Preventing and treating cancer with progesterone.
用孕酮预防和治疗癌症。
by Raymond Peat
“The energy of the mind is the essence of life.” Aristotle
“思想的能量是生命的精髓”
—亚里士多德
All through the last century, as more and more resources were devoted to solving “the cancer problem,” the death rate from cancer increased every year. Something was clearly wrong with the way the problem was being approached.
If you grind up a computer and dissolve it in acid, you can find out exactly what substances it was made of, but you won't learn from that information how the computer worked. Twentieth century biologists became fond of emulsifying cells and studying the soluble parts. By the end of the century, they had identified so many parts that the government was financing projects to use supercomputers to try to understand how the parts interacted.
If some essential information was lost in studying the parts, supercomputation isn't the way to find it. Even with infinite computing capacity, a description of the electrons on carbon and hydrogen atoms on amino acids in protein molecules won't lead to the reality of how those atoms would have functioned in the living state.
The image of a cell as a watery solution contained in an elastic membrane bag is still having a radically stupefying effect on biology and medicine. The idea that a cell can be understood by using a computer to model a network of interactions between genes and gene products is nothing more than a technologizing of the primitive understanding of life that was promulgated by the Weismann-Mendel-Morganist school. It was the dogmatic insistence of that genetic determinist school that cancer originated with a genetic mutation.
整个上个世纪，随着越来越多的资源被用于解决“癌症问题”，癌症的死亡率每年都在上升。解决这个问题的方法显然有问题。
如果你把电脑磨碎，并把它溶解在酸里，你就能确切地知道它是由什么物质组成的，但你不能从这些信息中了解电脑是如何工作的。二十世纪的生物学家开始喜欢乳化细胞和研究可溶性部分。到本世纪末，他们已经确定了如此多的部件，政府正在资助使用超级计算机的项目，试图了解部件是如何相互作用的。
如果在研究部件的过程中丢失了一些必要的信息，那么超级计算并不是找到这些信息的方法。即使有无限的计算能力，对蛋白质分子中氨基酸上的碳原子和氢原子上的电子的描述也无法揭示这些原子在生命状态下是如何工作的。
在生物学和医学上，细胞作为弹性膜袋里的水溶液的图像仍然具有根本的令人震惊的效果。利用计算机模拟基因和基因产物之间的相互作用网络，可以理解细胞，这种想法不过是韦斯曼-孟德尔-摩根主义学派所宣扬的对生命的原始理解的一种技术化。这是基因决定论学派的教条主义坚持认为癌症起源于基因突变。
By the middle of the 20th century, that dogma had excluded the most important parts of biology from the schools and the journals. Ideas of a developmental field, cellular coherence, and holistic cooperativity were denounced as unscientific vitalism. Returning to the idea of a “cancer field” is an essential first step in thinking realistically about preventing and treating cancer, but that idea has hardly progressed since the 1930s.
In the last few years, interest in cloning and stem cells and tissue regeneration has revived interest in studying the factors that contribute to the spatial and temporal ordering of cell growth.
The idea of a developmental field was a fundamental part of embryology in the first half of the 20th century. It was an empirical idea, supported most commonly by evidence that diffusing substances and secreted materials governed the differentiation of cells and tissues, but the form-generating effects of bioelectric fields were also often demonstrated, and there was some evidence that tissue radiations played a role. The extracellular matrix secreted by cells served to transmit information between cells, but its form was regulated by cells, and its structure was a factor governing the cells' differentiation.
Experiments in amphibians showed that regeneration of organs had a reciprocal relationship with the development of cancer–a tumor could be turned into a tail, for example, if it was grafted onto the stump following amputation of the tail, but factors that weakened regeneration could cause a tumor to develop. In these experiments, the normal organism's morphogenetic or epimorphic field overrode the disordered developmental field of the tumor.
In the absence of overriding external influences, the disordered system of the tumor, in which cells emitted many products of their disordered metabolism, could interfere with the normal functions of the organism. All of the products of the injured cells, including their altered extracellular matrix, constituted the cancer field.
The recent recognition of the “bystander effect” of radiation exposure, in which cells that haven't been irradiated undergo genetic changes or death when they are exposed to irradiated cells, has provided an opportunity to return to the “field” idea in cancer, because the stress-induced factors emitted by irradiated cells are the same toxic factors emitted by cells undergoing carcinogenesis from other causes, such as over-exposure to estrogen.
到了20世纪中叶，这种教条已经把生物学中最重要的部分排除在学校和期刊之外。关于发展领域、细胞一致性和整体协作的观点被谴责为不科学的活力论。回到“癌症领域”的观点是现实地思考预防和治疗癌症的重要的第一步，但自20世纪30年代以来，这一观点几乎没有进展。
在过去的几年里，对克隆、干细胞和组织再生的兴趣重新燃起了研究细胞生长的空间和时间顺序的因素的兴趣。
在20世纪上半叶，发育领域的概念是胚胎学的基本组成部分。这是一种经验的观点，最普遍的支持证据是扩散物质和分泌物质控制细胞和组织的分化，但生物电场产生的效应也经常被证明，有一些证据表明组织辐射发挥了作用。细胞分泌的细胞外基质起到细胞间信息传递的作用，但其形态受细胞调节，其结构是细胞分化的调控因素。
在两栖动物身上进行的实验表明，器官的再生与癌症的发展有着互惠关系——例如，如果在切除了尾巴之后将肿瘤移植到残肢上，它可以变成一条尾巴，但削弱再生能力的因素可能会导致肿瘤的发展。在这些实验中，正常生物体的形态发生或内形态场覆盖了肿瘤的紊乱发育场。
在缺乏主要的外部影响的情况下，肿瘤系统的紊乱，即细胞释放出许多代谢紊乱的产物，可能会干扰机体的正常功能。所有损伤细胞的产物，包括它们改变的细胞外基质，构成了癌细胞区。
最近人们认识到辐射照射的“旁观者效应”，即未受辐射的细胞在受到辐射细胞照射时发生基因变化或死亡，这为重新回到癌症的“场”观点提供了机会。因为受到辐射的细胞所释放的压力诱发因子与细胞因其他原因(如过度接触雌激素)发生癌变所释放的毒性因子相同。
H. J. Muller, one of T. H. Morgan's students and colleagues, studied the mutagenic effects of x-rays, and the genetic determinists argued that the random changes produced in the genetic material by ionizing radiation provided a model of the evolutionary process. Randomly altered genes and natural selection would explain everything, including cancer. Every time cells divide, their genes supposedly become more susceptible to random changes, so increased replication of cells would increase the risk of producing genetic changes leading to cancer. This idea is so simple and so widely believed that many people focus only on the rate of proliferation, and the random mutations that supposedly occur during proliferation, when they try to explain carcinogenesis. They feel that it's reasonable to discuss cancer without bothering to understand the physiology of the cell or the organism.
