✅Evidence-Based: Written by a Board-Certified Endocrinologist
In Comments and Controversies on Hormones Demystified, I laid out the case for why I needed to write this series of posts about T3. In this and other articles on the topic, I address the myriad claims and questions that have come up over the years in the Comments section of T3 Or Not T3 – Exploring The Controversy. Per my current Comment policy, I will aggressively moderate reader-generated content that doesn’t meet the standard. I would also ask you to restrict your thoughts, questions, and theories about T3 to the narrow subject of each post in the T3 Controversies Series. I believe this will make the reader experience better for everyone, allowing people to more easily find the information they need. Let’s get started on today’s subject! [HD: Note that today’s post has a lot of footnotes. I encourage you to read them, as I address many questions you may have in those.]
Question: When T3 (liothyronine) is added on to T4 (levothyroxine) therapy, how much T3 should I take1?
HD: I plan to keep the scope of my answer to this common question extremely narrow, as the topic lends itself to getting lost in the weeds. For the purpose of this discussion, we will focus on T3 add-on therapy – not desiccated thyroid hormone2 or T3-only therapy.
Focus on Normal Physiology First
In order to provide context for what a reasonable dose of T3 might be, it is critical to understand how much T3 is produced in euthyroid people3. Without getting into a detailed physiology lesson, the thyroid contributes roughly 5 micrograms (mcg) of T3 to the body’s pool, with the rest produced by peripheral conversion of T4 to T3 by deiodinase enzymes. The D2 enzyme (brain, pituitary, muscle, heart, brown adipose tissue) does the bulk of the heavy lifting, producing about 20mcg of T3 per day. The D1 enzyme (liver, kidney, thyroid) contributes a small amount to the T3 pool, about 5mcg/day4.
If my readers weren’t so intelligent, I’d probably just do a mic-drop after the preceding paragraph and call it a day. I know y’all wouldn’t be satisfied with that, but humor me for a minute, simply as a thought exercise. I’ve written extensively about widespread misconceptions regarding “conversion issues” and debunked alt med’s assertion that there are millions/billions of people out there who can’t make adequate amounts of T35.
The bottom line is: should someone have a specific defect somewhere along the pathway of thyroid hormone production, metabolism, transport, and/or action, their body will most likely compensate for that defect. Remember that the body is excellent at achieving and maintaining homeostasis; it can increase T4:T3 conversion, decrease thyroid hormone breakdown, increase thyroid hormone transport into the cell, upregulate thyroid hormone receptors, and increase thyroid hormone binding to receptors.
What About People Who Have No Thyroid?
What the body cannot do, however, is secrete T3 from the thyroid if the thyroid has been surgically removed. Therefore, I’d like to use that situation to form the basis of what might be a reasonable T3 dose. If the thyroid contributes about 5mcg of T3 per day, then it stands to reason that a dose delivering 5mcg should be a good starting point for most thyroidectomized people6.
In order to figure out how to deliver 5mcg of T3, I’ll paraphrase one particularly critical comment on my original T3 post: “What you put in your gob is not what you get in your blood.” This is more true for levothyroxine than for liothyronine, but it’s good to at least be familiar with the bioavailability of these drugs. Under perfect conditions (empty stomach and no interfering medications or food), about 80% of a levothyroxine dose is absorbed. Liothyronine has significantly better bioavailability – about 95% of a dose is absorbed, even in the presence of food.
Therefore, a 5mcg liothyronine pill will deliver 4.75mcg of T3 into the blood – pretty darn close to replacing the 5mcg that the absent thyroid was responsible for making.
At this time, I’d like to bring the discussion back around to my earlier, tongue-in-cheek implication that thyroidal T3 production is all you really need to know when choosing a dose of liothyronine. It is my opinion (based on published data as well as clinical experience) that people with postsurgical hypothyroidism are more likely than other subsets of hypothyroid folks to benefit from T3. I believe that this is due to loss of thyroidal T3 secretion and (for some people) the presence of the Thr92Ala SNP in the D2 gene7.
My point is: loss of thyroidal T3 production is likely to be the biggest “hit” the body can take when considering what could go wrong along the entire pathway of thyroid hormone production, metabolism, transport, and action. Any other defect in the pathway – consider re-reading my post about EDCs and impaired thyroid hormone action, for example – will likely provoke a compensatory response by the body.
