Ryan Smith
As the Founder TruDiagnostic, and formerly Tailor Made Compounding, I am passionate about applying my biochemistry and medical knowledge to create innovative solutions for the biomedical industry. I have over 10 years of experience in leading and developing startups, as well as providing consulting services to various biomedical clients.
I have successfully established TruDiagnostic as a cutting-edge company that offers personalized and preventive healthcare products and services through leveraging advanced technologies such as AI and genomics. Since starting in 2020, TruDiagnostic has created the largest private epigenetic database in the world with over 70,000 patients. We have also published over 30 academic papers and been awarded 10+ patents.
In addition to my startup work, I have consulted other companies where I support and advise various biomedical projects and initiatives, ranging from research and development, clinical trials, regulatory affairs, to quality assurance and compliance. My core competencies include startup development, entrepreneurship development, successful business ownership, biomedical innovation, and biochemistry expertise. I am always eager to learn new skills, explore new opportunities, and collaborate with other professionals in the biomedical field. My mission is to make a positive impact on the health and well-being of people and society.
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Podcast transcript:
Biological Age with Ryan Smith
[00:00:00] Welcome back to the urban monk, Dr. Pedram, Shojai excited to share Ryan Smith with you, Ryan. One of the brightest guys I’ve ever met. Uh, was in medical school, decided the same for me had gone pretty far down the line and became one of the leading researchers in the field of peptides. Uh, and is now running a lab, doing some of the coolest work I’ve ever seen around measuring biological age, looking at methylation pathways and DNA.
Uh, these guys are looking at a lot of data. And figuring out what it is that is actually working when it comes to reversing age, enjoy.
Dr Pedram Shojai: Good to see you, Ryan. I’m always excited to speak with you because you’re always up to something. And last time we talked, you had done so much already going from, your first generation, your third generation of this testing. So I’m really excited to share this with everyone here. By way of background I would love for them to just know how you ended up here because you’ve, it’s a [00:01:00] somewhat circuitous path and I’m happy you’re where you’re at, but if you could share that’d be great.
Yeah. And thanks for having me. First and foremost, I think I’m excited to always share this message and and definitely talk, I think in a like minded fashion. But but yeah, my, my journey to this place has been a little bit unique. For me, I started off doing biochemistries in undergrad, went to medical school past all my sort of schooling phase past my US only step one I got to the third year is where we started the clinical rotations and really just hated it.
I, I, Didn’t enjoy the medicine I was doing didn’t really think I was making a big impact. And and so got really obviously discouraged there and so decided to make a really big change and decided to quit and then about three months later I created a compound Pharmacy called Taylor made compounding, which is specializing in a couple of really unique molecules.
You really peptides in order to help treat a variety of different things, but aging included. And we grew that really fast. It was the fourth fastest growing company in health care went, several 100 employees within just three years, and it was a really good learning experience. [00:02:00] for me where I learned about the this field of preventative medicine, one that actually spoke to me I think a little bit more.
We ended up selling that company in 2020 really because we saw, I think the it was really exciting to see what was happening with biologic diagnostics particularly with DNA methylation, which is why we created True Diagnostics. So we sold that in 2020 and really launched True Diagnostic in July of 2020.
And that’s brought us to what we’re doing here today.
And what you’re doing today to me is just so fascinating and, it sits on this premise that, we can look at aging as a disease and that the biological clock can in fact be manipulated. Turn down however you want to say it. So let’s get into that on a high level, , aging is a disease and what biological clocks are, , historically the Horvath and all the different clocks that have come before we get to where we’ve arrived now.
Ryan Smith: Yeah, certainly. So I think that, the fundamental thing that I think anyone listening, they should know is that it’s certainly our belief that age is a [00:03:00] disease because it is the biggest risk factor for every chronic disease and death. So if you can really think of anything from Alzheimer’s to cardiovascular disease, diabetes, the biggest risk factor for all of those is still age.
And there’s a reason that we don’t see people in their thirties walking around with the same type of conditions or health consequences we see for people in their sixties or seventies. And this concept of age is one that has been, debated a long time as, is it a disease or is it a function that causes disease?
Or, what is it? And I think that really in 2013, this sort of concept started to change a little bit. And I think, as you mentioned, this really started with Dr. Steve Horvath from UCLA. Who created an algorithm that was trained to predict someone’s chronological age. And the implications at first were not necessarily health related, right?
They were used for forensics to see how old someone was, if they left their DNA at a crime scene. And then also at that time the Syrian refugee crisis was really I would say a big issue. And they were actually using this testing in parts of Europe to see if these people who were crossing borders were adults or [00:04:00] minors and then therefore eligible for asylum.
And and so they had consequences in an application, but it wasn’t necessarily a health application. And and so I think that’s a really cool concept just generally is that with molecular biomarkers in the blood, we can actually tell you how old you are, right? Chronologically. And there are really cool use case scenarios.
We just were I should say on HBO for where we’ve actually applied this to some real world, settings but it’s really not what we’re interested in. I think what we’re really interested. then is quantifying that risk that happens with aging, that sort of that biological risk.
And that’s really what happened with Dr. Horvath is that they started to use this in really large population cohorts. And they noticed a really interesting trend, which was that those people who were younger than their biological age or their chronological age were protected against negative health outcomes.
And those people who were older than they’re with their testing with this. testing where than their chronological age were negative risk outcomes. Basically, if you’re older with this test, you were more likely to develop negative outcomes. And so even though this was meant to be a chronological age predictor just [00:05:00] to tell you your birth date, it actually was measuring some part of biology that was really influencing the way that we develop or way that we get disease.
And so that was a really big breakthrough to think that we can actually measure that process of aging with a molecular biomarker and they can inform us about what’s going to happen to us as we get older.
Dr Pedram Shojai: There’s some interesting data that suggests, look, you look at a, heart disease, diabetes, you look at a lot of these kind of killers of humans, and you would assume that if you were to eradicate heart disease, then suddenly, the life expectancy goes up, so profoundly.
And the number was like two years or three years. And then you start looking at these, one at a time and you go, Oh my God, we’re playing whack a mole. And so it isn’t necessarily the heart disease, but. aging, something else that is making the body’s system start to wobble and fall apart. And so let’s talk about that.
Like what is that je ne sais quoi that we’re now starting to understand that actually is, this [00:06:00] vitalism that when it starts to collapse, we, start to experience all of this.
