Salt, energy, metabolic rate, and longevity
by Raymond Peat
In the 1950s, when the pharmaceutical industry was beginning to promote some new chemicals as diuretics to replace the traditional mercury compounds, Walter Kempner’s low-salt “rice diet” began to be discussed in the medical journals and other media. The diuretics were offered for treating high blood pressure, pulmonary edema, heart failure, “idiopathic edema,” orthostatic edema and obesity, and other forms of water retention, including pregnancy, and since they functioned by causing sodium to be excreted in the urine, their sale was accompanied by advising the patients to reduce their salt intake to make the diuretic more effective.
It was clear to some physicians (and to most veterinarians) that salt restriction, especially combined with salt-losing diuresis, was very harmful during pregnancy, but that combination became standard medical practice for many years, damaging millions of babies.
在20世纪50年代，当制药工业开始推广一些新的化学物质作为利尿剂来取代传统的汞化合物时，Walter Kempner的低盐“大米饮食”开始在医学杂志和其他媒体上被讨论。利尿剂用于治疗高血压、肺水肿、心力衰竭、“特发性水肿”、直立性水肿和肥胖，以及其他形式的水潴留，包括怀孕，由于它们的功能是导致钠在尿液中排泄，它们的销售伴随着建议患者减少盐的摄入量，以使利尿剂更有效。
一些医生(和大多数兽医)很清楚，限制盐的摄入，特别是结合失盐利尿，在怀孕期间是非常有害的，但这种结合成为多年来的标准医疗实践，损害了数百万婴儿。
Despite numerous publications showing that diuretics could cause the edematous problems that they were supposed to remedy, they have been one of the most profitable types of drug. Dietary salt restriction has become a cultural cliché, largely as a consequence of the belief that sodium causes edema and hypertension.
Salt restriction, according to a review of about 100 studies (Alderman, 2004), lowers the blood pressure a few points. But that generally doesn’t relate to better health. In one study (3000 people, 4 years), there was a clear increase in mortality in the individuals who ate less salt. An extra few grams of salt per day was associated with a 36% reduction in “coronary events” (Alderman, et al., 1995). Another study (more than 11,000 people, 22 years) also showed an inverse relation between salt intake and mortality (Alderman, et al., 1997).
尽管大量的出版物表明利尿剂可能会导致它们本应治疗的水肿问题，但它们一直是最有利可图的药物类型之一。饮食中盐的限制已经成为一个文化cliché，很大程度上是由于人们相信钠会导致水肿和高血压。
根据对大约100项研究的回顾(Alderman, 2004)，盐的限制可以降低血压几个点。但这通常与更好的健康无关。在一项研究(3000人，4年)中，吃盐少的人死亡率明显增加。每天多摄入几克盐与“冠状动脉事件”减少36%相关(Alderman等，1995)。另一项研究(超过11000人，22年)也显示了盐摄入量和死亡率之间的反比关系(Alderman, et al, 1997)。
Tom Brewer, an obstetrician who devoted his career to educating the public about the importance of prenatal nutrition, emphasizing adequate protein (especially milk), calories, and salt, was largely responsible for the gradual abandonment of the low-salt plus diuretics treatment for pregnant women. He explained that sodium, in association with serum albumin, is essential for maintaining blood volume. Without adequate sodium, the serum albumin is unable to keep water from leaving the blood and entering the tissues. The tissues swell as the volume of blood is reduced.
During pregnancy, the reduced blood volume doesn’t adequately nourish and oxygenate the growing fetus, and the reduced circulation to the kidneys causes them to release a signal substance (renin) that causes the blood to circulate faster, under greater pressure. A low salt diet is just one of the things that can reduce kidney circulation and stimulate renin production. Bacterial endotoxin, and other things that cause excessive capillary permeability, edema, or shock-like symptoms, will activate renin secretion.
