Skip to main content

Longevity Library · Lab reference

Written by Daniel Tagge, MD
Updated October 10, 2026
Reviewed October 12, 2026
32 sources · Measured in mg/dL

System: Mitochondria & Cellular Energy

MagnesiumSerum magnesium · RBC magnesium · Red blood cell magnesium

The cohorts agree: a serum magnesium in the lowest quartile, roughly below about 1.8 to 1.9 mg/dL, kept company with more atrial fibrillation, sudden cardiac death, heart failure and diabetes, risk sat lowest in the upper quartiles from about 2.0 to 2.4, and two expert groups have proposed raising the lower limit to 2.07 (0.85 mmol/L). Supplement trials moved blood pressure by about 2 mm Hg and glucose modestly, and red-cell magnesium, often preferred as a better measure of stores, has thin validation and no outcome literature of its own.

Serum magnesium holds about 0.3 percent of the body's magnesium, so it reports the regulated blood pool rather than the stores in bone and muscle. Laboratories print about 1.7 to 2.4 mg/dL as normal, a range drawn from a 1974 population distribution rather than from outcomes. The cohorts place the extra risk in the lowest quartile and the lowest risk in the upper half of that range, and the red-cell test the practice uses is a plausible but thinly validated proxy.

01 · The scale

Where the laboratory range and the evidence sit.

Consistent at the low end: the lowest quartile of serum magnesium, roughly below about 1.8 to 1.9 mg/dL, carried more atrial fibrillation, sudden cardiac death, heart failure and diabetes in the cohorts, and risk sat lowest in the upper quartiles from about 2.0 to 2.4. Supplement trials lowered blood pressure by about 2 mm Hg and improved glucose modestly; no trial has treated to a serum target, and no outcome study has used red-cell magnesium.

11.41.722.42.63

  1. Common laboratory reference range

    1.7 to 2.4 mg/dL · Typical US laboratories

  2. Hypomagnesemia by most laboratory cutoffs; low potassium and calcium, cramps and arrhythmia live here

    1 to 1.7 mg/dL · Jahnen-Dechent 2012

  3. Lowest quartiles of the cohorts: more atrial fibrillation, sudden cardiac death, heart failure and diabetes

    1.7 to 2 mg/dL · Khan 2013; Peacock 2010; Misialek 2013; Kieboom 2016; Lutsey 2014

  4. Inside the laboratory range but below the proposed 2.07 lower limit

    2 to 2.1 mg/dL · Rosanoff 2022; Elin 2010

  5. Upper quartiles of the cohorts, where risk sat lowest; above the proposed lower limit

    2.1 to 2.4 mg/dL · Kieboom 2016; Peacock 2010; Khan 2013; Kao 1999

  6. Top of the laboratory range; no cohort signal either way

    2.4 to 2.6 mg/dL · No cohort addresses this span separately

  7. High: usually reduced kidney function or magnesium-containing medicines; symptoms appear well above 3

    2.6 and above mg/dL · Jahnen-Dechent 2012

  • Laboratory range
  • Evidence supports
  • Guideline goal or unstudied
  • Higher risk in studies
Scale in mg/dL. Some laboratories report mmol/L; multiply mg/dL by about 0.41 for mmol/L. Red-cell magnesium is reported on its own scale, about 4 to 7 mg/dL. Bands show where studies found something, not a recommendation for any one person.

02 · What it is

What Magnesium measures.

Magnesium is the second most abundant cation inside cells after potassium and a cofactor in more than 600 enzymatic reactions, including energy metabolism and protein synthesis. About 99 percent of body magnesium sits in bone, muscle and soft tissue, roughly 53 percent in bone and 27 percent in muscle; about 1 percent is extracellular, with about 0.3 percent in serum and 0.5 percent in red blood cells.1,2Grade C

Serum magnesium is the test medicine uses, and it is a poor measure of stores: it does not correlate with tissue pools apart from interstitial fluid and bone, bone buffers the serum value from its exchangeable reserve, and people with a serum value inside the reference interval can carry a total body deficit. The reference standard is the magnesium load test, in which the share of an infused dose retained by the body is measured in 24-hour urine; a serum value below about 0.75 mmol/L (about 1.8 mg/dL) is useful for severe deficiency, and between 0.75 and 0.85 mmol/L the load test identifies deficient people.2,3,4Grade B

Intake is short for many Americans. About 50 percent consume less than the estimated average requirement, 48 percent of the US population consumed less than the required amount from food in 2005 to 2006 (down from 56 percent in 2001 to 2002), and by one NHANES reading 79 percent of US adults do not meet the recommended dietary allowance.5,6,7Grade B

03 · Origins

Where it came from, and where it sits in the network.

