Aging is not merely wear and tear but a cellular programming problem involving the 12 hallmarks of aging, including mitochondrial dysfunction, stem cell exhaustion, and loss of proteostasis; regenerative medicine approaches like partial epigenetic reprogramming using Yamanaka factors (OSK), MSCs, Muse cells, and PAX cells, along with exosomes and gene therapies such as follistatin, can potentially reverse cellular aging, though foundational lifestyle interventions (sleep, exercise, nutrition) remain essential for optimal outcomes.
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Aging Isn't Wear and Tear, It's a Programming Problem w/ Dr. Adeel Khan
Added:In today's episode of Adding Years, I'm joined by Dr. Adil Khan, a physician working at the intersection of longevity, regenerative medicine, and emerging biotechnology. We break down what stem cells and exoomes actually do, the difference between full and partial cellular reprogramming, the promise and uncertainty surrounding gene therapies like folstatin, and how proteomics and AI may help us understand how all of these interventions are working. This is a fascinating look at where longevity medicine is today and where it might be heading next.
Welcome to Adding Years, your road mapap to longevity, a playbook for living healthier and longer. I'm Josie. Along with being a certified personal trainer and longevity enthusiast, I am also a data and AI executive with four master's degrees, including one in AI from John's Hopkins. In each episode, I'll share simple technology and AI back strategies with practical steps that you can use to build your own longevity road map.
Dr. Khan, thank you so much for joining us today on the adding years podcast.
>> Yeah, thanks for having me. Excited to talk to you.
>> I do this for every single episode because I think a lot of the terminology that we use in longevity have a lot of conflation. So starting off strong, regenerative medicine, longevity medicine, functional medicine for you, how do you distinguish them and where does your work specifically sit? It actually sits in all three of those realms, interestingly enough, but as you mentioned, they're all kind of distinct areas, but interestingly, I think functional medicine is kind of a precursor to regenerative medicine. So functional medicine is this whole concept of treating the root cause and trying to get the body to heal from the fundamental principles of how physiology works and restoring restoring homeostasis which is balance in the body. And so the kind of evolution of that is regenerative medicine which is using cell therapy, gene therapy, tissue engineering and all these cutting edge technologies to restore function. So essentially getting tissue and cells to function the way they're supposed to because what happens with aging and this is where it ties into longevity because what happens with aging is ultimately cells become dysfunctional. Aging really is the loss of identity of the cell to do its job. Epigenetic drift is one of the terms that a lot of scientists use for that. And if we can restore function and remember the cell how to do its job, that's fundamentally helping to rejuvenate the cell and making your body functionally younger.
And that's where the field is really headed. Epigenetic reprogramming is a really hot topic which we can get into.
But that's why these fields are all kind of interconnected even though they mean different things and that's why it can be confusing for people. But I don't personally like the term functional medicine just so I think it's important to say because unfortunately functional medicine has a lot of pseudocience as well in it. And so you just have to be careful because there is a lot of supplement pushing and a lot of extra testing that's not always necessary. And so I personally like the approach of what's called systems biology. That's more of the scientific term what it says is your body is a system that works as a whole. And how do we restore that system? It's all interconnected, right?
Your your stomach is connected to your brain and it's connected to your heart and so on and so forth, right? It's all working as a system and it's just that whole paradigm shift as opposed to looking it as a fragmented individualized system which is what happens right now in the medical traditional medical system. Yeah.
>> Yeah. And I think that epigenetic reprogramming, how you said it is really interesting because I want to touch on a phrase that you had in your Substack because you wrote that aging is not a wear and tear problem, it's a programming problem. So can you unpack a little bit um more of what you mean because I think even healthconscious people think of aging as like rust accumulating on a machine that can't be helped, right?
>> Yeah. And there's a lot of medical conditions where doctors will just say, "Oh, you know, your knee's hurting. It's just wear and tear." But it's not. It's not just wear and tear. Actually, there's something called the 12 hallmarks of aging, which are fundamentally the underlying cellular processes driving this dysfunction in the cells. I'm not going to list all 12 because I think that usually will bore people, but just to give a few, uh, stem cell exhaustion is one of the hallmarks of aging. loss of proteostasis which is the proteins being able to do their job sas which is scessence associated secretary phenotype mitochondrial dysfunction these things are all interconnected in a sense as well what happens is these processes are kind of going array over time and we can start to now measure them before problems start and then potentially intervene and that's why longevity is becoming a really hot topic because it's no longer this inevitable decline of wear and tear it's this underlying process that's happening at a cellular level which we can now understand and measure and know how to intervene to potentially slow down the decline and that's part of the reason I think the field is exploding.
