Iodine

Iodine is a vital micronutrient required at all stages of life, with fetal life and early childhood being the most critical phases of requirement.

Iodine is an essential component of the hormones produced by the thyroid gland.

The thyroid gland uses iodine from food to make the two thyroid hormones, namely, triiodothyronine (T3) and thyroxine (T4).

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It also stores these thyroid hormones and releases them as they are needed.

Thyroid hormones, and therefore iodine, are essential for mammalian life.

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An iodine deficiency is strongly connected with the development of brain damage and neurocognitive impairment in children.

Iodine deficiency disorder (IDD) is the most common endocrinopathy in the world and also the most preventable cause of mental retardation [1].

In 1998, one-third of the worlds′ population lived in iodine-deficient areas [2].

The two major factors responsible for iodine deficiency disorder (IDD) are inadequate iodine intake and inadequate iodine utilization.

Iodine (as iodide) is widely but unevenly distributed in the earth’s environment.

Most iodide is found in the oceans (≈50 μg/L), and iodide ions in seawater are oxidized to elemental iodine, which volatilizes into the atmosphere and is returned to the soil by rain, completing the cycle.

The sole source of iodine is through diet, which in turn is dependent upon the iodine content of water and soil.

The coastal regions of the world are much richer in iodine content than the soils further inland, where the problem gets more compounded by continuous leaching of iodine from the soil [1].

Therefore, crops grown in such soil remain iodine deficient, and even the groundwater in these areas is deficient in iodine.

Iodine and The Human Body

Iodine is mostly concentrated in the thyroid gland.

A healthy adult body contains 15-20 mg of iodine, 70-80% of which is stored in the thyroid gland.

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The daily physiological requirement during adult life is 150 micrograms.

During pregnancy and lactation period is 200 micrograms, and during the neonatal period is 40 micrograms.

Normally, about 120 micrograms of iodide are taken up by the thyroid gland for the synthesis of thyroid hormones.

Iodine Metabolism

Iodine metabolism in the human body is facilitated through a series of stages involving the hypothalamus, pituitary, thyroid gland, and blood.

The thyroid gland plays a central role in the metabolism of iodine.

The gland comprises multiple follicles lined by follicular cells resting on a basement membrane.

The follicles are filled by a clear viscous material called colloid.

The colloid is a glycoprotein called thyroglobulin [3].

The 3 steps of iodine metabolism are the following:

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1st Step: Iodine Trapping

Iodine trapping is the first step in the metabolism of iodine.

This process involves the uptake of iodide from the capillaries into the follicular cells (thyroid epithelial cells) of the gland by an active transport system.

This occurs against chemical and electrical gradients by sodium/iodide symporters (NIS) found in the basolateral membrane of the follicular cells.

Symporters are integral membrane proteins that are involved in the transport of many different types of molecules across the cell membrane.

The energy required for this process is linked to the ATPase dependent Na+/ K+ pump, which is present in the plasma membrane of all human cells [4].

2nd Step: Production of Thyroglobulin

Synthesis and secretion of thyroglobulin is the second step.

It occurs by another independent process within the follicular cells.

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Particularly, the synthesis starts on the rough endoplasmic reticulum (RER) as peptide units of molecular weight of 330,000 g/mol.

Later these units combine into a dimer, followed by the addition of carbohydrate moieties, after which the molecule moves to the Golgi apparatus.

The completed thyroglobulin molecule contains about 140 tyrosine residues, which serve as a substrate for the synthesis of thyroid hormones [5].

The thyroglobulin is contained within small vesicles, which then move towards the apical surface of the plasma membrane, before being released into the follicular lumen.

3rd Step: Iodide Oxidation

The third step is the oxidation of iodide.

The iodide within the follicular cells moves towards the apical surface of the plasma membrane, to enter into the follicular lumen.

This transport is facilitated by a sodium independent iodide/chloride transporter protein called pendrin.

The iodide is then immediately oxidized to iodine by the thyroid peroxidase (TPO) enzyme.

This is followed by the organification of thyroglobulin, a process in which iodine is incorporated into thyroglobulin for the production of thyroid hormones.

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Iodination first occurs at position 3 to form monoiodotyrosine (MIT), and then at position 5 to form diiodityrosine (DIT).

Iodination of tyrosine is followed by a coupling reaction, whereby, two molecules of diiodityrosine (DIT) couple to form thyroxine (T4), and one molecule of monoiodotyrosine (MIT) couples with one molecule of diiodityrosine (DIT) to form triiodothyronine (T3) [5].

The reaction is catalyzed by the enzyme thyroid peroxidase (TPO) [6].

Thyroid hormones are then stored inside the thyroid follicles as colloid for several months.

The stored hormones can meet the body’s requirements for up to 3 months [5].