Therefore, it is my opinion that hypothyroid people who seem to require T3 supplementation should rarely require more than 5-10 micrograms per day.
But I Take More Than 5-10 micrograms of T3!
It is my opinion8 that the vast majority of people taking T3 do not truly need it. As such, many folks on T3 have been misdiagnosed as “non-converters” or even diagnosed inappropriately with hypothyroidism. When using a short half-life hormone such as T3, the body may perceive it as a stimulant, assuming that it is not truly needed as a replacement therapy. As with any stimulant, the initial good feeling tends to wane over the course of weeks to months. This often results in an endless cycle of dose escalation, which temporarily makes people feel better…until they gradually drift back toward baseline.
While the above explanation likely accounts for most people who inappropriately take higher doses of T3, I can think of some valid – but rare – reasons and one less-than-rare reason why people may require more.
First and most common, a large person with an absent thyroid may need a larger dose of T3. I don’t want to get mired in whether to use actual body weight or ideal body weight to calculate thyroid hormone dose requirements, because reality has taught me that the required dose is usually based on a number somewhere between actual and ideal weight. Suffice it to say that a tall person with a fair amount of body mass could conceivably require more than 10mcg per day of exogenous T3.
The trouble with the rest of the “reasons” for a higher T3 requirement is that they should be extraordinarily rare, but they’re typically invoked will-nilly by alt med enthusiasts who really want the thyroid to be the answer to their problems. I wrote about one such scenario in T3 Controversies: Can Impaired Thyroid Hormone Action be Treated with T3? In that post, I addressed the potential effects of Endocrine Disrupting Chemicals (EDCs) on thyroid hormone metabolism and action. I recommend (re)reading the whole post for context, but here is an excerpt elucidating the pitfalls of claiming “I need high-dose T3 because…EDCs:”
[Y]ou simply cannot invoke a “block” at a single point in the thyroid hormone metabolic pathway as the sine qua non of needing to give large doses of T3. Even multiple blocks in the pathway by different types of EDCs might not cause enough of an effect to be clinically apparent. The human clinical data in this space are thin, so I will have to explain my opinion on this matter using a combination of my clinical experience and knowledge of physiology.
In my opinion, here are the necessary conditions that would need to exist in order to see EDCs cause clinically meaningful hypothyroidism:
• The person has hypothyroidism, making them unable to ramp up production of thyroid hormone if required.
• The person has a high burden of EDCs with constant or recurrent exposure.
• Multiple different EDCs present in high concentrations will cause multiple blocks at different steps in the synthesis, conversion, transport, and intracellular action of thyroid hormone.
• These blocks will – at least at some of the steps – be complete or near-complete blocks, likely due to the high blood EDC concentration.
• Compensatory actions taken by the body will be inadequate due to the number and completeness of the blocks, thereby failing to increase thyroid hormone action at the cellular level.
I hate to beat a dead horse, but you must remember that the body has numerous mechanisms by which it can compensate for a deficiency or block in one or more parts of the pathway. So my usual answer to someone who thinks they’re special enough to fall outside the above guidelines is, “You don’t need high-dose T3 because…homeostasis.”
What About People with a Thyroid?
I’ve focused mainly on people with postsurgical hypothyroidism, because I believe that is the subset of hypothyroid people more likely to respond to T39. However, I do have patients with postablative hypothyroidism10 and autoimmune hypothyroidism11 who sometimes benefit from T3 add-on therapy.
In my opinion, the usual reason why fewer people in these latter categories will truly need T3 is because their thyroids are still capable of producing some. Obviously, the ability to produce T3 will correlate with how much thyroid tissue destruction has occurred. Hypothyroid people whose thyroids were completely destroyed by radioactive iodine might be more likely to benefit from T3. Similarly, those with Hashimoto’s might benefit from T3 once the majority of the thyroid has been destroyed.
Coming back to the main point of this post: regardless of what type of hypothyroidism you have, if you haven’t seen any benefit by the time you reach 10mcg of T3, it’s time to seriously reconsider whether you’re on the right path. If you continue to escalate the dose of T3 with no improvement or an improvement that wanes over weeks to months, T3 is almost certainly not the answer for you.
