Jod (Urin): the pathway in the body · Biomarker & Blood Analysis

Jod (Urin) is part of the pathway “Iodine”. This page shows the whole pathway; the station of Jod (Urin) is highlighted.

Where this laboratory value sits: Iodine in food — mostly as iodide. In food, iodine occurs mainly as iodide, for example in sea fish, seaweed, milk and iodised table salt. The body does not make iodine itself. Source 1

In brief

Iodine is a trace element that mostly enters the body as iodide in food and is largely excreted in urine. The thyroid gland builds it into its hormones thyroxine (T4) and triiodothyronine (T3). When little iodine is available, the thyroid draws more of it from the blood.

The pathway step by step

Each station states what the compound does there. Three signs: ↑ supplies — builds up or makes available · ↓ depletes — inhibits, consumes or withholds · ↕ both, depending on amount. Behind it stands what the statement rests on: established physiology, observed in studies, or contested. The signs do not grade; they name the direction.

1. Iodine in food → Iodide in blood In the small intestine, iodide passes almost completely into the blood and spreads through the body water. From there, the thyroid and some other tissues absorb it. The thyroid and kidneys share this pool. Source 1, 2↑ supplies Iodide in the blood is the shared pool that the thyroid and kidneys divide between them. Via NIS it also reaches the salivary glands, stomach lining and the lactating breast. established physiology Source 2
   ⚖ When the balance tips

   too much — If iodide in the blood rises sharply, the thyroid temporarily curbs hormone production (Wolff-Chaikoff effect); after a few days it absorbs less via NIS, and production resumes.

   too little — If there is little iodide in the blood, the pituitary releases more TSH; TSH brings more NIS into the thyroid cell membrane, which thus retains a larger share.

   established physiology · Source 2, 3

2. Iodide in blood → Iodide in urine The kidneys excrete most of the absorbed iodide in the urine. The amount in urine therefore mainly reflects intake over the last few days. What the thyroid does not absorb leaves the body this way. Source 1↓ depletes Iodide continuously leaves the body via the kidneys; what the thyroid does not absorb is excreted in this way. The amount in urine therefore follows intake rather than the store in the thyroid. established physiology Source 1
   ⚖ When the balance tips

   too much — If a lot of iodide arrives, the amount in the urine rises quickly with it; the kidneys do not hold back the excess.

   too little — If little iodide arrives, the amount in the urine falls. Because it varies strongly from day to day, a single measurement describes the last few days rather than the thyroid's store.

   established physiology · Source 1

3. Iodide in the cell → Iodide in the follicle Pendrin On the opposite side of the cell, the transporter pendrin releases iodide into the follicle space. This is where the thyroid stores the protein thyroglobulin. There it is ready for TPO to make hormone. Source 3↑ supplies In the follicle space, iodide is available to TPO at the cell surface. Hormone production takes place there, outside the cell interior and directly on the stored thyroglobulin. established physiology Source 3
   ⚖ When the balance tips

   too much — More iodide in the follicle does not bring unlimited hormone: TPO and the hydrogen peroxide provided set the limit.

   too little — If pendrin releases little iodide, less is available to TPO, and fewer iodinated units form on thyroglobulin.

   established physiology · Source 3

4. Iodide in the follicle → MIT and DIT TPO · Hydrogen peroxide, Haem (iron) Thyroid peroxidase (TPO) links iodine to tyrosine units of thyroglobulin, forming mono- and diiodotyrosine. For this, the enzyme needs hydrogen peroxide, supplied by DUOX2. With very much iodide, this step pauses temporarily. Source 3, 4↑ supplies Only iodination turns thyroglobulin into a hormone store. For this, TPO needs iodide, hydrogen peroxide from DUOX2 and haem iron in its active site at the same time. established physiology Source 3, 4
   ⚖ When the balance tips

   too much — If iodide in the cell rises sharply, it temporarily inhibits iodination by TPO (Wolff-Chaikoff effect); once uptake via NIS then falls, iodination resumes.

   too little — If little iodine is available, more MIT than DIT forms, and the thyroid makes proportionally more T3, which carries one iodine atom fewer than T4.

   established physiology · Source 2, 3, 4

5. MIT and DIT → T4 and T3 TPO The same TPO couples two iodinated units together. This forms thyroxine (T4) and, in smaller amounts, triiodothyronine (T3) – both still attached to the carrier protein. In the follicle they form a store for later release. Source 3↑ supplies T4 and T3 remain stored in thyroglobulin until they are called on. The follicle thus holds a store from which the thyroid can release hormone without first iodinating anew. established physiology Source 3
   ⚖ When the balance tips

   too much — If the store in thyroglobulin is well filled, hormone is called on as needed; a larger store does not speed up release, because release follows the TSH signal.

   too little — If little iodine is built in, fewer T4 residues form on thyroglobulin and the store shrinks; TSH then drives uptake and iodination harder.

   established physiology · Source 3, 2

6. T4 and T3 → T4 in blood Proteases The cell reabsorbs thyroglobulin. Proteases in the lysosome cut the hormones out, and the cell releases them into the blood; iodide from the remaining units is reused. TSH from the pituitary controls how much is released. Source 3↑ supplies T4 is the main form the thyroid releases; it circulates in the blood for a long time and is converted to T3 only in the tissues. The cell recovers iodide from MIT and DIT and builds it in again. established physiology Source 3, 5
   ⚖ When the balance tips

   too much — If a lot of T4 is present in the blood, the pituitary releases less TSH; the thyroid then absorbs less iodide and releases less hormone.

