Magnesium (Serum Magnesium): Understanding Your Blood Test Series

1. Overview: What this test reveals and why it is important

Magnesium is the fourth most abundant cation in the body and the second most abundant intracellular cation after potassium. It is a critical cofactor for over 300 enzymatic reactions, including:

· Energy production: ATP metabolism requires magnesium‑ATP complexes.

· Protein synthesis: Ribosomal function.

· Nucleic acid synthesis and repair: DNA and RNA polymerases.

· Neuromuscular excitability: Regulates ion channels (calcium, potassium) and neurotransmitter release.

· Cardiovascular health: Maintains normal cardiac conduction, vascular tone, and blood pressure.

· Bone structure: 50–60% of body magnesium is stored in bone.

· Glucose and insulin metabolism: Modulates insulin signalling.

Serum magnesium measures the extracellular magnesium concentration, which represents less than 1% of total body magnesium. It is a poor reflection of total body stores – significant intracellular depletion can exist with normal serum levels. Conversely, serum levels can be transiently low without true deficiency (e.g., during acute illness, after surgery).

Clinical utility:

· Assessment of deficiency: In patients with risk factors (malabsorption, alcoholism, diuretic use, proton pump inhibitors, critical illness, burns, diarrhoea, vomiting).

· Investigation of symptoms: Unexplained muscle cramps, tetany, seizures, cardiac arrhythmias (especially torsades de pointes), hypokalaemia, hypocalcaemia.

· Monitoring replacement therapy: In patients receiving intravenous magnesium or high‑dose oral supplements.

· Assessment of toxicity: In renal failure or excessive supplementation (rare).

Important principle: Magnesium is an acute‑phase reactant. Levels may fall during acute illness, stress, or surgery due to redistribution and increased renal loss. A low level in an acutely ill patient may not indicate chronic deficiency. Interpretation always requires clinical context and, ideally, concurrent measurement of calcium, potassium, and renal function.

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2. What does it measure

a. Units of measurement

· Milligrams per decilitre (mg/dL) – common in the United States.

· Milliequivalents per litre (mEq/L) – used in some clinical settings.

· Millimoles per litre (mmol/L) – used in many other countries.

· Conversion:

· 1 mg/dL = 0.411 mmol/L

· 1 mmol/L = 2.43 mg/dL

· 1 mEq/L = 0.5 mmol/L (for magnesium, valence = 2)

b. Normal Range

(Reference ranges vary slightly by laboratory; the following are general guidelines.)

Adults:

· Serum magnesium: 1.7–2.3 mg/dL (0.85–1.15 mmol/L)

· Ionised magnesium (free, biologically active): 0.54–0.67 mmol/L (rarely measured clinically).

Children:

· Infants: 1.5–2.2 mg/dL (0.75–1.10 mmol/L)

· Older children: Adult range.

Pregnancy:

· Physiological decline due to haemodilution and increased fetal demand.

· Third trimester: 1.4–2.0 mg/dL (0.7–1.0 mmol/L) is common.

· Interpret with gestation‑specific reference ranges if available.

Interpretation notes:

· Hypomagnesaemia: <1.7 mg/dL (<0.85 mmol/L). Severe: <1.0 mg/dL (<0.5 mmol/L).

· Hypermagnesaemia: >2.3 mg/dL (>1.15 mmol/L). Severe: >4.0 mg/dL (>2.0 mmol/L).

· Serum magnesium does not reflect tissue stores – normal levels can occur with marginal deficiency.

· Ionised magnesium is the physiologically active form and may be a better marker, but it is not widely available.

· Magnesium loading tests (measuring urinary excretion after intravenous load) can assess total body stores but are research tools, not routine.

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3. Other factors connected to this

a. Direct correlation (factors that directly lower or raise serum magnesium)

Factors that lower serum magnesium (hypomagnesaemia):

· Inadequate intake:

· Malnutrition, anorexia nervosa, alcoholism.

· Prolonged parenteral nutrition without magnesium.

· Refeeding syndrome – rapid influx of magnesium into cells during carbohydrate repletion.

· Malabsorption:

· Coeliac disease, inflammatory bowel disease (Crohn, ulcerative colitis), short bowel syndrome, cystic fibrosis, chronic pancreatitis.

· Bariatric surgery (especially malabsorptive procedures).

