Of the subclinical thyroid disorders, 73.8% are subclinical hypothyroidism and 26.2% are subclinical hyperthyroidism. Subclinical hypothyroidism is a common endocrine metabolic disorder characterized by elevated serum levels of thyroid stimulating hormone and normal levels of free thyroxine. The prevalence of subclinical hypothyroidism ranges from 4% to 10% of the population and can be as high as 15% to 20% in women over 60 years of age, with approximately 7.5% of women and 3% of men. Anti-thyroid antibodies can be detected in 80% of patients with subclinical hypothyroidism, and in 75% of these patients, TSH is less than 10 mIU/L. The etiology of subclinical hypothyroidism can be caused by chronic autoimmune thyroiditis, postpartum thyroiditis, iodine deficiency or excess, thyroid surgery, I-131 exposure, external radiation, infiltrative disease, and long-term use of certain medications, the most common of which is Hashimoto’s thyroiditis. Hashimoto’s thyroiditis. TSH has 98% sensitivity and 95% specificity for thyroid disease and is the most important indicator for screening and diagnosis of subclinical hypothyroidism. However, non-subclinical hypothyroidism can also cause elevated TSH, including: recovery from sick thyroid syndrome, pituitary TSH tumor, thyroid hormone resistance syndrome, primary hypoadrenocorticism, and abnormal TSH elevation caused by drugs such as Gastrodin, etc. Before diagnosing subclinical hypothyroidism, these causes of TSH abnormalities should be ruled out. Why does subclinical hypothyroidism require treatment? Subclinical hypothyroidism can be seen as a mild form of hypothyroidism, which can have mild hypothyroid-like symptoms and negative effects. Treating subclinical hypothyroidism can prevent patients from progressing to clinical hypothyroidism and avoid the risks of dyslipidemia; atherosclerosis; depressed mood, memory loss and weight gain. Certain patients may suffer from ovulatory dysfunction and infertility. If subclinical hypothyroidism is detected during pregnancy, it may affect the neuropsychological development of the fetus and fetal survival, and may cause hyperemesis and toxemia, so we advocate screening pregnant women and checking their thyroid function in infertility patients with a view to early treatment. Which patients need treatment? In 2004, the US Preventive Services Task Force suggested that treatment of subclinical hypothyroidism in patients with a history of prior Graves’ hyperthyroidism or TSH >10 may reduce symptoms, but most trials have shown no improvement in lipid levels with treatment. In 2004, the Endocrine Clinic Association stated that treatment of subclinical hypothyroidism could prevent hypothyroidism, but there is no definitive evidence to support the benefit of early treatment, nor is there clear evidence that treatment can improve survival, but treatment can improve lipid levels. The National Treatment Guidelines Clearinghouse also suggested that a TSH of 4.5-10 does not require treatment and that follow-up of TSH every 6 C and 12 months is sufficient, and that treatment can prevent progression of signs and symptoms. 2005 Joint Statement of the American Endocrine Society and the American Thyroid Association concluded that routine TSH screening should be performed in the general population and in women who are pregnant or planning a pregnancy; in subclinical hypothyroidism, TPOAb is a valuable test in subclinical hypothyroidism. Patients with subclinical hypothyroidism with TSH 5-10 mIU/L should also be treated; insufficient evidence of benefit from treatment is not the same as no benefit; there is less evidence to support treatment, but even less evidence that treatment is risky. In conclusion, treatment should be advocated for younger patients, TPOAb positive, elevated cholesterol, goiter, symptomatic, infertile, and pregnant patients with subclinical hypothyroidism. How is it treated? （We believe that there are 2 principles to be followed. One is that treatment needs to be stratified according to different ages and conditions. The second is to consider the clinical characteristics of the individual, not just the abnormal TSH results. (Individualized treatment) 1. For the general population of young people, especially patients with subclinical hypothyroidism with anti-TPOAb (+), our response is to treat and reduce TSH to below 2.5. People at normal high values (TSH 2.5-5 mIU/L) are more likely to develop hypothyroidism later. 2. There is no consensus on whether to treat or not to treat subclinical hypothyroidism patients who are elderly or/and have heart disease and the goals of treatment. It is relatively clear that treatment is not advocated for subclinical hypothyroidism patients over 85 years of age. Studies suggest that the distribution of serum TSH levels tends to increase with age, making the prevalence of subclinical hypothyroidism in the elderly overestimated. In the absence of antithyroid antibodies, hypothyroidism cannot be diagnosed in people over 70 years of age, even if TSH is above 6.0 mIU/L or even 7.0 mIU/L. We believe that thyroid hormone replacement therapy in such patients will instead cause a cardiac burden that can have side effects. The Chinese guidelines for the diagnosis and treatment of thyroid disease set the treatment target for elderly subclinical hypothyroidism at a TSH of 0.5-3.0 mIU/L, which is somewhat higher than the general young population. We believe that the treatment target for elderly and cardiac patients is set at the upper limit of the normal range of TSH. At the same time, individualization should be taken into account, and the heart burden should not be increased in elderly patients because of the need to lower TSH. 3. For pediatric patients, the treatment viewpoint is again different. TSH is