Leakiness, aging, and cancer
渗漏、衰老和癌症
by Raymond Peat
A thin layer of fibrin lining blood vessels provides a filtering barrier that helps to strengthen the wall and prevent other proteins from leaking out of the vessels, and it participates in repair processes when the blood vessel is broken.
血管内壁有一层薄薄的纤维蛋白，它提供了一个过滤屏障，帮助加强血管壁，防止其他蛋白质泄漏出血管，它还参与血管破裂时的修复过程。
Cellular energy metabolism is the basis for maintaining the barrier functions. Energy depletion causes the endothelial cells lining blood vessels to become excessively permeable.
细胞能量代谢是维持屏障功能的基础。能量消耗导致血管内皮细胞过度通透。
When the organism's resistance is low, proteins and fats that normally remain inside the bloodstream can escape into the extracellular matrix and enter cells, contributing to their stress and disorganization, and other materials can escape from cells and enter the bloodstream.
当机体抵抗力低下时，通常留在血液中的蛋白质和脂肪会逃逸到细胞外基质中，进入细胞，造成细胞的压力和紊乱，其他物质也会从细胞中逃逸，进入血液。
One of the simplest demonstrations of fibrin leakage is to shine a beam of light into the eye; the presence of fibrin and other inappropriate molecules diffuses the light, causing a “flare” in the aqueous compartment. Albumin, a small protein from the blood, is often seen in the urine during stress. The effects of that sort of leakage vary with each organ.
纤维蛋白渗漏的一个最简单的演示是用一束光照射眼睛;纤维蛋白和其他不适当分子的存在使光线漫射，在水腔中引起“耀斑”。白蛋白是血液中的一种小蛋白质，在压力大时，它常出现在尿液中。这种渗漏的影响因器官而异。
Fibrin is an essential structural and functional part of the organism, but when it escapes from the bloodstream it participates in the degenerative processes of inflammation, fibrosis, and tumor formation. (Its fragments stimulate secretion of inflammatory mediators: Hamaguchi et al., 1991.)
纤维蛋白是机体必不可少的结构和功能部分，但当它从血液中逃逸时，它参与了炎症、纤维化和肿瘤形成的退化过程。(其碎片刺激炎症介质的分泌:Hamaguchi et al.， 1991)。
In the hormonal environment dominated by estrogen, mild stresses such as exertion, or even restless sleep, allow toxins (and sometimes bacteria) from the intestine to enter the bloodstream, triggering a complex chain of events that create a systemic inflammatory state. Although these processes have been observed in many simple experiments, their implications are almost always neglected or denied or explained away. Incorporation of certain polyunsaturated fats into the tissues increases the leakiness of blood vessels, and amplifies the reactions to stresses and inflammatory stimuli.
在由雌激素主导的激素环境中，轻微的压力(如用力)，甚至不安分的睡眠，都会让毒素(有时是细菌)从肠道进入血液，引发一系列复杂的事件，造成全身炎症状态。尽管这些过程已经在许多简单的实验中被观察到，但它们的含义几乎总是被忽视、否认或解释掉。某些多不饱和脂肪与组织的结合增加了血管的渗漏，并放大了对压力和炎症刺激的反应。
Antioxidants, thyroid hormone, progesterone, and antiinflammatory agents, including glycine or gelatin, niacin, and saturated fats, can prevent, and in many cases reverse, these degenerative inflammatory processes.
抗氧化剂、甲状腺激素、黄体酮和抗炎剂，包括甘氨酸或明胶、烟酸和饱和脂肪，可以预防，并在许多情况下逆转这些退行性炎症过程。
Even a single celled organism has to keep its parts separate, and highly differentiated multicelled organisms have many special systems that serve to keep their parts separate, so the different tissues and organs can maintain their distinct functions.
即使是单细胞生物也必须保持各部分的分离，而高度分化的多细胞生物有许多特殊的系统来保持各部分的分离，所以不同的组织和器官可以保持它们不同的功能。
The movement of substances from blood to cell, and from cell to cell, is normally very tightly controlled, and when the systems that control those movements of water and its solutes are damaged, the tissues' structures and functions are altered. The prevention of inappropriate leakiness can protect against the degenerative processes, and against aging itself, which is, among other things, a state of generalized leakiness.
