I know how some of you good people like a bit of a thyroid labs puzzle - so I thought i might post up some of my recent results and see if you had any thoughts on them.
I have been diagnosed with Hashimoto’s and have been taking combination T3 / T4 therapy with levothyroxine and Tiromel T3 for a few months now.
I deliberately used a relatively high dose of T3 initially and a relatively low dose of T4 to try to flush reverse T3 out of my system to help overall thyroid function
This resulted in good levels of T3 (upper half of ref range) and low TSH (under 1) and I felt pretty good - but I noted that free T4 was below ref range - and thought I should at least try to get it in the reference range in case that made me feel better and for peace of mind.
So I increased the T4 from 50mcg a day to 100mcg a day and reduced T3 from 62.5 to 37.5mcg and waited 2 months to test
Usual precautions for the test: morning test – same 8-30am each time, fasted, no B-vitamins for 48-72hrs before the test, last T3 dose is taken 12 hrs before the test.
My GP called me in for a routine TSH test around 8-9 weeks after making the above dose change and TSH was v low 0.08 - but not entirely unexpected due to the combined T3/T4 regime.
But of course, the GP will not run a full thyroid panel so - in order to know if the low TSH is an indication of perhaps too much T4 or T3 I ran my own panel with Thriva 4 weeks later ( BTW they have an offer on – full thyroid panel, liver function test and lipid profile for £50)
The really odd thing is that these tests do not seem to line up well at all
I will outline the dose changes and test results below
Dosing : ( units = mcg)
Date/ T3 / T4
04/05/2020 62.5/50
13/10/20 37.5/100
Results : (T3,T4 units = pmol/L TSH = mIU/L)
Date / Free T3 /Free T4 /TSH
29/09/20 5.43 7.32 0.32
18/12/2020 only TSH 0.08
21/01/2021 4.1 13 2.17
(Antibodies both now back in the normal range - around 10-11iu - have been for 3yrs now)
If anyone has any ideas for why the TSH is so much higher in the January result than the December one - while on the same T3/T4 dose I would be interested in your thoughts
I was also a bit surprised to see that the free T3 reading dropped so much after reducing the Tiromel but doubling the levo – but I guess this just points to poor conversion?
thank you in advance for your input
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garz
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yep - it looks this way - but just seems odd that this latest result says high TSH and yet the last 2 results say the T3 was in the upper half of the range and TSH also low - no dose changes.
I deliberately used a relatively high dose of T3 initially and a relatively low dose of T4 to try to flush reverse T3 out of my system to help overall thyroid function
I hope you don't mind if I point out the misconceptions in this paragraph.
Firstly, high doses of T3 do not 'flush out' rT3. In fact, if your FT3 gets too high, it can increase your level of rT3.
rT3 is one of the body's safety precautions, to prevent FT3 levels going too high. But, it doesn't need 'flushing out'. It only stays in the body for about 2 hours before being converted to T2. It does not block T3 receptors - it has its own - and it does not affect conversion, nor cause symptoms.
There are many, many causes of high rT3 but only one of them has anything to do with thyroid, and that is when your FT4 is too high. And, in that case, all you need to do to lower rT3 would be to lower your dose of levo.
Secondly, reducing rT3 does not 'help over-all thyroid function'. It doesn't affect the thyroid in any way. But, in any case, if you're taking thyroid hormone replacement, your thyroid won't be functioning, anyway.
(Antibodies both now back in the normal range - around 10-11iu - have been for 3yrs now)
Does this mean that, in the past, your antibodies were above normal range? If so, it means you have Hashi's. And, Hashi's doesn't go away, whatever the antibodies do. The antibodies are not the disease, just an indication that you have it. They fluctuate all the time, but the Hashi's will always be there. And having Hashi's could have something to do with the variations in your results.
thanks for this interesting point of view. I would like to look into the mechanisms of Reverse T3 metabolism and function you mention with some further reading
can you point me towards references for the mechanisms you describe?
The thyroid gland secretes mostly T4 and very little T3. Most of the T3 that drives cell metabolism is produced by action of the enzyme named 5'-deiodinase, which converts T4 to T3. (We pronounce the "5'-" as "five-prime.") Without this conversion of T4 to T3, cells have too little T3 to maintain normal metabolism; metabolism then slows down. T3, therefore, is the metabolically active thyroid hormone. For the most part, T4 is metabolically inactive. T4 "drives" metabolism only after the deiodinase enzyme converts it to T3.
Another enzyme called 5-deiodinase continually converts some T4 to reverse-T3. Reverse-T3 does not stimulate metabolism. It is produced as a way to help clear some T4 from the body.
Under normal conditions, cells continually convert about 40% of T4 to T3. They convert about 60% of T4 to reverse-T3. Hour-by-hour, conversion of T4 continues with slight shifts in the percentage of T4 converted to T3 and reverse-T3. Under normal conditions, the body eliminates reverse-T3 rapidly. Other enzymes quickly convert reverse-T3 to T2 and T2 to T1, and the body eliminates these molecules within roughly 24-hours. (The process of deiodination in the body is a bit more complicated than I can explain in this short summary.) The point is that the process of deiodination is dynamic and constantly changing, depending on the body's needs.
