Oils in Context
by Raymond Peat
An oil researcher[0] spent 100 days eating what he considered to be the “Eskimo diet,” seal blubber and mackerel paste. He observed that his blood lipid peroxides (measured as malondialdehyde, MDA) reached a level 50 times higher than normal, and although MDA is teratogenic, he said he wasn't worried about fathering deformed children, because his sperm count had gone to zero. Evidently, he didn't have a very thorough understanding of the Eskimo way of life. In most traditional cultures, the whole animal is used for food, including the brain and the endocrine glands. Since unsaturated fats inhibit thyroid function, and since Eskimos usually have a high caloric intake but are not typically obese, it seems that` their metabolic rate is being promoted by something in their diet, which might also be responsible for protecting them from the effects experienced by the oil researcher. (According to G. W. Crile, the basal metabolic rate of Eskimos was 125% of that of people in the United States.)
一位石油研究员[0]花了100天的时间吃他认为是“爱斯基摩饮食”的海豹脂和鲭鱼酱。他观察到他的血脂过氧化物(测量为丙二醛，丙二醛)达到了正常水平的50倍，虽然丙二醛会致畸，但他说他并不担心成为畸形孩子的父亲，因为他的精子数量已经降为零。显然，他对爱斯基摩人的生活方式并没有很透彻的了解。在大多数传统文化中，整个动物被用作食物，包括大脑和内分泌腺。由于不饱和脂肪会抑制甲状腺功能，而且由于爱斯基摩人通常摄入高热量，但并不典型的肥胖，似乎“他们的新陈代谢率是由饮食中的某些东西促进的，这可能也有助于保护他们免受石油研究人员所经历的影响。”(G. W. Crile称，爱斯基摩人的基础代谢率是美国人的125%。)
People who eat fish heads (or other animal heads) generally consume the thyroid gland, as well as the brain. The brain is the body's richest source of cholesterol, which, with adequate thyroid hormone and vitamin A, is converted into the steroid hormones pregnenolone, progesterone, and DHEA, in proportion to the quantity circulating in blood in low-density lipoproteins. The brain is also the richest source of these very water-insoluble (hydrophobic) steroid hormones; it has a concentration about 20 times higher than the serum, for example. The active thyroid hormone is also concentrated many-fold in the brain.
吃鱼头(或其他动物的头)的人通常会消耗甲状腺，以及大脑。大脑是身体中胆固醇最丰富的来源，它与足够的甲状腺激素和维生素A一起，转化成类固醇激素孕烯醇酮、孕酮和脱氢表雄酮，与血液中循环的低密度脂蛋白的数量成比例。大脑也是这些非常不溶于水(疏水性)的类固醇激素最丰富的来源;例如，它的浓度大约是血清的20倍。活跃的甲状腺激素也成倍地集中在大脑中。
DHEA (dehydroepiandrosterone) is known to be low in people who are susceptible to heart disease [1] or cancer, and all three of these steroids have a broad spectrum of protective actions. Thyroid hormone, vitamin A, and cholesterol, which are used to produce the protective steroids, have been found to have a similarly broad range of protective effects, even when used singly. For example, according to MacCallum,
It has been shown that certain lipoid substances, especially cholesterine, can act as inhibiting or neutralizing agents toward such haemolytic poisons as saponin, cobra poison, etc., through forming with them an innocuous compound. Hanes showed that the relative immunity of puppies from chloroform poisoning is due to the large amount of cholesterin esters in their tissues. When artificially introduced into the tissues of adult animals a similar protection is conferred.[2]
众所周知，脱氢表雄酮(dehydroepiandrosterone，脱氢表雄酮)在易患心脏病[1]或癌症的人群中含量很低，而这三种类固醇都具有广泛的保护作用。用于生产保护性类固醇的甲状腺激素、维生素A和胆固醇也被发现具有同样广泛的保护作用，即使是单独使用。例如，根据麦卡勒姆的说法，
已有研究表明，某些脂类物质，特别是胆甾醇，可以通过与皂素、眼镜蛇毒等溶血毒素形成一种无害的化合物，起到抑制或中和作用。哈内斯表明，幼犬对氯仿中毒的相对免疫力是由于其组织中有大量的胆固醇酯。当人工注入成年动物的组织时，给予类似的保护。
A high level of serum cholesterol is practically diagnostic of hypothyroidism, and can be seen as an adaptive attempt to maintain adequate production of the protective steroids. Broda Barnes' work clearly showed that hypothyroid populations are susceptible to infections, heart disease, and cancer. [3]
高水平的血清胆固醇实际上可以诊断甲状腺功能减退，并可被视为一种适应性尝试，以维持足够的保护性类固醇的生产。Broda Barnes的研究清楚地表明甲状腺机能减退的人群易受感染、心脏病和癌症的影响。［3］
In the 1940s, some of the toxic effects of fish oil (such as testicular degeneration, softening of the brain, muscle damage, and spontaneous cancer) were found to result from an induced vitamin E deficiency. Unfortunately, there isn't much reason to think that just supplementing vitamin E will provide general protection against the unsaturated fats. The half-life of fats in human adipose tissue is about 600 days, meaning that significant amounts of previously consumed oils will still be present up to four years after they have been removed from the diet. [4] According to Draper, et al., [5]
20世纪40年代，人们发现鱼油的一些毒性作用(如睾丸退化、大脑软化、肌肉损伤和自发癌症)是由维生素E缺乏引起的。不幸的是，没有太多的理由认为仅仅补充维生素E就能对不饱和脂肪起到普遍的保护作用。人体脂肪组织中的脂肪的半衰期约为600天，这意味着，大量先前消耗的油脂在从饮食中去除后，仍将存在长达4年之久。根据Draper等人，[5]
, , , enrichment of the tissues with highly unsaturated fatty acids results in an increase in lipid peroxidation in vivo even in the presence of normal concentrations of vitamin E. Fasting for more than 24 hours also results in an increase in MDA excretion, implying that lipolysis is associated with peroxidation of the fatty acids released.
、、浓缩的组织高度不饱和脂肪酸会导致体内脂质过氧化增加甚至在正常浓度的维生素e .禁食24小时以上也导致MDA排泄增加,这意味着脂类分解与脂肪酸的过氧化反应释放有关。
According to Lemeshko, et al., it seems that this effect increases with the age of the animal. [6]
Lemeshko等人认为，这种效应似乎随着动物年龄的增长而增加。[6]
Commercial advertising (including medical conferences sponsored by pharmaceutical companies) and commercially sponsored research are creating some false impressions about the role of unsaturated oils in the diet. Like the man who poisoned himself with the “Eskimo diet,” many people focus so intently on avoiding one problem that they create other problems. Since I have discussed the association of unsaturated fats with aging, lipofuscin, and estrogen elsewhere, I will outline some of the other problems associated with the oils, especially as they relate to hormones.