产科医生Tom Brewer致力于教育公众产前营养的重要性，强调充足的蛋白质(尤其是牛奶)、卡路里和盐，这在很大程度上是导致孕妇逐渐放弃低盐加利尿剂治疗的主要原因。他解释说，钠与血清白蛋白有关，对维持血容量至关重要。如果没有足够的钠，血清白蛋白就无法阻止水分离开血液进入组织。当血容量减少时，组织就会膨胀。
在怀孕期间，减少的血容量不能给生长中的胎儿提供足够的营养和氧气，而减少的肾脏循环导致它们释放一种信号物质(肾素)，导致血液在更大的压力下更快地循环。低盐饮食只是可以减少肾脏循环和刺激肾素产生的事情之一。细菌内毒素和其他引起毛细血管通透性过度、水肿或休克样症状的东西会激活肾素的分泌。
The blood volume problem isn’t limited to the hypertension of pregnancy toxemia: “Plasma volume is usually lower in patients with essential hypertension than in normal subjects” (Tarazi, 1976).
Several studies of preeclampsia or toxemia of pregnancy showed that supplementing the diet with salt would lower the women’s blood pressure, and prevent the other complications associated with toxemia (Shanklin and Hodin, 1979).
It has been known for many years that decreasing sodium intake causes the body to respond adaptively, increasing the renin-angiotensin-aldosterone system (RAAS). The activation of this system is recognized as a factor in hypertension, kidney disease, heart failure, fibrosis of the heart, and other problems. Sodium restriction also increases serotonin, activity of the sympathetic nervous system, and plasminogen activator inhibitor type-1 (PAI-1), which contributes to the accumulation of clots and is associated with breast and prostate cancer. The sympathetic nervous system becomes hyperactive in preeclampsia (Metsaars, et al., 2006).
血容量问题不仅限于妊娠毒血症的高血压:“原发性高血压患者的血浆容量通常比正常人低”(Tarazi, 1976)。
几项关于子痫前期或妊娠毒血症的研究表明，在饮食中补充盐可以降低妇女的血压，并防止与毒血症相关的其他并发症(Shanklin和Hodin, 1979)。
多年来人们已经知道，减少钠摄入量会导致身体做出适应性反应，增加肾素-血管紧张素-醛固酮系统(RAAS)。该系统的激活被认为是高血压、肾脏疾病、心力衰竭、心脏纤维化和其他问题的一个因素。钠限制还会增加血清素、交感神经系统的活性和纤溶酶原激活抑制剂-1型(PAI-1)，这有助于凝块的积累，并与乳腺癌和前列腺癌有关。交感神经系统在子痫前期变得异常活跃(Metsaars, et al.， 2006)。
Despite the general knowledge of the relation of dietary salt to the RAA system, and its application by Brewer and others to the prevention of pregnancy toxemia, it isn’t common to see the information applied to other problems, such as aging and the stress-related degenerative diseases.
Many young women periodically crave salt and sugar, especially around ovulation and premenstrually, when estrogen is high. Physiologically, this is similar to the food cravings of pregnancy. Premenstrual water retention is a common problem, and physicians commonly offer the same advice to cycling women that was offered as a standard treatment for pregnant women–the avoidance of salt, sometimes with a diuretic. But when women premenstrually increase their salt intake according to their craving, the water retention can be prevented.
Blood volume changes during the normal menstrual cycle, and when the blood volume is low, it is usually because the water has moved into the tissues, causing edema. When estrogen is high, the osmolarity of the blood is low. (Courtar, et al., 2007; Stachenfeld, et al., 1999). Hypothyroidism (which increases the ratio of estrogen to progesterone) is a major cause of excessive sodium loss.
