Unsaturated fatty acids: Nutritionally essential, or toxic? 不饱和脂肪是必须营养还是毒？
by Raymond Peat
In 1929 George and Mildred Burr published a paper claiming that unsaturated fats, and specifically linoleic acid, were essential to prevent a particular disease involving dandruff, dermatitis, slowed growth, sterility, and fatal kidney degeneration.
1929年，乔治和米尔德丽德·伯尔发表了一篇论文，声称不饱和脂肪，特别是亚油酸，对于预防一种特殊疾病是必不可少的，这些疾病包括头皮屑、皮炎、生长迟缓、不育和致命的肾脏退化。
In 1929, most of the B vitamins and essential trace minerals were unknown to nutritionists. The symptoms the Burrs saw are easily produced by deficiencies of the vitamins and minerals that they didn't know about.
1929年，大多数维生素B和必需的微量元素还不为营养学家所知。伯尔夫妇看到的症状很容易因为他们不知道的维生素和矿物质的缺乏而产生。
What really happens to animals when the “essential fatty acids” are lacking, in an otherwise adequate diet?
如果在正常饮食中缺乏“必需脂肪酸”，动物会发生什么呢?
Their metabolic rate is very high.
Their nutritional needs are increased.
They are very resistant to many of the common causes of sickness and death.
They are resistant to the biochemical and cellular changes seen in aging, dementia, autoimmunity, and the main types of inflammation.
它们的代谢非常旺盛。
他们的营养需求增加了。
它们对许多常见的疾病和死亡原因具有很强的抵抗力。
它们能抵抗衰老、痴呆、自身免疫和主要炎症所引起的生化和细胞变化。
The amount of polyunsaturated fatty acids often said to be essential (Holman, 1981) is approximately the amount required to significantly increase the incidence of cancer, and very careful food selection is needed for a diet that provides a lower amount.
多不饱和脂肪酸的量通常被认为是必不可少的(Holman, 1981)，这大约是显著增加癌症发病率所需的量，对于提供较低量的饮食，需要非常谨慎的食物选择。
When I was studying the age pigment, lipofuscin, and its formation from polyunsaturated fatty acids, I saw the 1927 study in which a fat free diet practically eliminated the development of spontaneous cancers in rats (Bernstein and Elias). I have always wondered whether George and Mildred Burr were aware of that study in 1929, when they published their claim that polyunsaturated fats are nutritionally essential. The German study was abstracted in Biological Abstracts, and the Burrs later cited several studies from German journals, and dismissively mentioned two U.S. studies* that claimed animals could live on fat-free diets, so their neglect of such an important claim is hard to understand. (*Their bibliography cited, without further comment, Osborne and Mendel, 1920, and Drummond and Coward, 1921.)
Since 1927, others have demonstrated that the polyunsaturated fats are essential for the development of cancer (and some other degenerative diseases), but the Burrs' failed to even mention the issue at any time during their careers. How could they, studying fat-free diets, have missed an important contemporary publication, if I, 40 years later, saw it? There were very few publications on dietary fats in those years, so it was hardly possible to miss it.
当我在研究年龄色素、脂褐素及其由多不饱和脂肪酸形成时，我看到了1927年的一项研究，在该研究中，无脂肪饮食实际上消除了大鼠自发癌症的发展(伯恩斯坦和伊莱亚斯)。我一直在想，乔治和米尔德丽德·伯尔(George and Mildred Burr)是否知道1929年的那项研究，当时他们发表了多不饱和脂肪是营养必需品的声明。德国的这项研究被刊登在《生物学文摘》上，伯尔斯夫妇后来又引用了几份德国期刊上的研究，并轻蔑地提到了两项声称动物可以靠无脂饮食生存的美国研究*，所以他们忽视了如此重要的声明，令人难以理解。(他们的参考书目引用了奥斯本和孟德尔，1920年，德拉蒙德和科沃德，1921年，没有进一步评论。)
自1927年以来，其他人已经证明多不饱和脂肪是癌症(和一些其他退行性疾病)的发展所必需的，但伯尔夫妇在他们的职业生涯中甚至没有在任何时候提到过这个问题。他们在研究无脂饮食，怎么会错过当代的一份重要出版物，如果40年后我看到了它?在那些年里，关于膳食脂肪的出版物很少，所以不可能错过它。
When researchers at the Clayton Foundation Biochemical Institute at the University of Texas demonstrated that “Burr's disease” was actually a vitamin B6 deficiency, rather than a fatty acid deficiency, the issue was settled. Later studies failed to confirm the existence of the Burr disease caused by a deficiency of fatty acids, though many similar conditions were produced by a variety of other dietary defects. In 1938, a group in Burr's own laboratory (Brown, et al.) failed to produce dermatitis in a man during a six month experiment. Neither of the other major features of the Burr disease, male sterility and kidney degeneration, has been subsequently confirmed. The claim that polyunsaturated fatty acid deficiency caused sterility of male animals (“A new and uniform cause of sterility is shown”) was quickly dropped, probably because an excess of polyunsaturated fats was discovered to be an important cause of testicular degeneration and sterility.
德克萨斯大学克莱顿基金会生化研究所(Clayton Foundation Biochemical Institute at the University of Texas)的研究人员证明，“伯尔氏病”实际上是维生素B6缺乏，而不是脂肪酸缺乏，这个问题就解决了。后来的研究未能证实由缺乏脂肪酸引起的伯尔病的存在，尽管许多类似的情况是由各种其他饮食缺陷引起的。1938年，伯尔自己实验室的一个小组(布朗等人)在6个月的实验中未能使一名男子患上皮炎。伯尔病的其他主要特征，男性不育和肾脏退化，随后均未得到证实。多不饱和脂肪酸缺乏导致雄性动物不育的说法(“出现了一个新的、统一的不育原因”)很快就被推翻了，可能是因为发现多不饱和脂肪过多是睾丸退化和不育的重要原因。
One of the features of the Burrs' rats on the fat-free diet was that they ate more calories and drank much more water than the rats that received polyunsaturated fatty acids in their diet. They believed that the animals were unable to synthesize fat without linoleic acid, although in another context they cited a study in which the fat of rats on a fat-free diet was similar in composition to lard: “McAmis, Anderson, and Mendel [37] fed rats a high sucrose, fat-free diet and rendered the fat of the entire animal. This fat had an iodine number of 64 to 71, a fairly normal value for lard.”