So as as you said it is a program problem in the sense that the genes are the instructions right that's the blueprint and the instruction manual and then the epigenetics are kind of what turn on and turn off those genes. We can't change your genes but we can change your epigenetics right we can turn on and we can turn off certain genes. Exercise is technically epigenetic reprogramming in a way because it turns off cancer genes right and it turns on genes that protect your body from insulin resistance. So these are all just interventions that are reprogramming ourselves. And that's part of the reason I'm fascinated with regarded medicine is because to me it seems like it's going to be the frontier and it's going to have it's going to be the realm in which we have the breakthroughs which are going to allow us to cells. I really like that you mentioned exercise because when we hear anything that's like reprogramming, I think everybody really thinks like gene therapy or stem cell [clears throat] therapy, but it's also really great to know that there are less intensive interventions that allow us to do that.
And it's I think it's really interesting that how the media really only picks up on these very extreme protocols versus probably the the basic ones that you would prescribe to all of your patients, which is I'm going to guess eat well, exercise, and sleep to >> literally those things are going to fundamentally make you younger than any stem cell or gene therapy we have currently available. So, but that doesn't make for a sexy headline or clickbait. Yeah. So that's that's just how things work.
>> Yeah. I want to go back on to what you mentioned with the 12 hallmarks and originally how you said that you really want to think of it as a systems approach, right? So um can you see like what is the core through line let's say that really ties all of those hallmarks of aging together for you and how you approach treating it?
>> Yeah. I mean this is a hot area of debate among aging scientists. So I'm not going to, you know, claim that one hallmark is the most important, but if I had to pick a winner at this point, I do think it's the mitochondrial dysfunction and specifically what's called the mitochondrial DNA fidelity, which is basically the replication just as your as your cells replicate, your mitochondrial DNA has to replicate. And there there's something called polyurase gamma, which is an enzyme, which is kind of think of it as like the copying machine, which is responsible for copying that DNA to make sure that the right copy is made. And that over time can't do its job as well. And so the DNA then doesn't get copied properly and now starts making mistakes and those mistakes lead to more oxidative stress which is the free radicals that then start damaging cell membranes start damaging nuclear DNA and mitochondrial DNA and then that starts the whole downstream cascade events of everything else of the cells malfunctioning. So for example if a stem cell becomes exhausted which is one of the hallmarks of aging what was the upstream driver of that?
Ultimately, we think the upstream driver of that was metabolic in nature, which was a mitochondria inside of that stem cell not being able to do its job as it should have been. And so, if you can keep that mitochondria working, cuz mitochondria are really the batteries, right, of your body. And if you can keep them working, let's say theoretically infinitely, and they would never run out of doing their job or never make mistakes, then, you know, that's where things get interesting in terms of being able to extend lifespan. And that's why some companies are betting big on that.
There are mitochondrial transplantation companies and startups. You know, aging is so complicated and there's so many different factors to it. I I don't think if we can do mitochondriation just that alone will cure aging. But certainly I think it would take us in a step in the right direction. And I one of the other interesting things about you know the whole aging kind of shift one of the shifts I had at least in my thinking too is that it's also a problem with the wiring in the body. So this these are the neuromuscular junctions. So what happens is that the amount of neurons that intervate your muscles decrease significantly as you get older. And this is why it's kind of depressing sometimes if you if you look at the science like even if you lift heavy your whole life, you might add only a few years of extra strength as you get into your 70s and 80s because it doesn't matter at that 70s and 80s. You're you just you start losing those w that wiring. And so being able to keep that wiring I intact is also one of the areas that we haven't solved for yet. And I think it's going to be but again it's another area of research right now because if you can keep those if you can keep that wiring intact then you can recruit those muscles and maintain your muscle mass even in your 70s and 80s. Uh which as of right now we have no way of doing that.
>> I think it's really interesting because we went from really treating symptoms to trying to intervene now upstream like you mentioned trying to intervene at a higher level. And I know that this is something that you you deal with in your practice. What's the difference between a full epigenetic reprogramming um protocol and like a partial reprogramming protocol? Cuz I think that both terminologies are really out there a lot in social media and I want a clarification from a a professional.
Well, the you know the the problem with full reprogramming which is these Yamanaka factors, the OSK uh CMIC which were you know discovered in Japan and I think a lot of people have probably heard about them at this point. But what they the problem is when you have those transcription factors overexpressed for a period of time, they can take the cell back all the way to like an embryionic stem cell state. uh which means it kind of loses its identity and then it can also have the risk of tumors. Uh so those are two of the concerns with full reprogramming and that's why it never even though it was a big breakthrough in medicine the clinical applications of it even 20 years later since the discovery of it hasn't really happened uh you know still not really being used like it's under research there's some you know clinical trials starting to happen with they're called iPSC's induced puro stem cells but it's still very early days and I don't think that's necessarily going to be this solution but I think partial reprogramming is definitely much more promising which is potentially exposing cells to these OSK factors for a trans like a temporary period of time and taking them back a certain amount uh or using small molecules. They're even discovering small molecules. Uh there's one, you know, there's two or three startups uh that are, you know, retro sciences is one of them and there's a few others that are basically looking at small molecules that they've discovered which is super interesting if you think about it. It's almost like why do our our cells have this hidden code almost to make them younger and we just have to figure out what the right molecules or the right signals are to do that. The partial uh reprogramming is essentially taking it back to a certain certain level but not all the way back to like embryionic or and then that that's part of the reason why this whole exome and stem cell stuff is interesting because there's a lot of literature coming out.
