有效、营养、美味还是风险?探索用 FODMAP 饮食管理和治疗肠易激综合征

R. Valk, James Hamill, Mieke Valk
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摘要

肠易激综合征(IBS)是一种使人衰弱、复杂的慢性疾病,其发病机制、病理生理学和临床表现均受多种因素影响。肠易激综合征是最常见的肠脑交互障碍(DGBI),全球发病率从 7% 到 23% 不等。肠易激综合征会降低患者的生活质量,给患者带来沉重负担。此外,由于肠易激综合征的直接和间接医疗费用高达数十亿美元,因此给医疗系统和社会造成了巨大的损失。肠易激综合征的发病机制复杂且多因素。肠易激综合征的常见症状是腹胀、反复发作的腹痛、排气过多、便秘、腹泻或排便习惯交替。许多肠易激综合征患者将摄入特定食物与消化道症状的发作或加重联系起来。因此,许多肠易激综合征患者尝试用饮食疗法来治疗和控制他们的消化道症状。低可发酵低聚糖、双糖、单糖和多元醇(FODMAP)饮食是目前最有实证依据、国际公认的治疗肠易激综合征的可行一线饮食疗法。FODMAPs 是短链碳水化合物,在小肠中吸收不良或不完全,随后被结肠微生物群发酵,产生气体,如氢气、二氧化碳和甲烷。人们认识到有必要阐明 FODMAPs 是如何诱发消化道症状的,并了解 FODMAP 三阶段(限制、重新引入和个性化)饮食是如何发挥作用的。因此,本综述文章旨在阐明 FODMAPs 引起消化道症状的病理生理中枢和外周肠道相关机制,解释 FODMAP 膳食的实施,并强调和驳斥对 FODMAP 膳食长期安全性和风险的担忧。
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Efficacious, Nutritious and Delicious or Risky? Exploring the FODMAP Diet to Manage and Treat Irritable Bowel Syndrome
Irritable bowel syndrome (IBS) is a debilitating, complex, chronic disorder with a multifactorial etiopathogenesis, pathophysiology and clinical phenotype. IBS is the most common disorder of gut-brain interaction (DGBI), with a prevalence ranging from 7% to 23% globally. The burden of IBS on patients is considerable in terms of reduced quality of life. Furthermore, the costs to healthcare systems and society are substantial as IBS accounts for billions of dollars in direct and indirect medical costs. The pathogenesis of this DGBI is complex and multifactorial. Common symptoms of IBS are bloating, reoccurring episodes of abdominal pain, excessive flatus, constipation, diarrhea or alternating bowel habits. Many IBS patients have associated ingestion of specific foods with GI symptoms onset or exacerbation. Therefore, many IBS patients have attempted dietary therapy for the treatment and control of their GI symptoms. The low fermentable oligo-, di-, mono-saccharides, and polyols (FODMAP) diet is currently the most evidence-based and internationally accepted viable first-line dietary therapy for IBS. FODMAPs are short-chain carbohydrates that are poorly or incompletely absorbed in the small intestine and subsequently fermented by the colonic microbiota, leading to the production of gases, such as hydrogen, carbon dioxide, and methane. There is a recognized need to elucidate how FODMAPs induce GI symptoms and to understand how the 3-phase (restriction, re-introduction and personalization) FODMAP diet works. Hence, the objective of this review article is to elucidate the pathophysiological central and peripheral gut-related mechanisms through which FODMAPs cause GI- symptoms, to expound the implementation of the FODMAP diet and to highlight and confute concerns around the safety and risks of the FODMAP diet longterm.
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