伯尔斯的老鼠在无脂肪饮食中的特点之一是，他们比饮食中含有多不饱和脂肪酸的老鼠吃了更多的卡路里，喝了更多的水。他们认为动物不能合成脂肪没有亚油酸,尽管他们在另一个上下文中引用的一项研究中,老鼠的脂肪无脂饮食相似成分猪油:“McAmis、安德森和孟德尔[37]喂老鼠高蔗糖,无脂饮食和整个动物的脂肪。这种脂肪的碘含量在64到71之间，这是猪油相当正常的值。”
The “wasteful” food consumption, and the leanness of animals that weren't fed polyunsaturated fats became fairly common knowledge by the late 1940s, but no one repeated the Burrs' claim that the absence of those fatty acids led quickly to the animals' death. Meanwhile, “crazy chick disease” caused by feeding an excess of polyunsaturated fats, and a little later, “yellow fat disease,” caused by too much fish fat, were being recognized by farmers. In the 1950s, the seed oil industry created the anti-cholesterol diet culture, and a few decades later, without any new “Burr-like” publications, the omega minus 3 oils, especially fish oils, were coming to be represented as the overlooked essential fatty acids, which were capable of preventing the toxic effects of the original “essential” linoleic acid.
到20世纪40年代末，“浪费”的食物消费和不喂食多不饱和脂肪的动物消瘦已成为相当普遍的知识，但没有人重复伯尔夫妇的说法，即缺乏这些脂肪酸会很快导致动物死亡。与此同时，由于喂食过多的多不饱和脂肪而引起的“疯鸡病”，以及稍后由于鱼脂肪过多而引起的“黄脂肪病”，都被农民们所认识。在20世纪50年代，籽油工业创造了抗胆固醇饮食文化，几十年后，没有任何新的“伯尔式”出版物，omega - 3油，特别是鱼油，开始被代表为被忽视的必需脂肪酸，它们能够防止原始“必需”亚油酸的毒性作用。
Although the 1929 Burr paper is still often cited as proof of the essentiality of PUFA, Burr's younger colleague (at the University of Minnesota Hormel Institute), Ralph Holman, has cited an infant (1970), and a 78 year old woman (in 1969), who developed dermatitis while receiving fat-free intravenous feedings. Dermatitis, with dandruff, similar to Burr's disease, has been produced by various nutritional deficiencies besides vitamin B6, including a trace mineral deficiency and a biotin deficiency, so there is no valid reason to associate dermatitis with a fat deficiency. The cases of “EFA deficiency” produced by intravenous feedings that have been widely cited were probably the result of a deficiency of zinc or other trace mineral, since so-called “Total Parenteral Nutrition” was in use for many years before the trace minerals were added to the “total” formula. In 1975, I learned that our local hospital was putting all premature babies on what they called total intravenous feeding, without trace minerals, for weeks, or months. There is still more emphasis on polyunsaturated fat in intravenous feeding than on the essential trace nutrients.
尽管伯尔1929年的论文仍然经常被引用作为PUFA重要性的证据，伯尔的年轻同事(明尼苏达大学荷美尔研究所)拉尔夫·霍尔曼(Ralph Holman)引用了一个婴儿(1970年)和一个78岁的妇女(1969年)，她们在接受无脂肪静脉注射喂养时患上了皮炎。皮炎，带有头皮屑，类似于伯尔氏病，除了维生素B6之外，还由于各种营养缺乏而产生，包括微量矿物质缺乏和生物素缺乏，因此没有充分的理由将皮炎与脂肪缺乏联系在一起。由于所谓的“全肠外营养”使用多年后，微量元素才被添加到“全”配方中，因此静脉注射引起的“维生素A缺乏症”被广泛引用，可能是锌或其他微量元素缺乏症的结果。1975年，我了解到我们当地的医院对所有早产儿进行他们所谓的完全静脉喂养，不含微量矿物质，持续数周或数月。在静脉喂养中，多不饱和脂肪仍然比必需的微量营养素更受重视。
Holman and the Hormel Institute have been extremely influential in promoting the doctrine of the essentiality of PUFA, including fish oils and the omega -3 oils, but their best evidence, the Burr experiment, doesn't make their case. Far worse than that is the effect it has had in distracting attention from the profoundly toxic effects of the so-called essential fatty acids. Long after he should have known better, Holman was arguing that butter was a nutritionally inferior fat.
霍尔曼和荷美尔研究所在推广多不饱和脂肪酸(包括鱼油和欧米加-3油)的重要性方面有着极大的影响力，但他们最好的证据，伯尔实验，并不能证明他们的观点。更糟糕的是，它分散了人们对所谓的必需脂肪酸的毒性作用的注意力。早在他应该更了解真相之后，霍尔曼还在争论黄油是一种营养不良的脂肪。
When the Burrs were doing their study, Raymond Pearl was one of the most famous biologists in the country, and his “rate of living” theory of aging was very widely known. According to that theory, an organism has an intrinsic potential to produce a certain total amount of energy during its lifetime, and if it metabolizes at a higher than normal rate, its life span will be proportionately shorter than normal.
当伯尔夫妇在做他们的研究时，雷蒙德·珀尔是美国最著名的生物学家之一，他关于衰老的“活率”理论广为人知。根据这一理论，一个有机体在其一生中具有产生一定总能量的内在潜力，如果它的新陈代谢速度高于正常水平，那么它的寿命就会按比例比正常水平短。
There is general agreement that animals on a fat free diet have a very high metabolic rate, but the people who believe the “rate of living” theory will be inclined to see the increased rate of metabolism as something harmful in itself. It is clear that this is what the Burrs thought. They didn't attempt to provide a diet that provided increased amounts of all vitamins and minerals, in proportion to the increased metabolic rate.
人们普遍认为，吃无脂肪食物的动物新陈代谢率很高，但相信“活率”理论的人倾向于认为新陈代谢率的增加本身是有害的。很明显，这就是伯尔夫妇的想法。他们并没有试图提供一种饮食来增加所有维生素和矿物质的含量，并与新陈代谢率的增加成比例。
Pearl did an experiment, sprouting cantaloupe seeds in a dish with water. The sprouts that grew rapidly died sooner than those that grew more slowly. They died as soon as the nutrients stored in the endosperm had been consumed. Naturally, when nutrients are depleted, growth and metabolism must stop. If food and air and water are rationed, then slow metabolizers are going to live longer. But when nutritional needs are met, the organisms with the highest metabolic rate generally are healthier and live longer. In a study of nurses, those who habitually consumed the most calories lived longer than those who consumed the least. Even while Pearl was promoting his theory, other famous biologists, for example John Northrup in Jacques Loeb's lab at the Rockefeller Institute, were making observations that contradicted the rate of living theory. For example, around 1916, Northrup observed that fruit flies that metabolized at the highest rate lived the longest. Northrup was doing biology, Pearl was doing propaganda, following Weismannism.
