Sensitive Midwifery - Issue 44 - October 2019

Dimensions body iodine levels remaining stable throughout pregnancy. However, as one 2008 article notes, ‘in areas of even mild to moderate iodine deficiency, total body iodine stores, as reflected by urinary iodine values, decline gradually from the first to the third trimester of pregnancy. This dietary iodine deficiency results in impaired thyroid hormone synthesis.’ The risks of excess iodine While the dangers of iodine deficiency are evident, the risks of too much iodine are just as real. Acute iodine poisoning is rare, occurring only with doses of many grams, but symptoms are serious: fever; nausea and/or vomiting; diarrhoea; burning of the mouth, throat, and stomach; weak pulse; cyanosis; and coma. More generally, excess iodine intake (more than 1 100 mcg of iodine per day – with the recommended daily intake being 150 mcg) may cause thyroid dysfunction – and the elderly, pregnant and lactating women, as well as individuals with preexisting thyroid disease are more likely to experience adverse e ff ects. The Wol ff -Chaiko ff e ff ect This occurs in response to ingestion of large amounts of iodine, and sees the thyroid reducing thyroid hormone levels to protect against hyperthyroidism. While for adults and children this is temporary, fetuses and newborns have immature thyroid glands that have not developed this protective e ff ect, making them more susceptible to iodine-induced hypothyroidism. A study published in 2015 discovered an increased risk of maternal subclinical hypothyroidism and maternal hypothyroxinaemia associated with iodine excess, and warns that ‘excessive iodine exposure might also be detrimental to maternal thyroid health and recommends a lower limit for maternal iodine intake during pregnancy than that currently advised by the WHO’. Even the WHO, which takes pains to point out how important iodine is to infant survival and development, has acknowledged that ‘routine iodine supplementation in pregnancy may not be without risk’, with congenital hypothyroidism in newborns being linked to high maternal intakes of iodine. Interestingly, Oregon State University also ascribes iodine-induced goitre and hypothyroidism in newborns to high exposure to iodised antiseptics. A 2012 study looking at excess maternal iodine supplementation noted how fetuses and newborns are ‘more susceptible to iodine-induced hypothyroidism’, finding that: ‘Although infants recover normal thyroid function after acute iodine exposure (e.g., a few days of topical iodine application), continuous excessive iodine exposure to the fetal and neonatal thyroid gland may cause long-term harmful e ff ects on thyroid function.’ So what about salt? With iodine being so important to human growth and development, WHO and UNICEF have recommended universal salt iodisation – an easy, inexpensive method to eliminate iodine deficiency – as a global strategy. Following these recommendations, more than 120 countries around the world have implemented widespread salt iodisation. In South Africa, mandatory iodisation of table salt at 40–60 ppm was introduced in 1995. Within three years, a 1998 survey showed that optimal iodine nutrition was achieved nationally. A 2014 WHO review on the e ff ect and safety of salt iodisation to prevent iodine deficiency disorders found that ‘exposure to iodised salt was associated with reduced risk or prevalence of goitre, cretinism, low intelligence or low urinary iodine excretion, as well as increased mean IQ and increased median and mean urinary iodine excretion. There was no clear relationship between iodised salt and any adverse e ff ects, including increased hypothyroidism or hyperthyroidism.’ Despite this, the WHO still acknowledges that for some, there remains concern that large-scale salt iodisation could potentially result in excess iodine intake. Continued on page 32 31 eSensitive Midwifery Magazine Issue 44