Research progress of clinical nutrition in inflammatory bowel disease
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摘要:
炎症性肠病是一种病因尚不明确的慢性非特异性肠道炎性疾病, 包括溃疡性结肠炎及克罗恩病。炎症性肠病的发病机制复杂，包括遗传因素和环境因素，其中饮食是重要的环境因素之一。炎症性肠病患者通常会伴有营养不良及微量元素缺乏的表现。本文综述了近年来临床营养在炎症性肠病中的研究成果，分析了炎症性肠病的不同饮食治疗策略，为进一步研究炎症性肠病的预防与治疗策略提供参考。
Abstract:Inflammatory bowel disease is a chronic non-specific inflammatory disease of the gastrointestinal tract with unclear etiology, including ulcerative colitis and the Crohn's disease. The pathogenesis of inflammatory bowel disease is complex, involving genetic and environmental factors, and diet is one of the important environmental factors. Patients with inflammatory bowel disease often present with malnutrition and micronutrient deficiencies. This paper reviewed the research achievements of clinical nutrition in inflammatory bowel disease in recent years, analyzed the different dietary therapeutic strategies for inflammatory bowel disease, and provided reference for further research on the prevention and treatment of inflammatory bowel disease.
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炎症性肠病(IBD)是遗传、肠道微生物失调及环境因素和异常的宿主免疫反应之间相互作用的结果[1], 西方化的饮食和微生物失调是主要环境因素[2-3]。西方化饮食的特点是热量高但营养稀少，含有大量蛋白质和脂肪，但蔬果、豆类和全谷物含量较低[4]。目前，越来越多的超加工食品(UPF)被发现与IBD发病风险高有关[5-6]。UPF由精制的碳水化合物、糖、脂肪、分离蛋白和各种添加剂制成，西方化饮食和UPF可降低肠道微生物区系多样性，导致肠道菌群失调，从而引起IBD[7-8]。
1. IBD与临床营养素的关系
临床营养中3大产能营养素包括碳水化合物、蛋白质和脂肪。富含精制的碳水化合物、动物蛋白、饱和脂肪和加工食品的西方饮食会带来IBD的风险，而富含鱼类、坚果和纤维的地中海饮食(MD)可降低该风险[9-13]。
1.1 碳水化合物
OPSTELTEN J L等[14]研究发现摄入精制碳水化合物和高糖饮食与IBD的风险有关。FU T等[15]研究发现摄入不同类型的饮料对IBD的影响有差异，食用含糖饮料可显著增加克罗恩病(CD)的风险，但不会增加溃疡性结肠炎(UC)的风险，而食用不含其他添加剂的自制糖饮料或天然果汁与IBD风险之间没有关联。YAN J等[16]研究发现高糖饮食可增加肠道通透性，降低微生物多样性，减少单链脂肪酸，从而增加细菌数量导致肠道炎症的发生，因此建议在饮食中限制精制糖的摄入来预防IBD的发生。
研究[17-19]提示，总碳水化合物摄入量与IBD风险之间无关联。这可能是因为在总碳水化合物的摄入量中包括了膳食纤维素，也可能在膳食纤维素摄入量较低的前提下，糖和碳酸饮料的高摄入量才与IBD风险有关，表明膳食纤维素降低了IBD的风险[20]。
