Today I stumbled upon an interesting thing: T3 pooling, most often caused by low (sometimes high) cortisol levels.
The reason I stumbled upon it was because, our of sheer desperation, I decided to go down the t3 only route after reading several articles about rT3 dominance and, lately, "The paleo thyroid diet" by Elle Russ who basically got her life back on T3 only.
I have to stress right away that I have to self-diagnose and -medicate most of the time. What I do know is the following: for the past year or so, NDT has worked less well for me. I have had troublesome symptoms of both hypo and hyper.
I did well on NDT for years and thought I had found the right treatment for me when things suddenly started to change for the worse.
I have tried to self-medicate with T3 only and felt awful. So, I have concluded I do not have rT3 dominance.
No, I do NOT advocate self-diagnosing or -treating, I believe this should only be used as a last resort. But, sometimes, you have no choice.
Looking at my most recent labs, I can see that my Ft4 levels are at the very bottom of range on NDT, my FT3 levels about 75% through range, and my TSH (useless, granted) completely suppressed (<0.01). I have read a lot about rT3 dominance, and it seems those who suffer from it and have treated it successfully (anecdotal evidence) have had HIGH/over range FT4 levels. Mine are quite the opposite - at the very bottom of range.
So, low or very low FT4 levels do not seem common in people suffering from rT3 dominance.
Then, I stumbled upon an article about T3 pooling, and I realised ALL the symptoms described match mine: feeling hyper and hypo at the same time, having FT4 levels at the bottom of range, and highish FT3 levels, yet displaying hypo symptoms along with symptoms such as racing heart and anxiety. The most troublesome symptom in my case has been weight gain (+30 kilograms in less than a year).
It seems the most common cause of T3 pooling is low cortisol, but high cortisol and/or adrenaline levels can also cause this condition. What strikes me is that I felt worse when I tried T3 only, and people with T3 polling need to lower or even go off T3 completely until they have solved the underlying problem(s). Easier said than done, of course...!
I'm sorry to tell you this, but neither T3 pooling nor rT3 dominance really exist.
T3 has a half life of 24 hours in the blood. So, it doesn't stay around long enough to pool.
rT3 only stays around for about 2 hours before it is converted into T2, and then T1. And, it is inert, so not likely to make you put on weight.
What you could have is thyroid hormone resistance, meaning that even though you have good levels in the blood, it's not getting into the cells and therefore you stay hypo. And, all you can do about that is take extra large doses of T3. Sorry.
Yes, well, that's STTM for you. There are a lot of wrong things on there. To be taken with a large pinch of salt!
"I did well on NDT for years and thought I had found the right treatment for me when things suddenly started to change for the worse. "
"...I have tried to self-medicate with T3 only and felt awful."
I've read of others on here that this seems to happen to. You go on happily on a certain dosage of Levo, NDT, or whatever, maybe for many years and suddenly everything seems to go haywire. I suppose our bodies change as time goes on, or something triggers it.
I don't know much about taking T3 (I'm still Levo only and still trying to find the optimal dose) but I would have thought that Low T4 and highish T3 meant that you needed to add some T4 to your NDT, not suddenly go T3 only.
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Yes, that is what I have been thinking too...!
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T3 is much more powerful than levo, and more difficult to get adjusted to suit. If you went T3 only from taking a combination it's no wonder you felt ill. At least from what I've read. Our bodies take a long time to adjust to even a tiny change.
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Thanks, I could not agree more...!!!
Reasonably high T3 and low T4 seems to suggest you are converting T4 to T3 OK but the supply of T4 is too little to convert enough for your needs.
At least I think it does. greygoose does that make sense?
Could you post some recent test results (TSH, T3 and T4)? That may help to understand what is happening.
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I think that is true for people on T4 only drugs, but hardly for people on NDT...?
Anyway, here are my labs from last week, on 3 grains of NDT (ref ranges in brackets):
TSH 0.01 (0.2-4-2)
Free T3 3.4 (1.7-3.7)
Free T4 0.7 (0.7-1.5)
anti-TPO 11 (<6) when diagnosed with Hashi's in 2001 6333 UI/mL
anti-thyroglob 15 UI/mL (<4) when diagnosed with Hashi's 449 UI/mL
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It does seem as if you need either an increase in NDT or some T4 added
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Just curious: how can you tell if someone is converting T4 to T3 reasonably well but that the supply of T4 is low when someone is on NDT...I thought it was impossible to tell what comes from conversion and what comes from the drug itself once on anything containing T3?