generally high in normal children and adolescents, with a tendency to decrease with age. The normal upper limit of TSH in neonatal cord blood is 15-20 mIU/L. A study by Prof. Teng Weiping of China Medical University also found that TSH levels were significantly higher in the 12-19 years age group than in other age groups, and there was no significant difference in TSH levels between age groups above 20 years, which has been similarly reported in many foreign literature. Traditionally, it is believed that younger patients are at the stage of growth and development and we should give them replacement therapy to prevent the growth from being affected, but recently it has been reported that hormone replacement therapy in children with subclinical hypothyroidism does not have a growth promoting effect, although this result needs further confirmation. In several foreign trials, they followed up patients under 20 years of age with subclinical hypothyroidism, most of whom could regress naturally to normal without any treatment, while some remained at subclinical hypothyroid levels, and only a very small proportion became clinically hypothyroid. It would be inappropriate to treat all children with subclinical hypothyroidism for the sake of a very small percentage. Other experts suggest that patients with subclinical hypothyroidism with TSH greater than 20 mIU/L or those with clinical symptoms for whom replacement therapy is effective can be treated. We suggest that for children with subclinical hypothyroidism, TSH less than 10 mIU/L can be followed up and observed. 4. The TSH value gradually rises and reaches the high limit around 33 weeks; the TSH level increases before delivery. Because of this characteristic of TSH in pregnancy, we believe that we should not use the TSH range of the general population to measure TSH levels in pregnancy; if we use the criteria of the general population, it may lead to misdiagnosis and underdiagnosis. We should have normal ranges of TSH that are specifically applicable to pregnant women, and the TSH ranges should be different for different gestational weeks. In pregnant women, if subclinical hypothyroidism is diagnosed, it should be treated, and it is recommended to control it below 2.5 mIU/L in the first trimester because in early pregnancy, the fetal thyroid gland is not yet developed, and all the thyroid hormones needed for fetal growth and development come from the mother. This is the critical period for the development of the fetal brain and nervous system, so it is necessary to ensure sufficient supply of thyroid hormones from the mother, otherwise it will affect the fetus’ intellectual development and lower its IQ; in the second six months, it is recommended to control below 3.5, because the fetus can secrete some thyroid hormones by itself at this time. However, it should not be oversupplemented. If the TSH is too low after maternal treatment, resulting in hyperthyroidism, it will instead increase the rate of preterm delivery and miscarriage. Therefore, the treatment target for pregnant patients is set at 0.5 mIU/L-2.5 mIU/L (especially in the first 3 months of pregnancy). Treatment options: Treatment of subclinical hypothyroidism is the same as that of hypothyroidism. It can be treated with dietary therapy (iodine-containing foods) and, in some cases of subclinical hypothyroidism due to iodine deficiency, supplementation with iodine, the raw material for making thyroid hormones. However, it should be used with caution in patients with high TPOAB levels. Excessive iodine intake can trigger thyroiditis and worsen the degree of hypothyroidism. Oral thyroid hormone (drug) replacement therapy can also be used. Thyroid hormones can be divided into two types: one is levothyroxine (L-T4) and the other is thyroxine tablets (a biological preparation, a mixture of T3 and T4). We usually recommend the use of L-T4 for the treatment of patients, especially pregnant women. Since FT3 cannot pass through the placenta, the fetus relies on maternal FT4 to supply all the thyroid hormones it needs. Therefore, pregnant women with subclinical hypothyroidism should be treated with levothyroxine (L-T4) instead of thyroid tablets. Otherwise, there is a risk that excessive FT3 may suppress TSH, resulting in the illusion that TSH is less than 2.5 mIU/L, while the fetus does not have enough FT4, which may affect fetal mental development. For some patients with subclinical hypothyroidism who have been treated with sufficient T4 and still have symptoms, a combination of T3 + T4 therapy can be tried. It has been reported in the literature that the combination of T3 + T4 therapy may improve health status and may have an antidepressant effect, although this effect is not exact and more research is needed. Dosage of therapeutic drugs: The aim of thyroid hormone replacement therapy is to effectively restore the pool of thyroxine (T4) stores in the tissues. The principle of its administration is to obtain the best therapeutic effect with the smallest possible dose. The recommended dose of levothyroxine is 1-1.7 μg/kg/day, and the starting dose should be determined by the patient’s age, the presence of comorbidities and the severity of the disease. Young patients without significant clinical manifestations or comorbidities may be started on the full replacement dose. However, it is prudent to start with small doses, especially in elderly patients and those with cardiovascular disease. The dose should be increased by 25-50 μg every 4-8 weeks on top of 25 μg daily of L-T4. In conclusion, the treatment of subclinical hypothyroidism should be stratified and individualized according to age and status. For the average young patient, TSH control at 0.4-2.5 mIU/L; for the very old, mild TSH elevation is permissible.