How To Clear Out Damaging, Life-Shortening Zombie Cells In Just 2 Days A Month, A “Shotgun Formula” For Senescent Cells & More

My name is Ben Greenfield, and on this episode of the Ben Greenfield Life.

Podcast, Identifying and studying senescent cells is pretty hard, really. You have to do tissue biopsies to identify senescent cells and tissues. So because of that, there just hasn't been the amount of research on things that would be in that hermetic category for how they impact senescence. But intuitively, because these stressors are known to be a big part of this premature cellular senescence or stress induced senescence, my guess is that a lot of the things that we're trying to protect ourselves from by being biohackers and integrating these hermetic habits into our lifestyles would help at least slow down the accumulation.

Of senescent cell faith, family, fitness, health, performance, nutrition, longevity, ancestral living, biohacking, and a whole lot more. Welcome to the show.

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But a lot of people are not going about it the right way because they aren't actually paying attention to what's called senescence. Cellular senescence. Now senescent cells, as my guest on today's podcast is going to fill you in on in great nitty gritty detail are these cells that can accumulate in the body and accelerate aging. You get more of them as you get older. There are ways to get rid of them. So called senolytics and that's actually what my guest Dr. Gregory Kelly kind of specializes in. Like how do you clean up these senescent cells? How are they a problem in the first place? What do you do about them? And how do you ultimately live longer and have better health span and lifespan based on what you do Now? Greg is not only A naturopathic physician, he also develops products for Neurohacker Collective. That's a company that actually makes a like a nootropic smart drug kind of formula that I liked. I even wrote a book called Shapeshift. Shapeshift. And he studies nootropics, anti aging, regenerative medicine, weight management, chronobiology, which is kind of like circadian rhythm type of stuff. He has more than 30 different journal articles indexed on PubMed. He's published various articles on various aspects of natural medicine and nutrition. So he's a wealth of knowledge. He's never been on the show before, so see how this goes. You never know with first time guests. But anyways, everything that you hear is going to be@BenGreenfieldLife.com.

I know that's hard to spell, so let me spell it for you. S E N O L Y t I c BenGreenfieldLife.com Senolytic is where you can grab the show notes. So Greg, welcome to the show. Are you ready to talk about these so called zombie cells?

I am really excited today to share this with you and your audience.

Yeah. Does that annoy you, by the way, when people call senescent cells zombie cells? Because it's like everything in the body has a reason. And this, this is really something I want to ask you. Anyway, it's not like senescence is totally bad, right?

No, no. There's like most things and you'd be well aware of this context matters. So we'll get into a deep dive on that. But to answer your question, no, I think zombies is a good analogy for senescent cells especially what we'll really talk about, the subtype of them that accumulates as we get older. And the reason is twofold. There are cells that haven't died and can turn other cells into senescent cells. So you know, very akin to what you'd see in zombies in a movie or a book.

Okay. So basically they can be like cells that are almost dead, like a zombie, not quite dead, and wreaking havoc in the human body, to use the highly scientific terminology.

Absolutely, yes. So I think it's why I think it's the most widespread metaphor. At Neurohacker Collective we tend to go more for a gardening analogy and yellowing leaves and being a gardener and pruning senescent cells away. But it would still have some analogies. A gardener as an example, with leaves yelling on a plant. There's a couple of different issues that causes one, they can be a source to spread disease. Now to other more vibrant leaves. They use up resources and while they're there, you can't promote new growth. So in a sense, senescent cells would do those things in our tissues as well. And so I generally use that gardening yellowing leaves analogy instead of zombies. But they're both very appropriate.

Yeah, I guess it just depends if you're a green thumb person or a movie freak. The idea with the cell senescence is that these cells, from what I understand, they stop dividing, right? Like cellular senescence is just like the cessation of cell division. And I know there's a lot of stuff that can cause the cells to stop dividing, you know, like stress and oxidation and environmental toxins and things like that. But it kind of begs the question, like, why would the body have this built in mechanism in the first place? And the reason I asked that is where my mind goes, you know, unhampered cellular division with no brakes on it would technically be something that we kind of call cancer, right? Like, like this, this full on growth of cells with no breaks whatsoever. And so would, would cell senescence be built in as a mechanism in the body to keep us from getting cancer or something like that?

Yeah, it's definitely thought of as a stress response program. So I guess going back in time, the origin of the idea of what's now known as cellular senescence goes back to Hayflick in 1961. So before his work, there was this thought that if you put cells in a culture and as long as you gave them enough food and created a hospitable culture environment, they would just be immortal, they would grow forever. And what Hayflick found is that human cells, and they were fibroblasts that he used in that study, divided about 50 times before they essentially hit a wall. It wouldn't divide any further. So that's now known as the Hayflick limit. And that introduced this idea of cellular senescence, this idea that cells can get to a point with certain amounts of divisions where they'll just frankly say, like, I'm done, I'm not going to divide anymore and make any new cells. What then, like leaping forward to the 70s, the idea of telomeres, or telomeres, depending on, I guess the pronunciation, one's more British, one's more North American, were identified and became eventually known that it was the shortening of telomeres over time as cells copied themselves, that would cause this running into the Hayflick limit. And kind of one of the other things about the Hayflick limit, it Varies organism to organism, probably also even in humans, tissue to tissue. So that idea we could call replicative senescence. And my guess is that's at most really minor importance in aging. Fundamentally, even older people don't run out of the ability to create new cells and to have cells proliferate. But because of this kind of clock, with telomere attrition ticking down, shortening, shortening, shortening, there became this idea that senescent cells like that mechanism replicate of senescence was probably a pretty prominent part of aging. Now we're back in, well pre2010. What eventually they I guess early on thought is okay, well these cells are. So I guess telomere attrition in a simple sense would subject DNA to potential damage if it's copied. So cells enact this program called a DNA damage response. So the general idea was, okay, this makes sense, we shouldn't copy these cells if we might be copying damaged DNA, because that could promote cancerous cells. So this idea that senescence cells or cellular senescence was an anti cancer mechanism was fairly early on in the senescence thing. Now as times evolved and especially more recently, it's really nuanced. And so this is going to be way oversimplified. But just so we don't get too bogged down, when cells are precancerous, enacting the cellular senescence programs, probably beneficial in terms of preventing cells from going towards a damaged cell that could just copy itself over and over and over, become cancerous. But once cancer is developed, especially in older organisms, Solucionescence is probably a net negative. So again, context.