1.2 脂肪
研究认为n-6/n-3多不饱和脂肪酸的高比例与IBD风险相关，在西方饮食中，该比例可高达20∶1。n-3多不饱和脂肪酸有抗炎性，可能对IBD患者有益，但临床证据不足，仍需要更多的研究来验证n-3多不饱和脂肪酸对IBD患者的保护作用[21]。此外，有研究[22]提出鱼油中的二十二碳六烯酸对CD患者有益，但没有进一步的证据显示CD与总脂肪或特定脂肪之间的关联。
HIGASHIMURA Y等[23]研究显示油炸食品和UPF中普遍存在的反式脂肪酸也可以加剧肠道炎症。富含反式脂肪酸的饮食使肠道微生物区系严重失调，导致有害细菌繁殖，降低有益细菌的数量，从而促进肠道炎症的发展[24-25]。
1.3 蛋白质
TAYYEM R F等[26]研究发现，与健康人相比，IBD患者的饮食特点是蛋白质摄入量更高。动物研究[27]表明，高蛋白饮食后肠道微生物区系组成发生变化，进而导致氨基酸、硫化氢和支链脂肪酸等代谢产物的变化，导致肠道屏障功能和免疫反应受损，此外，高蛋白饮食可促进促巨噬细胞反应，从而加重肠道炎症。
高蛋白饮食，特别是红肉类食物，可增加患CD和UC的风险[28-32]。但有研究[31]报道虽然红肉摄入量高存在患病风险，但低肉摄入量对IBD并没有保护作用，也没有肠道微生物区系变化的证据。然而有研究[30]报道，高蛋白饮食无论是来自动物性食物的酪蛋白，还是来自牛奶或大豆的乳清，都会引起肠道炎症，即使蛋白质摄入量仅为健康推荐量的2倍, CD的患病风险也会增加。
2. IBD的营养治疗进展及饮食策略
目前尚未研发出针对IBD的特效药，对IBD患者的治疗目标主要是诱导、维持缓解，减少复发，除了药物和手术治疗，营养治疗也具有一定的疗效。饮食治疗的原则是去除食物来源的刺激因素，补充必需能量和营养，调整肠道的微生态环境，减少炎症并修复肠道黏膜的病变。
2.1 完全肠内营养
完全肠内营养(EEN)指通过口服或鼻胃管从液体营养配方中100%提供人体所需的营养，避免在6~8周内摄入其他食物。肠内营养的配方可分为氨基酸为主的要素配方、短肽为主的半要素配方及整蛋白为主的聚合物配方。要素配方的优点是不需要消化或稍微消化就可以被吸收，无渣或少渣，缺点是口味不佳。聚合物配方需要消化才能吸收，其制作成本更低，耐受性更好，更贴合普通人的饮食标准。
在儿童活动性CD的治疗中, EEN的使用得到了荟萃分析的支持[33]。营养学会已正式推荐EEN作为儿童CD的一线治疗方法[34]。但是，成人使用EEN依从性较低，在成人CD患者中应用EEN的证据不能令人信服[35]。
目前使用EEN的主要挑战是其适口性和长期耐受性差，这限制了其依从性和广泛应用的益处[33]。除了日本以外，EEN在成人CD患者中应用的很少[35]。若可以改善其耐受性的问题，将给CD治疗带来新的突破。
2.2 部分肠内营养(PEN)联合CD排除饮食(CDED)
PEN指患者在进行肠内营养的同时结合普通饮食的方案。LAMB C A等[36]不建议在成人CD患者中使用PEN作为维持治疗。MIELE E等[37]也不推荐单独使用PEN来治疗IBD。
克罗恩病排除饮食(CDED)指排除破坏肠道黏膜和引起微生物失调的特定饮食成分的方案。CDED方案在12周内分为2个阶段。第1阶段为期6周，旨在诱导缓解，含有可能导致微生物失调、增加肠道通透性或降低黏液层屏障的饮食成分的食品被排除或限制，包括调味品、调味汁、动物脂肪、面筋、乳制品、加工肉类、包装产品，以及含有某些单糖和乳化剂的产品。此外水果和蔬菜也受到限制，以减少纤维素暴露。在第2阶段，扩大了食物的种类，允许增加固定比例的全谷物、水果和蔬菜，并改善依从性[38]。
研究人员[38]尝试使用PEN联合CDED来治疗那些无法长期坚持EEN的患者，结果表明其对诱导儿童和年轻人轻至中度CD的缓解是有效的。SZCZUBEŁEK M等[39]也证实了其在成年患者诱导缓解方面的价值，与单用EEN方案相比, PEN联合CDED方案的有效性和耐受性更好[40]。
2.3 MD
MD是以摄入新鲜蔬果、五谷杂粮、橄榄油、坚果、鱼类和豆类为主，适量的乳制品(主要是奶酪和酸奶)，及少吃糖果、肉类及肉类制品的饮食风格[41-44]。
