A changing view on saturated fatty acids and dairy: from enemy to friend.

A changing view on saturated fatty acids and dairy: from enemy to friend.
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对饱和脂肪酸和乳制品的看法不断变化:从敌人到朋友。

DOI:
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发表时间:
2014
影响因子:
7.1
通讯作者:
A. Astrup
A. Astrup
中科院分区:
医学1区
文献类型:
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作者:
A. Astrup

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几乎所有国家的膳食指南都建议减少SFA作为降低心血管疾病(CVD)发病率和死亡率的关键干预措施。这已转化为建议,以减少摄入的主要来源的SFAs,即乳制品,肉类产品和鸡蛋。然而,最近对观察性研究和随机对照试验的荟萃分析不仅对这一建议的科学依据提出了质疑,而且实际上破坏了它。很明显,需要一种完全不同的方法,基于食物而不是营养素的建议。支持减少SFA的证据基于两步论证:“大量证据表明,大多数膳食SFA(A)的摄入量较高与血液总胆固醇和低密度脂蛋白(LDL)胆固醇(B)水平较高有关。较高的总胆固醇和低密度脂蛋白胆固醇水平(B)是心血管疾病的风险因素(C)(1)。大多数人会将上述声明解释为摄入SFA(A)和CVD(C)之间存在因果关系的证据,但实际上这是一种假设,即LDL胆固醇(B)浓度的增加总是会增加CVD(C)的风险。然而,膳食脂肪(和其他膳食成分)与CVD之间的关系要复杂得多,并且这种假设没有考虑LDL-胆固醇颗粒大小的重要性,对HDL胆固醇的影响以及动脉粥样硬化,血栓形成和血栓溶解过程的其他介质(2)。
Almost all national dietary guidelines recommend a reduction in SFAs as a key intervention to reduce incidence and mortality of cardiovascular disease (CVD). This has been translated into advice to reduce the intake of the major sources of SFAs, that is, dairy produce, meat products, and eggs. However, recent meta-analyses of both observational studies and randomized controlled trials not only have raised doubts about the scientific substantiation for this advice but have actually undermined it. It has become clear that there is a need for a completely different approach, with advice that is based on foods rather than on nutrients. The evidence to support reducing SFAs rests on a 2-step argument: ‘‘A strong body of evidence indicates that higher intake of most dietary SFA (A) is associated with higher levels of blood total cholesterol and low-density lipoprotein (LDL) cholesterol (B). Higher total and LDL cholesterol levels (B) are risk factors for CVD (C)’’ (1). Most would interpret the statement above as evidence of a causal relation between intake of SFAs (A) and CVD (C), but it is actually an assumption that increased concentrations of LDL cholesterol (B) will always increase the risk of CVD (C). The relation between dietary fats (and other dietary components) and CVD is, however, much more complex, and this assumption does not take into account the importance of LDL-cholesterol particle size, effects on HDL cholesterol, and other mediators of the atherosclerotic, thrombotic, and thrombolytic processes (2).
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