Okay, so, so would that mean. Because this is something I've been thinking about a little bit when it comes to senescence, it's kind of like the idea with protein, right? Like we don't necessarily want, especially later on in life, to excessively stimulate mtor, for example, or excessively cause anything that would, that would result in pro growth functions that might potentially cause cancer. And I'm not saying that older individuals can't benefit from like growth hormone precursors or, or peptides that simulate growth hormone releases or amino acids in forms of protein and enzymes that break down protein that allow them to better assimilate those amino acids. But at the end of the day, it appears that longevity is assisted with some amount of kind of slowing down this pro growth effect. Yet at a younger age, when fertility and muscle and a lot of things related to performance and replication of the human species should be prioritized, then we would actually want to really be engaged In a lot of pro growth activities that might accelerate aging later on in life. So that being said, let's say, and I know we'll get into these so called senolytics that can kind of get rid of senescent cells later on in our chat, but if you're young, should you be thinking twice about trying to shut down senescence so that you're able to grow and be fertile and everything?

What I would generally bucket senescence into, I mentioned there's the replicative senescence, the Hayflick's limit. But depending on what causes a cell to become senescent, basically to execute this software program, the cell will have really almost different structure and function. Several other areas where senescence is at least in the right amount good. One would be embryogenesis, the development in utero. Another would be placental aging. There's at least some research that suggests that senescence in the placenta, and this would be I guess somewhat controversial, but would be involved in the age of placental aging. But for sure, in these animal experiments it has to do with triggering labor. Pregnancy as an example, would be a time period where in general, I'm a believer in the precautionary principle. If something's not known to be safe in something like pregnancy, then you just wouldn't do it. Senolytics, I would say, would be something during pregnancy. No reason to take down potential downsides because senescent cells are definitely doing a few useful things during that time period. Wound healing would be another area where senescent cells are known to play a role. But even in that, it's more of a timing issue in both the embryogenesis and in wound healing. Think of it as a wave of senescent cells come in early on to do something good. So the senescent cells post, say like you just ran a marathon. That's quite a bit of muscular trauma, inflammation caused from that, there would be some need to repair and regenerate. So there'll be a wave of senescent cells that'll sweep in. They help attract macrophages, other aspects of the immune system to do the repair regeneration. And a week later they've been cleaned up, either by going through a falling off process called apoptosis, or, or by the immune system coming in and scavenging up, gobbling up any remaining senescent cells. What would be problematic is if that wave came and didn't recede and the senescent cells lingered. Then instead of helping the tissue repair and heal itself, it would actually hinder that. Okay, so because of that, I tend to use this idea of there's transient senescent cells, mostly beneficial, have a role doing a job, and then there's lingering ones, which are most of the times causing issues.

Okay, so what it sounds to me like, in a nutshell, is that for the most part, senescent cells are going to cause damage to the body and accelerate the onset of chronic disease due to the inflammation. And there may be some other things that they're causing that I'd love to hear in terms of what type of damage a senescent cell is actually causing. But at the same time, if you are pregnant, if you are potentially trying to heal a wound, I don't know, maybe you're a burn victim or something like that, if you have an existing tumor, and maybe if you're trying to repair a whole bunch of muscle damage, like, I don't know, maybe if you're a bodybuilder or something, then taking senolytics could potentially not be a good idea. But if you don't fall into those categories from a longevity or anti aging standpoint, having sensors, some form of a senolytic strategy could be a good idea.

I think that's fair, and that's how I would bucket it. But even say for the bodybuilder, periodic senescent or senolytic senescent clearance strategies might be advantageous. Maybe not in the couple days after something that you really put a lot of trauma on the muscles, but intermittently, I think would be potentially prudent.

A lot of the studies that I've seen, particularly on pharmaceuticals, for getting rid of senescent cells actually do, because you just mentioned not doing it all the time. It seems that they have these pulses, like a few times during the year that you would take senolytics, but it's not something you would use every day. Is that correct?

Yeah. And the way I think of it, you've had Walter Longo on your show before.

No, no, he's the fasting, mimicking diet guy, right?

Yeah. Yeah. So he was on our collective insights at one point. So the fasting, mimicking diet, just to give context, is something meant to replicate short periods of fasting. So his original research, going back to mice, I believe he would fast mice completely for two or three days. And some of the changes that he noticed would be it would promote autophagy, which is different than senescence, different than apoptosis, but another cellular response program. And it would also tend to selectively get rid of cells that were stressed, like senescent cells particularly, I believe he was measuring senescent immune cells like macrophages. He created that fasting, mimicking diet as a way to get the upside of short periods of fasting without some of the downside. Because at the time I think he was doing a lot of research with cancer patients and it was hard for some of them to even do a three day water fast. When I think of senolytics, especially in the sense of qualia senolytic, the product that neurohealthical collective created, these are things that are essentially mimicking short periods of fasting is how I would say they work based just mechanistically.

Because of that. Just like you wouldn't want to go on a water fast every day for the rest of your life. Doing senolytic compounds, generally speaking, is also something that's short periods like bursts to just mimic a signal and then let that signal take its role in the body, turning on and off genes, causing certain cells that are less important, like potentially senescent cells, to then go through this falling off process.

Okay, did you see the study? And I'm sure as somebody who's looked into senescent cells, you probably did. On, I think it was desanatib. I don't know if I'm pronouncing that properly with quercetin as like this 1,2 combo stack. At least that's the one that I've seen talked about a lot in the anti aging and longevity circles as kind of like what was the gold standard based on research to limit senescence. What do you think about that?

