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Query: UMLS:C0917816 (mental retardation)
 15,867 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hunger and malnutrition in Africa have been on the increase since the 1960s. During the 1970s, it is estimated that 30 million people were directly affected by famine and malnutrition. About 5 million children died in 1984 alone. In Mozambique during the 1983-84 famine, about 100,000 people perished. In Ethiopia, Sudan, Somalia, Liberia, and Angola armed conflicts compound the problem. Ethiopia alone had 9 million famine victims in 1983. The most common form of malnutrition in Africa is protein energy deficiency affecting over 100 million people, especially 30-50 million children under 5 years of age. Almost another 200 million are at risk. Iron deficiency, commonly called anemia, also affects 150 million people, mostly women and children. Iodine deficiency leads to disorders like mental retardation, cretinism, deafness, abortion, low resistance to disease, and goiter and this affects 60 million with about 150 million more at risk. Vitamin A deficiency causes blindness and low resistance to disease and affects about 10 million. Protein energy deficiency is treated by using donated foods in hospitals, rehabilitation centers, day care centers, and feeding centers. There are no community programs for anemia, or vitamin A or iodine deficiencies. Vaccines for preventing and drugs for treating diseases that cause malnutrition are imported. Therefore, African food and nutrition professionals met in 1988 and created the Africa Council for Food and Nutrition Sciences (AFRONUS) to eliminate famine and malnutrition in Africa. Activities have started in: 1) developing contacts between the workers in food and nutrition; 2) assessing the situation of food and nutrition in Africa; 3) developing an action plan; 4) implementing the plan; and 5) monitoring progress. Food and Nutrition Policy Guidelines have also been prepared by AFRONUS for food and nutrition workers. Africa has enough natural resources to solve the problem of hunger and malnutrition, but these resources have to be harnessed.
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PMID:Hunger and malnutrition: the determinant of development: the case for Africa and its food and nutrition workers. 139 7

It is well known that insufficient production of thyroid hormones during the fetal and neonatal period of development may result in permanent brain damage unless treatment with thyroid hormone is instituted very soon after birth. But congenital hypothyroidism is not the only situation in which brain damage may be related to insufficient thyroid function. Cretinism is the most severe manifestation of iodine deficiency disorders found in areas where iodine intake is greatly reduced. Some of the manifestations of cretinism suggest that the insult to the developing brain starts earlier than in the case of congenital hypothyroidism. Hypothyroxinemia of mothers with adequate iodine intake may also leave permanent, though less severe, mental retardation. For these reasons the possible role of maternal transfer of thyroid hormones during early fetal development have been reinvestigated, using the rat to obtain various experimental models. It has been shown that thyroid hormones are found in embryonic tissues before onset of fetal thyroid function and that thyroidectomy of the mother results in delayed development of the concepta. The concentrations of T4 and T3 in embryonic tissues from thyroidectomized dams were undetectable before the onset of fetal thyroid function, and still reduced in some tissues near term, despite the onset of fetal thyroid function. Treatment of control and thyroidectomized dams with methyl-mercaptoimidazole to block fetal thyroid function reduced thyroid hormone concentrations in fetal tissues near term, but this decrease could be partially avoided by infusion of physiological doses of thyroxine to the mothers. Iodine deficiency of the mothers resulted in thyroid hormone deficiency of the developing embryo, which was very marked until term in all tissues including the brain. The results strongly support a role of maternal thyroid hormones in fetal thyroid hormone economy both before and after the onset of the fetal thyroid function, at least in the rat. They also support a role of the hypothyroxinemia of iodine-deficient mothers in initiating the brain damage of the endemic cretin, a damage which would not be corrected once the fetal thyroid becomes active, as iodine-deficiency of the fetus would impair adequate production of hormones by its own thyroid, and maternal transfer would continue to be low.
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PMID:Fetal and maternal thyroid hormones. 329 61

