Re: T4 conversion. How does it work?

[Guest guest]

Hi this is a question I asked a GP a long time ago {I was being treated

on levo for a goitre] so not going by blood tests -at least I wasn't . She could

not tell me the answer but I did find that I certainly could not take enough T4

to become hyper as so much of it was being left unconverted. A normal thyroid

produces some T3 so I don't think you can become hyper on just T4 . When on T4

only you are at a disadvantage -you have to convert more T4 than somebody with a

normal working thyroid . I think there must be a limit to how much most people

can convert. I have been hyper from an overactive thyroid but a long long way

from this by being given only T4.Hope this is some help Best wishes

[Guest guest]

Hi - If my memory is working now -the endo told the GP that excess T4 was

excreted . When I asked Dr P -he said it made RT3 and blocked the receptors . So

no hyper from T4 only ? Best wishes

>

>

[Guest guest]

Hi ,

Absolutely agree with you and I really can't see how extra T4 would send anyone

hyper.... but what prompted my post was this quote in the middle of post 76588

from Sam sigler....

" I asked him if I could increase my dosage to 150 mcg and he was reluctant to

let

me do so as he was worried that he would push me into hyperthyroidism, but he

said to try as it couldn't hurt in the long run. "

These doctors amaze me, there is no reason, or logic... they simply don't

think things out....

I just wondered if I had missed the point somewhere and that perhaps there was

some miracle happening, whereby it was possible to get hyper on T4.....

x

>

> Hi - If my memory is working now -the endo told the GP that excess T4

was excreted . When I asked Dr P -he said it made RT3 and blocked the receptors

.. So no hyper from T4 only ? Best wishes

> >

> >

>

[Guest guest]

I would be interested to know, too! I should have asked him what he meant when

he said that, but didn't press it. In retrospect, I should have!

>

> Hi ,

>

> Absolutely agree with you and I really can't see how extra T4 would send

anyone hyper.... but what prompted my post was this quote in the middle of post

76588 from Sam sigler....

[Ed]

[Guest guest]

Hi,

I posted the opposite ages ago because I can't grasp T4 toxicosis? The majority

of people who are hyperthyroid have a high T4 which then pushes up their T3.

All atd's are monitored on the measurement of T4 and was the biggest cause of

my debates/fights with GP's and endo.

There's only something like 5% of people with Graves that present with T3

toxicosis

( also documented this can only happen in Graves) the rest have high T4 so I

kept

asking why they were basing atd's on my T4 when it wasn't high in the first

place

and practically bottomed out after a week on cbz.

They said because that's how it's done/monitored, folk with T3 hyper were in the

minority.

So I couldn't understand why you couldn't go hyper on T4, or why a high T4 on

meds was automatically converting to RT3 when the majority of hyperthyroid folk

have a high T4 to start with which causes their T3 to rise too?

I still can't get my head round how RT3 is diagnosed from a high T4, highish T3

without a test - or is RT3 always tested in those cases?

So I still don't understand why you couldn't go hyper on T4....just when I

thought I thought I had a grasp on this RT3 stuff.....why would T4 show low in

the blood - I

thought with RT3, T4 showed high, T3 could be high......which is where I was

confused in the first place - I thought that was hyper?

Love Tess x

>

> Hi everyone, am reposting my question with a new title as it got hijacked....

and no one replied, or no one knew the answer....

>

>

> I just read yet again in someones post, that the doctor didn't want to

increase

> T4 in case it sent her hyperthyroid.

>

> Normally your thyroid would make t4, which would circulate in your blood at a

> given level and some t3. When you need some energy, you either use the t3 that

> has been made by your thyroid, or you convert some of the T4 which is going

> round your blood into t3. When you have the right amount of T4 stored in

>

[Guest guest]

Hi ,

Hi everyone, am reposting my question with a new title as it got hijacked....and no one replied, or no one knew the answer.... :(I had started a reply yesterday, but then wound myself into knots, trying to explain – so second go.....

