|
果糖和脂肪肝 与葡萄糖相比，果糖与肥胖和糖尿病的关系更为密切。从营养的角度来看，果糖和葡萄糖都不含必需的营养素。作为甜味剂，两者都是相似的。与葡萄糖相比，果糖对人体健康特别恶劣，因为其在身体内具有独特的代谢作用。 葡萄糖和果糖代谢在许多重要方面有所不同。几乎人体内的每一个细胞都可以使用葡萄糖作为能量，而细胞则没有能力使用果糖。一旦进入人体，只有肝脏才能代谢果糖。在葡萄糖可以分散在整个身体作为能源使用的地方，果糖被定位为像导弹一样的肝脏。
果糖也是如此。大量摄取的果糖直接进入肝脏，因为没有其他细胞可以帮助利用或代谢，给肝脏带来巨大的压力。碳水化合物和胰岛素的水平可能比其他部分高10倍。因此，肝脏暴露于远远高于其他任何器官的碳水化合物 - 果糖和葡萄糖。 用锤子压下来，用针压下来的压力是不同的，所有的压力都是指向一个点的。蔗糖提供等量的葡萄糖和果糖。当葡萄糖被所有170磅的平均人体组织代谢时，等量的果糖需要仅由5磅肝脏代谢。这实际上意味着果糖与葡萄糖单独相比可能导致脂肪肝的20倍（胰岛素抵抗的关键问题）。这解释了有多少原始社会可以忍受极高的碳水化合物饮食而不发生高胰岛素血症或胰岛素抵抗。 肝脏将果糖代谢成葡萄糖，乳糖和糖原。这个果糖代谢系统没有限制。你越吃越多，你代谢。当有限的糖原储备充足时，过量的果糖通过从头脂肪生成直接变成肝脏脂肪。果糖超喂可使DNL增加5倍，用热量等量的果糖代替葡萄糖仅在8天内使肝脏脂肪增加38％。正是这种脂肪肝对胰岛素抵抗的发展至关重要。 果糖引起脂肪肝的倾向在碳水化合物中是独一无二的。脂肪肝直接导致胰岛素抵抗，引起高胰岛素血症 - 胰岛素抵抗的恶性循环。此外，果糖的这种有害作用不需要高血糖或血胰岛素水平来造成严重破坏。 此外，这种肥胖效应，因为它通过脂肪肝和胰岛素抵抗发挥作用，在短期内不能被看到，只能长期。 乙醇（酒精）的代谢与果糖非常相似。一旦摄入后，组织只能代谢20％的酒精，剩下80％直接输送到肝脏，在那里代谢为乙醛，从而刺激脂肪从头生成。底线是酒精很容易变成肝脂肪。 过量的乙醇消耗是众所周知的脂肪肝病因。由于脂肪肝是胰岛素抵抗的关键一步，过量使用乙醇也是发生代谢综合征的危险因素，这并不奇怪。 果糖和胰岛素抵抗 果糖过度摄入会引起胰岛素抵抗，早在1980年就已知道。健康受试者每天摄入超过1000卡路里的果糖，他们的胰岛素敏感性恶化了25％ - 只过了七天！每天给予额外1000卡路里的葡萄糖没有表现出类似的恶化。 最近的一项2009年的研究强化了果糖在健康志愿者中易诱发胰岛素抵抗。当Kool-Aid用葡萄糖或果糖增甜时，受试者被喂食其每日卡路里的25％。虽然这看起来很高，但许多人在饮食中消耗了这么高比例的糖。果糖，而不是葡萄糖组，已经增加了他们的胰岛素抵抗力，以至于他们将被临床分类为糖尿病前期。更为显着的是，这种发展只需要八个星期的果糖过量消费。 It only takes six days of excess fructose to cause insulin resistance. It only takes eight weeks to allow pre-diabetes to establish a beachhead. What happens after decades of high fructose consumption? The result is a diabetes disaster; precisely we are having right now. Fructose overconsumption stimulates fatty liver and leads directly to insulin resistance. There is definitely something sinister about overconsumption of fructose. Yes, Dr. Robert Lustig is correct. Sugar is a toxin. Toxicity factors Fructose is particularly toxic for several reasons. First, metabolism occurs solely within the liver, so virtually all ingested fructose becomes stored as newly created fat. In contrast, all cells can help metabolize glucose. Secondly, fructose is metabolized without limits. More ingested fructose leads to more hepatic de novo lipogenesis and more liver fat. No natural brakes exist to slow down over production of new fat. Fructose directly stimulates DNL independently of insulin, since dietary fructose has minimal effect on blood glucose or serum insulin levels. Fructose metabolism is less tightly regulated. Thus, it can overwhelm the export machinery of the liver leading to excessive buildup of fat in the liver. We’ll talk more about how the liver tries to rid itself of the newly created fat in the next chapter. Thirdly, there is no alternative runoff pathway for fructose. Excess glucose is stored safely and easily in the liver as glycogen. When needed, glycogen is broken back into glucose for easy access to energy. Fructose has no mechanism for easy storage. It is metabolized to fat, which cannot be easily reversed. While fructose is a natural sugar, and part of the human diet since antiquity, we must always remember the first principle of toxicology. The dose makes the poison. The body has the ability to handle a small amount of fructose. This does not mean it can handle unlimited amounts of it without adverse health consequences. Conclusions Fructose was once considered harmless because its low glycemic index. In the short-term, there are few obvious health risks. Instead, fructose exerts its toxicity mainly through long-term effects on fatty liver and insulin resistance. This effect is often