This article may well be one of the most important ones that I have ever written. It is especially important to those thyroid patients who plan on introducing some T3 into their treatment.
I discuss the content of the article in Recovering with T3, and even more so in The Thyroid Patient’s Manual. However, this article devotes a lot more space to this important topic.
Why do I say it is one of the most important things that I have written? When thyroid patient’s medication is being adjusted, it may be that some extra T4 medication or a little T3 medication might be added. It frequently takes a knowledgeable thyroid patient a long time to persuade their doctor, or endocrinologist, to consider adding some T3 thyroid hormone.
However, whether it is T4 or T3 that is added, the patient may get some benefit for a short time and then the symptoms return and they often feel just as bad as before the change. In some cases, there may not even be any benefit, or symptoms might quickly worsen.
The next meeting with the doctor frequently prompts the response, “Well, I did say that your thyroid hormones are already optimal”, or “I told you that the T3 would not make any difference”.
In defence of the doctors, or endocrinologists, some simply do not know any better. They do not understand what is going on, because no one has explained it to them.
This article explains WHY the change in thyroid medication can FAIL, and HOW to FIX it. As such, it is VERY IMPORTANT, as this occurs VERY FREQUENTLY.
Sometimes 2 + 2 does not equal 4 when dealing with thyroid hormones.
This blog post is relevant to those patients who are trying to feel healthier by increasing their thyroid medication, but find that this does not seem to work and can sometimes even make their results worse than they were before.
It also applies to those who are beginning to receive thyroid hormone treatment.
Patients that have ongoing hypothyroid symptoms often do need a higher FT3 level. This usually does need to be achieved by raising thyroid medication. However, there are some things to be aware of that may help avoid confusion.
The typical pattern
I have frequently observed two types of confusing responses that may follow an increase in any type of thyroid medication:
- Some patients may feel a lot better immediately. This can be more obvious when someone adds T3/Liothyronine. The individual is often convinced that this increase is going to be wonderful for them and that they will now continue to feel so much healthier. However, after 3-5 days, this initial benefit can disappear and they feel just as bad as they did beforehand.
- For some patients, an increase in T3 thyroid medication may make the patient feel more hypothyroid very quickly. This can also be due to the same mechanism as in 1.
Sometimes, when patients in either of these categories repeat their laboratory tests, they find that FT3 has not increased and it can even be lower than it was to begin with. Why is this?
This pattern is easy to understand when you realise that the conversion rate of FT4 to FT3 is not fixed – it is variable and regulated and I hope that this post will help to explain what happens.
Conversion from T4 to T3
Only unbound (free) thyroid hormones are able to enter our cells. Therefore, only Free T4 (FT4) can be converted to Free T3 (FT3). Once inside the cell walls, some of the FT4 will be converted to additional FT3.
T4 to T3 conversion occurs within every cell of the body. Most of the T3 in the blood comes from conversion within the cell walls of the thyroid gland, liver, kidneys, peripheral tissues, and the gastrointestinal tract.
All cells depend on taking some FT3 from the bloodstream and/or taking in FT4 and converting it to FT3. The cells vary substantially in their ability to convert FT4 to FT3 depending on what tissue they are part of.
This process of conversion requires the removal of an iodine atom from an FT4 molecule, so it is referred to as deiodination. There are enzymes produced in certain tissues (cells of the body), called deiodinase enzymes. It is through the action of two of these enzymes (D1 and D2 deiodinase) that FT4 is converted to FT3.
The brain, pituitary, heart, thyroid gland and skeleton muscle (peripheral tissues) use D2 to convert FT4 to FT3. The liver, kidneys and thyroid gland use D1.
D2 is significantly more efficient in converting FT4 to FT3 than D1. However, D1 deiodinase is very important in the clearance of Reverse T3 (rT3) by the liver. The liver clears rT3 through the deiodination of rT3 into T2, then T1 and T0 (which is excreted within a day). In some people, genetic defects associated with these enzymes can hamper conversion from T4 to T3, and rT3 clearance.
