Iodine deficiency symptoms

What are the symptoms of iodine deficiency?

According to the NIH, when iodine is insufficient, TSH stays high; this reflects the thyroid gland’s effort to capture more of the circulating iodine and leads to enlargement of the gland, that is, goiter. Goiter is generally the earliest clinical finding of iodine deficiency. If iodine intake falls below about 10–20 µg per day, hypothyroidism develops and is often accompanied by goiter. ^[1]

The guideline of TEMD (Society of Endocrinology and Metabolism of Türkiye) states that the symptoms and signs seen in hypothyroidism are not specific to hypothyroidism; the most common are dry skin, feeling cold easily, fatigue, voice changes and constipation. Weight gain, hair loss, forgetfulness, reduced concentration, depression, menstrual irregularities and muscle pain are also among the reported findings. ^[2] None of these symptoms alone shows iodine deficiency; causes of hypothyroidism also include Hashimoto’s thyroiditis, thyroid surgery and certain medications. ^[2]

In mild-to-moderate deficiency there may be no obvious complaint. The NIH reports that many pregnant women in the US may be taking in inadequate iodine without carrying a clear sign of deficiency, and that the effect of this on fetal development, if any, is unknown. ^[1]

Why is deficiency more important in pregnancy and infancy?

According to the NIH, iodine deficiency can cause irreversible effects in pregnancy and early infancy. Severe deficiency in pregnancy can cause serious neurodevelopmental disorders in the fetus, growth restriction, miscarriage and stillbirth; chronic and severe deficiency leads to cretinism in the womb (findings such as intellectual disability, deaf-mutism, motor spasticity and short stature). It reports that in infants and children, milder deficiency can also lead to neurodevelopmental deficits such as a slightly below-average IQ. The NIH also reports that mild-to-moderate maternal iodine deficiency has been found to be associated with an increased risk of attention deficit hyperactivity disorder in children; this association does not show causality. ^[1]

The TEMD guideline summarizes iodine deficiency disorders by life stage: in the fetus, miscarriage, stillbirth, congenital anomalies and cretinism; in the newborn, neonatal goiter and hypothyroidism; in children and adolescents, goiter and delayed mental and physical development; in adults, goiter, hypothyroidism and impairment of mental functions. ^[2] This list describes severe, population-level deficiency; in a randomized study, supplementation in mildly deficient pregnant women has not been shown to increase the child’s cognition (details are on the hub page).

Who is at risk in Türkiye today?

Rural settlements

In the 2007 status assessment study relayed by the TEMD guideline, median urinary iodine was 42 µg/L in rural schools and 147 µg/L in urban schools; the guideline attributes this to iodized salt use still being inadequate in small settlements. In the same study, 27.8% of children had urinary iodine below 50 µg/L. ^[2] In Yığılca, an area of severe iodine deficiency in the West Black Sea, six years after mandatory salt iodization, in 806 school children (aged 6–19), the goiter rate was found to be 20.3% at ages 6–12 and 23.8% at ages 13–19, and the hypothyroidism rate 10.4% and 18.9% respectively; median urinary iodine was 83 and 78 µg/L respectively. The authors state that goiter and iodine deficiency persist in the rural West Black Sea. ^[7]

Pregnant and breastfeeding women

In pregnant women, in addition to national data, there are individual city studies, and the results are not consistent:

Vural and colleagues also reported that deficiency was higher in infants of mothers with low socioeconomic and educational level, less household access to iodized salt and a higher number of births; in newborns the median was 96 µg/L and the deficiency rate was 51% (<100 µg/L). ^[3] The TEMD guideline writes that studies in pregnant women, limited in number and in the number of women, have increased in recent years, that a median of 77 µg/L was found in 3,543 pregnant women in Istanbul, and that although iodine is borderline adequate in many regions of the country, a serious proportion of deficiency is still found in pregnant women. ^[2] The study in Muğla, on the contrary, reports an adequate median and a high proportion in the “more than adequate” group; this single-city, 135-person hospital study shows regional difference and does not change the national picture.

Other risk groups

The NIH counts people who do not use iodized salt, pregnant women, people following vegan diets and people who consume few dairy products, seafood and eggs among the groups at risk of inadequate iodine. According to NHANES 2001–2006 data in the US, median urinary iodine was 100 µg/L in pregnant women who had not consumed dairy products in the previous 24 hours and 163 µg/L in those who had; urinary iodine was also lower in women restricting salt, and the likelihood of deficiency may be higher. ^[1] The TEMD guideline, assuming that the daily iodine intake of a pregnant woman consuming standard iodized salt in Türkiye averages 100–150 µg, writes that a pregnant woman who restricts salt needs separate support. ^[2]

How is iodine deficiency tested?

Why is urinary iodine not an individual test?

According to the TEMD guideline, more than 90% of dietary iodine is excreted in urine and excretion in feces is negligibly small; therefore urinary iodine gives an idea of the iodine a person took in over the last 24 hours. WHO, UNICEF and IGN recommend urinary iodine measurement to determine a population’s iodine status; in a population survey of at least 500 people a single randomly taken sample may be sufficient, but to determine a single person’s status, 12 or more samples taken on different days are needed. ^[2]

According to the criteria relayed by the NIH, iodine intake is adequate if median urinary iodine is 100–199 µg/L in children and adults, 150–249 µg/L in pregnant women and >100 µg/L in breastfeeding women; below 100 µg/L is inadequate in children and non-pregnant adults, and severe deficiency is defined as below 20 µg/L. ^[1] These thresholds apply to a group’s median. That a single spot urine result of a single pregnant woman comes out <150 µg/L does not mean individual deficiency, because, according to the TEMD guideline, it may be affected by diet, environmental factors, supplements and pregnancy-related increased clearance. ^[2]

TSH and other blood tests

The TEMD guideline states that marked TSH elevation is expected in advanced iodine deficiency; in severe iodine inadequacy, TSH may be normal, free T4 low and free T3 high. ^[2] A normal TSH therefore does not exclude mild iodine deficiency. The guideline states that people with symptoms consistent with hypothyroidism should be evaluated for thyroid function, while routine screening in people without symptoms is generally not recommended outside risk groups. ^[2]

Does selenium deficiency affect iodine deficiency?

The NIH’s selenium fact sheet reports that selenium deficiency may worsen iodine deficiency and increase the risk of congenital hypothyroidism in infants. ^[8] The role of selenium in thyroid hormone metabolism, the evidence in Hashimoto’s and Graves’ disease, and the upper limit are covered separately on the selenium page.

How certain is the evidence on deficiency?

The harm of severe deficiency and findings such as goiter are well documented. In Türkiye, median urinary iodine in school-age children rose with mandatory iodization; there are studies reporting deficiency in rural areas and in pregnant women, but the pregnancy studies give differing results and a single spot urine result does not prove individual deficiency. Organizations’ views on supplementation in pregnancy are given side by side on the hub page; this guide does not recommend a personal dose.