Magnesium belongs to the oldest chemistry in biology. It is the eighth most common element in the Earth's crust, the sea holds about 55 mmol/L of it against about 0.85 mmol/kg in human serum, and in plants it is the central ion of chlorophyll, which is why green vegetables are the main dietary source. Inside the cell it is the counter ion for ATP and for nucleic acids, so that the energy currency of every cell is in effect magnesium-ATP. The ribosome shows how far back this goes: the atomic structure of the large ribosomal subunit of an archaeon contains 116 magnesium ions bound mainly to ribosomal RNA, concentrated around the peptidyl transferase center where protein tails are absent, which the structural biologists read as a trace of the period before proteins existed, when metal ions alone stabilized RNA. A chronology built from the same structures finds that the earliest core of the ribosome may have assembled through magnesium-mediated RNA interactions, with proteins replacing magnesium ions as one moves outward through younger layers. The ion composition of the cell is itself an evolutionary record: cells hold far more potassium than modern or reconstructed ancient oceans, and one reading of that mismatch is that the first cells, lacking ion-tight membranes and pumps, took on the chemistry of their birthplace and have kept it since. Magnesium's place as the second intracellular cation after potassium sits inside that inheritance.2,8,9,10Grade C

The modern-intake story is a hypothesis, and the entry names it as one. The physiology review notes that processed foods carry much less magnesium than unrefined grain, that drinking water supplies about 10 percent of intake, and that boiling, processed food and demineralized soft water together strip much of the natural supply in industrialized countries; a separate review attributes the postulated rise in deficiency partly to a decline in the magnesium content of cultivated produce over the past century and a rise in processed-food consumption. The same authors caution that the estimates of lost mineral content rest on old data, that the USDA figures they cite had not been updated since 2000, and that the claim should be verified. What is measured, rather than inferred, is intake: about half of Americans eat less than the estimated average requirement. Whether that gap is new is the part that remains a hypothesis.2,11,5Grade C

In the body's network, magnesium sits under several systems this shelf measures separately. It stabilizes the ATP-generating reactions and the ATPases, including the sodium-potassium pump; it modulates insulin signal transduction, with lower intracellular magnesium common in people with diabetes; and the enzymes that synthesize and metabolize vitamin D are magnesium dependent, so that in a randomized trial of 180 adults magnesium raised 25-hydroxyvitamin D3 when the baseline level was near 30 ng/mL and lowered it when the baseline was higher. That is why a deficit shows up where it is not being looked for: severe hypomagnesemia usually travels with low potassium and low calcium, and the listed manifestations include arrhythmia, tremor, cramps, weakness and fatigue. On this shelf the same network connects magnesium to Vitamin D, to Fasting insulin and HbA1c, and to eGFR, because the kidney sets the serum value by what it excretes. A serum magnesium is a proxy for the regulated blood pool, kept steady by bone until the reserve runs low; a red-cell magnesium is a proxy for one intracellular compartment, chosen because it is easy to sample, and neither is a measure of the stores themselves.2,7Grade C

04 · The laboratory range

What a laboratory calls normal.

About 1.7 to 2.4 mg/dL for serum (some laboratories 1.6 to 2.6), and about 4.2 to 6.8 mg/dL for red-cell magnesium, depending on the laboratory.

The common serum interval of 0.75 to 0.95 mmol/L (about 1.82 to 2.31 mg/dL) was derived from the distribution of serum magnesium in the NHANES I population of 1974, not from clinical outcomes, and a normal population unknowingly includes people with a chronic latent magnesium deficit whose serum value is held up by bone.5,12Grade B

Two independent groups have designated 0.85 mmol/L (2.07 mg/dL) as the lower cutoff for hypomagnesemia, on the reasoning that lower values are associated with more diabetes and cardiovascular disease. When an international magnesium network collected 43 reference values from its members' hospitals and laboratories, only 2 met that cutoff; the rest were lower. No international consensus on the range exists.13,3,12Grade B

The red-cell range is a laboratory population interval, not an outcome-derived one. Red cells hold about 0.5 percent of body magnesium against about 0.3 percent in serum, which is the usual argument for preferring them; the systematic review of status markers found that red-cell magnesium, like serum and urine, responded to dietary manipulation, but drew that conclusion from limited data and called for higher-quality studies.11,14Grade C

05 · The evidence

What the studies support.

In the Atherosclerosis Risk in Communities cohort, 14,232 adults aged 45 to 64 were followed for an average of 12 years, with 264 sudden cardiac deaths. The highest quartile of serum magnesium, 1.75 mEq/L or more (about 2.1 mg/dL), carried a 38 percent lower risk than the lowest, 1.5 mEq/L or less (about 1.8 mg/dL), after full adjustment (hazard ratio 0.62), and the risk fell with each quartile. People above the median at both of two visits had a 42 percent lower risk; being above it at one visit only made no difference. The laboratory's own coefficient of variation was 3 percent, and the correlation between the two visits' values was 0.46.15Grade B

Atrial fibrillation follows the same pattern. In 14,290 ARIC participants followed a median of 20.6 years, with 1,755 new cases, the lowest quintile of serum magnesium, below 1.55 mEq/L (about 1.9 mg/dL), carried 34 percent more atrial fibrillation than the middle quintile, and the curve was L-shaped: no extra risk above the middle. Dietary magnesium showed no association. In 3,530 Framingham Offspring participants free of cardiovascular disease, with a mean serum magnesium of 1.88 mg/dL, the lowest quartile (1.77 or less) was about 50 percent more likely to develop atrial fibrillation over up to 20 years than the upper quartiles (hazard ratio 1.52), 9.4 against 6.3 cases per 1,000 person-years in the highest quartile (1.99 or more), with similar results after excluding people on diuretics.16,17Grade B