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Sorry, no idea. Hidden Forgot that you are on NDT. Probably you can't tell in that case xxxx
I'm failing to find the Paul Robinson quote that I wanted to post for you; so meanwhile, here's this:
The word 'Pooling' has been used a fair amount on the Internet. However, there is no substantive evidence for any real pooling. It is just good-high FT3 levels that are not being effective, for one reason or another. It is misleading term that different people interpret in different ways (sometimes in a rush to use hydrocortisone/HC). If I could be given $1 or £1 for every person that spoke to me and said, "I have been told I am pooling, and need to begin using hydrocortisone", I would be a rich man. What is always important to focus on is what is stopping a treatment working, fixing it, and getting the treatment to be successful.
Hidden I've now found the quote from PR that I was looking for, regarding the myth of pooling:
I think as soon as someone sees a moderate (mid range) or high (top of range or above) FT3 result and the person doesn't feel like running a marathon or three then they shout "you are likely to be 'pooling'". Well, that is a simplistic analysis and often wrong.
How can anyone tell that someone's T3 is not getting into the cells? Do they have a cell-wall-T3-o-meter? No they don't. They are ...... what is technically called...... guessing.
Anyone who takes T3 or who takes a fair amount of NDT will have decent to high levels of FT3 in the blood. This looks higher depending on the time the blood draw is done.
My FT3 is around 9. With a reference range of 3 - 6 approx. So .... am I 'pooling' ? .... well, some would say so .... but I am not.
No one can tell if pooling happens, or doesn't happen. No one can tell if someone is pooling at all. I am not even sure if it even exists.
What I do know is that people can have good looking FT3 results and still be hypo, because the signs and symptoms say they are. The reasons for some people remaining hypo (with cells that don't metabolise at the right rate due to thyroid hormone that isn't active enough) are MANY.
I listed 20 of these in the second book and numerous in the first (blue book).
Low cortisol can be one. It doesn't cause 'pooling' it just limits ATP generation through low glucose presence in the cells. Low iron, low B12, infections, gut absorption, high immune system activity are a few others. The list goes on.
No one can look at an FT3 result and conclude a damned thing re: 'pooling' or 'not pooling' .... It is a wholly redundant concept as far as I'm concerned. It doesn't help fix anything or determine a suitable treatment.
What is important ..... as always ...... are the signs and symptoms - they tell us whether the person is improving or not. At the end of the day that is the only thing that counts.
Some people need to get their T3 intake to a high level before they begin to feel well. These people (if they ever do an FT3 blood test) might find that they have high FT3. Some people might get well on T4 only, or on NDT, or on low doses of T3, and have FT3 levels in the middle or upper half of the reference range for FT3.
If we believe the idea of 'pooling', then any FT3 that is high might be assumed to be pooling. Clearly that isn't the case.
I just don't think measuring FT3, or any thyroid labs, is helpful when trying to manage T3 only dosing. The doses themselves need to be managed well, signs and symptoms need to be assessed, and other labs may well need to be done, especially if the person doesn't respond to treatment.
The notion or idea of 'pooling' has never helped me once in dealing with anyone using T3. I think it is an unhelpful idea.
"I just don't think measuring FT3, or any thyroid labs, is helpful when trying to manage T3 only dosing. The doses themselves need to be managed well, signs and symptoms need to be assessed, and other labs may well need to be done, especially if the person doesn't respond to treatment."
This helps to finally ameliorate my concerns about the much over range FT3 test result I received this week. I have RTH, my dose is 112.5mcg T3-only, assessed daily, still symtomatic but much less so ...and been somewhat concerned about a further increase.
Time to add another 6.25mcg me thinks!
A few more miles still to go over the humps and bumps of this thyroid journey!
Thanks for posting. I can see why this document looks quite feasible at first glance. Sadly, it is an appalling document, for many reasons.
I haven’t studied the role of cortisol in thyroid hormone action but some simple common-sense observations make this theory very unlikely. We would expect clinicians to have noticed severe thyroid dysfunction in patients with normal thyroid hormone levels and Addison’s Disease or Cushing’s Disease. Also, whilst there is very considerable diurnal variation in cortisol levels, about 3x as high early morning, we do not see a corresponding change in thyroid hormone activity.
The statement that ‘pooling’ is: ‘free T3 isn’t making it well to your cells’ (sic) is just plain silly. There is a very rare genetic condition ‘Allan-Herndon-Dudley syndrome’, a disorder of the MCT8 cellular transport protein that causes very severe hypothyroidism. However, any condition that stops T3 getting into cells will stop it getting into the hypothalamus and pituitary and thus lead to very high TSH levels. We should note that provided the patient is not taking exogenous hormone, all their T3 comes OUT of cells (as well as entering other cells). T3 is made in cells and converted from T4 in cells. Even a minor impairment of T3 entering cells will push up TSH, unless you can provide an explanation as to why it doesn’t affect pituitary cells.