By using this site and interacting with me and others in the Comments, you agree to abide by my Disclaimer. As a reminder, please restrict your comments and questions to the narrow topic at hand. There are plenty of opportunities to discuss additional hotly contested topics in my other posts in the ongoing T3 Controversies Series.
Image Credit: Photo by Altin Ferreira on Unsplash
- Today’s focus is on the total daily dose of T3, not how to divide up the doses. Note that optimal dosing of T3 would be accomplished via a sustained-release preparation, which is not currently commercially available. Therefore, T3 should be dosed 2-3 times/day. [↩]
- Most versions of desiccated thyroid hormone have a ratio of T4:T3 in the neighborhood of 4:1. [↩]
- This term refers to having normal thyroid function. [↩]
- The absolute numbers I’ve given will vary slightly depending on the source you read. I pulled my numbers from this source. Also keep in mind that the numbers will get smaller or larger with lighter or heavier people, respectively. [↩]
- Please read everything in the Thyroid category on this site before asking questions about conversion issues; I’ve covered this ground in numerous posts. If I haven’t covered your specific conversion-issue question yet, I probably will in a future T3 post. [↩]
- Keep in mind that people with postsurgical hypothyroidism may adequately compensate for the loss of thyroidal T3 via any of the mechanisms outlined in the preceding paragraph. This explains why only a small subset of these folks seems to do better with T3 add-on therapy. [↩]
- I discuss this single nucleotide polymorphism in more detail in Is TSH the Best Test? [↩]
- This opinion is based on years of weaning people off of T3, only to find that they feel no different off of it. [↩]
- Note: I am not saying these folks need T3; most will do fine with levothyroxine alone. But in those who do not feel well on T4 alone, they may benefit from adding T3. [↩]
- Previously treated with radioactive iodine for hyperthyroidism, leaving them with a non-functional or partially functional thyroid. [↩]
- Hashimoto’s thyroiditis [↩]
49 Replies to “T3 Controversies: How Much T3 Should I Take?”
Thank you again for taking the time to address this. I have shared before my horrible experience on 5mg T3 that included palpitations and high blood pressure. Because my thyroid has been damaged by radiation treatment for Hodgkin’s lymphoma, I may be at a full replacement dose of Synthroid. I feel very well. Is there any reason I should look at a very small dose of T3 again if I have a thyroidectomy this summer? How would you determine if a person without a thyroid needs T3? I am obviously concerned about taking it but want to optimize my health after surgery. Thank you so much for this information.
I have touched on this question in at least a couple of posts (two linked below), but I can speak briefly to the general question of how to know if someone needs T3. If a person with hypothyroidism has several unresolved/persistent symptoms that sound like hypothyroid symptoms, despite seemingly adequate T4 replacement (person feels the same regardless of where the TSH is within the normal range), and there are no other good competing explanations for the symptoms (sleep apnea, etc), then it’s reasonable to try T3. For the most part, T3 levels are unlikely to be helpful in making the determination of who needs/may benefit from T3 (see the post about T3 levels below):
T3 Controversies: Should T3 Levels Be Normal When Treating Hypothyroidism?
Optimizing Thyroid Hormone Replacement after Surgery
Good post. How does one know when the majority of the thyroid has been damaged from Hashimotos? Would a very high initial TSH be an indicator? Or would a thyroid ultrasound be needed. I’m still afraid to try adding T3 and would rather give T4 only as much a shot as possible. I also understand it’s best to take T3 twice a day (morning and 3pm), which is somewhat unfortunate that they only come in 5mcg pills (and I’ve heard they can be hard to split sometimes). Another thought that maybe helpful is what can be done to give your body the best chance of making use of the T3 or give your body a better shot at converting. Zinc, Selenium, and exercise, stress reduction to name a few. Of course be very careful if supplementing as both of those can be overdone and better to get through food.
When one reaches what appears to be a full replacement dose of levothyroxine (calculated by using the formula 1.6 micrograms of levothyroxine for every kg of body weight), then most of the damage has probably been done. That is not a universal truth, but it’s a reasonable way to think about it.
