Fats and degeneration 脂肪和退化 by Raymond Peat
50 years ago, in the first phase of marketing the polyunsaturated fatty acids (PUFA), linoleic acid was “heart protective,” and the saturated fats raised cholesterol and caused heart disease. 50年前，在多不饱和脂肪酸(PUFA)上市的第一阶段，亚油酸具有“保护心脏”的作用，而饱和脂肪会提高胆固醇，导致心脏病。 In the second phase, the other “essential fatty acid,” linolenic acid, was said to be even better than linoleic acid.
In the third phase, the longer chain omega -3 (omega minus three, or n minus three) fatty acids, DHA and EPA, are said to be even better than linolenic acid. 在第二阶段，另一种“必需脂肪酸”，亚麻酸，据说甚至比亚油酸更好。
在第三阶段，长链脂肪酸-3(-3，或n -3) DHA和EPA据说比亚麻酸更好。
Along the way, the highly unsaturated arachidonic acid, which we and other animals make out of the linoleic acid in foods, was coming to be identified with the “harmful animal fats.” But we just didn't hear much about how the amount of arachidonic acid in the tissues depended on the amount of linoleic acid in the diet.
在这个过程中，我们和其他动物从食物中的亚油酸中提取的高度不饱和的花生四烯酸，逐渐被认为是“有害的动物脂肪”。但是我们很少听说组织中的花生四烯酸的数量是如何取决于饮食中的亚油酸的数量的。
U.S. marketing dominates the world economy, including of course the communication media, so we shouldn't expect to hear much about the role of PUFA in causing cancer, diabetes, obesity, aging, thrombosis, arthritis and immunodeficiency, or to hear about the benefits of the saturated fats.
美国的市场主导着世界经济，当然包括传播媒体，所以我们不应该期望听到太多关于不饱和脂肪酸在癌症、糖尿病、肥胖、衰老、血栓形成、关节炎和免疫缺陷方面的作用，也不应该听到饱和脂肪的好处。
The saturated fats include the “tropical fats,” because they are synthesized in very warm organisms, and are very stable at those temperatures. Their stability offers some protection against the unstable PUFA.
饱和脂肪包括“热带脂肪”，因为它们是在非常温暖的生物体中合成的，在这些温度下非常稳定。它们的稳定性为不稳定的PUFA提供了一些保护。
Several of the degenerative conditions produced by the “essential fatty acids” can be reversed by use of saturated fats, varying in length from the short chains of coconut oil to the very long chains of waxes.
饱和脂肪的长度从短链的椰子油到长链的蜡都不同，它可以逆转由“必需脂肪酸”引起的一些退化状况。
When a person uses a drug, there is generally an awareness that the benefit has to be weighed against the side effects. But if something is treated as a “nutrient,” especially an “essential nutrient,” there is an implication that it won't produce undesirable side effects. 当一个人使用一种药物时，通常都意识到必须权衡利弊。但如果某种东西被当作“营养素”，特别是“必需营养素”，就意味着它不会产生不良的副作用。
Over the last thirty years I have asked several prominent oil researchers what the evidence is that there is such a thing as an “essential fatty acid.” One professor cited a single publication about a solitary sick person who recovered from some sickness after being given some unsaturated fat. (If he had known of any better evidence, wouldn't he have mentioned it?) The others (if they answered at all) cited “Burr and Burr, 1929.” The surprising thing about that answer is that these people can consider any nutritional research from 1929 to be definitive. It's very much like quoting a 1929 opinion of a physicist regarding the procedure for making a hydrogen bomb. What was known about nutrition in 1929? Most of the B vitamins weren't even suspected, and it had been only two or three years since “vitamin B” had been subdivided into two factors, the “antineuritic factor,” B1, and the “growth factor,” B2. Burr had no way of really understanding what deficiencies or toxicities were present in his experimental diet.
在过去的30年里，我问过几位著名的石油研究人员，有什么证据表明存在“必需脂肪酸”这种东西。一位教授引用了一篇关于一个孤独的病人在服用了一些不饱和脂肪后从疾病中恢复过来的文章。(如果他知道任何更好的证据，他会不提吗?)其他人(如果他们回答了的话)引用了“伯尔和伯尔，1929年”。令人惊讶的是，这些人可以把1929年的任何营养研究作为权威。这很像引用1929年一位物理学家关于制造氢弹过程的观点。1929年人们对营养学了解多少?大多数B族维生素甚至都没有被怀疑过，而“维生素B”被细分为两种因素，“抗尿症因子”B1和“生长因子”B2，也只是两三年前的事。伯尔无法真正了解他的实验饮食中存在哪些缺陷或毒性。
A few years after the first experiments, Burr put one of his “essential fatty acid deficient” rats under a bell jar to measure its metabolic rate, and found that the deficient animals were metabolizing 50% faster than rats that were given linoleic and linolenic acids as part of their diet. That was an important observation, but Burr didn't understand its implications. Later, many experiments showed that the polyunsaturated fats slowed metabolism by profoundly interfering with the function of the thyroid hormone and the cellular respiratory apparatus. Without the toxic fats, respiratory energy metabolism was very intense, and a diet that was nutritionally sufficient for a sluggish animal wouldn't necessarily be adequate for the vigorous animals.
在第一次实验的几年后，伯尔把他的一只“必需脂肪酸缺乏”的老鼠放在一个钟形罩下测量其代谢率，发现缺乏脂肪酸的老鼠的代谢速度比饮食中含有亚油酸和亚麻酸的老鼠快50%。这是一个重要的发现，但伯尔并不理解它的含义。后来，许多实验表明，多不饱和脂肪通过严重干扰甲状腺激素和细胞呼吸器官的功能而减慢新陈代谢。如果没有有毒脂肪，呼吸能量代谢就会非常剧烈，对于行动迟缓的动物来说营养充足的饮食对精力充沛的动物来说就不一定足够了。
Several publications between 1936 and 1944 made it very clear that Burr's basic animal diet was deficient in various nutrients, especially vitamin B6. The disease that appeared in Burr's animals could be cured by fat free B-vitamin preparations, or by purified vitamin B6 when it became available.A zinc deficiency produces similar symptoms, and at the time Burr did his experiments, there was no information on the effects of fats on mineral absorption. If a diet is barely adequate in the essential minerals, increasing the metabolic rate, or decreasing intestinal absorption of minerals, will produce mineral deficiencies and metabolic problems.
1936年至1944年间的几篇出版物明确指出，伯尔的基本动物饮食缺乏各种营养物质，尤其是维生素B6。在伯尔氏动物身上出现的疾病可以通过无脂维生素b制剂或纯化维生素B6来治愈。缺锌会产生类似的症状，在伯尔做实验的时候，没有关于脂肪对矿物质吸收的影响的信息。如果饮食中基本矿物质不足，增加代谢率，或减少肠道对矿物质的吸收，将产生矿物质缺乏和代谢问题。
Although “Burr's disease” clearly turned out to be a B-vitamin deficiency, probably combined with a mineral deficiency, it continues to be cited as the basis justifying the multibillion dollar industry that has grown up around the “essential” oils.
尽管“伯尔氏病”很明显是由于b族维生素缺乏，可能还伴有矿物质缺乏，但它仍然被认为是围绕“精油”发展起来的数十亿美元产业的依据。
Two years before Burr's experiment, German researchers found that a fat-free diet prevented almost all spontaneous cancers in rats. Later work showed that the polyunsaturated fats both initiate and promote cancer. With that knowledge, the people who kept claiming that “linoleic, linolenic, and maybe arachidonic acid are the essential fatty acids,” should have devoted some effort to finding out how much of that “essential nutrient” was enough, so that people could minimize their consumption of the carcinogenic stuff.
