Bleeding, clotting, cancer
出血、凝血、癌症
by Raymond Peat
The balance between bleeding and clotting is easily disturbed. The condensation and dissolution of the clotting protein, fibrinogen/fibrin, is a continuous process, sensitive to changes in stress, nutrition, and hormones. Clots form, locally or systemically, when fibrin is formed faster than it is dissolved. When fibrin is destroyed faster than it can be replaced, blood vessels become too permeable, and bleeding can occur more easily.
出血和凝血之间的平衡很容易被破坏。凝血蛋白(纤维蛋白原/纤维蛋白)的凝结和溶解是一个连续的过程，对应激、营养和激素的变化敏感。当纤维蛋白形成的速度快于溶解的速度时，局部或全身就会形成血栓。当纤维蛋白被破坏的速度快于其可被替代的速度时，血管就会变得渗透性太强，从而更容易发生出血。
Mental stress, exercise, estrogen, and serotonin activate both the formation and dissolution of clots.
Bleeding and clotting are not only very closely related with each other, such that a given stress can induce either or both, but the condensation and dissolution of the clotting protein are involved in edema, multiple organ failure, and the growth of cancers. The growth of tumors is as directly related to the clotting system as are thromboses and hemorrhages.
Disordered clotting contributes to maladaptive inflammation and to the “diseases” of aging and degeneration.
精神压力、运动、雌激素和血清素都能激活血栓的形成和溶解。
出血和凝血不仅彼此密切相关，例如给定的压力可以诱导其中之一或两者都有，而且凝血蛋白的凝结和溶解与水肿、多器官衰竭和癌症的生长有关。肿瘤的生长与凝血系统直接相关，就像血栓和出血一样。
凝血紊乱会导致适应性不良的炎症和衰老和变性的“疾病”。
Metabolic energy is the basic defense against the stress reactions that disrupt circulation, healing, and growth.
代谢能量是对破坏循环、愈合和生长的应激反应的基本防御。
“It is commonly known that the ESR (red cell sedimentation rate) of cancer patients is always high.”
“Thus far, completely unagglutinated blood has been found only in strictly healthy animals and men. No severely ill person has yet been seen who did not have intravascular agglutination of the blood and visibly pathologic vessel walls.” Melvin H. Knisely, et al., 1947)
“众所周知，癌症患者的红细胞沉降率总是很高。”
“到目前为止，只有在严格健康的动物和人身上发现了完全未凝集的血液。尚未见没有血管内凝集和明显病变血管壁的重症患者。”Melvin H. knisse等，1947)
When science became a sort of “profession,” in the 19th century, the old “natural philosophy” of Newton’s time began to subdivide into many specialties. At that time, medicine had some general theories to account for deviations from good health, such as the theory of the four humors and their balance, but as those general theories disappeared, they weren’t replaced by any single scientific understanding of the nature of good health and disease. Medical education has convinced doctors and the public that the reasons for suffering, disability and death are mostly known, and that when medical experts agree to give a condition a name, there must be some clear scientific evidence behind that disease name.
19世纪，当科学成为一种“职业”时，牛顿时代的旧“自然哲学”开始细分为许多专业。当时，医学上有一些一般性理论来解释健康的偏差，比如四种体液及其平衡理论，但随着这些一般性理论的消失，它们没有被任何对健康和疾病本质的单一科学理解所取代。医学教育已经使医生和公众相信，造成痛苦、残疾和死亡的原因大多是已知的，当医学专家同意给一种疾病命名时，这种疾病名称背后必须有一些明确的科学证据。
That mystique of diagnosing disease (specific, concrete, reified disease) was so strong that when Hans Selye noticed (in the 1930s) something that underlies all sickness (he first called it the “syndrome of being sick”), he was disregarded and disrespected, at least until his dangerous perceptions could be trimmed, distorted, and subsumed under some proper medical categories. Selye observed that stress causes internal bleeding (in lungs, adrenals, thymus, intestine, salivary and tear glands, etc.), but instead of trying to understand what that means for the control of sickness, the medical schools and journals have offered concrete, fragmentary, and false explanations for his observations. “Stomach acid” causes bleeding in the stomach and duodenum; stuff leaking out of the brain gets the blame for some cases of systemic bleeding, stuff leaking out of the uterus, for other cases, and so on. Selye’s observations have been rendered harmless (to medicine) by these falsely concrete explanations. While conventional medicine propagated its medical fantasies, it characterized Selye’s work as “controversial.”
诊断疾病(具体的、具体的、具体化的疾病)的神秘性如此之强，以至于当汉斯·塞利(Hans Selye)(在20世纪30年代)注意到所有疾病的基础(他最初称之为“生病综合症”)时，他被忽视和不尊重，至少在他危险的观点被修正、扭曲之前，归入适当的医学范畴Selye观察到压力会导致内出血(在肺、肾上腺、胸腺、肠、唾液腺和泪腺等)，但医学院和期刊并没有试图理解这对疾病控制意味着什么，而是为他的观察提供了具体的、零碎的和错误的解释。胃酸引起胃和十二指肠出血;从大脑中漏出的物质导致了一些全身出血的病例，从子宫中漏出的物质，还有一些病例，等等。由于这些错误的具体解释，Selye的观察结果(对医学)是无害的。在传统医学大肆宣扬其医学幻想的同时，它将Selye的工作描述为“有争议的”。
In many cases, “diagnosis” consists of what could, at best, be called an educated guess, with no attempt to find evidence to support it. Obviously, if every doctor in the country is guessing wrong about certain deadly conditions, lots of people will die, and no one will see the need to even study the subject, since it has a definite name and an explanation that seems to satisfy.
