The Science Behind a Systems-Based Endometriosis Supplement

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Full transcript of the original video, lightly edited for readability.

So it seems that I may have gone a little overboard on the last video. I know I got pretty deep pretty fast, and I may have gone a little over the top. Sometimes I do. I try my best to simplify things, but I don't do a good enough job sometimes. So the following explanation is the concepts behind our endometriosis supplement. Why it works and how it works. This applies both to the case of endometriosis and adenomyosis. So this isn't for anything else outside of these two conditions.

You see, the way that we look at it is that it like a house. A house is not stand if it doesn't have the appropriate support pillars. So if you keep weakening this base right here, the whole structure becomes less stable. And that's exactly how we should look at a condition such as endometriosis and adenomyosis when it's a network problem, not a singular inflammation problem, nor a one receptor problem, but as a disease structure being held up by several major biochemical pillars at once.

And endometriotic lesions behave like wounds moving through repeated tissue injury and repair. And the disease is supported by very specific pillars. Once you start to dissect it all. We have inflammation here, we have estrogen here, we have tissue remodeling, and then survival right here, which we will talk about. So when we go to the first pillar, we see inflammation. This is where you can find Cox, two prostaglandins, Inflammatory cytokines. This is where the pain chemistry lives, right? Cox two is over expressed.

Prostaglandin, E2 rises, and that same inflammatory pressure helps drive other genes involved in the second pillar, such as the star and sarmatase. So in other words, the inflammation is not just pain. It's part of a machinery that feeds off each portion, okay, the disease. Because estrogen is not really a problem. Estrogen exists in every single individual. It's if your machinery set up for it to be a normal response, or is it going to feed something else. So once we get this inflammatory action, it's going to push for aromatase to start enzyme, like we said, which is going to start an estrogen feedback loop.

You see, estrogen helps induce something known as estrogen receptor beta. Estrogen receptor beta is going to start pushing back over here. So all in all, it's already feeding off each other, these two pillars. Then this is where we kind of go down to the wound behavior. See, these lesions don't behave like quiet tissue. They are wounds that do not heal. It just. They keep reopening. This is where we start to get platelets, tumor growth factor beta, estrogen linked wound activity. Because that estrogen is gonna activate tumor growth factor beta, and it just becomes harder, deeper, more persistent over time.

The fibrosis, which eventually is gonna trigger the fourth pillar right here. And this is going to be survival, resistance, and, persistence. The lesions are going to stay because they remain biologically comfortable. They keep enough inflammatory support, enough hormonal support, and wound support just to avoid being cleared. This is typically, the body can get rid of these cells in normal individuals. However, since you have a mutated mechanism that allows a disease network to arrive, that's when you start to get to this situation.

Right. So the goal of vendors was never to be just hyper focused. The way you see, it's. It everyone looks at the hormone. Estrogen's the problem. Always estrogen driven. Estrogen is a feel. That's why we say it is estrogen driven, but not the way most people think. Estrogen is not the problem. It's the byproduct of a broken system. It's a framework that. Well, essentially, it's just using estrogen as fuel. So even if you take estrogen away, they're still machinery operating. So let's go on to the next portion.

We highlighted the four pillars. Now we must ask the question, how do we activate or deactivate these pillars to get that desired result? So which receptors are involved? Well, this is what we need to talk about. Receptor activation. You see, most people imagine the biology much too simply, and this includes some doctors as well. Receptor activation is just not an on and off binary switch. That's not really what's happening. It's more like a door that's always opening. It's opening this way, all the way this way.

Sometimes it's right here. Where the wall's at. But this is ultimately what's happening. It's always favour in one state or the other. Sometimes it's fully closed, sometimes it's somewhat closed, sometimes it's fully open. It just. It's not just on and off all the time. And this is a much better way of understanding it. And this is where we started to talk about stochastic processes and how this all works. And the previous model, we're talking about DIM and estrogen receptor beta. And this is something of key importance because when we start to look at it right, if we get DIM, it's gonna start binding to each receptor beta and it's gonna be shifting between these states.

Four total states exist. So bound, unbound, active and inactive. Sometimes the receptor can activate itself, mind you, so there's something to be, aware of. And this is the reason why we will get a little bit deeper into that and then the next section. But the goal is to make them spend more time in a desire activated state. This is what's known as active state occupancy. This is what it means. It's what fraction of the receptor population, or right here, as you can see, receptor beta is gonna spend time in the active state instead of the inactive one.

So this is what the model explicitly, explicitly states as the active state occupancy. It's overall what we're trying to accomplish here, okay? Because these are the overall states that receptors Can exist in. And mind you, estrogen receptor beta is not a background detail. It sits inside a well known and established feedforward disease loop. Increased estradiol helps induce estrogen receptor beta, which helps induce COX-2, and that drives PGE2. More inflammation, more growth. So changing receptor behavior is not just a receptor story.

