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How Diabetes Weight Loss Drugs (Ozempic, Trulicity) & GLP-1 Agonists Actually Work

And the GLP-1 no one is talking about…

Everyone is talking about GLP-1 agonists (diabetes drugs like Ozempic and Trulicity) right now for weight loss and blood sugar regulation, but what do we really know about them? In this video, I explain what GLP-1 agonists are, including the GLP-1 no one is talking about.

Video Transcript

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I think there are a couple of questions we have to ask about GLP-1… Why do all these people need more GLP-1 agonists to begin with? 

Well, today I want to discuss the GLP-1 no one is talking about – but first, let’s talk about the one that’s getting all the attention.


So within minutes of eating, the cells in your intestinal tract release this hormone called GLP-1. 

GLP-1 goes through the pancreas, decreases glucagon production, and it increases the release of insulin, especially the first phase of insulin response, which is preformed insulin. So that way as blood glucose is going up, insulin is rising with it so it doesn’t rise too high. 

The glucagon that’s typically released by the pancreas is what drives the liver to push out glucose so that our glucose is maintained in a fasted state. 

So when you’re eating a bunch of food, your body wants to kind of decrease the production of extra glucose because we’ve got glucose coming from our food. 

And what it’s thought with people that have high blood sugar, that have pre-diabetes and diabetes, is if you just give them a GLP-1 agonist, this medication that binds to these GLP-1 receptors, then you’ll get more shutdown of glucagon and more stimulation of insulin production, and that can help with weight loss and controlling blood sugar values. 


But I guess a couple of questions we have to ask is why was the GLP-1 low to begin with? Why was the GLP-1 they were making not working well enough, and is adding more GLP-1 to that system really the best scenario? 

I don’t know that that’s necessarily the case, but the most important thing is it doesn’t address the cause. And sure, some people don’t want to address the cause. We’re just trying to treat the problem. Maybe we don’t really care about the cause. 


But there’s another GLP that may have a bigger impact on why we don’t have GLP-1 being released appropriately to begin with – and that’s Central GLP. 

So GLP-1 that’s being talked about on TV commercials is the one that’s being released from the GI tract. Central GLP is what’s being made and released in the brain, and it impacts satiety signals. 

There’s this hormone called Leptin. When you’re storing extra calories in your adipose tissue, the adipose tissue releases Leptin. Leptin can increase the release of Central GLP. Leptin tells the brain, “Hey, we need to release this Central GLP-1” and that GLP-1 that’s released in the brain triggers greater satiety cues so that we’re not hungry. 

And so that’s kind of how this whole process should work. 


But this is an important piece: There’s something else that increases Central GLP-1 in the brain, and that is some type of chronic stress, emotional stress, or inflammatory trigger.

And that increased central GLP-1 increases the sympathetic nervous system, which is your fight or flight response. This then ends up decreasing your parasympathetic nervous system. So GI tract gets shut down, we’re in stress, we’re in danger, we don’t need to digest food, we’re going to get decreased intestinal function. 

And then that means, guess what? We’ll also get decreased GLP-1 in the digestive tract, which is the GLP-1 all these drugs are targeting. 

So maybe one of the reasons why these people with diabetes and blood sugar problems and obesity have low GLP-1 is because they’ve got some type of chronic stress or inflammatory process going on, and it’s impacting the central nervous system. 

And because they have decreased GLP-1 when they eat food, they have increased blood glucose levels because there’s not enough intestinal GLP-1 to rise insulin and not enough to turn off glucagon. And so the liver still keeps pumping out glucose. 

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That central GLP-1 can also activate the HPA axis. That’s the hypothalamus pituitary adrenal axis, which drives increased ACTH production, and that increases cortisol. 

Now, what is cortisol going to do? Cortisol is going to increase blood glucose production. And that’s not all…

That increasing of the central nervous, the sympathetic nervous system is going to increase epinephrine and other fight or flight catecholamines. What’s that going to do? It’s going to increase blood glucose. 


There’s another thing that we have to take into consideration when we have that stress and that inflammatory process in the brain. It increases the conversion of T4 to T3 in the paraventricular nucleus of the hypothalamus. That results in a lower TRH that results in a lower TSH and a decreased T4 to T3. 

So what that might look like on a blood panel is somebody having hypothyroid signs and symptoms, but a low TSH. And if TSH is the only thing, run TSH with a reflex to free T4. 

If TSH is low-normal, then the person could be complaining of hypothyroid symptoms. The person could be overweight, they could have blood sugar issues, but they’re going to have, if we did the rest of the panel, maybe their T4 and T3 levels are low. 

Lastly, when you have this decreased peripheral T4 to T3 conversion, because there’s less T4 in the system because there’s this inflammatory process going on, there’s less T3 in some of those peripheral cells and tissues like the GI tract. 

If there’s less T3 in those peripheral cells, it’s going to result in decreased insulin-dependent glucose transport in the cell, and so you’re going to have higher blood glucose. 


So what does all this mean? Maybe we’re focused on the wrong GLP-1 stimulation…

Maybe we have to think about what’s causing this whole process to shut down to begin with. Maybe the reason is that people have a lot of physical, chemical emotional stress that’s impacting their brain and causing their brain to shut down the digestive process on purpose because it needs to defend itself. 

So if we spend more time worrying about what’s happening, what’s creating that excessive stress load on our physiology, that would probably be the most important thing we could do. 

And maybe we wouldn’t need all of these medications that really don’t address the underlying issue. 

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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.