Sodium is an essential mineral of the human body and the major cation of the extracellular fluid.

It regulates fluid balance, blood pressure, and cellular homeostasis by regulating plasma volume and cellular transport.

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Sodium serves many physiological functions and is necessary for health.

Humans can obtain sufficient sodium from the low amounts present in many foods, including fresh meat, fish, and vegetables, but most of the sodium we now consume is added in food processing or at the table.

Sodium chloride (NaCl) or salt has also been used as a preservative for centuries and is now added for flavoring during food preparation.

Salt is an excellent preservative because it reduces the water activity of foods, which is the amount of unbound water available for microbial growth and chemical reactions.

Salt can also alter the texture of meats, such as in brining, which can produce a juicier product, while increasing the taste and palatability of the food.

The mean body content of sodium in the adult male is 92 gr., with half of this (46 gr.) being located in the extracellular fluid, 11 gr. being found in the intracellular fluid, and 35 gr. being found in the skeleton.

The concentration gradient between the extracellular and intracellular fluid is maintained by the activity of the sodium-potassium (Na+/K+) pump.

The sodium-potassium (Na+/K+) pump, found ubiquitously in all animal cells, transfers sodium and potassium, respectively, from inside to outside the cell, and vice versa, against the concentration gradient, using the energy supplied by ATP (adenosine triphosphate).

In the polarized cells of the renal tubular epithelium or the intestinal wall, sodium enters the cell from the tubular lumen or from the gut, through specific channels and other transport mechanisms.

Afterward, it is extruded from the cell into the adjacent capillaries, again, through the action of the sodium-potassium (Na+/K+) pump, which is mainly distributed on the basolateral sides of the cell.

In these types of epithelial cells, sodium transport is mostly facilitated along with other substrates, such as phosphates, amino acids, glucose, and galactose. 

Sodium Absorption and Metabolism

Sodium absorption occurs almost quantitatively in the distal small intestine and the colon.

Sodium balance in the body is closely linked to that of water and is finely maintained by the kidneys.

Here, the sodium filtered by the glomeruli is reabsorbed in a proportion ranging from 0.5% to 10% according to the needs at the tubular level, in which angiotensin II, norepinephrine, aldosterone, and insulin, stimulate reabsorption, whereas dopamine, cAMP (cyclic adenosine monophosphate), the cardiac natriuretic peptides (atrial natriuretic peptide and brain natriuretic peptide), and prostaglandins exert a natriuretic (sodium-excreting) effect.

Generally, small losses of sodium occur through feces and sweat, and these losses increase with increasing sodium intake, although part of them are obligatory.

Salt as a Preservative

Historically, the main reason for the addition of salt to food was for preservation.

Recently, because of the emergence of refrigeration and other methods of food preservation, the need for salt as a preservative has decreased.

Nevertheless, prior to refrigeration, salt was one of the best methods for inhibiting the growth and survival of undesirable microorganisms in food.

Despite modern-day advances in food storage, packaging techniques, and speed of transportation, which have largely diminished this role, salt still remains in widespread use for preventing rapid spoilage (and thus extending product shelf life), creating an inhospitable environment for pathogens, but also promoting the growth of desirable micro-organisms (probiotics) in various fermented foods and other products.

Salt’s excellent preservative properties derive from its ability to draw water out of food, inducing dehydration and cessation of water activity.

All living things require water and cannot grow in the absence of it, including bacteria and other microorganisms, which can cause food poisoning.

Salt’s efficacy to decrease the water activity of foods is possibly attributed to the ability of sodium and chloride ions to associate with water molecules (Fennema, 1996Potter and Hotchkiss, 1995).

Another speculated mechanism is that the addition of salt to foods may cause microbial cells to undergo osmotic shock, resulting in the loss of water from the cell, and thereby causing cell death or retarded growth (Davidson, 2012).

It has also been suggested that for some microorganisms, salt may limit oxygen solubility, interfere with cellular enzymes, or force cells to expend energy to exclude sodium ions from the cell, all of which can reduce the rate of growth (Shelef and Seiter, 2005).

Today, only a few foods are preserved solely by the addition of salt.

Yet, salt or sodium chloride still remains a commonly used component for creating an environment resistant to spoilage and inhospitable for the survival of pathogenic organisms in foods.

