Clearing Out the Cellular Clutter: with Dr. Gregory Kelly

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I'm JJ Virgin, PhD dropout. Sorry, mom turned four time New York Times bestselling author.

Yes, I'm a Certified Nutrition Specialist, Fitness hall of Famer, and I speak at.

Health conferences and trainings around the globe. But I'm driven by my insatiable curiosity.

And love of science to keep asking.

Questions, digging for answers, and sharing the information I uncover with as many people as I can. And that's why I created the well Beyond 40 podcast to synthesize and simplify the science of health into actionable strategies.

To help you thrive.

In each episode we'll talk about what's working in the world of wellness, from personalized nutrition and healing your metabolism to healthy aging and prescriptive fitness. Join me on the journey to better health so you can love how you look and feel right now and have the energy to play full out at 100.

We're about to dive into a topic that's not just fascinating, it's absolutely crucial for everyone who wants to age powerfully. And since you're listening, I know that's you. Right now we're in the middle of a health revolution and really at the heart of it, there is something called cellular senescence. Now I know that sounds like a mouthful. It was a mouthful to say. But stick with me because this could be the key to unlocking a level of vitality that you might have thought was long gone. Here's the thing.

As we age, our bodies accumulate these.

Worn out zombie like cells that refuse to die off like they're supposed to. They just hang around causing inflammation and.

Messing with our healthy cells.

It's like having a bunch of cranky energy vampires in your body, sucking the.

Life out of everything around them.

And guess what? This isn't just making us feel older. It's at the root of so many age related issues we've come to accept as normal. But here's where it gets exciting. On this episode we we're going to expose these cellular saboteurs and give you practical, science backed strategies to deal with them.

We're talking about potentially reversing years of cellular damage, boosting your energy, improving joint health, and maybe even turning back the.

Clock on some of those visible signs of aging we all dread. And to guide us through this mind blowing science. We have the brilliant Dr. Gregory Kelly with us now. Dr. Kelly isn't just any researcher. He's a heavyweight in the world of natural medicine and anti aging. He's a naturopathic physician, the vice president of product development at Neurohacker Collective, and the author of the book Shapeshift. Dr. Kelly has published hundreds of articles on natural medicine and nutrition, contributed to the textbook of natural medicine, and has over 30 journal articles indexed on PubMed. His expertise spans from nootropics to anti aging and regenerative medicine, and he's been a pioneer in the field of senolytics. That's the science of clearing out these problem cells.

He's been on the cutting edge of.

This research for years, even developing products to help us mere mortals benefit from these amazing breakthroughs.

In this episode, you're going to hear.

About the shocking truth behind these zombie cells and how they're impacting every aspect.

Of your health, from your joints to your brain function.

And on we're going to talk about why traditional anti aging approaches might be missing the mark and how targeting cellular senescence could be the game changer we've been waiting for. Dr. Kelly is going to share some practical, actionable steps you can start taking today to combat cellular aging no matter.

What stage of life you're in.

And let me tell you, some of these strategies, they're surprisingly simple. We're talking about compounds that might already.

Be in your kitchen.

We're also going to dive into the latest breakthroughs in senolytic science. Trust me, this isn't just about adding.

Years to your life. It's about adding life to your years.

We're talking about staying vibrant, active, and sharp well into your golden years.

So whether you're in your 40s and.

Starting to feel those first twinges of, wait, when did that start hurting?

Or you're well beyond that and looking forward to reclaiming some of that youthful vitality.

This episode is for you.

We're about to embark on a journey.

That could fundamentally change how you think about aging. So let's dive into this conversation with the amazing Greg Kelly and unlock the secrets to aging powerfully.

Are you ready?

Let's do this.

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Dr. Greg Kelly, I'm so excited to have you here in person.

Yeah, this worked out really wonderfully to be able to come here and do this face to face with you.

Yes, it did. Well, I knew I was in San Diego and I knew you were in San Diego, so we made it happen. And I'm very excited to dig into senescent cells, what they do, why we should be concerned about them, everything around longevity. So let's dig in and start with what the heck is a senescent cell?

Yeah. So can we start with a history lesson?

Of course we can. You be a little geek.

Yeah. Yeah.

Okay, good.

Like back, say, pre1961, there was this idea that if you had human cells in a petri dish and gave them the right nutrition, they were immortal, they would live forever. And then a researcher, Hayflick was one of them, Moorhead was the other, did a really brilliant study and they found out, no, that these cells would kind of divide up to about 50 times, hit a max, and then would not make any new cells. They would just die off. And that's what we would now call replicative senescence. And so the idea is, we know now, he didn't know then that as telomere length gets shorter and shorter, at some point they're short enough that a cell doesn't want to reproduce itself because it would potentially reproduce damaged DNA, we never want that. And so that idea that a cell will at some point basically become old and no longer make copies of itself became called cellular senescence. So for the listeners, the key idea is that we would have healthy cells that are doing their job. They were born, they're living, they're doing whatever they're doing. Maybe liver cells are doing one thing or something else. And those cells live their lifetime, die, and are replaced often by daughter or son cells that, that they divide and create. And like, on average. Right. We probably hear if you Google it, you'll see cells live for, on average seven years. But that's not particularly true. It's true. Ish. Right. It's an average. But liver cells, it's one to three years. Heart cells, it's about four decades. Muscle cells, about 15 years. Neurons are meant to last a lifetime. So for these cells that are born, go through their life, they eventually go through their own cellular death process. It's called apoptosis. It comes from a Greek word that means falling off, kind of in the sense of a fruit falling off a tree. So when you think of cellular senescence, it's somewhere between. It's a cell that's not quite this healthy live cell that's allowed to make copies of itself, but it's a cell that's resisting going through that form falling off process. So when you think of the idea of cellular senescence and aging, the simplest way is these are stress cells that are kind of aged, worn out, but they're still lingering in our tissues.

