We have a new paper submitted to Frontiers in Thyroid Endocrinology which has been passed by review and merely awaits editorial formal acceptance. It looks at the responses to T4 therapy separately in three classes of patients: Hashimoto's (autoimmune) thyroiditis, thyroid carcinoma, and large benign goitre. Within each class we find individually different responses to T4, and also basic differences when comparing treatment classes. So in any indiscriminate patient panel, you will find different responses in different classes, and different responses within each class. In short, the state and response to T4 of a patient with thyroiditis is different from one having had carcinoma, and different again from goitre. I infer from this that before treatment, epigenetic changes unique to each situation have altered gene expression differently. Patients are not just individuals as regards general response to T4 treatment, but also have on top of that individuality in which of the three classes they inhabit. It takes the concept of individual treatment and response, even to T4 only, one step further. NB we couldn't do the same for T3 because the multiple possibilities in combined treatment obscure any analysis and not many patients are on T3 only.
The paper should appear within the next month.
The paper title is:
Functional and Symptomatic Individuality in the Response to Levothyroxine Treatment
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diogenes
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I hope the NICE team will get to read it before the guidance is finalised as the oversimplification of the response to thyroid hormones/replacement is overwhelming...
I want to say that I am utterly amazed at the number of papers you and your colleagues have produced. The sheer amount of work that must have gone into them is astonishing.
The basic reason is that we have in our possession a huge database of patient treatment and history, involving every possible measured thyroid parameter, both chemical and structural, together with a detailed individual history of repeated patent presentation over many years. This is a goldmine wherever you look into it, and new interpretations can come easily because you have all the necessary data. Because few outside Germany & Japan perform in this way, and even fewer now perform like this, because of perceived TSH superiority, there is no chance elsewhere to conduct such analyses because the data is just not there to do so.
Thank you for your continued work in this field. I look forward to reading the paper. I know we comprise a small percentage of the hypo population, but I wonder if there's a reason why you didn't look at those with non-autoimmune hypothyroidism as a possible fourth cohort in your study?
Thank you for your feedback. So to turn that negative to good use, if I ever have the opportunity to discuss your paper and findings with a GP, I suppose I can at least add as a coup de grâce, "and as the cause of my own hypothyroidism is unknown, you definitely can't presume my response to T4 will perforce, be the same as anyone else's ......" 😂
Indeed, thank you, Thank You, THANK YOU! When some of us are up against those who deliberately choose to stare the evidence hard in the back of the neck (you can see where I'm based ), you and your colleagues give us hope. Wishing you the best in all that you do.
I've been saying this for years!
it's one of the most important aspects to Hypothyroidism but has been totally ignored as far as I know.
With regard to those with after surgery from a benign goitres for example, we are simply stuck into the same category for treatment as if we simply had an underperforming thyroid gland. Papers exist from years ago that indicate this treatment to be totally incorrect, eg:
I hope this new paper will be accepted universally as it shows how treatment for all of us could be improved dramatically for the patients as every patient is different and should therefore be treated differently.
Thank you to all the team, and to you in particular for sharing with us such a wealth of information....we are fortunate beyond words!
It would be wonderful if the nay sayers and doubters of (supraphysiological) T3-only treatment could be convinced of its efficacy. Sadly however, most patients concerned are left in a medical wilderness with self sufficiency usually the only route to escape; the result being (I assume) that there are no/few records available as a base line for research
Interestingly you say, "not many patients are on T3 only" .
Sadly we just don't know for sure....or, how many should but have not been treated.
The endo that I saw, just a couple of times, listened to what I said about my (self medicating) journey to much improvement on T3 only (currently 112.5mcg). He refused to consider any type of acquired thyroid hormone resistance, could not explain why this huge dose was working yet concluded that it was working for me and I should maintain the status quo.....but with the caveat that it was not what he would advise!
It is high time that those in the upper echelons of the thyroid world started listening to themselves, opening their minds, reading research papers...and joining up the dots.
They lack so much of what you and your team stand for!
"Individual treatment and response" as you say, is the key.
For clarity, the gene that affects T4 to T3 conversion is called DIO2 - that is, three letters and a number. Not D102 - a letter and three numbers. Not DI02 - two letters and two numbers.
The name comes from the enzyme that this gene affects which is a deiodinase. It removes an iodine atom from a thyroid hormone molecule - it deiodinates it.
On this forum we probably understand, but if you wish to look it up anywhere, it might help to get it right. If you are discussing with a doctor, and get it wrong, you are providing an excuse for them to dismiss what you say.
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