The organism can only be understood in its environments, and a cell can't be understood without reference to the tissue and organism in which it lives. Although the geneticists were at first hostile to the idea that nutrition and geography could have anything to do with cancer, they soon tried to dominate those fields, insisting that mutagens and ethnicity would explain everything. But the evidence now makes it very clear that environment and nutrition affect the risk of cancer in ways that are not primarily genetic.
Every tumor, like every person, has a uniqueness, but valid and practical empirical generalizations can be made, if we understand some of their properties and the conditions that govern their development and survival.
穆勒(H. J. Muller)是摩根(T. H. Morgan)的学生和同事之一，他研究了x射线的诱变效应，基因决定论者认为，电离辐射在遗传物质中产生的随机变化为进化过程提供了一个模型。随机改变的基因和自然选择可以解释一切，包括癌症。每次细胞分裂，它们的基因就会变得更容易受到随机变化的影响，所以细胞复制的增加会增加产生导致癌症的基因变化的风险。这个想法很简单，也很普遍，以至于很多人在试图解释癌变时，只关注增殖的速率，以及增殖过程中可能发生的随机突变。他们认为，讨论癌症而不必费心去理解细胞或有机体的生理学是合理的。
有机体只能在它所处的环境中被理解，而一个细胞如果不参考它所生活的组织和有机体就无法被理解。尽管起初遗传学家对营养和地理可能与癌症有任何关系的观点持反对态度，但他们很快就试图主导这些领域，坚持认为诱变剂和种族可以解释一切。但现在有证据表明，环境和营养对癌症风险的影响并不主要是由基因决定的。
每一种肿瘤，就像每个人一样，都有其独特性，但如果我们了解它们的一些特性和支配它们发展和生存的条件，就可以做出有效和实用的经验总结。
Percival Potts' observation of scrotal cancer in chimney sweeps eventually led to the study of soot carcinogenesis, and then to the study of the properties of the polycyclic aromatic hydrocarbons in soot. The similarities of those properties to estrogen's soon became apparent.
Over the decades, many studies have confirmed that prolonged, continuous exposure to estrogen is carcinogenic, and that progesterone offsets those effects.
Following the animal studies that showed that carcinogenesis by estrogen could be prevented or reversed by progesterone, studies of the endogenous hormones in women showed that those with a natural excess of estrogen, and/or deficiency of progesterone, were the most likely to develop uterine or breast cancers.
The Morganist school of genetic determinism moved into endocrinology with a doctrine that hormones act only through hormone receptors, proteins which activate certain genes.
Many researchers – physical chemists, biochemists, cytologists, embryologists, reproductive and developmental biologists, gerontologists, physiologists, neurologists, endocrinologists – were investigating estrogen's properties and actions, and had made great progress by the 1950s, despite the medical frauds being perpetrated by the estrogen industry (Rothenberg, 2005).
Percival Potts对烟囱清洁工中阴囊癌的观察，最终导致了对煤烟致癌机理的研究，然后是对煤烟中多环芳烃性质的研究。这些特性与雌激素的相似性很快就变得明显起来。
在过去的几十年里，许多研究已经证实，长期、持续地接触雌激素是致癌的，而孕酮可以抵消这些影响。
动物研究表明，雌激素的致癌作用可以被孕酮阻止或逆转，对女性体内内源性激素的研究表明，那些天生雌激素过多和/或孕酮不足的女性最有可能患子宫癌或乳腺癌。
摩根主义遗传决定论学派转向内分泌学，认为激素只能通过激素受体，即激活某些基因的蛋白质发挥作用。
许多研究人员——物理化学家、生物化学家、细胞学家、胚胎学家、生殖和发育生物学家、老年学家、生理学家、神经学家、内分泌学家——都在研究雌激素的特性和作用，并在20世纪50年代取得了很大进展，尽管雌激素行业正在实施医疗欺诈(Rothenberg, 2005)。
All of this complex and subtle work was of no interest to a small group of people who wanted to impose their genetic views onto biology.
The inventor of the estrogen receptor, Elwood Jensen, has written that the results of certain of his experiments “caused the demise of the transhydrogenation hypothesis and convinced all but the most diehard enzymologists that estradiol binds to a characteristic component of target cells to exert its physiological effect without itself being chemically altered.” The hypothesis he referred to was just part of a large fairly systematic international effort.
How he did away with the opposition, who were studying the complex metabolic actions of estrogen, was by synthesizing isotope-labeled estradiol and estrone, and claiming to observe that they weren't metabolically altered, as they produced their hormonal effect. Since the experiment was extremely expensive, and required the cooperation of the Atomic Energy Commission, it wasn't easily repeated. However, many experiments have subsequently demonstrated that practically every tissue in the body (and plants and bacteria) metabolize the estrogens, causing estradiol to change into estrone, and estrone, into estradiol. Jensen's decisive and historically crucial experiment was false.
But it served its purpose, and (with help from the pharmaceutical industry and government granting agencies) marginalized the work of those “enzymologists” and everyone else who persisted in studying the complex actions of estrogen.
The enzyme that converts the weaker estrone into the stronger estradiol is an important factor in determining estrogen's effects on a particular tissue. Progesterone is able to regulate the cell's metabolism, so that the oxidative pathway, forming estrone from estradiol, predominates. Estrogen-dominated tissues are likely to have a balance in the direction of reduction rather than oxidation, increasing the amount of the active estradiol.
所有这些复杂而微妙的工作对一小群想把自己的基因观点强加于生物学的人来说毫无兴趣。
雌激素受体的发明者埃尔伍德·延森他写道，他的某些实验结果“导致了转氢化假说的消亡，并说服了除最顽固的酶学家外的所有人，雌二醇与目标细胞的特征成分结合，在不发生化学改变的情况下发挥其生理作用。”他提到的假设只是一个相当系统的国际努力的一部分。
他是如何除掉那些研究雌激素复杂代谢作用的反对者的，就是通过合成同位素标记的雌二醇和雌酮，并声称观察到它们在产生激素作用时没有代谢改变。因为这个实验非常昂贵，而且需要原子能委员会的合作，所以很难重复。然而，后来的许多实验表明，实际上体内的每一个组织(包括植物和细菌)都能代谢雌激素，使雌二醇转化为雌酮，雌酮又转化为雌二醇。詹森决定性的、历史上至关重要的实验是错误的。
但它达到了它的目的，(在制药行业和政府授权机构的帮助下)边缘化了那些“酶学家”和所有坚持研究雌激素复杂作用的人的工作。
将弱雌酮转化为强雌酮的酶是决定雌激素对特定组织作用的重要因素。孕酮能够调节细胞的新陈代谢，因此氧化途径从雌二醇形成雌二醇占主导地位。雌激素主导的组织可能在减少而不是氧化的方向上有一个平衡，增加了活性雌二醇的数量。
The immediate effects of estrogen and progesterone on cells, that occur long before genes can be activated, were simply ignored or denied by the promoters of the estrogen receptor doctrine. Some of these excitatory or antiexcitatory effects are probably structural changes, that involve the mobilization of calcium inside cells, and the activation or inhibition of reactions involving phosphoric acid. Although they have been known for many years, they are always referred to as “novel” or “non-classical” effects, and are called “membrane effects,” because that's the only way the reductionists are able to identify changes that happen immediately throughout the cell.
