Water: swelling, tension, pain, fatigue, aging
水:肿胀、紧张、疼痛、疲劳、衰老
by Raymond Peat
I have spoken to many people who believe they should drink “8 glasses of water every day,” in addition to their normal foods, even if they don't feel thirsty. Many doctors still recite this dangerous slogan, but the addition of the qualifying phrase, “or other liquids,” has become common.
我和许多人交谈过，他们认为除了正常的食物外，他们每天应该喝“8杯水”，即使他们不觉得口渴。许多医生仍在背诵这一危险的口号，但加上“或其他液体”的限定短语已变得普遍。
The amount of water a person needs is extremely variable, depending on things such as metabolic rate, activity, and the temperature and humidity of the air. Working hard in hot, dry weather, it's possible to drink more than two quarts per hour for more than eight hours, without forming any urine, because all of the water is lost by evaporation. But in very hot, humid weather, a person with a low metabolic rate can be endangered by the smallest amount of water (e.g., “Meteorological relations of eclampsia in Lagos, Nigeria,” Agobe, et al., 1981).
一个人需要的水量是非常多变的，取决于代谢率、活动以及空气的温度和湿度等因素。在炎热干燥的天气里努力工作，你可能每小时喝两夸脱以上的水，持续八小时以上，而不会形成任何尿液，因为所有的水分都通过蒸发蒸发掉了。但在非常炎热、潮湿的天气中，代谢率低的人可能会受到少量水的威胁(例如，“尼日利亚拉各斯子痫的气象关系”，Agobe等人，1981)。
Most foods contain a considerable amount of water, usually more than 70% of their weight, and some water is produced in cells by metabolism. The function of water in the organism has been mystified and neglected because of some deeply rooted cultural images of the nature of organisms and their cellular make-up.
大多数食物含有大量的水，通常超过其重量的70%，有些水是在细胞代谢过程中产生的。水在生物体中的作用一直被迷惑和忽视，因为一些根深蒂固的文化形象，对生物体的本质及其细胞组成。
One silly image that has been perpetuated by schools and textbooks is that biochemistry consists of chemical reactions that occur in substances dissolved in water, and that the water is retained by cells because they are enclosed by an oily membrane, and because of the osmotic forces produced by the dissolved substances. Most grade school kids have seen an osmometer made from an egg, in which the egg causes a column of water to rise, and have heard the explanation that this has something to do with the way cells work. Membrane pumps are invoked to explain the differences in solute concentrations and “osmotic pressure” inside and outside cells. The story is that invisible things on the surface of a cell (in its “membrane”) force dissolved molecules to move in ways that they wouldn't move spontaneously by diffusion, and that water passively follows the “actively transported” solutes. But the evidence shows that both water and its solutes are regulated by the bulk phase of the cell, not its surface.
一个愚蠢的形象已经被学校和延续教科书是生物化学的化学反应发生在物质溶解在水中,水是由细胞保留,因为它们是封闭的油膜,由于产生的渗透力量溶解物质。大多数小学生都见过一个由鸡蛋制成的渗透计，鸡蛋使水柱上升，并听说这与细胞工作的方式有关。膜泵被用来解释细胞内外溶质浓度和“渗透压”的差异。这个故事是这样的:细胞表面(其“膜”)上看不见的东西迫使溶解的分子以它们不会通过扩散自发运动的方式运动，而水是被动地跟随“主动运输”的溶质运动的。但有证据表明，水和它的溶质都是由细胞的体积阶段而不是表面来调节的。
In some cultural settings, animism has a kind of charm (water sprites, and such), but in the culture of medicine and biology, the animistic conceptualization of cells and their mechanisms has been very destructive, because it gets in the way of coherent understanding of physiology. Practically every disease would be approached differently if the physiology of water and ions were allowed to advance beyond the animistic doctrines of mainstream medicine, such as the “membrane pumps.” If all the substances that are said to be “actively transported” by pumps into, or out of, cells are considered, the amount of energy required to operate the pumps is at least 15 times larger than the total energy available to cells. “Specific” pumps are commonly invoked even for novel synthetic chemicals, to explain their unequal distribution, inside and outside cells. In many biological situations water is ignored, but when it becomes an issue, its distribution is usually mechanistically subordinated to the solutes that are actively “pumped.”
在某些文化背景下，万物有灵论具有某种魅力(水精灵之类的)，但在医学和生物学文化中，万物有灵论对细胞及其机制的概念化具有非常大的破坏性，因为它妨碍了对生理学的连贯理解。如果允许水和离子的生理学超越主流医学的万物有灵论学说，比如“膜泵”，那么几乎每一种疾病都将以不同的方式处理。如果考虑所有所谓的被泵“主动输送”到细胞或被泵出细胞的物质，那么操作泵所需的能量至少要比细胞可获得的总能量大15倍。“特殊”泵甚至经常被用于新型合成化学品，以解释它们在细胞内外的不均匀分布。在许多生物环境中，水被忽略了，但当它成为一个问题时，它的分布通常在机械上服从于积极“泵送”的溶质。
Cells aren't osmometers, in the sense the textbooks say. They do control their water content, but no “membrane pumps” are needed. It's more accurate to think of the water of cells as being “dissolved in cells,” somewhat the way water is contained in jello or boiled eggs. The cell controls its hydration by the processes that control its structure, its metabolism, and movements, because water is part of its deepest structures and essential functions. The cell's adjustments to changes of hydration and volume appear to be regulated by contractile proteins and energy metabolism (Minkoff and Damadian, 1976).
细胞不是教科书上所说的那种渗透计。它们确实控制了水分含量，但不需要“膜泵”。更准确的说法是，细胞中的水“溶解在细胞中”，就像果冻或煮鸡蛋中的水一样。细胞通过控制其结构、新陈代谢和运动的过程来控制其水合作用，因为水是细胞最深层结构和基本功能的一部分。细胞对水合作用和体积变化的调节似乎是由收缩蛋白和能量代谢调节的(Minkoff和Damadian, 1976)。
Any stress or energy deficit that disturbs cellular structure or function disturbs the interactions among water, proteins, and other components of the cell. Excitation causes a cell to take up extra water, not by osmosis resulting from an increase in the concentration of solutes in the cell, or because the membrane has become porous, but because the structural proteins of the cell have momentarily increased their affinity for water.
任何扰乱细胞结构或功能的压力或能量不足都会扰乱水、蛋白质和细胞其他成分之间的相互作用。激发使细胞吸收额外的水，不是由于细胞中溶质浓度增加而产生的渗透作用，也不是因为细胞膜变得多孔，而是因为细胞的结构蛋白暂时增加了它们对水的亲和力。
This increased affinity is similar to the process that causes a gel to swell in the presence of alkalinity, and it is related to the process called electroosmosis, in which water moves toward a higher negative charge. Intense excitation or stress increases the cell's electrically negative charges, and causes it to become more alkaline and to swell. Swelling and alkalinity cause the cell to begin the synthesis of DNA, in preparation for cell division. Mitogens and carcinogens, including estrogen, cause cells to become alkaline and to swell, and substances that block the cell's alkalinization (such as the diuretics acetazolamide and amiloride) inhibit cell division. Prolonged alkaline stress alone can cause malignant transformation of kidney cells (Oberleithner, et al., 1991).
这种增加的亲和力类似于凝胶在碱度存在时膨胀的过程，它与电渗透过程有关，在电渗透过程中，水向更高的负电荷移动。强烈的激发或压力增加了细胞的负电荷，使其变得更碱性并膨胀。肿胀和碱性导致细胞开始合成DNA，为细胞分裂做准备。有丝分裂原和致癌物质，包括雌激素，导致细胞变碱性和膨胀，而阻止细胞碱化的物质(如利尿剂乙酰唑胺和阿米洛利)抑制细胞分裂。单独延长碱性应激可引起肾细胞的恶性转化(Oberleithner等，1991)。
The general idea of “stress” is useful, because it includes processes such as fatigue, osmotic pressure changes, disturbed pH, and the enzyme changes that follow, producing substances such as lactic acid, nitric oxide, polyamines, estrogen, serotonin, and many more specific mediators. But paying attention to the physical factors involved in a stress reaction is important, if we are to see the organism integrally, rather than as a collection of “specific biological mechanisms,” involving things like the pixie-powered “membrane pumps.”
