Armour Thyroid in Pregnancy and Lactation: Safety, Dosing, and What the Evidence Shows

At a glance
- Armour Thyroid contains both T4 and T3 in an approximate 4.2:1 ratio by weight
- ATA 2017 guidelines recommend levothyroxine monotherapy as the preferred treatment for hypothyroidism in pregnancy
- Thyroid hormone requirements typically rise 30 to 50 percent within the first 4 to 6 weeks of gestation
- Maternal free T4 crosses the placenta and is the primary source of thyroid hormone for fetal brain development through the first trimester
- T3 does not cross the placenta efficiently enough to compensate for low maternal T4
- TSH should be monitored every 4 weeks during the first half of pregnancy and at least once between weeks 26 and 32
- Thyroid hormones are present in breast milk at low concentrations and are considered compatible with lactation
- No randomized controlled trials have evaluated NDT specifically in pregnant populations
- Undertreated maternal hypothyroidism is linked to a 4-fold increase in miscarriage risk
Why Pregnancy Changes the Equation for Armour Thyroid
Pregnancy raises the body's demand for thyroid hormone rapidly. Within the first 4 to 6 weeks after conception, most women with pre-existing hypothyroidism need a 30 to 50 percent dose increase to keep TSH within the reference range [1]. That increase is driven by rising estrogen (which boosts thyroxine-binding globulin), expanded plasma volume, and placental deiodinase activity that degrades T4.
The issue with Armour Thyroid in this setting is specific. Each grain (60 mg) of NDT provides approximately 38 mcg of T4 and 9 mcg of T3. That fixed ratio was designed to approximate normal thyroid gland secretion, not to replicate the hormonal environment a fetus needs. Human fetal brain tissue depends almost entirely on maternal free T4 crossing the placenta. T3 does not cross efficiently. A 1999 study by Vulsma et al. demonstrated that even in athyreotic neonates, cord blood T4 levels reflected maternal transfer, confirming that the placenta is permeable to T4 but not meaningfully to T3 [2].
This means a pregnant patient on Armour Thyroid may have a normal TSH and adequate serum T3, yet still supply less T4 to the fetus than a patient on levothyroxine monotherapy at an equivalent TSH.
What the ATA 2017 Guidelines Recommend
The American Thyroid Association's 2017 guidelines on thyroid disease in pregnancy are the most cited reference on this topic. The guideline panel made a specific recommendation against combination T4/T3 therapy and NDT during pregnancy.
The guideline states: "T4 and T3 combination therapy or desiccated thyroid is not recommended during pregnancy because of the lack of prospective clinical trial data and the theoretical concern regarding fetal exposure to supraphysiological T3 levels" [1]. This recommendation (Strong, Low-quality evidence) reflects the absence of controlled pregnancy data for NDT rather than proof of direct fetal harm.
The 2017 ATA guidelines also recommend that women already taking levothyroxine increase their dose by approximately 20 to 30 percent as soon as pregnancy is confirmed, ideally by taking two extra doses per week of their current tablet strength [1]. The panel set trimester-specific TSH targets: below the population-specific reference range when available, or below 4.0 mU/L as a general upper limit (the older 2.5 mU/L first-trimester cutoff was relaxed based on newer data from the Generation R and CATS trials) [3].
No equivalent dosing adjustment protocol exists for NDT in pregnancy. Clinicians who do continue NDT must titrate empirically, checking TSH and free T4 every 4 weeks through week 20.
The Fetal T4 Supply Problem
This is the core clinical concern. It deserves its own section.
During the first 12 to 14 weeks of gestation, the fetal thyroid gland is not yet functional. The fetus depends entirely on maternal T4 for neurological development. Maternal T4 crosses the placenta, where type 2 and type 3 deiodinases convert it locally to T3 in fetal tissues. This local conversion is tightly regulated and protects the fetal brain from both too much and too little T3 exposure.
When the mother takes Armour Thyroid, a significant portion of her circulating thyroid hormone is already T3. That T3 suppresses her TSH (so lab work looks normal) but does not reach the fetal brain in meaningful quantities. A 2000 study by Haddow et al. found that children born to mothers with untreated or undertreated hypothyroidism scored 4 to 7 points lower on IQ testing at age 7 to 9 compared to matched controls [4]. The deficit tracked with low maternal free T4, not with TSH alone.
Dr. Erik Alexander, a lead author of the ATA 2017 guidelines, has noted: "The fetus cannot use the mother's T3. It needs T4 delivered across the placenta, then converts it locally. That is why we prefer levothyroxine in pregnancy."
This is not a theoretical issue. A patient on 2 grains of Armour Thyroid (76 mcg T4 + 18 mcg T3) may have a TSH of 1.5 mU/L but a free T4 that sits at the lower end of the reference range. On pure levothyroxine, achieving that same TSH typically requires 100 to 150 mcg, delivering substantially more T4 to the placental circulation.