Cellular excitation involves an increase of intracellular calcium and the activation of phosphorylating enzymes in cells. Some experiments suggest (Improta-Brears, et al., 1999) that the estrogen receptor mediates estrogen's ability to mobilize calcium (leading to the activation of cell division, mitosis). Whether or not it does, the recognition that estrogen activates calcium, leading to activation of the phosphorylation system, should “cause the demise of” the “classical estrogen receptor” doctrine, because the phosphorylation system alters the expression of genes, much as the estrogen receptor was supposed to do by its direct actions. But before it alters the expression of genes, it alters the activities of enzymes. When estrogen activates calcium and phosphorylation independently of the estrogen receptor, the situation is even worse for the Jensen dogma.
雌激素和黄体酮对细胞的直接作用在基因被激活之前就已经存在了，但雌激素受体学说的发起者们完全忽视或否认了这种作用。其中一些兴奋性或抗兴奋性效应可能是结构变化，包括细胞内钙的动员，以及磷酸反应的激活或抑制。尽管人们已经知道它们很多年了，但它们总是被称为“新”或“非经典”效应，并被称为“膜效应”，因为这是还原论者能够识别细胞中立即发生的变化的唯一方法。
细胞兴奋包括细胞内钙离子的增加和细胞内磷酸化酶的激活。一些实验表明(Improta-Brears, et al.， 1999)雌激素受体介导雌激素调动钙的能力(导致细胞分裂和有丝分裂的激活)。,是否认识到雌激素激活钙,导致磷酸化系统的激活,应该引起的消亡”“经典雌激素受体”学说,由于磷酸化系统改变基因的表达,就像雌激素受体是应该做的直接行动。但在它改变基因表达之前，它会改变酶的活动。当雌激素激活钙和磷酸化独立于雌激素受体，情况更糟糕的Jensen教条。
Progesterone's opposition to those early excitatory effects of estrogen are so basic, that there shouldn't be any difficulty in thinking of it as an antiestrogen, that stops cell division primarily by opposing the excitatory effects of estrogen and other mitogens. Progesterone's opposition to the calcium-activating and phosphorylating effects of estrogen affects everything in the cell, according to the cell's specific nature.
But the reductionists don't like “nongenomic” explanations of anything, even when they are triggered by the estrogen receptor rather than by a membrane-event. So, to argue that progesterone's opposition to estrogen is general, it's necessary to examine each of estrogen's actions, where those actions are clearly known, and to evaluate progesterone's effects on the same events.
When a cell is stimulated or slightly stressed, homeostatic mechanisms are activated that help it to return to its normal resting state. The mobilization of calcium and the phosphorylation system is followed by increased synthesis of cholesterol and the formation of glucose from glycogen. Cholesterol itself is protective, and in some cells it is massively converted into progesterone, which is even more effective in restoring homeostasis.
In the ovary, the enzymes that synthesize cholesterol, along with the production of progesterone, are activated by the pituitary hormone, FSH, but also by estrogen. In the liver and uterus and vascular endothelium, which aren't specialized for the production of progesterone, stimulation by estrogen activates the enzymes to increase the formation of cholesterol.
黄体酮对雌激素早期兴奋作用的反对是如此的基本，所以认为它是一种反雌激素应该没有任何困难，它主要通过反对雌激素和其他有丝分裂原的兴奋作用来阻止细胞分裂。孕酮反对雌激素的钙激活和磷酸化作用，根据细胞的具体性质影响细胞中的一切。
但还原论者不喜欢对任何事情的“非基因组”解释，即使它们是由雌激素受体而不是膜事件触发的。因此，要论证孕激素对雌激素的反对是普遍的，就有必要检查雌激素的每一个作用，这些作用都是清楚的，并评估孕激素对相同事件的影响。
当细胞受到刺激或轻微的压力时，体内平衡机制就会被激活，帮助细胞回到正常的静息状态。钙的动员和磷酸化系统随后增加胆固醇的合成和糖原的形成。胆固醇本身具有保护作用，在一些细胞中，胆固醇大量转化为黄体酮，而黄体酮在恢复体内平衡方面更为有效。
在卵巢中，垂体激素FSH和雌激素会激活合成胆固醇和黄体酮的酶。在肝脏、子宫和血管内皮中，雌激素的刺激会激活酶，增加胆固醇的形成。
When cells are injured or seriously stressed, instead of being able to directly recover their normal quiescence, they may instead mobilize their systems for growing and replicating, to replace damaged or destroyed cells.
Prolonged exposure to estrogen, that can't be offset by the homeostatic factors, such as progesterone, typically causes cells to enter a growth phase. (But so do other excitatory processes, such as ionizing radiation.)
One of the basic reactions to injury is to shift the cell away from oxidative metabolism to glycolytic metabolism, which is inefficient, but can support cell division. Chemical stains show that during cell division cells are in a reduced state, with abundant sulfhydryl groups including reduced glutathione and protein sulfhydryls. This shift in itself increases the formation of active estradiol from estrone.
In the inflamed or estrogen dominated cell, enzymes such as the cyclooxidases (COX), that convert arachidonic acid into prostaglandins, are activated. Beta-glucuronidase and sulfatases are activated, and these cause intracellular estrogen to increase, by removing the water soluble sulfate and glucuronate portions from estrogens that had been inactivated. The detoxifying enzymes that attach those molecules to estrogen are inactivated in the estrogen dominated cell. The prostaglandin formed from arachidonic acid stimulates the formation of the enzyme aromatase or estrogen synthetase, that converts androgens into estrogen.
Those processes, initiated by excitation or injury, increase the amount of estrogen in the cell, which intensifies the excitation.
Progesterone opposes all of those processes, decreasing the amount of estrogen in the cell by modifying the activities of those five types of enzyme.
