I just finished reading Paul Robinson´s book "The Thyroid Patient´s Manual" and it states on p. 142: " If you have lost thyroid tissue through a thyroidectomy or through Hashimoto´s thyroiditis, you will also have lost a substantial amount of T4 to T3 conversion. The thyroid gland converts more T4 than any other tissue".
This contradicts everything I have read so far; it´s often said that T4 to T3 conversion is normal in hypothyroid patients as conversion takes place OUTSIDE the thyroid gland. That is, after all, the argument used by the medical community to prescribe T4 only drugs.
This seems to be in line with what most doctors claim, and that would be the reason (according to them) that conversion remains normal even in hypo patients. I have not found anything to back Robinson´s statements up; however, would not be willing to reject them either as he really seems to know what he is talking about...however, if what he saying is true, then patients who have had a TT would never be able to get along on levo only...yet, some do.
It looks questionable - primarily how substantial is the loss?
Within the thyroid gland, we make mono-iodo-tyrosine (MIT) and di-iodo-tyrosine (DIT).
Two molecules of DIT can combine to form T4.
One molecule of MIT and one of DIT can combine to form T3.
As I understand, that is the fundamental output of the thyroid gland itself.
However, I do believe that some T4 can be (and is) converted to T3 in a functioning thyroid gland. Though I do not know how much! Which is the core of the question. This nonetheless could be a critical part of the T3 supply.
Some tissues convert T4 to T3 which is used entirely within that tissue - I think that hair follicles are one such. Parts of the brain do their own local conversion.
On top of the ability of tissue to convert, we also need to consider what factors control conversion.
I read somewhere that, of the +/-10 mcg of T3 secreted from the thyroid gland every day, about half of it is produced directly by the thyroid gland and the rest comes from conversion within the gland. Meaning most of the T3 (30-50 mcg daily depending on source) is made elsewhere…from T4.
Does the 30-50 micrograms include T3 that is only used within cells? Or, indeed, only used within the brain? Or is it based on the T3 that does actually circulate?
I understood that both T4 & little T3 was made in the thyroid gland but the T3 was not converted from the T4 but synthesised directly from the iodination of thyroglobulin, etc, and iodine uptake.
These are then both released in response to TRH & TSH and further conversion takes place in many organs and tissues (mainly liver & gut) all regulated by the iodothyronine deiodinase enzymes. Conversion also happens in the pituitary gland but works in a slightly different way.
Many of us suffer low FT3 levels but if most T3 had to come directly from the thyroid gland as per PR claims, those of us without a thyroid gland might risk having hardly any. I agree it's a curious & bold statement he has made considering most of what he says makes sense.
The thyroid converts a little T4 to T3 and secretes about 15% of the total T3 but when TSH is high this can increase substantially. My view is that type-2 deiodinase (D2) is most important as it is the major source of T4 to T3 conversion, is increased when thyroid hormones are low and regulates low T3 levels, especially in the brain.
If you are missing a thyroid (and not on T3) you will have lower T3 levels. When this is compensated with a little more T4 it causes TSH to fall which reduces the rate of T4 to T3 conversion.
I feel that where the conversion takes place is important, not just the blood level of T3.
Thanks Jim, this is such a clear response and makes sense of why some of us feel worse and worse as Levothyroxine is increased. Please could you explain more about D2? What is it? Something in food? A hormone? Or what?
The deiodinases are enzymes that break down thyroid hormones. It is a very complex subject. This is a good introduction ncbi.nlm.nih.gov/books/NBK2... but even so it is a difficult subject that takes a lot of study.
Jim, are these enzymes ones we take in with food or enzymes naturally occurring within or produced by the body? I'm wondering if they are something we can influence, maybe increase if we have too few.
They are made by the body, they are also subject to a process called 'ubiquination' which reduces the half-life of the enzyme. The only way you can influence them is by not being sick or depressed and by not taking high levels of thyroid hormone (which you may need to).
Thanks Jim, what a great answer, aiming not to be sick or depressed. One more question please. What is a high level of thyroid hormone? I am prescribed 40 - 50 mcg Liothyronine per day, where does that come in high-to-low?
