American Journal of Clinical Nutrition:研究挑战了“饮食-心脏假说”——饱和脂肪诱导健康人群LDL-C升高可能是正常的而不是病理反应

2021-01-26 “心关注”公众号 “心关注”公众号

最新膳食脂质的均黏调试(HADL)模型对“饮食-心脏假说”提出了质疑,并解释了脂蛋白胆固醇的变化是一种自适应的稳态调节,有助于维持细胞膜的流动性,从而优化细胞功能。

关于饱和脂肪(SFAs)在健康和疾病中的作用,近年来一直是营养科学领域最大的一个争议话题。与多不饱和脂肪酸(PUFAs)相比,SFAs通常会增加循环中低密度脂蛋白胆固醇(LDL-C)的浓度,LDL-C是动脉粥样硬化性心血管疾病(ASCVD)的危险因素,这就是所谓的“饮食-心脏假说”。然而,在人类适应性生物学的背景下,很少有研究讨论控制饮食诱导的脂蛋白胆固醇动态的调节机制的目的。

近日,一项发表在《美国临床营养学杂志》(American Journal of Clinical Nutrition)上的研究中,来自挪威比约克内斯大学学院、奥斯陆大学医院和卑尔根大学的三位教授提出了一个新的模型,即膳食脂质的均黏调试(the homeoviscous adaptation to dietary lipids,HADL)模型,该模型解释了为什么这个对饮食指南有重大影响的“饮食-心脏假说”可能是错误的。

胆固醇是人体所有细胞的重要分子,细胞周围有一层控制细胞功能的液膜,细胞依靠吸收一定量胆固醇分子的能力,这样细胞膜就不会变得太硬或太流质。该模型建立的基础是,当饮食中的SFAs取代PUFAs时,细胞膜中所需的胆固醇就会减少。当摄入更多的PUFAs,包括Ω-3和Ω-6脂肪酸时,情况正好相反,这是因为饮食中的PUFAs进入细胞膜,使它们更具流动性。细胞通过吸收血液中的胆固醇来调节细胞膜的流动性。根据研究人员提出的模型,这就可以解释为什么当我们摄入更多的PUFAs时,血液胆固醇水平会下降。

细胞需要根据环境条件的变化来调整膜的流动性,例如获得不同类型的脂肪,这种现象被称为均黏调试(Homeoviscous Adaptation),在微生物、脊椎动物和人类皮肤细胞中都有描述。研究作者认为这是人类生理学的一个重要原则,我们的细胞通常能够根据膳食脂肪的变化来调节胆固醇含量。因此该模型被命名为膳食脂质的均黏调试(the homeoviscous adaptation to dietary lipids,HADL)模型。

营养研究通常关注身体的变化,但为什么血液胆固醇等变化的问题同样重要?这就是新的HADL模型发挥作用的地方,它提供了一种基于适应性人体生理学的解释。从HADL模型的角度,研究人员找到了合理的解释,为什么当饮食中的脂肪改变时,细胞需要改变胆固醇含量,从而改变血液中的胆固醇。

众所周知,动脉粥样硬化和心脏病的病因是多因素的。通过这一模型,研究人员建议将饮食对血液胆固醇的升高作用与和心脏病有因果关系的血液胆固醇升高分离开来。

该研究还讨论了心血管疾病患者LDL-C升高的其他原因,如轻度炎症和胰岛素抵抗。这表明,代谢紊乱引起的血胆固醇升高必须与饮食SFAs摄入的重大变化引起的血胆固醇升高分开。同时,研究还质疑了通过在饮食中添加PUFAs来降低血液胆固醇的益处,而不是解决根本原因。

研究人员指出,只有微弱的证据表明摄入过多的SFAs会导致心脏病,总体数据不一致、不可信,更何况缺乏合乎逻辑的生物学和进化论解释。此外,代谢紊乱患者在改变脂肪摄入量时,往往没有显示出预期的血胆固醇变化,这表明他们失去了正常的反应。HADL模型所依据的研究和推理表明,膳食脂肪对血液胆固醇的影响不是致病性反应,而是对饮食变化的完全正常甚至健康的适应。作者同时表示,虽然该模型是基于现有的细胞机制的知识,但仍然需要验证。

原始出处:

Marit Kolby Zincker et al, The homeoviscous adaptation to dietary lipids (HADL) model explains controversies over saturated fat, cholesterol, and cardiovascular disease risk. The American Journal of Clinical Nutrition (2020). DOI: 10.1093/ajcn/nqaa322.

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    2021-01-27 zhwj
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    2021-01-27 zll0628
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    2021-01-26 ms6000000156981277

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