果糖不会导致糖尿病是一种误解

Fructose not causing Diabetes is a misconception

　

~Dr.Gabriel Cousens

　

　

　

作为整个糖尿病讨论的一部分，存在一种误解，认为果糖不会导致糖尿病。这是一个很大的误解。果糖，尤其是高果糖玉米糖浆与糖尿病直接相关。当一个人对葡萄糖、蔗糖和/或果糖上瘾时，他们就会 依赖在糖代谢产生能量。

 

多年来，有限的传统“智慧”认为果糖不会影响血糖。这在表面上是准确的，但它的假设~因为果糖不会升高血糖， 因此它不会引起胰岛素抵抗，不会由于代谢过量的果糖而引起的代谢异常导致许多代谢疾病是不科学的。因此，它被错误地认为是比葡萄糖更安全的糖。这些都没有被证明是真的。

　

 

主要的区别在于果糖的代谢方式与葡萄糖不同。果糖通过肝脏代谢的速度比其他任何糖都要快得多。它也主要在肝脏中代谢。正因为如此，它还与高水平的非酒精性脂肪肝(NAFLD)和一种储存在肝脏和普通脂肪组织中的特殊脂肪(甘油三 酯)的快速积累有关。这不仅与 非酒精性脂肪肝有关，也与心脏病和高血压有关。葡萄糖与果糖(如蔗糖和高果糖玉米糖浆)结合，会加速果糖的吸收。

 

根据2011年3月发表的糖尿病、肥胖症和新陈代谢的最新研究，这些代谢差异进一步增强。该研究发现，下丘脑周围的皮质区对果糖的反应不同于对葡萄糖的反应。他们发现，在大脑扫描中，葡萄糖在20分钟内提高神经活动水平，而果糖在20分钟内降低神经活动水平。这是一个显著的极差; 再次强调，说明单糖的处理方式是不一样的。在这两个不同的区域，果糖和葡萄糖处理方式不同。

 

随着故事的深入，人们开始看到其他的研究。在这20年中，糖尿病的发病率增加了90%，与此同时，高果糖玉米糖浆在20世纪80年代被引入我们的集体饮食模式。代谢差异的另一部分是果糖比葡萄糖更容易转化为脂肪。高果糖饮食不仅与 非酒精性脂肪肝有关，而且高果糖玉米糖浆使用量的增加也与肥胖、糖尿病和代谢综合征的流行有关。

 

伊丽莎白·帕克斯(Elizabeth Parks)在2000年的《营养学杂志》(Journal of Nutrition)上发表文章说，果糖代谢的一个独特之处就是人类以惊人的速度从果糖中合成脂肪。一旦身体被训练成果糖代谢模式，就很难把它关掉。当葡萄糖进入系统时，身体会做出决定，是将其储存为脂肪，还是将其燃烧。果糖不会参与到这个决定中，而且会绕过燃烧，直接进入储存。越来越多的研究表明，高果糖玉米糖浆比血糖更快地转化为甘油三酯和脂肪组织。

 

果糖还干扰瘦素和胰岛素信号。这是一个问题，因为胰岛素和瘦素起着调节食物摄入的作用。果糖似乎混合了信号，导致食物摄入量增加和体重增加。高果糖玉米糖浆加糖食物也会导致糖尿病，因为它们含有高水平的复杂的羰基(糖尿病患者也会高)。果糖不含有酶、维生素或矿物质，所以最终会从身体中偷取营养素，尤其是镁、铜和铬。问题是，与葡萄糖相比，果糖对胃饥饿素没有影响，葡萄糖抑制胃饥饿素。胃饥饿素是一种向我们发出进食信号的激素。它被称为饥饿激素。果糖不会关闭它，所以它不会抑制食欲，而葡萄糖会减少胃饥饿素的分泌，从而减少食欲。当然，如果食欲不降下来，人就会发胖，变得肥胖。换句话说，果糖阻止瘦素发出停止进食和减少对甜食的渴望的信号。相反，果糖向我们的身体发出信号，让我们不停地进食和储存脂肪，从而导致肥胖。

 

蔗糖含有45% - 50%的葡萄糖和50% - 55%的果糖。与此相反，高果糖玉米糖浆高达80%的果糖和20%的葡萄糖，这是一个显著的区别。虽然它们每克都含有相同的热量，但差别更大。

过量果糖的代谢，与葡萄糖的代谢方式不同，是人类健康的一个普遍重大灾难。大量进入肝脏代谢的果糖会扰乱肝脏的葡萄糖代谢，以及与产生胰岛素抵抗相关的代谢途径和水平。

 

