hypokalemia

What is Hypokalemia

Hypokalemia or low potassium refers to a lower than normal potassium level in your bloodstream. Fortunately, most hypokalemia cases are mild. Potassium is an electrolyte (mineral). Potassium is the most abundant intracellular cation, is an essential nutrient that is naturally present in many foods and available as a dietary supplement. Potassium is present in all body tissues and is required for normal cell function because of its role in maintaining intracellular fluid volume and transmembrane electrochemical gradients 1. Potassium has a strong relationship with sodium, the main regulator of extracellular fluid volume, including plasma volume. Potassium helps carry electrical signals to cells in your body. It is critical to the proper functioning of nerve and muscles cells, particularly heart muscle cells. You get potassium through food. Your kidneys help to keep the right amount of potassium in your body. If you have chronic kidney disease, your kidneys may not remove extra potassium from the blood. Some medicines also can raise your potassium level. You may need a special diet to lower the amount of potassium that you eat.

Your body needs potassium to:

  • Build proteins
  • Break down and use carbohydrates
  • Build muscle
  • Maintain normal body growth
  • Control the electrical activity of the heart
  • Control the acid-base balance

Many people get all the potassium they need from what they eat and drink. Sources of potassium in the diet include:

  • Leafy greens, such as spinach and collards
  • Fruit from vines, such as grapes and blackberries
  • Root vegetables, such as carrots and potatoes
  • Citrus fruits, such as oranges and grapefruit

Hypokalemia is rarely caused by low dietary potassium intake alone, but it can result from diarrhea due to potassium losses in the stool. It can also result from vomiting, which produces metabolic alkalosis, leading to potassium losses in the kidneys. Hypokalemia can also be caused by refeeding syndrome (the metabolic response to initial refeeding after a starvation period) because of potassium’s movement into cells; laxative abuse; diuretic use; eating clay (a type of pica); heavy sweating; or dialysis 2.

The total amount of potassium in the adult body is about 45 millimole (mmol)/kg body weight (about 140 g for a 175 pound adult; 1 mmol = 1 milliequivalent [mEq] or 39.1 mg potassium) 3. Most potassium resides intracellularly, and a small amount is in extracellular fluid 4. The intracellular concentration of potassium is about 30 times higher than the extracellular concentration, and this difference forms a transmembrane electrochemical gradient that is maintained via the sodium-potassium (Na+/K+) ATPase transporter 4. In addition to maintaining cellular tonicity, this gradient is required for proper nerve transmission, muscle contraction, and kidney function.

Normally, your blood potassium level is 3.6 to 5.2 millimoles per liter (mmol/L). Although there is a slight variation, an acceptable lower limit for normal serum potassium is 3.5 mmol/L. Severity of hypokalemia is categorized as mild when the serum potassium level is 3 to 3.4 mmol/L, moderate hypokalemia when the serum potassium level is 2.5 to 3 mmol/L, and severe hypokalemia is when the serum potassium level is less than 2.5 mmol/L 5. A very low potassium level (less than 2.5 mmol/L) can be life-threatening and requires urgent medical attention.

Values obtained from plasma and serum may differ. Therefore, it is important to know the sampling source. Compared to plasma levels, serum levels are usually slightly higher due to delays in processing and/or the effect of clotting 6.

A variety of causes can result in hypokalemia. These causes can be placed into the following categories:

  1. Decreased potassium intake
  2. Transcellular shifts (increased intracellular uptake)
  3. Increased potassium loss (skin, gastrointestinal, and renal losses)

In general, hypokalemia is associated with diagnoses of cardiac disease, renal failure, malnutrition, and shock. Hypothermia and increased blood cell production (for example, leukemia) are additional risk factors for developing hypokalemia. There are subsets of patients that are susceptible to the development of hypokalemia. For instance, psychiatric patients are at risk for hypokalemia due to their drug therapy. Hypokalemia is also prevalent in hospitalized patients, in particular, pediatric patients, those who have a fever and those who are critically ill. Additionally, in developing countries, an increased risk of mortality is observed in children when severe hypokalemia is associated with diarrhea and severe malnutrition.