商业广告(包括制药公司赞助的医学会议)和商业赞助的研究对不饱和油在饮食中的作用产生了一些错误的印象。就像那个用“爱斯基摩饮食”毒害自己的人一样，许多人过于专注于避免一个问题，而导致了其他问题的产生。因为我已经讨论了不饱和脂肪与衰老、脂褐素和雌激素的关系，所以我将概述一些与油脂有关的其他问题，特别是与激素有关的问题。
Mechanisms and Essentiality: When something is unavoidable, in ordinary life, talking about “essentiality,” or the minimum amount required for life or for optimal health, is more important as an exploration into the nature of our life than as a practical health issue. For example, how much oxygen, how many germs (of what kinds), how many cosmic rays (of what kinds), would produce the nicest human beings? The fact that we have adapted to something—oxygen at sea level, microbes, or vegetable fats, for example–doesn't mean that we are normally exposed to it in ideal amounts.
机制和本质:在日常生活中，当一些事情不可避免时，谈论“本质”，或生命或最佳健康所需的最小量，更重要的是探索我们的生活本质，而不是作为一个实际的健康问题。例如，多少氧气，多少细菌(什么种类的)，多少宇宙射线(什么种类的)才能造就出最好的人?事实上，我们已经适应了某些东西——例如，海平面上的氧气、微生物或植物脂肪——但这并不意味着我们通常会以理想的数量接触到氧气。
Animals contain desaturase enzymes, and are able to produce specific unsaturated fats (from oleic and palmitoleic acids) when deprived of the ordinary “essential fatty acids,” [7] so it can be assumed that these enzymes have a vital purpose. The high concentration of unsaturated fats in mitochondria–the respiratory organelles where it seems that these lipids present a special danger of destructive oxidation–suggests that they are required for mitochondrial structure, or function, or regulation, or reproduction. Unsaturated fats have special properties of adsorption, [8] and are more soluble in water than are saturated fats. The movement and modulation of proteins and nucleic acids might require these special properties. As the main site of ATP production, I suspect that their water-retaining property might be crucial. When a protein solution (even egg-white) is poured into a high concentration of ATP, it contracts or “superprecipitates.” This condensing, water-expelling property of ATP in protein solutions is similar to the effect of certain concentrations of salts on any polymer. It would seem appropriate to have a substance to oppose this condensing effect, to stimulate swelling [9, 10] and the uptake of precursor substances. Something that has an intrinsic structure-loosening or water-retaining effect would be needed. The ideas of “chaotropic agents” and “structural antioxidants” have been proposed by Vladimirov [11] to bring generality into our understanding of the mitochondria. Lipid peroxides are among the chaotropic agents, and thyroxin is among the structural antioxidants. The known oxygen-sparing effects of progesterone [12, 13]would make it appropriate to include it among the structural antioxidants. The incorporation of the wrong unsaturated fats into mitochondria would be expected to damage the vital respiratory functions.
动物体内含有去饱和酶，当剥夺了普通的“必需脂肪酸”[7]时，动物能够产生特定的不饱和脂肪(从油酸和棕榈酸中)，因此可以假定这些酶有重要的作用。在线粒体中高浓度的不饱和脂肪表明它们是线粒体结构、功能、调节或繁殖所必需的。线粒体是呼吸细胞器，在这里，这些脂类似乎具有破坏性氧化的特殊危险。不饱和脂肪具有特殊的吸附性质，比饱和脂肪更容易溶于水。蛋白质和核酸的运动和调节可能需要这些特殊的性质。作为ATP产生的主要部位，我怀疑它们的保水性可能是至关重要的。当蛋白质溶液(甚至蛋清)被倒入高浓度的ATP中时，它会收缩或“超沉淀”。ATP在蛋白质溶液中的这种冷凝和排水特性类似于一定浓度的盐对任何聚合物的影响。似乎应该有一种物质来对抗这种冷凝效应，刺激膨胀[9,10]和前体物质的吸收。需要一些具有内在结构松散或保水效果的东西。弗拉基米罗夫[11]提出了“向混沌剂”和“结构抗氧化剂”的概念，使我们对线粒体的理解具有普遍性。脂质过氧化物是一种促混沌剂，甲状腺素是一种结构性抗氧化剂。已知的黄体酮的氧节约效应[12,13]将其列入结构抗氧化剂中是合适的。在线粒体中加入错误的不饱和脂肪可能会损害重要的呼吸功能。
Some insects that have been studied have been found not to require the essential fatty acids. [14]* According to reviewers, hogs and humans have not been shown to require the “essential” fatty acids. [15] In vitro studies indicate that they are not required for human diploid cells to continue dividing in culture. [16] According to Guarnieri, [17] EFA-deficient animals don't die from their deficiency. The early studies showing “essentiality” of unsaturated fats, by producing skin problems and an increased metabolic rate, have been criticized [18] in the light of better nutritional information, e.g., pointing out that the diets might have been deficient in vitamin B6 and/or biotin. The similar skin condition produced by vitamin B6 deficiency was found to be improved by adding unsaturated fats to the diet. A fat-free liver extract cured the “EFA deficiency.” I think it would be reasonable to investigate the question of the increased metabolic rate produced by a diet lacking unsaturated fats (which inhibit both thyroid function and protein metabolism) in relation to the biological changes that have been observed. Since diets rich in protein are known to increase the requirement for vitamin B6 [19] (which is a co-factor of transaminases, for example), the increased rate of energy production and improved digestibility of dietary protein on a diet lacking unsaturated fats would certainly make it reasonable to provide the experimental animals with increased amount of other nutrients. With increasing knowledge, the old experiments indicating the “essentiality” of certain oils have lost their ability to convince, and they haven't been replaced by new and meaningful demonstrations. In the present state of knowledge, I don't think it would be unreasonable to suggest that the optional dietary level of the “essential fatty acids” might be close to zero, if other dietary factors were also optimized. The practical question, though, has to do with the dietary choices that can be made at the present time.
研究发现一些昆虫不需要必需的脂肪酸。根据评论家的说法，猪和人还没有被证明需要“必需”脂肪酸。[15]体外研究表明，人类二倍体细胞在培养中继续分裂并不需要它们。据Guarnieri说，[17]efa缺乏的动物不会死于它们的缺乏。早期的研究表明，不饱和脂肪的“重要性”在于引起皮肤问题和代谢率的增加，这些研究受到了[18]更好的营养信息的批评，例如，指出饮食中可能缺乏维生素B6和/或生物素。研究发现，在饮食中添加不饱和脂肪可以改善因缺乏维生素B6而导致的类似皮肤状况。一种无脂肝脏提取物治愈了“脂肪酸缺乏”。我认为，研究缺乏不饱和脂肪(抑制甲状腺功能和蛋白质代谢)的饮食所产生的代谢率增加与已观察到的生物学变化之间的关系是合理的。众所周知，富含蛋白质的饮食会增加对维生素B6[19]的需求(维生素B6[19]是转氨酶的辅助因子)，在缺乏不饱和脂肪的饲粮中，能量产生率的提高和蛋白质的消化率的提高，当然可以为实验动物提供更多的其他营养物质。随着知识的增长，旧的实验表明某些油的“本质”已经失去了说服的能力，它们还没有被新的和有意义的证明所取代。在目前的知识水平下，我认为，如果其他饮食因素也得到优化，建议可选的“必需脂肪酸”水平可能接近于零是合理的。然而，实际问题与目前可以做出的饮食选择有关。
*If we followed Linus Pauling's reasoning in determining optimal vitamin C intake, this study of the linoleic acid content of the tissues of an animal which can synthesize it would suggest that we are eating about 100 times more “EFA” than we should.