   too little — If the thyroid releases little T4, TSH rises; tissues such as the brain at the same time increase DIO2 activity and make more T3 from the available T4.

   established physiology · Source 3, 5

7. T4 in blood → T3 in the target cell Deiodinases · Selenium In the tissues, deiodinases remove one iodine atom from T4; this produces T3, which binds to the thyroid hormone receptor. These enzymes carry selenium in their active site. Each tissue thus sets how much T3 acts. Source 5, 4↑ supplies T3 binds to receptors in the cell nucleus and switches on and off genes that set energy turnover and heat production. How much T3 arrives is regulated by the selenium-containing deiodinases in each tissue. established physiology Source 5, 4
   ⚖ When the balance tips

   too much — If a lot of T3 is present in the tissue, DIO3 converts more of it into inactive forms and DIO2 is curbed; each tissue thus limits the hormone action itself.

   too little — If little T3 is present, the target genes are read less often, and energy turnover and heat production slow down. If selenium is also scarce, the deiodinases convert T4 more slowly.

   established physiology · Source 5, 4

Further stations

• Iodine in food — mostly as iodide In food, iodine occurs mainly as iodide, for example in sea fish, seaweed, milk and iodised table salt. The body does not make iodine itself. Source 1↑ supplies Iodide from food is the raw material from which the thyroid builds its hormones. The body does not make iodine itself; what reaches the blood comes from what was eaten and drunk. established physiology Source 1
  ⚖ When the balance tips

  too much — If a lot of iodide arrives, excretion via the kidneys rises with it; most of it leaves the body again quickly in the urine.

  too little — If little iodide arrives, the amount in the urine falls; the thyroid then draws a larger share from the blood with more NIS.

  established physiology · Source 1, 2

• Iodide in the cell — thyroid follicular cell The sodium-iodide symporter (NIS) brings iodide from the blood into thyroid cells, using the sodium gradient across the cell membrane. Perchlorate, nitrate and thiocyanate bind to the same transporter. TSH sets how much NIS is available. Source 2, 6↑ supplies NIS concentrates iodide in the thyroid far above the level in the blood; the sodium gradient provides the energy for this. TSH determines how much NIS sits in the cell membrane. established physiology Source 2
  ⚖ When the balance tips

  too much — If there is a lot of iodide in the cell, the thyroid places less NIS in the membrane and so curbs further uptake after a few days.

  too little — If little iodide is available or perchlorate, nitrate or thiocyanate occupy the transporter, less iodide enters the cell; TSH then drives the production of NIS.

  established physiology · Source 2, 6

Cofactors in this pathway

• Selenium — Component of the deiodinases, which convert T4 to T3 in the tissues; it thus helps set how much T3 acts in the tissue Source 4, 5In the ORY catalogue as a laboratory value: Selen
• Iron — Haem iron in the active site of thyroid peroxidase (TPO); without haem, TPO forms no MIT or DIT Source 4, 3In the ORY catalogue as a laboratory value: Eisen
• Tyrosine — Building block of thyroglobulin to which TPO attaches the iodine; MIT, DIT, T4 and T3 arise from it Source 3In the ORY catalogue as a laboratory value: Tyrosin
• Sodium — Its gradient drives the sodium-iodide symporter (NIS); this lets the thyroid concentrate iodide Source 2In the ORY catalogue as a laboratory value: Natrium (intrazellulär)
• NADPH — Electron donor of DUOX2, which forms hydrogen peroxide for TPO; without hydrogen peroxide no iodination Source 3

Sources

1. Zimmermann MB, Andersson M. Assessment of iodine nutrition in populations: past, present, and future. Nutr Rev 2012 · PubMed 23035804
2. Portulano C, Paroder-Belenitsky M, Carrasco N. The Na+/I- symporter (NIS): mechanism and medical impact. Endocr Rev 2014 · PubMed 24311738
3. Carvalho DP, Dupuy C. Thyroid hormone biosynthesis and release. Mol Cell Endocrinol 2017 · PubMed 28153798
4. Köhrle J. Selenium, Iodine and Iron-Essential Trace Elements for Thyroid Hormone Synthesis and Metabolism. Int J Mol Sci 2023 · PubMed 36834802
5. Gereben B, Zeöld A, Dentice M et al. Activation and inactivation of thyroid hormone by deiodinases: local action with general consequences. Cell Mol Life Sci 2008 · PubMed 17989921
6. Serrano-Nascimento C, Nunes MT. Perchlorate, nitrate, and thiocyanate: Environmental relevant NIS-inhibitors pollutants and their impact on thyroid function and human health. Front Endocrinol (Lausanne) 2022 · PubMed 36339434

Whole pathway: Iodine

Related pathways

• Thyroid hormones — iodide in the cell
• Vitamin C — Selen, Eisen
• 8-OHdG — Selen, Eisen
• Borrelia — Selen, Eisen
• IgG antibodies to food — Selen, Eisen

As of 2026-09-16. Draft written by Claude to schema v2; sources checked in PubMed; expert review pending
Legal notice Privacy policy All biomarkers