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  • Sodium and chloride — major electrolytes of the fluid compartment outside of cells (i.e., extracellular) — work together to control extracellular volume and blood pressure. Disturbances in sodium concentrations in the extracellular fluid are associated with disorders of water balance. (More information)
  • Various mechanisms act on the kidney to ensure that the amount of sodium lost via renal excretion compensates adequately for the amount of sodium consumed, thereby maintaining sodium homeostasis. (More information)
  • Hyponatremia (abnormally low sodium concentrations in blood) is common among older adults and in individuals with hypertension, kidney disease, and heart disease. Hyponatremia also occurs in up to 30% of hospitalized patients. (More information)
  • Acute severe hyponatremia may lead to brain edema with neurologic consequences and be lethal if not promptly diagnosed and treated. Mild chronic hyponatremia with long-term adverse health effects, such as attention deficits, gait instability, falls, and bone loss and fractures, has been associated with cardiovascular morbidity and mortality. (More information)
  • In 2019, the National Academy of Medicine established an adequate intake (AI) for sodium of 1.5 grams (g)/day in adults, equivalent to 3.8 g/day of sodium chloride (salt). (More information)
  • The National Academy of Medicine established a Chronic Disease Risk Reduction Intake (CDRR) for sodium of 2.3 g/day (5.8 g/day of salt) for adults based on evidence of potential long-term health benefits on blood pressure and risk of hypertension and cardiovascular disease associated with reducing sodium intakes below this level. (More information)
  • Current sodium intakes of the US adult population far exceed the CDRR. Sodium has been identified as a nutrient of public health concern for overconsumption. (More information)
  • Excess dietary sodium is a major contributor to hypertension, which is a leading preventable risk factor for cardiovascular disease. Randomized controlled studies demonstrated that dietary sodium reduction (by 1.8 to 3.2 g/day) could lower blood pressure in subjects with elevated blood pressure. Yet, current evidence fails to support a decrease in cardiovascular morbidity and mortality with moderate sodium restriction in patients with hypertension. (More information)
  • Additional adverse health outcomes, including gastric cancer, osteoporosis, and kidney stones, have also been linked to sodium overconsumption. (More information)

Salt (sodium chloride) is essential for life. Total body sodium in an average 70-kg person is of about 4,200 mmol (~100 g), of which 40% is found in bone and 60% in the fluid inside and outside of cells (1). Total body chloride averages 2,310 mmol (~82 g), of which 70% is distributed in the extracellular fluid and the remaining is found in the collagen of connective tissue (1). Multiple mechanisms work in concert to tightly regulate the body's sodium and chloride concentrations. Although this review emphasizes the function and requirements of sodium, sodium and chloride ions work together to control extracellular volume and blood pressure (1).


Sodium (Na+) and chloride (Cl-) are the principal ions in the extracellular compartment, which includes blood plasma, interstitial fluid (fluid between cells), and transcellular fluid (e.g., cerebrospinal fluid, joint fluid). As such, they play critical roles in a number of life-sustaining processes. 

Maintenance of membrane potential

Sodium and chloride are electrolytes that contribute to the maintenance of concentration and charge differences across cell membranes. Potassium (K+) 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 10 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 Na+/K+ ATPase pumps. These pumps use ATP (energy) to pump sodium out of the cell in exchange for potassium (Figure 1). 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 (2-4).

Figure 1. A Simplified Model of the Na+/K+ ATPase Pump. Differences in concentrations of potassium ions across cell membranes create an electrochemical gradient known as the membrane potential. The concentration of potassium is typically 20 to 30 times higher inside compared to outside cells, whereas sodium is in higher concentration in the extracellular compared to intracellular compartment. Therefore, potassium ions diffuse easily out of cells and sodium diffuses easily into cells. The sodium/potassium ATPase pump is thus required to maintain the membrane potential by pumping sodium ions out of cells and potassium into cells. In the presence of magnesium, adenosine triphosphate (ATP) provides the energy to translocate three sodium ions and two potassium ions across the plasma membrane against their concentration gradients. The binding of ATP and magnesium allows the enzyme to adopt a confirmation that opens toward the cytoplasm for the binding and translocation of sodium ions. In turn, the binding of potassium ions induces the release of phosphate and magnesium and the translocation of potassium ions into the cytoplasm.

[Figure 1 - Click to Enlarge]

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 (5)

Maintenance of blood volume and blood pressure

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 (6). Below are descriptions of three mechanisms contributing to a larger multifactorial homeostatic control system that governs blood volume and blood pressure through regulation of sodium balance. These regulatory mechanisms are especially important for the control of sodium transport in various segments of the nephron (basic structural unit of the kidney), including the proximal and distal convoluted tubules, the thick ascending limb of the loop of Henle, and the collecting duct.

Renin-angiotensin-aldosterone system

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 (7).

