Electrolyte Imbalances in Eating Disorders
Electrolyte disturbances are common and serious medical complications of eating disorders, often caused by food restriction, purging, or malnutrition. This article explains how low potassium, sodium, magnesium, and phosphorus levels can affect the heart, kidneys, muscles, and brain — and how refeeding syndrome increases these risks. See how the providers at ACUTE manage electrolyte imbalances to support a safe recovery.
Eating Disorders & Electrolytes
Eating disorder behaviors such as food restriction and purging can lead to electrolyte imbalances, including potassium, sodium, magnesium and phosphorus deficiencies. These electrolytes are crucial for many vital bodily functions and contribute to the serious complications seen in patients with eating disorders, such as:
- Gastrointestinal problems
- Cardiovascular complications
- Renal (urinary) issues
- Nervous system complications
- Musculoskeletal problems
Electrolyte abnormalities are common in patients with eating disorders, and lab testing can help providers – whether general practitioners or specialists – identify covert eating disorders.
How Do Eating Disorders Cause Electrolyte Problems?
Food restriction
Individuals with eating disorders may restrict their food intake to lose weight or prevent weight gain. Food restriction decreases the intake of essential nutrients – including electrolytes – which are needed for normal cellular and organ function.
Self-induced vomiting
Self-induced vomiting is one of the most common purging methods for individuals with bulimia nervosa and the binge-eating and purging subtype of anorexia nervosa (AN-BP). It causes a direct loss of electrolytes through the expelled stomach contents.
Laxative use
People with eating disorders may misuse laxatives to compensate for food intake. Laxative use speeds up the loss of fluids and electrolytes from the lower gastrointestinal tract.
Diuretic use
Along with laxatives, patients with eating disorders may also use diuretics to purge. Diuretics increase urine production, leading the body to lose significant amounts of water along with essential electrolytes.
Common Electrolyte Problems
Hypokalemia (low potassium)
Hypokalemia is the most common electrolyte abnormality, with about 42% of patients with AN-BP, 14% of patients with the restricting subtype of anorexia nervosa (AN-R), 26% of patients with bulimia nervosa and 22% of patients with other specified feeding or eating disorder (OSFED) having hypokalemia in an inpatient or residential care setting.1
Hypokalemia more commonly develops due to excessive loss of potassium through vomit, stool, or urine without adequate replacement, but it can also occur during the refeeding process. Signs of low potassium can include:
- Constipation
- Nausea and vomiting
- Fatigue
- Heart palpitations or arrhythmias
- Muscle weakness, twitches, or cramps
- Tingling or numbness
- Rhabdomyolysis (muscle breakdown)
- Polyuria (excessive urination)
- Polydipsia (excessive thirst)
Why is potassium important?
Among other vital functions, potassium is the primary intracellular electrolyte that maintains the resting membrane potential of cells in the body, which is especially crucial for muscle and nerve function.
Hyponatremia (low sodium)
Low serum sodium is the second most common electrolyte disorder seen in patients with eating disorders. One study found that 17% of patients with AN-BP, 16% of patients with AN-R, 12% of patients with OSFED and 8.5% with BN experienced hyponatremia.1
Sodium is the main extracellular cation in the body, aiding in maintaining blood volume, cell volume and the function of nerves and muscles. Symptoms of hyponatremia may include:
- Nausea and vomiting
- Headache
- Confusion
- Loss of energy, drowsiness or fatigue
- Restlessness
- Irritability
- Muscle weakness, spasms or cramps
What causes hyponatremia?
Low sodium in eating disorders can be caused by several etiologies:
- Hypovolemia (dehydration from either reduced fluid intake or purging)
- Medications and excessive water intake (primary polydipsia)
Malnutrition is also linked to a decreased ability of the kidneys to excrete free water due to reduced solute intake.
Hypernatremia (high sodium)
Patients with eating disorders are also at risk of developing hypernatremia. This occurs for one of two reasons: either reduced water intake (dehydration) or diabetes insipidus. During refeeding, patients with malnutrition often experience increased urine output, and in severe cases, diabetes insipidus.
Hypomagnesemia (low magnesium)
The development of hypomagnesemia is generally poorly understood, but older studies suggest about a quarter of patients with eating disorders have hypomagnesemia.2 Hypomagnesemia can be caused by decreased oral intake, diarrhea or diuretic misuse.2
Additionally, approximately 16% of patients with anorexia nervosa, bulimia nervosa and OSFED develop hypomagnesemia within an average of 5 days after refeeding.2 Alcohol use disorder, a common co-occurring condition with eating disorder, is also a common cause of hypomagnesemia.
Symptoms of hypomagnesemia may include:
- Tremor
- Ventricular arrhythmias and other cardiac conduction abnormalities
- Nystagmus (abnormal eye movements)
- Muscle spasms and cramps
- Fatigue or weakness
- Abnormal bodily movements
- Confusion
- Seizures
Why is magnesium important?
Magnesium is an intracellular cation, with the largest stores found in bone, serving as a vital cofactor in most enzyme systems and involved in potassium and calcium metabolism. It is essential for muscle, nerve and cardiac function, among others. It is also a cofactor in all bodily reactions utilizing ATP (adenosine triphosphate), the main energy compound in our body that is largely composed of phosphorus.
Hypophosphatemia (low phosphorus)
Low serum phosphate is a key factor in developing refeeding syndrome but can sometimes occur beforehand. About 6% of patients with anorexia nervosa have hypophosphatemia on admission, which predicts hypophosphatemia during refeeding.2
However, the development of hypophosphatemia is most closely related to the lowest body mass index (BMI) on admission.2 A significantly higher number of patients develop hypophosphatemia during nutritional rehabilitation, occurring during the refeeding process when increased glucose intake from food stimulates insulin release, which then enhances phosphorus uptake and causes a depletion of extracellular phosphate.