*如果我们按照莱纳斯·鲍林的推理来确定最佳的维生素C摄入量，这项对动物组织中可合成维生素C的亚油酸含量的研究将表明，我们摄入的“必需脂肪酸”大约是我们应该摄入的100倍。
In evaluating dietary fat, it is too often forgotten that the animals' diet (and other factors, including temperature) affect the degree of saturation of fats in its tissues, or its milk, or eggs. The fat of wild rabbits or summer-grazing horses, for example, can contain 40% linolenic acid, about the same as linseed oil. Hogs fed soybeans can have fat containing over 30% linoleic acid. [20] Considering that most of our food animals are fed large amounts of grains and soybeans, it isn't accurate to speak of their fats as “animal fats.” And, considering the vegetable oil contained in our milk, eggs, and meat, it would seem logical to select other foods that are not rich in unsaturated oils.
在评估膳食脂肪时，人们常常忘记动物的饮食(和其他因素，包括温度)会影响其组织、牛奶或鸡蛋中脂肪的饱和程度。例如，野生兔子或夏季放牧的马的脂肪中含有40%的亚麻酸，与亚麻籽油大致相同。用大豆饲养的猪脂肪中亚油酸含量超过30%。考虑到我们大多数食用动物都被喂食大量的谷物和大豆，将它们的脂肪称为“动物脂肪”是不准确的。而且，考虑到我们的牛奶、鸡蛋和肉类中所含的植物油，选择不富含不饱和油的食物似乎是合乎逻辑的。
Temperature and Fat: The fact that saturated fats are dominant in tropical plants and in warm-blooded animals relates to the stability of these oils at high temperatures. Coconut oil which had been stored at room temperature for a year was found to have no measurable rancidity. Since growing coconuts often experience temperatures around 100 degrees Fahrenheit, ordinary room temperature isn't an oxidative challenge. Fish oil or safflower oil, though, can't be stored long at room temperature, and at 98 degrees F, the spontaneous oxidation is very fast.
温度和脂肪:饱和脂肪在热带植物和温血动物中占主导地位，这与这些油脂在高温下的稳定性有关。椰子油在室温下存放一年，无明显的酸味。由于种植椰子的温度通常在100华氏度左右，普通的室温不是氧化挑战。然而，鱼油或红花油不能在室温下长时间储存，而且在98华氏度下，自发氧化非常快。
Bacteria vary the kind of fat they synthesize, according to temperature, forming more saturated fats at higher temperatures.[21] The same thing has been observed in seed oil plants. [22] Although sheep have highly saturated fat, the superficial fat near their skin is relatively unsaturated; it would obviously be inconvenient for the sheep if their surface fat hardened in cool weather, when their skin temperature drops considerably. Pigs wearing sweaters were found to have more saturated fat than other pigs.[23] Fish, which often live in water which is only a few degrees above freezing, couldn't function with hardened fat. At temperatures which are normal for fish, and for seeds which germinate in the cold northern springtime, rancidity of fats isn't a problem, but rigidity would be.
根据温度的不同，细菌会合成不同种类的脂肪，在较高的温度下会形成更多的饱和脂肪在籽油植物中也观察到了同样的情况。虽然绵羊有高度饱和脂肪，但靠近皮肤的表面脂肪相对不饱和;如果在凉爽的天气里，当它们的皮肤温度大幅下降时，它们的表面脂肪变硬，这显然对绵羊来说是不方便的。研究发现，穿毛衣的猪比其他猪含有更多的饱和脂肪鱼类通常生活在仅高于冰点几度的水中，它们无法与硬化的脂肪一起工作。对于鱼类和在寒冷的北方春天发芽的种子来说，温度是正常的，在这样的温度下，脂肪的酸臭不是问题，但脂肪的硬度就会成为问题。
Unsaturated Fats Are Essentially Involved In Heart Damage: The toxicity of unsaturated oils for the heart is well established, [24, 25, 26] though not well known by the public.
不饱和脂肪本质上与心脏损害有关:不饱和油脂对心脏的毒性是众所周知的，[24,25,26]，但公众并不了解。
In 1962, it was found that unsaturated fatty acids are directly toxic to mitochondria. [27] Since stress increases the amount of free fatty acids circulating in the blood (as well as lipid peroxides), and since lack of oxygen increases the intracellular concentration of free fatty acids, stored unsaturated fats would seem to represent a special danger to the stressed organism. Meerson and his colleagues [18] have demonstrated that stress liberates even local tissue fats in the heart during stress, and that systematic drug treatment, including antioxidants, can stop the enlargement of stress-induced infarctions. Recently, it was found that the cardiac necrosis caused by unsaturated fats (linolenic acid, in particular) could be prevented by a cocoa butter supplement. [29] The author suggests that this is evidence for the “essentiality” of saturated fats, but points out that animals normally can produce enough saturated fat from dietary carbohydrate or protein, to prevent cardiac necrosis, unless the diet provides too much unsaturated fat. A certain proportion of saturated fat appears to be necessary for stability of the mitochondria. Several other recent studies show that the “essential” fatty acids decrease the P/O ratio, or the phosphorylation efficiency, [30]the amount of usable energy produced by cellular respiration.