Ryan Smith: Yeah, absolutely. And to be honest with you, it’s hard to put a finger on what exactly that is, or even how to define it. Whenever I would. say in 2020, there was really a big push to start categorizing these things into hallmarks of aging. Things like telomere shortening or epigenetic dysregulation or nutrient sensing and to try and classify these many different changes that happen with age, which make us more likely to develop these outcomes, but also less likely to be able to cope against maybe any type of damage that were occurring.
And so this is they started with these nine hallmarks of aging and now even just years later we’re up to 15 or 16. So if there’s one thing to take away, it’s that aging is really complex and it happens across every organ system, across every molecular process. And that can be really discouraging for aging researchers because it is so complicated.
The question is, where do we start? And That’s really been what we’ve tried to do as an approach is to [00:07:00] take all of those little and different changes, but to take it in a big picture format so we can quantify where someone’s at and predict where they’re going to go. And so one of the ways that we validate that is.
by doing things like predicting time until death, right? Overall lifespan is a really important metric that incorporates a lot of those disease related criteria and incorporates all those really complex related changes. And so that tends to be one way that, that we create ways to measure but also then document if we’re actually correct.
And so there were a lot of different changes, but the one that we think is probably the most influential is what we’re measuring, which is DNA methylation.
Dr Pedram Shojai: So what, for the lay person, what is DNA methylation? What are you measuring in particular? And how does that tell us what it is that we’re wanting to hear here?
Ryan Smith: Yeah. So I think that the best way to start this conversation is with something everyone knows, which is DNA, right? Everyone knows that they have a DNA sequence, which is completely unique to them as an individual. And this DNA is the same in every cell in your body, [00:08:00] right? So if you’re looking at your heart, your skin, your liver, it’s the same sequence, but obviously those tissues we’re talking about, your heart and your liver are very different, right?
They’re behaving extremely differently. And so how does this make sense to us, right? How do we have something that our DNA encodes for. And that’s the same in every tissue, but our tissues are very different. And the answer to that is by our genetic expression. So are even though we all have the unique sequence that is the same across ourselves, what DNA is actually turned on or turned off in each type of cell can be remarkably different.
And for instance, our skin is expressing things to make it function like skin and our heart is expressing things to function like heart. And the way that it does that is by those on or off switches on the DNA. And that’s really what we’re measuring with what epigenetics is. Epi stands for above.
So above the genome, we’re looking at those changes that sort of control regulation. But in particular, when we’re talking about DNA methylation, we’re talking about that off switch by attaching little sort of molecules to, to cytosines in our DNA, we are able to [00:09:00] turn off that DNA.
So basically it doesn’t go from DNA to RNA, which then creates those peptides and proteins of our body. And so that off switch is really what we’re measuring. And this is a very complex topic because for every single cell in our body, there are 29 million locations in our they can become methylated.
And again, every cell is different and it can change throughout time. So unlike genetics, which is the same in every tissue and at every point in your life methylation is incredibly dynamic and changing. And that’s exactly why we can start to see patterns that tend to change as we get older and associate those patterns.
to age related change. And so that’s really what we’re looking at is the off switches. Whenever we’re doing this testing and when most researchers are doing this testing, they’re looking at right around 950, 000 locations on your DNA to tell you what percentage is methylated.
Dr Pedram Shojai: And so you start getting this data and this is, now we’re talking about a big data, Deal here, right? This isn’t something you’re doing on the back of a napkin. You’re getting 950, 000 locations [00:10:00] times, , , a lot of inputs. And then how are we starting to understand how to read these tea leaves?
I know that you just did a study with like 50, 000 people at Harvard. And so you got a lot, you got a lot of information that you guys had to crunch. How does this turn into something useful for us?
Ryan Smith: Yeah. And, I can understand maybe people being a little bit frustrated with concepts like AI and machine learning because it just seems like a black box, right? It seems like a way to explain everything away without actually having to explain it. But really, that’s what we’re doing is we’re looking just for patterns.
And we’re looking for those patterns and so much data that it’s almost impossible to do again by hand or even with The human mind. And so we need ways to look at that. And so what we’re basically doing is looking at what changes at what regions are the most prevalent in big groups of people.
And looking at what those changes are. And by looking at those patterns, we can start to see really unique associations. But it’s not just with aging. And I think that with DNA methylation as a biomarker, we can [00:11:00] see a lot of really interesting things. So as I, this is a biomarker that goes way beyond just aging, but it’s I think the importance of aging is what’s driven.
This is one of the biggest areas of research with DNA and epigenetics because we know aging is such a big problem and has such a broad applicability. So what we’re really looking for patterns that happen as we get older and particularly those patterns, which might predispose us to more disease outcomes than than other patterns, which might be protective against those outcomes.
Dr Pedram Shojai: So as we start to. Become aware of these patterns. What do when I met you, maybe four years ago, you had a lot less data and you were still finding some very interesting results with what people are doing. And look, you’ve tested all the biohackers. You’ve looked at a lot of data to know what’s working, right?
You got the scoreboard in front of you, right? We would assume diet, exercise, lifestyle would be on there. How much do you see lifestyle as a lever, how big of a lever, and then we can talk about the, the [00:12:00] stuff people take like the rapamycins.
Ryan Smith: Yeah, I think that definitively probably lifestyle factors. So things like sleep exercise those play major impacts in, in, in this type of analysis. If you look at disease related markers and predisposition the effect size for exercise, sleep and activity, it just, through the roof.
And original analyses of these clocks look that about 30 percent was heritable. So around 30 percent is based on your factors. We might not be able to change as much, but 70 percent are based on factors we can. And because of the way that we’ve evolved biologically, a lot of that is due to again what our environment.
So not just, our exercise and nutrition, but even other factors that we’re exposed to, such as the amount of greenness or pollution markers. And so all of this plays an impact. And again, it can be difficult to tease out what is making an impact first or what is, causal versus correlative.
Especially when there’s so many different things that affect our lifestyle nowadays. But we’re starting to see those trends. And I would say that exercise and nutrition [00:13:00] are very big levers were able to pull.
Dr Pedram Shojai: How much so compared to, , wonder drug A, B, or C? Because, , it’s very easy to come up with some hyperbolic promise and say this is the pill and, historically, Nothing’s really come close enough to exercise, sleep and lifestyle intervention. So just curious if you’re seeing anything even coming close to those, because to me, those are obvious, the obvious first levers.