So you mentioned telomere length. Yeah, let's talk about that. Just since you threw it out there. I always like to get the terms. And I still remember when I had my telomere length tested, when they didn't really know what to do about having. I was like, well, this was not helpful. This just made me worse. Now I'm more stressed because I have short telomeres. So talk about what those are.

Yeah, so telomeres, this is more like a common use definition. But at the end of strands of DNA, there would be some things that aren't copied. So the genetics that don't get copied and that they're often described almost like the tips on our shoelaces, those things that prevent them from fraying. So that's what telomeres would be. They're the things at the end of DNA that would prevent the strand from unraveling. And each time DNA is copied, you lose a little bit of the length of telomeres. And if that length gets Short enough, then there's what's called a DNA damage response. But fundamentally that means is the cell will become senescent because it doesn't. We don't want it to make a new copy.

So is there a way then, would you look at telomere length to be able to identify senescent cells?

So in the old days, they probably would have said yes, because think of cellular senescent or senescent cells as a category. And different things can cause a cell to become senescent. In the old days, it was thought that the main reason was telomeres, so that once telomeres got short enough, a cell would become senescent so that it wouldn't. And now that would be a category of senescence called replicative senescence. But what they eventually discovered is all kinds of other things can cause a cell to become senescent. When telomeres are completely fine, what would those things be? So that category would be called stress induced premature senescence. So long before the cell was worn out because of telomeres, something prematurely stressed it and caused it. So these can be things like mitochondrial dysfunction, which I'm sure you've talked about on your show before. Issues with nutrients that surround the cell can be toxicity, radiation. Really think of the things that stress us on a whole body level stress our cells. And if a cell gets stressed to a certain point, it has to respond. And this would just be the way I think about like, you know, a cell gets stressed. You know, it's resilient. It's got this. It goes through door number one and just gets fitter, tougher, like, you know, builds up its antioxidant defenses. If stress is more than that, it's going to go through door number two. And door number two means it took some damage on. So in cellular damage, you're talking about proteins getting gunked up like tangled up, or organelles like mitochondria being damaged. Door number two is where autophagy comes in as an example of something that repairs damage or processes in our cells that repair damage. Nad has a molecule like part of its link to longevity is its fuels and DNA repair. That's door number two. Stress took some damage, but we can fix it. Door number three would be the damage is so much it's not repairable. And that's door number three is a senescent cell.

Got it. So we have the cell that went to the gym and got stronger. We have the cell that like, maybe was under tremendous stress in a moldy house and got some autophagy and was able to get rid of some of that. And then we have the cell that's just got a bunch of damage and she's sitting there.

Right.

And so those senescent cells are just sitting there. They're not doing any good.

Yeah. So most things are contextual. So the way that we would describe it at Qualia is think of there's transient senescent cells and there's lingering ones. So get to the transient ones first because transient ones can do some good things. So like imagine a listener maybe on the show is 25 or 30, they decide to.

This show's called well Beyond 40.

Okay, well Beyond. So like a super healthy Beyond 40.

All of us, everyone listening is super healthy.

And well beyond 40 does something like, you know, more exercise than you're used to and creates some inflammation, some damage. So that will cause an increase in senescent cells. And in a young person, what you would have seen is five days, a week later, those would have been transient. They would have kind of bloomed and then died off. They would have gone through that falling off process, apoptosis. But what happens as we get older? So the well beyond 40 listeners, they linger. And what that means is they resist that falling off process. So we create them, but they just stay long past their use by date, if that makes sense.

Okay, so they're hanging out. They shouldn't be. If you were younger, you would have gotten rid of them.

Correct.

You still would get rid of some of them, I would think with exercise. Because of the poptosis from exercise. Right.

So exercise without question helps prevent the accumulation of senescent cells in muscle tissues, whether.

Well, you said muscle tissues. So.

Yeah, because things in the body, there's this weird thing, is that responses tend to be tissue specific. So sometimes things will have a generalized response. But you know, sometimes, you know, like insulin resistance would be a classic thing. Like a type 2 diabetic, just before often being identified, will lose a bunch of weight. Like that's often a trigger that causes their diagnosis. And what's happening then is their, their muscle cells have been insulin resistant for a while. Their fat cells for a long time weren't. So they were sucking in, you know, the things to turn into fat. And at that point there's their fat cells also said like, we've had enough two. Right. So things, you know, ultimately happen on a tissue level, but exercise for sure, for listeners prevents some degree of cellular senescence.

I will always plug exercise into anything, wherever I can, like the exercise benefit. So you have these senescent cells then, that are accumulating more in someone as they age. So, you know, how does that. How would one know that they have this going on?

And.

And how does that. Does aging causes senescent cells, or does senescent cells cause the aging?

So those are great questions. Let's take the latter one first.

I love to throw too many questions at once. Yeah, no, no, Sorry about that.

