In my last post, I alluded to my and others’ questions around the effects of COVID-19 and the vaccines on reproductive health. In my research to discover whether or not the latest booster was right for me, I wanted to go deeper into an article I read by Aviva Romm, MD, an integrative women’s health practitioner, trained first as an herbalist and midwife, who has written multiple books I adore (Hormone Intelligence, The Adrenal Thyroid Revolution). This article focuses on changes in women’s menstrual cycles, which in my observations took some time to receive validation and attention (and then, all of a sudden, did). Anyway, as someone with a family history of hypothyroidism, it was this paragraph about the thyroid that stood out to me:
“We also know that COVID-19 infection can have some impact on thyroid function, and there’s a relationship between your thyroid and your menstrual cycles. The authors of one study found that abnormal thyroid function – especially low TSH – is common in patients with COVID-19. (In fact, about 15-30% of hospitalized COVID-19 patients will have detectable new-onset thyroid dysfunction.) They concluded that although more research is needed, it’s possible that COVID triggers systemic immune activation that can cause inflammation in the thyroid, subacute hyperthyroidism, or acute hypothyroidism. Thyroid conditions like these are known contributors to menstrual cycle issues. The thyroid not only affects metabolism and weight, but it also interferes with the production of other hormones, including estrogen and progesterone, and can cause infertility, miscarriage, irregular cycles, skipped periods, heavy periods, cognitive problems, and much more.”
The second link is to an article published by the Baylor College of Medicine that explains that infection with COVID-19 can lead to acute hypothyroidism in something called “non-thyroidal illness syndrome,” characterized by low T3 or TSH and triggered by the release of pro-inflammatory cytokines. Alternatively, infection can lead to acute subclinical hyperthyroidism. Several cases have also reported subacute thyroiditis, or inflammation and pain in the thyroid that is thought to be autoimmune and possibly caused by invasion of the ACE2 receptor by the virus. Which led me to… What is the ACE2 receptor?
A quick Google search taught me that ACE2 stands for angiotensin-converting enzyme 2 and that these receptors are located in the heart, lungs, and other parts of the body, including those involved in the female reproductive system (notably, ovaries, although it turns out these receptors are also located in the male reproductive system — not trying to leave anyone out!). Frontiers in Physiology (I do love Frontiers — they have a journal for everything) dedicates an entire research topic to the impact of COVID-19 on the human reproductive system. One article serves as the most comprehensive review of literature on this topic to date that I’ve found. It explains that ACE2 regulates the expression of several peptides, including angiotensin II and Ang(1-7), which are involved in maturation of oocytes, ovulation, and “all stages of follicular development, suggesting a role in fertility.” Notably, the vagina and cervix do not express ACE2. Infection with COVID-19 has also been implicated indirectly in obstetric outcomes including pregnancy loss, preterm birth, neonatal NICU admission, and more, at least in part through a mechanism compromising the placenta.
Interestingly, there is also a body of research around the immunomodulatory effects of estrogen, supporting a stronger immune response in females than in males. Women are known to have “a stronger innate and adaptive immune response to viral infection,” as this article explains in detail, although it also notes that “While androgens like testosterone are known to be immunosuppressive, oestrogen tends to be more versatile in its character, and may enhance or deplete immune response, based on its concentration, distribution, and expression of its receptors.”
This one is worth a read, but I’ll call out two points:
· Women appear to experience higher phagocytic activity (from white blood cells calls neutrophils and macrophages), more robust responses from T cells (CD4+ and CD8+), and increased production of antibodies that remain in circulation longer, too.
· Estrogen has been shown to dampen production of pro-inflammatory cytokines, preventing cytokine storm syndrome.
More research is needed into gender-specific responses to COVID-19, the effects of COVID-19 on pregnancy (the research is limited and divided), and the effects of COVID-19 vaccines on reproductive health (so far, I have only read that the vaccines do not compromise fertility).
Tell me what you’re seeing and link me to any research you’re reading!
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