Abdelhamid Asmaa S, Martin Nicole, Bridges Charlene, Brainard Julii S, Wang Xia, Brown Tracey J, Hanson Sarah, Jimoh Oluseyi F, Ajabnoor Sarah M, Deane Katherine Ho, Song Fujian, Hooper Lee
Norwich Medical School, University of East Anglia, Norwich Research Park, Norwich, Norfolk, UK, NR4 7TJ.
Cochrane Database Syst Rev. 2018 Nov 27;11(11):CD012345. doi: 10.1002/14651858.CD012345.pub3.
Evidence on the health effects of total polyunsaturated fatty acids (PUFA) is equivocal. Fish oils are rich in omega-3 PUFA and plant oils in omega-6 PUFA. Evidence suggests that increasing PUFA-rich foods, supplements or supplemented foods can reduce serum cholesterol, but may increase body weight, so overall cardiovascular effects are unclear.
To assess effects of increasing total PUFA intake on cardiovascular disease and all-cause mortality, lipids and adiposity in adults.
We searched CENTRAL, MEDLINE and Embase to April 2017 and clinicaltrials.gov and the World Health Organization International Clinical Trials Registry Platform to September 2016, without language restrictions. We checked trials included in relevant systematic reviews.
We included randomised controlled trials (RCTs) comparing higher with lower PUFA intakes in adults with or without cardiovascular disease that assessed effects over 12 months or longer. We included full texts, abstracts, trials registry entries and unpublished data. Outcomes were all-cause mortality, cardiovascular disease mortality and events, risk factors (blood lipids, adiposity, blood pressure), and adverse events. We excluded trials where we could not separate effects of PUFA intake from other dietary, lifestyle or medication interventions.
Two review authors independently screened titles and abstracts, assessed trials for inclusion, extracted data, and assessed risk of bias. We wrote to authors of included trials for further data. Meta-analyses used random-effects analysis, sensitivity analyses included fixed-effects and limiting to low summary risk of bias. We assessed GRADE quality of evidence.
We included 49 RCTs randomising 24,272 participants, with duration of one to eight years. Eleven included trials were at low summary risk of bias, 33 recruited participants without cardiovascular disease. Baseline PUFA intake was unclear in most trials, but 3.9% to 8% of total energy intake where reported. Most trials gave supplemental capsules, but eight gave dietary advice, eight gave supplemental foods such as nuts or margarine, and three used a combination of methods to increase PUFA.Increasing PUFA intake probably has little or no effect on all-cause mortality (risk 7.8% vs 7.6%, risk ratio (RR) 0.98, 95% confidence interval (CI) 0.89 to 1.07, 19,290 participants in 24 trials), but probably slightly reduces risk of coronary heart disease events from 14.2% to 12.3% (RR 0.87, 95% CI 0.72 to 1.06, 15 trials, 10,076 participants) and cardiovascular disease events from 14.6% to 13.0% (RR 0.89, 95% CI 0.79 to 1.01, 17,799 participants in 21 trials), all moderate-quality evidence. Increasing PUFA may slightly reduce risk of coronary heart disease death (6.6% to 6.1%, RR 0.91, 95% CI 0.78 to 1.06, 9 trials, 8810 participants) andstroke (1.2% to 1.1%, RR 0.91, 95% CI 0.58 to 1.44, 11 trials, 14,742 participants, though confidence intervals include important harms), but has little or no effect on cardiovascular mortality (RR 1.02, 95% CI 0.82 to 1.26, 16 trials, 15,107 participants) all low-quality evidence. Effects of increasing PUFA on major adverse cardiac and cerebrovascular events and atrial fibrillation are unclear as evidence is of very low quality.Increasing PUFA intake probably slightly decreases triglycerides (by 15%, MD -0.12 mmol/L, 95% CI -0.20 to -0.04, 20 trials, 3905 participants), but has little or no effect on total cholesterol (mean difference (MD) -0.12 mmol/L, 95% CI -0.23 to -0.02, 26 trials, 8072 participants), high-density lipoprotein (HDL) (MD -0.01 mmol/L, 95% CI -0.02 to 0.01, 18 trials, 4674 participants) or low-density lipoprotein (LDL) (MD -0.01 mmol/L, 95% CI -0.09 to 0.06, 15 trials, 3362 participants). Increasing PUFA probably has little or no effect on adiposity (body weight MD 0.76 kg, 95% CI 0.34 to 1.19, 12 trials, 7100 participants).Effects of increasing PUFA on serious adverse events such as pulmonary embolism and bleeding are unclear as the evidence is of very low quality.
AUTHORS' CONCLUSIONS: This is the most extensive systematic review of RCTs conducted to date to assess effects of increasing PUFA on cardiovascular disease, mortality, lipids or adiposity. Increasing PUFA intake probably slightly reduces risk of coronary heart disease and cardiovascular disease events, may slightly reduce risk of coronary heart disease mortality and stroke (though not ruling out harms), but has little or no effect on all-cause or cardiovascular disease mortality. The mechanism may be via TG reduction.