Instead of finding pseudo-reasons for the bleeding abnormalities caused by stress, it would be good to look freshly at the nature of blood and its circulation. It might turn out that it’s a way to expand our understanding of the stress reaction.
在许多情况下，“诊断”最多只能被称为一种有根据的猜测，而没有试图找到证据来支持它。显然，如果这个国家的每个医生对某些致命疾病的猜测都是错误的，那么很多人就会死亡，甚至没有人会认为有必要研究这个学科，因为它有一个明确的名称和一个似乎令人满意的解释。
与其为压力引起的异常出血寻找伪原因，不如重新审视一下血液及其循环的本质。这可能是一种扩展我们对压力反应理解的方式。
Most people are aware of some of the variations of bleeding and clotting that occur commonly. Bleeding gums, nose-bleeds, menstruation and its variations, and the spontaneous bruising (especially on the thighs) that many women have premenstrually, are familiar events that don’t seem to mean much to the medical world. Sometimes nose-bleeds are clearly stress-related, but the usual “explanation” for that association is that high blood pressure simply blows out weak blood vessels. Bleeding gums are sometimes stress related, but high blood pressure is seldom invoked to explain that problem.
大多数人都知道一些常见的出血和凝血的变化。牙龈出血、流鼻血、月经及其变化，以及许多女性经前出现的自发淤青(尤其是大腿上的淤青)，这些都是大家熟悉的事情，对医学界似乎没什么意义。有时，流鼻血显然与压力有关，但通常的“解释”是，高血压只是吹出了虚弱的血管。牙龈出血有时与压力有关，但高血压很少被用来解释这个问题。
The whole issue of blood vessel fragility is usually disposed of as a “genetic trait,” or a result of old age. This is part of a general tendency to think of the blood vessels as an anatomically fixed, “congenital,” and genetically determined system. At least until recently, nearly all physicians have called aneurysms “congenital defects.” But varicose veins are merely low-pressure analogs of arterial aneurysms, and they obviously develop under specific conditions, such as pregnancy and malnutrition. Spider veins are another anatomical variation that commonly appears under the influence of estrogen. Subarachnoid hemorrhages, which can put pressure on the brain, are usually considered to result from a ruptured aneurysm, and these hemorrages are twice as common in women as in men, and probably result from a hormone imbalance.
血管脆弱的整个问题通常被认为是一种“遗传特征”，或者是老年的结果。一般倾向于认为血管是解剖学上固定的、“先天性的”和遗传决定的系统，这是其中的一部分。至少直到最近，几乎所有的医生都把动脉瘤称为“先天性缺陷”。但是静脉曲张仅仅是低压动脉瘤的类似物，它们显然是在特定的条件下形成的，比如怀孕和营养不良。蜘蛛静脉是另一种解剖学变异，通常出现在雌激素的影响下。蛛网膜下腔出血会对大脑造成压力，通常被认为是由动脉瘤破裂引起的，而这种出血在女性中的发生率是男性的两倍，可能是激素失衡造成的。
Menstrual bleeding is a good place to start the investigation of bleeding problems, since its relatively harmless abnormalities are physiologically related to some very serious health problems, such as pregnancy bleeding, abruptio placentae, and eclampsia. Women who die from eclampsia have been found to have massively clotted blood vessels in their brains, but the variety of names for the pregnancy disorders have prevented most people from thinking of pregnancy as a time when there is a high risk of the “thrombohemorrhagic disorders,” a time when the clotting system is under stress. (For about fifteen years after Selye coined the term, only he and some Russians were publishing research on it, and Americans still don’t show much interest in the subject.)
月经出血是开始调查出血问题的好地方，因为它相对无害的异常与一些非常严重的健康问题，如妊娠出血、胎盘早剥、子痫等生理相关。妇女死于惊厥已经发现大量凝结的血管在他们的大脑,但怀孕的各种名称的障碍阻止大多数人想怀孕的时候有一个高风险的“出血性障碍,”在凝血系统压力。(在Selye创造了这个词后的大约15年里，只有他和一些俄罗斯人发表了关于这个词的研究，而美国人仍然对这个话题不太感兴趣。)
Women with a chronic menstrual problem resulting from progesterone deficiency often continue to bleed each month even when they are pregnant, and these women tend to develop toxemia, and to have a high incidence of pregnancy complications, and to deliver premature, poorly developed babies.
由于黄体酮缺乏而导致的慢性经期问题的妇女即使在怀孕期间，每月也会持续出血，这些妇女往往会出现毒血症，怀孕并发症的发生率很高，并会早产，产下发育不良的婴儿。
In 1933 James Shute was recommending the use of vitamin E for preventing the clotting problems associated with pregnancy, that often lead to miscarriage. He based his work on animal studies, that led to vitamin E’s being known as the “fertility vitamin.” Later, his sons Wilfred and Evan reported that vitamin E could prevent heart attacks, birth defects, complications of diabetes, phlebitis, hypertension, and some neurological problems.
