012] in CD, it retains a nonuniform transmural extension along any part of the gastrointestinal tract . The current paradigm of IBD pathogenesis comprises a combination of aberrant immune response, genetic susceptibility, gut dysbiosis, and environmental factors such as smoking, antibiotics, oral contraceptives, and diet [Abraham and Cho, 2009;Chapman-Kiddell et al., 2010]. The Westernization of lifestyle and diet, with considerably higher Marruganti/Discepoli/Gaeta/Franciosi/ Ferrari/Grandini Caries Res 2 DOI: 10.1159/000519170 intake of refined sugars, was appointed as a key factor in the escalating incidence of IBD across Europe and the rest of the world [Ooi et al., 2016]. ...
Article
Full-text available
Objective: The present review aimed to systematically evaluate the occurrence of caries in patients with inflammatory bowel disease (IBD), either Crohn's disease (CD) or ulcerative colitis (UC), compared to healthy controls. Materials and methods: MEDLINE (PubMed), Embase, Google Scholar, LILACS, and Cochrane Library electronic databases were screened. Caries experience was measured through the Decayed, Missing, Filled Teeth (DMFT) index. The weighted mean difference (WMD) with 95% confidence interval was calculated between IBD patients and healthy controls. Results: Six studies were selected for the inclusion in the systematic review, 5 of which were also included in the quantitative synthesis of data. The WMD in the DMFT index between IBD and healthy subjects was 3.04 (1.52, 4.56) (p = 0.10). Subgroup analysis showed no difference (p = 0.31) between CD (2.52 [0.54, 4.49]) and UC (4.01 [1.52, 4.56]) subjects. Conclusions: There is a remarkably higher past and present occurrence of dental caries in subjects with IBD than healthy controls. This result should encourage clinicians to include oral health preventive programs in the overall treatment plan of IBD patients.
... Diet is suspected to be an environmental factor involved in the etiology of IBD [5]. Experimental models show that diet may contribute to gut inflammation through several mechanisms including antigen presentation, alteration of gut permeability, and changes in the composition of the gut microbiota [5][6][7]. ...
Article
Full-text available
Scientific evidence shows that dietary patterns are associated with the risk of IBD, particularly among unhealthy and Western dietary patterns. However, Western dietary patterns are not exclusive to Western countries, as Jordanians are steadily moving towards a Western lifestyle, which includes an increased consumption of processed foods. This study aims to investigate the association between dietary patterns and the risk factors for IBD cases among Jordanian adults. This case-control study was conducted between November 2018 and December 2019 in the largest three hospitals in Jordan. Three hundred and thirty-five Jordanian adults aged between 18–68 years were enrolled in this study: one hundred and eighty-five IBD patients who were recently diagnosed with IBD (n = 100 for ulcerative colitis (UC) and n = 85 for Crohn’s disease (CD)) and 150 IBD-free controls. Participants were matched based on age and marital status. In addition, dietary data was collected from all participants using a validated food frequency questionnaire. Factor analysis and principal component analysis were used to determine the dietary patterns. Odds ratios (OR) and their 95% confidence interval (CI) were calculated using a multinomial logistic regression model. Two dietary patterns were identified among the study participants: high-vegetable and high-protein dietary patterns. There was a significantly higher risk of IBD with high-protein intake at the third and fourth quartiles in the non-adjusted model as well as the other two adjusted models. In contrast, the high-vegetable dietary pattern shows a significantly protective effect on IBD in the third and fourth quartiles in all the models. Thus, a high-vegetable dietary pattern may be protective against the risk of IBD, while a high-protein dietary pattern is associated with an increased risk of IBD among a group of the Jordanian population.
... 14 Among environmental factors, food is reported as a possible trigger of UC; mechanisms through which food seems to potentially induce intestinal inflammation include direct dietary antigens, changes in the gut microbiome, and effects on gastrointestinal permeability. 15 The present case, indeed, developed UC in the colon graft placed outside the gastrointestinal tract, therefore not exposed to food antigens and with a microflora likely different from the enteric one. This fact may be explained by the involvement of the neovagina as a consequence of a systemic autoimmune response of all colonic tissue to an exposure in the colon. ...
Article
Full-text available
The case of a toddler with long-channel cloaca, mild chronic kidney disease (CKD) due to renal dysplasia, and early onset of ulcerative colitis (UC) is herein reported. The patient underwent definitive repair of cloaca, that included vaginal elongation with colon, at 5 months of age and was admitted for episodes of vaginal bleeding at 22 months of age. A vaginoscopy revealed a severe inflammation of the colonic neovagina. As rectal bleeding was also noticed, she underwent a colonscopy that showed the same macroscopic inflammatory picture. Neovaginal and colonic biopsies confirmed UC. The mother turned out to be affected by UC since adolescence. The patient is now on oral therapy with mesalazine and topical steroid and mesalazine in the neovagina. The association between cloaca and inflammatory bowel disease (IBD) is anecdotal, but the family history of IBD should be considered when planning the surgical reconstruction of patients with cloaca. In this patient, the occurrence of UC may require a new neovagina in the future and the concomitance of CKD may complicate the overall management due to the potential nephrotoxicity of drugs used for UC therapy.
... Upon examining the "Western" diet, mechanisms such as insulin resistance, modification of intestinal permeability and the effect of sulfur compounds from protein have been identified A c c e p t e d M a n u s c r i p t as contributors to intestinal inflammation [15]. For example, increased intake of polyunsaturated fatty acids and animal fat has been linked to an increased incidence of UC and CD, and relapse in patients with UC [16][17][18][19]. ...
Article
Full-text available
Inflammatory bowel disease (IBD), Crohn’s disease and ulcerative colitis, cause inflammation of the digestive tract. It is estimated that about three million Americans and, globally, over six million individuals, suffer from IBD. While most physicians, especially gastroenterologists, are experts in the function and pathology of the gastrointestinal tract, factors such as nutrition science education and training, bandwidth, culture, language, and the longitudinal nature of dietary care, represent some of the barriers to receiving optimal nutritional guidance. Remote dietary expert counseling, an emerging solution that has been further highlighted by the COVID-19 pandemic, can improve IBD patients’ nutritional status, avoid food triggers, and reduce the frequency and severity of exacerbations.
... 42 Experimental models showed that diet contributed to gut inflammation through several mechanisms including antigen presentation, alteration of gut permeability, and changes in the composition of the gut microbiota. [42][43][44] The Mediterranean diet has long been accepted as an example of a well-balanced diet but a gold-standard "Mediterranean diet" is lacking. 45 At least 16 countries border the Mediterranean Sea, variation in Mediterranean diet among these countries as well as among regions within the same country is well known. ...