TSH stimulates deiodinase so a low TSH will reduce deiodinase. The catch 22 for many people is that they have poor conversion because their TSH is lower than normal (for their fT3, fT4 levels). If they take some T3 it pushes their TSH (and deiodinase) even lower. You can't win and so just have to take high doses of L-T3.
High hormone levels stimulate type-1 deiodinase which converts T4 to T3 and T4 to rT3 in organs such as the liver and kidneys but this doesn't do anything for tissues such as the brain and muscles which tend to rely more on type-2 deiodinase for local regulation of T3.
Why does it work ok with a fully functioning thyroid but all go wrong on thyroid hormone therapy - is it down to exquisite fine tuning that is impossible on a daily tablet?
As TSH falls the RATE of conversion falls. But as fT4 falls (and TSH rises) there is less T4to convert. So, there is probably a sweet spot where you get optimal conversion. This is probably where most doctors target, high normal fT4 and average fT3. Really they should give a little liothyronine so that normal healthy T3 and T4 levels are achieved.
High doses of levothyroxine will give high fT3 levels but this is mainly from type 1 deiodinase rather than type 2 deiodinase which controls cellular T3 levels.
The science isn’t exact and it comes down to personal experiment. Also I would avoid high fT4 levels are there is evidence it can lead to increased risk of cancer, I will post about this in a month or two.
Selenium deficiency will reduce deiodinase and this will push up TSH as the hypothalamus, pituitary have reduced response to T4. I wouldn’t think that restoring normal selenium levels would help. It’s not scientific but I’ve never seen a post on this forum where someone had sufficient deficiency that deiodinase was affected and TSH, fT3 recovered with supplements.
Well, if I have to choose between feeling well and risking cancer, I prefer feeling well even if that means high T4 levels. For the same reason- quality of life - I take estrogen even if that slightly increases the risk of cancer.
Can you please provide links to this? I would like to know how high levels we are talking about here. I tried to find this info but the only thing I came across was an article saying that cancer patients had higher levels of T4, but not that T4 itself was the cause of cancer (so the high T4 levels could in theory have been caused by cancer and not the other way around).
I will post about it in a month or two, I don’t want to divert from the subject of this post. The problem I have is that I’ve always thought it is OK to have levothyroxine monotherapy with high normal fT4 giving average fT3. Recent research suggests this is not OK. I don’t want to go into details until I have prepared a balanced presentation but I’m no longer comfortable with patients having above average fT4 as it carries risks. I’ll try and get things ready ASAP but I’m having to complete some decorating at home so that we can reinstall some radiators before it gets too cold!
But you also advocate an in-range TSH, and many people on any amount of T3 will have a very low or even suppressed TSH...so not sure how you are supposed to combine T3 and T4 while keeping your TSH in range?
That’s the problem! Endocrinologists need to find ways of restoring the axis so that patients can have normal fT3, fT4 and TSH. They aren’t bothered about it.
I advocate trying to keep TSH normal, at least for a few months because a subnormal TSH causes problems. I accept, and advocate, T3 therapy where necessary that leads to a very low TSH. My TSH is low because I needed high dose hormone for many years, I wish my TSH would pick up.
I think that going back to an "euthyroid" state is virtually impossible. We have to assume our thyroids and bodies will never be the same as before, and accept that no treatment will ever be a perfect substitute for the organ we've lost.
True. I was thinking of patients who have a functioning thyroid but are hypothyroid because their thyrotroph is under performing, less obvious central hypothyroidism. It also applies to those whose thyroid has failed, if they produce less TSH than expected they will have poor conversion and do badly on levothyroxine.
Very true and well said! I remember so well what the doctor who diagnosed me over 20 years ago said...that when your thyroid gland becomes dysfunctional you won´t notice it, not like you would notice it when your heart or liver or pancreas stops working. He said that hypothyroidism was perfectly treatable and that I would never notice any difference once on levo. I have found that not to be true...I can live a normal life, provided I am my own doctor and take what I need to feel functional (which is not levo), but it will still never be the same as when my own thyroid gland worked properly. Now, I need much higher FTs and a suppressed TSH to even function. Not what nature intended, no...but that just proves to me that we cannot achieve a euthyroid state once hypothyroid - at least not if we are to maintain all lab results - TSH, FT4, FT3 - within range. Also, I take issue with the word "treatable". To me, that suggests curing the disease. A UTI is treatable. Hypothyroidism is not. It is at best manageable...with the right drug(s) or combination of drugs.
