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Let’s Talk Thyroid Lab Interpretations: Suppressing TSH and Applying a T3 “Bandaid”

A case study from a real client and my recommendations…

The lab values we’re looking at today are from a client who had a very limited thyroid panel run. This client had some hypothyroidism symptoms (tiredness, fatigue, weight gain), so they were prescribed T3 medication but felt that the symptoms were getting worse.

Video Transcript

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This is a recent case where a client asked me to give an opinion on their labs.

(Now keep in mind I don’t prescribe, this is just my opinion, and I would rarely ever run this limited of a thyroid panel.)

If you listen to my podcast, you hear me say a lot that I think we need a more comprehensive thyroid panel on a regular basis, and in context with the rest of the labs so we can find out what the effect is at the tissue level. 

Okay, so this is a person who’s got some signs of hypothyroidism. They’re tired, they’re fatigued, they’ve got some mild weight gain. Some of those classic symptoms.

So they go to a primary care physician. The primary care physician runs a TSH with reflex to free T4. 

Her TSH is functionally low. It’s below 1. Doctor says you don’t have a thyroid problem, move on, eat less, exercise more. You know the story. 

So then she does go to a functional or integrative MD, and this is the panel that they run: a TSH, free T4, free T3, reverse T3, and TPO antibodies (no total T4, no total T3, no T3 uptake).

And so I think this is an incomplete panel when you run it, but let’s just kind of go through what was there. TSH is 0.62. The free T4 is 1.26, a free T3 at 2.21, reverse T3 at 15.3, and a TPO at 55. 

So the physician said, listen, you’re not converting T4 to T3. You’ve got Hashimoto’s thyroiditis, you have hypothyroidism, and you don’t convert T4 to T3. So we’re going to give you T3. 

So the person started out with five micrograms of T3, didn’t feel great, not much improvement. So they increased the dose to 10 micrograms of T3, and she noticed some more significant weight gain and other symptoms, and she just felt like she was getting worse.

So here are the follow-up labs. TSH is now 0.41. The free T4 is 0.9, free T3 is 2.3. Reverse T3 is 11.4, TPO antibodies have gone up (still no total T4 total, T3, T3 uptake), and the free T4 and to free T3 ratio has gone up. It’s still low but has gone up. Optimal ratio is usually somewhere around 0.31 to 0.34.


So what they want to do is give her even more T3, they think they’re on the right path, and these numbers are starting to look better, but the person’s feeling worse. They went from 5 micrograms to 10 micrograms, the weight’s already going up and they’re not feeling good. 

So they wanted my opinion. And so when we take a look at this first panel, my first question for this person would be, why is this low? She doesn’t have optimal levels of T3, free T3. I don’t know what the totals are, but my concern is why is this number low?

I would look at a low TSH at 0.62 and start to think, is this a person with an inflammatory process going on? 

And the inflammation is increasing the conversion of T4 to T3 at the person’s hypothalamus and HPA axis, and that is resulting in lower TSH? So I would assume if I have a lower TSH, then I’m secondary to an inflammatory mechanism going to have reduced conversion of T4 to T3. 

So I don’t look at this as necessarily broken physiology. A reverse T3 of 15.3, everybody uses different numbers here. I use that range 18 as the higher end of the range, but we can’t be dogmatic about this number. I don’t know why that’s elevated.

I look at these numbers and I wonder with a suppressed TSH and a free T4, with a low TSH, this person may not really be making a lot of T4… So a reverse T3 at 15.3, that actually might be technically a little bit higher than it should be, but without the totals, I really don’t know.

But I do know they have TPO antibodies, so I know there’s some level of thyroiditis going on here and an inflammatory process. 

So I think what’s going on here is – this person doesn’t have low production or an inability to produce thyroid hormone, necessarily – they have an inflammatory suppression of T4 or T3 production, and they have inflammation impacting the conversion of T4 to T3.

I think I talked about all of these, but the big thing here is would adding T3 solve the person’s problem? Is this broken physiology, that they can’t convert T4 to T3?

Or is this the immune system and inflammatory system saying, “Hey, we need to slow down the metabolism, and reduce the conversion of T4 to T3 so we can defend against something”?

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Now, this clinician might’ve been thinking, “Well, if their free T3 is low, I’ll just give them T3. I’m going to try and optimize their physiology, and then I’ll start worrying about what’s creating the immune inflammatory process.”

So this is on 10 micrograms of T3, and they’re looking at this TSH at 0.41. The client is concerned that it’s lower, but the clinician isn’t. And the reason the clinician, because they know that if they give T3, it’s going to suppress TSH. I’m assuming they know that free T4 has dropped. 

Now why is free T4 dropped? One of the reasons it’s dropped is because this person’s getting T3 that’s going to suppress TSH production even further. And if I suppress TSH production, then I’m going to have lower T4 generated from the gland. 

Now because the person’s not measuring total T4, they may have had low T4 total to begin with, and now it may be actually even lower. We don’t have a T3 uptake or anything. You should keep in mind that anytime both free hormones are low, you have to be wondering, is it because I’m not making enough or because those hormones are stuck on the binding globulins?

Now they were happy that free T3 went up, but is that really good? 

Well, one of the things you have to keep in mind is this person took the T3 right before they did the blood draw. So we’re measuring some of the T3 that they took the morning before the draw. 

This ratio actually makes it look like this is better conversion, but it’s not. This is measuring some of the T3 they took just earlier in the morning. 

So this isn’t better conversion necessarily when you’re taking T3, you can’t really compare it when you’re not taking T3. It’s not actually what the cells are converting.

The reverse T3 went down, and the physician thought this was good because they’re probably under the thought process that reverse T3 blocks T3 from working, which it doesn’t. 

I’m actually concerned that the reverse T3 went down, because that means you’re suppressing the thyroid gland’s ability to make T4. And so with less T4, there’s less T4 to be converted into both T3 and reverse T3. So I’m not happy with either one of those numbers in this situation. 

I think the reason the person feels worse is because we’ve suppressed their TSH further. That means they probably have less T4 to support the tissues. We are actually creating a more hypothyroid state here, and we’re trying to bandaid it with T3. 

But by suppressing the thyroid gland, we’re going to lose out on the amount of T4 because remember, most of all, the T4 in the body is made at the thyroid gland and then it’s converted in the peripheral tissue. Some T3 is made at the thyroid gland, but most of it’s converted into peripheral tissue. 


So if I suppress TSH with T3 in this situation, plus the inflammation that was probably suppressing it, now I get decreased gland production. 

The T3 medication is actually creating a glandular hypothyroid state. 

I’m going to have less circulating T4, and remember, there’s a lot more T4 in circulation than T3.

So I think what’s what the person’s trying to do here is not the right strategy. I don’t think more thyroid hormone is the answer. This would be a case where I would want to run a more complex thyroid panel to see what the totals look like. I don’t think this is the person should be on T3 medication at all. 

My recommendation to this clinician would be to get her off of the T3 medication, do a more complex thyroid panel, look at a more complex blood panel so you can see the context, and start working with that client to identify what’s causing the cell stress and inflammatory response. 

By addressing that, not only will there probably be reduced thyroid thyroiditis, there will probably be better conversion of T4 to T3 and the thyroid gland will start to work and function better and the person’s symptoms will improve.

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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.