As I see it, the short answer to your question – if I have understood your question correctly – is: If you take in more T4 than the body can handle, then the body's protective mechanism will come into force....first the body is trying to rid itself of the excessive T4 by raising the metabolism higher and higher, making the heart and all the organs work overtime - thereby pushing the body into hyperthyroidism as a result of thyrotoxicosis - whilst at the same time it tries to reduce the excessive T4 by converting more of it than usual into rT3, which results in blocking the uptake of FT3 into the cells. So I'd assume that an excess of T4 would eventually result in hyperthyroid symptoms whilst the patient remains hypothyroid, because an excess of rT3 might prevent sufficient FT3 from getting into the cells.

And this is the long-winded answer.....Normally your thyroid would make t4, which would circulate in your blood at agiven level and some t3. When you need some energy, you either use the t3 thathas been made by your thyroid, or you convert some of the T4 which is goinground your blood into t3. When you have the right amount of T4 stored inyour blood, the TSH drops and you don't make as much.I may be wrong, but the way I understand this whole business, the TSH does not drop as the T4 in the blood goes up, but the demand for more needed thyroid hormone comes from the cellular (not blood) level. So effectively it is the level of T3 inside the cells that regulates a demand for more TSH, not the level of T4.

The way I envisage it in my mind is that the cells send a demand for more T3 to the hypothalamus in the brain when their T3 levels drop – The hypothalamus then secretes TRH to the pituitary, which is the signal for the pituitary gland to produce TSH and send it to the thyroid gland.... this is the signal for the thyroid to secrete T4 and a little `readymade' T3 into the bloodstream. The T4 should then be converted into T3 as needed, and the T3 gets into the cells, etc.....

If you take levothyroxine, it circulates in your blood and when you have enoughthe tsh drops. If you have too much, you make reverse t3 which breaks down theexcess t4 and gets rid of it.As I said above, I believe it is not the T4, but the T3 that regulates the TSH output – but yes, if faced with excessive T4, the body will partially attempt to rid itself of the T4 excess by converting it into rT3, and in my view that poses one of the dangers of a T4-only therapy. It is easy to overdose on T4, because you would not feel the overdose for several days as it builds up, unless you were very sensitive. If you up the T4, the body will first respond by raising the metabolism as much as possible, and there comes a point where the body can no longer cope, and then it rids itself of the excessive T4 by converting it into rT3 – and rT3 will block FT3 from getting into the cells. The result is that the patient will become thyrotoxic – all the excessive and unusable hormones will be stored in the liver as toxins and the whole system will have to work very hard to rid itself of those toxins....

Even if a full blood test including FT3 were done at that stage, it would not give you the obvious answers, because – and this is the point - rT3 in a normal blood test will show up as FT3, since both have the same chemical formulation – rT3 is just the mirror image of FT3. So your TFT would show a low or suppressed TSH, high normal or above normal FT4 and high normal or above FT3.... and the patient would feel pretty rotten, I'd think...

So where, in taking too much levothyroxine would you be making too much t3,which is what you have when you are hyper?

I am hoping that the above explains it....

Surely just having t4 in the blooddoesn't mean you automatically convert it to t3. ???

No, not automatically, as I understand it – The conversion from T4 to T3 happens on demand from the cells, - although some patients have conversion problems and then the T4 mostly stays T4, the cells don't get the needed amount of T3, and the patient will become thyrotoxic (with hyper- as well as hypothyroid symptoms) from an excess of T4 and at the same time be hypothyroid from a lack of T3 in the cells. I would imagine in such a case the TSH would be elevated, the FT4 also high and the FT3 low..... although you would not see this very often, I don't think. I remember one of our members presenting such a TFT some time ago.... her doctor never got to the bottom of her problem, nor did he appear bothered, if I remember correctly.

If you did convertautomatically then you'd be hyper as soon as you got any t4, t4 would alwaysshow low in the blood and t3 would be high....

I agree – I can't imagine such a scenario.... I just can't fathom how taking too much t4 could lead to hyper, there isanother step involved which tells your body to do the conversion to t3 when youneed it..... any ideas on this?