And even before getting to that, let's just tie exercise in one more time. So what would I mention that young animal exercises a lot. They'll make some senescent cells and they'll do something good, right? They call in the immune cells, they help to repair damage. They're gone really quickly. And any stragglers the immune system finds and gobbles up in older animals, they've done these experiments. So what happens as we age is called anabolic resistance. Very similar to the idea of insulin resistance, that our muscle, the tissue, becomes resistant to the anabolic signals, which are like exercise, right. Weightlifting, getting enough protein, and the right kinds of.

I wish there was a way that we could look at anabolic resistance similar to how. I mean, we can. You can clearly tell insulin resistance. You can clearly do a lab test and see it. Be so cool if we could do that for anabolic resistance. Because I just am sure that if someone is eating optimal protein and exercise and has been doing that consistently, that they must. Their rate of anabolic resistance would be so much different.

For sure. Yeah.

Okay.

And then wrapping up that story, so they decided, okay, well, let's look to see if senescent cells play a role in anabolic resistance in animals. And sure enough, they did. And what I think it was, the researchers that came out of Buck Institute of Aging kind of framed it like, oh, like when a young animal exercises intensely, there's some senescent cells, but it's like an explosion of them are created in the old animals. And that 100% they contributed to the. The anabolic resistance. And when they did something called the senolytic, which we'll get to later, it helped remove the senescent cells and then reverse that anabolic resistance. So they started responding in a healthy way. So that kind of wraps that story up. But then you would ask, well, how would we know? And that's the really hard question to answer. The senescent cell cellular senescence is pretty new science. And the only way to really tell if senescent cells are in a tissue is to do a biopsy, which they do in animals. And then even then, the scientists have to do the right kind of treatments to those cells to identify, like, yes, this is a senescent cell.

And again, it would be tissue specific.

Yeah.

And as we age, do we tend to get them in certain tissues more than others, or do we not know that?

So it was originally thought that it was. They thought more in terms of what cell types than tissue, but that the cells most prone to it were immune cells, one, because they're everywhere. Another one would be called fibroblast. And there are connective tissue cells. So fibroblasts are in our skin, they're in our joints, they're between tissues. They're a connective tissue type of cell. And then endothelial cells, which are linear vessels and arteries. So those ones originally, they thought with the prime candidates. But at this point, I had mentioned earlier that neurons are supposed to last a lifetime. Like, in theory, they should never be able to become senescent because they don't divide in the first place. But even neurons can become senescent if they're stressed enough. So, long story short, all cell types can become senescent. What would definitely be true is, as we get older, we accumulate more and more in all of our tissues, organs, all cell types. But it might be uneven. You know, most things happen. Kind of an Achilles heel type of sense. Like, we all have our. Our weak points, Whether that's genetic, old injuries, you know, trauma, you name it. So really, the way that I would say the first, like, kind of sanity check is, you know, in a person, is there some part that feels like it's aging faster than the rest? And if the answer is yes, there's, I would say, good odds, given what we know from animal research and biopsies, that there's probably senescent cells contributing.

So when you're saying this, I'm thinking then arthritis, vision loss, wrinkling, like, these all seem like signs of senescent cells. Would they be.

They definitely contribute to all of those. Really, you know, like, all the things we think of that come with the onset of aging visibly. And then functionally, Senescent cells to date seem like they track with all of those. And whether they're the, like, the cause or not, I would say, without question, they contribute. And part of it. There's almost like two big camps within the longevity community and have been for a long time. One would be their idea is the main reason we age is because the accumulation of damage. And then there's a bunch of theories that go with that. Another is we. It's called programmed aging. Or things that basically we're designed to create offspring. And then after that we've done our job, we can get all the software just runs differently. Senescent cells clearly are in that first one because they're a type of damage. I mentioned earlier that they're fundamentally unrepairable cells because of the amount of stress and damage. But there's also evidence that as we get older, our genes cause us to produce more. So they seem like an output of programmed aging as well. So I think those theories aside, the one thing we can safely say is as I'm sitting here speaking with you, I'm a 62 and a half year old Greg. This version of Greg likely has more senescent cells all throughout my body than 30 year old Greg would have had. Exactly which cell and tissue has way more. Some have been pruned away, maybe in other tissues that we just don't have the science to know yet.

Well, I hope you really put your foot on the gas pedal for this science. It would seem clear as I'm listening, I'm like, all right, so the obvious question as you're listening to all of this is how do we slow this down, stop it, like, what do we need to do here? Because this could have a dramatic impact on our rate of aging.

Yeah. And so can I talk about a couple quick studies to bring that up? So senescent cells, like I mentioned, kind of origins back 1961. By the 70s, they named them senescent cells. By the mid-80s, telomeres had been identified. And then in the early 2000s, one of the researchers at Buck Institute discovered that senescent cells secrete so like they give off what are called sasp. SASP factors. But it stands for senescence associated secretory phenotype. And phenotype just means like a characteristic. So like a characteristic of lingering senescent cells is that they put out chemicals in the environment around them and those tend to be really inflammatory and cause all kinds of havoc. So that got scientists at places like Buck Institute and Mayo Clinic way more interested in senescent cells. And you've probably heard the idea of zombie cells.

Yes, that's what I was just going to ask you. So those signals going in, recruiting.