大量的蔬菜、水果是MD的特性，不仅含有丰富的膳食纤维和微量营养素，还是生物酚的主要来源。酚类成分具有抗氧化和抗炎的特性，对IBD有潜在的治疗作用[45-46]。橄榄油也是MD方案中抗氧化和抗炎活性的主要来源[46]。MOZAFFARI H等[47]研究发现鱼类摄入量高可降低CD风险，同时饮食中较高的omega-3多不饱和脂肪酸可降低UC风险。SCAIOLI E等[48]给UC患者服用n-3多不饱和脂肪酸的主要成分二十碳五烯酸(EPA), 结果发现与安慰剂相比, EPA可以降低粪便降钙素原的水平，且没有发生严重的不良事件。
KHALILI H等[41]报道MD可降低患CD的风险，且不受性别、年龄、教育水平、体质量指数和吸烟等因素的影响。AMROUSY D E等[49]报道MD可改善儿童和青少年轻中度活动期IBD的临床评分和炎症标志物水平。对于绝大多数患者来说，MD可能是一种更可行的饮食模式，需要进一步验证其对亚洲IBD患者的疗效。
2.4 低“可发酵寡糖、二糖、单糖和多元醇”饮食
“可发酵寡糖、二糖、单糖和多元醇”的英文缩写是FODMAP(Fermentable, 发酵; Oligosaccharides, 寡糖; Disaccharides, 二糖; Monosaccharides, 单糖; Polyols，多元醇)。低FODMAP饮食指限制可发酵寡糖、二糖、单糖和多元醇含量高的食物。
低FODMAP饮食不仅对肠易激综合征患者有益[50], 还对缓解期IBD患者出现的胃肠道症状有效，特别是腹胀、腹泻、腹痛、乏力和恶心，但对便秘没有影响[51-52]。此外，低FODMAP饮食可以改善疾病活动性，降低粪便降钙素原和C反应蛋白等促炎标记物，提高IBD患者的生活质量[53-55]。需要注意的是，长期坚持低FODMAP饮食，可能会增加IBD患者营养不良的风险[56]。由于低FODMAP饮食尚缺乏足够的证据，其获益性尚不明确，不推荐给有功能性胃肠道症状的IBD患者[57]。
2.5 抗炎饮食(AID)
AID包括限制特定的碳水化合物，如精制或加工的复合碳水化合物和乳糖; 增加益生元、益生菌和富含有助于恢复肠道菌群平衡的成分的食物的摄入; 增加富含omega-3多不饱和脂肪酸的食物摄入量，同时减少总脂肪和饱和脂肪酸的摄入量; 评估患者的饮食结构并监测潜在的营养缺乏; 修改食物质地以改善营养吸收(均质、煮熟、碾碎)。AID需要限制加工的复合碳水化合物，其可能会增加卡路里摄入不足和体质量减轻的风险。而CD和UC患者在实践中都更倾向于食用更多的精制谷物，这增加了AID实施的难度。此外，限制乳制品有可能导致钙和维生素D缺乏症，并导致蛋白质摄入量不足。
为了评价饮食的炎症性，研究人员提出了一些计算炎性指数的方法。饮食炎症指数(DII)由45种食物参数估算得分，如各种脂肪、微量营养素、酒精、花青素、黄酮类、大蒜、生姜等[58]。经验膳食炎症指数(EDII)是根据18个食物类别的加权得分，包括与炎症呈正相关的加工肉类、红肉、精制谷物、饮料和西红柿，以及与炎症呈负相关的啤酒、茶、咖啡、深黄色和绿叶蔬菜等[59]。DII和EDII评分均为正和负，分别反映了促炎饮食和抗炎饮食。
LAMERS C R等[60]报道在CD患者中，DII与疾病活动性呈正相关，然而这种关联在UC患者中并不显著。VAGIANOS K等[61]使用DII和EDII方法观察饮食改变对粪便降钙素原和IBD症状的影响，结果表明EDII评分的增加与粪便降钙素原的升高和IBD症状的加重有关，但未观察到DII评分与粪便降钙素原或IBD症状之间的关联。研究[62]表明DII和EDII评分与疾病活动性无关，可能不是所有的食物参数都包括在DII和EDII中。
OLENDZKI B C等[63]报道IBD患者接受AID 4周或更长时间后，临床症状都有所减轻，并能够停用至少1种以前的药物。最近一项研究[64]推出格罗宁根抗炎饮食(GrAID), GrAID包含的食物种类比其他饮食模式(如MD、低FODMAP饮食、AID)要多，这为IBD患者选择或避免某种食物提供了依据。目前对AID的研究十分有限，还需更多的实践来证明其有效性。
2.6 特定碳水化合物饮食(SCD)