Potassium Food Sources

Many foods contain potassium. All meats (red meat and chicken) and fish such as salmon, cod, flounder, and sardines are good sources of potassium. Soy products and veggie burgers are also good sources of potassium.

Vegetables including broccoli, peas, lima beans, tomatoes, potatoes (particularly their skins), sweet potatoes, and winter squash are all good sources of potassium.

Fruits that contain significant amounts of potassium include citrus fruits, cantaloupe, bananas, kiwi, prunes, and apricots. Dried apricots contain more potassium than fresh apricots.

Milk, yogurt, and nuts are also excellent sources of potassium.

People with kidney problems, particularly those on dialysis, should not eat too many potassium-rich foods. The health care provider will recommend a special diet.

It is estimated that the body absorbs about 85%–90% of dietary potassium 7. The forms of potassium in fruits and vegetables include potassium phosphate, sulfate, citrate, and others, but not potassium chloride (the form used in salt substitutes and some dietary supplements) 8.

Selected food sources of potassium are listed in Table 2.

The Food and Nutrition Center of the Institute of Medicine recommends these dietary intakes for potassium, based on age:

INFANTS

  • 0 to 6 months: 0.4 grams a day (g/day)
  • 7 to 12 months: 0.7 g/day

CHILDREN and ADOLESCENTS

  • 1 to 3 years: 3 g/day
  • 4 to 8 years: 3.8 g/day
  • 9 to 13 years: 4.5 g/day
  • 14 to 18 years: 4.7 g/day

ADULTS

  • Age 19 years and older: 4.7 g/day

Women who are producing breast milk need slightly higher amounts (5.1 g/day). Ask your doctor what amount is best for you.

Table 1. Adequate Intakes (AIs) for Potassium*

AgeMaleFemalePregnancyLactation
Birth to 6 months400 mg400 mg
7–12 months860 mg860 mg
1–3 years2,000 mg2,000 mg
4–8 years2,300 mg2,300 mg
9–13 years2,500 mg2,300 mg
14–18 years3,000 mg2,300 mg2,600 mg2,500 mg
19–50 years3,400 mg2,600 mg2,900 mg2,800 mg
51+ years3,400 mg2,600 mg

Footnote: *The Adequate Intakes (AIs) do not apply to individuals with impaired potassium excretion because of medical conditions (e.g., kidney disease) or the use of medications that impair potassium excretion.

[Source 9 ]

Table 2. Selected Food Sources of Potassium

FoodMilligrams
(mg) per
serving
Percent
DV*
Apricots, dried, ½ cup1,10131
Lentils, cooked, 1 cup73121
Prunes, dried, ½ cup69920
Squash, acorn, mashed, 1 cup64418
Raisins, ½ cup61818
Potato, baked, flesh only, 1 medium61017
Kidney beans, canned, 1 cup60717
Orange juice, 1 cup49614
Soybeans, mature seeds, boiled, ½ cup44313
Banana, 1 medium42212
Milk, 1%, 1 cup36610
Spinach, raw, 2 cups33410
Chicken breast, boneless, grilled, 3 ounces3329
Yogurt, fruit variety, nonfat, 6 ounces3309
Salmon, Atlantic, farmed, cooked, 3 ounces3269
Beef, top sirloin, grilled, 3 ounces3159
Molasses, 1 tablespoon3089
Tomato, raw, 1 medium2928
Soymilk, 1 cup2878
Yogurt, Greek, plain, nonfat, 6 ounces2407
Broccoli, cooked, chopped, ½ cup2297
Cantaloupe, cubed, ½ cup2146
Turkey breast, roasted, 3 ounces2126
Asparagus, cooked, ½ cup2026
Apple, with skin, 1 medium1956
Cashew nuts, 1 ounce1875
Rice, brown, medium-grain, cooked, 1 cup1544
Tuna, light, canned in water, drained, 3 ounces1534
Coffee, brewed, 1 cup1163
Lettuce, iceberg, shredded, 1 cup1023
Peanut butter, 1 tablespoon903
Tea, black, brewed, 1 cup883
Flaxseed, whole, 1 tablespoon842
Bread, whole-wheat, 1 slice812
Egg, 1 large692
Rice, white, medium-grain, cooked, 1 cup542
Bread, white, 1 slice371
Cheese, mozzarella, part skim, 1½ ounces361
Oil (olive, corn, canola, or soybean), 1 tablespoon00