Yeah, so the like. So you'll sometimes hear the idea of zombie cells for senescent cells. And part of that is what I mentioned earlier. Right. They're not quite live healthy cells in the sense that they don't make offspring, but they're resisting going through cellular death. So they're Stuck in this limbo. So that's kind of one reason right there somewhere in between like a zombie would be. But the other reason is because of those SASP factors. Because what can happen is those can stress out otherwise healthy cells and turn them into new senescent cells so they can zombify neighbors in a sense. So with that recognition, all of a sudden it's like, oh, these are probably even more important. We always figured they had something to do with aging. But if they can cause, we'd call it inflammaging. If they can cause that and change the behavior of other healthy cells, we should look more closely. That led to a study around 2009 where they did a transgene experiment. Think of it as they genetically modified. I think it was a mice line to be all through the aging process. Fundamentally what would happen is they would find and remove senescent cells with these gene modifications and found that those animals just aged way better than animals where senescent cells were allowed to build up at the time. I think that really ignited the interest in like, is there another non that degree of intervention that we could do? Which led in 2015 to some scientists at Mayo Clinic and Scripps Institute of Aging writing a paper where they had identified that two compounds, one's quercetin, which I'm sure you would have taken. Maybe, I would guess.

Well, I've been taking full disclosure. I've been on senolitics since it came out. Oh, okay. And yes, I've been on it, on it, on it, on it. And you know, I met James and Daniel years ago, so I get the benefits of it. Which we'll talk about. Yeah, yeah. But I don't want to jump the gun.

Yeah. So anyways, they, you know, they identified corcitin in this medication, dasatinib, as compounds that could help these lingering senescent cells finally go through that falling off process and decided to call compounds that did that senolytics. So that was around 2000. So.

But these senolytic compounds that do this, from what I've read, they're tissue specific or are they global? Like when you take quercetin, does it go out and scavenge everything or is it NIS specific?

Yes, that's a great question. So in that original study, what they found is that they didn't look at every tissue, but they started off looking at what happens in a cell culture. An in vitro study. But then they gave these compounds to animals and looked and what they found was quercetin worked for endothelial cells in that experiment and worked in, I think it was bone marrow, but wasn't active as a sinolytic compound in adipose tissue or fat tissue in those animals where dasatinib wasn't so active in the ones where quercetin worked, but worked in fat cells. Had the idea right from the get go that we should stack things together. That stack D and Q is how usually I would think of it has been the most used stack for trying to remove senescent cells when you would read studies to date. And it's because there's a complementary. And I think, you know, for going with just the natural senolytic compounds, like, you know, what's in qualia senolytic, which we'll talk about. That's why we stacked things together. Because something can be a senolytic, but that doesn't mean what you mentioned, it can't necessarily go everywhere in the body and do that.

Is there anything, you know, like autophagy where we know exercise or extended fast could trigger autophagy? Is there anything like that, that. That is a synolytic? Are there any lifestyle things or is it all more nutrients that do this?

So the only work I know of is Valter Longo and his fasting mimicking diet, which Prolon is the commercial thing that people can buy and take. And the fasting mimicking diet is something you do intermittently, usually like five days.

Have you done it?

Yeah, yeah, several times.

I never got past day three.

Okay. And I've also done things where I try to kind of on my own, like hack it and do like my own, because there's a few principles that go with it. And I'm. One of the things I've seen him mention in, in like talking, his book is that senescent immune cells after about day three start to be pruned away.

Well, it's a good thing I like senolytics because I never got past day three. So there you go. It's way easier.

I think autophagy starts happening earlier, you know, like 24 to 48 hours. Some autophagy, you know, so that I think of autophagy as something that would prevent the cell from becoming senescent. But I think, you know, for immune cells. But his, his protocol, the fasting mimicking diet may not work for muscle senescent cells or other ones, but for the immune system, I think that would be. But other than that, I'm not aware of anything. And in part it's hampered just because it's, it's Such a new field and does require biopsies that, you know, there's just not a lot. There's nowhere near the amount of science on what might prevent or reverse it. Outside of senolytics that's been investigated today.

Would looking at something like highly sensitive C reactive procedures protein be an indicator that you've reduced senescence? Maybe.

So right now, there's a bunch of trials that are in progress, and there's like, fisetin is in quiocinolytic. Some of them are using just fisetin alone. Because one of the things the Mayo and Scripps Institute researchers found eventually, I think it was 2018, they published, is that fisetin seemed better than quercetin. It worked in tissues where quercetin didn't. It seemed to be more powerful on its own. And so some of those studies are trying to figure out what would be things we should look at that might infer that.

So quercetin plus fisetin. Fisetin alone was more powerful than quercetin plus fisETIN or quercetin. Fisetin is more powerful than quercetin, but it would seem like you put the two together, you'd have more firepower than just.

Yeah, so it was the latter. Like, fisetin alone was more powerful in their experiment than quercetin alone and worked in a tissue where quercetin wasn't active. But what happens in science often is like the D and Q I mentioned, that's being studied now. Fisetin is being studied, but almost no one studied. I know, Stacked together.

So frustrating because that's not how nature works. You know, it's not in a vacuum. Well, you hear this, and it's obvious. I remember when I first started looking at this, I'm like, well, this seems like an obvious thing that I'd want to be doing. Why wouldn't I want to do this all the time?

