维生素E，如同孕酮和阿司匹林，作用于细胞调节系统，以防止炎症和不适当的兴奋。由于不受控制的兴奋会导致破坏性氧化，这些物质能够防止这些形式的氧化反应。

容易被氧化和还原的分子可以作为抗氧化剂发挥作用，而维生素E在许多化学环境中确实起到了这种抗氧化剂的作用。然而，将其视为其众多有益生物学效应的解释是极具误导性的。这种推理方式曾促使抗氧化剂类致癌物BHT和BHA被用作食品添加剂和“抗衰老”补充剂，还有许多其他化学品因其抽象的抗氧化功能而被推广。

认识到维生素E的真正价值将对营养学和医学产生深远的影响。

在确定刑事或民事法律责任时，“应当知道”这一概念被广泛认可和使用。在科学领域，尤其是涉及数百万人的生命和健康时，知情责任至关重要。政府和行业的科学机构应为其为自身利益而隐藏、破坏或忽视的信息承担责任。美国政府设有专门机构来起诉研究欺诈行为，但当欺骗成为常态时，这一概念的应用范围过于狭窄，几乎毫无意义。此外，由于政府控制着法院系统，即使其罪行众所周知，政府机构及其官员也不会被起诉。

“50多年前，安大略省伦敦市的埃文·舒特博士（Dr. Evan Shute）就提倡将维生素E作为心脏病的有效治疗方法。他的开创性主张在当时并未被医学界广泛接受，但最近的流行病学研究和临床试验已经证实了他的观点。”

政治科学家已经认识到，大型企业如何“俘获”原本用于监管它们的政府机构。而专业期刊的编辑委员会比政府机构更容易被“俘获”，并且它们对行业的影响甚至可能更有价值。

如果科学研究影响到某个行业的计划，而该行业又控制了期刊和资助研究的机构，那么科学就可以被操控，使其符合行业利益。

在20世纪40年代，雌激素产业已经意识到，维生素E研究正在影响其核心利益。

曼哈顿计划（制造原子弹的项目）也培养了一代科学和官僚狂热分子，他们为了推动自己的项目和职业发展，忽视了公众健康和安全，并改变了科学运作的方式。与此同时，制药行业利用其财力和政治影响力，改变了医学的实践和教学方式，其对全球健康的影响可与核工业相媲美。

维生素E的早期研究与雌激素产业的对抗

1933年，医生R.J. Shute 已经意识到妊娠毒血症或子痫（preeclampsia）的问题。特别是在营养不良的女性中，许多妊娠会因循环系统问题（如周期性出血、血栓、中风和高血压）而变得复杂，这些问题经常导致流产或早产，幸存的婴儿也面临许多健康问题。

当时，雌激素和维生素E都在被广泛研究，尽管生育酚（tocopherol）分子的确切结构直到1936-1937年才被确定。研究发现，维生素E能够改善动物的生育能力，并防止胚胎或胎儿在子宫内死亡，因此它被称为“抗不育维生素”。利用它来预防女性流产的想法一定曾吸引过许多研究人员。

20世纪30年代的动物研究也显示，雌激素具有许多毒性作用，包括导致不孕、胚胎死亡、结缔组织异常以及过度凝血。Shute医生和他的儿子Wilfred 和 Evan 认为维生素E是一种抗雌激素物质，他们发现它在预防妊娠凝血疾病方面非常有效。

其他研究人员也注意到，孕酮（progesterone）可以抵抗雌激素的毒性作用，而维生素E表现出了类似孕酮的效果，因此被称为“孕酮节约剂”（progesterone-sparing agent）。

Shute兄弟后来开始将维生素E用于治疗更广泛的循环系统疾病，而不仅仅是孕妇的问题——血栓、静脉炎、高血压、心脏病和糖尿病等疾病都对大剂量的维生素E治疗有良好反应。

雌激素产业的应对

维生素E这个名字表明它是第五种被发现的维生素因子，它在1922年被命名，尽管其化学结构尚未被确立。公众很快接受了某些食物成分对生命和健康至关重要的观点，因此到1940年，几乎所有医生都推荐使用营养补充剂。

然而，如果维生素E对人体健康至关重要，并且部分作用是通过抑制雌激素来实现的，那么合成雌激素行业就面临了一个问题。

爱德华·伯内斯（Edward L. Bernays）早已在商业上取得成功，他教授企业和政府如何“制造同意”（engineering consent）。他曾帮助政府策划支持美国参战一战的宣传，随后又为烟草行业工作。他策划了一场“自由火炬”复活节游行，成千上万的女性在游行中吸烟，以此象征男女平等。美国医学协会（AMA）的编辑甚至帮助烟草行业设计宣传，声称吸烟对健康有益。