Ryan Smith: Yeah, no, I think that I always go back to even animal studies. Some of the baseline information which we can learn a lot. And still even in animal studies, mouse studies in particular, it doesn’t look like anything has been more effective than simple caloric restriction. Caloric restriction is again, eating just food.
fewer calories than you’re burning every single day. And that has shown lifespan and healthspan related increases that in a lot of animal species, but also in humans. And so it seems to be our baseline target of, are we doing better than this? And I would say that the models that we’re seeing from an epigenetic [00:14:00] aging perspective core restriction definitively works.
It’s one of those things We usually tell people as a baseline, this is something that will work no matter who you are or where you’re at in your health journey. Because it’s so reliably effective at reducing some of these clocks. Not all of them, but some of the clocks the good clocks, I should say, but with that being said, we are seeing some other now I would say interventional therapies.
Coming close to that. Coming close to that effect size. I think that we’ve still yet to prove this out on a really large scale or, looking at outcome data, but it takes time to develop that outcome data because we need people to develop those outcomes, right? But if we look at at even just short periods of time, we see some things that are actually approaching the level of significance of what we see of caloric restriction.
Dr Pedram Shojai: So here’s the thing you get to actually see, right? One of my favorite things about working with Ryan back in the day was like, he actually knows what’s working cause he’s seeing data from, thousands and thousands of patients across, the country and the world.
And , obviously you would perk up when you saw, statistically significant results. , what are the top five interventions if you [00:15:00] will?
Ryan Smith: Yeah. So I think that my, my answer to this won’t be a purely scientific one. And I want to mention that because I’m getting my data from a lot of sources, right? Some of them are just looking at our 35, 000 patients and looking at trends. Others are looking at, studies where we actually look at a person take their measurements, then do an intervention and look at an outcome.
So for any of the scientists out there, this might be a little all over the place. But with that being said, I think that there are some clear trends, probably number one of which is a drug which is, on everyone’s minds. And, in the zeitgeist lately, which is rap rap, my son is A drug which has been shown to extend lifespan and a lot of animal models is still having some initial studies in humans, but typically used for organ transplant medication as a way to prevent your body from rejecting an organ transplant from another donor.
And so it’s an off label product, which is used for aging, but it looks to definitively be helpful in reversing age of a lot of these clocks.
Dr Pedram Shojai: Amazing.
Ryan Smith: I dunno. Yeah. , sorry. I’m happy to go on, but I didn’t know if we [00:16:00] might wanna dive in there
Dr Pedram Shojai: Yeah, so what, rapamycin, this isn’t something you pick up at the drugstore, right? So I know biohackers are, getting access to it. How much of this is commercially available to, , the listeners of this summit and how much of this is still just , either you know a guy or, interesting but not for me yet.
That’s
Ryan Smith: Yeah, I think that rapamycin is not without side effects. So it absolutely is something that should be managed by a physician. And is can be dis but by pharmacies. But it’s actually readily available. If you have a physician who. know, I would say knows about aging. Generally they know about implementing rapamycin and it’s readily available.
It’s also relatively cheap, less than 100 a month at most dosing. And so it, for something that has such a big impact, that’s a relatively good cost efficacy. But it is new and most of your physicians are probably not familiar with it within the realm of aging. Most of them are familiar with it.
probably as a transplant medication, which has way different dosing protocols and strategies. And so [00:17:00] it’s not something that your regular GP will know, but it is now getting a level of access because people are even creating companies that are just offering this in telemedicine formats.
Dr Pedram Shojai: interesting. And then what are people notice? You could see aging clocks Starting to turn, which is, , obviously very interesting for the work that you’re doing, but are there any known biological effects or people running faster or people, what kind of performance, what kind of, is their skin getting better?
Like what would people notice with this?
Ryan Smith: Yeah, so in the case of rapamycin it not, it’s probably not gonna help with performance. But with that being said, there are certainly features of skin, as you mentioned, which definitely improved. So one of the things that rapamycin has been known to do is to act as a little bit of a senolytic.
And that can be a a complex topic. But basically, as our cells have damage, sometimes they have a damage off switch where they’re meant to just not proliferate anymore and not make the damage more widespread, but just to pause. Some people call them zombie like cells because [00:18:00] they’re still alive and active, but they’re not actually proliferating.
And that’s this process we call senescence. And when this happens, ourselves to start to secrete a lot of inflammation. And this happens especially in skin. And so there have been some really good trials showing that even rapamycin as a topical product just applied onto your skin might improve wrinkles and skin collagen and firmness.
And so it definitely has some aspects that people would notice probably aesthetically. But I think that the majority of what they will notice is really not a lot. It’s betting on lowering or inhibiting this one enzyme that tends to be hyper proliferative or cause hyper growth and differentiation.
And by slowing that process down, it tends to have better effects across the board. So you might not notice anything immediately, but across several years and especially several decades, I think that most people probably would.
Dr Pedram Shojai: And that’s the challenge with. Kind of America and the West in general is, , instant gratification. So doing something that the data suggests is good for you, but you don’t see any immediate results. It’s hard to have staying power [00:19:00] for a lot of people that said it’s really important to understand that reversing aging downstream has huge implications for morbidity, mortality, and all these things that we’re starting to just understand.
What about. The stem cells. There’s so much hyperbole. There’s so much salesmanship and so much stuff. You’ve seen a lot of these results. What’s promising. What’s not. I don’t need you to bad mouth people, are you seeing results in, in that? area.
Ryan Smith: stem cells are difficult because unfortunately we might all talk about stem cells, but there are lots of different types of stem cells. You can get stem cells from your adipose tissue. For instance, you can get stem cells from your bone marrow. You could even use umbilical stem cells or fetal stem cells from other people.
And not all stem cells are the same. And so as a result, this can make it very difficult to evaluate one stem cell regimen from another. And so we did a stem cell analysis longitudinally [00:20:00] with a group in Pakistan, got amazing results. We did a stem cell result with a group in the U S and got almost no change.
And the data on stem cells is remarkably varied, but I think that if we’re talking about aging and we’re talking about particularly cells, stem cells, I think I’d be remiss if I didn’t talk about one of the most exciting things that I think is out there which is re cellular reprogramming.