物质从血液到细胞，以及从一个细胞到另一个细胞的运动，通常是受到严格控制的，当控制水及其溶质运动的系统遭到破坏时，组织的结构和功能就会发生改变。防止不适当的渗漏可以防止退化过程，也可以防止老化本身，这是一种普遍渗漏的状态。
When cells' energy is depleted, water and various dissolved molecules are allowed to move into the cells, out of the cells, and through or around cells inappropriately. The weakened cells can even permit whole bacteria and similar particles to pass into and out of the blood stream more easily.
当细胞的能量耗尽时，水和各种溶解的分子被允许进入细胞，离开细胞，不适当地穿过或围绕细胞。被削弱的细胞甚至可以让整个细菌和类似的颗粒更容易地进出血液。
One of the earliest investigators of the effects of stress and fatigue on nerves and other cells was A.P. Nasonov, in the first half of the 20th century. A.S. Troshin (1956) has reviewed his work in detail. He showed that in cells as different as algae and nerve cells, fatigue caused them to take up dyes, and that the dyes were extruded, if the cells were able to recover their energy. When nerve cells are excited for a fraction of a second, they take up sodium and calcium, but quickly eliminate them. Prolonged excitation, leading to fatigue, can gradually shift the balance, allowing more substances to enter, and to stay longer.
20世纪上半叶，A.P.纳索诺夫(A.P. Nasonov)是最早研究压力和疲劳对神经和其他细胞影响的人之一。A.S. Troshin(1956)详细回顾了他的作品。他指出，在像藻类和神经细胞这样不同的细胞中，疲劳会使它们吸收染料，如果细胞能够恢复它们的能量，染料就会被挤压。当神经细胞兴奋了几分之一秒，它们会吸收钠和钙，但很快就会消除它们。长时间的兴奋，导致疲劳，可以逐渐改变平衡，允许更多的物质进入，并停留更长时间。
When nerves or other cells are quickly killed with heavy metals such as osmium, the metals are visible in a layer at the surface, which is sometimes taken as evidence of a “cytoplasmic membrane,” but if the cells have suffered oxygen deprivation or have been injured by X-rays, the metal will be visible as a grey color evenly distributed through the cell. The deposition of the metal occurs when it reacts with electrons. In the relatively vital cell, the heavy metal stops at the surface, and is mostly reduced there, but the devitalized cell presents no structural or chemical barrier to the entry of the metal, and the reactive electrons appear to be evenly distributed through the cell. Oxygen deprivation, X-irradiation, and other stresses cause the cell to be unable to use electrons to produce energy, and instead the electrons are available to react destructively with whatever may be available. While Nasonov showed that dyes and even particles enter energetically depleted cells, newer techniques are able to show that the leaky cells are structurally disrupted by the excessive reduction of their proteins, by excited electrons and free radicals.
当神经或其他细胞被锇等重金属迅速杀死时，这些金属会出现在细胞表面的一层，这有时被认为是“细胞质膜”的证据，但如果细胞遭受缺氧或被x射线损伤，这种金属会以灰色的颜色均匀地分布在整个细胞中。当金属与电子反应时就会沉积。在生命力相对较强的细胞中，重金属停留在细胞表面，并主要在那里被还原，但失去生命力的细胞对金属的进入没有结构上或化学上的障碍，而活性电子似乎均匀地分布在整个细胞中。缺氧、x射线照射和其他压力导致细胞不能利用电子产生能量，相反，电子可以与任何可能的物质发生破坏性反应。当纳索诺夫证明染料甚至粒子进入能量耗尽的细胞时，更新的技术能够证明泄漏的细胞在结构上是被蛋白质的过度还原、被激发的电子和自由基破坏的。
In the 1970s, experimenters found that muscles from vitamin E deficient animals released their enzymes when washed in a saline solution, more easily than did the muscles from vitamin E replete animals. Other experiments around the same time showed that reducing the ATP of muscles caused a similar loss of their ability to retain their proteins.
在20世纪70年代，实验人员发现维生素E缺乏的动物的肌肉在盐水中洗涤时比维生素E充足的动物的肌肉更容易释放酶。大约在同一时间的其他实验表明，减少肌肉的ATP会导致它们失去保留蛋白质的能力。
Over the years, many experiments have established, both in vitro and in vivo, that fatigue, stress, aging, and inflammation cause cells to lose their normal constituents, but also to allow foreign materials to enter more easily.