在伯尔进行实验的两年前，德国研究人员发现，无脂饮食几乎可以预防大鼠的所有自发癌症。后来的研究表明，多不饱和脂肪会引发和促进癌症。有了这些知识，那些一直声称“亚油酸、亚麻酸，也许还有花生四烯酸是必需脂肪酸”的人，应该花点精力去弄清楚多少“必需营养素”才是足够的，这样人们就可以尽量减少对致癌物质的摄入。
Between the first and second world wars, cod liver oil was recommended as a vitamin supplement, at first as a source of vitamin A, and later as a source of vitamins A and D. But in the late 1940s, experimenters used it as the main fat in dogs' diet, and found that they all died from cancer, while the dogs on a standard diet had only a 5% cancer mortality. That sort of information, and the availability of synthetic vitamins, led to the decreased use of cod liver oil.
第一次和第二次世界大战之间,鱼肝油是推荐的维生素补充剂,起初的维生素a,以及后来的维生素a和d。但在1940年代末,实验者用它作为主要的脂肪在狗的饮食,发现他们都死于癌症,而吃标准饮食的狗的癌症死亡率只有5%。这类信息，以及合成维生素的可用性，导致了鱼肝油使用量的减少。
But around that time, the seed oil industry was in crisis because the use of those oils in paints and plastics was being displaced by new compounds made from petroleum. The industry needed new markets, and discovered ways to convince the public that seed oils were better than animal fats. They were called the “heart protective oils,” though human studies soon showed the same results that the animal studies had, namely, that they were toxic to the heart and increased the incidence of cancer.
但大约在那个时候，由于从石油中提取的新化合物取代了油漆和塑料中使用的种子油，种子油行业陷入了危机。该行业需要新的市场，并找到了让公众相信种子油比动物脂肪更好的方法。它们被称为“心脏保护油”，尽管人类研究很快就显示出与动物研究相同的结果，即它们对心脏有毒，并增加癌症的发病率。
The “lipid hypothesis” of heart disease argued that cholesterol in the blood caused atherosclerosis, and that the polyunsaturated oils lowered the amount of cholesterol in the blood. Leaving behind the concept of nutritional essentiality, this allowed the industry (and their academic supporters, such as Frederick Stare at Harvard) to begin promoting the oils as having drug-like therapeutic properties. Larger amounts of polyunsaturated fat were supposed to be more protective by lowering the cholesterol, and were to be substituted for the saturated fats, which supposedly raised cholesterol and increased heart disease, producing atherosclerotic plaques in the blood vessels and increasing the formation of blood clots.
心脏病的“脂质假说”认为，血液中的胆固醇导致动脉粥样硬化，而多不饱和油降低了血液中的胆固醇含量。抛开营养的重要性这一概念，制药行业(以及他们的学术支持者，如哈佛大学的Frederick Stare)开始宣传这种油具有药物般的治疗特性。大量的多不饱和脂肪被认为可以通过降低胆固醇来起到更大的保护作用，并被用来替代饱和脂肪，饱和脂肪被认为会提高胆固醇，增加心脏病，在血管中产生动脉粥样硬化斑块，并增加血栓的形成。
Since all ordinary foods contain significant amounts of the polyunsaturated fats, there was no reason to think that, even if they were essential nutrients, people were likely to become deficient in them. So the idea of treating the seed oils as drug-like substances, to be taken in large amounts, appealed to the food oil industry.
由于所有普通食品都含有大量的多不饱和脂肪，因此没有理由认为，即使它们是必需的营养物质，人们也有可能缺乏它们。因此，把这种种子油当作药物一样，可以大量食用的想法吸引了食用油行业。
Prostaglandins, which are produced in the body by oxidizing the polyunsaturated fatty acids, provided an opportunity for the drug industry to get involved in a new market, and the prostaglandins offered a new way of arguing for the nutritional essentiality of linoleic and related acids: A whole system of “hormones” is made from these molecules. Since some of the prostaglandins suppress immunity, cause inflammation and promote cancer growth, some people have divided them into the “good prostaglandins” and the “bad prostaglandins.”
前列腺素在体内通过氧化生产多不饱和脂肪酸,为医药行业提供了一个机会参与一个新的市场,和主张的前列腺素提供了一种新的方式亚麻油酸和相关的营养重要性酸:“荷尔蒙”的整个系统是由这些分子。由于一些前列腺素抑制免疫力，引起炎症和促进癌症生长，一些人把它们分为“好前列腺素”和“坏前列腺素”。
PGI2, or prostacyclin, is considered to be a good prostaglandin, because it causes vasodilatation, and so drug companies have made their own synthetic equivalents: Epoprostenol, iloprost, taprostene, ciprostene, UT-15, beraprost, and cicaprost. Some of these are being investigated for possible use in killing cancer.
PGI2，或称前列环素，被认为是一种很好的前列腺素，因为它会导致血管扩张，所以制药公司已经制造了他们自己的合成等品:Epoprostenol, iloprost, taprostene, ciprostene, UT-15, beraprost，和cicaprost。其中一些药物可能用于杀死癌症，目前正在进行研究。
But many very useful drugs that already existed, including cortisol and aspirin, were found to achieve some of their most important effects by inhibiting the formation of the prostaglandins. It was the body's load of polyunsaturated fats which made it very susceptible to inflammation, stress, trauma, infection, radiation, hormone imbalance, and other fundamental problems, and drugs like aspirin and cortisone, which limit the activation of the stored “essential fatty acids,” gain their remarkable range of beneficial effects partly by the restraint they impose on those stored toxins.
但是许多已经存在的非常有用的药物，包括皮质醇和阿司匹林，被发现通过抑制前列腺素的形成来达到一些最重要的效果。是身体的多不饱和脂肪的负荷使它非常容易受到炎症、压力、创伤、感染、辐射、激素失衡和其他基本问题的影响，以及阿司匹林和可的松等药物，它们限制了储存的“必需脂肪酸”的激活，之所以能获得显著的有益效果，部分原因是它们抑制了储存的毒素。
Increasingly, the liberation of arachidonic acid from tissues during stress is seen as a central factor in all forms of stress, either acute (as in burns or exercise) or chronic (as in diabetes or aging). And, as the fat stores become more toxic, it seems that they more readily liberate the free fatty acids. (For example, see Iritani, et al., 1984)
越来越多的人认为，压力时组织中花生四烯酸的释放是各种压力的核心因素，无论是急性(如烧伤或运动)还是慢性(如糖尿病或衰老)。而且，随着脂肪储存的毒性越来越大，它们似乎更容易释放出游离脂肪酸。(例如，参见Iritani等人，1984)
During this same period, a few experimenters were finding that animals which were fed a diet lacking the “essential” fatty acids had some remarkable properties:They consumed oxygen and calories at a very high rate, their mitochondria were unusually tough and stable, their tissues could be transplanted into other animals without provoking immunological rejection, and they were very hard to kill by trauma and a wide variety of toxins that easily provoke lethal shock in animals on the usual diet. As the Germans had seen in 1927, they had a low susceptibility to cancer, and new studies were showing that they weren't susceptible to various fibrotic conditions, including alcoholic liver cirrhosis.
在同一时期，一些实验人员发现，喂食缺乏“必需”脂肪酸的饲料的动物具有一些显著的特性:他们消耗氧气和热量非常高的速度,他们的线粒体异常艰难的和稳定的,他们的组织可以移植到其他动物没有引发免疫排斥,他们很难杀死的创伤和各种各样的毒素,容易引发动物平时饮食中致命的冲击。正如德国人在1927年所看到的，他们患癌症的几率很低，新的研究表明，他们不容易患各种纤维化疾病，包括酒精性肝硬化。
In 1967 a major nutrition publication, Present Knowledge in Nutrition, published Hartroft and Porta's observation that the “age pigment,” lipofuscin, was formed in proportion to the amount of polyunsaturated fat and oxidants in the diet. The new interest in organ transplantation led to the discovery that the polyunsaturated fats prolonged graft survival, by suppressing the immune system. Immunosuppression was considered to have a role in the carcinogenicity of the “essential” fatty acids.