But I feel quite a lot better than I did for decades before treatment - my depression has vanished completely and it was really awful. I wonder when I was euthyroid if ever! I do feel pretty good.
They are and generally T3 therapy (or combination) carries no additional risk pubmed.ncbi.nlm.nih.gov/269... (you can get the full paper from Sci-Hub).
So it must be possible on NDT to get good levels. I was ok for years on 1.25 grains then suddenly it wasn’t enough any more, it has been a job to get to some sort of equilibrium again. I find 1.75 works best at the moment. I wonder why it changed like that. Optimisation is a trickle lark if you ask me.
This is what I also understand from reading a lot about T4 to T3 conversion. But, I´m surprised that Robinson would be wrong since he seems very knowledgeable about thyroid matters...but, the fact remains, I have never seen anywhere else that most of the T4 to T3 conversion takes place INSIDE the thyroid gland itself so I doubt he is right about that.
I believe thyroidal T4 to T3 conversion can increase substantially when TSH is high and also the thyroid manufactures proportionally more T3. Of course when medicated TSH is not allowed to go very high. I haven't read the book so I can't really comment in detail.
Therefore, a thyroid is not just a T3 synthesis factory, it’s also arguably one of our body’s most powerful T4-T3 conversion machines. It rivals the role of the liver in thyroid hormone conversion.
From an interpretation of the work of our own Diogenes et al, at:
That´s interesting, I have found many very good articles on the Canadian site. What surprises me is that, if the thyroid gland plays such an important role in the T4 to T3 conversion, most doctors seem unaware of it.
I can' vouch for that as a GP told me - when he said my T4 was too low (I take T3 alone) and I said but I take T3 alone doctor - his response was 'T3 converts to T4!'.
I said 'No doctor that's wrong'.
What chance have patients recovering their health when GPs know little of how to restore patients' health and this forum has been a stalwort for those who have a connection to the internet. There must be many who do not have that support and remain unwell with disabling symptoms. Some also may be unable to work and I think a few members on this forum have lost their jobs.
Yea I thought I had read something to that effect! Thanks for reminding us 👍🏽 If all these other organs were merrily converting T4 to T3 surely life without a thyroid gland and no synthetic hormones would be possible when we know all too well it isn’t.
I guess the other issue is how “convertible” is the synthetic T4 we take in Levothyroxine. There may be conversion issues with the synthetic that are not relevant to the biological conversion of natural T4 produced in a healthy person.
Is there any evidence for this? I am sure helvella said that to all intents and purposes the synthetic T4 is the same as natural T4. I thought poor digestion or fillers might make it difficult to absorb. I guess our own T4, when we make it, did not have to get to where it was needed via the digestive system
The molecular structure of synthetic and endogenous T4 is identical with the exception of the sodium atom - though the effect of that is likely minor or irrelevant.
But the issues like compounds formed in levothyroxine tablets, the effects of the excipients in several ways, impurities in the active pharmaceutical ingredient, etc., all have potential for affecting us.
As too, that our own drip feeds from our thyroid, whereas taking a tablet is a sudden change. Typically, our daily dose appearing within a very short time, with another peak around 48 hours later of T3 formed from that levothyroxine.
Levothyroxine itself is very close to insoluble in water or acidic solutions. Absorption is affected by so many factors. Yes, a major issue.
I think it has been mooted about T3 as well tgat the synthetic and natural products are different, but I tend to think helvella knows what he’s talking about where molecules (and a whole lot more) are concerned. All the other things he listed could make a huge difference to absorption. I guess taking a tablet every day is a rather blunt tool when compared to the beauty of a fully functioning thyroid gland able to adjust the dose every second of the day to suit ones needs.
I agree! The body supposedly cannot tell the difference between synthetic T3 and T4 and the hormones the thyroid gland produces. That´s why the body is able to convert levothyroxine to T3 just like it would thyroxine. But, as you say, it´s different to take it as a pill or have the thyroid gland produce it as needed...I wonder if the fact that synthetic hormones are not bound to proteins (unlike NDT and our own hormones) also makes a difference, especially re T3, which is then much more rapidly absorbed...?