尽管人们普遍知道膳食盐与RAA系统的关系，以及Brewer和其他人将其应用于预防妊娠毒血症，但应用于其他问题的信息并不常见，如衰老和应激相关的退行性疾病。
许多年轻女性周期性地渴望盐和糖，尤其是在排卵前后和月经前，此时雌激素水平较高。从生理学上讲，这与怀孕时对食物的渴望类似。经前水潴留是一个常见的问题，医生们通常会向骑行女性提供与孕妇标准治疗相同的建议——避免盐，有时使用利尿剂。但是，如果月经前的女性根据自己的渴望增加盐的摄入量，就可以防止水潴留。
在正常的月经周期内，血容量会发生变化，当血容量低时，通常是因为水已经进入组织，导致水肿。当雌激素高时，血液的渗透压就低。(Courtar等，2007;Stachenfeld等，1999)。甲状腺功能减退(增加雌激素和孕酮的比例)是过量钠流失的主要原因。
The increase of adrenalin caused by salt restriction has many harmful effects, including insomnia. Many old people have noticed that a low sodium diet disturbs their sleep, and that eating their usual amount of salt restores their ability to sleep. The activity of the sympathetic nervous system increases with aging, so salt restriction is exacerbating one of the basic problems of aging. Chronically increased activity of the sympathetic (adrenergic) nervous system contributes to capillary leakage, insulin resistance (with increased free fatty acids in the blood), and degenerative changes in the brain (Griffith and Sutin, 1996).
The flexibility of blood vessels (compliance) is decreased by a low-salt diet, and vascular stiffness caused by over-activity of the sympathetic nervous system is considered to be an important factor in hypertension, especially with aging.
限盐导致肾上腺素增加有许多有害影响，包括失眠。许多老年人已经注意到，低钠饮食扰乱了他们的睡眠，而吃正常量的盐可以恢复他们的睡眠能力。交感神经系统的活动随着年龄的增长而增加，所以限制盐的摄入加剧了衰老的一个基本问题。交感神经系统(肾上腺素能)活动的长期增加有助于毛细血管渗漏、胰岛素抵抗(血液中游离脂肪酸增加)和大脑的退行性变化(Griffith和Sutin, 1996)。
低盐饮食降低了血管的灵活性(顺应性)，交感神经系统过度活跃引起的血管僵硬被认为是高血压的一个重要因素，特别是随着年龄的增长。
Pregnancy toxemia/preeclampsia involves increased blood pressure and capillary permeability, and an excess of prolactin. Prolactin secretion is increased by serotonin, which is one of the substances increased by salt restriction, but prolactin itself can promote the loss of sodium in the urine (Ibarra, et al., 2005), and contributes to vascular leakage and hypertension.
妊娠毒血症/子痫前期包括血压升高、毛细血管通透性增加和催乳素过量。5 -羟色胺是限盐增加的物质之一，催乳素的分泌可通过5 -羟色胺增加，但催乳素本身可促进尿中钠的流失(Ibarra, et al.， 2005)，导致血管渗漏和高血压。
In pregnancy, estrogen excess or progesterone deficiency is an important factor in the harmful effects of sodium restriction and protein deficiency. A deficiency of protein contributes to hypothyroidism, which is responsible for the relative estrogen excess.
Protein, salt, thyroid, and progesterone happen to be thermogenic, increasing heat production and stabilizing body temperature at a higher level. Prolactin and estrogen lower the temperature set-point.
The downward shift of temperature and energy metabolism in toxemia or salt deprivation tends to slow the use of oxygen, increasing the glycolytic use of sugar, and contributing to the formation of lactic acid, rather than carbon dioxide. In preeclampsia, serum lactate is increased, even while free fatty acids are interfering with the use of glucose.
在怀孕期间，雌激素过多或孕激素缺乏是限制钠摄入和蛋白质缺乏的一个重要因素。缺乏蛋白质会导致甲状腺功能减退，而甲状腺功能减退是雌激素相对过剩的原因。
蛋白质、盐、甲状腺和黄体酮碰巧是产热的，增加了热量的产生，并将体温稳定在一个较高的水平。催乳素和雌激素降低温度设定值。
在毒血症或缺盐的情况下，温度和能量代谢的下降往往会减缓氧气的使用，增加糖的糖酵解作用，并促进乳酸的形成，而不是二氧化碳的形成。在子痫前期，即使游离脂肪酸干扰葡萄糖的使用，血清乳酸也会增加。
One way of looking at those facts is to see that a lack of sodium slows metabolism, lowers carbon dioxide production, and creates inflammation, stress and degeneration. Rephrasing it, sodium stimulates energy metabolism, increases carbon dioxide production, and protects against inflammation and other maladaptive stress reactions.
