Nutritional Deficiencies - Health Concerns

Iodine - updated: 01 December 2008

The disorders induced by iodine deficiency

Thyroid. 1994 Spring;4(1):107-28

Delange F.

This paper reviews present knowledge on the etiology, pathophysiology, complications, prevention, and therapy of the disorders induced by iodine deficiency. The recommended dietary allowances of iodine are 100 micrograms/day for adults and adolescents, 60-100 micrograms/day for children aged 1 to 10 years, and 35-40 micrograms/day in infants aged less than 1 year. When the physiological requirements of iodine are not met in a given population, a series of functional and developmental abnormalities occur including thyroid function abnormalities and, when iodine deficiency is severe, endemic goiter and cretinism, endemic mental retardation, decreased fertility rate, increased perinatal death, and infant mortality. These complications, which constitute a hindrance to the development of the affected populations, are grouped under the general heading of iodine deficiency disorders (IDD). At least one billion people are at risk of IDD. Iodine deficiency, therefore, constitutes one of the most common preventable causes of mental deficiency in the world today. Most of the affected populations live in mountainous areas in preindustrialized countries, but 50 to 100 million people are still at risk in Europe. The most important target groups to the effects of iodine deficiency from a public health point of view are pregnant mothers, fetuses, neonates, and young infants because the main complication of IDD, i.e., brain damage resulting in irreversible mental retardation, is the consequence of thyroid failure occurring during pregnancy, fetal, and early postnatal life. The main cause of endemic goiter and cretinism is an insufficient dietary supply of iodine. The additional role of naturally occurring goitrogens has been documented in the case of certain foods (milk, cassava, millet, nuts) and bacterial and chemical water pollutants. The mechanism by which the thyroid gland adapts to an insufficient iodine supply is to increase the trapping of iodide as well as the subsequent steps of the intrathyroidal metabolism of iodine leading to preferential synthesis and secretion of triiodotyronine (T3). They are triggered and maintained by increased secretion of TSH, which is ultimately responsible for the development of goiter. The acceleration of the main steps of iodine kinetics and the degree of hyperstimulation by TSH are much more marked in the pediatric age groups, including neonates, than in adults, and the development of goiter appears as an unfavorable side effect in the process of adaptation to iodine deficiency during growth. The most serious complication of iodine deficiency is endemic cretinism, a syndrome characterized by irreversible mental retardation together with either a predominant neurological syndrome or predominant hypothyroidism, or a combination of both syndromes

Publication Types:

• Review

Increased risk of maternal thyroid failure with pregnancy progression in an iodine deficient area with major iodine deficiency disorders

Thyroid. 1999 Jan;9(1):19-24

Vermiglio F, Lo Presti VP, Castagna MG, Violi MA, Moleti M, Finocchiaro MD, Mattina F, Artemisia A, Trimarchi F.

In an effort to assess the impact of moderate iodine deficiency on maternal thyroid function during pregnancy, we measured serum thyrotropin, total and free thyroid hormones, thyroid-binding globulin (TGB) at 8, 14, 20, 29, and 36 weeks of gestation, along with urinary iodide excretion, in 10 healthy women from a moderately iodine deficient region (group A), and compared them with 6 women from an iodine sufficient region (group B). Serum total thyroxine (T4) fell significantly in group A, and was significantly lower than in group B at 29 and 36 weeks (p<0.05). TBG saturation was significantly lower in group A throughout pregnancy, and declined in both groups as pregnancy progressed. Free thyroxine (T4) and triiodothyronine (T3) concentrations fell in both groups, and FT4 values were significantly lower in group A than group B in the third trimester (p<0.05). Urinary iodine excretion was lower in group A women with respect to group B and did not vary significantly in either group as gestation progressed. The serum T3/T4 molar ratio increased through pregnancy only in group B. Thyrotropin concentrations rose in both groups through pregnancy, and were higher in group A at term (p< 0.01). The incidence of isolated hypothyroxinemia or biochemical hypothyroidism doubled (30% to 70%) between midgestation and term in group A, suggesting that moderate iodine deficiency may result in maternal thyroid failure during the later stages of pregnancy.

Publication Types:

• Study

Hypothyroidism

Lancet. 2004 Mar 6;363(9411):793-803

Roberts CG, Ladenson PW. Roberts CG, Ladenson PW.

