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The Thyroid Paradigm Shift: Part 1

How we can start helping people with hypothyroidism by shifting our perspective…

Here I explain why we need to shift away from thinking about hypothyroidism as just a problem with the thyroid gland, to looking inside cells. Hypothyroidism symptoms are caused by a lack of thyroid hormone binding to receptors inside the cells, which is why many people show signs before any glandular destruction is evident.

Video Transcript

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Today on this edition of Thyroid Thursday, we’re talking about the paradigm shift, and this is the thought process that I think a lot of people need to start having when it comes to how to address and help people with hypothyroidism.

We need to start thinking about hypothyroidism, not from a gland perspective necessarily, but from what’s happening within the cells.  Because it’s actually a lack of or reduced thyroid hormone binding to receptors inside the cells that causes our signs and symptoms.

So the cell typically operates in one of two modes. 

The cell is either in a low-stress state, or what we call a homeostatic state, and the primary goal of the cell is to manufacture. So it’s bringing in nutrition, it’s building proteins and peptides and proteins and hormones and neurotransmitters, and your tissues are making skin, you’re making hair, and you’re feeling good, and you’re burning up a lot of the energy. The energy you bring in is getting used to make stuff to keep the body healthy, and keep it functioning and running optimally. 

The other state the cell runs in is what we call an allostatic state, and that’s an excessive stress state. So whether there’s reduced resources, reduced oxygen, whether there’s a toxin, an organism, whether there’s emotional stress or trauma, there’s lots of different things that can create too much stress on the cell, too much demand on the cell, reduced energy to the cell, and that triggers what we call the cell danger response. 

And the cell behaves totally differently, whether it’s in a manufacturing homeostatic state or an allostatic state where it’s more in cell defense and the manufacturing processes are turned down.

(01:46):

In the low-stress state, the cell’s in homeostasis, so there’s lots of manufacturing. Inflammation is actually downregulated. The cells are very sensitive to glucose, very sensitive to insulin. So you don’t have high glucose, you don’t have high insulin. The cells are able to burn fats for fuel because the mitochondria are cranking out at high output, and there’s plenty of T3 inside the cell, and you’re not going to feel tired and fatigued and hypothyroid, okay? You’re not going to have dry skin, you’re not going to have constipation, you’re not going to have all that symptomatology.

(02:20):

But when a cell starts to perceive excessive stress, it now has to shift its function. So instead of manufacturing things, it’s going to slow down the metabolism and look for whatever’s causing the threat, the danger, whatever that danger signal is. 

And so in an allostatic state, we see decreased manufacturing. We make fewer amino acids into peptides and proteins. Neurotransmitter production with sex hormone regulation goes down. We see an increase in inflammation, and we all think inflammation’s bad, but actually inflammation is a protective mechanism. We also see glucose and insulin resistance.

So for all of you who have been told you have glucose or insulin resistance, pre-diabetes or diabetes, and you’re exercising and you’re eating low carb, higher levels of fat and protein, and yet you still have insulin resistance or glucose resistance, it’s not because of necessarily what you’re doing. It’s because your cells are perceiving some type of cell stress or danger.

There’s reduced fat burning, so you’re not going to burn fat as fuel, you’re going to store fat. You’re going to primarily burn glucose and carbohydrates as a fuel source.

(03:34):

And part of this whole allostatic process is the downregulation of thyroid metabolism inside the cell, and reduced T3 inside the cell. Why?

Because T3 increases the manufacturing process. High levels of T3 inside the cell turn down the immune defense inflammatory processes. T3 inside the cell helps support glucose transport and insulin signaling. T3 in the cell is critical to burning fats efficiently. 

(04:07):

So when there is cell stress or cell danger response, the cells, instead of converting T4 into T3, there’s a favoring of converting the T4 into something called reverse T3 and T3 into something called T2. 

Now, that’s a whole nother discussion. I’ve got other videos on the impact of T2. There are different forms of T2. Some of it is functional,  but from a simplistic standpoint, when there is homeostasis, there’s higher conversion of T4 to T3 in most of the cells. 