The thyroid gland contributes about 25% of our circulating T3. This occurs through T3 production and T4 to T3 conversion within the thyroid. Consequently, the thyroid production of T3, and its conversion of FT4 to FT3, provide a large proportion of the available T3 in the body. Even if the thyroid gland produced no hormones of its own, it would still convert some of the FT4, that is present in the blood that flows through it, into FT3. The thyroid gland is like a little machine that sits in the blood flow, converting FT4 to FT3.
FT4 to FT3 conversion requires adequate amounts of the right deiodinase enzymes. These enzymes are heavily dependent on the mineral selenium in their construction. Consequently, it is important to have enough selenium in the diet or through supplements. The conversion process is also dependent on levels of B12, zinc, ferritin, and iodine.
D3 deiodinase enzymes convert FT4 into Reverse T3 (rT3). Although rT3 itself only has a minor effect in reducing the level of D2 enzymes, it is a possible marker for problems. This is because when rT3 is high, there is likely to be a higher level of D3 enzymes. D3 enzymes hinder FT3 from binding with receptors in the cell nuclei, i.e. they block the effect of T3. In some ways, rT3 can be seen as a ‘T3 blocker’, but it is really the D3 enzymes that are doing this. If the thyroid patient is not improving in terms of their symptoms after thyroid medication raises, and rT3 appears to be rising without much improvement in FT3, then this suggests that any T4 medication may not be converting well to T3.
Both level of TSH and of T3 have an effect on the regulation of the deiodinase enzymes and therefore on conversion rate.
Let me deal with TSH first. The thyroid gland has TSH receptors within it. The thyroid uses TSH to regulate its production of T4 and T3. The thyroid produces less of its own T4 and T3 when TSH goes lower. The thyroid produces more T4 and T3 when TSH is higher.
Importantly, the thyroid also makes fewer D2 and D1 deiodinase enzymes when TSH is lower, and more enzymes when TSH is higher. So, the conversion rate of FT4 to FT3 within the thyroid gland is lower when TSH is reduced. The Conversion rate is higher with higher TSH. Researchers call the process of adjusting the level of deiodinase enzymes up-regulation (making more) or down-regulation (making fewer).
The takeaway here is that the more D2 and D1 deiodinase enzymes there are, the better the conversion rate from FT4 to FT3, i.e. more FT3 is produced from conversion. The fewer D2 and D1 deiodinase enzymes there are the lower the conversion, i.e., less FT3 is produced from conversion. This is the process that up-regulates and down-regulates conversion. So, the conversion rate is not fixed at all – it is variable and regulated.
Other tissues than the thyroid have TSH receptors too. Brown adipose tissue, found in various parts of the body also contains TSH receptors. This tissue will also up-regulate its deiodinase enzyme production with higher TSH and down-regulate it with lower TSH. The conversion rate from FT4 to FT3 will be adjusted in the same way as in the thyroid gland, i.e. less FT3 will be produced from conversion with lower TSH, and more FT3 will be produced with higher TSH.
According to thyroid researchers, is it likely that there are other tissues in the body with TSH receptors. The cells of the heart, fat, and bone are thought to have TSH receptors, and it is likely that more locations will be discovered over time.
TSH is not the only factor involved in how the cells decide to regulate conversion. As FT3 levels increase D2 enzymes are down-regulated, and D3 enzymes are up-regulated, so conversion rate from FT4 to FT3 is lowered and conversion rate from FT4 to rT3 is increased. As FT3 levels fall, the D2 enzymes are up-regulated, and the D3 enzymes are down-regulated, thus increasing FT4 to FT3 conversion and lowering FT4 to rT3 conversion.
Conversion from FT4 to FT3, and from FT4 to rT3, is regulated and variable. Conversion rate is different from person to person. Conversion rate also varies for an individual person during the day, and this conversion rate changes with the addition of thyroid medication.
I attach research references at the end of this post for those of you who wish to see even more detail.
So, that is the really technical bit. What is interesting is how this information can be used and what it means to you!