1962年，人们发现不饱和脂肪酸对线粒体有直接毒性。由于压力增加了血液中循环的游离脂肪酸(以及脂质过氧化物)的数量，而且由于缺氧增加了细胞内游离脂肪酸的浓度，储存的不饱和脂肪似乎对受到压力的生物体是一种特殊的危险。Meerson和他的同事[18]已经证明，压力甚至可以在压力下释放心脏局部组织脂肪，包括抗氧化剂在内的系统药物治疗可以阻止压力引起的梗死扩大。最近，研究发现不饱和脂肪(特别是亚麻酸)引起的心脏坏死可以通过补充可可脂来预防。作者认为，这是饱和脂肪“必要性”的证据，但指出，动物通常可以从饮食中的碳水化合物或蛋白质中产生足够的饱和脂肪，以防止心脏坏死，除非饮食中提供太多的不饱和脂肪。一定比例的饱和脂肪似乎对线粒体的稳定是必要的。最近的其他几项研究表明，“必需”脂肪酸降低了P/O比率，或磷酸化效率，[30]细胞呼吸产生的可用能量。
There has been some publicity about a certain unsaturated fat, eicosapentaenoic acid, or EPA, which can have some apparently protective and anti-inflammatory effects. A study in which butter was added to the animals' diet found that serum EPA was elevated by the butter. The investigator pointed out that other studies had been able to show increased serum EPA from an EPA supplement only when the animals had previously been fed butter. [31]
有一些关于某种不饱和脂肪，二十碳五烯酸(EPA)的宣传，它有一些明显的保护和消炎作用。一项在动物饮食中添加黄油的研究发现，血清EPA因黄油而升高。研究人员指出，其他研究表明，只有当动物之前被喂食黄油时，EPA补充剂才会增加血清EPA。[31]
Intense lobbying by the soybean oil industry has created the widespread belief that “tropical oils” cause heart disease. In a comparison of many kinds of oil, including linseed oil, olive oil, whale oil, etc., palm oil appeared to be the most protective. The same researcher [32] more recently studied palm oil's antithrombotic effect, in relation to platelet aggregation. It was found that platelet aggregation was enhanced by sunflowerseed oil, but that palm oil tended to decrease it.
豆油行业的激烈游说使人们普遍相信“热带油”会导致心脏病。与亚麻籽油、橄榄油、鲸鱼油等多种油相比，棕榈油似乎是最具保护作用的。[32]研究员最近研究了棕榈油与血小板聚集有关的抗血栓作用。结果表明，葵花籽油促进血小板聚集，而棕榈油则有降低血小板聚集的趋势。
Much current research has concentrated on the factors involved in arterial clotting. Since the blood moves quickly through the arteries, rapid processes are of most interest to those workers, though some people do remember to think in terms of an equilibrium between formation and removal of clot material. For about 25 years there was interest in the ability of vitamin E to facilitate clot removal, apparently by activating proteolytic enzymes.[33] Unsaturated fats' ability to inhibit proteolytic enzymes in the blood has occasionally been discussed, but seldom in the U.S. The equilibrium between clotting and clot dissolution is especially important in the veins, where blood moves more slowly, and spends more time.
目前许多研究都集中在动脉凝血的相关因素上。由于血液在动脉中快速流动，这些工作人员对快速过程最感兴趣，尽管有些人确实记得要考虑血栓形成和清除之间的平衡。大约25年来，人们对维生素E促进凝块清除的能力感兴趣，显然是通过激活蛋白水解酶。[33]不饱和脂肪抑制血液中蛋白水解酶的能力偶尔被讨论过，但在美国很少。凝血和凝血溶解之间的平衡在静脉中尤其重要，因为静脉中的血液流动更慢，停留时间更长。
. . . the slower blood flows the greater its predisposition to clotting. However, this intrinsic process, leading to fibrin production, is slow, taking up to a minute or more to occur. Thrombosis as a result of stasis, therefore, occurs in the venous circulation; typically in the legs where…venous return is slowest. In fact, many thousands of small thrombi are formed each day in the lower body. These pass via the vena cava into the lungs where thrombolysis occurs, this being a normal metabolic function of the organ. [34]
。。血液流动得越慢，就越容易凝结。然而，这个导致纤维蛋白生成的内在过程是缓慢的，需要一分钟或更长时间才能发生。血栓形成是由于淤滞，因此，发生在静脉循环;通常在腿部，那里静脉回流最慢。事实上，下体每天都有成千上万的小血栓形成。血栓通过腔静脉进入肺，溶栓发生的地方，这是器官的正常代谢功能。[34]
In the Shutes' research in the 1930s and 1040s, vitamin E and estrogen acted in opposite directions on the clot-removing enzymes.[33] Since estrogen increases blood lipids, and increases the incidence of strokes and heart attacks, it would be interesting to expand the Shutes' work by considering the degree of saturation of blood lipids in relation to the effects of vitamin E and estrogen on clot removal. Estrogen's effect on clotting is very complex, since it increases the ratio of unsaturated to saturated fatty acids in the body, and increases the tendency of blood to pool in the large veins, in addition to its direct effects on the clotting factors.
在20世纪30年代和10世纪40年代舒特夫妇的研究中，维生素E和雌激素对凝块清除酶的作用方向相反由于雌激素会增加血脂，并增加中风和心脏病发作的发生率，因此，考虑到血脂的饱和程度与维生素E和雌激素对血块清除的影响，将是有趣的，舒特的工作扩大。雌激素对凝血的影响是非常复杂的，因为除了它对凝血因子的直接影响外，它还增加了体内不饱和脂肪酸和饱和脂肪酸的比例，增加了血液在大静脉中聚集的趋势。
Immunodeficiency and Unsaturated Fats: Intravenous feeding with unsaturated fats is powerfully immunosuppressive [35] (though it often was used to give more calories to cancer patients) and is now advocated as a way to prevent graft rejection. The deadly effect of the long-chain unsaturated fats on the immune system has led to the development of new products containing short and medium-chain saturated fats for intravenous feeding. [36] It was recently reported that the anti-inflammatory effect of n-3 fatty acids (fish oil) might be related to the observed suppression of interleukin-1 and tumor necrosis factor by those fats. [37] The suppression of these anti-tumor immune factors persists after the fish oil treatment is stopped.