珀尔做了一个实验，在一个有水的盘子里发芽哈密瓜种子。长得快的芽比长得慢的芽死得早。在胚乳中储存的营养一被消耗掉，它们就死亡了。自然地，当营养物质耗尽时，生长和新陈代谢就必须停止。如果食物、空气和水都限量供应，那么新陈代谢缓慢的人会活得更久。但是，当营养需求得到满足时，新陈代谢率最高的生物体通常更健康，寿命更长。在一项针对护士的研究中，那些习惯消耗最多卡路里的人比消耗最少卡路里的人活得更长。即使在珀尔推广他的理论时，其他著名的生物学家，例如洛克菲勒研究所雅克·勒布实验室的约翰·诺斯鲁普，也进行了与生命速率理论相矛盾的观察。例如，在1916年左右，诺斯鲁普观察到新陈代谢率最高的果蝇寿命最长。诺斯鲁普在研究生物学，珀尔在做宣传，遵循维斯曼主义。
The idea of extending life span by slowing metabolism and growth was a logical implication of the “rate of living” theory of aging, and it's an idea that is still popular. Many people have supposed that eating less would slow metabolism. Caloric restriction does extend the life span of many species, but it generally preserves the high metabolic rate of youth, so that at a given age the calorie-restricted animal has a higher rate of oxygen consumption per gram of body weight than the unrestricted eaters.
通过减缓新陈代谢和生长来延长寿命的想法是衰老“活率”理论的逻辑暗示，这个想法现在仍然很流行。许多人认为吃得少会减缓新陈代谢。热量限制确实延长了许多物种的寿命，但它通常保持了年轻动物的高代谢率，因此在给定的年龄，热量限制的动物每克体重的耗氧量比不限制的食者要高。
Roy Walford, a gerontologist who wrote about extending the human life span to 120 years by caloric restriction, spent 30 years limiting his diet to about 1600 calories, with little animal protein, almost no saturated fat–fish once or twice per week, poultry or beef about once, and a fat free milkshake for breakfast–and after about 15 years, began developing a degenerative brain disease, ALS, one of the nerve diseases involving lipid peroxidation and excitotoxicity. When he died from the disease, he had lived a year longer than the normal life expectancy.
罗伊-老年病学家，延长了人类寿命到120年通过热量限制。30年间每天摄入大约1600卡路里，吃很少动物蛋白质，几乎没有饱和脂肪——鱼一次或每周两次，家禽或牛肉。早餐吃无脂肪奶昔。大约15年后，他开始发展为退行性脑疾病，ALS，一种涉及脂质过氧化和兴奋性毒性的神经疾病。他死于这种疾病时，只比正常预期寿命多活了一年。
V. Stefannson, one of the early polar explorers, spent a winter living entirely on caribou meat, and felt that it had prevented the scurvy that had killed so many of the other explorers, who had counted on fruit and vegetables to prevent it. But he believed that meat was a metabolic stimulant that made people age prematurely, as Pearl's rate of living theory predicted. Stefannson said that Eskimo women were getting old in their twenties, and that at the age of 60 they looked as old as Europeans did at 80. He was a well informed anthropologist, and his observations were probably accurate. The Eskimos he observed ate large amounts of fish, and other unsaturated fats, and sometimes ate highly decayed fish. An accelerated rate of aging would be expected from such a diet, because of the toxic lipid peroxides.
早期的极地探险者之一v·斯蒂芬森(V. Stefannson)有一个冬天完全靠驯鹿肉维生，他觉得驯鹿肉可以预防坏血病。其他许多探险者都曾死于坏血病，而他们都是靠水果和蔬菜来预防坏血病的。但他认为，肉类是一种代谢兴奋剂，会让人过早衰老，正如珀尔的生命速度理论所预测的那样。斯蒂芬森说，爱斯基摩妇女在20多岁的时候就开始变老，60岁的时候看起来和80岁的欧洲人一样老。他是一位消息灵通的人类学家，他的观察可能是准确的。他观察到的爱斯基摩人吃大量的鱼和其他不饱和脂肪，有时还吃高度腐烂的鱼。由于有毒的脂质过氧化物，这样的饮食会加速衰老。
Calorie-restricted animals (on a diet of normal composition) have a lower degree of fat unsaturation in their mitochondria as they age, preserving the relatively more saturated fats of youth.
限制热量摄入的动物(饮食成分正常)随着年龄增长，其线粒体中的脂肪不饱和程度较低，保留了年轻时相对较多的饱和脂肪。
Birds' mitochondrial fats are much less polyunsaturated than those of mammals, and birds' metabolic rates are much higher, and they live much longer than mammals of a similar size.
鸟类的线粒体脂肪比哺乳动物的多不饱和脂肪酸少得多，鸟类的代谢率也高得多，它们的寿命也比同等体型的哺乳动物长得多。
With aging, the highly peroxidizable fatty acids, arachidonic and docosahexaenoic acid, increase greatly in a variety of tissues, and lipid peroxidation increases with aging. Peroxidation slows mitochondrial respiration, lowering the metabolic rate. Caloric restriction slows the accumulation of the highly unsaturated fatty acids in mitochondria, and reduces peroxidation.
随着年龄的增长，各种组织中高过氧化物脂肪酸花生四烯酸和二十二碳六烯酸大幅度增加，脂质过氧化也随着年龄的增长而增加。过氧化作用减慢线粒体呼吸，降低代谢率。限制热量可以减缓线粒体中高度不饱和脂肪酸的积累，并减少过氧化作用。
Over the years, it has become evident that the polyunsaturated fats are not very compatible with a high rate of metabolism, though they are necessary for organisms that live at low temperatures and metabolize slowly, such as fish and vegetables. The saturated fats solidify at low temperature; beef fat is very stiff at refrigerator temperature, and in a fat fish, such stiffness would be lethal.
Even some hibernating rodents can stay alive with their body tissues close to the freezing point, and their stored fats have to be unsaturated. When their diet doesn't allow them to store enough polyunsaturated fat, they fail to go into hibernation. This is probably a clue to some of the general biological effects of the PUFA.
尽管多不饱和脂肪对低温环境下代谢缓慢的生物体(如鱼和植物)来说是必需的，但多年来，多不饱和脂肪显然与高代谢率并不相容。饱和脂肪在低温下会凝固;牛肉的脂肪在冰箱温度下非常坚硬，而对于肥美的鱼来说，这种坚硬是致命的。
即使是一些冬眠的啮齿动物也能在接近冰点的身体组织下存活，而且它们储存的脂肪必须是不饱和的。当它们的饮食不能储存足够的多不饱和脂肪时，它们就不能进入冬眠。这可能是PUFA的一些一般生物学效应的线索。
A series of studies about 20 years ago showed that the functions of the thyroid hormone are all inhibited by unsaturated fats, with the inhibition increasing in proportion to the number of unsaturations (double bonds) in the fat molecule.