· Increased losses (gastrointestinal):

· Chronic diarrhoea, vomiting, fistulas, nasogastric suction.

· Laxative abuse.

· Increased losses (renal):

· Diuretics: Loop diuretics (furosemide, bumetanide) and thiazide diuretics – increase urinary magnesium excretion.

· Osmotic diuresis: Uncontrolled diabetes mellitus (glycosuria).

· Alcohol: Acute and chronic use increases renal magnesium loss.

· Medications:

· Proton pump inhibitors (PPIs): Long‑term use (>1 year) is associated with hypomagnesaemia; mechanism unclear.

· Aminoglycosides, amphotericin B, cisplatin, ciclosporin, tacrolimus, pentamidine – cause renal magnesium wasting.

· Epidermal growth factor receptor (EGFR) inhibitors (cetuximab, panitumumab) – cause hypomagnesaemia.

· Hypercalcaemia: Calcium competes with magnesium for reabsorption in the thick ascending limb.

· Post‑obstructive diuresis.

· Genetic: Gitelman syndrome, Bartter syndrome – rare tubulopathies.

· Redistribution:

· Acute illness / stress / surgery: Catecholamines drive magnesium into cells.

· Refeeding syndrome: As above.

· Hungry bone syndrome: After parathyroidectomy for hyperparathyroidism – rapid bone uptake of magnesium and calcium.

· Insulin therapy: Insulin shifts magnesium into cells.

· Acute pancreatitis: Saponification of magnesium with fatty acids in the peritoneum.

· Endocrine:

· Hyperaldosteronism, hyperthyroidism, hyperparathyroidism – increase renal magnesium loss.

· Diabetes mellitus: Poor control increases urinary loss.

· Pregnancy / lactation: Increased demands.

Factors that raise serum magnesium (hypermagnesaemia):

· Excessive intake:

· Iatrogenic: Intravenous magnesium (e.g., for pre‑eclampsia, asthma, torsades de pointes).

· Oral supplements: High‑dose magnesium salts (especially magnesium oxide and sulphate) – usually causes diarrhoea before toxicity.

· Antacids / laxatives: Magnesium‑containing products (e.g., milk of magnesia).

· Reduced excretion:

· Chronic kidney disease (CKD): Most common cause. Risk increases as eGFR falls below 30 mL/min.

· Adrenal insufficiency (Addison's disease): Mineralocorticoid deficiency impairs magnesium excretion.

· Hypothyroidism: Reduced renal blood flow.

· Lithium therapy: May increase magnesium reabsorption.

· Other:

· Hypoparathyroidism.

· Familial hypocalciuric hypercalcaemia.

· Volume depletion / dehydration: Haemoconcentration.

b. Indirect correlation (factors that influence magnesium interpretation or cause artefactual changes)

· Timing of test: Fasting samples are preferred to minimise postprandial variation.

· Infection / inflammation / stress: Serum magnesium falls; measure CRP concurrently.

· Pregnancy: Physiological decline; do not overdiagnose deficiency.

· Albumin levels: Magnesium is not significantly protein‑bound (~30% bound), so hypoalbuminaemia has less effect than on calcium.

· Sample handling: Avoid haemolysis (magnesium is released from red cells, falsely elevating levels). Use serum separator tubes.

· Age: Newborns have slightly lower levels; adult levels achieved by 1 year.

· Circadian rhythm: Minor; not clinically significant.

· Medications: As above.

· Renal function: Always interpret magnesium in the context of eGFR.

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4. Disorders related to abnormal values

a. When magnesium is low (hypomagnesaemia – clinically significant)

Clinical manifestations of magnesium deficiency:

Neuromuscular manifestations include muscle cramps, fasciculations, tremor, tetany, a positive Chvostek sign, a positive Trousseau sign, weakness, and hyperreflexia.

Cardiovascular manifestations include ECG changes such as prolonged PR and QT intervals, ST segment depression, and flat or inverted T waves. Arrhythmias may include atrial fibrillation, ventricular tachycardia, and torsades de pointes (polymorphic ventricular tachycardia). Hypertension is also associated.

Metabolic disturbances include hypokalaemia that is refractory to potassium replacement, as magnesium is required for renal potassium conservation, and hypocalcaemia refractory to calcium replacement, as magnesium deficiency impairs parathyroid hormone secretion and action.