1933年，詹姆斯·舒特推荐使用维生素E来预防与怀孕有关的凝血问题，这通常会导致流产。他的工作基于动物研究，这导致维生素E被称为“生育维生素”。后来，他的儿子威尔弗雷德(Wilfred)和埃文(Evan)报告说，维生素E可以预防心脏病、出生缺陷、糖尿病并发症、静脉炎、高血压和一些神经问题。
Later, referring to the decades of hostility of the medical establishment to vitamin E, Dr. Shute said “…an obstetrician was unduly hardy and audacious to try it.” The spectrum of vitamin E’s protective effects (like those of aspirin) has been consistently misrepresented in the medical literature.
后来，在提到医疗机构几十年来对维生素E的敌意时，舒特博士说:“……一位产科医生非常大胆地尝试了一下。”在医学文献中，维生素E的保护作用范围(就像阿司匹林的保护作用)一直被歪曲。
Hematomas in many organs (pituitary, kidney, pancreas, liver, even around the abdominal muscles) can occur because of hormone imbalances in these difficult pregnancies. Tom Brewer’s demonstration that a good diet, with abundant protein, can prevent and cure pregnancy toxemia, is practically unknown in the medical world, though a protein deficiency has been shown to increase the risk of blood clots under many other circumstances besides pregnancy.
许多器官(脑下垂体、肾脏、胰腺、肝脏，甚至腹部肌肉周围)都可能出现血肿，因为在这些困难的妊娠中，激素失衡会导致血肿。汤姆·布鲁尔(Tom Brewer)的论证表明，富含蛋白质的良好饮食可以预防和治疗妊娠毒血症，这在医学界几乎是未知的，尽管有证据表明，在怀孕之外的许多情况下，缺乏蛋白质会增加血栓的风险。
Abruptio placentae (premature detachment of the placenta) has often been blamed on the use of vitamin E, because of vitamin E’s reputation for preventing abnormal clotting, though the evidence tends to suggest instead that vitamin E (like aspirin) reduces the risk of pregnancy-related hemorrhaging.
One of the deadly clotting conditions related to childbirth has been called “pregnancy anaphylaxis,” but it is more often called “amniotic fluid embolism,” despite the fact that amniotic fluid injected intravenously is harmless (Petroianu, et al.), and only by grinding up and injecting massive amounts of the pregnancy membranes can the clotting system be disturbed. The term is really a criminal misnomer, serving to blame a preventable clotting/shock disorder on the patient.
胎盘早剥(胎盘过早脱离)经常被归咎于维生素E的使用，因为维生素E以防止异常凝血而闻名，尽管有证据倾向于表明维生素E(像阿司匹林一样)可以降低妊娠相关出血的风险。
其中一种与分娩有关的致命凝血疾病被称为“妊娠过敏反应”，但它更常被称为“羊水栓塞”，尽管事实是羊水静脉注射是无害的(Petroianu等)，而且只有碾碎并注射大量的妊娠膜才能扰乱凝血系统。这个术语实际上是犯罪用词不当，将可预防的凝血/休克障碍归咎于患者。
“Consumption coagulopathy” refers to the bleeding that follows excessive activation of the clotting system, combined with a defensive dissolving of the clots, when finally the fibrinogen or other elements of the clotting system have been depleted, consumed. A blood test can show when clot degradation products are being produced too rapidly, even while a person has no symptoms, so there should be time for the accelerated clotting to be controlled, before major thromboses and bleeding and shock have developed.
“消耗性凝血病”是指当最终凝血系统中的纤维蛋白原或其他成分被消耗殆尽时，凝血系统过度激活并结合了凝血块的防御性溶解而导致的出血。血液测试可以显示何时凝块降解产物产生过快，即使患者没有任何症状，因此在出现重大血栓、出血和休克之前，应该有时间控制加速凝块。
In 1936 Albert Szent-Gyorgyi reported that some chemicals in lemon juice, which he called vitamin P (or citrin), would prevent purpura, subcutaneous capillary bleeding. By 1938, he had decided that citrin, (which he now called bioflavonoid) probably wasn’t a vitamin, and that its action was more like that of a drug, substituting for a natural regulatory factor that was missing. Later research has confirmed that view, showing that the bioflavonoids inhibit the enzyme hyaluronidase, which degrades the “ground substance” of connective tissues. At least one natural endogenous inhibitor of hyaluronidase has now been identified. The basement membrane that surrounds and unites the endothelial cells of capillaries is largely hyaluronic acid and collagen. It isn’t thrombogenic (Buchanan, et al.), despite the common belief that collagen is intrinsically a clot instigator. The breakdown of this ground substance is involved in growth and reproduction, so an excess of bioflavonoids in the diet could conceivably interfere with fertility and fetal development. Some bioflavonoids have been prescribed for menstrual problems, and are probably useful when the physiological inhibitor isn’t adequate.