当细胞受伤或受到严重压力时，它们不能直接恢复正常的安静状态，而是会调动自身系统进行生长和复制，以替代受损或破坏的细胞。
长期暴露在无法被体内平衡因子(如孕酮)抵消的雌激素中，通常会导致细胞进入生长阶段。(但其他兴奋过程，如电离辐射，也是如此。)
对损伤的一个基本反应是将细胞从氧化代谢转移到糖酵解代谢，这是低效的，但可以支持细胞分裂。化学染色显示细胞分裂时细胞处于还原状态，含有丰富的巯基，包括还原型谷胱甘肽和蛋白质巯基。这种转变本身就增加了雌酮中活性雌二醇的形成。
在炎症或雌激素为主的细胞中，酶，如将花生四烯酸转化为前列腺素的环氧化酶(COX)，被激活。β -葡萄糖醛酸酶和硫酸酯酶被激活，通过去除雌激素中已灭活的水溶性硫酸盐和葡萄糖醛酸部分，从而导致细胞内雌激素增加。将这些分子与雌激素结合的解毒酶在雌激素主导的细胞中被灭活。由花生四烯酸形成的前列腺素刺激芳香化酶或雌激素合成酶的形成，将雄激素转化为雌激素。
这些过程，由兴奋或损伤引起，增加细胞中的雌激素的数量，从而加强兴奋。
黄体酮反对所有这些过程，通过改变这五种酶的活动来减少细胞中的雌激素。
Although many kinds of protein (including enzymes) bind estrogen, the protein that Jensen called “the estrogen receptor” is largely responsible for the ability of the uterus and breasts to retain high concentrations of estrogen. Various kinds of stimulation or stress (including heat and oxygen deprivation) cause its appearance, and estrogen itself increases the amount of the estrogen receptor in a cell. The estrogen receptor doesn't just “activate genes,” as the Jensen dogma claimed. For example, the estrogen receptor directly binds and inactivates the “tumor suppressor” p53 protein, which otherwise would restrain the replication of damaged cells.
Progesterone causes the estrogen receptor to be eliminated. (Batra; Boling and Blandau; Resko, et al.)
Among the cell activating factors, other than estrogen, are proteins that are considered to be “oncogenes,” because of their involvement in cancer. Several of these proteins are activated by estrogen, inhibited by progesterone. The term “oncogene” refers to any gene that contributes to the development of cancer, but it is so burdened by ideology that it shouldn't be used as if it had a simple clear meaning.
A variety of proteins promote cell activity and replication, under the influence of estrogen. The “composite transcription factor activating protein 1,” AP-1 which integrates the effects of other transcription factors, is important in a variety of cell types, and its activity is increased by estrogen and decreased by progesterone.
When the “progesterone receptor” lacks progesterone, it has the opposite effect of progesterone, and this feature has been used propagandistically, by infecting cells with a virus carrying the progesterone receptor protein, and then suggesting that the disturbed functions of the cell reflect a potential effect of progesterone. The receptor, lacking progesterone, tells the cell that it has a progesterone deficiency, but too many molecular endocrinologists are trying to say that the receptor protein is the same as the progesterone.
虽然许多种类的蛋白质(包括酶)都与雌激素结合，但延森称之为“雌激素受体”的蛋白质在很大程度上负责子宫和乳房保持高浓度的雌激素。各种刺激或压力(包括热和缺氧)导致它的出现，而雌激素本身增加了细胞内雌激素受体的数量。雌激素受体不只是“激活基因”，正如Jensen教条所说。例如，雌激素受体直接与“肿瘤抑制因子”p53蛋白结合并使其失活，否则p53蛋白将抑制受损细胞的复制。
黄体酮导致雌激素受体被排除。(巴特拉;怕冷和Blandau;Resko等)。
在细胞激活因子中，除了雌激素，还有蛋白质，它们被认为是“致癌基因”，因为它们与癌症有关。其中一些蛋白质被雌激素激活，而被孕酮抑制。“致癌基因”一词指的是任何有助于癌症发展的基因，但它背负着太多的意识形态负担，以至于它不应该被当作一个简单明确的含义来使用。
在雌激素的影响下，多种蛋白质促进细胞活性和复制。AP-1是“复合转录因子激活蛋白1”，它整合了其他转录因子的作用，在多种细胞类型中都很重要，它的活性在雌激素中增加，在孕酮中降低。
当“孕酮受体”缺乏孕酮时，它具有孕酮相反的作用，这一特性已经被宣传使用，通过携带孕酮受体蛋白的病毒感染细胞，从而提示细胞功能的紊乱反映了孕酮的潜在作用。受体，缺乏孕酮，告诉细胞它有孕酮缺乏，但太多的分子内分泌学家试图说受体蛋白和孕酮是一样的。
The generality of the process of excitation/activation can be clearly seen in the effects of the nerve-inhibiting GABA and the nerve-exciting glutamate or NMDA. In cultured breast cancer cells, GABA inhibits growth, NMDA increases growth. As in the brain, progesterone supports the actions of GABA, and opposes those of NMDA or the excitatory amino acids, while estrogen in general promotes the effects of the excitatory amino acids, and opposes those of GABA.
Both the excitatory amino acids and a peptide that promotes inflammation, tumor necrosis factor (TNF), activate the enzyme which makes estrogen, aromatase. Estrogen, by activating NF kappaB, increases the formation of TNF, which in itself can promote the growth and metastasis of cancer. Various antiinflammatory agents, including aspirin, progesterone, testosterone, saturated fats, and glycine, can inhibit the production of NF kappaB.
An enzyme that has been thought of mainly in relation to the brain is catechol-O-methyl transferase, which is inhibited by estrogen (producing effects similar to cocaine), leading to brain excitation.The enzyme detoxifies catecholestrogen (Creveling, 2003), protecting cells from DNA damage (Lavigne, et al., 2001). When the activity of this enzyme is low, there is increased risk of breast cancer (Matsui, et al., 2000). Progesterone increases its activity (Inoue and Creveling, 1991, 1995).
兴奋/激活过程的普遍性可以从抑制神经的GABA和刺激神经的谷氨酸或NMDA的作用中清楚地看到。在培养的乳腺癌细胞中，GABA抑制生长，NMDA促进生长。在大脑中，孕酮支持GABA的作用，反对NMDA或兴奋性氨基酸的作用，而雌激素一般促进兴奋性氨基酸的作用，反对GABA的作用。
兴奋性氨基酸和一种促进炎症的肽，肿瘤坏死因子(TNF)，都激活了制造雌激素的酶，即芳香化酶。雌激素通过激活NF kappaB，增加TNF的形成，其本身就能促进肿瘤的生长和转移。各种抗炎药物，包括阿司匹林、孕酮、睾酮、饱和脂肪和甘氨酸，都能抑制NF - kappaB的产生。
一种被认为主要与大脑有关的酶是儿茶酚- o -甲基转移酶，它被雌激素抑制(产生类似可卡因的效果)，导致大脑兴奋。这种酶可以解毒儿茶酚雌激素(Creveling, 2003)，保护细胞免受DNA损伤(Lavigne等，2001)。当这种酶的活性较低时，乳腺癌的风险就会增加(Matsui, et al.， 2000)。孕酮增加其活性(Inoue和Creveling, 1991, 1995)。
Another enzyme system that affects the body's reactions to stress and modifies processes of inflammation and growth, the monoamino-oxidases, is affected oppositely by estrogen and progesterone. Estrogen's effects are partly mediated by increased formation of serotonin, progesterone's, by decreasing it. Histamine is another promoter of inflammation that is increased by estrogen, decreased by progesterone.
