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Why Is My T3 Low?

Four reasons your T3 and free T3 are low, even though you’re on thyroid medication.

This is a question I get asked all the time and see often in my practice. Here are four reasons I’ve identified why your T3/fT3 levels might be low despite taking thyroid medication (and why taking more T3 won’t help).

Video Transcript

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I’ve talked about this topic here before and even on my podcast, Thyroid Answers, but if people keep asking, I think it’s worth continuing to cover.

So I had someone ask me why their T3 and free T3 (fT3) levels are low, even though they’re taking sufficient levels of T4 and T3 medication. 

When they finally found a practitioner who would provide T3 medication along with the T4 medication, they thought this was going to be the thing to fix their condition. Because if their gland is atrophied, then getting adequate amounts of T4 and T3 to replace what the gland makes should have made this person feel better. 

Unfortunately, their concern is that, once they took T3, it only provided maybe three to five days of benefit before the benefits seemed to taper off, and then they would need more T3, they’d feel better temporarily and then it would taper off and then they would get more T3. The benefits would be there for a bit, but then taper off, and then they finally just didn’t feel good at all on the dose of additional T3. So they’re really confused. 


Now, there are people in our space that talk about, well, the thyroid gland makes T4 and T3, so you have to take a medication that has both T4 and T3, and there’s a bunch of these glandular products out there. Some people are taking compounded T4 and T3, but still don’t feel well. 

So I think the question from this person was really, why is it that adding T3 to the system doesn’t seem to help long-term?


Keep in mind, that the thyroid gland makes about 5-10 micrograms of T3 per day, and there are about 30 micrograms of T3 made per day overall. Most of that occurs in the peripheral tissues. 

Some tissues use deiodinase 1 to convert T4 to T3, and others use deiodinase 2 to convert T4 to T3 inside their cells. So they’re bringing T4 from the bloodstream into the cell,  and the cells determine, “Do I want to increase my metabolism or decrease the metabolism based on everything that’s going on in the environment?” 

If the cell wants to increase metabolism, it converts more of that T4 to T3. If it wants to slow its metabolism, it can deactivate that T4 to reverse T3. 

So let’s say somebody’s got hypothyroidism, they’ve been placed on thyroid medication, T4-only, but they don’t feel good. Their T3 and free T3 levels are still low. They go to somebody who then provides the T3 and it only provides temporary benefit. 

Why would their T3 or free T3 be low when they’re taking T4-only medication? And should we be giving people T3 medication when T3/free T3 levels seem to be low?


So there are really four primary possibilities why, if you have hypothyroidism and you’re on sufficient T4 replacement therapy, your T3 and free T3 levels would still be low…

One, you have a deiodinase 2 polymorphism. 

So deiodinase 2 is the enzyme inside cells and tissues that converts T4 to T3. Some people have a polymorphism, which is an alteration of the gene that then results in a reduced ability to convert T4 to T3.

How many people have this is questionable, but it’s a possibility. So how would you know for sure? You could get genetic testing done that looks at the deiodinase 2 gene(DIO2). And then what would you do in that situation? 

Well, there’s two options. One, you could provide additional T3; option two, you could provide co-factors that might help that conversion of T4 to T3 and potentially make that polymorphism work a little bit better.

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Two, you’re probably in the “gray zone” with your T4 dosing. 

So typically, when you provide T4 that’s sufficient and there’s no cell stress response in the tissues (cells are in homeostasis), the cells will bring the T4 into the cell and convert it to T3.

However, if you exceed the amount of T4 in the bloodstream (by taking too much T4 medication), then what happens is too much T4 in the bloodstream can deactivate the enzyme deiodinase 2. So you get reduced peripheral conversion of T4 to T3. 

Now, why would the body do that? You start to see rising levels of T4 in the bloodstream, the hypothalamus gets saturated, and one of the things that can happen then is the body says, “Whoa, we’re starting to get too much T4 in the bloodstream. Let’s reduce the conversion of T4 to T3 to prevent a hyperthyroid state.” And so you get an upregulation of deiodinase 3, which is the deactivating hormone.

I call this the “gray zone” for T4 medication. You are taking more T4 medication than you may need, but you’re not taking such excessive amounts of T4 medication that you might divert deiodinase 1 from its primary role.

Deiodinase 1 is the enzyme that primarily metabolizes reverse T3 and gets it out of the system. It does do some conversion of T4 to T3, but that’s not its primary goal. Its primary goal is to metabolize reverse T3. And so if this system becomes flooded with way too much T4, then what happens is deiodinase 1 says, “Hey, forget that reverse T3. I’ve got to start deactivating some of these excessive amounts of T4.” 

The fastest way to get thyroid hormone out of the system is to convert it to T3 because the half-life of T4 is about seven days, but the half-life of T3 is about 24 hours. And so the fastest way to slow down this hyperthyroid state that’s been induced by too much T4 medication is to divert deiodinase 1 from its primary job of metabolizing reverse T3, and change it to convert T4 to T3.

So in that situation, if you’re in the gray zone with T4 medication, you’ll initially see a drop in T3. But then if you bump up to excessive amounts of T4 medication, you’ll see an elevation of T4 AND T3 because it’s just too much. You’re now in a true hyperthyroid state with the medication.


The third reason you’d see a low T3 or free T3 is that there’s some type of cell stress, excessive cell stress, cell danger response going on in cells, and they don’t want to upregulate the metabolism. 

I talk about this all the time. Cells operate either from a low-stress state, where their primary role is manufacturing and they need a lot of T3; OR they operate from a high-stress state, in which they want to reduce the conversion of T4 to T3 inside the cells to slow down the manufacturing and ramp up cell defense.

So if you have cells and tissues that are in a high-stress downregulation of the metabolism, if you replace what the gland was supposed to be making with T4, that T4 is probably not going to convert to T3 in high levels. That’s why your T3 would be low. 

But when a regular doctor sees that T4 to T3 conversion is low, then they come in with T3 medication and just think they’re going to top off the tank. 

The problem is that the cells and tissues don’t want more T4 and T3 in a high-stress state. More T3 medication might help temporarily, but then the cell figures out, “Oh, we got to deactivate this stuff. We don’t want to increase metabolism,” and your T3 levels taper off again. 


And then the fourth reason might be that there’s a combination of these factors. 

Maybe you do have genetic polymorphism, maybe you’re on too much thyroid hormone replacement, and maybe you have a cell danger response all at the same time or some combination of those things. 

So if you don’t feel well on the appropriate level of T4 for your size, for your age, for your body weight, and you see low T3 and free T3 levels, it’s likely that there’s some type of cell stress response or maybe a combination of these factors.

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Hi, I’m Dr. Eric Balcavage, owner and founder of Rejuvagen. If you’re struggling with health issues or have questions, let’s chat. You can schedule a 15-minute call with me to get started.