Hyper but resistant.

Why, when cells are resistant to eg. T3, can taking it produce the symptoms of excess. If it is not being absorbed, then how can it have an effect? How can you tell the difference between resistance and just taking too much?

[helvella Administrator Thyroid UK]

I suggest you have a good read of this chapter:

Reduced Sensitivity to Thyroid Hormone

Resistance to thyroid hormone (RTH), a syndrome of reduced responsiveness of target tissues to thyroid hormone (TH) was identified in 1967 (1). An early report proposed various mechanisms including defects in TH transport, metabolism and action (2). However, with the identification of TH receptor (TR) ß gene mutations 22 years later (3, 4), the term RTH become synonymous with defects of this gene (5). Subsequent discoveries of genetic defects that reduce the effectiveness of TH through altered cell membrane transport (6, 7) and metabolism (8) have broadened the definition of TH hyposensitivity to encompass all defects that can interfere with the biological activity of a chemically intact hormone secreted in normal or even excess amounts. In this revised chapter, we have retained the acronym RTH to denote the syndrome produced by reduced intracellular action of the active TH, T3. The term of reduced sensitivity to TH (RSTH) is used to denote reduced effectiveness of TH in the broader sense.

<much more by following link>

thyroidmanager.org/chapter/...

Rod

[shaws Administrator]

This may help too.

web.archive.org/web/2010122...

web.archive.org/web/2010122...

[Heloise]

thyroid-rt3.com/backgrou.htm

This has quite a big of information beginning with tissue resistance. I understood that it takes a while for T3 to reenter receptors taken over by reverse T3 if that was the initial problem.

[Hidden]

Both Dr. Peatfield and Dr. Skinner say, as far as I can tell, that if one is resistant to thyroid hormones, when eg. T3 or T4 are taken, they can produce symptoms of excess if the absorbtion problem isn't dealt with. But this is because they are too high in the blood, but still not getting into the tissues. But if they aren't getting into the tissues, how can they produce symptoms of excess? I have read the articles you all suggested. These seem to suggest, logically to me, that this would just produce high levels in the blood and not symptoms of excess. Drs. Skinner and Peatfield seem to contradict this. However they aren't talking about genetic resistence. Please help. I am confused.

[bbarrowes]

I also have this question. I have been diagnosed with resistance to thyroid hormone, but did not test positive for the THRB set of genetic defects. I am currently on 550 micrograms of T3 per day. It does not seem to be doing much for me. And every time I raise the dose by 50 ug/day, I feel awful for a few days, then I feel basically as good as I did before raising the dose.

What is going on? How can I feel worse when raising the dose if the T3 isn't working int he forst place? I am starting to feel some effects, like not as cold, but overall, I don't feel better. Still fatigued, listless, depressed, slow reflexes (c.f. thyroflex, 180ms), etc.