Iodine deficiency

Iodine deficiency is a lack of the trace element iodine, an essential nutrient in the diet. It may result in metabolic problems such as goiter, sometimes as an endemic goiter as well as congenital iodine deficiency syndrome due to untreated congenital hypothyroidism, which results in developmental delays and other health problems. Iodine deficiency is an important global health issue, especially for fertile and pregnant women. It is also a preventable cause of intellectual disability. Iodine is an essential dietary mineral for neurodevelopment among children. The thyroid hormones thyroxine and triiodothyronine contain iodine. In areas with little iodine in the diet, typically remote inland areas where no marine foods are eaten, deficiency is common. It is common in mountainous regions where food is grown in iodine-poor soil. Prevention includes adding small amounts of iodine to table salt, a product known as iodized salt. In areas of deficiency, iodine compounds have also been added to other foodstuffs, such as flour, water, and milk. Seafood is also a well known source of iodine. In the U.S., the use of iodine has decreased over concerns of overdoses since the mid-20th century as the iodine antagonists bromine, perchlorate and fluoride have become more ubiquitous. In particular, around 1980 the practice of using potassium iodate as dough conditioner in bread and baked goods was gradually replaced by the use of other conditioning agents such as bromide. Iodine deficiency resulting in goiter occurs in 187 million people globally as of 2010 (2.7% of the population). It resulted in 2700 deaths in 2013, up from 2100 deaths in 1990.

Signs and symptoms

Goiter

A low amount of thyroxine (one of the two thyroid hormones) in the blood, due to lack of dietary iodine to make it, gives rise to high levels of thyroid stimulating hormone (TSH), which stimulates the thyroid gland to increase many biochemical processes; the cellular growth and proliferation can result in the characteristic swelling or hyperplasia of the thyroid gland or goiter. In mild iodine deficiency, levels of triiodothyronine (T3) may be elevated in the presence of low levels of levothyroxine, as the body converts more of the levothyroxine to triiodothyronine as compensation. Some such patients may have a goiter, without an elevated TSH. The introduction of iodized salt since the early 1900s has eliminated this condition in many affluent countries; however, in Australia, New Zealand, and several European countries, iodine deficiency is a significant public health problem. It is more common in developing countries. Public health initiatives to lower the risk of cardiovascular disease have resulted in lower discretionary salt use at the table. Additionally, there is a trend towards consuming more processed foods in Western countries. The non-iodized salt used in these foods means that people are less likely to obtain iodine from adding salt during cooking. Goiter is said to be endemic when its prevalence in a population is > 5%, and in most cases, goiter can be treated with iodine supplementation. However, if a goiter is untreated for around five years, iodine supplementation or thyroxine treatment may not reduce thyroid gland size because the thyroid is permanently damaged.

Congenital iodine deficiency syndrome

Congenital iodine deficiency syndrome, previously known as cretinism, is a condition associated with iodine deficiency and goiter, commonly characterized by mental deficiency, deafness, squint, disorders of stance and gait and stunted growth due to hypothyroidism. Paracelsus was the first to point out the relation between goitrous parents and their mentally disabled children. As a result of restricted diet, isolation, intermarriage, etc., as well as low iodine content in their food, children often had peculiar stunted bodies and retarded mental faculties, a condition later known to be associated with thyroid hormone deficiency. Diderot, in his 1754 Encyclopédie, described these patients as "crétins". In French, the term "crétin des Alpes" also became current, since the condition was observed in remote valleys of the Alps in particular. The word cretin appeared in English in 1779. While reporting recent progress towards overcoming iodine-deficiency disorders worldwide, The Lancet noted: "According to World Health Organization, in 2007, nearly 2 billion individuals had insufficient iodine intake, a third being of school age." A conclusion was made that the single most preventable cause of intellectual disability is that of iodine deficiency.

Fibrocystic breast changes

There is preliminary evidence that iodine deficiency enhances the sensitivity of breast tissue to estrogen. In rats treated with estradiol, iodine deficiency has been shown to lead to changes similar to benign breast changes that are reversible by increased iodine in the diet. In a few studies, iodine supplementation had beneficial effects (such as reducing the presence of breast cyst, fibrous tissue plaques, and breast pain) in women with fibrocystic breast changes. Protective effects of iodine on breast cancer have been postulated from epidemiologic evidence and described in animal models. Given the antiproliferative properties of iodine in breast tissue, molecular iodine supplementation has been suggested as an adjuvant in breast cancer therapy.

Risk factors

Following is a list of potential risk factors that may lead to iodine deficiency:

Low dietary iodine Selenium deficiency Pregnancy Exposure to radiation Increased intake/plasma levels of goitrogens, such as calcium Sex (higher occurrence in women) Smoking tobacco Alcohol (reduced prevalence in users) Oral contraceptives (reduced prevalence in users) Perchlorates Thiocyanates Age (for different types of iodine deficiency at different ages)

Pathophysiology Iodine accounts for 65% of the molecular weight of T4 and 59% of T3. There is a total of 15–20 mg of iodine in the human body, primarily concentrated in thyroid tissue and hormones. Thirty percent of iodine is distributed in other tissues, including the mammary glands, eyes, gastric mucosa, choroid plexus, arterial walls, the cervix, and salivary glands. In the cells of these tissues, iodide enters directly by sodium-iodide symporter (NIS).

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