Thyroid and Pregnancy

Thyroid and Pregnancy

Anil Kumar



Anil Kumar, PhD  | Last updated Sep 19, 2018

Thyroid in pregnancy is required for baby’s development, mother’s health, and normal pregnancy. It is especially important for development of an infant’s central nervous system. Because the baby’s thyroid is not fully developed until second trimester, a mother’s thyroid requirements increase during pregnancy. The levels fluctuate significantly in the first half of pregnancy when the baby is entirely dependent on mother’s thyroid hormones. The role of thyroid in pregnancy is very complex. The most common questions being asked are: what should my thyroid levels be to get pregnant or how thyroid levels change during pregnancy? Here we attempt to answer these question based on the available scientific research on thyroid in pregnancy.


Thyroid levels during pregnancy chart


More from our blogs: Thyroid and Youhow thyroid impacts everyone | Thyroid and Iodineunderstand the role of iodine in thyroid healthAll About Thyroidbrief summary of thyroid disorder, deficiency symptoms, and more | At Home Thyroid Testa test that measures TSH, free T4, free T3, and TPO.

  • A baby’s thyroid is not fully developed until weeks 18–20 of pregnancy and the T4 hormone supply comes from the mother
  • Mother’s free thyroxine (fT4) concentrations increase and TSH concentrations decrease from approximately eighth week through the first half of pregnancy
  • In first trimester, the high concentrations of pregnancy hormone, hCG (human chorionic gonadotropin), increase thyroid hormone production and suppress TSH levels
  • Pregnancy requires an increase in mother’s thyroid hormone production to ensure sufficient thyroid hormone is available for the mother and baby, mainly because:
    • The fetus relies on mother’s thyroid hormone which increases the T4 requirement
    • The protein that binds T4, thyroxine-binding globulin (TBG), increases in concentrations binding even more T4
    • The mother’s urinary excretion of iodine increases which leaves less iodine for thyroid hormone production
    • The placenta’s enzyme (type 3 de-iodinase) deactivates some of the T4
  • These changes might expose pre-existing mild thyroid dysfunction during pregnancy
  • The presence of TPO (thyroid peroxidase) antibodies can significantly impact the pregnancy and child development as the antibodies indicate autoimmune disease in mother
  • Maternal T4 levels seem to affect the fetal development and TSH levels seem to affect maternal health (as TSH can not pass through placenta)
  • TSH reference intervals of 0.1–2.5 mIU/L for the first trimester and of 0.2–3.0 mIU/L for the second trimester are recommended (De Groot 2012)
  • Screening of thyroid function is not expensive because in western countries all pregnant women have a standardized blood sample test at 8–12 weeks’ gestation, and positive patients largely benefit from a cheap, safe, and effective treatment



Thyroid in pregnancy

How common is thyroid dysfunction during pregnancy?


  • The prevalence of thyroid dysfunction during pregnancy is common—about 2%–4% of all pregnancies have some form of thyroid related issues (Krassas 2010)
  • Risk of thyroid problems during pregnancy vary significantly and can affect both the mother and the child
  • Overt or clinical hypothyroidism (with elevated concentrations of TSH with low concentrations of free T4) occurs in about 0.2% to 0.6% of pregnant women (Medici 2015)
  • Based on the birth figures of 2012, if all pregnant women from the United States, the UK, or The Netherlands were screened, the conservative annual number of cases with overt hypothyroidism (TSH > 10 mIU/L) would be 25,000, 4500, and 1000 respectively (Pop 2014)
  • Maternal subclinical or mild hypothyroidism (elevated concentrations of TSH with normal concentrations of free T4) is more prevalent, as it occurs in 3.5% to ~18% of all pregnancies (Abalovich 2007)—however the numbers vary depending on what range of TSH your doctor defines as subclinical hypothyroidism
  • The combination of high TSH concentration and positivity of TPO (thyroid peroxidase) antibody seems to synergistically increase the risk of adverse pregnancy results; data suggest occurrence of TPO antibody in roughly one-third of pregnant women who have subclinical hypothyroidism (Casey 2006)
  • Overt or clinical hyperthyroidism is fairly uncommon in pregnancy
  • Pregnancy data collected for 4199 women (Pop 2014) showed the prevalence of overt or clinical hypothyroidism (a TSH >10 mIU/L) was just 26 (0.62%) but a surprisingly 96% had (highly) elevated TPO antibodies
  • Pathological hyperthyroidism (mainly Graves disease and toxic nodules or goiters) during pregnancy is not very common, with a frequency of 0.4% to 1% before pregnancy and a frequency of approximately 0.2% during pregnancy (Cooper 2013)
  • Gestational or pregnancy-related hyperthyroidism (biochemically defined by high levels of free T4 and low levels of TSH) is much more frequent and is diagnosed in about 1% to 3% of pregnancies (Cooper 2013)
  • In published data (Casey 2006), subclinical hyperthyroidism (TSH levels below 1.75 ng/dL or 0.42 mIU/L) were found to be 1.7% in 25,765 pregnant women; among them, 0.4% had an elevated fT4 levels (which was similar to non-pregnant women in same age group of around 25 years)
  • It was also found that women with subclinical hyperthyroidism were less likely to be obese than women with TSH values between the 5th and 95th percentile (+/- 2 std dev). This positive relationship between TSH values and BMI has been well studied, it is hypothesized to represent an altered energy balance due to increased thermogenesis in obese women (Iacobellis 2005)
  • Subclinical or mild hyperthyroidism has not been associated with any of the commonly known adverse pregnancy outcomes (Casey 2006)