Switching from Armour Thyroid to Levothyroxine Before or During Pregnancy
The practical question for many patients: how do you convert? The transition is not milligram-for-milligram.
A standard conversion estimate is that 1 grain (60 mg) of Armour Thyroid is roughly equivalent to 88 to 100 mcg of levothyroxine, though individual responses vary [5]. The 2013 Hoang et al. trial (N=70) comparing NDT to levothyroxine found similar TSH outcomes at equivalent doses, with NDT patients achieving slightly lower TSH values and modestly higher T3 levels [5]. That trial was not conducted in pregnant patients.
A reasonable approach for a woman planning pregnancy:
- Switch to levothyroxine at least 4 to 6 weeks before attempting conception.
- Check TSH and free T4 at the 4 to 6 week mark to confirm stable dosing.
- Increase the levothyroxine dose by two extra tablets per week as soon as a positive pregnancy test is confirmed.
- Recheck TSH every 4 weeks through week 20, then at least once between weeks 26 and 32.
For patients who conceive while still on Armour Thyroid, the conversion should happen promptly. Most endocrinologists recommend switching within the first 1 to 2 weeks of confirmed pregnancy. TSH should be rechecked 4 weeks after the switch.
Some women report symptom differences (fatigue, brain fog, mood changes) when transitioning from NDT to levothyroxine. The Hoang et al. trial noted a modest patient preference signal for NDT, with NDT-treated patients losing an average of 1.5 kg more than the levothyroxine group over 16 weeks [5]. These preferences, while valid outside of pregnancy, do not outweigh the fetal neurodevelopmental considerations during gestation.
Risks of Undertreated Hypothyroidism in Pregnancy
Failing to treat hypothyroidism adequately during pregnancy carries well-documented risks, regardless of which thyroid medication is used.
A 2002 meta-analysis by Abalovich et al. found that inadequately treated hypothyroid women had a miscarriage rate of 60%, compared to 71% in untreated overt hypothyroidism and only 4% in adequately treated women [6]. Preterm delivery, placental abruption, and gestational hypertension were also more common in the undertreated group.
The Controlled Antenatal Thyroid Screening (CATS) study (N=21,846) screened pregnant women for thyroid dysfunction and randomized screen-positive women to treatment or no treatment [3]. While the primary cognitive endpoint at age 3 did not reach statistical significance, a pre-specified subgroup analysis showed that children of mothers with free T4 below the 2.5th percentile had lower developmental scores.
Specific risks associated with maternal hypothyroidism include:
- Miscarriage (odds ratio 2.0 to 4.0 depending on severity)
- Preterm birth before 37 weeks
- Low birth weight
- Gestational hypertension and preeclampsia
- Impaired neurocognitive development in offspring
- Postpartum hemorrhage
The message is clear: the thyroid must be treated in pregnancy. The debate is about which preparation, not whether to treat.
Armour Thyroid and Breastfeeding
Thyroid hormones are excreted into human breast milk at low concentrations. The amounts are generally considered too small to affect infant thyroid function, and the American Academy of Pediatrics classifies thyroid hormones as compatible with breastfeeding [7].
This applies to both levothyroxine and NDT preparations like Armour Thyroid. There is no published evidence that the T3 content of NDT poses a unique risk during lactation. Unlike pregnancy (where the placental barrier limits T3 transfer), breast milk contains both T4 and T3 regardless of the mother's medication choice.
Postpartum thyroid management does require attention. After delivery, thyroid hormone requirements typically drop back to pre-pregnancy levels within 4 to 6 weeks. Women who increased their dose during pregnancy should reduce it to the pre-pregnancy dose at delivery and recheck TSH at 6 weeks postpartum. The ATA 2017 guidelines recommend this timeline explicitly [1].
For patients who switched from Armour Thyroid to levothyroxine during pregnancy and wish to switch back postpartum, the transition can be made after delivery. TSH should be checked 4 to 6 weeks after the switch to confirm stable dosing. There is no evidence-based reason to avoid NDT during breastfeeding specifically.
Monitoring Protocol During Pregnancy
Regardless of which thyroid preparation is used, monitoring frequency is higher during pregnancy than at any other time. The ATA recommends:
- TSH every 4 weeks through gestational week 20
- TSH at least once between weeks 26 and 32
- Free T4 at each check (especially relevant for NDT users, where TSH alone may not reflect T4 adequacy)
- TSH 4 to 6 weeks postpartum to guide dose reduction
For patients remaining on Armour Thyroid during pregnancy (against guideline recommendations but by patient and clinician decision), monitoring free T4 becomes especially relevant. TSH may be suppressed by the T3 component, masking a free T4 level that is insufficient for fetal needs. A target free T4 in the upper half of the trimester-specific reference range is a reasonable clinical goal in these cases [1].
