← Nutrients · Metabolic Health

Sodium

ElectrolyteFoundationalTransportElectrochemical

Not just "salt": the gradient that runs your nerves, heart and nutrient absorption.

At a glance

Essential · don't fear salt
Strong human evidence

How to take it

  • About 3–5 g of sodium a day (1¼–2¼ tsp of salt, counting what's already in food), more if you sweat a lot
  • Salt your food, especially if you cook at home
  • Also: cheese, olives, bone broth
details ↓

Watch out

  • Both too little (under ~3 g) and too much (over ~7 g) go with more heart events

Signs you're low

  • Headache, confusion
  • Seizures in severe cases
details ↓
The Research

Mechanisms, studies and evidence grades for each claim above.

Keeps you hydrated

Water moves toward wherever dissolved particles are most concentrated. Sodium is the main particle in the fluid outside cells: blood plasma and the fluid between cells. So the amount of sodium in the body largely decides how much water stays outside cells, and that sets blood volume.1

The body defends this with two linked systems:

That second system is why very low salt intake isn't free. In a Cochrane analysis of 82 trials, cutting sodium reliably raised renin and aldosterone, and also raised noradrenaline, cholesterol and triglycerides. Meanwhile it lowered blood pressure by only about 0.4 mmHg in people with normal pressure.2 The body treats a low-salt diet as a volume threat and stays in a stress response to hold onto sodium.

↑ back to summary

Lets nerves fire

Every cell keeps sodium about 10 times more concentrated outside than inside. The sodium-potassium pump does this by pushing 3 sodium out for every 2 potassium it brings in, and it uses a large share of the body's resting energy, around half of the brain's. That gradient is stored energy, like water behind a dam.

A nerve signal spends it. When a neuron is stimulated, voltage-gated sodium channels open for about a millisecond and sodium rushes in. That flips the inside of the membrane from negative to positive, which opens the next set of channels further along. The signal travels down the nerve as a chain reaction. Hodgkin and Huxley worked out this mechanism in squid nerve in 1952 and won a Nobel Prize for it.3 Local anaesthetics like lidocaine work by blocking those sodium channels.

What happens when blood sodium falls. Low blood sodium (hyponatremia) makes water move into brain cells, so they swell inside the skull. Severe or fast drops cause headache, confusion, seizures and coma.4 Even mild, chronic hyponatremia that was thought to cause no symptoms isn't harmless. Among emergency patients with mild chronic hyponatremia, 21% had come in because of a fall, against 5% of matched controls. When tested, their attention and balance were measurably worse while their sodium was low than after it was corrected. The researchers found the impairment comparable to what they measured in volunteers after drinking alcohol.5

↑ back to summary

Powers the heart's rhythm

A heart muscle cell fires the same way a nerve does. A fast rush of sodium through its own sodium channels (Nav1.5) starts each beat and sets how quickly the electrical wave spreads across the heart.3 Then the sodium gradient powers a second step. The sodium-calcium exchanger lets 3 sodium ions in to push 1 calcium ion out, which is how the heart muscle relaxes between beats. So sodium is involved both in triggering the beat and in resetting it.

Sodium also keeps up blood volume, which is what the heart pumps. Too little volume means lower filling pressure, lightheadedness when you stand up and a faster heart rate to make up for it. That is a common, fixable problem in endurance athletes and people on low-salt or ketogenic diets, where the kidneys excrete more sodium.1

↑ back to summary

Pulls nutrients into cells

The sodium gradient doesn't only power nerves. Cells also use it to pull nutrients in against their own concentration gradients. A transporter in the gut lining, SGLT1, carries 2 sodium ions and 1 glucose (or galactose) molecule into the cell together. Sodium flowing "downhill" drags glucose "uphill," so glucose is absorbed even after the gut contents run low.6 Several amino acid transporters work the same way. Vitamin C enters through its own sodium-coupled transporters: SVCT1 in the gut and kidney, and SVCT2 in the brain, eyes and other tissues that concentrate it.7

This is why oral rehydration solution works. Adding a little glucose to salty water lets SGLT1 pull both sodium and water into the body, even during cholera diarrhoea. The Lancet called it potentially the most important medical advance of the 20th century. It also explains why a pinch of salt in water hydrates better than plain water during heavy sweating. See Vitamin C.

