1. What is iodine?
Iodine (atomic weight 126.9) is a natural chemical element of the earth (like oxygen, hydrogen, and iron). It occurs in a variety of chemical forms, the most important being: iodide (I-); iodate (IO3-), and elemental iodine (I2).
It is present in fairly constant amounts in seawater but its distribution over land and fresh water is uneven. Deficiency is especially associated in areas like high new mountains (e.g., Himalayas, Andes, Alps) and areas of frequent flooding, but many other areas are also deficient (e.g., Central Africa, Central Asia, much of Europe).
Iodine is an essential component of the hormones produced by the thyroid gland.
2. Why do we need iodine?
Iodine is an essential dietary nutrient for humans because it is a key component of the chemical structure of thyroid hormones. We need iodine because thyroid hormones are essential to human life.
The thyroid is a butterfly-shaped gland in the lower front part of the neck. It produces two hormones (thyroxine known as T4, and triiodothyronine known as T3), which have important functions throughout the body. The hormones are released into the bloodstream and carried to target organs, particularly the liver, kidneys, muscles, heart, and developing brain, where they influence their functions.
Our bodies must have adequate levels of thyroid hormone, and thus iodine, to grow and develop normally. This is why iodine is especially important during pregnancy, infancy, and childhood. But it is also important during adult life, for normal metabolism and function.
3. How much iodine should we get?
A teaspoon of iodine is all a person requires in a lifetime, but because iodine cannot be stored for long periods by the body, tiny amounts are needed regularly.
Several international groups have made recommendations, which are fairly similar. WHO and UNICEF recommend the following daily amounts:
Age 0-5 years: 90 micrograms (mcg)/day
Age 6-12 years: 120 mcg
Older than 12 years: 150 mcg
Pregnant and lactating women: 250 mcg
The Food and Nutrition Board, Institute of Medicine also sets the tolerable upper limits of the daily iodine intake as 1.1 mg (1100 mcg) for adults, with proportionately lower levels for younger age groups.
4. How is Iodine distributed in the environment?
Iodine (as iodide) is widely but unevenly distributed in the earth’s environment. In many regions, leaching from glaciations, flooding, and erosions have depleted surface soils of iodide, and most iodide is found in the oceans. The concentration of iodide in sea water is approximately 50 µg per liter.
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. However, iodine cycling in many regions is slow and incomplete, leaving soils and drinking water iodine depleted. Crops grown in these soils will be low in iodine, and humans and animals consuming food grown in these soils become iodine deficient. In plant foods grown in deficient soils, iodine concentration may be as low as 10 ppb dry weight, compared to 1 ppm in plants from iodine-sufficient soils.
Iodine deficiency in populations residing in low-iodine areas will persist until iodine enters the food chain through addition of iodine to foods (e.g. iodization of salt) or dietary diversification introduces foods produced outside the iodine-deficient area.
5. What are sources of dietary iodine?
Most of the iodine we consume comes from what we eat and drink. The native iodine content of most foods and beverages is low. In general, commonly consumed foods provide 3 to 80 µg per serving.
Foods of marine origin have higher iodine content because marine plants and animals concentrate iodine from seawater. Iodine in organic form occurs in high amounts in certain seaweeds. Inhabitants of the coastal regions of Japan, whose diets contain large amounts of seaweed, have remarkably high iodine intakes amounting to 50 to 80 mg/day. Salt water fish and seafood have high natural iodine content, but their contribution to the overall dietary iodine intake is modest unless consumed every day.
Freshwater fish reflect the iodine content of the water where they swim, which may be deficient. Other foods vary tremendously in iodine content, depending on their source and what may have been added. Plants grown in iodine-deficient soil do not have much iodine, nor do meat or other products from animals fed on iodine-deficient plants.
Because the breast concentrates iodine, milk and dairy products are usually a good source of iodine.
Dietary supplements often contain iodine. Certain health foods, such as some types of kelp, contain large amounts of iodine. But one of the most important source of Iodine presently is Iodized salt.
6. What is Iodized salt?
Iodized salt is a special case. Common salt (sodium chloride) does not naturally contain iodine. Iodine is added deliberately as one of the most efficient ways of improving iodine nutrition. In countries in which salt is iodized, it is generally the major dietary contributor to iodine intakes, i.e. household salt or salt used in food production.
WHO recommends levels of 20-40 mg iodine per kg salt. According to label declarations, commercially available iodized salt contains iodine in the range of 15-80 mg iodine per kg salt. Either potassium iodide or potassium iodate is used to fortify salt.
Boiling, baking, and canning of foods manufactured with iodized salt cause only small losses (10%) of iodine content.
Fortunately, due to Iodized salt, our India has shifted from an Iodine deficient country to an adequate Iodine country with 71.1% households consuming Iodized salt now.
