Stimulating post from Canadian Thyroid Campaign - Thyroid UK

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Stimulating post from Canadian Thyroid Campaign

I was very taken with Tania Smith's blog on the way in which the hegemony of TSH as a primary measure of thyroid function came about historically. She conducted a mock interview with the developer of the first TSH test (Utiger) in the 60's. She brings out the conflicted views of Utiger as to how TSH could be used, and the drawbacks against it as an only test, together with its sensitivity to T3 dosing. Utiger himself was ambivalent and uncertain at tne end of what conclusion to draw, but ultimately he made the fatal error of suppressing his doubts and promoting TSH as THE frontline screen, with the results we see today (he was a revered figure). Its a beautiful look at scientific history and how an eminent scientist, who tried to be honest, at the end succumbed to his own propaganda.

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Link for this blog post :

thyroidpatients.ca/2019/09/...

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Thank you diogenes - I generally cite him, in terms of his view of still treating the patient not the TSH - and have today copied this for quotes etc... for my 'Friends in the North'. I was hoping for comments from you. :-)

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Utiger lived in his time and worked under the restricted knowledge of his time. When he finally formed his definitive (and accepted universally) opinion that TSH testing was sufficient for diagnosis "because of its exquisite sensitivity" he made that decision based on the following simple idea. This idea still forms the basis of testing today. It is that pituitary TSH stimulates the thyroid to produce T4 (and effectively T4 only). T4 is then converted by the body into T3, which is the active hormone. T4 and T3 feedback to the pituitary to control TSH production. This describes the thyroid as a simple factory producing T4 as the raw material that the body converts. When the thyroid is lost, this model simply says that giving enough T4 by mouth will restore the situation to where it was in health. that is, the healthy T4/T3/TSH will be fully restored in all respects. This simple concept is the basis of modern day thyroid testing.

It is however wrong. Utiger did not know of the fact that the thyroid is not just a factory producing the raw material T4. It also produces a portion of the active hormone T3. This makes the thyroid into a lot more than a factory, but a finetuning instrument to direct and control the rest of the body's T3 production from T4. The decline of the thyroid is countered by a TSH-stimulated increase in T3 production by the gland (as the T4 production declines and body T4-T3 conversion diminishes because of that). If fact, when the thyroid is nearly dead but not quite, its production of T3 is more than the bodys conversion to T3 of what small amount of T4 is being made. Rather than beinga passive bystander, the dying thyroid does its utmost to maintain the T3 status quo, until it finally expires. It largely fine-controls T3 production, not the body.

With this scenario, the naive idea presently held simply does not work, and the implications for T4 treatment now fundamentally change. This leads to the problems of T4 dsing for members of this forum and the need for additional T3.

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Thank you so much diogenes - much appreciated. I'm sure I've already replied to this... apologies if I have ;-)

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Thanks for that interesting info. I feel sorry for my poor thyroid going through that - desperately pumping out T3 to keep me going it got pretty rocky in the final stages then it finally fizzled out just prior to treatment. I often wondered how on earth I kept going, now I know.

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Well worth checking out all Tania’s blogs on thyroid matters!

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This probably isn’t the thing I should be taking away from this great blog post—but I can’t help it.

“Overeating can cause T3 to rise.”

I didn’t know that. I probably should have figured it out—after all, I knew that starving/dieting can cause T3 to fall.

But is this another reason why so many hypothyroid patients are overweight? It’s not just that our metabolisms are shot to hell, it’s because our bodies are prompting us to take in more calories in an attempt to raise our T3 levels?

And the effect would presumably be exacerbated in anyone who is under-treated by their doctor courtesy of the “exquisite sensitivity of the TSH”?

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My thoughts exactly Jazzw I was just about to ask the same question. At present my appetite is horrendous I feel hungry almost as badly as I did when I was very overtly hypothyroid. Normally I don’t have much of an appetite but I have been repeatedly poorly this year with one infection after another, which has coincided with this strange increase in appetite. I am trying to do a pin prick blood test to get my freeT3 reading but it has been a disaster I can’t get one drop out of my finger ends (despite huge efforts to make it flow out easily) which appear to be virtually devoid of a blood supply! It might explain the hideous nails....so I can’t check the levels to see where they lie until I can get a venous draw sorted 🙄 that part of the article about increased appetite and T3 was very interesting to me. The rest was great too.