Estrogen's effects in the nervous system go beyond the production of cocaine-like hypomania, or chorea, or epilepsy, and include the activation of the basic stress hormones, increasing the formation in the hypothalamus of pro-opiomelanocortin (POMC), which is a precursor of ACTH to activate the adrenals, and endorphins (“endogenous opiates”), which stimulate growth processes. Both endorphins and ACTH can be found in tumors such as breast cancer. The ACTH stimulates the production of cortisol, that protects against some of the immediate causes of inflammation and growth, but that contributes to the loss of resistance, and increases estrogen synthesis.
A protein called the sigma receptor, known for its role in cocaine's action, binds progesterone, and can inhibit the growth of cancer. Some anesthetics have similar effects on tumors, acting through this protein. The sigma receptor, in association with progesterone or pregnenolone, is protective against the excitatory amino acids.
The extracellular medium changes during the development of a tumor. Irritated hypoxic cells, and estrogen-stimulated cells, increase their production of collagen, and the increase of collagen interferes with normal cell functions. Progesterone reduces the formation of collagen, and probably contributes to its removal.
Naloxone or naltrexone, which blocks the actions of the endorphins and morphine, is being used to inhibit the growth of various kinds of cancer, including breast cancer and prostate cancer. Leptin (which is promoted by estrogen) is a hormone produced by fat cells, and it, like estrogen, activates the POMC-related endorphin stress system. The endorphins activate histamine, another promoter of inflammation and cell division.
另一种影响身体对压力的反应并改变炎症和生长过程的酶系统是单氨基氧化酶，它受到雌激素和孕酮的相反影响。雌激素的作用部分是通过增加血清素的形成来调节的，而孕激素则通过减少血清素的形成来调节。组胺是另一种炎症促进剂，雌激素增加，孕酮减少。
雌激素在神经系统的影响超出了生产cocaine-like轻度躁狂,或舞蹈病或癫痫、激活的,包括基本的压力荷尔蒙,增加形成的下丘脑pro-opiomelanocortin (POMC),这是一种前体激活肾上腺的ACTH和内啡肽(“内源性鸦片”),刺激生长过程。内啡肽和促肾上腺皮质激素都可以在乳腺癌等肿瘤中发现。促肾上腺皮质激素刺激皮质醇的产生，皮质醇可以防止炎症和生长的直接原因，但它会导致抵抗力的丧失，并增加雌激素的合成。
一种名为sigma受体的蛋白质，因其在可卡因作用中的作用而闻名，它与孕酮结合，可以抑制癌症的生长。一些麻醉剂通过这种蛋白质对肿瘤有类似的作用。西格玛受体与孕酮或孕烯醇酮相结合，对兴奋性氨基酸起保护作用。
细胞外培养基在肿瘤的发展过程中发生变化。受刺激的缺氧细胞和雌激素刺激的细胞，增加了它们的胶原蛋白的生产，而胶原蛋白的增加干扰了正常的细胞功能。孕酮可以减少胶原蛋白的形成，并可能有助于胶原蛋白的去除。
纳洛酮或纳曲酮，可以阻止内啡肽和吗啡的活动，被用来抑制各种癌症的生长，包括乳腺癌和前列腺癌。瘦素(由雌激素促进)是由脂肪细胞产生的一种激素，它和雌激素一样，激活与pomc相关的内啡肽应激系统。内啡肽会激活组胺，这是另一种促进炎症和细胞分裂的物质。
Progesterone opposes those various biochemical effects of estrogen in multiple ways, for example by inhibiting the ACTH stress response, by restraining cortisol's harmful actions, and by inhibiting leptin.
Mediators of the radiation bystander effect include NO, TNF, COX, and prostaglandins. These are produced by other things that cause inflammation and injury, including estrogen.
Cell division, when it is part of the body's continuous renewal and adaptation, isn't a source of mutations or degeneration, but when it is induced by the mediators of inflammation produced in response to injury, it leads to inherited changes, loss of differentiated function, and eventually to genetic instability.
When cell division is so disturbed that the number of chromosomes becomes abnormal, the instability of these cells decreases their ability to survive, but when the causes of the inflammation persist, they will continue to be replaced by other abnormal cells. The toxic products of dying cells can reach a point at which the debris can't be removed, adding to the injury and inflammation. The damaged bystander cells spread their influence through a cancer field, injuring more cells.
One of the “field” effects of cancer is the stimulation of new blood vessel development, angiogenesis. Lactic acid stimulates the formation of new blood vessels, the secretion of collagen, and tumor growth. Low oxygen, nitric oxide, carbon monoxide, prostaglandins and other products of tissue stress can stimulate the growth of new blood vessels, at the same time that they stimulate tumor growth and impair oxidative metabolism. Several of these agents promote each other's activity.
孕酮通过多种方式对抗雌激素的各种生化效应，例如通过抑制ACTH应激反应，通过抑制皮质醇的有害行为，以及通过抑制瘦素。
辐射旁观者效应的介质包括NO、TNF、COX和前列腺素。这些物质是由其他引起炎症和损伤的物质产生的，包括雌激素。
细胞分裂，当它是身体持续更新和适应的一部分时，不是突变或退化的来源，但当它是由响应损伤而产生的炎症介质诱导时，它会导致遗传变化，分化功能的丧失，最终导致遗传不稳定。
当细胞分裂受到干扰，染色体数量变得异常时，这些细胞的不稳定性降低了它们的生存能力，但当炎症的原因持续存在时，它们将继续被其他异常细胞所取代。死亡细胞的有毒产物会达到碎片无法被清除的程度，从而加剧损伤和炎症。受损的“旁观者”细胞将其影响扩散到癌细胞区，从而损伤更多的细胞。
癌症的“场”效应之一是刺激新血管的发展，血管生成。乳酸刺激新血管的形成、胶原蛋白的分泌和肿瘤的生长。低氧、一氧化氮、一氧化碳、前列腺素等组织应激产物能刺激新血管的生长，同时刺激肿瘤生长，损害氧化代谢。其中一些因子可以促进彼此的活动。
Therapeutic thinking has been influenced by the doctrine of the mutant cell as the initiator of cancer, leading to the idea that only things which kill the cancer cells can cure cancer. But when the body stops activating the processes of inflammation and growth, normal processes of tissue repair have an opportunity to eliminate the tumor. Even the fibroblasts which normally secrete collagen can participate in its removal (Simoes, et al., 1984). Something as simple as eliminating lactate can change their functions.