One of the main mechanisms by which they work is that they actually help to increase OSK transiently uh which means for a temporary period of time and that's why they have a rejuvenation effect on the cell. It seems like you read my mind on the next level of questions that I wanted to ask. Um because you know when you were talking about stem cells, I know that that is such a hot topic right now. Like such a hot topic. Everybody's talking about it.
You specifically I know use um mells rather than the the typical MSC's that I think most clinics are leveraging. Can you walk us through a little bit on why this specific approach makes sense to you? Yeah, it's a long story but I think it's important to share and which is that the professor who coined the term meenal stem cells as you name MSC's he came up with that term in 1991 and at the time he thought that these cells were capable of differentiating into any type of cell in your body which is one of the kind of raw definitions of a stem cell because it has ability to self renew and has ability to divide into new types of tissue. And so, but then in 2017, he kind of he wrote a paper later saying that, well, I was wrong. Uh, let's name it to medicinal signaling cells. It's now no longer stem cell because they're signaling well because meaning they're not actually regenerating new tissue. They're reducing inflammation, which can still be helpful, but the the the reality is when you put these MSC's in your body, 90% plus of them are going to die. That doesn't mean they can't have an effect.
And of course, we've used MSE and there's still clinics having success.
But to me, it's always about consistency of results and how do we achieve the most reliable outcomes. I was involved in a clinical trial in Canada using MSC's uh for osteoarthritis uh for knee and hip arthritis. That's how I got into the whole stem cell world. And so I was researching and obviously reading and just being my obsessive personality, I just kept, you know, going down the rabbit hole and kind of figuring out that wait a minute, I'm not actually treating patients with stem cells. But I realized, you know, obviously during my research that these are I felt like I was misleading almost. And then I I saw all these clinics in like Panama, in, you know, overseas and even in the US being like, "Come to our stem cell clinic." And then I'm like, "Wait, this is kind of misleading people. These aren't really doing what they're saying they're doing." Cuz everyone thinks when you're putting new stem cells in your body, they're going to turn to new cells and regenerate. They're not. They're going to send signals to your body's own stem cells. And those own stem cells, indogenous stem cells may help to repair and regenerate and create a micro environment for your own body to heal.
So it's recruiting your body's own innate mechanisms. So it's a different concept than saying that, you know, than what people think is going on. And so I was I I I came across immune cells a couple years ago when one of my patients told me about it. And I I just got curious and I went to Japan. I met with you know, Professor Dazawa who's the one who discovered them. And then I got fascinated by this whole idea that there's a subset inside of those MSEs that are naturally occurring and they're just one to two% of the population and they've been there the whole time. We just didn't know until 2010 when she discovered them by accident as many discoveries in medicine are that they are this unique subop or subset that can survive better that are pur potent so they can turn to anything in your body and they have a homing mechanism. So meaning they can find the areas of damage and go there with just infusions and they don't get trapped in the lungs as easily with IV which is very important for longevity because when we do longevity treatments we're doing introvenous and a lot of these just get trapped in the lungs. Now one of the other interesting things which is something I haven't talked about as much but I think it's also important to people to know is in 2013 there was another group in UCLA that discovered like muse like cells from the fat and they they called them amus so adapose derived mucells but then they later renamed them to pack cells blurry potent atapose derived stem cells and the reason was because they've realized that they're a bit they're slightly different from mucels they're still like similar in that they're stress enduring, they're pur potent, but a lot of them are actually even smaller in size than mu cells. Uh so mucels are like 10 to 15 microns and then pax cells are sometimes like 7 to n microns which is important because the pax cells being smaller in size means that there's going to be potentially even less trapped in the lens. So it's just an interesting uh interesting discover, you know, it's just interesting to me that there was these two discoveries that were pretty similar in time. Uh but neither of them were really well talked about and not many people knew about them. I believe I was, you know, kind of the first one to talk about it with Chris Hemsworth when he did a post about it and then of course a lot of people since then have started talking about the mouse and now they're becoming more popular which is great to see. uh but not many people know about the PAX house and that's something I want to educate people on too just so people know about their options you know and then they can obviously decide based and there's there's differences in pricing and there's differences you know those type of considerations are also important I think so cuz my whole vision with this stuff is how do you make it as accessible as possible to people not necessarily just giving people what's the most expensive treatment you know what I mean >> well since we're on the topic what what scenario would you recommend between the mu cells and the pack cells other than maybe is it a price differentiation?