measured in decades, leading to considerable debate. Sucrose or high fructose corn syrup, with roughly equal parts of glucose and fructose, therefore plays a dual role in obesity and type 2 diabetes. These are not simply ‘empty calories’. It is something far more sinister as people are slowly coming to realize. Glucose is a refined carbohydrate that directly stimulates insulin. However, much of it can be directly burned for energy leaving only smaller amounts to be metabolized at the liver. Nevertheless, very high consumption of glucose may also lead to fatty liver. The effects of glucose are immediately obvious in the blood glucose and insulin responses. Fructose overconsumption directly produces fatty liver, which in turn directly creates insulin resistance. Fructose is five to ten times more likely than glucose to cause fatty liver. This sets off a vicious cycle. Insulin resistance leads to hyperinsulinemia, to ‘overcome’ this resistance. However, this backfires, as the hyperinsulinemia, made worse by the attendant glucose load, leads to further insulin resistance. Sucrose therefore stimulates insulin production both in the short term and in the long term. In this way, sucrose is far, far more menacing than starches that contain glucose, such as amylopectin. Looking at the glycemic index, the effect of glucose is obvious, but the effect of fructose is completely hidden. This fact has long misled scientists to downplay the role of sugar in obesity. The additional fattening effect of insulin resistance festers for years or even decades before it becomes apparent. Short-term feeding studies completely miss this effect. A recent systemic analysis, by analyzing many studies lasting less a week, concluded that fructose shows no special effect outside of its calories. But fructose’s effects, as well as obesity, develop over decades, not weeks. If we were to analyze only short-term studies of smoking, we might make the same mistake and similarly conclude that smoking does not cause lung cancer. Cutting back on sugars and sweets has always been the first step in weight reduction in virtually all diets throughout history. Sucrose is not simply empty calories or refined carbohydrates. It is far more hazardous, since it stimulates both insulin and insulin resistance simultaneously. Our ancestors have always known this fact, even if they did not know the physiology. We have tried to deny this during our 50-year obsession with calories. In our effort to blame everything on calories, we have not recognized the inherent danger of fructose overconsumption. But the truth cannot be denied forever, and there was a price for ignorance. We paid for the caloric pied piper with the twin epidemics of type 2 diabetes and obesity. But the uniquely fattening effect of sugar has finally been recognized once again. This was a long repressed truth. So, when Dr. Lustig presented his lecture on a lonely stage in 2009 and declared that sugar was toxic, the world listened with rapt attention. Because this professor of endocrinology was telling us something we already, instinctively knew to be true. Despite all the platitudes and the reassurances that sugar was not a problem, the world already knew, in its heart, the real truth. Sugar is a toxin.
|
|
|
当大量的葡萄糖被吃掉时，它实际上循环到身体的每个细胞，帮助分散这个负荷。肝脏以外的身体组织代谢百分之八十摄取的葡萄糖。身体中的每一个细胞，包括心脏，肺，肌肉，大脑和肾脏都可以帮助自己喝到这种无所不能的葡萄糖自助餐。这只剩下百分之二十的肝脏进入葡萄糖负荷。这些葡萄糖中的大部分都被转化成糖原来储存，留下少许葡萄糖作为新脂肪生产的基质。