Symptoms of hypophosphatemia may include:
- Musculoskeletal pain
- Ventricular arrhythmias
- Edema
- Confusion
- Irritability
- Numbness or reflexive weakness
Why is phosphorous important?
Phosphorus plays a vital role in all intracellular processes and the structural integrity of cells. Hypophosphatemia can cause:
- Diaphragmatic muscle fatigue
- Respiratory failure
- Bursting of red blood cells as they circulate through the bloodstream (hemolysis)
- Rhabdomyolysis (skeletal muscle injury)
- Edema
- Seizures (i.e., refeeding syndrome)
Complications of Electrolyte Abnormalities
Heart problems
Low serum potassium can lead to heart problems, including QT interval prolongation.2 QT interval prolongation may increase the risk of dangerous arrhythmias, such as sudden cardiac death, deadly cardiac arrhythmias and myocardial fibrosis.2 Hypophosphatemia can also affect the heart, potentially causing systolic heart failure and arrhythmias.
Rhabdomyolysis
Both hypokalemia and hypophosphatemia can lead to rhabdomyolysis (cell death in muscles), a condition that can be life-threatening.2When skeletal muscle tissue is disrupted, it results in the breakdown of muscle fibers, which releases various proteins and electrolytes into the bloodstream and surrounding areas, causing::
- Elevated creatine kinase
- Electrolyte imbalances
- Acute renal failure
- Compartment syndrome, a condition of tissue injury due to significant edema that compromises blood flow
Bone disease
Prolonged hypophosphatemia causes osteopenia, osteoporosis, rickets, or osteomalacia because of reduced bone mineralization.3 Hypomagnesemia also likely plays a role in decreasing bone mineral density.
Delayed gastrointestinal transit
Without adequate potassium, the smooth muscle of the intestines and colon become weak and unable to move stool, delaying gastrointestinal transit and resulting in:3
- Paralytic ileus (inability of the intestines to contract normally)
- Constipation
- Abdominal distention
- Nausea
Hypokalemic nephropathy
Chronic potassium depletion can cause significant negative effects in the kidney, known as hypokalemic nephropathy.2Hypokalemic nephropathy is estimated to affect between 15-20% of patients with anorexia nervosa.2 The cause of hypokalemic nephropathy is believed to be due to renal vasoconstriction, decreased medullary blood flow, and impaired renal angiogenesis caused by hypokalemia. This condition can progress to end-stage renal disease requiring hemodialysis.
Refeeding syndrome
Refeeding syndrome is a potentially lethal complication comprised of the various clinical complications that develop due to a shift in fluids and electrolytes that occurs in significantly malnourished patients receiving artificial refeeding.
Treating Electrolyte Disturbances
Correcting hypokalemia
Correcting potassium depends on severity and whether or not metabolic alkalosis is present. Critically low levels of potassium (<2.5 mEg/L) generally require both intravenous and oral potassium. Higher levels (>2.5 mEg/L) in patients that are asymptomatic and have no ECG changes can usually be corrected more slowly with oral potassium supplementation. Dehydration and hypomagnesemia also need to be corrected.2
Supplementing sodium
Correction of hyponatremia can be done through the following methods:
- IV fluids
- Increased salt intake
- Pharmacologic intervention
- Improved nutritional status
The chosen intervention depends on the etiology and severity. Too aggressive a correction of hyponatremia can, although rarely, lead to a condition called central pontine myelinolysis (CPM), which may cause potentially irreversible neurologic problems.
Mild hyponatremia generally self-corrects with cessation of purging and nutritional rehabilitation.2 For sodium <125 mEq/L, patients should be treated with a slow intravenous infusion of isotonic saline, increasing sodium no more than 4 to 6 mEq/L over a 24-h period to prevent CPM.2
Severe hyponatremia <118 mEq/L requires transfer to the intensive care unit for closer monitoring and potential renal consultation for administration of a medication called desmopressin which can help the sodium from being corrected too quickly.2
Correcting magnesium
For symptomatic, severe hypomagnesemia (<1.2 mg/dL), IV replacement is generally recommended, but for milder hypomagnesemia, oral repletion can be started at 400–800 mg twice daily.2
Supplementing phosphorous
Failure to adequately treat hypophosphatemia can lead to refeeding syndrome. Treating hypophosphatemia during the refeeding process can require thousands of milligrams of oral phosphorous. For levels <2 mg/dL, patients should be treated inpatient with both intravenous and oral phosphorus.2
Finding Treatment for Electrolyte Imbalances
Electrolyte imbalances from eating disorders can lead to serious, even life-threatening complications, but with the right medical care, they are treatable. If you or a loved one are experiencing severe electrolyte imbalances, it’s important to receive medical stabilization and guided nutrition therapy from experienced professionals.
References
- Mehler, P. S., Blalock, D. V., Walden, K., Kaur, S., McBride, J., Walsh, K., & Watts, J. (2018). Medical findings in 1,026 consecutive adult inpatient–residential eating disordered patients. International Journal of Eating Disorders, 51(4), 305–313. https://www.acute.org/medical-findings-1026-consecutive-adult-inpatient-residential-eating-disordered-patients
- Puckett, L. (2023). Renal and electrolyte complications in eating disorders: a comprehensive review. Journal of Eating Disorders, 11(1). https://www.acute.org/renal-and-electrolyte-complications-eating-disorders-comprehensive-review
- Mehler PS and Andersen AE (eds.). 2022. Eating Disorders: A Comprehensive Guide to Medical Care and Complications (fourth edition). John Hopkins University Press.