This is a good question, I had a total thyroidectomy in 2019 after thyroid storm, had graves also had high antibodies, I tried T4 for over 10 months felt dreadful couldn't operate normally was bed bound most days, my bloods showed varying values, from one being hypo to the rest hyper.. The endo said I had an absorbtion problem (I have colitis) she put me on T3.. I started low at 10mg and built up I'm now on 25mg was on 35mg..(i have other problems which I'm trying to address at the minute over range calcium and parathyroid hormone) but my T4 is 2)...range 11.00.. 22.00pmol).. My T3 is 5.9)... Range.. 3.10..6.8).my TSH is.. 0.05)...range.. 0.30..4.50..ive been on T3 for probably 11 months or so.. So I wonder what happens to T4 if your on T3 only? When I tried to increase to 35mg by 5mg every 6 wks I was taken to A&E with a resting heart rate of 133 the doc said I was over medicated, I'm on 25mg T3 now and my T3 is 5.9...but T4 low and TSH low... I'm confused as to what to do... I'm now wanting to have 2 wks off T3, re do my thyroid bloods just to see what they come bk as, ( obviously over range calcium and parathyroid hormone are having an affect on me but my gp keeps on insisting I'm over medicated and T3 is not working for me,🤷♀️.. I don't feel hypo at all in fact I do feel a bit hyper, tremor, sweating but these are also associated with hyperparathyroidism to🤦♀️... I wonder if my surgeon got all my thyroid out??? Can having a bit of thyroid left cause you to go hyper? how would you know if any thyroid was left?? sorry to put this to you but I'm totally lost with all of this, I try to read everything I can on thyroid medication/disease ect... I'm going round in circles and feel so ill(but that's probably hyperparathyroidism)
I would imagine that even a tiny bit of thyroid left could in theory leave you hyper. Robinson writes in his book (p. 144): "Even if TSH is fully suppressed, there will be some remaining, basal level of thyroid gland secretion of thyroid hormone. However, the effect of thyroid medication is that gradually, over time, this basal secretion will reduce".Did you have a total thyroidectomy, or was the intention to leave a portion of your thyroid gland intact? If you´ve had a TT, I would imagine there is no endogenous thyroid hormone production so that any symptoms would have be caused by the replacement hormones...!
I imagine you´d need an ultrasound to determine if there is any thyroid tissue left.
I hope members who´ve had a thyroidectomy will reply as I´m certainly no expert on the subject!
However, Paul Robinson stresses that hypocortisolism (and sometimes hypercortisolism) will mess thyroid hormone treatment up and result in hyper symptoms when your thyroid hormone levels indicate you are undermedicated. On T3 only, your FT4 will be very low or undetectable, but you need enough T3 to compensate for the loss of T4.
He lists the following reasons for T3 only not working:
- not being on enough T3 (increasing too slowly , or having a doctor dosing by the TSH)
- not absorbing T3 properly, or not absorbing enough of it (caused by low stomach acid or gut issues, as well as taking calcium or iron with thyroid meds)
- too much T3 - usually by raising it too quickly (NB: hypocortisolism and low iron can masquerade as too much T3!)
- taking T3 once daily instead of multidosing
- low B12, low folate, low vitamin D
- it simply is not right for you.
I´m sure not all of the above applies to you, but just to give you an idea how many possible explanations there are!
The point about one daily dose vs multidosing is controversial as some claim T3 should be taken in one go, while others claim it should be multidosed (at least twice, sometimes three or four times daily). But, I would imagine one single daily dose of this potent hormone requires your adrenal glands to be in good shape...!
When your T3-only dosage is ideal, these are the symptoms and signs to expect (Robinson p. 144):
- you should feel well, with no hypo symptoms
- your body temp should be normal for you
- blood pressure should be normal for you
- heart rate should be normal for you
- TSH can be at bottom of range or suppressed
- FT4 is likely to be at bottom of range or totally suppressed
- FT3 is likely to be at top of range or well over the top of it. He stresses that the reference range for FT3 applies to patients on T4-only drugs and should not be used to contrain T3 dosage for patients on T3-only
He also mentions that rT3 will be very low on T3 only, but new research shows that rT3 does NOT block the action of free T3 so not sure that comment is valid anymore.
