Hello all,
I had my appt with the TUK friendly consultant. In the first instance he has raised my T4 as my TSH is around 3.
I agree with this course of action but when I raised my concern that it would send my T4 over range he wasn't concerned with that.
Given my conversion rate is poor I'd need T4 well over range to get a good T3.
Perhaps I'm just looking for things to worry about 🤣 but is there any concern about an over range T4?
Thanks all! 🌱
I have been in more or less same position with one of the endocrinologist in the team I’m seeing. My ft3 is only just over bottom of range and ft4 is actually at the top. I’m still feeling hypo but they said to up levo. When I shared my concerns over going into rt3 I got no response. It’s very worrying and I’m sorry I can’t help.
You do not need to worry about rT3. It won't do anything to you. A certain percentage of T4 always converts to rT3 anyway, so there's always some in your system. It's just that when the FT4 gets to a certain level (different for everyone) it starts converting to more rT3 than T3, to stop you going 'hyper'. But, that does mean that you need more and more T4 to raise your FT3.
The majority of doctors have never even heard of rT3, so I wouldn't expect them to be concerned. But, rT3 is inert, and only stays around for a couple of hours before it is converted into T2. It does not block T3 receptors, as used to be thought. It has its own receptors, so no need to worry on that point. 
That’s not what I have been reading which is why it worrying.
Dee there are a lot of articles out there re RT3 which are no longer relevant. At one time not so long ago it was thought that RT3 blocked the T3 receptor cells and blocked T3 from getting into them. More recent research has disproven this theory and we now know that RT3 has its own receptors and its own function. However not all articles will reflect this and there are some supposed gurus out there who still have a mis-conception of RT3.Too be honest that is how I judge the validity of an article, on how the writer explains RT3.
Would appreciate a link if you have one
i can't remember which one of the many thyroidpatient.canada articles has the best reference for 'new proof of rT3 having it's own receptors' ....it might be in one of the following .. (but she 's written so many, and my filing system is rubbish, sorry )
thyroidpatients.ca/2019/11/... RT3 inhibits T4-T3 conversion. How worried should we be?"[Post updated May 2, 2021]
Many thyroid patients have acquired concerns about Reverse T3 (RT3) by reading Kent Holtorf’s web pages.
Likely even more have learned by reading Reverse T3 information on the Stop the Thyroid Madness (STTM) thyroid patients’ website, which has been influenced by Holtorf, whom they cite.
On the positive side, both of these websites share a lot of rich resources and truths that have helped many thyroid patients, including myself.
I’m grateful to them. I don’t want to be cruel toward our benefactors.
But we need to continue learning together in thyroid patient communities. Learning includes humbly admitting and fixing mistakes and problems when they’re pointed out. Love of truth is the basis of trust.
Before I attempt to reduce the fear of Reverse T3 to reasonable levels in this post, I want to make clear my stance on Reverse T3 and its testing. It’s a moderate stance:
Yes, higher levels of Reverse T3 often go hand in hand with illness and poor T4 conversion. But you can have low or no RT3 in blood and still be ill. RT3 is a signal that can mean many things depending on health status and T4 and T3 supply.
Yes, RT3 testing can inform us about thyroid hormone metabolism. But there are three major enzymes involved in thyroid hormone metabolism. Imbalance between the enzyme that creates most RT3 and the enzyme that clears most RT3 tells us something about what these enzymes are doing to RT3, not necessarily what RT3 is doing to the enzymes. Cause and effect become blurred.
Yes, Reverse T3 testing can be a useful test for resolving puzzles and confirming problems in thyroid therapy (see part 2 of this post). But it does not have to be tested routinely if you have the wisdom to interpret Free T3 and Free T4.
When claiming Reverse T3 is a powerful inhibitor of T4-T3 conversion, Holtorf takes a fragment of a quotation from a 1977 article and magnifies its significance.
Holtorf’s teachings on Reverse T3 have been lifted by many web pages without enough careful investigation. It’s gone viral long ago. It’s cemented in thyroid internet lore.
It’s not entirely Holtorf’s fault, and it’s gotten out of hand. Such beliefs have fostered unnecessary Reverse T3 paranoid obsession. I’ve seen the signs of it in online thyroid patient support communities.
RT3 obsession has led to some patients and doctors in US and Canada doing Reverse T3 testing too frequently, often charged to the patient’s own credit card.
Some believe RT3 absolutely essential for a “complete thyroid lab test.” But ideally a complete thyroid lab test would include a T2 test and a Triac test, and the list could go on and on.
Decisions based on exaggerated blame of Reverse T3 for “causing” low T3 and illness can sometimes lead to reducing T4 dosing too far and compensating with T3 dosing. A temporary shift away from T4 dosing and toward T3 dosing will lower RT3. But in the long term, appropriate FT4 levels can still support an individual patient despite RT3 levels.