Article
Full-text available
Objective Many dietary and lifestyle factors are found to be associated with the pathogenesis of IBD. The purpose of this study is to review the dietary and lifestyle factors associated with IBD. In addition, too, this review attempts to investigate the association between dietary patterns and IBD risk and compare lifestyle factors among IBD patients. Methods Google Scholar and PubMed were searched together with relevant journals for Englishstudies from September 2018 to August 2020. The original studies which evaluated the lifestyle factors and dietary patterns as risk factors for inflammatory bowel disease were included. Results Several studies in IBD were discussed and highlighted the independent effects of various dietary and lifestyle factors on the risk of IBD. Forty-nine articles met the inclusion criteria and indicated that dietary factors tend to play a pivotal role in the disease etiopathogenesis and course. However, research on food and IBD is contradictory. Conclusion An excessive intake of sugar and animal fat is considered a risk factor for the development of IBD, whereas a high fiber diet and high intake of fruits and vegetables may play a protective effect. The role of lifestyle factors in IBD is crucial. Amply of evidence suggested that smoking is a causative agent in CD while it is protective against UC. Stress, depression, vitamin D deficiency, and impaired sleep have all been associated with incident IBD. A diet with a modified carbohydrate composition, a semi-vegetarian diet, a diet low in protein and fat, and a diet low in fermentable oligosaccharides, disaccharides, monosaccharides, and polyols should be taken into consideration for IBD patients.
... Besides, accurately capturing dietary intake comes with difficulties since there are potential interactions between nutrients and because it might be affected by the physical form of foods [16]. Therefore, it is not surprising that unambiguous dietary advice has not been developed yet [285,286]. ...
Article
Full-text available
Diet plays a pivotal role in the onset and course of inflammatory bowel disease (IBD). Patients are keen to know what to eat to reduce symptoms and flares, but dietary guidelines are lacking. To advice patients, an overview of the current evidence on food (group) level is needed. This narrative review studies the effects of food (groups) on the onset and course of IBD and if not available the effects in healthy subjects or animal and in vitro IBD models. Based on this evidence the Groningen anti-inflammatory diet (GrAID) was designed and compared on food (group) level to other existing IBD diets. Although on several foods conflicting results were found, this review provides patients a good overview. Based on this evidence, the GrAID consists of lean meat, eggs, fish, plain dairy (such as milk, yoghurt, kefir and hard cheeses), fruit, vegetables, legumes, wheat, coffee, tea and honey. Red meat, other dairy products and sugar should be limited. Canned and processed foods, alcohol and sweetened beverages should be avoided. This comprehensive review focuses on anti-inflammatory properties of foods providing IBD patients with the best evidence on which foods they should eat or avoid to reduce flares. This was used to design the GrAID.
... Dietary components and microbial imbalance may trigger inflammation. [6][7][8][9] Experimental and clinical data provide strong evidence of the role of bacterial microbiota in IBD and pro-inflammatory and anti-inflammatory taxa have been described. [10] Bacterial dysbiosis in mucosa and stool was reported as predictor in the diagnosis of IBD including CD but with conflicting results on the relative accuracy of different samples. ...
Article
Background: Studies have reached different conclusions regarding the accuracy of dysbiosis in predicting the diagnosis of Crohn's disease (CD). The aim of this report is to assess the utility of mucosal and fecal microbial dysbiosis as predictors in the diagnosis of this condition in Saudi children. Methods: Tissue and fecal samples were collected prospectively from children with final diagnosis of CD and from controls. Bacterial DNA was extracted and sequenced using Illumina MiSeq chemistry. The abundance and diversity of bacteria in tissue and fecal samples were determined in relation to controls. Sparse logistic regression was calculated to predict the diagnosis of CD based on subject's microbiota profile. Results: There were 17 children with CD and 18 controls. All children were Saudis. The median age was 13.9 and 16.3 years for children with CD and controls respectively. Sex distribution showed that 11/17 (65%) of the CD and 12/18 (67%) of the control subjects were boys. The mean area under the curve (AUC) was significantly higher in stool (AUC = 0.97 ± 0.029) than in tissue samples (AUC = 0.83 ±0.055) (P < 0.001). Conclusions: We found high AUC in mucosal and fecal samples. The higher AUC for fecal samples suggests higher accuracy in predicting the diagnosis of CD.
... In CEABAC10 transgenic mice, the Western diet, which is considered a risk factor for CD development [13], increases AIEC capacity to colonize the gut mucosa, and then to trigger inflammation [14,15]. The Western diet is poor in fibers and rich in total fat, especially saturated fatty acids and n-6 polyunsaturated fatty acids (PUFAs), and in refined sugars and animal proteins. ...
Article
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The Western diet, rich in lipids and in n-6 polyunsaturated fatty acids (PUFAs), favors gut dysbiosis observed in Crohn's disease (CD). The aim of this study was to assess the effects of re-balancing the n-6/n-3 PUFA ratio in CEABAC10 transgenic mice that mimic CD. Mice in individual cages with running wheels were randomized in three diet groups for 12 weeks: high-fat diet (HFD), HFD + linseed oil (HFD-LS-O) and HFD + extruded linseed (HFD-LS-E). Then, they were orally challenged once with the Adherent-Invasive Escherichia coli (AIEC) LF82 pathobiont. After 12 weeks of diet, total energy intake, body composition, and intestinal permeability were not different between groups. After the AIEC-induced intestinal inflammation, fecal lipocalin-2 concentration was lower at day 6 in n-3 PUFAs supplementation groups (HFD-LS-O and HFD-LS-E) compared to HFD. Analysis of the mucosa-associated microbiota showed that the abundance of Prevotella, Para-prevotella, Ruminococcus, and Clostridiales was higher in the HFD-LS-E group. Butyrate levels were higher in the HFD-LS-E group and correlated with the Firmicutes/Proteobacteria ratio. This study demonstrates that extruded linseed supplementation had a beneficial health effect in a physically active mouse model of CD susceptibility. Additional studies are required to better decipher the matrix influence in the linseed supplementation effect. Citation: Plissonneau, C.; Sivignon, A.; Chassaing, B.; Capel, F.; Martin, V.; Etienne, M.; Wawrzyniak, I.; Chausse, P.; Dutheil, F.; Mairesse, G.; et al. Beneficial Effects of Linseed Supplementation on Gut Mucosa-Associated Microbiota in a Physically Active Mouse Model of Crohn's Disease. Int. J. Mol. Sci. 2022, 23, 5891. https://doi.org/10.3390/ ijms23115891 Academic Editors: Massimiliano Gasparrini and Luca Mazzoni
... Western diet, rich in sugar, animal proteins, and polyunsaturated fatty acids (PUFAs), might predispose to IBD [53][54][55][56]. Several studies have shown that the Western diet promotes intestinal inflammation via modulation of barrier integrity and the gut microbiome, resulting in altered gut homeostasis [53,[57][58][59][60][61][62][63]. A high-sugar diet affected the intestinal epithelial integrity in mice, increased their susceptibility to dextran sodium sulfate (DSS)-induced colitis, and altered their gut microbiome [64]. ...
