Is plain water enough, or do you also need electrolytes?

The three electrolytes that matter most:

Sodium is the primary electrolyte lost in sweat. In a 20-year follow-up of the Trials of Hypertension Prevention, there was a direct linear association between sodium intake and mortality, with no evidence of a J-shaped relationship². Athletes, people following ketogenic or low-carb diets, and those who fast regularly need substantially more sodium than sedentary individuals eating standard diets.

Potassium works in partnership with sodium to regulate fluid balance and nerve signaling. Most Americans consume far less potassium than the recommended 4,700 mg/day — data from NHANES show the average intake is only about 2,640 mg/day⁴. Potassium-rich foods include avocados, bananas, potatoes, and spinach, but supplementing the gap can be challenging through diet alone.

Magnesium is involved in over 300 enzymatic reactions including muscle contraction, nerve function, and energy production. Subclinical magnesium deficiency is widespread, affecting an estimated 50-80% of the population, largely due to depleted soil mineral content and processed food consumption³. See our Magnesium page for a deep dive into the different forms and their specific uses.

Signs of electrolyte imbalance include:

• Muscle cramps, especially at night or during exercise
• Brain fog and difficulty concentrating
• Persistent fatigue that sleep does not resolve
• Heart palpitations or irregular heartbeat
• Headaches, particularly in the morning
• Dizziness upon standing

Who needs to pay extra attention: Anyone who sweats heavily (athletes, outdoor workers, sauna users), follows a ketogenic or low-carb diet (insulin drives sodium retention — when insulin drops, sodium excretion increases sharply), practices intermittent or extended fasting, or drinks large amounts of plain water without food.

Rosner and Kirven (2007) reviewed exercise-associated hyponatremia (EAH) in the Clinical Journal of the American Society of Nephrology. EAH occurs when athletes drink excessive amounts of hypotonic fluid (plain water) relative to sodium losses during prolonged exercise. They documented cases in marathon runners, triathletes, and military personnel where serum sodium dropped below 135 mmol/L, with severe cases below 120 mmol/L producing cerebral edema, seizures, and in rare cases, death. The mechanism is straightforward: sweat contains 20-80 mmol/L of sodium, and replacing this loss with sodium-free water progressively dilutes plasma sodium. Their review concluded that the advice to "drink as much as possible" during exercise is actively dangerous and should be replaced with guidance to drink to thirst and include sodium¹.

Cook et al. (2016) published a 20-year follow-up of the Trials of Hypertension Prevention examining sodium intake and all-cause mortality, using urinary sodium excretion measured in multiple 24-hour urine samples from pre-hypertensive adults aged 30 to 54 years. Among 2,974 participants not assigned to an active sodium intervention, 272 deaths occurred, and there was a direct linear association between average sodium intake and mortality: hazard ratios were 0.75, 0.95, 1.00 (reference), and 1.07 for intakes of <2,300, 2,300 to <3,600, 3,600 to <4,800, and ≥4,800 mg/24 h, and 1.12 per 1,000 mg/24 h (95% CI 1.00 to 1.26; p = 0.05). The authors found no evidence of a J-shaped or nonlinear relationship; they reported an increased risk of mortality for high sodium intake and a direct relationship with total mortality, even at the lowest levels of sodium intake. They concluded that the results are consistent with a benefit of reduced sodium and sodium/potassium intake on total mortality over a 20-year period².

De Baaij et al. (2015) published a comprehensive review of magnesium physiology in Physiological Reviews. They detailed magnesium's role as a cofactor for over 300 enzymes, including those involved in ATP synthesis, DNA replication, and neuromuscular excitability. Intracellular magnesium regulates potassium and calcium channel function, directly linking magnesium status to muscle cramping, cardiac rhythm, and neurological function. They documented that serum magnesium (the standard clinical test) reflects only 0.3% of total body magnesium, meaning deficiency can be present with "normal" lab values. They identified modern agriculture, food processing, and certain medications (proton pump inhibitors, diuretics) as major contributors to widespread subclinical deficiency³.

Cogswell et al. (2012) analyzed NHANES data from 2003-2008 and found that the average American adult consumes approximately 3,400 mg of sodium and only 2,640 mg of potassium per day — nearly the inverse of what evolutionary biology and clinical guidelines suggest. The sodium-to-potassium ratio, rather than absolute sodium intake alone, may be the more important determinant of cardiovascular risk. Their data showed that fewer than 2% of U.S. adults meet the potassium adequate intake recommendation of 4,700 mg/day. This imbalance, driven largely by processed food consumption, may be more consequential than sodium excess alone⁴.