多年来，许多体外和体内实验都证实，疲劳、压力、老化和炎症会导致细胞失去其正常成分，但也会让外来物质更容易进入细胞。
When I was working on my thesis, around 1970, investigating the effects of aging on the metabolism of the uterus, I found that the changes occuring during aging were (in all the ways I tested) the same as those produced by X-irradiation, excess estrogen, oxygen deprivation, excess polyunsaturated fats, and vitamin E deficiency.
当我在我的论文工作,大约在1970年,研究老化的影响子宫的新陈代谢,我发现在衰老过程中发生的变化(在所有的方面我测试)产生的相同X-irradiation,多余的雌激素,缺氧,多余的多不饱和脂肪,维生素E缺乏症。
Although everyone working in the lab was familiar with the appearance of the uterus from old hamsters (they are typically large, stiff, and bluish), everyone was surprised when I suggested that the aged uteri seemed to function as if they were under the influence of a considerable amount of estrogen. Everyone was familiar with the medical textbook doctrine that “menopause is caused by estrogen deficiency.” In humans, gynecologists know about “Chadwick's sign,” the fact that the uterine cervix turns blue or purple during pregnancy, and everyone knows that blood is blue when it's deprived of oxygen, so it's surprising that estrogen's effect on tissue oxygenation isn't widely recognized.
尽管在实验室工作的每个人都熟悉老仓鼠子宫的外观(它们通常是大的，僵硬的，蓝色的)，但当我说老的子宫似乎在相当数量的雌激素的影响下发挥作用时，每个人都感到惊讶。每个人都熟悉医学教科书的教条“更年期是由雌激素缺乏引起的。”在人类中，妇科医生知道“查德威克症”，即子宫颈在怀孕期间会变成蓝色或紫色，每个人都知道血液在缺氧时是蓝色的，所以雌激素对组织氧化的作用没有被广泛认识是令人惊讶的。
When estrogen is given to an animal, it almost instantly causes capillaries to become leaky, allowing water to move out of the blood stream, and at the same time, estrogen causes cells to take up water. Both of these processes are the same as the early effects of oxygen deprivation. In the normal reproductive cycle, the surge of estrogen lasts only a few hours, and normal permeability is quickly restored by increasing progesterone. During those intermittent short exposures to estrogen, there isn't a massive leakage of serum proteins into the tissues. During the time of estrogenic influence, all kinds of cells are influenced, with the excitatory equilibrium of nerve cells, glandular cells, and immune system cells being shifted, lowering the threshold of excitation, or prolonging the excited state.
当雌性激素被注射到动物体内时，它几乎会立即导致毛细血管漏水，让水分流出血液，同时，雌性激素会导致细胞吸收水分。这两个过程与缺氧的早期影响是一样的。在正常的生殖周期中，雌激素的激增只会持续几个小时，而通过增加孕酮，正常的渗透性很快就会恢复。在这些间歇的短暂雌激素暴露期间，没有大量的血清蛋白泄漏到组织中。在雌激素影响期间，各种细胞都受到影响，神经细胞、腺细胞、免疫系统细胞的兴奋平衡发生改变，兴奋阈值降低，或兴奋状态延长。
Anything that causes inflammation causes a similar loss of water from the blood, as it is taken up by swelling cells. If inflammation is generalized, it causes circulatory shock, because the volume of the blood has become insufficient to serve the organism's needs. One of Hans Selye's earliest observations of the effect of an overdose of estrogen was that it causes shock.
任何引起炎症的东西都会导致血液中的水分流失，因为水分会被肿胀的细胞吸收。如果炎症蔓延，就会引起循环休克，因为血液容量已经不足以满足机体的需要。汉斯·塞利耶(Hans Selye)对过量雌激素影响的最早观察之一是，它会导致休克。
Although water loss causes the blood to become more viscous under the influence of estrogen, the plasma becomes hypotonic, meaning that it contains fewer osmotically active solutes than normal; some of the sodium that helps to maintain the blood's osmotic balance is lost through the kidneys, and some is taken up by the red blood cells and other cells. The osmotic imbalance of the blood causes tissue cells to take up more water, contributing to their increased excitability. In many cases, the vascular leakage of inflammation and shock can be corrected by using osmotically active substances, such as starch solutions, gelatin, or concentrated sodium chloride.
