Higher cortisol levels reduce TSH (through the effect on the hypothalamic-pituitary system). A reduced TSH does two things:
- For those patients with working thyroid tissue, lower TSH will decrease thyroid hormone production.
- Lower TSH also reduces T4 to T3 conversion, resulting in even less T3 (active thyroid hormone)
Lower cortisol levels increase TSH. An increased TSH does two things:
- For those patients with working thyroid tissue, higher TSH will increase thyroid hormone production.
- Higher TSH also increases T4 to T3 conversion, resulting in even more T3. Studies have found that in severe cortisol deficiency, the TSH and FT3 are often high. Cortisol (HC) supplementation in these people, normalises the TSH and FT3.
We do know that cortisol and T3 are both required to increase mitochondrial energy production. So a lack of cortisol is likely to reduce T3’s effectiveness in the mitochondria. But there are probably other mechanisms at work, yet to be discovered
T3 and cortisol both need to be at good levels. Cortisol increases T3-effect, and T3 increases cortisol-effect – they are in a partnership within the cells. T3 helps to keep cortisol levels up as it stimulates the hypothalamic-pituitary system more than T4. This latter point is why thyroid medications that contain T3 help to keep cortisol levels higher. Low cortisol is very common in thyroid patients, as many have lower T3 levels during the day and in the night than they had when they were well (for reasons I have discussed in my books and in various other blog posts). For all the reasons above, it should be clear that with low cortisol, T3 does not work as effectively as it should do. High cortisol also causes problems and can reduce the effectiveness of T3 within the cells, hence thyroid patients with high cortisol often complain of feeling hypothyroid even when they appear to have reasonable FT3 levels.
However, I know of no evidence whatsoever that T3 is less able to enter cells when cortisol is low. That would require low cortisol to affect the T3 transporter molecules in the cells’ membranes. There is no evidence that low cortisol does this, and I do not know of any researchers who believe this (and I have spoken to some about this specifically). I stated this clearly in the first edition of Recovering with T3. I said that cortisol was not required to allow FT3 to enter the cells.
If someone comes to me and says that their FT3 level seems quite good or high, but they are not feeling well still, it simply means that there is another problem that needs to be resolved. If low cortisol is behind the problems, it can result in slightly higher FT3 due to the mechanism that I have described above.
The bottom line is that a high FT3 on a T3 combination treatment is not unusual, and this does not mean the T3 is not getting into the cells (‘pooling’ as some people call it). The T3 is still getting into the cells. The issue is simply that having enough FT3 is no guarantee that metabolism is going to work correctly. Many other things need to also be right, including the cortisol level, as T3 and cortisol work synergistically.
As I stated in the opening paragraph here, low cortisol does have some effect on raising TSH, which also increases T4 to T3 conversion. So, people whose cortisol is low may get a small amount of extra FT3 from this. But their cellular FT3 will also be a little higher too. It isn’t that the T3 cannot reach the cells.
When someone is still not feeling well, and their FT3 levels look good to high, it could be assumed that T3 is not getting into the cells. There are many reasons for metabolic rate not to be correct, including low cortisol.
However, low cortisol does not prevent the entry of T3 into the cells. The ‘pooling’ concept may scare some patients to rush into cortisol supplementation because many thyroid patients have come to associate this word with low cortisol issues. Yet, there can be many reasons for thyroid treatment not working. Yes, these need to be resolved. However, the reason for thyroid treatment not working is not always low cortisol.
A good FT3 level does not mean the T3 is not available in the cells – it will be. I have written about many reasons for thyroid treatment not working properly in my latest book, The Thyroid Patients Manual. Please see:
https://paulrobinsonthyroid.com/the-thyroid-patients-manual/ for more information on the book.
If someone is on too much thyroid hormone treatment, but it is not working well, and the issue that fixes the problem is resolved, they can feel hyper-thyroid. This is not a sudden rush of FT3 into the cells – the FT3 is already there! It is simply that they were taking too much thyroid hormone, to begin with. The issue that has been resolved has simply allowed the biologically active T3 to do its job.
It is important to not rush into using synthetic cortisol (HC, Cortef, adrenal glandulars), as soon as thyroid treatment is not working and FT3 appears to be good-high. Cortisol needs to be tested fully (cortisol saliva testing and an 8:00 am morning cortisol test), and other vitamins and minerals need testing – see The Thyroid Patient’s Manual for details on these.
The word ‘Pooling’ has been used a fair amount on the Internet. However, there is no evidence to support this idea. It is just another Internet myth that has been spread for too long. 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.
To make matters even clearer, there is new research as of 2021 that has actually tested whether hydrocortisone has an inhibitory effect on T3 transport into cells. They discovered that LOW doses of hydrocortisone do not inhibit T3 transport into cells via the MCT8 transporter, but HIGH levels do inhibit T3 transport into the cells. Also, Dexamethasone, a steroid that also activates cortisol’s receptors, is more potent than hydrocortisone as an MCT8 transport inhibitor.
These recent research findings confirm that the ‘pooling’ idea is incorrect. The research is saying that high cortisol levels actually prevent some level of T3 transport into the cells and that low levels of cortisol do not do this. See Cosmo et al, 2021: “Dexamethasone and Some Commonly Used Drugs Inhibit MCT8-mediated T3 Transport in Vitro.” This might go some way to explaining why some patients with low cortisol do not respond well to hydrocortisone, as it might inhibit T3 entry into the cells.
I hope you found this helpful.