Anti-diuretic hormone

Secretion of anti-diuretic hormone (ADH; also known as arginine vasopressin [AVP]) by the posterior pituitary gland is stimulated by a significant decrease in blood volume or pressure. In conjunction with the renin-angiotensin-aldosterone system, ADH stimulates epithelial sodium channels (ENaC) in apical cell membranes along kidney nephron distal tubules to increase the reabsorption of sodium and water (8).

Dopaminergic system

Dopamine is produced from L-DOPA in the kidney proximal tubules and acts on dopamine receptors distributed along the proximal tubules and the thick ascending limbs of the loop of Henle to regulate sodium transport. Dopamine promotes sodium excretion (natriuresis) by inhibiting the Na+/H+ exchanger and Na+/phosphate (Pi) co-transporter in apical cell membranes and the Na+/bicarbonate (HCO3-) co-transporter and Na+/K+ ATPase in basolateral cell membranes. The inhibitory effect of dopamine on Na+/K+ ATPase is enhanced by the natriuretic hormone, atrial natriuretic peptide (ANP), which is secreted by heart muscle cells into the circulation (9).


Hyponatremia, defined as a serum sodium concentration ([Na+]) <136 mmol/liter (mM), may result from increased fluid retention (dilutional hyponatremia) or increased sodium loss. Inadequate sodium intakes rarely result in hyponatremia, even in those on very low-salt diets, because the kidneys increase the excretion of water in order to maintain serum osmolality (i.e., electrolyte-water balance). The results of the 1999-2004 US National Health And Nutrition Examination Survey (NHANES) indicated an overall prevalence of hyponatremia of 1.9% in a US population representative sample of 14,697 participants aged 18 and older (10). Hyponatremia was found to be more prevalent among older individuals (3.1% in those aged 65 to 84 years) and in those suffering from hypertension (2.9%), diabetes mellitus (3.3%), coronary heart disease (CHD; 2.6%), stroke (3.6%), chronic obstructive pulmonary disease (COPD; 3.9%), cancer (3.4%), and psychiatric disorders (2.9%) (10). Hyponatremia is also common in hospitalized patients, with an estimated 15%-30% having mild hyponatremia (serum [Na+]: 130-135 mM) and up to 7% having moderate-to-severe hyponatremia (serum [Na+] <130 mM) (11).

Causes of hyponatremia

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 (see also Exercise-associated 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. Too severe restriction of dietary sodium intake in renal patients with hypertension and congestive heart failure might also result in harmful body depletion of sodium (1).

Exercise-associated hyponatremia

Exercise-associated hyponatremia (EAH) is dilutional hyponatremia occurring in individuals competing in endurance (up to 6 h in duration) and ultra-endurance (>6 h in duration) exercise events, such as marathons, Ironman triathlons, mountain bike races, hiker treks, and open-water ultra-distance swimming events. Of note, symptomatic EAH has been increasingly reported in shorter events, such as half-marathons and sprint triathlons. The development of hyponatremia during or up to 24 h after intense and/or sustained physical activity has been linked to fluid overload due to excessive water intakes, impaired urinary water excretion due to persistent ADH secretion, and very low or very high ambient temperature (12). Risk factors include pre-exercise hyperhydration, use of non-steroidal anti-inflammatory drugs (NSAIDs), and prolonged exercise (>4 h) (reviewed in 12).

Signs and symptoms of hyponatremia

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 (13)

Chronic mild hyponatremia has been associated with deficits in gait and attention, falls, and bone loss and fractures, especially in women and the elderly (14, 15). A recent 11-year prospective cohort study in over 3,000 men free of cardiovascular disease (CVD) also reported significantly higher risks of stroke, coronary heart disease, total CVD events, CVD-related mortality, and all-cause mortality in participants with mild-to-severe hyponatremia (serum [Na+] <139 mM) compared to those with serum [Na+] between 139 mM and 144 mM (16). In addition, in a meta-analysis of 81 observational studies in patients with diverse medical conditions (including cardiovascular disease, pulmonary infections,  and cirrhosis), the risk of mortality was found to be nearly three times greater in hyponatremic compared to normonatremic subjects (17). Improvement or normalization of serum [Na+] in hyponatremic subjects was associated with a reduced mortality rate in patients with diverse clinical conditions (18).

Drug interactions

Table 1 lists some medications that may increase the risk of hyponatremia (10, 19).