And so this is the idea that we can give cells a couple growth factors, any cell that we have in your body and actually revert it back to a pluripotent stem cell. And so this won a Nobel prize in 2012 for Dr. Yamanaka. And these growth factors actually called Yamanaka factors. And what they can do is they can go in and basically reset the epigenetic landscape.
For instance, cells that we test that might have an age of, let’s just say 45, we can then give them these Yamanaka factors, test them again and have their age be zero, essentially reset to normal. And there’ve been companies now that have been funded by people like Jeff Bezos for, multiple billions of [00:21:00] dollars who are specializing just in this application of trying to turn back the clock by resetting the epigenetics or that gene expression profile of our cells.
And even already in some early trials, they’ve been able. to even restore vision in mice who have gone blind as a result of applying this. So I’m incredibly excited about that as a technology. And really, the implication is that by resetting the epigenetics, we can almost do a factory reset like we would on our phones or our laptop.
And I think that holds a lot of promise still very early. But but it’s a way to take any cell. back to a pluripotent stem cell. And I think that’s really exciting.
Dr Pedram Shojai: What does that look like therapeutically? , it sounds like you could also turn Frankenstein loose. So how does that deploy? Do you take cells out? You reset them, you put them back in. Is it an infusion? I have no idea how this would even deploy.
Ryan Smith: It’s a good question. And you’re not the only one. I think there’s a lot of questions about how to best do this. I think that one of the biggest side effects in your analogy, this Frankenstein is cancer [00:22:00] development. These are growth factors. And taking cells back to a pluripotent stem cell mean that they could differentiate into any type of cell which might not be great.
And there are a lot of different applications. I actually think one of the most exciting applications, at least to start, it’s actually gonna be skin, right? It’s probably the most accessible organ system in your body. And and again, we have relatively good data to show that we can. look at and regenerate youthful phenotypes.
So there’s some companies that are not too far away from actually starting drug trials with the FDA to apply this to skin. But I think that probably one of the, one of the most exciting will be things like organ transplant, where we might be able to take some cells out or take even, regenerate organs as a result.
And then Just refuse an organ of a, someone who might have a diabetic issues with their pancreas or might have alcohol related fatty livers and then just grow them essentially identical new organs at younger ages for transplant. So I think that there’s a lot of applications. There’s even people who think this could be done just systemically.
system systemically with a couple injections or an I. V. Where you’re having [00:23:00] effects all over the body. So I think there’s a lot of different ways that people are going to be tackling this issue. And it’s going to start obviously in animals. So I think we’ll see some really cool things before we go forward.
And so I think that’s certainly a notable treatment. I wouldn’t say it’s obviously in my top five of the tried and true, but it’s still exciting. Nonetheless, Yeah.
Dr Pedram Shojai: Okay. Let’s keep working down that list. What else you got on your top five?
Ryan Smith: So going back to, I think just diet and nutrition and lifestyle. One of the things that was the biggest surprises for me, and I think I’ve talked to you about this before, is the impact of stress. And the way that, that even just small coping strategies like mindfulness and meditation can play a major impact.
In, in some of the first clocks, they’re pretty good at Horvath clock. We mentioned almost a third of those CPGs or those locations in the DNA were located at stress related signalers, gluco corticoid genes. So even already we know that stress plays a major role in impact. But even on my own personal journey, I can tell you that I used to be such a big doubter of mindfulness.
I used to be one of those people who says, is this, am I doing this right? Is this actually doing, doing what I’m supposed to [00:24:00] be doing? And I can tell you that stress just plays an incredible impact. Even your ability to emotionally regulate yourself has been shown to improve biological aging.
So how you cope with the world around you, even from a mental perspective is something that plays a major impact and something I was not expecting to see. But this mind body connection is certainly one that we can actually pick up molecularly.
Dr Pedram Shojai: Amazing. And how long before these interventions really start to show a positive signal? Because, people are like, oh, I tried meditating for a week, wasn’t for me. And some of the studies I’ve seen are incredibly short. Like a six week trial, all of a sudden you’re seeing all sorts of wonderful results.
So where’s the sweet spot?
Ryan Smith: Yeah. So there actually was a small epigenetic age trial in people after they had a heart attack. So myocardial infarction and it looked basically it took one group, put them on six weeks of mindfulness meditation. The other group did none. And in that comparison, we actually saw that the people who did mindfulness meditation over the course of six weeks had better epigenetic ages.
As a result, even other biomarkers of aging, [00:25:00] improved. telomere length as another. And so even short interventions, I would say that from an epigenetic trial at scale, probably the shortest time period that we’ve seen change has actually been eight weeks. And that’s another intervention that I think is probably worth mentioning, which is we did a comparison of vegan diets versus omnivore.
And we did see that vegan diets had a slightly more positive benefit. And we actually even did this in twins. So we took one twin again, genetically identical. We took one twin, put them on onboard diet, the other one on a vegan diet. And it looked like we had some age reduction related effects in that vegan group.
And across the different Types of treatments. It does look like plant based Mediterranean seems to be the better diet types. Then I would say just about anything else that we’re seeing outside of just overall caloric restriction. But combining those two, I think you have a really good caloric restriction and Mediterranean diets seem to be plant based diets seem to be really effective.
Dr Pedram Shojai: Amazing. And the implications of healthy microbiome and the butyrates and everything that come from that, I think are probably downstream. Like you’re, there’s so much to look at. , right [00:26:00] now you just know that the plant based did better than the animal based. , next 10 years we’ll sort out that data, one would assume.
Right.
Ryan Smith: Exactly. And we’re getting close now. It used to be that whether or not you were 10 years older or two years younger, we’d really recommend you the exact same treatment, all of these things that we know from these big meta analysis. But now aging is getting to a point and these aging clocks are getting to a point.
We don’t just, tell you where your age is, but also can tell you what’s driving that process. And that’s a big step forward to make it that personalized medicine component to actually tell you what’s driving that process. And and even that has just happened for us in the last four weeks. We just launched one of our new algorithms can actually tell you what metabolites, clinical values of proteomics are really driving that aging process on an individualized basis.
So we’re certainly getting there.
Dr Pedram Shojai: What are you seeing in that? Not to jump ahead, but , what are the major drivers that you’re, obviously this is a new, you just deployed the new algorithm and you’re seeing all sorts of interesting stuff, but is it the smoking? Is it the, , like , there’s gotta be some smoking guns here.