SCD最初在20世纪中期被用于治疗乳糜泻，后来被用于IBD的治疗。肠道内促炎微生物是由吸收不良的碳水化合物(如二糖和多糖)持久存在而产生的。因此，谷物、二糖和多糖食物受到严格限制。SCD允许的食物有大多数蔬菜、水果、非加工的肉类、蛋、海鲜、坚果、蜂蜜、自制发酵好的酸奶、健康油脂和一部分豆类。
研究[65]表明儿童IBD患者接受SCD治疗后营养摄入是充足的。大部分患者在严格SCD后病情得到改善，限制就会放松，一些SCD“非法”食物被逐渐添加到饮食中，如大米、燕麦、土豆等，这称为改良SCD。WAHBEH G T等[66]比较了7例儿童CD患者遵循SCD和改良SCD 26个月后情况发现，所有患者C反应蛋白、白蛋白和红细胞压积已正常化，粪便降钙素原轻度升高，但黏膜未见完全愈合。对于大多数轻中度CD患者来说，SCD并不优于MD[67]。因为患者在遵循MD时感觉更轻松，这意味着饮食模式不仅要有效，而且要容易坚持。
2.7 植物性饮食
植物性饮食是以植物为基础的全食，包括蔬菜、水果、豆类、种子和坚果，限制肉类、乳制品、鸡蛋、油及精制和加工食品的摄入。植物性饮食富含膳食纤维和多酚，动物蛋白和脂肪含量低，可以增加肠道微生物多样性，从而减轻肠道炎症。
乳蛋半素食联合英夫利昔单抗这一疗法除了能降低CD患者疾病活动性和C反应蛋白，促进黏膜愈合，还可以提高重症UC患者的缓解率，降低结肠切除率。此外，植物性饮食也对预防UC复发有效。然而，长期植物性饮食可能会导致维生素B12和其他微量营养素的缺乏，这可能会影响植物性饮食治疗IBD的有效性。
3. 总结与展望
国内外的研究结果表明，西方化饮食和一些饮食成分与IBD发病率上升有关。适宜的饮食可以纠正IBD患者的营养不良，达到缓解临床症状，修复肠道黏膜，减少病情复发的作用。但目前对IBD患者的饮食治疗还是保守和慎重的，除了对活动期CD患者进行专门的EEN外，目前少有高质量的证据来为IBD的治疗提供最佳的饮食建议。IBD饮食的研究设计需要考虑不同人种、人群地域特点及生活习惯的差别，不合理地限制或增加某种营养物质的摄入都不利于疾病的康复，这些都需要进一步的前瞻性证据。
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[1] LIMKETKAI B N, MULLIN G E, LIMSUI D, et al. Role of vitamin D in inflammatory bowel disease[J]. Nutr Clin Pract, 2017, 32(3): 337-345. doi: 10.1177/0884533616674492
[2] CHIBA M, NAKANE K, KOMATSU M. Westernized diet is the most ubiquitous environmental factor in inflammatory bowel disease[J]. Perm J, 2019, 23: 18-107.
[3] LI T, QIU Y, YANG H S, et al. Systematic review and meta-analysis: association of a pre-illness Western dietary pattern with the risk of developing inflammatory bowel disease[J]. J Dig Dis, 2020, 21(7): 362-371. doi: 10.1111/1751-2980.12910
[4] SCHREINER P, MARTINHO-GRUEBER M, STUDERUS D, et al. Nutrition in inflammatory bowel disease[J]. Digestion, 2020, 101(Suppl 1): 120-135.
[5] NARULA N, WONG E C L, DEHGHAN M, et al. Association of ultra-processed food intake with risk of inflammatory bowel disease: prospective cohort study[J]. BMJ, 2021, 374: n1554.