Footnotes: *DV = Daily Value. The U.S. Food and Drug Administration (FDA) developed DVs to help consumers compare the nutrient contents of products within the context of a total diet. The DV for potassium used for the values in Table 1 is 3,500 mg for adults and children aged 4 and older 10. This Daily Value, however, is changing to 4,700 mg as the updated Nutrition and Supplement Facts labels are implemented 11. The updated labels and DVs must appear on food products and dietary supplements beginning in January 2020, but they can be used now 12. FDA does not currently require food labels to list potassium content unless a food has been fortified with this nutrient, but they do require potassium content to be listed on the updated label. Foods providing 20% or more of the Daily Value are considered to be high sources of a nutrient, but foods providing lower percentages of the Daily Value also contribute to a healthful diet.

[Source 9 ]

People who are being treated for hypokalemia may need potassium supplements. Your doctor will develop a supplementation plan based on your specific needs.

Note: If you have kidney disease or other long-term (chronic) illnesses, it is important that you talk to your provider before taking potassium supplements.

What causes hypokalemia?

Low potassium (hypokalemia) has many causes. The most common cause is excessive potassium loss in urine due to prescription medications that increase urination. Also known as water pills or diuretics, these types of medications are often prescribed for people who have high blood pressure or heart disease.

Vomiting, diarrhea or both also can result in excessive potassium loss from the digestive tract. Occasionally, low potassium is caused by not getting enough potassium in your diet.

Common causes of hypokalemia include:

  • Alcohol use (excessive)
  • Chronic kidney disease
  • Diabetic ketoacidosis
  • Diarrhea
  • Eating disorders (such as bulimia)
  • Excessive laxative use, which can cause diarrhea
  • Excessive sweating
  • Folic acid deficiency
  • Genetic disorders, such as hypokalemic periodic paralysis, Bartter syndrome
  • Low magnesium level
  • Medicines, such as diuretics (water pills) and certain antibiotics
  • Primary aldosteronism
  • Some antibiotic use
  • Sweating
  • Vomiting

Magnesium depletion can contribute to hypokalemia by increasing urinary potassium losses 13. It can also increase the risk of cardiac arrhythmias by decreasing intracellular potassium concentrations. More than 50% of individuals with clinically significant hypokalemia might have magnesium deficiency 14. In people with hypomagnesemia and hypokalemia, both should be treated concurrently 15.

Groups at risk of hypokalemia

Potassium inadequacy can occur with intakes that are below the AI but above the amount required to prevent hypokalemia. The following groups are more likely than others to have poor potassium status.

People with inflammatory bowel diseases

Potassium is secreted within the colon, and this process is normally balanced by absorption 16. However, in inflammatory bowel disease (including Crohn’s disease and ulcerative colitis), potassium secretion increases, which can lead to poor potassium status. Inflammatory bowel diseases are also characterized by chronic diarrhea, which can further increase potassium excretion 17.

People who use certain medications, including diuretics and laxatives

Certain diuretics (e.g., thiazide diuretics) that are commonly used to treat high blood pressure increase urinary potassium excretion and can cause hypokalemia 15. Potassium- sparing diuretics, however, do not increase potassium excretion and can actually cause hyperkalemia. Large doses of laxatives and repeated use of enemas can also cause hypokalemia because they increase losses of potassium in stool.