1936年，阿尔伯特·圣乔吉报道说，柠檬汁中的一些化学物质，他称之为维生素P(或柠檬酸)，可以预防紫癜，也就是皮下毛细血管出血。到1938年，他认定柑橘素(他现在称其为生物类黄酮)可能不是一种维生素，它的作用更像是一种药物，替代了一种缺失的自然调节因子。后来的研究证实了这一观点，表明生物类黄酮抑制了透明质酸酶，这种酶能降解结缔组织的“基质”。至少有一种天然内源性透明质酸酶抑制剂现已被鉴定。包围和连接毛细血管内皮细胞的基膜主要是透明质酸和胶原蛋白。它不是血栓形成的(Buchanan等人)，尽管人们普遍认为胶原蛋白本质上是血栓激发剂。这种基础物质的分解涉及到生长和繁殖，所以饮食中过量的生物类黄酮可能会干扰生育能力和胎儿发育。一些生物类黄酮已经被用于治疗月经问题，当生理抑制剂不足时可能有用。
Hyaluronidase is activated by shock, and also by estrogen. Both hyaluronidase and estrogen have been used in plastic surgery to “expand” tissue, weakening it and allowing it to be enlarged. During aging, hyaluronic acid (the major water-retaining component of connective tissue that’s broken down by hyaluronidase) decreases in the connective tissues, but increases in the blood stream. Shock allows hyaluronic acid to increase in the serum. Fragments of degraded hyaluronic acid are pro-inflammatory.
透明质酸酶可由休克激活，也可由雌激素激活。透明质酸酶和雌激素都被用于整形手术，以“扩大”组织，使其变弱并扩大。在衰老过程中，结缔组织中的透明质酸(被透明质酸酶分解的结缔组织的主要保水成分)减少，但在血流中增加。休克可使血清中的透明质酸增加。降解的透明质酸碎片是促炎的。
In the 1940s Hans Selye studied the steroid hormones in a comprehensive way, defining their actions and interactions. At that time he found that progesterone protected broadly against stress, and that a large dose of estrogen created a condition that duplicated the initial shock phase of the stress reaction. Later animal studies showed that estrogen quickly causes enlargement of the adrenal glands, followed by bleeding, and, with large and continuous doses, death of the adrenal cells.
20世纪40年代Hans Selye对类固醇激素进行了全面的研究，定义了它们的作用和相互作用。当时他发现黄体酮能有效地抵御压力，而大量的雌激素会产生一种与压力反应最初的休克阶段相同的状况。后来的动物研究表明，雌激素会迅速导致肾上腺增大，随后出血，并在大剂量和连续剂量下导致肾上腺细胞死亡。
Estrogen promotes vascular permeability by a variety of mechanisms. Serotonin, histamine, lactic acid, and various cytokines and prostaglandins contribute to the leakage stimulated by estrogen, trauma, irradiation, poisoning, oxygen deprivation, and other factors that can induce shock. Even exercise, mental stress, and aging can increase the tendency of capillaries to leak.
雌激素通过多种机制促进血管通透性。血清素、组胺、乳酸、各种细胞因子、前列腺素等都是雌激素、创伤、照射、中毒、缺氧等诱发休克的因素。即使是运动、精神压力和衰老也会增加毛细血管渗漏的趋势。
Progesterone and cortisol protect against shock and stress partly by maintaining the resistance and integrity of the capillaries, preventing leakage of blood materials into the tissues. The maintenance of the capillary barrier probably also prevents substances from the extracellular matrix from triggering the clotting systems.
孕酮和皮质醇通过维持毛细血管的抵抗力和完整性，防止血液物质渗漏到组织中来保护休克和压力。维持毛细血管屏障可能也会阻止来自细胞外基质的物质触发凝血系统。
Clots are formed when soluble fibrinogen polymerizes, condenses, and becomes insoluble. Even before the particles of fibrin become insoluble, a clot-dissolving system is continuously breaking it down into small peptides. These peptides tend to cause capillaries to leak. If a massive amount of fibrinogen and fibrin leak out of capillaries, clots are formed outside capillaries, and the peptides released in the process of cleaning up this debris contribute to further leakage, and to inflammation. The inflammation stimulates the production of collagen-rich connective tissue, and a fibrotic tissue replaces the functional tissues. Many of Hans Selye’s experiments explored the conditions in which inflammation, exudation, and fibrosis developed, sometimes ending with calcification of the region.
当可溶性纤维蛋白原聚合、凝结和不溶时，就形成了凝块。甚至在纤维蛋白颗粒变得不可溶之前，一个凝块溶解系统就在不断地将其分解成小肽。这些多肽会导致毛细血管渗漏。如果大量的纤维蛋白原和纤维蛋白从毛细血管中泄漏出来，血块就会在毛细血管外形成，而在清除这些碎片的过程中释放的肽会进一步泄漏，并导致炎症。炎症刺激胶原蛋白丰富的结缔组织的产生，纤维组织取代了功能性组织。Hans Selye的许多实验探索了炎症、渗出和纤维化发生的条件，有时以该区域的钙化结束。
The presence of fibrin in the extracellular matrix interferes with the differentiated functioning of cells, which depend on their contact with a normal matrix. When healing and regeneration occur in the normal matrix, the remodeling of the tissue involves the breakdown of collagen, which releases peptides with antiinflammatory, antiangiogenic and antiinvasive actions. When fibrin is present, the remodeling process releases peptides that increase cell growth, invasiveness, inflammation, and the production of new blood vessels, which in turn become leaky.
