Hi. Did anyone experience pooling T3? Was it due to high or low cortisol? How did you level your cortisol? I heard that magnesium is good for it.
I believe I'm pooling T3. My level in the blood is over range, but I don't think it's going to the cells as I'm not feeling slightly better for the moment, and I've read that it could be due to high cortisol. Any advice?
No such thing as pooling T3. That is a falsehood put about by mainly functional doctors who don't have the necessary expertise in the subject. Half of any T3 is lost in 1 day, and is either made up in health from T4 made by the thyroid or T4 (in those who can take it and maintain health) by mouth daily.
Oh. I got that information from STop the thyroid madness page. I thought it was a thing.
Yes it's one of those myths originating in the mists of time which has been absorbed in such sites as you quote as a given, when it isn't.
Desperation 😢
Do you have a better explanation/definition for inordinate levels of FT3 and not the corresponding elevation of metabolism?
In what circumstances of treatment (T4, T3 or combination)?
High FT3 can occur in either of two ways. One is that the patient is taking too much T4 or T3 or combination. The other is the rarer situation of T3 resistance, where there is a lack of receptors in the cells, so FT3 level has to be higher to get enough in for normal metabolism to work. This is like a doorway. A broad doorway lets people in without any crush at the entrance. A narrow one inhiibits passage so the crowd trying to get will be larger.
So you would suggest that she would feel better with an even larger dose of T3 unless she is already taking too much now.
And you don't think she is thyrotoxic with her symptoms.
I think we need more information and lab results.
A little common sense will show that 'pooling of T3' and 'T3 not getting into cells' is nonsense. Apart from T3 in tablets ALL T3 comes from cells. A lilttle T3 is made and secreted from thyroid cells, more T3 comes from diodinase which takes place in cells. The T3 has come out of cells and no doubt can go back in. If T3 was not entering cells TSH would go massively high as T3 would be unable to enter the pituitary or hypothalamus cells.
Hi Hypo, I've asked diogenes what he attributes to this situation. Can you tell us what you are taking for your thyroid condition assuming you are hypo? If you are taking T3 I would assume you might lower your dose so that is probably not the issue unless you decided to
add T3 to your T4 recently.
nahypothyroidism.org/thyroi...
When there is an excess of Reverse T3 in one’s system their metabolism slows leaving them feeling sluggish and tired. To counteract this, the body releases cortisol, also known as the stress hormone, to increase alertness and energy.
nahypothyroidism.org/thyroi...
Hi Heloise, I have been in NDT since September, as I saw a dr who said I was low in T3, and changed back to levo and added Cynomel 25mcg since mid January as NDT was too expensive. I was born without a Thyroid gland. I'm also taking vit D and K2, plus b complex. Also recently started magnesium (only a couple of days ago). I just don't feel any better considering my blood levels, and I'm trying to find the bottom of it.
Thank you Hypo,
I've listened, read, watched videos and other information about thyroid treatment for years. To tell the truth I think there is not total understanding of how the adrenal/thyroid coordination works. We do know that when the thyroid or metabolism is low, the adrenal gland has to step in otherwise ALL your energy goes down the drain.
So your adrenals start producing cortisol and adrenaline to keep your organs functioning. So usually the body compensates to protect vital organs first.
The important thing is probably not that your FT3 is too high but why you are feeling poorly in spite of it. Energy is produced through glycolysis so there may be a connection since we know we don't burn calories as we should with low thyroid.
I've been trying to look at this situation from more of a holistic view, heal the gut so it can produce all the nutrients your body needs. We are most likely overwhelmed with toxins which really can start with constipation (another element of low metabolism).
So we should start there. Magnesium can help with that and so many other processes so take good amounts.
Do you know your results from Dec. and later ones after making the switch? Did you reduce one grain of NDT when replacing with 25 mcg T3. Is it possible you are overdosing T3?
Hi. Yes my results are on my previous posts. I just changed straight from 3 grains to 125mcg levo and 25mcg t3 which is about the equivalent. My levels are now higher, because I increased my Levo to 150mcg as my t4 was at the lower part of the range but my t3 was 75% in range.