1967年，一份重要的营养刊物《营养知识》(Present Knowledge In nutrition)发表了哈特罗夫特和波尔塔的观察结果，即“年龄色素”脂褐素是与饮食中的多不饱和脂肪和氧化剂的数量成比例形成的。对器官移植的新兴趣导致发现多不饱和脂肪通过抑制免疫系统延长移植物存活。免疫抑制被认为在“必需”脂肪酸的致癌性中有作用。
Around the same time, there were studies that showed that unsaturated fats retarded brain development and produced obesity.
大约在同一时间，有研究表明，不饱和脂肪会阻碍大脑发育，导致肥胖。
Substances very much like the prostaglandins, called isoprostanes and neuroprostanes, are formed spontaneously from highly unsaturated fatty acids, and are useful as indicators of the rate of lipid peroxidation in the body. Most of the products of lipid peroxidation are toxic, as a result of their reactions with proteins, DNA, and the mitochondria. The age-related glycation products that are usually blamed on sugar, are largely the result of peroxidation of the polyunsaturated fatty acids.
与前列腺素非常相似的物质，被称为异前列腺素和神经前列腺素，是由高度不饱和脂肪酸自发形成的，可以用作体内脂质过氧化速率的指标。大多数脂质过氧化产物是有毒的，这是它们与蛋白质、DNA和线粒体反应的结果。与年龄相关的糖基化产物通常归咎于糖，主要是多不饱和脂肪酸的过氧化作用的结果。
Through the 1970s, this sort of information about the harmful effects of the PUFA was being slowly assimilated by the culture, though many dietitians still spoke of “the essential fatty acids, vitamin F.” By 1980, it looked as though responsible researchers would see the promotion of cancer, heart disease, mitochondrial damage, hypothyroidism and immunosuppression caused by the polyunsaturated fats as their most important feature, and would see that there had never been a basis for believing that they were essential nutrients.
在1970年代,这种信息PUFA被缓慢吸收的有害影响的文化,尽管许多营养师还谈到“必需脂肪酸,维生素f”到1980年,它看起来好像负责人员会促进癌症、心脏病、线粒体损伤,由多不饱和脂肪引起的甲状腺功能减退和免疫抑制是它们最重要的特征，并且会看到从来没有根据认为它们是必需营养素。
But then, without acknowledging that there had been a problem with the doctrine of essentiality, fat researchers just started changing the subject, shifting the public discourse to safer, more profitable topics. The fats that had been called essential, but that had so many toxic effects, were no longer emphasized, and the failed idea of “essentiality” was shifted to different categories of polyunsaturated fats.
但是，在不承认本质主义存在问题的情况下，肥胖的研究人员只是开始改变话题，将公众讨论转移到更安全、更有利可图的话题上。那些曾经被称为必需脂肪，但却有如此多的毒性作用的脂肪不再被强调，“必需脂肪”这一失败的概念也被转移到不同类别的多不饱和脂肪上。
The addition of the long chain highly unsaturated fats to baby food formulas was recently approved, on the basis of their supposed “essentiality for brain development.” One of the newer arguments for the essentiality of the PUFA is that “they are needed for making cell membranes.” But human cells can grow and divide in artificial culture solutions which contain none of the polyunsaturated fats, and no one has claimed that they are growing “without membranes.”
最近，在婴儿食品配方中添加长链高不饱和脂肪的做法获得了批准，理由是它们被认为“对大脑发育至关重要”。关于多不饱和脂肪酸的重要性的一个较新的论点是，“它们是制造细胞膜所必需的。”但人类细胞可以在不含多不饱和脂肪的人工培养液中生长和分裂，也没有人声称它们是在“没有膜”的情况下生长的。
The long chain fats found in fish and some algae don't interfere with animal enzymes as strongly as the seed oils do, and so by comparison, they aren't so harmful. They are also so unstable that relatively little of them is stored in the tissues. (And when they are used as food additives, it's necessary to use antioxidants to keep them from becoming smelly and acutely toxic.)
在鱼类和一些藻类中发现的长链脂肪对动物酶的干扰不像种子油那么强烈，所以相比之下，它们并没有那么有害。它们也非常不稳定，在组织中储存的相对较少。(当它们被用作食品添加剂时，有必要使用抗氧化剂来防止它们变臭和剧毒。)
When meat is grilled at a high temperature, the normally spaced double bonds in PUFA migrate towards each other, becoming more stable, so that linoleic acid is turned into “conjugated linoleic acid.” This analog of the “essential” linoleic acid competes against the linoleic acid in tissues, and protects against cancer, atherosclerosis, inflammation and other effects of the normal PUFA. Presumably, anything which interferes with the essential fatty acids is protective, when the organism contains dangerous amounts of PUFA. Even the trans-isomers of the unsaturated fatty acids (found in butterfat, and convertible into conjugated linoleic acid) can be protective against cancer.
当肉在高温下烧烤时，通常间距较大的PUFA双键相互迁移，变得更加稳定，因此亚油酸变成了“共轭亚油酸”。这种类似于“必需”亚油酸的物质在组织中与亚油酸竞争，并能预防癌症、动脉粥样硬化、炎症和正常多不饱和脂肪酸的其他作用。据推测，当生物体中含有危险数量的多不饱和脂肪酸时，任何干扰必需脂肪酸的东西都是保护性的。甚至不饱和脂肪酸的反式异构体(存在于乳脂中，可转化为共轭亚油酸)也能预防癌症。
In the 1980s the oil promoters were becoming more sophisticated, and were publishing many experiments in which the fish oils were compared with corn oil, or safflower, or soy oil, and in many of those experiments, the animals' health was better when they didn't eat the very toxic seed oils, that contained the “essential fatty acids,” linoleic and linoleic acids.
1980年代,石油推动者变得更加复杂,并出版许多实验的鱼油和玉米油相比,或红花,或豆油,和在许多实验中,动物的健康好当他们不吃有毒的种籽油,含有“必需脂肪酸”，亚油酸和亚油酸。
Besides comparing the fish oils to the stronger toxins, another trick is to take advantage of the same immunosuppressive property that had seemed troublesome, and to emphasize their ability to temporarily alleviate some autoimmune or allergic diseases. X-rays were once used that way, to treat arthritis and ringworm, for example.
除了将鱼油与更强的毒素进行比较外，另一个技巧是利用同样的免疫抑制特性，这似乎令人烦恼，并强调它们能够暂时缓解一些自身免疫或过敏性疾病。例如，x光曾被用于治疗关节炎和癣。
And, knowing that cancer cells have the ability to consume large amounts of fatty acids, they would test these fats in tissue culture dishes, and demonstrate that they were poisonous, cytotoxic, to the fast growing cancer cells. Although they caused cancer in animals, if they could be shown to kill cancer cells in a dish, they could be sold as anticancer drugs/nutrients, with the special mystique of being “essential fatty acids.” Strangely, their ability to kill cancer cells under some circumstances and to suppress some immunological reactions is being promoted in close association with the doctrine that these fats are nutritionally essential.
