Dietary Polyphenols in the Aetiology of Crohnʼs Disease and Ulcerative Colitis—A Multicenter European Prospective Cohort Study (EPIC)

Lu, Yunxia; Zamora-Ros, Raúl; Chan, Simon; Cross, Amanda J.; Ward, Heather; Jakszyn, Paula; Luben, Robert; Opstelten, Jorrit L.; Oldenburg, Bas; Hallmans, Göran; Karling, Pontus; Grip, Olof; Key, Timothy J.; Bergmann, Manuela M.; Boeing, Heiner; Overvad, Kim; Palli, Domenico; Masala, Giovanna; Khaw, Kay Tee; Racine, Antoine; Carbonnel, Franck; Boutron-Ruault, Marie Christine; Andersen, Vibeke; Olsen, Anja; Tjønneland, Anne; Kaaks, Rudolf; Tumino, Rosario; Trichopoulou, Antonia; Scalbert, Augustin; Riboli, Elio; Hart, Andrew

doi:10.1097/mib.0000000000001108

Cited by 47 publications

(28 citation statements)

References 29 publications

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“…Experimental evidence has suggested that polyphenols prevent colitis by inhibiting the biological process of oxidative stress and the associated damage to DNA, lipids, and proteins. The mechanism was to study proinflammatory proteins by affecting the mitogen‐activated protein kinase and transcription factor NF‐κB signaling pathway . In the present study, we found that the administration of polyphenols increased the biochemical parameters SOD and GSH‐Px in the serum and decreased MPO and NO in colon tissue.…”

Section: Discussionsupporting

confidence: 54%

Honey Polyphenols Ameliorate DSS‐Induced Ulcerative Colitis via Modulating Gut Microbiota in Rats

Zhao

Cheng

Zhou

et al. 2019

Molecular Nutrition Food Res

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Scope Ulcerative colitis (UC) is a multifaceted and recurrent immune disorder that requires long‐term potent pharmacological treatment. Honey, as a natural food of nourishment and pharmaceutical value, has been found to defend against colitis. Methods and results The effects of different constituents in honey are investigated on DSS‐induced colitis in rats. Rats are given DSS, sugars, honey, polyphenols, or SASP for a week, with blood and colon samples collected for the biochemical parameters and inflammation‐related gene analysis and colon contents for gut microbiota. The results show that pretreatments with honey polyphenols significantly improve SOD, GSH‐Px, NO, and MPO levels and reduce DSS‐induced colonic apoptosis, the colonic inflammatory cytokines IL‐6, TNF‐α, and TGF‐β1 accompanied by downregulation of IL‐1β, IL‐6, TNF‐α, and IFN‐γ gene and upregulation of IκB‐α gene. Furthermore, honey polyphenols and SASP show similar microbial community structure shifts and selective enrichment of key species. At the genus level, honey polyphenols significantly reduce the population of Bacteroides, Corynebacterium, and Proteus species. The correlation analysis indicates that colonic gene expression regulated by honey polyphenols is relative to the key species of gut microbiota. Conclusions Honey polyphenols improve intestinal inflammation and oxidative stress resistance via modulating gut microbiota, which is conducive to revealing the host–microbe interactions.

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Section: Discussionsupporting

confidence: 54%

Honey Polyphenols Ameliorate DSS‐Induced Ulcerative Colitis via Modulating Gut Microbiota in Rats

Zhao

Cheng

Zhou

et al. 2019

Molecular Nutrition Food Res

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“…95,152 Indeed, as part of the IBD European Prospective Cohort Study (IBD-EPIC study), many dietary factors have been associated with IBD onset. [153][154][155][156] Milk consumption was shown to be potentially associated with a decreased risk of developing CD (P = 0.23 for CD) but not with UC (P = 0.60), 154 whereas a role of flavones and resveratrol in the risk of developing CD was also observed. 155 The IBD-EPIC study findings also support a role for dietary linoleic acid in the etiology of UC.…”

Section: Table 1: Continuedmentioning

confidence: 99%

“…[153][154][155][156] Milk consumption was shown to be potentially associated with a decreased risk of developing CD (P = 0.23 for CD) but not with UC (P = 0.60), 154 whereas a role of flavones and resveratrol in the risk of developing CD was also observed. 155 The IBD-EPIC study findings also support a role for dietary linoleic acid in the etiology of UC. 155 In this cohort, obesity, as measured by body mass index (BMI), was not associated with the development of UC or CD.…”

