I’m JJ Virgin, PhD dropout, sorry mom, turned four time New York Times best selling 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.

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’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, Shape Shift.

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 to weight loss. And he’s been a pioneer in the field of synalytics. 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 are 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 twinges of, wait, when did that start hurting? Or you’re well beyond that and looking forward to reclaiming some of that useful 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 secret. To aging powerfully. Are you ready? Let’s do this.

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 in. Into senescent cells, what they do, why we should be concerned about them, everything around longevity.

Uh, so let’s dig in and start with, what the heck is a senescent cell?

Yeah. So can we start with a history lesson? Is that okay? Of course we can. Yeah. So can you be a little geek ? Yeah. Yeah. So, um, a little bit. Okay, good. Like back, say pre 1961, there was this idea that if you had human cells in a Petri dish.

and give 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, Um, 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, you know, basically become old and no longer make copies of itself became called cellular senescence. So for the listeners, the key idea is that we, we would have healthy cells that are doing their job. They were born, they’re living, they’re doing, you know, whatever they’re doing, maybe liver cells are doing one thing or on something else.

And those cells, you know, live their lifetime, die and are replaced often by, you know, daughter or son cells that. And, um, 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, uh, 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 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, you know, 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, um, telomeres, this is, you know, more like a, like a, um, like a common use definition, but at the end of, um, strands of DNA, there would be some things that aren’t copied, you know, so the genetics that don’t get copied are often described almost like the, 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, um, in the old days, they probably would have said yes. And, um, cause 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. 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 would, that category would be called stress induced premature senescence. So, uh, 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.

Um, issues with nutrients in, you know, that surround the cell can be, you know, toxicity, radiation. Really think of the things that stress us on a whole body level stress ourselves. And if a cell gets stressed To a certain point, it has to respond. And this, this is 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 fit, like 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, you know, like tangled up or organelles like mitochondria being damaged.

And door number two is where autophagy comes in as an example of something that repairs damage or. You know, processes in our cells that repair damage. So NAD has a molecule like part of its link to longevity is it’s, you know, fuels and DNA repair. So that’s door number two, like, you know, 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, 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 it’s just sitting there. Right. And so those senescent cells that are just sitting there, they’re not doing any good.

Yeah, so the um, like 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 for us because transient ones can do some good things. So like imagine, you know, 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, like well beyond 40. All of it. Everyone

listening is super

healthy and well beyond 40.

Like does something, like Like, you know, more exercise than you’re used to and create some inflammation, some damage. So that will cause an increase in senescent cells. And in a young person, what you would have seen is that 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, Um, 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. You still would get rid of some of them. I would think with exercise because of the apoptosis from exercise, right? So, um,

exercise without question helps prevent the accumulation of senescent cells and muscle tissues, whether it does muscle

tissue.

So 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, um, 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, you know, They’re fat cells also said like, we’ve had enough too, right?

So things, you know, ultimately happen on a tissue level, but, but exercise for sure for listeners prevents some degree of cellular senescence. It’s just I will always plug exercise into any,

anything, wherever I can, like the exercise benefits. So you have these senescent cells then that are accumulating more in someone as they age.

Yep. So, you know, how does that, how would one know that they have this going on, and how does that, does aging cause the 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, so I’m sorry about

that.

And even before getting to that, let’s just tie exercise in one more time. So what would, um, I mentioned 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. Um, they’re gone really quickly. And any straggler is the immune system finds and gobbles up.

In older animals, they’ve done these experiments. So what, um, 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. You know, 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. It’d be so cool if we could do that for anabolic resistance because I just am sure that if someone is eating optimal protein and exercising and has been doing that consistently, that they their rate of anabolic resistance would be so Much different. Oh, for sure.

Yeah.

So, okay. So, well, like, 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, you know, intensely, There’s, you know, some senescent cells, but it’s like an explosion of them are created in the old animals.

And that a hundred percent, they contributed to the anabolic resistance. And when they did something called a 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, you know, well, 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. Like the senescent cells, 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 fibroblasts, and they’re our 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 line of 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 in Achilles heel. Type of sense, like we all have our weak points, whether that’s genetic, old injuries, you know, trauma, you name it. So really the way that I would say that 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, um, vision loss, wrinkling, like these all seem like signs of senescent cells, would they be?