果糖对我们是有害的还有其他一些原因。综上所述，高果糖玉米糖浆在20世纪80年代的引入与几大健康灾难有关。总之,从整体的角度来看除了糖尿病管理,过多的果糖(每天25克),尤其是高果糖玉米糖浆与高血压、心脏病、糖尿病、肥胖和胰岛素抵抗代谢综合征,痛风、肾结石,非酒精性脂肪肝,大脑炎症,增加癌症、加速老化, 晚期糖基化终末产物增加的增加率有关。《英国医学杂志》(British Medical Journal)上的一项研究表明，糖、加糖软饮料和果糖与男性患痛风的风险显著相关。果糖促进并与肾结石增加有关，如前所述，非酒精性脂肪肝的显著增加。

 

从1970年到1990年，美国人的日常饮食中，高果糖玉米糖浆的摄入量增加了1000%，而高果糖玉米糖浆占我们食物中卡路里甜味剂的40%。在人类历史的大部分时间里，就像我之前提到的，人类的饮食中很少有果糖(大概每天15克，而且是周期性的)。主要是水果和蔬菜。如今，美国人的日常饮食中估计有81克果糖，这是人类过去的五倍之多。每天15到25克是安全的，但是人们已经超过了安全限度，每天摄取81克的果糖。由于过量 ，正如我之前解释的，身体变得果糖过载。人体并不能处理安全量三到五倍的果糖。如前所述，果糖代谢不同于葡萄糖，因为葡萄糖是主要的能量来源。葡萄糖主要用于ATP的产生。过量的葡萄糖会进入肝脏以碳水化合物的形式储存在肝脏中。与此相反，果糖代谢主要发生在肝脏，在肝脏中，果糖代谢会使代谢途径淤积，增加肝脏中甘油三酯的储存，因此过量的果糖对肝脏来说太多了。它会增加甘油三酯，激活动脉粥样硬化的 血脂，从而增加心血管的病理性血脂。

 

与先前的一些学说相反，增加的膳食果糖也与胰岛素抵抗和2型糖尿病有关。2004年，研究人员公布了与精制碳水化合物摄入量和糖尿病相关的数据。1997年，高果糖玉米糖浆和其他甜味剂的使用量比1909年增加了2100个百分点，并与更高的糖尿病发病率有关。因此，它与糖尿病流行的飙升有关。研究还阐明了果糖和葡萄糖在胰岛素抵抗中的区别。对照组与高果糖和高糖饮食相比较，甚至在一周后，与高糖组相比，果糖饮食的增加明显增加了胰岛素抵抗，而高糖组没有变化。过量的果糖也与高血压有关，它通过抑制位于血管壁的内皮一氧化氮合酶来实现这一点。这样，果糖就阻止了动脉中的基底扩张作用。

 

与葡萄糖相反，果糖在体内产生高浓度的脂肪和脂蛋白，并导致不健康的脂质。果糖的主要脂肪增加是甘油三酯。它也会转化为活化的甘油3磷酸(g-3-p)，这是将游离脂肪酸转化为甘油三酯所必需的。g-3-p越高，可以储存的脂肪就越多。它还会增加活化的APOB100，这是一种主要的脂蛋白，能将胆固醇运送到血管，并导致脂肪沉积。它减少了高密度脂蛋白，高密度脂蛋白有助于将致病的胆固醇从血管中带走并带回肝脏。

 

果糖过量最严重的一个方面是非酒精性脂肪肝（NAFLD)，它影响了高达30%的人口;非酒精性脂肪肝患者的果糖摄入量多出两到三倍。非酒精性脂肪肝与肝硬化和肝癌的高发病率相关。这当然会导致更高的肝癌死亡率。果糖噩梦最重要的一个方面是它创造了 晚期糖基化终产物(AGES)，如前所述。果糖比葡萄糖活跃10倍。其他研究表明，癌细胞使用果糖的 速率至少是葡萄糖的10倍，而癌细胞摄取的葡萄糖是正常细胞的10到50倍。

 

总的来说，数据表明长期摄入果糖会增加晚期糖基化终产物(AGES)，加速衰老过程。

 

应该完全避免果糖吗? 不。从历史上看，人体每天要处理15-25克的果糖。问题是，既然在美国，每天的平均摄入量是81克，我们该怎么做才能将其最小化呢?它有助于减少膳食果糖、果汁、高血糖水果、食糖和蜂蜜的来源;这些是基本的、相当简单、直接的方法。基本上，任何包装好的非有机食品都会含有高果糖玉米糖浆。此外，我们还有一个新的威胁叫做转基因生物(GMOs)。转基因产品(包括86%的玉米作为高果糖玉米糖浆的来源)是另一个非常严重的问题，因为它们被隐藏在标签游戏中。简单、安全的解决方案是只购买未加工的有机食品。