Thyroid Hormone Production

The colloid containing iodinated thyroglobulin undergoes endocytosis, whereby it is salvaged from the follicular lumen by epithelial cells.

This is facilitated via the thyroglobulin receptor megalin, which is present on the apical membrane of the epithelial cells.

The colloid now enters the cytoplasm in the form of colloid droplets, which move towards the basal membrane, possibly by way of microtubule and microfilament function.

The colloid droplets next fuse with lysosome vesicles, which contain proteolytic enzymes/proteases.

The proteases/proteolytic enzymes help digest the thyroglobulin molecule, releasing T4, T3, diiodityrosine (DIT), and monoiodotyrosine (MIT) into the cytoplasm.

While T4 and T3 diffuse via the basal surface into the bloodstream, monoiodotyrosine (MIT) and diiodityrosine (DIT) get rapidly deiodinated by the deiodinase enzymes.

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This mechanism helps to retrieve iodide, as well as tyrosine for recycling. In the bloodstream, T4 and T3 may circulate in the bound or free form.

While 99% of T4 and T3 circulate in the bound form, less than 1% circulates in an unbound (free) form.

The thyroid hormone-binding proteins include thyroxine-binding globulin (TBG), thyroxine-binding prealbumin (TBPA), and thyroxine-binding albumin (TBA).

The binding of hormones, apart from serving as a reservoir, also helps to prevent urinary loss of hormones.

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The unbound hormones are biologically active.

About 80 percent of circulating T3, the most active thyroid hormone is derived from the peripheral deiodination of the T4 hormone, mainly in the liver, kidneys, and intestines [7].

Thyroid secretion is regulated by the pituitary gland through TSH, which operates on a feed-back mechanism depending on the T4 levels in the blood.

A fall in T4 levels stimulates the pituitary to increase its TSH secretion, which in turn stimulates the thyroid gland to release T4 in the circulation to maintain normal levels of the hormone [8].

Iodine Excretion

The thyroid gland secretes 80 micrograms of iodine in the form of T3 and T4 hormones per day.

About 40 micrograms of iodine secreted appear in the extracellular fluid (ECF) per day.

T3 and T4 are metabolized in the liver, which releases about 60 micrograms of iodine into the extracellular fluid (ECF), and 20 micrograms of iodine into the bile to be excreted in stools.

On average, 365-480 micrograms of iodine get excreted in urine and 20 micrograms in stools per day [910].

Sweat is another potent source of iodine excretion, especially in athletes.

Since the thyroid possesses a remarkably efficient iodine-trapping mechanism, it normally maintains a gradient of 100:1 between the iodine content of thyroid cells and extra-cellular iodine, which explains why serum iodine is a very poor indicator of iodine status, except for severe deficiency [11]

Extrathyroid Actions of Iodine

While a major portion of iodine is concentrated in the thyroid gland, non-hormonal iodine is also found in a variety of body tissues, including mammary glands, eye, gastric mucosa, cervix, and salivary glands [12].

Except for mammary tissue, the function of iodine in these tissues is still not clear.

Accumulation of iodine in the breast plays an important role during breastfeeding in fetal and neonatal development.

Additionally, such iodine has been proven to exert an antioxidant effect. In the presence of hydrogen peroxide and peroxidase (free radicals), iodide acts as an electron donor, thereby decreasing damage by oxygen free radicals [1314].

On the contrary, breasts with inadequate iodine stores are prone to get damaged by accumulating high levels of malondialdehyde, a product of lipid peroxidation [1516].

Much like ascorbic acid, iodine concentrations as low as 15 micromoles (μmols), can have significant antioxidant effects [17].

This antioxidant effect of iodine could explain the therapeutic effects of seaweed baths or iodine-rich solutions that were historically used to treat many diseases [17].

Furthermore, animal studies have proven that iodine normalizes elevated adrenal corticosteroid hormone secretion related to stress, and reverses the effects of hypothyroidism on the ovaries, testicles, and thymus of thyroidectomized rats [1819].

Iodine may also play a role in immune function- it has been shown that when human leukocytes were placed in a medium containing 10-6 M iodide, they synthesize thyroxine [20].

Iodine Sources

Iodine is mostly obtained from food sources, particularly fish, seafood, dairy, iodized salt, and vegetables grown on iodine-rich soil.

The remaining requirement is met from drinking water.

Fish, such as cod and tuna, shrimp, and other seafood are great iodine sources.

Seaweeds, such as wakame, nori, dulse, and mekabu, widely used in some Asian cultures for making soups, salads, and condiments, are also great sources of the trace element.

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Some dairy products, such as milk, yogurt, and cheese also contain iodine.

Cottage cheese, in particular, is one of the best sources.

