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Nutrient Name: Magnesium.
Elemental Symbol: Mg.

Summary Table
Drug/Class Interaction TypeMechanism and SignificanceManagement
Beta-2-adrenoceptor agonist bronchodilators
Supplementation enhances albuterol efficacy and counters hypomagnesemia. Variable significance, ranging from minimal, preventive to significant, urgent.Coadminister.
Aminoglycoside antibiotics
Drug-induced tubular damage, impaired magnesium absorption. Magnesium important with extended therapy.Coadminister.
Amphetamines and stimulant medications
Magnesium salts may enhance drug retention and availability; drugs may elevate magnesium levels; mutual increased effect. Improved drug kinetics and enhanced Mg status and effect on Ca/Mg ratio may benefit clinical outcomes.Coadminister.
Monitor. Possible decrease of drug dose.
Amphotericin B

Hypomagnesemia caused by renal magnesium wasting and impaired reabsorption. Hydration and nutrients nephroprotective.Coadminister.
Monitor. Consider liposomal amphotericin B.
/ /
Minerals and bisphosphonate chelate; reduced absorption and bioavailability. Immediate onset, usually moderate severity, gradual effect.Modify timing to prevent chelation.
Calcium channel blockers
/ / / / / / /
Reduced ionic calcium availability to muscle cells; more hypotensive. Possible synergy. Caution: increased risk in pregnancy.Consider coadministration.
Closely monitor.
Cisplatin impairs renal tubules’ ability to conserve magnesium, resulting in clinically significant hypomagnesemia.Evaluate magnesium and potassium status, renal function.
Coadminister. Monitor.

Colchicine may impair absorption of magnesium and other nutrients, potentially causing depletion and adverse effects. Plausible mechanism, but minimal evidence.Consider supplementing with multivitamin/mineral formulation containing magenesium, with extended colchicine therapy. Separate intake.
Corticosteroids, oral
Magnesium depletion and impaired absorption. Associated with steroid-induced bone loss.Supplement minerals during extended steroids.
/ /
Severe hypomagnesemia, renal magnesium wasting, nephrotoxicity.Coadminister. Regularly monitor renal function and RBC Mg levels.
/ / /
Digoxin decreases Mg and increases loss, increasing risk of digitalis toxicity.
Magnesium and digoxin may chelate; reduced absorption and bioavailability of both. Immediate and potentially severe as well as cumulative depletion effects; potential mutual interference.
Coordinated use with separated administration. Closely monitor.
Diuretics, loop and thiazide
/ /
Diuretics inhibit magnesium absorption and increase excretion, amplifying potassium depletion. Cumulative adverse effect of mineral depletion; rapid correction may require intravenous or intramuscular administration of magnesium.Evaluate magnesium and potassium status, renal function. Coadminister long-term. Monitor.
Estrogen replacement therapy (ERT)
Oral contraceptives (OCs)
Exogenous estrogen may shift magnesium to soft tissue and bone, lowering serum levels and body stores. Magnesium depletion may amplify, and supplementation may moderate, possible adverse effects from PMS to bone and heart.Conservative to supplement for short-term and long-term preventive and protective effects.
/ /
Coadministration of intravenous magnesium sulfate may enable reducing analgesic dosage requirements, possibly by resetting nerve activation thresholds. Encouraging preliminary research indicates further study warranted, including trials using oral magnesium.Coadministration of magnesium, usually IV, may be beneficial. Closely monitor.
Fluoroquinolone/quinolone antibiotics
/ /
Magnesium and fluoroquinolones may chelate; reduced absorption and bioavailability of both. Evidence of potential interference derived from magnesium antacids.Adjust timing to avoid simultaneous or close oral administration.

