Regulation of Thyroid Hormone Metabolism in the Brain

Larsen, P. Reed

doi:10.1007/978-1-4613-0765-5_2

Cited by 2 publications

(2 citation statements)

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“…This paradoxical finding is explained by the fact that the direct effect of T4 on TSH suppression results from intrapituitary T4 to T3 conversion and the subsequent binding of T3 to the nucleus of the thyrotropes; in other tissues, the largest part of intracellular T3 originates from circulating T3 (130,131). These findings account for the observation in endemic goiter that normal serum T3 levels enable a patient to maintain an overall euthyroid status, but pituitary stimulation persists as long as the serum T4 level is depressed.…”

Section: Etiologymentioning

confidence: 99%

“…SCN (mg/dL)4.4 ± 0.3(119) 1.03 ±0.05(120) 12.7 ± 0.3(112) 182 ±5 (109) 3.6 ±0.2 (111) 0.35 ± 0.03 (111) 11.4 ±0.2 (204) 50 ± 1 (202) 8.2 ± 0.4 (201) 0.27 ± 0.01 (200) 1.8 ± 0.09 (130) 1.41 ±0.09 (128) 8.0 ± 0.5 (117) 196 ±6 (118) 14.0 ± 2.4 (120) 0.76 ± 0.03 (170) 7.4 ± 0.4 (83) 96 ±7 (84) 70.7 ± 13.1 (83) 0.66 ± 0.04(131) "In Brussels, Belgium and in the Ubangi endemic goiter area, Zaire. Results are given as mean ± SEM.…”

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The Disorders Induced by Iodine Deficiency

Delange¹

1994

Thyroid

561

447

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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.(ABSTRACT TRUNCATED AT 400 WORDS)

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Section: Etiologymentioning

confidence: 99%

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confidence: 99%

The Disorders Induced by Iodine Deficiency

Delange¹

1994

Thyroid

561

447

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Iodine Deficiency and the Brain

Hetzel

1999

Nutritional Neuroscience

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The effects of iodine deficiency on growth and development are known as the iodine deficiency disorders (IDDs). Most common is goitre at all ages, but most significant are the effects on brain development during pregnancy. The major effect of iodine deficiency is the clinical syndrome of endemic cretinism characterised in its fully developed form by mental defect, deaf mutism and spastic diplegia. This condition can be totally prevented by correction of the iodine deficiency before pregnancy. There is considerable variation in the degree of brain damage that occurs due to iodine deficiency in a given population. A meta-analysis of studies comparing iodine deficient populations with appropriate control groups reveals a mean loss of 13.5 IQ points. Experimental studies in the sheep, rat and marmoset confirm the effect of iodine deficiency on foetal brain development. They show that the effect is due to a slowing of neuroblast multiplication and differentiation and a consequent effect on neuroglial development. Iodine deficiency is now recognised as the most common cause of preventable brain damage in the world today. In 1990, the elimination of iodine deficiency as a cause of brain damage by the year 2000 was accepted by the UN system and substantial progress has been made since 1990 with the mass correction of iodine deficiency through Universal Salt Iodisation (USI).

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Regulation of Thyroid Hormone Metabolism in the Brain

Cited by 2 publications

References 40 publications

The Disorders Induced by Iodine Deficiency

The Disorders Induced by Iodine Deficiency

Iodine Deficiency and the Brain

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