制药行业开始采用类似手段推广雌激素，有时手法粗糙，但总是有效。他们将雌激素称为“女性激素”，并且在没有研究的情况下声称天然激素（包括雌激素和孕酮）在口服时无效。同时，制药公司培养了一批医生为雌激素的神奇功效背书。而维生素E的维生素地位则遭到否认，甚至在1970年代，大学的营养学教授仍在宣称“没有人需要维生素E”。

几乎所有显示维生素E对人体疾病有治疗效果的研究都无法发表，因此反对维生素E的声音很少需要公开发声。1981年，美国医学协会（AMA）的期刊发表了一篇文章，列举维生素E的“毒性”影响。然而，我阅读了所有被引用的文章，发现作者的论点是：每当维生素E产生某种生理变化，这种变化就被视为有害，即使原始研究认为这种效果是有益的。

尽管JAMA（美国医学协会期刊）最终被迫放弃烟草广告收入，但由于雌激素行业的大规模广告投放，它并未受到影响。JAMA显然不愿发表任何可能暗示维生素E、孕酮或甲状腺激素对抗雌激素有益的研究。

维生素E与雌激素的对抗作用

雌激素会导致子宫发生变化，阻碍胚胎着床，并减少胚胎的氧气供应，而维生素E则可以增加氧气供应。

我的论文导师A.L. Soderwall曾进行一系列实验，表明补充维生素E可以推迟中年仓鼠的不孕期。在我的实验中，维生素E增加了子宫中的氧气供应，纠正了由补充雌激素或衰老引起的氧气缺乏。孕酮也有类似的作用。

然而，在20世纪40年代，维生素E的官方定义被改变了。它的功能不再被描述为防止胚胎死亡、睾丸退化或大脑/肌肉退行，而是被重新定义为“抗氧化剂”，即防止不饱和脂肪酸氧化。

尽管一些研究人员继续认为维生素E可以防止血栓、心脏病、糖尿病和不孕不育，但医学界却声称动物实验的结果不能适用于人类，并认为“单纯的抗氧化剂”无法预防或治疗人类疾病。

维生素E实验表明，多不饱和脂肪酸（PUFA）具有生育抑制作用，但当时科学界尚未认识到这种作用与雌激素的抗生育作用有关。然而，要理解维生素E的作用，就必须考虑雌激素与PUFA之间的相互作用。它们的作用密切相关，并受到各种能量促进和稳定物质的抑制，包括饱和脂肪、孕酮、甲状腺激素、维生素E和阿司匹林。

雌激素会使毛细血管变得渗漏，而维生素E则能减少这种渗漏。雌激素增加血小板聚集，而维生素E则减少聚集。过量的雌激素和维生素E缺乏都会导致血栓，而血栓又会导致纤维化，而维生素E被证明可以预防和治疗纤维化疾病。

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Prostaglandins Leukot Essent Fatty Acids 1991 Oct;44(2):89-92. Inhibition of PGE2 production in macrophages from vitamin E-treated rats. Sakamoto W, Fujie K, Nishihira J, Mino M, Morita I, Murota S.

Int J Vitam Nutr Res 1990;60(1):26-34. The influence of vitamin E on rheological parameters in high altitude mountaineers. Simon-Schnass I, Korniszewski L. “The erythrocyte filterability was unaltered in the vitamin E group in comparison with baseline but was significantly impaired in the control group.”

Neurobiol Aging 1991 Jan-Feb;12(1):55-9. Aging and food restriction: effect on lipids of cerebral cortex. Tacconi MT, Lligona L, Salmona M, Pitsikas N, Algeri S. In experimental animals dietary restriction reduces the body weight increase due to aging, increases longevity and delays the onset of age-related physiological deterioration, including age-related changes in serum lipids. Little is known about the influence of food restriction on brain lipids, whose concentration and composition have been shown to change with age. We studied whether some biochemical and biophysical parameters of rat brain membranes, known to be modified with age, were affected by a diet low in calories, in which 50% of lipids and 35% of carbohydrates have been replaced by fibers. The diet was started at weaning and maintained throughout the animal’s entire life span. Animals fed the low calorie diet survived longer and gained less body weight than standard diet fed rats. Age-related increases in microviscosity, cholesterol/phospholipid and sphingomyelin/phosphatidylcholine ratios were reduced or restored to the levels of young animals in cortex membranes of 32 old rats fed the low calorie diet, while the age-related increase in mono- to polyunsaturated fatty acid ratios in phospholipids was further raised. In conclusion we have shown that a diet low in calories and high in fibers affects lipid composition in the rat brain, in a direction opposite to that normally believed to reduce age-related deterioration of brain functions.