Neurological manifestations include seizures (generalised or focal), lethargy, confusion, nystagmus, and ataxia.

Gastrointestinal manifestations include anorexia, nausea, and vomiting, which can be both a cause and an effect of deficiency.

Common causes of hypomagnesaemia:

Gastrointestinal causes include coeliac disease, Crohn disease, ulcerative colitis, short bowel syndrome, chronic diarrhoea, vomiting, laxative abuse, and bariatric surgery.

Renal causes include the use of diuretics (both loop diuretics and thiazide diuretics), alcohol consumption, long‑term proton pump inhibitor use, medications such as aminoglycosides, cisplatin, ciclosporin, and tacrolimus, genetic tubulopathies like Gitelman syndrome and Bartter syndrome, diabetic ketoacidosis, hyperaldosteronism, and hyperparathyroidism.

Nutritional causes include malnutrition, alcoholism, anorexia nervosa, and prolonged parenteral nutrition without magnesium.

Redistribution causes include refeeding syndrome, hungry bone syndrome, acute pancreatitis, and insulin therapy.

Endocrine causes include diabetes mellitus, hyperthyroidism, hyperparathyroidism, and hyperaldosteronism.

b. When magnesium is high (hypermagnesaemia – clinically significant)

Clinical manifestations of magnesium toxicity:

At serum levels between 2.3 and 3.0 mg/dL (0.95–1.25 mmol/L), patients are often asymptomatic. Between 3.0 and 4.0 mg/dL (1.25–1.65 mmol/L), symptoms may include nausea, flushing, drowsiness, hyporeflexia, hypotension, and bradycardia. Between 4.0 and 6.0 mg/dL (1.65–2.5 mmol/L), patients may experience lethargy, confusion, areflexia, muscle paralysis, and ECG changes such as PR prolongation and QRS widening. Between 6.0 and 8.0 mg/dL (2.5–3.3 mmol/L), complete heart block, respiratory depression, and coma can occur. Above 8.0 mg/dL (>3.3 mmol/L), cardiac arrest and asystole are imminent.

Common causes of hypermagnesaemia:

The most common cause is chronic kidney disease (CKD), where excretion is impaired. Iatrogenic causes include excessive intravenous magnesium administration, such as in the treatment of pre‑eclampsia, if not carefully monitored. Oral ingestion of large doses of magnesium‑containing antacids or laxatives, particularly in patients with CKD, can also cause toxicity. Other causes include adrenal insufficiency (Addison's disease), hypothyroidism, lithium therapy, familial hypocalciuric hypercalcaemia, and volume depletion or dehydration leading to haemoconcentration.

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5. Best way to address aberrant levels

Important principle: Magnesium levels are not treated in isolation. The underlying cause – deficiency due to malabsorption, diuretics, or alcoholism, or toxicity due to renal failure or excess intake – must be addressed.

a. Quick ways or using Medications

For hypomagnesaemia (deficiency):

The first step is to identify and treat the underlying cause. This may involve stopping or reducing offending medications such as diuretics or proton pump inhibitors if possible. Treating malabsorption with a gluten‑free diet for coeliac disease, immunosuppression for inflammatory bowel disease, or pancreatic enzyme replacement for chronic pancreatitis is essential. Managing alcoholism through abstinence and nutritional support, and improving glycaemic control in diabetes are also critical.

For mild to moderate deficiency in asymptomatic or mildly symptomatic patients, oral magnesium supplementation is appropriate. The preferred forms of magnesium, ranked by bioavailability and tolerability, include magnesium glycinate, which is highly bioavailable, well tolerated, and least likely to cause diarrhoea, making it ideal for long‑term use. Magnesium citrate is well absorbed but has a slight laxative effect, which can be useful if constipation is also present. Magnesium malate may be beneficial for fatigue and fibromyalgia. Magnesium taurate has been studied for cardiovascular benefits. Magnesium chloride has good absorption but may cause gastrointestinal upset. Magnesium lactate is also well absorbed.

Forms to avoid include magnesium oxide, which is poorly absorbed and acts primarily as a laxative, and magnesium sulphate in oral form, which is also poorly absorbed and causes diarrhoea. Magnesium with calcium or iron taken simultaneously should be avoided as these minerals compete for absorption; doses should be separated by at least two hours.

