Do T3-containing medications like pig thyroid suppress TSH out of proportion to what happens with equivalent doses of levothyroxine? Let’s hunt for evidence.
Some studies suggest that T4 monotherapy doesn’t normalize BMR; others say it’s fine. The jury may be out on this, but it’s nonetheless fascinating to look at the strength (or lack thereof) of the original studies using BMR to guide treatment.
In a new clinical trial, study participants preferred desiccated thyroid and T4/T3 combination therapy over T4 alone, but is there more to this than the conclusion?
Which sounds better to you: taking a physiologic dose of T3, or a heroic bolus that acts like an illicit stimulant? If you get your care from alt med, chances are you’ll be slammed with the latter.
In assessing whether there is value in monitoring T3 levels and restoring them to normal in hypothyroidism, I think it helps to return to first principles. And no, “more T3 is better” is not a first principle.
In this next post in the T3 Controversies series, we cover whether T3 therapy must be used to account for tissues that can’t make their own T3.
In this first post of my “T3 Controversies” series, I address the claim that there are acquired forms of tissue resistance to thyroid hormone, which can be treated with high-dose T3 therapy.