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868 lines
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<head>
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<title>
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Salt, energy, metabolic rate, and longevity
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</title>
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</head>
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<body>
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<h1>
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Salt, energy, metabolic rate, and longevity
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</h1>
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<p></p>
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<p>
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In the 1950s, when the pharmaceutical industry was beginning to promote some new chemicals as diuretics to
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replace the traditional mercury compounds, Walter Kempner"s low-salt "rice diet" began to be discussed in
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the medical journals and other media. The diuretics were offered for treating high blood pressure, pulmonary
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edema, heart failure, "idiopathic edema," orthostatic edema and obesity, and other forms of water retention,
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including pregnancy, and since they functioned by causing sodium to be excreted in the urine, their sale was
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accompanied by advising the patients to reduce their salt intake to make the diuretic more effective.
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</p>
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<p>
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It was clear to some physicians (and to most veterinarians) that salt restriction, especially combined with
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salt-losing diuresis, was very harmful during pregnancy, but that combination became standard medical
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practice for many years, damaging millions of babies.
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</p>
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<p>
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Despite numerous publications showing that diuretics could cause the edematous problems that they were
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supposed to remedy, they have been one of the most profitable types of drug. Dietary salt restriction has
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become a cultural cliché, largely as a consequence of the belief that sodium causes edema and hypertension.
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</p>
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<p>
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Salt restriction, according to a review of about 100 studies (Alderman, 2004), lowers the blood pressure a
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few points. But that generally doesn"t relate to better health. In one study (3000 people, 4 years), there
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was a clear increase in mortality in the individuals who ate less salt. An extra few grams of salt per day
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was associated with a 36% reduction in "coronary events" (Alderman, et al., 1995). Another study (more than
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11,000 people, 22 years) also showed an inverse relation between salt intake and mortality (Alderman, et
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al., 1997).
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</p>
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<p>
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Tom Brewer, an obstetrician who devoted his career to educating the public about the importance of prenatal
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nutrition, emphasizing adequate protein (especially milk), calories, and salt, was largely responsible for
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the gradual abandonment of the low-salt plus diuretics treatment for pregnant women. He explained that
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sodium, in association with serum albumin, is essential for maintaining blood volume. Without adequate
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sodium, the serum albumin is unable to keep water from leaving the blood and entering the tissues. The
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tissues swell as the volume of blood is reduced.
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</p>
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<p>
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During pregnancy, the reduced blood volume doesn"t adequately nourish and oxygenate the growing fetus, and
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the reduced circulation to the kidneys causes them to release a signal substance (renin) that causes the
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blood to circulate faster, under greater pressure. A low salt diet is just one of the things that can reduce
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kidney circulation and stimulate renin production. Bacterial endotoxin, and other things that cause
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excessive capillary permeability, edema, or shock-like symptoms, will activate renin secretion.
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</p>
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<p>
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The blood volume problem isn"t limited to the hypertension of pregnancy toxemia: "Plasma volume is usually
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lower in patients with essential hypertension than in normal subjects" (Tarazi, 1976).
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</p>
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<p>
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Several studies of preeclampsia or toxemia of pregnancy showed that supplementing the diet with salt would
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lower the women"s blood pressure, and prevent the other complications associated with toxemia (Shanklin and
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Hodin, 1979).
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</p>
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<p>
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It has been known for many years that decreasing sodium intake causes the body to respond adaptively,
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increasing the renin-angiotensin-aldosterone system (RAAS). The activation of this system is recognized as a
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factor in hypertension, kidney disease, heart failure, fibrosis of the heart, and other problems. Sodium
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restriction also increases serotonin, activity of the sympathetic nervous system, and plasminogen activator
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inhibitor type-1 (PAI-1), which contributes to the accumulation of clots and is associated with breast and
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prostate cancer. The sympathetic nervous system becomes hyperactive in preeclampsia (Metsaars, et al.,
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2006).
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</p>
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<p>
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Despite the general knowledge of the relation of dietary salt to the RAA system, and its application by
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Brewer and others to the prevention of pregnancy toxemia, it isn"t common to see the information applied to
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other problems, such as aging and the stress-related degenerative diseases.
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</p>
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<p>
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Many young women periodically crave salt and sugar, especially around ovulation and premenstrually, when
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estrogen is high. Physiologically, this is similar to the food cravings of pregnancy. Premenstrual water
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retention is a common problem, and physicians commonly offer the same advice to cycling women that was
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offered as a standard treatment for pregnant women--the avoidance of salt, sometimes with a diuretic. But
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when women premenstrually increase their salt intake according to their craving, the water retention can be
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prevented.
