Magnesium deficiency

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Magnesium deficiency
Other namesHypomagnesia, hypomagnesemia
Mg-TableImage.svg
Magnesium
Specialty Endocrinology
Symptoms Tremor, poor coordination, nystagmus, seizures [1]
Complications Seizures, cardiac arrest (torsade de pointes), low potassium [1]
Causes Alcoholism, starvation, diarrhea, increased urinary loss, poor absorption from the intestines, certain medications [1] [2]
Diagnostic method Blood levels < 0.6 mmol/L (1.46 mg/dL) [1]
Treatment Magnesium salts [2]
FrequencyRelatively common (hospitalized people) [2]

Magnesium deficiency is an electrolyte disturbance in which there is a low level of magnesium in the body. [3] Symptoms include tremor, poor coordination, muscle spasms, loss of appetite, personality changes, and nystagmus. [1] [2] Complications may include seizures or cardiac arrest such as from torsade de pointes. [1] Those with low magnesium often have low potassium. [1]

Contents

Causes include low dietary intake, alcoholism, diarrhea, increased urinary loss, and poor absorption from the intestines. [1] [4] [5] Some medications may also cause low magnesium, including proton pump inhibitors (PPIs) and furosemide. [2] The diagnosis is typically based on finding low blood magnesium levels, also called hypomagnesemia. [6] Normal magnesium levels are between 0.6 and 1.1 mmol/L (1.46–2.68 mg/dL) with levels less than 0.6 mmol/L (1.46 mg/dL) defining hypomagnesemia. [1] Specific electrocardiogram (ECG) changes may be seen. [1]

Treatment is with magnesium either by mouth or intravenously. [2] For those with severe symptoms, intravenous magnesium sulfate may be used. [1] Associated low potassium or low calcium should also be treated. [2] The condition is relatively common among people in hospitals. [2]

Signs and symptoms

Deficiency of magnesium can cause tiredness, generalized weakness, muscle cramps, abnormal heart rhythms, increased irritability of the nervous system with tremors, paresthesias, palpitations, low potassium levels in the blood, hypoparathyroidism which might result in low calcium levels in the blood, chondrocalcinosis, spasticity and tetany, migraines, epileptic seizures, [7] basal ganglia calcifications [8] and in extreme and prolonged cases coma, intellectual disability or death. [9] Magnesium deficiency is strongly associated with and appears to contribute to obesity, insulin resistance, metabolic syndrome, and type 2 diabetes, although the causal mechanism is not fully understood. [10] [4] [5]

Causes

Magnesium deficiency may result from gastrointestinal or kidney causes. Gastrointestinal causes include low dietary intake of magnesium, reduced gastrointestinal absorption or increased gastrointestinal loss due to rapid gastrointestinal transits. Kidney causes involve increased excretion of magnesium. Poor dietary intake of magnesium has become an increasingly important factor: many people consume diets high in refined foods such as white bread and polished rice which have been stripped of magnesium-rich plant fiber. [11]

Magnesium deficiency is common in hospitalized patients. Up to 12% of all people admitted to hospital, and as high as 60–65% of people in an intensive care unit (ICU), have hypomagnesemia. [12]

About 57% of the US population does not meet the US RDA for dietary intake of magnesium. [13] Kidneys are very efficient at maintaining body levels; however, if the diet is deficient, or certain medications such as diuretics or proton pump inhibitors are used, [14] or in chronic alcoholism, [15] levels may drop.

Deficiencies may be due to the following conditions:

Medications

Genetics

Metabolic abnormalities

Other

Pathophysiology

Magnesium is ubiquitous in the human body as well as being present in all living organisms and the ion is a known co-factor in over known 300 enzymatic reactions including DNA and RNA replication, protein synthesis, acting as an essential co-factor of ATP during its phosphorylation via ATPase. It is also extensively involved in intracellular signaling. [20] [25] It is involved in protein synthesis, regulating glucose, lipid and protein metabolism, muscle and nerve functioning, vascular tone (affecting blood vessel contraction, thus helping to regulate blood pressure), bone development, energy production, the maintenance of normal heart rhythm, and the regulation of glucose, among other important roles. [15] [25] Physiologically, it acts as a calcium antagonist. [25] Thus, the effects of low magnesium are widespread. Low magnesium intake over time can increase the risk of illnesses, including high blood pressure and heart disease, diabetes mellitus type 2, osteoporosis, and migraines. [15]