Renal impairment caused by foscarnet may be responsible for adverse effect on magnesium, calcium, potassium, and phosphorus. Depletion sequelae are common and can be rapid and severe.Frequently monitor magnesium and other electrolytes. Administer magnesium as indicated.
Diabetics tend toward magnesium deficiency; magnesium can improve insulin sensitivity and secretion. Both risks and benefits tend to increase gradually.Coadminister.
Lithium carbonate
Lithium and magnesium may compete. Concomitant intake may elevate magnesium levels but adverse effects unlikely. No indication of interference with drug activity.Monitor.
Macrolide antibiotics
Erythromycin and other macrolide antibiotics may interfere with absorption of magnesium and other nutrients, especially with extended treatment. Mechanism plausible but evidence preliminary or inconclusive.Consider nutrient supplementation with extended macrolide therapy. Separate intake.
/ /
Probable additive effect of magnesium, increasing diarrhea. Misoprostol's adverse effects on gastrointestinal tract may be aggravated.Temporarily avoid magnesium, if possible.
Neuromuscular blocking agents
/ / /
Magnesium salts can increase and prolong agent effects. Unintentional additive effects may be severe; coordinated use may allow lower drug doses.Assess magnesium status. Consider coadministration. Monitor closely.
Pentamidine can decrease magnesium levels and produce adverse effects, especially on cardiac function. Evidence minimal but mechanisms reasonable.Assess and monitor magnesium (and potassium) status initally and during treatment. Coadminister as indicated, possibly preventively.
/ / /
These agents tend to complex; may reduce magnesium absorption. Simultaneous intake may interfere with and inhibit activity of both agents. High doses of penicillamine for extended period can inactivate and deplete magnesium.Assess magnesium status. Adjust timing to separate oral administration if magnesium strategically necessary.
Antiarrhythmic drugs
/ / /
Quinidine-induced arrhythmias aggravated by electrolyte abnormalities; MgSO4 reverses torsades de pointes by unknown mechanism. Hypomagnesemia may increase quinidine adverse effects, especially with hypokalemia.Assess magnesium and potassium status. Consider coadministration. Monitor closely.
Sodium polystyrene sulfonate (SPSS)
SPSS may alter magnesium levels and contribute to depletion. Compensatory magnesium may prevent or reverse potential adverse effects. Evidence minimal but mechanism(s) plausible.Consider magnesium coadministration, especially if magnesium strategically significant.
Beta-1-adrenoceptor antagonists
/ / /
Magnesium salt may reduce drug absorption and availability; drug effect on magnesium (and other minerals) may increase adverse effects; MgSO4 reverses torsades de pointes by unknown mechanism. Intentional coadministration can be acute therapy or long-term supportive; unintentional interference may be gradual.Coordinated use may be beneficial but need separate administration; closely monitor.
Sulfonylurea Hypoglycemics
/ / / / /
Magnesium may increase drug activity on glucose. Diabetics tend toward magnesium deficiency; Mg can improve insulin sensitivity and secretion. Enhanced drug response may excessively lower glucose or may facilitate therapeutic strategy.Coadminister.
Monitor. Titrate drug dose.
Tetracycline antibiotics
/ / /
Tendency to chelate may reduce (or enhance) absorption of both; mixed evidence. Coadministration carries risk of (increased) adverse effects but may be efficacious in some uses.Adjust timing to separate oral administration if magnesium strategically necessary.
/ / /
Theophylline may deplete magnesium and aggravate magnesium status. Patient population tends to be magnesium deficient, and magnesium can support therapeutic outcome.Assess magnesium status. Consider coadministration. Monitor closely.
Warfairn Oral vitamin K antagonist anticoagulants
/ /
Binding and formation of chelate complexes may reduce absorption and activity of both agents. Evidence mixed but suggests negligible impact on drug activity, especially with separation of oral intake. Further research warranted.Separate intake by at least 2 hours. Monitor closely.
RBC, Red blood cell; PMS , premenstrual syndrome.
nutrient description

Chemistry and Forms

Magnesium ascorbate, magnesium aspartate, magnesium chloride, magnesium citrate, magnesium fumarate, magnesium gluconate, magnesium glycerophosphate, magnesium glycinate, magnesium hydroxide, magnesium malate, magnesium oxide, magnesium pidolate, magnesium succinate, magnesium sulfate.