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Re the blood supply - over the years people have had trouble getting blood from me. I've been advised to be well hydrated and to use a warm pack on the arm (where they'll take the blood). But I've never tried to do it with a finger prick so it may be different.

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You would not believe what I did to get the blood pumping 5k jog then 7 flights of stairs hot shower hand soak 24 hr concerted hydration hand pumping and swinging after 3 attempts in 3 different finger ends not even one decent drop!

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:( What a nuisance.

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That's a good theory, but many hypos have no appetite to speak of, and yet they still put on weight.

I find that my appetite has improved the higher my T3 has risen - I eat far more than I did when it was in my boots, and yet I'm not as large as I was then. So, I'm not sure that's correct. :)

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I wonder if it comes down to specific calorie sources - I'm driven to carbs. LCHF seems to lower T3 according the internet. :) That might be fine for a healthy person (a healthy adaptation) but not for the likes of us?

Or, likely it's individual. Certainly getting my T3 up hasn't noticeably affected my weight.

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Low carb affects conversion, yes. But, I don't know if calorie sources has anything to do with it. I somehow doubt it.

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But low carb is calorie source? Or am I misunderstanding?

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Ummm… I think I'm misunderstanding. lol

Low calorie diets affect conversion.

Low carb diets affect conversion.

But, you can have one without the other. Don't know if that answers your question.

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Yes, you can have low carb without low calorie.

If low carb lowers T3 (without also being low calorie) as some kind of normal adaptation for healthy people, then it might follow that it does for us too, and that we might be less able to cope with it. Or not, who knows!

Source of food seems to be at least somewhat important, at least for some people, as different foods have different hormonal effects.

Increasing my T3 hasn't had any beneficial effect on my weight or appetite, sadly.

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Well, yes, of course it affects hypos. I'm always saying to people: don't go too low carb because it will affect your conversion. I would imagine it affects hypos a lot more than healthy people.

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My mood is better when I eat a keto diet. I did some intermittent fasting and ended up unwell last year but people here thought I'd just been underdosed for a long time, so I'm not sure I can completely blame the IF. Might have tipped me over, though.

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Might, indeed.

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I will ask though, how to lose weight? A higher (and probably optimal, we'll find out soon) thyroid dose isn't making any difference. :( Keto did seem to help minimally - it reduced the hunger. Maybe IF is okay if I'm on a more optimal dose.

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I very much doubt that over-eating is the reason you've put on weight. And, the less you eat, the lower your nutrient levels. Is it actually fat causing the increase in weight? Or is it water-retention/mucin?

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Not water retention. I don't have any of the indents from socks etc.

I think it is likely to be overeating, in that my resting metabolic rate is rather low, but my appetite is normal. That's probably why I did better with keto - it did control the appetite issue.

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Should also say that even though I felt horrible, my FT3 was much the same as it had been for years - not very high in range. My TSH went very low though and as I felt so awful I sprung for the RT3 test which was very high.

It would be so interesting to try different diet options and get blood tests but not likely to happen.

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Gosh thinking back I would go days without eating anything or another problem was that I could not decide what to eat and after huge deliberation would simply give up on the idea completely. I do wonder sometimes if I was really hyper not hypo I was always on the go, hardly slept life was one big effort to dissipate excessive energy plus eating next to nothing. I was very thin too. I guess the antibodies they found led to the hypo diagnosis by that time I felt mostly hypo with occasional mad bursts of energy which I had come to regard as normal! I should dig out my old letters from guys to see what the numbers were. I do have one hyper sister the others are hypo.

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I was normally active as a young woman, and effortlessly slim. Active, but not like you're describing. And it was the 80s and we were all thinner then. I don't think I was hyper, but I wonder if my hormones were naturally higher in range.