I think the step you are looking for is the cells demand for T3. This demand is a combination of our environmental needs (to keep warm, for instance) and energy needed on a cellular level – if more energy is needed for whatever we are just about to do, the hypothalamus in the brain will sense that via feedback it gets from the cells and from the environment... and that set into motion what I described above – hypothalamus to pituitary – pituitary to thyroid – thyroid to blood, which takes the hormones through the body, converting T4 into T3 as needed – which is then taken up by the cells. A healthy body with a healthy thyroid would automatically keep a perfect balance of all this happening. We hypos have to regulate our own hormone input, preferably by listening to our bodies.

I can't guarantee that all of the above is correct, but this is the picture I have in my head about how the thyroid cycle works.

Love,

xx

[Guest guest]

Hi -I've just read your post . Please could you see if your reasoning

explains this -

TSH-3.0 T4-16 T3 borderline [6 weeks later] TSH- 3.6 T4-16 T3

abnormal It was the begining of the winter but as TSH went up 0.6 the T3

went down 0.6 and the T4 stayed virtually the same. This was also before any

treatment.

My conversion is poor so I just take T3 . Physically I just have less than

half my thyroid left and it seems to have given up completely. I first saw Dr P

when I was on 150-175 T4 which wasn't being converted properly making RT3 and

making me feel unwell [migraines etc ] Too much T4 but definitely not

hyper-[still swollen tongue ,brain fog etc] The more T4 I took the more RT3 and

the less getting to the cells -hence not getting hyper. For me the TSH seems

to depend on the T4 . Can this fit in your thinkng .Best wishes

[Guest guest]

Please could you see if your reasoning explains this -> TSH-3.0 T4-16 T3 borderline [6 weeks later] TSH- 3.6 T4-16 T3 abnormal It was the begining of the winter but as TSH went up 0.6 the T3 went down 0.6 and the T4 stayed virtually the same. This was also before any treatment.

Hi ,

I do not claim to be an expert, but looking at the figures and data you have given, I can't really see the sequence of events, which is rather important when trying to draw conclusions. I assume that you first had your operation, then were put on Levo, which did not suit you .... but thereafter your account gets a bit jumbled. You say you were on Levo when you first saw Dr. P., but also say you were on no medication when the blood tests were taken, yet now you are on T3 only, but don't give any test results since you've been on T3 only - so all I can look at is your test results, which – as you say – were taken whilst you were on no thyroid medication at all.... and under those circumstances they would make perfect sense : They show you were clearly hypothyroid at the time – rising TSH, low-ish FT4 and very low and falling FT3 .... your cells were starved of thyroid hormones, as apparently nothing much was getting in, hence your TSH was slowly rising, responding to your cells crying out for more. Your remaining half thyroid was still producing some T4 and responding to the TSH demand, but could not produce much, and your body was not converting what little T4 your thyroid gland was still secreting.

- If, however, you had been taking 150 - 175 mcg Levo at the time of those blood results, then those figures would not make any sense whatsoever to my mind.....

Too much T4 but definitely nothyper-[still swollen tongue ,brain fog etc] The more T4 I took the more RT3 andthe less getting to the cells -hence not getting hyper.

Yes, what you say makes sense. Your body was not converting the T4 into T3 but was making mostly rT3 to rid the body of the T4 excess; thereby you would experience symptoms of thyrotoxicosis from the excessive T4, but at the same time your cells would still have been deprived of T3, hence you would have felt pretty hypo and hyper at the same time and since many of the hypo symptoms and hyper symptoms overlap, you would have felt pretty awful all round, experiencing the worst of both worlds... – does this make sense?

Best wishes,

[Guest guest]

Hi ,

Thanks for that, you always explain things beautifully. I'm still stuck with

one bit..... the bit where if you take too much t4 the metabolism speeds up to

help you get rid of it.... does it? Really? Are there any scientific studies

on this? Why would the metabolism speed up to get rid of T4, why not just

break it down into reverse t3? Do we really have two methods of getting rid

of excess t4?

If we do have the two methods then that shows why docs believe we can go hyper

with too much t4.... as it converts into t3 (which our cells don't need and

haven't asked for). I personally can't see it and am off to have a look for

some research..... The reverse t3 I can understand perfectly....