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Other sodium-containing compounds with preservative effects, such as sodium nitrate, sodium phosphate, and sodium glutamate (MSG), are also used in the food supply, not solely for the purpose of spoilage prevention, but to improve the sensory properties of foods, through increasing saltiness, decreasing bitterness, increasing sweetness and other congruent flavor effects [93].

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Most products in the modern food supply are typically preserved by multiple hurdles that control microbial growth (Leistner, 2000), increase food safety, and extend product shelf life.

Salt, high- or low-temperature processing and storage, pH, redox potential, and other additives are examples of hurdles that can be used for preservation.

Most often, no single preservation method alone can create a stable product.

However, when combined, these methods result in a desirable, stable, and safe product.

For example, a food might be protected by a combination of salt, refrigeration, pH, and chemical preservatives.

Food Sources

Dietary sodium intake is the sum of the generally small amounts of sodium present naturally in some foods, with higher amounts being added during food preparation in the kitchen and at the table, and even greater amounts added to many foods during their industrial processing.

The mass percent composition of sodium in sodium chloride is 39% (1 g of sodium corresponding to ∼2.5 g of salt).

Additional, not negligible amounts of sodium may be acquired through oral or parenteral medications.

The sources of sodium intake can otherwise be divided into “discretionary” (from the salt added to food in the kitchen or at the table) and “non-discretionary” (the sodium present naturally in foods and that added during industrial food processing), the latter being mainly in the form of sodium chloride (NaCl), with about 10% being in the form of sodium glutamate (MSG), sodium bicarbonate (baking soda), sodium phosphate, etc.

The sodium content of foods is quite variable and depends on both the food source (e.g., animal foods naturally contain more sodium than plant foods), and the level of transformation undergone by the food itself.

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Foods naturally low in sodium are fruit, vegetables, oils, and cereals, with their content ranging from traces to ∼20 mg/100 g, with few exceptions.

Meat and fishery products naturally contain from 40 to 120 mg/100 g, but some shellfish, such as mussels and oysters, contain up to 500 mg/100 g.

Whole milk contains ∼50 mg/100 g.

The sodium content of processed foods varies depending on the amount of salt added during their preparation.

For example, bread may contain only traces to several hundred milligrams of sodium per 100 g (∼1.5–2 g of salt).

The sodium content of some traditional meats and cheeses is extremely high (up to 2500 mg/100 g), and so also is that of many frozen foods (up to 700 mg/100 g).

In most countries, cereals and cereal products, including bread, are the main source of non-discretionary sodium, followed by the meat/eggs/fish aggregate and by milk and dairy products.

The contributions to total sodium intake by fruit and vegetables are almost negligible [1].

Sodium content of natural and processed foods

Food itemDescriptionSodium content (mg/100 g)
BeefTopside, Roast, Lean and fat
Corned beef, Canned
Wheat bran flakes
CheeseHard, Average
Chick-peasDried, Boiled in unsalted water
Canned, Re-heated, Drained
PotatoRaw, Boiled in unsalted water
Canned, Re-heated, Drained
PeasRaw, Boiled in unsalted water
Canned, Re-heated, Drained
Potato chipsHomemade, Fried in blended oil
Oven chips, Frozen, Baked
SalmonRaw, Steamed
Sweet cornOn-the-cob, Whole, Boiled in unsalted water
Kernels, Canned, Re-heated, Drained
Canned in oil, Drained
Canned in brine, Drained
Comparison of the sodium content of some of the “natural” and processed foods [100

Global Intakes and History

In most of the world’s populations, sodium intake greatly exceeds the minimal physiological need, which is estimated to be 200-500 mg/day (about 0.5-1.25 g of salt per day) for healthy individuals [10].

Historically, however, sodium consumption has not changed dramatically over time.

It is believed that the relatively high sodium intake of almost all societies today became common between 5000–10,000 years ago [96].

It is speculated that food preservation was the main driver of high sodium consumption in the early days [98].

For example, in 300 B.C. the average daily sodium intake in certain parts of China was approximately 3000 mg Na/day (7.6 g NaCl/day) for women and 5000 mg Na/day (12.7 g NaCl/day) for men [97].

In his book “Neptune’s gift: a history of common salt”, Multhauf estimated that the average salt consumption in 1850 in Britain and France was about 4000–5000 mg of sodium per day (10.2–12.7 g of salt per day) [98], which is rather similar to the current intake of sodium [14].

