Hi there,I would love some help on understanding my test results.
I take a high level of T3 at 63mg and 75mg Levo (both reduced from higher levels as in previous post).
I followed all the protocols for testing and have got my results from Medichecks:
TSH: 0.01 (0.27 - 4.2) Abnormal
Free T3: 3.7 (3.1 - 6.8)
Free Thyroxine: 6.7 (12- 22) Abnormal
I was surprised my T3 was only just in range, and it looks like my T4 is too low. I suffer with fatigue, tiredness, hair falling out, weight gain amongst other things. I had my vitamins done a few weeks ago and posted on here and I think they looked OK.
I am now confused as to what to do and would really appreciate any help.
Thank you
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Misspinkdaisy
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Hi greygoose, I take all of my T3 and T4 together in the morning 3 hours before eating / drinking. I followed the protocol on here and took my Levo 24 hours before test and split my T3 into 3 doses the day before, with last dose 12 hours before test.
first post around 8 th July you were taking 75mg T3 + 125mg levothyroxine.
might be too soon to see/ feel the full effect of your large dose reduction yet.
Levo was 125mcg , reduced to 75mcg ~ 50mcg reduction.
T3 was 75mcg, reduced to 63mcg ~ 12mcg reduction.
I think you should probably just let things settle for at least a couple of months after such large change , and then retest .
edit ~ Also , because you didn't know what your fT4 and fT3 were on 150mcg levo before you added 75mcg T3 .. and because you didn't test on 125mcg levo +75mcg T3 before lowering dose ,..... it's a bit difficult to get a clear picture of what is going on.
Wow, that's a big dose, and this is the reduced version, and your labs show deficiency.
The body has safety mechanisms to prevent long term over medication and it involves metabolising thyroid hormones into inactive forms. This doesn't happen easily and I suspect you have cooked up a perfect storm with long term Levothyroxine that wasn't utilised correctly (common problem), eventually adding high levels of T3, common iron/nutrient deficiencies? and do you have chronic inflammation or other illnesses?
I think you need to keep reducing meds slowly to try eliminating some of those high levels. Until they are detoxed, your meds won't work.
Hi radd,Thanks for your response. I really just don't know what to think anymore. I just want to be well. I don't have chronic inflammation as far as I'm aware, and my vitamins were done recently and seemed OK. I suffer with anxiety but no other illnesses.
Wow, I really don't understand Radd's response. US guideline suggest dosing T3 at 50 to 75 mcg. The OP is taking 63 mcg and still has low T3. How is lowering liothyronine going to solve low T3? Perhaps drop the levo slowly and increase T3 until the person feels better.
Because the O/P isn’t on T3 mono therapy. When T4 and T3 is medicated as a combo the deiodinases respond differently to when someone medicates T3 alone.
Unused T4 when in large amounts will metabolise to RT3 and the responsible enzyme (D3) will congruently metabolise T3 to an inactive form of T2. Hence the low labs.
Of course there is a chance she has genuine thyroid resistance given that she was even able to raise to these amounts without the usual over medication symptoms, but in the interest of safety and considering her deterioration, I think I would rather reduce dose first to assess any improvements rather than take higher given her labs are so extraordinarily low.
Be marvellous to have our resident thyroid scientist's input at this stage diogenes
No, I mean 'congruently’, as in happening at the same time with no differentiation. Same as Tania Smith who explains the deiodinase behaviours here ... . .. thyroidpatients.ca/2019/11/...
You don't have to believe me. That's the beauty of the forum to invite all opinions and discovery (a bit {not} like House 😍 {I wish} .. 😁), but then ... ‘The three deiodinase enzymes, D1, D2 and D3 (regulated by genes Dio1, Dio2, and Dio3) are collectively responsible for customizing the levels of thyroid hormone signaling in all tissues across the human body. Two deiodinases convert T4 into T3, and two of the three can convert T4 into RT3. Then, the deiodinases cooperate to convert T3 and RT3 into three types of T2, then two types of T1, then finally T0 (T-zero)’ .. thyroidpatients.ca/2021/02/...