“压力”的一般概念是有用的，因为它包括疲劳、渗透压变化、pH值紊乱以及随之而来的酶变化等过程，产生乳酸、一氧化氮、多胺、雌激素、血清素和许多更具体的介质。但是，如果我们要从整体上看待这个有机体，而不是把它看作一系列“特定的生物机制”的集合，比如精灵动力的“膜泵”，那么关注应激反应中涉及的物理因素是很重要的。
When a cell shrinks under hyperosmolar conditions, its metabolism becomes catabolic, breaking down proteins and glycogen, and sometimes producing lactic acid, which results in an alkaline shift, increasing the cell's affinity for water, and causing it to return to normal size. A slight degree of hyperosmolarity increases the cell's metabolic rate.
Swelling in hypo-osmolar conditions, i.e,, with an excess of water, is anabolic, leading to cellular proliferation, and inhibiting the breakdown of protein and glycogen.
当细胞在高渗条件下萎缩时，它的代谢变成分解代谢，分解蛋白质和糖原，有时产生乳酸，乳酸导致碱性转移，增加细胞对水的亲和力，并使其恢复到正常大小。轻微的高渗会增加细胞的代谢率。
在低渗条件下，即水分过多时，肿胀是合成代谢，导致细胞增殖，抑制蛋白质和糖原的分解。
Respiring cells are always producing some water, by transferring hydrogen from fuel molecules to oxygen. Respiration also produces carbon dioxide, which in itself is a Lewis acid (meaning that it binds electrons, rather than releasing protons), that associates with cellular proteins, acidifying them in the process. A large amount of carbon dioxide can exist inside cells in the bound form. Acidified cytoplasm (like any other mostly acidic polymer-gel) releases water and sodium. (This process is physically analogous to the process of flushing a water softener with salt, or a demineralizer with acid, to reactivate it.)
呼吸细胞总是通过将氢从燃料分子转移到氧分子而产生一些水。呼吸作用也会产生二氧化碳，二氧化碳本身就是一种路易斯酸(意思是它结合电子，而不是释放质子)，它与细胞蛋白质结合，在这个过程中酸化细胞蛋白质。大量的二氧化碳可以以束缚的形式存在于细胞内。酸化的细胞质(就像其他大多数呈酸性的聚合物凝胶一样)释放出水和钠。(这个过程在物理上类似于用盐冲洗水柔软剂，或用酸冲洗除盐剂，以使其重新活化。)
Besides binding with the cytoplasm, the carbon dioxide can be changed into carbonic acid, by chemically combining with water. Carbonic acid is hydrophilic, and so it quickly leaves the cell, taking with it some of the oppositely charged ions, such as calcium and sodium. The formation of carbonic acid, which is constantly streaming out of the respiring cell, causes some water and some positively ionized metals to leave the cell, in an “active” process, that doesn't require any mysterious pumps.
除了与细胞质结合外，二氧化碳还可以通过与水的化学结合而变成碳酸。碳酸是亲水的，所以它会很快离开细胞，带走一些相反的离子，比如钙离子和钠离子。碳酸的形成，不断地从呼吸的细胞中流出，导致一些水和一些正离子金属离开细胞，这是一个“活跃的”过程，不需要任何神秘的泵。
As the blood passes through the lungs, carbon dioxide leaves the system, and as carbonic acid is converted to carbon dioxide, water is left behind in the blood, along with the counterions (of alkaline metals or earths), accounting for slight differences in pH and osmolarity between the bloodstream and the tissue cells. Some experiments suggest that the normal osmolarity of various tissues is 2 or 3 times higher than that of the blood, which is called “isosmolar” or isotonic.
血液通过肺部,二氧化碳离开系统,以及碳酸转化为二氧化碳、水是血液中留下,连同抗衡离子(碱性金属或地球),轻微的pH值和渗透性的差异占血液与组织细胞之间。有些实验表明，各种组织的正常渗透压比血液的渗透压高2或3倍，称为“等摩尔”或等渗。
The kidneys adjust the osmolarity of the blood by allowing water and solutes to leave the bloodstream, in proportions that usually keep the body fluids in balance with cells. The kidneys are able to compensate for many of the imbalances produced by stress and inappropriate diets, for example by forming ammonia and carbon dioxide, to compensate for imbalances in the alkalis and acids that are being delivered to the blood by other organs. Because of the kidneys' great ability to regulate the flow of solutes between the blood and the forming urine, the “membrane pumps” have great importance for medical nephrologists. But the more extreme the “active transport” is, the more obvious it becomes that processes other than “membrane pumps” are responsible.
肾脏通过允许水和溶质离开血液来调节血液的渗透压，其比例通常保持体液与细胞的平衡。肾脏能够弥补许多由压力和不适当饮食造成的失衡，例如通过形成氨和二氧化碳，来弥补由其他器官输送到血液中的碱和酸的失衡。由于肾脏有很大的能力来调节溶质在血液和形成的尿液之间的流动，“膜泵”对医学肾病学家有很大的重要性。但是，“主动运输”越极端，其作用就越明显，而不是“膜泵”。
Some lizards and sea birds have glands near their noses that are called salt glands, because of their ability to secrete salt. The salt gland is probably the most extreme case of active transport, but its physiology is very similar to the physiology of any other secretory gland or membrane, such as tear glands and sweat glands. The mechanism of salt excretion in these glands should really settle the issue of how active transport works, but most nephrologists, oculists, and medical researchers in general aren't interested in salt glands.
一些蜥蜴和海鸟的鼻子附近有一种腺体，叫做盐腺，因为它们有分泌盐的能力。盐腺可能是主动运输的最极端的例子，但它的生理机能与任何其他分泌腺或膜的生理机能非常相似，如泪腺和汗腺。这些腺体的盐排泄机制应该真正解决积极运输如何工作的问题，但大多数肾病学家、眼科医生和医学研究人员一般对盐腺体不感兴趣。
Carbon dioxide is the driving force in the salt gland. The constant formation of CO2, and its loss into the air, allows a high concentration of salt to be excreted. Blocking the interchange of CO2 and carbonic acid, with acetazolamide, or inhibiting the formation of CO2, prevents the excretion of salt.
Since respiratory metabolism, governed by the thyroid hormone, is our main source of carbon dioxide, it's obvious that thyroid deficiency should impair our ability to regulate water and solutes, such as salt. An organism that illustrates this function of thyroid is the young salmon, when it leaves a freshwater river to begin its life in the ocean. As it converts its physiology to tolerate the salty environment, its thyroid hormone surges. When it's mature, and returns to the fresh water to spawn, its prolactin rises sharply. In experiments with rodents, it has been found that drinking a large amount of water increases their prolactin, but the same amount of water, with added salt, doesn't.
二氧化碳是盐腺的驱动力。二氧化碳的不断形成和散失到空气中，使得高浓度的盐被排出体外。用乙酰唑胺阻断二氧化碳和碳酸的交换，或抑制二氧化碳的形成，可以防止盐的排泄。
由于受甲状腺激素控制的呼吸代谢是我们体内二氧化碳的主要来源，很明显，甲状腺不足会削弱我们调节水和溶质(如盐)的能力。说明甲状腺功能的生物是幼年鲑鱼，当它离开淡水河流，开始在海洋中生活时。当它改变生理机能以适应咸的环境时，它的甲状腺激素激增。当它成熟并返回淡水产卵时，它的催乳激素急剧上升。在对啮齿动物的实验中，人们发现大量饮水会增加它们的催乳素，但同样数量的水加上盐不会。
Hypothyroidism is typically associated with increased prolactin secretion. Hypothyroid people typically retain water, while losing salt, so the hypothyroid state is analogous to the salmon that has returned to the river, and to the mice that drink too much salt-free water.
甲状腺功能减退通常与催乳素分泌增加有关。甲状腺机能减退的人通常在失去盐的同时保持水分，所以甲状腺机能减退的状态类似于鲑鱼回到河里，以及老鼠喝了太多无盐水。
The typical hypothyroid person loses salt rapidly in the urine (and probably in the sweat, too, though that is usually diagnosed as cystic fibrosis), and retains water, diluting the urine less than normal. The reduced production of carbon dioxide, with increased susceptibility to producing lactate and ammonium, causes the cells to be more alkaline than normal, increasing their affinity for water. The rise of estrogen that usually accompanies hypothyroidism also increases intracellular pH, loss of sodium, and over-hydration of the blood.