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I was nuts, swimming and aqua jogging at the crack of dawn before work sports like running, badminton, weights every dinner time and every evening it was any of those or cycling. On a weekend I would cycle 70 miles with the cycle club and feel like I had done nothing and go and run 9 miles I might feel like I had done something a bit reasonable after all that. I was time trialling on the bike, running half marathon and 10k races as often as I could - believe you me it was mental. I had a bit of a return to it last summer riding 50 miles to work and back on the bike - gardening all day and getting up at 4am to water the allotment and working in it after work till nightfall c 10pm. I think the hot weather had something to do with it. It was very odd.

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So, you have Hashi's, then. That starts with a 'hyper' swing, and then you go hypo. And from then on, it can occasionally swing backwards and forwards between the two.

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Me? or TSH110? I never had an identifiable hyper phase.

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TSH110

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Yes according to Guys it was atropic autoimmune thyroiditis (they don’t use Hashis but I have read it requires you to have a goitre which I never had to my knowledge) after an initial hyperthyroid diagnosis. I seemed to be hyper for years at first then got more hypo episodes until the final mother of all hyper bouts (hence the erroneous hyperthyroid diagnosis) by which time I was a raving lunatic but at least I got treated as the eternal hypo set in and finally pulled through. The progression is a curious business and very bizarre to experience right to the final stages. I’m astounded a body could go through that and make such a recovery with the right thyroid hormone therapy. I still think a few things got boshed long term but I am pretty happy with my NDT life esp being depression free after decades of the black dog hounding me 😊

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Yes according to Guys it was atropic autoimmune thyroiditis

In other words: Ord's. Ord's is Hashi's without the goitre. That's what I've got. But, everywhere else in the world, they call them both Hashi's. It's just the UK that hates giving them the names of the men that discovered them: Hashimoto and Ord. :)

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Me too, but I recently read a paper that decided they were just different presentations of the same thing. If I remember next week I'll see if I can dig it up.

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Oh, I'm pretty sure it is, yes.

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I never knew it was called Ord’s - hats off to him! They claim a long descriptive name of the actual illness is better than calling it after the person who first described it. I think Ord’s is a darn sight easier than the technical mouthful guys insisted on using! I wonder why no goitre develops in some cases. I understand it is more unusual to not have one.

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I don't know. But, I shall be eternally grateful that I never had one! It's unlucky enough to have the disease, without walking round advertising it!

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My mother hid hers for years under a polo neck jumper how she coped in the summer I don’t know perhaps she was so cold she didn’t mind. It was so massive it nearly suffocated her before she got emergency chemotherapy which very luckily worked as an op was impossible due to its size. We asked fue years to see the doc about it but she would not go. Why she finally did is anyone’s guess. She was on oxygen it was so serious. It’s was NHL of the thyroid. She got 8 years of excellent quality life but it finally came back and took her the second time around. They are not a good look I can spot one a mile off. Yes we were lucky in our unluckiness!

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Sorry, what is NHL of the thyroid?

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I'd guess: Non-Hodgkin lymphoma .

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Ah, ok, thank you.

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Have just now added it to my Abbreviations and Acronyms document:

dropbox.com/s/og3lmxa1dqadb...

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Sorry I broke the rules there using acronyms - yes that is what I meant to say Non Hodgkin’s lymphoma

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Sorry I used the acronym which helvella has requested we avoid doing. I feel like a naughty child that has been caught out doing something wrong! It was Non Hodgkins lymphoma of the thyroid (as helvella has said) which is quite rare about 1 in 2 million I think so only about 30 cases a year

in uk if my understanding of the maths of it is correct. Another close relative has had it too.

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I'm so sorry to hear that. It's not something I know anything about.

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Quite few of my family have had Non Hodgkin’s lymphoma. If caught early it can respond well to treatment and in my mother’s case even when it was caught late, but she was very lucky, it did for my brother at 36. I have been tested for a genetic predisposition to it which I do have but they can’t screen for it you just have to guess your symptoms might be it and seek further investigations. Some people never get any symptoms or only one and the usual ones are a bit vague. I try not to expend much energy on fretting about it, it may never happen.