虽然水分流失导致血液在雌激素的影响下变得更粘稠，血浆变成低渗，这意味着它含有比正常更少的渗透活性溶质;一些帮助维持血液渗透平衡的钠会通过肾脏流失，而一些则会被红血球和其他细胞吸收。血液的渗透性不平衡导致组织细胞吸收更多的水分，从而增加了它们的兴奋性。在许多情况下，炎症和休克的血管渗漏可以通过使用渗透活性物质，如淀粉溶液、明胶或浓氯化钠来纠正。
The tissue water retention caused by estrogen, hypoxia, and stress is analogous to the swelling of gels and colloids, that is, it's governed by the state of the electrons and counterions in the system. Excitation, fatigue, or injury can cause a shift of pH toward alkalinity, causing water uptake and swelling.
由雌激素、缺氧和压力引起的组织水分保留类似于凝胶和胶体的膨胀，也就是说，它是由系统中电子和反离子的状态控制的。兴奋、疲劳或损伤会导致pH值向碱性转移，导致水分吸收和肿胀。
The blue color of the pregnant cervix, or of the uterus in an animal given an overdose of estrogen, indicates that the tissue isn't sufficiently oxygenated to maintain its normal red color, even though the flow of blood is increased. Some experimenters have noticed that newborn animals sometimes have the postural reflex (lordosis) that indicates an estrogenic state, and that suffocation can produce the same reflex. Irradiating animals with x-rays will also produce the whole range of estrogenic effects.
被注射过量雌激素的动物的子宫颈或子宫呈蓝色，表明即使血液流量增加，该组织也没有足够的氧气来维持其正常的红色。一些实验者注意到，新生的动物有时会有姿势反射(前凸)，这表明一种雌激素状态，而窒息可以产生相同的反射。用x射线照射动物也会产生各种各样的雌激素效应。
One of the features of the aged uterus that I studied was the age pigment, lipofuscin, a brown waxy material that accumulates in old or stressed tissues. Prolonged dosage with estrogen accelerates the formation of this pigment, which is largely derived from oxidized polyunsaturated fatty acids. Increased amounts of those fats in the diet, or a deficiency of vitamin E, or exposure to ionizing radiation, or oxygen deprivation, can also accelerate the formation of the age pigment. The presence of the pigment intensifies the effect of estrogen, since the pigment wastes oxygen by functioning as an oxidase enzyme.
我研究的衰老子宫的特征之一是衰老色素，脂褐素，一种在衰老或压力组织中积累的棕色蜡状物质。长时间服用雌激素会加速这种色素的形成，这种色素主要来自氧化的多不饱和脂肪酸。饮食中增加这些脂肪，或缺乏维生素E，或暴露于电离辐射，或缺氧，也会加速年龄色素的形成。色素的存在增强了雌激素的作用，因为色素通过氧化酶的功能消耗氧气。
Other tests that I did on aged, or estrogenized, uterine tissue indicated that several oxidative systems were activated; for example, the tissues showed an extremely high activity of the enzyme peroxidase, and a very intense reduction of a chemical dye (tetrazolium/formazan) that indicates the presence of reductive and oxidative activity, of the sorts caused by radiation and oxygen deprivation. These reductive and oxidative processes include the production of some free radicals that are capable of reacting randomly with polyunsaturated fatty acids.
我对衰老或雌激素化的子宫组织做的其他测试表明，一些氧化系统被激活;例如，这些组织表现出极高的过氧化物酶活性，一种化学染料(四唑/福马赞)的强烈还原，表明存在由辐射和缺氧引起的还原和氧化活性。这些还原和氧化过程包括一些自由基的产生，这些自由基能够与多不饱和脂肪酸随机反应。
The interactions between estrogen and the polyunsaturated fats are now coming to be more widely recognized as important factors in the inflammatory/hyperpermeable conditions that contribute to the development of heart and blood vessel disease, hypertension, cancer, autoimmune diseases, dementia, and other less common degenerative conditions.