So the idea of senolytic was coined by Mayo Clinic and Scripps Institute of aging researchers in 2015. And the original like stack that they identified was I would say dasatinib, but I'm not sure that that's the correct pronunciation either. And quercetin. And that combination was interesting because I guess stepping back, senescent cells are a category of things that all have in common this idea that they won't divide any longer. They also have some other characteristics in common. But many of the other characteristics, especially when you start to think structurally and functionally, can vary. So when we talk about like that, I would say developmental senesis, embryogenesis, placenta, those cells will have actually slightly different markers on them than these zombie cells we're talking about with aging as an example. Just like going back, the insight for this Scripps and Mayo researchers was that what we wanted to do was induce these cells to go through apoptosis, which literally translates as falling off in the sense that leaves or fruit falling off a plant. So apoptosis is the Greek word. And the idea was, okay, let's find things that mechanistically may shift the balance in cells from resisting going through that process to in favor of that. And so they identified several different candidates, eventually found that dasatinib was really useful as an example in their original research in adipose tissues, fat cells to get some senescent fat cells to complete this journey to falling off. Quercetin wasn't active in that, but was active in bone marrow and in, I think it was endothelial cells in that research. And the combination was active in places that each individually wasn't. So that created that stack, which is by far the most researched combination. I think fisetin, or sometimes pronounced fisetin, would be second, but not quite really even a close second. Yeah, I just would say dnq. The DNQ stack is by far the most used right now.

Somebody gave me the DNQ stack. They gave me a few days supply if I wanted to try it to clear senescent cells. I didn't take it. I looked into it, and for me as an athlete, I was a little bit concerned about this because apparently it can lower your blood cell count. And then the other side effect is diarrhea along with the anemia. And I don't know if that's common or if that's, you know, just something you don't need to worry about with low dosages or standard dosages or something like that. But are you familiar with side effects of that stack?

Dasatinib would be. It's a tyrosine kinase inhibitor. That's the category of drug it's in. And it's used particularly for blood cancers. And definitely in that context, like a lot of anti cancer drugs can have fairly significant side effects. So one of the, I guess again, the original idea from the researchers at Mayo and Scripps was, all right, well, dasatinib may not be a great thing to have people take every day. Maybe if you need to pulse it more frequently for cancer treatment, that's one thing. But let's see if we can shift this risk reward profile in a way that we get a much better risk reward ratio. Right from the get go, they had this idea, well, let's do what they called hit and run dosing. Instead of doing something every day, every day, hey, let's just do this intermittently. Let's give the D and Q stock for a couple days, give a window of time to recover for it and then do another cycle. So that idea of hit and run dosing was almost built in from the beginning as a way to take something that would otherwise not be a great thing to do in terms of at least the side effect profile, dasatinib. And let's figure out a way to do it in something that at least seems more prudent. And so even with natural compounds like fisetin as an example, I believe all of the studies. Well, let me say the last time I looked@clinicaltrials.gov for studies that were registered on fisitin as a senolytic, all of them were following some type of an intermittent dosing protocol.

Yeah. And again, that seems to be the case with a lot of these senolytic agents, whether the pharmaceuticals or the natural agents. Now, another couple of things that I've seen pop up for controlling senescent cells are two other kind of darlings of the anti aging or longevity community. Metformin and rapamycin. Have you looked into those at all as a senolytic?

Sometimes what you'll see in the cellular senescence community is this idea of senotherapeutics. So think of senolytics as one leg under the broader xenotherapeutic category, two other legs, One would be called cenomorphic, sometimes also called sinostatic or.

And the third leg of the stool would be the immune system. The idea of that middle leg, the xenomorphics, is are there things we can do that would protect cells that are near these things from becoming zombies? So rapamycin would, I think classically be thought of as more senomorphic than senolytic, if that makes sense. It's something that it impacts, obviously the MTOR pathway, which is very important in like senescent cell signaling as well. Like a big part of a cell choosing to become senescent or go from senescent to that falling off process has to do with nutrient sensing in the environment. So I guess getting back to your question, the general idea would be, or I would categorize rapamycin more as a xenomorphic, something that's helping essentially toughen up cells near senescent cells to make sure they don't also become senescent. Metformin. I've seen less on, and I would again put it more in that xenomorphic area. Again mostly because of what it's doing with nutrient signaling, but probably more on the glucose side than on the protein side. Like MTOR would be more amino acid signaling.

Okay, so based on this idea of either Senolytic agents that would kill off senescent cells or cenomorphic agents that would kind of like transform the environment the senescent cells are in. Are there things other than say, like over the counters or pharmaceuticals or nutrients that would limit senescence? I mean, you mentioned fasting, so I assume that would fall into the category. But what about a lot of other strategies that could exist out there, like, I don't know, cold therapy or sauna or light therapy or, or anything like that? Have any of those type of strategies been studied?

Very few of them. We can jump into a couple that have. But I guess first maybe we want to set the backdrop. We talked about telomere shortening, Hayflick limit, basically replicate of senescence. But shortly or relatively shortly after that was identified, what they also found in these cell cultures is that lots of things could cause premature senescence. Basically too much oxygen, too little oxygen, not enough nutrients, too much nutrients, ionizing radiation. So all of these things collectively tend to be pigeonholed in this idea of premature stress induced senescence. And my guess is that most of what we're talking about when we think of cellular senescence and aging has nothing to do with this Hayflick limit. It's these stress induced premature senescence that cells are going through long before they've run out of the ability to divide. So with that backdrop, the way I loosely think of them, how would a cell respond to stress? I bucket into a couple areas. The first thing it's going to be upregulate antioxidant defenses, create a fitter mitochondrial network, basically toughen itself up, make itself more resilient. And if stress is more than it can adapt to, then it will damage some things, like maybe some mitochondria, some other things inside a cell, like typically proteins. Right. So then what it will run is autophagy, which is a cleanup stress program. Let's recycle some of these damaged proteins and organelles and reuse those components to make better versions. And if stress is then more than could be dealt with. Something like with DNA repair, autophagy, that's when cellular senescence would get activated. It's like, okay, there's enough damage that let's just freeze things where they were so we can sort it out, but not so much damage that it's tripped it into apoptosis. Basically the cell is like, okay, like damage is so much, let's just get rid of this cell. And then if damage is even more than that, that's when necrosis, I'm sure you're familiar with that idea, right? Like apoptosis would be a cellular stress program. Like, it's very controlled. When necrosis is basically trauma just caused the cell to die accidentally. There's that continuum. When I think of things getting back to what you asked about cold therapy as an example, or some of these other things we do to build stress resilience, my intuition is those things on the continuum are going to make cells in that first category, right? Like we've made ourselves fitter, much more capable of dealing with a wide range of other stresses. Right. We've done something hormetic. And some of those things may help get rid of at least senescent cells in certain tissues. But that's far less known. And in part it's because identifying and studying senescent cells is pretty hard, really. You have to do tissue biopsies to identify senescent cells and tissues. So because of that, there just hasn't been the amount of research on things that would be in that hermetic category for how they impact senescence. But intuitively, because these stressors are known to be a big part of this premature cellular senescence or stress induced senescence, my guess is that a lot of the things that we're trying to protect ourselves from by being biohackers and integrating these hormetic habits into our lifestyles would help at least slow down the accumulation of senescent cells.