Tania Smith is a fellow hypo sufferer who can not tolerate Levo, and interprets thyroid medical papers that the standard lay-person (me) can not understand. She also collaborates with diogenes (the forums resident scientist) and Bianco.
Thanks for clearing that up. I knew you wouldn't take offense at being challenged.
I'm also a long time fan of Tania Smith and have corresponded with her. She explains Diogene's (I believe) work with Spina Thyr app which is generally ignored here.
I don't always agree with her. Her depiction of T3 mono therapy as a "wheelchair" is particularly concerning.
In my opinion Spina is good at measuring the efficiency of thyroid de-iodination at a cellular level, eg conversion, and best useful in disclosing hypothalamic dysfunction before thyroid hormone is medicated, and then a little useful when ambiguous results are obtained whilst medicating a more ‘normal/usual’ dose (as per Dr Blanchard), as opposed to the high amounts of T3 medicated by the O/P. I wouldn’t know how to interpret it or if it's possible!
As below 'Hey here's a novel thought, why not use the Spina Thyr app to investigate! (I know it's invalid if taking any form of T3.)'
You can't use Spina if you are medicating high amounts of T3. However, (and others might correct me but) I think you can use it if you are medicating T3 in an amount equal or lower than the amount your thyroid naturally secreted pre hypothyroidism/medicating, eg Dr Blanchard advocates only ever for 5mcg T3 alongside Levothyroxine.
'It is used for people in two conditions only: People who are on
No thyroid therapy, or
T4 monotherapy at the time of the lab test.
Any T3 dosing at levels higher than normal thyroidal T3 secretion, and even minimal T3 dosing within 12 hours prior to the lab test, will distort the results.'
It's not used on this forum much because many take T3. You also have to download the software when if you wanted a result you can just ask admin to input your numbers on Tania's FB group. I have never done it because I medicate NDT.
You should believe her because this is how the diodinases work. Plenty of articles out there about them.
I saw the OP post and immediately thought the same thing. She’s taking too much and D3 is converting her thyroid hormone into T2 and eliminating it to protect her. I did the same thing to myself. It’s not nice. It feels hopeless. The way out is slow reduction.
radd my current understanding from research of Thyroid hormone resistance is that TSH remains high and blood levels of the frees actually run high too, not low, so I think we can rule this out as a case of THR?
Yes, you are absolutely correct in the 'usual' sense but I was considering skewed signalling even beyond THR. The TSH could be acknowledging medicated thyroid hormones that aren't evident in the labs or is there some central hypo at play? 🤷♀️
Great discussion but sad it's at the expense of poor Misspinkdaisy 😞
If this is in reference to Spina thyr, it's been a while since I read the algorithms which make up the app. But I did read them. It took a while to absorb and alas, not much is left. Kinda like a iodine skin test...
Pituitary Resistance refers to resistance to TSH. Its presentation is the opposite to the usual reference to THR, eg thyroid hormones elevate in response to TSH not being appropriately shutoff. Peripheral tissues can become resistant to constant high levels of thyroid hormone and this is the same for all hormones, and easily recognised in 'insulin resistance' (constant excess insulin). It can also be seen with excess thyroid meds that constantly saturate receptors, particularly T3 and usually blood levels are high but not always.
Research generally refers to THR when defects in the receptors disallow good utilisation of thyroid hormone, eg cellular resistance (Jim writes about this a lot) but it can also refer to secondary genetic mutations such as those in transporters or components involved in other metabolic pathways of thyroid hormones, such as the lesser researched (so far) mutations in the TRH receptor (hypothalamus). I also read of 'cellular resistance' in the sense of an inability to convert due to inadequate essential cofactors (iron, Vit B12, etc) whether we have a thyroid gland or not. The terminology can be very muddled.