In recent years, Weissman’s “wear-and-tear” theory of aging, and Pearl’s “rate of living” theory have been clearly refuted by metabolic studies that are showing that intensified mitochondrial respiration decreases cellular damage, and supports a longer life-span.
Many dog owners are aware that small dogs eat much more food in proportion to their size than big dogs do. And small dogs have a much greater life expectancy than big dogs, in some cases about twice as long (Speakman, 2003).
了解这些事实的一种方法是，钠的缺乏会减缓新陈代谢，降低二氧化碳的产生，并导致炎症、压力和退化。换句话说，钠刺激能量代谢，增加二氧化碳的产生，并防止炎症和其他不适应的应激反应。
近年来，代谢研究明确驳斥了魏斯曼关于衰老的“磨损”理论和珀尔的“存活率”理论，这些研究表明，加强线粒体呼吸可以减少细胞损伤，支持延长寿命。
许多狗主人都知道，就体型而言，小狗比大狗吃更多的食物。小型犬的寿命比大型犬长得多，在某些情况下大约是大型犬的两倍(Speakman, 2003)。
Organisms as different as yeasts and rodents show a similar association of metabolic intensity and life-span. A variety of hamster with a 20% higher metabolic rate lived 15% longer than hamsters with an average metabolic rate (Oklejewicz and Daan, 2002).
Individuals within a strain of mice were found to vary considerably in their metabolic rate. The 25% of the mice with the highest rate used 30% more energy (per gram of body weight) than the 25% with the lowest metabolic rate, and lived 36% longer (Speakman, et al., 2000).
The mitochondria of these animals are “uncoupled,” that is, their use of oxygen isn’t directly proportional to the production of ATP. This means that they are producing more carbon dioxide without necessarily producing more ATP, and that even at rest they are using a considerable amount of energy.
像酵母菌和啮齿动物这样不同的有机体，在代谢强度和寿命方面也表现出类似的联系。一种代谢率高20%的仓鼠比平均代谢率的仓鼠寿命长15% (Oklejewicz和Daan, 2002)。
研究人员发现，同一品系小鼠的个体代谢率差异很大。代谢率最高的25%的小鼠比代谢率最低的25%的小鼠多消耗30%的能量(每克体重)，寿命长36% (Speakman, et al.， 2000)。
这些动物的线粒体是“分离的”，也就是说，它们对氧气的使用与ATP的产生不是直接成比例的。这意味着它们产生更多的二氧化碳，而不一定产生更多的ATP，而且即使在静止状态下，它们也在消耗大量的能量。
One important function of carbon dioxide is to regulate the movement of positively charged alkali metal ions, such as sodium and calcium. When too much calcium enters a cell it activates many enzymes, prevents muscle and nerve cells from relaxing, and ultimately kills the cell. The constant formation of acidic carbon dioxide in the cell allows the cell to remove calcium, along with the small amount of sodium which is constantly entering the cell.
When there is adequate sodium in the extracellular fluid, the continuous inward movement of sodium ions into the resting cell activates an enzyme, sodium-potassium ATPase, causing ATP to break down into ADP and phosphate, which stimulates the consumption of fuel and oxygen to maintain an adequate level of ATP. Increasing the concentration of sodium increases the energy consumption and carbon dioxide production of the cell. The sodium, by increasing carbon dioxide production, protects against the excitatory, toxic effects of the intracellular calcium.