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</p>
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<p>
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Blood volume changes during the normal menstrual cycle, and when the blood volume is low, it is usually
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because the water has moved into the tissues, causing edema. When estrogen is high, the osmolarity of the
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blood is low. (Courtar, et al., 2007; Stachenfeld, et al., 1999). Hypothyroidism (which increases the ratio
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of estrogen to progesterone) is a major cause of excessive sodium loss.
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</p>
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<p>
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The increase of adrenalin caused by salt restriction has many harmful effects, including insomnia. Many old
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people have noticed that a low sodium diet disturbs their sleep, and that eating their usual amount of salt
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restores their ability to sleep. The activity of the sympathetic nervous system increases with aging, so
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salt restriction is exacerbating one of the basic problems of aging. Chronically increased activity of the
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sympathetic (adrenergic) nervous system contributes to capillary leakage, insulin resistance (with increased
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free fatty acids in the blood), and degenerative changes in the brain (Griffith and Sutin, 1996).
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</p>
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<p>
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The flexibility of blood vessels (compliance) is decreased by a low-salt diet, and vascular stiffness caused
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by over-activity of the sympathetic nervous system is considered to be an important factor in hypertension,
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especially with aging.
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</p>
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<p>
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Pregnancy toxemia/preeclampsia involves increased blood pressure and capillary permeability, and an excess
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of prolactin. Prolactin secretion is increased by serotonin, which is one of the substances increased by
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salt restriction, but prolactin itself can promote the loss of sodium in the urine (Ibarra, et al., 2005),
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and contributes to vascular leakage and hypertension.
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</p>
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<p>
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In pregnancy, estrogen excess or progesterone deficiency is an important factor in the harmful effects of
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sodium restriction and protein deficiency. A deficiency of protein contributes to hypothyroidism, which is
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responsible for the relative estrogen excess.
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</p>
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<p>
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Protein, salt, thyroid, and progesterone happen to be thermogenic, increasing heat production and
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stabilizing body temperature at a higher level. Prolactin and estrogen lower the temperature set-point.
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</p>
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<p>
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The downward shift of temperature and energy metabolism in toxemia or salt deprivation tends to slow the use
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of oxygen, increasing the glycolytic use of sugar, and contributing to the formation of lactic acid, rather
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than carbon dioxide. In preeclampsia, serum lactate is increased, even while free fatty acids are
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interfering with the use of glucose.
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</p>
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<p>
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One way of looking at those facts is to see that a lack of sodium slows metabolism, lowers carbon dioxide
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production, and creates inflammation, stress and degeneration. Rephrasing it, sodium stimulates energy
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metabolism, increases carbon dioxide production, and protects against inflammation and other maladaptive
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stress reactions.
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</p>
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<p>
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In recent years, Weissman"s "wear-and-tear" theory of aging, and Pearl"s "rate of living" theory have been
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clearly refuted by metabolic studies that are showing that intensified mitochondrial respiration decreases
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cellular damage, and supports a longer life-span.
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</p>
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<p>
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Many dog owners are aware that small dogs eat much more food in proportion to their size than big dogs do.
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And small dogs have a much greater life expectancy than big dogs, in some cases about twice as long
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(Speakman, 2003).
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</p>
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<p>
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Organisms as different as yeasts and rodents show a similar association of metabolic intensity and
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life-span. A variety of hamster with a 20% higher metabolic rate lived 15% longer than hamsters with an
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average metabolic rate (Oklejewicz and Daan, 2002).
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</p>
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<p>
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Individuals within a strain of mice were found to vary considerably in their metabolic rate. The 25% of the
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mice with the highest rate used 30% more energy (per gram of body weight) than the 25% with the lowest
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metabolic rate, and lived 36% longer (Speakman, et al., 2000).
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</p>
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<p>
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The mitochondria of these animals are "uncoupled," that is, their use of oxygen isn"t directly proportional
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to the production of ATP. This means that they are producing more carbon dioxide without necessarily
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producing more ATP, and that even at rest they are using a considerable amount of energy.
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</p>
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<p>
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One important function of carbon dioxide is to regulate the movement of positively charged alkali metal
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ions, such as sodium and calcium. When too much calcium enters a cell it activates many enzymes, prevents
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muscle and nerve cells from relaxing, and ultimately kills the cell. The constant formation of acidic carbon
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dioxide in the cell allows the cell to remove calcium, along with the small amount of sodium which is
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constantly entering the cell.