In the Rotterdam Study, 9,820 adults with a mean age of 65 and a mean serum magnesium of 0.84 mmol/L (about 2.0 mg/dL) were followed for a median of 8.7 years. Each 0.1 mmol/L (about 0.24 mg/dL) higher serum magnesium carried an 18 percent lower risk of death from coronary heart disease. Values of 0.80 mmol/L or less (about 1.9 mg/dL) carried 36 percent more coronary death and 54 percent more sudden cardiac death than the reference of 0.81 to 0.88 (about 2.0 to 2.1); low magnesium went with slightly thicker carotid walls and a faster heart rate, but adjusting for both did not explain the association.18Grade B

Heart failure too. Among 14,709 ARIC participants followed a median of 20.6 years, with 2,250 new cases, the lowest magnesium category, 1.4 mEq/L or less (about 1.7 mg/dL), carried 71 percent more heart failure than the highest, 1.8 mEq/L or more (about 2.2), independent of race, sex and kidney function.19Grade B

Pooled across 16 prospective studies of 313,041 people, each 0.2 mmol/L (about 0.5 mg/dL) higher circulating magnesium carried 30 percent less cardiovascular disease (relative risk 0.70), with trends toward less ischemic heart disease (0.83) and fatal ischemic heart disease (0.61) that did not reach significance. A dose-response meta-analysis of 40 cohorts with more than a million participants found that each 100 mg a day of dietary magnesium went with 19 percent less type 2 diabetes, 22 percent less heart failure, 7 percent less stroke and 10 percent lower all-cause mortality, but no change in total cardiovascular disease (0.99) or coronary heart disease (0.92, not significant).20,21Grade A

Serum magnesium predicts diabetes. In 12,128 nondiabetic ARIC adults followed for 6 years, white participants showed a graded relationship: diabetes incidence rose from 11.1 to 22.8 per 1,000 person-years from the highest of six serum categories to the lowest, and the lowest category carried 1.76 times the adjusted odds of the reference of 0.95 mmol/L or more (about 2.3 mg/dL). Little or no association was seen in Black participants, and dietary magnesium predicted nothing in either group. Across 13 prospective cohorts of 536,318 people with 24,516 cases, the highest magnesium intake carried 22 percent less type 2 diabetes than the lowest, 14 percent less per 100 mg a day.22,23Grade B

The supplementation trials are smaller than the cohorts and their effects are modest. In 116 adults with prediabetes and hypomagnesemia, 382 mg of magnesium a day as a chloride solution for four months lowered fasting glucose to 86.9 mg/dL against 98.3 on placebo, left serum magnesium at 1.96 mg/dL against 1.60, and improved glucose status in 50.8 percent against 7.0 percent. Pooling 18 double-blind trials, magnesium lowered fasting glucose in people with diabetes (standardized mean difference minus 0.40, with 77 percent heterogeneity) and two-hour glucose in people at high risk (minus 0.35), with a trend in HOMA-IR that did not reach significance. Those trials enrolled people selected for low magnesium or for diabetes risk, not healthy adults with a mid-range value.24,25Grade A

On blood pressure, 34 randomized double-blind placebo-controlled trials with 2,028 participants, at a median dose of 368 mg a day for a median of three months, lowered systolic pressure by 2.00 mm Hg and diastolic by 1.78, while raising serum magnesium by 0.05 mmol/L (about 0.12 mg/dL) against placebo; about 300 mg a day or one month was enough to do both. The authors call the effect causal and small.26Grade A

Red-cell magnesium has no outcome literature of its own. None of the cohorts above measured it; the systematic review of status markers found only that it, like serum and urine, moved with dietary manipulation, from limited data; most red-cell studies are too short and do not validate the measure against other compartments such as urine or muscle; and cellular magnesium measurements frequently disagree with one another. In a 60-day randomized comparison of three supplement forms at 300 mg a day in 46 healthy adults, serum and urinary magnesium rose on citrate but red-cell magnesium did not differ between any group and placebo. The practice's red-cell threshold is therefore a judgment, and the page says so.14,11,4,27Grade C

06 · What moves it

The levers with evidence behind them.

What is listed here has been tested. The size of each effect, and the size of the study, are in the sentence, so a small effect reads as a small effect.

