Iodine and thyroid hormones during pregnancy and postpartum

Abstract

Iodine is a trace element essential for synthesis of the thyroid hormones, triiodothyronine and thyroxine. These hormones play a vital role in the early growth and development stages of most organs, especially the brain. The World Health Organization (WHO) has declared that, after famine, iodine deficiency is the most avoidable cause of cerebral lesions including different degrees of mental retardation and cerebral paralysis. The main function of iodine in vertebrates is to interact with the thyroid hormones. During pregnancy sufficient quantities of iodine are required to prevent the appearance of hypothyroidism, trophoblastic and embryonic or fetal disorders, neonatal and maternal hypothyroidism, and permanent sequelae in infants. Thyroid hormone receptors and iodothyronine deiodinases are present in placenta and central nervous tissue of the fetus. A number of environmental factors influence the epidemiology of thyroid disorders, and even relatively small abnormalities and differences in the level of iodine intake in a population have profound effects on the occurrence of thyroid abnormalities. The prevalence of disorders related to iodine deficit during pregnancy and postpartum has increased. Iodine supplementation is an effective measure in the case of pregnant and lactating women. However, it is not implemented and the problem is still present even in societies with theoretically advanced health systems. During pregnancy and postpartum, the WHO recommends iodine intake be increased to at least 200 microg/day. Side-effects provoked by iodine supplementation are rare during pregnancy at the recommended doses.

Hypothyroidism

“…Screening programs for neonatal congenital hypothyroidism indicate that it is present in approximately one case out of 3000 to 4000 live births (Klein et al, 1991). Seventy-eight percent were found to have an intelligence quotient (IQ) of over 85 when congenital hypothyroidism was diagnosed within the first few months after birth, 19% when it was diagnosed between 3 and 6 months, and 0% when the diagnosis was made 7 months after birth (Pérez-López, 2007). In a meta-analysis of seven studies (Derksen-Lubsen and Verkerk, 1996), a decrease of 6.3 IQ points was found among neonates who suffered hypothyroidism during pregnancy in comparison to the control group.…”

“…This discrepancy was understood only when it was demonstrated that in the DRC, iodine deficiency is aggravated by selenium deficiency and thiocyanate overload (see later section) (Delange et al, 1982;Vanderpas et al, 1990;Contempre et al, 1991). Also, during pregnancy, iodine deficiency produces hypothyroxinemia which consequently causes (1) thyroid stimulation through the feedback mechanisms of TSH, and (2) goitrogenesis in both mother and fetus (Pérez-López, 2007). For this reason, it seems that moderate iodine deficiency causes an imbalance in maternal thyroid homeostasis, especially toward the end of pregnancy, leading to isolated hypothyroxinemia suggestive of biochemical hypothyroidism.…”

“…Traditionally, research on the role of the thyroid hormones in brain development has focused on the postnatal phase and on identifying congenital hypothyroidism, which is the final result of the deficiency suffered throughout the pregnancy (Pérez-López, 2007). Iodine deficit during pregnancy produces an increase in perinatal mortality and low birth weight which can be prevented by iodated oil injections given in the latter half of pregnancy or in other supplementary forms (European Commission, 2002 .…”

Influencia de la hipotiroxinemia materna durante la gestación sobre el desarrollo psicomotor

“…Todavía hoy, el aporte insuficiente de este oligoelemento es la primera causa de retraso mental evitable en el mundo 1,2 .…”

“…Así, casi toda la T3 presente en los receptores nucleares de la corteza cerebral fetal desde el primer trimestre de embarazo se genera por la desyodación local de la T4 de origen materno 5 . De esta manera, las concentraciones séricas bajas de T4 libre materna desempeñan un papel fundamental en el desarrollo neurológico del feto, sobre todo durante el primer trimestre de gestación, porque no existe producción de hormona tiroidea fetal hasta la semana 20 de embarazo 2,[6][7][8][9][10] .…”