[6] VASSEUR P, DUGELAY E, BENAMOUZIG R, et al. Dietary patterns, ultra-processed food, and the risk of inflammatory bowel diseases in the NutriNet-santé cohort[J]. Inflamm Bowel Dis, 2021, 27(1): 65-73. doi: 10.1093/ibd/izaa018
[7] BROUSSARD J L, DEVKOTA S. The changing microbial landscape of Western society: diet, dwellings and discordance[J]. Mol Metab, 2016, 5(9): 737-742. doi: 10.1016/j.molmet.2016.07.007
[8] CUEVAS-SIERRA A, MILAGRO F I, ARANAZ P, et al. Gut microbiota differences according to ultra-processed food consumption in a Spanish population[J]. Nutrients, 2021, 13(8): 2710. doi: 10.3390/nu13082710
[9] ADOLPH T E, ZHANG J W. Diet fuelling inflammatory bowel diseases: preclinical and clinical concepts[J]. Gut, 2022, 71(12): 2574-2586. doi: 10.1136/gutjnl-2021-326575
[10] HOU J K, ABRAHAM B, EL-SERAG H. Dietary intake and risk of developing inflammatory bowel disease: a systematic review of the literature[J]. Am J Gastroenterol, 2011, 106(4): 563-573. doi: 10.1038/ajg.2011.44
[11] LEONE V, CHANG E B, DEVKOTA S. Diet, microbes, and host genetics: the perfect storm in inflammatory bowel diseases[J]. J Gastroenterol, 2013, 48(3): 315-321. doi: 10.1007/s00535-013-0777-2
[12] YAO C K, MUIR J G, GIBSON P R. Review article: insights into colonic protein fermentation, its modulation and potential health implications[J]. Aliment Pharmacol Ther, 2016, 43(2): 181-196. doi: 10.1111/apt.13456
[13] SPOOREN C E, PIERIK M J, ZEEGERS M P, et al. Review article: the association of diet with onset and relapse in patients with inflammatory bowel disease[J]. Aliment Pharmacol Ther, 2013, 38(10): 1172-1187. doi: 10.1111/apt.12501
[14] OPSTELTEN J L, DE VRIES J H M, WOOLS A, et al. Dietary intake of patients with inflammatory bowel disease: a comparison with individuals from a general population and associations with relapse[J]. Clin Nutr, 2019, 38(4): 1892-1898. doi: 10.1016/j.clnu.2018.06.983
[15] FU T, CHEN H, CHEN X J, et al. Sugar-sweetened beverages, artificially sweetened beverages and natural juices and risk of inflammatory bowel disease: a cohort study of 121, 490 participants[J]. Aliment Pharmacol Ther, 2022, 56(6): 1018-1029. doi: 10.1111/apt.17149
[16] YAN J, WANG L, GU Y, et al. Dietary patterns and gut microbiota changes in inflammatory bowel disease: current insights and future challenges[J]. Nutrients, 2022, 14(19): 4003. doi: 10.3390/nu14194003
[17] WANG F, FENG J R, GAO Q, et al. Carbohydrate and protein intake and risk of ulcerative colitis: systematic review and dose-response meta-analysis of epidemiological studies[J]. Clin Nutr, 2017, 36(5): 1259-1265. doi: 10.1016/j.clnu.2016.10.009
[18] KHADEMI Z, MILAJERDI A, LARIJANI B, et al. Dietary intake of total carbohydrates, sugar and sugar-sweetened beverages, and risk of inflammatory bowel disease: a systematic review and meta-analysis of prospective cohort studies[J]. Front Nutr, 2021, 8: 707795. doi: 10.3389/fnut.2021.707795
[19] ZENG L R, HU S, CHEN P F, et al. Macronutrient intake and risk of Crohn's disease: systematic review and dose-response meta-analysis of epidemiological studies[J]. Nutrients, 2017, 9(5): 500. doi: 10.3390/nu9050500
