The thyroid gland, located below the vocal cords and directly in front of the neck, is a butterfly-shaped endocrine organ. It secretes, stores and releases two thyroid hormones, iodothyronine (T3 for short) and thyroxine (T4 for short). Iodine is a necessary component of T3 and T4. The amount of T4 in the body is about 20 times greater than that of T3, and the half-life of T4 is longer than that of T3. L-T4 is the levothyroxine (L-T4) that hypothyroid patients take to supplement and replace T4, which will be discussed in more detail later. Both T3 and T4 are available in free form (less than 1% of the total) and bound to certain proteins (thyroid binding globulin), which is the difference between being a free-ranging individual and being part of a group and bound to a collective. The thyroid hormones affect almost all organ functions in the body, such as the metabolism of the three macronutrients (carbohydrates, proteins, fats), the growth and development of the fetus and infants (especially the development of the brain), the menstrual cycle, the dryness of the skin, body temperature, breathing, heart rate, the nervous system, muscles, weight, cholesterol, etc. Hypothyroidism is when the thyroid gland does not produce enough T3 or T4, while hyperthyroidism is when the thyroid gland produces too much T3 or T4. What factors influence the production of thyroid hormones (T3 and T4)? There is another endocrine organ called the “pituitary gland”, which is a very important organ about the size of a pea in our head. It is the apex of the thyroid gland and regulates the amount of T3 and T4 produced by the thyroid gland by secreting “thyroid stimulating hormone” (TSH for short). When the amount of T3 and T4 in the blood is low, the pituitary gland secretes more TSH to stimulate the thyroid gland to produce more; when the amount of T3 and T4 in the blood is high, the pituitary gland secretes less TSH to reduce the production of thyroid hormones. Pregnancy and the thyroid The hormonal changes in the body during pregnancy, mainly hCG and estrogen, can also have an effect on the thyroid gland. Human chorionic gonadotropin (hCG) mimics the “thyroid stimulating hormone” TSH and slightly stimulates the thyroid gland to produce more thyroid hormones (T3 and T4), which is most pronounced in the late first trimester when hCG levels are at their highest, and then as hCG levels drop rapidly T3 and T4 also drop. T4 also decreases. High levels of estrogen cause the liver to produce almost twice the amount of thyroid binding globulin, which binds free T3 and T4 stored in the thyroid gland and brings them into the bloodstream, thereby increasing the level of thyroid hormones in the blood. At the same time, the original free T3 and T4 in the blood are also bound by the extra thyroid binding globulin, resulting in a decrease in free T3 and T4 levels. The pituitary gland monitors the decreased free T3 and T4 and secretes more TSH resulting in increased TSH levels. The high TSH stimulates the thyroid gland to continue producing and secreting T3 and T4 to meet the bundle of extra thyroid binding globulin. Thyroid binding globulin increases from the 10th week of pregnancy, peaks at 20 weeks and is maintained until delivery. The above changes are normal. It is also clear from these changes that pregnancy increases the workload of the thyroid gland and raises the risk of thyroid conditions during pregnancy. Doctors will take the above factors into account to determine TSH and free T4 levels during maternity exams at different times of pregnancy. During the first 12 weeks of pregnancy, adequate levels of thyroid hormones (T3 and T4) are critical for fetal development because the fetus’ own thyroid gland is not developed at this time and depends on maternal thyroid hormones (T3 and T4) transmitted from the placenta to maintain development. Judging from the effect of hCG on the thyroid gland, T3 and T4 levels will naturally increase in the first trimester under the action of hCG, which shows how amazing the body’s own mechanism is! Pregnant women should have their thyroid function checked at their first maternity visit. If hypothyroidism is found at this time, it should be treated promptly to avoid affecting fetal development, especially mental development. There are two types of hypothyroidism in pregnant women: clinical hypothyroidism and subclinical hypothyroidism. The difference is that clinical hypothyroidism has obvious symptoms, such as extra weakness, extra coldness, constipation, memory loss, inability to concentrate, cramps, and a higher than normal TSH and lower than normal Free T4 in hypothyroidism. Subclinical hypothyroidism is actually a less severe form of hypothyroidism, with no obvious symptoms and a higher than normal TSH but normal Free T4 values. Clinical hypothyroidism should be treated aggressively at all times. For subclinical hypothyroidism, it should also be treated during pregnancy, mainly to ensure normal fetal development. Although Free T4 levels are normal in subclinical hypothyroidism, an excessive TSH indicates that the thyroid gland is overwhelmed and needs more stimulation to produce enough thyroid hormone. It is safe and necessary for pregnant women with clinical hypothyroidism, and for pregnant women with subclinical hypothyroidism to reduce the burden on the thyroid gland to avoid the development of clinical hypothyroidism. Untreated hypothyroidism during pregnancy may lead to: pre-eclampsia, anemia, miscarriage, low birth weight, and stillbirth. Regarding iodine supplementation: Pregnant women have a greater than usual need for iodine even if they do not have hypothyroidism. First, as mentioned above, both T3 and T4 need iodine to be synthesized in the thyroid gland, so the high demand for T3 and T4 during pregnancy leads to a high demand for iodine; second, the fetal thyroid gland also needs iodine to participate in the synthesis of thyroid hormones after it has developed well, causing additional demand. In addition, the excretory function of the kidneys is increased during pregnancy, resulting in more iodine being excreted from the body, requiring more iodine intake to ensure that enough iodine remains in the body. A daily intake of 220mcg of iodine is required during pregnancy, 290mcg during lactation, and only 150mcg during other periods. Pregnant women with clinical hypothyroidism or subclinical hypothyroidism should ensure that sufficient iodine is involved in the synthesis of thyroid hormones in the body to avoid an even lower thyroid hormone that is already low.