With respect to zinc, selenium, vit d, iron, iodine, vit A, etc., I will have future posts about this. Most people with normal diets in the United States, especially if they take a multivitamin on top of the normal diet, are not going to benefit much from extra supplementation to juice T4:T3 conversion.
Very interesting. I would be just about right there. However, I suppose it would depend on how well you absorb the medication. Someday maybe I’ll give a little bit a try, but I’m a bit worried about anxiety and such (that’s kind of a funny way of putting it)
Remember that the majority of people with no thyroid function at all do fine with T4 alone…
One thing I do feel like often needs supplementation is Vitamin D (not actually a vitamin really). It’s often deficient with hashimotos (mine was at 20). I take 5000 iu of D3 a day and I’m still only at 50 with a range of 30-100. lots of evidence on this one such as this: https://pubmed.ncbi.nlm.nih.gov/31557141/
Let’s table this particular discussion until I get there with another post. Thanks, Mike.
Very interesting. This point specifically:
The bottom line is: should someone have a specific defect somewhere along the pathway of thyroid hormone production, metabolism, transport, and/or action, their body will most likely compensate for that defect.
This is along similar lines as Chris Masterjohn and people with MTHFR genetic “issues”. It’s relatively simple to compensate.
Are you planning on future posts that will detail on what can be done to “assist” the body to compensate? That will help a lot for those that see your post and wonder “OK, what now?”.
One last question, you discuss T3 very well for people with their thyroid removed. What about those rare individuals with central hypothyroidism that produce zero TRH? Does their thyroid still make a bit of T3 even though they don’t release any T4?
Yes, agreed. I have touched on this a bit in the past; for example, avoiding EDCs will help the body compensate. I do also plan to talk more about addressing serious mineral/vitamin deficiencies that can negatively impact deiodinases and other aspects of thyroid hormone metabolism.
That’s a tough one, as central hypothyroidism may be partial as opposed to complete. In other words, even the rare person with subnormal TRH/TSH production may still make some. And, since the thyroid itself is normal, it can still produce some T3 in response to the stimulation. But let’s just say we’re talking about someone with zero TRH/TSH, for whatever reason. I think that the answer would be that that person would not make much T3 in the thyroid.
Do you think a “slow-release” compounded T3 will have the same about of T3 available as regular T3? This is what I was prescribed (before I read your posts about it!), 15mcg. I can’t say I’ve noticed massive improvements reducing my T4 and adding this dose, and my FT3 hasn’t really changed either. I’m wondering if I should try regular T3, on a smaller dose. I had my thyroid removed 6 yrs ago, and probably the only major complaint is feeling very slow mentally – “brain fog” as they call it in the alt-med world.
I think you meant to say “the same bioavailability as regular T3.” That’s a great question, and I can only guess as to the answer. Compounded products, as you know, usually have no published data (because there is no rigorous testing required of them) regarding pharmacokinetics/dynamics/etc. Assuming that the compounding pharmacy didn’t alter the active ingredient too much in the process of compounding, I would guess the oral bioavailability would be similar to pharmaceutical-grade liothyronine. But then there’s the issue of: does the compounded pill have the amount of T3 in it that is on the label? It could have anywhere from 0% of the active ingredient to several times the amount.
Yes, I meant to type “amount” instead of “about” – facepalm. 😛
I’m inclined the think the amount I’m getting isn’t so significant as my TSH isn’t suppressed.
Do you have a “target” range for FT3 and TSH results when working with LT3, a point where people have noticed an improvement? Presuming the patient has T3 at or below the reference range before starting T3.
No, not really, when it comes to T3 levels – I don’t believe they help. I decrease T4 a bit when I add in T3, aiming for a low-normal TSH and resolution of the “hypothyroid” symptoms. If symptoms fail to improve despite multiple dose adjustments and an “optimal” TSH, I usually think there is something else going on – it’s not the thyroid.
How should one interpret blood test results when they have no thyroid and are taking T3? I take 5mcg of liothyronine and 88mcg of levothyroxine, but my TSH is always suppressed (around 0.06). My PCP doesn’t seem to think it’s an issue as long as my free T3 and T4 results are normal (which they are).