The dose of elemental magnesium depends on the severity of deficiency. For mild deficiency or maintenance, 200–400 mg of elemental magnesium per day is appropriate. For moderate deficiency, 400–600 mg per day in divided doses may be needed. For severe, symptomatic deficiency, higher doses may be required, but the oral route may be limited by diarrhoea. Supplementation should continue until serum magnesium normalises and symptoms resolve, which typically takes two to four weeks for mild deficiency, though chronic depletion may require longer. Monitoring should include a repeat serum magnesium level after two to four weeks of therapy, along with assessment of symptom improvement in cramps, weakness, and arrhythmias.

For severe deficiency, symptomatic patients, those unable to absorb oral magnesium, or in specific therapeutic indications such as pre‑eclampsia, intravenous magnesium is required. Magnesium sulphate is used, with one gram providing approximately 98 mg of elemental magnesium (or about 4 mmol). A typical regimen is 4 to 8 grams intravenously over 24 hours, given in divided doses. For severe arrhythmia like torsades de pointes, 1 to 2 grams may be given as an intravenous push over one to two minutes, followed by an infusion. The dose must be reduced by 50 to 75 percent in patients with renal impairment. Monitoring during IV therapy includes rechecking serum magnesium six to twelve hours after the infusion, assessing deep tendon reflexes (hyporeflexia or areflexia indicates toxicity), and monitoring ECG, respiratory rate, and blood pressure.

It is also essential to correct concomitant deficiencies. Hypokalaemia often requires magnesium repletion first, as potassium replacement will be ineffective otherwise. Similarly, hypocalcaemia will not correct until magnesium is repleted.

For hypermagnesaemia (toxicity):

In mild, asymptomatic cases, all magnesium‑containing medications and supplements should be stopped. Ensuring adequate hydration with intravenous fluids if needed promotes renal excretion. Serum magnesium, renal function, and ECG should be monitored.

In moderate to severe, symptomatic cases, intravenous calcium gluconate at a dose of 1 to 2 grams given over 10 to 20 minutes antagonises the cardiac and neuromuscular effects of magnesium, although it does not lower the magnesium level itself. Intravenous fluids with a loop diuretic such as furosemide can increase renal magnesium excretion, but this is only effective if renal function is adequate. Haemodialysis is the most effective method for rapid removal of magnesium and is indicated in severe toxicity with renal failure, respiratory depression, or cardiac compromise.

Identifying and treating the underlying cause is also crucial. This may involve managing chronic kidney disease, reviewing and adjusting medications, or treating adrenal insufficiency if present.

Do not self‑prescribe high‑dose magnesium – can cause toxicity. All supplementation beyond standard multivitamin doses should be supervised.

b. Using Supplements or Holistic medicine

Magnesium is itself a supplement. The principles above cover therapeutic use. The following can support magnesium status and overall health.

To enhance magnesium absorption and utilisation, vitamin B6 (pyridoxine) may be beneficial. It can enhance magnesium absorption and cellular uptake. The active form, pyridoxal‑5‑phosphate, is preferred, at a dose of 25 to 50 mg per day. Vitamin D is also important, as magnesium is required for vitamin D activation, and conversely, vitamin D may increase intestinal magnesium absorption. Vitamin D3 (cholecalciferol) from lichen is the preferred form, at a dose of 600 to 2000 IU per day. Probiotics and prebiotics support gut health and may improve absorption in malabsorptive conditions. Preferred sources include fermented plant foods such as kimchi, sauerkraut, kombucha, miso, and tempeh, as well as standardised probiotic supplements with documented strains. Taurine, at a dose of 500 to 2000 mg per day, may enhance magnesium retention in cells and is often combined in supplements.

It is important to avoid taking high‑dose calcium or iron supplements simultaneously, as they compete for absorption. These should be spaced at least two hours apart from magnesium. Phytate‑rich foods such as unprocessed bran, whole grains, and legumes can inhibit magnesium absorption, but in a balanced plant‑based diet, food preparation techniques like soaking, sprouting, and fermentation reduce phytate content. These healthy foods should not be avoided; rather, adequate magnesium intake should be ensured.

Supplements to avoid in magnesium deficiency include high‑dose calcium and iron supplements, as noted. Synthetic folic acid and cyanocobalamin have no direct interaction but should be replaced with methylfolate and methylcobalamin respectively.

