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    <h1>Salt, energy, metabolic rate, and longevity</h1>
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<p class="nav"><span class="nav-left">Listed under <a href="/ray-peat.html">Ray Peat</a>.</span><span class="nav-right"><a href="/theme.html">Theme</a></span></p>
<p>From the <a href="https://raypeat.com/articles/articles/salt.shtml" target="_blank">original article</a> in 2007. Author: <a href="https://raypeat.com/" target="_blank">Ray Peat</a>.</p>
<p>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.</p>
<p>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.</p>
<p>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 clich&eacute;, largely as a consequence of the belief that sodium 
causes edema and hypertension.  </p>
<p>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).</p>
<p>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. </p>
<p>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.</p>
<p>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).</p>
<p>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). </p>
<p>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).</p>
<p>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.</p>
<p>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. </p>
<p>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.</p>
<p>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).</p>
<p>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.</p>
<p>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.</p>
<p>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. </p>
<p>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.</p>
<p>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. </p>
<p>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.</p>
<p>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.</p>
<p>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).</p>
<p>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).</p>
<p>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).</p>
<p>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.</p>
<p>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.</p>
<p>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.</p>
<p>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. </p>
<p>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).</p>
<p>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.</p>
<p>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).</p>
<p>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). </p>
<p>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.</p>
<p>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.</p>
<p>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.</p>
<p>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.</p>
<p>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.</p>
<p>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.</p>
<p>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.</p>
<p>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.</p>
<p>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). </p>
<p>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.)</p>
<p>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.</p>
<p>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.  
</p>
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