Yeah. So the. So the D part of D and Q is a really powerful immunomodulator medication. So when they were first doing this, the Bach and Mayo clinics were like, risk reward is how I would think of it. They were like, okay, what's a way we can do this that's more likely to be safe? Because one of these compounds we're using is a pretty powerful medication. And they came up with like, okay, well, let's do it intermittently. Which sometimes hear the idea, hit and run dosing. And the idea. The reason they thought that could work was because senescent cells are. This is my explanation. So the scientists Listening this is like a way simplification. But a senescent cell is resisting going through apoptosis. It's resisting going through that falling off process. There's certain proteins that are at the core of that. And I think of it as just their voters, right? And some are saying like, yes, fall off, and others saying no, no, no, hang on in tissues. And all we need to do is swing the vote enough to get enough voters to finally say, go through this falling off process. We don't have to do that every day, every day, every day. We just have to do it for that cell that one time and then it will kick into that process and finally go through the process it's been resisting and should have gone through. So because of that, it's sensible to do it intermittently. And like I said with the D and Q, you know, from a toxicity perspective, it made sense.

And.

One of my principles, because we were talking before the camera started rolling, is that, you know, there's just lots of information. We're bombarded often with it and sometimes we don't have the framework to understand it correctly. And I tend to think of the idea of first principles or principles, like I will filter information through my idea of like, well, what principles really matter for health? And one of them is, you know, it's like engineers would say signal to noise ratio. But like our senses, our vision, our hearing relies on things changing for it to detect and respond to it. So, you know, for listeners, imagine you were, you know, you're in a, a restaurant, there's a bunch of background noise. Our brain will tune all that out really quickly. But now if someone said, greg, at a table nearby, I'd probably hear them, right? Like that signal stood out from the background noise. And that's how our senses are designed, is to like detect signals out of noise. And if you take the insulin resistance that we talked earlier, someone that's insulin resistance will usually have way more insulin than, than an insulin sensitive person 24, 7. So the noise level is higher. So for the signal to stand out, you need now even a bigger spike of insulin, right? Because the way signal to noise ratios work, it's the proportional change. So like the story sometimes I use is, imagine in your home, back where you live, you find the darkest closet in your place. Go in there and there's no lights. And now you light one candle, you'll notice a huge difference. Now imagine someone else went in there, has 99 candles lit. You go in and light one more. It's like almost no difference. Maybe None. Right. So one candle doesn't mean anything. It's how something changes from the background and that background is always noise. So if you think of senolytics and the intermittent dosing, we're giving a huge signal in just a couple days that stands out from the background, where if conversely you're taking a small amount of quercetin or fisetin every day. Every day? Every day the signal's different. And part of the explanation for why things like quercetin and fisetin are senolytic is because they work on nutrient sensing pathways. Just like us. The senses on a cell are trying to detect changes in the world outside of them. So anyways, long story short, I think that intermittent dosing, while originally it was thought of as a way to avoid the potential downside of the D part of D and Q, it actually makes a lot of physiological sense, in a principle sense, like we want periodically to do something that creates a huge change to get the attention of our cells, specifically these stress cells.

I relate everything back to exercise. And you'd never do the same thing every day because your body would adapt and then that would be that.

Absolutely.

You gotta shift things around.

I think exercise like, you know, there's at qualia, we're like big into what we would call complexity science. But in living organisms it's complex adaptive systems. Right. And that adaptive piece is super important, right. That you know, our systems change the rules of the game as we play. And it's one why with exercise you want to not do the same thing every day and vary it and be prudent in how you design your.

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So you created this product, the senolytics, and I remember hearing you talking about this saying, I just knew that I wanted to have it and it was the right thing to make. I didn't think anyone would actually buy it. Yeah.

Yes. So 2015 was when that first Mayo Clinic and then I started following it and actually the next plant compound identified as acetolic was something called Piper longamine, which is from ayurvedic plant long pepper and Then fisonin, you know, 2018 was the third. So at this point I'm like, oh, that's three things that are plant compounds that I've used in one way or another. At some point in my time as a naturopathic doctor thought like, oh, like I would like to start taking at a minimum those three. And they just didn't exist. And in some of the places like Fight Aging or Longer City, you know, there was now starting to be people like, how do I get these things and put them together? And you know, so I would have been like minded, like, well, I want to run that experiment and take this. I think the risk to reward ratio is the kind I'm willing to accept. And so I think it was towards the end of 2019, I was talking to our CSO Chief Science Officer and our head of marketing at Qualia and said, we should make this product. I'd really like to take it personally. They're like, okay, well who would buy it? I don't know if anyone would buy it. No one knows about Sinolytics. Some biohackers for sure. I know would, you know, the people like me that are following this field, you know, would, you know, I'm sure some, you know, longevity focused doctors would use it. And they're like, well, that doesn't sound like a lot of people, Greg. Like, yeah, well, you know, I think maybe it's just a good thing for our brand, right, to stay like on the forefront of where I think the ball's heading. And so at the time I remember saying, like, like I'm certain in 2030 compared to now, like just entering 2020, many people will know about senescent cells and senolytics. And you know, I think like, if it was my company, Greg's company, we would make this product. And fortunately the decision makers also agreed and we made quality senolytic.

So what research have you guys done on this?

So, yeah, great question. So one of the things we always do at Qualia is when we, like I would think of them as prototypes before we would bring a product to market. We'll create, you know, a prototype, basically make the recipe and do a small pilot study.

I need to get in on the prototypes.

Sure. Well, definitely, you know, so usually that prototype, or before even that prototype phase, like I'll take them and a few other teams members. Well, just because we want to make sure like these are well tolerated. And then the we'll do then a pilot study. We'll make enough of the prototype to give people to Take for anywhere, depending on what the product's for, like qualia mind, you know, 12 days is sufficient.