When there’s excessive cell stress in the cells or in tissues in the body in general, there’s a general downregulation of T4 to T3 and a lower metabolism. 

Again, it’s an adaptive response in my opinion, and what I’ve read in all the literature. It’s what I talk about in the book that I wrote with Dr. Kelly Halderman, The Thyroid Debacle.

(05:01):

So when this allostatic state occurs, then in all of this manufacturing starts going down, inflammation goes up, glucose and insulin resistance occurs.

What starts to happen? Well, inflammation then starts to trigger and activate the immune system. And the immune system then can trigger the initiation of thyroiditis, which is the inflammation of the gland. Now, whether you call it thyroiditis or Hashimoto’s thyroiditis, I don’t think it really matters. I think it’s all the same thing. It’s just whether you’re TH1 or TH2 dominant, whether you’re making antibodies or not. But there still can be thyroiditis going on.

Once you have the activation of thyroiditis, you get decreased thyroid gland production, and you can actually go through episodes where there’s destruction of the gland. You get lots of thyroid hormone dumped out of the system, and then periods of time where there’s a lull and there’s reduced thyroid hormone being dumped into the bloodstream. So because there’s thyroid gland destruction, there’s decreased T4 and a reduction in T3 there. 

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(06:12):

There’s also a general reduction of T3 in the body, because most of the T3 is converted in the peripheral cells, some in the liver, some in the kidneys, some in the GI tract. So most of that T3 is going to start to become down-regulated because inflammation activates another hormone, called deiodinase 3. Deiodinase 3 is the hormone that converts or deactivates T4 to reverse T3, and deactivates T3 to T2. 

(06:47):

So now what we have is we have the gland making less thyroid hormone. We already had a cellular hypothyroid state. So this is why you could start having hypothyroid signs or symptoms even before anybody detects anything going on with the gland. We had the tissue hypothyroidism going on. Now we have the gland being damaged, and now we have even less hormone being available, which to some degree is an adaptive response.

(07:09):

But now we also have less T4 in the system. So not only do we have the cells not converting T4 to T3, but we also have less T4 entering the bloodstream. And now we can start to head into a full on glandular and tissue hypothyroid state.

Here we were just having an inflammatory-induced tissue hypothyroidism, but now we’ve got a global hypothyroidism because there’s just not enough thyroid hormone in the system.

(07:37):

Other things that come on is that when you have this glucose and insulin resistance, you increase the size and quantity of your white adipose tissue, which means you can start storing more calories as fat. 

Why would your body do that? 

Because if you’ve got this cell stress response going on and you have reduced T3 in the cell, the cell danger response wants to decrease glucose coming into the cell. It doesn’t want to provide resources for the threat. T3 is needed to help with that glucose transport.

(08:15):

So because there’s cell stress going on and because there’s decreased T3, glucose is having a harder time getting in the cell, even with the help of insulin. So glucose goes up in the bloodstream, insulin goes up in the bloodstream, and now you start storing more calories in your white adipose tissue. They need to enlarge and expand.

And so what happens is Vitamin D gets driven into your fat cells to help increase the quantity and size of your white blood cells. Now you can store more calories and you get fatter. This why a lot of people, when they get their 25 OHD tested, it’s low. They’re not truly vitamin D deficient. It’s just going into their fat cells to try and make more room in this inflammatory situation to store more calories. 

The other thing that happens is leptin goes up. Leptin should tell the brain, “Hey, you’re satisfied. You don’t need to eat more.” But after a period of time, you get so much leptin circulation that your brain starts to become leptin resistant, and so now your brain doesn’t get the signal that it’s satiated. Even though you may have just had a big meal, you’re still hungry. 

As leptin goes up, it starts increasing inflammation. That inflammation makes the conversion of T4 to T3 worse. You slow down the metabolism even more, and this becomes a vicious cycle. 

So then the question becomes, should you give thyroid hormone? Should it be T4? Should it be T3? Should it be both? How much do we give and is more thyroid hormone the solution? I answer those questions in part 2.

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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.