What are the implications?
What happens if a patient adds more T4 medication when their TSH is not fully suppressed yet?
After an increase in T4 medication, the effect will be that the T4 accumulates to create a new higher FT4 level over the next couple of months. TSH is likely to fall slightly. It may only be a small change but it is often significant. Most of the reduction in TSH will happen over the few weeks because that is when the biggest rise in FT4 will occur.
Until this change in TSH occurs, the patient will have more FT4 as a result of the increase in T4 medication, and this should produce more FT3. With a slight increase in FT3, the patient may feel an improvement in well-being. We know that FT3 is the active thyroid hormone and that research has shown that FT3 is the only laboratory test result that changes when symptoms adjust.
However, the lowering of TSH, and any increase in FT3, will tend to induce a reduction in the rate of conversion of FT4 to FT3 (due to the effect on down-regulation of the deiodinase enzymes described above). The production of T4 and T3 by the thyroid gland will also reduce due to the reduction of TSH. So, any initial improvement in the FT3 level will then reduce and more of the FT4 will go into rT3 instead.
So, as a result of the increase of T4 medication, the conversion rate of FT4 to FT3 will often become lower, as the T4 medication begins to raise FT4. Any initial increase in FT3, may then be lost.
Consequently, after a few days or a week of feeling better, the poor patient is often right back where they started and feeling poorly again.
Do you recognise that pattern?
For some patients, the regulation of conversion can act much faster. Even within hours of an increase in thyroid medication (especially T3), their conversion rate can lower. It is very patient specific. The person can either feel better, the same as they were before, or they can feel even more hypothyroid.
There are solutions and I will come to that in a moment.
Please also do not make the mistake that the pituitary must know exactly what it is doing and will ensure that we have the perfect levels of T4 and T3 – this is simply not true. The pituitary gland is perfectly capable of lowering TSH even when the person still does not have enough T3. In actual fact, a healthy thyroid gland is highly involved in ensuring the person has the right level of T3 for them. Once the thyroid is not functioning well, the pituitary gland cannot be relied upon to compensate for that with any confidence. This is a common misunderstanding.
What happens if a patient adds some T3 medication?
The same mechanism occurs when a little T3 is added alongside T4 medication. But the results can be even more pronounced.
When a thyroid patient begins to add T3 to T4 medication, in most cases, the first thing that happens is that FT3 levels increase.
FT3 levels rise and the thyroid patient often feels better! This is not a surprise, as T3 is the biologically active thyroid hormone. This improvement can, in some cases, last for 2 to maybe 7 days.
But the improvement is often not sustained. It is a top-up of T3 after all, so why shouldn’t it last?
The reason it frequently fails to last is due to the mechanism that I have explained above.
The lowering of TSH that comes with the increase in FT3, lowers the conversion rate of FT4 to FT3 (with more FT4 going into rT3). The extra FT3 alone, will also down-regulate conversion rate from FT4 to FT3. Consequently, for those patients who rely on some T4 medication (or some natural thyroid medication, or some T4 from their own thyroid gland), adding T3 medication can create an initial great result, which is then followed after some time by a lower conversion of FT4 to FT3. The circulating FT4 thyroid hormone that you have just does not convert to as much FT3 anymore. You have added extra T3, but you have lost some converted FT3!
The net result is often a good improvement of symptoms followed by FT3 dropping to a level that is just as low as it was, to begin with. Note: for those thyroid patients who are adding only small doses of T3, the addition of the T3 might be met by an immediate down-regulation of conversion. This can leave the patient no better than they were before adding the T3, and in some cases they can be even more hypothyroid.
Some of you reading this may have added T3 thyroid medication and felt that increase in FT3, but then after some days, they may then have found themselves back where they started in terms of symptoms.
This is a very frequent pattern.
For some, the worsening of conversion from FT4 to FT3 can occur very quickly, and they can feel more hypothyroid without ever having experienced any benefit of the added T3.