Ryan Smith: Oh, yeah. Yeah. I [00:27:00] think that’s a good place to start is we have a clear list of don’t deuce. That’s and that’s usually where we start is let’s eliminate bad behaviors because that can be a large proportion. And of course, I think that smoking, drinking, on average, people who have you know five or more drinks a week are on average 2.
2 years older than those people who don’t. And so smoking, drinking getting insufficient sleep or having insomnia like symptoms. All of those things are drivers. So I think that’s what we always start with in our recommendation list is the don’ts, the things we know definitively not to do.
And we have ways of even tracking those behaviors. So even with right now, with methylation, we can tell you how much you’re smoking. We can tell you how much you’re drinking. We can even tell you how much you smoked across your entire life. And actually that tends to be even more influential.
Our predictions tend to be more influential for disease and even self reported smoking status. So we can actually pick this up the damage up from some of these behaviors on a molecular signal. And in the case of smoking that never returns. Once you do smoking for a little bit. Those your methylation pattern is set essentially and can’t recover to the [00:28:00] status of someone who never smoked.
And so there’s some behaviors which look to be incredibly detrimental. But with that being said, I think that from another biomarker category, one of the biggest things that we’re seeing is just the importance of inflammation. And I’ve talked about this in relationships to synalytics, but just generally overall body inflammation tends to be a huge driving process of aging.
And I think that if I had to boil it down to just one term that is, every, everything seems to be connected to, it tends to be that one.
Dr Pedram Shojai: So the idea that inflammation is, , a signal that then tells the body, to age. How much of this do we know is related to mitochondria and the signaling that happens with the mitochondria, telling, system, , we’re still going or we’re shutting down.
Ryan Smith: Yeah, another great question. And one of my favorite sort of peptide related treatments is our mitochondrial enhancing products because the important thing about the mitochondria is they’re in every tissue and they supply the energy for every process. And so if you’re improving your mitochondria, you’re helping out across the [00:29:00] board.
But unfortunately, from an epigenetic perspective, there haven’t been a lot of studies which are looking at mitochondrial function and looking at epigenetic aging. Or, even taking that a step further, the mitochondria are unique in the fact that they actually have their own DNA, right? You share the mitochondrial DNA of your mother and her mother, right?
It’s passed down from The, that female lineage. And unfortunately we don’t have a lot of data connecting these two things because it’s sometimes very hard to address mitochondrial function. But if you look at some of the treatments that we know tend to have an effect, like exercise like rapamycin, like metformin, a lot of these work within the mitochondria as a direct mechanism.
So there’s certainly, I would say a connection and correlation there, but unfortunately, in terms of trying to figure out how much of a connection or what that driving process where there’s still a lot of work that needs to be done.
Dr Pedram Shojai: Yeah, seems it. It’s interesting how a lot of these different worlds are starting to converge and our understanding of what, what makes you better. You’re seeing it in your data. We don’t know why, but we see it, right? We see it. Okay. So [00:30:00] what other interventions are moving the needle from the data?
Ryan Smith: Yeah. So again, there are a couple of things that I also say we tend to see work for everyone. Vitamin D is one of those. Most people probably know vitamin D as that nutritional ingredient that’s made whenever you get exposure to the sun. And but most people in analysis tend to be vitamin D deficient.
And we can see that supplementing with that can have. some age reversal effects relatively rapidly. So vitamin D is one of those things that I think I recommend for everyone. And I think there are a couple other correlations we typically tend to see, which is that, omega three fatty acids again being an anti inflammatory sort of fat molecule also seem to have an effect.
And those two things I think across the board are very helpful. And then I think there’s some other more surprising related things nutritionally that I think also are really exciting. We’ve identified the carotenoids, right? And most people know these as, from carrots, right?
Tend to have a big anti inflammatory impact and now across multiple clocks have been identified as something that is highly correlated to better biological aging.
Dr Pedram Shojai: Interesting. Carrots.
Ryan Smith: Yeah. Just simple [00:31:00] carrots. Yeah. And in particular, it doesn’t beta carotenes, alpha carotenes people might be familiar with supplements like lutein which is mainly used for macular degeneration or eyesight.
That’s I think of most people have grown up learning about carrots, but they have anti inflammatory effects all over the body and have been certainly identified as a compound, which seems to have a lot of benefit.
Dr Pedram Shojai: Curious sulforaphane, anything on the aging clocks with that?
Ryan Smith: So it’s funny you mentioned that literally this morning. I just did a meta analysis in our cohort of sulfurophane. And the answer is yes. We are seeing some positive effects, but minor effect size. And in our, and this is in a cross sectional analysis, but the people who are taking sulfurophane tend to have a moderate better biological age.
So it is still significant, but it’s smaller in effect size.
Dr Pedram Shojai: Quick pause here to let you know that a lot of this stuff, the reason I started looking at biological age and the reason a lot of the biological age guys started coming to me was because turns out the mind body practices, the meditation the qigong. [00:32:00] The stuff that I learned in the monastery turns out that stuff really high impact on age reversal, really high impact on all this biological stuff. Who knew, I guess they did.
So just want to point your eyes to what I call the temple grounds. It’s where I teach the stuff that I brought from the different masters over the years, different lineages, Shaolin Taoists health. Uh, longevity performance, all these practices in an area of the urban monk academy, I call the temple grounds.
I teach it all there. It is the pure unadulterated teachings that I have passed down. This is the stuff that just works. If you really want to be well in life, do the practices. We’ll see the results back to the show.
Yeah, there’s, every week there’s something new, right? It’s this week, it’s the, , the du jour that comes into the health industry. And I love being able to have a scoreboard and look at what they’re actually doing. At least in this analysis, right? Aging, [00:33:00] right? And you’re looking at a very specific thing.
Okay, so downstream from this. You start to see changes in the biological clock from, , all these interventions that we talked about. How do these map out across to the diagnosis codes that people are suffering from right now? Like how are these correlating and why should this be supremely interesting to our listeners?
Ryan Smith: Yeah. This is this is where we really get to the utility, right? Why measure these things in the first place and how do we know they work? And so before I go into sort of their, how they actually, we know they make a difference, I think it’s important to talk about how we conduct these studies because at the end of the day, people might say, Hey, you’re measuring this, how do you know what actually works?