  • Green vegetables, nuts, seeds and whole grains

    raise intake; each 100 mg a day tracks with less diabetes and mortality in cohorts

    Chlorophyll makes green vegetables the main dietary source of magnesium; nuts, seeds and unprocessed cereals are also rich in it, dairy is low, and processed foods carry much less than unrefined grain. Across 40 cohorts each 100 mg a day of dietary magnesium went with 19 percent less type 2 diabetes and 10 percent lower all-cause mortality, and across 13 cohorts the highest intake carried 22 percent less diabetes than the lowest. Serum magnesium, though, did not track intake in ARIC, where dietary magnesium predicted neither diabetes nor atrial fibrillation.2,21,23,22Grade A

  • Magnesium supplements, in trials

    raise serum by about 0.1 mg/dL; lower blood pressure by about 2 mm Hg; improve glucose modestly in people with low magnesium or diabetes

    In the pooled blood-pressure trials a median of 368 mg a day for three months raised serum magnesium by 0.05 mmol/L (about 0.12 mg/dL) and lowered blood pressure by about 2 mm Hg. In adults with prediabetes and hypomagnesemia, 382 mg a day for four months lifted serum magnesium to 1.96 mg/dL against 1.60 and lowered fasting glucose by about 11 mg/dL relative to placebo. These are trial descriptions, not a recommendation; a supplement belongs in a conversation with a physician who knows the person's kidney function and medication list.26,24Grade A

  • Supplement form

    citrate absorbed better than oxide in one small trial; thin evidence

    In 46 healthy adults randomized to 300 mg a day of magnesium as citrate, an amino-acid chelate or oxide for 60 days, the organic forms were absorbed better than oxide by 24-hour urinary excretion, citrate produced the highest serum magnesium after one dose and after 60 days, and oxide did not differ from placebo. Red-cell magnesium did not change in any group. One trial of 46 people is the evidence; the forms question is largely unanswered.27Grade C

  • Acid-suppressing medicines, as a class

    lower it, especially with prolonged use and with loop diuretics

    In 9,818 Rotterdam Study participants, users of proton-pump inhibitors had twice the odds of hypomagnesemia (serum magnesium 1.44 mEq/L or less, about 1.75 mg/dL) and a serum value 0.022 mEq/L lower than non-users; the excess appeared only after prolonged use, and in people also taking a loop diuretic the odds rose to 7.22. Histamine-2 blockers showed a similar doubling. Pooling nine observational studies of 109,798 patients, proton-pump inhibitor use carried 1.43 times the risk of hypomagnesemia, 1.63 in the higher-quality studies.28,29Grade B

  • Diuretics, alcohol, diarrhea and uncontrolled diabetes

    lower it by urinary or intestinal loss

    Loop diuretics increase urinary magnesium excretion and thiazides may do so over the long run, while potassium-sparing diuretics conserve it; chronic alcohol consumption raises urinary magnesium loss and lowers muscle magnesium; chronic diarrhea, malabsorption and bowel surgery lose it from the gut; and diabetes, hyperthyroidism, hypercalcemia and aldosteronism raise excretion. The physiology review adds epidermal growth factor receptor inhibitors and calcineurin inhibitors to the drug list. The classes matter more than the names: a low value on any of these calls for a look at the medication list before a supplement.2,1Grade C

  • Reduced kidney function and magnesium-containing laxatives or antacids

    raise it

    The kidney sets the serum value: about 2,400 mg is filtered a day and 95 percent is reabsorbed, so in advanced chronic kidney disease the compensation fails and hypermagnesemia can develop, and magnesium-containing laxatives and antacids raise it further, particularly in older people with declining kidney function. Values above 1.07 mmol/L (about 2.6 mg/dL) turned up in 7.9 percent of 6,252 hospital patients, usually without noted symptoms; confusion, loss of reflexes and low blood pressure are reported at 3.7 to 4.9 mmol/L, about 9 to 12 mg/dL.2Grade C

07 · Reading it well

Caveats, and what belongs with a physician.

Serum misses stores. Only about 1 percent of body magnesium is extracellular and 0.3 percent is in serum; bone supplies the serum pool from a reservoir of which about a third is exchangeable, so a normal serum value can coexist with a total body deficit. The load test that is the reference standard has its own problems: in 88 healthy adults given 30 mmol intravenously over eight hours, mean retention was 6.3 percent with a standard deviation of 10.3, the normal range was wide, retention did not correlate with serum magnesium at all, and the test is unsuitable in kidney or intestinal disease and lacks a standardized protocol.2,3,30,4Grade B

Red-cell magnesium is a thinner measure than its reputation. It holds about 0.5 percent of body magnesium, moved with diet in a handful of supplementation and depletion studies, and has not been validated against urine, muscle or the load test in most of the studies that use it; its reference interval is a laboratory population range, and no cohort has followed it to an outcome.11,14Grade C

A single serum value is noisy for a marker this tightly held. In 60 healthy men, within-person biological variation was 3.2 percent against 7.4 percent between people, an index of individuality of 0.5, which means a meaningful change can occur inside the reference interval and a single determination is unlikely to say much about whole-body status; in ARIC the correlation between two visits was 0.46, and the sudden-death signal belonged to people who were above the median both times. Hemolysis raises the measured value, because red cells hold more magnesium than serum, and a recent supplement raises serum magnesium within a day.31,15,32,27Grade B

The cohorts cannot settle cause. Diuretics, diabetes and kidney handling all move serum magnesium and all move the outcomes; the ARIC investigators themselves noted that dietary magnesium predicted neither diabetes nor atrial fibrillation while serum did, and read that as a sign that compartmentalization and renal handling, rather than intake alone, sit behind the serum association. The sudden-death association weakened and lost significance once incident coronary disease was modeled along the way.22,16,15Grade B