The statement rT3 is ‘competing for the same cell receptors as T3’ is wrong. rT3 is inactive (as far as is known), it does not bind to thyroid hormone receptors. It does not block the action of T3.
The recommendation to take hydrocortisone or adrenal cortex is dangerous, it can lead to dependency on exogenous hormone and adrenal insufficiency. (I would exclude the treatment recommended by Dr Barry Durrant-Peatfield in this respect as he advocates very low doses. I don’t feel it’s of any use, but it is relatively harmless).
Whilst this blog is well intentioned it does much harm to the cause of thyroid patients. Unfortunately, an optimum way to get a good Google ranking is to write a regular blog and get lots of hits. This ranking may be desired for personal or business reasons but clearly it leads to a temptation to produce ‘copy’ on a regular basis, articles which may not be adequately researched.
I'm sorry, but would you care to elaborate on the following statement:
"The recommendation to take hydrocortisone or adrenal cortex is dangerous, it can lead to dependency on exogenous hormone and adrenal insufficiency. (I would exclude the treatment recommended by Dr Barry Durrant-Peatfield in this respect as he advocates very low doses. I don’t feel it’s of any use, but it is relatively harmless)".
I've read Dr. Peatfield's book, and he recommends 5 mg of prednisolone daily which is the equivalent of 20 mg of hydrocortisone. So a physiological dose - which would be all that is required under normal circumstances.
Do you have any scientific proof that PHYSIOLOGICAL (not supra physiological/therapeutic) doses of HC (or the equivalent doses of prednisolone) or adrenal cortex will shut down the adrenal glands for good?
My comment wasn't that clear. The dose recommended by Dr Peatfield is physiological, it can still create a dependency and a need for careful weaning off. The danger is that patients will take more, especially if in the form of 'glandulars' which tend not to have verified amounts of hormone. It also seems undesirable to take over the job of the adrenals as you want to keep them working, demands can vary substantially such as during illness. The reason I excluded Dr Peatfield is that in his presentations he always emphasized that low doses should be used, others are more vague. It's just possible that 'adrenal support' has some value (other than placebo) but unfortunately the proponents have been reluctant to carry out prospective placebo controlled trials. My impression is that other good thyroid doctors have had equal success without telling every patient they have 'adrenal fatigue'.
Doctors working with prednisolone or HC for adrenal fatigue, like Dr. Peatfield and also the Hertoghe doctors in Belgium, claim that doses up to 40 mg of HC, 10 mg of pred, or 8 mg of Medrol daily are considered safe. But I think that can turn out to be too much for some.
Although I doubt it will suppress adrenal function completely for good, I suspect it can leave the adrenals struggling in some patients who have taken so called physiological doses of prescription drugs for a long time, leaving them at least partially dependent on adrenal hormone replacement. I seem to recall Dr. Peatfield at least only recommends them for short-term use, but I know of Hertoghe doctors who prescribe them continuously.
Not sure about adrenal cortex/glandulars...do they contain enough hormones to suppress one's own adrenal glands? If that were the case, wouldn't they have been banned by now?
My feeling, and it's based on instinct rather than research is to only treat adrenals if there are signs of adrenal insufficiency. They can fail after long term severe hypothyrodism but I've never seen a comment on the fora about someone suffering such an effect.
Adrenals are highly reactive organs, they respond very rapidly to situations and it seems unwise to replace a hormone and thus partially shut down natural production (although not permanent).
A long time ago I looked for studies that measured cortisol, adrenaline and noradrenaline levels in hypothyroid patients. There were very few, quite old, but they tended to show levels were above average, probably because of reduced clearance. So, perhaps some hypothyroids have impaired adrenal function with good or even slightly elevated chronic levels but an inability to respond to sudden demands for high adrenal output. Unfortunately, chronic replacement therapy is likely to make this worse not better. The only solution is to treat the hypothyroidism and in a few very rare cases of adrenal insufficiency identify and treat it.
One thing I find interesting in this context is the supplement Thyroplex (man and woman) formulated by an anti-aging doctor who claims this product counteracts the age-related hormonal decline. It contains 1/4 grain of thyroid, 200 mg of adrenal glandular and 50 mg of either ovarian or testicular tissue (bovine). While it’s true that sex hormones decline with age, and thyroid hormone levels also maybe, I have never heard that adrenal function declines with age, at least not to the point of needing to take glandulars (it’s specifically pointed out that this product is intended for people without endocrine disease).
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