I looked at your other post. I know it's so difficult to analyze because of a million factors. First, your FT3 level at 7.7 isn't really exceptionally high, it's barely one point but as gg said, twelve hours is a long time for T3 to dissolve.
Were you doing very well on 3 grains?
Actually your T4 was perfect at 19.8.
Honestly, Hypo, I think your results look very good. Maybe your increase to 150 of T4 will work out in the end. That takes a couple of weeks to tell. But even that dose is not quite equivalent to your 3 grains. I go by the ratio of 100 mcgs T4=25mcgs T3.
Hi Heloise. Thank you very much for your insights and for the thread of information you have provided. I was doing ok, not great, but ok on 3 grains. Mainly mood wise. I have changed back to synthetic because I probably would have need to increase my NDT and it's just too expensive. The NDT contained 38mcg T4 and 9 mcg T3, so I based the conversion to synthetic from that. I increased the levo to 150 as my results from January showed lower t4 with above mid range t3 and wanted to see how much t3 I was converting naturally. I will leave the dose as it is for the moment, and keep taking my vits and magnesium and check again in 6 weeks. Thank you so much again.
i would strong urge you to ignore the nahypothyroidism website it is full of errors and misleading, it is not a National body or an academy in the usual sense of the word.
Specifically, it claims 'Reverse T3 and T3 compete for the same receptors throughout the body'. This is not true, reverse T3 does not bind to thyroid hormone receptors. Neither does it 'block active thyroid hormone from reaching cells'. As far as I know rT3 has no effect on T3 or T4 reaching or entering cells. 'Not only does it block receptor sites' - rT3 does not bind to receptors and so does not block them.
There is some evidence rT3 might inhibit type-2 deiodinase (D2) but I think this is inconclusive.
Nobody really knows how to interpret rT3 results and certainly not how to use it to diagnose the underlying condition. The NAH website will offer you an expensive rT3 assay.
Incbi.nlm.nih.gov/pmc/articl...
In this regard, the type 2 deiodinase (D2) catalyses T4 to T3 conversion and increases intracellular levels of T3 potentially leading to local thyrotoxicosis.
Is that overconversion with D2? Some have lowered doses of T4 and improved.
I don't know what either of those looks like in an FT3 test, do you?
The opposite is observed in cells expressing the type 3 deiodinase (D3), which depletes the cell of T3 by deiodination to T2 and can cause local hypothyroidism.
This is an excellent paper. In practice I think it would be very rare for D2 to lead to local thyrotoxicosis, certainly in people who are not taking thyroid hormone. If you lower your dose of L-T4 TSH will rise and stimulate D2 activity thus increasing local T3. I think this is why reducing L-T4 can help hypothyroid patients, especially with brain function. (When I use phrases like 'I think' or 'I guess' I intend to express uncertainty).
I believe D2 activity is reflected in the fT3 blood result. This is because I've noticed that patients who have a subnormal TSH (lower than you would expect) not only have a low normal fT4 but also a low normal fT3. Other patients with a low normal fT4 usually have an elevated TSH and mid-interval fT3. We would expect the higher TSH to increase D2 activity and we see it reflected in the normal fT3.
This is in part contradicted by a recent study by diogenes team ncbi.nlm.nih.gov/pubmed/318... which suggests most of this extra T3 comes from additional T3 secretion by the thyroid. This is a very difficult study to follow and I've yet to read it properly. I still feel that a lot of the T3 we see when patients reduce their L-T4 is coming from D2. My guess is that T3 from D2 predominates when TSH is within normal levels and thyroidal T3 takes over as TSH goes high. Sorry if I've gone too deep, in short a reduction in L-T4 should lead to more T3 from D2 as long at there is enough T4 and the pituitary is functioning normally.
Too much D3 will lower T3 especially in those cells that express D3, mostly in the brain. Excess D3 activity will also increase reverse T3 levels. Apart from taking too much T4 this can also occur in servere illnesses such as burn injury or cardiac arrest.
