Changes in the endocrine environment, changes in thyroid hormone metabolism, and changes in the autoimmune status of pregnant women during pregnancy are the main reasons for the occurrence of hypothyroidism. 1. Increase in thyroid binding protein (TBG) The significant increase in blood estrogen level during pregnancy causes an increase in synthesis of thyroid binding protein in the liver. The increase in TBG level causes a large amount of thyroxine to be bound in the blood and a decrease in free thyroxine, resulting in hypothyroidism. 2. The effect of human chorionic gonadotropin (hCG) on the thyroid gland. hCG peaks in the third trimester. hCG has a similar chemical structure to thyrotropin (TSH) and has a stimulating effect on thyroid cells. Due to the stimulating effect of hCG, feedback inhibits the pituitary thyroid axis, causing a decrease in blood TSH secretion. hCG also competitively inhibits the effect of TSH, causing a decrease in thyroxine synthesis. 3, iodine deficiency The kidney’s clearance of iodine increases during pregnancy, and the fetus has to obtain iodine from the mother to make thyroid hormones, so the body’s demand for iodine increases significantly. For pregnant women in iodine sufficient areas, iodine intake should be increased to 200ug/day to meet the needs. However, in iodine deficient areas, if the mother does not receive the required amount of iodine, the thyroid gland will develop pathological changes, resulting in hypothyroidism. 4. Effects of autoimmune thyroiditis Autoimmune thyroiditis is the main cause of clinical hypothyroidism and subclinical hypothyroidism in iodine-sufficient areas. In epidemiological surveys, the positivity rate of thyroid peroxidase antibodies in the female population was 13.0% and that of thyroglobulin antibodies was 11.2%. In iodine-sufficient areas, subclinical hypothyroidism during pregnancy is predominantly present in this population.