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In 2010, Bernstein and Willett [99] analyzed 38 studies, published between 1957 and 2003, which investigated sodium consumption, and found that individuals consistently consumed about 3700 mg of sodium per day (9.4 g of salt per day) throughout this period.

Despite the absence of any substantial increases in sodium consumption in the past centuries, it is commonly agreed that salt intake has remained too high, as people transitioned from preserved foods to modern processed foods [99].

Scientific evidence supports that, although small amounts of sodium are necessary for health, too much may cause health problems.

For example, because sodium affects fluid regulation, a high sodium intake may increase blood pressure through volume expansion.

However, there is some debate about how far salt intake should be reduced.

Current mean population sodium intake is about 3600 mg/day in the US [2], and the estimated global average is 3660-4000 mg/day [34], with a wide range across countries [5].

Recent guidelines in the US, Canada, and the UK call for lowering sodium consumption below 2300-2400 mg/day [678], but some organizations go even lower.

The American Heart Association (AHA) recommends no more than 2300 mg/day, but suggests an ideal limit of 1500 mg per day for most adults [9], especially those with high blood pressure.

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The World Health Organization (WHO) calls for <2000 mg/day [10].

Others conclude that the optimal range is much higher [1112]

Sodium Intake Recommendations

The recommendations for sodium intake issued by authoritative international sources are relatively consistent.

However, because of the lack of dose-response testing data, most national and international authorities have found it impossible to define a sodium average requirement or a recommended intake for the general population.

The available data suggest that the minimum sodium intake that prevents deficiency signs or symptoms is very low.

For most healthy individuals, physiological requirements for sodium are <500 mg/day.

Despite that, there is no doubt that a balanced and varied diet, like one that meets the need for other essential nutrients, contains a considerably higher amount of sodium than these levels.

As a result, rather than setting reference intakes for covering the minimum physiologic needs, most health authorities have found it convenient to set an adequate intake (AI) corresponding to a moderate intake of sodium, which is compatible with a varied diet and a healthy lifestyle.

Intakes at or above the adequate intake (AI), have a low probability of inadequacy.

An age-specific tolerable upper intake level (UL) or a standard dietary target have also been established by the same authorities, to indicate the need to reduce the intake of sodium for the prevention of cardiovascular disease (CVD), and other chronic degenerative diseases.

The goal for the general population is that sodium intake should be at least lower than the upper intake level (UL) or standard dietary target, although even lower levels of intake may be desirable [13].

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In 2010, the Nutritional Guidelines for Americans, based on the analysis of the Institute of Medicine (IOM), set an adequate intake (AI) of 1500 mg (or 3.75 g of salt) for all individuals aged 9–50 years, and a correspondingly lower level for children and older people, considering their lower calorie intake.

This amount was considered suitable for both genders. For adolescents and adults of all ages (≥14 years old), the Institute of Medicine (IOM) set the upper intake level (UL) at 2300 mg/d.

The upper intake level (UL) is the highest daily nutrient intake level that is likely to pose no risk of adverse health effects to almost all individuals in the population.

As intake increases above the UL, the risk of adverse effects increases.

The American Heart Association (AHA) provides recommendations consistent with the IOM 2006 document.

Recently, however, the new Institute of Medicine (IOM) Committee on the Consequences of Sodium Reduction in Populations has observed that the available evidence on the effects of reducing sodium intake to ≤1500 mg/day on direct health outcomes among individuals with diabetes, chronic kidney disease (CKD), or pre-existing cardiovascular disease (CVD), does not support recommendations to treat them differently from the general U.S. population.

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As a result, this committee redefined an adequate intake (AI) of 2300 mg (or 5.75 g of salt) per day for all adult individuals.

The recommendations by the U.K. Food Standard Agency (FSA) and the Sodium Working Group of the Minister of Health for Canada, are in line with those by the Institute of Medicine (IOM).

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The recent World Health Organization (WHO) guideline has set ≤2000 mg of sodium (5 g of salt) per day as a target for the general population, stating that this level is fully compatible with the prophylaxis of thyroid diseases caused by iodine deficiency, which can be prevented by the more extensive use of iodized salt [10].

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Given the presence of added salt in a wide range of commonly used food products, a clinically relevant food deficit of sodium is extremely unlikely to occur in healthy individuals.

Indeed, a deficiency of sodium does not happen under normal healthy conditions, even with diets very low in sodium.