典型的甲状腺机能减退患者在尿液中盐分流失迅速(可能在汗液中也有，尽管这通常被诊断为囊性纤维化)，并保留水分，使尿液的稀释程度低于正常水平。二氧化碳的产生减少，增加了产生乳酸和铵的敏感性，导致细胞比正常情况下更碱性，增加了它们对水的亲和力。通常伴随甲状腺功能减退的雌激素增加也会增加细胞内的pH值、钠的流失和血液的过度水合作用。
Hypothyroid muscles typically retain excess water, and fatigue easily, taking up more water than normal during exertion. In childhood, mild hypothyroidism often causes the leg muscles to swell and ache in the evenings, with what have been called “growing pains.” When the problem is more extreme, all the skeletal muscles can become very large (Hoffman syndrome), because of the anabolic effect of over-hydration. Enlargement of any muscle can result from the excessive hydration produced by thyroid deficiency, but when it happens to the muscles behind the eyes (Itabashi, et al., 1988), it often leads to a diagnosis of hyperthyroidism, rather than hypothyroidism.
甲状腺机能减退肌通常会保留多余的水分，容易疲劳，在运动时比正常肌需要更多的水分。在儿童时期，轻微的甲状腺功能减退症经常导致腿部肌肉晚上肿胀和疼痛，这被称为“生长痛”。当问题变得更严重时，所有的骨骼肌都可能变得非常大(霍夫曼综合症)，因为过度补水的合成代谢效应。任何肌肉的增大都可能是由于甲状腺机能缺乏引起的过多水合作用造成的，但当这种情况发生在眼睛后面的肌肉时(Itabashi等人，1988)，通常会被诊断为甲状腺机能亢进，而不是甲状腺机能减退。
The little kids with the Hoffman syndrome don't have the bloated myxedematous appearance that's often associated with hypothyroidism. They look athletic to a ridiculous degree, like miniature body-builders. But after a few weeks of treatment with thyroid, they regain the slender appearance that's normal for their age. The swollen state actually supports enlargement of the muscle, and the cellular processes are probably closely related to the muscle swelling and growth produced by exercise. The growth of the muscle cell during swelling seems to be the result of normal repair processes, in a context of reduced turnover of cellular proteins.
患有霍夫曼综合症的小孩没有肿胀的粘液水肿，而这通常与甲状腺功能减退有关。他们看起来运动到可笑的程度，就像微型健美者。但经过几周的甲状腺治疗后，他们恢复了正常年龄的苗条外貌。肿胀状态实际上支持肌肉的扩大，而细胞过程可能与运动产生的肌肉肿胀和生长密切相关。在肿胀期间肌肉细胞的生长似乎是正常修复过程的结果，在细胞蛋白质周转减少的背景下。
The people who believe in membrane pumps that maintain normal solute distributions by active transport know that the pumps would require energy (far more than the cell can produce, but they don't confront that issue), and so their view requires that they assign a great part of the cell's resources just to maintaining ionic homeostasis, and the result of that is that they tend to neglect the actual energy economy of the cell, which is primarily devoted to the adaptive renewal of the cell structure and enzyme systems, not to driving the systems that don't exist.
相信膜泵可以通过主动运输来维持正常的溶质分布的人知道，膜泵需要能量(远远超过细胞能产生的能量，但他们没有面对这个问题)，所以他们的观点要求他们分配一个伟大的一部分细胞的资源来维持离子稳态,结果就是他们往往忽略了细胞的实际能量经济，主要用于细胞结构和酶系统的适应性更新，而不是驱动不存在的系统。
The “anabolic” balance of the swollen cell is the result of decreased turnover of the cell's components. The higher rate of metabolism produced by adequate thyroid function maintains a high rate of renewal of the cell's systems, keeping the cell constantly adjusted to slight changes in the organism's needs. The evidence of a high rate of bone turnover is sometimes taken as evidence that thyroid can cause osteoporosis.
肿胀细胞的“合成代谢”平衡是细胞成分更替减少的结果。充足的甲状腺功能所产生的较高的新陈代谢速率维持了细胞系统的高更新速率，使细胞不断调整以适应机体需求的微小变化。高骨转换率的证据有时被认为是甲状腺可导致骨质疏松症的证据。
Later, in a more mature person, chronically fatigued and painful muscles that at one time would have been diagnosed as rheumatism, may be diagnosed as fibromyalgia. Most doctors are reluctant to prescribe thyroid supplements for the problem, but the association of elevated prolactin with the muscle disorder is now generally recognized.
后来，在一个更成熟的人，慢性疲劳和疼痛的肌肉曾经被诊断为风湿病，可能被诊断为纤维肌痛。大多数医生都不愿意为这个问题开甲状腺补剂，但催乳素升高与肌肉障碍之间的联系现在已被普遍认识。
The hypo-osmolar blood of hypothyroidism, increasing the excitability of vascular endothelium and smooth muscle, is probably a mechanism contributing to the high blood pressure of hypothyroidism. The swelling produced in vascular endothelium by hypo-osmotic plasma causes these cells to take up fats, contributing to the development of atherosclerosis. The generalized leakiness affects all cells (see “Leakiness” newsletter), and can contribute to reduced blood volume, and problems such as orthostatic hypotension. The swollen endothelium is stickier, and this is suspected to support the metastasis of cancer cells. Inflammation-related proteins, including CRP, are increased by the hypothyroid hyperhydration. The heart muscle itself can swell, leading to congestive heart failure.
Some of the nerve problems associated with hypothyroidism (e.g., carpal tunnel syndrome and “foot drop”) are blamed on compression of the nerves, from swelling of surrounding tissues, but the evidence is clear that hypothyroidism causes swelling in the nerve cells themselves. For example, in hypothyroidism, nerves are slow to respond to stimulation, and their conduction of the impulse is slow. These changes are the same as those produced by hyper-hydration caused by other means. Hypothyroid nerves are easily fatigued, and fatigued nerves take up a large amount of water. Swelling of the spinal cord is probably responsible for the “spinal stenosis” commonly seen in domestic animals and people; the mobility of intracellular water molecules is distinctly increased in patients with compression of the spinal cord (Tsuchiya, et al., 2003; Ries, et al., 2001).
甲状腺功能减退的低渗血，增加血管内皮细胞和平滑肌的兴奋性，可能是导致甲状腺功能减退的高血压的机制之一。低渗透血浆在血管内皮产生的肿胀导致这些细胞吸收脂肪，促进动脉粥样硬化的发展。广泛性渗漏影响所有细胞(见“渗漏”通讯)，并可能导致血容量减少，以及直立性低血压等问题。肿胀的内皮细胞更粘稠，这可能是支持癌细胞转移的原因。包括CRP在内的炎症相关蛋白因甲状腺功能减退、水合过度而增加。心肌本身会膨胀，导致充血性心力衰竭。
一些与甲状腺机能减退相关的神经问题(如腕管综合症和“足下垂”)被归咎于周围组织肿胀造成的神经压迫，但有证据表明，甲状腺机能减退会导致神经细胞本身肿胀。例如，在甲状腺机能减退症中，神经对刺激的反应较慢，冲动的传导也较慢。这些变化与其他原因导致的过度水化所产生的变化相同。甲状腺机能减退神经容易疲劳，疲劳神经耗水量大。脊髓肿胀可能是家畜和人常见的“椎管狭窄”的原因;脊髓受压患者细胞内水分子的流动性明显增加(Tsuchiya等，2003;Ries等，2001)。
The hyperhydration of hypothyroidism has been known to cause swelling and softening of cartilage, with deformation of joints, but somehow it has never dawned on surgeons that this process would lead to deformation of intervertebral disks.
众所周知，甲状腺机能减退的水化过度会导致软骨肿胀和软化，导致关节变形，但不知为何，外科医生从未意识到这一过程会导致椎间盘变形。
It has been known for a long time that hyperhydration can produce seizures; at one time, neurologists would test for epilepsy by having the patient drink a pint of water. Although there are many reasons to think that the hyperhydration produced by hypothyroidism is a factor in epilepsy, physicians have been very reluctant to consider the possibility, because they generally think of thyroid hormone as a stimulant, and believe that “stimulants” are necessarily inappropriate for people with epilepsy.
长期以来，人们都知道过度补水会导致癫痫发作;曾经有一段时间，神经学家会让病人喝一品脱的水来检测癫痫。虽然有很多理由认为甲状腺功能减退所产生的高水合作用是导致癫痫的一个因素，但医生一直很不愿意考虑这种可能性，因为他们一般认为甲状腺激素是一种兴奋剂，认为“兴奋剂”对癫痫患者来说必然是不合适的。
While it's true that the thyroid hormone increases sensitivity to adrenaline, its most noticeable effect is in improving the ability to relax, including the ability to sleep soundly and restfully. And it happens that increasing norepinephrine (the brain's locally produced form of adrenaline) helps to prevent seizures (Giorgi, et al., 2004).