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Fingers crossed it doesn't. :)

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A family member had one, but it went away when she was on levothyroxine. I can't say I recall seeing it - though her doc saw it as she walked into the office! so it must have been noticeable. She def doesn't have one now.

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Yes, they do sometimes just go away with levo. But, sometimes they don't!

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I imagine she was quite relieved when it diminished.

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I can imagine she was!

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Jazzw TSH110

My attention was caught by the overeating and higher T3 remarks. I've been weaving all this together with other stuff since I read it and probably managed to make a tapestry full of holes...

1) We know that hypothyroidism damages the gut and lots of us end up with low nutrients. Is there a possibility that the body urges us to eat because we are low in nutrients?

2) People have been brainwashed for decades to avoid saturated fats and eat loads of carbs, and also to be abstemious with meat, which contains more nutrients than, say, pizza, grains and pulses. There are several essential fat-soluble vitamins that I would guess are chronically low in the population as a whole as a result of low-fat dogma. Again I wonder if the body is urging us to eat because of lack of nutrients.

3) People who have switched to diets which contain high(ish) protein, high fat (including saturated fats), and much lower carbs than they have been used to for years have discovered that they have few or no urges to overeat after they have adapted to their new diet. They feel satisfied in a way that they never did on low fat, high carb diets. The change of diet also probably helps their nutrient levels and T3 levels.

4) People becoming hypothyroid are mainly female, and females have a habit of depriving themselves of food in the hope of staying thin, which will increase their risk of low nutrients. Under-eating lowers T3. This almost certainly makes women more prone to depression and anxiety. Perhaps the low T3 increases their TSH, and increases the chances of them becoming frankly hypothyroid.

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That is interesting and sounds sensible to me. I think women are also more complex hormonally so there is more possibilities for things to go wrong. I am sure our bodies must know when we are deficient in nutrients and there must be a mechanism to rectify matters or I can’t see how we could have survived for millions of years. I also wondered about T2 (as per recent research) being important in controlling weight which would be another driver to get T3 levels increased so more could be converted to T2.

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Hi. So is it the t3 that converts to t2 for definite?

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As far as I understand it is part of the diodinase process until it becomes T1 and is then excreted or maybe it is recycled. But the thyroid gland also makes some of its own T2 as well (and T1) but it seems no one knows how much or if it has any significance. I personally can’t think the thyroid gland makes it for fun but I’m no expert save what I have garnered from here and pointers given to articles, as a person with hypothyroidism who felt totally dire on T4 monotherapy but feels pretty good on NDT. I have a poor conversion DIO2 gene combination which might explain it. But seems to me there is a lot about this disorder that remains unelucidated to date. diogenes would be the one who would know

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Thankyou yes I suppose difficult, as where in the conversion process does it occur? And if it still converts the same through taking the thyroid supplements

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We classify thyroid hormone actions into classical and nonclassical. The classical actions are those of T4 and T3 which have receptors for them on the cells and act as the chief metabolic stimulators. T2 is produced from T3 and is a nonclassical effector. One important thing it does is the control of mitochondrial action (the energy producing units) in cells. T1 is merely regarded as a degradation production which ultimately breaks down into iodide which goes to the salivary gland and then into the thyroid for recycling to T4 and T3. There are probably many nonclassical actions of unusual thyroid hormones, of which there are at least 25.

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Thanks for the detailed info. Is that 25 thyroid hormones 😳 So in addition to the T 4-1 there are 21 others? Astounding, if I have understood right. I wonder how they were detected and I hope they are being studied. Oddly I had terrible pains in my salivary glands when I was untreated for my hypothyroidism. I had to give up vermouth in the days when I drank, that really set it off. Interesting the salivary glands are involved in thyroid hormone breakdown and recycling. Coincidence re the pains I got in them, I wonder. Something had to set it off, it was not spontaneous.