Although the angiogenic action of lactate has been known for several decades, some researchers believed that a specific anti-angiogenic peptide could be found which would stop the growth of cancer cells. The interest in angiogenesis tacitly acknowledges that there is a cancer field, but the faith that cancer could be cured only by killing the mutant cells seems to have guided the search for a single antiangiogenic substance. Such a substance would be toxic to normal tissues, since blood vessels are constantly being renewed.
The more advanced a tumor is, the more numerous the growth-promoting factors are likely to be, and the weaker the body's ability becomes to control them.
“突变细胞是癌症的始发者”的学说影响了治疗思维，导致了只有杀死癌细胞的东西才能治愈癌症的想法。但是，当身体停止激活炎症和生长过程时，正常的组织修复过程就有机会消除肿瘤。甚至正常分泌胶原的成纤维细胞也能参与其清除(Simoes等，1984)。像消除乳酸盐这样简单的事情就能改变它们的功能。
尽管乳酸的血管生成作用已经为人所知几十年了，但一些研究人员认为可以找到一种特定的抗血管生成肽，它可以阻止癌细胞的生长。对血管生成的兴趣默认了癌症领域的存在，但只有通过杀死突变细胞才能治愈癌症的信念似乎引导了对单一抗血管生成物质的研究。这种物质对正常组织是有毒的，因为血管在不断更新。
肿瘤越严重，促生长因子可能就越多，身体控制它们的能力就越弱。
The search for toxic factors to kill the cancer cells is unlikely to lead to a generally effective treatment. Even immunological approaches that think in terms of destroying a tumor might be misconceiving the nature of the problem. For example, the protein called “tumor necrosis factor” (TNF) or cachectin was discovered as a result of Lawrence Burton's work in the 1960s. He extracted proteins from the blood that could shrink some tumors in mice with amazing speed. In the right setting, TNF is involved in the destruction of tumors, but when other factors are missing, it can make them worse. Burton was focussing on factors in the immune system that could destroy cancer, but he ignored the basic problem of tissue degeneration that produces tumors which are complex and changing.
If the cancer-productive field is taken into account, all of the factors that promote and sustain that field should be considered during therapy.
Two ubiquitous carcinogenic factors that can be manipulated without toxins are the polyunsaturated fatty acids (PUFA) and estrogen. These closely interact with each other, and there are many ways in which they can be modulated.
For example, keeping cells in a well oxygenated state with thyroid hormone and carbon dioxide will shift the balance from estradiol toward the weaker estrone. The thyroid stimulation will cause the liver to excrete estrogen more quickly, and will help to prevent the formation of aromatase in the tissues. Low temperature is one of the factors that increases the formation of estrogen. Lactic acid, serotonin, nitric oxide, prostaglandins, and the endorphins will be decreased by the shift toward efficient oxidative metabolism.
寻找杀死癌细胞的有毒因子不太可能产生普遍有效的治疗方法。即使是免疫学的方法，从摧毁肿瘤的角度考虑，也可能误解了问题的本质。例如，劳伦斯·伯顿在20世纪60年代的工作中发现了一种名为“肿瘤坏死因子”(TNF)或cachectin的蛋白质。他从血液中提取的蛋白质可以以惊人的速度缩小老鼠体内的一些肿瘤。在正确的情况下，TNF参与肿瘤的破坏，但当其他因素缺失时，它会使肿瘤恶化。伯顿关注的是免疫系统中能够摧毁癌症的因素，但他忽略了产生复杂多变的肿瘤的组织退化这一基本问题。
如果癌症产生的领域被考虑在内，所有促进和维持该领域的因素都应该在治疗期间被考虑。
多不饱和脂肪酸(PUFA)和雌激素是两种无处不在且不需要毒素就能控制的致癌因素。它们彼此紧密地相互作用，并且有很多方式可以调节它们。
例如，让细胞与甲状腺激素和二氧化碳保持良好的氧合状态，将使平衡从雌二醇转向较弱的雌二醇。甲状腺刺激会导致肝脏更快地排出雌激素，并有助于防止组织中芳香化酶的形成。低温是增加雌激素形成的因素之一。乳酸、血清素、一氧化氮、前列腺素和内啡肽将因向高效氧化代谢的转变而减少。
Progesterone synthesis will be increased by the higher metabolic rate, and will tend to keep the temperature higher.
Thyroid hormone, by causing a shift away from estrogen and serotonin, lowers prolactin, which is involved in the promotion of several kinds of cancer.
Vitamin D and vitamin K have some antiestrogenic effects. Vitamin D and calcium lower the inflammation-promoting parathyroid hormone (PTH).
Eliminating polyunsaturated fats from the diet is essential if the bystander effect is eventually to be restrained. Aspirin and salicylic acid can block many of the carcinogenic effects of the PUFA. Saturated fats have a variety of antiinflammatory and anticancer actions. Some of those effects are direct, others are the result of blocking the toxic effects of the PUFA. Keeping the stored unsaturated fats from circulating in the blood is helpful, since it takes years to eliminate them from the tissues after the diet has changed. Niacinamide inhibits lipolysis. Avoiding over-production of lipolytic adrenaline requires adequate thyroid hormone, and the adjustment of the diet to minimize fluctuations of blood sugar.
The endorphins are antagonistic to progesterone, and when they are minimized, progesterone tends to increase, and to be more effective. The drugs naloxone and naltrexone, which block the effects of the endorphins, have several remarkable effects that resemble progesterone's. Naltrexone has been successfully used to treat prostate and breast cancer.
孕酮的合成会随着代谢速度的提高而增加，并且会倾向于保持较高的温度。
甲状腺激素，通过引起雌激素和血清素的转移，降低催乳素，催乳素与促进多种癌症有关。
维生素D和维生素K有一些抗雌激素作用。维生素D和钙可以降低促进炎症的甲状旁腺激素(PTH)。
如果旁观者效应最终要得到抑制，就必须从饮食中消除多不饱和脂肪。阿司匹林和水杨酸可以阻止多不饱和脂肪酸的许多致癌作用。饱和脂肪有多种抗炎和抗癌作用。有些影响是直接的，有些则是阻止多不饱和脂肪酸毒性作用的结果。防止储存的不饱和脂肪在血液中循环是有益的，因为在饮食改变后，需要数年时间才能将它们从组织中清除。烟酰胺抑制脂类分解。避免脂质肾上腺素的过度分泌需要足够的甲状腺激素，并调整饮食以尽量减少血糖的波动。
内啡肽对孕酮有拮抗作用，当内啡肽减少时，孕酮倾向于增加，更有效。药物纳洛酮和纳曲酮可以阻断内啡肽的作用，但也有一些类似孕酮的显著作用。纳曲酮已成功用于治疗前列腺癌和乳腺癌。
Opiates are still commonly used for pain relief in cancer patients, despite the evidence that has accumulated for several decades indicating that they promote inflammation and cancer growth, while suppressing immunity and causing tissue catabolism, exacerbating the wasting that commonly occurs with cancer. Their use, rather than alternatives such as procaine, aspirin, and progesterone, is nothing but a medical fetish.
