There seems to be an increasing awareness that something is wrong in diagnosing thyroid therapy sufficiency by TSH alone. This commentary is part of that discussion. However it still parrots the line that FT3 levels are unstable with T3 treatment, and that FT4 +TSH should remain the mainstay of treatment. They simply cannot grasp the contradictions in their approach or that fluctuating FT3 levels after taking in T3 do not indicate the problem they think it does - the body treats this as an average over time rather than a momentary hyper state followed by a hypo state with little normality in between.
Endocrinology
Triiodothyronine alongside levothyroxine in the management of hypothyroidism?
No. if the pharmacokinetics for T4 and T3 uptake are different, all this means is that the changes in FT4 and FT3 are different from each other in blood after taking a fixed dose of both. This would be a problem if the quick changes in T3 were really important. However the body doesn't react to such FT3 changes as fast as the authors assume, so that the apparent rapid change in FT3 takes time for the body to adjust, thus smoothing out the response to T3. Also new T3-analogues are being produced that slow down T3 changes. Additionally, NDT probably has T3 bound to thyroglobulin which takes time to break down and release the T4 and T3 by stomach digestion of the globulin.
If I see a change in FT3 results after a medication change and get worried it is going too low, does it mean I should wait longer then for the body to adjust my level?
Depends. On T4 only changes up or down should be gradual with plenty of time between changes. One could well aim to keep or attain FT3 in the higher part of its healthy range. With combination therapy, the outlook becomes one of how you feel on a given regimen. also on T3 only. In general I'd advocate trying to attain a higher in range FT3.
Yes, the tide is changing, we hope. However, having listened to Kristien Boleart and Pete Taylor, the other night debating, supposedly against and for the use of T3, I was very disappointed to find that there is still this overwhelming fear and lack of understanding regarding using T3. The point being missed in all the noise about T3 is individual need and optimal treatment for that individual. As someone who has been taking 60mcg of T3 for 11 years now, with no palpitations or other adverse side effects, it frustrates the hell out of me that the stance now is 10mcg pd ONLY. Yet again the ‘experts’ are falling into the narrow mindset trap of compartmentalising patients into type. So for decades we have been the type - ‘hypothyroid - needing T4 only'. Now, having acknowledged that, hmmm, this regime is not really working, there is a subset who are not getting well on T4. yet again they are falling into the same trap, now we have two types of hypoT patient. Those who are ok on T4 and those who are not. So now there is thinking that those who are not ok on T4 mono need some T3. So instead of this raising the question and need for research as to why some do not thrive on T4, they promote a new ‘set’ regime that is expected to be suitable for all within that subset, even though it is acknowledged that they don’t understand why T4 does not suit this group. So how can they decide that 10mcg pd along side a reduced level of T4 is going to be ok for all of this group. They already know that there are many still out here like myself already and successfully thriving on T3 mono and NDT. They are effectively continuing to gaslight us.
And KB could not answer the question as to what is so wrong with NDT when it was used successfully, without adverse effects, for decades prior to T4. I was totally disgusted at her weak attempt at humour likening it to the drug thalidomide, when she failed to come up with a reasonable answer. It is this attitude that draws questions regarding expertise and guidance!
They have learnt nothing from the failed T4 mono regime. Why can they still not understand the basic principle that we are NOT ALL THE SAME? We are individuals and have different genetics, different comorbidity, different needs.
They talk about needing a large scale study to assess once and for all any benefit of combination therapy. But this is not going to be the end of it. It will not go far enough, it is doomed to be another useless failing study before it starts. It will be a study that is already biased, based on what some current thinking is that 10mcg of T3 is enough, and that given with T4 should be all that anyone needs. This might be ok if all of us with hypoT had exactly the same reasons for having and developing this condition. If non of us had inherent or developed any other conditions.
Any study needs to be wider. To look at just what are the individuals needs. What are the starting points for these individuals. What other genetic polymorphisms/comorbidity do they have. Diabetes, adrenal issues, other AI conditions etc. Is there a correlation between other comorbidity/genetics and thyroid treatment needs.
To accept that 10mcg T3 only, is acceptable without further study and consideration is no better than saying T4 mono for all.
