Based on feeling awful on just levo and having keniesiology testing today the levo and westroid I took along both showed positive to take, it doesnt of course differentiate between the two
So thought maybe to take one levo 25 and add in the westeoid half grain to start? but grateful for advice on this please? my vitamins were ok except for calcium,
I'm having private bloods done soon also to confirm everything and to see if optimum levels
You may or may not think this all crackers, but I feel happy to think the ndt showed good for me at this time, bearing in mind I exist in a half life with constant fear sensations that plague me
Tomtske, can anyone advise please, shall I take the levo with westeoid, or take levo at night as previously and the westeoid apart? I know it's low starting dose
- maybe I'm better waiting to see free t3 level from bloods, although I know it will be in the lower part of the range by the waynInfeel
Jx
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I'm going to jump right in here, because it really worries me; and say that there is absolutely no scientific evidence to prove that "applied kinaesiology" can either diagnose illness or prognosticate what treatment is or isn't suitable, and our muscles have no capability whatsoever of reading a medicine container held in front of it and conclude that it's good or bad for you. Practitioners are either snake oil sellers or expert cold-readers, who in my mind, as a qualified therapist, prey on the desperate . Only a complete set of blood testing will identify which hormones, vitamins and minerals are measuring as deficient or in excess, in order to guide your supplementing decisions. If you believe your symptoms are indicating a deficiency of T3, why would you add levo to an NDT?
I watched the BBC six o'clock news last night. I don't know if or not you watched it?
It interviewed a women who had been taking T3 and was well and has now had it taken away.
The interview also wanted to know why the NHS were being charged such a large amount for the purchase of T3 and pointed out the price in other EU countries which the cost was just a few pound per packet.
I just hoped that somebody important in the government was watching but I doubt that?
• in reply to
Bunnyjean thank you for mentioning that. There is a powerful Facebook group thrusting ahead with its aim to achieve improved thyroid care, primarily, but not exclusively, through a shift from the TSH as a prime/sole indicator of thyroid health, and the "unbanning" of T3 and providing universal availability of both it and NDT. The creator of the group, and key others, have been doing stirling work to feed into the national consultation process etc; and members have been writing to their MPs, CCGs etc plus much more. After the provisional finding by the CMA that that particular make was massively overpriced, the pricing issue etc is being further considered by the relevant agency and Govt depts, so thankfully it isn't going to be possible to ignore this. If you're interested, you can join the FB group ITT (Improve Thyroid Treatment) Campaign.
Hi, in my experience Levo and NDT work well together. DTE alone is not physiologicaly suited to humans, pigs yes! Consider using DTE to add a physiologically normal level of T3 with however much levo you need for however much T4 your body manages best with. e. g. 50-70 µg Levo and half to One grain DTE to give 5-10 µg T3 which overall is something like having to take 100-150 µg Levo. Of course everyone's needs and progression is unique to them and should be established by regular frequent blood tests of TSH FT4 FT3 and a symptom diary. I take my Levo in split dose before bed, on waking and the DTE in 3 equall doses at the same time as the levo and at midday. It works for me!
EH? NDT (what you call DTE) is the "original" thyroid treatment and many humans do much better on it than on levo, since it contains T4, T3 and probably t2 and T1 also. I don't know that pigs go hypo. It's easiet to individualise your dose with T4 plus T3 than with NDT - and you need to buy both NDT or T3 yourself as the NHS won't prescribe, so really the choice is yours. I'd tend to go with with either T4 plus T3 OR NDT (or even NDT plus T3), not NDT plus T4, as many people seem to have problems with conversion from T4 to T3 so adding more T4 isn't often helpful.
desiccated porcine thyroid is not physiologically balanced for humans. Alone it will either tend to overdose T3 or under dose T4 when considered as a alternative to Levothyroxine for straightforward hypothyroidism. My endocrinologist is relaxed about desiccated in combination with Lerothyroxine, as am I, and I use it! It gives the best of both worlds in the absence of a conveniently packaged dose of synthetic T3 and T4 that can be easily titrated. Synthetic T3 isn't readily availably in doses small enough to reflect human physiologic.\ needs in straightforward replacement therapies. The drug companies have failed / neglected to develop a physiologically balanced combined pill for human hypothyroidism. And the NHS is increasingly reluctant to prescribe concomitant T3 , even where they were doing it? And yes farm animals can be hypothyroid!
