Iodine deficiency and development of brain

  title={Iodine deficiency and development of brain},
  author={Vani Sethi and Umesh Kapil},
  journal={The Indian Journal of Pediatrics},
  • V. Sethi, U. Kapil
  • Published 1 April 2004
  • Biology, Medicine
  • The Indian Journal of Pediatrics
Iodine is a trace element essential for the synthesis of triodothyronine (T3) and thyroxine (T4). Inadequate intake of iodine leads to insufficient production of these hormones, which play a vital role in the process of early growth and development of most organs, especially the brain. The neurological sequele of iodine deficiency are mediated by thyroid hormone deficiency, varying from minimal brain function to a syndrome of severe intellectual disability. All the basic processes of… 
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Thyroid hormones states and brain development interactions
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Free thyroxine levels in marginal iodine-deficient rats decreased after pregnancy in rats with marginal iodine deficiency, affecting the expression of related proteins in the brain of offspring.
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This review focuses on fluorosis and iodine deficiency disorders, two serious, highly prevalent metabolic disorders that are under-reported and addressed through structured national programmes, but the implementation unfortunately is in a compartmentalized manner.
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It was showed that women did not have enough knowledge regarding the importance of iodine in fetal brain development and evidence-based nursing is one approach that may enable future healthcare providers to manage the explosion of new literature and technology and ultimately may result in improved patient outcomes.
A Study on Renal Function Status of Patients with Hypothyroidism attending a Tertiary Care Hospital in North Bengal
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Iodine deficiency as a cause of brain damage
  • F. Delange
  • Medicine, Biology
    Postgraduate medical journal
  • 2001
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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It appears urgent to ensure the use of iodine supplements from before or very early in pregnancy, and to screen all women for hypothyroxinemia as early as possible, due to increasing evidence from epidemiological studies and patient reports that these hormones are already needed for orderly development during the first trimester.
Early effects of iodine deficiency on radial glial cells of the hippocampus of the rat fetus. A model of neurological cretinism.
The most severe brain damage associated with thyroid dysfunction during development is observed in neurological cretins from areas with marked iodine deficiency. The damage is irreversible by birth
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Though experimental work has primarily focused on the effects of thyroid hormones on the fetal brain, it is believed to be likely that fetal exposure to maternal hormones is under placental control, and that other components of this putative system are worthy of study.
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Experimental research and clinical studies have partially clarified the correlation between the maturation of the nervous system and thyroid function during the early stages of development; both a deficit and excess of thyroid hormones may lead to permanent anatomo-functional damage to the central nervous system.
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  • J. Lazarus
  • Medicine, Biology
    Thyroid : official journal of the American Thyroid Association
  • 1999
Recent data from Holland suggest that children born to mothers known to have circulating antithyroid peroxidase antibodies or from mothers with low normal free T4 concentrations measured at 12 weeks gestation have significant development impairment.
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It is suggested that iodine deficiency has an early effect on neuroblast multiplication and, if so, this could be important in the pathogenesis of the neurological form of endemic cretinism.
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The prenatal disturbances noted in this study may have wide-ranging consequences since they occur when neurotransmitters have putative neurotropic roles in brain development and may affect neurotransmission, thereby contributing to the behavioural dysfunction seen in adult progeny of hypothyroxinemic dams.
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