This test is most useful if any of these apply to you.
Lithium occurs naturally in drinking water and food, and your kidneys remove most of the amount you absorb. Urinary lithium can help investigate exposure from these sources, supplements, or medication. A single urine concentration also depends on dilution and kidney handling, so it can't tell you exactly how much you consumed.
For prevention and longevity, this remains an exploratory marker. Published population reference data exist, but they don't establish an optimal urine level or a threshold that diagnoses thyroid or kidney damage. Routine screening and repeated testing in healthy adults haven't been shown to improve health outcomes.
This test measures elemental lithium in a spot urine sample using ICP-MS. It's a sensitive method for measuring metals. The result combines lithium from different sources; it doesn't identify which water, food, supplement, or medication contributed it.
Water can be a substantial source where natural levels run high. In the Strong Heart Family Study, household tap-water lithium explained a meaningful share of the variation in urinary lithium among participating American Indian communities. Researchers adjusted urine results for dilution using creatinine. Average levels were similar at two visits about 15 years apart, though individual results varied.
One human study examined 202 women and adolescent girls in Andean villages with unusually high natural lithium exposure. Higher lithium in spot urine, after adjustment for dilution, was associated with lower free thyroxine and higher TSH in blood. Free thyroxine is a thyroid hormone. TSH signals the thyroid to make more hormone.
The pattern suggests an effect on thyroid function, but most participants' thyroid results remained within clinical reference intervals. The study didn't establish that lithium caused hypothyroidism in each person. Exposure included water and other environmental sources, and the findings don't establish a urine threshold for harm at ordinary dietary exposure.
In 642 adults with stable kidney transplants, higher total lithium excretion in 24-hour urine was associated with better outcomes over a median of 5.3 years. Each doubling was associated with about 46% lower risk of transplant failure and about 36% lower risk of death. The risk of blood creatinine doubling was about 27% lower, though that estimate was less certain. Associations persisted after adjustment for factors including starting kidney function and urine protein.
Higher excretion also tracked with greater calorie, plant-protein, and water intake. These were observations, not a trial of eating or drinking more. Diet, health, and kidney handling could contribute to the associations. The study measured total daily lithium loss, which isn't interchangeable with a spot urine concentration. It doesn't show that raising your urine lithium protects healthy kidneys or that a low result identifies a deficiency.
Most evidence about lithium-related kidney injury comes from prescription treatment. Vasopressin helps your kidneys conserve water. Lithium can reduce the kidneys' response to this hormone, producing more dilute urine. In 11 healthy volunteers, four weeks of lithium carbonate caused a small reduction in urine-concentrating ability. In a separate study of 217 people taking lithium, higher daily doses were associated with greater urine output and higher vasopressin levels.
Long-term treatment can also cause chronic kidney disease. The size of that risk varies with treatment duration, blood lithium levels, starting kidney function, and other health conditions. An Icelandic cohort found increased risk with higher average blood levels. A Swedish study comparing new lithium and valproate users found similar kidney outcomes between treatments during follow-up, while higher blood lithium was associated with acute kidney injury. These studies assessed medication exposure and kidney function; they didn't establish a urine lithium concentration that predicts injury.
Ordinary dietary exposure and prescription dosing differ greatly. Findings from either setting can't establish a beneficial or harmful urine target for the other.
A Portuguese study found no clear difference in urinary lithium between residents of regions with different suicide rates. It compared regional patterns, so it couldn't determine whether an individual's urine lithium predicted their mood or suicide risk.
A US study found lower cancer risk among people living where estimated groundwater lithium was highest, compared with where it was lowest. Exposure was assigned from geographic groundwater models, without measuring participants' urine or actual lithium intake. Geographic differences and exposure misclassification limit interpretation. This finding doesn't establish a cancer-preventive intake or urine level.
For prescription exposure, a large Danish study found no statistically clear increase in kidney or upper urinary tract cancer with long-term lithium use. Its estimate was imprecise, so some increase in risk couldn't be excluded. Urinary lithium has no established role in cancer screening.
Repeated measurements under comparable conditions may help investigate a suspected exposure change. A stable result doesn't prove safety, and a rise can reflect dilution, timing, kidney handling, or a change in intake. Urinary lithium hasn't been validated as a way to track nutritional adequacy, mood protection, or longevity.
Evidence-backed interventions that affect your Lithium level
Lithium is best interpreted alongside these tests.
Lithium is included in these pre-built panels.
See which minerals your body holds onto and which it flushes away, a research-grade look at your diet and kidney handling.
See which environmental metals your body is passing and how your essential minerals compare, from a single urine sample.
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