Our wish: May you be blessed with T3 sufficiency

At this time of year, many nonprofit organizations focus on the relief of poverty and hunger. But humans can also suffer T3 hormone poverty and hunger. We can’t be truly healthy without “enough” T3 in our bloodstream, our tissues, organs and cells. We can’t be healthy with “too much” T3 activity in cells, either. Well-regulated T3 supply is just like having well-regulated blood sugar levels and a healthy insulin response to blood sugar. Getting enough T3 is like getting enough macro- and micronutrients in our diet, without excess or imbalance. “Enough” also depends on the individual. Giving 1500 to 2500 …

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How do we get enough T3 into thyroid hormone receptors?

In thyroid disease and therapy, even when TSH is normalized, we can still be genuinely hypothyroid if we do not have enough T3 getting into our thyroid hormone receptors in cells throughout the body. Most people know there’s two ways we get T3 into our cells’ nuclei: From circulating Free T3, and From circulating Free T4 hormone that is converted into T3 at a variable rate. However, most doctors are not taught about our cells’ and tissues’ high priority for and dependence upon circulating T3, nor are they taught about the largest factor that can reduce T4’s local variable conversion …

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Caution: Doctors perform T3-ectomies without our consent

We all know a “thyroidectomy” is the surgical removal of a thyroid gland. Nobody removes a vital gland without a patient’s informed consent. If your medical system and doctor are ethical, you as a patient have the opportunity to weigh the risks and benefits of the procedure and give signed consent. We need to consider requiring doctors to get our consent for a “T3-ectomy.” What’s a T3-ectomy? In metabolically vulnerable human beings, the standard “TSH-normalized T4 monotherapy” programme causes the removal of a significant portion of vital circulating T3 hormone supply from a person’s bloodstream.  The idea of a T3-ectomy without consent …

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Principles and Practical tips for Reverse T3, FT3, FT4

This post follows up on several recent posts on the topic of Reverse T3 (RT3) and our thyroid hormone conversion enzymes, the three deiodinases. Here I’m providing some practical tips about Reverse T3 testing, test interpretation, and where we should be focusing our attention. In these posts, I aim to improve thyroid therapy by debunking myths about Reverse T3 hormone and replacing them with more complete understandings that can help us make wise therapy decisions together with our good scientific-minded thyroid doctors. In previous posts, I have proven that: Reverse T3 doesn’t actually have a role in “blocking” T3 from …

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Deiodinase Type 3, not RT3, plays the T3-blocking role

A lot of internet myths and misinformation surrounds Reverse T3 (RT3). Well-meaning people have attributed to the hormone a “T3-blocking” function. However, the enzyme deiodinase type 3 (D3) (NOT Vitamin D3, which is very different) is the main blocker of T3 hormone. Deiodinase type 3 (D3), regulated by the DIO3 gene, is the enzyme that rises to dominate in states of severe illness and states of excess T4 and/or excess T3. The role of D3 enzyme is two-fold: When D3 is working properly, it defends us from hyperthyroidism. It’s an intracellular defense mechanism. When D3 is temporarily upregulated in acute …

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