Pregnancy and your thyroid

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Pregnancy is undoubtedly a time of great change, mentally, emotionally and physically. One often overlooked area of change however is how pregnancy affects your thyroid, especially for individuals with pre-existing thyroid disease. Optimal thyroid function is ESSENTIAL for your baby’s health and development, as well as for your health and wellbeing throughout pregnancy. Let’s take a look at why:

Why Optimal Thyroid Function is Essential in Pregnancy

Firstly, it’s important to understand why healthy thyroid function is essential during pregnancy. Not only is healthy thyroid function required for the mother’s health and wellbeing, but it is also ESSENTIAL to foetal growth and development. In fact, thyroid dysfunction in pregnancy is a known risk factor for complications such as miscarriage, intrauterine growth restriction, pre-eclampsia, preterm birth and impaired neurological development.

As the baby does not start producing adequate quantities of its own thyroid hormone until midway through the second trimester, it is almost entirely dependent upon the mother’s supply of thyroid hormones until that point. As a result, numerous biochemical changes occur during pregnancy in order to provide adequate thyroid hormones to both the mother and the developing foetus. In fact, it is estimated that pregnancy necessitates an increase in thyroid hormone production by as much as 50%, which is why we must be supporting women throughout their pregnancies both nutritionally and with adequate thyroid monitoring.

Whilst hypothyroidism is much more common in women of reproductive age, an overactive thyroid during pregnancy can be just as problematic, which is why I recommend monitoring of thyroid function before, during and after pregnancy where possible, particularly if there is a history of thyroid disease.

What Happens in Pregnancy

It’s well-recognised that profound changes in thyroid physiology occur during pregnancy, and this must always be taken into account when assessing the thyroid results of a pregnant woman. The reference ranges that are applicable to non-pregnant women are not necessarily applicable during pregnancy, and a result which might be considered normal for a non-pregnant woman may not be normal for a pregnant individual. This is also why it’s essential to work with a healthcare professional who understands the importance of pregnancy and trimester-specific reference ranges, and can interpret thyroid function during pregnancy accordingly.

TSH - Thyroid Stimulating Hormone

One of the biggest changes we see with regards to thyroid function during pregnancy is the effect of pregnancy on TSH. The pregnancy hormone hCG is structurally very similar to TSH, and as a result, it exerts weak thyroid-stimulating effects. As hCG increases during the first trimester, we may therefore observe a small and transient increase in T4 production, resulting in a reciprocal decrease in TSH from around the 8th week of gestation. That said, research suggests there is a 20-40% increase in thyroid hormone requirements as early as the fourth week of gestation - For these reasons, it is well-recognised that TSH in pregnancy should be lower than that which is considered normal for non-pregnant individuals, and a reference interval of 0.1 - 2.5 mIU/L is recommended in the first trimester. According to the Royal Australian College of General Practitioners, failure to use an appropriate reference range for TSH may result in over-diagnosis of hyperthyroidism and under-recognition of hypothyroid states during pregnancy, both of which are potentially problematic.

Whilst discussing TSH, it’s important to note that in recent years some debate has arisen concerning the ideal upper limit of TSH during pregnancy. Notably, some researchers are calling not only for trimester-specific reference ranges, but more specifically, lab-specific reference ranges (Korevaar provides an interesting commentary on the topic in his 2018 article here). Whilst debate exists, the most important takeaway is that TSH must always be interpreted contextually and with consideration to the health status and medical history of individual concerned.

Thyroxine (T4)

As mentioned above, T4 levels tend to increase slightly in the first trimester and this is followed by a gradual decrease across the remainder of the pregnancy. In addition to the thyroid-stimulating effects of hCG, a number of other changes take place which account for this fluctuation.