Will get back when I've had time to have a look round......

xx

>

>

> Hi ,

If you take in more T4

> than the body can handle, then the body's protective mechanism will

> come into force....first the body is trying to rid itself of the

> excessive T4 by raising the metabolism higher and higher, making the

> heart and all the organs work overtime - thereby pushing the body into

> hyperthyroidism as a result of thyrotoxicosis - whilst at the same time

> it tries to reduce the excessive T4 by converting more of it than usual

> into rT3, which results in blocking the uptake of FT3 into the cells. So

[Guest guest]

>> Hi,> > I posted the opposite ages ago because I can't grasp T4 toxicosis? The majority of people who are hyperthyroid have a high T4 which then pushes up their T3. This is what i don't get.... how does t4 convert into t3 if it isn't told to via a message from the cells. Surely it can't change just because it's there?> All atd's (sorry what's an atd?) are monitored on the measurement of T4 and was the biggest cause of> my debates/fights with GP's and endo.> There's only something like 5% of people with Graves that present with T3 toxicosis> ( also documented this can only happen in Graves) the rest have high T4 so I kept> asking why they were basing atd's on my T4 when it wasn't high in the first place> and practically bottomed out after a week on cbz. > They said because that's how it's done/monitored, folk with T3 hyper were in the minority.> So I couldn't understand why you couldn't go hyper on T4, or why a high T4 on meds was automatically converting to RT3 when the majority of hyperthyroid folk> have a high T4 to start with which causes their T3 to rise too? ( How does it with no signal ffom the cells)> I still can't get my head round how RT3 is diagnosed from a high T4, highish T3> without a test - or is RT3 always tested in those cases? (Guesswork?)> So I still don't understand why you couldn't go hyper on T4 ( I thought you couldn't go hyper because you would get rid of the excess t4 with reverse t3, but Christna said earlier that maybe you convert some t4 to t3 and speed up just to use up the excvess t4. I'm off to find out if this is so)........just when I thought I thought I had a grasp on this RT3 stuff.....why would T4 show low in the blood - I> thought with RT3, T4 showed high, T3 could be high......which is where I was confused in the first place - I thought that was hyper? (T3 and reverse T3 just show on a blood test as T3. You have to specifically test for reverse t3.. This is why a high t3 doesn't always mean hyper, -it's not actually high t3, but high reverse t3 plus t3)> Gosh, if we're srtuggling so much and we have the condition, no wonder the endo's just don't know.... It's so confusing they must all fall asleep when the subject is covered in training xx

[Guest guest]

Hi , I did laugh at this.... endo's falling asleep! You do wonder don't

you.

This thread has been a fascinating read. How complex are the workings of the

body. Think I now understand a little more after reading this thread.

When I was first diagnosed hypothyroid 17 years ago my then GP told me I no

longer had a thryoid illness as she had sorted it with L-thyroxine. Just shows

she knew nothing at all.

Its been a struggle to get somewhere near well and no thanks to any NHS

doctor/endo. Just thanks to Sheila and Dr P. for starting me in the right

direction.

Judy

> Gosh, if we're srtuggling so much and we have the condition, no wonder

> the endo's just don't know.... It's so confusing they must all fall

> asleep when the subject is covered in training

>

> xx

>

[Guest guest]

