Limketkai Berkeley N, Iheozor-Ejiofor Zipporah, Gjuladin-Hellon Teuta, Parian Alyssa, Matarese Laura E, Bracewell Kelly, MacDonald John K, Gordon Morris, Mullin Gerard E
Division of Digestive Diseases, University of California Los Angeles, 100 UCLA Medical Plaza, Suite 345, Los Angeles, California, USA, 90095.
Cochrane Database Syst Rev. 2019 Feb 8;2(2):CD012839. doi: 10.1002/14651858.CD012839.pub2.
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.
To evaluate the efficacy and safety of dietary interventions on IBD outcomes.
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.
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.
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.
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.
炎症性肠病(IBD)包括克罗恩病(CD)和溃疡性结肠炎(UC),其特征为慢性黏膜炎症、频繁住院、不良的健康经济学状况以及生活质量受损。有假说认为饮食会影响IBD的活动。
评估饮食干预对IBD结局的疗效和安全性。
我们检索了Cochrane IBD小组专业注册库、CENTRAL、MEDLINE、Embase、科学引文索引、Clinicaltrials.gov以及世界卫生组织国际临床试验注册平台,检索时间从各库建库起至2019年1月31日。我们还浏览了纳入研究的参考文献列表、相关综述和指南。
我们纳入了比较饮食干预与其他饮食对IBD参与者影响的随机对照试验(RCT)。专门关注肠内营养、口服营养补充剂、医用食品、益生菌和肠外营养的研究被排除。
两位综述作者独立进行研究筛选、提取数据并使用偏倚风险工具评估偏倚。我们尽可能使用随机效应模型进行荟萃分析,并计算二分结局的风险比(RR)及相应的95%置信区间(CI)。我们使用GRADE评估证据的确定性。
该综述纳入了18项RCT,共1878名参与者。这些研究评估了针对活动期CD(6项研究)、非活动期CD(7项研究)、活动期UC(1项研究)和非活动期UC(4项研究)的不同饮食干预。饮食干预包括食用少量或完全排除一种或多种已知会引发IBD症状的食物组。由于干预措施和对照饮食各不相同,数据合并的范围有限。这些研究大多样本量不足。14项研究被评为高偏倚风险。其他研究被评为偏倚风险不明确。高纤维、低精制碳水化合物、低微粒饮食、低钙饮食、症状导向饮食和高度限制的有机饮食对活动期CD临床缓解的影响尚不确定。在4周时,低精制碳水化合物饮食组100%(4/4)的参与者实现缓解,而对照组为0%(0/3)(RR 7.20,95%CI 0.53至97.83;7名参与者;1项研究;极低确定性证据)。在16周时,低微粒饮食组44%(23/52)的参与者实现临床缓解,而对照组为25%(13/51)(RR 3.13,95%CI 0.22至43.84;103名参与者;2项研究;I² = 73%;极低确定性证据)。症状导向饮食组50%(16/32)的参与者实现临床缓解,而对照组为0%(0/19)(RR 20.00,95%CI 1.27至315.40;51名参与者;1项研究;极低确定性证据)(随访情况不明确)。在24周时,高度限制的有机饮食组50%(4/8)的参与者实现临床缓解,而对照组为50%(5/10)(RR 1.00,95%CI 0.39至2.53;18名参与者;1项研究;极低确定性证据)。在16周时,低钙饮食组37%(16/43)的参与者实现临床缓解,而对照组为30%(12/40)(RR 1.24,95%CI 0.67至2.29;8名参与者;1项研究;极低确定性证据)。低精制碳水化合物饮食、症状导向饮食和低红色加工肉类饮食对非活动期CD复发的影响尚不确定。在12至24个月时,低精制碳水化合物饮食组67%(176/264)的参与者复发,而对照组为64%(193/303)(RR 1.04,95%CI 0.87至1.25;567名参与者;3项研究;I² = 35%;低确定性证据)。在6至24个月时,症状导向饮食组48%(24/50)的参与者复发,而对照饮食组为83%(40/48)(RR 0.53,95%CI 0.28至1.01;98名参与者;2项研究;I² = 54%;低确定性证据)。在48周时,低红色和加工肉类饮食组66%(63/96)的参与者复发,而对照组为63%(75/118)(RR 1.03,95%CI 0.85至1.26;214名参与者;1项研究;低确定性证据)。在12个月时,由低双糖/谷物/饱和脂肪/红色和加工肉类组成的排除饮食组0%(0/16)的参与者出现临床复发,而对照组为26%(10/38)(RR 0.11,95%CI 0.01至1.76;54名参与者;1项研究;极低确定性证据)。症状导向饮食对活动期UC临床缓解的影响尚不确定。在6周时,症状导向饮食组36%(4/11)的参与者实现缓解,而常规饮食组为0%(0/10)(RR 8.,25,95%CI 0.50至136.33;21名参与者;1项研究;极低确定性证据)。基于艾伯塔省的抗炎饮食、无角叉菜胶饮食或无奶饮食对非活动期UC复发率的影响尚不确定。在6个月时,基于艾伯塔省的抗炎饮食组36%(5/14)的参与者复发,而对照组为29%(4/14)(RR 1.25,95%CI 0.42至3.70;28名参与者;1项研究;极低确定性证据)。无角叉菜胶饮食组12个月后30%(3/10)的参与者复发,而对照组为60%(3/5)(RR 0.50,95%CI 0.15至1.64;15名参与者;1项研究;极低确定性证据)。在12个月时,无奶饮食组59%(23/39)的参与者复发,而对照饮食组为68%(26/38)(RR 0.83,95%CI 0.60至1.15;77名参与者;2项研究;I² = 0%;低确定性证据)。纳入的研究均未报告与饮食相关的不良事件。
饮食干预对CD和UC的影响尚不确定。因此,无法就饮食干预在CD和UC中的利弊得出确凿结论。需要就IBD饮食干预的组成达成共识,并且需要更多的RCT来评估这些干预措施。目前,至少有五项正在进行的研究(估计招募498名参与者)。当这些研究结果可用时,本综述将进行更新。