二氧化碳的一个重要功能是调节带正电的碱金属离子的运动，如钠和钙。当过多的钙进入细胞时，它会激活许多酶，阻止肌肉和神经细胞放松，最终杀死细胞。在细胞中不断形成的酸性二氧化碳使细胞能够除去钙，以及不断进入细胞的少量钠。
当有足够的细胞外液钠,钠离子的不断向内运动到静息细胞激活酶,钠钾ATP酶,导致磷酸分解成ADP和ATP,刺激消费的燃料和氧气来维持一个适当的水平的ATP。增加钠的浓度会增加细胞的能量消耗和二氧化碳的产生。钠通过增加二氧化碳的产生，保护细胞内钙的兴奋性和毒性作用。
Hypertonic solutions, containing more than the normal concentration of sodium (from about twice normal to 8 or 10 times normal) are being used to rescuscitate people and animals after injury. Rather than just increasing blood volume to restore circulation, the hypertonic sodium restores cellular energy production, increasing oxygen consumption and heat production while reducing free radical production, improves the contraction and relaxation of the heart muscle, and reduces inflammation, vascular permeability, and edema.
Seawater, which is hypertonic to our tissues, has often been used for treating wounds, and much more concentrated salt solutions have been found effective for accelerating wound healing (Mangete, et al., 1993).
There have been several publications suggesting that increasing the amount of salt in the diet might cause stomach cancer, because countries such as Japan with a high salt intake have a high incidence of stomach cancer.
高渗溶液，含有高于正常浓度的钠(从大约正常浓度的2倍到正常浓度的8或10倍)，被用来抢救受伤的人和动物。高渗钠不仅能增加血容量以恢复循环，还能恢复细胞能量的产生，增加氧的消耗和热的产生，同时减少自由基的产生，改善心肌的收缩和松弛，减少炎症、血管通透性和水肿。
海水对我们的组织是高渗的，经常被用来治疗伤口，更浓的盐溶液被发现可以有效地加速伤口愈合(Mangete, et al.， 1993)。
有几篇文章指出，饮食中增加盐的摄入量可能会导致胃癌，因为像日本这样盐摄入量高的国家，胃癌的发病率很高。
Studies in which animals were fed popular Japanese foods–“salted cuttlefish guts, broiled, salted, dried sardines, pickled radish, and soy sauce”–besides a chemical carcinogen, showed that the Japanese foods increased the number of tumors. But another study, adding only soy sauce (with a salt content of about 18%) to the diet did not increase the incidence of cancer, in another it was protective against stomach cancer (Benjamin, et al., 1991). Several studies show that dried fish and pickled vegetables are carcinogenic, probably because of the oxidized fats, and other chemical changes, and fungal contamination, which are likely to be worse without the salt. Animals fed dried fish were found to have mutagenic urine, apparently as a result of toxic materials occurring in various preserved foods (Fong, et al., 1979).
研究显示，除了一种化学致癌物外，给动物喂食常见的日本食物——“咸墨鱼内脏、烤、咸、干沙丁鱼、腌萝卜和酱油”——表明，日本食物增加了肿瘤的数量。但在另一项研究中，仅在饮食中添加酱油(含盐约18%)并不会增加癌症的发病率，在另一项研究中，它可以预防胃癌(本杰明等人，1991)。几项研究表明，干鱼和腌菜是致癌的，可能是因为氧化脂肪、其他化学变化和真菌污染，如果没有盐，这些情况可能会更糟。喂鱼干的动物被发现有诱变尿，显然是由于各种腌制食品中存在有毒物质的结果(Fong等，1979年)。
Although preserved foods develop many peculiar toxins, even fresh fish in the diet have been found to be associated with increased cancer risk (Phukan, et al., 2006).
When small animals were given a milliliter of a saturated salt solution with the carcinogen, the number of tumors was increased with the salt. However, when the salt was given with mucin, it had no cancer promoting effect. Since the large amount of a saturated salt solution breaks down the stomach’s protective mucus coating, the stomach cells were not protected from the carcinogen. Rather than showing that salt causes stomach cancer, the experiments showed that a cup or more of saturated salt solution, or several ounces of pure salt, shouldn’t be ingested at the same time as a strong carcinogen.
Some studies have found pork to be associated with cancer of the esophagous (Nagai, et al., 1982), thyroid (Markaki, et al., 2003), and other organs, but an experiment with beef, chicken, or bacon diet in rats provides another perspective on the role of salt in carcinogenesis. After being given a carcinogen, rats were fed meat diets, containing either 30% or 60% of freeze-dried fried beef, chicken, or bacon. Neither beef nor chicken changed the incidence of precancerous lesions in the intestine, but the incidence was reduced by 12% in the animals on the 30% bacon diet, and by 20% in rats getting the diet with 60% bacon. Salt apparently made the difference.