Neurological examinations were made of 67 children and adults with congenital iodine-deficiency disorder (endemic cretinism) in four rural villages in highland Ecuador. There was a distinct and readily identifiable pattern of neurological deficits. These included, to varying degrees: deaf-mutism or lesser degrees of bilateral hearing-loss or dysarthria; spasticity, particularly involving the proximal lower extremities; mental deficiency of a characteristic type; and rigidity and bradykinesia. Not all of these elements were found in all cases. Less common features were strabismus, kyphoscoliosis and frontal-lobe signs. There were exceptional cases with hypotonia. In contrast, cerebellar function was largely spared, as were functions of emotion and attention, vegetative and autonomic functions, social interaction, and probably memory, except in the most severely involved.
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PMID:Neurological signs in congenital iodine-deficiency disorder (endemic cretinism). 401 26

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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PMID:The disorders induced by iodine deficiency. 805 57

Iodine deficiency is well known as a cause of several disorders such as endemic goiter and cretinism, along with a wide spectrum of psychoneurologic development disorders including endemic mental deficiency, which are generally correlated with damage to the fetus. Since as much as 40% of the Tanzanian population is at risk for iodine deficiency disorders (IDD) because they live in iodine-deficient areas, and although the effects of iodine deficiency on human reproduction in Tanzania have not been objectively studied, it is estimated that there are approximately 600,000 cretins and cretinoids in the country as a result of IDD. As a baseline study for future research on iodine deficiency and its effects on human reproduction in Tanzania, we assayed serum thyroxine (T4), triiodothyronine (T3), thyrotropin (TSH), and free thyroxine (FT4) in 93 clinically euthyroid pregnant women and 34 nonpregnant women as controls. Pregnancy was accompanied by significantly increased levels of total T3 and T4, decreased FT4, and increased TSH concentration in serum. However, biochemical euthyroidism (assessed by FT4 and basal TSH) was demonstrated in almost all (99%) of the pregnant subjects in conformity with most of the previous findings elsewhere. We conclude that pregnant Tanzanian women residing in areas without iodine deficiency experience changes in biochemical parameters of thyroid function similar to their counterparts in other places.
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PMID:Thyroid function studies in normal pregnant Tanzanian women. 865 71

Iodine deficiency is the most common preventable cause of mental deficiency. Remarkable success has been achieved by the use of iodised salt to correct this deficiency in many industrialised countries since 1920. The Government of India has adopted a strategy to iodise all edible salt in the country to overcome iodine deficiency. Universal salt iodisation is the principal public health measure for eliminating iodine deficiency disorders. Daily iodine intakes of up to 1000 micrograms, appear to be entirely safe. In India, the likelihood of exceeding this level is quite small. Iodised salt does not cause any side effects. Iodine in iodised salt does not carry risks for persons who are already iodine sufficient. iodisation of salt at the current level of fortification (15-30 ppm iodine) keeps intakes well within a safe daily range for all populations, irrespective of their iodine status.
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PMID:Human requirements of iodine & safe use of iodised salt. 867 43

Iodine deficiency disorders (IDD) are the world's single most significant cause of preventable brain damage and mental retardation. Data regarding IDD in upper Egypt are scarce and even lacking. The aim of the present work was to study the prevalence of IDD and some potential risk factors in upper Egypt. Using a two-stage cluster sampling technique, 6750 school children aged 8-10 years were screened for IDD through clinical examination of the thyroid gland and determination of urinary iodine, from three governorates in upper Egypt, namely Al-Minya (population of 3.3 million), Assyut (population of 2.9 million), and Suhag (population of 3.1 million). Iodine was determined in samples of soil and drinking water. Overall, the prevalence rate of goitre was 34.6 per cent. The median urinary iodine level for children with goitre was 5.04 micrograms/dl compared to 14.81 micrograms/dl among children free of goitre. Multiple logistic regression analysis showed that certain groups of school children were much more likely to develop goitre. They included females (OR = 3.07, 95 per cent CI = 2.78-3.39), children in households where drinking water had an iodine content of less than 0.5 microgram/100 ml (OR = 3.44, 95 per cent CI = 3.09-3.89), and children living in places where soil content of iodine was less than 0.2 microgram/100 g (OR = 2.67, 95 per cent CI = 2.30-3.10). We conclude that IDD is a severe public health problem in upper Egypt. The present situation in upper Egypt necessitates an urgent intervention programme.
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PMID:Iodine deficiency disorders among school children in upper Egypt: an epidemiologic study. 981 88

