The kiddies are squabbling again. This is about part 3 so far in Medscape. This link may not work for all. PR
medscape.com/viewarticle/83...
"Two leading US endocrine societies — the American Thyroid Association (ATA) and the American Association for Clinical Endocrinology (AACE) — are at odds over the specific advice that should be given to doctors regarding the use of triiodothyronine (so-called T3) in patients with hypothyroidism who do not fare well on levothyroxine treatment (T4) alone."
It seems to me that they don't recommend routine testing of T3 levels because they might discover how many people have low T3. And then they might have to treat people with T3. And that would be shocking.
The logic of the contributors to the article really escaped me.
PR, They need their heads banging together! They ought to be commissioning the research they claim is needed to help them make their minds up. Or, they could listen to their patients. Bottom line is it must be for the patient to decide whether to take T3 in order to feel well today with possible future adverse effects or not.
This comment suggests to me that they are determined to avoid TSH being suppressed at all costs "directly and indirectly may promote the overuse of combination T4/T3 therapy or overtreatment with T4."
This TSH-suppression-fear thing doesn't make sense to me. Under NORMAL circumstances, a high TSH indicates a high level of thyroid hormones which could be harmful. As far as I am aware, it is not the suppressed TSH istself that causes the problems but the cause of the suppressed TSH. Of course, in those of us on thyroid medication (and others) TSH is not representative of our actual thyroid status. Sometimes I wish the TSH test has never been invented!
Over the years I've come to the conclusion that everyone put of LEVO should once they are stable on that be given an FT3 test to see if there appears to be conversation factors. Then I think all other levels of vitamins, bloods etc to see if these are high enough to encourage conversation and supplemented accordingly. It's taken me about a year to improve after doing that and readings confirm that but still not, in my opinion, optimum. So I disagree in the article not doing routine full thyroid panel. However I do agree with patients who it is suggested to try T3 should be part of a clinical trial. Surely that can only be a good thing.
What does concern me slightly that reading some posts on here and comments elsewhere that some think they must be on T3 without the evidence to back it up or not giving the more conventional methods more time. If things then go horribly wrong not only is that detrimental to their own health but puts a black mark against combined therapy and mono therapy thus making it even harder to obtain for the people that really need it. We need properly conducted trials here by Endos with no connection whatsoever with Big Pharma.
Hence the petition 
I do agree. If someone is well on thyroxine and they are converting well enough to have good t3 levels, do they really need to add t3? For some people, adding t3 actually makes things worse. But there should be an option to try t3 for those who don't feel well on thyroxine. It's the lumping us all into one box approach that really sucks. We should be treated as individuals with individual needs.
Its exactly this sort of antediluvian thinking that is so dispiriting in its wooden repetition of accepted ideas (accepted that is until they aren't, and then woe betide those who remind about the previous errors, as it casts a poor light on the reputations of those who once thought otherwise). I and colleague Rudolf Hoermann are in both a good and bad position re this. The good is that we are both retired and therefore beholden to no one, and are not in the medical cabal that decides such matters. We do what we do in our own time, taking money from nobody. It actually costs (a little) but finding out really what is going on, without prejudice, is paramount. It should be what good science (even in medicine) is all about. The bad is that in not belonging to the cabal, the herd can and do turn their backs. But I hope members of this charity do realise that the facts can't be hidden for ever. From what I've taken in from the post above, our submission to Thyroid journal (US) where we specifically advocate both the measurement of FT3 in T4 therapy and the need to consider dual therapy where conversion is poor in the body, is going to get a dusty answer. Keep you posted.
Diogenes, you and Dr. Hoermann submitted to Mary Ann Liebert's Thyroid journal? If so that should be interesting although I suspect the reaction will be a cold one, but, you never know. PR
This is a deliberate "smoke out" tactic to see how the land lies in the US thyroid thinking at this moment in time given the rumblings in the post above. Though the likelihood of success may be small, we can always submit somewhere more understanding and up to date.
Diogenes, one of the reasons they fault NDT is because the 4:22-1 ratio, T4 to T3, is considered too high compared to the estimated output of the thyroid gland. However, Dr. Bianco in his video says that they estimate the total daily production of T3 at 30mcg, 5mcg from the thyroid, 5mcg from the liver and kidneys and 20mcg from extrathyroidal conversion. If you take that into account then the total daily production is closer to 100mcg T4 and 30mcg T3 which is a 3.33 to 1 ratio, a much closer ratio to NDT than just looking at the thyroid output which is usually quoted as somewhere between 10-1 to 20-1. I would think the total body production a more accurate figure to compare NDT too. I will grant that any thyroid medication is a poor substitute compared to what the body does naturally but I think comparing NDT to just the thyroid output is a warped perspective, one of many in endocrinology. Couple this with your concept about 'good convertors versus poor convertors' and I think they both help to explain NDT's success. PR
From our own indications I would estimate the direct thyroidal output of T3 as significantly higher than Bianco's estimate (up to 2 fold a greater proportional contribution) and also variable from person to person - that is, you have a spread reference range of outputs just as in every other parameter. The only way to find out directly is by measuring in healthy people using nonradioactive T4. I understand Johann Dietrich plans to do this later in the year. None of the above affects your argument about relative T4/3 production overall, just the proportions supplied by the various tissues and the gland.
Diogenes, that is something I've always been curious about. How to you accurately measure the output of the thyroid gland? Do you inject a marker into the gland and try to determine how much comes out, or is left in the gland after a certain time period? Counting molecules that the gland produces has got to be a rather tricky business. PR
The way to do it is (best) to give healthy volunteers a measured dose of 13-C labelled T4 (nonradioactive). You then sample the subjects with time to look at the way in which 13-C labelled T3 is produced. There will be a complex curve produced with time, and sophisticated statistical techniques can distinguish between direct glandular conversion of T4 to T3 and the slower conversion in the tissues. Thus you get a quick initial partial conversion and a slower later one. The two parts of the curve are then separated and analysed.
Advice needed on "normal range" for hypothyroidism
Advice on T3
"Many Over-the-Counter Thyroid Support Supplements Contain Thyroid Hormone"