He stresses that any dosage change (up or down) should not be more than a quarter pill (5 or 6.25 mcg of T3).
According to Robinson, it´s common for adults to need 40-80 mcg of T3 only daily (with some needing less and some more).
This comment is interesting: "The genomic effects of T3 in the cell nuclei could take weeks or months to fully occur. THis can be thought of restructuring or reprogramming the genes. So, sometimes it takes patience between increases, especially when the dosage is closer to a therapeutic level. The body needs time to adjust". ("The thyroid patient´s manual", p. 143).
I can recommend this book as it goes through all available treatment methods with their pros and cons, I have been reading a lot about thyroid disease for the past 20 years, but still feel I learnt a lot from Robinson.
That was interesting, I do mulit dose 10mg 8am..10mg 2pm..5mg 8pm..its interesting to note my last bloods done in march show my T3 at 5.9...range.. 3.10..6.8)...on 25mg of T3.... I feel if I go up anymore say 30mg what would that do to my T3... Would it not go over the range making me over active.. Another thing I've been having bloods done for pth and calcium the gp put a thyroid pannle in but didn't tell me this so I took my T3 as normal... 10mg 8am..10mg 2pm...blood test was at 3.35..id drank and eaten to... The results were... T3... 11.3...TSH..0.04...no T4 was done.., so would this suggest that I need to lower the T3 instead of increasing it.... Its all so confusing to me.. 🤦♀️🤦♀️
I am not on T3 only, but I will put some members in copy who are greygoose , shaws , and hopefully they will be able to tell you more, but I know you should leave 8-12 hours between taking T3 and having blood drawn, or your results will show a false high.
Having real problems 😢 although as I've said I don't think it's linked to my T3 meds, (pth raised, calcium raised) my bloods Done in March were, done at 9am, no food or drink only water last T3 tablet of 5mg was taken at 8pm.. And my (T3 was 5.9.. ranges...3.10...6.8) ....T4 was 2...ranges 11.00...22.00) ..TSH was 0.05 ranges... 0.30...4.50..so T3 appears to be at the top end of the range, with 25mg split into 10mg 8am..10mg 2pm..5mg 8pm..with the T4, TSH way at the bottom, I know this is normal for us who only take T3... But my gp, endos are insisting my symptoms are related to over medication, the endo wrote to me just last week saying... "Ms whitehead as said she wishes to remain on T3 treatment despite the advice from mr******regarding the risks of T3 treatment without T4" what makes me so angry greygoose... IS this is the very endo who took me off T4 because she said I was not doing good on it, I was not absorbing it.... She put me on T3... I feel I was doing OK on it.. Till I started with utter thirst, weeing more, bad bone pain, bad headaches, totally exhausted, insomnia, in April 2020....2 over range calcium, 2 over range pth,... I can't get it through to my gp it's not over medication 🤷♀️🤷♀️
They think it's over-medication because they're only looking at the TSH. That is often the way. And, I don't know what you can do about that. And, even if you'd left the recommended 8 to 12 hour gap between your last dose of T3 and the blood draw, the TSH would still be suppressed, because as you said yourself, that's the way it is with T3. Unless you can get that point through your GP's think head, he's going to carry on with his false beliefs because that's what he learnt in med school.
The thyroid and the parathyroids are two separate, independant systems.
Like Paul Robinson and greygoose point out, when on T3 only, you need to look at your FT3 levels, NOT your TSH or FT4, both of which are bound to be low or suppressed.I have never been on T3 only so would hesitate to give advice on that, but I notice you are nowhere near what Paul R considers a common replacement dose when on T3 only (40-80 mcg daily).
Remember what he says about current lab reference ranges applying to patients on levothyroxine only, not on any kind of alternative treatment.
But, as Greygoose points out, if your doctor does not know or won´t acknowledge that, there isn´t much you can do about it...so, you basically have three options: accept a dosage decrease that will most likely leave you even worse off than to begin with, find a new doctor, or self-medicate (if you decide T3 only is right for you). I have to admit I don´t know of many doctors in Europe working with T3 only...some will prescribe NDT or T3+T4, but they are few and far between...even more so in the UK, it would seem. So, unfortunately, it seems most patients requiring non-conventional therapy have to be willing to take matters into their own hands. Of course, you are not alone, you will always have the support of members here, and many will be able to give you advice on how to use and dose T3 only, but doctors may not be able to help you if they are only using the TSH to adjust your dosage.