雌性激素之间的相互作用和多不饱和脂肪现在来被广泛认为是重要的因素在炎症/高渗透条件导致心脏和血管疾病的发展,高血压、癌症、自身免疫性疾病、痴呆、和其它不太常见的退行性条件。
Estrogen increases lipid peroxidation, and maintains a chronically high circulating level of free fatty acids, mainly PUFA, activates the phospholipases that release arachidonic acid from cells leading to formation of prostaglandins and isoprostanes, and increases the enzymes that form the inflammation-promoting platelet activating factor (PAF) while suppressing the enzymes that destroy it, and increases a broad range of other inflammatory mediators, interleukins, and NF-kappa B.
雌激素增加脂质过氧化，并维持长期高水平的游离脂肪酸，主要是多不饱和脂肪酸，激活磷脂酶，从细胞中释放花生四烯酸，导致前列腺素和异前列腺素的形成，并增加形成炎症促进血小板激活因子(PAF)的酶，同时抑制破坏它的酶，并增加广泛的其他炎症介质，白细胞介素和NF-kappa B。
The leakage of enzymes out of cells and into the blood stream is recognized medically as evidence of damage to the organ that is losing them. Different combinations of enzymes are commonly considered to be evidence of a heart attack, or skeletal muscle damage, or liver disease, pancreatitis, prostate cancer, etc. But often the reason for the leakage isn't understood. Hypothyroidism, for example, causes leakage of enzymes, possibly mainly from the liver, but also from other organs. Excess estrogen, intense exercise, starvation, anything that increases lipid peroxidation and free radical production, such as drinking alcohol when the tissues contain polyunsaturated fats, can cause organs such as heart and liver to leak their components.
从医学上讲，酶从细胞中泄漏到血液中被认为是失去它们的器官受到损害的证据。酶的不同组合通常被认为是心脏病发作、骨骼肌损伤、肝病、胰腺炎、前列腺癌等的证据。但通常泄漏的原因还不清楚。例如，甲状腺机能减退会导致酶的泄漏，可能主要来自肝脏，但也可能来自其他器官。过量的雌性激素、剧烈运动、饥饿，以及任何增加脂质过氧化和自由基产生的行为，比如当组织中含有多不饱和脂肪时饮酒，都会导致心脏和肝脏等器官的成分泄漏。
The loss of enzymes increases the energy needed to stay alive, but it doesn't necessarily change the basic functions of the cell. (Though when mitochondrial enzymes leak out into the cytoplasm, the cell's energy metabolism is impaired, at least temporarily.) But the entry of catalytic materials from other tissues changes the organization of a cell, giving it conflicting instructions. In many situations, as L.V. Polezhaev and V. Filatov demonstrated, the substances released during stress and degeneration serve to stimulate healing and regeneration. But when the resources aren't available for full repair or regeneration, only a scar, or atrophic fibrosis, or a tumor will be formed.
酶的丧失增加了维持生命所需的能量，但并不一定会改变细胞的基本功能。(不过，当线粒体酶渗入细胞质时，细胞的能量代谢会受到损害，至少是暂时的。)但是来自其他组织的催化物质的进入改变了细胞的结构，给了它相互矛盾的指令。Polezhaev和V. Filatov证明，在许多情况下，压力和退化过程中释放的物质有助于促进愈合和再生。但当资源无法完全修复或再生时，就会形成疤痕、萎缩性纤维化或肿瘤。
In severe stress, intracellular fibrin deposits have been found in the heart and other organs, including the prostate gland. Deficiency of testosterone causes vascular leakage into the prostate. Fibrin promotes tumor growth, partly by serving as a matrix, partly by releasing stimulatory peptides.
在严重压力下，在心脏和其他器官，包括前列腺，发现了细胞内纤维蛋白沉积。睾酮缺乏会导致血管漏入前列腺。纤维蛋白促进肿瘤生长，部分是通过作为基质，部分是通过释放刺激肽。
Kidney disease, diabetes, pregnancy toxemia and retinal degeneration are probably the best known problems involving vascular leakage, but increasingly, cancer and heart disease are being recognized as consequences of prolonged permeability defects. Congestive heart failure and pulmonary hypertension commonly cause leakage of fluid into the lungs, and shock of any sort causes the lung to get “wet,” a waterlogged condition called “shock lung.” Simply hyperventilating for a couple of minutes will increase leakage from the blood into the lungs; hyperventilation decreases carbon dioxide, and increases serotonin and histamine. Hyperoxia itself contributes to lung injury, and exacerbates emphysema, though it is common to see patients breathing a high concentration of oxygen. Emphysema (which can be caused by hypothyroidism or hyper-estrogenism, and often can be cured by thyroid or progesterone) and many other respiratory problems are associated with capillary leakage. Cells of the lung and intestine are able to synthesize their own fibrin, apparently because of their special problems in preventing leakage. Prolonged systemic inflammation can lead to lung fibrosis, and fibrosis increases the likelihood of lung cancer.