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Nano- and microparticles are an implicit part of the human diet. They are unknowingly ingested with our food that contains them as additives or pollutants. However, their impact on human health is not yet understood and controversially discussed. The intestinal epithelial barrier shields our body against exogenous influences, such as commensal bacteria, pathogens, and body-foreign particles and, therefore, protects our body integrity. Breakdown of the intestinal epithelial barrier and aberrant immune responses are key events in the pathogenesis of inflammatory bowel disease (IBD). Epithelial lesions might enable systemic translocation of nano- and microparticles into the system, eventually triggering an excessive immune response. Thus, IBD patients could be particularly vulnerable to adverse health effects caused by the ingestion of synthetic particles with food. The food-additive titanium dioxide (TiO2) serves as a coloring agent in food products and is omnipresent in the Western diet. TiO2 nanoparticles exacerbate intestinal inflammation by activation of innate and adaptive immune response. Because of serious safety concerns, the use of TiO2 as a food additive was recently banned from food production within the European Union. Due to environmental pollution, plastic has entered the human food chain, and plastic microparticles have been evidenced in the drinking water and comestible goods. The impact of plastic ingestion and its resulting consequences on human health is currently the subject of intense research. Focusing on TiO2 and plastic particles in the human diet and their impact on epithelial integrity, gut homeostasis, and intestinal inflammation, this review is addressing contemporary hot topics which are currently attracting a lot of public attention.
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Background/aims: It is unclear whether IgG4-related immune responses to food can play a role in the pathogenesis of inflammatory bowel disease (IBD). The aim of the present study was to investigate the serum levels of IgG4 to common food antigens in patients with ulcerative colitis (UC), Crohn's disease (CD), and healthy controls. Materials and methods: Thirty-six patients with CD (n=12) or UC (n=24) and 36 sex- and age-matched healthy individuals (mean age, 49 years) participated in the study. Serum levels of IgG4 to 90 common food antigens were measured. The number of subjects with positivity, defined by cut-off values ≥0.7 U/mL, was compared. Results: Serum titers of IgG4 to salmon, onion, shrimp, cuttlefish, eel, millet, gluten, soybean, and coconut in patients with IBD were significantly or tended to be higher than those in the control group. Serum levels of IgG4 to salmon, millet, and onion in patients with CD were significantly or tended to be higher than those in the control group. Serum titers of IgG4 to cuttlefish and onion in patients with UC tended to be higher than those in the control group. The number of subjects with positivity to cod, tuna, mackerel, oat, pea, peanut, and coconut was significantly higher in patients with CD than in healthy controls. The number of subjects with positivity to kiwi and cuttlefish was significantly higher in patients with UC than in controls. Conclusion: Patients with IBD shows higher serum levels of IgG4 to diverse food antigens. Patients with CD present IgG4-related immune reactions to more foods than patients with UC.
Article
Strawberry (Fragaria chiloensis) is a major edible berry with various potential health benefits. This study determined the protective effects of whole strawberry (WS) against dextran sulfate sodium (DSS)-induced colitis in mice. In colitic mice, dietary WS reduced the disease activity index (DAI), prevented the colon shortening and spleen enlargement, and alleviated the colonic tissue damages. The abundance of pro-inflammatory immune cells was reduced by dietary WS in the colonic mucosa, which was accompanied by the suppression of overproduction of pro-inflammatory cytokines. Western blotting and immunohistochemical analysis revealed that dietary WS decreased the expression of pro-inflammatory proteins in the colonic mucosa. Moreover, dietary WS partially reversed the alteration of gut microbiota in the colitic mice by increasing the abundance of potential beneficial bacteria, e.g. Bifidobacterium and Lactobacillus, and decreasing the abundance of potential harmful bacteria, e.g. Dorea and Bilophila. Dietary WS also restored the decreased production of short chain fatty acids (SCFAs) in the cecum of the colitic mice. The results revealed the anti-inflammatory effects and mechanisms of dietary WS in the colon, which is critical for the rational utilization of strawberry for the prevention of inflammation-driven diseases.
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Background: Inflammatory bowel disease (IBD), 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. Diet has been hypothesised to influence IBD activity. Objectives: To evaluate the efficacy and safety of dietary interventions on IBD outcomes. Search methods: We searched the Cochrane IBD Group Specialized Register, CENTRAL, MEDLINE, Embase, Web of Science, Clinicaltrials.gov and the WHO ICTRP from inception to 31 January 2019. We also scanned reference lists of included studies, relevant reviews and guidelines. Selection criteria: We included randomized controlled trials (RCTs) that compared the effects of dietary manipulations to other diets in participants with IBD. Studies that exclusively focused on enteral nutrition, oral nutrient supplementation, medical foods, probiotics, and parenteral nutrition were excluded. Data collection and analysis: Two review authors independently performed study selection, extracted data and assessed bias using the risk of bias tool. We conducted meta-analyses where possible using a random-effects model and calculated the risk ratio (RR) and corresponding 95% confidence interval (CI) for dichotomous outcomes. We assessed the certainty of evidence using GRADE. Main results: The review included 18 RCTs with 1878 participants. The studies assessed different dietary interventions for active CD (six studies), inactive CD (seven studies), active UC (one study) and inactive UC (four studies). Dietary interventions involved either the consumption of low amounts or complete exclusion of one or more food groups known to trigger IBD symptoms. There was limited scope for data pooling as the interventions and control diets were diverse. The studies were mostly inadequately powered. Fourteen studies were rated as high risk of bias. The other studies were rated as unclear risk of bias.The effect of high fiber, low refined carbohydrates, low microparticle diet, low calcium diet, symptoms-guided diet and highly restricted organic diet on clinical remission in active CD is uncertain. At 4 weeks, remission was induced in: 100% (4/4) of participants in the low refined carbohydrates diet group compared to 0% (0/3) of participants in the control group (RR 7.20, 95% CI 0.53 to 97.83; 7 participants; 1 study; very low certainty evidence). At 16 weeks, 44% (23/52) of participants in the low microparticle diet achieved clinical remission compared to 25% (13/51) of control-group participants (RR 3.13, 95% CI 0.22 to 43.84; 103 participants; 2 studies; I² = 73%; very low certainty evidence). Fifty per cent (16/32) of participants in the symptoms-guided diet group achieved clinical remission compared to 0% (0/19) of control group participants (RR 20.00, 95% CI 1.27 to 315.40; 51 participants ; 1 study; very low certainty evidence) (follow-up unclear). At 24 weeks, 50% (4/8) of participants in the highly restricted organic diet achieved clinical remission compared to 50% (5/10) of participants in the control group (RR 1.00, 95% CI 0.39 to 2.53; 18 participants; 1 study; very low certainty evidence). At 16 weeks, 37% (16/43) participants following a low calcium diet achieved clinical remission compared to 30% (12/40) in the control group (RR 1.24, 95% CI 0.67 to 2.29; 83 participants; 1 study; very low certainty evidence).The effect of low refined carbohydrate diets, symptoms-guided diets and low red processed meat diets on relapse in inactive CD is uncertain. At 12 to 24 months, 67% (176/264) of participants in low refined carbohydrate diet relapsed compared to 64% (193/303) in the control group (RR 1.04, 95% CI 0.87 to 1.25; 567 participants; 3 studies; I² = 35%; low certainty