尽管腌制食品会产生许多特殊的毒素，但即使是饮食中的鲜鱼也被发现与增加癌症风险有关(Phukan等，2006年)。
当给小动物一毫升含有致癌物的饱和盐溶液时，肿瘤的数量随着盐的增加而增加。然而，当盐与粘蛋白一起服用时，它没有促进癌症的作用。由于大量的饱和盐溶液会破坏胃粘膜的保护层，胃细胞并没有受到致癌物质的保护。实验不是证明盐会导致胃癌，而是表明一杯或更多的饱和盐溶液，或几盎司的纯盐，不应该与强致癌物同时摄入。
一些研究发现猪肉与食道癌(Nagai, et al.， 1982)、甲状腺癌(Markaki, et al.， 2003)和其他器官癌有关，但一项在老鼠身上进行的牛肉、鸡肉或培根饮食的实验为盐在致癌中的作用提供了另一种视角。在给老鼠喂食致癌物后，老鼠被喂食含有30%或60%冻干炸牛肉、鸡肉或培根的肉类食物。牛肉和鸡肉都没有改变肠道癌前病变的发病率，但在吃30%培根的动物中发病率降低了12%，在吃60%培根的老鼠中发病率降低了20%。显然，盐起了作用。
Other protective effects of increased sodium are that it improves immunity (Junger, et al., 1994), reduces vascular leakiness, and alleviates inflammation (Cara, et al., 1988). All of these effects would tend to protect against the degenerative diseases, including tumors, atherosclerosis, and Alzheimer’s disease. The RAA system appears to be crucially involved in all kinds of sickness and degeneration, but the protective effects of sodium are more basic than just helping to prevent activation of that system.
A slight decrease in temperature can promote inflammation (Matsui, et al., 2006). The thermogenic substances–dietary protein, sodium, sucrose, thyroid and progesterone–are antiinflammatory for many reasons, but very likely the increased temperature itself is important.
A poor reaction to stress, with increased cortisol, can raise the body temperature by accelerating the breakdown and resynthesis of proteins, but adaptive resistance to stress increases the temperature by increasing the consumption of oxygen and fuel. In the presence of increased cortisol, abdominal fat increases, along with circulating fatty acids and calcium, as mitochondrial respiration is suppressed.
增加钠的其他保护作用是提高免疫力(Junger, et al.， 1994)，减少血管渗漏，缓解炎症(Cara, et al.， 1988)。所有这些作用都有助于预防退行性疾病，包括肿瘤、动脉粥样硬化和阿尔茨海默病。RAA系统似乎在所有疾病和退化中都起着至关重要的作用，但钠的保护作用更基本，而不仅仅是帮助防止该系统的激活。
轻微的体温下降可以促进炎症(Matsui等，2006)。生热物质——膳食蛋白质、钠、蔗糖、甲状腺和黄体酮——具有多种抗炎作用，但很可能温度升高本身很重要。
对压力的不良反应，包括皮质醇的增加，可以通过加速蛋白质的分解和重新合成来提高体温，但对压力的适应性抵抗则通过增加氧气和燃料的消耗来提高体温。在皮质醇增加的情况下，腹部脂肪增加，伴随着循环脂肪酸和钙，线粒体呼吸受到抑制。
When mice are chilled, they spontaneously prefer slightly salty water, rather than fresh, and it increases their heat production (Dejima, et al., 1996). When rats are given 0.9 per cent sodium chloride solution with their regular food, their heat production increases, and their body fat, including abdominal fat, decreases (Bryant, et al., 1984). These responses to increased dietary sodium are immediate. Part of the effect of sodium involves regulatory processes in the brain, which are sensitive to the ratio between sodium and calcium. Decreasing sodium, or increasing calcium, causes the body’s metabolism to shift away from thermogenesis and accelerated respiration.