For example, early in the first trimester, oestrogen stimulates the production of thyroxine binding globulin (TBG); a protein which binds to thyroid hormones in the blood and reduces their bioavailability. In addition, plasma volume increases dramatically during pregnancy, resulting in increased “dilution” (volume of distribution) of the available T4. The placenta is also rich in a type of enzyme called type 3 iodothyronine deiodinase, which degrades T4 and helps regulate supply of thyroid hormone to the foetus. Passage of T4 to the baby across the placenta also reduces the amount which is available to the mother. Lastly, pregnant women excrete more iodine in their urine than non-pregnant individuals, which means they require increased iodine intake in order to sustain T4 production.

In summary, this can be described as:

  • Decreased bioavailability of T4

  • Increased degradation of T4

  • Increased ‘dilution’ T4

  • Increased urinary iodine excretion (resulting in increased iodine requirements for thyroid hormone production

Together, these effects account for the dramatic alterations in thyroid hormone metabolism observed in pregnant women. They also help explain why up to 85% of women with pre-existing thyroid disease will need an increase in their thyroid medication dose during pregnancy, typically within the range of 30-50% (under the guidance of their GP, endocrinologist or obstetrician).

Triiodothyronine (T3)

T3 levels are generally considered less significant than T4 with respect to their effects on foetal development, as T3 does not cross the placenta. Instead, the baby produces T3 ‘locally’ via conversion of maternal T4 (and eventually, production of its own thyroid hormones). As a result, it is generally assumed that maternal T3 levels have little, if any, role in foetal development. This is also part of the reason why very little research has been conducted on the use of T3 therapy alone as a form of thyroid hormone replacement during pregnancy.

Despite this, adequate T3 levels during pregnancy are still essential for the mother’s health and wellbeing. For this reason, T3 assessment during pregnancy may still be very much beneficial, particularly for women displaying symptoms of hypothyroidism, those with pre-existing thyroid disease and those with results suggestive of poor peripheral thyroid hormone conversion.

What This Means

Ultimately, pregnancy is a time of unique change when it comes to thyroid function and physiology, and it is therefore important to work with a healthcare provider who understands these changes and can interpret thyroid function results appropriately within the context of pregnancy. From a nutritional perspective, women should be counselled on the importance of adequate dietary iodine intake during pregnancy, and supplementation to meet the recommended daily intake of 220 mcg should be advised where necessary.

Those with overt or subclinical hypothyroidism during pregnancy should be guided by their healthcare practitioner with regards to monitoring and thyroid hormone replacement, with RACGP recommending follow-up assessment of thyroid function within 4 weeks of commencing Thyroxine. In such cases, assessment of thyroid antibodies and iodine status may also prove beneficial. Women with pre-existing thyroid disease should undertake additional monitoring of their thyroid during pregnancy (with the guidance of a suitably-qualified healthcare practitioner), and adjustment of Thyroxine dosage should be considered where applicable. Ideally, those with pre-existing hypothyroidism should be monitored every 4-6 within the first half of pregnancy, in addition to at least once between weeks 26 and 32, as well as during the postpartum period.

Overt hyperthyroidism is estimated to occur in 0.4% of pregnancies, most commonly due to Graves’ disease or gestational thyrotoxicosis. Medications such as Propylthiouracil may be prescribed at the discretion of the endocrinologist or obstetrician, along with monitoring of thyroid function every 2-6 weeks during gestation. As TSH receptor antibodies may cross the placenta, RACGP also recommends their assessment at 28-32 weeks gestation in women with hyperthyroidism or a history of such. Thyroid monitoring should also occur for both the mother and baby in the postpartum period, in order for appropriate management strategies to be implemented where required.

Ultimately, the thyroid plays an essential role during foetal growth and development, and appropriate monitoring and assessment of thyroid function is essential for the wellbeing of both the mother and baby. It is imperative healthcare providers are cognisant of the biochemical and physiological changes that occur with respect to the thyroid during pregnancy, so they may provide appropriate recommendations and clinical assessment as required. Just as we monitor things like iron and haemoglobin during pregnancy, regular monitoring of thyroid function is recommended for women who are pregnant, trying to conceive or have recently given birth.

Niki x

Further Information and Sources