A new paper showing that soft gel or liquid T4 better controls T4 dose in patients with central hypothyroidism - accessible paper.
l-Thyroxine in an Oral Liquid or Softgel Formulation Ensures More Normal Serum Levels of Free T4 in Patients with Central Hypothyroidism
Salvatore Benvenga, Giovanni Capodicasa and Sarah Perelli
Original Research Context: L-thyroxine therapy of central hypothyroidism (CH) is guided by measurements of serum free thyroxine (FT4), which should be above the midnormal range value (MNRV). In some countries, novel formulations of oral L-thyroxine (liquid or softgel) ...
The paper is aimed only at those who can satisfactorily use T4 in therapy = the 80% or more. However it may also help those who need T3 also, by more efficiently getting T4 into the body and maybe reducing the T3 requirement.
Lack of TSH response doesn't affect T4-=T3 conversion negatively. In fact it may stimulate it so that what T4 there is made is converted as much as possible into T3 until it can no longer find enough T4 to do so. This happens during the protracted decay of a dying thyroid. After all, a lot of patients with this problem can use T4 therapy in exactly the same way as those with no thyroid. The body's response to inadequate T4 is always to ameliorate with better conversion. Of course if you are the unlucky one who has basic poor conversion then you must suffer insufficient FT3 production and need T3 supplementation.
Interesting. Are there any studies showing that, as I was told that low TSH affected conversion negatively and that was why mine was bad, but it sounds as though that is not true.
You will have one soon. We have shown that as the thyroid function decays, so the body's deiodinases are stimulated to convert more of what T4 is being made into T3 and this is directly proportional to how much working thyroid you have left. Thus FT3 is maintained as close to normal as long as possible, until so little working thyroid is left that the system suddenly collapses Since both T4 and T3 stimulate the pituitary, this means that you can continue to feel well because of normalised FT3 even though your thyroid is under stress, until such time of gland decay has been reached to pass over your unique threshold for feeling hypo effects. This will also occur with pituitary failure, because though TSH is lower, the same stimulation of deiodinases will occur for the same reason. As a guiding rule the body always tries to mitigate the adverse circumstances and never quietly lies down under attack.
My understanding is (or was) that TSH is a signalling mechanism to the Thyroid gland to increase or decrease its output of T4 and T3 (amongst other hormones).
A bit like a throttle pedal controlling the flow of fuel into an engine.
I have always been puzzled how the T4 to T3 conversion process is expected to make-up for the missing 20% of the body's T3 in patients on Thyroxine monotherapy.
It seemed to me that it was a wishful thinking assumption that the level of conversion is somehow increased to make-up for the shortage of T3, as I have not found any hard evidence of this to-date.
So, if TSH does actually play a role in normalising FT3 on T4 monotherapy, I (and I am sure many others) will be very interested to read about how this has been established and measured.
In that case, it will be appreciated if you can direct me to appropriate sources of the evidence, so that I can learn more about this.
Just to be clear, I am not questioning your answer, or that there is copious evidence.
It is just that I have not found such evidence in my 5-years of searching for, saving and reading a copious number of T3-related medical papers, articles, etc.
Either I have been looking in the wrong places, or not using the the appropriate search criteria, or both.
Its a complex mechanism but we discovered a feedforward positive T3-TSH "shunt" mechanism which when T3 is lacking, promotes the activity of deiodinases to produce more T3. Its all in our several papers to explain what is happening. We're engaged in writing a paper which demonstrates clearly that as the thyroid gland deteriorates (and its T3 production falls as well as T4) the body's deiodinases take over as best they can to substitute for the lack of direct T3 production by increasing T4-T3 conversion. All our earlier papers have described this in detail and will reward careful reading.
What is the evidence that 80% or more can satisfactorily use T4 in therapy?
From the large numbers of patients on this and other forums looking for help, it is apparent that the majority of GPs and Endos use TSH as the primary indicator of so called 'normal' levels, while at the same time ignoring the symptoms of low T3 and, it seems, claiming that the patients are depressed, have chronic fatigue, menopause, etc.
My Endo (an exclusively thyroid specialist) told me that the there was no point in testing FT3 levels as it is meaningless (which, I presume, comes from the original BTF guidelines that she was reluctant to deviate from).
It seems that very few patients are able to have their FT3 tested, so how do the great and good in the NHS really know that 80% or more can satisfactorily use T4 to produce adequate FT3 levels when most do not have their FT3 tested?
Epidemiologically - that is the fraction of subjects who are satisfied with T4 monotherapy to the extent of never bothering their doctors and leading an apparently health life. This is not restricted to the UK, but to places like Germany where historically the attention to detail including FT3 measurement has shown this. There's no reason to think otherwise - indeed in olden times (the 80's) - all measurements were done until sensitive TSH took over to the deteriment of future diagnosis. Your endo is as ignorant as a child re FT3 and simply has no grasp of thyroidology.
Sadly, my wife falls into the 80% and feels better when her FT4 is a little over-range, as this increases her FT3 to just below mid-range.
However, using the BTF guidelines as their reference, her GPs insist that low TSH and 'high' FT4 signifies that she is over-medicated and, consequently, reduce her Levothyroxine dose, resulting in a drop in her FT3 level and reduced level of energy.
So, are you suggesting that it is not just the increase in Levothyroxine dose that results in an increase in FT3, but also the consequent reduction in TSH?
As I mention above, I am not questioning your answers, but I am looking for some clarity
Some bedtime reading, but there's lots more if you want it:
Advances in applied homeostatic modelling of the relationship between thyrotropin and free thyroxine
•November 2017
•PLoS ONE 12(11):e0187232
•DOI
•10.1371/journal.pone.0187232
Dual control of pituitary thyroid stimulating hormone secretion by thyroxine and triiodothyronine in athyreotic patients
•July 2017
•Therapeutic advances in endocrinology and metabolism 8(6):83-95
•DOI
•10.1177/2042018817716401
Homeostatic Control of the Thyroid–Pituitary Axis: Perspectives for Diagnosis and Treatment
•November 2015
•Frontiers in Endocrinology 6(177)
•DOI
10.3389/fendo.2015.00177
Homeostatic Equilibria Between Free Thyroid Hormones and Pituitary Thyrotropin Are Modulated By Various Influences Including Age, Body Mass Index and Treatment.
•June 2014
•Clinical Endocrinology 81(6):907-15
•DOI
•10.1111/cen.12527
TSH Measurement and Its Implications for Personalised Clinical Decision-Making
•December 2012
•Journal of Thyroid Research 2012(2):438037
•DOI
•10.1155/2012/438037
Most of these are open access but if not Louise Roberts has copies.
Central hypothyroidism is the affect of the pituitary not functioning. Whenever this happens your thyroid is not the issue. The pituitary gland is. Central hypothyroidism is all in your head!! 🤔 pituitary gland wise! So, as in my case my pituitary is not making the TSH to tell your thyroid to make t4. T3 is in the basement and will remain there because of pituitary malfunction, not the thyroid in central hypothyroidism. This is what makes CH different from “normal” hypothyroidism. Also, it takes longer to get the correct dosage right, Me? It’s been almost one year and I’m still crazy!
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