To receive more information about up-to-date research on micronutrients, sign up for the free, semi-annual LPI Research Newsletter here.
Salt (sodium chloride) is essential for life. The tight regulation of the body's sodium and chloride concentrations is so important that multiple mechanisms work in concert to control them. Although scientists agree that a minimal amount of salt is required for survival, the health implications of excess salt intake represent an area of continued investigation among scientists, clinicians, and public health experts (1).
Sodium (Na+) and chloride (Cl-) are the principal ions in the fluid outside of cells (extracellular fluid), which includes blood plasma. As such, they play critical roles in a number of life-sustaining processes (2).
Maintenance of membrane potential
Sodium and chloride are electrolytes that contribute to the maintenance of concentration and charge differences across cell membranes. Potassium is the principal positively charged ion (cation) inside of cells, while sodium is the principal cation in extracellular fluid. Potassium concentrations are about 30 times higher inside than outside cells, while sodium concentrations are more than ten times lower inside than outside cells. The concentration differences between potassium and sodium across cell membranes create an electrochemical gradient known as the membrane potential. A cell's membrane potential is maintained by ion pumps in the cell membrane, especially the sodium, potassium-ATPase pumps. These pumps use ATP (energy) to pump sodium out of the cell in exchange for potassium (diagram). Their activity has been estimated to account for 20%-40% of the resting energy expenditure in a typical adult. The large proportion of energy dedicated to maintaining sodium/potassium concentration gradients emphasizes the importance of this function in sustaining life. Tight control of cell membrane potential is critical for nerve impulse transmission, muscle contraction, and cardiac function (3, 4).
Nutrient absorption and transport
Absorption of sodium in the small intestine plays an important role in the absorption of chloride, amino acids, glucose, and water. Similar mechanisms are involved in the reabsorption of these nutrients after they have been filtered from the blood by the kidneys. Chloride, in the form of hydrochloric acid (HCl), is also an important component of gastric juice, which aids the digestion and absorption of many nutrients (2, 5).
Because sodium is the primary determinant of extracellular fluid volume, including blood volume, a number of physiological mechanisms that regulate blood volume and blood pressure work by adjusting the body's sodium content. In the circulatory system, pressure receptors (baroreceptors) sense changes in blood pressure and send excitatory or inhibitory signals to the nervous system and/or endocrine glands to affect sodium regulation by the kidneys. In general, sodium retention results in water retention and sodium loss results in water loss (4, 5). Below are descriptions of two of the many systems that affect blood volume and blood pressure through sodium regulation.
In response to a significant decrease in blood volume or pressure (e.g., serious blood loss or dehydration), the kidneys release renin into the circulation. Renin is an enzyme that splits a small peptide (Angiotensin I) from a larger protein (angiotensinogen) produced by the liver. Angiotensin I is split into a smaller peptide (angiotensin II) by angiotensin converting enzyme (ACE), an enzyme present on the inner surface of blood vessels and in the lungs, liver, and kidneys. Angiotensin II stimulates the constriction of small arteries, resulting in increased blood pressure. Angiotensin II is also a potent stimulator of aldosterone synthesis by the adrenal glands. Aldosterone is a steroid hormone that acts on the kidneys to increase the reabsorption of sodium and the excretion of potassium. Retention of sodium by the kidneys increases the retention of water, resulting in increased blood volume and blood pressure (4).
Anti-diuretic hormone (ADH)
Sodium (and chloride) deficiency does not generally result from inadequate dietary intake, even in those on very low-salt diets (5).
Hyponatremia, defined as a serum sodium concentration of less than 136 mmol/liter, may result from increased fluid retention (dilutional hyponatremia) or increased sodium loss. Dilutional hyponatremia may be due to inappropriate anti-diuretic hormone (ADH) secretion, which is associated with disorders affecting the central nervous system and with use of certain drugs (see Drug interactions). In some cases, excessive water intake may also lead to dilutional hyponatremia. Conditions that increase the loss of sodium and chloride include severe or prolonged vomiting or diarrhea, excessive and persistent sweating, the use of some diuretics, and some forms of kidney disease. Symptoms of hyponatremia include headache, nausea, vomiting, muscle cramps, fatigue, disorientation, and fainting. Complications of severe and rapidly developing hyponatremia may include cerebral edema (swelling of the brain), seizures, coma, and brain damage. Acute or severe hyponatremia may be fatal without prompt and appropriate medical treatment (6).