[20] RACINE A, CARBONNEL F, CHAN S S M, et al. Dietary patterns and risk of inflammatory bowel disease in Europe: results from the EPIC study[J]. Inflamm Bowel Dis, 2016, 22(2): 345-354. doi: 10.1097/MIB.0000000000000638
[21] SCAIOLI E, LIVERANI E, BELLUZZI A. The imbalance between n-6/n-3 polyunsaturated fatty acids and inflammatory bowel disease: a comprehensive review and future therapeutic perspectives[J]. Int J Mol Sci, 2017, 18(12): 2619. doi: 10.3390/ijms18122619
[22] CHAN S S, LUBEN R, OLSEN A, et al. Association between high dietary intake of the n-3 polyunsaturated fatty acid docosahexaenoic acid and reduced risk of Crohn's disease[J]. Aliment Pharmacol Ther, 2014, 39(8): 834-842. doi: 10.1111/apt.12670
[23] HIGASHIMURA Y, TANAKA Y, TAKAGI T, et al. Trans-unsaturated fatty acid activates NLRP3 inflammasome in macrophages and exacerbates intestinal inflammation in mice[J]. Biochem Biophys Res Commun, 2020, 529(2): 243-250. doi: 10.1016/j.bbrc.2020.06.005
[24] GE Y T, LIU W, TAO H T, et al. Effect of industrial trans-fatty acids-enriched diet on gut microbiota of C57BL/6 mice[J]. Eur J Nutr, 2019, 58(7): 2625-2638. doi: 10.1007/s00394-018-1810-2
[25] LI C, ZHANG Y H, GE Y T, et al. Comparative transcriptome and microbiota analyses provide new insights into the adverse effects of industrial trans fatty acids on the small intestine of C57BL/6 mice[J]. Eur J Nutr, 2021, 60(2): 975-987. doi: 10.1007/s00394-020-02297-y
[26] TAYYEM R F, QALQILI T R, AJEEN R, et al. Dietary patterns and the risk of inflammatory bowel disease: findings from a case-control study[J]. Nutrients, 2021, 13(6): 1889. doi: 10.3390/nu13061889
[27] KOSTOVCIKOVA K, COUFAL S, GALANOVA N, et al. Diet rich in animal protein promotes pro-inflammatory macrophage response and exacerbates colitis in mice[J]. Front Immunol, 2019, 10: 919. doi: 10.3389/fimmu.2019.00919
[28] JANTCHOU P, MOROIS S, CLAVEL-CHAPELON F, et al. Animal protein intake and risk of inflammatory bowel disease: the E3N prospective study[J]. Am J Gastroenterol, 2010, 105(10): 2195-2201. doi: 10.1038/ajg.2010.192
[29] LUGLIO G, RISPO A, IMPERATORE N, et al. Surgical prevention of anastomotic recurrence by excluding mesentery in Crohn's disease: the SuPREMe-CD study- A randomized clinical trial[J]. Ann Surg, 2020, 272(2): 210-217. doi: 10.1097/SLA.0000000000003821
[30] CHEN L L, WANG J Y, YI J, et al. Increased mucin-degrading bacteria by high protein diet leads to thinner mucus layer and aggravates experimental colitis[J]. J Gastroenterol Hepatol, 2021, 36(10): 2864-2874. doi: 10.1111/jgh.15562
[31] RUBIN K H, RASMUSSEN N F, PETERSEN I, et al. Intake of dietary fibre, red and processed meat and risk of late-onset Chronic Inflammatory Diseases: a prospective Danish study on the diet, cancer and health cohort[J]. Int J Med Sci, 2020, 17(16): 2487-2495. doi: 10.7150/ijms.49314
[32] DONG C, CHAN S S M, JANTCHOU P, et al. Meat intake is associated with a higher risk of ulcerative colitis in a large European prospective cohort study[J]. J Crohns Colitis, 2022, 16(8): 1187-1196. doi: 10.1093/ecco-jcc/jjac054
[33] NARULA N, DHILLON A, ZHANG D N, et al. Enteral nutritional therapy for induction of remission in Crohn's disease[J]. Cochrane Database Syst Rev, 2018, 4(4): CD000542.