Scientifically true, but it always seems empirically that people who don't get on with levo alone need far more T3 than we are told the human thyroid gland normally produces in order to achieve decent free T3 levels. The tiny t3 doses that would mirror what we are told we would naturally produce generally do sweet FA - which is probably why there is so much "evidence" that T3 is not useful.
Agreed, Angel_of_the_North . We rely more on peripheral deiodination than gland production of T3, not that you'd know that from the poor quality research into combination treatment.
where is the evidence that physiologically comparable (to thyroid secretion) supplementation of T3 does nothing useful?
Are the people who don't get on with Levo and changing to some form of T3 Supplementation measuring at least FT3,TSH and FT4 every 6 weeks and keeping detailed diaries of physical symptom observations to accumulate profound empirical evidence?
Part of the problem with managing this is over reliance on often confusing anecdotal 'evidence' and often repeated opinions, which have lost their originating evidence (if there was any). The complexity and individual variation needs detailed empirical observations over long periods to identity variable factors and subsequent statistical analysis to find meaningful relationships.
No one appears to be doing such research, or interested in doing it!
Hashihouseman I think Diogenes addressed the issue of T4-T3 proportions in porcine desiccated thyroid on the forum a few weeks ago. The human body will take the T4 it needs for conversion (assuming one can convert efficiently) and the rest will be deiodinated to RT3, the waste product. The fact that pig thyroids produce more T3 in the gland than humans do isn't really relevant. Or at least, it becomes relevant if NDT/DTH doesn't provide the individual human patient with enough T3, and that patient is also a poor converter.
I haven't found any scientific research that talks about that or evidences the assumptions behind it.... Can anyone on here link to the research that sheds more light on this. All the research I have seen indicates that homeostasis is demand led rather than continually adapting to excess supply. Hyperthyroidism is partly a consequence of our limited allostasic potential to ameliorate excess endogenous T3. Euthyroid individuals are unlikely to produce the excess of T3 possible with high doses of desiccated. The Naturopathic solution to homeostatic peturbation is surely mimicing Euthyroid hormone synthesis with exogenous replacement as closely as practicable....?
I hadn't seen this discussion till now. The sequence is that the thyroid produces about on average 20% of the T3 that is present in the body. The remaining 80% comes from T4 conversion in the tissues. Therefore the body only produces what extra T3 is needed to satisfy demand overall. In health, if the thyroid slightly falls in production, body conversion makes up for it. If the thyroid is lost, the body has to do it all - that is work harder to make up for the loss of direct T3 supply. If T4 only is supplied then for some people, the tissues can't convert enough to satsify needs at any T4 level - if added too much T4, the conversion is actually inhibited, and T4 is diverted to rT3 to avoid what the body sees as a toxin. Thus from this argument alone, the T4/T3 ratio is different in therapy than in health. So if this change is tolerated, so this applies to NDT which similarly has an apparently improper ratio of T4 to T3. But it is not the ratio that matters, but the actual T3 in the body derived from the amount of the combinations of T3 supplied direct and T4 conversion. So long as the NDT dose doesn't by this combination produce too much T3, then all is well. One can disregard the T4 as being the inactive reservoir.
Also as my own body has produced 'not bad' levels of t4 and free t3 but under the half way with the t3, I have struggled with it, as just really felt I needed a bit more of free t3 going on
A question which may seem obvious to those in the know, do you still need t4 and t3 in the middle to top third of range, when it is tested WITHOUT any supplementing at all, or is this only when on meds?
The answer lies in what you are taking. If only T4, then normally you'd need high-normal or just above-normal FT4 to get an adequate FT3 (upper third normal). But again we have to be careful. In health some people were healthy with quite low FT3. These are "sensitives" to T4 therapy - its easy to overdose them. They are the opposite of the "insensitives" who had high FT3 in health. On the other hand if you are taking NDT, then you'll achieve acceptable FT3 with lower FT4. And of course on T3 only, hardly any FT4 at all.
Thank you diogenes for your input again which is much appreciated and so fascinating.
