Low sodium, known medically as hyponatremia, happens when blood sodium drops below 135 mmol/L (the normal range is 135 to 145 mmol/L). It’s one of the most common electrolyte problems, and the causes range from drinking too much water to serious organ disease. In most cases, the issue isn’t that you’re losing sodium. It’s that your body is holding onto too much water, diluting the sodium you have.
How Your Body Controls Sodium
Sodium levels are really about water balance. Your brain constantly monitors the concentration of your blood and adjusts a hormone called ADH (antidiuretic hormone) to keep things in range. When your blood gets too concentrated, ADH tells your kidneys to hold onto water. When it’s too dilute, ADH drops, and your kidneys flush out the extra water as dilute urine.
Problems start when this system misfires. If ADH stays elevated when it shouldn’t be, your kidneys keep reabsorbing water even though your blood is already dilute. That extra water pulls your sodium concentration down. This is the core mechanism behind many causes of low sodium, whether the trigger is a medication, a disease, or overhydration during a marathon.
Medications Are a Leading Cause
Drugs are one of the most common and overlooked reasons sodium drops. The biggest offenders are diuretics (water pills), antidepressants, anticonvulsants, and antipsychotics. Among cases of severe drug-induced hyponatremia, thiazide diuretics and thiazide-like drugs account for roughly 23% of cases, making them the single most common medication trigger. Loop diuretics contribute about 9%.
Antidepressants, particularly SSRIs, cause low sodium by triggering inappropriate ADH release. They account for about 9% of severe cases. Certain seizure medications, especially carbamazepine and oxcarbazepine, are the most frequently implicated anticonvulsants. Older antipsychotics carry a higher risk than newer ones. Even a common antibiotic combination (trimethoprim-sulfamethoxazole) can cause moderate to severe sodium drops in a dose-dependent way.
If you’re on any of these medications and get blood work showing low sodium, the drug is worth discussing with your prescriber. In many cases, switching to an alternative or adjusting the dose resolves the problem.
Drinking Too Much Water
It sounds counterintuitive, but overhydration is a straightforward path to low sodium. Your kidneys can normally flush out 500 to 1,000 mL of water per hour. Add in sweat and other losses, and most people can handle up to 1,000 to 1,500 mL per hour before water starts to build up. But when intake exceeds that capacity, or when ADH stays elevated and prevents the kidneys from producing dilute urine, the excess water dilutes your sodium.
This is especially relevant for endurance athletes. Exercise-associated hyponatremia has been reported in nearly every form of endurance activity, from marathons to long hikes. The pattern is usually excessive water intake combined with elevated ADH levels triggered by the physical stress of exercise. During intense activity, ADH can reduce the kidneys’ ability to excrete water by as much as two-thirds compared to normal. The safest approach is to drink based on thirst rather than following a fixed schedule. If you weigh more after an hour of exercise than when you started, you’ve been drinking too much.
Heart Failure and Liver Disease
Both congestive heart failure and advanced liver cirrhosis cause a type of low sodium where the body is actually holding onto too much of both sodium and water, but water even more so. The result is dilutional hyponatremia: the total amount of sodium in your body may be normal or even high, but the sheer volume of extra fluid makes it seem low on a blood test.
In cirrhosis, the mechanism is well understood. Portal hypertension (increased pressure in the liver’s blood vessels) causes widespread blood vessel dilation, which makes the body think its circulating volume is too low. In response, the brain activates several compensatory systems, including ADH, the renin-angiotensin-aldosterone system, and the sympathetic nervous system. All of these drive the kidneys to retain sodium and water aggressively. As cirrhosis progresses, the kidneys lose their ability to excrete excess water, and ADH release becomes uncoupled from its normal triggers. Water builds up, and sodium concentration falls.
Heart failure follows a similar logic. The heart’s weakened pumping reduces effective blood flow, triggering those same compensatory hormones. The body retains fluid, leading to edema and swelling alongside low sodium readings.
SIADH: When the Hormone System Misfires
The syndrome of inappropriate antidiuretic hormone (SIADH) is one of the most common causes of low sodium in hospitalized patients. In this condition, ADH stays elevated even when blood sodium is already low and the body has no reason to hold onto water. The kidneys keep reabsorbing water, diluting sodium further, while blood volume stays normal or high.
SIADH can be triggered by lung diseases, brain injuries, infections, certain cancers, and many of the medications mentioned earlier. It’s considered “euvolemic” hyponatremia, meaning the person doesn’t look obviously swollen or dehydrated. That makes it trickier to recognize without blood and urine tests.
Vomiting, Diarrhea, and Fluid Loss
When you lose a lot of fluid through vomiting, diarrhea, or heavy sweating, you lose both water and sodium. But if you replace those losses with plain water or other low-sodium fluids, you dilute whatever sodium remains. The body also responds to the volume loss by ramping up ADH, which holds onto water and compounds the problem.
Conditions that cause “third-spacing,” where fluid shifts into body cavities or tissues (as in pancreatitis or bowel obstruction), can have the same effect. The sodium isn’t gone from your body, but it’s trapped in places where it can’t maintain normal blood levels.
Poor Diet and Heavy Alcohol Use
A condition sometimes called “beer potomania” shows how diet and drinking habits can combine to tank sodium levels. First described in 1972, it occurs in people who drink large amounts of beer while eating very little food. Beer has almost no solute (dissolved particles), and alcohol suppresses protein breakdown, reducing the amount of waste products delivered to the kidneys. Your kidneys need those waste products to generate concentrated urine and excrete excess water efficiently.
In documented cases, patients drinking 9 to 20 cans of beer daily with minimal food intake had an osmole intake of only about 225 to 250 mOsm per day. At that low solute load, any fluid intake beyond 3 to 4 liters per day will overwhelm the kidneys’ ability to clear the water, resulting in dilutional hyponatremia. A similar mechanism, sometimes called “tea and toast syndrome,” affects elderly people who eat very little protein and drink mostly tea or water.
Hormonal and Kidney Conditions
Addison’s disease (adrenal insufficiency) reduces levels of aldosterone, a hormone that tells the kidneys to retain sodium. Without enough aldosterone, the kidneys waste sodium in the urine. Hypothyroidism can also contribute to low sodium, though the mechanism is less direct and may involve reduced kidney function and altered ADH regulation. Kidney disease itself, whether acute or chronic, impairs the organ’s ability to balance sodium and water, and nephrotic syndrome (a condition where the kidneys leak protein) can cause sodium dilution through fluid shifts.
How Low Sodium Affects the Body
The symptoms of low sodium are primarily neurological because the brain is especially vulnerable to changes in water balance. When sodium drops, water moves into brain cells by osmosis, causing them to swell. Early symptoms include nausea, headache, muscle cramps, weakness, and lethargy. Some people feel restless or disoriented. If sodium falls further or drops very quickly, the consequences become severe: seizures, coma, and in extreme cases, respiratory arrest.
Even mild, chronic low sodium causes real problems. Research has linked sodium levels around 126 mmol/L (modestly below normal) with gait instability, attention deficits, and a significantly increased risk of falls and fractures. There’s also an association with osteoporosis. These effects are easy to dismiss as aging or general fatigue, which means mild hyponatremia often goes unrecognized.
One important nuance: correcting sodium too quickly is dangerous in its own right. Rapid correction can cause osmotic demyelination syndrome, which damages nerve insulation in the brain and can lead to difficulty swallowing, speaking, or moving. This is why severe hyponatremia is always treated carefully and gradually in a hospital setting.