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Yeah. And you'd have to do it in pretty much every tissue because. So like as an example that going back to that original D and Q study, there was bone marrow. They looked at endothelial cells. They looked at adipose tissue. They looked at. And dasatinib was active with adipose tissues, not with the other ones. Of course it didn't. Vice versa. There's no simple assay. Buck Institute is one of the leading researchers in cellular senescence and senolytics. What they would typically do even in a cell culture, they there's no one thing they can look at in that culture and say, okay, this is a senescent cell and this isn't. Now senescent cells, to a trained eye might look slightly different, so they could potentially visibly see a difference in some. But what they'll usually look for is an enzyme called beta galactosidase that synoptic cells tend to give off that enzyme, but it's not 100% sensitive for senescent cells. They'll stain cells for that. I believe if they turn blue with the right stain, that's a marker that, oh, this enzymes disproportionately in this cell. But then they'll look for other markers. Like P16 is a good one, which is a protein that some cells give off. If cells are positive for P16, they're much more likely to be a senescent cell. So fundamentally what the scientists would do is they would look for cells that have a grouping of characteristics.

Yeah, well, based on the fact that you see a high secretion of pro inflammatory cytokines and higher levels of inflammation with senescence, you could probably at least do like, because it'd be pretty easy to get a blood inflammation analysis of Levels of homocysteine and fibrinogen and CRP and a host of other inflammatory markers. And that might give you a clue, at least, that you might have a high rate of cellular senescence.

Yeah, correct. There's a lab in Atlanta called Ginfinity that has a blood panel, and that's what they're looking for. They're looking for betos galactosidase. They're also looking for these inflammatory cytokine markers in the blood. Last time that I talked with the founder there, they were also looking at nad. The idea being because inflammation tends to gobble up a lot of nad, that NAD might be an indirect way of guessing as whether there's a big burden of senescent cells and tissues throughout the body.

Okay, so do you think that if someone were taking nad, that would be one good anticellular senescence strategy?

Yeah, I think, at least to some extent, NAD or NAD boosters would be, again, thought of as being in that xenomorphic category, things that. If the cell doesn't have enough nad, then. So mitochondrial dysfunction, as an example, would be one of the things known to cause premature cellular senescence. So things that support healthy mitochondria, and NAD would be in that category, would tend to make a cell, again, fitter, so that it can resist stress and not execute this senescent cell program.

Okay, got it. Now, there are a wide variety of compounds that I see that you've looked into in the senolytic formulation you guys have been working on. You actually sent me some. I think it was, like, two months ago. It came in this little white box, and the instructions were just to take the pills. I forget how many there were. It wasn't a small number. How many pills were there?

Yeah, a daily dose is six capsules.

Yeah. So you take six capsules on day one, six capsules on day two, and then you're just kind of done. And so I tried that. I just did one. From what I understand, the protocol is you're supposed to do two days out of the month. Every month? Yeah.

Yes, that's our general recommendation. We've done two small pilot studies where we had people do it more frequently than that. So we did three cycles over the course of about a month. So two days on, 12 days off. Two days on, 12 days off. So that's the most frequent that I would have anyone do it. And the most, I guess, slowest amount I would recommend would be to do the two days once a quarter. But our general recommendation and what we use ourselves is the once A month, two days.

And have you been getting results back from people in terms of anything like heart rate variability or telomere length or these DNA methylation clocks or anything like that?

Telomere length I wouldn't expect to have anything to do with. Again, that's that Hayflick limit, a very different type of. What's that? Replicative senescence. So I don't think that would be a useful marker. I've talked to Ryan Smith at Trueage, some people at Clock foundation that do the Grimage epigenetic test using DNA methylation, and then some people in the longevity community. But the consensus is that DNA methylation is just not a useful way to measure senescent cells because senescent cells just don't exhibit the same types of DNA methylation patterns. So what we've opted for is to tend to look much more at subjective things. As an example, because it's so hard to directly measure senescent cell, short of taking biopsies. Some of the pharma companies that are developing their own senolytic, in this case drug candidates, have tried to figure out ways to look at things. Again, what you suggested, inflammatory markers in the blood, is one that is in some studies, but several studies have looked at. Do you know the Womack scale? Is that a scale you've ever run across in research?

No. Tell me about it.

So Womack is. I think it's Wisconsin, Ontario. I can't remember the rest of it, but it's basically an osteoarthritis scale.

Like a pain scale?