Hi,This is what i don't get.... how does t4 convert into t3 if it isn't told to via a message from the cells. Surely it can't change just because it's there?When you had your hyper phase did you not get high T4 and T3? http://www.ehealthmd.com/library/hyperthyroidism/hye_whatis.htmlsorry what's an atd? Anti thyroid drug....Carbimazole or PTU.How does it with no signal ffom the cells? Cells respond to thyroid hormone with an increase in metabolic activity. Metabolic activity, or metabolism, is a term used to describe the processes in the body that produce energy and the chemical substances necessary for cells to grow, divide to form new cells, and perform other vital functions.If you think of each cell in the body as a car, then thyroid hormoneacts as if you were tapping on the accelerator pedal. Its message is "go."I thought you couldn't go hyper because you would get rid of the excess t4 with reverse t3, but Christna said earlier that maybe you convert some t4 to t3 and speed up just to use up the excvess t4. I'm off to find out if this is soI'm googling too...trying to grasp Rt3 again(T3 and reverse T3 just show on a blood test as T3. You have to specifically test for reverse t3.. This is why a high t3 doesn't always mean hyper, -it's not actually high t3, but high reverse t3 plus t3)This is the bit - if they're using guesswork and not a test - how can hyper be ruled out or vice versa - is the TSH suppressed with RT3 as well? Here's more on hyperthyroid - http://www.mercksource.com/pp/us/cns/cns_hl_adam.jspzQzpgzEzzSzppdocszSzuszSzcnszSzcontentzSzadamfullzSzadam_encyzSz1zSz000356zPzhtmhttp://www.suite101.com/lesson.cfm/19330/2897/4Thyroid hormones initiate a chain of molecular events or gene expressions when the active form of the hormone interacts with specific cell receptors and subcellular components of various organs.These receptors have been found in the liver, brain, heart, spleen, testis, kidney and anterior pituitary gland with the liver having the largest number of receptors and the pituitary the least. In summary, active or free thyroid hormone molecules react with specific cell components or binding sites on specific organs. Here, they initiate specific cellular changes, such as energy production, that are also influenced by genes and other factors.To complicate matters, the receptor sites for thyroid hormone are shared with other substances, such as other hormones, including the hormone vitamin D. This is why someone with hyperthyroidism who has the same thyroid hormone levels as another individual will not have identical symptoms.Thyroid hormones stimulate many metabolic processes, including energy expenditure and the basal metabolic rate, including digestion, and the metabolism of lipids, carbohydrates, drugs, proteins and minerals. Thyroid hormone is necessary for the proper functioning of other glands and organs. People deficient in thyroid hormone typically have low levels of other hormones.When levels of either FT4 or FT3 are low, symptoms of hypothyroidism occur. When levels of either FT4 or FT3 are high, symptoms of hyperthyroidism occur. For diagnosing these disorders, blood tests for FT4 and FT3 are superior to tests for T4 and T3 since the latter two tests are influenced by binding protein levels.When FT3 is elevated and FT4 is normal, this form of hyperthyroidism is called T3 thyrotoxicosis. T3 thyrotoxicosis is a common occurrence in hyperthyroidism caused by Graves' disease and also toxic multinodular goiter.In the next section you'll learn about one of the body's major axis systems and how it regulates thyroid hormone levels.Off to google again and if I can't get to grips with RT3 this time....I'm giving up.....at least we try to understand though....unlike the endo's.Love Tess xx> >> > Hi,> >> > I posted the opposite ages ago because I can't grasp T4 toxicosis? The> majority of people who are hyperthyroid have a high T4 which then pushes> up their T3. This is what i don't get.... how does t4 convert into> t3 if it isn't told to via a message from the cells. Surely it can't> change just because it's there?> > > All atd's (sorry what's an atd?) are monitored on the measurement of> T4 and was the biggest cause of> > my debates/fights with GP's and endo.> > There's only something like 5% of people with Graves that present with> T3 toxicosis> >

[Guest guest]

Hi ,

I found this http://www.ncbi.nlm.nih.gov/pubmed/668639 then re read your post,

think I'm getting it now?

When Hyper T4 you get the hyper symptoms, too much Thyroxine gives an initial

burst of metabolism but then with both a defence mechanism kicks in to stop any

more FT3 being produced and this is RT3?

Then problems are caused because the RT3 blocks the FT3 from working and causes

more hypo symptoms but some hyper ones too because the TT3 will be floating

about the blood making them Toxic? This leaves the unlucky 5% with T3 Toxicosis

with no defence mechanism which is why we're (or was in my case) more

likely to go nuts and although rare, have a higher risk of thyroid storm. Am I

nearly there lol.................

Love Tess

>

>

> Hi ,

>

>

>

> Hi everyone, am reposting my question with a new title as it got

> hijacked....

> and no one replied, or no one knew the answer....