Prolonged endurance exercise and hyponatremia
Hyponatremia has recently been recognized as a potential problem in individuals competing in very long endurance exercise events, such as marathons, ultramarathons, and Ironman triathlons. In 1997, 25 out of 650 participants in an Ironman triathlon (almost 4%) received medical attention for hyponatremia (7). Participants who developed hyponatremia during an Ironman triathlon had evidence of fluid overload despite relatively modest fluid intakes, suggesting that fluid excretion was inadequate and/or the fluid needs of these ultradistance athletes may be less than currently recommended (8). It has been speculated that the use of non-steroidal anti-inflammatory drugs (NSAIDs) may increase the risk of exercise-related hyponatremia by impairing water excretion (9), but firm evidence is presently lacking.
In 2004, the Food and Nutrition Board of the Institute of Medicine established an adequate intake level (AI) for sodium based on the amount needed to replace losses through sweat in moderately active people and to achieve a diet that provides sufficient amounts of other essential nutrients (5). This recommended intake level is well below the average dietary intakes of most people in the U.S.
|Adequate Intake (AI) for Sodium, with Estimated Sodium Chloride (Salt) Equivalence|
Males and Females
|Adults||71 years and older||1.2||3.0|
Epidemiological studies, conducted mainly in Asian countries, indicate that high intakes of salted, smoked, and pickled foods increase the risk of gastric cancer (10,11). Although these foods are high in salt, they may also contain carcinogens, such as nitrosamines. For more information on nitrosamines and cancer, see the article in the Linus Pauling Institute Fall/Winter 2000 Research Newsletter. Additionally, populations with high intakes of salted foods tend to have low intakes of fruits and vegetables, which are protective against gastric cancer (12). The risk of developing stomach cancer is increased by chronic inflammation of the stomach and infection by the bacteria, Helicobacter pylori. High concentrations of salt may damage the cells lining the stomach, potentially increasing the risk of H. pylori infection and cancer-promoting genetic damage. Although there is little evidence that salt itself is a carcinogen, high intakes of certain salted foods, such as salted fish, may increase the risk of gastric cancer in susceptible individuals (11, 13, 14).
Osteoporosis is a multifactorial skeletal disorder in which bone strength is compromised, resulting in an increased risk of fracture. Nutrition is one of many factors contributing to the development and progression of osteoporosis. Increased salt intake has been found to increase urinary excretion of calcium. Each 2.3 gram increment of sodium (5.8 grams of salt; NaCl salt) excreted by the kidneys draws about 24-40 milligrams (mg) of calcium into the urine (15). Salt intake has been associated with biochemical markers of bone resorption in some studies but not in others. In general, cross-sectional studies have not found an association between sodium intake and bone mineral density (BMD) (16). However, a 2-year study of postmenopausal women found that increased urinary sodium excretion (an indicator of increased sodium intake) was associated with decreased BMD at the hip (17). More recently, a longitudinal study in 40 postmenopausal women found that adherence to a low sodium diet (2 grams/day) for six months was associated with significant reductions in sodium excretion, calcium excretion, and aminoterminal propeptide of type I collagen, a biomarker of bone resorption. However, these associations were only observed in women with baseline urinary sodium excretions equal to or greater than 3.4 grams/day (i.e., the mean sodium intake for the U.S. adult population) (18). Long-term prospective studies are needed to determine whether decreasing salt intake has clinically significant effects on BMD and fracture risk in individuals at risk for osteoporosis. For more information on osteoporosis, see the article on Calcium.
Most kidney stones contain calcium as a main constituent. Although their cause is often unknown, abnormally elevated urinary calcium (hypercalciuria) increases the risk of developing calcium stones (19). Increased dietary salt has been found to increase urinary calcium excretion, and this effect may be more pronounced in patients with a history of calcium-containing kidney stones (20). A large prospective study that followed more than 90,000 women over a 12-year period found that women with a sodium intake averaging 4.9 grams/day (12.6 grams/day of salt) had a 30% higher risk of developing symptomatic kidney stones than women whose sodium intake averaged 1.5 grams/day (4.0 grams/day of salt) (21). However, a similar study in men did not find an association between sodium intake and symptomatic kidney stones (22). Clinical studies have shown that salt restriction reduces urinary calcium in individuals with a tendency to form calcium stones (23), and a five-year randomized trial of two different diets in men with recurrent calcium oxalate stones found that a diet low in salt and animal protein significantly decreased stone recurrence compared to a low calcium diet (24).