evidence). At 6 to 24 months, 48% (24/50) of participants in the symptoms-guided diet group relapsed compared to 83% (40/48) participants in the control diet (RR 0.53, 95% CI 0.28 to 1.01; 98 participants ; 2 studies; I² = 54%; low certainty evidence). At 48 weeks, 66% (63/96) of participants in the low red and processed meat diet group relapsed compared to 63% (75/118) of the control group (RR 1.03, 95% CI 0.85 to 1.26; 214 participants; 1 study; low certainty evidence). At 12 months, 0% (0/16) of participants on an exclusion diet comprised of low disaccharides / grains / saturated fats / red and processed meat experienced clinical relapse compared to 26% (10/38) of participants on a control group (RR 0.11, 95% CI 0.01 to 1.76; 54 participants; 1 study; very low certainty evidence).The effect of a symptoms-guided diet on clinical remission in active UC is uncertain. At six weeks, 36% (4/11) of symptoms-guided diet participants achieved remission compared to 0% (0/10) of usual diet participants (RR 8.25, 95% CI 0.50 to 136.33; 21 participants; 1 study; very low certainty evidence).The effect of the Alberta-based anti-inflammatory diet, the Carrageenan-free diet or milk-free diet on relapse rates in inactive UC is uncertain. At 6 months, 36% (5/14) of participants in the Alberta-based anti-inflammatory diet group relapsed compared to 29% (4/14) of participants in the control group (RR 1.25, 95% CI 0.42 to 3.70; 28 participants; 1 study; very low certainty evidence). Thirty per cent (3/10) of participants following the carrageenan-free diet for 12 months relapsed compared to 60% (3/5) of the participants in the control group (RR 0.50, 95% CI 0.15 to 1.64; 15 participants; 1 study; very low certainty evidence). At 12 months, 59% (23/39) of milk free diet participants relapsed compared to 68% (26/38) of control diet participants (RR 0.83, 95% CI 0.60 to 1.15; 77 participants; 2 studies; I² = 0%; low certainty evidence).None of the included studies reported on diet-related adverse events. Authors' conclusions: The effects of dietary interventions on CD and UC are uncertain. Thus no firm conclusions regarding the benefits and harms of dietary interventions in CD and UC can be drawn. There is need for consensus on the composition of dietary interventions in IBD and more RCTs are required to evaluate these interventions. Currently, there are at least five ongoing studies (estimated enrollment of 498 participants). This review will be updated when the results of these studies are available.
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Ulcerative colitis (UC) is a complex chronic, immune-mediated inflammatory disorder of the colon. Factors associated with increased risk of UC include diet, particularly Western diet influences in newly industrialized nations, medications, and lifestyle factors that may influence the host's microbiome or immune response to antigens. Although much evidence identifying potential genetic and host-related factors is currently available, there are still many unanswered questions. As the global UC incidence and prevalence continues to increase, there are multiple opportunities for continued investigation to clarify our understanding of UC, identify potential predictors of disease severity, response to therapy, and novel therapeutic targets.
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Background: Inflammatory bowel diseases (IBDs) are chronic gastrointestinal diseases that negatively affect the enjoyment of food and engagement in social and cultural gatherings. Such experiences may promote psychosocial challenges, an aspect of IBD often overlooked and under-supported in clinical settings and research. Objectives: This study explored the psychosocial experiences that young adults with IBD have with food via a qualitative patient-led research process. Methods: Trained patient researchers conducted this study by engaging peers via semi-structured interviews and focus groups in a three-step co-design process. Participants (n = 9) identified the research topic (SET), explored the topic and identified emerging themes (COLLECT), refined themes and made recommendations for healthcare system change (REFLECT). Results: Themes that emerged included: 'Experimenting with Food', 'Evolution Over Time', 'Diet Changes are Emotional' and 'Role of Stigma'. Participants identified the significance and frustrations of repeated testing and experimenting with food compatibility, and noted nuances in food relationships as they gain knowledge and experience over time. They emphasized the importance of maintaining a sense of hope throughout and wished to impart this to newly diagnosed patients. Conclusion: Participants experience numerous psychosocial challenges as they strive to manage their diet, noting gaps in support available from IBD practitioners. Participants made practical recommendations for healthcare system change to improve patient outcomes, highlighting the importance of sharing stories and collaboratively including patients in the development of new services and protocols. Authors recommend further research in this area to build a body of knowledge and support that helps IBD patients maintain hope while navigating challenges with food. Patient or public contribution: The first four authors on this paper were the lead researchers in this study's design and analysis and identify as patients; they conducted the research with this identity at the forefront following a peer-to-peer research model. These authors were mentored by patient researchers who also contributed to the manuscript, and the research process itself was co-lead and directed by other patient participants and consultants. Results and recommendations coming from this paper came directly from patient participants.
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Inflammatory bowel disease (IBD) is a chronic recurring inflammation of the intestine which can be debilitating for those with intractable disease. However, the etiopathogenesis of inflammatory bowel disorders remains to be solved. The hypothesis that mitochondrial dysfunction is a crucial factor in the disease process is being validated by an increasing number of recent studies. Thus mitochondrial alteration in conjunction with previously identified genetic predisposition, changes in the immune response, altered gut microbiota, and environmental factors (eg, diet, smoking, and lifestyle) are all posited to contribute to IBD. The implicated factors seem to affect mitochondrial function or are influenced by mitochondrial dysfunction, which explains many of the hallmarks of the disease. This review summarizes the results of studies reporting links between mitochondria and IBD that were available on PubMed through March 2021. The aim of this review is to give an overview of the current understanding of the role of mitochondria in the pathogenesis of IBD.
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Background and aim: Peyer's patches (PPs) play a major role in intestinal mucosal immunity; however, their role in ulcerative colitis (UC) is not well investigated. We evaluated endoscopic features of PPs on narrow-band imaging with magnifying endoscopy (NBI-ME) and investigated their association with clinical factors. Methods: We prospectively recruited 105 patients with UC, 18 with Crohn's disease (CD), 16 with disease control (DC), and 33 healthy control (HC) subjects at 3 institutions from 2014 to 2017. NBI-ME images of the villi of PPs were evaluated according to the Villi Index, and patients were divided into the Villi Index low (L-) and high (H-) types. The 1-year sustained clinical remission rate was evaluated between L- and H-type PPs in patients with UC. Results: The proportions of patients with H-type PPs were significantly higher among UC, CD, and DC patients than among HC patients (P = 0.0125, 0.018, 0.0007). In UC, age, gender, endoscopic score, and extent of disease involvement were not significantly different between L- and H-type PPs, whereas the sustained clinical remission rate was significantly higher in L-type PPs than in H-type PPs (88% [57/65] vs. 65% [17/26], P = 0.019). Multivariate analysis revealed that the L-type of PPs was a significant factor for sustained clinical remission (odds ratio 3.8, 95% confidence interval 1.1-12.9, P = 0.033). Conclusions: Patients with UC showed endoscopic alterations in PPs on NBI-ME, and highly altered appearance of PPs can be associated with a high risk of clinical relapse in patients with UC.
