Al-Khudairy Lena, Hartley Louise, Clar Christine, Flowers Nadine, Hooper Lee, Rees Karen
Division of Health Sciences, Warwick Medical School, University of Warwick, Coventry, UK, CV4 7AL.
Cochrane Database Syst Rev. 2015 Nov 16(11):CD011094. doi: 10.1002/14651858.CD011094.pub2.
Omega 6 plays a vital role in many physiological functions but there is controversy concerning its effect on cardiovascular disease (CVD) risk. There is conflicting evidence whether increasing or decreasing omega 6 intake results in beneficial effects.
The two primary objectives of this Cochrane review were to determine the effectiveness of:1. Increasing omega 6 (Linoleic acid (LA), Gamma-linolenic acid (GLA), Dihomo-gamma-linolenic acid (DGLA), Arachidonic acid (AA), or any combination) intake in place of saturated or monounsaturated fats or carbohydrates for the primary prevention of CVD.2. Decreasing omega 6 (LA, GLA, DGLA, AA, or any combination) intake in place of carbohydrates or protein (or both) for the primary prevention of CVD.
We searched the following electronic databases up to 23 September 2014: the Cochrane Central Register of Controlled Trials (CENTRAL) on the Cochrane Library (Issue 8 of 12, 2014); MEDLINE (Ovid) (1946 to September week 2, 2014); EMBASE Classic and EMBASE (Ovid) (1947 to September 2014); Web of Science Core Collection (Thomson Reuters) (1990 to September 2014); Database of Abstracts of Reviews of Effects (DARE) and Health Technology Assessment Database, and Health Economics Evaluations Database on the Cochrane Library (Issue 3 of 4, 2014). We searched trial registers and reference lists of reviews for further studies. We applied no language restrictions.
Randomised controlled trials (RCTs) of interventions stating an intention to increase or decrease omega 6 fatty acids, lasting at least six months, and including healthy adults or adults at high risk of CVD. The comparison group was given no advice, no supplementation, a placebo, a control diet, or continued with their usual diet. The outcomes of interest were CVD clinical events (all-cause mortality, cardiovascular mortality, non-fatal end points) and CVD risk factors (changes in blood pressure, changes in blood lipids, occurrence of type 2 diabetes). We excluded trials involving exercise or multifactorial interventions to avoid confounding.
Two review authors independently selected trials for inclusion, extracted the data, and assessed the risk of bias in the included trials.
We included four RCTs (five papers) that randomised 660 participants. No ongoing trials were identified. All included trials had at least one domain with an unclear risk of bias. There were no RCTs of omega 6 intake reporting CVD clinical events. Three trials investigated the effect of increased omega 6 intake on lipid levels (total cholesterol, low density lipoprotein (LDL-cholesterol), and high density lipoprotein (HDL-cholesterol)), two trials reported triglycerides, and two trials reported blood pressure (diastolic and systolic blood pressure). Two trials, one with two relevant intervention arms, investigated the effect of decreased omega 6 intake on blood pressure parameters and lipid levels (total cholesterol, LDL-cholesterol, and HDL-cholesterol) and one trial reported triglycerides. Our analyses found no statistically significant effects of either increased or decreased omega 6 intake on CVD risk factors.Two studies were supported by funding from the UK Food Standards Agency and Medical Research Council. One study was supported by Lipid Nutrition, a commercial company in the Netherlands and the Dutch Ministry of Economic Affairs. The final study was supported by grants from the Finnish Food Research Foundation, Finnish Heart Research Foundation, Aarne and Aili Turnen Foundation, and the Research Council for Health, Academy of Finland.
AUTHORS' CONCLUSIONS: We found no studies examining the effects of either increased or decreased omega 6 on our primary outcome CVD clinical endpoints and insufficient evidence to show an effect of increased or decreased omega 6 intake on CVD risk factors such as blood lipids and blood pressure. Very few trials were identified with a relatively small number of participants randomised. There is a need for larger well conducted RCTs assessing cardiovascular events as well as cardiovascular risk factors.
欧米伽6在许多生理功能中起着至关重要的作用,但关于其对心血管疾病(CVD)风险的影响存在争议。关于增加或减少欧米伽6摄入量是否会产生有益效果,证据相互矛盾。
本Cochrane系统评价的两个主要目的是确定以下措施的有效性:1. 增加欧米伽6(亚油酸(LA)、γ-亚麻酸(GLA)、二高-γ-亚麻酸(DGLA)、花生四烯酸(AA)或任何组合)的摄入量,以替代饱和脂肪或单不饱和脂肪或碳水化合物,用于CVD的一级预防。2. 减少欧米伽6(LA、GLA、DGLA、AA或任何组合)的摄入量,以替代碳水化合物或蛋白质(或两者),用于CVD的一级预防。
我们检索了截至2014年9月23日的以下电子数据库:Cochrane图书馆中的Cochrane对照试验中心注册库(CENTRAL)(2014年第12期第8卷);MEDLINE(Ovid)(1946年至2014年9月第2周);EMBASE经典版和EMBASE(Ovid)(1947年至2014年9月);科学引文索引核心合集(汤森路透)(1990年至2014年9月);效果评价文摘数据库(DARE)、卫生技术评估数据库以及Cochrane图书馆中的卫生经济学评价数据库(2014年第4期第3卷)。我们检索了试验注册库和综述的参考文献列表以获取更多研究。我们未设语言限制。
干预措施的随机对照试验(RCT),表明有意增加或减少欧米伽6脂肪酸,持续至少六个月,且纳入健康成年人或CVD高风险成年人。对照组未接受任何建议、未补充任何物质、给予安慰剂、控制饮食或维持其常规饮食。感兴趣的结局为CVD临床事件(全因死亡率、心血管死亡率、非致死性终点)和CVD风险因素(血压变化、血脂变化、2型糖尿病的发生)。我们排除了涉及运动或多因素干预的试验以避免混淆。
两位综述作者独立选择纳入试验、提取数据并评估纳入试验的偏倚风险。
我们纳入了四项RCT(五篇论文),共随机分配了660名参与者。未识别出正在进行的试验。所有纳入试验至少有一个领域的偏倚风险不明确。没有关于欧米伽6摄入量的RCT报告CVD临床事件。三项试验研究了增加欧米伽6摄入量对血脂水平(总胆固醇、低密度脂蛋白(LDL-胆固醇)和高密度脂蛋白(HDL-胆固醇))的影响,两项试验报告了甘油三酯,两项试验报告了血压(舒张压和收缩压)。两项试验(其中一项有两个相关干预组)研究了减少欧米伽6摄入量对血压参数和血脂水平(总胆固醇-LDL-胆固醇和HDL-胆固醇)的影响,一项试验报告了甘油三酯。我们的分析发现,增加或减少欧米伽6摄入量对CVD风险因素均无统计学显著影响。两项研究由英国食品标准局和医学研究理事会资助。一项研究由荷兰的商业公司Lipid Nutrition和荷兰经济事务部资助。最后一项研究由芬兰食品研究基金会、芬兰心脏研究基金会、阿尔内和艾丽·图尔嫩基金会以及芬兰科学院健康研究理事会提供资助。
我们未发现研究考察增加或减少欧米伽6对我们的主要结局CVD临床终点的影响,且证据不足表明增加或减少欧米伽6摄入量对血脂和血压等CVD风险因素有影响。识别出的试验极少,随机分配的参与者数量相对较少。需要进行规模更大、实施良好的RCT来评估心血管事件以及心血管风险因素。