Magnesium has several effects:

Potassium

Low potassium levels are usually associated with hypomagnesemia. Low magnesium levels act to inhibit the sodium-potassium pump (Na-K-ATPase) which normally pumps sodium to the extracellular space and potassium into the intracellular space, using ATP as energy to pump both cations against their concentration gradient, to maintain relatively high levels of potassium in the intracellular compartment and high levels of sodium in the extracellular space. [25] Hypomagnesemia also causes activation of the Renal outer medullary potassium channel (ROMK), a potassium channel which causes potassium losses in the urine via the cortical collecting duct in the kidney. [25] And hypomagnesemia prevents low potassium levels from activating the sodium-chloride cotransporter (NCC) and downregulates NCC levels, which prevents sodium and chloride reabsorption from the kidney tubule. [25] The inhibition of the sodium-potassium pump results in more potassium remaining in the extracellular space (interstitial fluid and plasma). And this potassium is then lost as blood is filtered in the kidney as ROMK channel activation causes potassium losses in the cortical collecting duct and NCC inhibition causes decreased sodium-chloride reabsorption by kidney tubules, with subsequent increased sodium-chloride (and water) delivery to the distal tubule, and associated diuresis and kaliuresis (kidney potassium loss in the urine). [25] Overall, the net effect of low magnesium levels in the body is renal potassium losses (in the urine), thus clinically, low potassium levels are often refractory to supplementation without also correcting low magnesium levels. [25] [31]

Patients with diabetic ketoacidosis should have their magnesium levels monitored to ensure that the serum loss of potassium, which is driven intracellularly by insulin administration, is not exacerbated by additional urinary losses. [ citation needed ]

Calcium

Release of calcium from the sarcoplasmic reticulum is inhibited by magnesium. Thus hypomagnesemia results in an increased intracellular calcium level. This inhibits the release of parathyroid hormone, which can result in hypoparathyroidism and hypocalcemia. Furthermore, it makes skeletal and muscle receptors less sensitive to parathyroid hormone. [12]

Arrhythmia

Magnesium is needed for the adequate function of the Na+/K+-ATPase pumps in cardiac myocytes, the muscles cells of the heart. A lack of magnesium inhibits reuptake of potassium, causing a decrease in intracellular potassium. This decrease in intracellular potassium results in tachycardia.[ citation needed ]

Pre-eclampsia

Magnesium has an indirect antithrombotic effect upon platelets and endothelial function. Magnesium increases prostaglandins, decreases thromboxane, and decreases angiotensin II, microvascular leakage, and vasospasm through its function similar to calcium channel blockers.[ citation needed ] Convulsions are the result of cerebral vasospasm. The vasodilatatory effect of magnesium seems to be the major mechanism.

Asthma

Magnesium exerts a bronchodilatatory effect, probably by antagonizing calcium-mediated bronchoconstriction. [32]

Neurological effects

Diabetes mellitus

Magnesium deficiency is frequently observed in people with type 2 diabetes mellitus, with an estimated prevalence ranging between 11 and 48%. [33] Magnesium deficiency is strongly associated with high glucose and insulin resistance, which indicate that it is common in poorly controlled diabetes. [34] Patients with type 2 diabetes and a magnesium deficiency have a higher risk of heart failure, atrial fibrillation and microvascular complications. [35] Oral magnesium supplements has been demonstrated to improve insulin sensitivity and lipid profile. [36] [37] [38] A 2016 meta-analysis not restricted to diabetic subjects found that increasing dietary magnesium intake, while associated with a reduced risk of stroke, heart failure, diabetes, and all-cause mortality, was not clearly associated with lower risk of coronary heart disease (CHD) or total cardiovascular disease (CVD). [39]

Homeostasis

Magnesium rich foods include cereals, green vegetables (with magnesium being a main component of chlorophyll), beans, and nuts. [25] It is absorbed primarily in the small intestine via paracellular transport; passing between intestinal cells. Magnesium absorption in the large intestine is mediated by the transporters TRPM6 and TRPM7. [25]

