Thyroid disorders are common in women, and in my practice I have consistently seen them associated with subfertility, poor egg quality, and miscarriage. These conditions have often thought to occur because of the embryo’s dependence on its mother’s thyroid hormone for its own metabolism. Until the embryo reaches 12 weeks of age, it can’t make thyroid hormones on its own and is dependent on the mother for these crucial factors that support its growth.
In addition, there’s a strong link between premature menopause, low ovarian reserve (low egg count), and Hashimoto’s (Autoimmune) thyroiditis. This link appears to be related to cross-reactivity between the thyroid and the ovary.
Egg quality impairment is common in women with PCOS as well, and thyroid dysfunction has a high prevalence in this group too.
This new studydelved beyond autoimmune factors to look at how thyroid hormones themselves affect the growth and development of healthy eggs, and the production of female hormones.
Researchers were interested in the direct impact of the hormones T3 and T4 on the growth and development of the ovarian follicles. These support healthy oocytes (eggs) and produce the vast majority of key female sex hormones.
Ovulation and Egg Quality
It is important to understand that the cells that surround the egg—the ovarian follicles—not only support the oocyte itself, but are also responsible for the majority of women’s estrogen, progesterone, and testosterone production.
In this study, they looked at the ovary’s cellular metabolism, and how this can be impacted by thyroid hormones. This study was completed on cultured rat ovarian follicles, which have striking similarities with human follicles.
Researchers exposed the hormone-producing follicles housing the eggs to the hormones T4 and T3.
T4 is the most abundant thyroid hormone, though it is often though to be largely metabolically inactive.
This belief has been challenged recently, however, as T4appears to have certain metabolic actions of its own. This study provided us with a bit more information showing that T4 is not an entirely inactive hormone.
Regardless, we have long known T3 to be by far the most powerful metabolically active thyroid hormone. It causes the majority of thyroid-related metabolic effects to occur.
When the ovarian follicles were exposed to T3 over the course of this study, they underwent a 40 percent increase in follicle volume.
This appeared to be due to a 33 percent decrease in the ovary’s granulosa cells‘ death rate when exposed to T3.
Granulosa Cells and Their Role in PCOS
The follicles’ granulosa cells make large quantities of estrogen during the follicular phase of a woman’s cycle, and have often been found to be under-active or dysfunctionally active in PCOS*. These same types of ovarian cells make progesterone during the cycle’s luteal phase. Clearly, if these cells’ function is deficient, there can be major impacts on follicle health. This in turn causes deficits in estrogen and progesterone production.
Thyroid and The Ovary
This is not the first time that thyroid hormones’ effects on the ovaries have been studied.
It has been demonstrated that hyperthyroidism or hypothyroidism significantly reduces the number of healthy follicles.  Replacing thyroid hormones has been found to markedly increase the number of healthy antral follicles—the types of follicles that are actively able to make hormones, and house a healthy egg .
In this study in particular, T4 appeared to be less effective at keeping the granulosa cells alive than T3, showing significance only at a higher concentration. That said, this difference is consistent with the fact that T3 is at least 10 times more effective than T4. This implies that both hormones are needed at optimal levels.
Overall, optimizing thyroid health has numerous benefits for metabolism, mood, and cardiovascular health. It is also clear that optimal thyroid function is crucial for ovarian health, egg quality, and overall female hormonal regulation..
- Canipari, R., Mangialardo, C., Di Paolo, V. et al.J Endocrinol Invest (2018)https://doi.org/10.1007/s40618-018-0912-2