People with pica

Pica is the persistent eating of non-nutritive substances, such as clay. When consumed, clay binds potassium in the gastrointestinal tract, which can increase potassium excretion and lead to hypokalemia 2. Cessation of pica combined with potassium supplementation can restore potassium status and resolve symptoms of potassium deficiency.

Hypokalemia pathophysiology

Potassium is predominantly intracellular where it is the most abundant cation and involved in cell regulation and several cellular processes. The fraction of potassium in the extracellular fluid is small. Therefore, plasma or serum levels are not a reliable indicator of total body potassium stores. Potassium homeostasis is maintained through a combination of adjustments in acute cellular shifts between the extracellular and intracellular fluid compartments, renal excretion and, to a lesser extent, gastrointestinal losses.

Hypokalemia can occur as a result of decreased potassium intake, transcellular shifts (increased intracellular uptake) or increased potassium loss (skin, gastrointestinal and renal losses). Decreased potassium intake, in isolation, rarely results in hypokalemia due to the ability of the kidneys to effectively minimize potassium excretion. However, reduced intake can be a contributor to hypokalemia in the presence of other causes, such as malnutrition or diuretic therapy. Cellular uptake of potassium is promoted by alkalemia, insulin, beta-adrenergic stimulation, aldosterone and xanthines, such as caffeine. Most cases of hypokalemia result from gastrointestinal (GI) or renal losses. Renal potassium losses are associated with increased mineralocorticoid-receptor stimulation such as occurs with primary hyperreninism and primary aldosteronism. Increased delivery of sodium and/or non-absorbable ions (diuretic therapy, magnesium deficiency, genetic syndromes) to the distal nephron can also result in renal potassium wasting. gastrointestinal losses are a common cause of hypokalemia with severe or chronic diarrhea being the most common extrarenal cause of hypokalemia 18.

Hypokalemia signs and symptoms

In most cases, hypokalemia is found by a blood test that is done because of an illness, or because you are taking diuretics. It is rare for hypokalemia to cause isolated symptoms such as muscle cramps if you are feeling well in other respects. Clinical symptoms of hypokalemia do not become evident until the serum potassium level is less than 3 mmol/L unless there is a precipitous fall or the patient has a process that is potentiated by hypokalemia. The severity of symptoms also tends to be proportional to the degree and duration of hypokalemia. Symptoms resolve with correction of the hypokalemia.

Significant muscle weakness occurs at serum potassium levels below 2.5 mmol/L but can occur at higher levels if the onset is acute. Similar to the weakness associated with hyperkalemia, the pattern is ascending in nature affecting the lower extremities, progressing to involve the trunk and upper extremities and potentially advancing to paralysis. Affected muscles can include the muscles of respiration which can lead to respiratory failure and death. Involvement of GI muscles can cause an ileus with associated symptoms of nausea, vomiting, and abdominal distension. Severe hypokalemia can also lead to muscle cramps, rhabdomyolysis, and resultant myoglobinuria. Periodic paralysis is a rare neuromuscular disorder, which is inherited or acquired, that is caused by an acute transcellular shift of potassium into the cells. It is characterized by potentially fatal episodes of muscle weakness or paralysis that can affect the respiratory muscles.

Hypokalemia can result in a variety of cardiac dysrhythmias. Although cardiac dysrhythmias or ECG changes are more likely to be associated with moderate to severe hypokalemia, there is a high degree of individual variability and can occur with even mild decreases in serum levels. This variability is dependent on concomitant factors such as magnesium depletion, digitalis therapy, among others. Moreover, characteristic ECG changes do not manifest in all patients. The ECG changes that occur are T-wave flattening initially, followed by ST depression and the appearance of a U wave that can be difficult to distinguish from the T wave. The U wave is often seen in the lateral precordial leads of V4 to V6. Prolongation of the PR and QT interval can also occur. Risk of arrhythmias is highest in older patients, those with heart disease and those receiving digoxin or antiarrhythmic drugs. Administration of anesthesia in the setting of hypokalemia is also a risk for dysrhythmias and impaired cardiac contractility but more so with acute rather than chronic hypokalemia.