而且，知道癌细胞有能力消耗大量的脂肪酸，他们会在组织培养皿中测试这些脂肪，并证明它们是有毒的，对快速生长的癌细胞是细胞毒性的。虽然它们会引起动物的癌症，但如果它们能在培养皿中杀死癌细胞，它们就可以作为抗癌药物/营养物质出售，因为它们具有作为“必需脂肪酸”的特殊魔力。奇怪的是，它们在某些情况下杀死癌细胞和抑制某些免疫反应的能力，与这些脂肪是营养必需品的学说密切相关。
Arachidonic acid is made from linoleic acid, and so those two oils were considered as roughly equivalent in their ability to meet our nutritional needs, but a large part of current research is devoted to showing the details of how fish oils protect against arachidonic acid. The “balance” between the omega -3 and the omega -6 fatty acids is increasingly being presented as a defense against the toxic omega -6 fats. But the accumulation of unsaturated fats with aging makes any defense increasingly difficult, and the extreme instability of the highly unsaturated omega -3 fats creates additional problems.
花生四烯酸是由亚油酸制成的，因此这两种油被认为在满足我们营养需求的能力上大致相当，但目前的大部分研究都致力于展示鱼油如何防止花生四烯酸的细节。欧米加-3和欧米加-6之间的“平衡”越来越被认为是对有毒的欧米加-6脂肪的防御。但是，随着年龄的增长，不饱和脂肪的积累使防御变得越来越困难，而高度不饱和脂肪酸-3的极端不稳定性又带来了额外的问题。
PUFA and x-rays have many biological effects in common. They are immunosuppressive, but they produce their own inflammatory reactions, starting with increased permeability of capillaries, disturbed coagulation and proteolysis, and producing fibrosis and tumefaction or tissue atrophy. This isn't just a coincidence, since ionizing radiation attacks the highly unstable polyunsaturated molecules, simply accelerating processes that ordinarily happen more slowly as a result of stress and aging.
多不饱和脂肪酸和x射线有许多共同的生物学效应。它们具有免疫抑制作用，但它们会产生自身的炎症反应，开始时毛细血管通透性增加，凝血和蛋白水解紊乱，并产生纤维化、肿胀或组织萎缩。这不仅仅是一个巧合，因为电离辐射攻击高度不稳定的多不饱和分子，只是加速了通常由于压力和老化而发生得更慢的过程。
Prolonged stress eventually tends to be a self-sustaining process, impairing the efficient respiratory production of energy, converting muscle tissue to amino acids, suppressing the thyroid, and activating further mobilization of fatty acids. Fatty acids are mobilized from within the structure of cells by phospholipases, and from fat tissues by other lipases.
长期的压力最终倾向于成为一个自我维持的过程，损害有效的呼吸生产能量，将肌肉组织转化为氨基酸，抑制甲状腺，并进一步激活脂肪酸的动员。脂肪酸由磷脂酶从细胞结构内动员，由其他脂肪酶从脂肪组织中动员。
The highly unsaturated fatty acids, as well as the ordinary “essential fatty acids,” act directly to increase capillary permeability, even without conversion into prostaglandins, and they interfere in many ways with the clotting and clot removal systems. The effects of PUFA taken in a meal probably disturb the clotting system more than the same quantity of saturated fat, contrary to many of the older publications. The PUFA are widely believed to prevent clotting, but when cod liver oil is given to “EFA deficient” animals, it activates the formation of clots (Hornstra, et al., 1989). An opposite effect is seen when a long chain fatty acid synergizes with aspirin, to restrain clotting (Molina, et al., 2003).
高不饱和脂肪酸，以及普通的“必需脂肪酸”，直接作用于增加毛细血管通透性，甚至不转化为前列腺素，它们以多种方式干扰凝血和凝块清除系统。与许多以前的出版物相反，在一餐中摄入多不饱和脂肪酸对凝血系统的影响可能比同样数量的饱和脂肪更大。多不饱和脂肪酸被广泛认为可以防止凝血，但当鱼肝油被给予缺乏脂肪酸的动物时，它会激活凝血块的形成(Hornstra等人，1989)。当长链脂肪酸与阿司匹林协同抑制凝血时，可以看到相反的效果(Molina等，2003)。
Fibrosis is a generalized consequence of the abnormal capillary permeability produced by things that disrupt the clotting system. Estrogen, with its known contribution to the formation of blood clots and edema and fibrosis and tumors, achieves part of its effect by maintaining a chronically high level of free fatty acids, preferentially liberating arachidonic acid, rather than saturated fatty acids.
纤维化是血管通透性异常的普遍结果，这是由破坏凝血系统的东西造成的。众所周知，雌激素对血凝块、水肿、纤维化和肿瘤的形成有贡献，它的部分作用是通过维持长期高水平的游离脂肪酸来实现的，优先释放花生四烯酸，而不是饱和脂肪酸。
Butter, beef fat, and lamb fat are the only mostly saturated fats produced on a large scale in the U.S., and the cheapness/profitability of the seed oils made it easy to displace them. But, in the face of the immense amount of propagandistic “health” claims that have been made against the saturated fats, it's instructive to look at some of their actual effects, especially on the clotting system, and the related fibrotic reactions.
黄油、牛油和羊肉油是美国大规模生产的主要饱和脂肪，而种子油的廉价/盈利性使其很容易被取代。但是，面对大量反对饱和脂肪的“健康”宣传，看看它们的一些实际影响是有益的，尤其是对凝血系统，以及相关的纤维化反应。
The saturated fatty acids are very unreactive chemically. Coconut oil, despite containing about 1% of the unstable PUFA, can be left in a bucket at room temperature for a year or more without showing any evidence of deterioration, suggesting that the predominance of saturated fat acts as an antioxidant for the unsaturated molecules. In the body, the saturated fats seem to act the same way, preventing or even reversing many of the conditions caused by oxidation of fats.
饱和脂肪酸在化学上非常不活泼。尽管椰子油中含有约1%的不稳定多不饱和脂肪酸，但在室温下，椰子油可以放在桶里一年或更长时间，而没有任何变质的迹象，这表明饱和脂肪对不饱和分子起到了抗氧化剂的作用。在人体中，饱和脂肪似乎也有同样的作用，可以防止甚至逆转许多由脂肪氧化引起的疾病。
The stress-induced liberation of arachidonic acid causes blood vessels to leak, and this allows fibrin to escape from the blood stream, into the basement membrane and beyond into the extracellular matrix, where it produces fibrosis. (Cancer, autoimmune diseases, and heart disease involve the same inflammatory, thrombotic, fibrotic processes as the nominal fibroses.) Scleroderma, liver cirrhosis, fibrosis of the lungs, heart, and other organs, and all the diseases in which fibrous tissue becomes dense and progressively contracts, involve similar processes, and the treatments which are successful are those that stop the inflammation produced by the oxidation of the polyunsaturated fatty acids.
压力诱导的花生四烯酸释放导致血管泄漏，这使得纤维蛋白从血流中逸出，进入基底膜，并进一步进入细胞外基质，在那里产生纤维化。(癌症、自身免疫性疾病和心脏病涉及的炎症、血栓、纤维化过程与名义上的纤维化相同。)硬皮病、肝硬化、肺、心脏和其他器官的纤维化，以及所有纤维组织变得致密和进行性收缩的疾病，都涉及类似的过程，而成功的治疗方法是阻止由多不饱和脂肪酸氧化产生的炎症。
Retroperitoneal fibrosis is now known to be produced by estrogen, and is treated by antiestrogenic and antiserotonergic drugs, but as early as 1940 Alejandro Lipschutz demonstrated that chronic exposure to very low doses of estrogen produced fibromas in essentially every part of the body. Earlier, Loeb had studied the action of large doses of estrogen, which produced fibrosis of the uterus, as if it had accelerated aging. Following Lipschutz' work, in which he demonstrated the “antifibromatogenic” actions of pregnenolone and progesterone, several Argentine researchers showed that progesterone prevented and cured abdominal adhesions and other fibrotic conditions, including retroperitoneal fibrosis.