My Blue Horizon thyroid genetic test tested the TRH (thyrotropin releasing hormone) and I have double impairments. Also impairment on the TSH receptor and TSH signalling gene . I suspect these are common mutations within the forum and why we can not achieve well being on Levothyroxine mono-therapy.
Sometimes when thyroid hormones aren’t working well the tendency is to keeping increasing the dose but unless it is THR in the true sense (eg genetic syndromes above ) this risks making matters worse.
diogenes has now suggested below Misspinkdaisy might suffer poor absorption and to try Liquid Levo to see if T4 levels can be raised. Because T3 conversion abilities can not be assessed until T4 levels are correct and supported by the appropriate cofactors, this essentially means T3 meds may not even be required but maybe additional gastric acid (Betaine HCL with pepsin).
Basically, the pituitary does not recognise the rising thyroid hormone levels so pumps out more and more TSH. Resulting in further rises of thyroid hormones...
Pituitary resistance to thyroid hormone-β (RTH-β) presents with the symptoms of hyperthyroidism with inappropriate secretion of thyroid stimulating hormone (TSH).
We report a case of a 46-year-old Chinese woman diagnosed with a thyroid nodule, with normal thyroid function. She underwent conventional subtotal thyroidectomy, and replacement therapy (levothyroxine) was used for as convention. However, it was later proven that she had pituitary resistance to thyroid hormone, as supra-physiological doses of levothyroxine were required to normalize TSH levels, which resulted in peripheral thyrotoxicity.
Pituitary resistance to thyroid hormone is a very rare cause of hyperthyroidism. It is characterized by normal, or elevated TSH concentration with high concentration of T3 and T4.
'Why would you reduce the levo when it's already way too low? That doesn't make much sense, either.'
FT4 can go low when medicating (high amounts of) T3 and I think the O/P has the ratio wrong 😬. If she reduced T3 meds, FT4 may rise.
Either medicate enough T3-mono therapy like yourself, or combine in lower amounts of T3 but higher FT4. For all those meds not be evidenced in labs, something is very amiss.
DI02 help converts T4 to T3, whereas DIO3 disallows conversion to happen in states of severe illness and/or excess T4/T3, by blocking T3 from entering the cell’s nucleus. Both deiodinases are influenced not only by environmental factors but each others activities, and also DI01.
For instance when T3 is low and DI03 is high, DI01 becomes down-regulated resulting in less T4-T3 conversion (even lower T3 levels) as well as not efficiently clearing RT3 from the blood.
DI03 can still dominate in the presence of low RT3 (ie, when there is not enough T4 to turn into excess RT3), and so still create low T3 levels through conversion to inactive T2.
Obviously an impairment in any genetics raises the probability of inefficient workings, although the body is often good at compromise. Have a look at Tania Smiths blogs on the Thyroid Canada website. They are fascinating.
That’s super interesting. I have the completely dodgy DIO2 genes - perfect DIO1 but not sure about DIO3 as I can’t find which alleles to look for.
I feel completely rubbish on T4 only no matter the dose. Need some T3. Labs show exactly what you’re suggesting. Without T3 I feel terrible. With T3 my labs show lower FT4 and FT3 which always baffled me. Never had a RT3 lab done but am going to soon.
I myself wouldn’t bother with the RT3 test as we can assume it's elevated if meds aren’t working. Money is better spent on tests and supplements that will help reduce RT3 and get thyroid hormones working more effectively.
When we have partial gland left FT4 often lowers (not always) when T3 meds are introduced as the body recognises we need to convert less. This is just one very small angle.
I can't comment as have no idea of your symptoms or labs. This is just general knowledge from reading Tania's site. If you wish for more members input/comments it would be better to start your own post 😊
I medicate relatively low amounts of T3 and this gives me clarity in my thinking and plenty of physical energy. If I take T3 levels any higher my brain freaks out! 🫠
I’m another one who would appear to go against your grain. I take 50mcg T3/day and 25mcg T4/day. I have tried cutting out the T4(levothyroxine) long enough for it to have disappeared from my body (around 6 weeks) and just rely on the T3, but I had to resume it as I felt more stable with it than without.