细胞外基质中纤维蛋白的存在干扰了细胞的分化功能，而细胞的分化依赖于细胞与正常基质的接触。当正常基质中发生愈合和再生时，组织的重塑涉及胶原蛋白的分解，释放具有抗炎、抗血管生成和抗侵袭作用的肽。当纤维蛋白存在时，重构过程释放多肽，增加细胞生长、侵袭性、炎症和新血管的产生，而新血管又变得渗漏。
Leakage of fluid out of the blood is one of the main features of shock, and at first it is mainly the loss of water and volume that creates a problem, by reducing the oxygenation of tissue and increasing the viscosity of the remaining blood. Blood becomes more concentrated during strenuous exercise, during the night, and in the winter, increasing the viscosity, and increasing the risk of strokes and other thrombotic problems. The absence of light causes the metabolic and hormonal changes typical of stress.
Tom Brewer and his associates showed that pregnancy toxemia involves inadequate blood volume, and that using extra sodium can alleviate the symptoms, including preventing albuminuria, one of the most characteristic signs of toxemia/preeclampsia. (Besides causing loss of albumin through leaky capillaries, estrogen also inhibits its synthesis by the liver; the loss of colloid osmotic pressure in hypoalbuminemia has many consequences, including disturbances of blood lipids.) Estrogen’s action in toxemia of pregnancy is paralleled by the fact that blood viscosity is highest at the time of ovulation during the normal monthly cycle.
从血液中漏出液体是休克的主要特征之一，最初主要是水分和体积的损失造成问题，通过减少组织的氧合和增加剩余血液的粘度。在剧烈运动期间，在夜间和冬季，血液会变得更加集中，增加粘度，增加中风和其他血栓问题的风险。缺乏光照会引起典型的代谢和激素变化。
Tom Brewer和他的同事指出，妊娠毒血症涉及血容量不足，使用额外的钠可以缓解症状，包括防止蛋白尿，这是毒血症/子痫前期最典型的症状之一。(除了通过毛细血管渗漏导致白蛋白流失外，雌激素还抑制肝脏合成白蛋白;低蛋白血症中胶体渗透压的丧失有许多后果，包括血脂紊乱。雌激素在妊娠毒血症中的作用与血液粘度在正常月经周期排卵时最高的事实是相对应的。
In the healthy person, some of the fibrin that is constantly being formed is deposited on the inside of blood vessels (and on the surfaces of blood cells), and this layer forms an important part of the capillary’s resistance to leaking. A.L. Copley, who pioneered the study of hemorrheology, called this the “endoendothelial layer.” This layer probably contains albumin, too, in close association with the (carbohydrate) “glycocalyx” of the endothelial cell surface. Disturbances that accelerate the formation and dissolution of the fibrin layer can be detected by an increase in the concentration of the fibrin degradation products (FDP, or D-dimers) in the blood, even before any symptoms have appeared.
在健康人体内，一些不断形成的纤维蛋白沉积在血管内部(和血细胞的表面)，这一层形成了毛细血管抵抗渗漏的重要组成部分。血液流变学研究的先驱A.L. Copley称其为“内皮层”。这一层可能也含有白蛋白，与内皮细胞表面的糖萼(碳水化合物)密切相关。通过血液中纤维蛋白降解产物(FDP或d -二聚体)浓度的增加，甚至在任何症状出现之前，就可以检测到加速纤维蛋白层形成和溶解的紊乱。
Although Selye described shock as the first (potentially lethal) phase of stress, usually followed by the corrective adaptive processes, it’s useful to think of aging in terms of a lingering partial state of shock, in which adaptation is less than perfect.
虽然Selye将休克描述为压力的第一个(可能致命的)阶段，通常随后是纠正性的适应过程，但将衰老视为一种挥之不去的部分休克状态是有用的，在这种状态下，适应并不完美。
The loss of blood volume through leaky capillaries tends to be self-aggravating. The concentrated and viscous blood doesn’t flow as well through the capillaries, and this energy deprivation leads to increased leakiness of the cells, and to swelling of the endothelial cells, decreasing the internal diameter of the small blood vessels. The energy-deprived state increases lactic acid, adrenaline, and free fatty acids, all of which contribute to increased leakiness and impaired circulation.
通过渗漏的毛细血管失血往往是自我加重。浓缩而粘稠的血液不能很好地流经毛细血管，这种能量的缺乏导致细胞的渗漏增加，内皮细胞的膨胀，小血管的内径减小。缺乏能量的状态会增加乳酸、肾上腺素和游离脂肪酸，所有这些都会增加渗漏和循环障碍。
In the bowel, the capillary malfunction increases the absorption of endotoxin, which intensifies the systemic energy problem. (Polyunsaturated oils, especially fish oil, damage the bowel capillaries, allowing more endotoxin to be absorbed.)