关于总多不饱和脂肪酸（PUFA）对健康影响的证据并不明确。鱼油富含ω-3多不饱和脂肪酸，植物油富含ω-6多不饱和脂肪酸。有证据表明，增加富含多不饱和脂肪酸的食物、补充剂或添加了多不饱和脂肪酸的食物摄入量可降低血清胆固醇，但可能会增加体重，因此对心血管的总体影响尚不清楚。
评估增加总多不饱和脂肪酸摄入量对成年人心血管疾病、全因死亡率、血脂和肥胖的影响。
我们检索了截至2017年4月的Cochrane系统评价数据库、MEDLINE和Embase，以及截至2016年9月的ClinicalTrials.gov和世界卫生组织国际临床试验注册平台，无语言限制。我们检查了相关系统评价中纳入的试验。
我们纳入了比较有或无心脑血管疾病的成年人中较高与较低多不饱和脂肪酸摄入量的随机对照试验（RCT），评估时间超过12个月或更长时间。我们纳入了全文、摘要、试验注册条目和未发表的数据。结局指标为全因死亡率、心血管疾病死亡率和事件、危险因素（血脂、肥胖、血压）以及不良事件。我们排除了无法将多不饱和脂肪酸摄入量的影响与其他饮食、生活方式或药物干预的影响区分开来的试验。
两位综述作者独立筛选标题和摘要，评估试验是否纳入，提取数据，并评估偏倚风险。我们写信给纳入试验的作者获取更多数据。荟萃分析采用随机效应分析，敏感性分析包括固定效应分析以及仅限于低偏倚风险汇总的分析。我们评估了证据的GRADE质量。
我们纳入了49项随机对照试验，共24272名参与者，试验持续时间为1至8年。11项纳入试验的汇总偏倚风险较低，33项试验招募的参与者无心脑血管疾病。大多数试验中基线多不饱和脂肪酸摄入量不明确，但报告的摄入量占总能量摄入的3.9%至8%。大多数试验给予补充胶囊，但8项试验给予饮食建议，8项试验给予补充食物如坚果或人造黄油，3项试验采用多种方法增加多不饱和脂肪酸摄入量。增加多不饱和脂肪酸摄入量可能对全因死亡率几乎没有或没有影响（风险分别为7.8%和7.6%，风险比（RR）为0.98，95%置信区间（CI）为从0.89至1.07，24项试验中的19290名参与者），但可能会使冠心病事件风险从14.2%略微降低至12.3%（RR 0.87，95% CI 0.72至1.06，15项试验中的10076名参与者），心血管疾病事件风险从14.6%略微降低至13.0%（RR 0.89，95% CI 0.79至1.01，21项试验中的17799名参与者），所有证据质量为中等。增加多不饱和脂肪酸摄入量可能会略微降低冠心病死亡风险（从6.6%降至6.1%，RR 0.91，95% CI 0.78至1.06，9项试验中的8810名参与者）和中风风险（从1.2%降至1.1%，RR 0.91，95% CI 0.58至1.44，11项试验中的14742名参与者，尽管置信区间包括重要危害），但对心血管疾病死亡率几乎没有或没有影响（RR 1.02，95% CI 0.82至1.26，16项试验中的15107名参与者），所有证据质量为低。增加多不饱和脂肪酸对主要不良心脑血管事件和心房颤动的影响尚不清楚，因为证据质量非常低。增加多不饱和脂肪酸摄入量可能会使甘油三酯略有降低（降低15%，MD -0.12 mmol/L，95% CI -0.20至-0.04，20项试验中的3905名参与者），但对总胆固醇（平均差（MD）-0.12 mmol/L，95% CI -0.23至-0.02，26项试验中的8072名参与者）、高密度脂蛋白（HDL）（MD -0.01 mmol/L，95% CI -0.02至0.01，18项试验中的4674名参与者）或低密度脂蛋白（LDL）（MD -0.01 mmol/L，95% CI -0.09至0.06，15项试验中的3362名参与者）几乎没有或没有影响。增加多不饱和脂肪酸摄入量可能对肥胖几乎没有或没有影响（体重MD 0.76 kg，95% CI 0.34至1.19，12项试验中的7100名参与者）。增加多不饱和脂肪酸对严重不良事件如肺栓塞和出血的影响尚不清楚，因为证据质量非常低。
这是迄今为止对随机对照试验进行的最广泛的系统评价之一，旨在评估增加多不饱和脂肪酸对心血管疾病、死亡率、血脂或肥胖的影响。增加多不饱和脂肪酸摄入量可能会略微降低冠心病和心血管疾病事件的风险，可能会略微降低冠心病死亡和中风的风险（尽管不能排除危害），但对全因或心血管疾病死亡率几乎没有或没有影响。其机制可能是通过降低甘油三酯实现的。