>

[Guest guest]

Hi thankyou for looking at my post -no I was not on anything when the

blood tests were taken . These results were 7 years after my partial

thyroidectomy -they did not put me on levo after my operation as my TSH's were

always in the 3's . I only got theseT3 results after 7 years -they only did TSH

before that . yes I agree I must have been producing some T4 but it was not

converting properly . Also since there seemed to be T4 there that is why the TSH

seemed to be in range {in the UK's reference range !!] Just shows how deceptive

the TSH test is . So TSH was linked to T4 which was going nowhere fast ? Using

levo lowered the TSH but I was starting at 3 - After the two tests I gave you

the T3 was not done. The levo did not work well and get rid of swollen

tongue,brain fog etc-so I take T3 and since it is DIY there are no blood tests

-just temp and pulse . Just to add -the feeling of too much T4 going nowhere

was not like being hyper . I thought hyper was too much T3 in your system -the

active hormone. The T4 can build up and make you feel ill but it is inactive ?

does the RT3 turn back to T4 and makes the T4 result seem okay and hence the

TSH ? Thankyou for helping to unravel what puzzles me Best wishes

[Guest guest]

Hi just read your post as well as 's Too much T4{inactive] in

the system is definitely a different feeling from being hyper -which I always

thought was too much T3 . If you are hyper surely it is too much T3 {active] I

should have thought it would be too much of an about turn for a hypo person to

convert so much T4 that they become hyper . I should have thought too many

people have conversion problems anyway and can't tolerate nearly enough T$ to

make the well -especially for the brain !!!! (Maybe my brain still isn't

getting enough T3 otherwise I would be able to work this out more clearly] Best

wishes

[Guest guest]

Hi , When I was diagnosed with Graves I thought T3 Toxicosis was Graves/

hyper, it was ages after that I was told I was in the minority, majority of

hyper was high T4 which made high T3. I had low T4 and high T3, I'm confused

again though

because if a defence thing kicks in and makes RT3 instead.....why the need for

atd's?

My brain can't take anymore in, I'll never understand it....and I'm not going to

try anymore....or I need more T3 too!!

Love Tess

>

> Hi just read your post as well as 's Too much T4{inactive] in

the system is definitely a different feeling from being hyper -which I always

thought was too much T3 .

>

[Guest guest]

Hi ,

Thanks for that, you always explain things beautifully....

Thank you, it's nice of you to say so, I just wish I could be more confident with what I am saying about this particular aspect. I am not claiming to be right about it all, it is only the way I understand what Dr. P. has said in his book.

I'm still stuck withone bit..... the bit where if you take too much t4 the metabolism speeds up tohelp you get rid of it.... does it? Really? Are there any scientific studieson this?

Please don't laugh, but that bit I have got on high authority, from US veterinarian Dr. Dodds; is the Dr. P. of the canine world . My dog was hypothyroid many years before it dawned on me that I was mirroring his symptoms and had been diagnosed hypothyroid myself, and my initial learning was on canine Hypothyroidism, which is not a lot different from the human version, only dogs have a much faster metabolism than humans and (presumably because of that) take about 8-10x the average human dosage when you take into the equation their weight vs ours. To the best of my knowledge though, a dog's thyroid – in principle – works in the same way as ours. Anyway, to cut the story short, I once asked Dr. Dodds back in 2007 if she had any explanation why my dog showed a low-ish T4 despite his exceptionally high thyroxine input, and this was (part of) her reply – (pasted from her email) –

Dear : The lower than anticipated T4 can have one or more of three logical explanations: 1) As calcium binds thyroxine and his raw diet has plenty of that, it retards absorption of the drug, and so post-pill T4 levels [assuming that they're being drawn at the correct 4-6 hrs the pill] will look lower than they eventually would become -- if you had any way to know when that peak level would be achieved. To avoid this variable, the pill should be given at least one hour before a calcium-rich meal -- and when testing thyroid levels, sample should be drawn 4-6 hrs after the pill.

2) At his current weight and age , the 0.8 mg BID dose seems quite high. When the dose is too high, the body excretes it faster to try to prevent thyrotoxicosis, so levels can appear lower and you're not getting the desired therapeutic effect.....

