I've reposted as I got confused over my readings and then have been talking to people through different posts. So thought might be good to start again.
I have no ferritin or B12 results as they didnt do them. Im waiting on vit D which was 17.9 two years ago ( very low, to osteoporosis point) (I also have previous B12 and ferritin results if any use). But my biggest problem is calculating the ratio of my FT3 and RT3 as the units of measurement are different. I have used both the STTM ratio converter and script essentials which do no have pmol/mL as an option.
My results:
TSH: <0.05 (0.15-3.2)
FT4: 15.8 (9.9-20.1)
RT3: 0.40 pmol/mL (0.14-0.54)
FT3: 6 pmol/L (2.7-7)
TPO: 267 (<35)
The RT3 is in mL not L and this is not a choice on STTM or scriptessentials. So I converted mL to L which gives me 400 and thus a ratio of 0.015. So what does this mean? I must be very bad I can only assume. Please help!
Thanks
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BexyLS
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Bex, if you go to the STTM ratio finder and put the figures in and then go back to the unit of measurement, you can put ml in one and L in the other. I think I tried a couple of times but It still comes out to 15.
Bexyl, I am sorry I cannot help at all with reverse T3. This is an excerpt from a link from Dr Lowe and, as far as I understand it, the reverse T3 rectifies quite quickly or, in illness, within 3 to 4 weeks.
If others have a different viewpoint, they will advise you. Go to the second question/answer. Extract:
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.
You rt3 is high, reguardless of what the ratio is. I have had consistently higher levels of rt3 for the past 13 months... my cortisol is on the low side. As much as i like Dr. Lowe, i am one of those who has a continuous issue. Inflammation can cause high rt3 levels..so many things can.
I'm not sure you can compare rT3 with fT3. I don't know but I assume rT3 is a measure of TOTAL reverse T3 but it doesn't tell you how much is free. Total rT3 is consistent with your result of 400 pmol/L. I don't even know if rT3 is bound to transport proteins like T3 and T4 are. I've read that rT3 binds to receptors like T3 does and so inactivates the receptors. I dont' know of any study of the relative binding potency of T3 and rT3. It does seem that rT3 opposes the effects of T3 but to what extent? Does anybody know?
It would be helpful if the labs reported it as frT3 or trT3 so we know if it's total or free. Perhaps you could ask the lab exactly what the figure measures. This would be a useful starting point for all of us.
It's known that rT3 is produced from T4 by type 3 deiodinase (D3) which increases as fT3 increases. More to the point it is known that type-1 deiodinase (D1) produces equal amounts of T3 and rT3. D1 increases with increasing levels of fT4, thus if fT4 is high D1 mitigates hyperthyroidism by producing more rT3 and less T3.
What I'm getting to is that I can't see the point of assaying rT3 until someone knows what the number means and can quatify its effect on thyroid hormone action. Of course high rT3 with lower fT3 suggests less thyroid hormone activity, but you will already be aware of this from your symptoms. I'm just suggesting we do not waste our money on this assay as so little is understood about rT3 at the moment.
A tiny fragment more information about rT3 that I accidentally fell over this evening. And it has still not percolated by brain what it all adds up to!
I've seen this abstract before and had the good sense not to bother with it!!! It looks at the activity of deiodinases and the thyroid hormone receptor mRNAs released in the endothelium and comes up with some surprising results. However, I don't think it matters much. Other research looks at the effects of deiodinases on levels of T3, rT3, T4 in the blood in response to levels of T3, T4 and TSH. This will involve the sum total of all deiodinases that affect blood levels of thyroid hormones and so I think give a much better overall picture.
Also we can't be absolutely certain of the role of intracellular deiodinase (D2), although I believe most of the T3 produced by D2 will spill out into the blood and so the blood test will give a reasonable indication of D2 activity. (Endocrinologists will tell you that the fT3 assay is meaningless because you don't know what is happening in the cells. If you say you might be hypothyroid in spite of normal hormone levels because you don't know what is happening in the cells, they will tell you that is not possible. Go figure.)
I don't think this reseach paper is of much practical value, it's really of academic value, at least until our understanding of thyroid hormone action has moved on a great deal.
I think it has practical value in as much as it enlightens Endocrinologists to the fact that you can be hypo at cell level while this does not manifest itself at blood level. This might result in a few more Endos understanding this fact and not leaving it all to the patient to convey this phenomena via his symptoms alone.
I haven't tried finding this paper, I think it is too obscure. Many organs have both deiodinase and all have receptors (I think all), so I'm not sure what the paper could add in practice. Bear in mind that we will have had these capabilities since birth (and to some extent before). Consequently, any thyroid problem that came along after birth is unlikely to be related to the contents of this paper.
The bit I did get from it is that different thresholds were present for the regulation of the different types of deiodonase but then Abstracts are (effectively) written by journalists at the journals, the real content is more largely written by researchers. I have met resarchers who complained bitterly of journalists insisting on abstracts that were contradictory or meaningless due to the desire to 'sell copy'.
I was already well versed on the 'interaxis circuits' in the Pituatory that make TSH unreliable, some recent stuff I have been reading on the de-iodinases and receptors gave fruther solid science to challenge that assumption. I would like to know much more about the science around the number of DIOs present in serum alluded to by this paper.
@Bexy- I think there's something wrong with your reported units -as such a high inverse ratio as you show would not have RT3 showing in range. The FT3 figure is OK.
There are so many different units to use for this -no wonder Docs veer away like wildfire!
You are right, the units are wrong. If we plug in the given values we get 4.0/408 which is absurd. This would be ~0. The result, in whatever units you use (so long as they are the same) should be >20.
This is not true for the TT3/TT4 ratio (another story) in that so called "ratio" they use TT3 in pg/mL and TT4 in mcg/dL. That is an historical "thing" they just use the units in which they are typically and have always been measured. So it is not a true ratio. (And nothing to do with Bexy's problem!)
The lab report should indicate the units. One has simialr issues with US vs UK reports for blood metabolites. rT3 can be reported in mg/dl, ug/l or mmol/l. It's always best when giving results here to state the units for that reason.
This is a fair comment, Jim- But! all the info on RT3 implies it is a serious problem existing to produce high levels. Illness, trauma or even ,dare I say poor thyroid function.
Because everything is not known about it doesn't make it useless to know.
Why are you more concerned to save people's money rather than advance understanding on RT3?
The more testing and enquiring that goes on the better as illustrated by many useful posts and tips on just this site.
I agree Trev, this ratio like many others should be reported by the Lab itself. They will then take account of the units they use for each metabolite and will give a normal range for the ratio too. So often with labwork, ratios are as useful as the actual metabolites. One can have two 'normal' results but a downright nasty ratio between them.
Maybe a good start would be to see if rt3 is high in range- with ft3 below halfway would indicate imbalance.
Taking thyrioid meds, of course, disrupts daily homeostasis -esp. T3 which shows up in a few hours.
One reason T3 is so effective, where needed- but medics seem transfixed by numbers and basically tend to hide lack of knowledge with the usual hints of increased age, lack of good lifestyle or depression.
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FT3/rT3
Does rT3 always have to be bottom-range in order not to have an rT3 problem?
FT3/rT3 ratio = 0.2 Not sure what this means
Is there any point in testing for rT3, fT4,fT3?