And the answer is. We know it because we’ve taken and done this analysis from samples which have been taken 40 years ago. And these happen in biobanks. So these biobanks have big university systems or big national systems have been able to take samples from individuals they’re treating and keep those samples.
For several years. And so now we can go to [00:34:00] a group like Harvard look at samples that have been taken decades ago and then look at what actually happened to those patients. So we can look, did they develop heart disease? Did they have a stroke? Did they, when did they die? Some of those things to see how effectively can we predict these outcomes.
And our ability to predict these outcomes is getting better than ever from an aging perspective. Right now, if we wanted to predict death with just your age, you It’s a relatively different, difficult thing to do, right? If you’re 99 years of age old, we can say it’s probably not too far off because we know that you’re way beyond the average lifespan.
But let’s just say, can we do that effectively for someone in their seventies? The average lifespan is still 77 ish. And you might say, if you’re going off the average lifespan, you could probably predict it with some degree of accuracy. But what about if you’re 50? Or what if you’re 30, right?
Where there’s a lot of room. And so with our newest algorithm with omegage we’ve actually been able to predict death within 10 years at a 92 percent accuracy. And compared to chronological age, we can only do that right around a 74 percent accuracy. So we’re getting much, much better at predicting these outcomes.
And what [00:35:00] we saw with this new algorithm is that we can actually out predict it. every disease versus previous measures of biological aging and by a wide margin. And especially way better than chronological age. And I think that should make people probably should understand that, right? I think that most people know someone in their seventies who looks like they’re 50 and probably knows someone in their fifties who looks like they’re 70.
And so you can probably tell outwardly, but we also need a way to. to have a consistent measuring stick than just how you look. And that’s what we’ve developed. And so right now our ability to break these negative outcomes are better than ever. I always like to use a statistic that was given in a presentation by Morgan Levine, which is that if everyone in the world were to reverse their biological aging by seven years, we’d be able to cut the incidence of disease in half.
50 percent of people would no longer be getting sick. And that is a I think. Hopefully what we’re trying to get everyone to aspire to is to start measuring this, start implementing the things that we have started to see work. Or maybe on an individualized basis work for you with retesting, get everyone to that seven year mark and have a massive [00:36:00] impact on disease worldwide.
Dr Pedram Shojai: As a quick aside, one of these days MetLife is going to call and try to buy you because the predictive, the predictive promise of being able to understand that is big for life insurance. And, , I wouldn’t be surprised if they had, I’ve already moved into this strong, right?
Ryan Smith: You’re right. I should say not met life in particular, but there are companies out there now that can use this testing to set a life insurance premium for you. And so it’s pretty sci fi. It’s something we’re not necessarily interested in doing, but it is out there.
Dr Pedram Shojai: Yeah and it would be a little Big Brother y, I mean it’s Big Brother y to begin with, but it would be very Big Brother y if there was nothing you can do about it. But if you can pull on the levers and through objective data show that you have moved your biological age, then your premiums should shift and, the outcomes should shift, which is also part of the promise is I’m also driving.
Ryan Smith: Yeah. And one of you again, I know it can be scary for some people but at the same time, it might finally be a way that we can finally incentivize preventative medicine. And, I think that a lot of people [00:37:00] know the U. S. healthcare system is in a bad spot. And a lot of that is because again, we’re putting money to treating disease and not preventative care.
And so if we can actually have an objective measure, which can help predict these outcomes and then be acted upon, and we can show that these actions actually improve outcomes, then we can finally maybe get some payer money behind it and really try and fix this place we are in healthcare. And so I think that’s certainly a goal for us and really.
demonstrates just the importance of preventive medicine and importance of age in that discussion.
Dr Pedram Shojai: And it’s a very different scoreboard, isn’t it? The not disease scoreboard of saying, Okay you’re under this number, come back when you’re worse has led to, , a chronic disease debacle that has really saddled the entire economy, frankly, , it’s not a good thing.
And so this scoreboard of what can I do to move my numbers and extend my lifespan I think offers a lot of promise, right? And seven years, you said was the magic number.
Ryan Smith: Yeah. Yeah. I [00:38:00] said, I think that number is always a little bit in flux as new and better methods of quantifying that come out. But yeah, I think that’s hopefully what one thing that everyone can shoot for. I always say, even as a baseline, I just want everyone to shoot for being younger with a biological measurement than they are chronologically.
If you can do that, I think that’s certainly a good thing. And there’s one, one thing I want to step back on and just help. People may be reflected, understand we’re talking a lot about disease. We’re talking a lot about death, but some people may say, why do I want to live an additional year longer or two years longer?
If it’s a poor quality of life. And so I want to distinctly mentioned one thing, which is that if you’re improving your biological age, you’re not just improving your risk of disease and death. You’re also improving your quality of life. So you’re improving things like your mental processing speeds and your I.
Q. Your ability to move about the world and have a proper balance or you have the muscle mass and even facial aging. We know that this is also impacted by the overall aging process. And so if you want to even look young forever, then this is again something that you can try and treat and have. We have some actually good pictures demonstrating that as well.
Dr Pedram Shojai: Yeah, that’s really [00:39:00] important, right? It’s because it’s the time with your grandkids. It’s the time to take those trips that , looked forward to, and now you can’t and the end of life. Currently, the model is it sucks, right? You park up on a golf course somewhere and , and just deteriorate away.
And that isn’t necessarily, , it doesn’t have that much sex appeal, right? But having the quality of life to be dancing and traveling and doing all the things can make a huge difference, right? So again, seven years, I want to understand, , you’ve seen a lot of this data. How many people, not numerically, but how often do you see somebody Go down seven years in their biological age.
How long does it typically take? How much work goes into hitting that magic number before 50 percent of chronic disease falls off?
Ryan Smith: Yeah. So I think that um, this is a hard question to answer mainly because, if someone’s healthy, if someone’s doing all the right things, taking their age down by seven years is going [00:40:00] to be definitively harder than someone who might be very unhealthy to start with. So it is relative about where you’re starting.
But I think that we have seen multiple year age reductions with even just a couple of different treatment regimens. And I think that but to go seven years in one single go between one measurement is a hard thing to do. And so to set expectations, I think that, Most people, that would be a relatively difficult thing to do in a single measurement.
But I think that what we see is that the people who implement strategies that are consistent about, positive health benefits and positive health regimens over time that starts to accumulate. And so it might not be something that can happen from in a single year, nor would we probably believe it, even if that were the data, right?
