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Functional Blood Chemistry Manual


Marker Name: Magnesium


Laboratory reference range: 1.6–2.6 mg/dL

Functional reference range: 2.0–2.6 mg/dL


Magnesium (Mg) is a cofactor for more than 300 enzymes, a constituent of bones and teeth, and needed by every cell. Magnesium is necessary for all enzymes that use and synthesize ATP and for enzymes involved in synthesis of RNA, DNA, proteins, and glutathione. Every cell uses magnesium for active transport of calcium and potassium ions across cell membranes, which is important for muscle and nerve function and normal heart rhythm. It helps regulate blood pressure, blood glucose, and levels of other nutrients including calcium, vitamin D, potassium, zinc, and copper.1-4

Assessing magnesium status is challenging because less than 1 percent of total magnesium is in blood serum—the rest is in bones and cells.3,5 Serum magnesium concentration is the most commonly used magnesium test, but this test is flawed because magnesium in blood serum is tightly regulated, and does not correlate well with overall magnesium status.6 Magnesium status is also evaluated by magnesium loading (tolerance) tests; total magnesium concentration in erythrocytes (RBCs), saliva, and urine; or total ionized magnesium concentration in blood, plasma, and serum. However, there is no single sufficient testing method for magnesium status; a better functional biomarker is needed.7,8

Magnesium balance is achieved primarily by small intestinal absorption and renal excretion and reabsorption. Unlike other ions, hormones do not substantially regulate urinary magnesium excretion, and magnesium content of bone is not readily mobilized into circulating magnesium. Instead, low plasma magnesium concentration triggers the kidney to lower magnesium excretion and prevent further depletion.9

High magnesium is uncommon but can be caused by insufficient renal function or very high magnesium intake. Slightly elevated magnesium can be caused by primary hyperparathyroidism, diabetic ketoacidosis, tumor lysis syndrome, drugs such as lithium, milk-alkali syndrome, adrenal insufficiency, and familial hypocalciuric hypercalcemia.10,11

Low magnesium is common. The primary cause of magnesium deficiency is low dietary intake; the vast majority of Americans consume well under their estimated average requirements (EAR).12 For low magnesium, also consider hyperthyroidism, heavy menstrual periods, excessive sweating, chronic stress, hungry bone syndrome, gastrointestinal magnesium loss (diarrhea, malabsorption, pancreatitis), renal magnesium loss (diabetes mellitus type 2, primary aldosteronism, hypercalcemia, renal tubular dysfunction, leptospirosis), certain drugs (proton pump inhibitors, diuretics), various genetic disorders, surgery, and other dietary factors (ketogenic diet, coffee, alcohol).9,10,13-15

For treatment of low magnesium, note that magnesium supplements list the amount of elemental magnesium per serving in the Supplement Facts panel, not the total weight of magnesium-containing compounds.1


High in:10,11

  • Renal insufficiency
  • Excessive magnesium ingestion
    • Parenteral magnesium treatment for severe preeclampsia or eclampsia in pregnant women
    • Very high dose ingestion of Epsom salt (magnesium sulfate)
    • Catharsis with magnesium-containing drugs (especially in children, the elderly, and those with gastrointestinal disease)
    • Magnesium enemas
    • Dead Sea water poisoning
  • Mild hypermagnesemia
    • Diabetic ketoacidosis
    • Tumor lysis syndrome
    • Lithium ingestion
    • Milk-alkali syndrome
    • Adrenal insufficiency
    • Familial hypocalciuric hypercalcemia
    • Some cases of primary hyperparathyroidism (though this condition can also result in low magnesium)

Low in:9,10,12-15

  • Inadequate dietary intake
  • Dietary factors (e.g., ketogenic diet, coffee, soda, alcohol, excessive sodium)
  • Hyperthyroidism
  • Heavy menstrual periods
  • Excessive sweating
  • Prolonged stress
  • Hungry bone syndrome (post parathyroidectomy)
  • States of gastrointestinal magnesium loss
    • Diarrhea
    • Malabsorption
    • Steatorrhea
    • Small bowel bypass surgery
    • Acute pancreatitis
  • States of renal magnesium loss
    • Chronic extracellular fluid volume expansion
      • Primary aldosteronism
    • Alcoholism
    • Diabetes mellitus type 2, especially if uncontrolled
    • Hypercalcemia
      • Primary hyperparathyroidism
    • Renal magnesium wasting due to tubular dysfunction
      • Recovery from acute tubular necrosis
      • Following renal transplantation
      • During a postobstructive diuresis
    • Leptospirosis
  • States of intravascular magnesium chelation
    • Following surgery
    • During liver transplantation
  • Genetic disorders
    • Mutation in the TRPM6 gene, which causes both primary intestinal hypomagnesemia and renal magnesium wasting
    • Familial primary renal magnesium wasting, a rare diagnosis of exclusion
      • Gitelman syndrome is the most common, caused by mutations in the SLC12A3 gene, which codes for the thiazide-sensitive sodium chloride cotransporter (NCC)
      • Familial hypomagnesemia with hypercalciuria and nephrocalcinosis (FHHNC), most often caused by mutations in the CLDN16 gene (also known as HOMG3 or PCLN1) and occasionally caused by mutations in the CLDN19 gene
      • Various less common genetic disorders
    • Drugs
      • Proton-pump inhibitors (e.g., omeprazole), especially when used for more than one year or when used concurrently with diuretics
      • Loop and thiazide diuretics
      • Aminoglycoside antibiotics
      • Amphotericin B
      • Cisplatin
      • Pentamidine
      • Cyclosporine
      • Antibodies targeting the epidermal growth factor (EGF) receptor (cetuximab, panitumumab, matuzumab)
      • Foscarnet therapy of cytomegalovirus chorioretinitis


High in:

  • Hypothyroidism
  • Impaired kidney function
  • Use of antacids with magnesium
  • Excessive supplementation with magnesium
  • Addison’s disease/adrenal insufficiency

Low in:

  • Magnesium deficiency
  • Malabsorption
  • Fluid loss
  • Many other disease states


  3. Rude RK. Magnesium. In: Coates PM, Betz JM, Blackman MR, Cragg GM, Levine M, Moss J, White JD, eds. Encyclopedia of Dietary Supplements. 2nd ed. New York, NY: Informa Healthcare; 2010:527-37.
  4. Rude RK. Magnesium. In: Ross AC, Caballero B, Cousins RJ, Tucker KL, Ziegler TR, eds. Modern Nutrition in Health and Disease. 11th ed. Baltimore, Mass: Lippincott Williams & Wilkins; 2012:159-75.
  5. Volpe SL. Magnesium. In: Erdman JW, Macdonald IA, Zeisel SH, eds. Present Knowledge in Nutrition. 10th ed. Ames, Iowa; John Wiley & Sons, 2012:459-74.
  6. Gibson, RS. Principles of Nutritional Assessment, 2nd ed. New York, NY: Oxford University Press, 2005.




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