Yes this is what I'm trying to get across to my gp/endo.... I'm on 25mg T3 split 3 times.... My T3 was 5.9....range... 3.10...6.80..so my T3 at 5.9 would not indicate over medication, as you say my gp/endo are consentration on the low T4, TSH.... But if my T3 is 5.9..at the top end would an increase in T3 not make it go in to over range?? Thus giving my gp the ammunition to still scream over medication,? is 25mg OK for me with a T3 of 5.9... I'd just like to see my bloods after not taking it for 2 weeks 🤷♀️
I understood that they can’t actually remove all of it even with a TT. A small stump is always left and some people might get the stump grow over a long time, say 30 years and it start producing again but it can’t really grow back as a proper organ again like a liver does for example. I think people here have had this happen and posted about it.
Ps. I should add that Robinson - a thyroid patient who himself ended up on T3 only after trying other options - stresses that T3 only should be the LAST RESORT. If T3 only doesn´t work for you, you could try NDT or a synthetic T3+T4 combo. You may not recover fully on levo only, but you may not need to be on T3 only either. The obvious advantage of a T3+T4 combo is that you can tweak the dosage, whereas NDT contains a fixed ratio of T3 and T4 which suits some but not others. Some people need quite a lot of T3, yet feel bad when their T4 levels drop too low, so they add a tiny dose of T4 to T3, while others need mostly T4 and only a little T3. You may be somewhere between LT4-monotherapy and T3 only therapy! Sometimes, a little goes a long way.
Did you feel really ILL on levo, or just hypo/still symptomatic?
Robinson writes that even small amounts of T4 made him ill, which is why he eventually switched to T3 only. He mentions he has DIO1 and DIO2 mutations (confirmed by lab analyses he ordered himself) causing him to produce faulty D1 and D2 deiodinase enzymes, leading to T4 to T3 conversion issues. So, in his case, taking T4 would not make much sense since he cannot convert it. However, in a person without the same conversion issues, combining T4 and T3 may make more sense.
The fact that most doctors have no clue when it comes to thyroid disease does not make life easier for us...! One thing that strucks me is that many doctors who DO think outside the box (like your endo who prescribed T3 for you) are still not knowledgeable enough to know what symtoms to look for, how to raise it, which symptoms could mask others, and how to decide if your are optimally treated. I think that is why Robinson´s book was such a "wow!" experience to me...finally someone who seems to know more than most doctors, and also able to explain it in a pedagogical manner.
Hi purpleCat71 ❤️I was on T4 for 10 months or so it made me really ill.. I started on 175mg..the endo reduced my dose after I was hyper, bloods showed this.. I eventually got to 50mg and again my bloods showed hyper.. I honestly don't know what that ment, the endo then said I was not absorbing🤷♀️.. So she put me on T3.. I started lower down 10mg then built up to 35mg..i have never felt hypo only hyper, the gp noticed this last year, before he found out I had no thyroid he said he thought I had hyperthyroidism 🙄 I then told him I had no thyroid (new doctor only been with the surgery a week) he was suprised that I looked so hyper, tremor, sweating ect... But I told him about the over range calcium and parathyroid hormone levels.. Which indicates primary hyperparathiyroidism, nothing to do with the thyroid, he checked my thyroid bloods and seemed OK with the levels... Only commenting on the very low TSH.. I then explained I was on T3 only, I started to feel better on the T3 I could get out of bed I got in to a sleep routine was doing OK... Then last year all the symptoms started of primary hyperparathiyroidism, weeing loads, thirst, bad headaches, bone pain, eventually got diagnosed with ostiopein in my spine, kidney stones, gal stones, calcium deposits in joints.. All point to primary hyperparathiyroidism untreated, I was diagnosed in 2004 with early onset of primary hyperparathyroidism so I recognised the symptoms right away, but the endo just discharge me saying I was now OK.. 🤷♀️ Think he was wrong, I then got diagnosed with cfs/me/fibro.. Wrong diagnosis I think.. Now I'm having the same problem in that the endos are saying I now don't have it because I had no calcium crystals in my urine, this test should not be used as a diagnosis alone of primary hyperparathiyroidism, I have wrote to the endo stating this... Don't expect a responce from her.. 🙄
So let me see if I got this right...you STARTED on 175 mcg daily and ended up on 50 mcg?! The latter is a starter dose. 175 mcg may be a maintenance dose for some.But, if you were on levo for only 11 months, did you decrease by 25 mcg every 6-8 weeks, or what did your doctor tell you to do?! Given the long half-life of levo, you need to raise or decrease it by 25 mcg every 6-8 weeks to give your FT4 levels time to stabilise. No matter how you did it, it seems strange that you went FROM 175 mcg TO 50 mcg...usually, it would be the other way around; ie, you start on 50 mcg, and then finally end up on 175 mcg (if your TSH, FT4, and FT3 warrant that).