Section: Table 1: Continuedmentioning

confidence: 99%

Determinants of IBD Heritability: Genes, Bugs, and More

Turpin

Goethel

Bedrani

et al. 2018

Inflammatory Bowel Diseases

140

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Defining the etiology of inflammatory bowel disease (IBD) continues to elude researchers, in part due to the possibility that there may be different triggers for a spectrum of disease phenotypes that are currently classified as either Crohn's disease (CD) or ulcerative colitis (UC). What is clear is that genetic susceptibility plays an important role in the development of IBD, and large genome-wide association studies using case-control approaches have identified more than 230 risk alleles. Many of these identified risk alleles are located in a variety of genes important in host-microbiome interactions. In spite of these major advances, the mechanisms behind the genetic influence on disease development remain unknown. In addition, the identified genetic risks have thus far failed to fully define the hereditability of IBD. Host genetics influence host interactions with the gut microbiota in maintaining health through a balance of regulated immune responses and coordinated microbial composition and function. What remains to be defined is how alterations in these interactions can lead to disease. The nature and cause of changes in the microbiota in patients with IBD are poorly understood. In spite of the large catalog of alterations in the microbiota of IBD patients, inflammation itself can alter the microbiota, leaving open the question of which is cause or effect. The composition and function of the gut microbiota are influenced by many factors, including environmental factors, dietary factors, and, as recent studies have shown, host genetic makeup. More than 200 loci have shown potential to influence the microbiota, but replication and larger studies are still required to validate these findings. It would seem reasonable to consider the combination of both host genetic makeup and the inheritance of the microbiota as interdependent heritable forces that could explain the nature of an individual's susceptibility to IBD or indeed the actual cause of IBD. In this review, we will consider the contribution of the host genetics, the microbiome, and the influence of host genetics on the microbiota to the heritability of IBD.

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“…Milk and milk product consumption was observed to be potentially related with a low risk of developing CD (p = 0.23) but not for with UC (p = 0.60) [224], whereas a role of flavones (C 15 H 10 O 2 ) and resveratrol (C 14 H 12 O 3 ) in the risk of triggering CD was also shown [225]. The IBD-EPIC study results also indicate dietary role for linoleic acid in the etiopathogenesis of UC [225]. According to this calculated study cohort, overweight, as measured by BMI (body mass index), was observed not consociated with the etiopathogenesis of either UC or CD, respectively [226].…”

Section: Dietary/nutritionmentioning

confidence: 91%

“…Intestinal mucosal microbiota composition is dependently influenced and modified by diet [221,222]. According to the IBD-EPIC (IBD European Prospective Cohort) Study, several dietary factors have been found to be related with IBD onset [223][224][225][226]. Milk and milk product consumption was observed to be potentially related with a low risk of developing CD (p = 0.23) but not for with UC (p = 0.60) [224], whereas a role of flavones (C 15 H 10 O 2 ) and resveratrol (C 14 H 12 O 3 ) in the risk of triggering CD was also shown [225].…”

Section: Dietary/nutritionmentioning

confidence: 99%

The Multifactorial Etiopathogeneses Interplay of Inflammatory Bowel Disease: An Overview

M’Koma

2018

Gastrointestinal Disorders

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The gastrointestinal system where inflammatory bowel disease occurs is central to the immune system where the innate and the adaptive/acquired immune systems are balanced in interactions with gut microbes under homeostasis conditions. This article overviews the high-throughput research screening on multifactorial interplay between genetic risk factors, the intestinal microbiota, urbanization, modernization, Westernization, the environmental influences and immune responses in the etiopathogenesis of inflammatory bowel disease in humans. Inflammatory bowel disease is an expensive multifactorial debilitating disease that affects thousands new people annually worldwide with no known etiology or cure. The conservative therapeutics focus on the established pathology where the immune dysfunction and gut injury have already happened but do not preclude or delay the progression. Inflammatory bowel disease is evolving globally and has become a global emergence disease. It is largely known to be a disease in industrial-urbanized societies attributed to modernization and Westernized lifestyle associated with environmental factors to genetically susceptible individuals with determined failure to process certain commensal antigens. In the developing nations, increasing incidence and prevalence of inflammatory bowel disease (IBD) has been associated with rapid urbanization, modernization and Westernization of the population. In summary, there are identified multiple associations to host exposures potentiating the landscape risk hazards of inflammatory bowel disease trigger, that include: Western life-style and diet, host genetics, altered innate and/or acquired/adaptive host immune responses, early-life microbiota exposure, change in microbiome symbiotic relationship (dysbiosis/dysbacteriosis), pollution, changing hygiene status, socioeconomic status and several other environmental factors have long-standing effects/influence tolerance. The ongoing multipronged robotic studies on gut microbiota composition disparate patterns between the rural vs. urban locations may help elucidate and better understand the contribution of microbiome disciplines/ecology and evolutionary biology in potentially protecting against the development of inflammatory bowel disease.

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Dietary Polyphenols in the Aetiology of Crohnʼs Disease and Ulcerative Colitis—A Multicenter European Prospective Cohort Study (EPIC)

Abstract: The data supports a potential role of flavones and resveratrol in the risk of developing CD; future aetiological studies should investigate these dietary components and further examine the potential for residual confounding.

Cited by 47 publications

References 29 publications

Honey Polyphenols Ameliorate DSS‐Induced Ulcerative Colitis via Modulating Gut Microbiota in Rats

Honey Polyphenols Ameliorate DSS‐Induced Ulcerative Colitis via Modulating Gut Microbiota in Rats

Determinants of IBD Heritability: Genes, Bugs, and More

The Multifactorial Etiopathogeneses Interplay of Inflammatory Bowel Disease: An Overview

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