Why Are NFL Players Having Early Heart Attacks? (Surprising)

There was a 3500 player study with the NFL. The players who half had 50% had had ACL tears, 50% had. Had. Not the, the 50% that had the ACL tears had a greater than 50% increase in severe cardiovascular disease. And they looked for kind of the smoking gun for what's, what's driving this. And what it came down to is, you know, you have increased chronic inflammation in that joint almost forever after that, after that traumatic tissue damage that you have with the, the injury and then the surgery. And that doesn't really go away, and it doesn't stay local. It, it impacts and impairs your cardiovascular endothelial tissue. And one of the measures that they use for cardiovascular endothelial tissue, which is just, just the kind of tissue on the inside of your blood vessels, is what they call a shear strength test. And so sheer strength is, is when you have pressure coming down the pipe of your, of your, your blood vessels, how much the, the more blood that's going through there, the more stress gets put on kind of at a, at a perpendicular angle angle to that endothelial tissue. And the, the sheer strength drops off when you have inflammation chronically in your body. And that's, that's when you start seeing stiffening those. That endothelial tissue can't, can't expand and deliver blood as easily. And, you know, part of the validation for this has been, let's go back and measure the tissue that's around this injury to validate that's what's driving it. And when we do, when we see somebody who's had an ACL tear, as an example professional athlete, they can be five years on or 10 years on, but when you measure the temperature of their quad above that unhealthy joint is 1 to 2 degrees colder than their, the one above their healthy joint. And it doesn't sound like a lot, but that, that's severely impacting the amount of oxygen and blood delivery to that tissue there. And so it essentially goes kind of really bad. Local inflammation impacts degrading tissue tearing down your cartilage, making you have worse outcomes from a mobility standpoint. And then you go regional and you look at the, the muscle tissue and it's getting worse blood delivery, worse oxygen delivery. And you go systemic and you looked at endothelial cardiovascular tissue, and the shear strength is dropping. This is, this is something that's crazy across all of these different parts of your body.

So really that's nature giving us the signal. Hey, pay attention. There's something that needs to be addressed here. And so people can go like 10, 15, 20 years plus with back pain. It's like, oh, it's just what it is. It's almost like this psychological excuse that. Because people are so overwhel, overwhelmed and busy. And you know what? I definitely fell into that in the past where there's so much going on. You know, you're a father, I'm a father. For the parents out there or for the busy single peeps, like, there's a lot to do during the day. There's a lot of stuff going on. And so unless pain is like, really screaming at you or debilitating you so that you can't do normal activities, sometimes the motivation, the internal locus of control to actually change what's. What's hurting cannot be there. It's like it has to bark at you so loud. But. But it's so fascinating what you said, because it can literally change the strength of the way that our heart feeds our body with fresh blood because of that local inflammation source. And this is where I think the photobiomodulation conversation for me is absolutely fascinating because think about what we would do back in the day, like, before you and I ever had computers, before there was phones, like, if we were to just pull the E bra and go back to, like, 1850.

Right.

If we were living in harmony with nature and we had had an injury, we would address it through being in sunlight, through using different mobility and massage. Or we would rest. Yes, we would actually be forced to rest because we couldn't go out and plow corn or whatever we were doing. So now it's like we lead these lives of, you know, computers and technology. And I feel like what Kineon is, is it's this answer. It's a Trojan horse for people to address the pain early, so. So that they don't have to wait decades before it actually makes their heart weaker.

Yes.

I didn't know that. That you could have a meniscus, or even for me, my elbow issue or anything at all that can actually make your heart weaker over time. That's freaking wild.