大约20年前的一系列研究表明，甲状腺激素的功能都受到不饱和脂肪的抑制，这种抑制程度与脂肪分子中不饱和(双键)的数量成正比。
When the tissues are saturated with those antithyroid fats, metabolism slows, especially when any stress, such as cold or hunger, increases the concentration of free fatty acids in the blood stream. Stress and hypothyroidism increase the formation of serotonin, which is an important factor in producing the torpor of hibernation, and lowering the body temperature. The polyunsaturated fatty acids themselves directly contribute to the formation of serotonin, for example by increasing the ability of tryptophan to enter the brain. In a certain cold climate, the PUFA are essential for hibernation, but under other conditions, the rodent would be able to continue gathering food and eating, instead of hibernating.
当组织中饱和了这些抗甲状腺脂肪时，新陈代谢就会减慢，特别是当任何压力，如寒冷或饥饿，会增加血液中游离脂肪酸的浓度。应激和甲状腺功能减退会增加血清素的形成，而血清素是导致冬眠的一个重要因素，还会降低体温。多不饱和脂肪酸本身直接促进血清素的形成，例如通过增加色氨酸进入大脑的能力。在某些寒冷气候下，多不饱和脂肪酸是冬眠所必需的，但在其他条件下，啮齿动物可以继续收集食物和食物，而不是冬眠。
The direct effects of the PUFA on the endocrine and nervous systems, as illustrated by the hibernating squirrel, interact with their effects on intercellular communication (including the formation of prostaglandins and related substances), and the effects of their oxidative breakdown products, such as acrolein. But the people who claim that they are absolutely, rather than conditionally, essential, base their argument on the idea that they are needed for the formation of prostaglandins and cell membranes. The fact that cells can replicate in fat free conditions shows that the argument from membranes is unfounded. The argument from prostaglandins is more complex, but has no firmer foundation.
多不饱和脂肪酸对内分泌和神经系统的直接影响，如冬眠的松鼠所示，与它们对细胞间通讯的影响(包括前列腺素和相关物质的形成)及其氧化分解产物(如丙烯醛)的影响相互作用。但是那些声称它们是绝对的，而不是有条件的，必不可少的人，他们的论点是基于前列腺素和细胞膜的形成需要它们。细胞可以在无脂肪条件下复制的事实表明，来自膜的论点是没有根据的。关于前列腺素的论点更为复杂，但没有更坚实的基础。
When a dose of PUFA is administered to a lizard, which isn't a hibernator, the lizard's body temperature is lowered by several degrees. There are probably many ways in which the PUFA produce that effect, besides increasing serotonin and decreasing thyroid. The PUFA are increased by estrogen, and they increase estrogen, and have some directly estrogen-like effects. Estrogen itself tends to lower body temperature and shift metabolism away from oxidative energy production. Aging, like estrogen, increases the body's content of the PUFA: Linoleic, linolenic, dihomo-gamma-linolenic, docosahexaenoic and docosapentaenoic acids are increased by age, and the longer chain acids increase more rapidly in women than in men (Bolton-Smith, et al., 1997). (Women are apparently relatively protected by progesterone, which inhibits lipolysis and prostaglandin formation, and protects the brain, thymus, and other tissues from lipid peroxidation and other effects of the PUFA.)
当给不是冬眠的蜥蜴注射多不饱和脂肪酸时，蜥蜴的体温会降低几度。除了增加血清素和减少甲状腺，多不饱和脂肪酸产生这种效果的方式可能有很多。多不饱和脂肪酸通过雌激素增加，增加雌激素，直接具有雌激素样作用。雌激素本身倾向于降低体温，使新陈代谢远离氧化能量的产生。像雌激素一样，衰老会增加身体的多不饱和脂肪酸含量:亚油酸、亚麻酸、二同-亚麻酸、二十二碳六烯酸和二十二碳五烯酸会随着年龄的增长而增加，而且女性体内较长链酸的增长速度要快于男性(Bolton-Smith等，1997)。(孕酮明显相对地保护了女性，它能抑制脂肪分解和前列腺素的形成，保护大脑、胸腺和其他组织免受脂质过氧化和多不饱和脂肪酸的其他影响。)
Aging involves a decreasing metabolic rate, an increased tendency toward inflammation, and a decreased ability to synthesize proteins. Inflammation contributes to the decreasing ability to use oxygen, and the slowed renewal of proteins combined with lower ability to produce energy impair the organism's ability to control peroxidative damage and inflammation.
衰老包括代谢率下降，炎症倾向增加，以及合成蛋白质能力下降。炎症会导致消耗氧气的能力下降，而蛋白质的更新速度减慢，再加上产生能量的能力降低，削弱了机体控制过氧化损伤和炎症的能力。
The fragments of deteriorating PUFA combine with proteins and other cell materials, producing immunogenic substances. The so-called “advanced glycation end products,” that have been blamed on glucose excess, are mostly derived from the peroxidation of the “essential fatty acids.” The name, “glycation,” indicates the addition of sugar groups to proteins, such as occurs in diabetes and old age, but when tested in a controlled experiment, lipid peroxidation of polyunsaturated fatty acids produces the protein damage about 23 times faster than the simple sugars do (Fu, et al., 1996).
降解的多不饱和脂肪酸碎片与蛋白质等细胞物质结合，产生免疫原性物质。所谓的“晚期糖基化终末产物”，被归咎于葡萄糖过量，主要来自“必需脂肪酸”的过氧化作用。名称、“糖化”,表明添加糖组蛋白,如发生在糖尿病和老年,但当测试在一个受控的实验中,多不饱和脂肪酸的脂质过氧化作用产生蛋白质损失约23倍的单糖(Fu, et al ., 1996)。
Several autoimmune disease models in animals (involving the eye, kidney, and pancreas) have been prevented by a deficiency of the EFA (Schreiner, et al., 1989, Bazan, et al., 1990, Benhamou, et al., 1995).
一些动物的自身免疫性疾病模型(包括眼睛、肾脏和胰腺)已经被EFA缺乏所预防(Schreiner，等人，1989,Bazan等人，1990,Benhamou等人，1995)。
Besides causing a general slowing of metabolism, aging and toxic PUFA have specific actions on the detoxifying system. The enzymes that help to detoxify PUFA and estrogen and serotonin are inhibited by both PUFA and estrogen. All systems, including blood vessels and the intestine, are made leaky by estrogen and the PUFA and their products. A reduced ability to regulate the excitatory amino acids, resulting from PUFA toxins, tends to produce excitotoxicity, damaging nerves (Ou, et al., 2002).
除了导致新陈代谢的普遍减缓，衰老和有毒的多不饱和脂肪酸对解毒系统有特定的作用。多不饱和脂肪酸、雌激素和血清素的解毒酶都被多不饱和脂肪酸和雌激素所抑制。所有的系统，包括血管和肠道，都是由雌激素和多不饱和脂肪酸及其产品造成的渗漏。多不饱和脂肪酸毒素导致调节兴奋性氨基酸的能力下降，容易产生兴奋性毒性，损伤神经(Ou等，2002)。
Although the interplay of the various types of nerve is very complex, a variety of experiments suggest that the PUFA are acting directly on serotonergic nerves, rather than just increasing the conversion of tryptophan to serotonin.