One cup (226 grams) of cottage cheese provides 65 mcg, while one ounce (1 slice) of cheddar cheese provides about 12 mcg of iodine.

Probably the easiest way to obtain iodine is by consuming iodized salt, which provides 75 mcg per gram.

If someone avoids excess salt, the use of iodine drops in the form of nascent iodine is recommended in cases where the diet is not plentiful in iodine.

Iodine is not toxic up to 1000 mcg per day for the majority of the population [24].

Concerning supplements, our pick is nascent iodine by Future Kind as it is: 1) Certified organic 2) Alcohol-free 3) Created from ancient salt deposits located more than 7,000 feet below the earth’s surface.

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Assessing Iodine Status

Four methods are generally recommended for the assessment of iodine nutrition in populations: urinary iodine concentration (UIC), the goiter rate, serum thyroid-stimulating hormone (TSH), and serum thyroglobulin (Tg).

These indicators are complementary: urinary iodine concentration (UIC) is a sensitive indicator of recent iodine intake (days), thyroglobulin (Tg) shows an intermediate response (weeks to months), while changes in the goiter rate reflect long-term iodine nutrition (months to years).

Since iodine is released from the body through urine, the best way to determine iodine deficiency across a large population is to measure the amounts of iodine in urine samples.

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The World Health Organization (WHO) defines iodine deficiency as a median urinary iodine concentration of less than 50 μg/L in a population [21].

Iodine Deficiency

Iodine Deficiency Disorder (IDD) is the most common endocrine disorder in the world, and also the most preventable cause of mental retardation [1].

Iodine Deficiency Disorder (IDD) is a term that collectively reflects the clinical and sub-clinical manifestations of iodine deficiency [21].

In 1998, one-third of the worlds′ population lived in iodine-deficient areas [2].

The two major factors responsible for iodine deficiency are inadequate iodine intake and inadequate iodine utilization.

Inadequate iodine intake may be secondary to the low iodine content of the soil, and consequently of the consumed food, or the low consumption of seafood dictated by its high cost and low availability.

On the other hand, the presence of goitrogens in certain foods may lead to inadequate iodine utilization.

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Goitrogens which get their name from the term ‘goiter’, which means enlargement of the thyroid gland, are substances that disrupt the production of thyroid hormones by interfering with iodine uptake in the thyroid gland [22].

This disruption triggers the pituitary to release thyroid-stimulating hormone (TSH), which then promotes the growth of thyroid tissue, eventually leading to goiter (enlarged thyroid).

Dietary Goitrogens

FoodsMechanism
Cassava, Lima beans, Linseed, Sorghum, Sweet potatoContain cyanogenic glucosides, which are metabolized to thiocyanates and compete with iodine for thyroidal uptake
Cruciferous vegetables: Cabbage, Kale, Cauliflower, Broccoli, Turnips, RapeseedContains glucosinolates- metabolites that compete with iodine for thyroidal uptake
Soy, MilletFlavonoids impair thyroid peroxidase activity
Nutrients
Selenium deficiencyAccumulated peroxides may damage the thyroid and deiodinase deficiency impairs thyroid hormone synthesis
Iron deficiencyReduces heme-dependent thyroperoxidase activity in the thyroid and may blunt the efficacy of iodine prophylaxis
Vitamin A deficiencyIncreases TSH stimulation and goiter through decreased vitamin A-mediated suppression of the pituitary TSHβ gene

Dangers of Iodine Deficiency

Since iodine is an indispensable component of T3 and T4 hormones, its deficiency interferes seriously with the synthesis of these hormones.

For some time, the thyroid compensates by releasing the hormones stored as components of thyroglobulin molecules.

But when stores get exhausted and blood levels of T4 start declining, the pituitary intervenes by increasing TSH output.

TSH stimulates the thyroid to increase the uptake of iodide and ensure the release of thyroid hormones in adequate amounts.

However, in a state of deficiency, when iodide uptake of thyroid is seriously hampered, TSH fails to promote the release of T4, ending up with hyperplasia of the follicular cells.

In a situation of severe iodine deficiency, while the levels of T4 remain low, the levels of TSH remain high.

Under continuing TSH stimulation in endemic areas, the thyroid gland undergoes hypertrophy and hyperplasia of follicular cells, and in the process, enlarges in size and appears as a goiter, which in certain cases may attain an enormous size.

The damage caused to the human body due to iodine deficiency is in actuality the result of thyroid hormone deficiency.

The effects of Iodine Deficiency Disorder (IDD) in humans are different depending on the stage of life [23].