[34] LIMKETKAI B N, GORDON M, MUTLU E A, et al. Diet therapy for inflammatory bowel diseases: a call to the dining table[J]. Inflamm Bowel Dis, 2020, 26(4): 510-514. doi: 10.1093/ibd/izz297
[35] WALL C L, DAY A S, GEARRY R B. Use of exclusive enteral nutrition in adults with Crohn's disease: a review[J]. World J Gastroenterol, 2013, 19(43): 7652-7660. doi: 10.3748/wjg.v19.i43.7652
[36] LAMB C A, KENNEDY N A, RAINE T, et al. British Society of Gastroenterology consensus guidelines on the management of inflammatory bowel disease in adults[J]. Gut, 2019, 68(Suppl 3): s1-s106. doi: 10.1136/gutjnl-2019-318484
[37] MIELE E, SHAMIR R, ALOI M, et al. Nutrition in pediatric inflammatory bowel disease: a position paper on behalf of the Porto inflammatory bowel disease group of the European society of pediatric gastroenterology, hepatology and nutrition[J]. J Pediatr Gastroenterol Nutr, 2018, 66(4): 687-708. doi: 10.1097/MPG.0000000000001896
[38] SIGALL-BONEH R, PFEFFER-GIK T, SEGAL I, et al. Partial enteral nutrition with a Crohn's disease exclusion diet is effective for induction of remission in children and young adults with Crohn's disease[J]. Inflamm Bowel Dis, 2014, 20(8): 1353-1360. doi: 10.1097/MIB.0000000000000110
[39] SZCZUBEŁEK M, POMORSKA K, KORÓLCZYK-KOWALCZYK M, et al. Effectiveness of Crohn's disease exclusion diet for induction of remission in Crohn's disease adult patients[J]. Nutrients, 2021, 13(11): 4112. doi: 10.3390/nu13114112
[40] LEVINE A, WINE E, ASSA A, et al. Crohn's disease exclusion diet plus partial enteral nutrition induces sustained remission in a randomized controlled trial[J]. Gastroenterology, 2019, 157(2): 440-450. e8. doi: 10.1053/j.gastro.2019.04.021
[41] KHALILI H, HÅKANSSON N, CHAN S S, et al. Adherence to a Mediterranean diet is associated with a lower risk of later-onset Crohn's disease: results from two large prospective cohort studies[J]. Gut, 2020, 69(9): 1637-1644. doi: 10.1136/gutjnl-2019-319505
[42] GODNY L, RESHEF L, PFEFFER-GIK T, et al. Adherence to the Mediterranean diet is associated with decreased fecal calprotectin in patients with ulcerative colitis after pouch surgery[J]. Eur J Nutr, 2020, 59(7): 3183-3190. doi: 10.1007/s00394-019-02158-3
[43] STRISCIUGLIO C, CENNI S, SERRA M R, et al. Effectiveness of Mediterranean diet's adherence in children with inflammatory bowel diseases[J]. Nutrients, 2020, 12(10): 3206. doi: 10.3390/nu12103206
[44] FIORINDI C, DINU M, GAVAZZI E, et al. Adherence to Mediterranean diet in patients with inflammatory bowel disease[J]. Clin Nutr ESPEN, 2021, 46: 416-423. doi: 10.1016/j.clnesp.2021.09.726
[45] HAGAN M, HAYEE B H, RODRIGUEZ-MATEOS A. (Poly)phenols in inflammatory bowel disease and irritable bowel syndrome: a review[J]. Molecules, 2021, 26(7): 1843. doi: 10.3390/molecules26071843
[46] LARUSSA T, IMENEO M, LUZZA F. Olive tree biophenols in inflammatory bowel disease: when bitter is better[J]. Int J Mol Sci, 2019, 20(6): 1390. doi: 10.3390/ijms20061390
[47] MOZAFFARI H, DANESHZAD E, LARIJANI B, et al. Dietary intake of fish, n-3 polyunsaturated fatty acids, and risk of inflammatory bowel disease: a systematic review and meta-analysis of observational studies[J]. Eur J Nutr, 2020, 59(1): 1-17. doi: 10.1007/s00394-019-01901-0
[48] SCAIOLI E, SARTINI A, BELLANOVA M, et al. Eicosapentaenoic acid reduces fecal levels of calprotectin and prevents relapse in patients with ulcerative colitis[J]. Clin Gastroenterol Hepatol, 2018, 16(8): 1268-1275, e2. doi: 10.1016/j.cgh.2018.01.036
[49] AMROUSY D E, ELASHRY H, SALAMAH A, et al. Adherence to the Mediterranean diet improved clinical scores and inflammatory markers in children with active inflammatory bowel disease: a randomized trial[J]. J Inflamm Res, 2022, 15: 2075-2086. doi: 10.2147/JIR.S349502
[50] GIBSON P R. History of the low FODMAP diet[J]. J Gastroenterol Hepatol, 2017, 32(Suppl 1): 5-7.