虽然不同类型的神经之间的相互作用非常复杂，但各种实验表明，PUFA直接作用于5 -羟色胺能神经，而不仅仅是增加色氨酸到5 -羟色胺的转换。
For example, a deficiency of the so-called essential fatty acids, EFA, makes animals more sensitive to some anesthetics, and more resistant to others. It makes them resistant to the anesthetics that act by promoting the actions of serotonin, but it prolongs the effects of those that don't act through serotonin, and these are the anesthetics such as xenon and nitrous oxide, that apparently act by stabilizing the structure of water, as described by Linus Pauling. Progesterone and the saturated fats seem to act partly through the stabilizing of cell water, and estrogen and the PUFA have opposing effects, creating cellular excitation while interfering with the stable cellular water structure.
Serotonin interferes with slow wave sleep, and promotes cortisol, both of which can be harmful to brain cells. (Hypothyroidism is one of the causes of a decrease in slow wave sleep.) Babies whose mothers' serum contained more DHA were more wakeful on their second day of life, than the babies of low-DHA mothers. The amide of oleic acid is a sleep promoter, with apparent antiserotonin activity (Yang, et al., 2003), and since oleic acid tends to be displaced by diets high in PUFA, this suggests another way in which the highly unsaturated fatty acids could promote serotonin's effects.
例如，所谓的必需脂肪酸EFA的缺乏，会使动物对某些麻醉剂更敏感，对其他麻醉剂更有抵抗力。这让他们抵抗行动的麻醉剂促进血清素的行为,但它延长那些不通过5 -羟色胺的影响,这些麻醉剂如氙和一氧化二氮,显然法案通过稳定的结构水,被莱纳斯·鲍林。孕酮和饱和脂肪似乎通过稳定细胞水发挥部分作用，而雌激素和多不饱和脂肪酸具有相反的作用，创造细胞兴奋，同时干扰稳定的细胞水结构。
血清素会干扰慢波睡眠，并促进皮质醇，这两者都对脑细胞有害。(甲状腺功能减退是慢波睡眠减少的原因之一。)母亲血清中含有更多DHA的婴儿在生命的第二天比母亲血清中DHA含量低的婴儿更清醒。油酸的酰胺是一种睡眠促进剂，具有明显的抗血清素活性(Yang, et al.， 2003)，由于油酸往往被富含多不饱和脂肪酸的饮食所取代，这表明高不饱和脂肪酸可以促进血清素的作用。
People who don't have a normal amount of slow wave sleep are likely to have slow reaction times when they are awake, and quickness of reactions is a good indicator of general intelligence.
Manufacturers of baby formulas are claiming that the highly unsaturated fatty acids accelerate brain development, but they neglect to mention studies that show either no effect, or retardation of development. In some of the tests that are used to measure infant development, a generalized state of arousal or anxiety could be interpreted as “more mature.”
In one experiment, animals that received less than 0.32% of their calories as EFA grew slightly less than rats on a standard diet, but their brains were as large as those of normal rats (Bruckner, et al., 1984). That is, their brain to body ratio was a little larger than normal, which is a typical feature of individuals with a higher metabolic rate. That result is very different from the claims of the baby food industry, that the brain is the organ most easily damaged by a PUFA deficiency.
那些没有正常的慢波睡眠的人在醒着的时候很可能反应较慢，而反应快是一般智力的一个很好的指标。
婴儿配方奶粉的制造商声称，高不饱和脂肪酸会加速大脑发育，但他们忽视了一些研究，这些研究表明，要么没有效果，要么发育迟缓。在一些用来衡量婴儿发育的测试中，普遍的觉醒或焦虑状态可以被解释为“更成熟”。
在一项实验中，食用少于0.32%的脂肪酸的动物比食用标准饮食的老鼠长得略少，但它们的大脑与正常老鼠一样大(Bruckner等人，1984)。也就是说，他们的大脑与身体的比例略高于正常水平，这是新陈代谢率较高的个体的典型特征。这一结果与婴儿食品工业声称的大脑是多不饱和脂肪酸缺乏最容易受损的器官的说法大相径庭。
One of the standard signs of toxicity is the enlargement of the spleen and liver, and that effect is produced by larger amounts of the EFA. The weight of the thymus is reduced by PUFA in the diet (Guimarães, et al., 1990). Thymus cells tend to be easily killed by a combination of stress and EFA, and bone marrow cells, though less sensitive than thymic cells, are damaged by lipid peroxidation of the PUFA. The effects of PUFA on the thymus were compared to those of radiation by Soviet researchers. Immunodeficiency, produced largely by damage to thymic cells, increases when larger amounts of PUFA are eaten for a prolonged time.
毒性的一个标准症状是脾脏和肝脏的肿大，而这种效果是由大量的脂肪酸产生的。饮食中的多不饱和脂肪酸可降低胸腺重量(Guimarães, et al.， 1990)。胸腺细胞容易被压力和必需脂肪酸的共同作用杀死，而骨髓细胞虽然没有胸腺细胞那么敏感，却会被多不饱和脂肪酸的脂质过氧化破坏。苏联研究人员将多不饱和脂肪酸对胸腺的影响与辐射的影响进行了比较。免疫缺陷主要是由胸腺细胞受损引起的，当长时间食用大量多不饱和脂肪酸时，免疫缺陷就会增加。
The growth and metastasis of a variety of tumors are inhibited by saturated fatty acids, and increased by fish oil–as much as 10 times in number of metastases, 1000 times in size (Griffini, et al., 1998).
饱和脂肪酸可抑制多种肿瘤的生长和转移，鱼油可使肿瘤转移数量增加10倍，肿瘤大小增加1000倍(Griffini等，1998)。
Mothers whose breast milk contains more long-chain n-3 fatty acids are more likely to have allergic children (Stoney, et al., 2004). (And children whose mothers are allergic have higher levels of DHA and EPA in their tissues.) These associations aren't mentioned by the manufacturers who speak of those fats as essential.
母乳中含有较多长链n-3脂肪酸的母亲的孩子更容易过敏(Stoney, et al.， 2004)。(母亲过敏的孩子的组织中DHA和EPA的含量更高。)生产商并没有提到这些关联，他们说这些脂肪是必需的。
When animals have been “deprived” of the EFA during gestation and nursing, and then given a standard diet, they develop larger bones, with a thicker cortex and more trabecular bone, both of which would suggest a lower level of stress. Many types of inflammation and stress are significantly reduced in “EFA deficient” animals. Inflammation caused by the injection of carrageenan is decreased, partly because of the absence of prostaglandins in these animals. The absence of the EFA protects against colitis and nephritis ( ). The kidneys are more effective in several ways in the deficient animals.