In contrast, an excess of sodium in food is common to most populations worldwide, because of both the salt added to products during food processing, and the widespread habit of adding additional amounts of salt in food preparation in the kitchen and at the table.

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This sodium excess is a recognized causative factor of hypertension and cardiovascular diseases (CVDs) [1516108], and also contributes to the development of:

  • Chronic kidney disease (CKD), as it increases oxidative stress, blood pressure, and the amount of protein in the urine (proteinuria), which is a major risk factor for the decline of kidney function and performance [103].
  • Gastric cancer, as sodium dissolves mucus and can destroy the mucosal barrier of the stomach. A damaged gastric mucosa offers little or no protection to carcinogens from foods, such as N-nitroso compounds. The damage caused by excessive salt intake may also increase gastric H. pylori colonization, a pathogen recognized to be one of the most important contributing factors to gastric cancer [94104]
  • Calcium nephrolithiasis (kidney stones), as increased sodium intake is associated with increased urinary excretion of calcium (hypercalciuria) and the formation of calcium oxalate stones [101105106107].
  • Low bone mineral density and osteoporosis, as sodium increases calcium excretion and higher calcium excretion is associated with lower bone mineral density (BMD), a predictor of osteoporotic fractures [95102].

A condition of true sodium (and water) depletion can occur only in pathologic conditions, such as primary adrenal insufficiency (Addison’s disease), sodium-losing kidney disease, hypoaldosteronism, extensive burns, chronic diarrhea, uncontrollable vomiting, extreme and prolonged sweating, diabetic ketoacidosis, excessive intake of diuretics, or continuous gastric suction.


Acute toxicity from excess sodium intake with the possibility of fatal outcome has been reported with the ingestion of huge amounts of sodium, such as 0.5–1 g of salt/kg body weight.

In certain pathologic conditions (e.g., heart failure, decompensated liver cirrhosis, and renal failure), sodium intake to levels routinely present in our diet (≥10 g/d) may lead to a dangerous increase in extracellular fluid (ECF) volume.

However, even under normal conditions, the intake of high amounts of sodium tends to favor, especially in predisposed individuals, an increase of extracellular fluid (ECF) volume and blood pressure (BP).

The biggest international, epidemiological study on the effects of dietary sodium on blood pressure- the Intersalt study [14] – showed that the higher the habitual consumption of sodium in a given population, the stronger the average blood pressure (BP) increase with age and the prevalence of hypertension.

Salt Sensitivity

Blood pressure responses to alterations in dietary sodium vary widely, leading to the concept of salt-sensitive and salt-resistant blood pressure [1718].

However, there are no standardized guidelines or firm blood pressure cut-offs for classifying individuals as having salt-sensitive blood pressure.

If blood pressure increases during a period of high dietary sodium, or declines during a period of low sodium intake, the individual is classified as salt-sensitive.

If there is no change in blood pressure with sodium restriction, the individual is characterized as salt-resistant.

However, for the time being, limited evidence supports the reproducibility of these responses to dietary salt [1920], and the concept of salt-sensitivity continues to apply until proven otherwise.

Research shows that salt-sensitivity in normotensive adults predicts future hypertension [2122], and salt-sensitive blood pressure has been associated with increased mortality [23].

Unfortunately, while there is academic interest in studying the pathophysiology of salt-sensitive blood pressure, there is less interest in its routine clinical assessment [24].

Recent Research on Sodium

Recent experimental and clinical studies have revealed major effects of sodium intake on endothelial function and potentially very important interactions between sodium intake and the immune system.

Excess sodium intake has also been associated with, the latter greater risk of gastric cancer, nephrolithiasis (kidney stones), and osteoporosis, due to increased urinary calcium losses favoring a negative calcium balance.

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Recent meta-analyses of randomized controlled trials on the effects of a moderate reduction in sodium intake, documented significant blood pressure (BP) reductions in adult hypertensive and normotensive individuals, as well as in children and adolescents [15].

Two meta-analyses of the prospective studies on the relationship between habitual salt intake and cardiovascular disease (CVD) morbidity and mortality have shown that higher salt intake is significantly associated with a greater risk of stroke and other cardiovascular events [1516].

However, as noted by the 2013 Institute of Medicine (IOM) ad hoc committee, the evidence for the impact of excess sodium intake on these hard endpoints is still primarily based on observational studies, most of which are influenced by important methodologic limitations.