Several lines of research, conducted over several decades, have suggested that sodium intake is causally related to blood pressure. Animal studies have provided much information on the physiology of this relationship. Of particular importance, a key animal experiment conducted in 26 adult chimpanzees, a species closely related to humans, showed that blood pressure levels rose and fell as a result of experimentally-induced high and low levels of sodium, providing strong evidence that higher sodium intake causes blood pressure to increase and reduced intake causes it to decrease (25).
In human studies, cross-cultural population studies comparing cultures with very low salt intake to those with high intakes, and observational studies, most of which were cross-sectional, have suggested that increased salt consumption is associated with higher levels of blood pressure. However, populations in cross-cultural studies may differ in a number of other ways that could affect blood pressure, and observational studies have varied in their ability to control for confounding factors (26). The largest and most rigorously designed observational study of sodium and blood pressure was INTERSALT, which studied more than 10,000 men and women in 32 countries. Both cross-population and within-population analyses supported the same conclusions, that sodium intake, measured by 24-hour urine collections, was associated with blood pressure (27). Subsequent analyses that used more sophisticated statistical techniques made the relationships even stronger than previously reported (28).
Clinical trials and meta-analyses on the effects of salt reduction on blood pressure
Many randomized clinical trials have examined the effect of dietary salt reduction on blood pressure in hypertensive and nonhypertensive people (please note that nonhypertensive does not necessarily mean normotensive [normal blood pressure] because the non-hypertensive blood pressure range could encompass what is now called pre-hypertensive). Several investigators have used a technique called meta-analysis to analyze the pooled data from many different trials to estimate the magnitude of the effect of dietary salt reduction on blood pressure (29-34). Estimates of the magnitude of the effect of dietary salt reduction on blood pressure did not differ substantially among the analyses, although the number and types of trials that were included in the various meta-analyses differed substantially. The Cochrane meta-analysis assessed the results of modest salt reduction from 20 trials in participants with high blood pressure and 11 trials in participants without high blood pressure. Modest salt reduction (by 1.7 to 1.8 g/day sodium, based on 24-hour urinary sodium excretions) decreased systolic and diastolic blood pressure by an average of 5.1/2.7 mm Hg in participants with hypertension and 2.0/1.0 mm Hg in participants without hypertension (34).
Of particular importance are the results of two large, long-term trials (more than two years in duration) that are the most relevant to clinical and public health practice, called TONE (35) and TOHP-Phase II (36). TONE showed that modest reduction in sodium intake by about 1.0 g/day resulted in better control of hypertension in older adults who initially were on blood pressure medication. TOHP-Phase II (the second of two hypertension prevention trials) showed that a similar level of sodium reduction not only reduced systolic and diastolic blood pressure by 1.2/1.6 mm Hg in overweight participants who did not have hypertension, but also reduced the onset of hypertension by 14% after four years (36). Although some clinicians have questioned the value of modest blood pressure reductions in hypertensive patients, overviews of observational studies and randomized trials suggest that reducing diastolic blood pressure by an average of 2 mm Hg in the U.S. population would reduce the prevalence of hypertension by 17%, the risk of a heart attack by 5%, and the risk of stroke by 15% (37). Thus, modest mean reductions in blood pressure may translate into significant public health benefits for the overall U.S. population.