In this post, I present Holtorf’s Reverse T3 claim and put it in perspective. "
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BY THYROIDPATIENTSCA on NOVEMBER 16, 2019
thyroidpatients.ca/2019/11/... deiodinase-type-3-plays-a-t3-blocking-function/ " The myth and the correction
Well-meaning people have attributed to the hormone RT3 a “T3-blocking” function.
This is a myth. Reverse T3 does not block T3 from entering cells, nor does it plug receptors and prevent T3 molecules from binding with them.
But science shows that the T3-blocking function is largely performed by Deiodinase Type 3 (D3), the enzyme that makes T4 into RT3 and also makes T3 into an inactive form of T2 called 3,3-T2.
Basically, the myth blames the child (RT3 hormone) for the father’s (D3 enzyme’s) activity."
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here is a link to the full list of thyroidpatient,canada articles
thyroidpatients.ca/home/sit... home/site-map/
You are amazing . 🙏 thank you
That’s typical first step…..see if you can tolerate high Ft4 in order to get higher Ft3
If you can tolerate, it’s easier than adding T3.
Dr Toft, past president of the British Thyroid Association and leading endocrinologist, states in Pulse Magazine,
"The appropriate dose of levothyroxine is that which restores euthyroidism and serum TSH to the lower part of the reference range - 0.2-0.5mU/l.
In this case, free thyroxine is likely to be in the upper part of its reference range or even slightly elevated – 18-22pmol/l.
Most patients will feel well in that circumstance.
But some need a higher dose of levothyroxine to suppress serum TSH and then the serum-free T4 concentration will be elevated at around 24-28pmol/l.
This 'exogenous subclinical hyperthyroidism' is not dangerous as long as serum T3 is unequivocally normal – that is, serum total around T3 1.7nmol/l (reference range 1.0-2.2nmol/l)."
(That’s Ft3 at 58% minimum through range)
You can obtain a copy of the articles from Thyroid UK email print it and highlight question 6 to show your doctor
please email Dionne at
tukadmin@thyroiduk.org
Thank you! This eased my mind. I had assumed that it can't be terrible to have an over range T4 because endo wasn't concerned at all but I'm a worrier!
My conversion has remained around 4.5 despite increases so doing some reverse engineering; I'd estimate I'd need T4 to be around 125% to achieve a T3 of 60%. Ish.
Hopefully that will be enough/tolerable. 🤞🏼
Thank you, SlowDragon.
Sadly page is unavailable
As I don’t want to hijack someone else’s post I will ask for links in another new one but thank you for trying 😊
Dee I think it is because I put two links up and they are putting them together to make 1.
i've had a look into this as i have very over range fT4. i'm not too worried, ( and if you can feel well using high fT4 to get enough fT3 , this is the easiest way to achieve it without all the hassle of getting T3/NDT , so being pragmatic, it's probably worth at least trying higher fT4 first before going to added T3 )
.... but i have found odd little bits of info which do possibly give some cause for concern .
( connections between the T4 and rT3 receptors and cancer proliferation)
But they are not specifically related to 'over-range' T4 , it is related to all T4 / rT3. But it does imply that more fT4 (and therefore more rT3) increases the risk.
It's complicated so you should read for yourself but i'll quote a bit of it.
This is from Thyroidpatients.canada.. but note ,it is discussing a study of terminal cancer patients who already had low fT4.. but reducing it further and replacing with T3 prolonged survival.
thyroidpatients.ca/2020/02/...
T4 cancer risk is found within reference range.
"....Again, it is “physiological” concentrations of T4 that activate cancer cell proliferation:
“T4 in physiological free hormone concentrations stimulates proliferation of cancer cells in vitro and in xenografts.”
“Physiological” concentrations mean within the normal statistical reference range.
T4 has a dose-dependent effect on a wide continuum. Hercbergs et al, 2019 say this:
“It is of note that there is a declining continuum of risk for free thyroxine levels from high supraphysiological (hyperthyroidism) to frank hypothyroxinemia and to blocking of the integrin avb3 thyroid hormone receptor, which would equate to a zero ambient free T4.”
Risk is absent when FT4 is absent or the receptor is blocked, but risk does not suddenly spike when FT4 rises above a statistical boundary.
According to Hercbergs and team, risk rises each pmol/L that your FT4 rises even within reference range.
This means that high-normal Free T4 presents relatively more cancer risk than low-normal Free T4.
Reverse T3’s activity
Even more recently, Reverse T3 has been proven active at this integrin receptor. In September 2019, Lin et al published an article confirming the following, which had previously been hypothetical:
“rT3 is known to bind to the thyroid hormone analog receptor on plasma membrane integrin αvβ3. This integrin is generously expressed by tumor cells and is the initiation site for the stimulation by L-thyroxine (T4) at physiological free concentrations on cancer cell proliferation.