[51] ZHAN Y L, ZHAN Y A, DAI S X. Is a low FODMAP diet beneficial for patients with inflammatory bowel disease?A meta-analysis and systematic review[J]. Clin Nutr, 2018, 37(1): 123-129. doi: 10.1016/j.clnu.2017.05.019
[52] POPA S L, POP C, DUMITRASCU D L. Diet advice for Crohn's disease: FODMAP and beyond[J]. Nutrients, 2020, 12(12): 3751. doi: 10.3390/nu12123751
[53] BODINI G, ZANELLA C, CRESPI M, et al. A randomized, 6-wk trial of a low FODMAP diet in patients with inflammatory bowel disease[J]. Nutrition, 2019, 67/68: 110542. doi: 10.1016/j.nut.2019.06.023
[54] BARBALHO S M, GOULART R A, ARANÃO A L C, et al. Inflammatory bowel diseases and fermentable oligosaccharides, disaccharides, monosaccharides, and polyols: an overview[J]. J Med Food, 2018, 21(7): 633-640. doi: 10.1089/jmf.2017.0120
[55] SIMÕES C D, MAGANINHO M, SOUSA A S. FODMAPs, inflammatory bowel disease and gut microbiota: updated overview on the current evidence[J]. Eur J Nutr, 2022, 61(3): 1187-1198. doi: 10.1007/s00394-021-02755-1
[56] GIBSON P R. Use of the low-FODMAP diet in inflammatory bowel disease[J]. J Gastroenterol Hepatol, 2017, 32(Suppl 1): 40-42.
[57] GRAMMATIKOPOULOU M G, GOULIS D G, GKIOURAS K, et al. Low FODMAP diet for functional gastrointestinal symptoms in quiescent inflammatory bowel disease: a systematic review of randomized controlled trials[J]. Nutrients, 2020, 12(12): 3648. doi: 10.3390/nu12123648
[58] SHIVAPPA N, STECK S E, HURLEY T G, et al. Designing and developing a literature-derived, population-based dietary inflammatory index[J]. Public Health Nutr, 2014, 17(8): 1689-1696. doi: 10.1017/S1368980013002115
[59] TABUNG F K, SMITH-WARNER S A, CHAVARRO J E, et al. Development and validation of an empirical dietary inflammatory index[J]. J Nutr, 2016, 146(8): 1560-1570. doi: 10.3945/jn.115.228718
[60] LAMERS C R, DE ROOS N M, WITTEMAN B J M. The association between inflammatory potential of diet and disease activity: results from a cross-sectional study in patients with inflammatory bowel disease[J]. BMC Gastroenterol, 2020, 20(1): 316. doi: 10.1186/s12876-020-01435-4
[61] VAGIANOS K, SHAFER L A, WITGES K, et al. Association between change in inflammatory aspects of diet and change in IBD-related inflammation and symptoms over 1 year: the Manitoba living with IBD study[J]. Inflamm Bowel Dis, 2021, 27(2): 190-202. doi: 10.1093/ibd/izaa052
[62] MIRMIRAN P, MOSLEHI N, MORSHEDZADEH N, et al. Does the inflammatory potential of diet affect disease activity in patients with inflammatory bowel disease[J]. Nutr J, 2019, 18(1): 65. doi: 10.1186/s12937-019-0492-9
[63] OLENDZKI B C, SILVERSTEIN T D, PERSUITTE G M, et al. An anti-inflammatory diet as treatment for inflammatory bowel disease: a case series report[J]. Nutr J, 2014, 13: 5. doi: 10.1186/1475-2891-13-5
[64] CAMPMANS-KUIJPERS M J E, DIJKSTRA G. Food and food groups in inflammatory bowel disease (IBD): the design of the Groningen anti-inflammatory diet (GrAID)[J]. Nutrients, 2021, 13(4): 1067. doi: 10.3390/nu13041067
[65] BRALY K, WILLIAMSON N, SHAFFER M L, et al. Nutritional adequacy of the specific carbohydrate diet in pediatric inflammatory bowel disease[J]. J Pediatr Gastroenterol Nutr, 2017, 65(5): 533-538. doi: 10.1097/MPG.0000000000001613
[66] WAHBEH G T, WARD B T, LEE D Y, et al. Lack of mucosal healing from modified specific carbohydrate diet in pediatric patients with crohn disease[J]. J Pediatr Gastroenterol Nutr, 2017, 65(3): 289-292. doi: 10.1097/MPG.0000000000001619
[67] LEWIS J D, SANDLER R S, BROTHERTON C, et al. A randomized trial comparing the specific carbohydrate diet to a Mediterranean diet in adults with Crohn's disease[J]. Gastroenterology, 2021, 161(3): 837-852, e9. doi: 10.1053/j.gastro.2021.05.047
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