Is it true that it’s safe to ignore the TSH when you take a supplemental dose of T3?
For most people, the answer is no – not safe. Remember that everyone likes to keep their thyroid hormone level in a certain portion of the normal range. If the TSH is low, it typically means that whatever level of T4/T3 one has achieved is too high.
Liothyronine peaks about 2-4 hours after ingestion, so if I happen to check a level (I usually do not), I check it then to make sure the peak isn’t too high. On 2.5mcg to 5mcg at a time, the peak is usually not that high.
This article was so well-written and tracks with my clinical practice. Thank you.
Maybe in another post you could comment on this, but I have read several papers about optimal T3 dosages. Most seem to take as a starting point the T4 dosage that produces an acceptable level of TSH. Then the idea is to reduce the T4 to allow for the T3. They also talk about maintaining a good ratio of T4/T3. When I played with the formulas, the resulting range of T3 is fairly narrow. No more than 10 mcg for an average person (based on weight).
That’s how I arrived to my current dosage: 7.5mcg of T3 twice a day (2.5 and 5) and 100 mcg of T4. Without T3, I used to take 120 of T4 for an average 1.5 TSH. It works for me so far.
This article had a good summary:
What was your TSH before you started on the T3 and what is it now? Do you monitor FT4 and FT3? Good to hear it’s working for you! I was wondering if the lowering of the T4 was needed or not.
I’ve written about the normal ratio of T4:T3 in humans, which is somewhere in the neighborhood of about 15:1, give or take. So yes, keeping the levothyroxine:liothyronine ratio somewhere around 10-20:1 is a pretty reasonable way to go about it. That also tends to mean – like you said – that the ultimate dosage of T3 never gets above about 10mcg total for the day.
If someone has a low-normal TSH on T4 alone, then backing off on the T4 dose a bit before adding the T3 is usually the way to go.
Very interesting. I’m wondering if the TSH is not very low (let’s say in the 2-3 range), if lowering the dose wouldn’t be necessary. I would think the discussion of this blog post may explain why some people don’t do well on the normal T4 only model. They are just in the end stage Hashimotos (or no thyroid/RI). I think as you’ve discussed it could be worth a trial. Just have to track it over 6 months to see if it works long term. My guess is the TSH maybe a bit lower on this combination. Maybe a goal of .5-1?
Usually, I reserve the initiation of T3 for someone who has already achieved an “optimal” TSH with T4 alone. Hence the need to drop the T4 dose a bit while adding in T3. However, if someone happens to have a TSH of 3-4 and – for whatever reason – we’re initiating T3 at that point, then it may not be necessary to touch the T4 dose, while adding in a small dose of T3 (usually 2.5mcg twice daily to start).
Thanks for the information. My Endocrinologist is willing to give me some T3 and lower my T4. I decided to wait and see since I’ve been feeling pretty good recently. My worry is my body will keep trying to compensate and I’ll go through another roller coaster trying to get things balanced. However, I will keep it in mind if things go south with my current treatment. I believe that lines up with what you speak of on T3. I think it’s worth a try assuming someone is in end stage hashimotos and still feeling bad.
Very informative, as usual! I believe you may have addressed this already, but would checking a person FT3 level 18 hours after dosing be useful? This is what my wife was doing and her T3 came back mid range or a tad higher. She started having syptoms of too much and backed off the dose. Her doc seemed to think her labs weren’t high enough to cause a problem. My thinking is that’s because it was tested after it left her system. And if tested at peak, it would show a very different level. Is this an accurate assumption?
Btw, she has since stopped taking T3, but her PA was saying she never saw high levels of T3 on her labs and thinks something else is going on. Recently her PA said she didn’t believe TSH was useful, after I said we would like to work towards normalizing her TSH, which is still below range. I’m beginning to think this practioner is is misguided.
Although I can’t speak to your wife’s situation, I can say that FT3 levels are heavily influenced by the type of replacement one is taking (T4 alone, T4 + small dose T3, desiccated thyroid) and when the level is drawn after a dose. While I wouldn’t expect tremendous fluctuations in T3 levels on T4 alone, I would expect large differences in people who take some type of T3 medication. Given that liothyronine shows its peak levels at 2-4 hours after ingestion, I would expect a level taken long after that to be lower.