They, 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. Transcripts provided by Transcription Outsourcing, LLC. 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 it’s 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. And senescent cells clearly are in that first one, right? Cause they’re a type of damage, right? I had 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 the, they seem like. Like an output of programmed aging as well. So, you know, I think, you know, those theories aside, the one thing we can safely say is like, 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 in, all throughout my body than 30 old Greg would have had like exactly, you know, which cell and tissue has, you know, way more, like some have been pruned away maybe, and 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, 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? Yes, please. So, um, so senescent cells, like I mentioned, kind of, you know, origins back 1961, you know, by the 70s, they named them senescent cells. By the, you know, mid 80s, telomeres had been identified.

Um, and then in the early 2000s, one of the researchers at Buck Institute. discovered that senescent cells secrete, so like they give off, um, 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. I’ve 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 you’ll sometimes hear the idea of zombie cells versus senescent cells. And part of that is what I mentioned earlier, right? They, 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? They’re somewhere in between like a zombie would be. But the other reason is because of those SAS 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, like, we’d call it inflammaging, in a sense. If they can cause that and change the behavior of other healthy cells, we should look more closely. And that led to a study around 2009 where they did a transgene experiment. So think of it as they genetically modified these, 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. So 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, um, quercetin, which I’m sure you would’ve taken.

Mm-Hmm. may, maybe, I would guess. Well, I’ve been taking

SLI for full disclosure. I’ve been on Sly and it came out. Oh, okay. And, um, yes, I’ve, I’ve been on it, on it, on it, on it. And, you know, I’ve met James and Daniel years ago. Um, so I, I get the benefits of it. Oh. Which we’ll talk about. Yeah. Yeah. Um, but I don’t wanna jump the gun on that.

Yeah.

So, um. So anyways, they, you know, they identified quercetin and this, uh, medication, dasatinib, as, um, compounds that could help these lingering exonescent cells finally go through that falling off process and decided to call compounds that did that senolytics. So that was around 2015. So, but these, these

senolytic compounds that do this, um, From what I’ve read, they’re tissue specific or are they global?

Like when you take quercetin, does it get, go out and scavenge everything or is it in a specific

tissue? That’s a great question. So in that original study, they, what they found is that they didn’t look at every tissue, but you know, they started off looking at what happens in a, you know, like a cell culture, an in vitro study, but then they gave these compounds to animals and, and looked.

And what they found was. Quercetin worked for endothelial cells in that experiment and worked in, I think it was, um, bone marrow, um, but wasn’t active as a seno litic 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.

So had the idea right from the, that we should stack things together so that, um, that stack d and q is how usually I would. Think of it as being the most used stack for, um, trying to remove senescent cells when you would read studies to date and it’s because there’s a complementarity. And I think, you know, for going with just the natural.

It’s like, you know, what’s in quality, is 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 book 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 is a senolytic? Are there any lifestyle things or is it all more nutrient driven?

So the only work I know of, um, is Walter 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.

Um, and then 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. Um, and I’m, one of the things I’ve seen him mention in, um, in, you know, like talking his book is that, um, senescent immune cells after about day three start to be, um, Well, pruned away.

Well, it’s a good thing. I like senolytics because I never got past day three. So there you go. Yes, this is

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 it is his protocol the fasting and making 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, um, 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. Um, that’s been investigated to

date. Would looking at something like highly sensitive C reactive protein be an indicator that you’ve reduced senescence, maybe?

It could be.

There’s um, so right now there’s a bunch of trials that are in progress and there’s um, like Vicetin isn’t quite as senolytic. Some of them are using just Vicetin alone because One of the things the Mayo and Scripps Institute researchers found eventually, I think it was 2018 they published, is that vicitin was seemed better than quercitin.

It was more, it worked in tissues where quercitin didn’t. It, you know, 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 So quercetin

plus feicetin, feicetin alone was more powerful than quercetin plus feicetin, or quercetin, feicetin is more powerful than quercetin, but it would seem like you put the two together, you’d have more firepower than just

Yeah, so the, yeah, so it was the latter, like feicetin alone was more powerful in their experiment than quercetin alone.

Okay. And worked in a tissue where quercetin wasn’t active. So, um, but what happens in science often is like the DNQ I mentioned, like that’s being studied. Now, vicitin is being studied, but almost no one’s studied them 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 um, so DNQ is a really powerful immunomodulator medication. They were first doing this, the, 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 saved? 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. Um, and which sometimes you’ll hear the idea of hit and run dosing. And the idea they, the reason they thought that could work was because senescent cells are.