当动物在怀孕和哺乳期间被“剥夺”了脂肪酸，然后给予标准饮食，它们会发育出更大的骨骼，更厚的皮质和更多的骨小梁，这两者都表明压力水平较低。许多类型的炎症和压力在“脂肪酸缺乏”的动物中显著减少。注射角叉胶引起的炎症减少，部分原因是这些动物体内缺乏前列腺素。EFA的缺乏可以预防结肠炎和肾炎()。肾脏在几个方面对缺陷动物更有效。
Shock, caused by the injection of endotoxin, which is 100% lethal to normally fed animals, is only 24% lethal to the deficient animals.
Poisons are much less harmful to deficient animals, for example, a cobra venom factor causes less tissue damage to their lungs.
Concussive trauma and burns cause much less damage to deficient animals.
注射内毒素引起的休克，对正常喂养的动物100%致死，而对缺乏喂养的动物仅24%致死。
毒素对有缺陷的动物的危害要小得多，例如，眼镜蛇毒液对肺的组织损伤较小。
脑震荡和烧伤对有缺陷的动物造成的伤害要小得多。
The endothelial lining of blood vessels is protected by saturated fats and oleic acid, damaged by polyunsaturated, and their barrier function is improved by the absence of PUFA.
饱和脂肪和油酸对血管内皮有保护作用，而多不饱和脂肪和油酸对血管内皮有破坏作用，多不饱和脂肪酸的缺失改善了血管内皮的屏障功能。
Alzheimer's disease, retinal degeneration, cataracts, and liver cirrhosis all involve reactions of oxidized PUFA with proteins. Saturated fats help to heal alcoholic liver cirrhosis.
阿尔茨海默病、视网膜变性、白内障和肝硬化都涉及氧化多不饱和脂肪酸与蛋白质的反应。饱和脂肪有助于治疗酒精性肝硬化。
The lesions of atherosclerosis and cataracts contain some of the same oxidized lipids as the age pigment itself. When large deposits of age pigment become visible, it's probably because the general reduction of metabolism and protein synthesis has interfered with the normal processes for removing debris. The age pigment contributes to degeneration by wasting energy and oxygen, weakening the antioxidation, antiglycation, and other defensive systems.
动脉粥样硬化和白内障的病变中含有一些与年龄色素相同的氧化脂质。当年龄色素的大量沉积变得可见时，可能是因为新陈代谢和蛋白质合成的普遍减少干扰了清除碎片的正常过程。老年性色素通过消耗能量和氧气，削弱抗氧化、抗糖基化和其他防御系统，从而导致退化。
The EFA amplify nearly all kinds of injury and stress, and the results of many recent publications make it look as though serotonin interacts harmfully with the EFA in most of these situations. The specific balance of polyunsaturated fatty acids, and their various breakdown products, from carbon monoxide, glyoxal, and acrolein, to the larger aldehydes and radicals, and the stress-induced substances such as serotonin, histamine, estrogens, can produce an immense variety of biological problems.
脂肪酸会放大几乎所有种类的伤害和压力，最近发表的许多研究结果表明，在大多数情况下，血清素与脂肪酸之间的相互作用似乎是有害的。多不饱和脂肪酸的特殊平衡，以及它们的各种分解产物，从一氧化碳、乙二醛、丙烯醛，到较大的醛和自由基，以及应激诱导的物质，如血清素、组胺、雌激素，可以产生各种各样的生物学问题。
When the various claims of an EFA “deficiency disease” or syndrome or symptom are examined, their inconsistency over the years makes skepticism seem increasingly justified. The Burrs' publications were typical of others, in failing to describe and account for the evidence that contradicted their claims. Claiming that certain fatty acids are essential, a scientific approach would require showing what was wrong with the experiments that showed that they were not essential, and especially, those that showed that they were positively harmful.
当各种EFA“缺乏症”或综合症或症状的说法被审查时，它们多年来的不一致使怀疑论似乎越来越有道理。伯尔夫妇的出版物是其他人的典型，没有描述和解释与他们的主张相矛盾的证据。声称某些脂肪酸是必需的，科学的方法需要证明那些表明它们不是必需脂肪酸的实验有什么问题，尤其是那些表明它们确实有害的实验。
In this culture that repeatedly makes such claims of essentiality, the growing number of reports of biological superiority of “deficient” animals suggests that nutritional research may be near the point at which it can resume the line of study begun by Northrup, Osborne, Mendel, Drummond, Bernstein, Elias, and others, that was interrupted for 60 years by industrial interests that promoted antiscientific opinions.
For example, in 1914 F.P. Rous showed that limiting food intake reduced the incidence of cancer, and then in 1915 and 1917, Osborne and Mendel showed that food restriction extended the fertility and longevity of female rats. The association between estrogen and cancer had become known during this time, and vitamin E, which was originally known as the fertility vitamin, was soon recognized to have antiestrogenic properties, as well as to prevent the deadly effects of excessive polyunsaturated fats in the diet. My endocrinology professor, A.S. Soderwall, who had found that excess estrogen prevented (or interrupted) pregnancy, demonstrated that increased vitamin E extended fertility in aging female rodents.
在这种反复强调重要性的文化中，关于“有缺陷”的动物在生物学上具有优越性的报道越来越多，这表明营养学研究可能已经接近可以恢复由诺斯鲁普、奥斯本、孟德尔、德拉蒙德、伯恩斯坦、埃利亚斯等人开始的研究路线的临界点。这一过程被推动反科学观点的工业利益中断了60年。
例如，1914年F.P. Rous表明限制食物摄入可以降低癌症发病率，然后在1915年和1917年，Osborne和Mendel表明限制食物摄入可以延长雌性老鼠的生育能力和寿命。在这个时期，雌激素和癌症之间的关系已经为人所知，而最初被称为生育维生素的维生素E，很快就被认为具有抗雌激素的特性，并能防止饮食中过多的多不饱和脂肪造成的致命影响。我的内分泌学教授a·s·索德沃尔(A.S. Soderwall)发现过量的雌激素可以阻止(或中断)怀孕，他证明了维生素E的增加可以延长老年雌性啮齿动物的生育能力。
By the time I began my research, it seemed clear that it had been the reduction of PUFA in the diet which, like the addition of vitamin E, had prevented sterility in the calorie restriction experiments, and that those treatments had limited the effects of estrogen in the aging organisms.
当我开始我的研究时，似乎很清楚的是，减少饮食中的多不饱和脂肪酸，就像添加维生素E一样，在卡路里限制实验中防止了不育，这些治疗也限制了衰老有机体中雌激素的作用。
Estrogen, by activating phospholipase A2, acts to amplify the toxic effects of PUFA in the tissues, and these effects increase with age, and with decreased amounts of thyroid and progesterone.