Iodine is a trace element essential for the synthesis of thyroid hormones. It is present in the human body in minute amounts (15-20 mg in adults). The thyroid is very sensitive to iodine deficiency in newborns and infants because of its very low iodine content. Daily iodine requirements in humans vary from 40 micrograms in neonates to 150 micrograms in adults. Iodine deficiency represents the first cause of avoidable mental deficiency in developed countries; it has not yet disappeared in Europe, especially in the East, where it is responsible for a high prevalence of goiter. Iodine deficiency during pregnancy increases the risk of neonatal transient hypothyroidism, with a high recall rate in programs of systematic screening for congenital hypothyroidism. Data available in France suggest that screening for iodine deficiency should be performed during pregnancy, and that the minimal iodine concentration in formula milk should be increased to 10 micrograms/100 kcal for term infants and 20 micrograms/100 kcal for premature infants. Iodine deficiency is ideally prevented by the use of iodized salt. Because of the risk of iodine overexposure and secondary transient hypothyroidism, the use of iodinated antiseptics must be avoided in premature babies and neonates as well as in pregnant and lactating women. The fight against iodine deficiency, associated with oral stable preventive iodine administration, decreases sharply the risk of thyroid cancer in case of nuclear exposure, by diminishing thyroid uptake of iodine radioactive isotopes.
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PMID:[Iodine nutrition in the infant. Committee on Nutrition of the French Society of Pediatrics]. 1066 89

This editorial reviews the impact of iodine deficiency (1) on thyroid function in pregnant women and neonates and (2) on the neurointellectual development of infants and children. All degrees of iodine deficiency (mild: iodine intake of 50-99 microg/day, moderate: 20-49 microg/day, and severe: <20 microg/day) affect thyroid function of the mother and the neonate as well as the mental development of the child. The damage increases with the degree of the deficiency, with overt endemic cretinism as the severest consequence. Maternal hypothyroxinaemia during early pregnancy is a key factor in the development of the neurological damage in the cretin. Selenium deficiency combined with iodine deficiency partly prevents the neurological damage but precipitates severe hypothyroidism in cretins. Iodine deficiency results in a global loss of 10-15 IQ points at a population level and constitutes the world's greatest single cause of preventable brain damage and mental retardation.
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PMID:Iodine deficiency as a cause of brain damage. 1126 81

Iodine deficiency is the leading cause of preventable mental retardation. Universal salt iodization (USI), calling for all salt used in agriculture, food processing, catering and household to be iodized, is the agreed strategy for achieving iodine sufficiency. This article reviews published information on programs for the sustainable elimination of the iodine deficiency disorders and reports new data on monitoring and impact of salt iodization programs at the population level. Currently, 68% of households from areas of the world with previous iodine deficiency have access to iodized salt, compared to less than 10% a decade ago. This great achievement, a public health success unprecedented in the field of noncommunicable diseases, must be better recognized by the health sector, including thyroidologists. On the other hand, the managers and sponsors of programs of iodized salt must appreciate the continuing need for greatly improved monitoring and quality control. For example, partnership evaluation of iodine nutrition using the ThyroMobil model in 35,223 schoolchildren at 378 sites of 28 countries has shown that many previously iodine deficient parts of the world now have median urinary iodine concentrations well above 300 microg/L, which is excessive and carries the risk of adverse health consequences. The elimination of iodine deficiency is within reach but major additional efforts are required to cover the whole population at risk and to ensure quality control and sustainability.
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PMID:Iodine deficiency in the world: where do we stand at the turn of the century? 1139 2


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