This is, 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. And there’s certain proteins that are at the core of that. And I think of it as just they’re voters, right?

And some are saying like, yes, fall off. And others saying no, no, no, no, like hang on in tissues. And. All we need to do is swing the vote enough to get the, the vote, 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& Q, You know, from a toxicity perspective, it made sense. And one of my principles, cause 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, like I, We’ll 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, um, 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, uh, you know, a restaurant, there’s a bunch of background noise, our brain will tune all that out. And 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 resistant will usually have way more insulin than a insulin sensitive person 24 7. 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 resistant will usually have way more insulin than a 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? Like, because the way signal to noise ratios work, it’s the proportional change. So like the story sometimes I use is imagine, you know, 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, like almost no difference, maybe none, right? It’s 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 of days that stands out from the background. Where if conversely, you’re taking a small amount of quercetin or feicetin every day, every day, every day, the signal’s different. And part of the explanation for why things like quercetin, feicetin are senolytic is because they work on nutrient sensing pathways.

So this, 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& 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 or specifically these stress cells.

I relate everything back to exercise. Yeah. And you’d never do the same thing every day because your body would adapt and then that would be that. Absolutely. You got to 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 why with exercise you want to, um, not do the same thing every day and vary it and be, you know, more flexible.

Prudent in how you design your programs.

So you created this product, the Sinalytics, and I remember hearing you talking about this saying, you know, 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.

So what, you know, so I, like 2015 was when, um, first Mayo Clinic and then I started following it and actually the next plant compound identified as a called piper longamine, which is from an Ayurvedic plant, long pepper.

And then vicin, you know, 2018 was the third. So at this point I’m like, oh, that’s three things that are, you know, plant compounds that I’ve used in one way or another at some point in my, you know, time as a naturopathic doctor. I 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 longicity, you know, there is now starting to be people like 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, you know, we should make this product, you know, I’d really like to take it personally. Um, and they’re like, Okay, well, who would buy it? I don’t know if anyone would buy it.

Like no one knows about Cetalytics. Like, um, you know, some biohackers for sure I know would, um, you know, the people like me that are following this field would, you know, I’m sure some, you know, longevity focus, um, doctors would use it. And, um, they’re like, well, that doesn’t sound like a lot of people, Greg.

And I’m like, yeah, well, um, 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, the ball’s heading. And so at the time I remember saying like, like I, I’m certain in 2030 compared to now, like just entering 2020, many people will know about senescent cells and senolytics.

And, um, 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 qualia sinalytic. 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.

Um, 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. So I need

to get in on the prototypes. Sure. Well, definitely.

Um, you know, so usually that prototype or before even that prototype phase, like I’ll take them and a few other team members, well, just cause 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 quality of mind. You know, 12 days is sufficient, but for some of the products Probably a mind

one, like Yeah, you’ll feel it quickly. Immediately.

Um, for this one it was, like, slower. So, um, we did a study where we recruited people that had some kind of joint issues.

Cause, as you mentioned earlier, like, joints are a super common thing that even, you know, by late thirties, 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 had joint issues. We had them take, you know, what’s now called quality analytic for two days, then take 12 days of not doing it.

Then. Take another two days, 12 days off, and then a final study. And why did you do the 2 12 2 12? So we did it, um, originally just because we found that more than about a month of a study, we just lose a lot of people. And even, you know, a month, there’s some people that just, you know, drop out, right, 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 percent improvement in their. Um, you know, discomfort, activities of daily living, flexibility, you know, like. So they did a,

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 we showed? Or is it not that it’s not fabulous to go, Oh, wow. Yeah. I don’t hurt like I used to.

Yeah. So at the time, you know, so this was playing out in the first half of 2020, I think. Um, and you know, so I got on the phone with, um, the founder of True Diagnostics, which is, you know, like they do the, um, the, some of the clocks, um, the, um, DNA methylation and asked him like, well, when will these work?

And he’s like, no, they, they, they, they, they, Cinescent cells are just their own thing. They’re not like the other cells that we’re measuring these patterns on. Um, you know, I talked to like another researcher and, um, 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 at QALY is test a product before, I actually went and did clinicaltrials. gov, where, like, studies are, um, put before they’re executed, right? That it’s a kind of a database for that. And looked like, okay, well, Big Pharma is investigating D and Q and some, you know, medication, potentially compounds.