The body contains about 25 grams of magnesium. [25] Of the body's magnesium, 50-60% is stored in bone, with the remainder, about 40-50%, being stored in muscle or soft tissue, with about 1% being in the plasma. [40] Therefore, normal plasma levels of magnesium may sometimes be seen despite a person being in a state of magnesium deficiency and plasma magnesium levels may underestimate the level of deficiency. Plasma magnesium levels may more accurately reflect magnesium stores when consideration is also given to urinary magnesium losses and oral intake of magnesium. [25]

Inside cells, 90-95% of magnesium is bound to ligands, including ATP, ADP, citrate, other proteins and nucleic acids. [25] In the plasma, 30% of magnesium is bound to proteins via free fatty acids, therefore elevated levels of free fatty acids are associated with hypomagnesemia as well as a possible risk of cardiovascular disease. [25]

The kidneys regulate magnesium levels by reabsorbing magnesium from the tubules. In the proximal tubule (at the beginning of the nephron, the functional unit of the kidney) 20% of magnesium is reabsorbed via paracellular transport with claudin 2 and claudin 12 forming channels to allow for reabsorption. [25] 70% of magnesium is reabsorbed in the thick ascending limb of the loop of Henle where claudins 16 and 19 form the channels to allow for reabsorption. [25] In the distal convoluted tubule, 5-10% of magnesium is reabsorbed transcellularly (through the cells) via the transporters TRPM6 and TRPM7. Epidermal growth factor and insulin activate TRPM6 and 7 and increase magnesium levels via increased renal reabsorption. [25]

Diagnosis

Magnesium deficiency or depletion is a low total body level of magnesium; it is not easy to measure directly. [41]

Blood magnesium

Typically the diagnosis is based on finding hypomagnesemia, a low blood magnesium level, [42] which often reflects low body magnesium; [6] however, magnesium deficiency can be present without hypomagnesemia, and vice versa. [41] A plasma magnesium concentration of less than 0.6 mmol/L (1.46 mg/dL) is considered to be hypomagnesemia; [1] severe disease generally has a level of less than 0.5 mmol/L (1.25 mg/dL). [2]

Electrocardiogram

The electrocardiogram (ECG) change may show a tachycardia with a prolonged QT interval. [43] Other changes may include prolonged PR interval, ST segment depression, flipped T waves, and long QRS duration. [1]

Treatments

Treatment of magnesium deficiency depends on the degree of deficiency and the clinical effects. Replacement by mouth is appropriate for people with mild symptoms, while intravenous replacement is recommended for people with severe effects. [44]

Numerous oral magnesium preparations are available. In two trials of magnesium oxide, one of the most common forms in magnesium dietary supplements because of its high magnesium content per weight, was found to be less bioavailable than magnesium citrate, chloride, lactate or aspartate. [45] [46] Amino-acid chelate was also less bioavailable. [47]

Intravenous magnesium sulfate (MgSO4) can be given in response to heart arrhythmias to correct for hypokalemia, preventing pre-eclampsia, and has been suggested as having a potential use in asthma. [1]

Food

Food sources of magnesium include leafy green vegetables, beans, nuts, and seeds. [48]

Epidemiology

Hypomagnesemia may be seen in 3-10% of the general population. [25] It is present in an estimated 10-30% of people with diabetes, 10-60% of hospitalized people and greater than 65% of people in the ICU. [25] [2] In hospitalized patients, hypomagnesemia is associated with an increased length of stay. And in those in an ICU, it is associated with a higher risk of requiring mechanical ventilation, and death. [49] [50] In population based cohort studies, chronic magnesium deficiency was associated with an increased risk of cardiovascular death and overall death. [25] [51]

History

Magnesium deficiency in humans was first described in the medical literature in 1934. [52]

Plants

A plant with magnesium deficiency Frangula alnus with magnesium deficiency.jpg
A plant with magnesium deficiency

Magnesium deficiency is a detrimental plant disorder that occurs most often in strongly acidic, light, sandy soils, where magnesium can be easily leached away. Magnesium is an essential macronutrient constituting 0.2-0.4% of plants' dry matter and is necessary for normal plant growth. [53] Excess potassium, generally due to fertilizers, further aggravates the stress from magnesium deficiency, [54] as does aluminium toxicity. [55]

