Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0025362 (mental retardation)
 15,878 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Micronutrients, mostly iodine and selenium, are required for thyroid hormone synthesis and function. Iodine is an essential component of thyroid hormones and its deficiency is considered as the most common cause of preventable brain damage in the world. Nowadays about 800 million people are affected by iodine deficiency disorders that include goiter, hypothyroidism, mental retardation, and a wide spectrum of other growth and developmental abnormalities. Iodine supplementation, under form of iodized salt and iodized vegetable oil, produced dramatic improvements in many areas, even though iodine deficiency is still a problem not only for developing countries. In fact, certain subpopulations like vegetarians may not reach an adequate iodine intake even in countries considered iodine-sufficient. A reduction in dietary iodine content could also be related to increased adherence to dietary recommendations to reduce salt intake for preventing hypertension. Furthermore, iodine intakes are declining in many countries where, after endemic goiter eradication, the lack of monitoring of iodine nutrition can lead to a reappearance of goiter and other iodine deficiency disorders. Three different selenium-dependent iodothyronine deiodinases (types I, II, and III) can both activate and inactivate thyroid hormones, making selenium an essential micronutrient for normal development, growth, and metabolism. Furthermore, selenium is found as selenocysteine in the catalytic center of enzymes protecting the thyroid from free radicals damage. In this way, selenium deficiency can exacerbate the effects of iodine deficiency and the same is true for vitamin A or iron deficiency. Substances introduced with food, such as thiocyanate and isoflavones or certain herbal preparations, can interfere with micronutrients and influence thyroid function. Aim of this paper is to review the role of micronutrients in thyroid function and diseases.
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PMID:Role of iodine, selenium and other micronutrients in thyroid function and disorders. 1959 17

Iodine deficiency remains a global concern for developing countries and some industrialised countries. Iodine deficiency is the most common cause of preventable mental retardation, posing a threat to the social and economic development of countries. Initiatives were developed and instituted to accelerate progress to achieve the goal of universal salt iodisation (USI). However, these efforts were not successful in eliminating iodine deficiency disorders (IDD) in some countries. Every year, 50 million children are born without the protection that iodine offers to the growing brain and body and about 18 million suffer some significant degree of mental impairment. The World Health Organization (WHO), United Nations Children's Fund (UNICEF) and non-governmental organisations assist to ensure that populations at risk have access to iodised salt. This paper will review the highlights of iodine deficiency and present the experiences in the various countries in Asia, i.e. assessments of the situation, action plans, and obstacles to implementation.
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PMID:Eliminating iodine deficiency: obstacles and their removal. 1990 47

Iodotyrosine deiodinase is a thyroidal enzyme that deiodinates mono- and di-iodotyrosines (MIT, DIT) and recycles iodine, a scarce element in the environment, for the efficient synthesis of thyroid hormone. Failure of this enzyme leads to hypothyroidism, goiter and mental retardation, a clinical phenotype yet described in the 1950s, whose diagnostic hallmark is the elevation of iodotyrosines in serum and urine. DEHAL1, the gene responsible for this activity, was recently isolated and the molecular basis for the iodotyrosine deiodinase deficiency (ITDD) unraveled. The current clinical picture of mutations in DEHAL1 mostly recapitulates the "classical" phenotype of ITDD, including the psychomotor deficits. This is probably due to the lack of expression of the disease at the beginning of life, which causes ITDD being undetected in current screening programs for congenital hypothyroidism. This worrying feature calls for efforts to improve the preclinical detection of iodotyrosine deiodinase deficiency in the neonatal time.
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PMID:Genetics and phenomics of hypothyroidism and goiter due to iodotyrosine deiodinase (DEHAL1) gene mutations. 2029 47