免疫缺陷和不饱和脂肪:静脉注射不饱和脂肪具有强大的免疫抑制35，现在提倡作为一种防止移植排斥的方法。长链不饱和脂肪对免疫系统的致命影响导致了含有短链和中链饱和脂肪用于静脉喂养的新产品的开发。最近有报道称，n-3脂肪酸(鱼油)的抗炎作用可能与这些脂肪对白细胞介素-1和肿瘤坏死因子的抑制有关。停止鱼油治疗后，这些抗肿瘤免疫因子的抑制仍在持续。
As mentioned above, stress and hypoxia can cause cells to take up large amounts of fatty acids. Cortisol's ability to kill white blood cells (which can be inhibited by extra glucose) is undoubtedly an important part of its immunosuppressive effect, and this killing is mediated by causing the cells to take up unsaturated fats. [38]
如上所述，压力和缺氧会导致细胞吸收大量的脂肪酸。毫无疑问，皮质醇杀死白细胞的能力是其免疫抑制作用的重要组成部分(这可以被额外的葡萄糖所抑制)，这种杀死作用是通过导致细胞吸收不饱和脂肪介导的。[38]
Several aspects of the immune system are improved by short-chain saturated fats. Their anti-histamine action [39] is probably important, because of histamine's immunosuppressive effects.[40] Unsaturated fats have been found to cause degranulation of mast cells.[41]The short-chain fatty acids normally produced by bacteria in the bowel apparently have a local anti-inflammatory action.[42]
短链饱和脂肪可以改善免疫系统的几个方面。他们的抗组胺作用可能是重要的，因为组胺的免疫抑制作用已发现不饱和脂肪可引起肥大细胞脱颗粒通常由肠道细菌产生的短链脂肪酸显然具有局部抗炎作用。
A recent discussion of “tissue destruction by neutrophils” mentions “a fascinating series of experiments performed between 1888 and 1906,” in which “German and American scientists established the importance of neutrophil proteinases and plasma antiproteinases in the evolution of tissue damage in vivo.” [43] MacCallum's Pathology described some related work:
. . . Jobling has shown that the decomposition products of some fats–unsaturated fatty acids and their soaps–have the most decisive inhibiting action upon proteolytic ferments, their power being in a sense proportional to the degree of unsaturation of the fatty acid. So universally is it true that such unsaturated fatty acids can impede the action of proteolytic ferments that many pathological conditions (such as the persistence of caseous tuberculous material in its solid form) can be shown to be due to their presence. If they are rendered impotent by saturation of their unsaturated group with iodine, the proteolysis goes on rapidly and the caseous tubercle or gumma rapidly softens.[44]
最近一篇关于“中性粒细胞对组织的破坏”的讨论提到“1888年至1906年间进行的一系列有趣的实验”，其中“德国和美国科学家确定了中性粒细胞蛋白酶和血浆抗蛋白酶在体内组织损伤演化中的重要性”。[43] MacCallum's Pathology描述了一些相关工作:
约布林已经证明，某些脂肪的分解产物——不饱和脂肪酸及其皂——对蛋白质水解发酵具有最决定性的抑制作用，它们的作用在某种意义上与脂肪酸的不饱和程度成正比。普遍的事实是，这种不饱和脂肪酸可以阻碍蛋白水解酵素的作用，因此许多病理状况(如干酪样结核物质以固体形式存在)可以被证明是由于它们的存在。如果它们的不饱和基团被碘饱和而变得无能为力，则蛋白质水解迅速进行，干酪结节或干酪胶迅速软化。
Another comment by MacCallum suggests one way in which unsaturated fats could block the action of cytotoxic cells:
This function of the wandering cells is, of course, of immediate importance in connection with their task of cleaning up the injured area to prepare it for repair. While the proteases thus produced are active in the solution of undesirable material, their unbridled action might be detrimental. As a matter of fact, it is shown by Jobling and Petersen that the anti-ferment known to be present in the serum and to restrict the action of the ferment is a recognizable chemical substance, usually a soap or other combination of an unsaturated fatty acid. It is possible to remove or decompose this substance or to saturate the fatty acid with iodine and thus release the ferment to its full activity. [45]
MacCallum的另一篇评论提出了一种不饱和脂肪可以阻止细胞毒细胞活动的方法:
漫游细胞的这种功能，当然与它们清理受伤区域、为修复做准备的任务有直接的重要性。虽然这样产生的蛋白酶在不需要的物质的溶液中是有活性的，但它们不受约束的作用可能是有害的。事实上，约布林和彼得森证明，已知存在于血清中的抑制发酵的抗发酵物质是一种可识别的化学物质，通常是肥皂或其他不饱和脂肪酸的混合物。可以去除或分解这种物质，也可以用碘使脂肪酸饱和，从而使发酵充分发挥其活性。[45]
Unsaturated Fats Are Essential For Cancer: The inhibition of proteolytic enzymes by unsaturated fats will act at many sites: digestion of protein, “digestion” of clots, “digestion” of the colloid in the thyroid gland which releases the hormones, the activity of white cells mentioned above, and the normal “digestion” of cytoplasmic proteins involved in maintaining a steady state as new proteins are formed and added to the cytoplasm. It has been suggested that inhibition of the destruction of intracellular proteins would shift the balance toward growth.[46] Cancer cells are known to have a high level of unsaturated fats,[47] yet they have a low level of lipid peroxidation;[48] lipid peroxidation inhibits growth, and is often mentioned as a normal growth restraining factor.[49]
不饱和脂肪对癌症至关重要:不饱和脂肪对蛋白水解酶的抑制会在许多部位起作用:消化蛋白质，“消化”凝块，“消化”甲状腺中释放激素的胶体，上述白细胞的活性，以及在新蛋白质形成并添加到细胞质时维持稳定状态的细胞质蛋白质的正常“消化”。有人认为，抑制细胞内蛋白的破坏将使平衡向生长方向转变众所周知，癌细胞具有高水平的不饱和脂肪，[47]，但它们具有低水平的脂质过氧化;[48]脂质过氧化抑制生长，常被认为是一种正常的生长抑制因子。
In 1927, it was observed that a diet lacking fats prevented the development of spontaneous tumors.[50] Many subsequent investigators have observed that the unsaturated fats are essential for the development of tumors. [51, 52, 53] Tumors secrete a factor which mobilizes fats from storage, [54] presumably guaranteeing their supply in abundance until the adipose tissues are depleted. Saturated fats–coconut oil and butter, for example–do not promote tumor growth.[55] Olive oil is not a strong tumor promoter, but in some experiments it does have a slightly permissive effect on tumor growth. [56, 57] In some experiments, the carcinogenic action of unsaturated fats could be offset by added thyroid, [57] an observation which might suggest that at least part of the effect of the oil is to inhibit thyroid. Adding cystine to the diet (cysteine, the reduced form of cystine, is a thyroid antagonist) also increases the tumor incidence.[58] In a hyperthyroid state, the ability to quickly oxidize larger amounts of the toxic oils would very likely have a protective effect, preventing storage and subsequent peroxidation, and reducing the oils' ability to synergize with estrogen.
1927年，人们发现缺乏脂肪的饮食可以防止自发肿瘤的发生许多随后的研究人员发现，不饱和脂肪对肿瘤的发展至关重要。[51,52,53]肿瘤分泌一种能调动储存脂肪的因子，[54]可能保证了它们的大量供应，直到脂肪组织耗尽。饱和脂肪——例如椰子油和黄油——不会促进肿瘤的生长橄榄油不是强肿瘤促进剂，但在一些实验中，它确实对肿瘤生长有轻微的纵容作用。[56,57]在一些实验中，不饱和脂肪的致癌作用可以通过添加甲状腺来抵消，[57]这一观察结果可能表明，油脂至少有一部分作用是抑制甲状腺。在饮食中添加胱氨酸(胱氨酸的减少形式，是一种甲状腺拮抗剂)也会增加肿瘤的发病率在甲亢状态下，快速氧化大量有毒油脂的能力很可能具有保护作用，防止储存和随后的过氧化作用，并降低油脂与雌激素协同作用的能力。
Consumption of unsaturated fat has been associated with both skin aging and with the sensitivity of the skin to ultraviolet damage, Ultraviolet light-induced skin cancer seems to be mediated by unsaturated fats and lipid peroxidation.[59]
不饱和脂肪的消耗与皮肤老化和皮肤对紫外线损伤的敏感性有关，紫外光诱导的皮肤癌似乎是由不饱和脂肪和脂质过氧化介导的。
In a detailed study of the carcinogenicity of different quantities of unsaturated fat, Ip, et al., tested levels ranging from 0.5% to 10%, and found that the cancer incidence varied with the amount of “essential oils” in the diet. Some of their graphs make the point very clearly: [52}
在一项关于不同数量的不饱和脂肪的致癌性的详细研究中，Ip等人测试了从0.5%到10%的不饱和脂肪水平，发现癌症发病率随饮食中“精油”的数量而变化。他们的一些图表非常清楚地说明了这一点:[52}
This suggests that the optimal EFA intake might be 0.5% or less.