Magnesium has an important role in photosynthesis because it forms the central atom of chlorophyll. [53] Therefore, without sufficient amounts of magnesium, plants begin to degrade the chlorophyll in the old leaves. This causes the main symptom of magnesium deficiency, interveinal chlorosis, or yellowing between leaf veins, which stay green, giving the leaves a marbled appearance. Due to magnesium's mobile nature, the plant will first break down chlorophyll in older leaves and transport the Mg to younger leaves which have greater photosynthetic needs. Therefore, the first sign of magnesium deficiency is the chlorosis of old leaves which progresses to the young leaves as the deficiency progresses. [56] Magnesium also acts as an activator for many critical enzymes, including ribulosebisphosphate carboxylase (RuBisCO) and phosphoenolpyruvate carboxylase (PEPC), both essential enzymes in carbon fixation. Thus low amounts of Mg lead to a decrease in photosynthetic and enzymatic activity within the plants. Magnesium is also crucial in stabilizing ribosome structures, hence, a lack of magnesium causes depolymerization of ribosomes leading to premature aging of the plant. [53] After prolonged magnesium deficiency, necrosis and dropping of older leaves occurs. Plants deficient in magnesium also produce smaller, woodier fruits.

Magnesium deficiency in plants may be confused with zinc or chlorine deficiencies, viruses, or natural aging, since all have similar symptoms. Adding Epsom salts (as a solution of 25 grams per liter or 4 oz per gal) or crushed dolomitic limestone to the soil can rectify magnesium deficiencies. An organic treatment is to apply compost mulch, which can prevent leaching during excessive rainfall and provide plants with sufficient amounts of nutrients, including magnesium. [57]

See also

Related Research Articles

<span class="mw-page-title-main">Diabetes insipidus</span> Condition characterized by large amounts of dilute urine and increased thirst

Diabetes insipidus (DI), alternately called arginine vasopressin deficiency (AVP-D) or arginine vasopressin resistance (AVP-R), is a condition characterized by large amounts of dilute urine and increased thirst. The amount of urine produced can be nearly 20 liters per day. Reduction of fluid has little effect on the concentration of the urine. Complications may include dehydration or seizures.

<span class="mw-page-title-main">Aldosterone</span> Mineralocorticoid steroid hormone

Aldosterone is the main mineralocorticoid steroid hormone produced by the zona glomerulosa of the adrenal cortex in the adrenal gland. It is essential for sodium conservation in the kidney, salivary glands, sweat glands, and colon. It plays a central role in the homeostatic regulation of blood pressure, plasma sodium (Na+), and potassium (K+) levels. It does so primarily by acting on the mineralocorticoid receptors in the distal tubules and collecting ducts of the nephron. It influences the reabsorption of sodium and excretion of potassium (from and into the tubular fluids, respectively) of the kidney, thereby indirectly influencing water retention or loss, blood pressure, and blood volume. When dysregulated, aldosterone is pathogenic and contributes to the development and progression of cardiovascular and kidney disease. Aldosterone has exactly the opposite function of the atrial natriuretic hormone secreted by the heart.

<span class="mw-page-title-main">Magnesium in biology</span> Use of Magnesium by organisms

Magnesium is an essential element in biological systems. Magnesium occurs typically as the Mg2+ ion. It is an essential mineral nutrient (i.e., element) for life and is present in every cell type in every organism. For example, adenosine triphosphate (ATP), the main source of energy in cells, must bind to a magnesium ion in order to be biologically active. What is called ATP is often actually Mg-ATP. As such, magnesium plays a role in the stability of all polyphosphate compounds in the cells, including those associated with the synthesis of DNA and RNA.