Variation in response to dietary sodium changes: salt sensitivity
There is considerable literature on variation in response of blood pressure to short-term changes in sodium intake (38, 39). However, classifying individuals based on their blood pressure response to salt changes, usually from an experimental protocol conducted just once, is extremely problematic. Like most physiological responses, there is a continuous, approximately normal distribution of responses of blood pressure to changes in salt intake (40). There is also variation in blood pressure from day-to-day, even when there is no change in diet (40). The classification of individuals as salt-sensitive or salt resistant has thus far not been based on population samples and has not yet been shown to be highly reproducible over time. Additionally, most of the protocols used in "salt sensitivity" studies involved extreme manipulations of sodium intake (sodium loading and sodium depletion) over a short time span of a few days or up to a week. There is no evidence that these very short-term studies have relevance to blood pressure changes occurring from long-term, gradual, and moderate changes in salt intake. Nonetheless, it is well known that certain subgroups of the population tend to have greater average blood pressure responses to changes in sodium intake. These include people who already have hypertension, older individuals, and African Americans (41). Research examining a genetic basis for salt sensitivity may eventually lead to better and reliable classification of individuals for salt sensitivity. Common variations in specific genes, known as polymorphisms, are currently under investigation and include those of genes whose products function prominently in the renin-angiotensin-aldosterone system (see Function) (42). Additionally, diet quality (e.g., the DASH diet; see below) and weight loss reduce blood pressure (43-45). Thus, environmental influences, in addition to genetic factors, likely contribute to salt sensitivity.
A multi-center, randomized feeding study, called the DASH (Dietary Approaches to Stop Hypertension) trial, demonstrated that a diet emphasizing fruits, vegetables, whole grains, poultry, fish, nuts, and low-fat dairy products substantially lowered blood pressure in hypertensive (systolic BP/diastolic BP: 11.4 mm Hg/5.5 mm Hg) and nonhypertensive people (3.5/2.1 mm Hg) compared to a typical U.S. diet (46). The DASH diet was markedly higher in potassium and calcium, modestly higher in protein, and lower in total fat, saturated fat, and cholesterol than the typical U.S. diet. However, sodium levels were kept constant throughout the study in order to better evaluate the effects of other dietary components. Subsequently, the DASH-sodium trial compared the DASH diet with a typical U.S. (control) diet at three levels of salt intake: low (2.9 grams/day), medium (5.8 grams/day; recommended as an upper limit by U.S. dietary guidelines), and high (8.7 grams/day; typical U.S. intake) (47). The DASH diet significantly lowered systolic and diastolic blood pressures in hypertensive and nonhypertensive people at each level of salt intake compared to the control diet. Reduction of salt intake resulted in an additional lowering of systolic and diastolic blood pressures. The combination of the DASH diet and reduced salt intake lowered blood pressure more than either intervention alone. Compared to the high-salt control diet, average blood pressure on the low-sodium DASH diet was decreased 8.9/4.5 mm Hg. The effect of salt reduction was greater in the control diet than in the DASH diet, suggesting that salt reduction may be more beneficial in those who consume typical U.S. diets. Results of the DASH trials support the idea that healthful dietary patterns offer an effective approach to the prevention and treatment of hypertension (48). Furthermore, a prospective cohort study in 88,517 middle-aged women followed for 24 years found that adherence to a DASH-style diet significantly lowered risk for coronary heart disease and stroke (49). More information about the DASH diet is available from the National Heart, Lung, and Blood Institute (NHLBI) of the National Institutes of Health (NIH).
The National High Blood Pressure Education Program and the National Heart, Lung, and Blood Institute of the NIH recommend consuming no more than 6 grams/day of salt (50), and the Food and Nutrition Board of the Institute of Medicine recently recommended that adults consume no more than 5.8 grams/day of salt (5) (see Safety). For more information regarding the U.S. dietary guidelines for salt intake, a statement from the National High Blood Pressure Education Program and a summary of the findings of a National Heart, Lung, and Blood Institute workshop on sodium and blood pressure are available online.
Target organ damage
Chronic hypertension damages the heart, blood vessels, and kidneys, thereby increasing the risk of heart disease and stroke, as well as hypertensive kidney disease. In a number of clinical studies, salt intake has been significantly correlated with left ventricular hypertrophy, an abnormal thickening of the heart muscle, which is associated with increased mortality from cardiovascular diseases (51). Recent research indicates that high salt intake may contribute to organ damage in ways that are independent of its effects on blood pressure (52-54). For example, studies in animals and humans have found increased salt intake to be associated with pathological changes in the structure and function of large elastic arteries that are independent of changes in blood pressure (55).