For senescent cells, how are they attempting to measure it? 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?

So

I’ve interviewed her on this podcast.

I am a big fan of hers and she’s 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, um, and I would look at this and go, you know, it 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? Um, then you have that and you’re just like, whoa. So I would think this would be a fantastic.

There’s a, like, there would be an equivalent questionnaire for men. That’s called the aging male syndrome scale. Um, but it’s kind of almost like a low T.

Yeah, but, but there, 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, I can’t. Lift my arm up, what, um, 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. When, 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 um, and I posted it on the Qualia X thing, but the gist of it was they looked at a whole bunch of like things with the gut microbiome and on a cellular level and found that there was huge changes in the mid 40s and the mid 60s for both men and women.

Hmm. So like on a cellular level, even if we’re not there 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. So, I mean, is there some kind of connection here with using synalytics and hormones? Is there anything there? So

that hasn’t been looked at. There’s been a couple animal studies that have been looked at what I would, what’s usually thought of as ovarian aging, because that’s like tied into what you were just discussing.

And senescent cells seem to definitely play a role in that. So you could

prolong 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 listeners, is completely like testimonials and if one may not actually matter, but we’ve had, that I know of, um, had six different women that have contacted qualia and said, Hey, I, After starting, um, Calliocenalytic, I, um, started my Menzies again.

Now, 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 rejuvenated that system.

Wow. They tied in. To the QIAC analytic, whether that was. Wow. There’s been, you know, like five or six isn’t a lot of people, but it’s starts to get interesting. It’s not one. Where you hear the same thing.

Well, it makes me wonder then, you know, when would the best time to start this be? Because you talked about, you know, looking at people as they were younger and they didn’t have the 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 put it. Like personally, think of it for Greg, if like, so 62 year old Greg, I take it the first weekend of every month. Like, that’s when we do it too. I think it’s a great investment.

I think there’s like worst case scenario, it’s, it doesn’t pay off, but I think there’s a really good chance that future Greg will say, thank you. Well, does, does

62 year old Greg notice any physical differences from taking it? So

the, the main thing I noticed. Fairly quickly. So I, I’ve, I’m confident I’ve taken quality analytic longer than anyone cause I took the very first prototypes.

So I had a headstart, um, but the very first thing I noticed was it unstuck me in my lifting that I, I’d 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. Um, 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, um, 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 nineties. I had a brief

sprint with Thorne too. Oh, and back

then they were, you know, professional only companies, but I went to a lot of the doctor 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. And, um, the last couple of 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.

Um, but otherwise I don’t have, like, I don’t have joint issues normally, like, you know, um, activities of daily living or, you know, discomfort. So I, 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. Um, 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, 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 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.

Um, 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, 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, Like this would be a super general recommendation, but you know, someone early thirties, mid thirties, it’s not like feeling any Achilles heel type of things, right? They, um, you know, then maybe do something like a qualia 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 tish, I don’t know, Are they real? Yeah. I don’t know, um, but on a real plant, you know, like we want the leaves to say vital and green. Um, but in the real world, sometimes plants get stressed, you know, leaves turn yellow and a yellowing leaf, think of as the, you know, something analogous to our senescent cell.

Um, what should happen is that yellow leaf should fall off the plant, but sometimes that doesn’t, right? And, you know, you go out and your plant has one yellow leaf and a week later there’s, you know, 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 senescent activity,

right? Yeah. Yeah. So the way You know, for someone mid thirties, 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 forties and older, older, like, okay, we, we probably have some yellow leaves. So, you know, we probably want to prune periodically and maybe more frequently. So younger Greg, if quite a scenalytic. 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 forties. Yeah. Well, I also was under ridiculous stress at 49. That just, so

when, in that study, even today, even though it wasn’t looking at senescence, just, you know, the, the huge shift in how our, um, biology changed in our mid forties, it just makes sense to me, we’d want to start doing for sure more and the.

Um, I presented this actually in one of the breakout sessions, like, it was on senescence, but I let in with, um, you know, if you were to Google, like, average age that people die, you’ll, maybe it’d be 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, like, life expectancy at 60. So, science would say, you know, 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 less. Um, 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’s would be thought of as like healthy years after age 60. And what the latest study was data from 2019, but yeah, 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, um, 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 their life 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. I always say that cause people are like, Oh, well, Oh no.