Stress and estrogen tend to produce alkalosis, while thyroid, carbon dioxide, and adequate protein in the diet help to prevent alkalosis.
Antihistamines and some of the antiserotonin drugs (including “dopaminergic” lisuride and bromocriptine) are sometimes useful in cancer treatment, but the safe way to lower serotonin is to reduce the consumption of tryptophan, and to avoid excessive cortisol production (which mobilizes tryptophan from the muscles). Pregnenolone and sucrose tend to prevent over-production of cortisol.
In the breast, COX-2 converts arachidonic acid into prostaglandins, which activate the enzyme aromatase, that forms estrogen from androgens. Until the tissues are free of PUFA, aspirin and salicylic acid can be used to stop prostaglandin synthesis.
阿片类药物仍被广泛用于缓解癌症患者的疼痛，尽管几十年来积累的证据表明，阿片类药物会促进炎症和癌症的生长，同时抑制免疫力，引起组织分解代谢，加剧通常发生在癌症中的损耗。它们的使用，而不是普鲁卡因、阿司匹林和黄体酮等替代品，只是一种医学癖好。
压力和雌激素容易引起碱中毒，而甲状腺、二氧化碳和饮食中适当的蛋白质有助于预防碱中毒。
抗组胺药和一些抗血清素药物(包括“多巴胺能”利尿苷和溴隐亭)有时在癌症治疗中有用，但降低血清素的安全方法是减少色氨酸的消耗，并避免过量的皮质醇产生(从肌肉中调动色氨酸)。孕烯醇酮和蔗糖有助于防止皮质醇的过度分泌。
在乳房中，COX-2将花生四烯酸转化为前列腺素，前列腺素激活芳香化酶，从雄激素中生成雌激素。在组织中没有多不饱和脂肪酸之前，可以使用阿司匹林和水杨酸来阻止前列腺素的合成。
Thyroid is needed to keep the cell in an oxidative, rather than reductive state, and progesterone (which is produced elsewhere only when cells are in a rapidly oxidizing state) activates the processes that remove estrogen from the cell, and inactivates the processes that would form new estrogen in the cell.
Thyroid, and the carbon dioxide it produces, prevent the formation of the toxic lactic acid. When there is enough carbon dioxide in the tissues, the cell is kept in an oxidative state, and the formation of toxic free radicals is suppressed. Carbon dioxide therapy is extremely safe.
In the 1930s, primates as well as rodents had been used in experiments to show the carcinogenic effects of estrogen, and the protective effects of progesterone.
By 1950, the results of animal studies of progesterone's anticancer effects were so clear that the National Cancer Institute got involved. But the estrogen industry had already been conducting its campaign against progesterone, and had convinced most doctors that it was inactive when taken orally, and so was inferior to their proprietary drugs that they called “progestins.” The result was that it was usually given by injection, dissolved in vegetable oil or synthetic solvents such as benzyl benzoate or benzyl alcohol, which are very toxic and inflammation-producing.
甲状腺是保持细胞处于氧化状态而不是还原状态所必需的，黄体酮(只有当细胞处于快速氧化状态时，其他地方才会产生黄体酮)激活了从细胞中移除雌激素的过程，并抑制了在细胞中形成新雌激素的过程。
甲状腺及其产生的二氧化碳可以防止有毒乳酸的形成。当组织中有足够的二氧化碳时，细胞保持氧化状态，有毒自由基的形成被抑制。二氧化碳疗法是非常安全的。
在20世纪30年代，灵长类动物和啮齿动物被用于实验，以证明雌激素的致癌作用和孕酮的保护作用。
到了1950年，黄体酮抗癌作用的动物研究结果非常清楚，美国国家癌症研究所(National Cancer Institute)也参与了进来。但是雌激素产业已经开始反对黄体酮，并说服大多数医生口服黄体酮是无效的，因此不如他们的专利药物“黄体酮”。结果是，它通常是注射给药，溶解在植物油或合成溶剂，如苯甲酸苄酯或苯甲醇，这是毒性和炎症的产生。
The NCI researchers (Hertz, et al., 1951) treated 17 women with visible cancers of the uterine cervix that had been confirmed by biopsies. They were given daily intramuscular injections of 250 mg of progesterone in vegetable oil. Although they described the treatment as “massive dosage with progesterone,” it didn't prevent menstruation in any of the women who had been menstruating before the treatment began. During a healthy pregnancy, a woman produces more progesterone than that.
Their article includes some photographs of cervical tumors before treatment, and after 31 days, 50 days, and 65 days of progesterone treatment. The improvement is clear. The examining physicians described softening of the tumor, and stopping of bleeding and pain.
“In eleven of the 17 treated patients visible and palpable evidence of regressive alteration of the tumor mass could be demonstrated. This consisted of (a) distinct reduction in size of the visible portion of the cancer as well as reduction of the palpable extent of the mass, (b) reduction in vascularity and friability of the visible lesion with a clearly demonstrable epithelization of previously raw surfaces and © markedly increased pliability of the previously rigid and infiltrated parametria.”
“In 10 cases there was associated with this type of gross change a reduction in, or complete cessation of vaginal bleeding and discharge.”
“Only one of the 17 patients showed active progression of the carcinomatous process while under the progesterone administration. The six patients whose lesions failed to show clearly demonstrable regressive changes showed minor alterations in size and vascularity of insufficient degree to be convincing to all clinical observers concerned. Nevertheless, none of the lesions under study appeared to be accelerated by progesterone.”
NCI的研究人员(Hertz等人，1951年)治疗了17名经活组织检查证实的可见子宫颈癌患者。他们每天肌肉注射250毫克植物油中的黄体酮。尽管他们将治疗描述为“大量使用黄体酮”，但它并没有阻止任何在治疗开始前就已经有月经的女性的月经。在健康的怀孕期间，女性产生的黄体酮比这多。
他们的文章包括治疗前、31天、50天和65天黄体酮治疗后宫颈肿瘤的一些照片。改善是明显的。检查医生描述了肿瘤的软化，出血和疼痛的停止。
“在17名接受治疗的患者中，有11名患者可以看到明显的肿瘤消退改变的证据。这包括(a)肿瘤可见部分的明显缩小，以及肿块可触及范围的缩小，(b)可见病变的血管密度和脆性降低，在以前的原始表面有明显的上皮化，©以前刚性和浸润性参数的柔韧性显著增加。”
“在10个病例中，这种类型的严重变化与阴道出血和分泌物的减少或完全停止有关。”
“在17名患者中，只有1名患者在服用黄体酮后，肿瘤进程出现了活跃的进展。6例患者的病变没有明显的退行性改变，其大小和血管状况的微小改变不足以使所有临床观察人员信服。然而，在研究中，黄体酮似乎没有加速病变。”
Observing very similar patients under similar conditions while they were waiting for surgery, but were not receiving progesterone, they saw no such regressions of tumors.
