Hashimoto’s thyroiditis (HT) is an autoimmune disorder where the immune system attacks the thyroid gland, often leading to hypothyroidism (low thyroid function). Infertility, defined as the inability to conceive or carry a pregnancy to term, is complexly related to HT. This connection involves two primary pathways: the disruption of hormone balance caused by low thyroid levels and the direct consequences of underlying immune system dysfunction. Understanding these pathways is important for optimizing reproductive health.
The Hormonal Cascade: How Hypothyroidism Affects Ovulation
Insufficient thyroid hormones (T3 and T4) resulting from HT disrupt the reproductive cycle. The thyroid directly influences the hypothalamic-pituitary-gonadal (HPG) axis, the master control system for reproduction. Low thyroid levels interfere with the rhythmic release of gonadotropin-releasing hormone (GnRH), altering the signaling of luteinizing hormone (LH) and follicle-stimulating hormone (FSH).
This hormonal imbalance can cause anovulation or irregular menstrual cycles. Hypothyroidism commonly increases thyrotropin-releasing hormone (TRH), stimulating the pituitary to secrete excessive prolactin. Elevated prolactin directly suppresses GnRH and gonadotropin release, further inhibiting ovulation. Hypothyroidism also alters estrogen metabolism and increases sex hormone-binding globulin (SHBG), creating an environment unfavorable for conception.
The Role of Thyroid Antibodies in Conception and Pregnancy
Beyond hormone deficiency, the presence of thyroid antibodies marks a distinct autoimmune component impacting reproductive outcomes. The most commonly measured marker is Thyroid Peroxidase Antibody (TPOAb), which signals immune activity against the thyroid gland. Studies show that even in women with normal thyroid hormone levels (euthyroid), TPOAb presence is associated with fertility challenges.
These antibodies signify systemic immune dysregulation that interferes with reproductive processes. TPOAb has been linked to issues with egg quality and diminished ovarian reserve. The autoimmune state can impair implantation and early fetal development by disrupting the immune tolerance required at the uterine lining and placenta. This immune activity is thought to compromise the development of a healthy placenta, contributing to subsequent pregnancy loss.
Specific Infertility and Pregnancy Risks Associated with Hashimoto’s
Hormonal disruption and autoimmune activity lead to several specific clinical outcomes for women with HT. Chronic anovulation and menstrual irregularities frequently hinder natural conception. Even when thyroid hormone levels are managed, the risk of recurrent miscarriage is substantially higher in women with HT.
The autoimmune environment also increases the risk of complications later in pregnancy, including preterm birth, preeclampsia, and placental abruption. For women undergoing assisted reproductive technologies (ART), such as in vitro fertilization (IVF), thyroid autoantibodies have been linked to reduced live birth rates. This suggests the antibodies create a barrier separate from the fertilization process itself.
Optimizing Thyroid Management for Reproductive Success
Effective HT management is a significant step toward improving reproductive outcomes, requiring stricter monitoring targets than general care. For women trying to conceive, medical guidelines recommend maintaining a serum TSH level below 2.5 mIU/L. This lower TSH threshold ensures optimal thyroid hormone availability for both the mother and the developing fetus.
Levothyroxine (LT4) therapy is the standard treatment used to achieve and maintain this target. Upon confirming pregnancy, the LT4 dose often needs immediate increase, sometimes by 25 to 50 micrograms daily, due to rapidly rising hormonal demands. Frequent TSH monitoring, especially during the first trimester, is necessary to adjust the dosage. However, for euthyroid, TPOAb-positive women with TSH below 2.5 mIU/L, starting LT4 therapy is generally not recommended as it does not increase the live birth rate.