Kidney function changes the meaning of the number in both directions. Low values in someone on a loop diuretic or an acid suppressant are a medication finding before a nutrition one, and a value above the laboratory range in someone with reduced kidney function or on magnesium-containing laxatives or antacids is the kidney's limit, not a surplus to celebrate. A supplement should wait on an eGFR.2,28Grade C

See a physician

  • A serum magnesium flagged low by the laboratory together with muscle cramps, tremor, numbness or tingling, palpitations or an irregular heartbeat, which can mean potassium and calcium are low as well.
  • A low value while taking a proton-pump inhibitor, another acid suppressant, or a loop or thiazide diuretic, where the medication, not a supplement, is the first question.
  • Chronic kidney disease or a reduced eGFR before any magnesium supplement is started, because the kidney is the only exit.
  • A value above the laboratory range, particularly with kidney disease or regular use of magnesium-containing laxatives or antacids, or any value with flushing, nausea, weakness, slowed reflexes or low blood pressure.
  • Persistent diarrhea, heavy alcohol use, or a low magnesium that will not correct, which point to a loss that needs a cause.

This page is education, not individual medical advice, and reading it creates no physician-patient relationship.

08 · Open questions

What the literature does not settle.

  • No trial has raised serum magnesium to a target in healthy adults with a mid-range value and measured heart rhythm, diabetes or death; the cohort signal in the lowest quartile has never been tested by randomization.
  • Whether the lower reference limit should move to 0.85 mmol/L (2.07 mg/dL), as two expert groups propose, is unsettled; no laboratory consensus body has adopted it, and the proposal rests on associations.
  • Red-cell magnesium has no outcome study, no agreed validation against the load test and no tested threshold; whether a red-cell value adds anything to a serum value read beside potassium, calcium and kidney function is unknown.
  • The supplement trials run about three to four months; whether a 2 mm Hg blood-pressure effect or a modest glucose effect persists, or changes outcomes, has not been shown.
  • Why serum magnesium predicted diabetes in white but not Black ARIC participants, and why intake tracks outcomes in some analyses while serum does not track intake, are open; the answers probably lie in kidney handling and compartments that serum cannot see.
  • Which supplement form, if any, matters is answered by one 60-day trial of 46 people.

10

Questions

11 · Sources

32 sources, read in full.

Numbered in the order they appear. Each line says what this page relies on from the paper; the link opens the record at PubMed or the publisher.

  1. 1.

    de Baaij JH, Hoenderop JG, Bindels RJ. Magnesium in man: implications for health and disease. Physiological Reviews. 2015. PMID 25540137. DOI 10.1152/physrev.00012.2014.

    Review · Magnesium is the second most abundant intracellular cation after potassium and is involved in over 600 enzymatic reactions; diuretics, EGFR inhibitors, calcineurin inhibitors and proton-pump inhibitors can cause hypomagnesemia; serum values are not generally determined.

  2. 2.

    Jahnen-Dechent W, Ketteler M. Magnesium basics. Clinical Kidney Journal. 2012. PMID 26069819. DOI 10.1093/ndtplus/sfr163.

    Review · About 99 percent of body magnesium is in bone, muscle and soft tissue, about 1 percent extracellular and 0.3 percent in serum; magnesium is the central ion of chlorophyll and the counter ion of ATP; serum does not reflect stores; the load test is more sensitive but unstandardized; diuretics, alcohol, diarrhea and diabetes lower it, and kidney failure, laxatives and antacids raise it.

  3. 3.

    Elin RJ. Assessment of magnesium status for diagnosis and therapy. Magnesium Research. 2010. PMID 20736141. DOI 10.1684/mrh.2010.0213.

    Review · Only 1 percent of body magnesium is in blood, yet serum magnesium is the predominant test; the traditional reference interval is flawed by normal people in chronic negative balance; recommends 0.85 mmol/L as the lower limit.

  4. 4.

    Arnaud MJ. Update on the assessment of magnesium status. British Journal of Nutrition. 2008. PMID 18598586. DOI 10.1017/S000711450800682X.

    Review · No simple accurate test of total body magnesium exists; serum below 0.75 mmol/L is useful for severe deficiency and a loading test identifies deficient subjects between 0.75 and 0.85; the loading test seems to be the gold standard but is unsuitable in kidney or intestinal disease; cellular magnesium measurements frequently disagree.

  5. 5.

    Costello RB, Elin RJ, Rosanoff A, et al.. Perspective: The Case for an Evidence-Based Reference Interval for Serum Magnesium: The Time Has Come. Advances in Nutrition. 2016. PMID 28140318. DOI 10.3945/an.116.012765.

    Review · About 50 percent of Americans consume less than the estimated average requirement; the 0.75 to 0.95 mmol/L interval came from the NHANES I (1974) distribution, not from outcomes; subclinical deficiency can exist within it.

  6. 6.