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So far as I am aware, the thyroid makes virtually no T2. Individual thyroid cells might convert T3 (and rT3) into T2 - just like any other cell of the body.

I have often said, I think at least some comments about T2 and T1 in the thyroid have confused diiodotyrosine (DIT) and monoiodotyrosine (MIT) with T2 and T1 respectively. DIT and MIT diiodotyrosine are precursors of T4 and T3. They are created in the thryoid gland. Two DIT molecules join to make T4. One MIT and one DIT molecule join together to make T3.

Even if the thyroid did make T2 (and T1), the amount that has ever been reported in the bloodstream is minuscule. Far more T2 must be produced by conversion of T3 and rT3.

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One of the studies did say T2 was many times more effective than T3 In some actions. I presume that only small amounts are needed by comparison to T3. If hardly any is in the bloodstream is that the T2 converted from T3 and RT3 as well as whatever minisucule amount the thyroid makes? Is the thyroid part such a small amount it is undetectable or is it simply impossible to know the true derivation of any T2? I wonder if there is any clever way to know maybe using those with no thyroid on a range of T3 doses. I suspect it is all so individual it is a non starter. If it is being generated elsewhere in the body as well, it sounds like a tough one to unravel to me. How did they measure it in all those dreadful T2 rat studies?

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Both T3 and rT3 convert to T2 (and then T2 converts to T1, but we don't seem to know what that does).

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Thanks

Maybe its Important or not, you feel there has to be a god given reason for it? maybe this distorted when its not brought about the natural route?

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Having done well on Armour for a couple of years, would it not be preferable to use a product containing them all?

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We don't actually know if NDT contains all thyroid hormones, we just assume it does, as only the T4 and T3 levels are stated and regulated

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How can it not if pigs thyroid make it like human thyroid does? I thought that the better weight control experienced by those in NDT is thought by some to be related to the T2 it is proported to contain. What I don’t get is what is supposed to happen to it why should it magically evaporate when the T4 and T3 do not. Or is it thought that it is deliberately removed in processing? Has it ever been measured anywhere, or who said it existed in the first place and why - were they just kidding us....what was the claim based on? If it can’t be measured does that mean it can’t possibly exist? Given that a tiny dose change caused big changes in TSH in those studied perhaps tiny doses of T2 and T1 have an effect too. Does anyone actually know one way or the other?

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Thank you for that - I never did well on Levo - ill after weeks of taking it - indicative of, as Dr S and Dr P both Feb and May 2010 respectively said, I needed T3 {Dr P saying T3 alone for life]. Just that small amount of T3 in Amour made a difference. T3 alone... again, good for a while.

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Makes sense to me after all Mother nature has been perfecting it for a very considerable amount of time, men in white coats making synthetic isolates have just a been at it for a mere nanosecond by comparison although they’d have you believe they have improved on nature I simply don’t buy it - I call it arrogance.

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Yes, and I've done better on NDt than levo, but we're not pigs and the hormone composition isn't the same. I'm not sure that 'natural' is important. I think for some of us levo is just incomplete and it may be that more human composition of synthetics may be better than natural animal hormones? No way to tell without research.

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But the research demonstrates that synthetic hormones are not as effective as NDT in normalising free T3. If our Thyroid strives against all else to keep free T3 within very narrow parameters - look what diogenes says even when it is in the final throes it keeps pumping out as much T3 as it can - then the hormone therapy that most closely mimics this is to my mind superior and what I’d want as a first line treatment ie NDT . Also the T4/T3 proportions are not a fixed ratio they vary greatly from individual to individual with some of us actually having ratios similar to the pig. In addition this ratio is not fixed, it is dynamic so the body supply of thyroid hormones is constantly fine tuned to meet changing needs with free T3 levels being the driver of the thyroid hormone production. That means there must be mechanisms to fine tune the ratios to suit the needs of the body. I presume rT3 must be part of that fine tuning. I also presume that these mechanisms must continue functioning despite the thyroid failing partially

