I just came across this website that claims that
"it is useful to determine T3 and T4 in 24-hour urine for hypothyroid symptoms if blood levels are normal. This test can also be used to check the effect of an adopted therapy."
Has anyone heard of this before?
I have been wondering that myself. The doctors who order it claim that the 24 h urine analysis tells us how much hormones the body actually uses on cellular level, not just how much is available in the blood. That not only applies to thyroid hormone, but also cortisol, sex hormones, and growth hormone. Other doctors claim that 24 h urine analyses don´t tell us anything useful, so it´s not easy to know what to think...the doctors who tend to prescribe them are functional/integrative/alternative/anti-aging doctors who prescribe body-identical hormones. I find these tests prohibitively expensive so have been trying to find out if they are indeed necessary, but opinions differ...
This study states that it is an unreliable test:pubmed.ncbi.nlm.nih.gov/182...
As a standalone test, I wouldn't trust such an expensive thing.
However, I'm skeptical too. Maybe a new approach to understanding thyroid hormone metabolism and action and helpful in some cases (as long as my doctors don’t blindly obey the TSH-dogma I am fine with blood tests, so far).
Thanks for your thoughts.
I've never seen any evidence that urine levels of thyroid hormones are any better than serum measurement. Indeed, the urine tests are usually validated by comparison with serum levels! This link claims: "However, in practice, the level of T3 (and T4) in 24-hour urine shows better correlation with the symptoms, particularly in early stage hypothyroidism." without giving any evidence. I've never seen any study that compares the comparative link between urine and serum T3, T4 levels and symptoms. It's possible that someone with hypothyroid signs and symptoms who have normal serum hormone levels might have abnormal urine levels - by chance. The opposite could occur but it would be very unusual to measure urine levels, find they are normal and then measure serum levels.
There are many confounding factors. Thyroid hormones are eliminated by many routes, some T3, T4 is converted to metabolites such as sulphates, some is eliminated in urine and some in faeces. Logically one would have to measure total elimination by all routes to achieve a valid result.
T3/T4 (free or total) ratios, T3/rT3 (free or total T3) ratios are useless. They vary according to hormone levels. If our fT4 is high we convert less T4 to T3 (and vice versa). There are also genetic differences in individual ratios. More importantly it matters whether the T3 is coming from type-1 (D1) or type-2 (D2) deiodinase, the latter takes place near the cell nucleus and is crucial in organs such as the brain. D1 activity increases in hyperthyroidism and is thought to protect against excess hormone activity. T3 from both D1 and D2 end up in the blood and via the kidneys in the urine.
I wouldn't waste money on urine testing. The results are likely to be random. The only consistent result is a smaller bank balance.
Oh, I wouldn't spend my money on this test either, I was just curious about your thoughts. Your explanation makes perfect sense to me, thank you for your comprehensive answer.
‘The only consistent result is a smaller bank balance’ 😂Is there a good (but not too technical) explanation of how the various deiodinase work that you can point me to?
ThyroidPatientsCanada is a well respected and well referenced site for understanding the technicalities , so perhaps try some of these ( still complicated , but they have got pictures .. so i find them useful for visualising what's going on) : thyroidpatients.ca/2019/01/... thyroid-hormone-conversion
thyroidpatients.ca/2021/01/... journey-metabolism
thyroidpatients.ca/2021/02/... 7-lessons-thyroid-hormone-deiodinases
thyroidpatients.ca/2021/08/... complete-pathway-map-t4-t3
or look at some of the other articles in this site list under the heading 'deiodinases' thyroidpatients.ca/home/sit... site-map
I give some explantion here ibshypo.com/index.php/where... where I emphasise that it is important to look at which deiodinase is producing the T3, where T3 is coming from not just how much T3 there is. The diagram from thyroidmanager is very useful. It's a difficult subject, just take your time looking at it. The thyroid patients Canada is a good source of information also (most websites are not, some are misleading).
Wow, how interesting! I'm curious to see more details, it seems you are still working on this page, right? Thank you for sharing.
I thought I’d finished it! There are links in blue at the bottom of each page that goes on to the next bit.
The 5 bullets at the very bottom of the page made me think there was something to be added. Nevertheless: Great work!
Oh. They are standard links to social media to enable people to share the webpage. I don't use social media!
A look at the footer shows that you are using a WordPress template. Sometimes they don't work the way we want them to at first. This explains why I thought the page was waiting for more content. My suggestion would be to disable these bullets with some inline CSS if there is no other way to exclude social media.
I put them in deliberately because it was easy. I'll have a think about it. I used to be a computer programmer before I became hypo. and would never use a package such as Wordpress if I had my full cognitive ability back. Apologies to everyone else for our drifting off topic.
I know what you mean, I also no longer program commercially, but only for my own purposes. On the other hand, I think WP has some advantages, and we don't need to invent the wheel twice. So why not use it?
Anyway, it was nice to share some off-topic information, I hope we have not bored other people with this technical excursion. 😉
Hi jimh111, it’s taken me some time to go through this, but it’s incredibly helpful, thank you!Reading suggests that TSH regulates deiodinase activity in the brain (& elsewhere) which leaves me wondering why we aim for a low or suppressed TSH (along with good T3 T4 ofc)? Am I missing something or misunderstanding?
Most patients with primary hypothyroidism seem to do well with a fairly normal TSH (e.g. 0.5 - 2.0) and mid-interval fT3 and fT4. If patients are given levothyroxine monotherapy they need higher fT4 levels to achieve average fT3. This causes TSH to be lower and hence there is impaired deiodinase with lower tissue T3 levels. Thus, they end up needing above average fT3, fT4 to compensate and a very low TSH. The answer is to give a little T3, usually as liothyronine.
However, I believe many of the patients on this forum have a pituitary that is not producing enough TSH, perhaps because their TSH was suppressed during autoimmune thyroiditis and hasn't recovered. Often in these cases the TSH also has lower bioactivity. These patients will have a TSH lower than expected and near zero when fT3, fT4 are reasonable. I'm in this situation and need higher doses of liothyronine (40 - 50 mcg) than normal which gives me a slightly high fT3. I would prefer to have normal hormone levels, it would be safer, but I can't get my pituitary to respond normally.
We should not aim for a low TSH or above average fT3, fT4. As a rough guide it's reasonable to initially target average fT3, fT4 (with levo and a little lio). Depending on the response to treatment higher hormone levels may be needed but we shouldn't see these levels as something to aim for.
The more I read the more I agree, particularly given the various representations in my family (hashis, graves & 2 who have similar representation as you pre-treatment), plus fatigue/ibs/brain fog in the younger generation who are not yet diagnosed
Thank you for documenting so thoroughly, it is incredibly helpful and provides potential areas of follow-up for us
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