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Future studies should try to overcome these limitations, and ideally, a randomized controlled trial designed to describe the effects of different degrees of long-term sodium reduction on hard health outcomes should be implemented.

Dangers of Sodium Overconsumption

There is evidence that in the absence of increased blood pressure, elevated dietary sodium can adversely affect multiple target organs and tissues [25], including the vasculature, heart, kidneys, bones, and areas of the brain that control autonomic outflow.


Rodent studies demonstrated impaired endothelial function during sodium loading, without alterations in blood pressure [26, 272829].

Sodium loading in normotensive men reduced endothelial function [30], and sodium restriction in adults with elevated blood pressure improved endothelial function [31].

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Additionally, high sodium impairs endothelial function in normotensive salt-resistant humans, providing support for a blood-pressure-independent effect of sodium on the endothelium [3233].

Sodium’s deleterious effects on endothelial function likely results from the increased production of reactive oxygen species [3433], such as superoxide [3536], resulting in reduced nitric oxide bioavailability.

Cell culture studies support that high sodium exposure stiffens endothelial cells and damages the glycocalyx (a glycoprotein/glycolipid covering that surrounds the cell membranes of some bacteria, epithelial, and other types of cells) [37].

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Animal studies show that elevated dietary sodium can increase arterial stiffness, independent of blood pressure [38].

In human studies, increased arterial stiffness was observed in groups consuming a higher sodium intake, independent of blood pressure [3940].

This increased stiffness is likely related to the profibrotic effects of transforming growth factor-β [41].

Endothelial cells throughout the vasculature and glomeruli respond to increased dietary salt intake with increased production of transforming growth factor-β (TGF-β) [42].

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TGF-β signaling is broadly accepted as a strong stimulator of renal and vascular fibrosis (scar tissue creation- pathological connective tissue deposition).

Thus, high dietary sodium stiffens the arteries and glomeruli, and reducing dietary sodium lowers arterial and glomerular stiffness in hypertensive patients [4344].

Heart and Kidneys

Increased blood pressure is a major risk factor for left ventricular hypertrophy; high dietary sodium may increase left ventricular wall thickness [45] and mass [46], independent of hypertension status.

For example, among a cohort of healthy adults with minimal hypertension, those with the highest sodium excretion – an indication of increased sodium intake – had greater left ventricular mass [46].

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High aldosterone levels may also be important in mediating the effect of dietary salt on left ventricular mass [47].

A 12-month sodium restriction intervention in hypertensive patients has been shown to reduce left ventricular hypertrophy [48].

Currently, there are a limited number of studies of subjects without kidney disease, but evidence suggests that high sodium is associated with reduced renal function [49].

Sodium loading in spontaneously hypertensive rats (inbred laboratory rats used as an animal model of essential hypertension to study cardiovascular disease) increased renal vascular resistance, glomerular pressure, serum creatinine, and proteinuria; sodium loading also caused a decline in single-nephron plasma flow.

This decline in renal function was observed with only a minimal additional increase in blood pressure [50], meaning that the kidney-damaging effects of increased sodium intake do not always coincide with significant increases in blood pressure.

Sodium restriction has also been shown to reduce both protein excretion and blood pressure in black hypertensive patients [51].

Similarly, in the LowSalt chronic kidney diseases (CKD) study [52], low salt intake reduced proteinuria, albuminuria, and blood pressure.


Sodium may affect brainstem nuclei that control blood pressure [53].

Chronically elevated dietary sodium may “sensitize” sympathetic neurons in the rostral ventral lateral medulla of rodents [545556], causing a greater sympathetic response to a variety of stimuli [57], including skeletal muscle contraction [58].

This increased responsiveness has been associated with increased blood pressure variability, even without an elevation in average blood pressure [59]; this is relevant due to the association of blood pressure variability with target organ damage [60].

Even in the absence of increased blood pressure, chronically increased sympathetic outflow may have deleterious health effects on multiple organs.

Sodium and Blood Pressure

Multiple meta-analyses and systematic reviews of randomized controlled trials (RCTs) have shown a strong positive association between sodium intake and systolic blood pressure [6162, 63, 64, 65, 66, 67] and a significant reduction in systolic blood pressure with sodium restriction [1568].

A recent meta-analysis of 103 randomized interventions confirmed these results, showing a linear association between salt restriction and systolic blood pressure.

The reduction was larger with older age, among blacks, and among hypertensive patients [6970].