现在已知腹膜后纤维化是由雌激素引起的，可以用抗雌激素和抗血清素药物治疗，但早在1940年，Alejandro Lipschutz就证明，长期暴露于极低剂量的雌激素会在身体的每个部位产生纤维瘤。早些时候，勒布研究了大剂量雌激素的作用，它会导致子宫纤维化，好像它加速了衰老。在Lipschutz的研究中，他证明了孕烯醇酮和孕酮的“抗纤维瘤”作用，随后几位阿根廷研究人员表明孕酮可以预防和治疗腹部粘连和其他纤维化疾病，包括腹膜后纤维化。
Since estrogen produces both leakiness of the capillaries and excessive formation of fibrin, its effects will be seen first in the organs where it concentrates, but eventually anywhere capillaries leak fibrin. Estrogen activates the phospholipase which liberates arachidonic acid, and progesterone inhibits that phospholipase. 由于雌激素既会造成毛细血管的渗漏，又会造成纤维蛋白的过度形成，所以它的影响首先会在它集中的器官中表现出来，但最终会在毛细血管渗漏纤维蛋白的任何地方显现出来。雌激素激活磷脂酶释放花生四烯酸，而孕酮抑制磷脂酶。
As the fat tissues become more burdened with arachidonic acid, they release it more easily in response to moderately lipolytic stress signals. This could explain the increased levels of free fatty acids and lipid peroxidation that occur with aging. In animals that are “deficient” in the polyunsaturated fatty acids, adrenalin doesn't have the lipolytic effect that it does in animals on the standard diet. With aging, there is not only a tendency to have chronically higher free fatty acids in the blood, but for those fatty acids to be more unsaturated. The phospholipids of mitochondria and microsomes become more unsaturated with aging (Laganiere and Yu, 1993, Lee, et al., 1999). In the human retina there is a similar accumulation of PUFA with aging (Nourooz-Zadeh and Pereira, 1999), which implies that the aged retina will be more easily damaged by light.
当脂肪组织背负更多的花生四烯酸时，它们更容易释放花生四烯酸，以响应适度的脂解应激信号。这可以解释随年龄增长而增加的游离脂肪酸和脂质过氧化水平。在多不饱和脂肪酸“缺乏”的动物体内，肾上腺素没有标准饮食动物体内的脂解作用。随着年龄的增长，血液中不仅有长期高游离脂肪酸的趋势，而且这些脂肪酸的不饱和程度也会更高。线粒体和微粒体的磷脂随着老化变得更加不饱和(Laganiere和Yu, 1993, Lee, et al.， 1999)。在人的视网膜中，随着年龄的增长，也有类似的PUFA积累(Nourooz-Zadeh和Pereira, 1999)，这意味着老化的视网膜更容易受到光的损伤。
Several studies suggest that a high degree of unsaturation in the fats is fundamentally related to the aging process, since long lived species have a lower degree of unsaturation in their fats. Caloric restriction decreases the age-related accumulation of the fatty acids with 4 and 5 double bonds.
一些研究表明，脂肪的高度不饱和从根本上与衰老过程有关，因为长寿物种的脂肪不饱和程度较低。热量限制降低了4和5双键脂肪酸的年龄相关积累。
Although publicity has emphasized the anti-inflammatory effects of fish oil, experiments show that it is extremely effective in producing alcohol-related liver cirrhosis. Breakdown products of polyunsaturated fats (isoprostanes and 4-HNE) are found in the blood of people with alcoholic liver disease (Aleynik, et al., 1998). In the absence of polyunsaturated fats, alcohol doesn't produce cirrhosis. Saturated fats allow the fibrosis to regress:
虽然宣传已经强调了鱼油的抗炎作用，但实验表明，它在产生与酒精有关的肝硬化方面非常有效。酒精性肝病患者血液中可发现多不饱和脂肪(异前列腺素和4-HNE)的分解产物(Aleynik等人，1998年)。在不含多不饱和脂肪的情况下，酒精不会导致肝硬化。饱和脂肪使纤维化消退:
“A diet enriched in saturated fatty acids effectively reverses alcohol-induced necrosis, inflammation, and fibrosis despite continued alcohol consumption. The therapeutic effects of saturated fatty acids may be explained, at least in part, by reduced endotoxemia and lipid peroxidation….” (Nanji, et al., 1995, 2001)
“即使持续饮酒，富含饱和脂肪酸的饮食也能有效逆转酒精诱导的坏死、炎症和纤维化。饱和脂肪酸的治疗效果可以解释，至少部分，通过减少内毒素血症和脂质过氧化….(Nanji等，1995,2001)
In these studies, the animals were switched from fish oil to either palm oil or medium chain triglycerides (a major fraction of coconut oil). In other studies, Knittel, et al. (1995), show that fibrinogen, in “a clotting-like process,” is involved in the development of liver fibrosis, and that this appears to provide a basis for the growth of additional extracellular matrix.
在这些研究中，将动物从鱼油换成棕榈油或中链甘油三酯(椰子油的主要成分)。在其他研究中，Knittel等人(1995)指出，纤维蛋白原在“一种类似凝血的过程”中参与了肝纤维化的发展，这似乎为额外的细胞外基质的生长提供了基础。
Brown, et al. (1989), discussed this developmental process (leaky capillaries, fibrosis) in relation to wound healing, lung disease, and tumor growth.
The relatively few studies of fish oil and linoleic acid that compare them with palmitic acid or coconut oil have produced some very important results. For example, pigs exposed to endotoxin developed severe lung problems (resembling “shock lung”) when they had been on a diet with either fish oil or Intralipid (which is mostly linoleic acid, used for intravenous feeding in hospitals), but not after palmitic acid (Wolfe, et al., 2002). Brown等人(1989)讨论了这种发展过程(毛细血管渗漏、纤维化)与伤口愈合、肺部疾病和肿瘤生长的关系。
很少有研究将鱼油和亚油酸与软脂酸或椰子油进行比较，得出了一些非常重要的结果。例如，暴露于内毒素的猪在食用鱼油或脂肪内酯(主要是亚油酸，用于医院静脉喂养)时出现了严重的肺问题(类似“休克肺”)，但在棕榈酸之后没有出现(Wolfe等人，2002年)。
Eating low-fat seafood (sole, whitefish, turbot, scallops, oysters, lobster, shrimp, squid, etc.) once in a while can provide useful trace minerals, without much risk. However, fish from some parts of the ocean contain industrial contaminants in the fat, and large fish such as tuna, swordfish, Chilean sea bass and halibut contain toxic amounts of mercury in the muscles. Chilean sea bass (Patagonian toothfish) is very high in fat, too.
偶尔食用低脂海鲜(比目鱼、白鱼、大菱鲆、扇贝、牡蛎、龙虾、虾、鱿鱼等)可以提供有用的微量矿物质，没有太多风险。然而，来自海洋某些地区的鱼类脂肪中含有工业污染物，而金枪鱼、旗鱼、智利海鲈鱼和大比目鱼等大型鱼类的肌肉中含有大量有毒的汞。智利黑鲈(巴塔哥尼亚犬牙鱼)的脂肪含量也很高。
About ten years ago I met a young man with a degenerative brain disease, and was interested in the fact that he (working on a fishing boat) had been eating almost a pound of salmon per day for several years. There is now enough information regarding the neurotoxic effects of fish oil to justify avoidance of the fatty fish.
大约十年前，我遇到了一个患有退行性脑疾病的年轻人，我对他(在渔船上工作)几年来每天吃几乎一磅鲑鱼的事实很感兴趣。现在有足够的关于鱼油神经毒性作用的信息来证明避免食用脂肪多的鱼是合理的。
Some of the current advertising is promoting fish oil to prevent cancer, so it's important to remember that there are many studies showing that it increases cancer.