But for some other Qualia mind, one like, yeah, you'll feel quickly, immediately, for.

This one, it was like slower. So we did a study where we recruited people that had some kind of joint issues, because, as you mentioned earlier, like, joints are a super common thing that even, you know, by late 30s, some people are starting to struggle with age joints. And, you know, as we get older, more and more people do. So we recruited people that have joint issues. We had them take, you know, what's now called quality senolytic for two days, then take 12 days of not doing it, then take another two days, 12 days off, and then a final.

And why did you do the 2:12,212?

So we did it originally just because we found that more than about a month of a study, we just lose a lot of people. And even a month, there's some people that just drop out. It's just the nature of it. So we felt that that approach would get us the most people that actually completed the study. And what we saw was about a 60% improvement in their, you know, discomfort, activities of daily living, flexibility, you know, like.

So they did a subjective rating scale.

Correct.

But is there any other way to look at this? Like, again, like looking at inflammation, Is there any lab tests would show it or is it not that it's not fabulous to go, oh, wow, yeah, I don't hurt like I used to is.

Yeah. So at the time, you know, so this was playing out in the. The first half of 2020, I think. And, you know, so I got on the phone with the founder of True Diagnostics, which is like, they do the. Some of the clocks, the DNA methylation, and asked him like, well, will these work? And he's like, no. Senescent cells are just their own thing. They're not like the other cells that we're measuring these patterns on. I talked to another researcher and bottom line, there was just nothing objective that anyone felt like in the blood would be a good indication. And so since one of the things we're always trying to do acquire is test a product before, I actually went into ClinicalTrials.gov where studies are put before they're executed. Right. It's kind of a database for that and looked like, okay, well, Big Pharma is investigating D and Q and some medication, potentially compounds for senescent cells. How are they attempting to measure it? And so one of the things, the most common thing I saw was joints and Then this subjective questionnaire that we.

Chose to use, I think, of this syndrome. I don't know if you. Have you heard Dr. Vonda Wright talk at all?

Yeah, I have.

So I've interviewed her on this podcast. I am a big fan of hers. And she also happens to live nearby, which is fun. And she is an orthopedic surgeon who went through menopause. And what she identified is which every menopausal woman will say, oh, yeah, that's a thing. Is this menopausal musculoskeletal syndrome because of estrogen dropping and becoming inflamed. And I would look at this and go, you know, just puts the fire on any osteoarthritis that you have. It's like, you know, if you had a little bit, which anyone who's been active, who doesn't. Right. Then you have that, and you're just like, whoa. So I would think this would be a fantastic.

Yeah. There would be an equivalent questionnaire for men that's called the Aging Male Syndrome Scale, but it's kind of almost like.

A low T. Yeah, but they're. You know, it's so different for men and women. Men don't fall off the cliff. Women, all of a sudden, it's like, what just happened here? You know, men, it's this, like, slow, slow kind of sliding into home. Right. Women wake up and they're like, I cannot. Like, I can't lift my arm up. What the heck happened?

Yeah, no, it's for sure. There's crazy differences in how not discounting.

Because I love men and have a great husband and not discounting that they go through their things.

Yeah. But. So there was this. Actually, I just saw in the medical news this morning over coffee when I was catching up on things, and I posted it on the Qualia X thing. But the gist of it was they looked at a whole bunch of things with the gut microbiome and on a cellular level and. And found that there was huge changes in the mid-40s and the mid-60s for both men and women. So, like, on a cellular level, even if we're not physically feeling it, there's these transition times where, like, things drastically change. And I think with women, it's really visible because of menopause, but it's happening to men. They're not feeling it, but their cells are also having these crazy changes at around those same times.

Interesting. Is there some kind of connection here with using senolytics and hormones? Is there anything there.

That hasn't been looked at? There's been a couple animal studies that have been looked at what's usually thought of as ovarian aging because that's tied into what you were just discussing. Senescent cells seem to definitely play a role in that.

So you could prolong the. You could keep yourself from going into menopause potentially. Because I know they're looking at other things to do that.

And one of the. So this for listening is completely like testimonials. N of one may not actually matter, but we've had that I know of had six different women that have contacted qualia and said, hey, after starting qualiacinolytic I started my menses again like I did now.

Were they, were they mad at you?

So they talked to our customer service, but my impression was no, they were more curious. Like have you heard this from anyone else?

Yeah. Is it that we've got to coach people to understand that's really a good thing. Like keep this as long as you can.

It would seem like something for those women, something changed that rejuvenates that system that they tied in to the qualia senolytic, whether that was what caused it or not. But there's been like five or six is in a lot of people. But it starts to get interesting. It's not one where you hear the same thing.

Well, it makes me wonder then when would the best time to start this be? Because you talked about looking at people as they were younger and they didn't have these senolytic cells, the senescent cells building up. At what age is this something that should be part of the protocol?

So it's a great question and I can only tell you how I would like personally think of it for Greg if like so 62 year old Greg, I take it the first weekend of.

Every month, that's when we do it too.

I think it's a great investment. I think there's like worst case scenario, it doesn't pay off. But I think there's a really good chance that future Greg will say thank you.

Well, does 62 year old Greg notice any physical differences from taking it?