Thyroxine in pregnancy (T4 and fT4)


  • More than 99% of T4 is bound to thyroid hormone-binding proteins (TBG) and not freely available
  • Therefore T4 concentrations are highly dependent on changes in TBG concentrations; the T4 concentrations are more variable during early pregnancy than free T4 concentrations
  • Differences in the concentrations of free T4 explain more clearly the variation in concentrations of TSH than concentrations of free T4 do (8.0% for free T4 versus 2.5% for T4); this suggests that free T4 reflects the function of the hypothalamic–pituitary–thyroid axis more accurately than T4 (Glinoer 1990)
  • During early pregnancy, the free T4 is associated with adverse pregnancy and child outcomes, not T4 (Glinoer 1990)
  • Research suggests that free T4 is a more useful index of thyroid function during early pregnancy than T4 (Korevaar 2016)




Risk-factors affecting thyroid in pregnancy


Thyroid hormones versus BMI during pregnancy


  • Higher BMI is associated with higher TSH concentrations (Han 2015), lower free T4 concentrations, higher free T3 (Knight 2016), and a higher T3:T4 ratio
  • A Finnish study reported shift in the TSH upper limits with BMI which suggests higher BMI is more susceptible to hypothyroidism (upper TSH limit of 2.86 mIU/L for BMI of 20-25 kg/m2 versus 3.50 mIU/L for BMI >30 kg/m2) (Mannisto 2011); the prevalence of overt hypothyroidism in very obese mothers (BMI >40 kg/m2) was found to be 11.8% (Michalaki 2006)
  • Factors affecting thyroid health during pregnancy include genetic, dietary, environmental and cultural factors; differences in maternal thyroid function between and within different ethnic populations during pregnancy have been well studied (Walker 2005, Benhadi 2011, La’ulu 2011)
  • A higher proportion of African-American women had subclinical hyperthyroidism than did Hispanic women (3% versus 1.6%); African-American women have higher serum levels of the pregnancy hormone (hCG) than white or Hispanic women
  • Smoking has only limited effects on mean TSH and fT4 concentrations during pregnancy; a Finnish study of pregnant women found that smokers had TSH concentrations identical to those of nonsmokers (1.02 mIU/L), whereas there was a small difference in fT4 concentrations (15.02 vs 15.24 pmol/L) (Mannisto 2012); however, smoking can negatively affect pregnancy in other ways beyond thyroid dysfunction



Overt hypothyroidism and pregnancy


  • Overt maternal hypothyroidism is one of the biggest concerns during pregnancy; it is known for higher risk of pregnancy complications, including premature delivery, low birth weight, miscarriage and pre-eclampsia , as well as a higher risk of detrimental effects on fetal neuro-development.
  • A large case–control study demonstrated that children born to women with untreated hypothyroidism have a 7-point reduction in IQ compared with children whose mothers were euthyroid (healthy thyroid levels) (Haddow 1999); these children also had delays in motor skill development, language development and attention at 7 to 9 years of age
  • Surprisingly, no data suggest that women with adequately treated hypothyroidism have an increased risk of pregnancy complications compared with women with normal thyroid function (Korevaar 2017)
  • The transfer of mother’s T4 to the fetus is essential for optimal fetal brain development, and levothyroxine supplementation is most common treatment for overt hypothyroidism