The developmental and physiological significance of the type of fatty acid in the diet has been established for a long time, but cultural stereotypes and commercial interests are threatened by it, so it can't be discussed publicly. 目前一些广告宣传鱼油可以预防癌症，所以重要的是要记住，有很多研究表明它会增加癌症。
饮食中脂肪酸类型的发育和生理意义已经确立很长时间了，但文化刻板印象和商业利益受到威胁，因此不能公开讨论。
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Transplantation 1995 Sep 27;60(6):570-7. The effect of dietary polyunsaturated fatty acids (PUFA) on acute rejection and cardiac allograft blood flow in rats.Haw MP, Linnebjerg H, Chavali SR, Forse RA. “The immunosuppressive effect of dietary PUFA warrants further investigation, and their use as a possible adjunctive treatment in organ transplantation should be considered.”
Dtsch Med Wochenschr. 2003 Jun 20;128(25-26):1395-8. [Rare cause of chronic abdominal pain: retractile mesenteritis] [in German] Hermann F, Speich R, Schneemann M. “Retractile mesenteritis is a rare cause of chronic abdominal pain with variable symptoms. Its aetiology is unknown. In case of bowel ischemia a surgical approach is preferred, milder forms may be treated with immunosuppressive agents as well as oral progesterone. Progesterone has exhibited positive effects on fatty tissue with successful treatment in desmoid tumors and retroperitoneal fibrosis. Here in we could demonstrate its safe and efficient use in a patient with retractile mesenteritis.”
Mech Ageing Dev 2001 Apr 15;122(4):427-43. Effect of the degree of fatty acid unsaturation of rat heart mitochondria on their rates of H2O2 production and lipid and protein oxidative damage. Herrero A, Portero-Otin M, Bellmunt MJ, Pamplona R, Barja G. “Previous comparative studies have shown that long-lived animals have lower fatty acid double bond content in their mitochondrial membranes than short-lived ones. In order to ascertain whether this trait protects mitochondria by decreasing lipid and protein oxidation and oxygen radical generation, the double bond content of rat heart mitochondrial membranes was manipulated by chronic feeding with semi-purified AIN-93G diets rich in highly unsaturated (UNSAT) or saturated (SAT) oils. UNSAT rat heart mitochondria had significantly higher double bond content and lipid peroxidation than SAT mitochondria. They also showed increased levels of the markers of protein oxidative damage malondialdehyde-lysine, protein carbonyls, and N(e)-(carboxymethyl)lysine adducts.” “These results demonstrate that increasing the degree of fatty acid unsaturation of heart mitochondria increases oxidative damage to their lipids and proteins, and can also increase their rates of mitochondrial oxygen radical generation in situations in which the degree of reduction of Complex III is higher than normal. These observations strengthen the notion that the relatively low double bond content of the membranes of long-lived animals could have evolved to protect them from oxidative damage.”
Biochem J. 1994 May 15;300 ( Pt 1):251-5. Regulation of fibrinolysis by non-esterified fatty acids. Higazi AA, Aziza R, Samara AA, Mayer M. “Examination of the fatty acid specificity showed that a minimal chain length of 16 carbon atoms and the presence of at least one double bond, preferably in a cis configuration, were required for inhibition of the fibrinolytic activity of plasmin.”
Science. 1976 Feb 27;191(4229):861-2. Nicotinic acid reduction of plasma volume loss after thermal trauma. Hilton JG, Wells CH. Intravenous administration of nicotinic acid to the anesthetized dog prior to thermal trauma reduced plasma loss at 10 minutes after burn from 7 milliliters per kilogram to less than 2 millimeters per kilogram. During the next 50 minutes plasma loss was the same in treated and untreated animals. An additional dose of nicotinic acid 30 minutes after burn prevented this further loss.
Z Gesamte Inn Med. 1976 Oct 15;31(20):838-43. [Age-dependence of catecholamine effects in man. IV. Effects of specific inhibitors on the lipolytic action of alpha and beta adrenergics] [in German] Hoffmann H.
Neurochem Res. 2000 Feb;25(2):269-76. Cortical impact injury in rats promotes a rapid and sustained increase in polyunsaturated free fatty acids and diacylglycerols. Homayoun P, Parkins NE, Soblosky J, Carey ME, Rodriguez de Turco EB, Bazan NG. “At day one, free 22:6 and 22:6-DAGs showed the greatest increase (590% and 230%, respectively). These results suggest that TBI elicits the hydrolysis of phospholipids enriched in excitable membranes, targeting early on 20:4-phospholipids (by 30 min post- trauma) and followed 24 hours later bypreferential hydrolysis of DHA-phospholipids. These lipid metabolic changes may contribute to the initiation and maturation of neuronal and fiber track degeneration observed following cortical impact injury.”
Thromb Res. 1989 Jan 1;53(1):45-53. Normalization by dietary cod-liver oil of reduced thrombogenesis in essential fatty acid deficient rats. Hornstra G, Haddeman E, Don JA.
Radiographics. 2003 Nov-Dec;23(6):1561-7. CT Findings in Sclerosing Mesenteritis (Panniculitis): Spectrum of Disease. Horton KM, Lawler LP, Fishman EK.
Nutr Cancer. 1985;7(4):199-209. Isomeric fatty acids and tumorigenesis: a commentary on recent work.Hunter JE, Ip C, Hollenbach EJ. “Neither epidemiological nor experimental studies published to date have demonstrated any valid association between trans fatty acid ingestion and tumorigenesis. A recent study showed that under controlled conditions, a fat with a high content of trans fatty acids did not promote the development of mammary tumors induced in rats by 7,12-dimethylbenz[a]anthracene to any greater extent than did a comparable fat with a high content of cis fatty acids. In addition, in this study a high trans fat was less tumor promoting than was a blend of fats that simulated the dietary fat composition of the United States and had a lower level of trans fatty acids.”
Medicina (B Aires). 1978 Mar-Apr;38(2):215. [Progesterone and retroperitoneal fibrosis] [in Spanish] Introzzi A.[Letter]
Cancer Res. 1985 May;45(5):1997-2001. Requirement of essential fatty acid for mammary tumorigenesis in the rat. Ip C, Carter CA, Ip MM. “Mammary tumorigenesis was very sensitive to linoleate intake and increased proportionately in the range of 0.5 to 4.4% of dietary linoleate.”
Biochim Biophys Acta. 1984 Nov 6;802(1):17-23.Activation of bovine platelets induced by long-chain unsaturated fatty acids at just below their lytic concentrations, and its mechanism. Kitagawa S, Endo J, Kametani F.
Clin Exp Metastasis 2000;18(5):371-7. Promotion of colon cancer metastases in rat liver by fish oil diet is not due to reduced stroma formation. Klieveri L, Fehres O, Griffini P, Van Noorden CJ, Frederiks WM. “Recently, it was demonstrated that dietary omega-3 polyunsaturated fatty acids (PUFAs) induce 10-fold more metastases in number and 1000-fold in volume in an animal model of colon cancer metastasis in rat liver.”
Folia Haematol Int Mag Klin Morphol Blutforsch. 1977;104(1):1-10. [Review: hemorrhagic diathesis resulting from acute exposure to ionizing Radiation] [Article in German] Krantz S, Lober M. The symptoms of the acute radiopathy are chiefly characterized by a severe blood coagulation disorder. The main results and problems of research work on this haemorrhagic diathesis are shortly reviewed.
Prostaglandins. 1978 Apr;15(4):557-64. Prostaglandin I2 as a potentiator of acute inflammation in rats.Komoriya K, Ohmori H, Azuma A, Kurozumi S, Hashimoto Y, Nicolaou KC, Barnette WE, Magolda RL.
