Abstract Thyroid disorders, including both thyroid dysfunction and thyroid autoimmunity (TAI), are prevalent in women of reproductive age and may impair fertility through hormonal and immune-mediated mechanisms. This review synthesizes current evidence and underlying mechanisms regarding the impact of thyroid dysfunction, particularly subclinical and overt hypothyroidism, and TAI on female fertility and outcomes of assisted reproductive technology (ART). While overt thyroid dysfunction clearly affects reproductive physiology, the role of subclinical hypothyroidism (SCH) and euthyroid TAI remains controversial. Despite limited supporting evidence, levothyroxine (LT4) is widely used in clinical practice, often initiated at TSH thresholds of 2.5 mIU/L to define SCH and commence treatment. However, recent data suggest that implementing such thresholds may not be associated with improved fertility outcomes, and there is a growing tendency to adopt higher TSH cut-offs for diagnosis and treatment in the preconception setting. ART introduces additional considerations, with thyroid status and autoimmunity potentially influencing ovarian response, embryo quality, and pregnancy outcomes. In light of these uncertainties, treatment decisions increasingly rely on individualized assessment of thyroid function, antibody status, and reproductive context.
Unuane et al. (2026) studied this question.