Subclinical hypothyroidism and pregnancy


  • Similar to overt hypothyroidism, subclinical or mild hypothyroidism is associated with a higher risk of pregnancy loss, placental abruption, premature delivery, pre-eclampsia and neonatal death (Sheehan 2015, Maraka 2016, Negro 2014); however, the ranges for subclinical hypothyroidism need to be carefully defined as values may vary significantly between studies and various labs
  • Evidence from large population studies indicates that subclinical hypothyroidism is not associated with any adverse neurobehavioral results in the baby (Korevaar 2016)
  • Thyroid autoimmunity is a major risk factor for subclinical hypothyroidism (Medici 2012) and studies show approximately one-third of women with subclinical hypothyroidism are found positive for TPO antibodies (Casey 2006, Korevaar 2017)
  • Combination of subclinical hypothyroidism and TPO antibody positivity is associated with a higher risk of adverse pregnancy results, such as miscarriage, gestational diabetes mellitus (glucose intolerance during pregnancy) and premature delivery (Korevaar 2013, Karakosta 2012, Liu 2014, Ying 2016)
  • Combination of high concentrations of TSH and TPO anti-bodies increases the risk of adverse pregnancy results compared with the presence of only high TSH concentrations or TPO antibodies; also, for women who are TPO positive are at higher risk already for TSH concentrations even in the high-normal range (in most studies for concentrations of TSH >2.5mIU/L)
  • One study showed that a large percentage of pregnant women with high serum thyrotropin concentrations subsequently had clinically apparent hypothyroidism; because the symptoms associated with hypothyroidism are nonspecific, the condition can be difficult to diagnose, as reflected by the five-year median time to diagnosis in these women (Haddow 1999)



Thyroid preoxidase antibodies, autoimmune diseases and pregnancy


  • TPO (thyroid peroxidase) antibodies are a marker of thyroid autoimmunity and they are the most important risk factor for thyroid dysfunction during pregnancy
  • Research shows women who are TPO positive have higher TSH concentrations, lower free T4 concentrations, and a higher risk of thyroid dysfunction during pregnancy than women who are TPO negative (Thangaratinam 2011, Medici 2012).
  • Intriguingly, being TPO positive by itself is associated with an elevated risk of miscarriage and premature delivery (Korevaar 2013)
  • Data show that women who are TPO antibody positive should be considered a high-risk group for thyroid-related adverse results, especially if TSH concentrations are elevated or in the higher end of the normal range (Korevaar 2017)
  • In one study, the presence of high serum concentrations of thyroid peroxidase (TPO) antibodies in 77 percent of the women with hypothyroidism indicates that chronic autoimmune thyroiditis was the most frequent cause of hypothyroidism (Haddow 1999)



Subclinical hyperthyroidism and pregnancy


  • Subclinical hyperthyroidism is not associated with any adverse pregnancy results (Casey 2006); in one large study where a total of 25,765 women underwent thyroid screening and delivered single babies and of these, 433 (1.7%) were considered to have subclinical hyperthyroidism (below 1.75 ng/dL or 0.42 mIU/L); pregnancies in women with subclinical hyperthyroidism were less likely to be complicated by hypertension
  • Most cases of pregnancy related subclinical hyperthyroidism are of short term and of physiological nature making it hard to collect enough scientific data
  • Few studies have shown that higher free T4 concentrations are associated with reduced birth weight and reduced child cognitive function (Korevaar 2013, Haddow 2014)