在肠内，毛细血管功能障碍增加了内毒素的吸收，加剧了全身能量问题。(多不饱和油脂，尤其是鱼油，会破坏肠道毛细血管，让更多的内毒素被吸收。)
In the uterus, increased viscosity of the blood impairs the delivery of oxygen and nutrients to the fetus, retarding its development. Dilution of the blood under the influence of progesterone reduces the hematocrit, helping to compensate for the viscosity; in toxemic pregnancies this isn’t sufficient to maintain normal viscosity and perfusion.
在子宫内，血液粘度的增加会阻碍氧气和营养物质的输送，从而阻碍胎儿的发育。在孕酮的影响下，血液的稀释降低了红细胞压积，有助于补偿粘度;在中毒妊娠中，这不足以维持正常的粘度和灌注。
In the brain, hyperviscosity contributes to dementia. In the lung, to edema and reduced oxygenation (“shock lung,” “wet lung,” respiratory distress; this lung edema is a major cause of mortality in pregnancy). In the pancreas, to inflammation, and to the release of proteolytic enzymes, impairing the clotting system even more.
在大脑中，高粘度会导致痴呆。在肺内，以水肿和氧合减少(“休克肺”、“湿肺”、呼吸窘迫;肺水肿是妊娠期死亡的主要原因)。在胰腺，炎症和蛋白水解酶的释放，更严重地损害了凝血系统。
During the development of cancer, hyperviscosity (and the associated hypoxia) contributes to the tumor’s deranged metabolism, tending to increase its production of ammonia, clotting factors, and other stress-inducing toxins.
在癌症的发展过程中，高粘度(和相关的缺氧)会导致肿瘤代谢紊乱，增加氨、凝血因子和其他应激诱导毒素的产生。
Factors that increase the fluidity of the blood protect against all of the thrombohemorrhagic conditions, and are especially protective against the estrogen-promoted cancers. Progesterone decreases the production of fibrinogen, and increases the volume of the blood and the flexibility of the red blood cells, increasing the ability of blood to flow freely, and it also decreases the leakiness of capillaries. Hypothyroid people (who tend to have low progesterone and high estrogen) are highly susceptible to heart disease and cancer, and have abnormally viscous blood. Hyperthyroid people have unusually fluid blood. Hypothyroidism increases the leakiness of capillaries, and decreases the amount of albumin in the blood. Albumin itself decreases the permeability of blood vessels.
增加血液流动性的因素可以预防所有的血栓出血性疾病，尤其是雌激素促进的癌症。孕酮减少纤维蛋白原的产生，增加血液容量和红细胞的灵活性，增加血液自由流动的能力，它也减少毛细血管的渗漏。甲状腺机能减退的人(孕激素水平低而雌激素水平高的人)极易患心脏病和癌症，并且血液异常粘稠。甲状腺机能亢进的人有异常的液体血液。甲状腺机能减退会增加毛细血管的渗漏，并减少血液中的白蛋白量。白蛋白本身会降低血管的通透性。
In hypothyroidism and under the influence of estrogen, there is a chronic increase of free fatty acids, and the free fatty acids are an important factor in increasing the production of fibrinogen (Pickart), and in blocking fibrinolysis (Lindquist, et al.). If the body’s stores of fat are largely polyunsaturated fats, the free fatty acids will combine with the fibrin as it polymerizes, making the clots especially resistant to dissolution.
In the 1940s, Melvin Knisely noticed that all seriously sick people had “sludged” blood, that can be observed microscopically in the small blood vessels on the surface of the person’s eye. The cells tend to stick together, producing a sludgy appearance and slow flow. This probably corresponds to increased viscosity of the plasma, increased red cell sedimentation rate, increased fibrinogen, decreased albumin, and decreased thyroid and progesterone. Clumped red cells, when separated under the microscope, appear to be bound together by fine filaments, possibly of fibrin.
在甲状腺功能减退和雌激素的影响下，游离脂肪酸慢性增加，游离脂肪酸是增加纤维蛋白原生产(Pickart)和阻断纤维蛋白溶解(Lindquist, et al.)的重要因素。如果身体储存的脂肪主要是多不饱和脂肪，游离脂肪酸将在纤维蛋白聚合时与纤维蛋白结合，使凝块特别难以溶解。
在20世纪40年代，梅尔文·克尼斯注意到所有重病的人都有“淤积”的血液，这可以通过显微镜在人眼睛表面的小血管中观察到。细胞倾向于粘在一起，产生一种泥状的外观和缓慢的流动。这可能与血浆粘度增加、红细胞沉降率增加、纤维蛋白原增加、白蛋白减少、甲状腺和孕酮减少有关。凝结的红细胞在显微镜下分离时，似乎被细丝(可能是纤维蛋白)结合在一起。
Aspirin is known to have a variety of anticancer activities, including the prevention of metastasis, and some people have reasoned that the clotting process simply helps migrating cancer cells to become anchored. However, the clotting process is normally part of the healing and repair processes, and I think the role of the fibrin clotting system in cancer is that the breakdown products of fibrin are growth-promoters, and that their presence in the extracellular matrix in large quantity, distorting the normal composition of the matrix, is what causes the formation of a tumor. It’s the leakage of the fibrin into the extracellular matrix that leads to the development of tumors.