7. What happens if we don’t get enough iodine?
Iodine deficiency has multiple adverse effects on growth and development in animals and humans. These are collectively termed the Iodine Deficiency Disorders (IDD), and are one of the most important and common human diseases. They result from inadequate thyroid hormone production due to lack of sufficient iodine.
Pregnancy-related problems: Iodine deficiency is especially important in women who are pregnant or nursing their infants. Severe iodine deficiency in the mother has been associated with miscarriages, stillbirth, preterm delivery, and congenital abnormalities in their babies. Thyroid hormones are essential for normal development of the brain. This is why the most damaging consequences of iodine deficiency are on fetal and infant development. If a fetus or newborn is not exposed to enough thyroid hormone, it may have permanent mental retardation, even if it survives. Low birth weights and decreased child survival also result from iodine deficiency. Iodine in this age group is also linked with growth. Iodine influences growth through its effects on the thyroid.
Iodine deficiency also causes Goiter and Hypothyroidism.
8. What is Cretinism?
Cretinism is a very severe degree of this brain damage; it includes permanent dense mental retardation, and varying degrees of additional developmental defects such as deaf mutism, short stature, spasticity, and other neuromuscular abnormalities.
Although new cases of cretinism are now rare, iodine deficiency still affects around 25% of the global population and can impair cognitive development. A meta-analysis of 18 studies concluded that moderate-to-severe iodine deficiency reduces mean IQ scores by 13.5 points. Iodine deficiency is thus considered the most common cause of preventable mental retardation worldwide.
9. What happens if we get too much iodine?
In the 1940s, Wolff and Chaikoff reported that high iodide exposure in rats resulted in a transient inhibition of thyroid hormone synthesis lasting approximately 24 hours (now known as the acute Wolff-Chaikoff effect), and that with continued administration of iodide, normal thyroid hormone synthesis resumed (escape from the acute Wolff-Chaikoff effect).
Iodine-induced hyperthyroidism, or the Jöd-Basedow phenomenon, represents a failure of the acute Wolff-Chaikoff effect. It occurs most frequently in individuals with a history of nodular goiters, which are most common in iodine deficient regions. In affected individuals, the nodules may escape the body’s usual controls, and they can start making too much thyroid hormone when their dietary iodine increases. In turn, failure to escape from the acute Wolff-Chaikoff effect results in iodine-induced hypothyroidism, when large amounts of iodine block the thyroid’s ability to make hormones.
Chronic excessive iodine intake may also result from ingestion of foods or supplements with very high iodine content such as kelp, or where there is high iodine content in drinking water.
Iodine excess is undesirable, but its consequences are not nearly so severe as those of iodine deficiency. Therefore, concern about iodine excess is not a reason to stop or avoid consumption of iodized salt.
10. How can we tell if we are getting the right amount of iodine?
Usually you as an individual won’t know how much iodine you are getting. You can make a rough calculation, based on (1) whether you use iodized salt; (2) how much salt you eat; (3) whether you take vitamins that contain iodine (many contain 150 mcg); and (4) whether you eat much meat, dairy products, or seafood.
For populations, a better way to learn the iodine intake is to measure the amount of iodine in representative urine samples. Most (more than 90%) of the iodine you ingest eventually comes out in the urine. Thus, the concentration of iodine in the urine, even in casual samples, is a good marker for iodine nutrition. Urine iodine concentration varies with fluid intake, so the established ranges have limited use for casual samples from an individual, but they are good for assessing a population group, because individual variations tend to average out. A median urinary iodine concentration between 100 and 200 mcg/L is ideal.
Routine laboratory tests of thyroid function are not as helpful as the urinary iodine concentration in assessing a population. The serum TSH (thyroid stimulating hormone or thyrotropin) is a test that is widely used clinically to assess thyroid function in individuals. TSH is released into the blood stream by the pituitary (an endocrine control gland at the base of the brain) in response to the amount of thyroid hormone in the blood stream. TSH tells the thyroid how much to work. It bases this decision on how much thyroid hormone is present in the blood. When blood thyroid hormone is low, serum TSH increases and this can be used as a measure for inadequate thyroid hormone production. The serum TSH is the most widely used test for diagnosing thyroid disease in individuals. However, the serum TSH is less valuable in recognizing iodine deficiency, because it can increase but still remain within the normal range.
An exception is the blood TSH in newborns. Most developed countries have a system of newborn screening, either with the blood TSH or thyroxine, to recognize congenital hypothyroidism. About one out of 4,000 newborns has congenital deficiency of thyroid hormone production, usually because the thyroid is absent or fails to develop properly. This newborn screening is important because prompt treatment with thyroid hormone can prevent most or all of the consequences of inadequate thyroid hormone on brain development.
Thyroid size (goiter):
Thyroid size is also a useful marker of iodine nutrition, because the iodine-deficient thyroid enlarges, as described above.