Is T3 medication the answer?
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Here’s the listener question I’m answering today: If reverse T3 is high and total T3 and free T3 are low, why isn’t it a good idea just to give the person T3 medication to kind of help with their signs and symptoms while you look for the root cause of why the cells aren’t converting T4 to T3?
I think this is a great question, and if you give somebody 5 or 10 micrograms and they feel better and it doesn’t create any negative consequences, it’s great, it’s fine.
But usually, that’s not the case, and most people only feel better temporarily.
There’s also this assumption that there are no negative consequences from adding T3, but there are, and I’ll go through them in this video.
Keep in mind that the enzyme that can deactivate T4 to reverse T3 inside the cells is called deiodinase 3. If that is upregulated due to some type of cell stress, cell danger inflammatory response, then that same enzyme will deactivate T3 as well. And so one of the reasons why people may temporarily feel good on T3 is that if deiodinase 3 is deactivating T4, less T4 is being converted to T3 inside the cell.
Many people think, hey, if I just give the T3 that the cells aren’t making, then I should be good. But remember that the deiodinase 3 enzyme can also deactivate the T3 to one of a couple forms of T2, which then may result in the cells and the tissues having to work even harder than they were before to deactivate this hormone that maybe the body didn’t want to begin with.
So I think this makes sense on paper that, hey, if we just top off the tank, if we just give what the body can’t make, it should work. You should feel good.
And the analogy I typically use is that if you have kids and you’ve told them to go clean their room and you go up to the room an hour or two later and it’s not clean, you wonder why they didn’t do it.
We’re pretty naive when it comes to the physical body, and we assume that anything that’s not going the way we want it to is “broken physiology.” And I don’t think that’s the case. I think the cells and tissues work adaptively.
If they sense that, hey, there’s low danger, then their primary role is manufacturing. If they sense danger, their primary role is cell defense, and there are consequences as a result of that.
It may not feel good to us, and we assume that the body’s broken, and this reduced conversion of T4 to T3 or the slowdown in the metabolism is just broken, and we can just fix it with some type of medication.
But in many cases, what’s going on inside the cells and tissues inside the body is not broken. The body’s saying, “Hey, there’s cell stress, there’s cell danger. We don’t want to increase the metabolism that could support the threat. We want to downregulate the metabolism and support the defense.”
Those signs and symptoms we are experiencing, although uncomfortable, are not really bad things. Yes, a fever doesn’t feel good, and inflammation in the body doesn’t feel good, but the body’s typically not producing them willy-nilly. They’re producing them because there’s a reason.
So when I look at somebody’s reduced conversion of T4 to T3, which I see many times, I ask is this an adaptive issue, or is this somebody who cannot do it because of some genetic polymorphism? And I think in the vast majority of cases, it is an adaptive response, not broken physiology.
So saying that, why wouldn’t we just give somebody T3 and make ’em feel good? Well, because it doesn’t last.
So they take a small dose of T3, maybe 5 micrograms, and they feel a little bit better. And then the problem is that benefits start to taper off.
Why? Because the same enzymes that were deactivating T4 to reverse T3 are now deactivating T3 to T2, and we feel the same signs and symptoms over some time.
So yeah, then the person says, well, I felt good temporarily, let me get a stronger dose. And now they’re on 10 micrograms and they’re like, okay, I feel a bit better. But it only lasts a short time because the body does the same thing. It says, “Well, here’s more T3, we got to deactivate that.”
And so they start riding this roller coaster of needing stronger and stronger doses.
What you should know is that not all the cells and tissues regulate thyroid hormones the same. And especially in allostasis (high stress) some of the cells and tissues that are more involved with the defense physiology are going to be upregulated and the cells and tissues and systems that aren’t as important for cell defense are going to be downregulated.
What does that mean?
When you start pumping in more thyroid hormone (T3) that the body might not want, you could upregulate the hyperthyroid cell danger response signaling even more. That means you can even induce some hyperthyroid symptomatology.
The other thing that can happen is if you’re already taking T4 medication, if there is still some thyroid hormone production by the gland and you start putting more and more T3 into the system chasing these really good symptoms, you may suppress TSH which could shut the gland off altogether requiring an even greater need for T4 medication over time.
So if somebody gives you T3 and you feel fantastic, that’s great.
But if you add T3 and you feel good temporarily, but then you need a stronger and stronger dose, the reason is probably because there’s some type of cell stress, cell danger response.
You’re spending too much time chasing symptoms, maybe creating more problems and not really addressing the real issue.
So is there a reason you couldn’t just give somebody T3 when they’re having reduced T4 to T3 conversion on T4 medication only?
There’s no reason you couldn’t do that. But be aware of some of the consequences… I just kind of said these, but I’ll go through again.
One: if cells didn’t want to make thyroid hormone to begin with, they didn’t want to increase the conversion of T4 to T3 to begin with, and now you add the T3 that they didn’t want, now they’re going to have to work even harder to deactivate T3. And that requires energy, energy that they may not have much of.
So you could actually create a combination of more hyperthyroid and hypothyroid type symptoms.
Two: not all cells and tissues regulate T4 and T3 the same.
So adding T3 can cause some cells to become more hyper, especially anything that’s involved with that fight or flight system. You can develop brain fog, insomnia, and heart palpitations.
And then three: adding in T3 may cause suppression of TSH and a greater need for more T4 therapy long-term.
The challenge then becomes that a lot of docs won’t run total T4 or total T3. They’ll run TSH, free T4, and free T3, and assume that means that there’s enough total hormone in the system.
Many times as people start ratcheting up their T3 dose, there’s a lower and lower level of T4 in the system, and that can often contribute to more symptomatology.
So if high reverse T3 and low T3 or free T3 are seen on a lab report, then is T3 medication the answer?
In many cases, I don’t think adding T3 medication is the answer if you’re trying to address the root cause issues to begin with.
But if you’re seeing a physician who’s just trying to manipulate blood values, providing T3 and taking that T3 right before the blood draw will show improved lab levels. And if you’re a person who’s just trying to manage symptoms only, yeah, take a bunch of T3 and see if you feel better.
To me, it doesn’t matter, as long as you feel functionally well, you feel symptomatically, well, you feel great. I don’t care what you take.
But if you’re on T4 only, and you have high reverse T3 and low total T3 and free T3, and somebody says, “Hey, we need to give you a bunch of T3 to optimize your thyroid physiology or optimize the blood levels,” that means they’re assuming that pumping more T3 into the system is going to optimize the T3 levels, and it may not.
If the body’s in homeostasis, maybe it does help. But if the body is in allostasis (high stress), more T3 is likely going to upregulate the sympathetic nervous system, and downregulate the parasympathetic nervous system, and you’ll probably still have more symptoms.