>> It's a cost. It's a cost thing. Yeah, it is. Yeah, it's basically the pack cells are easier to make cuz they're they don't require cell passages. So, they're basically just you just take adapose tissue and you don't have to culture and expand them. So, the process is only takes 48 hours and atapose tissue is plentiful. Everyone who there's lots of people giving fat from lipo section and uh things like that and so it's very easy to source. Of course, umbilical core tissue is easy to source too uh for the other type of mucels, but it the cost is a lot higher because you have to use bioreactors and there's a culture expansion process that takes weeks. So that is the main differentiation. I personally use both in my in in our clinical practice in in Cabo and Mexico and then you know in Dubai and places like that. But I haven't seen meaningfully different results between the two. So I try to just be honest with people and say you know these are how the cells work. They're both very similar. uh you know if you want just the pure mucells the Japanese mucells we have those if you're okay to use the you know the pack cells then we can use those most people it comes down to cost uh you know there may be some people who just want one or the other but I think that's usually the biggest factor >> one of the really interesting things of your explanation of your education of stem cell therapy is that how you describe stem cell therapy is honestly how I have heard exoomes being kind of you know sold to the consumer as and how I think about exoome really is this is how I educated myself is is if I put it in one word it's like the signal without the cell right so how do you really think about the exoome um mechanism and how would you use an exoome versus a stem cell in a protocol >> yeah I mean that's the interesting thing right if you think about it MSE's are very similar to exoomes or just a signal but the signal for the MSE's can stay there for longer it can stay there potentially for you know a few weeks before your body clears it out whereas exoomes are gone within probably 1 to 2 days we think so the signal is very transitory and that's why the signal is not as potent uh and so with exoomes you may need more frequent treatments so for example if you're doing it for longevity perhaps you might based off you know we don't know there's obviously this is an emerging area and I think there has to be more research done but it might be something you have to do every couple months uh versus stem cells you know we see data coming back now saying, you know, maybe every 6 months or every year seems to be enough to kind of slow down that aging process. So, it's just more frequent treatments is how it fit in.
And I I think the best explanation that I was given by one of my scientist friends and which I really like is I always say the exoomes is kind if you if you say the stem cells is like the chicken meat, you know, in if you if you have like a broth, right? And you're you have the soup, the soup, the entire soup is what's called the secret or secret.
And then a fraction of that is called the exoomes. So it's the broth, you know, it's part of the broth that has the nutrients and the signals in there.
But interestingly, I think sacrone is going to start to become more popular just because the issue with secret before was that it was hard to standardize and exoomes are easier to because they're smaller fraction of it.
So it's easier to standardize. But now the technology has improved and there's groups that really creating high quality secrets and mucus as well where you have all the microRNAs and proteins and kind of the entire signaling cascade that the cells would have. So they're potentially more well-rounded and although we don't know yet, but that's just my prediction.
>> Very cool. I'm going to I'll follow up with you in a year about the prediction and then I'll ask for some recommendations if the prediction comes true >> for sure. Um, okay. So, I'm going to get to one topic within this world that I think is very much um sensationalized, let's say, probably because there's a lot of prominent figures who have received it. Uh, followatin gene therapy. Can you help explain what it's doing on a molecular level, what that delivery mechanism is, what the use case for longevity is, and how you either use it in a protocol together with stem cells or separately? Yeah, I you know I was very excited when I first heard about it when I I it was about three years ago with a company called Mini and they they're called Minico because they basically created this gene therapy from a plasmid which is derived from Ecoli bacteria but that plasmid is basically just like a circle with it's a backbone kind of DNA and they're able to use that plasmid to insert a particular gene into your body and why use a plasmid because plasmids are very inert uh meaning they're not going to cause immune responses. Uh they're not going to migrate to somewhere and cause issues and that's what makes them very safe.