Table 1. Medications that Increase the Risk of Hyponatremia
Medication Family Examples
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
Carbamazepine (Tegretol)
Chlorpropamide (Diabinese)
Clofibrate (Atromid-S)
Cyclophosphamide (Cytoxan)
Desmopressin (DDAVP; nasal or oral)
Lamotrigine (Lamictal)
Oxytocin (Pitocin)
Vincristine (Oncovin)

The Adequate Intake (AI) for Sodium

In 2019, the Food and Nutrition Board (FNB) of the National Academy of Medicine revised the Dietary Reference Intakes (DRIs) for sodium (20). The FNB did not find sufficient evidence to determine an Estimated Average Requirement (EAR) and derive a Recommended Dietary Allowance (RDA). Instead, they established an adequate intake (AI) for sodium (Table 2; 20). Considerations accounted for by the FNB for establishing an AI for sodium included that the available evidence was insufficient to identify adverse health effects associated with low dietary sodium intakes and that there was substantial evidence suggesting potential long-term health benefits associated with reducing habitual sodium intakes below 2,300 mg/day (see The Chronic Disease Risk Reduction Intake for sodium). The AI could not be derived from the average dietary intakes of apparently healthy people in the US since average intake levels are well above 2,300 mg/day (see Sources).

Table 2. Adequate Intake (AI) for Sodium and Sodium Chloride (Salt)
Life Stage Age Males and Females
Sodium (mg/day)
Males and Females
Salt (mg/day)*
Infants  0-6 months 110 280
Infants  7-12 months  370 930
Children  1-3 years  800 2,000
Children 4-8 years  1,000 2,500
Children  9-13 years  1,200 3,000
Adolescents  14-18 years  1,500 3,800
Adults  19 years and older 1,500 3,800
Pregnancy 14-50 years 1,500 3,800
Breast-feeding 14-50 years 1,500 3,800
*The AI for salt corresponds to the AI for sodium multiplied by 2.5.


Most of the sodium and chloride in the diet comes from salt (21). Very little sodium occurs naturally in food. Instead, sodium is added to make certain foods shelf stable, and it is ubiquitously used in the US food supply such that all food groups contribute to sodium intake levels (21). It has been estimated that 75% of the salt intake in the US is derived from salt added during food processing or manufacturing, rather than from salt added at the table or during cooking (22). The lowest salt intakes are associated with diets that emphasize unprocessed foods, especially fruit, vegetables, and legumes. Combined data of the US National Health And Nutrition Examination Surveys (NHANES) 2007-2008 and 2009-2010 indicated average dietary sodium intakes of 3,100 mg/day in children (ages, 3-18 years), 3,800 mg/day in adults (ages, 19-50 years), and 3,300 mg/day in older adults (>50 years) (23). Usual intakes were estimated to be 4,400 mg/day and 3,100 mg/day in adult men and women (ages, 19-50 years), respectively. Overall, sodium intakes among males of all age groups were found to be 20%-45% higher than among females (23). These intakes are well above the sodium Chronic Disease Risk Reduction Intake (CDRR) of 2,300 mg/day (see The Chronic Disease Risk Reduction Intake for sodium).

Table 3 lists the sodium content (in milligrams [mg]) of some foods that are high in salt, and Table 4 lists some foods that are relatively low in salt. Most sodium is consumed in the form of sodium chloride (salt). The salt content of foods can be calculated by multiplying the 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 sodium content of foods, search USDA's FoodData Central.

Table 3. Some Foods that are High in Sodium and Salt Content
Food Serving Sodium (mg) Salt (mg)
Cereal, corn flakes 1 cup 182 445
Cereal, bran flakes 1 cup 216 540
Dill pickle 1 spear 283 707
Bread, whole-wheat 2 slices 291 727
Bread, white 2 slices 344 860
Hot dog (beef) 1 409 1,022
Cheese spread, pasteurized 1 ounce 416 1,040
Fish sandwich with tartar sauce and cheese 1 sandwich 582 1,455
Tomato juice, canned, with salt added 1 cup (8 fl. ounces) 615 1,537
Chicken noodle soup, canned 1 cup 789 1,972
Macaroni and cheese, box 1 cup 869 2,173
Corned beef hash 1 cup 972 2,430
Pretzels, salted 2 ounces (10 pretzels) 1,029 2,572
Ham, minced 3 ounces 1,059 2,647
Potato chips, salted 8 ounces (1 bag) 1,196 2,990
Sunflower seeds, dry roasted, with salt added 1 ounce 1,703 4,257
Table 4. Some Foods that are Relatively Low in Sodium and Salt Content
Food Serving Sodium (mg) Salt (mg)
Olive oil 1 tablespoon 0 0
Orange juice, frozen 1 cup (8 fl. ounces) 0 0
Almonds, unsalted ¼ cup 0.3 0.8
Popcorn, air-popped, unsalted 1 cup 1 3
Pear 1 medium 2 5
Mango 1 fruit 4 10
Tomato 1 medium 6 15
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, without salt added 1 cup (8 fl. ounces) 24 60
Carrot 1 medium 42 105

The daily value (DV) for sodium is less than 2,400 mg. The % DV included on the Nutrition Facts label of packaged foods and beverages is meant to help consumers make informed choices and consider the foods with low (≤5% DV per serving) rather than high (≥20% DV per serving) sodium content (24).