    Rosanoff A, Weaver CM, Rude RK. Suboptimal magnesium status in the United States: are the health consequences underestimated?. Nutrition Reviews. 2012. PMID 22364157. DOI 10.1111/j.1753-4887.2011.00465.x.

    Review · Almost half (48 percent) of the US population consumed less than the required amount of magnesium from food in 2005 to 2006, down from 56 percent in 2001 to 2002.

  7. 7.

    Dai Q, Zhu X, Manson JE, et al.. Magnesium status and supplementation influence vitamin D status and metabolism: results from a randomized trial. American Journal of Clinical Nutrition. 2018. PMID 30541089. DOI 10.1093/ajcn/nqy274.

    Randomized trial · Enzymes that synthesize and metabolize vitamin D are magnesium dependent; in 180 adults, magnesium raised 25-hydroxyvitamin D3 when baseline 25(OH)D was near 30 ng/mL and lowered it at higher baselines; per NHANES, 79 percent of US adults do not meet the RDA for magnesium.

  8. 8.

    Klein DJ, Moore PB, Steitz TA. The contribution of metal ions to the structural stability of the large ribosomal subunit. RNA. 2004. PMID 15317974. DOI 10.1261/rna.7390804.

    Laboratory method study · The large ribosomal subunit of Haloarcula marismortui contains 116 magnesium ions bound mainly to rRNA, abundant around the peptidyl transferase center where protein tails are absent, suggesting metal ions stabilized RNA in the evolutionary period before proteins.

  9. 9.

    Hsiao C, Mohan S, Kalahar BK, Williams LD. Peeling the onion: ribosomes are ancient molecular fossils. Molecular Biology and Evolution. 2009. PMID 19628620. DOI 10.1093/molbev/msp163.

    Laboratory method study · A shell-by-shell chronology of the large subunit suggests the early peptidyl transfer center formed through magnesium-mediated assembly of RNA, with proteins replacing magnesium ions from the center outward over evolutionary time.

  10. 10.

    Mulkidjanian AY, Bychkov AY, Dibrova DV, Galperin MY, Koonin EV. Origin of first cells at terrestrial, anoxic geothermal fields. Proceedings of the National Academy of Sciences of the United States of America. 2012. PMID 22331915. DOI 10.1073/pnas.1117774109.

    Review · All cells contain much more potassium, phosphate and transition metals than modern or reconstructed ancient oceans; because the first cells lacked ion-tight membranes and pumps, their ion composition may reflect their habitat, with a high potassium-to-sodium ratio.

  11. 11.

    Workinger JL, Doyle RP, Bortz J. Challenges in the Diagnosis of Magnesium Status. Nutrients. 2018. PMID 30200431. DOI 10.3390/nu10091202.

    Review · Only 0.8 percent of magnesium is in blood (0.3 percent serum, 0.5 percent red cells); most red-cell studies are short and not validated by inter-compartmental sampling; attributes postulated deficiency partly to soil and processing while cautioning that the mineral-decline data are old and need verifying.

  12. 12.

    Micke O, Vormann J, Kraus A, Kisters K. Serum magnesium: time for a standardized and evidence-based reference range. Magnesium Research. 2021. PMID 34463286. DOI 10.1684/mrh.2021.0486.

    Review · A reference range of 0.75 to 0.95 mmol/L (1.82 to 2.31 mg/dL) is common; serum is maintained by release from body pools; values below 0.85 mmol/L are associated with increased health risks.

  13. 13.

    Rosanoff A, West C, Elin RJ, et al.; MaGNet Global Magnesium Project. Recommendation on an updated standardization of serum magnesium reference ranges. European Journal of Nutrition. 2022. PMID 35689124. DOI 10.1007/s00394-022-02916-w.

    Consensus statement · Two independent groups set 0.85 mmol/L (2.07 mg/dL) as the low cutoff; of 43 collected laboratory values only 2 met it; no international consensus range exists; normal populations include people with chronic latent magnesium deficit.

  14. 14.

    Witkowski M, Hubert J, Mazur A. Methods of assessment of magnesium status in humans: a systematic review. Magnesium Research. 2011. PMID 22064327. DOI 10.1684/mrh.2011.0292.

    Systematic review and meta-analysis · Across 21 publications, serum, red-cell and urinary magnesium responded to dietary manipulation; data were limited and higher-quality studies are needed.

  15. 15.

    Peacock JM, Ohira T, Post W, Sotoodehnia N, Rosamond W, Folsom AR. Serum magnesium and risk of sudden cardiac death in the Atherosclerosis Risk in Communities (ARIC) Study. American Heart Journal. 2010. PMID 20826254. DOI 10.1016/j.ahj.2010.06.012.

    Prospective cohort · In 14,232 adults over 12 years with 264 sudden cardiac deaths, the highest quartile (1.75 mEq/L or more) had hazard ratio 0.62 versus the lowest (1.5 or less); above the median at both visits, 42 percent lower risk; laboratory CV 3 percent, visit-to-visit correlation 0.46.

  16. 16.