But the issue with plasmas historically was very low efficacy. Meaning you would put the plasmid in your body and it would disappear in like you know like 2 days. And so mini figured out how to make it stay longer in your body in a safe way. Uh now that so that allowed it to stay potentially for 6 months to a year. And so you could do this uh platform now you have this vector or platform technology to administer different genes. And so why would you want to administer different genes into your body because there are certain things that decrease you know as you get older. So for example phostatin is a biioidentical peptide hormone that your body makes that basically is kind of like the break for how much muscle you can put on. If the increase your follow statin, you're kind of taking the break off a little bit, meaning you're increasing your ability's body to increase the muscle increase muscle mass. It essentially inhibits something called myostatin. And uh those people in the bodybuilding world know about myostatin inhibitors because everyone's been obsessed with that concept since the '9s, but no one's ever been able to make it work, you know. Uh and and just to give that put that in a real world example who want you know those those Belgian blue cows that are super jacked they're they're basically have a myio jam a genetic mutation where they don't make myostatin and there's some people who have said you know like a lot of bodybuilding champions likely have genetic mutations too where they just don't make a lot of myostatin that's why they're able to become honest they look like Belgian blue cows they just kind of humongous right and so this isn't going to make you humongous cuz it's not like we're taking we're not knocking the gene out, right? We're just we're just adding the gene that's like and so it potentially increases the ability to put on muscle. We started using this 3 years ago. It got some traction with because Brian Johnson did it as well and that you know that created a bit of a buzz around it, you know, and I I still like Mini Circle as a company and I think they have a lot of potential. Uh but you know the reality is with their technology after doing it for hundreds of people the results are very mixed. uh meaning for some people it works great and other people it just does nothing uh and it's quite expensive and so I think it's honestly unless you have that kind of money to just like blow and it doesn't matter to you which there are people right there are people out there who are like that and they don't care they're just like yeah I'll try it and and I think those are the right people to do that type of therapy but if you want a more reliable vector uh it's it's going to be AAV adino associated virus and the reason is because AAVs are the most well studied They've been studying since the 90s and you know they got a and and there and and you know for for for those who haven't heard there's just been an IND approved by the FDA so meaning investigational drug use uh is David Sinclair's company using an AAV OSK uh and if we you remember earlier from our conversation OSK is those transcription factors that can reprogram. So now they're putting this on a AEV vector and they're injecting it into eyes to to try to reprogram and make the, you know, help with retinal diseases or degenerative diseases of the eye. And so you can take that same vector and instead of using OSK, you can use false statin and you can inject it into muscles throughout your body and you have a much more reliable vector to increase your body's fall statin production and inhibit myostatin and increase muscle mass. So this has you know based off the data and again this hasn't been done for thousands of people it's been done for you know a couple hundred at this point uh but based off the data that the team has they're called triple uh triple helix uh and and their company has basically uh shown it about 95% efficacy from the data that they shared with me which is quite high meaning most like the vast majority of people will notice a difference and by efficacy I mean you know um significant increase in strength muscle mass uh you know you can use dexa scan hands before and after to confirm that. Um, I personally just did it just being trans, you know, I've done both, the mini circle one I the first time I I did notice something, but it it only lasted a few months and then the second time I didn't notice anything. I did about four weeks ago, the AEV, and it's been a very meaningful difference. And I've been training naturally, you know, as a bodybuilder and a powerlifter for 15 years or so, and so I know my body pretty well, and I'm already feeling a lot stronger, which is very exciting for a meatthead like myself. So, it's fun to feel stronger in the gym and see my body and my I can really see my physique changing as well. So, it's going to be really fascinating to see how much muscle I can put on personally, but uh but I think, you know, I think this is a much more reliable method. And I think AEVs are going to become more mainstream obviously now that, you know, there's a company like Sinclair's and and all these people talking about it.
>> Uh that's super interesting. I didn't know a lot of the information that you shared and I think that our listeners will find that really interesting and I'm looking forward to learning more about it and doing some research after our conversation. You were talking a lot about results and data and tracking.
What does evidence actually look like for you in the longevity protocols that you're you're running for your patients?
Yeah, I mean look, in an ideal world, we would have like longitudinal randomized clinical trials and years of data that we're able to uh discern from with these cutting edge therapies, but we just don't. And so, the best we can do is try to at least create hypothesis from the from the real world evidence that we're gathering. And unfortunately, a lot of these clinics don't really publish or they don't really they're not really transparent about what their like stem cells are actually doing in the body.
You know what I mean? And so, you know, we've done a few case reports with epigenetic clocks with generation lab being the main one that we work with.
And generation lab uses something called biological noise. Uh, which is essentially if you think of if you if you think of your body as a symphony uh playing music, static would be equivalent to biological noise. The static kind of getting in the way of that beautiful music. And so that static that noise is being it entropy. it can be measured Dr. Professor Arena Convoy's technology and they can measure that and from that they can they can correlate it with different organ system aging and your biological age. Now, it's not perfect, right? And so, I think it's a useful tool to kind of track at least to see it's kind of like the analogy to say like if you use a broken scale and you use the same scale and you repeat your weight, at least you're using the same scale, you know? Not to say that it's it's broken, but it's just not perfect.
You know what I mean? It's not >> the direction you can at least >> Exactly. It can give you direction Exactly. It can give you directionality, but it can't but you can't you can't say, "Oh, I reversed my aging 10 years."
