Clinical importance of n-3 fatty acid-rich diet and nutritional education for the maintenance of remission in Crohn's disease

Tsujikawa, Tomoyuki; Satoh, Junko; Uda, Katsuhiro; Ihara, Takashi; Okamoto, Toshihiko; Araki, Yoshio; Sasaki, Makoto; Fujiyama, Yoshihide; Bamba, Tadao

doi:10.1007/s005350050021

Cited by 30 publications

(28 citation statements)

References 7 publications

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“…69,70 Other approaches have been unconvincing, particularly interventions specifically with n-3 PUFAs, 71 but such studies have uncertain rele vance to the use of diets high in n-3 PUFA-rich foods, which have their advocates, alas without high-quality evidence of benefit. 72 Reducing microparticle intake was unsuccessful in l owering r emission rates over 4 months in a well-powered RCT. 73 One disease that might represent a phenotype of Crohn's disease is orofacial granulomatosis.…”

Section: Ulcerative Colitismentioning

confidence: 99%

Dietary management of IBD—insights and advice

Halmos

Gibson

2015

Nat Rev Gastroenterol Hepatol

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The current general interest in the use of food choice or diet in maintaining good health and in preventing and treating disease also applies to patients with IBD, who often follow poor or nutritionally challenging dietary plans. Unfortunately, dietary advice plays only a minor part in published guidelines for management of IBD, which sends a message that diet is not of great importance. However, a considerable evidence base supports a focused and serious attention to nutrition and diet in patients with IBD. In this Review, a step-wise approach in the evaluation and management of these patients is proposed. First, dietary intake and eating habits as well as current nutritional state should be documented, and corrective measures instituted. Secondly, dietary strategies as primary or adjunctive therapy for the reduction of inflammation and/or prevention of relapse of IBD should be seriously contemplated. Thirdly, use of diet to improve symptoms or lessen the effects of complications should be considered. Finally, dietary advice regarding disease prevention should be discussed when relevant. An increasing need exists for applying improved methodologies into establishing the value of current and new ways of using food choice as a therapeutic and preventive tool in IBD.

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Section: Ulcerative Colitismentioning

confidence: 99%

Dietary management of IBD—insights and advice

Halmos

Gibson

2015

Nat Rev Gastroenterol Hepatol

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“…On the other hand, eicosanoids such as leukotriene B4 (LTB4) and thromboxane A2 (TXA2) are produced in the arachidonic acids cascade by n-6 fatty acids, which are a group of polyvalent unsaturated fatty acids. LTB4 and TXA2 are assumed to be the inflammatory substances that cause Crohn's disease [12,13]. LTB4 acts as the inflammatory mediator, which induces the liberation and adhesion of leukocyte, and TXA2 coagulates the platelet, and constricts the blood vessels.…”

Section: Discussionmentioning

confidence: 99%

“…N-3 fatty acids competitively inhibit the metabolism of n-6 fatty acids and have a close affinity to the rate-limiting enzymes. LTB5, TXA3 and other n-3 fatty acid metabolites are synthesized with a higher priority to cause anti-inflammatory activity [2,12]. Accordingly, for Crohn's disease, the ratio of n-6/n-3 is more important than the amount of fat in the enteral nutrient formulations.…”

Section: Discussionmentioning

confidence: 99%

Histoimmunological Evaluation for the Efficacy of Entero Nutrient Containing n-3 Fatty Acids in TNBS Rat Colitis Model

Yokoyama

Nakajima

Itō

et al. 2006

J. Clin. Biochem. Nutr.

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Summary Inflammatory bowel disease (IBD) is a chronic disease of the digestive tract, with complicated and multifactoral etiology. An exaggerated intestinal immune response to otherwise innocuous stimuli plays a key role in the pathophysiology of this intestinal disorder. Nutritional intervention is an important therapy for patients with IBD. But the ratio of n-3 and n-6 fatty acids on the modulation of intestinal inflammation is not clear. Interleukin-16 (IL-16) is a pleiotrophic cytokine secreted mainly by CD8 + T cells. The properties of IL-16 suggest that it may be involved in pathophysiological process of chronic inflammatory diseases. The aim was to determine the effect of an n-3 fatty acid-rich diet (RACOL ® ) on the expressions of cytokines and mucosal integrity in trinitrobenzene surufonic acid (TNBS) induced rat colitis. 7 week-male Wistar rats were divided into 4 groups. 1. Normal laboratory diet (n = 10), 2. RACOL ® diet only (n = 10), 3. TNBS induced colitis with normal laboratory diet (n = 10), 4. TNBS induced colitis with RACOL ® diet (n = 10). TNBS induced colitis rats were given an intracolonic injection of 50 mg of TNBS dissolved in 50% ethanol. From day 2, rats were fed 80 kcal/day of RACOL ® and/or normal laboratory diet, and sacrified on the 14 th and the 28 th days. One hour before sacrifice, 0.2 mg/g/rat of BrdU was injected. The expressions of BrdU labeled cells, tumor necrosis factor (TNF)-α, interferon (IFN)-γ and IL-16 were studied by the ABC staining method and DAB staining lesions in colonic mucosa were estimated by an image analyzer system. Apoptosis was assessed by the TUNEL method. Macroscopic and histological findings were classified by the Morris and Vilaseca method. TNBS application increased colonic epithelial cell proliferation, but nutrition by RACOL ® reduced this stimulation. Number of apoptosis cells was also increased by TNBS application, but nutrition of RACOL ® reduced the number of apoptosis cells, which had been increased by TNBS treatment. The expressions of cytokines had been increased in TNBS-colitis rats, but were reduced by the RACOL ® . In conclusion, the effect of nutrition by n-3 fatty acid-rich diet, RACOL ® , is an important treatment through the inhibition of inflammatory mediators, and colonic hyper-proliferation.

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“…Treatment of CD with supplemental fish oil has been demonstrated to reduce the occurrence of relapse. Tsuijikawa and coworkers 14 suggest that the n-3 polyunsaturated fatty acids, taken up in competition with n-6 polyunsaturated fatty acids, decrease the induction of inflammatory eicosanoids such as leukotriene B4 and control inflammation. Others found that supplementation with omega-3 fatty acids delayed relapse.…”

Section: In Youthmentioning

confidence: 98%