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The Thyroid Paradigm Shift: Part 2

Discussing the real reason most people will plateau on thyroid medication (T4, T3, T2, or a combo)…

Continuing our discussion on the Paradigm Shift of thyroid physiology. This explains why some patients will always plateau on their thyroid medication, no matter what dose or type they take.

Video Transcript

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This is Part 2 of the paradigm shift (click here for Part 1), and we just got done talking about how the cell operates differently in homeostasis, which is a low-stress state, and allostasis, which is a high-stress state.

In a homeostatic state, the primary function of the gland is manufacturing the cells and tissues of the body, making proteins, making peptides, making hormones, making neurotransmitters, detoxing things, burning up fat and extra calories, and making cells and cell membranes. That’s the primary focus.

When there’s excessive cell stress, danger is perceived by the cells, and the cells start to stiffen their cell membranes. They start to release inflammatory molecules, they decrease bringing glucose and other micronutrients into the cell that might support whatever the threat is. 

So we get micronutrients that can actually build up in the bloodstream, but inside the cells, the cells are deficient. Is it a deficiency inside the cells? No, it’s an adaptive change.


One of the biggest things we start to see is glucose and insulin resistance, and I said that a lot of people, they’re told they’re pre-diabetic or diabetic, even though they don’t eat a lot of glucose. 

How could I be insulin resistant and pre-diabetic or diabetic if I barely eat any carbohydrates? It’s not what you’re doing wrong. It is that there’s some type of inflammatory process going on and the cells are resisting glucose, and this is an adaptive response. 

So what does the body do in those times of danger? When the cells are resisting the glucose, it shuttles the glucose into your white adipose tissue. Now, your white adipose tissue doesn’t really burn fat as a fuel, it doesn’t help generate heat efficiently. What it does is just store it as extra calories. So glucose is heading into your fat cells. Fat cells are starting to enlarge. 


Then, something called vitamin D… that you should get from the sun, not from a supplement bottle, not from food, there’s very little vitamin D in food. It’s really only in cold water fish, because we were meant to get it from sun exposure… 

So we get our vitamin D. Vitamin D gets converted to 25 Vitamin D, and that vitamin D and 25 Vitamin D can go to the fat cells, and it’s going there for a purpose.  One of the things it can help do is increase the size and number of white adipose tissues. 

What’s the benefit of that? Well, if I’ve got to store a bunch of calories inside my white adipose tissue, it’s going to start to get crowded, and the more stuff I stick in there, the more inflammation that creates the crowding of all that material in there can start to create inflammation.


Vitamin D comes in there to increase the size of the white blood cell, the white adipose tissue. It increases the number of the white adipose tissue, and now what happens is we can store more calories. 

Is that good or bad? Well, in animal studies, what they did is they knocked out the vitamin D receptor inside those fat cells, and guess what? Those animals couldn’t get fat because they couldn’t store more calories.


But as you store more calories in the fat cells, the fat cells release leptin. Leptin then goes through the brain, and it should tell the brain that you’re satiated. You don’t need to eat more. It’s time to start increasing the metabolism.

But as this starts to build up the amount of stuff you store increases, and we increase leptin, we get too much leptin in circulation, the brain starts to become leptin resistant.

When the brain is leptin resistant, it doesn’t listen to the signal that we’re storing extra calories as fat. And so even though we just had a big meal, we want something more to eat. This is how somebody who’s obese can honestly think they’re still hungry. They’re still starving even though they have so much extra calorie on them to be able to run off of.


When leptin starts to go up, that increases inflammation. If you have increased inflammation, you have increased activation of the immune system, which could aggravate thyroiditis. 

You have increased inflammation, which decreases the conversion of T4 to T3, increases the deactivation of T4 to reverse T3, and increases the deactivation of T3 to T2. And then we wind up with more slowing down of the metabolism at some point.

Now we have so much damage and destruction of the gland, that now the gland can’t produce thyroid hormone anymore. You officially get diagnosed with primary hypothyroidism and somebody wants to give you a drug.


Now, the number one drug that most doctors will provide is T4, and there’s different forms of T4.

What doctors believe will happen is that when they put T4 into the system, it’s going to result in a drop in TSH – and it can do that at the brain pretty quickly. The brain’s receptors are about 10 times more sensitive to T4 than the peripheral receptors. 

So the brain gets saturated with T4 pretty quickly, and as soon as it does, there’s a decreased release of TRH from the hypothalamus, therefore a decreased TSH, and decreased stimulation of the thyroid gland.

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Now, is that good or bad? Well, it all depends.

If the goal is to just let the gland get shut down and never have it try and recover, then that may be a great strategy, because now the thyroid gland doesn’t have to do any work. But you’re now dependent on the T4.

What most doctors assume is that if TSH comes down and comes back into range and the (free) T4 becomes normal, then they assume that the T4 that’s in circulation in the bloodstream means that the rest of the body is supported and saturated with thyroid hormone. 


And that might be the case if the person was in homeostasis. If they are, and there’s low stress, then that T4 is going to convert to T3, and they’re going to feel good, they’re going to function good, there’s not a problem. 


But if you’re in allostasis, high stress, then there’s a decreased conversion of T4 to T3 by the cells. 

So if I pump a whole bunch of T4 into the system that the body doesn’t really want, even though my TSH has been normalized… if doctors looked at free T3 and total T3, they would start to realize that this number is still low, and T3 is what makes us feel and function well. 

And so people continue to struggle in an allopathic model when they’re on T4 only if they have this allostatic state going on. 


Now, some people say, “Well, we need to give T4 AND T3,” because they look at both the total T4, free T4, free T3, total T3, and they say, “Listen, I can see this person’s not converting T4 to T3, so I’m going to give that person T4 and T3.

Now if you look at their blood work, their TSH will typically go really low because they’re providing T4 and T3. Their T4 may be normal, but their T3, depending on when you take the hormone before the blood draw, you’re going to see that their T3 levels are low. 

So most doctors will tell them to take the T3 before they go for the blood work because they want to see if that bolus of T3 they’re taking is sustaining their blood levels of T3.


But what they’re assuming is that if there’s enough T4 and T3 in the blood, that it’s going to diffuse into the cells and make you feel and function well. 

And initially, every time you get a new dose of medication, a lot of times it makes you feel better… but then it plateaus. 

But keep in mind, if the person’s in allostasis and we give them T4, we know the cells favor the deactivation of T4 to reverse T3, not to T3. And if we give them T3, the same enzyme Deiodonase 3 is going to favor the deactivation of T2. 

Now, there is a form of T2 that can still support the metabolism, but people wind up ramping up T2 levels just like they ramped up T4 levels here. Any time they still don’t feel well, then there’s a whole camp that says, well, if that’s not working, we’ll just give T3. If that doesn’t work, we’ll give T2.

The reality is, if you agree with me that this is probably an adaptive response, then this is where we need to put our time.  What’s causing the excessive cell stress?

Is it trauma? Is it organisms? Is it decreased breathing? Is it hypoxia, respiration issues? Is it infections? What is it? 

When you start addressing this and we start shifting the person from allostasis to homeostasis, it really doesn’t matter what you give – the T4 to T3 just conversion works.

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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.