Iodine deficiency (ID) is the world's single most important preventable cause of brain damage and mental retardation. Iodine deficiency disorders (IDDs) is a public health problem in 130 countries, affecting 13% of the world population. The simplest solution to prevent the IDD is to consume iodized common salt every day. In India, significant progress has been achieved toward elimination of IDD, in the last 30 years. Satisfactory levels of urinary iodine excretion and iodine content of salt have been documented by the research surveys conducted by research scientists. The results indicate that we are progressing toward elimination of IDD. IDD is due to a nutritional deficiency, which is prima-rily that of iodine, in soil and water. IDD is known to re-appear if the IDD Control Program is not sustained. To ensure that the population continues to have intake of adequate amount of iodine, there is a need of i) periodic surveys to assess the magnitude of the IDD with respect to impact of iodized salt (IS) intervention; ii) strengthening the health and nutrition education activities to create demand for IS and iii) development of a monitoring information system (MIS) for ensuring that the adequately IS is available to the beneficiaries.
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PMID:Successful efforts toward elimination iodine deficiency disorders in India. 2127 62

Iodine is a trace element in the human body, its only known function is the synthesis of thyroid hormones. Effects of iodine deficiency, termed iodine deficiency disorders (IDD), include endemic goiter, hypothyroidism, cretinism, decreased fertility rate, increased infant mortality and mental retardation. 2.2 billion people worldwide are at risk for IDD. Of these, 30-70% have goiter and 1-10% have cretinism. Two decades ago the I.R. Iran was among the countries most severely affected by iodine deficiency, but during the last two decades has made much progress in the development of universal salt iodization strategies and IDD prevention, and since 1996 meets all WHO/UNICEF/ICCIDD criteria for the sustainable elimination of iodine deficiency.
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PMID:Appropriate iodine nutrition in Iran: 20 years of success. 2128 73

Iodine Deficiency Disorders (IDD) are one of the biggest worldwide public health problem of today. Their effect is hidden and profoundly affects the quality of human life. Iodine deficiency occurs when the soil is poor in iodine, causing a low concentration in food products and insufficient iodine intake in the population. When iodine requirements are not met, the thyroid may no longer be able to synthesize sufficient amounts of thyroid hormone. The resulting low-level of thyroid hormones in the blood is the principal factor responsible for the series of functional and developmental abnormalities, collectively referred to as IDD. Iodine deficiency is a significant cause of mental developmental problems in children, including implications on reproductive functions and lowering of IQ levels in school-aged children. The consequence of iodine deficiency during pregnancy is impaired synthesis of thyroid hormones by the mother and the foetus. An insufficient supply of thyroid hormones to the developing brain may result in mental retardation. Brain damage and irreversible mental retardation are the most important disorders induced by iodine deficiency. Daily consumption of salt fortified with iodine is a proven effective strategy for prevention of IDD.
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PMID:Health consequences of iodine deficiency. 2174 17

Iodine is in the crucial parts of two hormones of T4 and T3 produced by the thyroid glands which are essential for all the aspects of human metabolisms. It is demonstrated that iodine deficiency can be considered as sole cause of many thyroid abnormalities including mental disorders. Iodine deficiency of sufficient degree to cause hypothyroidism during fetus life and early infancy will be accompanied with brain abnormality possibly to the stage of mental retardation. The iodine deficiency among subjects in their early stage of childhood is not as severe as those in their fetus or infancy. In adult subjects the sever iodine deficiency can be also associated with mental disorders due to the direct side effects of hypothyroidism occurred by lack of iodine. The clinical manifestation of iodine deficiency show itself with psychological disorders in adult subjects. The status of iodine within blood can be evaluated through measurement of urinary iodine level and the low urinary concentration is an indicative of hypothyroidism. Mental retardation and brain damage due to iodine deficiency can be prevented if iodine supplementation prescribed duly on time.
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PMID:A review on the metabolic disorders of iodine deficiency. 2190 53