So you see, we’re all different and no one regime fits all. You just hope you get the medical backup that you need to be able to find the best levels for you.
My TSH is undetectable (0.005mIU/L Range: 0.27-4.2), my FT4 is way below range (4.9pmol/L R: 12-22) but my FT3 is at the top of the range (6.3pmol/L R: 3.1-6.8).
Occasionally, medics, especially GPs throw a wobbler over these results but the endo is ok (with the usual reservations about osteoporosis and AF, neither of which have posed any problems so far) with it, however, the main point is that I feel well on this.
Why do you think I need to get "medical back up"? I'm already running my "doctor" and he does what I command!
Seriously all I need is the guy to rubber stamp my prescription. I take care of testing and dosing levels myself. He is so swamped with vaccine injured people he's happy to let me do my own thing.
So do I, but new GPs looking at my blood test results throw wobblers until I tell them I’m doing all this “under the supervision of my endo” at which stage they shrug their shoulders and say “oh, ok then…” It just helps to keep the peace and them off my back!
As usual, what an informative post. It is like you are solving crimes - laughing, the line drawing is so interesting in content and analysis. As always - grateful Detective Radd.
Oh complicated .. .. liver enzymes raise for numerous reasons, one being too little thyroid hormone to drive hepatic function but thyroid hormone is also converted in the liver so an under functioning liver will provide less conversion.
Leptin can protect against high lipids but if elevated can drive liver inflammation as in NAFLD. Leptin, insulin, sex hormones and thyroid hormones all influence metabolism, body fat distribution and each other.
Leptin is secreted as weight is gained to signal to the hypothalamus there is enough energy (fat) stores and the hypothalamus then stimulates metabolic processes to reduce hunger, increase resting metabolism and lipolysis (fat breakdown). However, we get resistance to leptin the same as resistance to any other hormone including insulin and T3.
Leptin resistance is sensed as ‘starvation’ mode and when negative changes happen to the deiodinase enzymes that dictate how our body uses our thyroid meds (same as happens on a calorie deficient diet or anorexia).
I wouldn't bother with an RT3 test but concentrate on eating clean to support the liver, frequent low carb meals to help stabilise blood sugar levels, and maybe support adrenals. My own liver support is milk thistle but as others have pointed out it can have negative connotations regarding thyroid hormones if too much is taken.
My ALP 185 (max 104) is up higher and Alt at 80 (max is 35) but since I am on t3 30mcg the alp and alt has been higher.
I was on milk thistle before about 800mg but stopped a couple of months ago that and the enzymes have gone higher. I stopped as read on here re endocrine disrupters. I take t3 4 times a day at present so not idea when to take the milk thistle. Before I was taking milk thistle all the time during the day spaced out not realising but my t3 was ridiculously low (2.1 before t3) and on t3 30mcg last result was 4.8 (4.1 to 6.8)
I am on NAC 1800mg and liposomal glutathione 750mg
But … Mercury was 126 reading max is 0 to 25 and arsenic is high . Toxicology specialist said they don’t want to do chelation so I have been trying to detox myself but obviously not working. Awaiting new mercury results.
Re leptin - resistant- I am trying to figure out since t3 I have got very fat lower body.
Also urea is high as peeing non stop and thirsty but my Hab1c is 37 so not high
Chouchou1234 I take milk thistle and it has been a marvel for me! It has stopped me needing to take androgen blocking medication. I saw there was something on here about it being harmful to thyroid but I think it’s great stuff!
I think, I hope, that what I posted didn't just say it is harmful to thyroid. Rather that the issues are more complex. Primary message being not to dive in and take it without having read further and considered the issues.