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</p>
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<p>
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When there is adequate sodium in the extracellular fluid, the continuous inward movement of sodium ions into
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the resting cell activates an enzyme, sodium-potassium ATPase, causing ATP to break down into ADP and
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phosphate, which stimulates the consumption of fuel and oxygen to maintain an adequate level of ATP.
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Increasing the concentration of sodium increases the energy consumption and carbon dioxide production of the
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cell. The sodium, by increasing carbon dioxide production, protects against the excitatory, toxic effects of
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the intracellular calcium.
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</p>
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<p>
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Hypertonic solutions, containing more than the normal concentration of sodium (from about twice normal to 8
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or 10 times normal) are being used to rescuscitate people and animals after injury. Rather than just
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increasing blood volume to restore circulation, the hypertonic sodium restores cellular energy production,
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increasing oxygen consumption and heat production while reducing free radical production, improves the
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contraction and relaxation of the heart muscle, and reduces inflammation, vascular permeability, and edema.
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</p>
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<p>
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Seawater, which is hypertonic to our tissues, has often been used for treating wounds, and much more
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concentrated salt solutions have been found effective for accelerating wound healing (Mangete, et al.,
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1993).
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</p>
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<p>
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There have been several publications suggesting that increasing the amount of salt in the diet might cause
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stomach cancer, because countries such as Japan with a high salt intake have a high incidence of stomach
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cancer.
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</p>
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<p>
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Studies in which animals were fed popular Japanese foods--"salted cuttlefish guts, broiled, salted, dried
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sardines, pickled radish, and soy sauce"--besides a chemical carcinogen, showed that the Japanese foods
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increased the number of tumors. But another study, adding only soy sauce (with a salt content of about 18%)
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to the diet did not increase the incidence of cancer, in another it was protective against stomach cancer
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(Benjamin, et al., 1991). Several studies show that dried fish and pickled vegetables are carcinogenic,
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probably because of the oxidized fats, and other chemical changes, and fungal contamination, which are
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likely to be worse without the salt. Animals fed dried fish were found to have mutagenic urine, apparently
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as a result of toxic materials occurring in various preserved foods (Fong, et al., 1979).
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</p>
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<p>
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Although preserved foods develop many peculiar toxins, even fresh fish in the diet have been found to be
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associated with increased cancer risk (Phukan, et al., 2006).
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</p>
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<p>
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When small animals were given a milliliter of a saturated salt solution with the carcinogen, the number of
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tumors was increased with the salt. However, when the salt was given with mucin, it had no cancer promoting
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effect. Since the large amount of a saturated salt solution breaks down the stomach"s protective mucus
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coating, the stomach cells were not protected from the carcinogen. Rather than showing that salt causes
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stomach cancer, the experiments showed that a cup or more of saturated salt solution, or several ounces of
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pure salt, shouldn"t be ingested at the same time as a strong carcinogen.
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</p>
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<p>
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Some studies have found pork to be associated with cancer of the esophagous (Nagai, et al., 1982), thyroid
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(Markaki, et al., 2003), and other organs, but an experiment with beef, chicken, or bacon diet in rats
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provides another perspective on the role of salt in carcinogenesis. After being given a carcinogen, rats
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were fed meat diets, containing either 30% or 60% of freeze-dried fried beef, chicken, or bacon. Neither
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beef nor chicken changed the incidence of precancerous lesions in the intestine, but the incidence was
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reduced by 12% in the animals on the 30% bacon diet, and by 20% in rats getting the diet with 60% bacon.
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Salt apparently made the difference.
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</p>
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<p>
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Other protective effects of increased sodium are that it improves immunity (Junger, et al., 1994), reduces
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vascular leakiness, and alleviates inflammation (Cara, et al., 1988). All of these effects would tend to
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protect against the degenerative diseases, including tumors, atherosclerosis, and Alzheimer"s disease. The
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RAA system appears to be crucially involved in all kinds of sickness and degeneration, but the protective
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effects of sodium are more basic than just helping to prevent activation of that system.
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</p>
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<p>
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A slight decrease in temperature can promote inflammation (Matsui, et al., 2006). The thermogenic
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substances--dietary protein, sodium, sucrose, thyroid and progesterone--are antiinflammatory for many
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reasons, but very likely the increased temperature itself is important.