<span class="mw-page-title-main">Hydrochlorothiazide</span> Diuretic medication

Hydrochlorothiazide, sold under the brand name Hydrodiuril among others, is a diuretic medication used to treat hypertension and swelling due to fluid build-up. Other uses include treating diabetes insipidus and renal tubular acidosis and to decrease the risk of kidney stones in those with a high calcium level in the urine. Hydrochlorothiazide is taken by mouth and may be combined with other blood pressure medications as a single pill to increase effectiveness. Hydrochlorothiazide is a thiazide medication which inhibits reabsorption of sodium and chloride ions from the distal convoluted tubules of the kidneys, causing a natriuresis. This initially increases urine volume and lowers blood volume. It is believed to reduce peripheral vascular resistance.

<span class="mw-page-title-main">Hyperkalemia</span> Excess potassium in the blood

Hyperkalemia is an elevated level of potassium (K+) in the blood. Normal potassium levels are between 3.5 and 5.0 mmol/L (3.5 and 5.0 mEq/L) with levels above 5.5 mmol/L defined as hyperkalemia. Typically hyperkalemia does not cause symptoms. Occasionally when severe it can cause palpitations, muscle pain, muscle weakness, or numbness. Hyperkalemia can cause an abnormal heart rhythm which can result in cardiac arrest and death.

<span class="mw-page-title-main">Electrolyte imbalance</span> Abnormality in the concentration of electrolytes in the body

Electrolyte imbalance, or water-electrolyte imbalance, is an abnormality in the concentration of electrolytes in the body. Electrolytes play a vital role in maintaining homeostasis in the body. They help to regulate heart and neurological function, fluid balance, oxygen delivery, acid–base balance and much more. Electrolyte imbalances can develop by consuming too little or too much electrolyte as well as excreting too little or too much electrolyte. Examples of electrolytes include calcium, chloride, magnesium, phosphate, potassium, and sodium.

<span class="mw-page-title-main">Hypokalemia</span> Medical condition with insufficient potassium

Hypokalemia is a low level of potassium (K+) in the blood serum. Mild low potassium does not typically cause symptoms. Symptoms may include feeling tired, leg cramps, weakness, and constipation. Low potassium also increases the risk of an abnormal heart rhythm, which is often too slow and can cause cardiac arrest.

<span class="mw-page-title-main">Loop diuretic</span> Diuretics that act along the loop of Henle in the kidneys

Loop diuretics are pharmacological agents that primarily inhibit the Na-K-Cl cotransporter located on the luminal membrane of cells along the thick ascending limb of the loop of Henle. They are often used for the treatment of hypertension and edema secondary to congestive heart failure, liver cirrhosis, or chronic kidney disease. While thiazide diuretics are more effective in patients with normal kidney function, loop diuretics are more effective in patients with impaired kidney function.

<span class="mw-page-title-main">Amiloride</span> Medication

Amiloride, sold under the trade name Midamor among others, is a medication typically used with other medications to treat high blood pressure or swelling due to heart failure or cirrhosis of the liver. Amiloride is classified as a potassium-sparing diuretic. Amiloride is often used together with another diuretic, such as a thiazide or loop diuretic. It is taken by mouth. Onset of action is about two hours and it lasts for about a day.

<span class="mw-page-title-main">Chlortalidone</span> Thiazide-like diuretic drug

Chlortalidone, also known as chlorthalidone, is a thiazide-like diuretic drug used to treat high blood pressure, swelling, diabetes insipidus, and renal tubular acidosis. Because chlortalidone is effective in most patients with high blood pressure, it is considered a preferred initial treatment. It is also used to prevent calcium-based kidney stones. It is taken by mouth. Effects generally begin within three hours and last for up to three days. Long-term treatment with chlortalidone is more effective than hydrochlorothiazide for prevention of heart attack or stroke.

<span class="mw-page-title-main">Thiazide</span> Class of chemical compounds

Thiazide refers to both a class of sulfur-containing organic molecules and a class of diuretics based on the chemical structure of benzothiadiazine. The thiazide drug class was discovered and developed at Merck and Co. in the 1950s. The first approved drug of this class, chlorothiazide, was marketed under the trade name Diuril beginning in 1958. In most countries, thiazides are the least expensive antihypertensive drugs available.