 

15到25克的果糖相当于2个香蕉，1.5到2个中等大小的木瓜，4个葡萄柚，4个菠萝，5个猕猴桃，一些枣子，1个芒果，或者每天半杯无花果干。要注意的一件事是，大多数甜味剂都是有问题的，其中包括agave，它经常被发现含有高果糖玉米糖浆。(其中一些甚至被FDA发现 ）。我不建议用果糖代替葡萄糖或葡萄糖代替果糖。高果糖玉米糖浆是一种未结合的果糖，因此比水果果糖更具致病性，而水果果糖与其他糖类结合在一起。减少碳水化合物摄入的最有力和最主要的方法就是减少所有的白糖，所有的果糖来源(除了25克水果)，主要吃绿叶蔬菜、蔬菜、非淀粉类、纤维性碳水化合物、豆芽和海产蔬菜。这是摆脱长期、高碳水化合物饮食和高果糖碳水化合物饮食的危险的简单方法。

 

重新训练身体停止对甜食的渴求相对容易些。当进入1.0阶段的饮食或绿色果汁禁食(不含水果或谷物，只吃不含淀粉的蔬菜、坚果、种子和海洋蔬菜)时，身体自然会调整其编程，减少瘦素。因此，我们自然地摆脱了瘦素抵抗，不再渴望甜食，因为我们关闭了那些有害的代谢途径。对许多人来说，即使是蔬菜也开始尝起来是甜的，这很好。当瘦素抵抗减弱时，对甜食的渴望也会大大减少。再说一遍，除了当一个人少吃糖，身体从表观遗传程序到瘦素激素程序，都渴望更少的糖之外，没有什么真正的诀窍。更深层次的回答是你必须足够爱自己才能改变你的饮食。

　

　

 

这篇文章摘自加布里埃尔·库森斯(Gabriel Cousens)博士的《糖尿病有治愈方法》(There is a Cure for Diabetes)一书

　

https://s.click.taobao.com/oCymNMw

https://s.click.taobao.com/lBxmNMw

　

　

Fructose and Diabetes

　

　

 11/28/2014     Blog, Health and Wellness     Diabetes, diabetes causes, diabetic diet, fatty liver, fatty liver disease, fructose, fructose and diabetes, fructose and obesity, nafld, signs of diabetes, what causes diabetes, what is diabetes, what is fructose

This article is an extract from the book There Is a Cure for Diabetes, by Dr. Gabriel Cousens

　

 

As part of the overall diabetes discussion, there lurks the misconception that somehow fructose does not contribute to diabetes. This is a major misunderstanding. Fructose is directly associated with diabetes, especially high-fructose corn syrup. When one is cellularly addicted to glucose, sucrose, and/or fructose, they become stuck in sugar metabolism for making energy.

 

For years, limited and conventional “wisdom” has held that fructose does not affect your blood sugar. This is accurate on a superficial level but unscientific in its assumption that because fructose does not raise blood sugar, it does not affect insulin resistance and cause many metabolic disease problems from the metabolic abnormalities associated with metabolizing an excess amount of fructose. It is therefore falsely deemed a safer sugar than glucose. None of this has been proven to be true. A primary difference is that fructose is metabolized differently than glucose. Fructose is metabolized much more rapidly than any other sugar into fat via the liver. It is also primarily metabolized in the liver. Because of this it has also been associated with a high level of nonalcoholic fatty liver disease (NAFLD) and a rapid accumulation of a particular kind of fat (triglycerides) that is stored in both the liver and general fat tissue. This is related not only to NAFLD but also to heart disease and hypertension. Glucose, when combined with fructose (as in sucrose and high-fructose corn syrup), accelerates fructose absorption. These metabolic differences are further enhanced in light of recent research reported in the March 2011 Diabetes, Obesity and Metabolism, which found that cortical areas around hypothalamus in the brain responded differently to fructose than to glucose. They found that in brain scans, glucose raised levels of neuronal activity for 20 minutes, while fructose dropped neuronal activity for about 20 minutes. This is a significant and polar difference; again, making the point that simple sugars are not handled the same. In these two different areas, then, fructose and glucose are handled differently. As one goes a little further with this story, one begins to see some other pieces. The incidence of diabetes increased about 90 percent in the two years, which coincided with the introduction of high-fructose corn syrup into our collective dietary patterns in the 1980s. Another part of the metabolic difference is that fructose is more lipogenic than glucose. High fructose diets have not only been linked to NAFLD, but this rising amount of high-fructose corn syrup use has also been associated with the rising epidemics of obesity, diabetes, and metabolic syndrome.