Hypomagnesemia often occurs with and may worsen hypokalemia especially in the presence of chronic diarrhea, alcoholism, genetic disorders, diuretic use and chemotherapy. Both promote the development of cardiac dysrhythmias. The combination of hypokalemia and hypomagnesemia are associated with an increased risk of torsades de pointes, particularly in individuals receiving QT-prolonging medications. Additionally, hypomagnesemia can increase urinary potassium losses thus lowering the serum potassium level, as well as, prevent urinary potassium reabsorption thereby impeding potassium repletion.

Lastly, prolonged hypokalemia can cause structural and functional changes in the kidney that include impairing concentrating ability, increased ammonia production, altered sodium reabsorption and increased bicarbonate absorption. Hypokalemia can also result in glucose intolerance by reducing insulin secretion.

A small drop in potassium level often does not cause symptoms, which may be mild, and may include:

  • Constipation
  • Feeling of skipped heart beats or palpitations
  • Fatigue
  • Muscle damage
  • Muscle weakness or spasms (cramps)
  • Tingling or numbness

A large drop in potassium level may lead to abnormal heart rhythms, especially in people with heart disease. This can cause you to feel lightheaded or faint. A very low potassium level can even cause your heart to stop.

Hypokalemia complications

Abnormal heart rhythms (arrhythmias) are the most worrisome complication of very low potassium levels, particularly in people with underlying heart disease.

Talk to your doctor about what your blood test results mean. You may need to change a medication that’s affecting your potassium level, or you may need to treat another medical condition that’s causing your low potassium level.

Hypokalemia diagnosis

Your doctor will order a blood test to check your potassium level. Normal range is 3.6 to 5.2 mEq/L (3.6 to 5.2 mmol/L).

Other blood tests may be ordered to check levels of:

  • Glucose, magnesium, calcium, sodium, phosphorous
  • Thyroid hormone
  • Aldosterone

An electrocardiogram (ECG) to check the heart may also be done.

Diagnostic evaluation involves assessment of urinary potassium excretion and assessment of acid-base status. Assessment of urinary potassium excretion can help distinguish renal losses from other causes of hypokalemia. Measurement of potassium excretion is ideally done via a 24-hour urine collection. Excretion of more than 30 mEq of potassium per day indicates inappropriate renal potassium loss. Alternative methods for measurement include a spot urine potassium concentration or urine potassium-to-creatinine ratio. A urine potassium concentration of greater than 15 mmol/L or a ratio greater than 13 mEq/mmol of creatinine, respectively, also indicates inappropriate renal potassium loss. After determining the presence or lack of renal potassium wasting, assessment of acid-base status should then be determined. The existence of metabolic acidosis or alkalosis with or without renal potassium wasting can further narrow the differential diagnosis. Aside from diagnostic evaluation, assessment of serum magnesium level, muscle strength, and electrocardiographic changes is warranted as the latter two would warrant immediate intervention.

Hypokalemia treatment

Treatment of hypokalemia is directed at the underlying cause and may include potassium supplements. Don’t start taking potassium supplements without talking to your doctor first. The overarching goals of therapy for hypokalemia are to prevent or treat life-threatening complications, replace the potassium deficit, and to diagnose and correct the underlying cause.

Therapeutic urgency depends on the severity of hypokalemia, the existence of comorbid conditions and the rate of decline of serum potassium levels. Elucidating the cause of hypokalemia and understanding whether it is secondary to transcellular shifts or a potassium deficit is also essential. Regardless, potassium replacement is indicated in most cases of hypokalemia, especially in those related to renal or GI losses. The presence of concomitant hypomagnesemia should also be investigated and corrected if present. In the presence of hypomagnesemia, hypokalemia can be refractory to potassium replacement alone 19.

If your condition is mild, your doctor will likely prescribe oral potassium pills. If your condition is severe, you may need to get potassium through a vein (IV).