虽然甲状腺激素确实增加了对肾上腺素的敏感性，但它最显著的效果是提高了放松的能力，包括睡得安稳安稳的能力。增加去甲肾上腺素(大脑中局部产生的肾上腺素)有助于防止癫痫发作(Giorgi等，2004)。
Cell swelling increases the sensitivity of nerves, and hyperosmotic shrinkage lowers their sensitivity. Increasing carbon dioxide helps to reduce the hydration of tissue (for example, the hydration and thickness of the cornea are decreased when carbon dioxide is increased), and increasing carbon dioxide is known to inhibit epileptic seizures. Another diagnostic trick of neurologists was to have the patient hyperventilate; it would often bring on a seizure. The diuretic acetazolamide, which increases the body's carbon dioxide and reduces water retention, is very effective for preventing seizures.
细胞肿胀增加了神经的敏感性，而高渗收缩降低了神经的敏感性。增加二氧化碳有助于减少组织的水合作用(例如，当二氧化碳增加时，角膜的水合作用和厚度会减少)，众所周知，增加二氧化碳可以抑制癫痫发作。神经学家的另一个诊断技巧是让病人过度呼吸;这通常会导致癫痫发作。利尿剂乙酰唑胺能增加体内二氧化碳含量，减少水分滞留，对预防癫痫发作非常有效。
The sleep-inducing effect of salty food is probably related to the anti-excitatory effects of hyperosmolarity, of adequate thyroid function, and of carbon dioxide.
高盐食物的睡眠诱导作用可能与高渗透压的抗兴奋作用、充足的甲状腺功能和二氧化碳有关。
Degenerative diseases, especially cancer, heart disease, and brain diseases, are less prevalent in populations that live at a high altitude. When oxygen pressure is low, the lungs lose carbon dioxide more slowly, and so the amount of carbon dioxide retained in the body is greater. If the basic problem in hypothyroidism is the deficient production of carbon dioxide causing excessive loss of salt and retention of water, resulting in hypo-osmotic body fluids, then we would expect people at high altitude to have better retention of salt, more loss of water, and more hypertonic body fluids. That has been observed in many studies. The increased rate of metabolism at altitude would be consistent with the relatively active “catabolism” of the slightly hyperosmotic condition.
退行性疾病，尤其是癌症、心脏病和脑部疾病，在高海拔地区的人群中不那么普遍。当氧分压较低时，肺部二氧化碳的释放速度较慢，因此体内保留的二氧化碳量也较大。如果甲状腺功能减退的根本问题是缺乏生产的二氧化碳造成过多的盐和水潴留,导致高渗体液,然后我们希望人们在高海拔有更好的保留盐,更多的损失的水,和高渗体液。这在很多研究中都被观察到。高原地区代谢速率的增加与轻度高渗病相对活跃的“分解代谢”相一致。
After the drug companies began, in the late 1950s, marketing some newly discovered (thiazide) diuretics, which cause sodium to be lost in the urine, their advertising campaigns created a cultish belief that salt caused hypertension. They convinced a whole generation of physicians that pregnant women should limit salt in their diet, take a diuretic preventively, and restrict calories to prevent “excessive” weight gain. Millions of women and their babies were harmed by that cult.
20世纪50年代末，制药公司开始推销一些新发现的(噻嗪类)利尿剂，这种利尿剂会导致钠在尿液中流失。他们说服了整整一代的医生，孕妇应该限制饮食中的盐，预防性服用利尿剂，并限制热量摄入，以防止“过度”增重。数以百万计的妇女和她们的婴儿受到了这种邪教的伤害。
Pre-eclampsia and pregnancy toxemia have been corrected (Shanklin and Hodin, 1979) by both increased dietary protein and increased salt, which improve circulation, lower blood pressure, and prevent seizures, while reducing vascular leakiness. The effectiveness of increased salt in pre-eclampsia led me to suggest it for women with premenstrual edema, because both conditions typically involve high estrogen, hyponatremia, and a tendency toward hypo-osmolarity. Estrogen itself causes sodium loss, reduced osmolarity, and increased capillary leakiness. Combined with a high protein diet, eating a little extra salt usually helps to correct a variety of problems involving edema, poor circulation, and high blood pressure.
通过增加饮食中的蛋白质和盐，改善血液循环，降低血压，防止癫痫发作，同时减少血管渗漏，子痫前期和妊娠毒血症已经得到纠正(Shanklin和Hodin, 1979)。增加盐对子痫前期的疗效让我建议对经前水肿的女性使用盐，因为这两种情况通常涉及高雌激素、低钠血症和低渗透倾向。雌激素本身会导致钠流失，降低渗透压，增加毛细血管渗漏。再加上高蛋白饮食，多吃一点盐通常有助于纠正各种问题，包括水肿、血液循环不良和高血压。
The danger of salt restriction in pregnancy has hardly been recognized by most physicians, and its danger in analogous physiological situations is much farther from their consideration.
在怀孕期间限制盐的危险几乎没有被大多数医生认识到，它在类似的生理情况下的危险远远没有被他们考虑。
One of the things that happen when there isn't enough sodium in the diet is that more aldosterone is synthesized. Aldosterone causes less sodium to be lost in the urine and sweat, but it achieves that at the expense of the increased loss of potassium, magnesium, and probably calcium. The loss of potassium leads to vasoconstriction, which contributes to heart and kidney failure and high blood pressure. The loss of magnesium contributes to vasoconstriction, inflammation, and bone loss. Magnesium deficiency is extremely common, but a little extra salt in the diet makes it easier to retain the magnesium in our foods.
当饮食中没有足够的钠时会发生的一件事就是合成更多的醛固酮。醛固酮减少了钠在尿液和汗液中的流失，但这是以钾、镁、可能还有钙的流失为代价的。钾的流失会导致血管收缩，从而导致心力衰竭、肾衰竭和高血压。镁的缺乏会导致血管收缩、炎症和骨质疏松。镁缺乏是非常常见的，但饮食中多吃一点盐会让我们更容易保留食物中的镁。
Darkness and hypothyroidism both reduce the activity of cytochrome oxidase, making cells more susceptible to stress. A promoter of excitotoxicity, ouabain, or a lack of salt, can function as the equivalent of darkness, in resetting the biological rhythms (Zatz, 1989, 1991).
黑暗和甲状腺功能减退都会降低细胞色素氧化酶的活性，使细胞更容易受到压力的影响。兴奋毒性的促进剂，ouabain，或盐的缺乏，在重置生物节律方面可以起到等同于黑暗的作用(Zatz, 1989, 1991)。
Bone loss occurs almost entirely during the night, and the nocturnal rise in cortisol and prolactin has strongly catabolic effects, but many other pro-inflammatory substances also rise during the night, and are probably the basic cause of the increased catabolism. Increased salt in the diet appears to improve some aspects of calcium metabolism, such as reducing parathyroid hormone and increasing ionized calcium, when the diet is deficient in calcium (Tordoff, 1997).
骨流失几乎完全发生在夜间，夜间皮质醇和催乳素的升高具有强烈的分解代谢作用，但许多其他促炎物质也在夜间上升，这可能是分解代谢增加的基本原因。在饮食中增加盐似乎改善了钙代谢的某些方面，如减少甲状旁腺激素和增加离子钙，当饮食中的钙缺乏(Tordoff, 1997)。
The kidneys can produce large amounts of carbon dioxide and ammonia, in the process of preventing the loss of electrolytes, while allowing acid to be lost in the urine. The ammonia is produced by the breakdown of protein. During stress or fasting, the loss of tissue protein can be minimized by supplementing the minerals, potassium, sodium, magnesium, and calcium. Salt restriction can cause aldosterone to increase, and excess aldosterone causes potassium loss, and increases the use of protein to form ammonia (Norby, et al., 1976; Snart and Taylor, 1978; Welbourne and Francoeur, 1977).
在防止电解质流失的过程中，肾脏可以产生大量的二氧化碳和氨，同时允许酸在尿液中流失。氨是由蛋白质分解产生的。在压力或禁食期间，可以通过补充矿物质，钾，钠，镁和钙来减少组织蛋白的损失。盐的限制会导致醛固酮增加，过量的醛固酮会导致钾的流失，增加蛋白质形成氨的使用(Norby等，1976;史纳特和泰勒，1978年;韦尔本和弗朗索瓦，1977)。
Aldosterone secretion increases during the night, and its rise is greater in depressed and stressed people. It inhibits energy metabolism, increases insulin resistance, and increases the formation of proinflammatory substances in fat cells (Kraus, et al., 2005). During aging, salt restriction can produce an exaggerated nocturnal rise in aldosterone.
