An essential mineral behind more than 300 enzymes. Your cells can't use energy without it.
Mechanisms, studies and evidence grades for each claim above.
ATP is the cell's energy currency, but free ATP is not what enzymes actually use. Almost all ATP inside a cell is bound to a magnesium ion, and that Mg-ATP pair is the form that fits into the enzymes that spend it. The magnesium sits between ATP's phosphate groups, holding them in the right shape and spreading out their negative charge, so the last phosphate can be broken off and handed to another molecule. Without magnesium, ATP is like a full battery with no terminals.1
That is why magnesium shows up in more than 600 enzyme reactions. These include every kinase (an enzyme that moves a phosphate from ATP onto something else), the key steps of glycolysis, the enzyme that makes ATP in mitochondria, and the polymerases that copy DNA and RNA. It also holds ribosomes together so they can build proteins. Magnesium is not a booster for energy metabolism. Energy metabolism can't run without it.1
The body holds about 24 g, roughly half in bone and nearly all the rest inside cells. Less than 1% is in the blood. So a normal blood test does not rule out low tissue stores. Serum magnesium is kept in range by pulling from bone and adjusting how much the kidneys hold back.1
↑ back to summaryMagnesium calms nerve cells in two ways:
Human trials. In a double-blind trial, 46 older adults with insomnia took 500 mg of magnesium or placebo daily for 8 weeks. The magnesium group fell asleep faster, slept more efficiently and scored better on an insomnia scale. Their melatonin rose and their cortisol fell.2 A 2023 systematic review found the overall evidence encouraging but thin. The trials are small, mostly in older adults, and observational links between magnesium intake and sleep are mixed.3
Who it's likely to help. People whose intake is low, which is common in older adults, will probably notice it. People already getting enough from food probably won't. The glycinate form adds glycine, which has its own sleep effect (see Glycine).
↑ back to summaryA muscle contracts when calcium floods into the muscle fibre from its internal store and lets the actin and myosin filaments grab each other. It relaxes when pumps (which run on Mg-ATP) push the calcium back into storage. Magnesium works against calcium at several points. It competes with calcium for the binding sites that switch on contraction. It slows the calcium release channel. And it powers the pumps that clear calcium away. When magnesium is truly low, muscle and nerve get twitchy: tremor, spasms and, in severe cases, tetany (sustained cramping).1 Low magnesium also drains potassium and makes blood calcium hard to correct, because magnesium is needed for the kidney to hold onto potassium and for the parathyroid gland to release its calcium-raising hormone (PTH).
But cramp pills mostly don't work. A 2020 Cochrane review of randomised trials concluded that magnesium is unlikely to give meaningful protection from the ordinary night cramps of older adults. The evidence in pregnancy is conflicting, and no trials have tested exercise cramps.4 The mechanism is real when someone is deficient. Most everyday cramps just aren't caused by low magnesium. See Calcium and Potassium.
↑ back to summaryEach heartbeat is an electrical wave that depends on potassium flowing back out of heart cells to reset them. Magnesium matters to that reset in two ways. It runs the sodium-potassium pump (as Mg-ATP), which restores the potassium gradient after each beat. It also controls some of the potassium channels that let potassium out. Low magnesium therefore delays the reset (a long QT interval on an ECG) and makes extra beats more likely. Because low magnesium also drains potassium, the two often fall together.1
Clinical evidence. Intravenous magnesium is the standard first treatment for torsades de pointes, a dangerous rhythm tied to a long QT. Whether giving magnesium to people who aren't deficient prevents arrhythmias is less clear. An early meta-analysis of 20 trials found that magnesium given around heart surgery cut atrial fibrillation from 28% to 18%.5 But when a later analysis kept only the five double-blind trials where AF was the main outcome, the effect disappeared. The smaller trials had overstated it.6 The fair summary is that correcting a deficiency protects the heart, and topping up a normal level isn't proven to add more.
↑ back to summaryWhen insulin binds its receptor, the receptor switches itself on by adding phosphate groups to its own inner tail. That step is a kinase reaction, which needs Mg-ATP. Several steps further down the signal also use magnesium-dependent kinases. With low magnesium inside the cell, the receptor signals weakly and muscle and fat take up less glucose: that is insulin resistance at the molecular level. The relationship runs both ways. High blood sugar makes the kidneys lose more magnesium, so diabetes and low magnesium tend to feed each other.1
Human evidence. A meta-analysis of 13 prospective cohorts (536,318 people) found a 22% lower risk of type 2 diabetes in the highest magnesium intakes, and 14% lower risk per extra 100 mg/day. The link was clearest in overweight people.7 In double-blind randomised trials, magnesium supplements lowered fasting glucose in people with diabetes and improved glucose and insulin sensitivity in people at high risk.8 The cohort data can't separate magnesium from the whole foods that carry it, but the trials suggest the mineral itself contributes.
↑ back to summaryIn animals, magnesium deficiency triggers inflammation fast. Immune cells become primed, more calcium leaks into cells and inflammatory cytokines rise, partly through NMDA receptors and calcium signalling.1 Whether supplements calm inflammation in people depends on the starting point. A meta-analysis of 11 randomised trials found no overall effect on CRP (a blood marker of inflammation). But in people whose CRP started above 3 mg/L, the usual cutoff for raised inflammation, magnesium lowered it by about 1.1 mg/L.9 That matches the rest of this page: magnesium fixes what a shortage broke and does little when status is already fine.
↑ back to summaryThe RDA is 310–420 mg/day, depending on sex and age. The body can't make it, and refining grain strips most of it out, which is why surveys find many adults fall short. Bioavailability varies by form. Organic salts (glycinate, citrate) are absorbed better than inorganic magnesium oxide.1
Early signs are vague: tiredness, weakness, poor appetite. As it gets worse: muscle twitches, cramps and tremor; abnormal heart rhythms; anxiety and poor sleep; and low potassium and calcium that won't correct until magnesium is replaced.1 The most common causes are diuretics, long-term acid-blocking drugs (PPIs), heavy drinking, poorly controlled diabetes and chronic diarrhoea.