众所周知，阿司匹林具有多种抗癌活性，包括预防转移，一些人推断，凝血过程只是帮助迁移的癌细胞被固定。然而,凝血过程通常愈合和修复过程的一部分,而且我认为癌症是纤维蛋白凝血系统的作用,纤维蛋白分解产物的生长促进剂,,他们的存在在大量细胞外基质,扭曲的正常组成矩阵,是导致肿瘤形成的原因。正是纤维蛋白漏入细胞外基质导致了肿瘤的发生。
Heparin, a natural anticoagulant, is currently being tested as an anticancer agent.
肝素是一种天然抗凝血剂，目前正作为一种抗癌剂进行试验。
All of the factors that promote stable oxidative energy production protect against the coagulative derangements, largely by preventing capillary leakage, and it now seems that these processes protect against cancer as well as protecting against all of the stress-related degenerative and inflammatory diseases.
所有促进稳定氧化能量产生的因素，主要是通过防止毛细血管渗漏，来防止凝固性紊乱，现在看来，这些过程可以防止癌症以及所有与压力相关的退行性和炎性疾病。
Since hyperventilation can increase capillary leakage and cause the blood to become more concentrated, breathing carbon dioxide (breathing in a bag) should help to restore capillary function.
Since the blood becomes more concentrated, viscous, and clottable during the night (especially during long winter nights), the risk of a heart attack or stroke would probably be reduced by drinking orange juice before getting out of bed (and at bed-time), to dilute the blood and decrease adrenaline and the free fatty acids, which contribute to the increased tendency to form clots in the morning. (Assanelli, et al., discuss the importance of adrenaline in morning/winter sudden death; Antoniades and Westmoreland show that the availability of glucose can override major promoters of clotting and bleeding.)
由于过度换气会增加毛细血管的渗漏，使血液变得更集中，呼吸二氧化碳(在袋内呼吸)应该有助于恢复毛细血管功能。
因为血液变得更加集中、粘性和夜间clottable(特别是在漫长的冬夜),心脏病发作或中风的风险可能会减少喝橙汁在起床之前(在晚上),稀释血液,降低肾上腺素和游离脂肪酸,这就增加了早晨血栓形成的趋势。(Assanelli等人讨论了肾上腺素在清晨/冬季猝死中的重要性;Antoniades和Westmoreland的研究表明，葡萄糖的可用性可以压倒凝血和出血的主要促进因素。)
Things to reduce the stress-related coagulopathies: Sugar and niacin to minimize the liberation of fatty acids, progesterone and thyroid to protect against estrogen and to avoid hypoglycemia (which increases adrenaline and free fatty acids and accelerates clotting), magnesium and gelatin (or glycine), to protect against intracellular calcium overload and hypoxia, and vitamin E and salicylic acid for antiinflammatory effects, are major nutrients that protect the circulatory system against clotting, bleeding, edema, and tumefaction.
减少应激相关凝血疾病的方法:糖和烟酸，以减少脂肪酸的释放，黄体酮和甲状腺，以防止雌激素和避免低血糖(增加肾上腺素和游离脂肪酸，加速凝血)，镁和明胶(或甘氨酸)，以防止细胞内钙超载和缺氧，抗炎作用的维生素E和水杨酸是保护循环系统不凝血、出血、水肿和肿胀的主要营养物质。
Even on the mornings that you don’t drop dead, there is reduced adaptive capacity and functional impairment before eating breakfast. For example, men who went for a run before breakfast were found to have broken chromosomes in their blood cells, but if they ate breakfast before running, their chromosomes weren’t damaged.
即使在你没有倒地的早晨，在吃早餐之前也会有适应能力下降和功能障碍。例如，在早餐前跑步的男性被发现血细胞中的染色体已经损坏，但如果他们在跑步前吃早餐，他们的染色体没有损坏。
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Pediatr Crit Care Med. 2000 Jul;1(1):65-71. Administration of autologous fetal membranes: Effects on the coagulation in pregnant mini-pigs. Petroianu GA, Toomes LM, Maleck WM, Friedberg C, Bergler WF, Rufer R. “A hallmark of the so-called amniotic fluid embolism is the induction of coagulation defects. Entry of meconium-free autologous amniotic fluid into the circulation, however, is innocuous.” “Animals received 2 g FM [fetal membranes] (shredded and suspended in lactated Ringer's solution) via an ear vein. However, the full clinical picture of amniotic fluid embolism and disseminated intravascular coagulation could not be elicited despite the high dose of FM used.”
Am J Physiol. 1976 Apr;230(4):996-1002. Free fatty acids and albumin as mediators of thrombin-stimulated fibrinogen synthesis. Pickart LR, Thaler MM. “Mobilization of FFA in mice, triggered with an injection of thrombin, was followed within 24 h by a 2.5-fold increase in fibrinogen synthesis and a 30% increase in plasma fibrinogen concentration.”“Injection of exogenous defatted albumin into mice before thrombin injection prevented the FFA-associated rise in fibrinogen synthesis and plasma concentration.” “These studies indicate that the FFA/ALBUMIN RATIO MAY PLAY A MAJOR ROLE IN THE REPLENISHMENT OF FIBRINOGEN AFTER PERIODS OF RAPID DEFIBRINOGENATION.”