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, Human keratinocytes are commonly grown in culture with a serum-free medium. Under these conditions, keratinocytes become essential fatty acid deficient (EFAD), as determined by gas chromatographic analysis of cell phospholipid fatty acid composition. Exposure of EFAD keratinocytes for 2 hr to concentrations of t-butyl hydroperoxide (tBHP) up to 2 mM did not result in toxicity assessed by lactate dehydrogenase (LDH) release and only a small indication of lipid peroxidation assessed by the release of thiobarbituric acid-reactive substances (TBARS). Addition of 10 microM linoleic acid (LA) to serum-free medium alleviated the EFAD condition by increasing the phospholipid content of LA and its elongation and desaturation products, arachidonic acid and docosatetraenoic acid. Exposure of LA-supplemented keratinocytes to tBHP resulted in significant LDH (at 1 and 2 mM tBHP) and TBARS (tBHP concentration dependent) release. TBARS release was also significantly elevated in unexposed LA-supplemented keratinocytes (basal release). Co-supplementation with the antioxidant, alpha-tocopherol succinate (TS) prevented tBHP (1 mM)-induced LDH release in LA-supplemented cultures. TS supplementation also attenuated the effect of tBHP on TBARS release, but when compared to TS-supplemented EFAD cultures, LA supplementation still led to increased tBHP-induced TBARS release. Keratinocyte cultures are potentially useful as an alternative to animals in toxicology research and testing. It is important, however, that the cell model provide a response to toxic insult similar to that experienced in vivo. Our results suggest that fatty acid and antioxidant nutrition of cultured keratinocytes are important parameters in mediating the toxic effects of lipid peroxidation.

Cancer Lett 1997 Jan 1;111(1-2):179-85. Subcutaneous, omentum and tumor fatty acid composition, and serum insulin status in patients with benign or cancerous ovarian or endometrial tumors. Do tumors preferentially utilize polyunsaturated fatty acids? Yam D, Ben-Hur H, Dgani R, Fink A, Shani A, Berry EM.

AC Chan, J. of Nutrition, 1998 “The response-to-injury hypothesis explains atherosclerosis as a chronic inflammatory response to injury of the endothelium, which leads to complex cellular and molecular interactions among cells derived from the endothelium, smooth muscle and several blood cell components. Inflammatory and other stimuli trigger an overproduction of free radicals, which promote peroxidation of lipids in LDL trapped in the subendothelial space. Products of LDL oxidation are bioactive, and they induce endothelial expression and secretion of cytokines, growth factors and several cell surface adhesion molecules. The last-mentioned are capable of recruiting circulating monocytes and T lymphocytes into the intima where monocytes are differentiated into macrophages, the precursor of foam cells. In response to the growth factors and cytokines, smooth muscle cells proliferate in the intima, resulting in the narrowing of the lumen. Oxidized LDL can also inhibit endothelial production of prostacyclin and nitric oxide, two potent autacoids that are vasodilators and inhibitors of platelet aggregation. Evidence is presented that vitamin E is protective against the development of atherosclerosis. Vitamin E enrichment has been shown to retard LDL oxidation, inhibit the proliferation of smooth muscle cells, inhibit platelet adhesion and aggregation, inhibit the expression and function of adhesion molecules, attenuate the synthesis of leukotrienes and potentiate the release of prostacyclin through up-regulating the expression of cytosolic phospholipase A2 and cyclooxygenase. Collectively, these biological functions of vitamin E may account for its protection against the development of atherosclerosis.”

6: Early Hum Dev 1994 Nov 18;39(3):177-88 Vitamin A and related essential nutrients in cord blood: relationships with anthropometric measurements at birth. Ghebremeskel K, Burns L, Burden TJ, Harbige L, Costeloe K, Powell JJ, Crawford M. Institute of Brain Chemistry and Human Nutrition, Queen Elizabeth Hospital for Children, London, UK. Following the advice given by the Department of Health to women who are, or may become pregnant, not to eat liver and liver products because of the risk of vitamin A toxicity, the concentrations of vitamins A and E, and copper, magnesium and zinc in cord blood were investigated. The study was conducted in Hackney, an inner city area of London. Esters of vitamin A were not detected in any of the samples, indicating that there was no biochemical evidence of a risk of toxicity. Indeed, vitamin A correlated significantly with birthweight, head circumference, length, and gestation period. There was also a significant positive relationship between zinc and birthweight. In contrast, copper showed a negative correlation with birthweight and head circumference. Vitamin E and magnesium were not associated with any of the anthropometric measurements, although magnesium showed an increasing trend with birthweight. The data suggest that most of the mothers of the subjects studied may have been marginal with respect to vitamins A and E and zinc. In those with low birthweight babies. a higher intake would have improved their nutritional status and possibly the outcome of their pregnancy. For these low-income mothers, liver and liver products are the cheapest and the best source of vitamins A and E, haem iron, B vitamins and several other essential nutrients; hence the advice of the Department of Health may have been misplaced.