or fully, a bit like TSH actually serving no real purpose but the signalling still remaining intact without any thyroid function. To claim NDT is the wrong proportion to what our thyroid once made (when we don’t even know what that value actually was and it was not constant anyway) so it cannot be as good a synthetics does not hold water. Why do I feel perfectly normal on it if it is not at the correct proportions to give me health? T4 monotherapy most certainly did not restore my health at any dosage. I have poor T4 to T3 conversion to make matters worse for me and perhaps I am more pig than human in my thyroid hormone needs but I find that improbable. I believe our bodies are quite able to get to a euthyroid state on NDT

and have some measure of fine tuning T4 and T3 ratios tho obviously not as good as a real fully functioning thyroid. As it varies so much from person to person perhaps NDT is not best for everyone but given the obvious importance to health of freeT3 levels being properly maintained that is the one I intend to stay on. I would even surmise it is probably better for the majority than synthetic monotherapy or combination therapy. In addition it is far easier to get the correct dose and you don’t event even need to faff about with blood tests. For me the downside is feeling bad about the pigs dying to keep me alive. I was a vegetarian of many years.

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Are you able to point me to the research you refer to? Both the one that says that NDT normalises T3 more as well as the one that talks about the variation in T3/T4 in humans? (What can I say, I'm a nerd... lol at myself) I'd be interested to hear if NDT was compared to comparable T3/T4 therapy, or just T4, and at what doses.

I am not trying to say that synthetics are better (or worse, for that matter) - I haven't personally seen research that has convinced me of anything either way. I don't think that synthetic T4 is bad, just an incomplete treatment.

I know that when my TSH was 1 on T4 alone, I was unwell. I felt better on NDT, and I've always assumed it was the T3 component that helped.

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The one article was linked to on here but can I find it - aaargh! It was done in the USA I think at a hospital and they compared NDT to synthetic combination therapy on patients who did not do well on T4 only if my memory serves me well. They did detailed analysis of blood results and the NDT patient’s were much closer to normal (ie no thyroid problems) euthyroid readings than the synthetic T4 T3 group. They also scored higher on QoL questionnaires so not only were the blood results better so was their opinion of how they actually felt. Mind you there would be individual variations so the worst on NDT might feel less good than the best on synthetics. It was a very interesting and readable study which seems to have disappeared without trace. I might post to see if anyone remembers it and has a link to it. It was fairly recent I checked all helvella post goibgvback over a year and diogenes but drew a blank - humanbean is next!

The other study was posted by diogenes (very hard going despite having fantastic info) and I think his papers discuss it too they are easy to get on with. It just demonstrates that the action of the thyroid is very dynamic with free T3 protected above all else and how this is achieved. Thyroid hormones are pulsed out in mini bursts and rise and fall throughout the day and night as shown in graphs. So nothing is static or fixed and it can change according to circumstance in addition to the diurnal ebb and flow.

I’ll put the link to that paper.

I think TSH of 1 is quite high if you are hypothyroid. Toft recommends between 0.2 and 0.5 which is what my endocrinologist aimed for. I still felt unwell and my free T3 was low but freeT4 high. So I was not converting well. Other members of my family with hypo love their Levo and feel great in it so I was really gutted after 9 months of horrible struggle to still feel dreadful. I tried taking more but just felt wired all the time so no dose worked. I suffered it for 2years and became suicidal so decided I had nothing to loose with NDT - it started improving matters within days and as I gradually increased the dose I felt better and finally normal again. I am interested that T4 only does not seem to restore anyone’s blood levels back to healthy levels where NDT does. I think the ramifications must be significant over time given the vital role T3 appears to play in every cell in the body. Not having enough must have long term consequences for health.

I wonder if you would have felt ok on a higher dose of T4 but quite frankly I think you are better off sticking with NDT.

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That's possible. I was probably undermedicated on both but better on NDT.

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Glad you are feeling better on NDT. Did I post yiu the thyroid Patient Advocacy guide to correct dosing with it? It is very helpful.