Yes. It's crazy. And I think you've nailed it, though. I think one of the other things that we see a lot of that's really. It's kind of heartbreaking is that you see people just ascribing this to age. Like, I'm just old. I'm just going to have this pain. And, you know, part of our job is to educate and say, you don't have to. You can get out of this you know, it takes consistency. It's not going to happen in a week when you've had, the longer you've had it, the, and the more damaging that trauma has been to the tissue in the first place, the longer treatment like this takes to, to help you. And you know, we've, we've committed to our users to be able to keep it, keep it as long, as long as you're using it, keep it as long as you can. If you ever feel like you're not getting the results that you were expecting out of it, send it back to us. We're not here to sell devices. We're here to change your life. So it's, you know, that again, that's our commitment as a company is, is the mission for moving that needle. We, we don't want to be forcing something onto you. We, we get a lot of skepticism about like, oh, like. And reasonably, I, I think if you think about it from an outside looking in, it sounds incredible. Like I'm going to shine light on my body and I'm going to have physiological adaptations because of that. It, it, you know, even when I started looking at this from a medical research standpoint, that sounds, that sounds incredible. And so I can appreciate the skepticism. But when you get, now I think over 6,500 studies that we've cataloged and then kind of drilled down into and kept all of the dosing data from that, because it's one of the things that you've mentioned, and I think it's worth diving into a little bit is when you're out in sunlight, you're also getting infrared light. There's different ways to get light and there's different reasons that we've developed these photoacceptors in our body to be, that do trigger different signaling impacts. And you know, the difference with using photobiomodulation is that you can essentially work backwards from what you want to do or what you want to achieve from result and trigger the photoacceptors that you need to, at the right level with the right number of photons to be able to do that. That's essentially where we've spent tens of thousands of hours with our technical team is building out these mathematical models and then baselining them with physiological responses. And there are a number of different existing kind of off the shelf models. One of the ones we started with. So how, how just to kind of describe how most red light or laser therapy devices are dosed, most of them are dosed more from an engineering standpoint. So there's there's two metrics that are used quite commonly with particularly the commercial and really most of the medical level devices that are out in the market. That's irradiance and power density, optical power density. And that's essentially how much light's coming out of the device and how much light's hitting your skin. Those are interesting and to some degree give you a rough order of magnitude understanding of the light that you're, you're dosing with. What we wanted to start with and hold ourselves accountable to a higher standard for this was start from what you want to do, start from what you want to impact from a photoacceptor standpoint. We know which photoacceptors want to, we're trying to trigger, we know how many photons we need to be able to deliver to those, and we know essentially how light we can model mathematically. And the models are getting more and more complex. So I say that we can model mathematically how light distributes through tissue. And that's what we've done is we started with kind of off the shelf models of we want to trigger these photoacceptors at these level of tissue to be able to get the best results. We build the model to that and then we use again, what's gotten us into the optical sensor side of things is we use existing optical sensors to be able to measure what's happening within the physiology. And that gives us, we can't measure every photo acceptor output downstream signaling, but the larger ones we can. And so when we make our mathematical model, we build that and say, here's what we're delivering to this depth and here's what we're expecting for the outcome for serum nitric oxide, which is something that we increase as an example, then we can measure the serum nitric oxide. And if it's up or down, we have to go back in and understand with our dosing or what drove that difference with the physiology relative to what our mathematical model was predicting.

Is the serum nitric oxide one of the ways that it calms down the inflammatory cytokines or is that something different?

It does from a more macro level. It opens up the blood vessels. So when we're interacting with hemoglobin, our infrared wavelengths interact with heme core kind of based molecules like hemoglobin. And so hemoglobin is a carrier molecule that carries oxygen and nitric oxide in the body. When we reduce the affinity of nitric oxide to binding sites on hemoglobin, it dumps a bunch of the nitric oxide into the blood vessels and your endothelial tissue takes that on. And what's been very interesting and we have, we have one of our friendly companies that does sensors for this is there's almost kind of a paradigm shift in how people are thinking about cardiopulmonary function where it's been kind of a two molecule oxygen and carbon dioxide kind of paradigm. And then shifting into the nitric oxide one being built into this. There's these, there's some really smart people doing some really cool work in this space. But for us the main thing is that when you reduce that affinity and you kind of cleave the nitric oxide from the hemoglobin, you do this in a form called, there's a number of different forms of nitric oxide in a form called S nitrocetiol, which is very effective at increasing or dilating the, the blood vessels. And so when you dilate those blood vessels, you provide more oxygen, more blood to these areas where you do have chronic inflammation and you'd like to be able to get that out. This is one of the signaling molecules and one of the impacts that we have there. There are other ones that are cellular level where there's another heme based protein called cytochrome C oxidase that's part of your oxidative phosphorylation chain in your mitochondria or in the kind of phospholipid bilayer or cell wall of your mitochondria. Yes, we trigger that as well. And that's that the downstream signaling from that is essentially to, to balance and I would say reduce in most cases, but it actually, the literature shows us that it's, it's. If your oxidative stress is very high, it's not healthy for you. If your oxidative stress is very low, it's not healthy for you. And what we found is this actually balances that, that oxidative stress at a cellular level.

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