  • Pregnancy: Spontaneous abortions, Stillbirths, Maldevelopment of fetal brain, Increased perinatal morbidity and mortality, Birth of cretins.
  • Neonate: Neonatal goiter, Neonatal hypothyroidism, Endemic neurocognitive impairment, Increased susceptibility of the thyroid gland to nuclear radiation.
  • Childhood: Goiter, Low IQ, Impaired learning, Mental retardation, Delayed motor development, Stunted Growth, Apathy, Muscular disorders, Paralysis, Speech and hearing defects, High perinatal mortality, High infant mortality.
  • Adolescent: Mental retardation, Growth retardation
  • Adult and all ages: Goiter with its complications, Hypothyroidism, Increased susceptibility of the thyroid gland to nuclear radiation, Apathy, Impaired mental function, Reduced work output.

Iodine Toxicity

The recommended dietary allowance (RDA) of iodine for adults is 150 micrograms/day, 220 to 250 micrograms/day for pregnant women, and 250 to 290 micrograms/day for breastfeeding women [25].

It is believed that up to 1,000 mcg or 1 mg/day is safe for most people [26].

The sources of excess iodine may be due to the overconsumption of iodized salt, drinking water, milk rich in iodine, seafood, certain seaweeds, and dietary supplements containing iodine [27].

Ingestion of over 1.1 milligrams/day of iodine may be harmful and can lead to acute and/or chronic toxicity.

Iodine excess can cause subclinical or overt thyroid dysfunction in patients with specific risk factors, including those with pre-existing thyroid disease, the elderly, fetuses, and neonates.

The effects of excess iodine are variable among individuals and relate to the individuals’ underlying thyroid status [28].

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Iodine toxicity may lead to thyroiditis (inflammation of the thyroid gland), hypothyroidism (underproduction of thyroid hormones), hyperthyroidism (overproduction of thyroid hormones), and thyroid papillary cancer [29].

Clinical features of iodine toxicity from oral ingestion can range from mild to severe.

Mild symptoms consist of gastrointestinal upset (GI) upset, nausea, vomiting, and diarrhea, which may progress to delirium, stupor, and shock.

Rarely, it can even prove fatal [30].

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Excessive Iodine Consumption in Japan

Traditional Japanese food contains significant amounts of dietary iodine.

The Japanese possibly consume at least 7,000 mcg of iodine daily from kombu alone [31].

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It has been estimated that the Japanese consumption of dietary iodine exceeds the upper safety limit of 1 mg by approximately 5-14 times [1].

These higher levels appear to have no suppressive effect on the thyroid function in normal individuals, yet excess iodine intake could cause problems in patients with thyroid nodules, hyperthyroidism, and autoimmune thyroid disease (i.e., Hashimoto’s thyroiditis) [1].

On the contrary, it has been interestingly observed that Japanese women who consume a high iodine content diet have a low incidence of benign and malignant breast disease.

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However, this protective advantage is lost in the same ethnic group once they immigrate to other countries [323334].

Japan also has a low incidence of autoimmune thyroiditis [35].

Stadel has postulated that given the geographical distribution of iodine deficiency, there is a low incidence of cancers of the prostate, endometrium, ovary, and breast in populations consuming diets with high iodine content [36].

Conclusion

Iodine is an essential micronutrient that plays a pivotal role in human metabolism.

It is oxidized to produce iodine-containing thyroid hormones, namely, triiodothyronine (T3) and thyroxine (T4).

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Thyroid hormones are necessary for controlling growth, metabolism, body temperature, and many other bodily functions.

They are also crucial for fetal and neonatal brain development [37].

The recommended daily intake of iodine for adults is 150 mcg per day.

The best sources of iodine include fish, seafood, dairy, iodized salt, and vegetables grown on iodine-rich soil.

Iodine metabolism occurs in different tissues of the body, including the hypothalamus, pituitary, thyroid gland, and blood.

70-80% of iodine is stored in the thyroid gland, but is also present in other tissues, where its action remains unknown.

Iodine deficiency has long been recognized as a global health problem, and still remains a leading cause of preventable fetal brain damage [38].

Iodine deficiency can create serious complications depending on the stage of life of the person (i.e., pregnancy, neonates, children, adolescents, adults, elderly).

For example, iodine deficiency in pregnancy leads to hypothyroidism and impaired infant neurobehavioral and cerebral development [39].

Because >90% of ingested iodine is excreted in the urine, iodine urinary excretion is the best indicator of recent iodine intake and status.

The upper limit of iodine intake is 1,000 mcg or 1 mg/day, although the Japanese population consumes multiple times that quantity with positive health benefits, including reduced risk of certain cancers and autoimmune thyroid conditions, such as Hashimoto’s.

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About George Kelly

George Kelly M.Sc is a Sports Nutritionist, Functional Nutritional Therapy Practitioner (FNTP), and Metabolic Type expert. He is the CEO and lead author of Metabolic Body.


References

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