肾脏疾病、糖尿病、妊娠毒血症和视网膜变性可能是涉及血管渗漏的最著名的问题，但越来越多的癌症和心脏病被认为是长期通透性缺陷的后果。充血性心力衰竭和肺动脉高压通常会导致液体漏入肺部，任何类型的休克都会导致肺变得“湿”，这种被水浸湿的情况称为“休克肺”。简单地用力呼吸几分钟会增加血液向肺部的渗漏;过度换气减少二氧化碳，增加血清素和组胺。高氧本身会导致肺损伤，并加剧肺气肿，尽管病人呼吸高浓度氧气是很常见的。肺气肿(可由甲状腺功能减退或雌激素过多引起，通常可通过甲状腺或孕酮治愈)和许多其他呼吸问题都与毛细血管渗漏有关。肺和肠的细胞能够合成它们自己的纤维蛋白，显然是因为它们在防止渗漏方面的特殊问题。长期的全身炎症会导致肺纤维化，而肺纤维化会增加肺癌的可能性。
The inflammatory state that causes exaggerated cellular permeability is very closely related to “hyperventilation,” the loss of too much carbon dioxide. The release of serotonin during hyperventilation isn't the only cause of vascular leakage; the carbon dioxide itself is an essential factor in regulating the state of cellular electrons and in maintaining cellular integrity. Hyperventilation, like the shift from oxidative to glycolytic energy production that typifies estrogenized or stressed cells or cancer, raises intracellular pH. In the case of mast cells, increasing alkalinity causes them to release histamine (Alfonso, et al., 2005), but similar “alkaline-induced exocytosis” seems to occur in all stressed tissues.
导致细胞通透性过度的炎症状态与“过度通气”(失去过多的二氧化碳)密切相关。过度换气时血清素的释放并不是血管渗漏的唯一原因;二氧化碳本身是调节细胞电子状态和维持细胞完整性的重要因素。换气过度,就像从氧化转变为糖酵解能量生产,完全是雌激素主导或强调细胞或癌症,提高细胞内博士在肥大细胞的情况下,增加碱性会使他们释放组胺(阿方索,et al ., 2005),但类似“碱性引导的胞外分泌”似乎发生在所有强调组织。
The blood platelets that become incontinent and leak serotonin in the absence of carbon dioxide are undergoing the same structural stresses experience by endothelial cells, smooth muscle cells, mast cells and all other cells when carbon dioxide is depleted. Although it has been about 70 years since Yandell Henderson made it clear that supplemental oxygen should be combined with carbon dioxide, mechanical ventilation in hospitals is still causing lung injury resulting from hyperventilation, i.e., the absence of carbon dioxide. A similar misunderstanding of biology was involved in the use of dialysis to treat kidney disease. Until recently, commercial dialysis fluids contained acetate and/or racemic lactate instead of bicarbonate, because of the difficulty of preparing bicarbonate solutions, and the result was that very prolonged dialysis would damage the brain and other organs. (Veech and Gitomer, 1988, Veech and Fowler, 1987.) Dialysis has been seen to increase lung permeability Bell, et al., 1988).
在没有二氧化碳的情况下，血小板失禁并泄漏血清素，当二氧化碳耗尽时，内皮细胞、平滑肌细胞、肥大细胞和所有其他细胞都经历了同样的结构压力。虽然自从Yandell Henderson明确指出辅助氧气应与二氧化碳结合已经有70年的历史了，但医院的机械通气仍然会因为过度通气(即缺乏二氧化碳)而导致肺损伤。使用透析治疗肾脏疾病也涉及到类似的生物学误解。直到最近，商业透析液中都含有醋酸盐和/或外消位乳酸盐，而不是碳酸氢盐，因为制备碳酸氢盐溶液很困难，结果是长时间的透析会损害大脑和其他器官。(Veech和Gitomer, 1988; Veech和Fowler, 1987)透析可增加肺通透性Bell等人，1988)。
Amyloidosis produced by chronic dialysis affects all organs, but its effects are best known in the brain, heart, kidneys, and lungs. Serum amyloid-A is one of the acute phase proteins, like C-reactive protein (CRP), that are produced by inflammation. Estrogen, radiation and other stresses increase those pro-inflammatory acute phase proteins, and decrease protective albumin, which is called a “negative acute phase protein,” since it decreases when the other acute phase proteins increase. The liver is the major source of the acute phase proteins, and it is constantly burdened by toxins absorbed from the bowel; disinfection of the bowel is known to accelerate recovery from stress.
