As a result, iodine deficiency is the most common cause of goiter, hypothyroidism, and mental deficiency worldwide. See "Iodine deficiency disorders". Sources of excess iodine include over-the-counter and prescription medications that may be ingested or applied to the skin or vaginal mucosa, radiographic contrast agents, and dietary supplements kelp, seaweed table 1.

In the context of a person's usual dietary iodine intake, the amount of iodine in many of these substances is very large. As an example, a patient undergoing vascular imaging may receive several thousand mg of organic iodide.

Those substances that contain organic iodide are partially deiodinated to form inorganic iodide, the form that has thyroidal actions. Some of these substances that are deiodinated to form inorganic iodine, such as amiodarone, are stored in fat and may provide excess iodide for months after the last dose is administered.

Why UpToDate? Product Editorial Subscription Options Subscribe Sign in. Learn how UpToDate can help you. Select the option that best describes you. View Topic. Font Size Small Normal Large. Iodine-induced thyroid dysfunction. Formulary drug information for this topic.

Inadequate levels or overconsumption of iodine can lead to or worsen thyroid disease, as well as cause other significant health concerns. When you consume iodine, it is quickly absorbed and entered into your bloodstream.

Your thyroid, which has tiny cells that capture the circulating iodine, takes in and oxidizes it so it can begin to be used to create triiodothyronine T3 and thyroxine T4 —thyroid hormones that make their way throughout the body to regulate metabolism and ensure healthy functioning of the heart, brain, and other organs.

While the major portion of iodine is concentrated in the thyroid gland, the nonhormonal iodine is found in a variety of body tissues including the mammary glands, the eyes, the gastric mucosa, the cervix, and the salivary glands.

Levels of T3 and T4—as well as thyroid stimulating hormone TSH , which is influenced by the two—that are out of normal ranges can lead to issues such as hypothyroidism and hyperthyroidism, and the complications related to having an underactive or overactive thyroid.

This can occur for a number of reasons, including taking in too little or too much iodine. According to the Food and Nutrition Board of the National Academies formerly the National Academy of Science , the recommended dietary allowance RDA for iodine in the United States ranges anywhere from 90 mcg per day for toddlers to mcg for teens and adults.

Considering that one cup of plain low-fat yogurt contains about 75 mcg, 3 ounces of fish sticks contain about 54 mcg, a cup of cooked pasta contains about 27 mcg, and a quarter teaspoon of iodized salt contains about 71 mcg, that's generally an easy amount for most people to consume.

Excess iodine, however, can be particularly dangerous in these women. Most Americans have no trouble meeting the recommended intake of iodine because of the iodization of salt in the United States and incorporation of iodine-rich foods such as the following:.

Supplements e. potassium iodide, sodium iodide, kelp and iodine-containing herbs, such as bladderwrack, are other sources that can be considered.

Since iodine is needed to make thyroid hormone, diminished levels can lead to hypothyroidism low thyroid function. Iodine deficiency is also linked to the development of goiter thyroid enlargement. The impact of too little iodine reaches further.

Children born to mothers with severe iodine deficiency can suffer from stunted growth, severe and irreversible intellectual disabilities, and problems with movement, speech, and hearing.

Even mild iodine deficiency during pregnancy can lead to subtle intellectual deficits, although many children improve with iodine supplementation.

Mild iodine deficiency can also cause miscarriage. Fibrocystic breast disease , a benign condition characterized by lumpy, painful breasts mostly in women of reproductive age, is also associated with iodine deficiency. At a global scale, roughly 2 billion people are classified as having iron deficiency, of which around 50 million have clinical symptoms.

Even so, 21 countries have insufficient iodine in their diets, according to research from the Iodine Global Network.

These not only include developing countries like Madagascar, Mali, Cambodia, Haiti, Lebanon, and Tajikistan, but also developed countries like Norway, Israel, Finland, and Germany. The risk of iodine deficiency in the United States has long been considered small due to the implementation of salt iodization starting back in the s.

However, recent research suggests that mild-to-moderate iodine deficiency is, in fact, common in the U. and appears to be increasing. population had a urine iodine concentration UIC of under in , meaning that they met the definition of being iodine deficient. There are certain risk factors that may account for such deficiencies, not only in the United States but other developed and developing countries:.

Changing dietary habits have fueled increasing rates of iodine deficiency in the United States. The overall reduced use of table salt has been led by health concerns about sodium and high blood pressure.

At the same time, there has been an increased demand among consumers for sea salt, which is naturally low in iodine. Some healthcare providers are almost knee-jerk in their insistence that anyone with a thyroid problem requires iodine supplementation; alternative healthcare providers may recommend iodine-containing herbs, like kelp or seaweed.

This can be particularly risky, in part because iodine supplements can interact with several types of drugs, including anti-thyroid drugs used to treat hyperthyroidism.

Taking high doses of iodine with anti-thyroid medications can have an additive effect and could cause hypothyroidism. If iodine deficiency isn't the cause of hypothyroidism, then iodine supplements won't be helpful.

You'll want to be very careful about upping your iodine intake unless you and your healthcare provider have some very strong evidence that you're deficient.

This is especially true if you're pregnant or planning to become pregnant. Given the strong link between iodine and thyroid health, it's reassuring to learn that iodine deficiency is rare in the United States and other developed countries where iodized salt is used.

Indeed, as an International Journal of Molecular Sciences study reported in , iodine excess is currently a more frequent occurrence in these places. This, though, is not without concern.

For some people with abnormal thyroid glands, excessive iodine can trigger or worsen hypothyroidism. While initially, you may have more energy, high doses can cause an "iodine crash" that leaves you feeling exhausted and achy within a few days.