Can I ask how much the TSH level affects conversion? For instance, If a persons FT4 level is at the top of the range, but FT3 near bottom with TSH very low, say as in my case 0.07, is it possible that by reducing levo the TSH will rise and therefore FT3 will rise also?
I'm thinking that maybe someone whose FT3 is naturally low and therefore does not need higher FT3 levels might do well by reducing levo and letting the TSH do the work of pushing up the FT3. Could this work?
Control of TSH is though both T4 and T3. So if FT4 is near the top of range and FT3 near the bottom, the sum of both might be the same so the effect on TSH is also the same. However, if you have too much T4, there is a feedback which actually inhibits T4-T3 conversion so paradoxically you would be worse off than if you were taking less T4. In this case you'd see high rT3 because the body gets rid of unwanted T4 that way. If however you weren't taking too much T4 and your situation is as you say it is, I'd suspect poor T4-T3 conversion, and a failed attempt to get enough FT3 by the T4 dose which puts you high in the FT4 range. So if you lower the T4 dose, your TSH may rise, but your FT3 will fall. Matters will then be even worse. FT4/FT3 ratios of greater than say 4.5 for a given dose of T4 only should rouse suspicions of poor conversion.
My situation is that I tried T3 for a month whilst lowering levo slightly and felt much improved but came to the conclusion that I was reacting to one of the fillers (tight-chest, wheezing etc). Been off the T3 now for a couple of weeks, allergy symptoms gone but have not increased the levo back up as I feel really well, far better than I have for ages.
I've read many time of these boards that people notice an improvement when lowering or coming meds altogether, but this is temporary only, but I wonder if there is any scientific explanation for that.
....the very same question I wanted to ask! I felt so depressed and anxious on levo I felt I should take to try that as first port of call, now I'm well reduced I feel fab, my old self however I know it's temporary as read this, and that there is a scientific reason for,this, I don't think it's a physcological reason!
I'd just like to mention though that it gets forgotten at times that we are as good as our gut quite often, as without absorbing the right vits and minerals also, most is a lost cause, correct me if I'm wrong, it's the Whole thing for sure, it's quite daunting when a beginner
Hoping that when it's all evened out and balance restored it's easier to maintain
Cheery and back with blood results shortly, and also how much is influenced negatively by out of sort adrenals x
And me too forever summer, but caused by the German name of Levo, walkork or similar,
I got cataagh and wheezing and cough, it was difficult caused by the filler and couldn't continue, jynintuition knew this one although toldmit couldn't be true, as haven't had this with teva or mercury brand
Can't speak for t3 - yet
My gut feeling was to top up a bit of t3, it told at the time to take ndt
(Minefield when your brain won't go and lurching through day by day !!!!
Thanking you, I'm awaiting blood results and all will hopefully be revealed, although I'm now wondering if you are referring to whether or not levo has been taken?
I have before and after results anyway and adrenal saliva x4 so will really appreciate expert words xxx
Sorry Helleva I e read up a bit on combination t3 and 4
I quite fancy this or separate t3, I was out off t3 - is it a bit risky dosewise, what's the worst? As yes, can add it in to the prescribed levo as clutter said
This is a really interesting discussion to have here because clarity in the basic physiology and kinetics of TH metabolism underlies the issues and subtleties of individual variation. The more people who actually experience the conditions who can feed the discussion the better; because it is unlikely that many endocrinologists actually experience the sensations and challenges of hypothyroidism and hormone replacement and often fail to even try and explain the difficulties let alone diagnose and support individual needs and alternative hormone replacement regimes.
Sometimes the lack of endocrinologist support seems rooted in negative altitude, and / or negligence in considering relevant and recent research which increasingly points at the possibility of narrow individual tolerance to hormone concentrations around the personal set point of thyroid homeostasis which contribute to considerable variation in the treatment response.
In contributing to the discussion my experience of finding the least worst replacement regime was helped the most by aiming my replacement therapy at ratios both in dosing and resultant blood levels that mimic empirical euthyroid conditions. So, the starting point for some form of exogenous T3 for me is a realistic approximation to the amount of thyroidally secreted T3 Someone of my size / weight / status would likely produce.