　

 

One of the unique things about fructose metabolism, according to Elizabeth Parks in the Journal of Nutrition (2000), is the surprising speed with which humans make fat from fructose. Once the body is trained in the fructose metabolic pathways, it is difficult to turn it off. The body makes a decision when glucose enters the system whether to store it as fat or to burn it. Fructose does not get involved in this decision and bypasses burning, going directly to storage. More and more research is showing that high-fructose corn syrup converts more quickly to triglycerides and adipose tissues than blood glucose. Fructose also interferes with leptin and insulin signaling. That is a problem because insulin and leptin act, as previously discussed, as regulators of food intake. Fructose seems to mix up the signaling, resulting in increased food intake and weight gain. High-fructose corn syrup sweetened foods also contribute to diabetes because they have high levels of complex carbonyls (also high in people with diabetes). Fructose does not contain enzymes, vitamins, or minerals, so it ends up stealing nutrients from the body, particularly magnesium, copper, and chromium. Problematically, fructose has no effect on ghrelin, as compared to glucose, which suppresses ghrelin. Ghrelin is a hormone that signals us to eat. It is called the hunger hormone. Fructose does not turn it off, so it does not suppress the appetite, whereas glucose decreases ghrelin secretion in a feedback loop that decreases appetite. Naturally, if the appetite does not slow down, one will gain weight and become obese. In other words, fructose blocks the leptin message to stop eating and to decrease cravings for sweets. Instead, fructose signals our bodies to keep eating and store fat, which leads to obesity.

 

Sucrose is 45–50 percent glucose and 50–55 percent fructose. In contrast to this, high-fructose corn syrup can be as high as 80 percent fructose and 20 percent glucose, which is a significant difference. Although they both contain the same calories per gram, there are more differences. Metabolism of excess fructose, which is metabolized differently than glucose, is a general major disaster for human health. High amounts of fructose going to the liver to be metabolized disturbs glucose metabolism in the liver as well as uptake pathways and levels of metabolic pathways that are associated with creating insulin resistance.

 

Fructose is quite detrimental to us for a number of additional reasons. Taking an overview, the introduction of high-fructose corn syrup in the 1980s has been associated with several major health disasters. In summary, from a holistic perspective beyond diabetes management, excess fructose (over 25 grams daily) and particularly high-fructose corn syrup have been causally associated with increasing rates of high blood pressure, heart disease, diabetes, obesity and insulin resistance metabolic syndrome, gout, kidney stones, NAFLD, brain inflammation, increased cancer, accelerated aging, and increased AGEs. One study in the British Medical Journal suggests that sugar, sweetened soft drinks, and fructose were significantly associated with increased risk of gout in men. Fructose encourages, and is connected with, increased kidney stone and, as previously mentioned, a significant increase in cases of NAFLD. Between 1970 and 1990, there was a 1,000 percent increased intake of high-fructose corn syrup in the average American diet, and it comprises 40 percent of the caloric sweeteners added to our foods. Throughout most of human history, as I mentioned before, humans rarely had much fructose in their diets (probably 15 grams daily and it was periodic). It was mostly from fruits and vegetables. Today, there is an estimated 81 grams of fructose daily in the American diet, which is up to five times greater than the amount humans used to have. Fifteen to 25 grams daily is safe, but people have gone beyond safe limits with 81 grams of fructose daily. As a result of this excess, the body, as I explained earlier, becomes fructose overloaded. The body is not designed to handle three to five times the safe fructose amount. As already pointed out, fructose metabolism is different from glucose in that glucose is a primary source of energy. Glucose goes primarily to ATP production. Excess glucose may go to the liver to be stored in the liver as carbohydrates. By contrast, fructose metabolism takes place primarily in the liver, where it will sludge the metabolic pathways and will increase triglyceride storage in the liver so the overabundance is too much for the liver. It raises triglycerides, activates the atherogenic lipid profile, and therefore increases the cardiovascular pathogenic profile.