Overt hyperthyroidism and pregnancy


  • During pregnancy, two major types of overt hyperthyroidism can occur:
    1. a rare pathological form that mainly affects women with Graves disease (or diseases characterized by autonomous thyroid hormone production, e.g., multinodular toxic goiter or toxic adenomas)
    2. a form with transient elevations in thyroid function due to high pregnancy hormone (hCG) levels that typically peak around the 10th week of pregnancy
  • Pregnancy related hyperthyroidism occurs in 0.3–1.0% of all pregnant women (as defined by a TSH concentration <2.5th percentile and a free T4 concentration above the 97.5th percentile, i.e. 2 std dev) (Casey 2006, Korevaar 2013, Springer 2009)
  • In the first type, estimated prevalence rates in western countries are 0.5-1.3% for pre-existing Graves disease, 0.05% for new-onset Graves disease, and 0.1% for autonomous thyroid hormone production (Cooper 2013, Carle 2011)
  • The disease often presents with clear biochemical abnormal signs (e.g., suppressed TSH concentrations with high free T4 concentrations typically above 1.5x the upper limit of normal), it has clear symptoms such as palpitations, tremor or anxiety, and it is associated with a high risk of negative pregnancy results
  • Several studies have linked the pathological forms of pregnancy hyperthyroidism to a higher risk of pre-eclampsia, preterm (early) birth, low birth weight and maternal heart failure (Cooper 2013, Sheffield 2004, Sahu 2010, Luewan 2011, Millar 1994, Pillar 2010)
  • A large American study compared 417 women diagnosed with hyperthyroidism during pregnancy with ~217,000 controls and found that women diagnosed with hyperthyroidism had a 1.8x higher risk of pre-eclampsia (Mannisto 2013)
  • Women diagnosed with hyperthyroidism also had a 1.2x higher risk of threatened preterm birth, a 1.8x higher risk of late preterm birth and a 3.7x higher risk of maternal admission to intensive care compared with control participants; a similar study from Denmark showed that women diagnosed with hyperthyroidism have higher risks of miscarriage, stillbirth, preterm birth, lower birth weight and having a child with attention deficit hyperactivity disorder than control participants (Anderson 2014, Anderson 2013)
  • Overall, women with hyperthyroidism had a 3.9x higher risk of pre-eclampsia, a 2.2x higher risk of fetal growth restriction, a 1.7x higher risk of preterm birth and a 3.6x higher risk of induction of labor than control participants (Aggarwal 2014)
  • Some of these women do not have symptoms of hyperthyroidism, whereas others are classified as being transiently thyrotoxic and require treatment with therapeutics such as propranolol to relieve their symptoms



Thyroid related risk factors during pregnancy

Thyroid dysfunction during pregnancy is associated with an increased risk of various adverse outcomes, including miscarriage, lower than normal fetal growth, hypertensive disorders, early delivery, and a decreased child IQ (Krassas 2010). Below we discuss each of these risks in detail for thyroid in pregnancy.

Thyroid and risk of pregnancy loss


  • Mothers with subclinical or mild hypothyroidism are at an increased risk of pregnancy loss (Medici 2015)
  • Studies show women with serum TSH concentrations of 2.5–5.0 mIU/L had a 6.1% risk of pregnancy loss, compared to 3.6% in women with a TSH concentration below 2.5 mIU/L (Negro 2010)
  • There is a linear correlation between TSH concentrations and pregnancy loss as shown by a Dutch cohort study of 2497 pregnant women, in which it was shown that the incidence of miscarriage and fetal and neonatal death (combined into child loss) increased by 80% by every doubling of the maternal TSH concentration; although data were limited to 27 cases (Benhadi 2009)
  • Data from UK with 202 pregnancies of miscarriage or fetal loss and 3592 normal pregnancies showed pregnancies complicated by child loss had higher mean TSH and lower fT4 concentrations, and a higher prevalence of TSH concentrations (Ashoor 2010)
  • Early-pregnancy TSH concentrations (>95th percentile) were associated with an increased 3.66-times risk of miscarriages in an Australian pregnancy cohort (Schneuer 2012)



Thyroid and risk of premature delivery


  • Study of 17,298 pregnant women showed subclinical hypothyroidism (elevated TSH and normal free T4) was associated with a slightly increased risk of premature delivery at <34 weeks (4% vs 2.5%); borderline significantly associated with prematurity <32 weeks (2.5 vs 1%), and not associated with prematurity <36 weeks (7 vs 6%) (Casey 2005)
  • When TPO antibodies were present, a 1.9x and 2.5x increased risk of premature delivery at <37 and <34 weeks, respectively was seen among women with a TSH >4.0 mIU/L; however, no associations were seen with TSH >2.5 mIU/L
  • Studies in women presenting for prenatal care, subclinical hyperthyroidism (n=433) was not associated with prematurity <=36, <=34, and <=32 weeks (Casey 2006); subclinical hyperthyroidism (n=224 cases) was not associated with prematurity <37 and <34 weeks either (Mannisto 2009)



Thyroid and child IQ


  • The main benefit—an increase of approximately 4 points in IQ scores — would occur in the children of women with serum thyrotropin concentrations at or above the 98th percentile (Haddow 1999)
  • A secondary benefit would be reduced morbidity for women who were systematically identified and treated