So the main thing I noticed fairly quickly. So I'm confident I've taken quality analytic longer than anyone because I took the very first prototypes so I had a head start. But the very first thing I noticed was it unstuck me in my lifting that I kind of reached a plateau and then to move past that I was just feeling like inflammation would build up before I would be able to really unstuck. And I got unstuck the other thing I noticed and I don't do many trade shows anymore, but I saw you, I think it was at Dave's biohacker show, you know, so I was on my feet at a booth for, you know, a long part of a couple days. Much younger Greg did a lot of trade shows. I worked for Thorne way, way back in the late 90s.

I had a brief sprint with Thorne too.

And back then they were, you know, professional only companies. But I went to a lot of the Dr. Trade shows and you know, so that was 20, say 24 plus years ago. And even back then I mentioned earlier like, you know, we all have our Achilles heel. Like where I would always feel things are my knees and my low back. I would just feel the stiffness build up. And the last couple trade shows I've gone to that, it hasn't built up anywhere how my brain remembers it having built up decades ago. So I don't know if that's related, but that's where I think it's the, the things that would normally tax my body in ways that I'm not used to. I seem to resist better, but otherwise I don't have like, I don't have, you know, joint issues normally like, you know, activities of daily living or you know, discomfort. So I didn't have anything that I, you know, could really pay attention to in the way someone like we recruited for our study would. And the way I think about it is that senescent cells, and some of the scientists would agree with this, probably have a threshold effect. Meaning if we have an amount of senescent cells, maybe in say our joints that are below a certain amount, we're probably not going to experiencing anything from them. It's only when they accumulate past that threshold that they cause a lot of problems. So the goal always is to prevent things from going above, from accumulating.

So is that like you start at age 30, you start at age 40, or is it like someone who's got maybe was, I'm speaking for myself, like did really dumb sports as a six foot tall person. I did gymnastics, acrobatics and point ballet and broke a foot, broke an ACL multiple times, trashed a hip. I mean so I'm like a little bionic at this point. But I wonder, you know, is there an age where you'd start to want to look at this and, or is it something that if you've had an orthopedic history, would you have an accumulation of more senescent cells because of that? And it could help you with some of the osteoarthritis.

Yeah. So I think anything that caused us to be stressed disproportionately or at a much younger age probably built up some senescent cells, more than we should have at that age in that location in our body. So this would be a super general recommendation, but someone early 30s, mid-30s, that's not feeling any Achilles heel type of things that maybe do. Do something like koia senolytic once a quarter or, you know, once every six months like you would. Almost a periodic fast, like, you know, I'm. I'm just gonna. And the analogy we use at Qualia is being a gardener and pruning a plant. So we've got these lovely. Ish. I don't know.

Are they real? Yeah, I don't know.

But on a real plant, you know, like, we want the leaves to, say, vital and green. But in the real world, sometimes plants get stressed. Leaves turn yellow, and a yellowing leaf think of as something analogous to our senescent cell. What should happen is that yellow leaf should fall off the plant. But sometimes that doesn't. Right. And you go out and your plant has one yellow leaf, and a week later there's three or four more. And then before you know it, that whole plant is struggling. So a good gardener will then prune those leaves off before they can, you know, zombify other leaves.

So that's a great metaphor for. I mean, that is just showing a senescence activity, right?

Yeah. So the way, you know, for someone mid-30s, I would think, oh, like you still want to be a good gardener and prune these away, like, long before they're causing problems. You just don't have tons of leaves like your listeners. You know, now we're in our 40s and olders, older, like, okay, we probably have some yellow leaves, so we probably want to prune periodically, maybe more frequently. So younger. Greg, if quiocinolytic was around and I was my mid-40s, I would still be taking it once a month.

It seems like the perfect. When you talk about that hormonal rejuvenation like, this seems like the perfect thing. I wish I'd had this when I was in my 40s. Yeah, well, I also was under ridiculous stress at 49, at just so when.

In that study, even today, even though it wasn't looking at senescence, just, you know, the huge shift in how our biology changed in our mid-40s. It just makes sense to me. We'd want to start doing for sure more and The I presented this actually in one of the breakout sessions like it was on senescence. But I let in with, you know, if you were to Google like, you know, you know, average age that people die, you'll maybe 78 for women, 76 for men, like somewhere in there. But a better way to think about it, like, is how many years we live after age 60. So life expectancy at 60, so science would say, and on average in North America, if we make it to age 60, we make it to about 82 on average. Right. Some people more, some people, people less. And then what's more important and what I think most of your listeners care about is, okay, well, how much of that time am I going to be healthy and getting to live my life my way? And that would be thought of as healthy years after age 60. And what the latest study was data from 2019. But about. So say we live 22 years on average. About seven of those were in some degree of disability. Right. That's the average person. Right. So, you know, some of us obviously feel like we've invested well, you many of the listeners and that we're going to get better than that. But I think first and foremost for me, it's like, okay, I want to make sure you know me. But other more and more other people really chisel into that seven years of, you know, poor health at the end. Right. So that right up until the end, they get to live the exactly their way. And the only way that really happens is doing more things healthy and starting younger. Like, that doesn't happen because of doing things when the system's already breaking down.

However, whenever you can start, this is great. Yeah, I always say that because we're.

Like, oh, well, oh, no.

I'm like, no, no. Like, if you're listening to this, I'm imagining it seems like, you know, again, it's 40 plus. But whenever you can start this because I always hear that, well, I guess it's too late for me to start exercise. Nope. No, it's not.

No, it's never too late. It's easier to prevent things than to manage.