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The purpose of this review is to combine evidence from studies based on environmental impacts on inflammatory bowel disease. The review reflects the environmental factors influencing the incidence of IBD, and also considers the predictors that modify the course of the diseases.
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Extra virgin olive oil (EVOO) is often associated with anti-inflammatory and antioxidant properties. Its effects on inflammatory conditions such as Ulcerative Colitis (UC) however has yet to be defined. As such, we aimed to conduct a systematic review and meta-analysis of studies investigating olive-based interventions in UC. A comprehensive database search for randomized controlled trials was performed between 9 th July 2018 and 16 th August 2018. Studies identified from search alerts were included up to the 22 nd of June 2020. Both individuals living with UC at any disease stage and murine models of UC were included in this review. No human trials meeting the eligibility criteria were identified, while nineteen animal studies comprised of 849 murine models of UC were included in this review. Pooling of the data could not be performed due to heterogeneous outcomes, however general trends favouring olive-based interventions were identified. Milder disease expression including weight maintenance, reduced rectal bleeding and well-formed stools favouring olive-based interventions was statistically significant in 16/19 studies, with moderate-to-large effect sizes (ESs −0.66 (95% CI −1.56, 0.24) to −12.70 (95% CI −16.8, −8.7)). Olive-based interventions did not prevent the development of colitis-like pathologies in any study. In conclusion, effects of olive-based interventions on murine models of UC appear promising, with milder disease outcomes favouring the intervention in most trials and effect sizes suggesting potential clinical relevance. However, the lack of published randomized controlled human trials warrants further investigation to determine if these effects would translate to individuals living with UC.
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Hospitalizations are a time when providers often have uncertainty about what to feed patients with inflammatory bowel disease (IBD). While there are many trials evaluating the role of diet in the management of IBD, the role of diet for the hospitalized patient is less clear. The hospitalization may serve as an opportunity to educate patients about the role of diet, try different diets, and develop dietary recommendations for after discharge. Here, we review the literature for dietary considerations during hospitalizations and acute settings, as well as upon discharge. Patients with IBD benefit from screening and nutritional support for malnutrition and nutritional deficiencies. Enteral nutrition and exclusion diets are promising as induction and maintenance therapies, but no specific recommendations during hospitalization for adult patients are available currently. There are very few reasons to enforce bowel rest or clear liquids other than bowel obstruction, uncontrolled sepsis, or need for urgent or emergent surgery; most patients – including many with penetrating or stricturing disease - benefit from feeding in whichever capacity is tolerated, with enteral and parenteral nutrition used as needed to reach nutritional goals. Future studies are needed to define how the use of different diets can influence the outcomes of patients hospitalized for IBD.
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Adherent-invasive Escherichia coli (AIEC) is an opportunistic pathogen associated with major inflammatory bowel disease, Crohn disease, and ulcerative colitis. Unfavorable conditions push commensal AIEC to induce gut inflammation, sometimes progressing to inflammation-induced colon cancer. Recently, zebrafish have emerged as a useful model to study human intestinal pathogens. Here, a zebrafish model to study AIEC infection was developed. Bath inoculation with AIEC resulted in colonization and tissue disruption in the zebrafish intestine. Gene expression of pro-inflammatory markers including interleukin-1β (IL-1β), tumor necrosis factor alpha (TNFα), interferon-γ (IFNγ), and S100A-10b (akin to human calprotectin) in the zebrafish intestine was significantly induced by AIEC infection. The probiotic E. coli Nissle 1917 (EcN) was tested as a therapeutic and prophylactic against AIEC infection and reduced AIEC colonization, tissue damage, and pro-inflammatory responses in zebrafish. Furthermore, EcN diminished the propionic-acid-augmented hyperinfection of AIEC in zebrafish. Thus, this study shows the efficacy of EcN against AIEC in an AIEC-zebrafish model.
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A high salt diet (HSD) is often associated with a high risk for a variety of diseases, such as obesity and cardiovascular disease. Previous studies have demonstrated that an HSD enhances Th17 responses and increases the severity of autoimmune diseases. In this study, we investigated the effects of HSD (4% NaCl w/w) on colitis in IL-10-/- mice by comparing it with IL-10-/- mice on a normal salt diet (NSD, 1% NaCl w/w). The colonic epithelial barrier integrity in IL-10-/- mice, as well as differentiated Caco-2 cells exposed to high NaCl and proinflammatory cytokines, was also evaluated. Surprisingly, an HSD significantly ameliorated macroscopic colitis, improved the intestinal permeability of FITC-dextran, and decreased multiple proinflammatory cytokines in the colonic mucosa of IL-10-/- mice. While occludin and claudin-1, two major tight-junction proteins, were markedly down-regulated in IL-10-/- mice, HSD effectively restored their expressions. In Caco-2 cells, proinflammatory cytokines (TNF-α and IL-1β) potently decreased the expression of occludin and claudin-1 regardless of salt conditions [0.9% (standard), 1.2%, or 1.5% NaCl]. Under high salt conditions (1.5% NaCl), transepithelial electrical resistance (TEER) was elevated, while the addition of IL-10 further downregulated occludin and claudin-1 expressions by ~50% and lowered TEER. These findings suggest that, in the absence of IL-10, HSD promotes intestinal epithelial integrity and exerts an anti-inflammatory role as demonstrated by alleviated colitis in IL-10-/- mice. Moreover, Caco-2 data indicate that, in an inflammatory environment and under high NaCl conditions, IL-10 may play a proinflammatory role by disrupting colonic epithelial integrity and thus further promoting inflammation.
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Dietary microparticles are non-biological, bacterial-sized particles. Endogenous sources are derived from intestinal Ca and phosphate secretion. Exogenous sources are mainly titanium dioxide (TiO2) and mixed silicates (Psil); they are resistant to degradation and accumulate in human Peyer's patch macrophages and there is some evidence that they exacerbate inflammation in Crohn's disease (CD). However, whether their intake differs between those with and without CD has not been studied. We aimed to identify dietary microparticle sources and intakes in subjects with and without CD. Patients with inactive CD and matched general practice-based controls (ninety-one per group) completed 7d food diaries. Intake data for dietary fibre and sucrose were compared as positive controls. All foods, pharmaceuticals and toothpastes were examined for microparticle content, and intakes of Ca and exogenous microparticles were compared between the two groups. Dietary intakes were significantly different between cases and controls for dietary fibre (12 (SD 5) v. 14 (sd 5) g/d; P=0.001) and sucrose (52 (sd 27) v. 45 (sd 18) g/d; P=0·04) but not for Ca. Estimated median TiO2 and Psil intakes (2·5 and 35mg/individual per d respectively, totalling 1012–1013 microparticles/individual per d) were broadly similar to per capita estimates and while there was wide variation in intakes between individuals there was no significant difference between subjects with CD and controls. Hence, if exposure to microparticles is associated with the inflammation of CD, then the present study rules out excess intake as the problem. Nonetheless, microparticle-containing foods have now been identified which allows a low-microparticle diet to be further assessed in CD.