3) Just doing a T4 alone is inadequate, because T4 levels can be suppressed by any other illness present -- like his IBD --making levels look lower than they really are. As a minimum you need to insist upon a T4 and freeT4 measurement. Alternatively, you could send us a separated serum sample to test the whole thyroid profile. See www.hemopet.com under "Services" for the test form and instructions.

Since thyroid hormone is supposed to raise the metabolism and the only way (I know of) to excrete thyroxine from the blood stream is by speeding up the metabolism to `get it through the system', I would imagine that this is what indeed happens. I don't know of any scientific studies though. Did you come across anything useful in your search?

Why would the metabolism speed up to get rid of T4, why not justbreak it down into reverse t3? Do we really have two methods of getting ridof excess t4?Back in those days I had no idea that rT3 even existed, but I would guess that if there were moreT4 in the system than it can handle, the second protective mechanism is to convert into rT3 what can't be expelled quickly enough any other way. A small amount of T4, from what I have read, is always converted into rT3 anyway, even during the `normal' conversion process, so perhaps that is just a progression ??

Hi ,

no I was not on anything when theblood tests were taken . These results were 7 years after my partialthyroidectomy -they did not put me on levo after my operation as my TSH's werealways in the 3's . I only got theseT3 results after 7 years -they only did TSHbefore that .

I am speechless....that is disgraceful (( - poor you. Your GP or endo have a lot to answer for !

yes I agree I must have been producing some T4 but it was notconverting properly . Also since there seemed to be T4 there that is why the TSHseemed to be in range {in the UK's reference range !!] Just shows how deceptivethe TSH test is . So TSH was linked to T4 which was going nowhere fast ?

I tried to find anything further on this matter in Dr. Peatfield's book, but was unable to find any specific passage that refers to exactly which thyroid hormone regulates the amount of TSH. From one of his table-drawings it looks as if it were a combination of things - circulating T4 and T3 as well as the sensory input from the environment - trigger the hypothalamus to release TRH to the pituitary, which in turn then pushes out TSH to the thyroid. In his text he says (quote): The function of the thyroid, in us and all mammals, is to regulate all the processes of energy release within the individual cells and in the body as a whole. (The thyroid hormones also act as growth hormones controlling tissue growth and development in early life). This what we mean when we talk about metabolism. Metabolism is the rate at which we produce and use energy (unquote).... and then he goes all scientific about molecules and chains of carbon and hydrogen atoms, combining with oxygen forming carbon dioxide and water and that this is apparently the chemical energy all cells live on - besides T3, I guess (?) ... I really find chemistry such a struggle (

So the best I can imagine from that is that it is not just T3 alone as I assumed, but all of the sensory input from cells, blood, environment and energy demand is somehow deciphered and processed by the hypothalamus and this gland holds all the strings and decides whether or not any more thyroid hormone is needed and secretes TRH accordingly; perhaps this is why Dr. Peatfield describes the hypothalamus as "the composer of the wonderful symphony of life".

Using levo lowered the TSH but I was starting at 3 - After the two tests I gave youthe T3 was not done. The levo did not work well and get rid of swollentongue,brain fog etc

Yes, I am afraid it's the same old sad story about the FT3 not being done... Do you know by any chance how low the amount of 150-175 mcg Levo dropped your TSH and how high your FT4 went at that time?

....so I take T3 and since it is DIY there are no blood tests-just temp and pulse . Just to add -the feeling of too much T4 going nowherewas not like being hyper .

I appreciate that, because although you may have had some hyper symptoms without even realizing is, you were – despite a presumably "normal" or even high FT4 – still severely hypothyroid with all the associated symptoms, since hardly any T3 was getting inside your cells. Effectively it is the lack of T3 in our cells that renders us hypo, even if the FT4 or TSH look "normal". A "full tank" (of T4) is no use unless there is a means of getting that fuel into the engine to drive the car.