醛固酮的分泌在夜间增加，在抑郁和有压力的人体内增加得更大。它抑制能量代谢，增加胰岛素抵抗，增加脂肪细胞中促炎物质的形成(Kraus, et al.， 2005)。在衰老过程中，限制盐的摄入会导致醛固酮的夜间升高。
During the night, there are many changes that suggest that the thyroid functions are being blocked, for example a surge in the thyroid stimulating hormone, with T4 and T3 being lowest between 11 PM and 3 AM (Lucke, et al., 1977), while temperature and energy production are at their lowest. This suggests that the problems of hypothyroidism will be most noticeable during the night.
在夜间，有许多变化表明甲状腺功能被阻断，例如促甲状腺激素激增，T4和T3在晚上11点到凌晨3点之间最低(Lucke, et al.， 1977)，同时温度和能量生产处于最低水平。这说明甲状腺功能减退的问题在夜间最为明显。
Rheumatoid arthritis and asthma are two inflammatory conditions that are notoriously worse during the night. Melatonin has been reported to be higher in patients with severe asthma and rheumatoid arthritis, and to promote the secretion of a variety of other pro-inflammatory substances. The peak of melatonin secretion is followed by the peak of aldosterone, and a little later by the peak of cortisol.
类风湿性关节炎和哮喘是两种炎症，它们在夜间会变得更加严重。据报道，褪黑激素在严重哮喘和类风湿关节炎患者中较高，并促进多种促炎物质的分泌。褪黑激素分泌的高峰之后是醛固酮分泌的高峰，稍晚一点是皮质醇分泌的高峰。
The use of bright light (which suppresses melatonin) to treat depression probably helps to inhibit the production of aldosterone, which is strongly associated with depression.
使用强光(抑制褪黑激素)治疗抑郁症可能有助于抑制醛固酮的产生，而醛固酮与抑郁症密切相关。
Both aldosterone and melatonin can contribute to the contraction of smooth muscle in blood vessels. Constriction of blood vessels in the kidneys helps to conserve water, which is adaptive if blood volume has been reduced because of a sodium deficiency. When blood vessels are inappropriately constricted, the blood pressure rises, while organs don't receive as much blood circulation as they need. This impaired circulation seems to be what causes the kidney damage associated with high blood pressure, which can eventually lead to heart failure and multiple organ failure.
醛固酮和褪黑素都能促进血管平滑肌的收缩。肾脏血管的收缩有助于保存水分，这在由于钠缺乏而导致血容量减少的情况下是适用的。当血管不恰当地收缩时，血压就会上升，而器官就不能获得足够的血液循环。这种循环受损似乎是导致高血压引起肾脏损伤的原因，高血压最终会导致心力衰竭和多器官衰竭。
Progesterone, which helps to maintain blood volume (partly by preventing vascular leakiness, preventing excessive sodium loss and by supporting albumin synthesis) antagonizes aldosterone. Aldosterone antagonists are now being recognized as effective treatments for hypertension, water retention, congestive heart failure, arrhythmia, diabetes, kidney disease, and a great variety of inflammatory problems. (Synthetic drugs to antagonize aldosterone are most effective when they are most like natural progesterone.) Since aldosterone contributes to fibrosis of the heart and kidneys (nephrosclerosis), progesterone, the “antifibromatogenic steroid,” should be helpful for those problems that have been considered irreversible. Aldosterone appears to contribute to the hyperglycemia of diabetes itself, and not just to its complications, by interfering with the interactions of insulin and cortisol (Yamashita, et al., 2004).
黄体酮，有助于维持血容量(部分通过防止血管渗漏，防止过量钠流失和支持白蛋白合成)拮抗醛固酮。醛固酮拮抗剂现在被认为是有效的治疗高血压，水潴积，充血性心力衰竭，心律失常，糖尿病，肾脏疾病和各种各样的炎症问题。(合成药物对抗醛固酮最有效时，他们最像天然黄体酮。)由于醛固酮有助于心脏和肾脏纤维化(肾硬化)，黄体酮，“抗纤维瘤性类固醇”，应该有助于那些被认为是不可逆转的问题。醛固酮似乎通过干扰胰岛素和皮质醇的相互作用，促进了糖尿病本身的高血糖，而不仅仅是其并发症(Yamashita等，2004)。
One of progesterone's fundamental actions is to cause estrogen “receptors” to disintegrate; hypertonicity has this effect in some situations. Estrogen's effects are largely produced by increased tissue hydration.
黄体酮的基本作用之一是导致雌激素“受体”分解;高渗在某些情况下有这种作用。雌激素的作用主要是由增加的组织水合作用产生的。
Aldosterone causes cells to take up sodium, while increasing their pH, i.e., raising their alkalinity (Mihailidou and Funder, 2005). Intracellular sodium has long been known to be a factor, along with swelling and alkalinity, in stimulating cell division (Cone and Tongier, 1971). A lack of salt stimulates the formation of serotonin, which in turn stimulates aldosterone synthesis–that is, a sodium restricted diet activates processes that cause cells to take up sodium inappropriately, in a situation reminiscent of the calcium deficient diet causing inappropriate calcification.
醛固酮导致细胞吸收钠，同时增加它们的pH值，即提高它们的碱性(Mihailidou和Funder, 2005)。长期以来，细胞内钠一直被认为是刺激细胞分裂的一个因素，与肿胀和碱性一起(Cone和Tongier, 1971)。盐的缺乏会刺激血清素的形成，而血清素反过来又会刺激醛固酮的合成——也就是说，限制钠的饮食会激活导致细胞不恰当地吸收钠的过程，这让人想起钙的缺乏会导致不恰当的钙化。
Aldosterone, like stress or hypo-osmolarity, activates the enzyme (ODC) which produces the polyamines, that promote cell division, and that can probably account for some of the harmful effects of excessive aldosterone.
Eating salty food around bedtime usually has a sleep-inducing effect, and it helps to maintain blood volume (which tends to decrease during the night), and to restrain the nocturnal rise of aldosterone, and other indicators of stress or inflammation. Eating gelatin, which lacks tryptophan, will reduce the formation of serotonin, and is likely to limit the formation of aldosterone.
醛固酮，像压力或低渗透压一样，会激活产生多胺的酶(ODC)，促进细胞分裂，这可能是过量醛固酮的一些有害影响的原因。
睡前吃咸的食物通常有催眠的作用，它有助于维持血容量(往往在夜间减少)，并抑制夜间醛固酮的上升，以及其他压力或炎症的指标。食用缺乏色氨酸的明胶会减少血清素的形成，并可能限制醛固酮的形成。
Pregnenolone can sometimes very quickly allow swollen tissues to release their water. This function is probably closely related to its antifibromatogenic function, since swelling and leaking set the stage for fibrosis.
孕烯醇酮有时可以非常迅速地让肿胀的组织释放水分。这种功能可能与其抗纤维瘤的功能密切相关，因为肿胀和渗漏是纤维化的基础。
Hyperosmotic sodium chloride solutions (e.g., 7.5%) are being used more often for treating trauma and shock, because the concentrated solution increases blood volume by removing water from the extravascular spaces, unlike the “isotonic” saline (0.9% sodium chloride), which usually adds to the edema by leaking out of the blood vessels.
高渗氯化钠溶液(例如，7.5%)更多地用于治疗创伤和休克，因为浓缩液通过从血管外间隙中除去水分来增加血容量，而“等渗”盐水(0.9%氯化钠)通常通过漏出血管而增加水肿。
A 5% sodium chloride solution is effective for promoting healing of damaged corneas, and solutions of 5% to 10% sodium chloride are effective for accelerating the healing of wounds and ulcers. Other hypertonic solutions, for example glucose or urea, have been used therapeutically, but sodium chloride seems to be the most effective in a variety of situations.
5%氯化钠溶液能有效促进受损角膜的愈合，5% ~ 10%氯化钠溶液能有效促进伤口和溃疡的愈合。其他高渗溶液，如葡萄糖或尿素，已用于治疗，但氯化钠似乎在各种情况下最有效。
Thyroid hormone, by maintaining oxidative metabolism with the production of carbon dioxide, is highly protective against excessive water retention and loss of sodium and magnesium.