That's like just not true. You know what I mean? like it's not that doesn't mean you're going to live 10 years longer. It doesn't mean uh that you've extended your lifespan by 10 years like that's we can't say that based off that data. Now the more accurate and more robust version of this is proteomics which is you know one of the areas that I think I've I shared my excitement with you on because it's really a hot area in longevity and in medicine in general because proteomics is basically the prote proteins are the end product of gene expression right and so protein is the functional expression of how your body is actually working proteins are the things that are doing the job right now they so That's a way to kind of gauge how's your body actually working in this present moment. And the issue with proteomics historically was at it was just too expensive. You'd have to use max mass spectrometry and you'd have to go send it to like a CRO which is like >> or >> uh yeah, you know, so historically, yes, it was a blood, but then you'd have to centrifuge the plasma and then you'd have to store it at minus 80 and then send it let's say 5 years ago or 10 years ago that would cost like $10,000 plus dollars. You know what I mean? And then like no one's going to pay that much for I mean you know very few people will pay that much for it's just a test right and then a company called Somcan had their own you know so Soma logic they had their own kind of database that they they work with proteomics and they were able to give you you know 13,000 proteins and but you'd have to kind of do this whole process of centrifuging it and the plasma and storing it and sending it and that would be like $5,000 which I think was still out of the price range of most people are willing to spend on a test for longevity.
Uh and then this company called Sedona Health was able to get that down to $500. Uh and you know if you want a phabotamist to come your come to your house and it's extra it's like 600. So but the point is they got it down to onetenth of what was available previously and that is very impressive obviously number one. Uh but number two, what they also did was they built a biological AI backend which is basically training this AI on kind of all of humanity's knowledge on biology. So that when you get these protein biomarkers is able to link them to pathways. So it's not just like okay you got these thousand biomarkers now what it's like no okay okay this is what pathway these are the protein signatures that link to these pathways and now you're able to not only know what's wrong but but why it's wrong and what you can do to prevent it from getting worse or how you can intervene and so for example they've shown with neurodeenerative risk their platform can predict outpredict the bleeding other platform by 80 times in terms of predicting your risk of developing the neuro degen neuro degeneration condition. So you can now intervene much more earlier number one and you can more accurately diagnose that this may be a problem for you down the road. One of the other examples I can give is like, you know, like let's say you have like a sleep issue, right?
And so if you go to your traditional kind of doctor, you know, they if you're a woman, they might check your hormones, they might check your magnesium, you know, things like that, and you know, do some basic blood work like thyroid, iron, things like that. And then they may make some recommendations. But let's say if that all comes back normal, then they might just be like, uh, you know, try some melatonin, try some meditation, and hopefully, you know, hopefully you can sleep. But there's there's six distinct biological pathways that are linked to sleep and there's different protein signatures that can be linked to that. And so like inflammation like oxidative stress and so now if you do the proteomics you can figure out which pathway exactly is disregulated and then make a specific personalized plan based off that. So now for for diagnostically it can also be helpful but then also for longevity interventions the proteomic clocks for organ age clocks is it's more accurate than epigenetic clocks uh in terms of tracking the data and this is because they've been trained they use you know they have this UK bio bank they have this Chinese kadoui bank and these private banks and they use all these like over you know hundreds of thousands of patients on which this data has been extracted from in terms of linking protein you know the proteomics data to outcome like mortality data.
>> So for Sedona is essentially two two fe two twofold right. So it has the test that's available at a much lower cost but I think then the real value is what you were talking about is it has access to a lot of data and it's able to run an a heavy analysis and generate insights and intervention. Can you clarify a little bit more on how Sedona's model works that you were talking about? Yeah, I I think actionability is one of the biggest things which means it gives you insight onto what's actually wrong and what you can do about it as opposed to just being like okay I've done this blood test and you know like for example there's a company you know called function health where you can do like these 200 you get all these different biomarkers and but it doesn't really give you details on the biological pathway so you don't really have like a lot of people do that test and they're just like okay now what do I do and so this gives you more actionability uh and then it gives you also So the ability to track the interventions that you're doing. So for example, uh let's say you're doing peptides like peptides have obviously become super hot and a lot of people are doing them, but like there isn't a lot of human clinical data uh for a lot of peptides, right? Like the ones that people are using like BPC or TB4, copper peptide and things like that. And so a lot of it's just or mice data and we don't really know what it's doing at a cellular level. So for example with Sedona they're doing pilot projects right now with a bunch of clinics where they people are on these peptide protocols and then they they run the tests you know every like month or every two months and then we're doing a pilot project by Sedona as well uh where we're using the pack we we're using the pack stem cells and the mucells to basically see how it actually changes the proteomic aging clocks like the organ system aging uh before and after and then we can kind of get at least some idea of how these things are actually working. M and I'm going to ask a question because I think this comes up a lot especially with AI companies nowadays. So if somebody asked you what what how different is that if I just take a lot of all of my tests all of my labs and feed it into chat GPT or claude what would the difference or differentiation be for Sedona for from a consumer and patient perspective?