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Inflammatory bowel disease has become more common in developed countries this century. Mayberry et al reported incidences of Crohn’s disease in Wales of 0.18 cases/105/year in the 1930s and 5.95 cases/105/year in the 1970s.1 We investigated the prevalence of inflammatory bowel disease at age 26 years in a nationally representative birth cohort. Associations of sex and social class with risk of the disease have previously been shown,1–3 and these were also investigated.
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Thirty-two patients with Crohn's disease were treated with a fibre-rich, unrefined-carbohydrate diet in addition to conventional management and followed for a mean of four years and four months. Their clinical course was compared retrospectively with that of 32 matched patients who had received no dietary instruction. Hospital admissions were significantly fewer and shorter in the diet-treated patients, who spent a total of 111 days in hospital compared with 533 days in the non-diet-treated control group. Whereas five of the controls required intestinal operation, only one diet-treated patient needed surgery. This is in strong contrast to general experience with this disease. Treatment with a fibre-rich, unrefined-carbohydrate diet appears to have a favourable effect on the course of Crohn's disease and does not lead to intestinal obstruction.
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Thirty newly diagnosed patients with Crohn's disease were interviewed about their habitual, pre-illness diet and compared with 30 healthy controls, matched for age, sex, social class, and marital status. The patients ate substantially more refined sugar, slightly less dietary fibre, and considerably less raw fruit and vegetables than the controls. A diet high in refined sugar and low in raw fruit and vegetables precedes and may favour the development of Crohn's disease.
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The 1-day food intakes of 1,338 women, aged 19 to 50, who were respondents in the 1985 Continuing Survey of Food Intake by Individuals, were studied. The energy, nutrient, and food intake patterns of smokers, those how had quit smoking, and those who had never smoked cigarettes were compared. Mean energy intakes of smokers (1,627 kcal), those who had never smoked (1,620 kcal), and those who had quit at least 1 year before the interview (1,719 kcal) were not significantly different. Self-reported body weight was significantly different between never-smokers and smokers (p less than .01) and quitters (p less than .05) only for the oldest category of women (ages 41 to 50 years). The consumption of fruits (p less than .001) and vegetables (p less than .01) was significantly lower and the intake of eggs (p less than .01), sugars (p less than .001), regular carbonated soft drinks (p less than .01), coffee (p less than .001), and alcoholic beverages (p less than .001) was significantly higher for women smokers than for non-smokers. After controlling through regression analysis for physical activity, health status, and demographic characteristics, we found that smokers, compared with never-smokers, had significantly lower protein (p less than .04), dietary fiber (p less than .001), vitamin C (p less than .001), and thiamin (p less than .01) intakes and higher cholesterol (p less than .02) intakes per 1,000 kcal.
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Previous studies have consistently found strong positive associations between refined sugar intake and Crohn's disease (CD) and recently between smoking and CD. As refined sugar intake and smoking are themselves associated we have enquired about smoking and added sugar intake (AS) and smoking in CD using a postal questionnaire sent to 104 CD patients and 153 community controls. Smoking and AS were associated with one another. After adjusting for AS, smoking showed a significant association with CD with a relative risk of 1.8. After adjusting for smoking habit, AS was also strongly associated with CD in never and exsmokers and in a dose response pattern, with the relative risks for no AS, less than 50 g/day and greater than 50 g/day being respectively 1.0, 1.8, and 4.6 (chi 2 = 12.1; p less than 0.005). No association between CD and AS was evident in smokers. The AS relationship was supported by a separate association between frequency of confectionery consumption and CD. These findings indicate that while smoking and AS are individually associated with CD combined exposure results in no further increase in risk, suggesting that they may operate through a common mechanism.
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A population case controlled study of smoking habits at the time of diagnosis was done in 260 patients with ulcerative colitis and 144 with Crohn's disease. Smokers had a decreased risk of acquiring ulcerative colitis in comparison with never smokers (relative risk 0.7) which appeared to be dose dependent. In former smokers a rebound effect was seen, especially in former heavy smokers, where the risk was sharply increased (relative risk 4.4). No sex difference was recorded. Smoking doubled the risk of acquiring Crohn's disease without any dose dependent pattern. In former smokers a non-significantly increased risk was observed. This might be caused by a carry over effect after stopping smoking, however, which possibly is reduced by time. No sex difference was seen.
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Previous studies have suggested that an association exists between smoking habit and both ulcerative colitis and Crohn's disease. We reported studies of the diets before illness of patients who developed both types of inflammatory bowel disease. The patients who developed Crohn's disease had a high intake of refined sugar and a low intake of fibre from fruit. We now report the smoking behaviour of these patients and relate it to their dietary habits.
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Sera from patients with ulcerative colitis (51), Crohn's disease (30), hypolactasia (13), untreated adult coeliac disease (11), irritable colon syndrome (24), and sera from 38 healthy control subjects were tested for antibodies to the principal cow's milk proteins-casein, alpha-lactalbumin, and beta-lactoglobulin. The red-cell-linked antigen-antiglobulin reaction was used to determine the titres of direct agglutinating antibodies and IgA and IgG incomplete antibodies. Apart from patients with coeliac disease, direct agglutinating antibodies were found infrequently and then in low titres. Approximately 50% of subjects had low titres of IgA and IgG antibodies. However, the titres found in sera from patients with ulcerative colitis did not differ from those found in the control subjects or in patients with Crohn's disease, hypolactasia, or irritable colon syndrome. Patients with untreated coeliac disease frequently had high antibody titres to the milk proteins. In all subjects tested, incomplete antibodies of IgA or IgG immunoglobulin class occurred with equal frequency. The frequent occurrence in adults of low titres of antibodies to the milk proteins may be due to continued absorption of minute amounts of protein. Absorption of allergens may be facilitated by mucosal damage, such as that of coeliac disease, with stimulation of antibody production. At the present time, however, there is little evidence to suggest that milk allergy is a factor in the aetiology of ulcerative colitis.
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The mean daily intake of dietary fiber, sugar, starch, fat, protein, and total energy was determined in 35 patients with Crohn's disease and 70 normal controls by obtaining individual dietary histories. For each patient with Crohn's disease there were two controls, matched for age, sex, and socioeconomic background. In the patients with Crohn's disease the mean dietary fiber intake was established as 26.6 ± 1.4 g/day, compared to 22.3 ± 0.9 g/day in the controls, and was thus significantly higher (P < 0.05). When compared with the controls, the patients with Crohn's disease also exhibited a significantly higher consumption of sugar (156 ± 14 versus 91 ± 5 g/day (P < 0.001)), starch (211 ± 10 versus 170 ± 9 g/day (P < 0.01)), and total energy ( 14.4 < 0.7 versus 12.3 ± 0.5 MJ/day (P < 0.01)).