All the research and creditable academic papers I have seen indicate between 6 and 9 µg of direct T3 that my thyroid gland would have delivered, and presumbly for some good reason! So why not aim at replacing that !? Even though that amount of T3 is only about 20% of the overall free T3 in circulation it nevertheless has some functionality in that it is part of the euthyroid state, which does not rely on 100 % T3 from T4 conversion. And, even if this is only functionally significant as part of the homeostatic feedback pathways it may be one of the missing links in optimising efficacy and efficiency of exogenous T4 replacement...
Given that all the representative analysis of thyroid kinetics indicates that my healthy thyroid gland would produce about 100 µg T4 as well as 6-9 µg of T3, the daily ratio of T4:T3 could reasonably be assumed to be between 11-14:1 and this is the aim I take. Interestingly the outcome ratios and stable TSH and symptom experiences for me are, so far, associated with an 8-10:1 T4:T3 ratio i.e. needing more T3 than the euthyroid model suggests. And the 4.2:1 ratio in the desiccated preparation caused thyrotoxicity in me from excess T3 in chasing Stable TSH which was manifest at every empirical perspective. So, yes, the T4:T3 ratio is different in therapy than health in my case, and I have a DIO2 gene polymorphism that could explain that.
The discussion and perhaps a way forward for some is that mimicing euthyroid hormone secretion ratios could be helpful and that Desiccated thyroid may be an an easier way to add small amounts of T3 than by prescriptions of synthetic T3. This could also help by conferring other potential benefits of the natural thyroid while helping to avoid overdose of either T3 or T4. The only caveat I can see is that this proposition assumes the continuing difficulties of obtaining low dose synthetic T3 prescriptions and lack of combination Synthetic preparations in any dose ! (surely an oversight of market potential ?)
The current 'either or' paradigm of desiccated or synthetic thyroid hormone replacement falls into the trap of excess.
Excess T4 , which even fully conjugated still seems impossible to disregard as an inert resevoir since all Levothyroxine absorbed is initially at least Free T4 and exerts physiological effects and feedback loop influence in a way in which the demand led secretion does not and is part of an active dynamic equilibrium between total and free T4.
Excess T3, from doses of desiccated thyroid sufficient to elevate free T4 and stabilise TSH carries a straightforward risk of thyrotoxicity, hyperthyroidism from exogenous T3. The only exception to this may be where for whatever person specific reason the T3 in desiccated is not excessve for a particular individual as proven by regular and frequent blood level checks of free T3, free T4 and TSH.
Combining desiccated and synthetic preparations may be a preferable alternative or solution for the challenges of starting combined hormone therapy. Even a cynical endocrinologist may support such strategies given the guidelines in the European Thyroid Association 2012 review paper which concludes
' it is suggested to start combination therapy in an L-T4/L-T3 dose ratio between 13:1 and 20:1 by weight (L-T4 once daily, and the daily L-T3 dose in two doses). Currently available combined preparations all have an L-T4/L-T3 dose ratio of less than 13:1, and are not recommended..'
So, while some of us may not optimise on 20:1 or 13:1 or even 10:1 combining desiccated preparations having a 4:1 ratio with Levothyroxine to increase the ratio to something more suitable may have the potential to utilize the best of both worlds.
In my experience, the lack of endocrinologist support seems always to be due to the lack of contact between thyroid patient and endocrinologist.
In my own case, I don't think that any word starting "endo-" has ever been uttered when I have been with a GP about my thyroid. Certainly not in conjunction with "refer". This is in no way unusual - "simple" cases are usually classed as GP-managed.
In another case, the endocrinologist ensured that his lackey registrar passed on his complete lack of interest, unwillingness to help, and absolute lack of human empathy to someone in desperate need of help. Despite the GP knowing he was out of his depth, the patient was sent back to GP care.
There have been combination products in at least 10:1 and 4:1 ratios. The USA product Thyrolar is a 10:1 product but has not actually been available for many years.
But you do not need to use so much NDT as to normalise FT4 and TSH, whilst then overdosing on T3. As either an inert precursor (T4) or indirect signaller (TSH), the levels of these are irrelevant so long as the T3 given in the NDT restores FT3 to normal (whatever that is for the individual). If FT4 is also doing something then there is enough there to do its business.
