1.What is hypothyroidism? Please popularize the knowledge about hypothyroidism? A: The full name of hypothyroidism is hypothyroidism, which refers to the inability of the thyroid gland to produce enough thyroid hormones to meet the normal needs of the body due to various reasons. The clinical manifestations of hypothyroidism include fear of cold, reduced sweating, dry skin, sluggish expression, slowed heart rate, loss of appetite, dry stools and fatigue. The prevalence of clinical hypothyroidism is about 1%, more common in women than in men, and the prevalence increases with age. Hypofunction begins in the fetus or newborn and is referred to as cretinism; in children before the onset of pro-spring development, it is called juvenile hypothyroidism; in adults, it is called adult hypothyroidism. In severe cases, it can cause mucinous edema, and in more serious cases, it can cause mucinous edema coma. 2.Is hypothyroidism hereditary? A: Hypothyroidism is mostly an autoimmune disease. Autoantibodies are formed in the acquired environment, provided that the antigen invades. But why some people produce antibodies after bacterial and viral infections and some people do not? This means that there is a certain genetic susceptibility, that is, some people are particularly sensitive to certain antigens and will produce antibodies once they are exposed. This genetic susceptibility may be inherited. (Note that it is not a genetic disease, but a sensitivity to antigens). Further, hypothyroidism is a polygenic disease in which the genetic susceptibility as well as the onset of the disease is determined by a combination of multiple genetic loci, which raises the question of probability. For example, if 50 genes are associated with that susceptibility, as soon as 35 genes are passed down, the offspring develop the disease. Suppose the mother has the disease and carries 36 genes, and she passes 18 genes to half of the offspring, and the father has no disease and less than 35 genes, if 17 genes are passed down, the offspring will have 18+17=35 susceptibility genes and will be susceptible to the disease. If the father passes down 16 related genes, the offspring will have 18+16=34 susceptibility genes and will not develop the disease. Therefore, it is difficult to say whether it is hereditary or not, and the probability of heredity has yet to be further studied. 3.How to treat hypothyroidism and what are the precautions for treatment during pregnancy? A: Hypothyroidism treatment: The general principle is that hypothyroidism treatment uses substitution therapy. The amount of substitution needs to be individualized according to the degree of hypothyroidism and the patient’s own condition. For mild hypothyroidism, no special treatment is generally needed. Diet therapy can be used to supplement iodine, the raw material for thyroid hormone production, by eating appropriate seafood (this applies to patients with low antibodies); while for moderate and severe hypothyroidism, thyroid hormone replacement therapy must be used. Of course, the specific dosage needs to vary from person to person. Young patients should have their thyroid function reviewed regularly, and according to the index, the medication should be adjusted. sTSH is generally recommended to be controlled below 2.5 IU/ml, with an optimal range of 1-2. Elderly patients do not require too much supplementation, as long as sTSH is controlled within normal levels again. Hypothyroidism is generally irreversible and requires lifelong replacement therapy. Precautions during pregnancy: Patients with hypothyroidism who have not been treated with isotopes for six months can become pregnant after their thyroid function is normal. The pregnant mother needs to monitor her thyroid function monthly and adjust her medication dose in time to ensure the safety of the fetus and mother. The most important of the thyroid function is FT4, because only Ft4 can cross the placenta and supply the needs of fetal development; Ft3 and TSH cannot cross the placenta, so they are only corrective indicators. The requirement of maternal Ft4 in pregnancy is to adjust to normal midline or above to ensure sufficient Ft4 for fetal development, which requires TSH below 2.5. Especially the first 3 months of pregnancy is a critical period for fetal neurological development. Since Ft4 is 0.02% of total T4, the measurement error is large and is corrected by TSH. as long as 1 of Ft4 and Ft3 is elevated, TSH is lower; if TSH is high, it means that neither Ft3/Ft4 is high, although the Ft4 measurement may be in the normal range. Thyroid hormone replacement during