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</p>
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<p>
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A poor reaction to stress, with increased cortisol, can raise the body temperature by accelerating the
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breakdown and resynthesis of proteins, but adaptive resistance to stress increases the temperature by
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increasing the consumption of oxygen and fuel. In the presence of increased cortisol, abdominal fat
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increases, along with circulating fatty acids and calcium, as mitochondrial respiration is suppressed.
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</p>
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<p>
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When mice are chilled, they spontaneously prefer slightly salty water, rather than fresh, and it increases
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their heat production (Dejima, et al., 1996). When rats are given 0.9 per cent sodium chloride solution with
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their regular food, their heat production increases, and their body fat, including abdominal fat, decreases
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(Bryant, et al., 1984). These responses to increased dietary sodium are immediate. Part of the effect of
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sodium involves regulatory processes in the brain, which are sensitive to the ratio between sodium and
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calcium. Decreasing sodium, or increasing calcium, causes the body"s metabolism to shift away from
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thermogenesis and accelerated respiration.
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</p>
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<p>
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Regulating intracellular calcium by increasing the production of carbon dioxide is probably a basic
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mechanism in sodium"s protection against inflammation and excitatory cell damage and degeneration.
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</p>
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<p>
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Cortisol"s suppression of mitochondrial respiration is closely associated with its ability to increase
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intracellular calcium. Cortisol blocks the thermogenic effects of sodium, allowing intracellular calcium to
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damage cells. With aging, the tissues are more susceptible to these processes.
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</p>
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<p>
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The thermogenic effects of sodium can be seen in long-term studies, as well as short. A low-sodium diet
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accelerates the decrease in heat production that normally occurs with aging, lowering the metabolic rate of
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brown fat and body temperature, and increasing the fat content of the body, as well as the activity of the
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fat synthesizing enzyme (Xavier, et al., 2003).
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</p>
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<p>
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Activation of heat production and increased body temperature might account for some of the GABA-like
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sedative effects of increased sodium. Increasing GABA in the brain increases brown fat heat production
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(Horton, et al., 1988). Activation of heat production by brown fat increases slow wave sleep (Dewasmes, et
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al., 2003), the loss of which is characteristic of aging. (In adult humans, the skeletal muscles have
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heat-producing functions similar to brown fat.)
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</p>
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<p>
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Now that inflammation is recognized as having a central role in the degenerative diseases, the fact that
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renin, angiotensin, and aldosterone all contribute to inflammation and are increased by a sodium deficiency,
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should arouse interest in exploring the therapeutic uses of sodium supplementation, and the integrated use
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of all of the factors that normally support respiratory energy production, especially thyroid and
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progesterone. Progesterone"s antagonism to aldosterone has been known for many years, and the synthetic
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antialdosterone drugs are simply poor imitations of progesterone.
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</p>
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<p>
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But the drug industry is interested in selling new drugs to block the formation and action of each of the
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components of the RAAS, rather than an inexpensive method (such as nutrition) to normalize the system.
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</p>
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<p><h3>REFERENCES</h3></p>
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<p>
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J Hum Hypertens. 2002 Dec;16(12):843-50. <strong>Salt supresses baseline muscle sympathetic nerve activity
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in salt-sensitive and salt-resistant hypertensives.</strong>
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Abrah"o SB, Tinucci T, Santello JL, Mion D Jr.
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</p>
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<p>
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Neuropharmacology. 1986 Jun;25(6):627-31. <strong>Activation of thermogenesis of brown fat in rats by
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baclofen.</strong> Addae JI, Rothwell NJ, Stock MJ, Stone TW.
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</p>
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<p>
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Hypertension 25: 1144-1152, 1995:<strong>
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Low urinary sodium is associated with greater risk of myocardial infarction among treated hypertensive
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men.</strong> Alderman MH, Madhavan S, Cohen H, Sealey JE, Laragh JH
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</p>
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<p>
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The National Health and Nutrition Examination Survey (NHANES I). Lancet 351: 781-785, 1998: <strong>Dietary
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sodium intake and mortality,</strong> Alderman MH, Cohen H, Madhavan S.
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</p>
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<p>
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Clin Exp Hypertens A. 1982;4(7):1073-83.<strong>
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Aortic rigidity and plasma catecholamines in essential hypertensive patients.</strong> Alicandri CL,
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Agabiti-Rosei E, Fariello R, Beschi M, Boni E, Castellano M, Montini E, Romanelli G, Zaninelli A, Muiesan G.