How can free T4 ever be irrelevant? The whole body whole thyroid system has evolved, empirically at least, into a balance of T4, T3, TSH and the rest. T3 and T4 have different attributes and functions and are not just simply swappable by hormonal value factoring. For example, sufficient free T 3 to maintain some target of TSH will lead to gradual depletion of total T4, reduction in hormonal buffering capacity , lack of plasma T4 for intracellular conversion, predispose to uncomfortable and natural circadian rythyms of free T3 (short half life etc.) and potentially confusing and uncomfortable effects on TSH. And then there's the risk of thyrotoxicity and cardiac anomalies. T3 led therapy is a rollercoaster without the buffer of someway normal total T4. Blood levels of so called normal T3 are snapshots of a much more rapidly and a changing scene than T4 and smoothing peaks and troughs in free T3 is either reliant on frequent split level dosing which can completely overpower any potential for autonomous homeostasis, or on the bodies allostatic mechanisms which could struggle to keep free T3 and TSH levels in a benign state.
I think you are rather barking up the wrong tree. First both T3 and T4 almost equally control TSH production. Second I don't understand what you mean by hormone buffering. Someone on T4 therapy only can often only achieve adequate FT3 if their FT4 is high in range or just above. The FT4 level is quite different from their healthy state, so since the therapy is successful we can say that FT4 levels are not so important compared with FT3. Furthermore, hypothyroid symptoms are only correlated with low normal or low FT3, and neither FT4 nor TSH. If a patient on T4 therapy cannot make enough T3 by conversion, then T3 has to be given to get the FT3 up to a desirable level. That's I'm afraid the only solution if adequate FT3 can't be achieved otherwise. Then one has a combination of what conversion the body can achieve + the extra T3 to attain satisfactory levels of FT3. I agree that T3 therapy is tricky but it can be controlled by multiple dosing through the day to minimise peaks and troughs in FT3. I've also advocated for a long time slow release T3 to help matters. Temporary hyperthyroid peaking is not desirable but anecdotally doesn't seem to be too important, and the biochemical responses will be slower and therefore damp out the peaks and troughs. So in short, FT3 is the target and FT4 is much more flexible - if it wasn't therapy of any sort would be enormously difficult.
Total T4 and, commensurately, freeT4 are the hormonal buffer for freeT3 by way of being consistently available for conversion regardless of supply side irregularities and thus help prevent crashing into a wall of critically low T3. Otherwise, in the case of exogenous T3 dependency, one missed dose could cause noticeable craving / shock and after a few missed doses hypothyroid symptoms would escalate to very unpleasant levels without a T4 buffer. T4 is also a significant part of the signaling and overall allostatic response mechanism which is very hard to emulate by T3 focused daily dosing. I know I’ve tried both ways.
I'm not arguing that it is best or desirable that T3 only be an optimal therapy - merely that the actual level of T4 acompanying it doesn't matter so long as there is some. But I also believe and some members of TUK might confirm, that T3 only can be managed without apparent side effects.
I think your definition of a buffer is raher strange. I'd rather liken T4 to the tank of fuel (inert) which is changed on demand to combustion chemicals (active). The tank is merely a reservoir in this regard, and whether it is full, half empty etc doesn't matter if the demand can be met.
Except it’s not inert, there’s an active dynamic equilibrium between total t4 and free t4 and free t4 levels have physiological effects as part of the allostatic feedback loops not just as a precursor for T3 production wherever and whenever it’s needed. Given Most cellular requirements for T3 are supplied by deiodinisation which is fed by active transport of t4 from plasma rather than simply being bathed in extracellular t3. It may be an unecessary stretch to create a T3 heavy replacement regime at the expense of inadequate T4 replacement and only necessary if there is chronic incapacity with intracellular diodinisation e.g. unusually disabled enzyme activity because of a profound polymorphism. Defining t4 replacement needs as ‘some’ being enough isn’t scientific or helpful.