This mechanism is important to be aware of and can make all the difference in getting thyroid hormone dosage correct for the person.
Unfortunately, all too often what happens is that a thyroid patient has persuaded their doctor to allow them to add some extra T3. When they go back and say that it has not made any difference, the doctor just tells them that they did not expect it to, or that the T3 just does not suit them! Sometimes the T3 prescription is stopped and the trial is over! This happens a lot!
However, if adding some T3, results in a clear improvement that then disappears, one has to suspect the above mechanism is operating. If the person feels more hypothyroid quickly, and signs and symptoms also suggest they are more hypothyroid, then the mechanism described here has to be suspected.
In this situation, there are also solutions that I am about to discuss.
This is a big clue that the patient does need higher FT3! So, it should be seen as encouraging and not disheartening.
What can be done if this pattern of feeling better then worse again after a thyroid increase happens to you?
Excluding other common problems may be helpful. Running the full iron panel is a good idea. Having a cortisol saliva test and 8:00 am morning cortisol blood test is also sensible, as is testing other things that might be low like B12, folate, vitamin D, etc. See my blog post on B12 though, please.
If the patient is on T4 medication (Levothyroxine/Synthroid) only, one approach is to continue to increase the T4. Eventually, TSH may get sufficiently low that an increase does provide extra T3. But this depends on how well the patient converts FT4 to FT3.
If T3 medication has been added, a good way forward is to slowly increase the T3 content of thyroid medication using 2-4 divided doses. This can frequently resolve problems. Eventually, the addition of the T3 is sufficient to actually add and retain extra FT3. The T3 content may sometimes be T3 or NDT (depending on which is most appropriate).
It may also be very necessary to reduce the amount of T4-based medication that you are taking, whilst increasing the T3 medication. This can switch the balance to more T3, without having the same suppressive effect on TSH. By lowering the T4 medication, and having increased the T3 medication, can avoid any increase in rT3 (and the presence of more D3 deiodinase enzymes that actually block the effectiveness of the FT3).
When TSH is very low, or when the FT4 to FT3 conversion rate is as low as it is going to get, the mechanism described here ceases to operate. However, if T4 has not been lowered, it is still possible to have issues with rT3/D3 deiodinase enzymes when T3 is added, so the T4 medication might need to be reduced (sometimes a LOT).
Sometimes, if the rT3 level of the patient remains very high (a marker of high D3 deiodinase enzyme levels), bigger reductions of T4 may be needed.
Sometimes, this lowering, or cutting, of T4 medication, may need to be VERY substantial. I have worked with thyroid patients who clearly have poor FT4 to FT3 conversion and high rT3, and I have had to suggest the T4 content of their medication be reduced by 50%. In some cases, it may need to be a 75% reduction. Patients can be very reluctant to do this. Doctors can be even more reluctant to do this. However, it is often the only way to improve and retain a higher level of FT3, without having rT3 get incredibly high.
It is all about getting the right balance of T4 and T3 medication for the individual thyroid patient.
Importantly, research has now shown that a suppressed TSH when on thyroid treatment is acceptable. It does not mean the person is hyperthyroid or thyrotoxic. A suppressed TSH in a thyroid patient under treatment with thyroid medication is an entirely different situation to a patient who is not on thyroid medication. Unfortunately, many doctors and endocrinologists are still not making use of this research!
My latest book ‘The Thyroid Patient’s Manual’ covers both the mechanism described here and the research explaining that a suppressed TSH is safe when a patient is on thyroid medication (if there are no symptoms or signs of hyperthyroidism). I also wrote about this mechanism ten years ago when I wrote ‘Recovering with T3’.
A simple analogy
If any reader is struggling to take in the above information on the first read, this analogy might help. Imagine a large glass of water that is completely full to the brim, but not quite overflowing yet. If a golf ball is lowered into the glass and falls to the bottom, some of the water will spill over the top of the glass. The water that falls on the surface is displaced by the volume of the golf ball. The only easy way to add the golf ball, without spilling any water, would be to empty some of the water first.
