背景:已经观察到饱和脂肪酸(SFA)摄入量与Lp(a)浓度之间的反比关系;但是,这种影响还没有量化。
目的:目的是确定在没有动脉粥样硬化性心血管疾病(ASCVD)的成年人中,服用SFA是否会改变Lp(a)水平。
方法:对没有ASCVD的成年人中比较低SFA饮食和高SFA饮食的随机对照试验进行系统评价和荟萃分析。PubMed,Cochrane临床试验中央注册中心,ClinicalTrials.gov,到2023年10月,搜索了WebofScience数据库和登记册。较低与较低饮食之间Lp(a)的标准化平均差使用随机效应荟萃分析确定SFA较高(能量百分比[%E])。还进行了分析,以检查用碳水化合物(CHO)代替SFA的效果,单不饱和(MUFA),多不饱和(PUFA),或反式脂肪酸(TFA)。
结果:总计,在系统搜索中确定了6,255种出版物。26篇出版物报告了27项随机对照试验,包括1,325名参与者和49名饮食比较,包括在内。较低与较低之间的SFA平均差较高的SFA饮食为7.6%E(3.7%-17.8%E)。在较低的SFA饮食之后,与较高的SFA饮食相比,Lp(a)浓度较高(SMD0.14[95CI:0.03,0.24])。亚组分析显示,在用CHO(试验=8,n=539;SMD0.21[95CI:0.02,0.40])或TFA(试验=8,n=300;SMD0.32[95CI:0.17,0.48])代替SFA后,Lp(a)较高。当MUFA(试验=16,n=641;SMD0.04[95CI:-0.08,0.16])或PUFA(试验=8,n=415;SMD0.09[-0.04,0.22])替代SFA时,未观察到Lp(a)的差异。
结论:在没有ASCVD的个体中,与较高的SFA饮食相比,较低的SFA饮食适度增加Lp(a)。这种效应似乎是由用CHO或TFA代替SFA引起的。需要研究饮食诱导的Lp(a)变化的动脉粥样硬化,以告知脂质/脂蛋白紊乱的饮食管理。(PROSPERO注册号:CRD42020154169)。
BACKGROUND: An inverse relationship between saturated fatty acid (SFA) intake and Lp(a) concentration has been observed; however, there has been no quantification of this effect.
OBJECTIVE: The objective was to determine if SFA consumption alters Lp(a) levels among adults without atherosclerotic cardiovascular disease (ASCVD).
METHODS: A systematic review and meta-analysis of randomized controlled trials contrasting a lower SFA diet(s) with a higher SFA diet(s) among adults without ASCVD was conducted. PubMed, Cochrane Central Register of Clinical Trials, ClinicalTrials.gov, and Web of Science databases and registers were searched through October 2023. The standardized mean difference in Lp(a) between diets lower vs. higher in SFA (percent of energy [%E]) was determined using random-effects meta-analysis. Analyses were also conducted to examine the effect of replacing SFA with
carbohydrates (CHO), monounsaturated (MUFA), polyunsaturated (PUFA), or trans fatty acids (TFAs).
RESULTS: In total, 6,255 publications were identified in the systematic search. Twenty-six publications reporting 27 randomized controlled trials, including 1,325 participants and 49 diet comparisons, were included. The mean difference in SFA between lower vs. higher SFA diets was 7.6% E (3.7% - 17.8% E). After lower SFA diets, Lp(a) concentration was higher (SMD 0.14 [95%CI: 0.03, 0.24]) compared to higher SFA diets. Subgroup analyses showed higher Lp(a) following diets where SFA was replaced by CHO (trials=8, n=539; SMD 0.21 [95%CI: 0.02, 0.40]) or TFAs (trials=8, n=300; SMD 0.32 [95%CI: 0.17, 0.48]). No differences in Lp(a) were observed when MUFA (trials=16, n=641; SMD 0.04 [95%CI: -0.08, 0.16]) or PUFA (trials=8, n=415; SMD 0.09 [-0.04, 0.22]) replaced SFA.
CONCLUSIONS: Lower SFA diets modestly increase Lp(a) compared to higher SFA diets among individuals without ASCVD. This effect appeared to be driven by replacement of SFA with CHO or TFA. Research investigating the atherogenicity of diet induced Lp(a) changes is needed to inform dietary management of lipid/lipoprotein disorders. (PROSPERO Registration number: CRD42020154169).