Excessive intakes of sodium chloride lead to an increase in extracellular fluid volume as water is pulled from cells to maintain normal sodium concentrations outside of cells. However, as long as water needs can be met, normally functioning kidneys can excrete the excess sodium and restore the system to normal (1). Ingestion of large amounts of salt may lead to nausea, vomiting, diarrhea, and abdominal cramps (25). Hypernatremia, defined as serum sodium concentrations ([Na+]) >145 mM, is much less common than hyponatremia and rarely caused by excessive sodium intake (e.g., from the ingestion of large amounts of seawater or intravenous infusion of concentrated saline solution) (26). Hypernatremia generally develops from excess water loss (e.g., burns, respiratory infections, renal loss, osmotic diarrhea, hypothalamic disorders) or reduced water intake, frequently accompanied by an impaired thirst mechanism (6). Symptoms of hypernatremia with evidence of dehydration from excessive water loss may include dizziness or fainting, low blood pressure, and diminished urine production. Severe hypernatremia ([Na+] >158 mM) may result in altered mental status, lethargy, irritability, stupor, convulsions, and coma. Acute brain shrinkage can lead to intracranial and subarachnoid hemorrhage (26).

The Dietary Reference Intakes (DRIs) for sodium were recently revised by the Food and Nutrition Board of the National Academy of Medicine (20). Using a new expanded DRI model, the National Academy of Medicine did not find sufficient evidence of adverse toxicological effects of excessive sodium intake; therefore, they did not establish a tolerable upper intake level (UL) for sodium (20).

Health risks of excess dietary sodium


Normal blood pressure is defined by a systolic blood pressure below 120 mm Hg and a diastolic blood pressure below 80 mm Hg, often noted <120/80 mm Hg (27). Currently, about one-third of US adults have hypertension (blood pressure levels ≥140/90 mm Hg), and another one-third have elevated blood pressure (prehypertension, corresponding to levels ≥120/80 mm Hg and <140/90 mm Hg) that places them at risk for hypertension (28). 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 disease (29). Several lines of research, conducted over the last decades, have provided evidence of a relationship between sodium consumption and health outcomes. For instance, observational cohort studies, like the well-designed International Study of Salt and Blood Pressure (INTERSALT), have associated excess sodium intake with a progressive increase of blood pressure with age (30, 31). Further, a number of intervention studies, including the Trial of Nonpharmacologic Interventions in the Elderly (TONE), Trials Of Hypertension Prevention (TOHP), and Dietary Approaches to Stop Hypertension (DASH)-sodium, have demonstrated that dietary sodium reduction could effectively prevent or improve hypertension among population subgroups at elevated risk (see Blood pressure clinical trials).

Salt sensitivity: Blood pressure responses to short-term changes in sodium intake are heterogeneous. Indeed, some individuals have little-to-no change in blood pressure in response to sodium manipulation and are identified as "salt-resistant." In contrast, individuals who experience a greater change in blood pressure following dietary sodium manipulation are labeled "salt sensitive" (32, 33). Most of the protocols used in salt sensitivity studies involve extreme manipulations of sodium intake (sodium loading and sodium depletion) over a short timespan of a few days or up to one week. A typical controlled isocaloric intervention may include a two-phase, randomized, cross-over seven-day dietary sodium manipulation with a high-sodium diet (6.9 to 8.1 g/day) and a very-low-sodium diet (0.5 g/day). Salt resistance is often defined as a change of ≤5 mm Hg in 24-h mean arterial pressure (MAP) between a high-sodium diet and a low-sodium diet. Conversely, salt sensitivity is defined by changes of >5 mm Hg in MAP between high- and low-sodium diets (34).

About 26% of normotensive and 51% of hypertensive individuals are estimated to be salt sensitive (35). Salt sensitivity among normotensive subjects has been found to predict future hypertension (36, 37). Long-term prospective cohort studies also provided substantial evidence suggesting that sensitivity to salt may be an independent risk factor for cardiovascular disease (reviewed in 38). Salt sensitivity involves greater sodium reabsorption in the kidney proximal tubules and higher glomerular filtration rate (GFR) on a high-sodium diet than salt resistance. The rise in blood pressure is thought to compensate high sodium and fluid retention by triggering increased renal excretion. Conversely, salt resistance is associated with adequate excretion of excess sodium such that consumption of large amounts of sodium does not markedly increase blood pressure (1).