pregnancy must be pure T4 (e.g. Eugenol-L-T4), it is not recommended to choose thyroid tablets because thyroid tablets are dried and ground thyroid gland from animals, which contains both T4 and T3. with more T3 supplementation, TSH will drop, masking the Ft4 deficiency. Also during pregnancy, total T3 total T4 is elevated because TBG (thyroid binding globulin) is elevated during pregnancy. Total T4 is 1.5-2 times higher in pregnancy than in non-pregnancy. After 6-7 months of pregnancy, as the fetus develops and grows, the amount of Ft4 required gradually increases, and the amount of supplemental eugenol (L-T4) should be gradually increased at this time to ensure that the TSH is below 2.5. Therefore, it is necessary to check the nail function every month. 4.What are the symptoms that indicate hypothyroidism and can it be self-tested? A: Hypothyroidism can be self-tested. When the following ten symptoms appear, consider the possibility of hypothyroidism, and recommend to go to the hospital: easy to get sleepy, low physical strength and energy; slow thinking, hard to concentrate, memory loss; weight gain; dry skin; nails become brittle, gray, easy to break; often feel cold; easily depressed and depressed; easy to bowel movement; feel stiff and painful muscles and bones, numbness in hands, increased blood pressure or heartbeat 5. How to prevent hypothyroidism, such as from diet and medicine? A: Prevention of the cause of cretinism: In endemic cretinism, iodine deficiency in pregnant women during the embryonic period leads to insufficient production of maternal thyroid hormones, and the fetus does not receive an adequate supply is the key to the onset of the disease. Pregnant women with no other positive antibodies and simple iodine deficiency can be supplemented with iodine (more iodine-containing foods) – for mild cases – or with finished products (eugenol, L-T4) – for both mild and moderate cases. Sporadic cretinism, mostly caused by certain autoimmune thyroid diseases in pregnant women, is prevented by identifying the cause. Try to avoid excessive doses of antithyroid drugs during pregnancy in hyperthyroid mothers to prevent the development of hypothyroidism, and consider adding eugenol if necessary to keep TSH below 2.5, preferably between 1 and 2. And avoid other medications that cause goiter. Eugenol must be supplemented during pregnancy in hypothyroid mothers to keep TSH below 2.5, especially during the first 3 months of pregnancy. The need for iodine supplementation in the diet depends on the cause of hypothyroidism. In case of hypothyroidism after isotope treatment of hyperthyroidism, pregnant women who are still positive for TRAb during pregnancy should avoid iodine diet. After all, what the fetus needs is mainly the finished thyroxine (FT4) made by the mother and not iodine. Otherwise, it is easy to cause a recurrence of hyperthyroidism, or the need for eugenol fluctuates too much to be controlled. If the hypothyroidism is caused by other reasons and TRAb is negative, iodine is not contraindicated. Prevention of hypothyroidism in adults: timely treatment of thyroid diseases that easily cause hypothyroidism, such as Hashimoto’s thyroiditis, even if the thyroid function is normal at that time, because the antibody is still positive, it will continue to destroy the thyroid gland and eventually lead to hypothyroidism, so it is necessary to adjust the immunity, lower the antibody and eliminate the factors that destroy the thyroid gland as soon as possible. For example, in subthyroiditis, viral destruction leads to rupture of a large number of thyroid follicles, which can be painful, while some patients eventually lead to hypothyroidism. Therefore, during the treatment process, in addition to symptomatic pain relief, hormones should be used early to stabilize the thyroid cell membrane and reduce breakage to prevent future hypothyroidism from arising. It is also necessary to treat the root cause, anti-inflammatory and anti-viral, to get rid of antigens and reduce the immune response from the source. For hypothyroidism caused by surgical treatment of thyroid disease or radioactive 131 iodine treatment of hyperthyroidism, due to surgical removal or isotope destruction of part of the thyroid follicles (like a factory for thyroid hormone production), the remaining thyroid gland is not sufficient to produce enough hormone for normal use by the body and needs to be replaced by exogenous thyroid hormone (eugenol, L-T4) to make up for it. All cases of moderate hypothyroidism or above require lifelong eugenol replacement. 