I mean, the best time I was lifting weights with the high school football team when I was 16 because there was no gyms for girls. And that was the best time to start. The second best time is now. Right. And same with the senolytics. I would have loved to have started them in my 40s. But you hadn't gotten it together yet. Guess the science wasn't there. But now that they're here, this is now the next best time to start. So we have a little. We have a little offer, I think, for everybody listening too, and the ebook the Science of Senolytics. So we have the Science of Senolytics and we also have a qualia. 15% off qualia, off any qualia order. So very exciting. And I am going to put all of that@jjvirgin.com forward/now. They're going to have to learn how to spell this Cinnolytics. So I'm going to spell it out. It's S E, N O L Y T I C s j j virgin.com synolytics it will be in the show notes with this, with the coupon code. But I. This, this is. I've been really digging into this. I listened to all the podcasts you'd done on Citolytics because I was like, let's dig into this. Because I literally started taking it, not knowing anything about it. My husband Tim got it from you guys, and I was like, all right. You know, he just, every of each month he gives it to me. And, you know, one of the interesting things that you don't think about is that you don't hurt anymore. It's why it's super important. And back when I used to do a lot of work with people one on one, I always had them rate all of their things before we started. Their energy, their pain. Right. All of it. Because a couple months later they go, nothing happened. And you're like, are you kidding me? You look perform like a totally different person. And, you know, I didn't really think about it, but Tim and I used to joke about this because we'd sit down on the couch and go, oof. You know, get off the couch.

Oof.

And that's what I say about this, is like, no more oofs. You just stop that stuff. And for someone who tore her ACL at 17, literally broke a foot doing gymnastics at 21. I mean, just dumb things. Five knee surgeries, a total hip replacement, Total knee replacement. I have another one coming. And so for me to not have joint pain that I've had literally my whole life is pretty remarkable. Like, it's a huge, you know, I mean, if you could even take your arthritic pain down 20%, you'd take it. But to take it down like 80, 90%, it's pretty substantial.

Yeah, yeah, that's. You'd asked about studies. We followed up that original study with a placebo study. And we saw again, we recruited people with joint issues and saw 65% improvement on average. So some people more, some people less.

65% is crazy. What drugs get that without doing damage?

Yeah, same like that intermittent, you know, when we're doing that study again, but this time waiting a full month between to see what happens with the longer wow window. But yeah, so that seems an area that to date we've consistently seen good things.

That's exciting. Well, because everyone has a little of that going on, but they don't have to. All right, I just have to ask, you may not be able to tell me, but what's new and exciting over at Qualia?

So as we're recording this, we spent a lot of the beginning of 2024 going back into nootropic ingredients. And we wanted to. We've always thought of ourselves more like a software company model where, you know, like you launch a 1.0 and then a 2.0. And so we've been calling it Qualia Mind 2.0, but that is about to launch. I think officially it goes on sale September 7th. So that's exciting for us to, you know, get to share what we think is a new, improved quality of mind, that it's one fewer capsules and was more effective in our study compared to the original quality of mind. We also had a magnesium product that went through our beta testing that we're super excited as a team to start taking.

Magnesium is one everybody needs to take. Might not sound sexy, but it is, it is the under. If you look at that Vitamin D with K Omega 3s and magnesium pretty much across the board.

Yeah. So those.

And then we're doing what's exciting about this Magnesium.

Yeah. So, like one of the things that we acquire, like, you know, we'll, we take our products, but then sometimes we'll be taking things that we don't make. And so magnesium was something that many of us were taking. And then at one point we all got together, like, we should make a magnesium, since we're taking it and we think we can make one that's better than anything that's out there. So there's going to be a blend of nine different types of magnesium in it. One thing that I think people take for granted is that we know that soils are depleted. We don't get as much magnesium in our diet unless we're really, really impeccable. But it used to be that evolutionarily we would have got a maybe 15 or 20% of our magnesium from water. You know, so think of, you know, magnesium rich mineral waters would still have it. But because many of us purify water to get out the crab, we also lose the magnesium. And whether it was food or water, magnesium always came with trace minerals. So one of the things I wanted in Laquagia magnesium was a layer of remineralization to go with it. So there's 70 plus trace minerals. There's another ingredient that helps our body retain magnesium because you always hear like, oh, I want bioavailable magnesium, but we want to hang on to what we absorbed as well. Right, the retention. So yeah. So I think people that try it are going to love our new Qualia magnesium when it's available in October.

Exciting. Yeah, I think Lauren mentioned that. All right, well to remind everyone again, jjvirgin.com synolytics S E N O L Y T I C S and there you will be able to get the ebook on senolytics. And you will also get a Coupon code for 15 off anything you want from qualia. And this one's so easy to take. I mean literally. That's what we do beginning of each month. Yes.

Yeah, I know quite a few people do it like you and I. The first weekend of the month comes around, I do quite senolytic and those days I generally take off from taking any other supplements.

So it's a. Oh wait, you just threw that at me. Should we be doing that?

Oh no, it definitely doesn't have to. I just like, like you mentioned, even with exercise, like it's good to de load and detrain. So those become a deloading supplement. Del Day for me for my regular things. And then I just do quality senolytic.

There you go, another little pearl. Thank you. Well, thank you so much for being here.

My pleasure. Thanks for having me.

Be sure to join me next time for more tools, tips and techniques you can incorporate into everyday life to ensure you look and feel great and are built to last. Check me out on Instagram, Facebook and.

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