General caution: Supplements are adjunctive. Magnesium therapy itself is the primary intervention.

c. Using Diet and Foods (following a plant‑forward, ecologically sustainable approach)

Diet is the foundation of maintaining adequate magnesium status. A well‑designed plant‑based diet is naturally rich in magnesium.

Excellent primary plant sources of magnesium include dark leafy greens such as spinach, Swiss chard, kale, collard greens, and beet greens. One cup of cooked spinach provides approximately 157 mg of magnesium, which is about 40 percent of the daily value. Pumpkin seeds (pepitas) are also excellent, with one ounce providing about 150 mg of magnesium, or 35 percent of the daily value. Nuts, particularly almonds and cashews, are good sources; one ounce of almonds provides around 80 mg of magnesium. Seeds such as hemp seeds, chia seeds, flaxseeds, and sunflower seeds are also rich; one ounce of hemp seeds provides about 100 mg of magnesium. Legumes including black beans, kidney beans, chickpeas, lentils, and edamame are excellent; one cup of cooked black beans provides approximately 120 mg of magnesium. Soy products like tofu and tempeh are good sources, with half a cup of firm tofu providing about 50 mg of magnesium. Whole grains such as quinoa, brown rice, oats, barley, and millet are also important; one cup of cooked quinoa provides about 118 mg of magnesium. Bananas, avocados, dark chocolate (with at least 70 percent cocoa), dried fruits like figs and apricots, and potatoes with skin are additional sources.

Fungi and algae are encouraged. Mushrooms such as shiitake, crimini, and portobello provide moderate amounts, with one cup of cooked mushrooms offering 20 to 30 mg of magnesium. Spirulina and chlorella, at one tablespoon (10 grams), provide 20 to 30 mg of magnesium.

Biotechnology and lab‑grown options, such as precision‑fermented proteins like mycoprotein and animal‑free dairy proteins, may be fortified with magnesium, though this is an emerging area.

Dairy and eggs are permitted but not emphasised. One cup of yoghurt provides about 30 mg of magnesium, and eggs provide about 5 mg each. They are not necessary for adequate intake.

Meat, poultry, and fish are deliberately omitted. Effective plant‑based alternatives exist to meet all magnesium requirements. Animal products are relatively poor sources of magnesium compared to plants, making plant sources superior.

To enhance magnesium absorption from plant foods, techniques such as soaking, sprouting, and fermenting are valuable. Soaking legumes, grains, and seeds for 8 to 24 hours before cooking reduces phytate content. Sprouting lentils, chickpeas, and mung beans dramatically reduces phytate and increases mineral bioavailability. Fermenting foods such as tempeh, miso, and sourdough bread allows microbial phytase to break down phytate. Pairing magnesium‑rich foods with vitamin B6, which is found in many of the same foods like spinach, nuts, seeds, and legumes, may also help. Adequate protein intake supports overall mineral status. It is also advisable to avoid taking high‑dose calcium and iron supplements with meals, as they compete for absorption.

Foods to avoid or separate from magnesium‑rich meals include high‑dose calcium and iron supplements, as well as coffee and tea, as tannins may inhibit absorption. These beverages are best consumed between meals.

Sample magnesium‑rich plant‑based meals include spinach and pumpkin seed pesto pasta made with whole wheat pasta, a pesto of spinach, pumpkin seeds, basil, olive oil, garlic, and nutritional yeast, served with steamed broccoli. A black bean and quinoa burrito bowl can be made with black beans, quinoa, roasted sweet potatoes, avocado, corn, salsa, and lime. Tofu and vegetable stir‑fry with firm tofu, broccoli, bell peppers, snap peas, and carrots in a ginger‑soy sauce, served with brown rice, is another option. Oatmeal with hemp seeds, chia seeds, sliced banana, and almond butter makes a hearty breakfast. Chickpea and spinach curry with tomatoes, onions, coconut milk, and spices, served with quinoa, is a flavourful dinner. A simple trail mix of almonds, pumpkin seeds, dark chocolate chips, and dried apricots is a convenient snack.

What to avoid or severely limit includes ultra‑processed foods and refined carbohydrates, which are low in magnesium and high in phytates. Excess alcohol impairs magnesium absorption and increases urinary loss. High‑dose calcium supplements without magnesium can exacerbate magnesium deficiency. Smoking cessation, while not dietary, improves overall health.