Chapter
This chapter provides an overview of nutritional epidemiology for those unfamiliar with the field. The field of nutritional epidemiology developed from an interest in the concept that aspects of diet may influence the occurrence of human disease. Although it is relatively new as a formal area of research, investigators have used basic epidemiologic methods for more than 200 years to identify numerous essential nutrients. The most serious challenge to research in nutritional epidemiology has been the development of practical methods to measure diet. Because epidemiologic studies usually involve at least several hundred and sometimes hundreds of thousands of subjects, dietary assessment methods must be not only reasonably accurate but also relatively inexpensive. Epidemiologic approaches to diet and disease and the interpretation of epidemiologic data are discussed.
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A multisite, hospital-based, case-control study examined the risk of ulcerative colitis in relation to dietary factors, smoking and drinking habits, past history of diseases, and childhood factors. Information was obtained from self-administered patient questionnaires. Study subjects included 101 ulcerative colitis patients who were 10-39 years old at the time of disease onset, which was within the previous 3 years, and 143 control subjects. Combined consumption of Western foods (bread for breakfast, butter, margarine, cheese, meats, and ham and sausage) was significantly related to an increased risk of ulcerative colitis (trend, p = 0.04). Margarine (as an individual Western food item) was positively associated with ulcerative colitis (trend, p = 0.005). There was also a tendency toward positive association of bread for breakfast with ulcerative colitis (trend, p = 0.07). The risk did not measurably vary with the consumption of typical Japanese foods, vegetables and fruits, confectioneries, or soft drinks. As compared with lifelong nonsmokers, current smokers tended to have a decreased risk of ulcerative colitis and former smokers had an increased risk. There was no association between breastfeeding in infancy and the risk of ulcerative colitis.
Article
Recent data have revealed that the plasma concentration of inflammatory mediators, such as tumour necrosis factor-α (TNF-α) and interleukin-6 (IL-6), is increased in the insulin resistant states of obesity and type 2 diabetes, raising questions about the mechanisms underlying inflammation in these two conditions. It is also intriguing that an increase in inflammatory mediators or indices predicts the future development of obesity and diabetes. Two mechanisms might be involved in the pathogenesis of inflammation. Firstly, glucose and macronutrient intake causes oxidative stress and inflammatory changes. Chronic overnutrition (obesity) might thus be a proinflammatory state with oxidative stress. Secondly, the increased concentrations of TNF-α and IL-6, associated with obesity and type 2 diabetes, might interfere with insulin action by suppressing insulin signal transduction. This might interfere with the anti-inflammatory effect of insulin, which in turn might promote inflammation.
Article
The human large intestine contains a microbiota, the components of which are generically complex and metabolically diverse. Its primary function is to salvage energy from carbohydrate not digested in the upper gut. This is achieved through fermentation and absorption of the major products, short chain fatty acids (SCFA), which represent 40-50% of the available energy of the carbohydrate. The principal SCFA, acetate, propionate and butyrate, are metabolized by the colonic epithelium (butyrate), liver (propionate) and muscle (acetate). Intestinal bacteria also have a role in the synthesis of vitamins B and K and the metabolism of bile acids, other sterols and xenobiotics.
Article
A constant relationship between certain Summary diseases in different geographical areas or in different socio-economic groups suggests some related ætiological factor. Benign and malignant lesions of the large bowel which show such a relationship are examined, and it is suggested that there is epidemiological and other evidence to incriminate low-residue diet as a major ætiological factor.
Article
Patients with Crohn’s disease show an increased consumption of refined sugar compared to controls. It was speculated that the frequent occurrence of Crohn’s disease in developed countries might be related to a high intake of refined sugar. In contrast, others suggested margarine consumption to play a role in the etiology of Crohn’s disease, the hypothesis being based on the seemingly simultaneous onset of margarine consumption and the first reports of granulomatous ileitis and the similarities in their geographic distribution. Both hypotheses, however, have not been subjected to a rigorous epidemiologic analysis. In the present study, the per capita consumption of refined sugar and margarine were correlated with the incidence and mortality of Crohn’s disease from different countries. The time trends of mortality from Crohn’s disease were compared to those of sugar and margarine intake. Two weak correlations were found between the geographic distribution of sugar and margarine consumption and mortality from Crohn’s disease, the correlations resulting from the difference between two types of countries. Compared to Canada, the United States and most countries from Northern Europe on one side, Japan and most Mediterranean countries on the other side were characterized by low consumption of the two nutrients as well as low mortality from Crohn’s disease. No consistent pattern was found, however, within each group of countries. No significant correlation was found between sugar or margarine consumption and the incidence of Crohn’s disease. The time trends of Crohn’s disease in different countries were not matched by similar time trends of either sugar or margarine consumption. The different epidemiologic behavior of the two nutrients and Crohn’s disease indicates that variations in their dietary intake were not responsible for the geographic and temporal patterns of Crohn’s disease. Other factors must be sought to explain the characteristic epidemiology of Crohn’s disease.Copyright © 1988 S. Karger AG, Basel
Book
This book is intended to increase understanding of the complex relationships between diet and the major diseases of western civilization, such as cancer and atherosclerosis. The book starts with an overview of research strategies in nutritional epidemiology-a relatively new discipline which combines the knowledge compiled by nutritionists during this century with the methodology developed by epidemiologists to study the determinants of disease with multiple etiologies and long latent periods. A major part of the book is devoted to methods of dietary assessment using data on food intake, biochemical indicators of diet, and measures of body size and composition. The reproducibility and validity of each approach and the implications of measurement error are considered in detail. The analysis, presentation, and interpretation of data from epidemiologic studies of diet and disease are discussed. Particular attention is paid to the important influence of total energy intake on findings in such studies. As examples of methodologic issues in nutritional epidemiology, three substantive topics are examined in depth: the relations of diet and coronary heart disease, fat intake and breast cancer, and Vitamin A and lung cancer.
Article
120 patients with Crohn’s disease, 100 with ulcerative colitis and controls matched for age and sex were interviewed by questionnaire. Questions related to current and past sugar and milk intake and consumption of some breakfast cereals. Patients with Crohn’s disease ate significantly more sugar than either controls or patients with ulcerative colitis at the time of interview. Their use of sugar had changed little since the onset of symptoms.