Gerontology 1993;39(1):7-18. Modulation of membrane phospholipid fatty acid composition by age and food restriction. Laganiere S, Yu BP. H.M. “Phospholipids from liver mitochondrial and microsomal membrane preparations were analyzed to further assess the effects of age and lifelong calorie restriction on membrane lipid composition.” “The data revealed characteristic patterns of age-related changes in ad libitum (AL) fed rats: membrane levels of long-chain polyunsaturated fatty acids, 22:4 and 22:5, increased progressively, while membrane linoleic acid (18:2) decreased steadily with age. Levels of 18:2 fell by approximately 40%, and 22:5 content almost doubled making the peroxidizability index increase with age.” “We concluded that the membrane-stabilizing action of long-term calorie restriction relates to the selective modification of membrane long-chain polyunsaturated fatty acids during aging.”
Medicina (B Aires). 1978 Mar-Apr;38(2):123-32. [Effective treatment of several types of fibromatosis with progesterone. Fibrous mediastinitis, desmoid tumors, paraneoplastic fibrosis] [in Spanish] Lanari A, Molinas FC, Castro Rios M, Paz RA.
Medicina (B Aires). 1979 Nov-Dec;39(6):826-35. [Progesterone in fibromatosis and atherosclerosis][in Spanish] Lanari A.
Free Radic Biol Med 1999 Feb;26(3-4):260-5. Modulation of cardiac mitochondrial membrane fluidity by age and calorie intake. Lee J, Yu BP, Herlihy JT. “The fatty acid composition of the mitochondrial membranes of the two ad lib fed groups differed: the long-chain polyunsaturated 22:4 fatty acid was higher in the older group, although linoleic acid (18:2) was lower. DR eliminated the differences.” “Considered together, these results suggest that DR maintains the integrity of the cardiac mitochondrial membrane fluidity by minimizing membrane damage through modulation of membrane fatty acid profile.”
Lipids 2001 Jun;36(6):589-93. Effect of dietary restriction on age-related increase of liver susceptibility to peroxidation in rats. Leon TI, Lim BO, Yu BP, Lim Y, Jeon EJ, Park DK.
Acta Chir Scand. 1976;142(1):20-5. Induction of endogenous fibrinolysis inhibition in the dog. Effect of intravascular coagulation and release of free fatty acids. Lindquist O, Bagge L, Saldeen T. “In all groups subjected to infusion of thrombin an increase in plasma free fatty acids (FFA) was observed. The role of this increase for the development of fibrinolysis inhibition was tested by infusion of norepinephrine alone and in combination with nicotinic acid. Norepinephrine caused an increase of FFA after 2 hours and in urokinase inhibitor activity after 24-48 hours. Both of these were diminished by high doses of nicotinic acid, indicating that the release of FFA rather than intravascular coagulation might be the principal mechanism underlying the occurrence of fibrinolysis inhibition following trauma.”
Proc Natl Acad Sci U S A 1990 Nov;87(22):8845-9. Incorporation of marine lipids into mitochondrial membranes increases susceptibility to damage by calcium and reactive oxygen species: evidence for enhanced activation of phospholipase A2 in mitochondria enriched with n-3 fatty acids. Malis CD, Weber PC, Leaf A, Bonventre JV.
Prostaglandins Leukot Essent Fatty Acids 1994 Jul;51(1):33-40. Suppression of human T-cell growth in vitro by cis-unsaturated fatty acids: relationship to free radicals and lipid peroxidation. Madhavi N, Das UN, Prabha PS, Kumar GS, Koratkar R, Sagar PS.
Clin Exp Metastasis 1998 Jul;16(5):407-14. Diminution of the development of experimental metastases produced by murine metastatic lines in essential fatty acid-deficient host mice. Mannini A, Calorini L, Mugnai G, Ruggieri S.
Biochem Pharmacol. 1990 Mar 1;39(5):879-89. Histamine release from rat mast cells induced by metabolic activation of polyunsaturated fatty acids into free radicals. Masini E, Palmerani B, Gambassi F, Pistelli A, Giannella E, Occupati B, Ciuffi M, Sacchi TB, Mannaioni PF.
Journal of Lipid Research, Vol. 44, 271-279, February 2003. Arachidonic acid and prostacyclin signaling promote adipose tissue development : a human health concern? F. Massiera, P. Saint-Marc, J. Seydoux , T. Murata , T. Kobayashi , S. Narumiya , P. Guesnet, Ez-Zoubir Amri, R. Negrel and G. Ailhaud1.
Infection. 1994 Mar-Apr;22(2):106-12. Influence of dietary (n-3)-polyunsaturated fatty acids on leukotriene B4 and prostaglandin E2 synthesis and course of experimental tuberculosis in guinea pigs.Mayatepek E, Paul K, Leichsenring M, Pfisterer M, Wagner D, Domann M, Sonntag HG, Bremer HJ.
Biochim Biophys Acta 1994 Sep 15;1214(2):209-20. Reinvestigation of lipid peroxidation of linolenic acid. Mlakar A, Spiteller G. “Thus, a great number of previously unknown lipid peroxidation products was detected. It is assumed that these compounds also occur–at least as intermediates–in lipid peroxidation processes in mammalian tissue.”
Prostaglandins Leukot Essent Fatty Acids. 2003 May;68(5):305-10. Synergistic effect of D-003 and aspirin on experimental thrombosis models. Molina V, Arruzazabala ML, Carbajal D, Mas R.
Chem Res Toxicol. 2001 Apr;14(4):431-7. Defining mechanisms of toxicity for linoleic acid monoepoxides and diols in Sf-21 cells. Moran JH, Mon T, Hendrickson TL, Mitchell LA, Grant DF.
J Biochem (Tokyo). 1977 Aug;82(2):529-33. Effects of free fatty acids on fibrinolytic activity. Muraoka T, Okuda H. A novel method for the estimation of fibrinolytic activity is proposed. In this method, a fibrin clot suspension is used as a substrate (fibrin is known to be a physiological substrate of plasmin). The fibrin clot suspension was prepared by homogenization of human fibrin clots. With this method, we found that free fatty acids inhibited the plasmin activity, and long-chain, unsaturated free fatty acids had a particularly strong inhibitory action on plasmin. As regards the mechanism of the inhibitory action, free fatty acids may not inhibit complex formation between plasmin and fibirin, but may make it impossible for plasmin to act on fibrin due to deformation of the surface of the fibrin clot.
Alcohol Clin Exp Res. 1986 Jun;10(3):271-3. Dietary factors and alcoholic cirrhosis. Nanji AA, French SW.
Gastroenterology. 1995 Aug;109(2):547-54. Dietary saturated fatty acids: a novel treatment for alcoholic liver disease. Nanji AA, Sadrzadeh SM, Yang EK, Fogt F, Meydani M, Dannenberg AJ.
J Pharmacol Exp Ther. 1996 Jun;277(3):1694-700. Medium chain triglycerides and vitamin E reduce the severity of established experimental alcoholic liver disease. Nanji AA, Yang EK, Fogt F, Sadrzadeh SM, Dannenberg AJ.
Hepatology. 1997 Dec;26(6):1538-45. Dietary saturated fatty acids down-regulate cyclooxygenase-2 and tumor necrosis factor alfa and reverse fibrosis in alcohol-induced liver disease in the rat. Nanji AA, Zakim D, Rahemtulla A, Daly T, Miao L, Zhao S, Khwaja S, Tahan SR, Dannenberg AJ.
J Pharmacol Exp Ther. 2001 Nov;299(2):638-44. Dietary saturated fatty acids reverse inflammatory and fibrotic changes in rat liver despite continued ethanol administration. Nanji AA, Jokelainen K, Tipoe GL, Rahemtulla A, Dannenberg AJ.