甲状腺激素通过维持氧化代谢和二氧化碳的产生，对过度的水分保留和钠、镁的流失具有高度的保护作用。
Sometimes doctors recommend that constipated people should drink extra water, “to soften the stool.” The colon is where water is removed from the intestinal contents, and when it is inflamed, it removes too much water. Several decades ago, it was recognized (Orr, et al., 1931) that hypertonic saline, given intravenously, would stimulate intestinal peristalsis, and could be used to treat paralytic ileus and intestinal obstruction.
有时医生会建议便秘的人多喝水，“以软化大便”。结肠是水从肠道内容物中被排出的地方，当它发炎时，它排出太多的水。几十年前，人们认识到(Orr, et al.， 1931)静脉注射高渗盐水可刺激肠道蠕动，可用于治疗麻痹性肠梗阻。
When water is taken orally, it is absorbed high in the intestine, long before it reaches the colon, so the recommendation to drink water for constipation can produce a situation that's the opposite of intravenous hypertonic saline, by diluting the blood. Using a hypertonic salt solution as an enema can have the same beneficial effect on the intestine as the intravenous treatment.
当水被口服时，在到达结肠之前，水就在肠道被高度吸收了，所以建议便秘时喝水可能会产生与静脉内高渗盐水相反的情况，因为它会稀释血液。使用高渗盐溶液作为灌肠剂可以对肠道产生与静脉注射相同的有益效果。
Constipation physiology is probably analogous to the physiology of congestive heart failure, in which muscles are weakened and fatigued by swelling.
便秘生理学可能与充血性心力衰竭的生理学类似，在充血性心力衰竭中，肌肉因肿胀而减弱和疲劳。
In recent decades, the prevalence of congestive heart failure has increased tremendously, so that it is now often called an epidemic. Hyponatremia (too little salt, or too much water) is a recognized “risk factor” for congestive heart failure. In the failing heart, the muscle cells are swollen, causing the heart wall to stiffen, weakening its ability to pump. Osmotically shrinking the cells can restore their function.
The swollen heart, like any muscle, loses the ability to quickly and completely relax, and so it doesn't fill adequately between contractions. Elastic tissues, such as arteries and lungs, stiffen when they are over-hydrated, losing their normal functions. In small blood vessels, swelling narrows the channel, increasing resistance to the flow of blood.
近几十年来，充血性心力衰竭的发病率急剧上升，所以现在经常被称为流行病。低钠血症(盐太少或水太多)是充血性心力衰竭公认的“危险因素”。在衰竭的心脏中，肌肉细胞肿胀，导致心脏壁变硬，削弱了心脏的供血能力。通过渗透收缩细胞可以恢复它们的功能。
肿胀的心脏，就像任何肌肉一样，失去了快速和完全放松的能力，所以它不能在收缩之间充分填充。动脉和肺等弹性组织在水分过多时就会变硬，失去正常功能。在小血管中，肿胀会使通道变窄，增加血液流动的阻力。
When people force themselves to drink a certain amount of water every day, even when they don't feel thirsty, they are activating complex adaptive processes unnecessarily. Thirst is the best guide to the amount of fluid needed.
当人们强迫自己每天喝一定量的水，即使他们不觉得口渴，他们是在不必要地激活复杂的适应过程。口渴是饮水量的最佳指南。
When extra water consumption is combined with a low salt diet–as physicians have so often recommended–a healthy person can adapt easily, but for a hypothyroid person it can have disastrous effects.
当额外的饮水与低盐饮食结合在一起时——正如医生经常建议的那样——一个健康的人很容易适应，但对甲状腺机能减退的人来说，这可能会造成灾难性的影响。
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http://raypeat.com/articles/articles/water.shtml
水：肿胀、紧张、疼痛、疲劳、衰老
我与许多人交谈过，他们认为除了正常的食物外，应该每天喝“8 杯水”，即使不感到口渴。许多医生仍然背诵这个危险的口号，但加上限定词“或其他液体”已变得很普遍。
一个人需要的水量变化很大，这取决于代谢率、活动以及气温和湿度等因素。在炎热干燥的天气里努力工作，可以在超过 8 小时内每小时饮用超过 2 升的水，而不会形成尿液，因为所有的水都会因蒸发而流失。但是在非常炎热、潮湿的天气中，代谢率低的人可能会受到最小量水的危害（例如《尼日利亚拉各斯的子痫气象关系》Agobe 等人，1981 年）。
大多数食物都含有相当数量的水分，通常超过重量的 70%，一些水分是在细胞中通过代谢产生的。由于有机体性质及其细胞构成的一些根深蒂固的传统形象，水在有机体中的功能一直被神秘化和忽视。
学校和教科书一直在流传的一个愚蠢的形象是，生物化学由溶解在水中的物质发生的化学反应组成的，水被细胞保留是因为被油性膜包围，由于产生的渗透力通过溶解的物质。大多数小学生都见过用鸡蛋制成的渗透压计，鸡蛋会导致水柱上升，据说这与细胞的工作方式有关。膜泵被用来解释细胞内外溶质浓度和“渗透压”的差异。这隔故事是细胞表面（在其“膜”中）不可见的东西迫使溶解的分子以不会扩散自发运动方式移动，水被动地跟随“主动运输”的溶质。但有证据表明，水及其溶质均受细胞体相的调节，而不是其表面。