Physiology and Function

Magnesium functions as a structural cofactor or as an allosteric activator of enzyme activity in more than 300 enzyme reactions in the body, including those related to the transfer of phosphate groups, all reactions that require adenosine 5′-triphosphate (ATP; i.e., mitochondrial oxidative phosphorylation), glycolysis, fatty acid oxidation and amino acid metabolism, and the replication and transcription of DNA, synthesis of RNA, and translation of messenger RNA (mRNA). Magnesium is the second most abundant intracellular cation and the fourth most prevalent cation in the body. The normal body magnesium content is approximately 1000 mmol, or 22·66 g, of which 50% to 60% resides in bone. Magnesium affects many cellular functions, including transport of potassium (K+) and calcium (Ca++) ions, and modulates signal transduction, energy metabolism, and cell proliferation. The magnesium cation (Mg++) is also required for cellular energy metabolism and plays an important role in cell proliferation and membrane stabilization, nerve signal transduction, ion transport, and calcium metabolism. Magnesium decreases coagulation and acts as a calcium channel blocker. Magnesium regulates the absorption of calcium and is involved in the structural integrity of bones and teeth. If it is deficient in the bones, the bones may be dense but brittle because of poor trabecular integrity. Magnesium regulates the contractility of cardiac muscle. It is concentrated 18 times greater in heart muscle than in the bloodstream, and decreased levels in heart tissue increase susceptibility to coronary spasms. Magnesium has a relaxing effect on smooth muscle and may be helpful in relaxing the smooth muscle of the bronchioles and the arterioles. Consequently, magnesium deficiency can produce a variety of metabolic abnormalities and clinical consequences.

Serum magnesium concentration is maintained within a narrow range by the small intestine and kidneys. Total body magnesium (TBMg) depends mainly on gastrointestinal absorption and renal excretion. Many factors regulate magnesium absorption. Intestinal absorption is inversely proportional to the amount ingested. As calcium intake decreases, Mg++absorption increases. Magnesium absorption occurs primarily in the jejunum and ileum via active carrier-mediated transport (partly dependent on vitamin D and parathyroid hormone [PTH]) and passive diffusion. The rate of magnesium absorption varies from as low as 24% to as high as 85%. Plasma Mg++concentration is the major regulator of magnesium reabsorption within the kidney, serving as the principal organ in magnesium regulation. About 100 mg is excreted daily into the urine. In contrast to other ions, 60% to 70% of Mg++reabsorption occurs in the thick ascending loop of Henle. Even so, the distal tubule is the major site of magnesium regulation, although it normally reabsorbs only 10% of filtered Mg++. Both hormonal and nonhormonal factors influence Mg++reabsorption in the loop of Henle and distal tubule, including PTH, calcitonin, glucagon, and vasopressin levels; magnesium restriction; acid-base changes; and potassium depletion. In plasma magnesium self-regulatory processes, the Ca++/Mg++-sensing receptor induces inhibition of loop transport in response to hypermagnesemia, whereas hypomagnesemia stimulates transport. Hypercalcemia and the rate of sodium chloride reabsorption can also influence reabsorption. Under conditions of magnesium deprivation, both organs increase their fractional absorption of the nutrient. Magnesium distribution constantly but gradually shifts between stores in bone or muscle and the extracellular fluid (ECF). In situations of magnesium depletion, resulting in negative magnesium imbalance, ECF will give up the initial losses, and serum Mg++concentrations will rapidly fall. A compensatory reduction will then occur in urinary Mg++concentrations unless there is magnesium wasting for other reasons. Finally, over several weeks, equilibration utilizing the bone stores will take place.

nutrient in clinical practice

Known or Potential Therapeutic Uses

Magnesium has primarily been used in, and investigated for, the treatment of cardiovascular disease, diabetes, migraine, muscular spasm and irregular contractility, osteoporosis, and premenstrual syndrome. Usage ranges from daily dietary and supplemental intake to intravenous infusion for critical care. The value of this mineral in promoting health and treating disease is gradually coming into greater appreciation, as are the implications of its involvement in interactions with pharmaceutical agents. For example, a recent large study confirmed that greater levels of dietary magnesium intake appear to be associated with a reduced risk of coronary heart disease. 1