雌激素通过激活磷脂酶A2，增强多不饱和脂肪酸在组织中的毒性作用，这些作用随着年龄的增长以及甲状腺和孕酮的减少而增加。
Antioxidants can slightly retard the cumulative degenerative effects of the fats interacting with estrogen, serotonin, and other mediators of inflammation, but real elimination of the degenerative diseases will require an exploration of the effects of the entire series of lipid signalling substances derived from the saturated and omega minus 9 fatty acids.
抗氧化剂可以稍微延缓脂肪与雌激素、血清素和其他炎症介质相互作用的累积退化效应，但是，真正消除退化性疾病需要探索从饱和脂肪酸和ω - 9脂肪酸衍生的整个系列脂质信号物质的影响。
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Lipids. 1997 Sep;32(9):979-88. Modulation of adjuvant-induced arthritis by dietary arachidonic acid in essential fatty acid-deficient rats. Chinn KS, Welsch DJ, Salsgiver WJ, Mehta A, Raz A, Obukowicz MG. “Controlled feeding of linoleic acid (LA) or arachidonic acid (AA) to essential fatty acid-deficient (EFAD) rats was used to define the relationship between dietary AA and the inflammatory response evoked during adjuvant-induced arthritis.” “Compared to rats fed the standard laboratory chow diet (Control), edema in the primary hind footpads was decreased by 87% in EFAD, 71% in EFAD + 1x AA, 45% in EFAD + 10x AA, and 30% in EFAD + 0.5x LA. The decrease in edema in the footpads of EFAD rats was nearly identical to the decrease in edema in the footpads of Control rats dosed with indomethacin. Hind footpad edema correlated with the final AA plasma level and eicosanoid levels extracted from hind footpad tissue, but not with neutrophil infiltration.”
J Nutr. 1996 Jun;126(6):1534-40. Dietary (n-9) eicosatrienoic acid from a cultured fungus inhibits leukotriene B4 synthesis in rats and the effect is modified by dietary linoleic acid. Cleland LG, Gibson RA, Neumann MA, Hamazaki T, Akimoto K, James MJ.
J Nutr. 1981 Nov;111(11):2039-43. Effects of dietary fatty acids on delayed-type hypersensitivity in mice. Dewille JW, Fraker PJ, Romsos DR. Effects of an essential fatty acid deficient (EFAD) [0% corn oil (CO)] diet and a diet high in polyunsaturated fatty acids [PUFA (50% CO)] on one aspect of in vivo T cell function [delayed-type hypersensitivity (DTH)] were assessed. After a 70-day feeding trial, DTH was reduced by 30% in mice fed the EFAD diet, but the response of mice fed the high PUFA diet equaled that of control mice fed a diet containing 13% CO. The time required for the EFAD diet to reduce DTH was 42 days. Although consumption of the EFAD diet reduced DTH, this reduction was rapidly reversed, within 7 days, by switching the EFAD mice to the control diet. These results indicate that :1) consumption of the EFAD diet reduces one aspect of in vivo T cell function (DTH), but the effect can be reversed by refeeding the control diet; and 2) a high PUFA diet does not adversely affect DTH.
Biochem. J., 1917, xi, 325. A comparative study of tumour and normal tissue growth. Drummond, JC
J. Physiol. 1920, liv, p. xxx, Proc. Physiol. Soc. Nutrition on diets practically devoid of fats. Drummond, JC.
J. Gerontol. 30(6), 647-54, 1975, “Rat brain fatty acid composition: effect of dietary fat and age,” Eddy, D. E., and D. Harman.
J Biol Chem 1996 Apr 26;271(17):9982-6. The advanced glycation end product, Nepsilon-(carboxymethyl)lysine, is a product of both lipid peroxidation and glycoxidation reactions. Fu MX, Requena JR, Jenkins AJ, Lyons TJ, Baynes JW, Thorpe SR.
Pediatrics 31:171-192, 1963. Hansen AE, Wiese HF, Boelsche AN, Haggard ME, Adam DJD, Davis H.
Am J Clin Nutr 49:290-300, 1982. Holman RT, Johnson SB, Hatch TF.
Cancer Res. 45(5), 1997-2001, 1985. “Requirement of essential fatty acids for mammary tumor,” Ip, C., et al.
Food and Nutrition Board. 1989. Recommended Dietary Allowances 10th ed. Washington, DC: National Academy of Sciences. p 48.
Am J Clin Nutr. 2004 Nov;80(5):1167-74. Docosahexaenoic acid concentrations are higher in women than in men because of estrogenic effects. Giltay EJ, Gooren LJ, Toorians AW, Katan MB, Zock PL. “The proportion of DHA was 15 +/- 4% (x +/- SEM; P < 0.0005) higher in the women than in the men. Among the women, those taking oral contraceptives had 10 +/- 4% (P = 0.08) higher DHA concentrations than did those not taking oral contraceptives. Administration of oral ethinyl estradiol, but not transdermal 17beta-estradiol, increased DHA by 42 +/- 8% (P < 0.0005), whereas the antiandrogen cyproterone acetate did not affect DHA. Parenteral testosterone decreased DHA by 22 +/- 4% (P < 0.0005) in female-to-male transsexual subjects. Anastrozole decreased estradiol concentrations significantly and DHA concentrations nonsignificantly (9 +/- 6%; P = 0.09). CONCLUSION: Estrogens cause higher DHA concentrations in women than in men, probably by upregulating synthesis of DHA from vegetable precursors.”
J. American Geriatrics Soc. 24(1) 292-8, 1976, “Free radical theory of aging: effect of dietary fat on central nervous system function,” Harman, D., et al.
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J Theor Biol. 2005 May 21;234(2):277-88. Epub 2005 Jan 24. On the importance of fatty acid composition of membranes for aging. Hulbert AJ.
Biochim Biophys Acta. 2005 Jan 5;1686 3:248-54. Perinatal essential fatty acid deficiency influences body weight and bone parameters in adult male rats. Korotkova M, Ohlsson C, Gabrielsson B, Hanson LA, Strandvik B. Department of Pediatrics, Goteborg University, The Queen Silvia Children's Hospital, SE 41685 Goteborg, Sweden. [email protected] Fetal and postnatal nutrition have long-term effects on the risk for development of diseases late in life in humans and animals. The aim of the present study was to investigate the effect of dietary deficiency of essential fatty acids (EFA) in the perinatal period on later body weight and bone mass. During late gestation and throughout lactation, rats were fed a control or an EFA-deficient (EFAD) diet. At 3 weeks of age the offspring were weaned onto an ordinary chow and followed until adult age. The mean body weight of adult rats receiving the EFAD diet during the perinatal period was significantly increased from 12 weeks of age compared to the controls (P<0.05). Analysis by peripheral quantitative computerized tomography (pQCT) at 44 weeks of age showed that the trabecular volumetric bone mineral density (BMD) of the femur was significantly decreased (P<0.05) but the cortical bone mineral content, cortical area, and cortical thickness were increased (P<0.05) in the EFAD group of rats. The length of the femur was not affected. In conclusion, neonatal EFA deficiency was in adult rats associated with increased body weight and significant changes in both cortical and trabecular bone. The results indicate that regulatory mechanisms related to bone mass seemed to be programmed by EFA in the perinatal period. The nature of this modulation needs to be identified.
