Nutrients 2014, 6(1), 382-390; doi:10.3390/nu6010382
Paolo Ghirri *, Sara Lunardi and Antonio Boldrini
Department of Clinical and Experimental Medicine, Neonatal Intensive Care and Neonatology Unit, via Roma 55, Pisa 56126, Italy; E-Mails: email@example.com (S.L.); firstname.lastname@example.org (A.B.)
Author to whom correspondence should be addressed; E-Mail: email@example.com; Tel./Fax: +39-050-992529.
Received: 27 October 2013; in revised form: 29 November 2013 / Accepted: 20 December 2013 /
Published: 20 January 2014
Iodine deficiency can be defined as the world’s greatest single cause of preventable brain damage. Fetal and neonatal hypothyroidism, caused by iodine deficiency can be prevented prior to conception and then during pregnancy and lactation when an adequate iodine supplementation is ensured. Extremely low birth weight preterm babies risk having a negative iodine balance status in the first weeks of life, exacerbating the hypothyroxinaemia of the prematurity. It is important to ensure that these babies are provided with an adequate iodine intake from the first days of life. Mothers and newborns should avoid environmental iodine excess during pregnancy or lactation.
Iodine deficiency can be defined as the world’s greatest single cause of preventable brain damage. Important in the synthesis of thyroid hormones, iodine plays a major role in the early growth and development of many organs, particularly the brain and the central nervous system, and in many metabolic pathways. Consequently iodine insufficiency occurring during pregnancy and early infancy, if the maternal/fetal or neonatal thyroid is no longer able to produce enough thyroid hormones, can impair neuro-cognitive development.
Urinary iodine (UI) is a sensible marker of recent iodine intake but it is not reliable for individual diagnosis and treatment as it would be necessary to collect repeated urine samples from an individual over a period of time in order to evaluate its iodine status. Goiter rate, serum TSH, or Tg levels as well are used to assess the iodine status in a population, while thyroid hormones measurement remains a fairly unprecise methodology for the detection of iodine deficiency.
Further research will be useful for better defining methods of assessment of iodine intake and iodine status . Prevention of fetal and neonatal hypothyroidism, caused by iodine deficiency, starts prior to conception and then continues during pregnancy and lactation ensuring an adequate iodine supplementation. Studies on healthy preterm and full-term newborns lead to believe that the iodine intake required to maintain a positive balance are 15 µg/kg/day in full-term newborns and 30 µg/kg/day, and up to 60 µg/kg/day, in preterm babies. In the term newborn, an adequate iodine intake is granted from the first days of age if he or she is formula fed or breastfed by an adequately supplemented mother. Extremely low birth-weight preterm babies (newborns with a birth weight below 1000 g) are at risk of having a negative iodine balance status in the first weeks of life, exacerbating the hypothyroxinaemia of prematurity. It is important that an adequate iodine intake is provided for these babies from the first days of life, nevertheless, neither parenteral nutrition or formula milk completely fulfill iodine requirements. On the other hand, iodine antiseptics should be avoided during pregnancy or lactation and in the newborn: a “free from iodine excess” environment in Obstetrics and Neonatology Units should be assured as far as possible.
More studies are required in order to clearly demonstrate the real benefits deriving from supplementation of preterm formulas [18,28], as well as further large prospective studies are urgently required to exactly define, not only the short term advantages, but also the long term positive effects (for example, on mental development) [29,30] so that a universally accepted iodine supplementation plan in preterm babies can be put in place.
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