Earlier observations suggested that certain subgroups of the population, including African Americans, older individuals (>45 years), and hypertensive patients, tended to have greater average blood pressure responses to changes in sodium intake (38). Nevertheless, a recent meta-analysis of randomized controlled trials found marginal ethnic differences in blood pressure response to sodium reduction (for at least one week) compared to previously reported data (39). Research examining a genetic basis for salt sensitivity may eventually lead to better and reliable classification of individuals for salt sensitivity. Yet, at present, the analyses of common variations (known as polymorphisms) in the sequence of specific genes involved in sodium retention by the kidney failed to show consistent results (reviewed in 40). A recent meta-analysis of nine observational studies failed to show significant associations between specific gene polymorphisms in the renin-angiotensin-aldosterone system and blood pressure response to salt (41). Other polymorphisms in genes like those coding for G-protein coupled receptor kinase type 4 (GRK4), epithelial sodium channels (ENaC) and regulators, or α-adducin may favor sodium retention by the kidney, hence predisposing to blood pressure sensitivity to salt (reviewed in 40). Finally, in addition to genetic predispositions, factors like diet quality (e.g., the DASH diet) and body weight probably influence blood pressure sensitivity to salt (38).

Blood pressure clinical trials: Of particular importance are the results of long-term multicenter trials that are the most relevant to clinical and public health practice, i.e., TONE (42), TOHP (43), and DASH (Dietary Approaches to Stop Hypertension)-sodium. TONE showed that modest reduction in sodium intake by about 1.0 g/day (~2.5 g/day of salt) resulted in a better control of hypertension in older adults who initially were on blood pressure medication (42). TOHP-Phase II (the second of two hypertension prevention trials) showed that a similar level of sodium reduction significantly reduced systolic (but not diastolic) blood pressure by 1.2 mm Hg in overweight participants with prehypertension after three years and limited the onset of hypertension by 18% after four years compared to usual care (no dietary intervention) (43, 44). Adherence to the DASH diet, which emphasizes fruit, vegetables, whole grains, poultry, fish, nuts, and low-fat dairy products, was found to substantially lower systolic/diastolic blood pressures by 11.4/5.5 mm Hg in hypertensive and 3.5/2.1 mm Hg in normotensive people compared to a typical US diet (45). The DASH diet is also markedly higher in potassium and calcium, modestly higher in protein, and lower in total fat, saturated fat, cholesterol, red meat, sweets, and sugar-containing beverages than the typical US diet. The DASH-sodium trial compared the DASH diet to a typical US (control) diet at three levels of sodium intake: low (1.5 g/day, current AI), intermediate (2.3 g/day, recommended as an upper level by US dietary guidelines), and high (3.2 g/day, typical US intake) levels (46). At each level of sodium intake, systolic and diastolic blood pressures were systematically lower in (pre)hypertensive people (blood pressure >120/80 mm Hg) consuming the DASH diet compared to the control diet. Reduction of sodium intake also significantly reduced blood pressure in hypertensive consumers of either the DASH diet or the typical US diet. Yet, in prehypertensive participants, the blood pressure-lowering effect of sodium reduction was only significant in those consuming the typical US diet; sodium reduction failed to reduce blood pressure in all prehypertensive participants assigned to the DASH diet, with the exception of African Americans. Compared to the high-salt control diet, average blood pressure in (pre)hypertensive participants on the low-sodium DASH diet was decreased by 8.9/4.5 mm Hg. Results of the DASH trials support the idea that sodium reduction in the context of a healthful dietary pattern offers an effective approach to the prevention and treatment of hypertension (47).

A majority of randomized clinical trials have examined the effect of dietary sodium reduction on blood pressure in (pre)hypertensive rather than in normotensive (normal blood pressure) people. A recent meta-analysis assessed the results of modest sodium reduction from 22 trials in 990 participants with hypertension (blood pressure ≥140/90 mm Hg) and 12 trials in 2,240 participants without hypertension (blood pressure <140/90 mm Hg). A modest sodium reduction by 1.8 g/day (equivalent to 4.4 g/day of salt; based on 24-hour urinary sodium excretions) for at least four weeks decreased systolic and diastolic blood pressure by an average of 5.4/2.8 mm Hg in subjects with hypertension and 2.4/1.0 mm Hg in those without hypertension (48). Another pooled analysis of eight randomized controlled studies demonstrated a dose-response relationship between sodium reduction (by 1.8 to 3.2 g/day) and blood pressure in subjects with blood pressure over 130/80, but there was no such relationship in subjects whose blood pressure was below 130/80 (49).

The 2015-2020 Dietary Guidelines for Americans concurred with the 2013 American Heart Association (AHA)/American College of Cardiology (ACC) Guideline to recommend that individuals who would benefit from blood pressure lowering, particularly prehypertensive and hypertensive adults, should follow the DASH eating pattern to lower sodium intakes (50). Recommendations include sodium intakes of no more than 2.4 g/day, further sodium intake reduction to 1.5 g/day for an even greater blood pressure-lowering effect, or a reduction is sodium intake of at least 1 g/day if sodium intakes of 1.5 g/day or 2.4 g/day cannot be achieved (50, 51).

More information about the DASH diet is available from the National Heart, Lung, and Blood Institute (NHLBI) of the National Institutes of Health (NIH).