Cardiovascular disease (CVD)
Only a few studies have investigated the effects of sodium reduction on cardiovascular disease and on mortality, with mixed results (56-61). In general, the studies suggest a direct association, particularly the studies that used urinary sodium as a measure of sodium intake (56-58). In the TONE study, there was a trend toward reduced cardiovascular disease in participants assigned to the sodium reduction intervention (35). Importantly, a recent study found that participants initially without hypertension who were enrolled in the sodium interventions in the two previous TOHP trials had 25% reduction in cardiovascular events 10-15 years later compared with the control groups (62). Subsequent analyses from this TOHP follow-up study showed that the sodium-potassium ratio was associated with increased risk of cardiovascular disease in a dose-response relationship (63), providing complementary evidence for the adverse association between salt intake and cardiovascular disease.
Most of the sodium and chloride in the diet comes from salt. It has been estimated that 75% of the salt intake in the U.S. is derived from salt added during food processing or manufacturing, rather than from salt added at the table or during cooking. The lowest salt intakes are associated with diets that emphasize unprocessed foods, especially fruits, vegetables, and legumes. Recent surveys have found that the average dietary salt intake in the U.S. is 7.8-11.8 grams/day for adult men and 5.8-7.8 grams/day for adult women (5). These figures may be underestimations since they did not include salt added to food at the table.
The tables below list the sodium content (in milligrams [mg]) of some foods that
are high in salt and some foods that are relatively
low in salt. Since the majority of sodium and chloride
intake comes from salt, dietary salt content can be estimated by multiplying sodium content by 2.5.
Example: 2,000 mg (2 g) of sodium x 2.5 = 5,000 mg (5 g) of salt.
For more information on the nutrient content of foods, search the USDA food composition database.
|Food||Serving||Sodium (mg)||Salt (mg)|
|Bread, whole-wheat||2 slices||264||660|
|Bread, white||2 slices||340||850|
|Cereal, corn flakes||1 cup||266||665|
|Cereal, bran flakes||1 cup||293||733|
|Dill pickle||1 spear||300||800|
|Hot dog (beef)||1||510||1,300|
|Tomato juice, canned (salt added)||1 cup (8 fl. ounces)||650||1,600|
|Fish sandwich w/ tartar sauce & cheese||1 sandwich||940||2,400|
|Corned beef hash||1 cup||1,000||2,500|
|Pretzels, salted||2 ounces (10 pretzels)||1,000||2,500|
|Potato chips, salted||8 ounces (1 bag)||1,200||3,000|
|Macaroni and cheese, canned||1 cup||1,300||3,300|
|Canned, chicken noodle soup||1 cup||1,400||3,400|
|Food||Serving||Sodium (mg)||Salt (mg)|
|Olive oil||1 tablespoon||0||0|
|Orange juice (frozen)||1 cup (8 fl. ounces)||0||0|
|Popcorn, air-popped (unsalted)||1 cup||1||3|
|Almonds (unsalted)||1 cup||1||3|
|Pear, raw||1 medium||2||5|
|Fruit cocktail, canned||1 cup||9||23|
|Brown rice||1 cup, cooked||10||25|
|Potato chips, unsalted||8 ounces (1 bag)||18||45|
|Tomato juice, canned (no salt added)||1 cup (8 fl. ounces)||24||60|
Excessive intakes of sodium chloride lead to an increase in extracellular fluid volume as water is pulled from cells to maintain normal sodium concentrations. However, as long as water needs can be met, normally functioning kidneys can excrete the excess sodium and restore the system to normal (50). Ingestion of large amounts of salt may lead to nausea, vomiting, diarrhea, and abdominal cramps (64). Abnormally high plasma sodium concentrations (hypernatremia) generally develop from excess water loss, frequently accompanied by an impaired thirst mechanism or lack of access to water. Symptoms of hypernatremia in the presence of excess fluid loss may include dizziness or fainting, low blood pressure, and diminished urine production. Severe hypernatremia may result in edema (swelling), hypertension, rapid heart rate, difficulty breathing, convulsions, coma, and death. Hypernatremia is rarely caused by excessive sodium intake (e.g., the ingestion of large amounts of seawater or intravenous infusion of concentrated saline solution). In end-stage renal failure (kidney failure), impaired urinary sodium excretion may lead to fluid retention, resulting in edema, high blood pressure, or congestive heart failure if salt and water intake are not restricted (2, 65).
