This is a post I did not expect to be writing, but I may be about to join the T3 crowd for good. This post is mostly descriptive, and is intended as an update, given my previous assertions that I am well on T4 alone.
Latest blood test showed a drop in fT3 to 5.1 pmol/L (3.1 - 6.8). This is despite my fT4 being maintained at a high value of 24 pmol/L (12 - 22). TSH is up to 1.7 mIU/L (0.27 - 4.2). This is not a significant change, yet the trend is concerning to me.
These results may be perfectly adequate for some patients, however my body is used to a rapid metabolism which has been present since birth.
For an as yet unknown reason, my ability to convert T4 to T3 seems to be declining. I will seek nutritional panels, however nothing has changed since my last set which showed good levels of D3, B12, and B9.
Furthermore, I still supplement with 400% RDA of Selenium (combination of sodium selenite and selenomethionine). Selenium deficiency is therefore highly unlikely.
Some symptoms such as cold intolerance and dry skin are returning, with some noticeable fatigue.
In addition to this, my twin brother (monozygotic, identical) has had a thyroid function test, he has no symptoms and his euthyroid blood test results thus serve as a useful baseline for where mine should be.
My brothers blood test results show his fT4 to be 18, fT3 to be 5.9 (same ranges and unit as above). To me this suggests that I need to reduce my T4/levothyroxine dose and introduce T3/liothyronine.
Thus, I am trialling reducing 75mcg of thyroxine per day, to once every 2 days, resulting in 37.5mcg.
In addition, I shall add 12.5mcg Liothyronine. With a suggested relative potency of around 3-4 times that of thyroxine, this should result in a total equivalent thyroxine dose of 75mcg, unchanged from my previous regimen. If the potency is closer to 4 times, then a slight increase in overall exogenous thyroid hormone will occur.
I am hoping to reduce my fT4 and increase fT3 to match that of my euthyroid twin brother.
I shall post an update in a few weeks time, but at present it seems I shall require combination thyroid hormone replacement.
It is notable that the origin of my hypothyroidism is not fully determined still. It is equally likely to be hypopituitarism (secondary) as it is autoimmune (primary).
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anonymous45
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How very useful to have an identical twin! You have a good plan there, I’m just not sure the tests are as reliable as you assume. They all have a margin of error, a confidence interval. Your results and your brothers could lie within the margin of error of each other’s test. I wouldn’t trust one test each, I’d want at least two, taken at same time of day under same conditions.
Also, we can’t assume that someone that is treated will measure the same as someone who is not ingesting hormone. And if either of you were incubating or recovering from another condition, or taking other medication this could affect the test results.
Thyroid balance is not a simple science, it’s a balance of science and instinct /experience. Giving too much weight to one or other can lead the wrong way (as many have discovered at the hands of medics who adjust to the test). However, I acknowledge that you also refer to hypo symptoms and these should definitely inform the decisions you take, as you indicate they are.
That’s a big drop in Levo you are planning. And you will probably feel the 12.5mcg addition of T3, if not straight away, then later. T3 can be a bit tricky to get right so not worth introducing unless you have to.
What do you mean by good levels of vits etc. They need to be optimal which I would expect to be better that good. Have you had folate and ferritin recently as well?
"Latest blood test showed a drop in fT3 to 5.1 pmol/L (3.1 - 6.8). This is despite my fT4 being maintained at a high value"
Maintaining your T4 level at a high value could be the very reason that your FT3 is dropping, in that there may be a reprioritisation of T4 conversion to RT3 over T3 in order to deal with that excess of thyroxine.
I don't know much about genetics generally and twin genetics particularly to have an educated view on your sibling's blood test results necessarily being the exemplar for you; but it is a fact that small changes in DNA can and do happen, so identical twins do have a few differences; and while they share the same genes, they sometimes differ in how these genes are expressed. You'll probably be more aware than I, of the research that's been done comparing gene expression in pairs of identical twins in which only one twin has a disease, and looking at how the environment or other factors interact with genes to increase disease risk. It could be that at a certain point in their lifetime, a twin with a disease got epigenetic modifications of certain genes that didn’t happen in the healthy twin, and of course, epigenetic changes can occur randomly or from environmental influences. So you are already different, you are the twin with the disease and your sibling is the one without. Even if you could guarantee that your euthyroid brother is entirely free of those small DNA differences and/or post-natal effects such that his thyroid blood test results now would have matched yours when you were euthyroid, you aren't euthyroid now and he is, you aren't disease-free, he is; so chasing his results may be fruitless and misleading (and presumably you don't know what your own results would have been, pre-developing hypothyroidism). Wouldn't it make more sense to adjust meds and optimise all aspects of your health, so that you feel well and are symptom-free, and let your hormone levels be what they need to be, as a person with hypothyroidism, for that to be the case.
My symptoms began several months after a serious illness that had me in bed with a high fever for around a week, despite ibuprofen and paracetamol.
Symtpom wise, my GP thinks it could have been viral menginitis or EBV. Either one can result in endocrine issues. That is likely the trigger in my case!
Hypothyroidism may of course, be triggered by illness (there can be both post-viral and post-bacterial thyroiditis for instance, from which can arise both temporary and permanent hypothyroidism); and additionally, non-thyroidal illness can trigger changes in existing hypothyroidism through the same mechanism I mentioned earlier, whereby there is an increase in reverseT3 as a protective response.
Firstly T3 does not suit everyone. Also gentle cardio exercise can counter periods of fatigue. I have a twin and they do not take T3.
T3 normally comes as 20mcg scored tablets, that are halved to give divided dose, to avoid T3 flare, hot flush, palpitations etc.
I would suggest opposite - a step by step change, as my consultant's practice; replace T4 by T3 in ratio 50mcg by divided dose of 20 mcg . BUT to begin with only take the early morning 10mcgT3 + 50mcgT4 (see what happens) and then after a couple of weeks introduce after noon (empty stomach) second half of T3. The objective is allow your tissues/organs to transition. T3 is more than 'more potent', also is similar in result to a stimulant. If you have an over-reaction, don't stop, instead try alternate days of T4+T3/original dose T4 and latterly alternate days of afternoon second T3.
So try exercise or diet changes / rule-out blood pressure or recent other medication changes first.
I engage in regular exercise and consider myself relatively fit, on good days I am able to do a lot without much fatigue, and do not have issues with body temperature or low heart rate.
On bad days, I have noticed a return of notable bradycardia, sometimes being as low as 40-45, my resting heart rate should normally be around 55-65.
I have not noticed a stimulant effect, but I do note an increase in appetite (good) and often greater warmth within a few hours of a T3 dose.
At present I am taking 6.25mcg (1/4 of 25mcg) in the morning, and an additional quarter in the afternoon if I feel my symptoms require it.
I realise that a big drop in T4 might induce more symptoms, however I am keen to reduce my fT4 more quickly as I have now deduced it is probably too high and is counter productive. Over the next 2 weeks, the existing fT4 in my blood will reduce by about half, and thus I can calculate the required equivalent days on/off to achieve similar to 50mcg until I get a change of prescription.
Depending on the outcome of my trial, I will likely ask to have my dose reduced to 50mcg and then retest all 3 hormones again after 6 weeks.
My blood pressure is on the low side only when I experience bradycardia, I am still investigating whether low cortisol is also playing a part, as I've had 2 largely contrasting morning serum cortisol tests, one about half of what it should be (235) and the other around 550 which is normal. However the normal test indicates that Addisons is unlikely, thus the query with my GP about pituitary involvement.
To further complicate matters, a slightly elevated prolactin and significantly low DHEA-S results adds hormonal elements to the puzzle.
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