This is diogenes post with a really good article by Lindner and link to it, that I mentioned.

healthunlocked.com/thyroidu...

The Canadian doc for the site mentioned on this post title is really good such clear and informative articles a big thyroid penny dropped for me reading her stuff - from fuzzy to sharp focus comprehension in a few sentences, she is good. diogenes is a fan too.

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I get you on that one, yet the pigs would have died in any event. <3 As we will, before our time, if these damned endos keep on influencing... :-(

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Yes I tell myself the NDT is just a biproduct of meat eating - every last part of the poor piggy winkle is used apparently. I’m with you on having life expectancy reduced by those crazies in white coats who think we don’t deserve a quality of reduced life either

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I think I have read somewhereT1 does something but quite what I have forgotten - I am sure it was in a very technical paper - perhaps it was a postulation.

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Is be interested to read it if you find it.

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I will try but it was pretty impenetrable plus I might be wrong!

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Post away, no problem. Sometimes someone else will understand other parts and you can sort of put them together to understand more.

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I have this somewhere, spent a while looking - would really appreciate if you can find and I'll post if I do. :-)

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I can only find a mention of T1 being involved in MS and motor neurone disease on a Thyroid Patient Advocacy discussion but can find nothing scholastic to back that claim up. Jury’s out then. Plenty on T2 though and it was believed it did nothing too. It appears it does rather a lot in fact!

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The number of papers which even mention T1 (as monoiodothyronine) AND multiple sclerosis is pretty small.

ncbi.nlm.nih.gov/pubmed/?te...

And most mentions I could find of the literal characters "T1" AND multiple sclerosis were actually referring to "ratio of T1- and T2-weighted signal intensities" (related to Magnetic Resononace Imaging) or similar.

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I did wonder if the MRI machinations had been confused with the thyroid hormone leading to incorrect claims for T1 having a function other than a necessary stage of thyroid hormone breakdown and recycling. Do you think that has happened?

Did you get anything for motor neurone they have a different name for it in the states which I had not realised after someone who had it but I forget the name which I am sure you will know.

On a different matter I have a famous thyroid person for your list but a) I can’t find the list to check if she is there b) I can’t find a relevant post to respond to with the info c) I was too scared to send you a PM in case it incurred your wrath!

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I found just as little for Motor Neurone Disease and T1.

The USA call it Amyotrophic Lateral Sclerosis, I think. Or Lou Gehrig's disease.

Send a PM! Info like that is welcome - it is discussion which is (generally) better in the open. :-)

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I feel like I eat more calories than I "need" (exhibit A: weight gain!; exhibit B: my measured low resting metabolic rate) and it's rare (annual?) for me to feel like I've overeaten. I particularly crave fast energy (carbs, bread) even though I know my mood is better when I eat low carb and high fat.

That doesn't surprise me at all, if it turns out we are driven to eat to feel better.

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Hi yes can relate to times I have eaten to try and feel better! It's like filling up a hole, maybe the opinions that we are filling an emotional hole when we do this runs a bit deeper?

Dr S Myhill is strong advocate for paoloketogenic diet which is simply plain eating, no carbs, butter, lard protein, veggies - quite interesting read on her website

I had wondered if she was talking to ALL including hypo

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I tried all Dr Ms advice and FODMAP but was either undiagnosed overt hypo or T4 monotherapy that was of little use to me. I hadn’t felt hunger for 6 years at diagnosis. Hyperglycaemic incidents but no hunger,

Now I take NDT and have a number of issues properly diagnosed and medicated my diet is almost exclusively carnivore (MCAS means I am down to a handful of foods and IBD means most veg are out) the inflammation is down, weight is down a bit but my body shape has changed completely. No longer puffy and with a stomach roll. And hungry. Always weird to be weighed and be declared the same no. when my body is so very different even if still wheelchair and bed-based.

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I'm eating loads of gluten things just now to do a coeliac test but I'm looking forward to eating a better diet again. Adequate meat (2-3 times recommended, lol) is not negotiable in my diet to get enough iron. I do like vegetables and they don't seem to cause problems so I'll keep on with them. Glad to hear you've had some improvements with your own diet.