    Misialek JR, Lopez FL, Lutsey PL, et al.. Serum and dietary magnesium and incidence of atrial fibrillation in whites and in African Americans--Atherosclerosis Risk in Communities (ARIC) study. Circulation Journal. 2013. PMID 23047297. DOI 10.1253/circj.cj-12-0886.

    Prospective cohort · In 14,290 adults over a median 20.6 years with 1,755 atrial fibrillation cases, the lowest quintile (below 1.55 mEq/L) had hazard ratio 1.34 versus the middle quintile, with an L-shaped curve; dietary magnesium was not associated.

  17. 17.

    Khan AM, Lubitz SA, Sullivan LM, et al.. Low serum magnesium and the development of atrial fibrillation in the community: the Framingham Heart Study. Circulation. 2013. PMID 23172839. DOI 10.1161/CIRCULATIONAHA.111.082511.

    Prospective cohort · In 3,530 adults with mean serum magnesium 1.88 mg/dL, the lowest quartile (1.77 or less) had hazard ratio 1.52 for atrial fibrillation versus the upper quartiles over up to 20 years; 9.4 versus 6.3 cases per 1,000 person-years against the highest quartile (1.99 or more).

  18. 18.

    Kieboom BC, Niemeijer MN, Leening MJ, et al.. Serum Magnesium and the Risk of Death From Coronary Heart Disease and Sudden Cardiac Death. Journal of the American Heart Association. 2016. PMID 26802105. DOI 10.1161/JAHA.115.002707.

    Prospective cohort · In 9,820 Rotterdam adults over a median 8.7 years, each 0.1 mmol/L higher serum magnesium carried hazard ratio 0.82 for coronary death; 0.80 mmol/L or less carried 1.36 for coronary death and 1.54 for sudden cardiac death versus 0.81 to 0.88; mean 0.84 mmol/L.

  19. 19.

    Lutsey PL, Alonso A, Michos ED, et al.. Serum magnesium, phosphorus, and calcium are associated with risk of incident heart failure: the Atherosclerosis Risk in Communities (ARIC) Study. American Journal of Clinical Nutrition. 2014. PMID 25030784. DOI 10.3945/ajcn.114.085167.

    Prospective cohort · In 14,709 adults over a median 20.6 years with 2,250 heart failure events, serum magnesium of 1.4 mEq/L or less carried hazard ratio 1.71 versus 1.8 or more, unmodified by race, sex or kidney function.

  20. 20.

    Del Gobbo LC, Imamura F, Wu JH, de Oliveira Otto MC, Chiuve SE, Mozaffarian D. Circulating and dietary magnesium and risk of cardiovascular disease: a systematic review and meta-analysis of prospective studies. American Journal of Clinical Nutrition. 2013. PMID 23719551. DOI 10.3945/ajcn.112.053132.

    Systematic review and meta-analysis · Across 16 studies of 313,041 people, each 0.2 mmol/L higher circulating magnesium carried relative risk 0.70 for cardiovascular disease, with non-significant trends for ischemic heart disease (0.83) and fatal ischemic heart disease (0.61); dietary magnesium per 200 mg a day carried 0.78 for ischemic heart disease.

  21. 21.

    Fang X, Wang K, Han D, et al.. Dietary magnesium intake and the risk of cardiovascular disease, type 2 diabetes, and all-cause mortality: a dose-response meta-analysis of prospective cohort studies. BMC Medicine. 2016. PMID 27927203. DOI 10.1186/s12916-016-0742-z.

    Systematic review and meta-analysis · Across 40 cohorts with more than a million participants, each 100 mg a day of dietary magnesium carried relative risks of 0.81 for type 2 diabetes, 0.90 for all-cause mortality, 0.78 for heart failure and 0.93 for stroke, with no association for total cardiovascular disease (0.99) or coronary heart disease (0.92).

  22. 22.

    Kao WH, Folsom AR, Nieto FJ, Mo JP, Watson RL, Brancati FL. Serum and dietary magnesium and the risk for type 2 diabetes mellitus: the Atherosclerosis Risk in Communities Study. Archives of Internal Medicine. 1999. PMID 10527292. DOI 10.1001/archinte.159.18.2151.

    Prospective cohort · In 12,128 nondiabetic adults over 6 years, white participants showed a graded rise in diabetes from 11.1 to 22.8 per 1,000 person-years from the highest to the lowest of six serum magnesium categories, adjusted odds 1.76 in the lowest versus 0.95 mmol/L or more; no association in Black participants; dietary magnesium not associated.

  23. 23.

    Dong JY, Xun P, He K, Qin LQ. Magnesium intake and risk of type 2 diabetes: meta-analysis of prospective cohort studies. Diabetes Care. 2011. PMID 21868780. DOI 10.2337/dc11-0518.

    Systematic review and meta-analysis · Across 13 cohorts of 536,318 people with 24,516 cases, the highest magnesium intake carried relative risk 0.78 for type 2 diabetes versus the lowest, 0.86 per 100 mg a day.

  24. 24.