I do believe TSH gets a bit trickier when on combination medication. However, on T4 only I believe it is helpful. While doctors tend to not use FT4 and FT3, I think there is some insight to be gained by having them… [HD: Redacted, reader-to-reader advice with which I don’t agree.] …One thing I will say is your PA doesn’t appear to be following the normal conventional doctor guidance. However, this is an area where I do believe reliance on TSH can be tricky (combination therapy). Hope she has some better luck!
Thanks HD and Mike,
She is now off of T3 meds and feels much better, until recently. She tested mid to high on her FT4 with very low TSH. And she’s now having mild hyper symptoms. Her recent dose change will put her dose at Synthroids recommended dose per/weight. It’s only 6 mcg less, but as I understand T4 has a narrow therapeutic window. So hopefully she’ll be closer or on the mark with the latest change.
She never got her TSH normalized before stating combo therapy ( it’s been low for years) and since Supplemental T3 didn’t work anyway, thought we should back up and do this right. As I mentioned her PA doesn’t think TSH is useful. But we have seen her TSH move up on different doses, so the needle does move, so to speak.
Are you familiar with Kenneth Blanchard? He was a thyroid expert who advocated that optimal treatment for most hypothyroid people would comprise mostly T4 together with a very small amount of T3, in the range of 0.5 – 1.5mcg per day (T4:T3 ratio about 50:1). He felt that while pure T4 worked best for some people, most patients benefited from such an addition of a small dose of T3. He felt the reason T3 therapy so often doesn’t work neither in studies nor anecdotally is because its usually way overdosed.
He thought that the T3 secreted by the thyroid gland probably played an important role that could not be replicated by peripherally synthesized T3 and that in patients with an underactive thyroid gland, treatment should aim to compensate for the reduced glandular output of both T4 and T3.
Anyway it seems quite in line with what you are proposing here.
One thing that confuses me on the T3 dosages is they start at 5 mcg. I don’t understand why they don’t make it in smaller doses.
In Germany the lowest dose is even 20 mcg, its absurd, but I guess there is not much motivation to change the formulations because of the widespread belief that T3 has no place in the treatment of hypothyroidism anyway. That is some self-fulfilling prophecy, make only wildly unphysiological doses of T3 available, then marvel at why administering them doesn’t seem to be helping.
But I’ve heard that these doses actually harken from an earlier time when T3 pills were designed to be used as a total replacement for T4 therapy, which didn’t pan out, but the dosing remained.
Very fair points.
I’ve heard of him, but mostly in the context of people quoting him to me in the Comments. I don’t know if he did any actual studies of dosing T3 like that (I’ve not seen any), but my inclination would be to have a healthy dose of skepticism. Similar to how i feel about proponents of giving supraphysiologic doses of T3, I would need to hear a cogent explanation – supported by data – of why subphysiologic doses would be helpful.
I don’t think he ever went into detail on the rationale behind this dose, its simply what he found worked best in his patients. I’d guess for most hypothyroid people who simply have an underactive gland, they still produce glandular T3 but somewhat less than a healthy person, so a subphysiologic dose could just help to compensate for this deficit. Or it could be that these subphysiologic doses are less likely to cause an unphysiologic spiking of circulating T3 levels that would trigger negative feedback mechanisms. The gland produces 5 mcg daily, but only about 0.20 mcg per hour, so taking 5 mcg in one would be very different from what a healthy gland would do.
Interesting rationale. I suppose if one could get their hands on 1mcg T3 pills and take 1mcg every 2-3 hours for 5 doses in a day, it would be interesting to see if that works any better than 2.5mcg twice daily.
In her book “Living well with hypothyroidism” from 2000, thyroid patient advocate Mary Shomon interviews Dr. Blanchard. It would seem he advocated 2-5% of T3. So, if a patient was on 100 mcg of levo and remained symptomatic, he would prescribe 2-5 mcg of T3 daily, depending on the patient´s needs. He claimed NDT contains way too much T3 for humans. Also, Dr. B used a specialized compounding pharmacy to make sure the T3 was provided in sustained-release form.