The photographs and descriptions of the changes in the tumors were remarkable for any cancer study, but to have been produced by a treatment that didn't even alter the patients' menstrual cycle, the reader might expect the authors to discuss their plans for further studies of such a successful method.
But instead, they concluded “We do not consider the regressive changes observed to be sufficient to indicate the use of progesterone as a therapeutic agent in carcinoma of the cervix.”
(Their research was supported by a grant from the American Cancer Society.)
If the researchers had bothered to test progesterone on themselves or on animals, they would have discovered that it is fully active when taken orally, dissolved in oil, and that nontoxic saturated fats could have been used. Progesterone anesthesia was very well known at that time, so it would have been reasonable to use doses that were at least equivalent to the concentrations present during pregnancy, even if they didn't want to use doses that would approach the anesthetic level. The total daily doses could have been about ten times higher, if they had been given orally as divided doses.
The solvent issue continues to impede research in the use of progesterone for treating cancer, but the main problem is the continuing belief that “the cancer cell” is the problem, rather than the cancer field. Substances are tested for their ability to kill cancer cells in vitro, because of the basic belief that mutated genes are the cause of the disease. When progesterone is tested on cancer cells in vitro, the experimenter often sees nothing but the effects of the solvent, and doesn't realize that nearly all of the progesterone has precipitated in the medium, before reaching the cancer cells.
在相似的条件下观察相似的病人，当他们等待手术，但没有接受黄体酮，他们没有看到肿瘤的这种退化。
对于任何癌症研究来说，肿瘤变化的照片和描述都是值得注意的，但由于是由一种甚至没有改变患者月经周期的治疗方法产生的，读者可能会期待作者讨论他们对这种成功方法的进一步研究计划。
但相反，他们总结道:“我们不认为观察到的退行性变化足以表明使用孕酮作为宫颈癌的治疗药物。”
(他们的研究得到了美国癌症协会(American Cancer Society)的资助。)
如果研究人员费心在自己或动物身上测试黄体酮，他们就会发现，口服时，黄体酮完全活跃，溶解在油中，而且可以使用无毒的饱和脂肪。黄体酮麻醉在当时非常有名，所以使用至少与怀孕期间相同浓度的剂量是合理的，即使他们不想使用接近麻醉水平的剂量。如果按分剂量口服，每天的总剂量可能会高出十倍。
溶剂问题继续阻碍使用孕酮治疗癌症的研究，但主要问题是人们仍然相信“癌细胞”才是问题，而不是癌症领域。由于人们普遍认为突变的基因是导致癌症的原因，这些物质在体外对其杀死癌细胞的能力进行了测试。当孕酮在体外对癌细胞进行测试时，实验者通常只看到溶剂的作用，而没有意识到几乎所有的孕酮在到达癌细胞之前已经在培养基中沉淀了。
The cancer industry began a few years ago to combine chemicals for chemotherapy, for example adding caffeine to paclitaxel or platinum (cisplatin), or histamine to doxorubicin, but they do it simply to increase the toxicity of the chemical to the tumor, or to decrease its toxicity to the patient. Doctors sometimes refer to combined chemotherapy as a “shotgun approach,” meaning that it lacks the acumen of their ideal silver bullet approach. If cancers were werewolves, the cancer industry's search for more refined killing technologies might be going in the right direction. But the genetic doctrine of cancer's origin is just as mythical as werewolves and vampires.
A safe physiological approach to cancer, based on the opposition of progesterone to estrogen, would be applicable to every type of cancer promoted by estrogen, or by factors which produce the same effects as estrogen, and that would include all of the known types of cancer. Estrogen acts even on cells that have no “estrogen receptors,” but estrogen receptors can be found in every organ.
As estrogen's non-feminizing actions are increasingly being recognized to include contributions to other kinds of disease, including Alzheimer's disease, heart disease, and rheumatoid arthritis, the idea of the bystander effect, and the field of cellular degeneration, will eventually clear the way for a rational use of the therapeutic tools that already exist.
癌症行业几年前开始联合化学药物进行化疗，例如在紫杉醇或铂(顺铂)中加入咖啡因，或在阿霉素中加入组胺，但他们这么做只是为了增加化学药物对肿瘤的毒性，或降低其对患者的毒性。医生有时把联合化疗称为“霰弹疗法”，意思是它缺乏理想的银弹疗法的敏锐。如果癌症是狼人，那么癌症产业对更精细的杀伤技术的探索可能正朝着正确的方向发展。但是癌症起源的基因学说就像狼人和吸血鬼一样神秘。
一种基于黄体酮与雌激素对立的安全的治疗癌症的生理学方法，将适用于由雌激素促进的所有类型的癌症，或与雌激素产生相同效果的因素，这将包括所有已知类型的癌症。雌激素甚至作用于没有“雌激素受体”的细胞，但雌激素受体可以在每个器官中找到。
随着雌激素的非女性化作用被越来越多的人认识到包括对其他疾病的影响，包括阿尔茨海默病，心脏病，风湿性关节炎，旁观者效应，以及细胞变性，最终将为合理使用现有的治疗工具扫清道路。
There are several types of drug—carbonic anhydrase inhibitors, to increase carbon dioxide in the tissues, lysergic acid derivatives, to block serotonin and suppress prolactin, anti-opiates, antiexcitotoxic and GABAergic agents, anesthetics, antihistamines, anticholinergics, salicylic acid derivatives—that could probably be useful in a comprehensive therapy for cancer, but their combinations won't be explored as long as treatments are designed only to kill.
Preventing or correcting disturbances in the morphogenetic field should be the focus of attention.
有几种类型的药物——碳酸酐酶抑制剂，增加组织中的二氧化碳，麦角酸衍生物，阻止血清素和抑制催乳素，抗阿片类药物，抗兴奋毒性和gaba能剂，麻醉剂，抗组胺，抗胆碱能剂，水杨酸衍生物——这可能在癌症的综合治疗中有用，但只要治疗的目的是杀死人，它们的组合就不会被探索。
防止或纠正形态发生领域的干扰应成为关注的焦点。
http://raypeat.com/articles/articles/cancer-progesterone.shtml