Where is your evidence that T4 has an important direct physiological effect and on what? The body isn't controlled by any part of the equilibrium beween bound and free T4 or bound and free T3 - this is simply a passive automatic twoway equilibrium that responds to any celllular demands automatically. The body is controlled not by T4 levels themselves, but by controlling (increase or decrease) in the activity (amount) of the deiodinases that convert T4 to T3. And there are three different deiodinases each with their own response to challenge. Of course if there's no T4, then there's no T3 either. However, when the thyroid gland is failing, the body reacts by activating T4-T3 deiodinase to maintain FT3 production as close as possible to normal. This can go on to a great distance, until the thyroid is almost dead, when the T4 tank is so depleted that pressing on the accelerator however hard (deiodinase activation) can't produce the T3 needed. Both T4 and T3 control TSH about equally - mole for mole - so that in the failing gland, T3 increasingly dominates the control mechanism. The role of T4 as I've explained is largely as a precursor supply for T3 and can have only minor direct physiological roles.
I agree it doesn’t matter if the tank in your analogy is half full but it could matter a lot if the tank is running on empty or is repeatedly being drained faster than it is filled. It could also matter if there is physiological stress incurred by having an overflowing tank (too much ft4) or having to struggle with sucking on low levels in the tank, which is why the tank analogy is over simplistic for a non-linear complex enzyme dependent system with active transport components affected by complex feedback loops.
Thanks for these. The argument isn't futile and this is the place to have such discussions. and yes they should be evidenced based with nuanced and valuable differences in interpretation. Of course if you think it is merely argumentative or truly futile it's not rude to ignore posts. The issue over T4 levels we were discussing isn't as cut and dried as you put it based on the evidence I have seen and which I will place in my reply to your last post on that after I have read the references you have given me.
Hillwoman thanks for this clarification via Diogenes. It totally bears out my “anecdotal” experience of feeling fully well on NDT, very unwell on Levothyroxine, and increasingly better with each reduction in levothyroxine and increase in NDT as I swapped from one to the other. My anecdotal evidence is good enough to prove it to me that NDT suits me much better than levothyroxine
It's one of those things that yes you do go when desperate maybe but it is something maybe not to be knocked so harshly, as John Lennon said,mdont knock unless you try 😊 For me, I feel the reaction and that's enough
Having bloods done shortly and will be interesting to compare ( I'm not guloabke enough not to do the scientific alongside, I use the whole spectrum as for me we are made up a lot more intricately than just blood numbers etc, marvellous as they are, there probably are folk walking around fit and healthy with a 4.2 tsh, all unique as they say
Hi Jeppy I'm glad you're getting your bloods done shortly. Yes, we are unique, and having something that sits outside the average can simply mean we are normally an outlier in that respect, or it can indicate a problem.
At the urging of one particular friend over the years, I've definitely tried kinesiology, and a number of similar, other random & whacky "treatments" myself, (although I don't think you can universally apply don't knock it until you try, it to everything - there are things that you just don't need to try at all to know they're a very bad idea), so I do speak from experience. My friend twice refused surgery for her grapefruit-sized tumour, turning instead to a "psychic surgeon". She was only 52 when one of her sons rang to tell me she was dead from the tumours that had spread throughout her body; and they were locked in a legal battle to get back their mother's assets from the wholly unsuitable and devious "soulmate" she had married on the validation of another "therapist". The mind is a powerful thing, but desperately susceptible to being misled at times - for instance, if we accidently touch an iron that we believe to be switched on, the pain experienced can be just as real as if the iron really was hot instead of stone cold.
.... meant to say, I just feel so fed up with the depression, panic that I experience which I do believe is hormone related , both the sex ones and the thyroid, not just one thing, I seriously need to feel better sooner not later, spirits and patience worn out while life passes me by
So by adding a bit of ndt with what I take now, levo, I'm hoping will indicate that the t3 in it will lift, if it blends that is, no harm there really
Cup-cake7 this is exactly what I did but used 1/4 grain instead of 25mcg Levo slowly swapping over to NDT. I started feeling much better within 3 days and kept going with replacing Levo knowing if it did not go well I could easily pull out. I never needed to pull out. I used the thyroid patient advocacy guidelines but Stop the thyroid madness have good ones too that you could follow I will put up links for you
I think it is advised to sort out adrenal problems before taking NDT but I am not sure if I had any and the NDT helped with my unresolved hypo symptoms. Others here are more knowledgable about adrenal issues and I hope they will advise
This is the info on stop the thyroid madness about it:
Hi all thanks so much for replies, clear as mud now 😱😊. Mixed thoughts, And this is why I like keniesiology at times as it irons out for me these dilemmas, I just forgot to do this joint testing with her.