I thought hyper was too much T3 in your system -theactive hormone. The T4 can build up and make you feel ill but it is inactive ? Yes, that is my understanding too, although it is not quite so black and white. Not everybody has conversion problems, and if there were none, then taking too much T4 would convert into too much T3 and the person would become hyperthyroid. I certainly did get classic hyperthyroid symptoms when I overdosed on Levo. For someone like you, who has conversion problems, the T4 just builds up in blood and liver and becomes toxic waste.

....does the RT3 turn back to T4 and makes the T4 result seem okay and hence the TSH ?

Nope, I don't think it works like that. I would guess that rT3, like unused T4, would become toxic waste in the body and the liver and kidneys will have to work hard to do the detox.....- but that's a guess, perhaps Nick knows more about that?

Hi Tess,

Then problems are caused because the RT3 blocks the FT3 from working and causesmore hypo symptoms but some hyper ones too because the TT3 will be floatingabout the blood making them Toxic? This leaves the unlucky 5% with T3 Toxicosiswith no defence mechanism which is why we're (or was in my case) morelikely to go nuts and although rare, have a higher risk of thyroid storm. Am Inearly there lol.................

Yep, I'd imagine it's something like that, which, I would imagine, must be 100x worse than `just' getting toxic from too much T4. Makes you angry, doesn't it, that most of our doctors aren't able to work all this out and treat us properly..... – and with that thought I am off to my own GP now to receive the verdict from a bucket full of my blood .... GP felt generous and ordered everything under the sun for me.... wonder if the FT3 will have been done this time ;o)) <bg>

Love,

xx

[Guest guest]

Thanks ,

Hope you got on ok with your blood tests, I got all confused again earlier

thinking

why give out atd's then but looked it up again and some folk are hyper with a T4

way way up in 30's or more. Then there's the antibodies which the atd's help -

so

thanks again.....I'm understanding it at last ;-)

Love Tess xx

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>

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[Guest guest]

Found this on the temperature Syndrome about T4 conversion to T3 and rT3.

http://www.wilsonssyndrome.com/eManual/Chapters/01Basics.cfm#i20

I not sure what people think of Dr 's protocol but I must say I found the

supplements very effect. The only problem is the cost of delivery which stopped

me purchasing.

Judy

[Guest guest]

Hi -thankyou for your explanation . Looks like what the endo said

-excess T4 is excreted and Dr P -it makes RT3 are just bits of the explanation

.. After I started levo there

are a couple of blood tests

on 50 T4----TSH-1.5 T4 19.2

on 75 T4----TSH-1.37 T4 18.5 These results have no relationship to my

state of health -I was in fact getting worse faster than the T4 was increased

-this was going in to the winter-I think you need more T3 for the cells and the

T4 wasn't been converted . The GP then stopped blood tests as the T3 wasn't

coming back. As far as I can see the TSH was useless and the T4 probably showed

I wasn't converting . I saw Dr P a few months later and its improved from there.

Yes I have made a large number of waves . Best Wishes

[Guest guest]

Many thanks for posting this link, Judy.... I haven't had time to read it properly yet, but already I found several things in there that I didn't know......

http://www.wilsonssyndrome.com/eManual/Chapters/01Basics.cfm#i20 for instance:

5' deiodinase has two jobs. It converts T4 to T3, and it converts RT3 to T2.5 deiodinase (as opposed to 5' deiodinase) is the enzyme that converts T4 to RT3.

2. More T4 is converted to RT3 than to T3. The fact that serum RT3 concentrations are lower than those of T3 reflects its more rapid metabolic clearance.3. And, >95% of the body's production of RT3 occurs peripherally. 4. Like RT3, T2 is physiologically inactive.

Under stress the body converts T4 less to T3 and more to RT3 to conserve energy. With less T3, the cells of the body slow down. This makes it clear that there is a peripheral autoregulatory mechanism as well as the glandular one that regulates T4 production.

It is clear there is also a peripheral autoregulatory mechanism as well as a glandular one. This is because under conditions of significant physical, or emotional stress, the amount of T4 that is converted peripherally to the active T3 can drop by 50%. And at the same time, the amount of T4 converted to the inactive RT3 can increase by 50%.T4 to T3 conversion is inhibited by stress,......

I'm looking forward to reading it properly tomorrow – thanks )

Love,

xx