Thromb Haemost. 1995 Jul;74(1):391-5. Tissue factor expression in human leukocytes and tumor cells. Rickles FR, Hair GA, Zeff RA, Lee E, Bona RD. “Tissue factor (TF) exists in a cryptic form [i.e. without procoagulant activity (PCA)] in peripheral blood monocytes and quiescent tissue macrophages but is expressed constitutively in most human tumor cells.” “The regulation of TF synthesis in cells is complex and new information from transfection studies suggests that changes in cellular glycosylation pathways impair cell surface expression of functional TF.” “The importance of carbohydrate modification of TF is reviewed.”
Nature 138: 32 (1936). Selye, H. A Syndrome produced by diverse nocuous agents.
Int J Microcirc Clin Exp. 1996 Sep-Oct;16(5):266-70. Hyperventilation enhances transcapillary diffusion of sodium fluorescein. Steurer J, Schiesser D, Stey C, Vetter W, Elzi MV, Barras JP, Franzeck UK.
Lancet. 1991 Jul 6;338(8758):9-13. Seasonal variations in fibrinogen concentrations among elderly people. Stout RW, Crawford V. “Mortality and morbidity in elderly people are higher in winter than in summer months, with seasonal variations in rates of both fatal and non-fatal myocardial infarction and stroke.” “Significant seasonal effects were found for fibrinogen, plasma viscosity, and HDL cholesterol (p less than 0.003, Bonferroni adjustment). Plasma fibrinogen concentrations showed the greatest seasonal change and were 23% higher in the coldest six months compared with summer months. Fibrinogen was significantly (p less than 0.05) and negatively related to core body temperature and all measures of environmental temperature.” “Those living in institutions had greater changes in plasma fibrinogen than those living in the community. The seasonal variation in plasma fibrinogen concentration is large enough to increase the risk of both myocardial infarction and stroke in winter.”
Akush Ginekol (Mosk). 1989 Jan;(1):43-6. [Coagulative activity of the amniotic fluid][Article in Russian] Tersenov OA, Mikhaleva IV, Usol'tseva VA, Byshevskii Ash. “An ultracentrifugation study has shown thromboplastin to be the only blood coagulating agent, present in the amniotic fluid (AF). Its AF level shows no correlation to the rate of intrapartum or early postpartum thrombohemorrhagic complications….”
Metabolism. 1989 May;38(5):471-8. Effects of hypothyroidism on vascular 125I-albumin permeation and blood flow in Rats. Tilton RG, Pugliese G, Chang K, Speedy A, Province MA, Kilo C, Williamson JR. “Effects of hypothyroidism on vascular 125I-albumin permeation and on blood flow were assessed in multiple tissues of male Sprague-Dawley rats rendered hypothyroid by dietary supplementation with 0.5% (wt/wt) 2-thiouracil or by thyroidectomy.” “After 10 to 12 weeks of thiouracil treatment, 125I-albumin permeation was increased significantly in the kidney, aorta, eye (anterior uvea, choroid, retina), skin, and new granulation tissue….”
Clin Nutr. 2001 Aug;20(4):351-9. Effect of eicosapentaenoic acid (EPA) on tight junction permeability in intestinal monolayer cells. Usami M, Muraki K, Iwamoto M, Ohata A, Matsushita E, Miki A.
Carcinogenesis. 2003 Jun;24(6):1009-13. Epub 2003 Mar 28. Tissue factor signal transduction in angiogenesis. Versteeg HH, Peppelenbosch MP, Spek CA. Tissue factor (TF), a 47-kDa transmembrane glycoprotein, is a principal regulator of oncogenic neoangiogenesis and controls therefore the cancerous process. Although originally identified as a component of the coagulation cascade, it has become clear that TF functions as a cytokine-like receptor and this notion was confirmed by the discovery of coagulation-independent actions of TF (which include regulation of tumour growth, embryonic and oncogenic blood vessel formation as well as regulation of inflammation and sepsis). In accordance, TF-mediated signal transduction events are readily detected and the elucidation of the underlying molecular mechanisms has recently seen spectacular progress and it is now understood that the role of TF in angiogenesis is both coagulation-dependent and independent. The recent evidence for this emerging insight will be the subject of this review.
Semin Thromb Hemost. 2003 Jun;29(3):317-20. Occurrence of components of fibrinolytic pathways in situ in laryngeal cancer. Wojtukiewicz MZ, Sierko E, Zacharski LR, Rozanska-Kudelska M, Zimnoch L.
Semin Thromb Hemost. 2003 Jun;29(3):239-46. Malignancy as a solid-phase coagulopathy: implications for the etiology, pathogenesis, and treatment of cancer.Zacharski LR.
Thromb Res. 2003 Jun 1;110(4):213-4. Heparin treatment of malignancy: the case for clinical trials in colon cancer. Zacharski LR.
Anticancer Res. 2003 May-Jun;23(3C):2789-93. Low-molecular-weight heparin in oncology. Zacharski LR, Loynes JT.
Cancer Lett. 2002 Dec 1;186(1):1-9. Anticoagulants in cancer treatment: malignancy as a solid phase coagulopathy. Zacharski LR.
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