 

Increased dietary fructose, contrary to some earlier teachings, is also associated with insulin resistance and Type-2 diabetes. In 2004, researchers released data correlating refined carbohydrate intake and diabetes. The use of high-fructose corn syrup and other sweeteners was 2,100 percent higher in 1997 than in 1909 and was associated with a higher rate of diabetes. It is thus correlated with the skyrocketing diabetes epidemic. Research was also done to clarify the difference between fructose and glucose in insulin resistance. Controls were compared with high fructose and high glucose diets, and even after one week, those with increased fructose diets significantly increased insulin resistance, as compared to the high glucose group, which had no change. Fructose in excess has also been linked to hypertension, and it does this by inhibiting a key enzyme called endothelial nitrous oxide synthase, located in blood vessel walls. In this way, fructose blocks the basodilation effect in the arteries.

 

Contrary to glucose, fructose creates a high concentration of fats and lipoproteins in the body and contributes to unhealthy lipid profiles. One major lipid increase with fructose is the triglycerides. It also converts to activated glycerol 3 phosphate (g-3-p), which is needed to convert free fatty acids into triglycerides. The more g-3-p one has, the more fat one can store. It also increases the activated APOB100, a primary lipoprotein that carries cholesterol to blood vessels and leads to fatty deposits. It decreases the high-density lipoproteins, which help take pathogenic cholesterol away from the vessels and back to the liver.

 

　

　

One of the most serious aspects of fructose excess is NAFLD, which effects up to 30 percent of population; people with NAFLD are found to eat two to three times more fructose. NAFLD is associated with higher rates of cirrhosis and liver cancer. This of course leads to higher death rates from liver disease. A most important aspect of this fructose nightmare is its creation of advanced glycation end products (AGEs), as already stated. Fructose is 10 times more active in creating these AGEs than glucose. Other research shows that cancer cells will use fructose at least 10 times more actively than glucose, which, in itself, is up to 10 to 50 times the normal cell usage for glucose. Data suggests, in general, that long-term fructose consumption increases AGEs and accelerates the aging process.

 

Should one avoid fructose entirely? No. The body historically is designed to handle 15–25 grams of fructose daily. The question is, what can one do to minimize it since, in the United States, the average intake is 81 grams daily? It is beneficial to minimize sources of dietary fructose, fruit juices, high glycemic fruits, table sugar, and honey; these are your basic and rather simple, straightforward approaches to this. Basically, any packaged product that is not labeled organic will contain high-fructose corn syrup. Additionally, we have a new threat called genetically modified organisms (GMOs). GMO products (which include 86 percent of corn as a source of high-fructose corn syrup) are another very serious concern because they are so hidden in the labeling games. The easy, safe solution is purchase only unpackaged, organic foods. Fifteen to 25 grams of fructose is equivalent to about 2 bananas, 1.5–2 medium-sized papayas, 4 grapefruits, 4 pineapples, 5 kiwis, a few dates, 1 mango, or a half cup of dried figs per day. One of the things to be aware of is that most sweeteners are problematic, including agave, which has often been found to be laced with high- fructose corn syrup. (Some of this was even caught by the FDA.) I recommend avoiding agave, as “organic agave” brands are 59–60 percent fructose, which may be equal to or worse than some high-fructose corn syrup combinations. This is why I recommend avoidance of all fructose products when following a low-carbohydrate diets—not just glucose. I am not recommending substituting fructose for glucose or glucose for fructose. High-fructose corn syrup is an unbound fructose and is therefore more pathogenic than fruit-based fructose, which is bound to other sugars. The strongest and main way to cut down carbohydrates in our intake is simply to cut out all white sugar, all fructose sources (except for 25 grams of fruit), and eat mainly leafy greens, vegetables, nonstarchy, fibrous carbohydrates, sprouts, and sea vegetables. That is the simple way to move away from the dangers of a long-term, high complex carbohydrate diet and high-fructose carbohydrate diet. It is relatively easy to retrain one’s body to stop craving sweets. When moving into a Phase 1.0 diet or green juice fasting (no fruit or grains—only nonstarchy vegetables, nuts and seeds, and sea veggies), the body naturally readjusts its programming to a decrease in leptin. Thus we move naturally out of leptin resistance and no longer crave sweets, as we turn off those destructive metabolic pathways. For many, even greens begin to taste sweet, which is nice. When leptin resistance decreases, sweet cravings also decrease immensely. Again, there is no real trick to this other than when one eats less sugar, the body craves less sugar from the epigenetic program down to leptin hormonal programming. The answer on a deeper level is that you have to love yourself enough to want to change your diet.

　

 

This article is an extract from the book There Is a Cure for Diabetes, by Dr. Gabriel Cousens

　

 

http://treeoflifecenterus.com/fructose-and-diabetes/