发布日期：2017年5月5日

原文地址：www.virtahealth.com

这里有一个有趣的悖论。在过去的四十年里，营养政策的制定者越来越多的劝诫我们：少吃饱和脂肪。由于这一坚持不懈的信息，普通民众相信就算如果没有明确的毒性，饱和脂肪至少也是不健康的。

此外，天然含有饱和脂肪的食物，如牛肉、猪肉、奶制品、鸡蛋、巧克力和热带植物的油，也被认为是不健康的。矛盾的是，随着反对饱和脂肪的声音越来越大，支持这一假设的科学已经陷入混乱。我们难道应该逆来顺受的接受这个在科学上已经无效的结论？

饱和脂肪会导致心脏病吗？

前后两代的研究人员试图证明食用饱和脂肪会导致心脏病。但这个假设并不是坚如磐石。其相关的科学数据并没有变得更有说服力，反而越来越多地漏洞百出（除了漏洞之外，几乎不剩什么有价值的东西）。

例如，近年来多个荟萃分析（Meta- analyses）对大量人群进行了细致的跟踪，时间长达几十年。研究了他们吃什么和因为什么原因去世[1-4]。所有这些都表明，饮食饱和脂肪摄入量与心脏病或各种原因死亡的风险之间没有一致的关联。

事实上，这些研究中一些结果恰恰相反——饮食饱和脂肪摄入量与动脉粥样硬化或中风呈负相关。有趣的是，他们还表明，当膳食饱和脂肪减少并被碳水化合物取代时，一个人发生冠状动脉事件的风险会增加。

这正是问题所在。

通过激发人们对饱和脂肪的恐惧，人们可能会选择低脂肪、高碳水化合物的食物。事实上，这是正在发生的事情。根据一项政府资助的调查，[5]美国人减少了饱和脂肪的摄入，并用更多的碳水化合物来弥补能量缺口。在肥胖和糖尿病发病率飙升的同时，这种将饱和脂肪换成碳水化合物的饮食转变也同时发生。

这可能是个巧合，但更可能是一个极其不幸的“意外”后果。

饮食中的饱和脂肪会影响血液中饱和脂肪的水平吗？

我们想说的是：我们所学到的关于膳食脂肪的很多知识都是错误的。但这怎么可能——那些得到大批科学家支持的明智决策者都弄错了这一切？

这是一个很长的故事，一个很好的开始是阅读加里·陶布斯（Gary Taubes）[6]的《好卡路里，坏卡路里》（good Calories，Bad Calories）和尼娜·泰科尔兹（Nina Teicholz）[7]的《关于脂肪的大惊喜》（The Big Fat Surprise），这两位都是备受尊敬的调查记者。

简而言之，50年前，人们发现病变的冠状动脉含有大量的胆固醇和饱和脂肪。明尼苏达大学的安塞尔·凯斯（Ancel Keyes）教授假设，饮食中这两种营养素过多是原因——也就是说，他的假设是建立在有缺陷的概念上的，即“你吃什么就生长出什么”（you are what you eat）。

随后的研究也显示，血液中饱和脂肪的水平可以预测未来的心脏病[8-11]和糖尿病病例[12-15]，这似乎支持了凯斯的假设。

不过，这里的关键问题是：“从食物中摄入的饮食饱和脂肪和血液中的饱和脂肪水平之间的确切关系是什么？”

对于那些仍然相信“你吃什么就生长出什么”的人来说，答案很简单。从这个简单的答案可以看出，没有人想在臀部或动脉中积累饱和脂肪。这是如此本能的逻辑，以至于大多数人，包括许多著名的营养学研究人员，都懒得质疑它。

简言之，当前国家政策“不要吃饱和脂肪”是建立在一个简单的结论上。然而，科学证据清楚地表明，膳食饱和脂肪的摄入量和血清饱和脂肪的水平几乎没有相关性。

因此，我们建议大家摒弃这种有缺陷的肤浅结论，代之以：你的身体由食物中留存的物质组成。（you are what you save from what you eat.）

是什么导致血液中饱和脂肪含量高？

如果膳食饱和脂肪摄入量与我们血液中的饱和脂肪水平几乎没有关系，那又是什么呢？事实上，有确凿的证据表明，从食物中摄入的碳水化合物是血清饱和脂肪水平的主要决定因素。

我们之所以知道这一点是因为高质量的实验结论。例如：两个受人尊敬的研究小组[16,17]向参与者提供了经过仔细测量的、保持体重不变的高碳水化合物或中等碳水化合物饮食。在这两项研究中，高碳水化合物饮食中饱和脂肪的血液水平急剧上升，尽管它们的脂肪含量很低。