↑ back to summary

How much: the U-shaped curve

Official targets (under 2.3 g sodium/day, or 1.5 g for some groups) assume that less is always better. Large outcome studies don't support that. In the PURE study, sodium was estimated from urine in about 100,000 people across 17 countries. The lowest rate of death and cardiovascular events was at 3–6 g sodium per day. Both higher intakes (≥7 g) and lower intakes (<3 g) were linked to more events, and the low end looked worse. Under 3 g carried a 27% higher risk, against 15% for over 7 g.8 A study of 28,880 high-risk patients found the same J-shape, with the lowest risk at 4–6 g/day.9 A meta-analysis of 25 cohorts (274,683 people) found that both low and high sodium intakes were linked to higher death rates than usual intake.10

Most people already eat in the 3–5 g range. That's about 1¼–2¼ tsp of salt in total, counting salt already in food. People who eat mostly home-cooked, unprocessed food can end up well below that unless they salt their food, and so do people who sweat heavily.

Limits of the evidence. These are observational studies, and some of the extra risk at low intakes may come from sick people eating less overall. The defensible conclusion is that no randomised trial has shown that cutting sodium below about 3 g/day reduces deaths, while the hormonal costs of doing so are measured. People with salt-sensitive hypertension or heart failure are the exception and should follow their own doctor's advice.

Top foods

↑ back to summary

Deficiency effects

Low blood sodium is usually caused by holding too much water rather than eating too little salt. Common causes are drinking large volumes during endurance events, diuretics (especially thiazides), SSRIs and some other drugs, and conditions that raise ADH.4 Symptoms go from headache, nausea and fatigue to confusion, unsteadiness, seizures and coma. A low total-body sodium with normal blood levels is a different problem. It shows up as low blood volume: lightheadedness on standing, cramps, fatigue and poor exercise tolerance. It is common at the start of a ketogenic diet and in heavy sweaters.

↑ back to summary

References

  1. Palmer BF, Clegg DJ. Physiology and pathophysiology of potassium homeostasis. Adv Physiol Educ 2016;40:480–490 (sodium–potassium balance, RAAS and renal handling). PMID 27756725
  2. Graudal NA, Hubeck-Graudal T, Jürgens G. Effects of low sodium diet versus high sodium diet on blood pressure, renin, aldosterone, catecholamines, cholesterol, and triglyceride. Cochrane Database Syst Rev 2020;12:CD004022. PMID 33314019
  3. Hodgkin AL, Huxley AF. A quantitative description of membrane current and its application to conduction and excitation in nerve. J Physiol 1952;117:500–544. PMID 12991237
  4. Adrogué HJ, Madias NE. Hyponatremia. N Engl J Med 2000;342:1581–1589. PMID 10824078
  5. Renneboog B, Musch W, Vandemergel X, et al. Mild chronic hyponatremia is associated with falls, unsteadiness, and attention deficits. Am J Med 2006;119:71.e1–8. PMID 16431193
  6. Wright EM, Loo DDF, Hirayama BA. Biology of human sodium glucose transporters. Physiol Rev 2011;91:733–794. PMID 21527736
  7. Takanaga H, Mackenzie B, Hediger MA. Sodium-dependent ascorbic acid transporter family SLC23. Pflügers Arch 2004;447:677–682. PMID 12845532
  8. O'Donnell M, Mente A, Rangarajan S, et al. Urinary sodium and potassium excretion, mortality, and cardiovascular events. N Engl J Med 2014;371:612–623. PMID 25119607
  9. O'Donnell MJ, Yusuf S, Mente A, et al. Urinary sodium and potassium excretion and risk of cardiovascular events. JAMA 2011;306:2229–2238. PMID 22110105
  10. Graudal N, Jürgens G, Baslund B, Alderman MH. Compared with usual sodium intake, low- and excessive-sodium diets are associated with increased mortality: a meta-analysis. Am J Hypertens 2014;27:1129–1137. PMID 24651634