Biochem Biophys Res Commun. 1987 Jun 30;145(3):1185-91. Anti-lipoperoxidation action of food restriction. Laganiere S, Yu BP. “Chronic food restriction inhibited the age-related increase of malondialdehyde production and lipid hydroperoxides in liver mitochondrial and microsomal membranes of ad libitum fed Fischer 344 rats. The anti-lipoperoxidation action of food restriction could not be attributable to the changes in membrane lipid content nor vitamin E status. Restricting calories modified membrane fatty acid composition by increasing linoleic acid and decreasing docosapentaenoic acid content in both membranes.”
Lipids 22(3), 133-6, 1987.. “Effects of parenteral nutrition with high doses of linoleate on the developing human liver and brain,” Martinez, M., and A. Ballabriga.
J Nutrit 10:63(1935). “The effect of retarded growth upon length of the life span and upon the ultimate body size.” McCay, CM., Crowell, MF., and Maynard, LA.
McCollum EV. 1957. A History of Nutrition. Boston: Houghton Mifflin. p 374.
J Clin Invest 73:272-276,1984. Neuringer M, Connor WE, Van Petten C, Barstad L.
J. Biol. Chem., 1912, xii, 81. Feeding experiments with fat-free food mixtures. Osborne, TB., Mendel, LB.
Science 45:294-295. (1917). “The effect of retardation of growth upon the breeding period and duration of life in rats.” Osborne, TB., Mendel, LB., and Fey, EL.
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.”
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.
Neurobiol Aging. 1982 Fall;3(3):173-8. Lipid peroxides in brain during aging and vitamin E deficiency: possible relations to changes in neurotransmitter indices. Noda Y, McGeer PL, McGeer EG. “Lipid peroxide levels, were found to be significantly higher in brains of 18 month old as compared to 4 month old rats, with particularly large increases occurring in the olfactory bulb, globus pallidus, cerebral cortex and caudate-putamen (CP). Eighteen month old rats fed a vitamin E deficient diet for 9 months before sacrifice had lipid peroxide levels significantly higher than age-matched controls in the cerebral cortex, hippocampus and hypothalamus.” “Age-related decreases were seen in choline acetyltransferase, acetylcholinesterase and 3H-QNB binding in some but not all brain regions, while GABA transaminase and MAO showed age-related increases.” “As compared with controls, vitamin E deficient rats showed decreases of 38% in cortical 3H-DHA binding, of 33% in 3H-QNB binding in the CP and of 23% and 12% in choline acetyltransferase in the CP and cerebellum, respectively.”
J Immunol, 1989 Nov 15, 143:10, 3192-9. The antiinflammatory effects of essential fatty acid deficiency in experimental glomerulonephritis. The modulation of macrophage migration and eicosanoid metabolism. Schreiner GF, Rovin B, Lefkowith JB.
Br J Nutr. 2003 Aug;90(2):385-94. Dietary docosahexaenoic acid-induced production of tissue lipid peroxides is not suppressed by higher intake of ascorbic acid in genetically scorbutic Osteogenic Disorder Shionogi/Shi-od/od rats. Sekine S, Kubo K, Tadokoro T, Maekawa A, Saito M.
Cancer Res. 2004 Sep 15;64(18):6482-8. Estrogen enhances angiogenesis through a pathway involving platelet-activating factor-mediated nuclear factor-kappaB activation. Seo KH, Lee HS, Jung B, Ko HM, Choi JH, Park SJ, Choi IH, Lee HK, Im SY.
Clin Exp Allergy. 2004 Feb;34(2):194-200. Maternal breast milk long-chain n-3 fatty acids are associated with increased risk of atopy in breastfed infants. Stoney RM, Woods RK, Hosking CS, Hill DJ, Abramson MJ, Thien FC.
Proc Natl Acad Sci U S A. 1988 Aug;85(16):6137-41. Essential fatty acid deficiency prevents multiple low-dose streptozotocin-induced diabetes in CD-1 mice. Wright JR Jr, Lefkowith JB, Schreiner G, Lacy PE.
Mech Ageing Dev. 2005 May 10; [Epub ahead of print] Membrane alteration as a basis of aging and the protective effects of calorie restriction. Yu BP.
Acta Paediatr 1996 Jun;85(6):679-83. Phospholipid fatty acids in cord blood: family history and development of allergy. Yu G, Kjellman NI, Bjorksten B.
Fiziol Cheloveka. 2005 Mar-Apr;31(2):108-15. [Age-related changes in lipid peroxidation in various regions of the central nervous system] [Article in Russian] Volchegorskii IA, Shemiakov SE, Telesheva IB, Malinovskaia NV, Turygin VV.
Surg Today. 2003;33(8):600-5. Beneficial effects of n-9 eicosatrienoic acid on experimental bowel lesions. Yoshida H, Soh H, Sando K, Wasa M, Takagi Y, Okada A. PURPOSE: Dietary fortification of n-9 polyunsaturated fatty acids (PUFA) or 5,8,11-eicosatrienoic acid (ETrA) as well as n-3 PUFA might contribute to the suppression of leukotriene B4 (LTB4) synthesis and thereby reduce inflammatory bowel lesions. As a result, the effect of an ETrA-enriched diet on experimental bowel lesions was examined in this study. METHODS: In Expt. 1, rats were freely fed either an ETrA-enriched or a standard diet. After 7 days of feeding, acute bowel lesions were induced by the subcutaneous injection of 10 mg/kg indomethacin. In Expt. 2, chronic bowel lesions were made by performing subcutaneous injections of 7.5 mg/kg indomethacin twice. After the first injection, the rats were freely fed either an ETrA-enriched or a standard diet for 7 days. RESULTS: In both experiments, the rats fed an ETrA-enriched diet showed increased levels of ETrA in the plasma and intestinal mucosa, and a decreased inflammation score. However, there was no significant decrease in plasma and intestinal mucosal LTB4 in the ETrA-enriched diet-fed rats. CONCLUSION: These results suggest that the dietary supplementation of ETrA may have both prophylactic and therapeutic effects on experimentally produced bowel lesions. Further investigations are necessary to clarify the effects of ETrA on bowel lesions and its mechanisms.