Butter and coconut oil contain significant amounts of the short and medium-chain saturated fatty acids, which are very easily metabolized,[60] inhibit the release of histamine,[39] promote differentiation of cancer cells,[61] tend to counteract the stress-induced proteins,[62] decrease the expression of prolactin receptors, and promote the expression of the T3 (thyroid) receptor. [63] (A defect of the thyroid receptor molecule has been identified as an “oncogene,” responsible for some cancers, as has a defect in the progesterone receptor.)
这表明最佳的脂肪酸摄入量可能是0.5%或更少。
黄油和椰子油中含有大量的短链和中链饱和脂肪酸，这是非常容易代谢的，[60]抑制组胺的释放，[39]促进癌细胞的分化，[61]倾向于抵消应激诱导蛋白[62]，降低催乳素受体的表达，促进T3(甲状腺)受体的表达。63
Besides inhibiting the thyroid gland, the unsaturated fats impair intercellular communication,[64] suppress several immune functions that relate to cancer, and are present at high concentrations in cancer cells, where their antiproteolytic action would be expected to interfere with the proteolytic enzymes and to shift the equilibrium toward growth. In the free fatty acid form, the unsaturated fats are toxic to the mitochondria, but cancer cells are famous for their compensatory glycolysis.
除了抑制甲状腺，不饱和脂肪损害细胞间通讯[64]，抑制与癌症相关的几种免疫功能，并在癌细胞中高浓度存在，它们的抗蛋白水解作用预计会干扰蛋白水解酶并使平衡向生长方向转变。在游离脂肪酸形式下，不饱和脂肪对线粒体是有毒的，但癌细胞以代偿性糖酵解而闻名。
By using lethargic connective tissue cells known to have a very low propensity to take up unsaturated fats [65] as controls in comparison with, e.g., breast cancer cells, with a high affinity for fats, it is possible to show a “selective” toxicity of oils for cancer cells. However, an in vivo test of an alph-linolenic acid ester showed it to have a stimulating effect on breast cancer.[66] Given a choice, skin fibroblasts demonstrate a very specific preference for oleic acid, over a polyunsaturated fat.[67]
通过使用不活跃的结缔组织细胞作为对照，已知结缔组织细胞吸收不饱和脂肪的倾向性很低[65]，而乳腺癌细胞对脂肪的亲和性很高，这就可能显示出油脂对癌细胞的“选择性”毒性。然而，α -亚麻酸酯的体内试验表明它对乳腺癌有刺激作用。[66]如果可以选择，皮肤成纤维细胞表现出对油酸的特别偏爱，而不是多不饱和脂肪[67]。
Even if unsaturated fats were (contrary to the best evidence) selectively toxic for cancer cells, their use in cancer chemotherapy would have to deal with the issues of their tendency to cause pulmonary embolism,their suppression of immunity including factors specifically involved in cancer resistance, and their carcinogenicity.
即使不饱和脂肪(与最好的证据相反)对癌细胞有选择性的毒性，在癌症化疗中使用不饱和脂肪也必须处理它们引起肺栓塞的倾向，它们对免疫的抑制，包括与癌症抵抗有关的特定因素，以及它们的致癌性等问题。
Brain Damage And Lipid Peroxidation: When pregnant mice were fed either coconut oil or unsaturated seed oil, the mice that got coconut oil had babies with normal brains and intelligence, but the mice exposed to the unsaturated oil had smaller brains, and had inferior intelligence. In another experiment, radioactively labeled soy oil was given to nursing rats, and it was shown to be massively incorporated into brain cells, and to cause visible structural changes in the cells. In 1980, shortly after this study was published in Europe, the U.S. Department of Agriculture issued a recommendation against the use of soy oil in infant formulas. More recently, [68]pregnant rats and their offspring were given soy lecithin with their food, and the exposed offspring developed sensorimotor defects.
脑损伤和脂质过氧化:当怀孕的老鼠被喂食椰子油或不饱和籽油时，摄入椰子油的老鼠生出的婴儿大脑和智力正常，但摄入不饱和籽油的老鼠大脑更小，智力更低。在另一项实验中，用放射性标记的大豆油喂喂奶的老鼠，结果显示大豆油大量进入脑细胞，并在细胞中引起明显的结构变化。1980年，这项研究在欧洲发表后不久，美国农业部发布了一项建议，反对在婴儿配方中使用豆油。最近，[68]怀孕的大鼠及其后代在食物中加入了大豆卵磷脂，暴露在外的后代出现了感觉运动缺陷。
Many other studies have demonstrated that excessive unsaturated dietary fats interfere with learning and behavior, [70, 71] and the fact that some of the effects can be reduced with antioxidants suggests that lipid peroxidation causes some of the damage. Other studies are investigating the involvement of lipid peroxidation in seizures.[72]
许多其他研究已经证明，过多的不饱和脂肪会干扰学习和行为[70,71]，而抗氧化剂可以降低其中一些影响的事实表明，脂质过氧化会造成一些损害。其他研究正在调查脂质过氧化在癫痫发作中的作用。[72]
The past use of soy oil in artificial milk (and in maternal diets) has probably caused some brain damage. The high incidence of neurological defects (e.g., 90%) that has been found among violent criminals suggests that it might be worthwhile to look for unusual patterns of brain lipids in violent people.
过去在人造牛奶(和母亲的饮食)中使用豆油可能造成了一些脑损伤。在暴力罪犯中神经系统缺陷的高发生率(例如，90%)表明，在暴力人群中寻找不同寻常的脑脂模式可能是值得的。
There have been a series of claims that babies' brains or eyes develop better when their diets are supplemented with certain unsaturated oils, based on the idea that diets may be deficient in certain types of oil, Some experimenters claim that the supplements have improved the mental development of babies, but other researchers find that the supplemented babies have poorer mental development. But the oils that are added to the babies' diets are derived from fish or algae, and contain a great variety of substances (such as vitamins) other than the unsaturated fatty acids, and the researchers consistently fail to control for the effects of such substances.