Thyroid hormones (TH) are critical for growth and development and particularly brain development. There are numerous environmental agents that lead to marginal reductions of circulating TH. Although it is clear that severe developmental hypothyroidism is profoundly detrimental to neurodevelopment, there is less information regarding the consequences of modest degrees of thyroid. The impact of low level TH disruptions induced by environmental contaminants has not been defined. This paper is a synopsis from four invited speakers who presented at the 13th International Neurotoxicology Association meeting held in Xi'an, China during the summer of 2011. An overview of the role of TH in brain development and a review of human and animal data on the neurological sequelae of disruption of the thyroid axis in the pre- and early post-natal periods were presented by Mary Gilbert and Joanne Rovet. Iodine deficiency, a common cause of TH insufficiency and mental retardation in many countries, including China, was addressed by Zupei Chen. In this presentation the current incidence of iodine deficiency and neurological outcome in China and the efficacy of recently implemented iodinization programs to eliminate this cause of mental retardation were reviewed. Joanne Rovet described the impact of TH disruption during pregnancy and under conditions of congenital hypothyroidism. Children born with normal thyroid function, but who experienced TH insufficiency in the womb, display subtle cognitive impairments and abnormalities in brain imaging. Despite early detection and treatment, deficiencies also exist in children born with thyroid disorders. Different patterns of cognitive effects result from prenatal versus postnatal TH insufficiency. Mary Gilbert reported on the effects of environmental contaminants with thyroid disrupting action on brain development in animals. Results of neurophysiological, behavioral, structural and molecular alterations that accompany modest perturbations of the thyroid axis were reviewed. Noriyuki Koibuchi described molecular targets of TH-mediated signalling accompanying exposure to persistent organic pollutants. Both polychlorinated biphenyls (PCBs) and polybrominated diphenyl ethers (PBDEs) are prevalent environmental contaminants that disrupt TH signalling at the receptor level. This action by these chemical classes could contribute to the negative impact of these chemicals on brain function. In summary, epidemiological, preclinical and animal research has clearly identified the critical role of TH in brain development. Additional work is required to understand the impact of low level perturbations of the thyroid axis to evaluate the risk associated with environmental contaminants with thyroid action.
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PMID:Developmental thyroid hormone disruption: prevalence, environmental contaminants and neurodevelopmental consequences. 2213 53

Globally, about 2 thousand million people are affected by iodine deficiency. Although endemic goitre is the most visible sign of iodine deficiency, its most devastating consequence is brain damage causing mental retardation in children. The relationship between iodine deficiency and brain damage was not clearly established until the 1980s when the term iodine deficiency disorders (IDDs), which encompass a spectrum of conditions caused by iodine deficiency, was introduced. This paradigm shift in the understanding of the clinical consequences of iodine deficiency led to a change in iodine deficiency assessment. The median urinary iodine excretion level has been recommended as the preferred indicator for monitoring population iodine deficiency status since 2001. The 2007 WHO urinary iodine data in schoolchildren from 130 countries revealed that iodine intake is still insufficient in 47 countries. Furthermore, about one-third of countries lack national estimates of the prevalence of iodine deficiency. The picture that has emerged from available data worldwide over the past two decades is that IDDs are not confined to remote, mountainous areas in developing countries, but are a global public health problem that affects most countries, including developed countries and island nations. The recognition of the universality of iodine deficiency highlights the need to develop and apply new strategies to establish and maintain sustainable IDD elimination and strengthen regular monitoring programmes.
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PMID:The changing epidemiology of iodine deficiency. 2247 32

Radioactive iodine (RAI) is used effectively in the treatment of hyperthyroidism and thyroid cancer, but it is contraindicated during pregnancy. RAI treatment during pregnancy can lead to fetal hypothyroidism, mental retardation and increased malignancy risk in the infant. Pregnancy tests must be performed before treatment in all women of reproductive age. However, at times, RAI is being used before ruling out pregnancy. We herein present a male newborn infant with congenital hypothyroidism whose mother was given a three-week course of methimazole therapy for her multiple hyperactive nodules and subsequently received 20 mCi RAI during the 12th week of her pregnancy. The patient was referred to our neonatology unit at age two weeks when his thyrotropin (TSH) level was reported to be high in the neonatal screening test. Physical examination was normal. Laboratory investigations revealed hypothyroidism (free triiodothyronine 1.55 pg/mL, free thyroxine 2.9 pg/mL, TSH 452 mU/L, thyroglobulin 20.1 ng/mL). The thyroid gland could not be visualized by ultrasonography. L-thyroxine treatment was initiated.
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PMID:Congenital hypothyroidism due to maternal radioactive iodine exposure during pregnancy. 2267 71


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