我们[18]进行了一项减肥研究，期间我们每天摄入32至84克不等的饱和脂肪，同时也用“健康“的碳水化合物来弥补饮食脂肪减少时的能量差异。

在血液甘油三酯和胆固醇酯中，当摄入高碳水化合物、极低脂肪的饮食时，血液饱和脂肪水平呈上升趋势，尽管由于饮食受到能量限制，导致体脂减少。

从表面上看，这似乎是一个悖论；但稍加思考，这是有道理的。高碳水化合物摄入通过两件事来促进饱和脂肪水平的提高。

首先，碳水化合物刺激身体制造更多的胰岛素，从而抑制饱和脂肪的氧化。因此，当胰岛素水平高时，饱和脂肪往往被储存而不是作为燃料燃烧。

其次，高碳水化合物的摄入促进了肝脏中饱和脂肪的合成。这对于胰岛素抵抗的个体来说尤其如此，在我们最近的书中被描述为“碳水化合物不耐受”。[19]

胰岛素抵抗使肌肉更难吸收和利用血糖，从而导致肝脏更容易将膳食碳水化合物转化为身体的脂肪。因此，氧化减少和增加饱和脂肪合成导致饱和脂肪在血液和组织中的积累。那么罪魁祸首显然不是饮食饱和脂肪本身，而是摄入了超过身体能有效管理的，更多的碳水化合物。

碳水化合物耐受性的阈值因人而异，而且在一生中也会发生变化。因此，那些纤瘦的模特宣传她们在吃低脂饮食，实际是她们可以耐受碳水，但这并不意味着适合你。当模特们50岁时，新陈代谢发生变化时，这也可能不再适合她们了。

饱和脂肪的安全性

你可能会问，如果摄入饱和脂肪不会对身体产生有害影响，这是否意味着这类脂肪完全没有问题？我们的回答是，营养科学非常复杂，所以要小心非黑即白的答案。

尽管膳食饱和脂肪摄入量与慢性病风险无关，但血液中较高的饱和脂肪水平确实会带来问题。正如我们所指出的，每个个体对任何一种饮食的反应都有很大的差异，如果易感个体同时选择摄入高水平的碳水化合物和饱和脂肪，这一点可能尤为重要。

因此，人们需要测试其对摄入的碳水化合物和饱和脂肪的正确量，以满足个性化的代谢耐受度。

除了上文提到的高碳水化合物饮食会增加饱和脂肪的血液水平的研究之外，我们还进行了两项研究[20，21]，允许6-12周的时间适应中等碳水化合物或极低碳水化合物饮食。

这些都不是非常低热量的饮食，低碳水化合物饮食天然的含有相当高的脂肪，饱和脂肪的摄入量是对照组中（中等碳水化合物饮食组）的饱和脂肪的2-3倍。

结果非常惊人：与低脂饮食相比，低碳水化合物、高脂肪饮食显著降低了饱和脂肪的血液水平。

我们的数据表明，这是因为低胰岛素水平加速了所有脂肪（尤其是饱和脂肪）的氧化；再加上膳食碳水化合物的相对缺乏，意味着没有太多碳水化合物转化为饱和脂肪。因此，从身体的角度来看，低碳水化合物饮食可以降低血液饱和脂肪水平，且该水平与饮食摄入的饱和脂肪无关。

总结

因此，我们以一种充满希望的语气结束这段关于可怜的、被践踏的饱和脂肪的“悲惨”经历。是的，在发达国家，饮食中的饱和脂肪仍然是许多健康问题被假定的“凶手“。

然而，我们现在知道，营养政策制定者以提高血液饱和脂肪水平的罪名起诉了错误的宏观营养素（宏观营养素包括碳水化合物，脂肪和蛋白质）。

如果我们能摒弃“你吃什么就生长什么”这句话，也许营养机构会拓宽他们的视野，考虑其他的“凶手“并对整体健康和疾病做出贡献。

有令人信服的证据表明，饮食碳水化合物对身体处理饱和脂肪的方式有重要影响。因此，饱和脂肪，无论是在体内制造的还是在饮食中食用的，在高水平饮食碳水化合物的帮助和怂恿下更容易积累，尤其是在胰岛素抵抗的个体中（如2型糖尿病或代谢综合征）。