Article
To define epidemiologic and clinical characteristics of newly diagnosed pediatric inflammatory bowel disease (IBD) in a large population-based model. All pediatric gastroenterologists providing care for Wisconsin children voluntarily identified all new cases of IBD during a 2-year period. Demographic and clinical data were sent to a central registry prospectively for analysis. The incidence of IBD in Wisconsin children was 7.05 per 100,000, whereas the incidence for Crohn's disease was 4.56, more than twice the rate of ulcerative colitis (2.14). An equal IBD incidence occurred among all ethnic groups, and children from sparsely and densely populated counties were equally affected. The majority (89%) of new IBD diagnoses were nonfamilial. This study provides novel, prospective, and comprehensive information on pediatric IBD incidence within the United States. The surprisingly high incidence of pediatric IBD, the predominance of Crohn's disease over ulcerative colitis, the low frequency of patients with a family history, the equal distribution of IBD among all racial and ethnic groups, and the lack of a modulatory effect of urbanization on IBD incidence collectively suggest that the clinical spectrum of IBD is still evolving and point to environmental factors contributing to the pathogenesis.
Article
To evaluate the role of dietary factors in the etiology of inflammatory bowel disease (IBD), we conducted a multicenter hospital-based case-control study in a Japanese population. Cases were IBD patients aged 15 to 34 years [ulcerative colitis (UC) 111 patients; Crohn's disease (CD) 128 patients] within 3 years after diagnosis in 13 hospitals. One control subject was recruited for each case who was matched for sex, age, and hospital. A semiquantitative food frequency questionnaire was used to estimate preillness intakes of food groups and nutrients. All the available control subjects (n = 219) were pooled, and unconditional logistic models were applied to calculate odds ratios (ORs). In the food groups, a higher consumption of sweets was positively associated with UC risk [OR for the highest versus lowest quartile, 2.86; 95% confidence interval (CI), 1.24 to 6.57], whereas the consumption of sugars and sweeteners (OR, 2.12; 95% CI, 1.08 to 4.17), sweets (OR, 2.83; 95% CI, 1.38 to 5.83), fats and oils (OR, 2.64; 95% CI, 1.29 to 5.39), and fish and shellfish (OR, 2.41; 95% CI, 1.18-4.89) were positively associated with CD risk. In respect to nutrients, the intake of vitamin C (OR, 0.45; 95% CI, 0.21 to 0.99) was negatively related to UC risk, while the intake of total fat (OR, 2.86; 95% CI, 1.39 to 5.90), monounsaturated fatty acids (OR, 2.49; 95% CI, 1.23 to 5.03) and polyunsaturated fatty acids (OR, 2.31; 95% CI, 1.12 to 4.79), vitamin E (OR, 3.23; 95% CI, 1.45 to 7.17), and n-3 (OR, 3.24; 95% CI, 1.52 to 6.88) and n-6 fatty acids (OR, 2.57; 95% CI, 1.24 to 5.32) was positively associated with CD risk. Although this study suffers from the shortcoming of recall bias, which is inherent in most retrospective studies (prospective studies are warranted to confirm the associations between diet and IBD risk), the present findings suggest the importance of dietary factors for IBD prevention.
Article
The consumption of sugar and sugar-containing foods in 32 patients with recently diagnosed Crohn's disease was significantly greater than in matched controls; the assessment was made by a questionnaire and depended upon patients recalling their eating habits. In a further study of 16 patients with Crohn's disease, all food eaten over 5 days was weighed and recorded, and no significant difference was found in the consumption of carbohydrate, protein, fats, or sugars, although the consumption of added sugars in patients was greater than controls. Patients who participated in both studies significantly reduced their intake of added sugar, and this was not found to correlate with either total intake of monosaccharides and disaccharides or the total carbohydrate consumption. The increased consumption of added sugar in patients with Crohn's disease does not appear to be related to other dietary abnormalities and may simply reflect a deficiency in perception of sweet taste in patients with this condition.
Article
1. Ulcerative colitis is frequently due to food allergy—in at least sixty-six per cent of cases. 2. The resemblance between the mucosal lesions of ulcerative colitis and allergic reactions in the skin is quite obvious. 3. The pathological findings in early ulcerative colitis are identical with those demonstrated in allergy experiments in humans and animals. Their progression would produce the severe, later lesions. 4. The symptoms of ulcerative colitis are easily explainable on an allergic basis. 5. Proctoscopic and roentgenological examinations can be used to demonstrate the effect of allergenic foods and the improvement on their withdrawal from the diet. 6. Treatment based on allergic considerations has produced results which are better than those based entirely on an infective etiology.
Article
The mean daily intake of dietary fiber, sugar, starch, fat, protein, and total energy was determined in 35 patients with Crohn's disease and 70 normal controls by obtaining individual dietary histories. For each patient with Crohn's disease there two controls, matched for age, sex, and socioeconomic background. In the patients with Crohn's disease the mean dietary fiber intake was established as 26.6 +/- 1.4 g/day, compared to 22.3 +/- 0.9 g/day in the controls, and was thus significantly higher (P less than 0.05). When compared with the controls, the patients with Crohn's disease also exhibited a significantly higher consumption of sugar 156 +/- 14 versus 91 +/- 5 g/day (P less than 0.001), starch (211 +/- 10 versus 170 +/- 9 g/day (P less than 0.01)), and total energy (14.4 +/- 0.7 versus 12.3 +/- 0.5 MJ/ day (P less than 0.01)).
Article
The breakfast habits in adult life of 34 patients with Crohns disease were compared with those of 68 matched controls. Cornflakes were being eaten at least weekly by 23 of the patients (67--6%) at the time that their symptoms began, compared with 17 (25%) of the controls at the corresponding time. Only one of the 34 patients had not eaten cornflakes at all, compared with half of the controls. A significant but weaker association was found between Crohn's disease and the eating of wheat cereals. However, in both patients and controls the taking of cornflakes and of wheat cereals were correlated, and the observed preponderance of wheat eating among the patients was almost entirely ascribable to this association of habits. Eating of rice cereals and of porridge was not associated with Crohn's disease, though it was correlated with eating cornflakes. There was an excess of bran eaters among the propositi, but this, too, was attributable to their being also cornflake eaters. Other breakfast foods were taken with equal frequency, and omission of breakfast was equally common. Six of the 68 controls, but none of the patients, ate cornflakes later in the day but not at breakfast. The results need confirmation. There was no evidence that bias could have caused the correlation found. The association of Crohn's disease with the eating of cornflakes is strong and unlikely to be indirect. Variable digestive secretory behaviour after waking may play a part in determining susceptibility to Crohn's disease.
Article
The nutritional habits of 63 patients with Crohn's disease (C.d.) were explored by means of questionnaires and compared with a control group of 63 persons matched as to age, sex and social status. Before the disease was recognized patients with C.d. consumed 742 grams/week (g/w) sweets and 1380 g/w pastries, during the disease 482 g/w sweets and 905 g/w pastries. The controls only consumed 285 g/w sweets and 563 g/w pastries. The differences between both groups are highly significant. There existed no significant difference in the intake of other foodstuffs such as proteins, fats, vegetables or alcohol. The high intake of refined carbohydrates in patients with C.d. may be partly responsible for its increasing incidence in the developed countries. This might be due to the sugar content as such and/or the food additives.