Endothelial dysfunction

Early studies in animals and humans reported that high-salt intake was associated with pathological alterations in the structure and function of large elastic arteries, independent of changes in blood pressure (reviewed in 52). Endothelial dysfunction is considered to be an early step in the development of atherosclerosis. Alterations in the structure and function of the vascular endothelium that lines the inner surface of all blood vessels are associated with the loss of normal nitric oxide (NO)-mediated endothelium-dependent vasodilation. Endothelial dysfunction results in widespread vasoconstriction and coagulation abnormalities. The measurement of brachial artery flow-mediated dilation (FMD) is often used as a functional marker of endothelial function; FMD values are inversely correlated with the risk of future cardiovascular events (53).

The link between sodium intake and cardiovascular disease has traditionally involved hypertension. Yet, recent investigations in salt-resistant normotensive individuals have reported that dietary sodium loading could impair endothelial function independent of changes in blood pressure (54, 55). A study using controlled dietary sodium conditions also demonstrated that a high-sodium diet (6.9 g/day for one week) reduced brachial artery FMD to the same extent in salt-sensitive and salt-resistant normotensive participants (56). On the other hand, a three-week dietary sodium intake of 3 g following a baseline intake of 2.4 g/day of sodium did not lower FMD in 36 untreated (pre)hypertensive adults with baseline FMD values significantly lower than those usually observed in healthy normotensive subjects (57). Circulating markers of endothelial function and low-grade inflammation were unchanged; only urinary sodium excretion and systolic blood pressure increased (57).

In healthy normotensive adults in whom FMD significantly decreased following a meal containing 1.5 g of sodium, potassium supplementation (1.5 g) could limit high sodium-induced FMD reduction in the postprandial state (58, 59). In a 12-week, randomized, cross-over study in 25 overweight/obese and normotensive subjects, a diet containing 2.3 g/day reduced FMD after two days and for six weeks, compared to a diet containing 3.5 g/day (60). In another randomized, cross-over, placebo-controlled trial, dietary sodium restriction (1.2 g/day vs. 3.5 g/day) for five weeks significantly lowered systolic (but not diastolic) blood pressure by 12 mm Hg and increased FMD by 68% in 17 (pre)hypertensive subjects (mean age, 62 years) (61). The improvements in both blood pressure and endothelial function suggest that sodium restriction has a strong potential for reducing CVD risk by preserving the vasculature.

Cardiovascular morbidity and mortality

A high dietary sodium intake is a risk factor for cardiovascular disease. A pooled analysis of 13 prospective cohort studies in 177,025 participants followed for 3 to 17 years found greater risks of cardiovascular disease (+17%) and stroke (+23%) with an average difference of 2 g of sodium (5 g of salt) between higher and lower daily consumption across the studies (62). Higher sodium intakes were also found to be associated with an increased risk of stroke (+24%) — but not with the risk of cardiovascular disease or coronary heart disease — in a more recent meta-analysis of 10 prospective cohort studies and randomized controlled trials (63).

A meta-analysis of randomized controlled studies examined the effect of dietary sodium reduction on cardiovascular events and mortality (64). Dietary interventions aiming at reducing sodium intake failed to demonstrate an effect on all-cause mortality in hypertensive and non-hypertensive individuals. Current evidence also fails to support a decrease in cardiovascular morbidity and mortality in patients with hypertension (64). Likewise, the Centers for Disease Control and Prevention (CDC)-sponsored 2013 report on Sodium Intake in Populations by the US Institute of Medicine (IOM; renamed the National Academy of Medicine) indicated that evidence was scarce and of poor quality to assess whether sodium intakes below 2.3 g/day may lower the risk of heart disease, stroke, and all-cause mortality in the general US population (65). In addition, the IOM committee found no evidence of benefits but some evidence of potential harm in reducing sodium intakes to 1.5 g/day-2.3 g/day in individuals with diabetes mellitus, kidney disease, or cardiovascular disease (65). However, in a recent review of the literature, the US Agency for Healthcare Research and Quality (AHRQ) identified low strength evidence to suggest that sodium reduction could decrease the risk of a composite measure of cardiovascular outcomes (seven trials) and the risk of combined cardiovascular morbidity and mortality (eight trials) (66).

Gastric cancer

In the evidence-based report, Food, Nutrition, Physical Activity, and the Prevention of Cancer (2007), the World Cancer Research Fund/American Institute for Cancer Research concluded that salt was a probable cause of stomach cancer (67). A recent meta-analysis of seven prospective cohort studies in nearly 270,000 participants showed a 68% greater risk of gastric cancer with the highest versus lowest salt intake level (68). Findings from observational studies, conducted mainly in Asian countries, also suggested an increased risk of gastric cancer with high intakes of salted foods, pickled foods, and processed meat products (68-70). Low intakes of fruit and vegetables, which are protective against gastric cancer, in populations with high intakes of salted foods might also contribute to increasing the risk of gastric cancer (69, 71).