Possible Uses

Alcohol withdrawal, angina, anxiety, asthma, atherosclerosis, autism, cardiac arrhythmias, cardiomyopathy, cardiovascular disease, celiac disease, chronic fatigue syndrome (CFS), chronic obstructive pulmonary disease (COPD), congestive heart failure, constipation, Crohn's disease, depression, diabetes mellitus, dysmenorrhea, eclampsia, eosinophilia-myalgia syndrome, epilepsy, fatigue, fibromyalgia, gastrointestinal spasms or cramping (acute), glaucoma, hearing loss (especially noise-related), hyperactivity, hypercholesterolemia, hypertension, hypocalcemia, hypoglycemia, hypokalemia, insomnia, intermittent claudication, kidney stones, lead toxicity, low levels of high-density lipoprotein (HDL) cholesterol, menopause, migraine, mitral valve prolapse, muscle cramping (especially nocturnal), multiple sclerosis, myocardial infarction (acute), osteoporosis, premenstrual syndrome (PMS), Raynaud's disease, retinopathy, sickle cell disease, stress response, stroke, torticollis, toxemia of pregnancy, urinary urge incontinence.

Deficiency Symptoms

There is significant disagreement as to the prevalence of clinically significant, although possibly subclinical, magnesium deficiency among the healthy subpopulations in developed societies. Nevertheless, the incidence of inadequate magnesium nutriture among susceptible subpopulations is widely recognized. A survey conducted by the U.S. Department of Agriculture showed that the daily dietary magnesium intake of many Americans (up to 75%) falls below the recommended dietary allowance (RDA), 2 which would mean that magnesium is among the most commonly deficient nutrients in that population. Suboptimal magnesium intake adversely affects a wide range of tissues, particularly those of the heart, nerves, and kidneys; many experts would say that all tissues are compromised by such a status. A diet high in processed and packaged foods tends to be magnesium poor because magnesium is found predominantly in whole, unprocessed foods.

Hypomagnesemia is frequently encountered in hospitalized patients and is seen in up to two thirds of patients admitted to intensive care units. 3 One survey of predominantly female urban African Americans found a 20% overall prevalence of magnesium deficiency. 4 Chronic degenerative diseases, such as diabetes, hyperlipidemia, hypertension, renal disease, asthma, and heart failure, are often associated with, and even potential causes of, magnesium deficiency, usually resulting from loss of magnesium from the gastrointestinal (GI) tract or the kidney. Alcoholism, severe burns, and other debilitative or traumatized states are also strongly linked to compromised magnesium status. Other GI causes include protein-calorie malnutrition, intravenous administration of Mg-free fluids and total parenteral nutrition, acute or chronic watery diarrhea, short bowel syndrome, bowel fistula, acute pancreatitis, continuous nasogastric suctioning, malabsorption steatorrhea, and extensive bowel resection. A rare inborn error of metabolism (primary intestinal hypomagnesemia), characterized by a selective defect in magnesium adsorption, is another known cause. The renal causes include Bartter's and Gitelman's syndromes, postobstructive diuresis, post–acute tubular necrosis, renal transplantation, and interstitial nephropathy. 5-8Hypomagnesemia may also accompany other disorders, including phosphate depletion, hungry-bone syndrome after parathyroidectomy, correction of chronic systemic acidosis, postobstructive nephropathy, renal transplantation, and the diuretic phase of acute tubular necrosis. 6 Many medications, particularly aminoglycosides, furosemide, and amphotericin-B, can also cause or contribute to magnesium depletion.