No worries there's another I can pop to see soon, he has been so helpful to get me on road to recovery as without him I'd not have known I had a leaky gut and was intolerant to a few things, that I took away from my diet at the time - and enabled me to loose two stones which is hard as we know, for daughters sept wedding, I've brought most back into diet now that gut has healed and acid more balanced -
Wish I'd seen the news! Il see if in catch up unsure the news is
No it will be water of a ducks back no doubt 😔 My lovely late mum used to say 'no one see,s to really care!
On the basis that the amounts of T2 and T1 are not controlled, and desiccated thyroid only has extremely low quantities of each of them, I have my doubts that they make any meaningful difference.
It feels as if people mention them as a disinguishing feature of desiccated thyroid without full understanding of quanities and proven effects.
helvella but why are they made in the thyroid of pigs or humans or I presume every mammal? Nobody knows!
I can only assume they are good for us or simply benign but I wonder why waste energy on making them if they do not serve some useful purpose. Maybe one day elucidation will come.
Well it looks like T2 does do things but most is not from the thyroid as you said.
Within the thyroid, there is a "soup" of compounds. Including, as we know, T4 and T3.
T4 and T3 are produced by the joining of Diodotyrosine (DIT) and Monoiodotyrosine (MIT) molecules which are also present in the soup. Two DITs join to make T4 - the majority reaction. One DIT and one MIT join to make T3 - the next most-important reaction. Just sometimes two MITs join to make T2.
There will also be T2 and T1 within the individual cells of the thyroid - produced by deiodinating T3 to T2, and T2 to T1. Just as in the rest of the body.
I am not convinced that the small T2 and T1 quantities in the thyroid - and released from the thyroid into the bloodstream - are of any relevance. They might have some importance but I am not yet convinced. They could effectively be just impurities with no real role.
I have all too often seen people suggest that T2 and T1 are pre-cursors of T3 and T4. This seems to me to be a lack of understanding - it is DIT and MIT that are the prescursors. Just the other day I saw this mistake trumpeted across some academic Wiki site - with no obvious means of contacting them to let them know they are wrong.
Further, when people go on and on about T2 and T1, well, if they are so important and have a profound impact, we surely need to control their levels? We don't want too little, nor too much, of them. Proclaiming that some product does (or does not) contain T2 and T1 without knowing how much is delivered, how much is required, and what impact it has doesn't really help.
I entirely understand that everyone wants to know and understand why desiccated thyroid has such a different impact on somany. But speculation as to why should remain so.
I think it very likely that T2, T1 and some other members of the thyroid hormone family with prove to be important.
helvella thanks for that info I did find it odd to read that T2 helped in T4 to T3 conversión seemed a bit upside down but not being a scientist in the beginners mind the possibilities are many in the experts they are few...you might say. I think for me the T3 in NDT is probably key to me feeling better on it but I would need to try synthetic T3 and T4 to see if I get the same result - which as things stand with NHS and T3 is not looking promising as an option. My genetics seem to indicate partial T4 to T3 conversion problems. It intrigues me because other family members feel/felt fine on levo alone so I wonder why I do not.
The other thing that puzzles me is if your thyroid has died are the other bits of the body making T3 and T2 and maybeT1 all ticking away happily on their own and could this lead to interesting treatment options for our condition if I understand it correctly that the hormones are made in other body tissue.
Also, there is every reason to question whether the delivery of T4 and T3 from desiccated thyroid is the same as from synthetic combinations. (Assuming the same amounts are present to begin with!)
Different delivery (e.g. as simple as faster/slower) could have a significant impact.
Jeppy Our thyroids produce T1,2,3,4, & Calcitonin, so neither T1 or T2 is alien to us. As Helvella implies, there has been a paucity of information about T1 and T2, but here are a few random quotes from various sources/research to get your researching juices going:
"T3 acts on the nucleus to influence the expression of genes involved in the regulation of cellular metabolism and mitochondria function; T2, on the other hand, acts by directly influencing the mitochondrial energy-transduction apparatus. A molecular determinant of the effects of T3 could be uncoupling protein-3 (UCP-3), while the cytochrome-c oxidase complex is a possible target for T2. In conclusion, it is likely that iodothyronines regulate energy metabolism by both short-term and long-term mechanisms, and that they act in more than one way in affecting mitochondrial functions."