Clinical manifestations do not occur with mild to moderate hypokalemia; thus, repletion is not urgent. Mild to moderate hypokalemia is typically treated with oral potassium supplements. Providing 60 to 80 mmol/day in divided doses over days to weeks is usually sufficient. Oral supplementation can irritate GI mucosa leading to bleeding and/or ulceration but is associated with a lower risk of rebound hyperkalemia. It should be taken with plenty of fluids and food. Potassium chloride is the preferred formulation for replacement therapy in most cases. Increasing dietary potassium is not usually adequate to treat hypokalemia because most of the potassium contained in foods is coupled with phosphate. A majority of cases of hypokalemia involve chloride depletion and respond best to replacement with potassium chloride. Intravenous (IV) repletion is administered if oral therapy is not tolerated.

Replacement therapy must be given more rapidly with severe hypokalemia or when clinical symptoms are present. Potassium chloride of 40 mmol given every 3 to 4 hours for 3 doses is preferred. Rapid correction can be provided via oral and/or IV formulation. IV administration is preferred in the setting of cardiac dysrhythmias, digitalis toxicity and recent or ongoing cardiac ischemia. Pain and phlebitis usually occur with peripheral IV infusions when infusion rates exceed 10 mmol per hour. There is also a risk of rebound hyperkalemia when rates exceed a dose of 20 mmol per hour. In general, 20 mmol per hour of potassium chloride will increase serum potassium levels by an average of 0.25 mmol per hour. Potassium should not be given in dextrose-containing solutions because dextrose will stimulate insulin secretion which then exacerbates the hypokalemia. Serum potassium levels should be checked every 2 to 4 hours. Potassium repletion can occur more slowly once the serum potassium level is persistently above 3 mmol/L or clinical symptoms have resolved. Regardless of severity, careful monitoring of serum potassium levels is required as the development of hyperkalemia is common in hospitalized patients.

The potassium deficit varies directly with the severity of hypokalemia. Every decrease in serum concentration of 0.3 mmol/L accounts for a reduction of approximately 100 mmol in total body potassium stores. Accurate quantification is difficult, especially in instances where transcellular shifts are the cause of hypokalemia. Therefore, careful monitoring is required to prevent hyperkalemia from excessive supplementation.

The goal of potassium replacement in the context of renal or GI losses is to immediately raise serum potassium concentration to a safe level and then replace the remaining deficit over days to weeks. A potassium-sparing diuretic should also be considered when the etiology of hypokalemia involves renal potassium wasting as potassium replacement therapy alone may not suffice.

The presence of an acid-base disorder needs to be established as management may differ for etiologies of hypokalemia caused by redistribution of potassium from the extracellular fluid into cells (redistributive hypokalemia). When paralysis or cardiac dysrhythmias are present, in this setting, potassium repletion should be considered. Rebound hyperkalemia is a potential complication of potassium therapy when redistributive hypokalemia is the cause of hypokalemia. As the initial process causing redistribution resolves or is corrected, the transfer of potassium from intracellular to extracellular fluid in conjunction with potassium repletion can result in hyperkalemia. Potassium repletion in patients with periodic paralysis carries a high risk of rebound hyperkalemia. Regardless of etiology, careful monitoring of serum potassium levels is required due to an increased risk of hyperkalemia during replacement therapy.

If you need diuretics, your doctor may:

  • Switch you to a form that keeps potassium in the body. This type of diuretic is called potassium-sparing.
  • Prescribe extra potassium for you to take every day.

Eating foods rich in potassium can help treat and prevent hypokalemia. These foods include:

  • Avocados
  • Baked potato
  • Bananas
  • Bran
  • Carrots
  • Cooked lean beef
  • Milk
  • Oranges
  • Peanut butter
  • Peas and beans
  • Salmon
  • Seaweed
  • Spinach
  • Tomatoes
  • Wheat germ

Hypokalemia side effects

In severe hypokalemia cases, life-threatening paralysis may develop, such as with hypokalemic periodic paralysis.