>> Yeah the the difference is the biological AI it's kind of giving it like a map. So is claude and chatbd don't have that map to link these different protein biomarkers. So for example if you have like four it can because they give you over a thousand like proteins right and then it can figure out patterns and it can figure out patterns that claude and chat GPT wouldn't be able to figure out because they have they don't have that training background that Sedona's built. And so this is the equivalent of like, you know, let's say you went to a new city and you needed to you would just figure out where to go by just walking and making mistakes and then just figuring out, okay, no, I got to go this way versus having a map to guide you on where to go. Uh, that's kind of like the difference between using Claude and using the Sedona platform. So it's able to much quicker figure out connections between different patterns.
>> Got it. So it has a lot of the context and a proprietary model that's specifically trained on proteomics that's allowing it to be very focused and become a subject matter expert which we know that a lot of the general the frontier models are very good generic models but lack a little bit when it comes to specificity. So you have that specificity within within Sedona.
>> Exactly. Yeah. And that's why they like to call it biological AI.
>> I like that. I like that. It sounds like really futuristic and kind of like >> well it's the direction we need to head in. I think it empowers people, right?
Because eventually, you know, the vision of Sedona is to make these tests even cheaper. Then you can in real time you can always measure how your body's doing and how different interventions are working, right?
>> And I think that that's really important because like you said, there's a lot of people experimenting in the longevity space. people are doing peptides, taking a lot of supplements, doing a lot of IVs, doing all kinds of things. If a healthy individual who's listening, who's generally they they're optimizing their basics, they have the sleep, the exercise, the nutrition, the stress in place, but wants to really start thinking about regenerative medicine.
What would you recommend as being the entry point for them? Yeah, I mean, you know, I've seen regenerative medicine work amazing for some people and this is even with, you know, with the mucosels or stem cell or pack cells like the second generation cells and for other people it just does nothing. And so I'm always and my curiosity always drives me to figure out why doesn't it work for some people and how do we optimize our body as best as possible? And I think the foundation is like you said is is never going to change and that stuff is still the most important. But the other layer that we can add to that is you know this functional genomics. Uh we talked about proteomics but functional genomics as well. There's a there's a scientist uh named Dr. Mansour who's you know well-known clinical geneticist. and he's figured out, you know, which genes are kind of the most important when it comes to optimizing your heart health, your brain, your hormones, and understanding everyone's own blueprint to make a personalized plan for them on supplements and even, you know, nutrition and lifestyle. And so, I think when you have that stuff set, then you're much more likely to get a better outcome and a much more robust response to these regenerative medicine therapies. So I think it's important to not think of them as a magic bullet and they don't really fundamentally change anything without you doing the laying the groundwork first. I think that's that's what I've seen at least in my experience and I think a lot of clinics will just throw stem cells at you because you know it's I guess you know because it's lucrative and it's not cheap and so but my approach is much more holistic and I really believe if we want this field to become more mainstream and democratize it uh you have to show people real results and that it's not just like this you know cuz you know stem cells in general have a bad reputation now they're starting to become I think better because like the results are getting um more consistent, but at the same time, there's still a lot of what we would call predatory uh clinics where they're just not really doing things that are based in science and a lot of just heavy marketing. And I think it's important to kind of differentiate between the two. And that's why, you know, I'm so excited about this proteomics project because to me that'll give us at least some real world data. We're not we don't have the means to do double blind randomized clinical trials because those cost millions of dollars, but but at least this is something to give us some idea of how this works.
>> Nice. So if I just condense it a little bit, it's really understand your baseline, right? If you have the foundation, still understand your baseline. So that because there is a isn't a onesizefitsall approach when it comes to medicine.
>> Yeah. Exactly. And this and the main mechanisms by which the stem cells work is mitochondria DNA transfer and mphagy.
So it comes back to what we talked about earlier which is one of the root drivers of aging. We want to get your mitochondria optimized and that's how also you can do that through lifestyle and yes there might be certain supplements or peptides that can support that but ultimately it comes back to those basics.
>> So for our listeners who were hoping you know they didn't have to exercise or eat well and get some stem cells. That's bad news for them. Unfortunately, I can tell you because I have seen patients reports and what I've seen clinically is really it's actually kind of interesting is that the stem cells just wear off a lot quicker. Like so for example, if they're doing it for long say say they don't sleep well, they don't exercise, they do the stem cells, but then the results just last a couple months and then you know they disappear. Like whereas people who do all the foundational things, it seems like the results last longer. So it's one interesting thing I'd observed.