Gastroenterology 1995 Apr;108(4):1124-35. Accumulation and cellular localization of fibrinogen/fibrin during short-term and long-term rat liver injury. Neubauer K, Knittel T, Armbrust T, Ramadori G “Fibrinogen/fibrin deposition in damaged livers was studied by immunohistology.” “Immunohistology showed striking amounts of fibrinogen and fibrin deposits in pericentral necrotic areas (short-term damage) and within fibrotic septa (long-term damage).” “The results show fibrinogen/fibrin deposition during short-term liver injury and liver fibrogenesis, which may suggest the involvement of a “clotting-like process” in short-term liver damage and liver fibrosis. The data might indicate that fibrin/fibronectin constitute a “provisional matrix,” which affects the attraction and proliferation of inflammatory and matrix-producing cells.”
Ophthalmic Res. 1999;31(4):273-9. Age-related accumulation of free polyunsaturated fatty acids in human retina. Nourooz-Zadeh J, Pereira P.
Chem Res Toxicol. 2002 Mar;15(3):367-72. Formation of cyclic deoxyguanosine adducts from omega-3 and omega-6 polyunsaturated fatty acids under oxidative conditions. Pan J, Chung FL.
Radiobiologiia. 1985 Nov-Dec;25(6):763-7. [Mechanism of circulatory disorders in animals irradiated at high doses] [in Russian] Pozharisskaia TD, Vasil'eva TP, Sokolova EN, Alekseeva II. Some data are reported on pathoanatomical changes, a status of the microcirculatory channel and the coagulogram of animals affected by high doses of ionizing radiation. The signs of disseminated intravascular blood coagulation have been revealed.
J Biol Chem. 1998 May 29;273(22):13605-12. Formation of isoprostane-like compounds (neuroprostanes) in vivo from docosahexaenoic acid. Roberts LJ 2nd, Montine TJ, Markesbery WR, Tapper AR, Hardy P, Chemtob S, Dettbarn WD, Morrow JD.
Nutr Cancer 1995;24(1):33-45. Effects of linoleic acid and gamma-linolenic acid on the growth and metastasis of a human breast cancer cell line in nude mice and on its growth and invasive capacity in vitro. Rose DP, Connolly JM, Liu XH
Arch Toxicol. 1997;71(9):563-74. Impaired cellular immune response in rats exposed perinatally to Baltic Sea herring oil or 2,3,7,8-TCDD. Ross PS, de Swart RL, van der Vliet H, Willemsen L, de Klerk A, van Amerongen G, Groen J, Brouwer A, Schipholt I, Morse DC, van Loveren H, Osterhaus AD, Vos JG.
Nutr Cancer 1998;30(2):137-43. Effects of dietary n-3-to-n-6 polyunsaturated fatty acid ratio on mammary carcinogenesis in rats. Sasaki T, Kobayashi Y, Shimizu J, Wada M, In'nami S, Kanke Y, Takita T. “An increase in the n-3/n-6 ratio did not suppress the incidence or reduce the latency of mammary tumor development. The number and weight of mammary tumors per tumor-bearing rat tended to be large in the group with an n-3/n-6 ratio of 7.84 compared with those in the other groups. As the n-3/n-6 ratios were elevated, the total number and weight of tumors increased gradually.”
J. Biol. Chem. 1940 132: 539-551. Essential fatty acids, vitamin B6, and other factors in the cure of rat acrodynia. H. Schneider, H. Steenbock, and Blanche R. Platz
Science. 1988 May 20;240(4855):1032-3. Essential fatty acid depletion of renal allografts and prevention of rejection. Schreiner GF, Flye W, Brunt E, Korber K, Lefkowith JB.
Physiol Bohemoslov. 1990;39(2):125-34. Proportion of individual fatty acids in the non-esterified (free) fatty acid (FFA) fraction in the serum of laboratory rats of different ages. Smidova L, Base J, Mourek J, Cechova I.
Placenta. 2003 Nov;24(10):965-73. Augmented PLA(2)Activity in Pre-eclamptic Decidual Tissue-A Key Player in the Pathophysiology of 'Acute Atherosis' in Pre-eclampsia? Staff AC, Ranheim T, Halvorsen B.
Acta Neurochir Suppl (Wien) 1994;60:20-3. Mechanisms of glial swelling by arachidonic acid. Staub F, Winkler A, Peters J, Kempski O, Baethmann A.
Arch Biochem Biophys. 1991 Aug 15;289(1):33-8. A possible mechanism of mitochondrial dysfunction during cerebral ischemia: inhibition of mitochondrial respiration activity by arachidonic acid. Takeuchi Y, Morii H, Tamura M, Hayaishi O, Watanabe Y.
J Drug Target. 2003 Jan;11(1):45-52. Modulation of tumor-selective vascular blood flow and extravasation by the stable prostaglandin 12 analogue beraprost sodium. Tanaka S, Akaike T, Wu J, Fang J, Sawa T, Ogawa M, Beppu T, Maeda H.
Am J Clin Nutr. 2003 May;77(5):1125-32. Effect of individual dietary fatty acids on postprandial activation of blood coagulation factor VII and fibrinolysis in healthy young men. Tholstrup T, Miller GJ, Bysted A, Sandstrom B.
Biochem Soc Trans. 2003 Oct;31(Pt 5):1075-9. Regression of pre-established atherosclerosis in the apoE-/- mouse by conjugated linoleic acid. Toomey S, Roche H, Fitzgerald D, Belton O.
Int J Biochem Cell Biol. 2003 May;35(5):749-55. Increased muscle proteasome activities in rats fed a polyunsaturated fatty acid supplemented diet.Vigouroux S, Farout L, Clavel S, Briand Y, Briand M. “Changes in the proteasome system, a dominant actor in protein degradation in eukaryotic cells, have been documented in a large number of physiological and pathological conditions.” “With the polyunsaturated fatty acid enriched diet, the chymotrypsin-like and peptidylglutamylpeptide hydrolase activities increased by 45% in soleus and extensor digitorum longus (EDL), and by 90% in the gastrocnemius medialis (GM) muscle. Trypsin-like activity of the proteasome increased by 250% in soleus, EDL and GM.” “Proteasome activities and level were less stimulated with a monounsaturated fatty acid supplemented diet.” “Unsaturated fatty acids are particularly prone to free radical attack. Thus, we suggest that alterations in muscle proteasome may result from monounsaturated and polyunsaturated fatty acid-induced peroxidation, in order to eliminate damaged proteins.”
J Am Coll Nutr. 2000 Aug;19(4):478S-486S. Conjugated linoleic acid and bone biology. Watkins BA, Seifert MF. “Recent investigations with growing rats given butter fat and supplements of CLA demonstrated an increased rate of bone formation and reduced ex vivo bone PGE2 production, respectively.”
Ups J Med Sci. 1979;84(3):195-201. Effect of nicotinic acid on the posttraumatic increase in free fatty acids and fibrinolysis inhibition activity in the rat.Wegener T, Bagge L, Saldeen T. Nicotinic acid effectively inhibited the posttraumatic increase in both free fatty acids (FFA) and fibrinolysis inhibition activity (FIA) in the blood in rats, indicating that FFA might be involved in the posttraumatic increase of FIA. The FIA in the liver was greater than that in other organs studied and was increased in the posttraumatic phase. The possible role of the liver in the posttraumatic increase of FIA is discussed.
Am J Physiol Regul Integr Comp Physiol. 2001 Mar;280(3):R908-12. CLA reduces antigen-induced histamine and PGE(2) release from sensitized guinea pig tracheae. Whigham LD, Cook EB, Stahl JL, Saban R, Bjorling DE, Pariza MW, Cook ME.
Toxicol Appl Pharmacol 1993 May;120(1):72-9. Essential fatty acid deficiency in cultured human keratinocytes attenuates toxicity due to lipid peroxidation. Wey HE, Pyron L, Woolery M.
Nutrition. 2002 Jul-Aug;18(7-8):647-53. Dietary fat composition alters pulmonary function in pigs.Wolfe RR, Martini WZ, Irtun O, Hawkins HK, Barrow RE
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