特别是针对上述有基础代谢问题的庞大人群，这个一刀切的建议，即“积极降低饱和脂肪摄入量，期望降低血液饱和脂肪水平”，从理性角度来看是无效的，而且可能适得其反。

考虑到我们目前肥胖和糖尿病的流行，我们无法承受这个有缺陷的、过于简单的饮食政策。

应用的文献

1. Siri-Tarino PW, Sun Q, Hu FB, Krauss RM. Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease. Am J Clin Nutr. 2010 Mar;91(3):535-46.
2. Jakobsen MU, O’Reilly EJ, Heitmann BL, Pereira MA, Bälter K, Fraser GE, Goldbourt U, Hallmans G, Knekt P, Liu S, Pietinen P, Spiegelman D, Stevens J, Virtamo J, Willett WC, Ascherio A. Major types of dietary fat and risk of coronary heart disease: a pooled analysis of 11 cohort studies. Am J Clin Nutr. 2009 May;89(5):1425-32.
3. Skeaff CM, Miller J. Dietary fat and coronary heart disease: summary of evidence from prospective cohort and randomised controlled trials. Ann Nutr Metab. 2009;55(1-3):173-201.
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5. Centers for Disease Control and Prevention (CDC). Trends in intake of energy and macronutrients–United States, 1971-2000. MMWR Morb Mortal Wkly Rep. 2004 Feb 6;53(4):80-2.
6. Taubes, G. Good Calories, Bad Calories. Knopf, September 25, 2007.
7. Teicholz N. The Big Fat Surprise. Simon & Schuster; May 2014
8. Miettinen TA, Naukkarinen V, Huttunen JK, Mattila S, Kumlin T. Fatty-acid composition of serum lipids predicts myocardial infarction. Br Med J (Clin Res Ed). 1982 Oct 9;285(6347):993-6.
9. Simon JA, Hodgkins ML, Browner WS, Neuhaus JM, Bernert JT Jr, Hulley SB. Serum fatty acids and the risk of coronary heart disease. Am J Epidemiol. 1995 Sep 1;142(5):469-76.
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11. Yamagishi K, Nettleton JA, Folsom AR; ARIC Study Investigators. Plasma fatty acid composition and incident heart failure in middle-aged adults: the Atherosclerosis Risk in Communities (ARIC) Study. Am Heart J. 2008 Nov;156(5):965-74.
12. Wang L, Folsom AR, Zheng ZJ, Pankow JS, Eckfeldt JH; ARIC Study Investigators. Plasma fatty acid composition and incidence of diabetes in middle-aged adults: the Atherosclerosis Risk in Communities (ARIC) Study. Am J Clin Nutr. 2003 Jul;78(1):91-8.
13. Warensjö E, Risérus U, Vessby B. Fatty acid composition of serum lipids predicts the development of the metabolic syndrome in men. Diabetologia. 2005 Oct;48(10):1999-2005.
14. Hodge AM, English DR, O’Dea K, Sinclair AJ, Makrides M, Gibson RA, Giles GG. Plasma phospholipid and dietary fatty acids as predictors of type 2 diabetes: interpreting the role of linoleic acid. Am J Clin Nutr. 2007 Jul;86(1):189-97.
15. Patel PS, Sharp SJ, Jansen E, Luben RN, Khaw KT, Wareham NJ, Forouhi NG. Fatty acids measured in plasma and erythrocyte-membrane phospholipids and derived by food-frequency questionnaire and the risk of new-onset type 2 diabetes: a pilot study in the European Prospective Investigation into Cancer and Nutrition (EPIC)-Norfolk cohort. Am J Clin Nutr. 2010 Nov;92(5):1214-22.
16. Raatz SK, Bibus D, Thomas W, Kris-Etherton P. Total fat intake modifies plasma fatty acid composition in humans. J Nutr. 2001 Feb;131(2):231-4.
17. King IB, Lemaitre RN, Kestin M. Effect of a low-fat diet on fatty acid composition in red cells, plasma phospholipids, and cholesterol esters: investigation of a biomarker of total fat intake. Am J Clin Nutr. 2006 Feb;83(2):227-36.
18. Volk BM Kunces LJ, Freidenreich DJ, Kupchak BR, Saenz C, Artistizabal JC, Fernandez ML,
 Bruno RS, Maresh CM, Kraemer WJ Phinney SD, Volek JS. Effects of Step-Wise Increases in Dietary Carbohydrate on Circulating Saturated Fatty Acids and Palmitoleic Acid in Adults with Metabolic Syndrome. PLOS ONE | DOI:10.1371/journal.pone.0113605 November 21, 2014
19. Volek J, Phinney SD. The Art and Science of Low Carbohydrate Living. Beyond Obesity, May 2011.
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原文地址：www.virtahealth.com