Hypomagnesemia is known to produce a wide variety of clinical presentations. Clinically, neuromuscular hyperexcitability may be the first symptom to manifest in individuals with hypomagnesemia. Magnesium deficiency is associated with hypocalcemia and hypokalemia, fatigue, lethargy and apathy, anxiety, insomnia, irritability, weakness, convulsions, delirium and coma, muscle spasm, tremor and tetany, high blood pressure, atherosclerosis, cardiomyopathy, cardiac spasm, cardiac arrhythmias, tachycardia, supraventricular ectopy, sudden cardiac death, insulin resistance, sugar cravings, nerve conduction problems, anorexia, nausea, vomiting, abdominal pains, paralytic ileus, dysmenorrhea, PMS, and poor nail growth. 5,9-12

Dietary Sources

The magnesium content in foods varies widely, as does the soil content of magnesium. Nuts (almonds, cashews, Brazil), soybeans, brewer's yeast, buckwheat, and wheat bran are rich sources of magnesium, with 200 to 400 mg per 100 g of food.

Moderate sources include corn, peas, carrots, barley, oats, rye, wheat, rice bran, pecans, filberts, pistachios, black walnuts, green leafy vegetables (kale, endive, chard beet tops), celery, alfalfa, figs, apples, lemons, peaches, almonds, whole grains (millet, cornmeal, wheat germ, barley, buckwheat, oats), tahini, sunflower seeds, brown rice, sesame seeds, black-eyed peas, lima beans, tofu, lentils, potato, sweet potato, peas, brussels sprouts, broccoli, cauliflower, avocado, dates, banana, blueberries, grape juice, cantaloupe, orange juice, and milk.

Nutrient Preparations Available

  • Magnesium citrate, magnesium gluconate, and magnesium lactate are more soluble and bioavailable than magnesium oxide.
  • Magnesium chloride is more soluble than magnesium oxide, gluconate, citrate, hydroxide, and sulfate and does not require stomach acid for solubility, but its use is limited because of its hygroscopic properties.
  • Magnesium hydroxide (milk of magnesia).
  • Magnesium sulfate (Epsom salts).

Dosage Forms Available

Capsule, liquid, powder, spray, tablet, injectable (prescription only), intravenous (inpatient).

Dosage Range


Dietary: 300 to 400 mg/day (Dietary Reference Intake; DRI)

Pregnant or lactating females: 450 to 550 mg/day (DRI)

Supplemental/Maintenance: 250 to 500 mg/day.

Pharmacological/Therapeutic: 50 to 2500 mg/day; 5 to 6 g have been used under close medical supervision.

Toxic: Single doses of 800 mg may cause diarrhea. Significantly lower doses can be toxic in renally impaired individuals.

Pediatric (<18 Years)

Dietary: Infants, 0-6 months: 50 mg/day (DRI)

Infants, 7-12 months: 70 mg/day (DRI)

Children, 1-10 years: 150 to 250 mg/day (DRI)

Adolescents, 11-18 years: 300 to 400 mg/day (DRI)

Supplemental/Maintenance: Not established.

Pharmacological/Therapeutic: Not established.

Toxic: Not established.

Laboratory Values

Consensus is lacking as to what constitutes an abnormally low plasma magnesium concentration [Mg++] and how to best assess magnesium depletion in critical tissues. Some authorities contend that measuring serum magnesium concentration and urinary magnesium excretion is usually sufficient in most cases to diagnose magnesium deficiency. 5 However, serum magnesium is a very poor indicator of how much magnesium is actually in the tissues, particularly cardiac tissue, which normally has much higher concentrations of magnesium than typical of serum. Measuring white blood cell (WBC) magnesium may provide a more sensitive indicator of tissue levels. An anionic magnesium measurement, pioneered by Drs. Burton and Bella Altura at Down-State University of New York in Brooklyn, appears to be a considerably more accurate indicator of tissue levels of magnesium than either WBC or red blood cell (RBC) measurements. Koivisto and other researchers at Helsinki University Hospital in Finland assert that spot serum ionized magnesium reveals depletion poorly, and that the most reliable method for evaluating magnesium status is the magnesium loading test. In cases of depletion, uptake of magnesium is increased by 20% to 50%, reaching 6% of normal magnesium status; normally, it represents less than 1% of the TBMg. 13 A recently developed in vitro blood load test using a magnesium-stable isotope appears to offer an accurate assessment of magnesium status, based on initial animal research. 14 Sublingual buccal cell scrapings analyzed with x-ray fluorescence spectroscopy, developed by Burton Silver, have been shown to correlate well with cardiac tissue levels; this is considered the best clinically available test by many magnesium experts. 15

Urinary Magnesium

  • Urinary magnesium provides a sensitive measure of magnesium status.
  • Deficiency: Excretion of less than 1 mmol/day indicates magnesium deficiency.
  • Leukocyte magnesium levels may reflect tissue levels.
  • Normal range: 3.0 to 4.0 ±0.09 fmol/cell.