"Two iodothyronines have been identified as effectors of the actions of thyroid hormones on energy metabolism: 3′,3,5-triiodo-L-thyronine (T3) and 3,5-diiodo-L-thyronine (T2). Both have significant effects on BMR, but their mechanisms of action are not identical. T3 acts on the nucleus to influence the expression of genes involved in the regulation of cellular metabolism and mitochondria function; 3,5-T2, on the other hand, acts by directly influencing the mitochondrial energy-transduction apparatus. A molecular determinant of the effects of T3 could be uncoupling protein-3 (UCP-3), while the cytochrome-c oxidase complex is a possible target for 3,5-T2. In conclusion, it is likely that iodothyronines regulate energy metabolism by both short-term and long-term mechanisms, and that they act in more than one way in affecting mitochondrial functions."
“3,5-T(2) exerts metabolic effects on energy expenditure, on both lipid beta-oxidation and leucine metabolism in hypothyroid rats. We conclude that 3,5-T(2) is a metabolically active iodothronine.”
"T2/100 g BW (grams per body weight) affects G6PD activity 3-5 times more than the same dose of T3. These data provide the first evidence that T2 is a factor capable of regulating G6PD activity."
"Not only triiodo-L-thyronine, but also diiothyronines are active in regulating the energy metabolism. They influence resting metabolism in rats with 3, 5-diiodo-L-thyronine seeming to show a clearer effect."
Looks like T2 does lots of good things after all but most is made in the body tissues not from the thyroid so your stuck with it and NDT will only add a neglible amount to what your body is already making
Desiccated thyroid can be a lifesaver. Some people seem do thrive on it. Others seem better on alternatives (whether T4-only, T4/T3 combination or T3-only).
I am always concerned when people are pushed towards desiccated thyroid and they feel they must change to it, and stick with it, for some misguided reason such as it being "natural".
Take what works. Although the healthcare systems can make it difficult to have access to every possibility, that is what we need. Then choose what works.
In my view, the amounts of T2 and T1 in desiccated thyroid are likely so small as to be irrelevant. But I could be wrong.
Ready-made combination medicines are available in some countries (e.g. Germany and Greece) - but not the UK. And, so far as I can remember, not the USA these days. "compounding" pharmacies and/or "specials" suppliers could, no doubt, supply a combined product if asked - and paid handsomely. Yes - they would all be prescription-on ly in the UK.
However, I see little or no difference between a combined medicine and taking both T4 and T3 in separate tablets.
Thankyou as you have gone to great length above , unsure if Helleva was saying emphasis on them is heightened, in answer to query, don't know
With respect I was trying to determine in simple measure if an added dose of any of these t numbers has negative or adverse influence in the system, im not clever enough sadly to know and picking the experts advice on it who have probably done it for years
I do have a lot of brain fog and anxiety going on as a regular thing and really grateful for straightforward facts I guess xx
I'm not so gullible, I'm just not so black and white I guess, so mewhere down the middle, I have a couple of reverse stories where alternative medicine meaning not the usual nhs drugs,have turned others lives around. It's one of those, could discuss all day I suppose😊
All for everything ! Looking forward to bloods to see in black and white improvement, here's hoping! At least I've stopped falling asleep in lay bys so it has been turning it around
I'm now so depressed and this is all part of,the journey I suppose, hard to live with this in a world I have to be bright and breezy!!!!
Cup-cake7 pot has been used medicinally since at least the time of the Greeks I am sure it has some beneficial attributes but taking it everyday for kicks is not for me!
..... and none of it can change the world !! We have a very poorly tenant with terminal cancer so his partner has been on a search for the cannabis oil - more difficult to find apparently. We are feeling so sad as he only came home last night and was stretchered into their house .... meanwhile there is a heavy cloud of sadness hovering over the olive grove. So young at 53. Each day is precious ....
Cup-cake7 I hope the oil works I think the trouble with using it for kicks long term is that it can induce paranoia for some unlucky users. It is very powerful and seems to have many unique medicinal uses.
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Dosage advice on levo only??
Doseage advice please 
Latest bloods, advice on B12 and Levo dose please?
Levo and Armour - still feeling rotten - need advice please.
