Many people believe that thyroxine suppressive therapy, or TSH suppressive therapy, is an integral and important part of postoperative thyroid cancer, which I personally believe may be a pseudo-proposition. First of all, let’s understand the basis of thyroxine suppression therapy, because differentiated thyroid cancer cells retain the function of thyroid follicular epithelial cells to some extent, and their growth pattern depends on thyroid stimulating hormone (TSH), which is the TSH receptor expressed on the membrane surface of cancer cells, in response to TSH stimulation, and the cancerous tissue proliferates and recurs. Therefore, the therapy was designed to suppress serum TSH levels by taking supraphysiological doses of thyroxine with the aim of reducing tumor recurrence. Although differentiated thyroid cancer is a disease derived from the endocrine organ thyroid, its occurrence, development, treatment and prognosis are in fact not exactly or even unrelated to endocrine. Why is TSH suppression therapy widely promoted by most of the medical community? The incidence of thyroid cancer has increased dramatically in the last 20 years, and the demand for treatment in our domestic general hospitals or primary hospitals has increased dramatically, but due to the scattered sources of the disease and the extremely uneven treatment levels, the search for a unified and reasonable standardized treatment method has become an urgent need for hospitals around the world. With the reform and opening up, various advanced elements from the West were introduced, and the “Guidelines for the Diagnosis and Treatment of Thyroid Cancer” led by the American Thyroid Association Physicians were introduced to China by enthusiastic scholars more than ten years ago. It has indeed greatly advanced the treatment of thyroid cancer in China, and soon became a generally accepted guideline blueprint for most doctors. The majority of patients are treated in general hospitals in China, and TSH suppression therapy has become one of the widely delivered guiding messages for thyroid cancer treatment that “most” people are convinced of. The strong recommendation for TSH suppression of thyroid cancer recurrence and metastasis comes from a number of clinical statements made by American endocrinologists. A careful study of some of the authoritative foreign literature from the early days until now influences that while the observation that suppression of pituitary TSH production is associated with low recurrence rates is almost always based on results from relatively uncontrolled (e.g., it is difficult for endocrinologists to understand the extent to which highly inconsistent surgical criteria can influence recurrence rates) retrospective studies or multivariate analyses, and presents the correlation obsessively as causal , and in many existing clinical analyses, such correlation conclusions obtained are usually interpreted simply as a result of inhibiting the effectiveness of the treatment. These bases are actually based more on the inference that the high or low TSH may only reflect the endocrine functional status of the tumor glandular follicles or residual bands in relation to the endocrine function, without any significant correlation with the tumor regression, and even if correlated, it is not causal! In other words, it may inhibit the proliferation of glandular follicle cells, but not the biological behavior of tumor, that is, it cannot inhibit the “switch” of mutated oncogene (the mechanism of carcinogenesis is irreversible). In this sense, trying to prevent or control tumor recurrence through TSH suppression therapy is probably a false proposition! In fact, this is not my personal opinion either. Many foreign experts and scholars have long had different views or criticisms on guidelines related to TSH suppression therapy, and several of these issues have been questioned, especially the inconsistent surgical criteria, the impact of radioiodine therapy, standardization of thyroxine preparations, sensitivity of TSH assays, and the level of TSH suppression. The evidence from domestic studies is actually scarce, especially in the field of endocrinology and nuclear medicine, and most of them cite the established results of well-known foreign experts, which are easily compiled into reviews by senior scholars, while many young scholars and postgraduates repeatedly confirm and publish the established conclusions of “suppression therapy” using logical thinking and methods that are already framed. What is the role of thyroxine? According to more than 60 years of experience in oncology treatment at the National Cancer Center and the observation and analysis of the most well-preserved and longest-tracked treatment data, as well as my own experience in thyroid cancer treatment for nearly 40 years, all thyroid cancer treatment basically does not require low TSH or even subthyroidism, but only requires thyroxine supplementation within the normal physiological requirements, and there is no clinical evidence of TSH suppression and reduction of There is no clinical evidence that TSH suppression is associated with reduced recurrence rate or mortality, and the treatment effect is comparable to the concurrent data from abroad. Five years ago, a series of thyroid cancer recurrence cases was observed in relation to TSH suppression status. The results are shown in the table below. The observations suggest that the lower TSH, made possible by the excess thyroxine, did not effectively inhibit tumor recurrence, but perhaps only inhibited functional proliferation of thyroid cancer follicles. This means that tumor recurrence is not dependent on the level of TSH, but more clinical results suggest a clear relationship with meticulous and accurate diagnosis at the initial consultation and precise and standardized surgical treatment. Does the patient ultimately benefit? More clinical evidence is needed, but given the ethical issues involved and the testing capabilities necessary for a large number of studies, it is unlikely that randomized controlled trials will be conducted after TSH suppression in the future, and further clinical data will likely remain observational. The hope is that TSH suppression therapy will improve treatment outcomes, a strategy that many scholars are revisiting, and from long-term observations, there is a lack of high-level evidence of improved prognosis, except in patients with very advanced disease, and instead the negative effects may outweigh the benefits. I believe that the complex and not yet fully understood endocrine function of humans is difficult to be completely replaced by exogenous thyroxine, and in fact most female patients, with endocrine alterations or early menopause, enter middle and old age more or less accompanied by some underlying pathology such as cardiovascular disease, and that medically induced hyperthyroidism produced by long-term thyroxine administration can lead to adverse outcomes such as osteoporosis, fractures and cardiovascular disease, including atrial fibrillation, which are more harmful than the long-term risks associated with past treatment. In recent years, dual risk stratification has been proposed to set more refined management goals for PSH control and lower suppression is required only for high-risk patients, but so far there is also no uniform understanding or specific criteria. Therefore, it is recommended that the lowest possible amount of thyroid hormone be used to maintain close to the upper limit of normal values. Most of the recommendations of the “guidelines” can be useful references for the overall treatment of thyroid cancer, but care must be taken to avoid replicating the whole concept of suppression, which should be removed from the list, so that patients can be freed from the long-term confusion and worry of overly strict and elaborate TSH suppression. The above is only my personal advice, which may be different from the “mainstream” opinion that my friends have heard, so please decide to accept what you think is relatively correct according to your own perception and judgment!