6.What do I need to pay attention to in terms of diet after I have hypothyroidism? A: The occurrence of hypothyroidism has a great relationship with diet and nutrition. (1) Supplement the appropriate amount of iodine (kelp, nori, iodized salt, iodized soy sauce, iodized eggs and bread with iodine), and avoid using goiter substances (such as cabbage, cabbage, rape, cassava, walnuts, etc.). It should be noted that for hypothyroidism after isotope treatment for hyperthyroidism, TRAb is still positive, so iodine must be avoided; patients with Hashimoto’s thyroiditis will experience an increase in antibodies after taking high iodine foods, so iodine is not avoided, but eating more is also discouraged. (2) Supply sufficient amount of protein (eggs, dairy, various kinds of meat, fish; vegetable protein can be complementary, such as various kinds of soy products, soybeans, etc.). (3) Limit fat and cholesterol-rich diet (cream, animal brain and offal). (4) supply rich vitamins. 7.Is it possible to get pregnant with hypothyroidism? A: If you have hypothyroidism, you can get pregnant as long as you make up for it (normal thyroid function). During pregnancy, you should always take enough thyroid hormone and monitor your thyroid function every month because as the fetus grows up, the amount of Ft4 needed increases month by month. In hypothyroidism, thyroid hormone synthesis is not sufficient, and the body is less likely to conceive. Even if you get pregnant, because thyroid hormone is necessary for growth and development, the deficiency in early pregnancy will cause fetal neurological development disorders, leading to cretinism; in late pregnancy, hypothyroidism, the fetal growth and development is delayed. Therefore, to get pregnant with hypothyroidism, the prerequisite is to make up enough thyroid hormones. If you make up enough, you will be the same as normal people. 8.Can hypothyroidism heal completely on its own? A: The thyroid follicular cells are the factory floor for the production and storage of thyroid hormones. The destruction of the thyroid gland due to various reasons, such as post-surgical hypothyroidism (surgery to remove part of the thyroid tissue), post-isotope hypothyroidism (radioactive destruction of part of the thyroid tissue, surgery without incision), Hashimoto’s thyroiditis (antibody destruction of part of the thyroid tissue), and subthyroiditis (virus destruction of part of the thyroid tissue), all lead to the reduction of the factory floor for the production of thyroid hormones. fewer factory shops for thyroid hormones. The destroyed thyroid follicles are irreversible and can only be compensated for by what remains. If there is little destruction, the remaining thyroid cells can compensate and the thyroid function can still be normal. If there is more destruction, even if the thyroid gland is compensated, the remaining thyroid gland will not be able to produce enough to replace it, and the thyroid function will show hypothyroidism, and it will need external help to replace the thyroid hormone for life. Overdose of anti-thyroid medication for hyperthyroidism leads to pharmacological hypothyroidism, which is restored by drug reduction. Because the medication does not destroy the thyroid cells (factory floor), but only inhibits the synthesis of thyroid hormone (let the machine turn slower and produce less), the production will be restored when the medication is reduced, so the medication hypothyroidism is reversible. 9.Can hypothyroid patients breastfeed? A: Hypothyroidism patients can breastfeed, and it has little effect on the baby. The amount of thyroid hormone through the breast milk is very small, and the eugenol replacement is only substituted to the normal level of thyroid function, and normal breastfeeding can be done after delivery. Usually hypothyroid patients take eugenol replacement when they are pregnant. During pregnancy, as the fetus grows, the amount of Ft4 needed gradually increases, reaching a peak before delivery. Once delivery occurs and the fetus, which was originally sharing Ft4 in the body, has left, maternal thyroid hormone may be increased or even overdosed. Therefore, it is recommended to review the thyroid function 48-72 hours after delivery (when the mother reaches equilibrium) and adjust the dose of Eugenol in time. If hyperthyroidism occurs during breastfeeding in hypothyroid patients, the amount of T4 in the breast milk will be increased regardless of the overdose of eugenol or the recurrence of true hyperthyroidism, and the newborn’s own thyroid development will be affected, so we must wait until the thyroid function is normal before breastfeeding.