Thyroid and other pregnancy related risks


  • Hypertensive disorders, including pregnancy related hypertension and (pre)eclampsia, are common during pregnancy and are an important cause of maternal and fetal morbidity and mortality (Bellamy 2007)
  • Both hypo- and hyperthyroidism have vascular effects, including endothelial cell dysfunction (Klein 2001), and are associated with an increased risk of hypertensive disorders during pregnancy in limited studies conducted so far
  • Study of the correlation between free T4 and birth weight in a population-based cohort (without any overt thyroid dysfunction) found a statistically significant negative relation between fT4 and birth weight (Shields 2011)
  • Study of Dutch pregnant women confirmed above result that high-normal fT4 concentrations are associated not only with lower mean birth weights, but also with more SGA (small size for gestational age or smaller babies) and lower than 2500-g newborns (Medici 2013); however, these children do not suffer from more labor/delivery complications (Haddow 2014).
  • Low birth weight is a risk factor for cardiovascular and psychiatric diseases in later life (Barker 2006; Gale 2004)



Hypothyroxinemia and pregnancy


  • Hypothyroxinemia in pregnancy is defined as normal TSH and low free T4 value (below the 2.5th percentile or 3-std dev lower)
  • In 3,659 mother–child pairs from a prospective birth cohort, maternal hypothyroxinemia (defined as a TSH <2.5 mIU/L with free T4 <5th percentile) was associated with a 1.8x higher risk of expressive language delay at both 18 & 30 months of age (Henrichs 2013)
  • In same study, hypothyroxinemia was associated with a 2x higher risk of nonverbal cognitive delay;
  • Follow-up data subsequently revealed that maternal hypothyroxinemia (free T4 <5th percentile and TSH <2.5 mIU/L) was associated with a non-verbal IQ that was 4.3 points lower in these children at 6 years of age (Ghassabian 2014); free T4 concentrations <10th percentile were associated with a child IQ that was 1.5–3.8 points lower than that associated with maternal free T4 concentrations in the middle 80 percentiles (Korevaar 2016)
  • A Spanish study involving 1,643 mother–child pairs showed that a clear relationship existed between low maternal free T4 concentrations and mental score–at 14 months of age, infants whose mothers had free T4 concentrations during pregnancy <10th percentile, <5th percentile and <2.5th percentile had an IQ that was 2.4, 3.4 and 4.2 points lower, respectively, than that of children whose mothers had gestational free T4 concentrations above these cut-offs (Julvez 2013)
  • Maternal hypothyroxinemia has also been associated with a higher risk of other neurocognitive child outcomes that are a postnatal marker of intra-uterine brain development–one study showed that, compared with normal pregnancy levels, maternal hypothyroxinemia (defined as a TSH <2.5 mIU/L and a free T4 <5th percentile) is associated with a 2.6x higher risk of clinical symptoms of autism spectrum disorder in both boys and girls at a median age of 6 years (Roman 2013)
  • An investigation comparing 1,010 patients with schizophrenia with matched controls reported that maternal hypothyroxinemia (defined as a TSH between the 5th and 95th percentiles and a free T4 ≤10th percentile) in early pregnancy was associated with a 1.7x higher risk of schizophrenia (diagnosed at a mean age of 19.1 years (Gyllenberg 2016)
  • Maternal hypothyroxinemia is also associated with other childhood outcomes reflective of suboptimal prenatal brain development, such as attention deficit hyperactivity disorder, slower reaction times, suboptimal school performance and lower grey matter and cortical volumes (Finken 2013, Modesto 2015, Pakkila 2015, Korevaar 2016)



Hypothyroxinemia vs subclinical hypothyroidism


  • While subclinical hypothyroidism is associated with various negative pregnancy results, hypothyroxinemia is predominantly associated with negative neurobehavioral outcomes in the child (Korevaar 2013)
  • Studies suggest that subclinical hypothyroidism or maternal TSH concentrations better reflect maternal thyroid status whereas maternal free T4 concentrations better reflect thyroid hormone availability for the fetus, independent of TSH concentrations (Korevaar 2016, Henrichs 2013, Julvez 2013)
  • The results of studies associating hypothyroxinemia with adverse pregnancy outcomes, such as premature delivery or pre-eclampsia, are not very consistent (Korevaar 2013, Casey 2007, Mannisto 2010)



Iodine and thyroid

Iodine is an essential component of the thyroid hormones, T4 and T3, contributing 65% and 59% of their respective molecular weights

