Minerals >> Iodine Deficiency

Iodine deficiency is now accepted as the most common cause of preventable brain damage in the world. According to the World Health Organization (WHO), iodine deficiency disorders (IDD) affect 740 million people throughout the world, and nearly 50 million people suffer from some degree of IDD-related brain damage. The spectrum of IDD includes mental retardation, hypothyroidism, goiter, and varying degrees of other growth and developmental abnormalities . Nearly 2.2 million people throughout the world live in areas of iodine deficiency and risk its consequences. Major international efforts have produced dramatic improvements in the correction of iodine deficiency in the 1990's mainly through the use of iodized salt and iodized vegetable oil in iodine deficient countries. For more information on the international effort to eradicate iodine deficiency visit the Web sites of the International Council for Control of Iodine Deficiency Disorders (ICCIDD) or the WHO.

Thyroid enlargement, or goiter, is one of the earliest and most visible signs of iodine deficiency. The thyroid enlarges in response to persistent stimulation by TSH (see functions). In mild iodine deficiency, this adaptation response may be enough to provide the body with sufficient thyroid hormone. However, more severe cases of iodine deficiency result in hypothyroidism. Adequate iodine intake will generally reduce the size of goiters, but the reversibility of the effects of hypothyroidism depends on an individual's stage of development.  Iodine deficiency has adverse effects in all stages of development, but is most damaging to the developing brain. In addition to regulating many aspects of growth and development, thyroid hormone is important for the myelination of the central nervous system, which is most active before and shortly after birth. 

The effects of iodine deficiency by developmental stage

Prenatal development: Fetal iodine deficiency is caused by iodine deficiency in the mother. One of the most devastating effects of maternal iodine deficiency is congenital hypothyroidism, a condition that is sometimes referred to as cretinism and results in irreversible mental retardation. Congenital hypothyroidism occurs in two forms, although there is considerable overlap between them. The neurologic form is characterized by mental and physical retardation and deafness. It is the result of maternal iodine deficiency that affects the fetus before its own thyroid is functional. The myxedematous or hypothyroid form is characterized by short stature and mental retardation. In addition to iodine deficiency, the hypothyroid form has been associated with selenium deficiency and the presence of goitrogens in the diet that interfere with thyroid hormone production (see Goitrogens). 

Newborns and infants: Infant mortality is increased in areas of iodine deficiency, and several studies have demonstrated an increase in childhood survival when iodine deficiency is corrected . Infancy is a period of rapid brain growth and development. Sufficient thyroid hormone, which depends on adequate iodine intake, is essential for normal brain development. Even in the absence of congenital hypothyroidism, iodine deficiency during infancy may result in abnormal brain development and, consequently, impaired intellectual development.

Children and adolescents: Iodine deficiency in children and adolescents is often associated with goiter. The incidence of goiter peaks in adolescence and is more common in girls. School children in iodine deficient areas show poorer school performance, lower IQs, and a higher incidence of learning disabilities than matched groups from iodine-sufficient areas. A recent meta-analysis of 18 studies concluded that iodine deficiency alone lowered mean IQ scores in children by 13.5 points.

Adults: Inadequate iodine intake may also result in goiter and hypothyroidism in adults. Although the effects of hypothyroidism are more subtle in the brains of adults than children, recent research suggests that hypothyroidism results in slower response times and impaired mental function.

Pregnancy and lactation: Iodine requirements are increased in pregnant and breastfeeding women. Iodine deficiency during pregnancy has been associated with increased incidence of miscarriage, stillbirth, and birth defects. Moreover, severe iodine deficiency during pregnancy may result in congenital hypothyroidism in the offspring (see Prenatal development) . Iodine deficient women who are breastfeeding may not be able to provide sufficient iodine to their infants who are particularly vulnerable to the effects of iodine deficiency. A daily prenatal supplement providing 150 mcg of iodine will help to ensure that pregnant and breastfeeding women consume sufficient iodine during these critical periods.

Because iodine deficiency results in increased iodine trapping by the thyroid, iodine deficient individuals of all ages are more susceptible to radiation-induced thyroid cancer as well as to iodine-induced hyperthyroidism . 

Nutrient Interactions

Selenium deficiency can exacerbate the effects of iodine deficiency. Iodine is essential for the synthesis of thyroid hormone, but selenium-dependent enzymes (iodothyronine deiodinases) are also required for the conversion of thyroxine (T4) to the biologically active thyroid hormone, triiodothyronine (T3) . Deficiencies of vitamin A or iron may also exacerbate the effects of iodine deficiency.

Goitrogens

Some foods contain substances that interfere with iodine utilization or thyroid hormone production, known as goitrogens. The occurrence of goiter in the Democratic Republic of Congo has been related to the consumption of casava, which contains a compound that is metabolized to thiocyanate and blocks thyroidal uptake of iodine. Some species of millet and cruciferous vegetables (for example, cabbage, broccoli, cauliflower, and Brussel sprouts) also contain goitrogens. The soybean isoflavones, genistein and daidzein, have also been found to inhibit thyroid hormone synthesis . Most of these goitrogens are not of clinical importance unless they are consumed in large amounts or there is coexisting iodine deficiency. Recent findings also indicate that tobacco smoking may be associated with an increased risk of goiter in iodine deficient areas.

Individuals at risk of iodine deficiency

While the risk of iodine deficiency for populations living in iodine-deficient areas without adequate iodine fortification programs is well recognized, concerns have been raised that certain subpopulations may not consume adequate iodine in countries considered iodine-sufficient. Vegetarian and nonvegetarian diets that exclude iodized salt, fish, and seaweed have been found to contain very little iodine. Urinary iodine excretion studies suggest that iodine intakes are declining in Switzerland, New Zealand, and the U.S., possibly due to increased adherence to dietary recommendations to reduce salt intake. Although iodine intake in the U.S. remains sufficient, further monitoring of iodine intake has been recommended.

The Recommended Dietary Allowance (RDA)

The RDA for iodine was reevaluated by the Food and Nutrition Board (FNB) of the Institute of Medicine in 2001. The recommended amounts were calculated using several methods, including the measurement of iodine accumulation in the thyroid glands of individuals with normal thyroid function. These recommendations are in agreement with those of the International Council for Control of Iodine Deficiency Disorders, the World Health Organization, and UNICEF. 

See also:

• Iodine Deficiency: the common cause of brain damage

• Iodine & Diseases: Radiation-induced thyroid cancer

• Iodine & Disease Treatment: Fibrocystic breast condition

• Iodine Functions: essential component of the thyroid hormones

• Iodine Safety: Acute toxicity

• Iodine Sources: Food sources & Supplements

Bee Pollen
 

Royal Jelly
 

Viagra