Regulating intracellular calcium by increasing the production of carbon dioxide is probably a basic mechanism in sodium’s protection against inflammation and excitatory cell damage and degeneration.
Cortisol’s suppression of mitochondrial respiration is closely associated with its ability to increase intracellular calcium. Cortisol blocks the thermogenic effects of sodium, allowing intracellular calcium to damage cells. With aging, the tissues are more susceptible to these processes.
当老鼠被冷冻时，它们自发地更喜欢微咸水而不是淡水，这增加了它们的热量产生(Dejima等人，1996)。当老鼠在日常食物中加入0.9%的氯化钠溶液时，它们产生的热量会增加，身体脂肪(包括腹部脂肪)会减少(Bryant等，1984)。这些对增加膳食钠的反应是立竿见影的。钠的部分作用涉及到大脑的调节过程，大脑对钠和钙的比例非常敏感。减少钠，或增加钙，会导致身体的新陈代谢偏离生热作用，加速呼吸。
通过增加二氧化碳的产生来调节细胞内钙可能是钠保护细胞免受炎症和兴奋性细胞损伤和退化的基本机制。
皮质醇对线粒体呼吸的抑制与其增加细胞内钙的能力密切相关。皮质醇会阻止钠的生热作用，让细胞内的钙破坏细胞。随着年龄的增长，组织更容易受到这些过程的影响。
The thermogenic effects of sodium can be seen in long-term studies, as well as short. A low-sodium diet accelerates the decrease in heat production that normally occurs with aging, lowering the metabolic rate of brown fat and body temperature, and increasing the fat content of the body, as well as the activity of the fat synthesizing enzyme (Xavier, et al., 2003).
Activation of heat production and increased body temperature might account for some of the GABA-like sedative effects of increased sodium. Increasing GABA in the brain increases brown fat heat production (Horton, et al., 1988). Activation of heat production by brown fat increases slow wave sleep (Dewasmes, et al., 2003), the loss of which is characteristic of aging. (In adult humans, the skeletal muscles have heat-producing functions similar to brown fat.)
Now that inflammation is recognized as having a central role in the degenerative diseases, the fact that renin, angiotensin, and aldosterone all contribute to inflammation and are increased by a sodium deficiency, should arouse interest in exploring the therapeutic uses of sodium supplementation, and the integrated use of all of the factors that normally support respiratory energy production, especially thyroid and progesterone. Progesterone’s antagonism to aldosterone has been known for many years, and the synthetic antialdosterone drugs are simply poor imitations of progesterone.
钠的热效应可以在长期和短期的研究中看到。低钠饮食加速了通常随年龄增长而产生的热量的减少，降低了棕色脂肪的代谢率和体温，增加了身体的脂肪含量，以及脂肪合成酶的活性(Xavier等，2003)。
热生产的激活和体温的升高可能是钠增加产生的一些gaba样镇静作用的原因。大脑中GABA的增加会增加棕色脂肪热量的产生(Horton等人，1988)。棕色脂肪产生热量的激活会增加慢波睡眠(Dewasmes, et al.， 2003)，慢波睡眠的丧失是衰老的特征。(成年人骨骼肌的产热功能类似于棕色脂肪。)
现在，炎症被认为在退行性疾病中具有核心作用，肾素、血管紧张素和醛固酮都有助于炎症，并因钠缺乏而增加，这一事实应该引起人们对探索钠补充剂的治疗用途的兴趣，以及所有支持呼吸能量产生的因素的综合使用，尤其是甲状腺和孕酮。孕酮对醛固酮的拮抗作用已经为人所知很多年了，而合成的抗醛固酮药物仅仅是孕酮的拙劣模仿。
But the drug industry is interested in selling new drugs to block the formation and action of each of the components of the RAAS, rather than an inexpensive method (such as nutrition) to normalize the system.
但是制药业感兴趣的是销售新药来阻止RAAS的形成和每个成分的作用，而不是通过廉价的方法(如营养)来使系统正常化。
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