In this analogy, the water is the FT4 and the golf ball is the FT3. The spilt water is the rT3 that is forced out due to the added golf ball (FT3). It is not possible to keep the existing amount of water and yet still add the golf ball, i.e., you often cannot get added FT3, without extra rT3, just by adding T3 to the existing dosage of T4 medication (if conversion is not excellent).
For those thyroid patients that do NOT have an excellent conversion of T4 to T3, their glass is already completely full and adding T3 to any current T4 dose is going to raise rT3 and lower the FT4 to FT3 conversion further. Lowering the T4 dose often makes the addition of T3 more feasible. This might well need to be repeated if more additional T3 is still needed. This is not a perfect analogy but it conveys the essence of the issue and the solution.
Note: MANY thyroid patients have poor FT4 to FT3 conversion.
2 + 2 does not always equal 4 with thyroid hormones
Adding some T4 or even T3 medication to your existing dosage may not always increase your FT3 level.
However, knowledge is power! In this case, it helps to set expectations, and helps patients and doctors to understand this response, if it occurs, and know what the next steps might be.
It can be a tricky balancing act, but knowing this at the outset should help greatly to get to a working dosage of thyroid medication that alleviates your symptoms – which is what we all want.
As ever, I hope this information may be of some help.
At the end of this blog post are some additional research references for those interested. I also wrote a blog post a long time ago on this same topic that I will reference here for completeness:
https://paulrobinsonthyroid.com/effect-of-tsh-on-conversion-of-t4-to-t3/
Best wishes, Paul
Additional research references:
Experiments have also been done with the livers and kidneys of rats that have been removed from their bodies. The livers and kidneys were kept alive and the experiments suggest that the addition of TSH can also affect conversion rate in these organs:
“Effect of thyrotropin on conversion of T4 to T3 in perfused rat liver”
Ikeda, Takeuchi, Ito, Murakami, Mokuda, Tominaga, Mashiba.
See: Life Sciences, Volume 38, Issue 20:1801-1806, 1986
URL: http://www.ncbi.nlm.nih.gov/pubmed/3010024
and
“Effect of TSH on conversion of T4 to T3 in perfused rat kidney”
Ikeda, Honda, Murakami, Kuno, Mokuda, Tokumori, Tominaga, Mashiba.
See: Metabolism, Volume 34, Issue 11:1057-1060, 1985.
URL: http://www.ncbi.nlm.nih.gov/pubmed/4058310
Note: in these last two experiments, T4 medication was added to the rats’ livers and kidneys. There was a control group of livers/kidneys in which no TSH was added and a group that had TSH added. Upon addition of extra TSH, the level of FT3 in the this group increased, suggesting that TSH was affecting the deiodinase up-regulation. Liver and kidney tissues are not supposed to have TSH receptors within them, so more research in this area is required.
This paper highlights that D2 and D3 are expressed in a dynamic balance, in which the expression of one enzyme is regulated in coordination with that of the other, to tightly control intracellular FT3 levels to provide the cell with what it thinks it requires at the time. So, FT3 level is definitely a factor in how the regulation of conversion is done. Adding T3 medication will change the FT3 content and very often the FT4 to FT3 regulation via the deiodinase enzymes will adjust as a result:
“The deiodinases and the control of intracellular thyroid hormone signaling during cellular differentiation”
Monica Dentice a, Alessandro Marsili b, AnnMarie Zavacki b, P Reed Larsen b, Domenico Salvatore a,c,⁎
See: Biochim Biophys Acta. 2013 Jul;1830(7):3937–3945. doi: 10.1016/j.bbagen.2012.05.007
URL: https://pmc.ncbi.nlm.nih.gov/articles/PMC3670672/
Further research papers illustrating the way in which FT4 to FT3 conversion is not fixed but variable and regulated:
“Homeostatic equilibria between free thyroid hormones and pituitary thyrotropin are modulated by various influences including age, body mass index and treatment”
Hoermann, Midgley, Giacobino, Eckl, Wahl, Dietrich, Larisch.