Serum Ionized Magnesium

  • Serum ionized magnesium is a superior index, compared to serum levels, because the ionized portion of blood magnesium is not affected by variables that alter serum proteins.
  • Normal range: 0.5 to 0.66 mmol/L.

Serum Magnesium

  • Serum magnesium is an insensitive index of body magnesium stores; levels fall only with advanced deficiency.
  • Normal range: 0.75 to 1.05 mmol/L.
  • Occasionally, parenteral magnesium load test can be used to assess magnesium status.

safety profile


Magnesium has a very high therapeutic index, and hypermagnesemia is rare and usually iatrogenic, most commonly after intravenous (IV) magnesium, resulting from magnesium-containing laxatives or antacids, or rarely with intramuscular (IM) injection. Magnesium excess and toxicity most often result in diarrhea, drowsiness, weakness, and lethargy but may lead to depression of the central nervous system (CNS) and possibly death. Those most at risk are the elderly and patients with GI disorders or renal insufficiency. 16 Treatment of hypermagnesemia primarily consists of discontinuation of magnesium intake and introduction of calcium administration, but hemodialysis may be necessary in some cases.

Nutrient Adverse Effects

General Adverse Effects

Toxicity from oral ingestion of magnesium supplements is highly improbable in individuals with normal renal function, other than the potential for osmotic diarrhea. Clinical manifestations of hypermagnesemia include hypotension, nausea, vomiting, urinary retention, bradycardia, respiratory depression, depressed mental status, and electrocardiographic (ECG) abnormalities. Diarrhea is the most common adverse effect from oral magnesium supplements but is not associated with parenteral administration. Excessive oral magnesium intake can actually lead to a magnesium deficiency if it causes chronic diarrhea. Magnesium also competes with calcium and may induce a calcium deficiency if calcium intake levels are already low. About 800 mg of elemental magnesium will generally cause loose stools, but some individuals may tolerate much higher doses. Different forms of magnesium, such as magnesium glycinate, may be tolerated better as well. Slow-release forms of magnesium (e.g., Slo-mag), may be helpful in elevating the intracellular levels of magnesium. Individuals with kidney failure must be cautious about magnesium supplementation because they may experience elevated serum levels with associated toxicity symptoms.

Intravenous magnesium, because of its effect on smooth muscles, may cause hypotension along with dizziness and fainting. It may also cause respiratory depression or depletion of potassium with high doses and rapid infusion.

Intramuscular injections can often be painful and may cause a persistent lump if injection does not go deep enough to reach the muscle tissue. After the magnesium is loaded into the syringe, a small amount of 2% lidocaine can be drawn into the tip of the syringe to ease the reaction.

Adverse Effects Among Specific Populations

Gitelman's syndromes.

Pregnancy and Nursing

No problems have been reported with normal intake during pregnancy and lactation.

Infants and Children

No problems have been reported with normal intake in infants and children.


Individuals with impaired kidney function can accumulate magnesium, which is potentially fatal. Some medications, such as aminoglycosides and amphotericin-B, cause both renal tubular damage and magnesium depletion patterns.

Individuals with high-grade atrioventricular blocks or bifascicular blocks must avoid magnesium supplementation because it could slow cardiac conduction.