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I like your comment on filling an emotional hole possibly being a lot more profound in implication than we might realise. A lot of emotional terms we use are heavily allied to eating and digestion. I think the skin and guts come from the same basic tissue in the embryo (of the three main types) our stomachs are supposed to blush when our face does. How unexpected is that?

No lard or bone broth for me tho! Never liked meat even as a child.

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Interesting, are you saying in other words that the gut 'quality' is defined in the womb, sorry if misreading 🙈

Yes when low emotionally I've often turned to nice thing and chocolate, but is this also about the whole,hormone thing, it's a complicated affair LoL

Gut healing is vital isn't it, however you manage to heal it

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There are three types of cells or layers in the early stages of foetal development that differenciate into the major parts of the body. The skin and guts develop from one type the skeleton from another abd the brain and nervous system from the third (I think I have got that right) so the skin and digestive system gave the same origin and are linked in unusual ways. I guess the skin holds the outward expression of emotion like blushing. But think of expressions like fed up to the back teeth, butterflies in my stomach, sick to the pit of my stomach, bricking it (excuse the underlying meaning which is a tad vulgar) all describe an emotional state via digestive association.

I believe chocolate has antidepressant qualities plus lots of iron so it does have interesting qualities as well as being horribly moreish Fruit and Nut is my weakness interestingly the nuts are almonds which contain high levels of magnesium of which I deffo have deficiencies, dreadful cramp in the night for example and the fruit must be good for us 😎 plus it dies not cause such a high sugar spike in the blood than pure chocolate so it’s bad but not the baddest!

I totally agree about gut healing more and more research supports how fundamental it is to health

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Yes. Eating sweets is a way to self-medicate depression and/or anxiety. verywellmind.com/why-do-i-c...

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Sugar definitely made me feel better at a time when I was trying to get off an antidepressant much too fast (at a recommended pace). It would have been worth the ill effects from the sugar if I'd been able to get off properly then, but sadly it failed.

I read something at the time that talked about glucose and the brain and it made sense then.

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I was so lucky I was able to stop antidepressants by the recommended gradual reductions. I have heard it can be very difficult. I was on two different types for quite some time. The first time I felt like I had been blasted up to the stars and was amazed such drugs could be legal! They did some strange things to me I wasn’t depressed anymore but I was decidedly unreal in every way! The second type were not as space rocket 🚀 as the first. In the end they both stopped working and I got a bit aggressive. NDT cured all the depression without the spaced out stuff/nasty and it has not stopped working either.

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Yes there are some who can get off at the rapid pace recommended, and I'm very happy that you were one of them!

Sadly, there are also those who think they've got off safely at the recommended pace but we (at a support forum I use online) see a lot of delayed withdrawals, so we also see people who crash and go back on, or go onto another drug. They tell people they got off the drugs safely, which is a pity as it reinforces the rapid pace. Still, as you say, some people do get off them at the rapid pace.

I don't get the unreality, but I did get some nasty side effects, and it was very distressing to discover that I could not stop the AD, and had instead to deal with physical damage from the meds while slowly, slowly getting off.

Now, I've been told by well meaning friends that the fact that I am having such a hard time getting off the AD means that they are working (and by implication, maybe I need to keep taking them). I say, well then, why is it that while withdrawal after a dose cut is rough, why do I settle down to a better point than I was before I cut the dose in the first place?

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They may be working but working on quite what? I bet no one really knows. I was reading there are sleep deprivation and sleep advancement programs being used to try and target depression which seem to target the same systems as antidepressants and are effective for some. It sounds interesting and possibly less damaging (if done correctly as sleep deprivation persay is not good for us for sure) than anti depressants especially as they seem to be addictive or difficult to stop (may not be the same thing) in some people.

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I've also seen that thought about sleep deprivation. There isn't a lot of compelling evidence that I've seen, as to whether they SSRIs work better than placebo. I agree, I don't think they know what they really do.

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