In 2004, the Food and Nutrition Board of the Institute of Medicine established an upper level of sodium intake (UL) of 2.3 grams/day (5.8 grams/day of salt) for adults based on the adverse effects of high sodium intakes on blood pressure, a major risk factor for cardiovascular and kidney diseases (5). It should be noted that the UL for sodium may be lower for those who are most sensitive to the blood pressure effects of sodium, including older people, African Americans, and individuals with hypertension, diabetes, or chronic kidney disease. The UL values for sodium and salt in different age groups are listed in the table below.
|Tolerable Upper Intake Level (UL) for Sodium, with Estimated Sodium Chloride (Salt) Equivalence|
|Age Group||UL for Sodium (g/day)||Salt (g/day)|
|Infants 0-12 months||Not Determined*||Not Determined*|
|Children 1-3 years||1.5||3.8|
|Children 4-8 years||1.9||4.8|
|Children 9-13 years||2.2||5.5|
|Adolescents 14-18 years||2.3||5.8|
|Adults 19 years and older||2.3||5.8|
*Not determined. Intake should be from food or formula only.
The following drugs may increase the risk of hyponatremia (abnormally low blood sodium concentration) (6):
|Families of Medications Associated with Hyponatremia|
|Diuretics||Hydrochlorothiazide, Furosemide (Lasix)|
|Non-steroidal anti-inflammatory drugs (NSAIDs)||Ibuprofen (Advil, Motrin), Naproxen sodium (Aleve)|
|Opiate derivatives||Codeine, Morphine|
|Phenothiazines||Prochlorperazine (Compazine), Promethazine (Phenergan)|
|Serotonin-reuptake inhibitors (SSRIs)||Fluoxetine (Prozac), Paroxetine (Paxil)|
|Tricyclic antidepressants||Amitriptyline (Elavil), Imipramine (Tofranil)|
|Individual Medications Associated with Hyponatremia|
|Desmopressin (DDAVP; nasal or oral)|
There is strong and consistent evidence that diets relatively low in salt (5.8 grams/day or less) and high in potassium (at least 4.7 grams/day) are associated with decreased risk of high blood pressure and the associated risks of cardiovascular and kidney diseases. Moreover, the DASH trial demonstrated that a diet emphasizing fruits, vegetables, whole grains, nuts, and low-fat dairy products substantially lowered blood pressure, an effect that was enhanced by reducing salt intake to 5.8 grams/day or less and most enhanced by reducing salt intake to 3.8 grams/day. Limiting salt intake to 3.8 grams/day should be the aim. The Linus Pauling Institute recommends a diet that is rich in fruits and vegetables (at least 5 servings/day) and limits processed foods that are high in salt.
Older adults (> 50 years)
Diets low in salt (3.8 grams/day or less) and rich in potassium (at least 4.7 grams/day) are likely to be of particular benefit for older adults, who are at increased risk of high blood pressure along with its associated risks of cardiovascular and kidney diseases. Since sensitivity to the blood pressure-raising effects of salt increases with age, diets that are low in salt and high in potassium may especially benefit older adults.
Written in February 2004 by:
Jane Higdon, Ph.D.
Linus Pauling Institute
Oregon State University
Updated in November 2008 by:
Victoria J. Drake, Ph.D.
Linus Pauling Institute
Oregon State University
Updated and Reviewed in November 2008 by:
Eva Obarzanek, Ph.D, M.P.H., R.D.
Research Nutritionist (Retired)
Prevention and Population Sciences Program
Division of Cardiovascular Sciences
National, Heart, Lung, and Blood Institute (NHLBI)
Copyright 2001-2014 Linus Pauling Institute
The Linus Pauling Institute Micronutrient Information Center provides scientific information on the health aspects of dietary factors and supplements, foods, and beverages for the general public. The information is made available with the understanding that the author and publisher are not providing medical, psychological, or nutritional counseling services on this site. The information should not be used in place of a consultation with a competent health care or nutrition professional.
The information on dietary factors and supplements, foods, and beverages contained on this Web site does not cover all possible uses, actions, precautions, side effects, and interactions. It is not intended as nutritional or medical advice for individual problems. Liability for individual actions or omissions based upon the contents of this site is expressly disclaimed.
Thank you for signing up for the LPI Research Newsletter; this newsletter is available at: http://lpi.oregonstate.edu/nswltrmain.html