Hypokalemia prognosis

Taking potassium supplements can usually correct the problem. In severe cases, without proper treatment, a severe drop in potassium level can lead to serious heart rhythm problems that can be fatal.

References
  1. Stone MS, Martyn L, Weaver CM. Potassium intake, bioavailability, hypertension, and glucose control. Nutrients 2016;8
  2. Bailey JL, Sands JM, Franch HA. Water, electrolytes, and acid-based metabolism. In: Ross AC, Caballero B, Cousins RJ, Tucker KL, Ziegler TR, eds. Modern Nutrition in Health and Disease. 11th ed. Baltimore, MD: Lippincott Williams & Wilkins; 2014:102-32.
  3. Preuss HG, Clouatre DL. Sodium, chloride, and potassium. In: Erdman JW, Macdonald IA, Zeisel SH, eds. Present Knowledge in Nutrition. 10th ed. Washington, DC: Wiley-Blackwell; 2012:475-92.
  4. Hinderling PH. The pharmacokinetics of potassium in humans is unusual. J Clin Pharmacol 2016;56:1212-20.
  5. Castro D, Sharma S. Hypokalemia. [Updated 2019 Feb 17]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2019 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK482465
  6. Gallo de Moraes A, Surani S. Effects of diabetic ketoacidosis in the respiratory system. World J Diabetes. 2019 Jan 15;10(1):16-22
  7. Stone MS, Martyn L, Weaver CM. Potassium intake, bioavailability, hypertension, and glucose control. Nutrients 2016;8.
  8. He FJ, MacGregor GA. Beneficial effects of potassium on human health. Physiol Plant 2008;133:725-35
  9. Potassium. https://ods.od.nih.gov/factsheets/Potassium-HealthProfessional
  10. U.S. Food and Drug Administration. Guidance for Industry: A Food Labeling Guide. https://www.fda.gov
  11. U.S. Food and Drug Administration. Food Labeling: Revision of the Nutrition and Supplement Facts Labels Federal Register 81(103):33894-33895. 2016.
  12. U.S. Food and Drug Administration. Food Labeling: Revision of the Nutrition and Supplement Facts Labels and Serving Sizes of Foods That Can Reasonably Be Consumed at One Eating Occasion; Dual-Column Labeling; Updating, Modifying, and Establishing Certain Reference Amounts Customarily Consumed; Serving Size for Breath Mints; and Technical Amendments; Proposed Extension of Compliance Dates. Federal Register 2017;82:45753-6. https://www.federalregister.gov/documents/2017/10/02/2017-21019/food-labeling-revision-of-the-nutrition-and-supplement-facts-labels-and-serving-sizes-of-foods-that
  13. Rude RK. Magnesium. In: Coates PM, Betz JM, Blackman MR, et al., eds. Encyclopedia of Dietary Supplements. 2nd ed. London and New York: Informa Healthcare; 2010:527-37.
  14. Huang CL, Kuo E. Mechanism of hypokalemia in magnesium deficiency. J Am Soc Nephrol 2007;18:2649-52.
  15. Viera AJ, Wouk N. Potassium disorders: Hypokalemia and hyperkalemia. Am Fam Physician 2015;92:487-95
  16. Barkas F, Liberopoulos E, Kei A, Elisaf M. Electrolyte and acid-base disorders in inflammatory bowel disease. Ann Gastroenterol 2013;26:23-8.
  17. Musto D, Rispo A, Testa A, Sasso F, Castiglione F. Hypokalemic myopathy in inflammatory bowel diseases. J Crohns Colitis 2013;7:680.
  18. Shao W, Ayub S, Drutel R, Heise WC, Gerkin R. QTc Prolongation Associated With Psychiatric Medications: A Retrospective Cross-Sectional Study of Adult Inpatients. J Clin Psychopharmacol. 2019 Jan/Feb;39(1):72-77
  19. Skogestad J, Aronsen JM. Hypokalemia-Induced Arrhythmias and Heart Failure: New Insights and Implications for Therapy. Front Physiol. 2018;9:1500
Health Jade