The upstream mechanisms of insulin/IGF-1 signaling, low-grade inflammation, adipokine imbalance, and TSH-related stimulation are likely shared across sexes; however, effect magnitudes may diverge in postmenopausal women owing to (i) greater reliance on adipose aromatase–derived estrogen, (ii) lower sex hormone–binding globulin (SHBG) in MetS increases bioavailable estradiol, and (iii) estrogen receptor (ER) and G-protein-coupled estrogen receptor (GPER) signaling within thyroid tissue [27,28,29]. This evidence concerns the gene ESR1 and metabolic syndrome.