At the moment all I can do is view the abstract as it is paywalled. BUT it strongly questions the observational studies that link various disease outcomes to subclinical hypothyroidism. Now there is an agenda here that links on to the accusation of too many thyroid tests done in SCH. However, I hope I can eventually download this to get more information. However, if at the same time it questions links said to occur between AF and OP and thyroid function I would be quite in favour. I fear however it will be very selective in its criticisms of trials that it rightly wants to discredit. Briefly, sauce for the goose is sauce for the gander. If you criticise quite rightly observational trials as alleging cause and effect, you have to extend your analysis to those relationships you cling to as being real. These include TSH suppression v OP and AF risk which fall under the same cloud of suspicion.
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diogenes
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SCH is subclinical hypothyroidism, OP is osteoporosis and AF is atrial fibrillation. They take so long to type if they come up frequently that I abbreviate.
I thought this comment in the paper encapsulated the misunderstanding of the links between FT4, FT3 and TSH. They put together FT4 and FT3 as defining euthyroidism with normal TSH. They fail to understand that a low FT3 and high FT4 does not so define, regardless of the TSH. If FT3 is the driver, then it has to be the correct set point concentration for euthyroidism to be so proven.
Therefore,
increased T4 concentrations coincide with decreased
T3 concentrations, which leads to a net euthyroid status,
as reflected by the absence of an association with thyroidstimulating
Diogenes can you please elucidate a little more, and explain the ramifications of the above quote. If this conclusion of the paper (that you paste here) were put into wider medical practice, then what outcomes would follow for treatment? Would endos / GPs be observing FT3 levels more and TSH less? And if so, how would our medication then change? And do you think this would be a positive change?
The problem in their attitude is simple. At base they believe that TSH in the reference range strictly defines euthyroidism. This is regardless of what the FT4 and FT3 levels are with respect to their ranges. However everyone has their own unique healthy range for FT4 and FT3. If you are outside this especially for FT3, but still maybe in the reference range (low) you are NOT euthyroid whatever the TSH may say. The increase in FT4 accompanying the lower FT3 because of temporary reduced conversion will control the TSH but this is telling you nothing, if you rely on TSH alone as a measure of health. Therefore as you say, FT3 should be the determinant of successful treatment and not TSH. If someone can't attain a sensible FT3 with T4 therapy alone, then they obviously can't convert well enough, and need T3 supplementation. Never mind the TSH.
I don’t even know what my T3/4 levels have been since I developed Hashimoto’s so this is a useful spur to keep tabs and figure out where the happy medium is.
Massive generalisation ahead .. I that all medical research into thyroid problems as a whole is utilitarianism taken to the Nth degree - conducted in the spirit of “it’s for your own good”, rather than for the lived reality and benefit of the patient. I read a lot of medical research into other areas of health and don’t spot this paternalistic attitude elsewhere. Where does it come from?
And on this point, I would love to meet a doctor - endo or otherwise - who actually has hypothyroidism / Hashimoto’s and can join up the two worlds.
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