For the record, one should be skeptical of any compounding pharmacy claiming to make a sustained release T3. It is more likely than not that the product either isn’t sustained release, or that each batch has highly variable durations of action, or both. To date, there is no FDA-approved sustained release T3 product.
I find it odd that the thyroid gland reportedly produces about 100 mcg of T4 per day, but the total amount of T3 produced per day in the whole body, including what is converted from T4, is supposedly only 30-40 mcg. Does thyroxine fill some other purpose in the body or what happens to the remaining 70% of T4 that is not converted to T3? Am I missing something obvious? Google was of no help here.
Really good point – I never thought about it that way. My best guess is that – from an evolutionary perspective- the body likes having a stable pool of T4 to draw from. That way, in times of inadequate nutrition/lack of iodine supply, T3 can continue to be produced as needed. As for the T4 that isn’t converted to T3, about 1/3 of it is metabolized to rT3 and 1/3 is metabolized via other pathways.
But your question about WHY so much extra T4 is produced is good, and I don’t know the answer to that.
Another great article that fits with my experience prescribing the various thyroid medications. I have requested to many of my patients that they read your posts when info about T3/NDT from alt-med websites is referenced. Thanks!
I am wondering if T3 should be taken twice a day. My endo said no need to split my dose up.
I can’t tell you what to do, but I have written about the dosing schedule for standard T3 preparations. It is typically dosed twice daily, very occasionally thrice daily, because of its short half-life. However, many people take it once daily because it’s inconvenient to take the second dose in the afternoon, or because it’s a pain to split the 5mcg pill.
Wow, that was a fast response! Thank you!
My Endo dropped my t4 dose and started me on T3 with 1/2 of the 25mcg a day. And I suddenly have the awareness of my heart beating, especially when I lay down at night, (even though I took my 12.5mcg in the morning). It worries me because I don’t think I should feel my heart beating so strongly and occasionally I also get one hard big pump. Besides these issues I feel so much better, with more energy and am working out everyday and don’t hit the mid day exhaustion. I feel so much lighter on my feet and thinner in my middle section (bloating that I had on T4 only is gone, which I’ve struggled with my whole life). I guess I need to contact my endo again to get adjusted. If you have any advice, I’m all ears. Thank you for your blog of realness. 😉
I have to ask, not to jump on someone else’s post. I was on NP thyroid for about 4 years. After that, I went to a new Doctor Who put me on tirosint and then added liothyronine. It went great for the first couple of months and then panic attacks and anxiety set in. My numbers are hypo but I can’t seem to tolerate even 1mcg without anxiety of some kind. Ideas?
Your work helps middle aged women like me get off this insane thyroid ride. I got to the point that if it rained, I blamed my thyroid. At 45, after being lured into the magical world of naturopathic remedies, I am finally beginning to see the bigger picture thanks to your knowledge, expertise, and experience you are kind enough to share. I am on a mega dose of T3 (of course I feel better jacked up on T3!) but It’s a dead end and you have helped me understand why.
Thank you, Rebecca. I appreciate that feedback, and I wish you the best.
My Endo has just suggested I halve the T4 from 200mcgs to 100mcgs and commence 5 mcgs T3 BD.
Does that sound reasonable?
My TSH is always suppressed regardless of T4 Dose.
I had Thyroidectomy 5/6 40yrs ago.
M.B. ( Australia )
I had radiation ablation 20 years ago and initially was on armor thyroid. Later, Levothyroxine alone, but was very fatigued and gained a lot of weight. My endo then put me on 5 mcg of T3 and 112 mcg of T4 (recently increased by 1/2 tab once a week due to high tsh labs). I occasionally experienced heart palpitations over the years, and she stated that can happen with T3 but not to worry and rx’d beta blockers. I haven’t been followed by an endo in many years and I now experience cyclic heart palpitations that occur mid week for a day or two and then disappears. They can be very intense and sometimes I can see my chest moving as my heart beats. Is it the T3 that is causing this or the recent increase of T4? Or, can thyroid nodules cause this problem? It’s taking months to get scheduled with an endo and gp is saying stay the course. Feels like I may stroke out before I get an appointment with someone to properly evaluate what’s going on.