在某些文化背景下，万物有灵论具有某种魅力（水精灵等等），但在医学和生物学文化中，万物有灵论对细胞及其机制的概念化具有很大的破坏性，因为妨碍了连贯理解生理学。如果允许水和离子的生理学超越主流医学的有灵论学说，例如“膜泵”，那么几乎每种疾病都会以不同的方式处理。如果考虑到所谓通过泵“主动运输”进出细胞的物质，那么操作泵所需的能量至少是细胞可用总能量的 15 倍。即使是新型合成化学品，通常也会调用“特定”泵，解释其在细胞内外分布不均。在许多生物情况下，水被忽略了，但当水成为一个问题时，水的分布通常在机械上从属于其主动“泵送”的溶质。
就像教科书所说的，细胞不是渗透压计，确实控制了含水量，但不需要“膜泵”。将细胞的水想象为“溶解在细胞中”更准确，有点像果冻或煮鸡蛋中的水。细胞通过控制其结构、代谢和运动的过程来控制其水合作用，因为水是细胞最深层结构和基本功能的一部分。细胞对水合作用和体积变化的调整似乎受到收缩蛋白和能量代谢的调节（Minkoff 和 Damadian，1976）。
扰乱细胞结构或功能的任何压力或能量不足都会扰乱水、蛋白质和细胞其他成分之间的相互作用。激发导致细胞吸收额外的水，不是由于细胞中溶质浓度增加导致的渗透作用，也不是因为膜变得多孔，而是因为细胞的结构蛋白暂时增加了对水的亲和力。
这种增加的亲和力类似于导致凝胶在碱性状态下膨胀的过程，与称之为电渗的过程有关，其中水向更高的负电荷移动。强烈的激发或压力会增加细胞的负电荷，使其变得更加碱性并膨胀。膨胀和碱性导致细胞开始合成 DNA，为细胞分裂做准备。有丝分裂原和致癌物，包括雌激素，会导致细胞变成碱性并膨胀，而阻碍细胞碱化的物质（如利尿剂乙酰唑胺和阿米洛利）会抑制细胞分裂。单独的长期碱性压力可导致肾细胞的恶化（Oberleithner，等，1991）。
“压力”的一般概念是有用的，因为包括疲劳、渗透压变化、pH 值紊乱和随后的酶变化等过程，产生乳酸、一氧化氮、多胺、雌激素、血清素等物质更具体的介质。但是，如果从整体上看待有机体，而不是作为“特定生物机制”的集合，则关注压力反应中涉及的物理因素很重要，这些“特定生物机制”涉及诸如微小驱动的“膜泵”之类。
当细胞在高渗条件下收缩时，代谢变成分解代谢，分解蛋白质和糖原，有时会产生乳酸，这会导致碱化，增加细胞对水的亲和力，使其恢复正常大小。轻微的高渗性会增加细胞的代谢率。
低渗条件下的膨胀（例如水过量）是合成代谢的，导致细胞增殖，抑制蛋白质和糖原的分解。
呼吸细胞总是通过将氢从燃料分子转移到氧来产生一些水。呼吸也会产生二氧化碳，本身就是一种路易斯酸（意味着结合电子，而不是释放质子），与细胞蛋白质结合，在此过程中酸化。大量的二氧化碳以结合形式存在于细胞内。酸化的细胞质（像其他主要为酸性的聚合物凝胶一样）释放水和钠。（这个过程在物理上类似于用盐冲洗软水剂、或用酸冲洗除盐剂，以重新激活的过程。）
除了与细胞质结合外，二氧化碳还可以通过与水的化合转化为碳酸。碳酸是亲水的，因此会迅速离开细胞，带走一些带相反电荷的离子，例如钙和钠。不断从呼吸细胞中碳酸的形成流出，导致一些水和一些带正电的金属离开细胞，这是一个“主动”的过程，不需要任何神秘的泵。
当血液通过肺部时，二氧化碳离开系统，当碳酸转化为二氧化碳时，水与反离子（碱金属或矿物质）一起留在血液中，导致 pH 值略有不同，以及血流和组织细胞之间的渗透压。一些实验表明，各种组织的正常渗透压比血液高 2 或 3 倍，称为“等摩尔”或等渗。
肾脏通过允许水和溶质离开血流来调节血液的渗透压，其比例通常使体液与细胞保持平衡。肾脏能够补偿由压力和不当饮食产生的许多不平衡，例如通过形成氨和二氧化碳，以补偿由其他器官输送到血液中的碱酸失衡。由于肾脏具有调节血液和形成尿液之间溶质流动的强大能力，“膜泵”对于医学肾病学家来说非常重要。但是“主动运输”越极端，“膜泵”以外的过程就越明显。
有些蜥蜴和海鸟的鼻子附近有一种腺体，称为盐腺，因为能够分泌盐分。盐腺可能是主动运输最极端的例子，但其生理学与任何其他分泌腺或膜的生理学非常相似，例如泪腺和汗腺。这些腺体中的盐排泄机制应该真正解决主动运输如何工作的问题，但大多数肾病学家、眼科医生和医学研究人员通常对盐腺不感兴趣。
二氧化碳是盐腺的驱动力。二氧化碳的不断形成，排放到空气中，使得高浓度的盐分被排出体外。用乙酰唑胺阻断 二氧化碳 和碳酸的交换，或抑制二氧化碳 的形成，防止盐的排出。
由于由甲状腺激素控制的呼吸代谢是体内二氧化碳的主要来源，因此很明显，甲状腺功能低下会损害身体调节水和溶质（例如盐）的能力。说明甲状腺功能的有机体是年轻的鲑鱼，当鲑鱼离开淡水河流开始在海洋中生活时，转变生理机能以耐受咸味环境时，甲状腺激素会激增。当鲑鱼成熟，回到淡水产卵时，催乳素急剧上升。在对啮齿动物的实验中，发现喝大量的水会增加催乳素，但同样量的水加盐不会增加。
甲减通常与催乳素分泌增加有关。甲减患者通常会保留水分，同时会失去盐分，因此甲减的状态类似于回到河流的鲑鱼，以及喝太多无盐水的小鼠。
典型的甲减患者在尿液中会迅速失盐（也可能在汗液中失盐，尽管这通常被诊断为囊性纤维化），并且会保留水分，稀释尿液的程度低于正常水平。二氧化碳的产生减少，产生乳酸和铵的敏感性增加，导致细胞比正常细胞更具碱性，增加对水的亲和力。通常伴随甲减的雌激素升高也会增加细胞内的 pH 值、钠流失和血液的过度水合。
甲减患者肌肉通常会保留过多的水分，容易疲劳，在运动时会比正常情况下吸收更多的水分。在儿童时期，轻度甲减通常会导致腿部肌肉在晚上肿胀和疼痛，这就是所谓的“生长痛”。当变得更严重时，由于过度水合的合成代谢作用，所有骨骼肌都会变得非常大（霍夫曼综合症）。任何肌肉的增大都可能是由甲状腺功能缺乏引起的过度水合作用引起的，但当其发生在眼睛后面肌肉时（Itabashi 等人，1988 年），通常会导致诊断为甲亢，而不是甲减。
患有霍夫曼综合症的孩子没有通常与甲减有关的肿胀粘液性水肿外观，看起来运动到可笑的程度，就像小健美运动员一样。但经过几周的甲状腺治疗后，恢复正常的苗条外观。肿胀状态实际上支持肌肉的增大，而细胞过程可能与运动产生的肌肉肿胀和生长密切相关。在细胞蛋白质周转减少的情况下，肿胀期间肌肉细胞的生长似乎是正常修复过程的结果。
相信通过主动运输维持正常溶质分布的膜泵的人，知道膜泵需要能量（远远超过细胞可以产生的能量，但他们不面对这个问题），因此他们的观点要求分配细胞资源的很大一部分只是用于维持离子稳态，结果是往往忽略了细胞的实际能量经济，这主要致力于细胞结构和酶系统的适应性更新，而不是驱动不存在的系统。
肿胀细胞的“合成代谢”平衡是细胞成分更新减少的结果。由充足的甲状腺功能产生的较高的代谢率维持细胞系统的高更新率，使细胞不断调整以适应生物体需求的微小变化。高骨转换率的证据有时被视为甲状腺能导致骨质疏松症的证据。
后来，一个成人曾经被诊断为风湿病的长期疲劳和疼痛的肌肉可能被诊断为纤维肌痛。大多数医生不愿意为这个问题开出甲状腺补剂，但现在普遍认为催乳素升高与肌肉疾病有关。
甲减症的低渗性血液，增加血管内皮和平滑肌的兴奋性，可能是导致甲减症高血压的机制。低渗透血浆在血管内皮中产生的肿胀导致这些细胞吸收脂肪，从而导致动脉粥样硬化的发展。全身渗漏影响所有细胞（参见“渗漏”通信内容），并可能导致血容量减少和直立性低血压等问题。膨胀的内皮更粘稠，可能支持癌细胞的转移。包括 CRP 在内的炎症相关蛋白会因甲减过度水合而增加。心肌本身会膨胀，导致充血性心力衰竭。
一些与甲减相关的神经问题（例如腕管综合征和“足下垂”）被归咎于周围组织肿胀导致的神经受压，但有证据表明甲减症会导致神经细胞本身肿胀。例如，在甲减症中，神经对刺激的反应很慢，冲动传导很慢。这些变化与其他方式引起的过度水合作用所产生的变化相同。甲减的神经很容易疲劳，疲劳的神经会吸收大量的水分。脊髓肿胀可能是家畜和人常见的“椎管狭窄”的原因；脊髓受压患者细胞内水分子的流动性明显增加(Tsuchiya等，2003;Ries等，2001)。
众所周知，甲减的过度水合会导致软骨肿胀和软化，伴有关节变形，但不知何故，外科医生从未意识到这一过程会导致椎间盘变形。