<span class="mw-page-title-main">Glycosuria</span> Medical condition

Glycosuria is the excretion of glucose into the urine. Ordinarily, urine contains no glucose because the kidneys are able to reabsorb all of the filtered glucose from the tubular fluid back into the bloodstream. Glycosuria is nearly always caused by an elevated blood sugar level, most commonly due to untreated diabetes. Rarely, glycosuria is due to an intrinsic problem with glucose reabsorption within the kidneys, producing a condition termed renal glycosuria. Glycosuria leads to excessive water loss into the urine with resultant dehydration, a process called osmotic diuresis.

<span class="mw-page-title-main">Gitelman syndrome</span> Genetic kidney disorder

Gitelman syndrome (GS) is an autosomal recessive kidney tubule disorder characterized by low blood levels of potassium and magnesium, decreased excretion of calcium in the urine, and elevated blood pH. It is the most frequent hereditary salt-losing tubulopathy. Gitelman syndrome is caused by disease-causing variants on both alleles of the SLC12A3 gene. The SLC12A3 gene encodes the thiazide-sensitive sodium-chloride cotransporter, which can be found in the distal convoluted tubule of the kidney.

<span class="mw-page-title-main">Metabolic alkalosis</span> Increase in blood pH due to imbalance in hydrogen ion and bicarbonate concentrations

Metabolic alkalosis is an acid-base disorder in which the pH of tissue is elevated beyond the normal range (7.35–7.45). This is the result of decreased hydrogen ion concentration, leading to increased bicarbonate, or alternatively a direct result of increased bicarbonate concentrations. The condition typically cannot last long if the kidneys are functioning properly.

<span class="mw-page-title-main">Metolazone</span> Chemical compound

Metolazone is a thiazide-like diuretic marketed under the brand names Zytanix, Metoz, Zaroxolyn, and Mykrox. It is primarily used to treat congestive heart failure and high blood pressure. Metolazone indirectly decreases the amount of water reabsorbed into the bloodstream by the kidney, so that blood volume decreases and urine volume increases. This lowers blood pressure and prevents excess fluid accumulation in heart failure. Metolazone is sometimes used together with loop diuretics such as furosemide or bumetanide, but these highly effective combinations can lead to dehydration and electrolyte abnormalities.

<span class="mw-page-title-main">Bartter syndrome</span> Medical condition

Bartter syndrome (BS) is a rare inherited disease characterised by a defect in the thick ascending limb of the loop of Henle, which results in low potassium levels (hypokalemia), increased blood pH (alkalosis), and normal to low blood pressure. There are two types of Bartter syndrome: neonatal and classic. A closely associated disorder, Gitelman syndrome, is milder than both subtypes of Bartter syndrome.

<span class="mw-page-title-main">Milk-alkali syndrome</span> Medical condition

Milk-alkali syndrome (MAS), also referred to as calcium-alkali syndrome, is the third most common cause of hypercalcemia. Milk-alkali syndrome is characterized by elevated blood calcium levels, metabolic alkalosis, and acute kidney injury.

<span class="mw-page-title-main">Dent's disease</span> Medical condition

Dent's disease is a rare X-linked recessive inherited condition that affects the proximal renal tubules of the kidney. It is one cause of Fanconi syndrome, and is characterized by tubular proteinuria, excess calcium in the urine, formation of calcium kidney stones, nephrocalcinosis, and chronic kidney failure.

A renal diet is a diet aimed at keeping levels of fluids, electrolytes, and minerals balanced in the body in individuals with chronic kidney disease or who are on dialysis. Dietary changes may include the restriction of fluid intake, protein, and electrolytes including sodium, phosphorus, and potassium. Calories may also be supplemented if the individual is losing weight undesirably.

<span class="mw-page-title-main">Idiopathic hypercalcinuria</span>

Idiopathic hypercalcinuria (IH) is a condition including an excessive urinary calcium level with a normal blood calcium level resulting from no underlying cause. IH has become the most common cause of hypercalciuria and is the most serious metabolic risk factor for developing nephrolithiasis. IH can predispose individuals to osteopenia or osteoporosis, and affects the entire body. IH arises due to faulty calcium homeostasis, a closely monitored process, where slight deviations in calcium transport in the intestines, blood, and bone can lead to excessive calcium excretion, bone mineral density loss, or kidney stone formation. 50%-60% of nephrolithiasis patients suffer from IH and have 5%-15% lower bone density than those who do not.

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