Yeah, pain activities of daily living. So ease of getting in and out of cars, going up stairs, things like that, as well as some areas of flexibility. So that's widely used in any to do with joint pain. So you'll find studies of glucosamine that use the Womack scale and the same with lots of medications. So several of the senolytic studies registered on ClinicalTrials.gov use that and then recruit people with some degree of osteoarthritis. So that idea of subjective. Is this making a difference in your ability to do activities of daily living has been fairly common, just as a default thing since there's no great easy blood marker for it. And so what we tend to focus on, especially because in the supplement world, as you would well know, so we're really limited in terms of what types of claims we can make to structure function. Right. So we have to avoid things that would be preventing treating disease. So what we at Neurohacker Collective do is we'll recruit people and then we'll have them do some type of validated questionnaire that looks at things that would be more the positive characteristics of healthier aging, like are you better able to perform activities of daily living after a few cycles of quality analytic. And we've seen positive results in that. We've seen positive results in areas of energy, emotional well being, stress in general, and then individually, I think senescent cells can impact different people quite differently. That's definitely true in research. And part of the reason they think so would be this idea of a threshold effect. So below a certain amount of senescent cells in tissue, other mechanisms may accommodate enough so that we're not subjectively or objectively experiencing the negative effect of the growing amount of the equivalent of yellow leaves in that tissue. But once we cross that threshold, then they're much more problematic. That also makes it very individual how it's experienced because, I mean, I'll be 61 next month, but I'm like, at least I feel like I'm a pretty healthy 61. Right. I'm not limited. I don't have things consistent with inflammation. So how I might experience it might be vastly different than someone that's my age, 60, and that's much more limited.

Okay, yeah, that makes sense. I want to get into some of the ingredients that you have in this senolytic formula, because I hadn't seen some of these before. And a lot of them, like a lot of compounds that you'll find in supplements, they have their special brand name. And then the actual ingredient is revealed later. But one that leapt out to me right off the bat, obviously, was this thing called Sen active, because I think you have what maybe was it 10 or so ingredients in this formula?

10, if you count that as two.

It would be fair to do that because it's a brand ingredient. But it has two compounds in it. One is Noto ginseng, which is used very prominently in Chinese traditional medicine. And then a sweet rose chestnut extract would be the other part of Synactiv.

Okay, so what do those do?

So Synactiv is the company that has made and studied Synactiv, has done about 10 studies on it, some in vitro, some in animals and some in humans. But the human ones have focused on exercise. So the Synactiv has originally was positioned as something to take acutely before exercise to help recovery. What they then found is that. And I guess stepping back, so you know, I mentioned stress of all types can cause some senescent cells. You know, you and I talked about earlier that senescent cells, the transient ones, also play a role in wound healing. Things like that repair regeneration. So one of the things with intense exercise is that we'll naturally create some senescent cells. Because of that, the company that makes senactive at one point decided, well, let's just look post exercise and in people that have taken Synactiv or placebo to see how quickly the senescent cells that are made are cleared. What they found is that they were cleared much more efficiently. In people that took Synactiv. You have this on one side, this ingredient that's positioned as exercise recovery, better performance. Then one of its mechanisms just turned out it helped get rid of senescent cells in muscle tissues. One of the reasons I think that's super important with age is sometimes it's called anabolic resistance. But think of the like akin to insulin resistance. As we get older, muscles become much more resistant to the same things that would stimulate much better growth in a 20 year old. As an example, exercise, but also like protein intake. And so one of the studies I think that was really cool and I've seen another group replicate it, is that this anabolic resistance in old mice, what they did in this particular study is they had young mice, old mice had both. Intense exercise, looked for senescent cells after, within I think it was seven days in the young mice, all the senescent cells had been cleared out. They did their job and they were gone. But in the old mice, two weeks later, there was still a bunch lingering. In that particular study, they gave the D and Q stack to the old mice and it got rid of that and help rejuvenate the muscle tissues. So everything from fibers to hypertrophy. I think one of the big challenges with aging is we're all going to have this anabolic resistance. And so things that might support our muscle in getting rid of lingering senescent cells, to me makes just a lot of sense. Hence synactive.

Okay, so synactive is basically ginseng and sweet chestnut rose. Two different things used in traditional Chinese medicine.

Yeah, and specifically notogensing, which is in the Panax family, but different than Panax ginseng.

Okay, got it. Now, you mentioned that something like the ginseng could be useful for staving off sarcopenia or muscle loss. If, if I were to take your senolytic ingredient, is there a proper timing? Like, should I go work out after I take it on those two days out of the month? Should I prioritize getting a good strength training session? You'd also Mentioned that some strategies like fasting might pair well with senolytic agent. So should I instead fast and go easy or is there like a gold standard activity level that someone should have on the two days that they take this stuff?

So I wouldn't pretend to know that I can just have my intuitions and things. I've self experimented with and know some other people. But getting to synactive specifically they've done that acutely before intense exercise. So I don't think that matters personally. If I was, you know, had done intense exercise a few days later, maybe after a week would be when I would time the senolytic. But just to make it easy on myself, I know I do it the first weekend of every month. It's just easier to put into my protocol at that point in terms of then stacking other behaviors. I do know some people that have done it on days that they're doing maybe their monthly. As an example fasting behavior where they're doing a water fast or something more into the fasting mimicking diet. I've done that too. I've done it on times where I don't do that and I don't think anyone really knows is there and to what degree there might be advantages of stacking things or timing things differently. What I tend to go back to is Wango's work the fasting mimicking diet person. One of the things that he reported pretty early on and again this was before he would have come up with what became known as the fasting mimicking diet, but just had animals that were water fasting for a few days. And his lab was very focused on cancer and autoimmunity. But some of the cancer studies would have then found that okay, you do this short fasting for a couple days and what that does again promote autophagy. He almost described it as for healthy cells, it would almost be like putting a shield around them. It would make them more stress resilient. But for cells that were already maybe on the tipping point of I'm senescent, should I or shouldn't I go through this falling off process. It would tip them into apoptosis. The same with more damaged cells even than senescent cells. And so then the aftermath of that in the recovery, one, you would make regrow fitter cells, but two, the unhealthy cells. So in that case the cancer cells were much more susceptible to the chemotherapy than they would have been before doing this short fasting window. So when I tend to think of the qualia senolytic I personally Think of it as something that's more mimicking this idea of a short fast. And this is a complete guess. So one of the pathways that things like fisetin, quercetin, luteolin, ring quality, senolytic are known to impact, it's the PI 3K AKT MTOR pathway. So it's a nutrient signaling pathway. And there's also like an MTOR direct through amino acids. But this pathway, my intuition and I could be so wrong on this. But evolutionarily, when would your guess be that we would have consumed potentially a lot of things like thistin, quercetin, much more than in a normal diet?