长期以来，人们就知道过度水合会导致癫痫发作。有一段时间，神经科医生会通过让病人喝一品脱水来检测癫痫。尽管有很多理由认为甲减产生的水合过多是癫痫的一个因素，但医生们一直很不愿意考虑这种可能性，因为他们普遍认为甲状腺激素是一种兴奋剂，认为“兴奋剂”不一定适合癫痫患者。
虽然甲状腺激素确实会增加对肾上腺素的敏感性，但其最显著的效果是提高放松的能力，包括安然入睡的能力。增加去甲肾上腺素（大脑局部产生的肾上腺素）有助于预防癫痫发作（Giorgi 等人，2004 年）。
细胞膨胀增加了神经的敏感性，而高渗性收缩降低了敏感性。增加二氧化碳有助于减少组织的水合作用（例如，当二氧化碳增加时，角膜的水合作用和厚度会减少），已知增加二氧化碳可以抑制癫痫发作。神经科医生的另一个诊断技巧是让患者过度换气，经常会引起癫痫发作。利尿剂乙酰唑胺可增加体内二氧化碳并减少水分潴留，对预防癫痫发作非常有效。
咸味食物的睡眠诱导作用可能与高渗性、充足的甲状腺功能和二氧化碳的抗兴奋作用有关。
退行性疾病，尤其是癌症、心脏病和脑部疾病，在生活在高海拔地区的人群中不太普遍。当氧气压力低时，肺排出二氧化碳的速度更慢，因此保留在体内的二氧化碳量更多。如果甲减症的根本问题是二氧化碳产生不足导致盐分流失过多和水分潴留，导致体液渗透性低下，那么期望高海拔地区的人有更好的盐分保留，更多的水分流失，以及更多的高渗体液。这已在许多研究中观察到。在高海拔地区增加的代谢率将与轻微高渗状态的相对活跃的“分解代谢”相一致。
在 1950 年代后期，制药公司开始销售一些新发现的（噻嗪类）利尿剂，这些利尿剂会导致钠在尿液中流失，他们的广告宣传创造了一种歪曲信仰，即盐会导致高血压。他们说服了整整一代的医生，孕妇应该限制饮食中的盐分，预防性地服用利尿剂，限制热量以防止“过度”增加体重。数以百万计的妇女及其婴儿受到这种歪曲伤害。
先兆子痫和妊娠毒血症已通过增加膳食蛋白质和增加盐分得到纠正（Shanklin 和 Hodin，1979），这可以改善循环、降低血压和预防癫痫发作，同时减少血管渗漏。在先兆子痫中增加盐分的有效性，使我建议将其用于经前水肿的女性，因为这两种情况通常都涉及高雌激素、低钠血症和低渗透压倾向。雌激素本身会导致钠流失、渗透压降低和毛细血管渗漏增加。结合高蛋白饮食，多吃一点盐通常有助于纠正包括水肿、血液循环不良和高血压在内的各种问题。
大多数医生几乎没有认识到怀孕期间限盐的危险，而在类似的生理情况下，其危险也远远超出了他们的考虑。
饮食中钠含量不足时发生的一件事是合成更多的醛固酮。醛固酮导致尿液和汗液中钠的流失减少，但是以增加钾、镁和可能的钙的流失为代价来实现的。钾的流失会导致血管收缩，从而导致心脏和肾脏衰竭以及高血压。镁的流失会导致血管收缩、炎症和骨质流失。缺镁极为常见，但饮食中多一点盐就会更容易保留住食物中的镁。
黑暗和甲减都会降低细胞色素氧化酶的活性，使细胞更容易受到压力。兴奋性毒性的促进剂、哇巴因或缺盐，在重置生物节律时可以起到相当于黑暗的作用（Zatz, 1989, 1991）。
骨质流失几乎全部发生在夜间，皮质醇和催乳素的夜间升高具有强烈的分解代谢作用，但许多其他促炎物质也在夜间升高，这可能是分解代谢增加的根本原因。当饮食缺钙时，增加饮食中的盐似乎可以改善钙代谢的某些方面，例如减少甲状旁腺激素和增加离子钙（Tordoff，1997）。
在防止电解质流失的过程中，肾脏会产生大量的二氧化碳和氨，同时让酸从尿液中流失。氨是由蛋白质分解产生的。在压力或乏食期间，可以通过补充矿物质、钾、钠、镁和钙来最大限度地减少组织蛋白的损失。限盐会导致醛固酮增加，过量的醛固酮会导致钾流失，增加蛋白质的使用以形成氨（Norby 等人，1976；Snart 和 Taylor，1978；Welbourne 和 Francoeur，1977）。
醛固酮分泌在夜间增加，在抑郁和压力大的人群中上升幅度更大，抑制能量代谢，增加胰岛素抵抗，增加脂肪细胞中促炎物质的形成（Kraus 等，2005）。在衰老过程中，限盐会导致醛固酮夜间过度升高。
在夜间，有许多变化表明甲状腺功能正在受阻，例如促甲状腺激素激增，T4 和 T3 在晚上 11 点到凌晨 3 点之间最低（Lucke 等人，1977），而体温度和能量产生处于最低水平。这表明甲减的问题在夜间最为明显。
类风湿性关节炎和哮喘是众所周知的夜间恶化的两种炎症。据报道，严重哮喘和类风湿性关节炎患者的褪黑激素含量较高，促进多种其他促炎物质的分泌。褪黑激素分泌高峰之后是醛固酮高峰，接着是皮质醇高峰。
使用强光（抑制褪黑激素）治疗抑郁症可能有助于抑制与抑郁症密切相关的醛固酮的产生。
醛固酮和褪黑激素都可以促进血管平滑肌的收缩。肾脏血管的收缩有助于保存水分，如果血容量因缺钠而减少，这是适应性的。当血管收缩不当时，血压会升高，而器官则无法获得所需的血液循环。这种循环受损似乎是导致与高血压相关的肾脏损伤的原因，最终可能导致心力衰竭和多器官衰竭。
黄体酮有助于维持血容量（部分通过防止血管渗漏、防止过度钠流失和支持白蛋白合成）拮抗醛固酮。醛固酮拮抗剂现在被认为是高血压、水潴留、充血性心力衰竭、心律失常、糖尿病、肾病和多种炎症问题的有效治疗方法。（拮抗醛固酮的合成药物与天然黄体酮最相似时最有效。）由于醛固酮会导致心脏和肾脏纤维化（肾硬化），黄体酮（即“抗纤维瘤类固醇”）应该有助于解决认为不可逆转的问题。醛固酮似乎会导致糖尿病本身的高血糖，而不仅仅是并发症，
黄体酮的基本作用之一是使雌激素“受体”分解；在某些情况下，高渗性会产生这种影响。雌激素的影响主要是由增加的组织水合作用产生的。
醛固酮使细胞吸收钠，同时增加 pH 值，即提高碱性（Mihailidou 和 Funder，2005 年）。长期以来，人们都知道细胞内钠与膨胀和碱度一起是刺激细胞分裂的一个因素（Cone 和 Tongier，1971 年）。缺盐会刺激血清素的形成，进而刺激醛固酮的合成，也就是说，限钠饮食会激活导致细胞不适当摄取钠的过程，这种情况让人想起缺钙饮食导致不适当的钙化。
醛固酮与压力或低渗透压一样，会激活产生多胺的酶 (ODC)，从而促进细胞分裂，这可能是醛固酮过量的一些有害影响的原因。
在睡前吃咸的食物通常具有诱导睡眠的作用，有助于维持血容量（夜间趋于减少），抑制醛固酮的夜间升高，以及其他压力或炎症指标。食用缺乏色氨酸的明胶会减少血清素的形成，并可能限制醛固酮的形成。
孕烯醇酮有时可以很快让肿胀的组织释放水分。该功能可能与其抗纤维瘤功能密切相关，因为肿胀和渗漏为纤维化奠定了基础。
高渗氯化钠溶液（如 7.5%）更常用于治疗创伤和休克，因为浓缩溶液通过从血管外空间除水来增加血容量，而“等渗”盐水（0.9% 氯化钠）通常会通过从血管中渗出而加重水肿。
5%氯化钠溶液可有效促进受损角膜愈合，5%至10%氯化钠溶液可有效加速伤口和溃疡愈合。其他高渗溶液，例如葡萄糖或尿素，已用于治疗，但氯化钠似乎在各种情况下最有效。
甲状腺激素通过产生二氧化碳来维持氧化代谢，对防止过多的水潴留和钠、镁的流失具有高度保护作用。
有时医生建议便秘的人应该多喝水“以软化大便”。结肠是从肠道内容物中去除水分的地方，发炎时会去除过多的水分。几十年前，人们认识到（Orr，等，1931）静脉内给予高渗盐水会刺激肠蠕动，可用于治疗麻痹性肠梗阻。
喝水之后，水在肠道中的高处吸收，远在到达结肠之前，所以建议喝水治疗便秘会产生一种与静脉注射高渗盐水相反的情况，稀释了血液。使用高渗盐溶液作为灌肠剂可以对肠道产生与静脉内治疗相同的有益效果。
便秘生理学可能类似于充血性心力衰竭的生理学，其中肌肉因肿胀而变弱和疲劳。
近几十年来，充血性心力衰竭的患病率急剧增加，因此现在通常被称为流行病。低钠血症（盐太少或水太多）是公认的充血性心力衰竭的“危险因素”。在衰竭的心脏中，肌肉细胞肿胀，导致心脏壁变硬，削弱其泵血能力。渗透性收缩细胞可以恢复其功能。
与任何肌肉一样，肿胀的心脏失去了快速完全放松的能力，因此在两次收缩之间不能充分填充。弹性组织，如动脉和肺，在水分过多时会变硬，失去正常功能。在小血管中，肿胀会使通道变窄，增加血液流动的阻力。
强迫自己每天喝一定量的水，即使不感到口渴，也在不必要地激活复杂的适应过程。口渴是确定所需液体量的最佳向导。
当额外的饮水量与低盐饮食相结合时，正如医生经常推荐的那样，一个健康的人可以很容易地采用，但对于甲减的人来说，可能会产生灾难性的影响。