有一系列的声称，当婴儿的饮食中添加某些不饱和油时，他们的大脑或眼睛发育得更好，这是基于饮食中可能缺乏某些类型的油的观点。但其他研究人员发现，补充维生素的婴儿的智力发育较差。但是，添加到婴儿饮食中的油来自鱼类或藻类，除了不饱和脂肪酸外，还含有多种物质(如维生素)，而研究人员一直未能控制这些物质的影响。
It has shown that it is probably impossible to experience a detectable deficiency of linoleic acid outside of the laboratory setting,[69] but the real issue is probably whether the amount in the normal diet is harmful to development. Until the research with animals has produced a better understanding of the effects of unsaturated oils, experimenting on human babies seems hard to justify.
研究表明，在实验室环境之外，可能不可能检测到亚油酸缺乏[69]，但真正的问题可能是，正常饮食中的亚油酸含量是否对发育有害。在对动物的研究对不饱和油的作用有了更好的了解之前，在人类婴儿身上做实验似乎很难证明这一点。
Marion Diamond, who has studied the improved brain growth in rats given a stimulating environment (which, like prenatal progesterone, produced improved intelligence and larger brains), observed that in old age the “enriched” rats' brains contained less lipofuscin (age pigment).[73] It is generally agreed that the unsaturated oils promote the formation of age pigment. The discovery that stress or additional cortisone (which, by blocking the use of glucose, forces cells to take up more fat) causes accelerated aging of the brain[74] should provide new motivation to investigate the antistress properties of substances such as the protective steroids mentioned above, and the short-chain saturated fats.
马里恩·戴蒙德(Marion Diamond)研究了给予刺激环境(如产前孕激素，能提高智力并使大脑更大)的大鼠大脑发育的改善。她观察到，在老年时期，“丰富的”大鼠大脑中含有的脂黄素(年龄色素)更少。[73]人们普遍认为，不饱和油脂促进衰老色素的形成。压力或额外的可的松(通过阻止葡萄糖的使用，迫使细胞吸收更多的脂肪)导致大脑加速衰老[74]的发现应该为研究物质的抗压力特性提供新的动力，如上文提到的保护类固醇和短链饱和脂肪。
Essential for Liver Damage: Both experimental and epidemiological studies have shown that dietary linoleic acid is required for the development of alcoholic liver damage.[75] Animals fed tallow and ethanol had no liver injury, but even 0.7% or 2.5% linoleic acid with ethanol caused fatty liver, necrosis, and inflammation. Dietary cholesterol at a level of 2% was found to cause no harm,[76] but omitting it entirely from the diet caused leakage of amino-transferase enzymes. This effect of the absence of cholesterol was very similar to the effects of the presence of linoleic acid with ethanol.
肝损害的必要条件:实验和流行病学研究均表明，膳食亚油酸是酒精性肝损害发生的必要条件。[75]动物喂食动物脂和乙醇没有肝损伤，但即使0.7%或2.5%的亚油酸与乙醇，也会引起脂肪肝、坏死和炎症。研究发现，2%的饮食胆固醇水平不会造成伤害[76]，但完全从饮食中排除胆固醇会导致氨基转移酶的泄漏。没有胆固醇的影响与亚油酸与乙醇的影响非常相似。
Obesity: For many years studies have been demonstrating that dietary coconut oil causes decreased fat synthesis and storage, when compared with diets containing unsaturated fats. More recently, this effect has been discussed as a possible treatment for obesity.[77] The short-chain fats in coconut oil probably improve tissue response to the thyroid hormone (T3), and its low content of unsaturated fats might allow a more nearly optimal function of the thyroid gland and of mitochondria. A survey of other tropical fruits' content of short and medium chain fatty acids might be useful, to find lower calorie foods which contain significant amounts of the shorter-chain fats.
肥胖:多年来的研究表明，与含有不饱和脂肪的饮食相比，食用椰子油会导致脂肪合成和储存减少。最近，这种效应被认为是治疗肥胖的一种可能方法。[77]椰子油中的短链脂肪可能改善组织对甲状腺激素(T3)的反应，其低含量的不饱和脂肪可能使甲状腺和线粒体的功能更接近最佳。对其他热带水果中短链和中链脂肪酸含量的调查可能会对寻找含有大量短链脂肪的低热量食物有用。
Other Problem Areas: The presence of palmitate in the lung surfactant phospholipids[78] suggests that maternal overload with unsaturated fats might interfere with the formation of these important substances, causing breathing problems in the newborn. The bone-calcium mobilizing effect of prostaglandins suggests that dietary fats might affect osteoporosis; the absence of osteoporosis in some tropical populations might relate to their consumption of coconut oil and other saturated tropical oils. The steroids which occur in association with some seed oils might be nutritionally significant, in the way animal hormones in foods undoubtedly are. For example, soy steroids can be converted by bowel bacteria into estrogens. R. Marker, et al., found diosgenin (the material in the Mexican yam from which progesterone, etc., are derived) in a palm kernel, Balanites aegyptica (Wall).[79] Another palm fruit also contains sterols with anti-androgenic and anti-edematous actions.[80, 81]
其他问题领域:肺表面活性剂磷脂中棕榈酸酯的存在[78]表明，母亲过量的不饱和脂肪可能会干扰这些重要物质的形成，导致新生儿呼吸问题。前列腺素的骨钙动员作用提示膳食脂肪可能影响骨质疏松症;一些热带地区的人口没有骨质疏松症可能与他们食用椰子油和其他饱和热带油有关。与某些种子油相关的类固醇可能具有重要的营养意义，就像食物中的动物激素无疑具有重要的营养意义一样。例如，大豆类固醇可以被肠道细菌转化为雌激素。R. Marker等人在一种名为埃及Balanites aegyptica (Wall)的棕榈仁中发现了薯蓣皂苷元(一种在墨西哥山药中提取黄体酮的物质)[79]。另一种棕榈果也含有甾醇，具有抗雄激素和抗水肿作用。(80、81)
If the amount of ingested unsaturated fats (inhibitors of protein digestion) were lower, protein requirements might be lower.
The similar effects of estrogen and of polyunsaturated fats (PUFA) are numerous. They include antagonism to vitamin E and thyroid, to respiration and proteolysis; promotion of lipofuscin formation and of clot formation, promotion of seizure activity, impairment of brain development and learning; and involvement in positive or negative regulation of cell division, depending on cell type.
