Radioactive iodine therapy has the advantage of being highly effective, safe and inexpensive compared to other methods. Hypothyroidism is divided into early-onset hypothyroidism and late-onset hypothyroidism. Some early onset hypothyroidism is only temporary. Temporary hypothyroidism usually occurs within the first 6 months after 131I treatment. When hypothyroidism occurs or persists for more than 6 months after 131I treatment, it is likely to develop into permanent hypothyroidism and should be treated with thyroid hormone replacement therapy. In some cases, it continues as permanent hypothyroidism. There are various explanations for the occurrence of early onset hypothyroidism, mainly thought to be due to the high sensitivity of the individual to 131I. 1. The patient’s high sensitivity to 131I treatment leads to the destruction of too much thyroid tissue and permanent hypothyroidism occurs. In some patients, some cells are damaged by a certain amount of radiation and are in a state of “stasis”, but these cells are not necrotic, but only temporarily lose their function, resulting in a short period of hypothyroidism, when these cells recover from the state of stasis, hypothyroidism will be eliminated. 2. The hyperthyroidism before 131I treatment makes the pituitary secretion of TSH suppressed for a long time and the response is delayed. After a few months, the pituitary-thyroid axis returns to normal function and the hypothyroidism is eliminated. Hypothyroidism that occurs 1 year after taking 131I is called late onset hypothyroidism (distant hypothyroidism, permanent hypothyroidism). Permanent hypothyroidism is the only significant complication of 131I therapy. The causes of late onset hypothyroidism are not well understood, but there are some possibilities as follows: 1. After 131I treatment, some cells that are slightly damaged by radiation do not lose their function, but the cell division cycle slows down, the number of divisible generations decreases, and at a certain point they stop dividing and die prematurely, leading to late onset hypothyroidism. This is a distant biological effect of ionizing radiation, and is related to the treatment dose. 2. After 131I treatment, some thyroglobulin may escape due to thyroid follicle destruction, resulting in the development of antibodies to the thyroid gland, causing chronic potential damage to the thyroid gland and late onset hypothyroidism. 3. The natural history of hyperthyroidism can lead to spontaneous onset of hypothyroidism. Spontaneous hypothyroidism has been found to occur in GD without any treatment or in those who have stopped taking ATD for several months or even years, but the incidence of this hypothyroidism is much lower than in those who have been treated with 131I. It is possible that spontaneous hypothyroidism is the result of GD evolving into HD, and since both GD and HD are autoimmune diseases, they can evolve into each other.