![hormone type 3 hormone type 3](http://333oee3bik6e1t8q4y139009mcg.wpengine.netdna-cdn.com/wp-content/uploads/2009/11/Estrogen_3Types.png)
I can easily forgive people for being reluctant to talk about them. I understand why people don’t talk about deiodinases. In fact, many of the blogs and websites that blame RT3 do not even use the word “deiodinase.” Most people who support anti-RT3 theories do not understand the three deiodinase enzymes (D1, D2 and D3). Any excuse that shifts blame when RT3 is low can also be used to minimize the blame when RT3 is high. There’s a logic problem with these blame-shifting excuses. When high levels of circulating RT3 cannot be blamed, they often blame iron, cortisol, or non-compliance to a therapeutic protocol.
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However, these theories fail to explain major contradictions in a logical or scientific manner. RT3 must be implicated in a crime against T3 hormone, right? On the other hand, they also see the association between low-normal RT3 levels during T3-inclusive thyroid therapy and the alleviation of illness and hypothyroid symptoms. They see the association between high or high-normal RT3 levels, high RT3:T3 ratios, illnesses and/or hypothyroid symptoms. Many of these well-meaning people are intelligent and clinically observant. They are then echoed by thyroid patient communities and spread widely in online thyroid patient support groups.īut saying something a million times online does not make it truer. RT3-blocking claims are persuasively explained by vivid metaphors and graphics in many celebrity physicians’ blogs, videos, and books. It has even been claimed that RT3 functions as a “metabolic brake.” The analogy of the brake pedal versus the gas pedal seems perfectly reasonable, but it’s just not scientifically correct. It has now become a strong belief among many that high-normal RT3 levels and high RT3:T3 ratios in blood can block T3 transport into cells, hinder the enzymes that perform T4-T3 conversion, and plug receptors in the nucleus and prevent T3 from binding to them. It’s because so many people are convinced by and are quite satisfied with widely-circulating RT3-blaming theories and the concept of RT3 dominance. Why isn’t the truth about D3’s T3-blocking role being trumpeted from the rooftops? It just happens to be the case that RT3 is a byproduct of D3 overactivity when there’s enough T4 supply to drive RT3 high. It always performs both at the same time, but it prefers to inactivate T3 most of all because T3 interacts more readily with the enzyme.Įssentially, hypothyroid symptoms are not caused by RT3 gain, but by intracellular T3 loss. But the most harmful D3 role is the second one, the less visible T3-diminishing role, because T3 is the most active thyroid hormone.ĭ3 enzyme cannot choose between its T4-inactivating and T3-inactivating roles, because that’s how its machinery works. The more visible role is the first one, the production of measurable RT3 that shows up in test results. It converts T3 to an inactive form of T2 called 3,3′-T2.However, the enzyme deiodinase type 3 (D3) is the main blocker of T3 hormone.ĭ3 is the enzyme that rises to dominate in states of severe illness and states of excess T4 and/or excess T3. Well-meaning people have attributed to the hormone Reverse T3 (RT3) a “T3-blocking” function. Home › Thyroid hormone conversion › Deiodinase Type 3 › Deiodinase Type 3, not RT3, plays the T3-blocking roleĭeiodinase Type 3, not RT3, plays the T3-blocking roleīy thyroidpatientsca on Novem