Well, thinking seasonally, I don't know, during the spring and summer, that's probably true.

Right? Because these things are pretty widespread in the plant kingdom. But quercetin is actually named after oak trees. Quercus is the oak genus. And like onions would be another area that quercetin is well known to be in relatively high amounts. But in something like onions, it aggregates that basically the things we throw away when we tend to cook with onions. Right. The skins, you know, the bottom part, you know, the stems, that type of thing. Same with fisetin. Right. Like fisetin would tend to aggregate much more in outer parts of plants, leaves, things like that. So I was reading recently about the Dutch famine from World War II, and one of the things that mentioned in that was that because of that, you know, people were eating, you know, tree bark, leaves, grass, like those are classically famine foods that no one would choose to eat, but they're used to, you know, during famines to get something. And so my guess is that, you know, these things like fisetin, quercetin, so again, quercetin would also be in bark trees as an example is that they're sending almost a famine message when we really drastically increase the amount in our diet like we would in the amounts that are used as senolytics and then causing this nutrient signaling pathway, this pi3kt mtor to basically say, okay, the environment is really bad. I need to prioritize getting rid of cells that aren't that important. And senescent cells are the things most sacrificed.

Interesting. Okay, so you have fisetin and quercetin both in the senolytic. And you mentioned one other polyphenol like compound, what was it?

Luteolin.

Luteolin.

So luteolin and all of them have in common that they're really yellow. So one thing people notice if they take qualiocinolytic, the capsules are transparent and they're this really like pretty light yellow color. And fissin, quercetin, luteolin, they're all very yellow pigments.

Yeah, yeah. When I interviewed Dr. Mercola at one point, he was telling me about this so called autophagy tea that he'll drink at night. And he has a few different compounds in there, including one special form of T bark called Paul D Arco, which is a precursor to nad. But then he mentioned now he actually has a lot of these, I think it was quercetin and fisetin were included in there as something that he takes in the evening to enhance autophagy. So these are acting on multiple mechanisms of aging, including that fasting, mimicking type of strategy that you were talking about earlier. You also list, along with the quercetin, the fisetin and the luteolin that you have in the compound, soybean seed extract. Now, a lot of people in the health sector are of course concerned about soy. They think it might give them man boobs or cause excess estrogen or something like that. But fill me in on why you would include soybean seed extract in there and whether or not that could be concerning for some people.

The extract we use is standardized for soy isoflavones. And in a single dose, it would be about twice the daily dose that someone following, say, a Japanese diet would normally get. And the reason we have soy iseoflavones in there, milk thistle as well, goes back to really think almost mechanisms. So originally, when the Mayo Clinic and Scripps were trying to figure out what compounds might cause cells that were senescent to go through this falling off process, they looked through the research and said, okay, well, these are candidates. Like, they look mechanistically like they'll act on again, maybe that pathway I just mentioned, the PI 3K AKT MTOR, you have your fisetin, luteolin, quercetin that act on that pathway. But then they also looked at other pathways. Tyrosine kinases, specifically Src3kinase, another grouping called efferens. Those things also can prompt the cell to go from deciding to linger to choosing to go through this apoptosis pathway. And so what we did was on the Norhacker Collective science team side was something very similar. We were like, okay, are there compounds that aren't being used as senolytics, but that do some of these same mechanisms that would be complementary with things like quercetin and fisetin and hence the soy isoflavones and the milk thistle? And for people that are concerned about the man's boobs. So isoflavones, again, it's just two days a month. So one, I think it's way over exaggerated that these things, especially in dietary amounts, are problematic. But it's again, part of the idea of polycinolytic is we're just doing this two days a month. So for someone concerned about taking soy isoflavones consistently in the diet, that would be a very different concern than just taking a dose of them twice a month.

Okay, got it. And you list those. You kind of like chunk your ingredients into three categories. Adaptogens, polyphenols, and herbal tonics. We just covered the polyphenols, the fisetin, the quercetin, the soybean seed extract, and luteolin as four things that have been studied as senolytic agents. And then for adaptogens, that synactive, that ginseng that we talked about earlier, that falls into that category. What other adaptogens are you including?

Well, I think we categorize the Piper longum extract into that bucket as well. So Piper longum is a really interesting plant. My background, before becoming a naturopathic doctor, I did a master's degree in Southeast Asian studies. So specifically Thailand was my area of expertise. And my degree, I focused a lot on medical and nutritional anthropology. The Thai traditional medical system borrows heavily from Ayurveda, because when Buddhism came from India to Thailand, they brought Ayurveda with it as well. One of the classic trilogies of ingredient stacks in Ayurveda, but also in Thai tradition medicine, is the combination of ginger with black pepper and with long pepper. Now, some of the role would maybe be we would think of those things as bioenhancers, things that make other things work a bit better. But long pepper, of those three is the one that's least known in the US as an example, but widely used in Ayurveda as something that would be a rasayana.

What'd you call it? A rasayana.

Yeah. So it's akin to how we think of adaptogens, but it would more translate as a rejuvenator. And one of the interesting things about Piper longum is one, it tastes a lot like black pepper. I mean, the seeds can be almost used interchangeably, except long pepper is even more pungent. And the reason is because it has something called Piper longamine that's not found black pepper. And it turns out that Piper longamine is also senolytic, but in different tissues than where quercetin and fissatin have been shown to be senolytic at this point. It's been in things like, as an example, intervertebral discs, joints, things like that, where it's much more active.

That's interesting. I didn't know there was a difference between bioperine and Piper longamine because a lot of times you'll see bioperine combined with things like turmeric or curcumin to enhance the absorption. But it sounds to me like what you're saying is Piper longamine could do the same thing, but it's also potentially a senolytic compound.

Yeah. So bioperine, piperine is the generic word for that. So long pepper, light black pepper, and some other Piper species will also have the bioperine type of molecule of piperine. Piper longamine would be a different alkaloid and distinctive to the Piper longum plant. And maybe not a bioenhancer, but doing completely different things. So it looks like it helps again, that idea of cenomorphic toughen up cells so that they wouldn't become zombified by nearby neighbors. But also it's senolytic in different ways than some of these other compounds and in potentially different tissues.