    Guerrero-Romero F, Simental-Mendía LE, Hernández-Ronquillo G, Rodriguez-Morán M. Oral magnesium supplementation improves glycaemic status in subjects with prediabetes and hypomagnesaemia: A double-blind placebo-controlled randomized trial. Diabetes and Metabolism. 2015. PMID 25937055. DOI 10.1016/j.diabet.2015.03.010.

    Randomized trial · In 116 adults with prediabetes and hypomagnesemia, 382 mg of magnesium a day for four months lowered fasting glucose to 86.9 versus 98.3 mg/dL, raised serum magnesium to 1.96 versus 1.60 mg/dL, and improved glucose status in 50.8 versus 7.0 percent.

  25. 25.

    Veronese N, Watutantrige-Fernando S, Luchini C, et al.. Effect of magnesium supplementation on glucose metabolism in people with or at risk of diabetes: a systematic review and meta-analysis of double-blind randomized controlled trials. European Journal of Clinical Nutrition. 2016. PMID 27530471. DOI 10.1038/ejcn.2016.154.

    Systematic review and meta-analysis · Across 18 double-blind trials, magnesium lowered fasting glucose in people with diabetes (SMD minus 0.40, I2 77 percent) and two-hour glucose in people at high risk (SMD minus 0.35), with a non-significant trend in HOMA-IR.

  26. 26.

    Zhang X, Li Y, Del Gobbo LC, et al.. Effects of Magnesium Supplementation on Blood Pressure: A Meta-Analysis of Randomized Double-Blind Placebo-Controlled Trials. Hypertension. 2016. PMID 27402922. DOI 10.1161/HYPERTENSIONAHA.116.07664.

    Systematic review and meta-analysis · Across 34 trials of 2,028 adults, a median 368 mg a day for a median three months lowered systolic pressure 2.00 mm Hg and diastolic 1.78, raising serum magnesium by 0.05 mmol/L; 300 mg a day or one month sufficed.

  27. 27.

    Walker AF, Marakis G, Christie S, Byng M. Mg citrate found more bioavailable than other Mg preparations in a randomised, double-blind study. Magnesium Research. 2003. PMID 14596323.

    Randomized trial · In 46 healthy adults on 300 mg a day for 60 days, citrate and amino-acid chelate were absorbed better than oxide by urinary excretion, citrate gave the highest serum magnesium after one dose and after 60 days, oxide did not differ from placebo, and erythrocyte magnesium did not differ among groups.

  28. 28.

    Kieboom BC, Kiefte-de Jong JC, Eijgelsheim M, et al.. Proton pump inhibitors and hypomagnesemia in the general population: a population-based cohort study. American Journal of Kidney Diseases. 2015. PMID 26123862. DOI 10.1053/j.ajkd.2015.05.012.

    Prospective cohort · In 9,818 Rotterdam adults, proton-pump inhibitor use carried odds ratio 2.00 for hypomagnesemia (1.44 mEq/L or less), only after prolonged use, and 7.22 with concurrent loop diuretics; histamine-2 blockers carried 2.00.

  29. 29.

    Cheungpasitporn W, Thongprayoon C, Kittanamongkolchai W, et al.. Proton pump inhibitors linked to hypomagnesemia: a systematic review and meta-analysis of observational studies. Renal Failure. 2015. PMID 26108134. DOI 10.3109/0886022X.2015.1057800.

    Systematic review and meta-analysis · Across nine observational studies of 109,798 patients, proton-pump inhibitor use carried pooled relative risk 1.43 for hypomagnesemia, 1.63 in higher-quality studies.

  30. 30.

    Gullestad L, Midtvedt K, Dolva LO, Norseth J, Kjekshus J. The magnesium loading test: reference values in healthy subjects. Scandinavian Journal of Clinical and Laboratory Investigation. 1994. PMID 8171268. DOI 10.3109/00365519409086506.

    Laboratory method study · In 88 healthy adults given 30 mmol of magnesium intravenously over eight hours, mean retention was 6.3 percent (SD 10.3), retention did not correlate with serum magnesium, and the normal range was wide.

  31. 31.

    Djurhuus MS, Gram J, Petersen PH, Klitgaard NA, Bollerslev J, Beck-Nielsen H. Biological variation of serum and urinary magnesium in apparently healthy males. Scandinavian Journal of Clinical and Laboratory Investigation. 1995. PMID 8571086. DOI 10.1080/00365519509075394.

    Laboratory method study · In 60 healthy men, within-subject variation of serum magnesium was 3.2 percent and between-subject 7.4 percent, index of individuality 0.5; a single determination is unlikely to assess whole-body status.

  32. 32.

    Lippi G, Salvagno GL, Montagnana M, Brocco G, Guidi GC. Influence of hemolysis on routine clinical chemistry testing. Clinical Chemistry and Laboratory Medicine. 2006. PMID 16519604. DOI 10.1515/CCLM.2006.054.

    Laboratory method study · In serially hemolyzed samples, hemolysis produced a consistent overestimation of magnesium, potassium, phosphorus and several enzymes, roughly in proportion to the degree of lysis.

Related

Keep reading.

Reading a number well is the start of the work, not the end of it. If you would like a physician to read yours over time, Explore working with Dr. Tagge.