Animal studies suggested that high concentrations of salt may damage the cells lining the stomach, potentially increasing the risk of bacterial infection by Helicobacter pylori (72, 73) and cancer-promoting genetic damage (74). The colonization by H. pylori is a recognized risk factor for gastric cancer. Case-control studies examining the potential interaction between salt intake and H. pylori infection in the risk of gastric cancer have provided mixed results (75-78). Although there is little evidence that salt itself is a carcinogen, high intakes of salted foods may increase the risk of gastric cancer in individuals infected with H. pylori or exposed to gastric carcinogens (67). Salty foods, like processed meat, cured meat, and salted fish, contain high levels of nitrosated compounds that may contribute to increasing the risk of gastric cancer (67).


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. Dietary sodium is a major determinant of urinary calcium loss (79). High-sodium intake results in increased loss of calcium in the urine, possibly due to competition between sodium and calcium for reabsorption in the kidneys or by an effect of sodium on parathyroid hormone (PTH) secretion (see the article on Calcium). Every 1-g increment in sodium (2.5 g of salt) excreted by the kidneys has been found to draw about 26.3 mg of calcium into the urine (79). A study conducted in adolescent girls reported that a high-salt diet had a greater effect on urinary sodium and calcium excretion in White compared to Black girls, suggesting differences among ethnic groups (80). In adult women, each extra gram of sodium consumed per day is projected to produce an additional rate of bone loss of 1% per year if all of the calcium loss comes from the skeleton.

A number of cross-sectional and intervention studies have suggested that high-sodium intakes are deleterious to bone health, especially in older women (81). In particular, high-sodium intake in conjunction with low-calcium intake may be especially detrimental to bone health (82-84). A two-year longitudinal study in postmenopausal women found increased urinary sodium excretion (an indicator of increased sodium intake) to be associated with decreased bone mineral density (BMD) at the hip (85). Linear regression analysis estimated that BMD could be maintained by reducing sodium intake to a level of 2.3 g/day and by increasing calcium intake to 1.2 g/day. A second longitudinal study in postmenopausal women found that habitual sodium intake of approximately 3 g/day was not detrimental to BMD over three years of follow-up (86). Notably, the average calcium intake in this study population was 1.3 to 1.5 g/day — slightly above the RDA for calcium in women over 50 years. Another study in 40 postmenopausal women found that adherence to a low-sodium diet (2 g/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). Yet, these associations were only observed in women with elevated baseline urinary sodium excretions (87). Finally, in a randomized, placebo-controlled study in 60 postmenopausal women, potassium citrate supplementation prevented an increase in calcium excretion induced by the consumption of a high-sodium diet (≥5 g/day of sodium) for four weeks (88)

Kidney stones

Most kidney stones are composed of calcium oxalate or calcium phosphate. Subjects with an abnormally high level of calcium in the urine (hypercalciuria) are at higher risk of developing kidney stones (a process called nephrolithiasis) (89). A large prospective cohort study that followed more than 90,000 women over a 12-year period found that women with a sodium intake averaging 4.9 g/day (12.6 g/day of salt) had a 30% higher risk of developing symptomatic kidney stones than women whose sodium intake averaged 1.5 g/day (3.8 g/day of salt) (90). Because urinary calcium excretion is increased by high sodium intakes (79), dietary sodium restriction may reduce the risk of stone formation, especially in patients with a history of kidney stones, by limiting calcium excretion (91). A five-year, randomized intervention study that enrolled 120 men with idiopathic hypercalciuria (mean age, 45 years) reported that those assigned to a normal-to-high calcium (1.2 g/day) and low-sodium diet (1.2 g/day) had a 49% reduced risk of kidney stone recurrence compared to those on a low-calcium diet (~0.4 g/day) (92).

The Chronic Disease Risk Reduction Intake

In 2004, the Food and Nutrition Board (FNB) of the National Academy of Medicine (formerly, the Institute of Medicine [IOM]) established a tolerable upper intake level (UL) of 2.3 g/day sodium (5.8 g/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 (93). The 2015-2020 Dietary Guidelines for Americans report also recognizes that excess sodium consumption poses potential health risks and emphasizes the reduction of sodium intake in the context of a healthful dietary pattern, following the UL set by the IOM panel (50).

In a 2019 update of the Dietary Reference Intakes (DRIs) for sodium, the National Academy of Medicine made use of a new expanded DRI model (20). As a consequence, only evidence of a toxicological risk associated with excessive sodium intakes was considered to establish a UL for sodium (20), whereas previously the UL for sodium was based on evidence of any type of adverse effects (93). In addition, the evidence of the relationship between sodium intake levels, blood pressure, and cardiovascular disease — considered toward establishing a UL in the previous report — has now been reviewed to establish a new DRI category, namely the Chronic Disease Risk Reduction Intake (CDRR) for sodium (20).