That's because high iodine intake can initiate and exacerbate infiltration of the thyroid by lymphocytes, the white blood cells that accumulate due to chronic injury or irritation. In addition, large amounts of iodine block the thyroid's ability to make thyroid hormones.

A study in the journal Endocrinology and Metabolism found that more-than-adequate or excessive iodine levels are unsafe and may lead to hypothyroidism and autoimmune thyroiditis Hashimoto's thyroiditis , chronic lymphocytic thyroiditis , especially for people with recurring thyroid disease.

Women who take too much supplemental iodine during pregnancy may give birth to babies with congenital hypothyroidism, a thyroid deficiency that, if left untreated, can lead to mental, growth, and heart problems, according to a study published in The Journal of Pediatrics. While iodine poisoning is rare, the overconsumption of iodine can be just as problematic as consuming too little.

While iodine can be detected in urine, relying on such a test is not helpful, since 90 percent of the iodine you ingest is quickly expelled. The steps in this process are as follows: [31]. Thyroglobulin Tg is a kDa , dimeric protein produced by the follicular cells of the thyroid and used entirely within the thyroid gland.

More specifically, the monatomic anionic form of iodine, iodide I — , is actively absorbed from the bloodstream by a process called iodide trapping. This introduces 1—2 atoms of the element iodine , covalently bound, per tyrosine residue.

Coupling of DIT to MIT in the opposite order yields a substance, r-T 3 , which is biologically inactive. Thyroxine is believed to be a prohormone and a reservoir for the most active and main thyroid hormone T 3.

Thyrotropin-releasing hormone TRH is released from hypothalamus by 6 — 8 weeks, and thyroid-stimulating hormone TSH secretion from fetal pituitary is evident by 12 weeks of gestation , and fetal production of thyroxine T 4 reaches a clinically significant level at 18—20 weeks.

brain development abnormalities caused by maternal hypothyroidism. If there is a deficiency of dietary iodine , the thyroid will not be able to make thyroid hormones. Most of the thyroid hormone circulating in the blood is bound to transport proteins , and only a very small fraction is unbound and biologically active.

Therefore, measuring concentrations of free thyroid hormones is important for diagnosis, while measuring total levels can be misleading.

Thyroid hormone in the blood is usually distributed as follows: [ citation needed ]. Despite being lipophilic, T 3 and T 4 cross the cell membrane via carrier-mediated transport, which is ATP-dependent.

T 1 a and T 0 a are positively charged and do not cross the membrane; they are believed to function via the trace amine-associated receptor TAAR1 TAR1, TA1 , a G-protein-coupled receptor located in the cytoplasm. Another critical diagnostic tool is measurement of the amount of thyroid-stimulating hormone TSH that is present.

Contrary to common belief, thyroid hormones cannot traverse cell membranes in a passive manner like other lipophilic substances. The iodine in o -position makes the phenolic OH-group more acidic, resulting in a negative charge at physiological pH.

However, at least 10 different active, energy-dependent and genetically regulated iodothyronine transporters have been identified in humans.

They guarantee that intracellular levels of thyroid hormones are higher than in blood plasma or interstitial fluids.

Little is known about intracellular kinetics of thyroid hormones. The thyroid hormones function via a well-studied set of nuclear receptors , termed the thyroid hormone receptors.

These receptors, together with corepressor molecules, bind DNA regions called thyroid hormone response elements TREs near genes. This receptor-corepressor-DNA complex can block gene transcription.

Triiodothyronine T 3 , which is the active form of thyroxine T 4 , goes on to bind to receptors. This leads to recruitment of coactivator proteins and RNA polymerase , activating transcription of the gene. More recently genetic evidence has been obtained for a second mechanism of thyroid hormone action involving one of the same nuclear receptors, TRβ, acting rapidly in the cytoplasm through the PI3K.

Thyroxine and iodine stimulate the apoptosis of the cells of the larval gills, tail and fins in amphibian metamorphosis , and stimulate the evolution of their nervous system transforming the aquatic, vegetarian tadpole into the terrestrial, carnivorous frog.

In fact, amphibian frog Xenopus laevis serves as an ideal model system for the study of the mechanisms of apoptosis. Further information: Thyroid function tests. Triiodothyronine T 3 and thyroxine T 4 can be measured as free T 3 and free T 4 , which are indicators of their activities in the body.

Preterm births can suffer neurodevelopmental disorders due to lack of maternal thyroid hormones, at a time when their own thyroid is unable to meet their postnatal needs. Iodine uptake against a concentration gradient is mediated by a sodium—iodine symporter and is linked to a sodium-potassium ATPase.

Perchlorate and thiocyanate are drugs that can compete with iodine at this point. Compounds such as goitrin , carbimazole , methimazole , propylthiouracil can reduce thyroid hormone production by interfering with iodine oxidation. Contents move to sidebar hide.

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Main article: Thyroid hormone receptor. png References. Retrieved 20 May Textbook of Surgery. CRC Press. ISBN Retrieved 6 August WedMD LLC. Retrieved 2 May The American Journal of Physiology. doi : PMID ISSN PMC American Society for Biochemistry and Molecular Biology.

Archived from the original on 19 March Retrieved 4 July Retrieved 7 October World Health Organization model list of essential medicines: 21st list Geneva: World Health Organization. License: CC BY-NC-SA 3.

The Journal of Clinical Endocrinology and Metabolism. Angewandte Chemie. Retrieved 27 March JAMA: The Journal of the American Medical Association. Hormone Research. S2CID The Journal of Family Practice. Boron; Emile L.