No one aging is a hard thing to beat. No one has beat it yet, right? No one is. lived to, to an age that is, you know, astounding and we can say they can beat aging. And so it is a hard thing to beat. It’s probably the biggest competition we could ever do. And so with that being said we want to be measured about this.
We want to find interventions that have, a [00:41:00] quarter year age reduction, an eighth of a year age reduction, because those things add up, especially if we could do them across our lifespan. And So sometimes it can be hard to have those multiple year age reversals. But they’re out there, one, one person as a celebrity that most people probably heard about in their aging journey is Brian Johnson.
He is a sort of a tech entrepreneur who made a good amount of money and is able to really focus on aging. It’s this. primary fight or endeavor. He just even released yesterday that he was doing some things with his dad. Actually, one of the really exciting things which is called plasma exchange or young plasma, taking plasma from younger individual and putting it into older.
And we saw some really multi year age reductions with a couple treatments of that. And so I think there are certainly some things out there which make us excited, but it is hard. I think you need to implement some of these strategies consistently and for a long time to really have some of that benefit.
Dr Pedram Shojai: Okay, but let’s look at the long math on this, right? Say you’re 50 60 years old and you know You’re starting to feel the wobble of some chronic disease some of these kind of diagnosis codes [00:42:00] coming up you were pre diabetic and now you’ve crossed over and all that and so if it took you two years, three years to start, , layering on all these interventions to get to that seven years.
I wouldn’t quite call it time travel, but you are doing something very significant. So what does that look like in that kind of multi year approach to really address that number?
Hey, I just want to remind you. This event is winding down. This is the last day. Upgrade. Now keep this interview, keep access to the transcripts. Keep all of the bonuses that come with this summit. Do not miss out on this. This is a, an opportunity to save 50% on all of this information. Take it home, take vitality home, and also support the work that we’re doing here back to the show.
Ryan Smith: Yeah, absolutely. And so that’s actually one of the reasons one of our outputs is not just an age. It is a pace of aging to tell you on average, how many biological per years are you aging? [00:43:00] And the idea that is if we consistently age at a 0. 7 or 0. 8 biological year per year basis, we can slowly but definitively start to reduce that process, right?
Reduce that aging process. So that, if someone has been aging at 0. 75 percent their entire lives, but, by the time they get to a hundred years of age, they were body would only be 75 years of age. And so that’s a major difference. And so we like that pace of aging because it’s a more intermediate factor.
But really it adds up over time. And so if you can keep that low for as long as possible, it’s a little bit like compound interest. We see it get your rate of aging get accelerated as you get older. So if you can keep it low for a long period of time, you can reduce that sort of upward curve that can really have that problem.
And so the rate of aging is one of the things we really like to shoot for. And if you can keep it low, then it can have some major benefits across several different years.
Dr Pedram Shojai: I love that now there’s A feedback loop that allows us to know what’s working better. How often do [00:44:00] people retest or should they be retesting to know that what they’re doing is working so they can tack on the right trajectory?
Ryan Smith: Yeah. So I know that a lot of people who are interested in aging might be very interested in doing everything they can do to tackle this immediately including multiple tests to see what’s working. But sometimes that can give us. I would say information that we might act on, and it might be the wrong information.
And so we recommend a slow and steady pace to this type of thing, usually doing a testing once every six months or once every year, just to see what is helping or hurting or where you’re at. Some tests we do have some tests particularly that you need in pace of aging, which is more intermediately responding to change.
And so if you really want to test, how a certain medication or a certain diet or lifestyle intervention is doing, we recommend you could probably do that one as. most frequently. It’s every 12 weeks, but we still recommend putting a little bit time in there to make sure the signal we’re detecting is true biological signal.
And not just a confounding factor for something you might have eaten or done at a certain point of the day. So usually I would say six months [00:45:00] is usually that frequency for testing.
Dr Pedram Shojai: Love it. What is the testing like? Like I know you guys send kits, like just help the audience understand what this test looks like and feels
Ryan Smith: yeah. So with epigenetics, we did talk about tissue type being an important factor. And so unfortunately, We do not do saliva based testing. So this is still trying to get a blood sample first. But the good news is that this can still be done at home. It’s just a finger stick blood spot where we take a few drops of blood on a blood spot card.
And then you basically send that back to us in the mail. It takes about two weeks once we get the sample for us to do our analyses and then you have your reports available. So it really can be done with a sort of at home test. And we can still get really reliable results in that manner.
Dr Pedram Shojai: Yeah, I love that. And the good news is once you have that, you’ll have a baseline of where you’re at. You’ll understand where to go now. How much does your system and listen, I’ve known you for years and things have evolved as we’ve gone here. But how much does the system kind of generate [00:46:00] scientifically anchored recommendation vehicle, if you will.
So people know what to do with this stuff.
Ryan Smith: Okay. Yeah, so so I will be honest. That’s one thing that we have not really added to our platform. And the reason being is that we hate to make recommendations which may not be working for you as an individual. And a lot of this information can be quite complex. And so we really try and break it down.
So we do what we really try and do is We don’t want to sell the solution as well, right? We want to make sure that our test is as good as it can possibly be and is not confounded by us, selling you a solution that we, we might try and implement. So we try and be agnostic about the recommendations.
But with that being said, we’d love to provide education. So we do have a, on our website, even though. full list of clinical trials, which have shown positive associations to age. So you can look at, the diet changes, you can look at the stress of maintenance changes or the supplements or nutrition.
So we do a lot of clinical studies but we don’t put the recommendations directly on the report. So we always will help you educate. If you ever come to us, you can always ask and we’ll provide lots of evidence. [00:47:00] Always having evidence back recommendations. But we don’t do it necessarily on the port.
I think that now. that we’ve progressed so far, that will probably change in the very near future. What we will give specific recommendations, especially now, because we can get individualized aging treatment. We can tell you which organ system, for instance, is aging fastest. And that might, I would say, predispose us to making much more personalized and better recommendations.
Eso I think that at the moment we probably don’t do that effectively, but certainly in the future will continue to do that.
Dr Pedram Shojai: Yeah. And there’s a big difference and I appreciate the stance that you take on that, but I think there’s a big difference between, the report saying you should probably take more selenium and say, , take, my, my pill, which is where I think a lot of these companies go and they try to vertically integrate and then,
you don’t know who to trust, right? So I appreciate the stance that you’re taking, but if, my report came out and said, dude, you need more sulforaphane, I’ll know to go look for it.