>> I mean and it makes sense, right? And you kind of have get what you put into it. It seems like >> Yeah. Exactly. Exactly.
>> But okay, so let's say now they've gotten the baseline and they can't do the full protocol. People have, you know, an option to do kind of an intervention. If what what do you think right now is kind of the highest evidence to cost ratio intervention that people can access >> like outside of the basics?
>> Mhm. They want to do something fancy, something sexy that they can post on social.
>> Yeah. I mean it's I you know if I think you know based off the data that I'm seeing right now I mean I I do think it's you know the infusion of these muciles and these pactiles they do seem to have a very consistent effect on reversing organ system you know aging which again it just it's a correlation thing but at least it gives us some idea and we see it consistently you know where before and after we have these results and you could I guess you could always argue it's regression to the and things like that. But I think when you see it over and over again, um that can help. And obviously like I think the proteomic data will be more it will be revealing as well. There was a Stanford study, it's not published yet, but just someone tweeted about it. So I I read it, I remember reading about it. It was like the 17-year long study on looking at, you know, epigenetic clocks and like, you know, like the Hovart clocks and things like that. And then they found that the immune system, you know, aging clocks that they were using that outputed it by like up to seven years, meaning that they could better predict like, you know, people dying and mortality. And so basically, if you can have and that was a long obviously a very long long um study. And so I think if you can have your immune system if if you can show that you're making your immune system functionally younger and work better, I think you're doing something very good for your body in terms of slowing down the aging process.
Now I think obviously we need you know there's gonna be more data and research that comes out to support that but that's the direction in which the field is heading you know just to come back you know tied back to what we were talking about earlier with mitochondria it's this whole concept of which is you know metabolism being your mitochondria and then of course your immune system there being the T- cells and B cells and your adapted immune system and being able to regulate and control how inflammation is being regulated and if your immune system is going to attack itself or go haywire and all these things right amosence which is when your immune system cells just basically stop doing their job uh is essentially you know one of the biggest drivers of aging >> a lot of vitamin C I guess >> vitamin D is probably more important actually sunshine and vitamin D >> that's that's very true it's uh but it's hard to get vitamin D for the modern person right I think we're going off topic but I feel like vitamin D is a is definitely one of those lowhanging fruits that's somewhat hard to attain because you know >> it is and and >> we don't go outside as much?
>> No, we don't. Exactly. And people just don't get like I think the easiest tip I can give there is 10 15 minutes first thing in the morning. Just go out and get your circadian rhythm in tune with the light and then spend, you know, sometime in the sun if you can. Depends where you live obviously, but >> probably not where you are in the summer.
>> Yeah, that you don't Yeah, you don't want to be out in Dubine the summer.
>> Um, all right. So, I really want to wrap it up with something more about your beliefs. So, what belief about aging or medicine did you have um that you had to kind of completely reverse over the course of your career?
>> Yeah, I've actually been thinking about this a lot recently. I think I used to well I know it's tricky. I think I you know with the the telomeir length and telomeir attrition you know that was so like touted as the if your telomeirs are longer you're going to live longer if your telmirs are shorter you're going to die earlier but that doesn't mean you're it doesn't correlate necessarily you know it's just one hallmark of aging and there's so much more to it and I think uh I was wrong about that and I got overly excited about the following with mini circle and I thought it was like the best thing ever because of that data but then I realized that doesn't necessarily correlate and now I've obviously changed my view a little bit on the therapy as well as the whole telmir kind of just being the end all be all.
>> I like that one because fun fact I did an epigenetic test and you know I had really good results in multiple a areas like my age good like my pace of aging came good but the one thing that was kind of negative was my telomeir length so I like hearing that. Yeah, [laughter] exactly. Good, good confirmation bias.
Don't worry about it.
>> Exactly. Exactly. I'm going to take it.
You know what? I want I'm going to live in my bias mindset for for that one data piece. But thank you so much for uh joining us, sharing all your insights. I really appreciated all of the different perspectives and the objectivity that you brought to the conversation.
>> Yeah, thanks. Thanks for having me. It was fun chatting.
Thank you for spending your time with me today on adding years, your road map to longevity. If you found this episode helpful, please follow or subscribe on your favorite podcast platform and consider leaving a review. Before we wrap up, a quick but important reminder.
Adding ears is forformational and educational purposes only and is not a substitute for professional medical advice, diagnosis, or treatment. Always consult your physician or qualified health care provider before making changes to your health regimen, supplements, or exercise routine. What you hear on this show reflects personal opinions, experiences, and not medical advice. I'm Josie, and this is Adding Years. Until next time, here's to living better, longer.
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