The incidence of hypertension also decreased following a sodium intake reduction intervention in the Trials of Hypertension Prevention II randomized controlled trial (RCT) [71].

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Strategies For Limiting Sodium Intake

Most people like some level of salt in their food.

Conceptually, there is a “bliss point”, where the effect of sodium on flavor is optimum.

However, this “bliss point” is malleable, and most people will adapt [72] to a reduction in dietary sodium [73].

Sudden sodium changes are harder to accept, but if the United States gradually moves to a diet with less sodium, many people will likely make the transition with little difficulty [727475].

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Approximately 75% of sodium in the diet comes from processed foods [767778] and used to prepare foods as ubiquitous as bread [79].

Sodium added during food preparation and at the table contributes less, about 11% [7377].

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Restaurants are also more likely to have saltier foods and more people are eating out in recent decades.

Market forces are a contributing factor to a large proportion of sodium in the diet, so without a societal approach, pressure on individual stakeholders is likely to be resisted.

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Food processing companies have marketed low-sodium alternatives without much success [79].

A partnership of food companies and restaurant associations with groups like the American Heart Association (AHA) is more likely to successfully change diets [80].

Efforts in countries, such as Finland and the United Kingdom have successfully reduced sodium [818283].

Several approaches may decrease dietary sodium intake: 

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1) Decrease the sodium content of foods 

2) A switch by the consumer from high-sodium to low-sodium foods by avoiding processed foods and reading labels 

3) Switch to substitute salts [84] 

4) Reduce sodium while increasing other flavors [75, 1] 

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5) Use engineering approaches to provide salty taste with less sodium, or food processing with less sodium [8584].

Nonetheless, the most important thing is that flavor must be maintained, because taste is the driving force behind salty foods [7386].

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A decrease in sodium from the current levels will represent a major change in our food supply and may happen more easily and successfully as a series of small steps over several years.

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Coordination between food companies, restaurants, and advocacy groups is crucial and currently lacking [73].

Importantly, increased dietary potassium (K+) intake should also be taken into consideration, as it has been shown to decrease salt sensitivity and positively affect blood pressure [87109].


Sodium is an essential nutrient involved in the maintenance of normal cellular homeostasis and the regulation of fluid and electrolyte balance, as well as blood pressure.

Its role is crucial for maintaining extracellular fluid volume, because of its important osmotic action, and is equally important for the excitability of muscle and nerve cells, as well as for the transport of nutrients and substrates through plasma membranes.

A high sodium consumption is, however, related to negative health effects such as hypertension [15], cardiovascular diseases [16108], stroke [110], chronic kidney disease [103], decreased bone mineral density [95], osteoporosis [102], and gastric cancer [94104].

In most of the world’s populations, sodium intake greatly exceeds the minimal physiological need, which for healthy individuals is set at <500 mg/day.

Although small amounts of sodium are necessary for health, too much may cause health problems, especially in people with pre-existing metabolic abnormalities (i.e., hypertension).

For example, because sodium affects fluid regulation, a high sodium intake may increase blood pressure through volume expansion.

However, still, there is some debate about how far salt intake should be reduced, especially concerning healthy individuals.

The current average sodium intake of the general population is about 3600 mg/day in the US [2], and the estimated global mean intake is 3660-4000 mg/day [34], with some variability across countries [5].

Recent guidelines in the US, Canada, and the UK call for lowering sodium consumption below 2300-2400 mg/day [678], but some official health organizations, such as the American Heart Association (AHA) and the World Health Organization (WHO) go even lower.

In industrialized countries, about 75% of sodium in the diet comes from manufactured (processed) foods and foods eaten away from home [77].

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Because of the weight of evidence in favor of salt reduction and the difficulties in organizing a clinical trial that will demonstrate the beneficial effects of reduced dietary sodium on hard health outcomes in normotensive people, most health authorities recommend a population-wide reduction in sodium intake.

However, reducing sodium, especially in processed foods, which represent the biggest source of sodium intake, can be a challenging task due to sodium’s specific functionality in terms of preservability, flavor, and associated palatability of foods.

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Consequently, reducing sodium will require a coordinated effort involving official health authorities, food producers and manufacturers, restaurants, and public policies aimed at education.

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About George Kelly

George Kelly M.Sc is a Sports Nutritionist, Functional Nutritional Therapy Practitioner (FNTP), and Metabolic Type expert. He is the CEO and lead author of Metabolic Body.