We're drifting away from the 'pooling' concept which doesn't exist!
Your surmise; it all depends on whether the patient has some working thyroid or none at all. In the first case, if TSH hasn't risen, D2 will still be the predominant factor in converting T4 to T3. But as the thyroid wanes in activity producing T4, then there is a corresponding rise in TSH which both inhibits the D2 activity because there's less T4 to convert, but is closely balanced by the thyroid's T3 output direct being raised by the higher TSH stimulation. The two nearly balance each other. When the gland is dead or nearly so, the whole balancing act goes and exogenous T4 has to take over. Note I am not making statements about the AMOUNT of D2, merely its capability of conversion given limited T4 substrate.
Yes, I would agree fully. The rate of D2 activity will increase with TSH but if there is little T4 there will be insufficient T3. It would be nice if more work was done on patients without a thyroid, an ideal opportunity to see how deiodinase works. The mechanism seems to work very well for maintaining serum fT3 levels. It might not work so well in the brain which is mostly dependent upon D2, brain T3 is not visible in blood tests.
My particular interest is what happens when TSH is subnormal i.e. the pituitary produces less TSH of less potency than it should, perhaps because the axis is down-regulated. This will mess up both serum T3 and T3 in tissues that rely on D2.
Patients treated with L-T4 (especially those without a thyroid) will have a higher fT4 / fT3 ratio. The standard approach is to give them a little more L-T4 to bring their fT3 back to normal. However, this will reduce their D2 activity and so perhaps render D2 dependent tissues hypothyroid. I believe this is so and such patients experience brain hypothyroidism with symptoms such as brain fog and sleep disturbance. I feel these patients need some T3.
When I have time I will try and lobby some research teams to carry out sleep studies on athyroetic patients receiving L-T~4 monotherapy. If this is causing brain hypothyroidism perhaps it will show up in sleep EEG traces. (Hypothyroid patients have less deep sleep than controls, so sleep pattern is a marker for brain thyroid status).
Yes, too deep for me, but I appreciate you analysis. And have we considered polymorphysms? In the end each patient will have to determine which thyroid treatment makes them feel better and I also encourage them to improve their gut health and hormone balance.
Hopefully research will keep making discoveries that explain all the dilemmas we face as hypothyroid patients.
And, ok, no pooling of T3!
My best to you.
D2 polymorphisms will make things a little worse but theoretically if you were to supply the same amounts of T3 and T4 as the thyroid produced the patient should be back where they were before they became hypothyroid. So, my view is that polymorphisms don't matter if the patient can get some T3. On the plus side this means that patients who do not have the polymorphism have almost as much need for T3 as those that do.
Forget all the complicated stuff the message is that 'pooling' doesn't exist and many patients need T3.
Also p for help to lower cortisol you can you aptogenic herbs such as ashwahganda, rhodolia, shatarvi or schissandra Berry extract 😊
Here's my 2 pennies worth:
There is no such thing as pooling. But you need an adequate amount of cortisol for the glucose in the cells to make energy. So you need enough cortisol and T3.
My experience with rT3 is this:
I am told that rT3 does not compete for receptors. But, the DIO3 that creates it can interfere with the effect of T3. And it all depends on the person. Eg... I was on 50mcg T4 and 30mcg T3. I wasn't doing great. In fact, my cortisol was the lowest it's ever been. (You need T3 to trigger the process to create cortisol.)
Because my TSH is suppressed, the DI03 gene is activated and creates the rT3.
So I've now dropped the T4 entirely. It's only been 3 weeks. But my blood pressure is coming back up (indicating more cortisol production) and I have far more energy.
Here is an article on rT3: thyroidpatients.ca/2019/11/...
That is the best explanation I've seen so far for why some people do better without T4.
Do you think there is a difference when the patient has had radioactive iodine treatment on their gland? Some have said they must take T4 for that reason.
Cortisol and insomnia
Cortisol
A little pooling
Genova cortisol saliva results 
