Deficiency symptoms

Short answer

Early magnesium deficiency presents with nonspecific complaints such as loss of appetite, nausea, fatigue and weakness; as it worsens, numbness, muscle contractions, seizures and rhythm disturbances may occur. In healthy people, symptomatic deficiency from low dietary intake alone is rare, because the kidneys reduce excretion. Diagnosis is made not from symptoms but by clinical evaluation and laboratory testing. ^[1]

What are the symptoms of magnesium deficiency?

According to the NIH, early symptoms are loss of appetite, nausea, vomiting, fatigue and weakness. As the deficiency worsens, numbness, tingling, muscle contractions and cramps, seizures, personality changes, abnormal heart rhythms and coronary spasm may appear. ^[1]

This list has an important limit: none of the symptoms is specific to magnesium. Fatigue, weakness or muscle contractions occur in many different problems; the presence of one of them does not mean deficiency. Cramps are a good example: they are a common complaint, and in a Cochrane review magnesium supplementation gave no clinically meaningful benefit for nocturnal cramps in older adults. This finding is consistent with the view that cramps alone do not point to magnesium deficiency. ^[4]

With symptoms such as seizures, fainting, palpitations or chest pain, a health facility rather than a general guide should be consulted.

Are low magnesium intake and hypomagnesemia the same thing?

No; the two concepts are separate. Low intake means that daily magnesium falls below the reference value. Hypomagnesemia is a serum magnesium measured in the blood below 0.75 mmol/L. The NIH distinguishes a state below the reference intake but above the amount that prevents overt deficiency as “inadequacy.” ^[1]

Low intake from foods does not automatically create symptomatic deficiency; when magnesium falls, the kidneys reduce urinary excretion. Overt deficiency usually arises when sustained low intake is combined with a condition in which absorption is reduced or losses are increased. ^[1]

Is a serum magnesium test enough to show deficiency?

Serum magnesium is the most common and easily accessible method; however, the NIH states that serum level correlates very little with total body magnesium or with levels in tissues. The reason is that less than 1% of body magnesium is in serum and the serum level is tightly controlled. The normal range is 0.75–0.95 mmol/L. ^[1]

• Alternatives exist, such as red blood cell, saliva and urine measurements, ionized magnesium and a “loading test”; none is considered sufficient alone.
• The NIH notes that laboratory tests together with clinical assessment may be needed for a comprehensive evaluation.
• In the US, magnesium is not part of routine electrolyte panels. In Türkiye, laboratory and ordering practices may vary; this guide does not determine which test should be requested. ^[1]

An example from Türkiye shows this limit. In a retrospective cross-sectional study reported from an internal medicine department of a medical school in Rize, based on data from 502 patients with type 2 diabetes, serum magnesium was significantly lower in those with poor glycemic control; however, the power of magnesium to predict glycemic control was limited (AUC 0.41), and the authors reported that serum magnesium alone is not a reliable indicator. A single-center cross-sectional study does not show cause and effect and is not representative of the whole country. ^[3]

What are the causes of magnesium deficiency?

The causes that stand out in the sources are reduced absorption or increased loss. ^[1]

• Gastrointestinal diseases: Crohn’s disease, celiac disease and other diseases causing chronic diarrhea or fat malabsorption; resection or bypass of the small intestine (especially the ileum).
• Type 2 diabetes: Insulin resistance and increased urinary magnesium excretion in diabetes; the mechanism appears to be that high glucose in the kidney increases urine output. In the Rize study above, serum level was also associated with the use of metformin and indapamide. ^[3]
• Alcohol dependence: Several mechanisms, such as poor nutrition, vomiting, diarrhea, fatty stools due to pancreatitis, kidney losses, and phosphate and vitamin D deficiency. ^[1]
• Older age: Lower intake, reduced absorption, increased kidney excretion, chronic diseases and medications. ^[1]
• Medications: Loop (furosemide, bumetanide) and thiazide (hydrochlorothiazide) diuretics increase urinary magnesium loss; potassium-sparing diuretics (amiloride, spironolactone) reduce excretion. Hypomagnesemia has been reported with long-term, generally more than one year, use of proton pump inhibitors. ^[1]

The PPI association is debated. In an updated review dated 2019 that examined 15 observational studies (129,347 participants), a meta-analysis of 14 studies showed that the risk of hypomagnesemia increased with PPI use (RR 1.44; 95% CI 1.13–1.76), but noted that because of large heterogeneity between studies (I² 85.2%) and differing cutoff values, no firm conclusion could be drawn. This finding is a reason not to stop the medication on one’s own but to discuss monitoring with a physician in long-term use. According to the NIH, the FDA recommends considering measuring serum magnesium before starting long-term PPI use and periodically afterward. ^{[2] [1]}

Detailed guideMagnesium guide: functions, reference intakes and safety→

How does magnesium deficiency affect calcium and potassium?

Because severe magnesium deficiency disturbs mineral balance, it can result in low serum calcium (hypocalcemia) and low serum potassium (hypokalemia). ^[1] That these three electrolytes are interlinked means magnesium may also come into question when investigating the cause of low calcium or potassium; the physician decides which tests to order.

The effect of magnesium deficiency on heart rhythm (rhythm disturbances, coronary spasm) is listed by the NIH among the symptoms of severe deficiency. ^[1]

Can excess magnesium be confused with deficiency?

High magnesium (hypermagnesemia) is the opposite of deficiency and its symptoms differ. According to the NIH, symptoms of toxicity generally develop after serum magnesium exceeds 1.74–2.61 mmol/L: hypotension, nausea, vomiting, facial flushing, urinary retention, ileus, depression and lethargy; as it progresses, muscle weakness, difficulty breathing, extreme low blood pressure, irregular heartbeat and cardiac arrest occur. ^[1] Because nausea, vomiting and weakness can occur in both deficiency and excess, starting or increasing magnesium supplements based on symptoms alone is not a safe approach.

In a healthy person, excess from foods poses no risk, because the kidneys increase excretion. Risk rises with laxatives and antacids containing very high amounts of magnesium (generally above 5,000 mg per day) and especially when kidney function is impaired. ^[1]

What is evaluated when magnesium deficiency is suspected?

• Symptoms and medications: How long the complaints have lasted, prescription medications in use (especially diuretics and PPIs), supplements, laxatives and antacids are useful information in a physician visit.
• Risk factors: Chronic diarrhea, bowel disease, diabetes, alcohol use and kidney disease change the evaluation.
• Test and cause first: Deficiency is not inferred from a symptom; the physician decides which test is appropriate.
• Self-started supplements: Magnesium may accumulate in kidney failure; high amounts of magnesium-containing laxatives and antacids have been linked to toxicity. ^[1]

In the treatment of magnesium deficiency, the amount, form and duration are determined by a physician according to the degree of deficiency and the underlying cause; this page does not offer a treatment plan.

Detailed guideWhich foods contain magnesium?→ Detailed guideMagnesium benefits and the limits of the evidence→ Detailed guideMagnesium forms: oxide, citrate, glycinate→ Detailed guideWhen to take magnesium→