I've finalised what I hope may be useful to some here as a document to leave with your doctor. On occasion it might ring bells.
To the doctor
To the doctor
. You and I are meeting to discuss my health problem that I suspect (know) is associated with hypothyroidism. I’m sure we both want to come to a conclusion and treatment that best suits my particular state of health. Therefore before we start, I’d like to put in front of you the ideas and concepts that modern thinking on thyroid function has developed. At the moment, it seems that TSH alone is used to monitor treatment and that thyroxine (T4) is regarded as the universally satisfactory treatment. It seems also that a decision as to satisfactory treatment by T4 is to place the patient’s TSH anywhere within the reference range for healthy people. This attitude is merely a statistically based one, and takes no account of my individuality in terms of my natural FT4, FT3 and TSH levels which all act together to define my unique health.. I put the following points to you:
1) In health, each person has their own unique set of blood concentration values for TSH, FT4 and FT3 which together interact to define their healthy state. T4 is the relatively inactive precursor of T3, the active hormone that defines health. Especially for FT4 and FT3 the values throughout life occupy a restricted region of the reference ranges typical of the individual, which are far more closely drawn within the range than the reference range that describes everyone. TSH is more variable, as throughout a day its values alter significantly, with a peak in the early hours of the night, thereafter declining through the day until the next peak. It is therefore important at what time of day TSH is measured
2) Therefore, as nearly as possible, therapy in disease should attempt to regain the values (most importantly) for FT3 that originally applied in health. After all it is the T3 in the body that drives metabolism and neither T4 nor TSH.
3) But we have a problem, because we don’t know what that was, because it wasn’t measured when we were healthy. Inevitably therefore finding the original situation is a matter of trial and error. But it is not acceptable merely to “normalise” my blood levels somewhere within the normal range, because I only occupy a tight region typical for me. Also we have a difficulty in that the doses of T4 are very crudely determined in 25 ug steps, whereas my healthy situation is much more closely defined.
4) So there arises a serious question. If I had an FT3 and FT4 unique to myself in health, which we don’t know, how am I to regain this by therapy on T4? Surely only by trial and error and my response to therapy. But since we’ve agreed that my optimum values are not the same as the entire range, it can’t be logically right to just put me in the normal range for any parameter (TSH, FT4 or FT3) and say that I am properly treated. It’s more complicated than that (open-mouthed doctor stunned by irrefutable logic !).
5) I’d now like to propose what I think you’ve been taught. That TSH from the pituitary stimulates the thyroid gland to produce T4. The T4 then goes into the circulation and is converted to T3 (the active hormone) as suitable for health. But my thyroid is damaged (lost). So you give me T4 to replace the lost T4 no longer supplied by the thyroid. In doing this you restore my TSH to what it was before I became ill. Therefore, get my TSH back somewhere in the normal range and all must be well (in ALL cases). Therefore all you need to measure is TSH.
6) Unfortunately, new studies show that is completely wrong. First TSH stimulates the thyroid to produce BOTH T4 and some T3. Both enter the bloodstream and some T4 is converted to T3 as you were taught. But now the FT3 that governs my health is made up from two sources, the thyroid and body conversion. And the thyroid’s direct contribution is very important even though it is apparently a minor contributor to T3 production overall.
7) The T3 produced by my thyroid direct is an important controller of the body’s conversion of T4. As my thyroid declines, it tries to keep its production of T3 as close to normal as possible, even though my T4 is lowered. So the level of FT3 from thyroid and body conversion is kept as close to natural as possible both by the thyroid’s attempt to maintain its T3 production and increased T4-T3 conversion rates by the body.. Only when the thyroid has virtually gone, does the whole system collapse and body conversion of T4 by therapy has to take over completely.
8) So, we have two different situations: one where I’ve got some thyroid left, and another where I have none at all. The treatment of these situations is entirely different. But we don’t know which situation I’m in (for those who haven’t had their thyroid completely removed/destroyed). So once again treatment has not to be by rigid biochemistry, but by trial and error until I achieve something closer to original health. This is subjective and not objectively obtained by biochemical results.
9) We are all different. Our thyroids are different in size, and differ in their production of T4 and T3. Some people’s thyroids produce more T3 direct and others less. The combination of this T3 and body T4 conversion sum up to produce health FT3 levels. When we lose our thyroid, then we lose the T3 produced by it. This has to be made up by extra T4 conversion from T4 therapy. But to get to this state, more T4 has to be given than the thyroid produced in health, to force the body’s conversion to make up the difference. This, because T4 suppresses TSH, will give a lower TSH to achieve this than when in health. Therefore the TSH range suitable for health is unsuitable for therapy. Values lower than the healthy range are therefore suitable and ineivtable for proper treatment control. In certain cases, undetectable TSH may occur if the conversion capability of the patient is sufficiently restricted – but given normal range FT3 this does not matter. Suppressed TSH when one has some working thyroid left means something quite different (and undesirable) as opposed to those with no working thyroid at all.
10) If someone, whose thyroid T3 constitutes a higher proportion of the total T3, loses their thyroid entirely, then the body T4 conversion from T4 mono therapy may not be able to make up for the loss of thyroid T3, however much T4 is offered. It is this minority of subjects who can never sufficiently recover using T4 alone. These are the patients who will need T3 in some form in therapy to restore the FT3 to their unique healthy level. I believe I may be one of these. This can be discovered by measuring my FT4 and FT3 on a given T4 dose. If the FT4/FT3 ratio is above 4.5/1 then this gives suspicion I am not converting the T4 to T3 sufficiently well and T3 may also need to be given.
11) All these complications mean that simply using T4 therapy to put me somewhere in the "normal" range for TSH or FT4 is insufficient. FT3 is the measure to use in therapy control as you and I do not know the exact level of thyroid destruction (omit if not applicable to you). It really is a matter of trial and error and more liberalism in therapy choices. Not only T3 but desiccated thyroid extract should not be ruled out. There are allegations that DTE is not well controlled as to hormone content. This is not true as the product has to obey the various Pharmacopeias and has adequate quality control by rigid requirements. Furthermore the allegation that DTE does not contain the “right” relative quantities of T4 and T3 is also a red herring. T4 mono therapy is even more nonphysiological than that, but is the preferred mode of treatment.
You cannot both argue that DTE is nonphysiological when T4 is even more so.
12) I hope these comments will help us both to achieve a satisfactory outcome as regards my treatment and reattainment of health
Front. Endocrinol., 22 December 2017 | doi.org/10.3389/fendo.2017....