Using the expanded DRI model, the National Academy of Medicine did not find sufficient evidence of adverse toxicological effects to establish a UL for sodium (20).

In contrast, substantial evidence from trials showing a lowering of the risks of hypertension and cardiovascular disease with reduction of sodium intakes was used to set a CDRR for sodium in apparently healthy adults at 2,300 mg/day (20). The CDRR for healthy adults means that a lowering of usual sodium intakes to at least 2,300 mg/day from higher levels is expected to reduce the risk of chronic disease.

The CDRR values for other ages/life stages have been extrapolated from the CDRR value set for adults using estimated energy requirements; these CDRR-based recommendations for each age/life stage are presented in Table 5.

Table 5. Sodium Chronic Disease Risk Reduction Intake (CDRR)-based Recommendations
Age Group Recommendation
Infants 0-12 months Not Determined
Children 1-3 years Reduce intakes if above 1,200 mg/day*
Children 4-8 years Reduce intakes if above 1,500 mg/day*
Children 9-13 years Reduce intakes if above 1,800 mg/day*
Adolescents 14-18 years Reduce intakes if above 2,300 mg/day*
Adults 19 years and older Reduce intakes if above 2,300 mg/day
*Extrapolated from the adult CDRR using estimated energy requirements.

Of note, in its 2013 report on Sodium Intake in Populations, the FNB committee considered that recommendations to population subgroups, including those who are most sensitive to the blood pressure effects of sodium, like older people (≥51 years), African Americans, and individuals with hypertension, diabetes mellitus, or chronic kidney disease, should be similar to those for the general US population (65). The IOM committee found no supportive evidence to recommend that these subgroups lower their sodium intake to 1.5 g/day or below (65). In contrast, the 2013 American Heart Association (AHA)/American College of Cardiology (ACC) Guideline on Lifestyle Management to Reduce Cardiovascular Risk advises adults with (pre)hypertension to consume no more than 2.4 g/day of sodium, further reduce sodium intake to 1.5 g/day for an even greater blood pressure-lowering effect, or reduce their daily intake by at least 1 g if sodium intakes of 1.5 g/day or 2.4 g/day cannot be achieved (51).

Finally, the 2010 IOM report on Strategies to Reduce Sodium Intake in the United States suggested that the US Food and Drug Administration (FDA) revisit the Generally Recognized As Safe (GRAS) status of salt added to processed food, restaurant food, and food additives, in order to reduce the salt content in the food supply and assist in achieving sodium intakes consistent with US Dietary Guidelines and IOM recommendations (21). These recommendations are currently being reviewed by the FDA (22).

Drug interactions

Taking sodium bicarbonate orally may reduce the efficacy of the antibiotic cefpodoxime and the antidiabetic drug chlorpropamide by limiting drug absorption or increasing drug urinary excretion. Intravenous administration of sodium bicarbonate may also reduce the effects of aspirin and the nasal decongestant pseudoephedrine. Excessive intake of sodium bicarbonate may increase the risk of hypokalemia (abnormally low blood potassium concentration) in patients taking potassium-depleting drugs like diuretics (e.g., hydrochlorothiazide, furosemide, or bumetanide), the anti-gout agent colchicine, and calcium- or magnesium-containing antacids (94).

Linus Pauling Institute Recommendation

There is strong and consistent evidence that diets relatively low in sodium (2.3 g/day or less) and high in potassium are associated with decreased risk of high blood pressure and the related risks of cardiovascular and kidney diseases. Moreover, the DASH trial demonstrated that a diet emphasizing fruit, vegetables, whole grains, nuts, and low-fat dairy products substantially lowered blood pressure, an effect that was enhanced by reducing salt intake to 2.3 g/day of sodium (5.8 g/day of salt). The Linus Pauling Institute recommends a diet that is rich in fruit and vegetables (at least 9 servings/day) and limits processed foods that are high in salt.

Older adults (>50 years)

Since sensitivity to the blood pressure-raising effect of salt increases with age, sodium reduction in the context of a healthful dietary pattern may especially benefit older adults, who are at increased risk of high blood pressure, cardiovascular disease, and kidney disease.

Authors and Reviewers

Originally written in 2001 by:
Jane Higdon, Ph.D.
Linus Pauling Institute
Oregon State University

Updated 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 in May 2016 by:
Barbara Delage, Ph.D.
Linus Pauling Institute
Oregon State University

Reviewed in December 2016 by:
Harry G. Preuss, M.D., M.A.C.N., C.N.S.
Professor of Biochemistry, Physiology, Medicine, and Pathology
Georgetown University Medical Center

Last updated 4/11/19  Copyright 2001-2024  Linus Pauling Institute


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