See: Clin Endocrinol (Oxf) (2014) 81:907–915. doi:10.1111/cen.12527
URL: https://www.researchgate.net/publication/263321383_Homeostatic_Equilibria_Between_Free_Thyroid_Hormones_and_Pituitary_Thyrotropin_Are_Modulated_By_Various_Influences_Including_Age_Body_Mass_Index_and_Treatment
“Recent Advances in Thyroid Hormone Regulation: Toward a New Paradigm for Optimal Diagnosis and Treatment”
Hoermann, Midgley, Larisch, Dietrich
URL: https://www.frontiersin.org/articles/10.3389/fendo.2017.00364/full
“Relational Stability in the Expression of Normality, Variation, and Control of Thyroid Function”
Hoermann, Midgley, Larisch & Dietrich.
URL: https://www.frontiersin.org/articles/10.3389/fendo.2016.00142/full
“Relational stability of thyroid hormones in euthyroid subjects and patients with autoimmune thyroid disease”
Hoermann, Midgley, Larisch, Dietrich.
Eur Thyroid J. 2016;5:171-179. doi:10.1159/000447967
URL: https://www.researchgate.net/publication/306267613_Relational_Stability_of_Thyroid_Hormones_in_Euthyroid_Subjects_and_Patients_with_Autoimmune_Thyroid_Disease
“Triiodothyronine secretion in early thyroid failure: The adaptive response of central feedforward control”
Hoermann, Pekker, Midgley, Larisch, Dietrich.
Eur J Clin Invest. 2020;50 doi:10.1111/eci.13192
To view please click here
finally:
“Effects of Thyrotropin on Peripheral Thyroid Hormone Metabolism and Serum Lipids”
Beukhof, Massolt, Visser et al.
Thyroid. 2018 Feb;28(2):168-174. doi: 10.1089/thy.2017.0330. Epub 2018 Feb 1.
URL:
https://pubmed.ncbi.nlm.nih.gov/29316865/
pls help me find what the issue is
You’ll need to use the Contact page on my website Marie.
I don’t have open discussions about individuals under my blog posts.
Best wishes, Paul
So just to get this right, sorry!, adding T3 is actually preventing conversion of T4.
Instead, increasing the T4 is the best possible route.
No, that is NOT what I’m saying.
What I am saying is that when someone adds either T4 or T3 medication they can sometimes find a short term benefit that then stops occurring, i.e. they feel better for some days and then go back to feeling just as bad.
Depending on whether the person needs more T4 or more T3 (this depends on how well they actually do convert the T4), the solution is often to keep increasing the T4 or the T3 medication. In the case of T3, sometimes any T4 meds that are also being taken need to be reduced.
So, it is explaining that the system is complex and just because after an increase the person feels bad again after some days this does not mean that there isn’t a good solution.
I would read the blog post again. Although it is a longish one I think I do explain it.
Best wishes, Paul
Aloha Dr. Robinson,
This post was fascinating, many details I haven’t ever learned before. I don’t know how to convince my doctor to lower my T4 med and up my T3. After going to a naturopath years ago, she thought I had conversion issues. I have tried nature throid, Armour, T4 only (felt many symptoms increase on this), T3 only (for a short time and got very shaky and heart palps), and combo of T4 & T3 which is what I’m currently on. My hair loss, cholesterol, and melasma has been a problem for years, but it is getting worse and worse. I’m so afraid I’ll be going bald eventually. I’ve been tested for my vitamins and minerals and none of them show that I am low in any of them. Taking the many supplements when I tried the naturopath for two years never improved my symptoms. I am just at a loss. My dr. just lowered my t3 med because I was having heart palps and random big thumps and fluttering. Based on what I learned in this post, I’m wondering if I should try to lower my T4 medication and up my T3, in hopes to increase my conversion and then up FT3 and get rid of hair loss and other issues. I just know that lowering my T3 by only 2.5 mcg, my hair shedding has doubled when I take a shower. I just was switched to this new dr. and she really doesn’t seem to care about my symptoms at all and will not order any more labs than FT4, TSH, & T3 and she doesn’t want me to test again for 9 months. I don’t have the money to go out of my HMO network and do a naturopath again or another endo. I’m very sad about all this. If you have any advice, I’d welcome it. My recent labs since my does was lowered are: TSH 1.55; FT4 1.1; T3 104ng. I am currently on levo: 50mcg Monday-Friday (nothing on weekends. And LeoT3: 7.5mcg (5mcg in AM & 2.5mcg in PM).