Lifestyle factors with proven benefit include stress reduction, as chronic stress increases magnesium loss. Mindfulness, meditation, yoga, and adequate sleep are helpful. Regular moderate exercise supports magnesium status, though excessive endurance exercise may increase losses.

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6. How soon can one expect improvement and the ideal time frame to retest

For oral magnesium supplementation, serum magnesium begins to rise within one to two weeks, with normalisation typically achieved by two to four weeks. Clinical symptoms such as muscle cramps and tetany may improve within days to weeks. Cardiac arrhythmias like torsades de pointes resolve within minutes of intravenous magnesium, while other arrhythmias improve over days to weeks with repletion. Hypokalaemia and hypocalcaemia may normalise within one to two weeks after magnesium correction. Retesting should occur at two to four weeks after starting oral therapy.

For intravenous magnesium, serum magnesium rises within minutes to hours. Retesting should occur six to twelve hours after the infusion, and then as clinically indicated.

For chronic deficiency due to malabsorption, alcoholism, or diuretic use, long‑term supplementation may be required. Retesting should occur every three to six months.

For hypermagnesaemia, after discontinuing magnesium and initiating treatment, serum magnesium normalises within one to three days in patients with normal renal function, or over days to weeks with dialysis.

The retesting interval summary is as follows: for deficiency on treatment, retest at two to four weeks, then at three to six months, and then annually if stable on maintenance. For chronic hypomagnesaemia, such as in patients on proton pump inhibitors or diuretics, retest every three to six months. During acute illness, do not retest until the illness has resolved. For hypermagnesaemia, retest daily until normalised, then as clinically indicated.

Do not retest magnesium more often than every one to two weeks for chronic repletion, as meaningful change does not occur faster.

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Conclusion

Magnesium is the unsung hero of cellular metabolism – the quiet cofactor that powers ATP, stabilises cardiac rhythm, relaxes muscle, and calms the nervous system. Its deficiency mimics and exacerbates every electrolyte disorder, rendering potassium and calcium replacement futile until magnesium is restored.

A low serum magnesium level is a diagnostic prompt: Is this malabsorption? Diuretics? Alcohol? Proton pump inhibitors? Gitelman syndrome? Or the refeeding syndrome after starvation? The answer directs therapy – oral glycinate for the outpatient, intravenous sulphate for the seizing patient, and, always, correction of the underlying cause.

A plant‑based, ecologically responsible diet – rich in dark leafy greens, pumpkin seeds, almonds, black beans, quinoa, and dark chocolate – is naturally abundant in magnesium. Soaking, sprouting, and fermenting unlock this mineral from its phytate bonds. There is no need for animal products; they are, in fact, inferior sources. The pumpkin seed, the spinach leaf, and the black bean are magnesium powerhouses, and their cultivation sustains the planet.

Magnesium is a number – a concentration, a level. The patient is a story of cramps, fatigue, palpitations, and resilience. Listen to the patient, not the number – but when the number is low and the story fits, act swiftly, decisively, and with precision.

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Note on dietary recommendations on this site:

For the sake of our environment we adhere to the following dietary preference hierarchy:

1. Plant‑based

2. Fungi / algae / fermented

3. Biotechnology / lab‑grown / cultures

4. Dairy / eggs

5. Meat / fish / poultry (only if no effective alternative exists)

Special notes on magnesium:

· Magnesium supplements: Choose highly bioavailable forms – magnesium glycinate, citrate, malate, taurate, or chloride. Avoid magnesium oxide.

· Plant‑based magnesium sources: Dark leafy greens (spinach, Swiss chard), pumpkin seeds, almonds, cashews, black beans, chickpeas, lentils, edamame, tofu, quinoa, oats, bananas, avocado, dark chocolate.

· Enhance absorption: Soak, sprout, or ferment legumes and grains; pair with vitamin B6; avoid high‑dose calcium or iron with meals.

· Medication interactions: Proton pump inhibitors, diuretics, and certain antibiotics can cause magnesium deficiency. Monitor levels if on long‑term therapy.

· Refeeding syndrome risk: In malnourished patients, monitor magnesium, potassium, and phosphate closely during nutritional repletion.

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