翻译转载于：www.gowiselife.com（重返人生网）

原文：

The Sad Saga of Saturated Fat

Published on 

May 5, 2017

Jeff Volek, PhD, RD

Stephen Phinney, MD, PhD

Here’s a fascinating paradox. Over the last four decades, nutrition policy makers have increasingly exhorted us to eat less saturated fat. As a result of this unremitting message, the general population believes this single nutrient, if not overtly toxic, will at least cause widespread bodily damage. Additionally, foods that naturally contain saturated fat, such as beef, pork, dairy, eggs, chocolate, and tropical oils, have been branded unhealthy. The paradox here is that as the drumbeat against saturated fats has increased, the actual science supporting this message has fallen into shambles. Should we all just be good citizens and swallow this advice, even if the science behind it can no longer pass muster?

Does saturated fat cause heart disease?

Two generations of researchers have tried to prove that eating saturated fat causes heart disease. Rather than growing stronger, as would be the case if this hypothesis were rock-solid, increasingly the scientific data is painting a picture more akin to low-fat Swiss cheese (i.e., not much there besides the holes). Take, for example, multiple recent meta-analyses of large populations followed carefully for decades, examining what they eat and what they die of [1-4] All show no consistent association between dietary saturated fat intake and risk for heart disease or death from all causes. In fact some of these studies show just the opposite – an inverse association of dietary saturated fat intakes and atherosclerosis or stroke. Interestingly, they also suggest that one’s risk for a coronary event increases when dietary saturated fat is reduced and replaced by carbohydrate.

Here’s the problem as we see it. By continuing to provoke fear about the harmful effects of saturated fat, the likely response is that people will seek out foods low in fat and higher in carbohydrate. And in reality, that’s exactly what appears to be happening. According to a government-funded survey, [5] Americans have decreased their consumption of saturated fat and replaced those calories with an even greater amount of carbohydrate. This dietary flip-flop of trading away saturated fat and replacing it with carbohydrate has occurred in the same time interval as rates of obesity and diabetes have rocketed skywards. This might be coincidence, or more likely it’s an extremely unfortunate unintended consequence.

‍

Does dietary saturated fat contribute to levels of saturated fat in the blood?

Okay, so what we’re essentially doing here is telling you that much of what we’ve been taught about dietary fat is wrong. How could this be – that all those wise policy-makers backed up by legions of academic scientists have gotten this all wrong? That’s a long story, and a good place to start would be to read Good Calories, Bad Calories by Gary Taubes [6] and The Big Fat Surprise by Nina Teicholz, [7] both highly regarded investigative journalists. In short, 50 years ago diseased coronary arteries were found to contain buildups of cholesterol and saturated fat. Professor Ancel Keyes of the University of Minnesota hypothesized that too much of these two nutrients in the diet were the cause – i.e., his hypothesis was built on the flawed concept that you are what you eat. Then came well done studies showing that blood levels of saturated fats predict future cases of heart disease [8-11] and diabetes, [12-15] thus appearing to support Keyes’ hypothesis. But this works only if you believe this flawed sound bite, a concept that doesn’t pass the red-face test.

Obviously, the key question here is, “what’s the precise relationship between dietary saturated fat and blood levels of saturated fat?” For people who still believe you are what you eat, the answer is easy. And it follows from that easy answer that no one wants to accumulate saturated fat on their hips or lining their arteries. This is so instinctively logical that most people, including many prominent nutrition researchers, haven’t bothered to question it. Simply put, the current national policy imperative “don’t eat saturated fat“ is based on a sound bite. The scientific evidence, however, clearly shows that dietary intake and serum levels of saturated fat show little if any correlation. Thus our advice that we banish this flawed sound bite and replace it with: you are what you save from what you eat.

‍

What causes high levels of saturated fat in the blood?

‍If dietary saturated fat intake has little to do with saturated levels in our blood, then what does? There is, in fact, sound evidence that dietary carbohydrate is a major determinant of serum saturated fat levels. We know this because two respected research groups [16,17] fed humans carefully measured, weight-maintaining diets either high in carbohydrate or moderate in carbohydrate. In both studies, blood levels of saturated fats went up dramatically on the high carb diets, even though they were very low in fat. We [18] performed a weight loss study during which we fed diets varying from 32 up to 84 grams of saturated fat per day, with “healthy carbohydrate” making up the energy difference when dietary fat was reduced. In blood triglycerides and cholesteryl esters, saturated fat levels trended upwards when the high carbohydrate, very low fat diet was consumed, despite the diet being energy restricted, causing ongoing body fat loss.