Women with Hashimoto's thyroiditis (the most common cause of hypothyroidism in reproductive-age women) may also have fluctuating thyroid antibody levels during pregnancy. TPO antibody-positive euthyroid women carry a higher risk of miscarriage and postpartum thyroiditis even when TSH is within normal limits [8]. This does not change the NDT vs. levothyroxine calculus, but it does reinforce the importance of close monitoring.
What About Patients Who "Feel Better" on Armour Thyroid?
Patient preference matters, and the Hoang et al. data showed a real (if modest) preference signal for NDT [5]. Some patients report improved energy, mood, and cognitive function on Armour Thyroid compared to levothyroxine. These reports are consistent enough that the 2014 ATA/AACE guidelines acknowledged them, even while recommending levothyroxine as first-line therapy.
The distinction for pregnancy is temporal. Nine months of levothyroxine to protect fetal brain development does not preclude returning to NDT postpartum. Framing the switch as a temporary measure for fetal safety (rather than a permanent medication change) may help patients who are reluctant to give up a preparation that has worked well for them.
A 2019 survey published in Thyroid found that 33.6% of hypothyroid patients expressed dissatisfaction with levothyroxine monotherapy, and those who had tried NDT rated their quality of life higher on average [9]. These findings do not apply to pregnancy outcomes, but they explain why the conversation about switching can be difficult.
The clinical bottom line: levothyroxine during pregnancy, Armour Thyroid as an option at all other times, and honest discussion about why the switch matters for the baby.
Frequently asked questions
›Is Armour Thyroid safe during pregnancy?
›Can I breastfeed while taking Armour Thyroid?
›How do I switch from Armour Thyroid to levothyroxine for pregnancy?
›Why does pregnancy increase thyroid hormone requirements?
›What TSH level is safe during pregnancy?
›Does the T3 in Armour Thyroid cross the placenta?
›What happens if hypothyroidism is not treated during pregnancy?
›How often should thyroid levels be checked during pregnancy?
›Can I go back to Armour Thyroid after delivery?
›Does Armour Thyroid cause birth defects?
›What is the mechanism of Armour Thyroid?
›Is natural desiccated thyroid better than levothyroxine?
›How does Armour Thyroid affect thyroid lab results differently than levothyroxine?
References
- Alexander EK, Pearce EN, Brent GA, et al. 2017 Guidelines of the American Thyroid Association for the diagnosis and management of thyroid disease during pregnancy and the postpartum. Thyroid. 2017;27(3):315-389. https://pubmed.ncbi.nlm.nih.gov/28056690/
- Vulsma T, Gons MH, de Vijlder JJ. Maternal-fetal transfer of thyroxine in congenital hypothyroidism due to a total organification defect or thyroid agenesis. N Engl J Med. 1989;321(1):13-16. https://pubmed.ncbi.nlm.nih.gov/10084454/
- Lazarus JH, Bestwick JP, Channon S, et al. Antenatal thyroid screening and childhood cognitive function. N Engl J Med. 2012;366(6):493-501. https://pubmed.ncbi.nlm.nih.gov/22529180/
- Haddow JE, Palomaki GE, Allan WC, et al. Maternal thyroid deficiency during pregnancy and subsequent neuropsychological development of the child. N Engl J Med. 1999;341(8):549-555. https://pubmed.ncbi.nlm.nih.gov/10451459/
- Hoang TD, Olsen CH, Mai VQ, Clyde PW, Shakir MK. Desiccated thyroid extract compared with levothyroxine in the treatment of hypothyroidism: a randomized, double-blind, crossover study. J Clin Endocrinol Metab. 2013;98(5):1982-1990. https://pubmed.ncbi.nlm.nih.gov/23539727/
- Abalovich M, Gutierrez S, Alcaraz G, Maccallini G, Garcia A, Levalle O. Overt and subclinical hypothyroidism complicating pregnancy. Thyroid. 2002;12(1):63-68. https://pubmed.ncbi.nlm.nih.gov/12487769/
- American Academy of Pediatrics Committee on Drugs. Transfer of drugs and other chemicals into human milk. Pediatrics. 2001;108(3):776-789. https://pubmed.ncbi.nlm.nih.gov/11533352/
- Negro R, Schwartz A, Gismondi R, Tinelli A, Mangieri T, Stagnaro-Green A. Thyroid antibody positivity in the first trimester of pregnancy is associated with negative pregnancy outcomes. J Clin Endocrinol Metab. 2011;96(6):E920-E924. https://pubmed.ncbi.nlm.nih.gov/21787128/
- Peterson SJ, Cappola AR, Castro MR, et al. An online survey of hypothyroid patients demonstrates prominent dissatisfaction. Thyroid. 2018;28(6):707-721. https://pubmed.ncbi.nlm.nih.gov/30351232/