I’m like, no, no. 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, cause 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 them. I mean, the

best time I was lifting weights with the high school football team when I was, 16 ’cause there was no gyms for girls.

Um, and that was the best time to start. The second best time is now . Right. And same with the lytics. I would’ve loved to have started them in my forties. I bet you hadn’t gotten it together yet. Yeah. I guess the science wasn’t there, but now that they’re here, this is now the next best time to start. So yeah, we have a little, we have a little offer I think for everybody listening too.

And, uh, the ebook, the Science of Lytics. So, we have the Science of Cynalytics and we also have a Qualia, 15 percent off Qualia, off any Qualia order, so, very exciting, um, and I am going to put all of that at jjvirgin. com forward slash, now they’re going to have to learn how to spell this, Cynalytics, so I’m going to spell it out, it’s S E N O L Y T I C S, jjvirgin.

com forward slash Cynalytics. It will be in the show notes. with this, with the coupon code. Um, but I, this, this is, I’ve been really digging into this. I listened to all the podcasts you’d done on Sitalytics cause I was like, let’s dig into this. Cause 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, beginning 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.

I get out of the, 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 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, if, if you could even take your, 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 what, um, you’d asked about studies.

We, we followed up that original study with a placebo study and we saw, um, again, we recruited people with joint issues and saw, um, um, 65 percent improvement on average. So some people more, some people less. 65

percent 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 window. But, um, yeah, so that, that seems an area that, that to date we’ve consistently seen good things. That’s exciting.

Well, cause 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, what’s new and exciting over at Qualia?

So,

um, 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 Qualumine 2. 0 but that, um, is about to launch, I think officially it goes on sale September 7th.

So, um, that’s exciting for us to, you know, get to share what we think is a new and improved. That’s one fewer capsules and, um, was more effective in our, our study compared to the original quality of mind. We’ve been, um, we also had a magnesium product that go, went through, um, our beta testing, um, that we’re super excited as a team to start taking.

We, magnesium, you know, is, It’s one everybody needs to

take. It might not sound sexy, but it is, it is the under, you look at that, vitamin D with K, omega 3s, and magnesium, pretty much across the board.

Yeah, so those um, and then we’re doing What’s exciting

about this magnesium?

Yeah, so, um, like one of the things that we acquire, like, you know, we’ll, you know, we take our products, but then sometimes we’ll be taking things that we don’t make.

And so magnesium, it 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.

Um, one thing that I think people take for granted is that, you know, we know that soils are depleted, we don’t get as much magnesium in our diet unless, you know, we’re really, really impeccable. Um, but it used to be that evolutionarily we would have got a, you know, maybe 15 or 20 percent of our magnesium from water.

Um, um, 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 the quality of magnesium was a layer of remineralization to go with it.

So there’s 70 plus trace minerals. There’s, you know, another ingredient that helps our body retain magnesium because you always hear like, Oh, like I want bioavailable magnesium, but we want to hang on to what we absorbed as well, right? Retention. So, um, yeah. So I think, you know, people that try it are going to love our new quality magnesium when it’s available in October.

Yeah, I think Lauren mentioned that. All right, well, to remind everyone again, jjvirgin. com forward slash SINOLYTICS, S E N O L Y T I C S. And, uh, there you will be able to get the e book on SINOLYTICS. And you will also get a coupon code for 15 percent off anything that you want from Qualia. And this one’s so easy to take.

I mean, literally that’s what we do at the beginning of each month. Yes.

Yeah, it’s, um, I know quite a few people do it like you and I, the first weekend of the month comes around, I do Qualia Senolytic, and those days I generally take off from taking any other supplements. So it’s, uh, Oh, wait, you just threw that at me.

Is, 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 de train. So those become a de loading supplement day for me for my regular things. And then I just do quality senolytic.

There you go. Another little pearl.

Thank you. 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 my website, jjvirgin. com. And make sure to follow my podcast at subscribetojj. com so you don’t miss a single episode.

And hey, if you’re loving what you hear, don’t forget to leave a review. Your reviews make a big difference in helping me reach more incredible women just like you to spread the word about aging powerfully after 40. Thanks for tuning in, and I’ll catch you on the next episode.

Hey, J. J. here, and just a reminder that the Well Beyond 40 podcast offers health, wellness, fitness, and nutritional information. That’s designed for educational and entertainment purposes only. You should not rely on this information as a substitute for, nor does it replace, professional medical advice, diagnosis, or treatment.

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