Thank you!
You are unlikely to be able to alter your conversion ability but you can increase your Free t3 without increasing Reverse T3 if T4 is lowered and T3 is increased. That is a tiny amount of T3 by the way. But T4 may need to be reduced to cope with more. Plus
Testing FT3, reverse T3 and FT4 is a useful tool to point out a conversion issue to a doctor. Total T3 is of no use whatsoever – only Free T3 does anything. FT3 needs to be in the right part of the range for you.
If you have tested TPOAb and TGAb and have had high antibodies OR have had some thyroid tissue removed then you will have lost conversion ability as the thyroid gland is the single biggest asset for conversion.
Testing DIO1 and DIO2 autoantibodies can also help to prove you have a conversion issue.
I would read my The Thyroid Patient’s Manual book – most of the information you require is in there. It also includes all the other factors that could be stopping FT3 from working.
Also:
https://paulrobinsonthyroid.com/dio1-and-dio2-gene-defects-and-testing-them-for-thyroid-patients-with-suspected-t4-to-t3-conversion-issues/
and
https://paulrobinsonthyroid.com/possible-causes-of-hair-loss-in-some-thyroid-patients/
and
https://paulrobinsonthyroid.com/only-free-t3-ft3-tracks-changes-in-symptoms-during-thyroid-treatment-research/
Best wishes, Paul
Hello Paul
Like most readers, I’ve come across your website as my functional doctor seems to be very limited in her knowledge and problem solving of thyroid treatment for me and I’ve hit a wall. Some background, I’m a 36 yo female with signs of hypo and had labs done to validate my 3 year suspicion which were dismissed by many conventional doctors who just tested TSH and T4 in the past only.
My July 2022 lab results showed:
TSH: 1.67
FT4: 0.8 (range 0.8-1.8)
FT3: 2.7 (range 2.3-4.2)
TPO: 1 (range < 9)
Functional dr felt I was hypo and potentially had conversion issues but didn’t go into detail. Treatment was NP thyroid at 15mg for 7 days then up the dose to 30mg. I was only able to last for 9 days on NP as I felt lethargic and slept ALL day, short of breath, muscle weakness and major bloat.
She then recommended I switch to Armour thyroid with the same dosage (15 mg for 7 days and then begin 30mg) I only had a few days break of no medicine in between but after a few days on Armour, I felt major anxiety in a physical manifestation unlike any other in my life. I experienced chest tightness, faint-like low blood sugar crashes, tightness in all muscles which became worse after minimal exertion as if my fascia was rock) jitteriness and loose stools. It exacerbated my underlying anxiety/depression in which my psychiatrist and I worked recently on treating successfully. I reached out to let her know and she suggested to stop medications for now and we would follow up in person on next steps. I also asked if adrenal stress or vitamin deficiencies could be a reason as to why I wasn’t responding well to NDT. She agreed to test the following minerals:
My lab results showed:
Magnesium: 2.0 (range 1.5-2.5)
Selenium: 117 (range 63-160)
Iodine: 24 (range 34-523)
Zinc: 58 (range 60-130)
B12: 522 (range 200-1100)
I stopped everything on Aug 5 and have yet to feel any better. Still in a fight or flight physical state. After meeting her yesterday disclosing this as well as seeing my deficiencies in iodine and zinc she was at a loss of how to treat me moving forward. She suggested maybe supplement with zinc and iodine but was not at all comfortable and does not prescribe synthetic thyroids due to her form of process but mentioned compounding. She left it up to me to decide how to proceed which in the end highlights her lack of knowledge and was a warning sign to me to discontinue seeing her.