What form of turmeric or curcumin are you using?

So we use a branded turmeric called Longvida and Lyntheat is interesting. One of the challenges with a lot of these compounds is bioavailability. Polyphenols just in general, you could say, have low bioavailability. One of the things that can help increase them is when more are given together, they tend to sneak more past the gut and the liver that way. But another is when specific compounds are made to be more bioavailable. Neuroscientists at one point, and I think it was at ucla, but it was one of the California studies, created Bongvita curcumin as a way to be a more bioavailable curcumin. And specifically they, in their original research targeted the brain and cognitive performance. We opted for that in part, like Neurohacker Collective. We love things that have been studied in the brain. But Longdita is, I think, branded as the cognitive curcumin of choice and optimized turmeric. But it's one of the more bioavailable forms of curcumin.

Speaking of the brain, do you use that in your other Qualia product, the Qualia mind, or any of your nootropics?

In the original, we call it OG Qualia or Two Step, which I know you took back in the Day we used curcumin in that, but I think that was Meriva, if I recall correctly, that we were using at that point, which is another really good one. But bereave is the one that's typically combined with the bioperine. Right. As the way to increase its absorption and bioavailability. The advantage of Long Vita is you don't need to do the bio enhancer with it.

Okay, and then you've got the other category. You have the polyphenols. Then you have the ones that we just talked about. Are those the adaptogens?

Yep.

Okay, and then what's the last category that you have? Like olive leaf extract and milk thistle and stuff like that?

I don't remember how we categorize it. I think we like tonic herbs. Again, those are interesting. So olive leaf as an example, and I know you're a big fan of olive oil. I've heard you mention that on your podcast and seen it in blogs multiple times. So olive's really cool because it has these unique polyphenols. The leaf tends to have more of one fruit, a bit more of another. The oil is going to have both in some amounts, but the one that's specifically in the leafs in a higher proportion has again shown senolytic potential in tissues where. Where some of these other polyphenols were not active. So I tend to go back to that original dasatinib and quercetin study where it's important to support multiple tissues with potentially different compounds that have seen a lyric activity in a broader base of compounds if we want to target health in more different tissues. That's the reason that the olive leaf is in there, by the way, related.

To the olive leaf. Just real quick, it reminds me of Rudolf Steiner's whole. I think it's called Anthroposophy or Anthroposophy, where he talks about how when you're consuming plants, particularly if you can get the root, the leaf and the fruit, you're going to get different components that target different parts of the body. Like the organs, I think might correspond to the roots and the leaves, to the appendages and the fruits, to the reproductive organs or something like that. But basically what you're saying is if I'm consuming, let's say, extra virgin olive oil, I'm getting a lot of the fruit component of the olive tree. But if I were to take olive leaf extract, I'm going to get a different profile of polyphenols and some of the things I wouldn't be getting from the extra Virgin olive oil.

Correct. You'd get much more oleuropene. I'm probably mispronouncing. It is in much higher amounts in the leaves and much lower amounts in the fruits and the oil. So you'd still get some, but a much lower dose than would trigger these nutrient sensing pathways to kind of do the short term fasting, mimicking to get a senolytic activity.

Okay, got it. I also noticed that you have milk thistle in there. Milk thistle is something you'll find a lot of like hangover remedies and you know, liver detoxification remedies. But why'd you include it in a senolytic formula?

Yeah, so milk thistle, I mean, I think it's in European traditional herbal medicine, has been used for, you know, since going back to the Romans as a liver tonic. But again, we included it largely for the same reason. We picked something like the soy isoflavones, the soybean seed extract. And it's because it does things in these. So I guess going back to like the idea of, you know, why does a cell stay senescent? Right. Why wouldn't it after it's frozen? And then like I said in wound healing, post exercise in a young person, you know, within a week these things have been cleared out. Right. So why hasn't some subsidy cells been removed? And one of the frameworks I've seen, at least in one review article was think in terms of removable and non removable senescent cells. It's the non removable ones that are problematic as we age. The removable ones did their job and now they've disappeared. What makes these cells non removable? And part of it is their ability to resist this falling off process, resist apoptosis. And they do that with a combination of things. There's incredible redundancy built into physiology. So one of the things they're often described as pro apoptotic and anti apoptotic proteins.

Pro apoptotic and anti apoptotic.

Yeah. And it's a family called the BCL2 Bax family. And at any given point in time there's, you know, we cells would have both expressed. It's the relative amounts that would choose the cell's fate. Like, you know, should I proceed through this journey to falling off or you know, am I healthy enough? So you have those proteins and then you have signaling pathways like we've talked about that can tip the balance and say, okay, the environment looks like it's more famine nutrient signaling cascade shift towards this pro apoptotic and then you have other pathways that also influence like these. I mentioned tyrosine kinases. So one of the things that milk thistle does is mechanistically, it works on a sub family of tyrosine kinases that are important in shifting the balance towards saying, okay, like weighing things out. It looks more like a famine. Let's go through egg apoptosis.

Okay.

But in a different way than quercetin or fisetin or some of these things in a way maybe more analogous to what dasatinib would do. Right. It's not really a dasatinib mimic. Right. It's a really healthy liver tonic herb. But mechanistically, it would be doing something more akin to what that does than what the polyphenols are doing.

Okay, that makes sense. So with this whole range of ingredients that are targeting multiple pathways of limiting or clearing senescent cell accumulation, you guys at neurohacker have noticed, you kind of tend to have a shotgun approach. You'll take all the stuff that's good for the brain and acts as a nootropic and put it in quality of mind and just put it all together as one mighty capsule or whatever. Same thing with this senolytic formula. Do you guys ever get called out on the fact that, well, nobody's ever proven that all this stuff put together might not interact with each other in some deleterious way or something like that?