Tania's paper I gave is a really useful indicator for both for and against milk thistle. The second part also indicates that a daily 700mg is a high dose. You were supplementing 800mg. I don’t think I have ever taken more than 200mg a day and usually less in a liver support combo.
I also love NAC but only take about 500mg a day and liposomal glutathione at 500mg. I have chelated mercury using DMSA under guidance as believe it was an inhibitory factor in my hormones working effectively.
Probably best to start a new post as O/P has already received a lot of replies not directly associated to her query. (She will receive a notification for 'every' reply).
Misspinkdaisy these bloods are such a mystery. The fact you have suppressed TSH with low frees AND such high dosing is a real conundrum.
I wonder if you need to “pick a lane.” People rarely do such an even split of T4 and T3, it might explain why the bloods are so unusual. Usually people have a dominant hormone they dose as say 80% T4, 20% T3 or 100% T3 or 100% T4. It could be that the T3 is dragging your T4 down, but your T3 dose is not enough to sustain you as a “T3 only” person.
For this to be thyroid hormone resistance I think we’d expect high TSH and frees… it’s like you have the opposite…
What are your signs and symptoms like? Waking temp, heart rate, BP etc.?
I think it would be wise to show these bloods to your GP/an endo. You definitely need to get a retest with a different lab, there is a possibility that Medichecks have simply made an error?!
On Reddit there is a forum called “ask a physician.” It could be worth posting there to get some opinions.
can you request liquid levothyroxine as it’s much more effective absorbing. It could be a gut issue. But your TSH is suppressed so I don’t get why when your levels are so low. Maybe further investigation. Pituitary possibly??
So you’re taking quite a lot of t3 and t4 and were taking more and it doesn’t seem to be working… when I was taking decent amount if t3 (25) and reduced to small amount of t4 (75) my t4 shot down to similar level to yours. I decided to increase the t4 right back up to have level in range as I felt better. If you have some conversion still that will also help your t3 level so you’ll be able to reduce your t3 - that does seem a huge dose for someone taking both t4 and t3. Don’t know your story as to why you went so high - but anyway it’s not working right now so I’d be trying again to start low on t3 -20 say - once you’ve had a week or two getting your t4 up. But hey I see lots of other bits of advice above - who knows!
It could be the results are wrong I stopped using medichecks.because I got some stupid low results. My gp rechecked them because they were that bad and got totally different ones. So it might be worth having them checked again if u can get it done
Thank you to everyone who has commented, I really appreciate it. I am, however, still thoroughly confused! I will try to process all the information before I decide what to do. I just want to be well. Thanks again
I've never understood why something that only lasts for around 8 hours in your system is prescribed/advised at one dose per day?
I take 25mcg 3 times daily, so that there's some knocking about at all times. When I remember of course! I never forget the night time one. I also take 50mcg T4, despite feeling much better on 100mcg. That's punishment for having the audacity to take T3 after my prescription was pulled.
I'm not a 100%, but I'm self treating my B12 deficiency at the mo, so have great hopes
T3 has a half-life of about 24 hours. That means that if you took 5 mcg at 8 o'clock this morning, by 8 o'clock tomorrow morning there will be abou 2.5 mcg left, minus what got into the cells. What gets into the cells stays there for about 3 days.
The misfit between what you've taken and the blood results indicate poor intestinal absorption. The TSH result means very little if you have no thyroid left. It would be interesting to know if liquid thyroxine medication raises your FT4 level - this would indicate poor uptake from tablets.
Yes oral (liquid) levothyroxine is available. It’s much better at absorbing but more expensive. My GP prescribed it for me no problem. I also take liothyronine T3 in tablet form Thybon Henning brand.
Not necessarily. The relationship between TSH and FT4/FT3 is quite different from health. Also, it could be that T3 absorption might be a bit better than T4. That would modulate the TSH, as T3 is a potent repressor.
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