Would you please be able to shed any light as I am doing my own research to understand what’s going on with me since I still feel terrible. The only literature she provided me to read was one on perimenopause which wasn’t so much on thyroid.
I appreciate your knowledge and insight as well as time in reviewing my comment. I look forward to your response. Thank you, Paul.
Best
Savannah
Hi Savannah,
I am surprised that your doctor did not try Levothyroxine meds first as your FT4 was very low and FT3 was low but at least crept into the range. I would have wanted to explore T4-Only doses first to see if you could get stable with enough FT3 on that medication.
A 30 mg trial of NDT meds is nothing – it isn’t very much at all. It is not what I would have suggested. Likely, TSH has got lower and with that you would have a lower conversion of T4 to T3.
I recommend reading ‘The Thyroid Patient’s Manual’ book. I think you will be able to see what you need to do having read it.
I would restart and try T4 meds first. You will have to be patient with them as they take a couple of months to stabilise.
Normally, I do 1-1 coaching but I am waiting for medical treatment myself. You can contact me via the Contact Us page on this website if you want to find out more about possible 1-1 work in the future. Your situation does not sound difficult to resolve.
Low levels of vitamins and minerals are common when someone is hypothyroid – they just don’t absorb things well. It isn’t the vitamins etc. causing the issue. They are the result of being hypothyroid.
Best wishes, Paul
I currently take 88 Levo and 20 cytomel and my labs came back almost 0 TSH, low t3 and low t4. We decided to increase my cytomel to 12.5 three times a day and lower my Levo a little to make up for the higher amount of cytomel. With my t4 being low should I not just leave the Levo at 88 or is it just converting to reverse t3. Just trying to understand with my t4 labs coming back just below normal.
Hi Lee, no one can guess if your T4 is not converting well as you haven’t tested rT3 (which can be done privately, even in the UK, if needed).
Personally, the easiest thing to do would be to increase both the Cytomel and the Levo and get both FT4 and FT3 higher and then see how you go. Given FT4 and FT3 are low this is a different scenario to the most common ones and different to the info in the blog post. Often Levo needs to be very high. The biggest threat to not getting this right would be if your doctor wants to not have TSH near zero. It may well need to be very low as in some people the TSH response can be maladapted or the pituitary can be sub-optimal in its function.
Best wishes, Paul
Hi Paul, Thank you for this really helpful article. I am a bit confused on how to raise your D1 and D2 levels if you have confirmed you have a conversion issue. I’ve confirmed I do have a conversion issue. I’m not on any medication and have been working with a functional medicine doctor for the past year. I’ve been eating only whole organic foods, moderate exercise, sleeping better, no sugar or alcohol. I’ve also addressed my SIBO and other digestion problems. Despite this, but my insulin is high (7.5) and I’m now per-diabetic (5.7) and my Thyroid levels have also gotten worse over this last year. My number are:
TSH – 4.0 (2.8 yr ago)
T4 – 1.44 (1.58 yr ago)
RT3 – 16.2 (16 yr ago)
T3 2.6 – (3.0 yr ago)
HbA1c – 5.7 (was 5.4)
Would you recommend starting medication at this point? My functional medicine doctor does not agree that medication should be used if there is a conversion issue. My traditional doctor would like to put me on T4 only. I’m still having hypothyroid symptoms and am not sure what to do. Thanks!! Lisa
Lisa,
There are no reference ranges for the labs above and I don’t know if the T3 is FT3 also. Without reference ranges they can’t be interpreted.
You can’t improve conversion very easily. Diet changes often don’t work to address this.
I can’t tell from the labs if you have poor conversion or not as the results aren’t complete with ranges and I don’t know if the T3 is FT3 or total T3 (total is of no use).
If you had poor conversion on no labs and you needed higher FT3 then only by adding some Liothyronine (T3) could you improve the situation.
Best wishes, Paul