There's a new paper out by the eminent (retired) thyroid scientist Prof W Wiersinga. In it he goes through in some detail the increasing present day realisation that T4 isn't adequate always for therapy and even NDT is discussed as a possible alternative. The paper is downloadable:
It is quite detailed but there are lots of comments that are useful to pick up on. This scientist has been supremely reticent in the past in bringing himself to believe in these conclusions so strongly, but now he has, I feel that progress in realising what has been done wrong for so long is beginning to break through. If he can make the change they all can.
T4 + T3 combination therapy: any progress?
October 2019 Endocrine 66(1):70-78
DOI: 10.1007/s12020-019-02052-2
Wilmar M. Wiersinga
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Citations
Written by
diogenes
Remembering
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The article ends with the obligatory: "can only be solved by doing many more clinical trials".
"Why should we conduct these trials" thinks Big Pharma "when it will be expensive, make lots of people well again and seriously damage our share price? But we dare not admit that publicly".
100K + members of HU Thyroid U.K. plus thyroid support groups In UK and throughout the world (I’m in touch with a group in South Africa) all saying levo is not enough-Id like an Endo to stand up today and try and say (with all this in mind) that Levo is all we need.
It’s demolishing TSH priority testing next.
Then the Pilo/Bunevicius <10mcg T3 daily, Construct which seems to be gaining more credence and must be stamped in, hard!
I also find that while deficiencies of some vitamins are seen by RMOC and others as obstructing full benefit from levo monotherapy, the NHS seems rarely to test levels of them and are even more reluctant to prescribe when deficiencies are found.. so contradictory.
My Gp told me last Dec that there were talks about not testing Vitamin D and such as it was not beneficial to do so. So obviously they are moving away from doing so. But, they know levels are important, might not want to issue but should not stop testing.
He has probably changed his mind reading your research papers and/or he has found that he or members of his family couldn't improve on levo alone if diagnosed as hypo.
I’m much more cynical. I’m waiting for a ‘new’ medication to be announced that is going to solve all our problems (not) and I will be wondering who will be benefiting from it financially when marketed instead of T4. Might explain why T3 needs to be pushed off market, bit like NDT was when they were marketing and promoting T4 decades ago (Knowing it was One of my theories from 3 years ago, still hanging on to it....time will tell.
Thank you for this Diogenes but I won’t be celebrating yet, not when I read: “One may thus question whether low serum T3 levels could be involved in persistent complaints, necessitating higher L-T4 doses to normalize T3 levels. This seems, however, not very likely.” And: “However, there is no good evidence that low serum T3 or low FT3/FT4 ratios are linked to persistent symptoms”. Yeah, right.
I don't expect a complete Damascene conversion right away. Realisation of the right situation has to be chipped away at steadily until the whole statue appears. It's enough for me that the 2012 European Guidelines (and by influence) the UK ones have been questioned as to their accuracy. That means revisiting them. I hope the new UK guidelines also take this into account. Only by redrawing the Guidelines is officialdom going to move.
There is so much data to support the case for T3 supplementation in addition to T4-only, what the Hell are they waiting for. You have hundreds of examples on this forum alone, it is no longer anecdotal.
Much of this appears to describe at least part of my thyroid journey and echoes many of my thoughts/suspicions....as no doubt many others here will also recognise.
I'm neither a medic nor a scientist, just another thyroid patient wadng through the treacle that is current thyroid care
I have the Dio2 snp /homozygous and by acting as my own guinea pig have discovered that I also must have a type of RTH. Lab results suggest this is not the consequence of known genetic mutations. The endo that I saw briefly was adament that RTH in any form was not a factor in my condition....yet could not explain why I can tolerate a supraphysiological dose of T3 without overstimulation!
.The author's words (follows) are encouraging
".Outcomes might be different by applying different selection criteria. New RCTs can be envisaged restricted to patients with persistent symptoms and/or specific genotypes like Thr92Ala DIO2. Other polymorphisms should be considered as well, like SNPs in the brain-specific thyroid hormone transporter OATP1C1 which have been associated with fatigue and depression but not with neurocognitive functioning or preference for T4 + T3 [1]. Interestingly, a Danish RCT found two SNPs (Thr92Ala DIO2 and rs17606253 MCT10 -monocarboxylate transporter 10) associated with favored treatment: preference for T4 + T3 therapy was 42% when both SNPs were absent, 63% if one SNP was present, and 100% if both SNPs were present [35]."
I am now T3-only and many of my symptoms have improved or disapeared, however fatigue and gut issues remain and so far I have been unable to resolve these, with resultant continuing reduced QOL
Taking 125mcg T3 has not signalled overmedication (heart rate, temp and BP) and my problem now is to find a dose that will provide adequateT3 for some tissues without over stimulating others.
I'm now wondering if "the brain-specific thyroid hormone transporter OATP1C1 which has been associated with fatigue and depression but not with neurocognitive functioning" is the culprit.
Alll very well but even with that information working out an appropriate dose remains a problem ...this is a welcome and useful paper.
However, for those of us depending on T3-only (and I understand that is not the subject here) it is only one link in a longer chain and "can only be solved by doing many more clinical trials" . That remains only part of the challenge.
That challenge isn't the science it is the weight of political power, the clout of high finance and the intransigence of the decision makers.
Apologies diogenes .....ranting seems to be my default setting these days!
Thank you for posting this, I hope it falls on ears that listen..
'Endocrinologists are frequently asked to consult on patients taking L-thyroxine (T4) who appear dissatisfied with their therapy. However, the use of combination therapy with liothyronine (T3) remains highly controversial with conflicting results from clinical trials. Recent scientific studies have provided new insight into the complex relationship between
serum and tissue thyroid hormone levels justifying a review of the evidence base for the use of T4+T3 combinations and the design of future clinical trials in this area.'
So slow. At least they’re thinking about it. Studies irrelevant. We know the answer for most hypo. Treat slowly and gently. T4 to feeling fine (consider brands formulation etc). Hyper first/no improvement? add t3 or try ndt. Still no joy T3 mono treatment. If that doesn’t work wait for Bianco’s slow release T3 to be clinically trialled.
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