Hypothyroidism is common, potentially serious, often clinically overlooked, readily diagnosed by laboratory testing, and eminently treatable. The condition is particularly prevalent in older women, in whom autoimmune thyroiditis is common. Other important causes include congenital thyroid disorders, previous thyroid surgery and irradiation, drugs such as lithium carbonate and amiodarone, and pituitary and hypothalamic disorders. Worldwide, dietary iodine deficiency remains an important cause. Hypothyroidism can present with nonspecific constitutional and neuropsychiatric complaints, or with hypercholesterolaemia, hyponatraemia, hyperprolactinaemia, or hyperhomocysteinaemia. Severe untreated hypothyroidism can lead to heart failure, psychosis, and coma. Although these manifestations are neither specific nor sensitive, the diagnosis is confirmed or excluded by measurements of serum thyrotropin and free thyroxine. Thyroxine replacement therapy is highly effective and safe, but suboptimal dosing is common in clinical practice. Patient noncompliance, drug interactions, and pregnancy can lead to inadequate treatment. Iatrogenic thyrotoxicosis can cause symptoms, and, even when mild, provoke atrial fibrillation and osteoporosis. We summarise present understanding of the history, epidemiology, pathophysiology, and clinical diagnosis and management of hypothyroidism.

Publication Types:

• Review

Iodine nutrition and neonatal hypothyroidism

Rev Med Brux. 1994 Nov-Dec;15(6):359-65

Delange F.

This paper summarizes the research activities and the actions conducted and implemented by the author during the past 30 years in the field of the disorders induced by iodine deficiency and by neonatal hypothyroidism. This work was conducted within the framework of the activities of the author in the Department of Pediatrics in Saint-Pierre Hospital. The work resulted in original contributions to epidemiology, etiopathogenesis, clinical manifestations, diagnostic procedures, complications, prevention and therapy of the disorders resulting from iodine deficiency or neonatal hypothyroidism. Special attention was devoted to the prevention of impairment of brain and intellectual development resulting from both conditions in the infant.

Publication Types:

• Review

Iodine deficiency in Europe and its consequences: an update

Eur J Nucl Med Mol Imaging. 2002 Aug;29 Suppl 2:S404-16

Delange F.

This paper updates the information on the prevalence of the disorders induced by iodine deficiency (IDD) in Europe. Thirty-two European countries were still affected by mild to severe iodine deficiency in the late 1990s. The most severely affected countries were in Eastern Europe, including Central Asia, but Western Europe was also still affected. National surveys recently conducted in 11 of these countries show that, with the exception of the Netherlands, none has yet reached a state of iodine sufficiency, though very significant improvement in the situation has been evidenced in many of them, e.g. Poland, Bulgaria and Macedonia. The consequences of persisting iodine deficiency are goitre, hyperavidity of the thyroid for iodide (which increases the risk of thyroid irradiation in the event of a nuclear accident) and subclinical hypothyroidism during pregnancy and early infant (with a concomitant risk of minor brain damage and irreversible impairment of the neuropsychointellectual development of offspring). Access to iodised salt at the household level in European countries affected by IDD increased from 5%-10% in 1990 to 28% in 1999. This constitutes encouraging progress. However, in terms of access of iodine-deficient countries to iodised salt, Europe remains the worst region in the world, as shown by the fact that the mean figure worldwide in 1999 was 68%. In Latin America it even reached 90%. Salt iodisation has to be further implemented in Europe. Until that goal is achieved, iodine supplementation in those groups most sensitive to the effects of iodine deficiency (pregnant and lactating women and young infants) will have to be considered in the most severely affected areas.

Publication Types:

• Review

Disorders due to iodine deficiency

Acta Clin Belg. 1990;45(6):394-411

Delange F.

1. An insufficient dietary supply of iodine results in the development of a variety of disorders of thyroid function and development of the fetus and young infants, grouped under the general heading of Iodine Deficiency Disorders, IDD. Endemic goiter constitutes the most spectacular disorder from the clinical and epidemiological point of view. However, the most serious consequence of iodine deficiency is the impact on neuro-intellectual development at a population level, varying from endemic mental retardation to the complete picture of endemic cretinism. 2. Considering that mental retardation due to iodine deficiency represents the longterm consequence of hypothyroidism occurring during the perinatal period, it is presently recognized that the target groups to the effects of iodine deficiency at a population level are, by order of priority, the fetus, the newborn, the pregnant woman, the child and, finally, the adult. 3. The newborn is more susceptible than the adult to the effects of iodine deficiency. Consequently, systematic screening for congenital hypothyroidism in endemic areas is a particularly sensitive index for detecting the presence and action of goitrogens in the environment and for monitoring the effects of programs of iodine prophylaxis. 4. IDD are particularly prevalent in developing countries. However, large areas or even countries in Europe are still obviously iodine deficient. For example, the iodine intake in adults in Belgium is 50 to 70 micrograms/day which is lower than the recommended dietary allowance for iodine (at least 100 micrograms/day). 5. IDD should be corrected on a world scale, including in Europe. Special attention should be devoted to the protection of mother and child. Within this framework, the iodine content of formula milk should be increased in Europe. 6. Finally, correction of iodine deficiency in Europe would decrease the avidity of the thyroid for iodide and, consequently, would constitute the most efficient preventive measure in case of nuclear fallout.

Publication Types:

• Review

Publication Types:

• Review