Wang Fan, Lin Xue, Zhao Qiu, Li Jin
Department of Gastroenterology, Zhongnan Hospital of Wuhan University, Wuhan, China.
Hubei Clinical Center & Key Lab of Intestinal & Colorectal Diseases, Wuhan, China.
J Gastroenterol Hepatol. 2017 Jan;32(1):19-27. doi: 10.1111/jgh.13416.
Fat intake is generally thought as a risk factor for onset of ulcerative colitis (UC), while epidemiological data had been controversial. This study aimed to evaluate the role of fat intake in the development of UC.
Comprehensive search in PubMed and Embase was conducted to identify all relevant studies, and the role of fat intake in the development of UC was quantitatively assessed by dose-response meta-analysis.
Nine studies (four case-control and five prospective cohort) were indentified with a total of 966 UC cases and 171 589 controls. No evidence of a nonlinear dose-response association was found between fat intake and UC risk. Overall, the summary relative risks (RR) for per 30 g increment/day were 1.023 (95%confidence interval [CI]: 0.963-1.087; I = 24%; n = 6) for total fat intake, 1.063 (95%CI: 0.845-1.337; I = 44.5%; n = 4) for saturated fat intake, 1.214 (95%CI: 0.911-1.618; I = 63.1%; n = 4) for monounsaturated fat (MUFA) intake, and 1.247 (95%CI: 0.948-1.640; I = 25.4%; n = 4) for polyunsaturated fat (PUFA) intake, respectively. Subgroup and sensitivity analyses showed inconsistent results on PUFA intake, which was significantly related with UC risk after adjusting for smoking (RR: 1.617, 95%CI: 1.045-2.502; I = 0%; n = 3). For PUFA and MUFA subtypes, no subtypes were significantly associated with UC risk (P > 0.05), and only docosahexaenoic acid showed a potential protective effect in the development of UC (RR for the highest versus lowest intake level: 0.642, 95%CI: 0.403-1.024; I = 34.4%; n = 3) CONCLUSIONS: This meta-analysis suggested a lack of association between fat intake and UC risk, and large-scale prospective designed studies are warranted to confirm our findings.
脂肪摄入通常被认为是溃疡性结肠炎（UC）发病的危险因素，然而流行病学数据一直存在争议。本研究旨在评估脂肪摄入在UC发生发展中的作用。
在PubMed和Embase中进行全面检索以识别所有相关研究，并通过剂量反应荟萃分析定量评估脂肪摄入在UC发生发展中的作用。
共纳入9项研究（4项病例对照研究和5项前瞻性队列研究），总计966例UC病例和171589例对照。未发现脂肪摄入与UC风险之间存在非线性剂量反应关联。总体而言，总脂肪摄入量每增加30g/天的汇总相对风险（RR）为1.023（95%置信区间[CI]：0.963 - 1.087；I² = 24%；n = 6），饱和脂肪摄入量为1.063（95%CI：0.845 - 1.337；I² = 44.5%；n = 4），单不饱和脂肪（MUFA）摄入量为1.214（95%CI：0.911 - 1.618；I² = 63.1%；n = 4），多不饱和脂肪（PUFA）摄入量为1.247（95%CI：0.948 - 1.640；I² = 25.4%；n = 4）。亚组分析和敏感性分析显示，PUFA摄入量的结果不一致，在调整吸烟因素后，PUFA摄入量与UC风险显著相关（RR：1.617，95%CI：1.045 - 2.502；I² = 0%；n = 3）。对于PUFA和MUFA亚型，没有亚型与UC风险显著相关（P > 0.05），只有二十二碳六烯酸在UC发生发展中显示出潜在的保护作用（最高摄入量与最低摄入量水平的RR：0.642，95%CI：0.403 - 1.024；I² = 34.4%；n = 3）。结论：这项荟萃分析表明脂肪摄入与UC风险之间缺乏关联，有必要开展大规模前瞻性设计研究以证实我们的发现。