Yeah. So I think that's fair. And it's one of the reasons that neurohara collected before. Like, I guess stepping back, our process is first create a hypothesis. Right. Try to understand the system, the mechanisms, things that may help restore homeostasis, where it would be prudent or provide a resource that's limited, like not enough choline in the diet for many people. So you'll see a couple brain bioavailable choline sources in qualiami, like the alpha GPC cognizant cytokoline as an example. That's step one. Then step two is we build it and try it ourselves. That's our initial proof of concept. Then if at that point it seems like the safety and tolerability is fine, then we'll do some type of a pilot study where we'll make a small batch of it, recruit volunteers, and then have them take a product. And only at. Only if it passes both safety and tolerability at that stage and seems beneficial based on whatever we're measuring. Typically, again, you know, we'll often use subjective questionnaires. Would we move a product to market and sell it to the wider public. So because of that, I feel like compared to most supplement companies, we have a bunch of safety and tolerability built in that a lot of other companies would never know about when they're combining multiple things together until after it was already being sold to people.

Yeah, yeah. So if somebody were to get their hands on this stuff, the senolytic and I'll put links in the shownotes@bengreenfieldlife.com senolytic and take it on a couple of days. About how many months in I've taken it two days out of every month. Would you start to notice stuff or is this more one of those things where you're just keeping your fingers crossed is going to help you live a long time?

So I think it's going to depend on someone's health. That's what we've seen so far. Like in general, I would say three cycles is what I would recommend taking. We've seen some people in our small studies and some customers, some people I know, like friends, family that have taken it, that have noticed something within 12 day dosing cycle, you know, often something that's been kind of a nagging type of annoyance issue, you know, musculoskeletal very commonly. So again, the idea with senescent cells is this idea of a threshold effect. Below a certain threshold in tissues, they may be there, they're not probably doing anything beneficial if they're lingering, but there's not enough equivalent of yellow leaves on the plant yet that the whole plant function is being jeopardized. We would still probably want to prune those away, but we may not be noticing anything because the threshold is low. Right. We still want to keep it low, still want to periodically prune away the equivalent of these yellowing leaves in our tissues. If it's already above that threshold in a tissue, then reducing it below that, often you'll see a big change in some subjective area because of that. There's just not one way that someone would experience it. And you know, someone like you that does all kinds of things to, you know, stay resilient, stay healthy. I mean, my expectation is you wouldn't notice anything. Right. It would be more, you know, just the concept of, oh, I'm going to be a good gardener and burn away some things before they become problematic. Where someone that's already having issues with things related to, say, immunosenescence, you know, like immune cells that have been senescent, issues with areas of musculoskeletal they're much more likely to notice something and notice it quickly.

Yeah, I was reading some of the reviews on your website about. Some people felt like their mind got a little bit more clear. Other people felt like they were recovering faster. Somebody else said they had just had less joint aches and pains. I don't know how many cycles these people took, but just the idea of taking it two days out of every month, to me it's pretty simple. It's not super expensive. What is it like 40 bucks for your first box and 70 bucks after. And I think we have some kind of a discount code too, but it's not like a super duper expensive supplement like some of these other stacks.

The truth is when we first made it, we're kind of on the nerdy end Biohacker collective and in that biohacker niche. And the truth is we made this thinking, okay, we really want to take it. There's just not something out there that we think would be as useful as the product that we could put out. We really honestly weren't expecting it would sell particularly robustly. Right. We were making this for a niche audience is how we thought of it. Maybe some doctors in the longevity space, a subset of biohackers. And to our surprise, within four weeks the product completely sold out.

I think we launched the end of June 2022. What we think is that one, there's not a lot that competes with it, but two, the idea of just having this product that you take two days a month is so easy to integrate for a person that's used to having to juggle taking a whole bunch of things every day. So that idea of the hit and run dosing, the intermittent nature of it just makes it so easy to do is what we found in our customer response to date.

Yeah, well, it seems like a pretty well formulated product. And again, I think we do work with Neurohacker to get you guys some kind of a discount on it that is above and beyond what you'll find on the website. So I will hunt that down and put it in the shownotes@bengreenfieldlife.com Senolytic if you're over there shopping around on their website and you got a little bit extra cash burning a hole in your pocket, that quality of mind stuff, the caffeine free version, mostly just because I like to have a cup of coffee or tea that's caffeinated in the morning, I don't want to over caffeinate myself is another one that I like quite a bit. So that'd be one of their other products that. That's, that's in my pantry. So it's called. It was a. It's just called Senolytic. Right, Gregory?

Yeah. Qualia. Senolytic.

Qualia. Senolytic. Longy. All right, cool. Well, I'll, I'll link to all this@bengreenfieldlife.com senolytic s e n O L Y T I C over there. You can also leave your comments, your questions, your feedback for me or for Greg and leave your own thoughts on senescent cells and anything else that you're curious about that we didn't cover in today's show. In the meantime, Gregory, thanks so much for coming on the show and sharing with us all things Senescence.

My pleasure. Thanks for having me today, Ben.

Awesome. All right, folks, I'm Ben Greenfield along with Gregory Kelly, signing up from BenGreenfieldLife.com have an amazing week. One thing you should know that's super cool is that on the evening of March 11th in Sedona, I'm hosting a VIP dinner that's catered by me and my family using a bunch of biohacked recipes from my boundless cookbook, live music, an intimate Q and A, and an absolutely unforgettable once in a lifetime taste bud entertaining experience where you just come and hang out with me. So we're hosting at our house with only 25 seats available. Things gonna fill up fast. The VIP dinner, only a select few. We want to keep this small, intimate, but super fun with amazing food. So if you want to get on the VIP dinner as a part of this event that I'm doing down in sedona, go to BenGreenfieldSpeaking.com Sedona Dinner BenGreenfieldSpeaking.com SedONA Dinner.

More than ever these days, people like you and me need a fresh, entertaining, well informed, and often outside the box approach to discovering the health and happiness and hope that we all crave. So I hope I've been able to do that for you on this episode today. And if you liked it or if you love what I'm up to, then please leave me a review on your preferred podcast listening channel, wherever that might be. And just find the Ben Greenfield life episode. Say something nice. Thanks so much. Means a lot.