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Iodine in the urine
Last reviewed: 05.07.2025

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Reference values (norm) of iodine excretion in urine are 100-500 μg/l.
Iodine is a microelement present in nature in trace amounts. The iodine content in drinking water is insignificant, so the main amount of this microelement enters the human body with food. The highest concentration of iodine is in seafood (approximately 800 μg/kg); seaweed is especially rich in iodine. Fish oil contains a lot of iodine. Usually, milk, eggs, meat and cereals are sources of iodine in the body. The required daily intake of iodine depends on a person’s age, amounting to 40 μg/day for infants and 150 μg/day for adults. During pregnancy, the need for iodine increases to approximately 200 μg/day.
Iodine, which enters the body with food in the form of iodide, is absorbed in the gastrointestinal tract. From the blood, it easily penetrates into various organs and tissues, partially depositing in lipids. The most significant part of iodine (up to 10-20%) is selectively absorbed by the thyroid gland. Iodine is excreted from the body mainly by the kidneys (up to 70-90%).
After entering the blood, inorganic iodine is actively captured by the thyroid gland, where its concentration is 30-40 times higher than in the blood. Iodide concentrated in the thyroid gland is oxidized into molecular iodine, which quickly binds to the remains of thyroglobulin, forming monoiodotyrosine and diiodotyrosine (the iodine organification phase). In the condensation phase, two diiodotyrosines combine to form T 4 or one mono- and one diiodotyrosine to form T 3. The main factor regulating the synthesis of thyroid hormones is thyroid-stimulating hormone (TSH). It affects all stages of iodine metabolism: it enhances the ability of the thyroid gland to concentrate iodine from the blood, accelerates iodination and the formation of hormones from the thyroglobulin molecule, changes the sites of iodination in thyroglobulin with the predominant formation of T3 and activates cysteine proteinases and cathepsins, which break down thyroglobulin.
When there is a deficiency of iodine in the body, the production of thyroid hormones becomes insufficient, which has many consequences, which are united by the term "iodine deficiency states". Such consequences include goiter, hypothyroidism, developmental delay, reproductive disorders, etc.
Up to 90% of ingested iodine appears in the urine, so urinary iodine excretion correlates with iodine status. Urinary iodine concentration can serve as an indicator that adequately reflects its consumption. Numerous studies have shown that the iodine concentration in a single portion of urine correlates well with the iodine level in 24-hour urine. However, iodine levels in individuals vary daily and even during the day and therefore cannot reflect the iodine status of the population as a whole. Urine iodine analysis is suitable only for epidemiological studies. The minimum number of samples should be at least 60. Due to the very uneven distribution of iodine levels in the urine of the subjects, it is better to estimate the median of urinary iodine excretion rather than the mean value. If the median exceeds 100 μg/L, then there is no iodine deficiency in this population.
The International Committee on Iodine Deficiency Disorders and WHO distinguish three degrees of iodine deficiency severity based on the median iodine level in the urine: 99-55 μg/L - mild; 49-20 μg/L - moderate; less than 20 μg/L - severe. When an excessive amount of iodine enters the body of a person with normal thyroid function, the synthesis of thyroid hormones transiently decreases (for about 48 hours). The acute inhibitory effect of iodine on the synthesis of thyroid hormones is called the Wolff-Chaikoff effect and is associated with an increase in the concentration of iodine in the thyroid gland itself. Then, despite the continued intake of large amounts of iodine, the synthesis of thyroid hormones is restored, providing a euthyroid state (due to a decrease in the uptake of iodide by the gland). Despite the existence of such an adaptive mechanism, excess iodine can cause hypothyroidism with or without goiter, as well as hyperthyroidism in susceptible individuals.