慢性透析引起的淀粉样变影响所有器官，但其影响在大脑、心脏、肾脏和肺部最为明显。血清淀粉样蛋白- a是一种急性期蛋白，与c反应蛋白(CRP)一样，由炎症产生。雌激素、辐射和其他压力增加了促炎急性期蛋白，减少了被称为“负急性期蛋白”的保护白蛋白，因为当其他急性期蛋白增加时，保护白蛋白减少。肝脏是急性期蛋白质的主要来源，它经常被肠道吸收的毒素所负担;肠道消毒可以加速压力恢复。
Seen from the perspective of the stress-leakage syndrome, any serious injury or sickness damages all organs. The exhaled breath is being used to diagnose inflammatory lung disease, since so many of the mediators of inflammation are volatile, but systemic diseases such as cancer and arthritis, and relatively minor stress can be detected by changes in the chemicals found in the breath. Polyunsaturated fats and their breakdown products–aldehydes, prostaglandins, isoprostanes, hydrocarbons, and free radicals–and carbon monoxide, nitric oxide, nitrite, and hydrogen peroxide are increased in the breath by most stresses. Both proline and glycine (which are major amino acids in gelatin) are very protective for the liver, increasing albumin, and stopping oxidative damage.
从压力渗漏综合征的角度来看，任何严重的损伤或疾病都会损害所有器官。呼出的气体被用来诊断炎症性肺病，因为许多炎症介质都是挥发性的，但系统性疾病，如癌症和关节炎，以及相对较小的压力可以通过呼吸中发现的化学物质的变化检测到。多不饱和脂肪及其分解产物——醛、前列腺素、异前列腺素、碳氢化合物和自由基——以及一氧化碳、一氧化氮、亚硝酸盐和过氧化氢在大多数压力下都会在呼吸中增加。脯氨酸和甘氨酸(明胶中的主要氨基酸)都对肝脏非常有保护作用，增加白蛋白，并阻止氧化损伤。
Saturated fats are protective against free radical damage and can reverse liver fibrosis. Thyroid hormone protects against excess estrogen, and can prevent or reverse fibrosis of the heart. Antiestrogens are widely effective against vascular leakage. Thyroid, progesterone, and testosterone are among the most effective natural antiestrogens, and they are curative in many conditions that involve vascular leakage. Progesterone and pregnenolone have been called the antifibromatic steroids, and it has been used to treat many inflammatory and fibrotic diseases, including cancer.
饱和脂肪能防止自由基损伤，并能逆转肝纤维化。甲状腺激素可以防止过量的雌激素，并可以防止或逆转心脏纤维化。抗雌激素对血管渗漏有广泛的疗效。甲状腺、孕酮和睾酮是最有效的天然抗雌激素，它们在许多涉及血管渗漏的情况下都有疗效。孕酮和孕烯酮被称为抗纤维化类固醇，它被用于治疗包括癌症在内的许多炎症和纤维化疾病。
The antiserotonin drugs are being increasingly used to treat fibrotic diseases, and other problems related to vascular leakage.
抗血清素药物正越来越多地用于治疗纤维化疾病和其他与血管渗漏有关的问题。
Anti-inflammatory and anticoagulant things, especially aspirin and vitamin E, protect against the accelerated turnover of fibrinogen/fibrin caused by estrogen and the various inflammatory states.
抗炎和抗凝药物，特别是阿司匹林和维生素E，可以防止雌激素和各种炎症状态导致的纤维蛋白原/纤维蛋白加速转换。
http://raypeat.com/articles/articles/leakiness.shtml
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本文出自Ray Peat 2005/05时事通讯 标题上面的文字是：
Folly is the cloak of knavery. ——威廉·布莱克