In the present studies, we show that rT3 caused increases of proliferation in vitro of 50% to 80% (P < 0.05-0.001) of human breast cancer and glioblastoma cells.
Conclusion: rT3 may be a host factor supporting cancer growth.”
To put this hormone in perspective, Reverse T3 is always present when T4 is present, but in much lower quantities than T4. Total RT3 normally constitutes less than 1% of the concentration of Total T4. (Burman et al, 1977). "
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There is also this one which i haven't read yet : thyroidpatients.ca/2018/08/... study-on-t4-and-t3-in-breast-cancer/
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This may be related ?, from diogenes healthunlocked.com/thyroidu...
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I also found this study of long term cognitive effects in patients on TSH supressive doses of T4,compared to those on lower t4 doses that did not supress TSH.. which interested me because the 'word selection anomia' they refer to is sometimes an issue for me. healthunlocked.com/thyroidu...
@tattybogle . Thank you I have saved this for a time of quiet. Need my head in the right place but it gives me hope. I am arranging a private scan for next month as I need to know if my thyroid is completely dead before I up my dose. Last thing I need is for the graves to kick in again and it’s impossible to get it done through endocrinologist. I have saved the whole post
I'm definitely going to read this when my brain feels a bit more switched on.
At present I'm reading it sideways to try and get the gist. 😂
Thank you Tatty. Much appreciated. 
Hi plant_ladyI was treated with thyroxine for 17 years and normal health was never restored completely. I got through those years with T4 at the top end or just over the reference range and with suppressed TSH. It was the only way I could live. Eventually I was referred to an endocrinologist, and treated with T3, which must have been what I needed all along. Now in my 60s my health is the best it’s ever been, but I have been diagnosed with atrial fibrillation(AF). I found out that high T4 is associated with AF and wonder if that’s the origin of my problems. So be aware, your doctor may not be that well informed, or may be trying to get around the difficulties of prescribing T3 currently. The ranges are only statistical things and you may have needs that are slightly different.
endocrinologyadvisor.com/ho...
Thank you for sharing.
My endo is private and has suggested prescribing NDT if more levo isn't the ticket so hopefully health isn't too far away. 🙏🏼
I will keep an awareness of AF though. What a stress it all is; trying to balance wellness against risk .
Hello Plant Lady ;
For what it's worth :
I'm with Graves Disease post RAI thyroid ablation in 2005 and treated for primary hypothyroidism in primary care with T4 Levothyroxine and in around 2014 started to become increasigly unwell and in an ever increasing circle of hypothyroid symptoms.
I was immeditely put on 100 mcg T4 after RAI and in primary care I felt better at 125mcg but this gave me a suppressed TSH so I was cut back to 100 mcg and prescribed anti depresants as some sort of consolation prize,
Finding little help from within the NHS I found this site and started my learning curve.
As advised on here, in July 2017 I arranged a full thyroid function test including reverse T3 :
My level of Reverse T3 came in well over range with comments from the private blood test doctor suggesting I talk this through with my doctor. Both my doctor and hospital endocrinologist dismissed this issue and I was refused both T3 - synthetic Liothyronine and NDT and told I was overmedicated because of my TSH being at 0.01:
There was no discussion to be had on my T3 only coming in at 25% through the the range when on the suggested dose of T4 at100 mcg. and the conversation was closed because my TSH was the only topic of conversation.
It is suggested by some specialists that if there is a high level of Reverse T3, which is surplus and unconverted T4 - the patient will likely do better on less T4 and to introduce T3 to compensate according - thereby allowing this build up of reverse T3 to unblock itself - rather than add to it with more T4 to chase a better, higher T3 level..
Imagine a pressure cooker - adjusting the cooking by turning the valve and allowing steam out - imagine a boiling saucepan - same principle when you replace the lid- half cocked - and the body adjusts itself from boiling over by pushing unconverted T4 into reverse T3 which is inert, and the body's way of regulating itself.
So, I suspect by my having been overactive, my reverse T3 would be high, but still high and over range 10 years later - probably the result of monotherapy with T4 only ??
I did try increasing my T4 up to 137.50mcg daily to try to achieve a better conversion, I managed a T3 at around 56% through the range but it fell away after a few weeks, as did the headache I had endured trying this experiment.
So, I'm now self medicating and 3 years into taking Natural Desiccated Thyroid and am much improved :
Whether my reverse T3 has now unblocked itself or not, is the question, but it hasn't affected my NDT working well and my dose is just 1 + 1/2 grains which equates to 57 T4 + 13.50 T3 : so a much lower dose of T4 than I ever imagined I would need to feel well.
I hope this explanation of a sort, helps in your understanding and puts your mind at rest.
Over range Serum Urea and Plasma Viscosity.
T3 over range
Below range T4 - normal TSH - Pituitary?
The Lab have lowered their Free T4 reference range
T3 over range?
