This is a Chinese analysis of the US NHANES data done by postgrads who presumably need to get some papers on their CVs.
They incorrectly refer to 'resistance to thyroid hormone', this term is formally reserved for reduced T3 binding to receptors. I'd prefer to use the term more loosely but the correct term in this case is 'impaired sensitivity to thyroid hormone'. End of pedantry.
If we look at Table 1 fT3 has the strongest association with reduced bone mass density (BMD), by a long long way. Other studies have found associations with fT3, fT4 and TSH, even in so called subclinical hyperthyroidism. We have to be careful here because sometimes when the thyroid is diseased or under attack the parathyroids are affected. So, we can't extrapolate what happens in disease to treatment with T3. Indeed, I do not know of any studies that show T3 has worse effects on bone than T4 at equivalent doses. I recently had a DEXA scan which gave similar results to seven years ago, I'm on high dose liothyronine. When I find where I've put the results I will put up a post.
I dislike the fT3/fT4 ratio because it should vary depending on fT4 levels. Anyway, if we look at Figure 2 (a) we can see that the fT3/fT4 ratio has negligible effect on lumbar BMD. 2 (b) is downright dishonest, the axes have been stretched. A massive change in fT3/fT4 ratio (from 0.2 to 1.0) results in a tiny reduction in lumbar BMD (from 1.04 to 1.02). Two percent difference!
The same comment applies to Figure 3. More elasticity to suit their agenda.
Figure 4 continues the diddling, demonstrating an incredibly weak effect. It does however show the much greater effect of a low BMI (the red line). It appears that people who are all skin and (not much) bone have a lower lumbar BMD. In England 0.6% of males and 1.1% of females have a BMI below 18.5. A little nourishment might solve the problem!
The authors say "we hypothesized that osteoporosis can be prevented and treated by modifying thyroid sensitivity". I think they mean sensitivity to thyroid hormone but this is yet to be achieved and I think a long way off.
This paper illustrates how many doctors are only interested in getting something published. They seem to have no interest in helping patients. There are so many useful studies that are needed but we keep getting this sort of stuff that is of no use to anyone and serves to obscure good research.
Diogenes, thanks for bringing this up and more important thanks for the good work your team does.
Trouble is that I'm extremely busy, with colleagues, in producing our upcoming eBook on thyroid control, diagnosis, treatment, and inconsistency of FT4/3 tests and don't look at passing MS's as closely as I normally do. Including a fight with Word, which after a few edits, removes access to what I'm doing. In future I have to save under a different name, and tiis infuriatingly expands my MS list. I believe that FT3/FT4 ratio has value in that it roughly indicates conversion in health and on T4 mono therapy. I think FT3 is very important in these cases, but conversion efficiency given by the ratio tells a lot more in addition
No problem. I'm amazed at the amount of work that goes into a study, or at least the studies that advance the science.
The fT3 / fT4 ratio is incredibly useful - when measured with a roughly average fT4. The problem occurs when the ratio is blindly used as a number with no context. If fT4 is low there simply isn't enough substrate to generate T3 and so the ratio is meaningless. Also, if fT4 is high type-1 deiodinase takes over, you might get a good ratio but this isn't the same as good levels of T3 that are derived close to the cell nucleus by type-2 diodinase.
I look at fT3 levels when fT4 is middling, if fT3 is low or low normal in this case you have a problem. For example, a recent study found that antibodies to a selenium transport protein reduces deiodinase. Who would have thought? The only clue would be a poor fT3 / fT4 ratio. Wise interpretation of the ratio is very useful but some doctors use it as a vital number regardless of hormone levels.
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