On its surface, this looks like a paradox; but with a little thought it makes sense. A high carbohydrate intake has two effects in the body that promote higher levels of saturated fat. First, carbohydrates stimulate the body to make more insulin, which inhibits the oxidation of saturated fat. Thus, when insulin levels are high, saturated fat tends to be stored rather than burned as fuel. Second, a high carbohydrate intake promotes the synthesis of saturated fat in the liver. This is particularly problematic for individuals with insulin resistance, characterized as “carbohydrate intolerance” in our recent book. [19]‍

Insulin resistance makes it harder for muscles to take up and use blood sugar, thus causing a higher propensity for the liver to convert dietary carbohydrate into body fat. This combination of decreased oxidation and increased synthesis of saturated fat therefore results in accumulation of saturated fats in the blood and tissues. The culprit then is clearly not dietary saturated fat per se, but rather consumption of more carbohydrate than an individual’s body can efficiently manage. This threshold of carbohydrate tolerance varies from person to person, and it can also change over a lifetime. Thus the skinny model promoting her particular version of a low fat diet may actually thrive on it herself, but that doesn’t mean that it’s right for you if you weren’t born skinny. And of course, it also may not even be right for her when she’s 50 and her metabolism has changed.

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The safety of saturated fat

So, you may be asking, if consumption of saturated fat is not associated with harmful effects on the body, does this mean that this class of fats is completely off the hook? Our response is that the science of nutrition is pretty complex, so beware of black and white answers. Whereas dietary saturated fat intake is unrelated to risk for chronic disease, higher saturated fat levels in the blood do appear to pose a problem. As we noted, there is a lot of variation between individuals in their responses to any one diet, and this may be particularly important if a susceptible individual chooses to consume high levels of carbohydrates and saturated fat. Thus there is an unmet need for tests that will guide individuals to the correct amounts of both carbohydrates and saturated fat to match their personal metabolic tolerances.

In addition to the studies mentioned above in which high carbohydrate feeding increased blood levels of saturated fats, we conducted a pair of studies [20, 21] allowing 6-12 weeks for adaptation to moderate carbohydrate or very low carbohydrate diets. Because these were not very low-calorie diets, the low-carb diets were naturally pretty high in fat, containing 2-3 fold greater intakes of saturated fat than the moderate carbohydrate diets used as controls. The results were pretty striking: compared to low-fat diets, blood levels of saturated fat were markedly decreased in response to the low carbohydrate, high fat diets. Our data indicates that this occurred because the low insulin levels accelerated the oxidation of all fats (and particularly saturated fat); plus the relative paucity of dietary carbohydrate meant there wasn’t much of it to be converted into saturated fats. Thus, from the body’s perspective, a low-carbohydrate diet reduces blood saturated fat levels irrespective of dietary saturated fat intake.

‍

In closing

And so we end this sad saga about poor, downtrodden saturated fats on a hopeful note. Yes, dietary saturated fat continues to be scapegoated as the presumptive cause of many health problems in developed countries. However we now know that nutrition policy makers have indicted the wrong nutrient for the crime of raising blood saturated fat levels. If we can just banish the phrase you are what you eat, however, perhaps the nutritional establishment would broaden their perspective to consider how other offenders determine blood saturated fat levels and contribute to overall health and disease.

There is convincing evidence that dietary carbohydrate exerts an important influence on how the body processes saturated fat. Thus, saturated fat, whether made in the body or eaten in the diet, is more likely to accumulate when aided and abetted by high levels of dietary carbohydrate, particularly in insulin-resistant individuals (as in type 2 diabetes or metabolic syndrome). Especially in these substantial segments of our population, a one-size-fits-all recommendation to aggressively lower saturated fat intake with the expectation of lowering blood saturated fat levels is intellectually invalid and likely to backfire. Given our current epidemics of obesity and diabetes, we can’t afford to continue diet policies based on a tragically flawed, simplistic sound bite.

‍The information we provide at virtahealth.com and blog.virtahealth.com is not medical advice, nor is it intended to replace a consultation with a medical professional. Please inform your physician of any changes you make to your diet or lifestyle and discuss these changes with them. If you have questions or concerns about any medical conditions you may have, please contact your physician.

Citations

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