Precautions and Warnings

Magnesium supplementation may theoretically alter glucose regulation to such a degree as to be problematic for individuals with hypoglycemia or diabetes. Gradual introduction and increase of dosage will generally prevent complications. Close supervision and regular monitoring may be appropriate.

interactions review

Strategic Considerations

Although oral magnesium, as with many minerals, can bind and reduce bioavailability of many medications, the primary interactions of clinical significance derive from depletion and deficiency of this critical nutrient. Dietary magnesium deficiency is relatively common in the modern world, much more than usually expected, and its implications penetrate many aspects of human physiology, with the cardiovascular lesions being the most common arena of adverse effects. Inadequate dietary intake may affect the young and the aged, the poor and the institutionalized, the alcoholic and the malnourished, but iatrogenic causes of magnesium depletion produce many of the most severe outcomes. Clinically significant alterations in serum concentrations of Mg++(and K+) not only are frequently observed in acute or severely ill patients, especially in emergency rooms or intensive care wards, but also are a common adverse effect of many medications. Accurate assessment of magnesium status can be elusive but is critical because many symptoms of magnesium deficiency are nonspecific, and their effective correction requires early detection and intervention. In particular, digitalis and diuretics can intensify an underlying magnesium deficiency, leading to cardiac arrhythmias that are refractory unless magnesium is integrated into the therapeutic regimen. Furthermore, magnesium functions in association with other key minerals in supporting cardiovascular homeostasis, and these nutrients must often be administered in concert. Diuretic-treated hypertensive patients are particularly susceptible to potassium depletion and a resulting increased incidence of ventricular ectopy and sudden death. In such cases, potassium administration alone is inadequate, and concomitant magnesium is essential to intracellular potassium repletion and cardiovascular stabilization. Individuals receiving diuretic therapy, especially those with congestive heart failure, are also prone to chloride loss leading to metabolic alkalosis; this state interferes with potassium repletion, and the combination of potassium, magnesium, and chloride is often appropriate.

Ultimately, the disruptions of magnesium availability and function have their greatest impact on those populations most at risk for their adverse consequences. Furthermore, because the primary adverse effects of magnesium intake occur in individuals with compromised renal function, it is important that kidney function be assessed initially and monitored regularly, along with magnesium status. Importantly, the pharmacokinetic interaction between magnesium and many medications, involving formation of chelated complexes, reduces absorption and bioavailability of both agents. Both the nutrient and the drug presumably play important roles in the therapeutic strategy, so the separation of their administration by 2 to 4 hours avoids the interference and enables both agents to express their full activity.

nutrient-drug interactions
Albuterol/Salbutamol and Related Beta-2-Adrenoceptor Agonists (Inhalant Bronchodilators)
Aminoglycoside Antibiotics
Amphetamines and Related Stimulant Medications
Amphotericin B
Calcium Channel Blockers
Corticosteroids, Oral
Digoxin and Related Cardiac Glycosides
Diuretics: Loop Diuretics and Thiazide Diuretics
Oral Contraceptives: Monophasic, Biphasic, and Triphasic Estrogen Preparations (Synthetic Estrogen and Progesterone Analogs)
Hormone Replacement Therapy (HRT): Estrogen-Containing and Synthetic Estrogen and Progesterone Analog Medications
Fluoroquinolone (4-Quinolone) Antibiotics, Particularly Ciprofloxacin
Lithium Carbonate
Macrolide Antibiotics
Neuromuscular Blocking Agents
Quinidine and Related Antiarrhythmic Drugs
Sodium Polystyrene Sulfonate
Sotalol and Related Beta-1-Adrenoceptor Antagonists (Beta-1-Adrenergic Blocking Agents)
Sulfonylurea Hypoglycemics
Tetracycline Antibiotics
Warfarin and Related Oral Vitamin K Antagonist Anticoagulants
theoretical, speculative, and preliminary interactions research, including overstated interactions claims
Histamine (H 2 ) Receptor Antagonists
Hydroxychloroquine and Chloroquine
Isoniazid and Related Antitubercular Agents
Magnesium-Containing Antacids
Metformin and Related Biguanides
Potassium-Sparing Diuretics
Sulfamethoxazole and Related Sulfonamide Antibiotics
nutrient-nutrient interactions
Vitamin B 1 (Thiamine)
Vitamin B 6 (Pyridoxine)
Vitamin D
Citations and Reference Literature
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