Under certain conditions, the conversion of T4 to T3 decreases, and more reverse T3 is produced from T4. Three of these conditions are food deprivation (as during fasting or starvation), illness (such as liver disease), and stresses that increase the blood level of the stress hormone called cortisol. We assume that reduced conversion of T4 to T3 under such conditions slows metabolism and aids survival.
Thus, during fasting, disease, or stress, the conversion of T4 to reverse-T3 increases. At these times, conversion of T4 to T3 decreases about 50%, and conversion of T4 to reverse-T3 increases about 50%. Under normal, non-stressful conditions, different enzymes convert some T4 to T3 and some to reverse-T3. The same is true during fasting, illness, or stress; only the percentages change--less T4 is converted to T3 and more is converted to reverse-T3.
The reduced T3 level that occurs during illness, fasting, or stress slows the metabolism of many tissues. Because of the slowed metabolism, the body does not eliminate reverse-T3 as rapidly as usual. The slowed elimination from the body allows the reverse-T3 level in the blood to increase considerably.
In addition, during stressful experiences such as surgery and combat, the amount of the stress hormone cortisol increases. The increase inhibits conversion of T4 to T3; conversion of T4 to reverse-T3 increases. The same inhibition occurs when a patient has Cushing's syndrome, a disease in which the adrenal glands produce too much cortisol. Inhibition also occurs when a patient begins taking cortisol as a medication such as prednisone. However, whether the increased circulating cortisol occurs from stress, Cushing's syndrome, or taking prednisone, the inhibition of T4 to T3 conversion is temporary. It seldom lasts for more than one-to-three weeks, even if the circulating cortisol level continues to be high. Studies have documented that the inhibition is temporary.
A popular belief nowadays (proposed by Dr. Dennis Wilson) has not been proven to be true, and much scientific evidence tips the scales in the "false" direction with regard to this idea. The belief is that the process involving impaired T4 to T3 conversion—with increases in reverse-T3—becomes stuck. The "stuck" conversion is supposed to cause chronic low T3 levels and chronically slowed metabolism. Some have speculated that the elevated reverse-T3 is the culprit, continually blocking the conversion of T4 to T3 as a competitive substrate for the 5’-deiodinase enzyme. However, this belief is contradicted by studies of the dynamics of T4 to T3 conversion and T4 to reverse-T3 conversion. Laboratory studies have shown that when factors such as increased cortisol levels cause a decrease in T4 to T3 conversion and an increase in T4 to reverse-T3 conversion, the shift in the percentages of T3 and reverse-T3 produced is only temporary.
Oh, if you want a good interpretation of thyroid hormones, don't go to a doctor! They know nothing about it.
Well, you didn't answer about the antibodies, so we still don't know if you have Hashi's.
Also, sorry if you've mentioned this somewhere else and I missed it, but do you always have your blood draw at the same time of day? Do you always fast and leave a gap of 24 hours between your last dose of levo and the blood draw?
yes, as stated in the first post - I was diagnosed with Hashimoto's 2016 - due to raised antibodies - however, antibodies dropped to NHS "normal" levels ( both are under 10iu) for the last 3 years and stayed there so unless we know an autoimmune flare can be occurring without any measurable increase in antibodies - then it seems odd that the last TSH reading should be high ( as high as when i only took Levo and no T3 at all) with no accompanying raised antibodies.
also as stated - i always have the blood draw taken at the same time of day - also always fasted state, always 12hrs from last T3 and no b vitamins for 2-3 days before each test just in case.
OK, just checking. When a thread starts to get long, one loses track.
Just because antibodies are low when tested, doesn't mean they couldn't have been high at other times. These levels are not all perfectly synchronised so that the Antibodies and TSH are high at the same time.
There is no direct link between TSH and antibodies. Antibodies are high just after an attack, when they come in to clean up the mess left behind. They DO NOT do the attacking. And, after an attack, the TSH will be low, following behind the Frees, which will have risen sharply. But the TSH moves slowly, and lags way behind the Frees. Then, as the Frees decrease, the TSH follows, and will be highest when the Frees are lowest - which is also when the antibodies should be lowest. But, they all move at their own pace.
So I increased the T4 from 50mcg a day to 100mcg a day and reduced T3 from 62.5 to 37.5mcg and waited 2 months to test
I think this was a big mistake. We only change one thing at a time, never both at once. Any changes to doses should be relatively small - usually 25mcg for Levo or even 12.5mcg when fine tuning, and 5mcg for T3. Retesting 6-8 weeks after each dose change. It takes time so it needs a lot of patience, it's frustrating, but it's the only way to get the right balance without missing our sweet spot.
yes, I do understand the principle of changing one thing at a time only - but my question is not so much around the method of dose changes - as ideas on the mechanisms that might explain such a change in TSH and to a lesser extent T3 in successive tests with no dose changes. rogue test?
autoimmune activity? though my antibody titers have been extremely low and stable for years in around half a dozen successive tests - and I would have thought this would be a fair indicator of the level of thyroid damaging activity .....
I think we may have our wires crossed here - the question I had is about why would the levels on my test be varying widely in the last month when the last change was over 3 months ago, irrespective of whether we think that change was a good idea or not.
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