Hi nikegirl ❤️The thyroid surgeon administered the T4 dose but after 4 weeks of sheer hell.. Very hyper symptoms he noted them sweating very bad, bad tremors insomnia just very unwell he decreased the T4.. By 25mg 6wks then again I was still hyper.. He said he couldn't help me anymore and put me over to the endo.. Who after the 11 months of me in sheer hell.. Looked at my bloods and took me off T4.. She put me on T3.. 125mg..(i should also mention I'm very bad with synthetic meds my gp noted this also I'm lactose intolerant my T3 meds are lactose free.. Teva brand) the gp and myself thought it better to introduce the T3 slowly that's why I started on 10mg and built up.. I got to 35mg but I started to be ill in April last year, I'm sure as I said my symptoms have nothing to do with over medication, a parathyroid surgeon in Oxford who looked over my recent parathyroid /calcium bloods said I need to see a surgeon 🤷♀️ I did last week... He dismissed me.. Its such a struggle when a parathyroid surgeon in Oxford says I have primary hyperparathiyroidism but endos and my surgeon up here in Cumbria say I havent, 😠😠😠😠
Birkie,Can I ask WHAT exactly prompted your doctor to switch you from levo to T3 only? Thinking about it, that seems like quite a drastic move...I´d imagine some doctors might be willing to try a T3+T4 combo in that case, but few doctors seem willing to go for T3 only...which is why many patients on T3 only self-medicate. When I reread your previous post, I see you say you had an "absorption problem" and that apparently was the reason the doctor switched you to T3 monotherapy...however, I am not sure T3 will solve the problem if the reason you are having digestive issues isn´t known. Without being an expert on T3 only-therapy, it´s my understanding that T3 only-therapy is usually the last resort when you don´t convert enough T4 to T3 after everything else has been tried. Another thing that strikes me is that now that your TSH is suppressed and your FT4 levels are low, your doctor is not happy with you being on T3 only, which seems to suggest she is not very knowledgeable...the only Dr. I know of who used T3 only therapy is Dr. Lowe in the US who shaws knows much more about than me so hopefully she will chime in. But you just cannot start a patient on T3 only and then freak out as soon as his or her TSH and FT4 levels drop.
But Paul Robinson clearly states that it is very difficult to find doctors willing and able to work with patients on T3 only. Even if I sound a bit cynical, I´d say that is another reason not to go on T3 only unless nothing else works for you. And it seems you have not explored other possibilities (NDT/T3+T4 combo).
Sorry if I got something wrong, there have been many posts back and forth!
Hi purpleCat71❤️I was on T4 after my thyroidectomy on 175mg prescribed by my surgeon, I felt very unwell and were hyper, I saw the surgeon again 4 wks later he noted the hyper symptoms and reduced the levo this went on until I was eventually on 50mg of levo.. Bering in mind I'd never seen any endo face to face, only spoke over the phone, my gp sent the bloods to the endo she came bk with absorbtion issues (I have colitis) she put me on T3 as she also said levo didn't seem to be working for me going by my blood results, I was not converting🤷♀️.. As I say I seemed to be doing OK on T3, it was just the over range calcium and parathyroid hormone last year things hit the fan, been the same since last year, very ill.. Although I'm sure it's hyperparathyroidism and nothing to do with thyroid meds.. 🤷♀️
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