To say that a 3 or even 6 month trial of 10mcg of T3 is enough is yet again falling the individual. It might be that for whatever reason this individual needs 20mcg, 30mcg... etc. They may never get well taking an inadequate dose. They may never get well including T4 in the regime. I personally know that T4 caused me debilitating migraine, CF and fibromyalgia symptoms. I don’t know why, it might be an adrenal problem, perhaps caused by long term failing T4 use. No one bothered to find out. What I do know is that stopping T4 stopped these symptoms, whenever I tried adding T4 they came back. When I stopped T4 altogether, for T3 mono, I got well. I know I am not alone getting well on T3. Why do our experts not want to speak to us, to find out why we are able to tolerate higher doses of T3? Before continuing to condemn us all to yet another failing regime?
Square brick into round holes comes to mind and it is the so called experts sitting there playing this game with peoples lives and wellbeing.
As someone who needs 75mcg T3-only to function I totally agree with your comments.
Had I not eventually discovered that I have a type of thyroid hormone resistance/ tissue hypothyroidism and need this treatment I would have continued to deteriorate.
I also had diagnoses of FM, CFS, IBS...all the usual suspects. Tests, scans, various treatments both NHS and private proved nothing...
I'm convinced that, based on the scare stories that prevail, they fear T3 and try to avoid it if at all possible.
Also, to change horses and run with wider T3 treatment is likely to put reputations at stake....that would never do!!!!
It's old old problem. An individual is not a statistic and has to be considered as an individual. No indivdual's FT4, FT3 or whatever encounters the whole of the healthy ranges in health. In all of these their blood levels only occupy a small fraction of the overall range possibilities. And it is the disregard of this situation that condemns diagnosis to be made by statistics. The medics first try to say that someone might need combination therapy and straightaway fall completely into the trap of treating by generalisation. It seems impossible for the medical field to consider a problem without then trying to select an arbitrary, singular, general average dose, rather than consider the individual needs of a patient. It's a mindset I find completely bewildering, as it is self-evidently bogus.
well people have been writing treatment guidelines for years that completely ignore the spike in fT4 after taking Levo (apart from vets, who seem to be taught that time of last dose needs to be taken into account)... OK T3 is 'active' so it matters more, but still.. it seems some people are only interested in 'spikes' when it suits them , and not interested when it doesn't.
Saw your post, read the paper, very quickly so might have missed bits. Then read your comment. Completely agree.
Is there any mileage in looking at T3 at the molecular level?
I mean, if we imagine every cell of the body requires one T3 molecule a day, it makes little or no difference to the individual cell whether that occurs all at once, or randomly across all cells spread over the whole day.
Indeed, it suggests that the differences could lie in whether the whole liver (for example) ramps up and works at peak rate for a short period due to T3 arriving all at once. Or just a part of the liver with the remainder "having a rest". That is, it will reflect in whole organism effects rather than individual cells which might not really care.
Looks like more people are starting to say " we've been thinking about this " rather than risk being left behind with the ostritches.
It makes a nice change to read sensible thoughts on what might be happening, and why we might all be different , without any of the dismissive attitudes we've become so used to reading ...... and lots of useful references papers... including 3 of yours
All very encouraging :
"Future clinical trials must support the application of individualised thyroid care, including pre-treatment thyroid function and the presence of polymorphisms in DIO2, and be of sufficient duration (at least 1 year) to provide support for long-term routine management outside the clinical trial setting.69Future perspectivesThe current management of hypothyroidism (TSH-directed monotherapy with LT4) leaves a substantial minority of patients with residual hypothyroid symptoms. A consensus is emerging among experts in thyroid management that the potential benefits of combination LT4 + T3 preparations has not been studied adequately in randomised clinical trials. One solution to this unmet medical need, in the opinion of the authors, could be administration of a free combination of T4 and T3, as this is more flexible than a fixed-dose combination. LT4 could be given once-daily, with T3 given twice (ideally, if serum T3 can be kept within normal limits) or three times daily. ........
.....better-standardised FT3 assays, with measurements made before ingestion of the day’s thyroid medication may provide a useful adjunct to thyroid care for patients "
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