如果摄入的不饱和脂肪(蛋白质消化抑制剂)的量较低，蛋白质需求可能会较低。
雌激素和多不饱和脂肪(PUFA)有很多相似的作用。它们包括对维生素E和甲状腺的拮抗，对呼吸和蛋白质水解的拮抗;促进脂褐素形成和血栓形成，促进癫痫活动，损害大脑发育和学习能力;以及参与细胞分裂的正调控或负调控，这取决于细胞类型。
These parallels suggest that the role of PUFA in reproduction might be similar to that of estrogen, namely, the promotion of uterine and breast cell proliferation, water uptake, etc. Such parallels should be a caution in generalizing from the conditions which are essential for reproduction to the conditions which are compatible with full development and full functional capacity. If a certain small amount of dietary PUFA is essential for reproduction, but for no other life function, then it is analogous to the brief “estrogen surge,” which must quickly be balanced by opposing hormones. The present approach to contraception through estrogen-induced miscarriage might give way to fertility regulation by diet. A self-actualizing pro-longevity diet, low in PUFA, might prolong our characteristically human condition of delayed reproductive maturity, and, if PUFA are really essential for reproduction, unsaturated vegetable oils could temporarily be added to the diet when reproduction is desired.
这些相似之处表明多不饱和脂肪酸在生殖中的作用可能与雌激素相似，即促进子宫和乳腺细胞增殖、水分吸收等。在将生殖所必需的条件概括为与充分发展和充分功能能力相适应的条件时，这种类比应当是一种谨慎。如果饮食中少量的多不饱和脂肪酸对生殖是必要的，而对其他生命功能没有作用，那么这就类似于短暂的“雌激素激增”，它必须迅速被相反的激素平衡。目前通过雌激素流产避孕的方法可能会取代饮食调节生育。一个自我实现的长寿饮食，低不饱和脂肪酸，可能会延长我们人类特有的延迟生殖成熟的状况，而且，如果不饱和脂肪酸确实是繁殖所必需的，当需要繁殖时，可以暂时在饮食中添加不饱和植物油。
Conclusions: Polyunsaturated fats are nearly ubiquitous, but if they are “essential nutrients,” in the way vitamin A, or lysine, is essential, that has not been demonstrated. It seems clear that they are essential for cancer, and that they have other properties which cause them to be toxic at certain levels. It might be time to direct research toward determining whether there is a threshold of toxicity, or whether they are, like ionizing radiation, toxic at any level.
结论:多不饱和脂肪几乎无处不在，但如果它们是“必需营养素”，就像维生素A或赖氨酸一样，是必需的，这还没有得到证实。很明显，它们对癌症是必不可少的，而且它们还有其他的特性，导致它们在一定程度上具有毒性。也许是时候进行直接研究，以确定是否存在毒性阈值，或者它们是否像电离辐射一样，在任何水平上都是有毒的。
Note:
A possible mitochondrial site for toxicity: In 1971 I was trying to combine some of the ideas of Albert Szent-Gyorgyi, Otto Warburg, W. F. Koch, and L. C. Strong. I was interested in the role of ubiquinone in mitochondrial respiration. In one experiment, I was using paper chromatography to compare oils that I had extracted from liver with vitamin E and with commercially purified ubiquinone. Besides using the pure substances, I decided to combine vitamin E with ubiquinone for another test spot. As soon as I combined the two oils, their amber and orange colors turned to an inky, greenish black color. I tested both bacterial and mammalian ubiquinone, and benzoquinone, and they all produced similar colors with vitamin E. When I ran the solvent up the paper, the vitamin E and the ubiquinone traveled at slightly different speeds. The black spot, containing the mixture, also moved, but each substance moved at its own speed, and as the materials separated, their original lighter colors reappeared. Charge-transfer bonds, which characteristically produce dark colors, are very weak bonds. I think this must have been that kind of bond. Years later, I tried to repeat the experiment, using “ubiquinone” from various capsules that were sold for medical use. Instead of the waxy yellow-orange material I had used before, these capsules contained a liquid oil with a somewhat yellow color. Very likely, the ubiquinone was dissolved in vegetable oil. At the time, I was puzzled that the color reaction didn't occur, but later I realized that a solvent containing double bonds (e.g., soy oil or other oil containing PUFA) would very likely prevent the close association between vitamin E and ubiquinone which is necessary for charge-transfer to occur. Since I think Koch and Szent-Gyorgyi were right in believing that electronic activation is the most important feature of the living state, I think the very specific electronic interaction between vitamin E and ubiquinone must play an important role in the respiratory function of ubiquinone. Ubiquinone is known to be a part of the electron transport chain which can leak electrons, so this might be one of the ways in which vitamin E can prevent the formation of toxic free-radicals. If it can prevent the “leakage” of electrons, then this in itself would improve respiratory efficiency. If unsaturated oils interfere with this very specific but delicate bond, then this could explain, at least partly, their toxicity for mitochondria. [“Electron leak” reference: B. Halliwell, in Age Pigments (R. S. Sohal, ed.), pp. 1-62, Elsevier, Amsterdam, 1981.]
注意:
一个可能的线粒体毒性位点:1971年，我试图结合阿尔伯特·圣-吉奥吉(Albert Szent-Gyorgyi)、奥托·华宝(Otto Warburg)、w·f·科赫(W. F. Koch)和l·c·斯特朗(L. C. Strong)的一些观点。我对泛素在线粒体呼吸中的作用很感兴趣。在一次实验中，我用纸色谱法将我从肝脏中提取的油脂与维生素E和商业纯化的泛素进行了比较。除了使用纯物质，我决定将维生素E和泛素酮结合在一起进行另一个测试点。当我把这两种油混合在一起时，它们的琥珀色和橙色就变成了墨绿色的黑色。我测试了细菌和哺乳动物的泛素酮和苯醌，它们都用维生素E产生了相似的颜色。当我用溶剂在纸上移动时，维生素E和泛素酮的移动速度略有不同。含有混合物的黑点也在移动，但每种物质都以自己的速度移动，当这些物质分离时，它们原来较浅的颜色又出现了。电荷转移键的特点是产生暗色，是非常弱的键。我想这就是那种联系。几年后，我试图重复这个实验，使用各种药用胶囊中的“泛素”。与我以前使用的蜡状黄橙色材料不同，这些胶囊含有一种有点黄色的液体油。很有可能，泛素溶解在植物油中。当时,我困惑,颜色反应没有发生,但后来我意识到溶剂含有双键(如豆油或其他石油包含PUFA)将很有可能防止维生素E和泛醌之间的密切联系是电荷转移发生的必要条件。由于我认为Koch和Szent-Gyorgyi认为电子激活是生命状态最重要的特征的观点是正确的，我认为维生素E和泛素酮之间非常具体的电子相互作用在泛素酮的呼吸功能中一定扮演着重要的角色。众所周知，泛素是电子传递链的一部分，它可以泄漏电子，所以这可能是维生素E可以防止有毒自由基形成的方式之一。如果它能防止电子“泄漏”，那么它本身就能提高呼吸效率。如果不饱和油干扰了这种非常特殊但微妙的连接，那么这就可以解释，至少部分地解释，它们对线粒体的毒性。[“电子泄漏”参考:B. Halliwell, in Age颜料(r.s. Sohal, ed.)， pp. 1-62, Elsevier, Amsterdam, 1981.]
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