Sarah Thompson
L.Ac., CFMP, Doula
@functionalmaternity
Summary
Recent studies have begun to connect thyroid function with poor labour outcomes. Hypothyroidism has been an under-researched part of maternal physiology because the definition of hypothyroidism in pregnancy is not well established. The guidelines for pregnancy reference ranges for thyroid indices are not well established within the obstetrical community, and there is some discrepancy between the American College of Obstetrics and Gynecology and the Endocrine Societies on what is normal in pregnancy. Recently, though, this has started to change thanks to emerging research surrounding the role of thyroid hormones and childbirth outcomes.
What the Research Has to Say?
A 2019 study on hypothyroidism and birth outcomes conducted a cross-sectional retrospective study on 718 cases. [1] They collected information from patients who had been diagnosed with hypothyroidism before or during their pregnancies. They recorded miscarriages, stillbirths, gestational hypertension, preeclampsia, placental abruption, delivery outcomes, and postpartum haemorrhage. Of these women 638 had live births, 38.8% had postpartum hemorrhage, and 23.4% delivered via cesarean. The greatest clinical finding was the increased association with postpartum haemorrhage. Postpartum haemorrhage was significantly associated with TSH levels > 2.5 mIU/L in preconception and third trimester.
Another study called the Consortium of Safe Labor Study was an observational, US cohort study of 12 clinical centres and 19 hospitals between 2002 – 2008. [2] It was designed to provide information on birthing statistics in the United States at the time. It covered 228,668 deliveries. Data was collected both through electronic medical records and discharge summaries. They found that women diagnosed with hypothyroidism had 1.5-fold odds of developing preeclampsia, increased risk of premature rupture of membranes (48% of those with autoimmune thyroiditis), decreased odds of presenting in spontaneous labour, increased odds of labour induction, increased odds of “failure to progress” diagnosis, increased odds of cesarean delivery after spontaneous onset of labour, increased risk of haemorrhage, and an increased risk of ICU admission due to haemorrhage. They also found that only 66% of those with preexisting hypothyroidism were monitored throughout their pregnancy, leaving 33% with unmanaged hypothyroidism.
Current Guidelines and Recommendations
| Organization | First Trimester | Second Trimester | Third Trimester | Additional Recommendations |
| American College of Obstetrics & Gynecology | 0.6 – 3.4 mIU/L | 0.37 – 3.6 mIU/L | 0.38 – 4.04 mIU/L | |
| The Endocrine Society | 0.1 – 2.5 mIU/L | 0.2 – 3.0 mIU/L | 0.3 – 3 mIU/L | + TPOAb testing if over 2.5 mIU/L |
| The European Thyroid Association | 0.1 – 2.5 mIU/L | 0.2 – 3.0 mIU/L | 0.3 – 3.5 mUI/L | |
| American Thyroid Association | 0.1 – 2.5 mIU/L | 0.2 – 3.0 mIU/L | 0.3 – 3.0 mIU/L | + Iodine testing if over 2.5 mIU/L |
How Thyroid Hormones Affect Birth Outcomes
In early pregnancy, hCG hijacks the maternal thyroid to stimulate an increase in thyroid hormone production. There are two subunits of hCG, hCGα and hCGβ. hCGβ is the subtype tested in a pregnancy test and is dominant in early pregnancy. It is also the form that has an affinity for thyroid-stimulating hormone receptors. There is a shift to higher hCGα around 12/13 weeks. Then an increase in the production of hCGβ from 20 weeks to term. This increases the production of thyroid hormones in preparation for labour.
In early pregnancy, thyroid hormones are required for fetal metabolism and function. The fetus cannot make its thyroid hormones until after 20 weeks gestation. After this point, the baby can make its own without relying heavily on maternal production.
So, what do these hormones do?
During the third trimester, the primary functions of thyroid hormones are preparing the mother for childbirth and postpartum. This includes functions such as galactopoietic actions, platelet production and activation, prostacyclin production, thromboxane production, the modification of the genetic expression of certain blood clotting factors, as well as the conversion of beta carotene to vitamin A.
Many of these functions directly influence the maternal body’s ability to clot correctly during and after childbirth. This connection may be a direct cause of the increase in postpartum haemorrhage rates seen in the studies.
Additionally, and left directly, thyroid hormones affect the metabolism of beta-carotene and retinol into retinoic acid. Retinoic acid acts on genetic expression. Including the genetic expression of oxytocin and oxytocin receptors. [3] In the third trimester, there is nearly a 6-fold increase in vitamin A receptors in the uterus.
All of these maternal actions are directly and indirectly affected by a decreased production of thyroid hormones. This may be the underlying cause of why studies, like those mentioned above, find a significant increase in childbirth complications in those with subclinical and clinical hypothyroidism presentations in the third trimester.
Links to other resources
Websites
WebsitesNIH | Thyroid Disease and Pregnancy
Tommy’s | Health Conditions and Planning a Family
Books
BooksReal Food for Pregnancy by Lily Nichols
Film Audio, Apps and Podcasts
Film Audio, Apps and PodcastsBaby Buddy app, created by the Best Beginnings Charity
References
- Kiran Z, Sheikh A, Malik S, et al. Maternal characteristics, and outcomes affected by hypothyroidism during pregnancy (maternal hypothyroidism on pregnancy outcomes, MHPO-1). BMC Pregnancy Childbirth. 2019;19(1):476. Published 2019 Dec 5. doi:10.1186/s12884-019-2596-9
- Männistö T, Mendola P, Grewal J, Xie Y, Chen Z, Laughon SK. Thyroid diseases and adverse pregnancy outcomes in a contemporary US cohort. J Clin Endocrinol Metab. 2013 Jul;98(7):2725-33. doi: 10.1210/jc.2012-4233. Epub 2013 Jun 6. PMID: 23744409; PMCID: PMC3701274.
- Larcher A, Neculcea J, Chu K, Zingg HH. Effects of retinoic acid and estrogens on oxytocin gene expression in the rat uterus: in vitro and in vivo studies. Mol Cell Endocrinol. 1995 Oct 30;114(1-2):69-76. doi: 10.1016/0303-7207(95)03643-l. PMID: 8674853.