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</p>
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<p>
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Anesth Analg. 1989 Dec;69(6):714-20.<strong>
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Hypertonic saline solution-hetastarch for fluid resuscitation in experimental septic shock.</strong>
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Armistead CW Jr, Vincent JL, Preiser JC, De Backer D, Thuc Le Minh.
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</p>
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<p>
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J Clin Invest. 1976 Feb;57(2):368-79.<strong>
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Thyroid thermogenesis. Relationships between Na+-dependent respiration and Na+ + K+-adenosine
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triphosphatase activity in rat skeletal muscle.</strong> Asano Y, Liberman UA, Edelman IS.
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</p>
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<p>
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Experientia Suppl. 1978;32:199-203.<strong>
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Increased cell membrane permeability to Na+ and K+ induced by thyroid hormone in rat skeletal
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muscle.</strong> Asano Y.
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</p>
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<p>
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Nephron 1986;44(1):70-4.<strong>
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Effect of sodium bicarbonate preloading on ischemic renal failure.</strong> Atkins JL <strong>Rats
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pretreated with sodium bicarbonate were functionally protected from the damage of bilateral renal artery
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occlusion.</strong>
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</p>
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<p>
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Cancer Res. 1991 Jun 1;51(11):2940-2.<strong>
|
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Inhibition of benzo(a)pyrene-induced mouse forestomach neoplasia by dietary soy sauce.</strong> Benjamin
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H, Storkson J, Nagahara A, Pariza MW.
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</p>
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<p>
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Am J Vet Res. 1990 Jul;51(7):999-1007. <strong>Effect of hypertonic vs isotonic saline solution on responses
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to sublethal Escherichia coli endotoxemia in horses.</strong> Bertone JJ, Gossett KA, Shoemaker KE,
|
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Bertone AL, Schneiter HL. <strong>". . .</strong>
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<strong>cardiac output was increased and total peripheral resistance was decreased during the hypertonic,
|
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compared with the isotonic, saline trial."</strong>
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</p>
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<p>
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Am J Physiol Endocrinol Metab. 2005 Sep;289(3):E429-38. Epub 2005 May 10. <strong>
|
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Long-term caloric restriction increases UCP3 content but decreases proton leak and reactive oxygen
|
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species production in rat skeletal muscle mitochondria.</strong>
|
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Bevilacqua L, Ramsey JJ, Hagopian K, Weindruch R, Harper ME.
|
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</p>
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<p>
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Int J Obes. 1984;8(3):221-31. <strong>Influence of sodium intake on thermogenesis and brown adipose tissue
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in the rat.
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</strong>
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Bryant KR, Rothwell NJ, Stock MJ.
|
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</p>
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<p>
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Braz J Med Biol Res. 1988;21(2):281-3. <strong>Effect of hyperosmotic sodium chloride solution on vascular
|
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permeability and inflammatory edema in rats.</strong>
|
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Cara DC, Malucelli BE.
|
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</p>
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<p>
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Experientia Suppl. 1978;32:25-32. <strong>Does cytoplasmic alkalinization trigger mitochondrial energy
|
|
dissipation in the brown adipocyte?</strong> Chinet A, Friedli C, Seydoux J, Girardier L.
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</p>
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<p>
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Am J Clin Nutr. 1993 Nov;58(5):608-13. <strong>Effects of infused sodium acetate, sodium lactate, and sodium
|
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beta-hydroxybutyrate on energy expenditure and substrate oxidation rates in lean humans.</strong>
|
|
Chiol"ro R, Mavrocordatos P, Burnier P, Cayeux MC, Schindler C, J"quier E, Tappy L.
|
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</p>
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<p>
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Nutr Metab Cardiovasc Dis. 2006 Mar;16(2):148-55. <strong>High- or low-salt diet from weaning to adulthood:
|
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effect on body weight, food intake and energy balance in rats.</strong> Coelho MS, Passadore MD,
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Gasparetti AL, Bibancos T, Prada PO, Furukawa LL, Furukawa LN, Fukui RT, Casarini DE, Saad MJ, Luz J,
|
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Chiavegatto S, Dolnikoff MS, Heimann JC.
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</p>
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<p>
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Reprod Sci. 2007 Jan;14(1):66-72.<strong>
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Orthostatic stress response during the menstrual cycle is unaltered in formerly preeclamptic women with
|
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low plasma volume.