Age versus urinary Iodine levels


  • For women of childbearing age, the median UI (urinary iodine) concentration remains at ~130ug/L and the prevalence of a UI concentration <50ug/L remains at about 15%.
  • The median UI concentrations for the general U.S. population 2007–2008 were 164ug/L (95% CI 154–173) (Caldwell 2011)
  • The recommended amount is 150 ug/day for adults, 200 ug/day for pregnant or lactating women, and lower amounts for children (Dunn 1998; International Council for Control of Iodine Deficiency Disorders, the World Health Organization, UNICEF, and the Food and Nutrition Board of the U.S. National Academy of Sciences)
  • In the combined dataset for 2005–2006 and 2007–2008 NHANES, 56.9% +/- 7.9% of pregnant women had a UI concentration <150ug/L (although sampling of only 184 women); the assessment of 100 pregnant women from Boston, Massachusetts demonstrated that 49% of them had a UI <150ug/L (Pearce 2004)
  • The health risk to the fetus from maternal iodine insufficiency is greatest during the first trimester because the fetus is reliant upon maternal iodine stores for thyroid hormone synthesis. A maternal median UI concentration <=50mg/L during the first half of gestation can cause thyroid abnormalities such as increased thyroid gland size and elevated TSH and thyroglobulin concentrations in the newborn (Glinoer 1995; Pederson 1993)
  • A maternal UI concentration >50ug/L during the second trimester, an increased thyroglobulin, and a decreased free T4 index can cause thyroid abnormalities in the newborn (Kung 2007; Kung 2000).
  • Iodine supplementation can decrease the prevalence of postpartum goiter from iodine deficiency caused by gestation and lactation (Glinoer 1992; Antonangeli 2002)
  •  Consequences of Iodine-deficiency-syndrome include goiter, cretinism, intellectual impairment, brain damage, mental retardation, stillbirth, congenital deformities, and increased perinatal mortality (CDC:
  • Iodine supplementation before pregnancy compared with iodine supplementation during pregnancy appears to decrease a woman’s risk for abnormal thyroid function tests (i.e., decreased free T4 and increased TSH) (Moleti 2008)
  • Individuals who were hypothyroid at this critical period frequently have permanent mental retardation, which cannot be corrected by later administration of thyroid hormone or iodine. Child survival is also threatened by iodine deficiency, and several studies show that neonatal mortality decreases, sometimes by 50% or more, when the deficiency is corrected (DeLong 97)
  • The damage is greater when iodine deficiency provokes hypothyroidism during fetal or early life, because thyroid hormone is necessary for proper development of the central nervous system, particularly its myelination (neuron sheath formation)
  • Iodine may have effects independent of the thyroid as clinical studies suggest that fibrocystic breast disease is sensitive to iodine nutrition and improves when supplemented, particularly with iodine (I2) rather than iodide (Ghent 1993)
  • Dairy and grain products are the primary sources of iodine in the American diet (Murray 2008); in US salt is iodized with potassium iodide, which is used by about 50%–60% of the U.S. population; only a small percentage of its salt from table salt because ~70% of dietary salt is derived from processed food, which uses mostly non-iodized salt (Dasgupta 2008)




  1. Thyroid disease in pregnancy: new insights in diagnosis and clinical management by Korevaar et al.Nature Reviews Endocrinology 13, 610-622, 2017
  2. Early pregnancy reference interval of thyroid hormone concentrations in a thyroid antibody-negative pregnant population by Männistö et al., Thyroid 21 (1), 291-298 2011
  3. Thyroid Function in Pregnancy: What is Normal? by Medici et al. Clin. Chem. 61:5, 2015
  4. Association of maternal thyroid function during early pregnancy with offspring IQ and brain morphology in childhood: A population-based prospective cohort study by Korevaar et al. Lancet 4 (1), 35-43, 2016
  5. 2017 Guidelines of the American Thyroid Association for the Diagnosis and Management of Thyroid Disease During Pregnancy and the Postpartum by Alexander et al. Thyroid 27 (3) 315-389, 2017
  6. Iodine Status of the U.S. Population, National Health and Nutrition Examination Survey, 2005–2006 and 2007–2008 by Caldwell et al. Thyroid 21 (4), 419-427, 2011


Disclaimer: For information purposes only—not to be used for diagnosis or to replace advice from a medical professional. An At Home Thyroid Test can be ordered from our site here. Please see the full list of our CLIA-certified at-home health tests at All our tests include physician’s prescription, free shipping, and physician-approved reports.