Our goal is to change the pressure inside a larger inflammatory loop. So when I say receptor activation, it's not that I'm talking about on and off binary. What I'm actually trying to get across is that we're trying to change the odds into a better state occupancy. That's not a disease territory. We want to get the system to spend more time in a healthy homeostasis, a healthier equilibrium. See, when you start to look at the body this way, that. That's a completely different level of thinking.

Okay, so we talked about receptor fluctuation and inactivation activation, so on and so forth. So how does this fit in? Stochastic processes, network topology. And where exactly does our endometriosis supplement fall into this? Frameworks. So let's address one thing first. What is stochastic processes? Stochastic processes mean that the system is moving with some randomness. Not chaos without rules, just randomness. Like a boat inside the sea. There's weather, there's waves. It's just moving around, floating in the water. It's being carried by the waves, maybe some of the wind.

It's always being pushed around, but not without patterns. There's. There's things we can map and the estrogen receptor beta model. Even so, if we focus from one receptor and we pull back and look at the majority of the receptors, there is drift and then there's noise. Drift is where we're trying to push the boat, the. Where we're trying to push your biochemistry. The noise is. Was trying to go against it. The waves is still trying to push back. It's fluctuating between moving a little forward and pushing you back.

That is what stochastic processes is. So let's talk about network topology. Network topology is the disease network, the pathways. You can think of this like roads, like your neighborhood highways, freeways, major intersections. This is where the traffic really happens in the disease. So when we look at endometriosis and adenomyosis, inflammation connects to estrogen, and estrogen connects to estrogen receptor beta, and that connects to Cox. Two platelets connect to estrogen overproduction, and then that connects it to wound, to fibromyalgia, to adhesions.

And so this is what network topology is. And the disease, it's just a giant web, right? As we discussed here. So this is what we start to look at, our very, very specific bioactive molecules that you can find in. In plants. And there's a reason we choose plants, but that's for another, different video. So one specific bioactive molecule might help with this note, another helps with this note, and then this note. And so the goal here is To help against this noise, we're trying to continue to push a direction, a drift.

So that would be like the boat is getting its sails up to continue to fight against the waves pushing it back. So the same way that one specific extract, like Rhodiola rosea, would help one specific node, we can't just focus on this node. We have to focus on major points. So these would be the receptors that are going to affect the four pillars. That is what network topology is. Okay, so how does stochastic processes and network topology fit into everything we've discussed?

Well, this is really the most important section of it all, because once you understand the system drifting, once you understand that things are always fluctuating, you really come to the conclusion that one push is never enough. The body is not like a park car, okay? It's more like the boat on the water that we spoke about. There is current that's always gonna push against the boat in the wrong direction. But you do to. To start to change and get to your destination.

You can't just correct it once and walk away. You gotta keep steering. You gotta keep adjusting the direction and start. Keep opposing the noise. This is what homeostasis is, and it's what the true context behind what a healthy body is. It's not a magical reset. It's not healthy right away. It's just pushing less and less time. In disease pathology, or Territory and more time in healthy territory. It's a balance going back and forth trying to find a fine equilibrium. It's still gonna fluctuate.

This is the reason for ligand input over time, or key input or bioactive molecules found in a supplement. You wanna make sure that as over time you're producing more and more of an effect, so you're getting to a destination. The inflammation is always gonna keep pushing, estrogen loops are always gonna keep pushing back. All of these lesion disease biology is always gonna try to push back. But our strategy and what we have done over the years is that we're always trying to shift the equilibrium, the balance.

We're trying to always fight against the noise until we find ourselves in a good balance. Right, so you initially people start right here and you move a forward, forward a little bit and then back, forward a little bit, then back and forward a little bit, then back. And the goal is to try to maintain your time in this area. This is how you actually handle endometriosis and adenomyosis. Because if we stop treating the disease like one broken switch, if we stop treating it like one specific approach or therapeutic, therapeutic protocol works, then you start to understand that it's a dynamic, drifting, self reinforcing network.

And you need to attack it with multiple pillars, not just one big blow. That's the whole concept. We've been here for seven years. We haven't Really marketed or done really anything. And yet we're still here. And there could only be one reason why. That is because this methodology works. It didn't work for my wife, and we are more than happy to go deeper into this. And mind you, this is actually much more deeper than I've presented. But I've tried to simplify the overall concepts that we have done to create ENDOLLS to what it is today.

Hope this helps. Let me know if you guys need a deeper or further explanation.