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</strong>Courtar DA, Spaanderman ME, Janssen BJ, Peeters LL.
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</p>
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<p>
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Life Sci. 1990;47(25):2317-22.<strong>
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Pharmacological evidence for involvement of the sympathetic nervous system in the increase in renin
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secretion produced by a low sodium diet in rats.
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</strong>
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Tkacs NC, Kim M, Denzon M, Hargrave B, Ganong WF.
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</p>
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<p>
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J Trauma. 1992 Jun;32(6):704-12; discussion 712-3. <strong>Effects of hypertonic saline dextran
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resuscitation on oxygen delivery, oxygen consumption, and lipid peroxidation after burn injury.</strong>
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Tokyay R, Zeigler ST, Kramer GC, Rogers CS, Heggers JP, Traber DL, Herndon DN.
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</p>
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<p>
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Pflugers Arch. 1976 Jun 22;363(3):219-22. <strong>Is the chemomechanical energy transformation reversible?
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</strong>Ulbrich M, R"egg JC.
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</p>
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<p>
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Experientia 1971 Jan 15;27(1):45-6. <strong>Stretch induced formation of ATP-32P in glycerinated fibres of
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insect flight muscle.</strong> Ulbrich M, Ruegg JC
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</p>
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<p>
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Front Biosci. 2007 Jan 1;12:2457-70.<strong>
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Maternal-fetal metabolism in normal pregnancy and preeclampsia.
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</strong>von Versen-Hoeynck FM, Powers RW.
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</p>
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<p>
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Br J Nutr. 2005 May;93(5):575-9. <strong>The effects of drinks made from simple sugars on blood pressure in
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healthy older people.</strong> Visvanathan R, Chen R, Garcia M, Horowitz M, Chapman I.
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</p>
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<p>
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Clin Cardiol. 1980 Oct;3(5):348-51. <strong>Sympathetic nervous system activity during sodium restriction in
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essential hypertension.</strong> Warren SE, Vieweg WV, O'Connor DT.
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</p>
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<p>
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Curr Heart Fail Rep. 2004 Jul;1(2):51-6. <strong>Efficacy of aldosterone receptor antagonism in heart
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failure: potential mechanisms.
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</strong>
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Weber KT.
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</p>
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<p>
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J Hypertens. 1996 Dec;14(12):1461-2. <strong>Is salt-sensitivity of blood pressure a reproducible
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phenomenon-commentary.</strong> Weinberger MH. Hypertension Research Center, Indiana University School
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of Medicine, Indianapolis 46202, USA.
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</p>
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<p>
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J Clin Invest. 1983 Apr;71(4):916-25. <strong>Stimulation of thermogenesis by carbohydrate overfeeding.
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Evidence against sympathetic nervous system mediation.</strong> Welle S, Campbell RG.
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</p>
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<p>
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Br Med J (Clin Res Ed). 1986 Jan 18;292(6514):168-70. <strong>Treatment of hyponatraemic seizures with
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|
intravenous 29.2% saline.</strong> Worthley LI, Thomas PD. "Five patients with severe hyponatraemia and
|
|
epileptiform seizures were given 50 ml of 29.2% saline (250 mmol) through a central venous catheter over 10
|
|
minutes to <strong>control seizures rapidly, reduce cerebral oedema, and diminish the incidence of permanent
|
|
neuronal damage.</strong>
|
|
|
|
The saline controlled seizures in all patients, increasing the mean serum sodium concentration by 7.4 (SD
|
|
1.14) mmol(mEq)/l and decreasing the mean serum potassium concentration by 0.62 (0.5) mmol(mEq)/l."
|
|
</p>
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|
<p>
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|
Metabolism. 2003 Aug;52(8):1072-7. <strong>Dietary sodium restriction exacerbates age-related changes in rat
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|
adipose tissue and liver lipogenesis.</strong> Xavier AR, Gar"falo MA, Migliorini RH, Kettelhut
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|
IC.<strong>"Taken together, the data indicate that prolonged dietary sodium restriction exacerbates normal,
|
|
age-related changes in white and BAT metabolism."</strong>
|
|
</p>
|
|
<p>
|
|
Geriatr Nurs. 1997 Mar-Apr;18(2):87-8. <strong>Is salt restriction dangerous for elders?</strong> Yen PK.
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</p>
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Copyright 2007. Raymond Peat, P.O. Box 5764, Eugene OR 97405. All Rights Reserved. www.RayPeat.comNot for
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