![]() ![]() Hercbergs and Davis and their team call this therapy “euthyroid hypothyroxinemia.” This name literally means the achievement of metabolically appropriate thyroid hormone supply (euthyroidism) despite having very low T4 (thyroxine) hormone levels (hypo-thyroxin-emia). They replaced these hormones with synthetic T3 hormone, which provides the active form of thyroid hormone that can maintain life and health even in the absence of T4. In Hercbergs and team’s recent preclinical study, cancer patients who were beyond all hope were able to extend their survival by significantly reducing their circulating T4 hormone and also the variable RT3 concentrations that it brings. In certain cancer patients, it can be a health risk to have high-normal T4 concentrations regardless of their concurrent T3 and TSH levels. The bad news for cancer patients with high-normal FT4 levels is that Davis, Hercbergs and their team of scientists have discovered that physiological concentrations of T4 hormone, as well as its inevitable byproduct of Reverse T3, act on receptors on the cell membrane called “integrin αvβ3,” and through this receptor, they can cause many types of cancers to grow. Not all cancer researchers have kept up with the developing scientific knowledge of this thyroid hormone receptor’s role in cancer, but Davis and Hercbergs’ team of researchers certainly have. Since 2005, research on this receptor has advanced. It turns out that T3 and T4 have different non-genomic signaling at this cell membrane receptor that are very significant to cancer because this receptor is highly expressed in cancers, and T4 signaling more directly affects cancer proliferation rates.Īll researchers prior to 2005 (and many other research teams since 2005) were ignorant of T4’s unique effects at this key thyroid hormone receptor. Their insights into this receptor clarified T4’s role (and RT3’s role) in thyroid hormone signaling. Davis and colleagues have been at the forefront of research that clarifies the effect of T3 versus T4 hormones in the context of cancers by focusing on a special cell membrane receptor for thyroid hormones.īack in 2005 (Bergh et al, 2005), Davis and Hercbergs’ research team announced the details of T3 and T4 activity at the “integrin” cell membrane receptor. Such reviews can muddy the science more than clarify it.įortunately, Aleck Hercbergs and Paul J. For example, a recent review of science since the 1940s attempted to reclassify research findings under poorly defined generalizations of “hypothyroidism,” “euthyroidism” or “hyperthyroidism” and variable “high T3” or “low T4” conditions (Krashin et al, 2019). For many decades, scientists have been studying the effect of thyroid hormones in promoting cancer proliferation.Ĭonfusion and contradictions often arise in “cancer & thyroid” research reviews because the relationship between cancer and thyroid hormones is very complex. ![]()
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