Ryan Smith: Exactly. So now we do, I would say, have some particular recommendations. For instance, we can quantify metabolites like [00:48:00] carotene dial, right? We talked about the importance of carotene. If we see that your carotene is, lower than we would like to see in the population, that’s a really easy recommendation we can make.
We can make similar recommendations for supplements like uridine. And so we’re starting to get to that level of personalized recommendations where we can definitely recommend things based on your profile. We’ll start to be incorporating it, but we have been, I would say, hesitant to make sure that we’re completely rooted in really good science.
But I think that now we feel very comfortable about that and we’ll start making some other recommendations. There’s other 11 other thing I want to just recommend, or I should say, talk about and discuss with the reporting, which is that as I mentioned earlier, epigenetics so we can do some other really interesting things with this reporting to give you some feedback about other areas of your life that might have be connected to aging or just connected general health.
Dr Pedram Shojai: I, what would that be?
Ryan Smith: Yeah. Epigenetics now can do everything from, I already talked about it predicting death, but we can also even tell you probably what zip code you’ve lived in most of your life based on pollution markers in your DNA. We can tell you how much you’ve [00:49:00] smoked across an entire lifetime.
We can tell you how much you’re currently drinking. We can tell you if you’re likely to lose weight with caloric restriction. We can do a lot of really interesting things, even quantifying nutritional metabolites like alpha ketoglutarate or spermidine or, some of these things that even NAD related metabolites.
So we can do a lot of really interesting things here. And I think that if there’s one big takeaway, it’s to certainly pay attention to aging as a risk factor, but secondarily to that, the DNA methylation will be a diagnostic that affects. every area of medicine, even agriculture. One of my favorite anecdotes is that with climate change broccoli is actually changing its genetic expression and now manifesting more like cauliflower.
Just from its epigenetic change to the changes due to the climate. And so this epigenetic processes important across multiple species. And as we start to learn those patterns, we’re going to be able to tell some really interesting things and make very precise recommendations, not just with aging, but even for cardiovascular disease or diabetes.
Right now, we can even subtype type diabetes into four different groups, each with different treatment recommendations and each [00:50:00] with different relative risk outcomes. So this is going to be a tool for personalized medicine across the board.
Dr Pedram Shojai: I’m curious, , happy to, do this dance with you as we go, but I’m curious about people who say go through EDTA chelation and some of these other interventions, not necessarily to add, but to reduce toxic load and what you’re seeing there.
Ryan Smith: Yeah. So I wish we had more data pre and post chelation because actually a heavy metal exposure has very clear and definitive signals on the DNA methylation. We can actually, just from your methylation profile, tell you what heavy metals you’ve most likely been exposed to. And even in our first report, we outlined this.
And so we don’t do it as much anymore. I think But we’re very interested in making some great predictors. But I think that, even in our big meta analysis of this Harvard cohort we talked about, we saw definitive links between aging and PFAS chemicals, right? Those forever chemicals that were exposed to we see xenobiotics, which is just these outside chemicals, right?
Those environmental exposures lighting up all over the place in terms of association. So we did see, for instance, BPA [00:51:00] is one of those things that would predispose people to aging. And we are getting these measurements and starting to associate but we, right now we’re not sure about the longitudinal journey, right?
If someone changes these factors or removes them, how much of an impact do they have? And, I think that there’s also A really great scientist at the University of Washington Michael Skinner, who does a lot of really interesting work about even pesticides and even the multi generational impacts it can have.
Where we might, for instance, for glyphosate a really popular pesticide. they saw no changes or no negative impacts on the epigenetics of the mice they were studying, but they didn’t even see any negative impacts on the second generation mice. But on the third generation mouse, they saw massive changes that were negative and predisposing to disease.
And so it can be quite scary sometimes, but it just it doesn’t mean that we should shy away from it. It means we should dive in and really find out how this is affecting and what we can do about it.
Dr Pedram Shojai: Yeah, you look at DDT and the generational, downstream effects. We didn’t know until we knew and then it was like, oh. Yeah, and these PFAS, I’ve been [00:52:00] looking at these kind of overlapping hockey sticks of, , the rise in the pesticides, the rise in the glyphosate and all this.
And then all of a sudden you start to see chronic disease and autism. And it’s almost. Scary how these overlap, right? And so if the aging clocks are also, , a reflection of this, then the question is, okay, what can we do and how do we change that? It’s too early to tell, but it’s still, to me, it’s just fascinating that we can look at all this now.
Ryan Smith: Without going too far down this rabbit hole, I will mention that there are things we call imprinted gene regions. And these are epigenetic patterns which are actually passed down from our parents and our grandparents. And so we can actually see epigenetic signals For instance, the people who were in the Holocaust or descendants of the Rwandan genocide.
And so we can actually see this. And one of my favorite studies was in mice where they exposed mice to the smell of cherries. And every time they did that, they would give them a slight shock. But even four generations later, when those the generations of. Mice still smell cherries, they would still have the shaking response.
And we know that some of these things take a long time to [00:53:00] manifest, but we’re starting to be able to untangle those signals and see how they all relate. And I think in particular these environmental chemicals are one of those things we can see in epigenetically that play a major impact.
Dr Pedram Shojai: I’m loving the work that you’re doing. I love that you’re on the bleeding edge of all this and seeing the data come in. And it’s encouraging that this scoreboard is showing up. The scoreboard is teaching us how to live more healthfully. And change the way we behave, change the way we consume stuff to, to move the needle in ways that are meaningful.
So the test is called True Age. You have, , a new algo that just got crunched. A lot of really interesting results that have come of it. We’ll have, , access to the tests here. I highly encourage it. It’s worth having this snapshot. It’s very enlightening. And the science is getting better and better.
And there’s also a look back. I did this, I don’t know, however many years ago, and that data is still relevant because the algos are learning and giving us more [00:54:00] information just on what I did then. And I like to do it every six months. I’m in the space, I’d like to know. But I think it’s just one of the many new innovations that are helping us change this paradigm.
And you’ve been at the forefront of it. Would love to talk about peptides in a future conversation and what you had seen for mitochondrial enhancement and all that. Maybe you could just give a couple nuggets on that before we cut out. Just ’cause you were the guy, you were the peptide guy.
Ryan Smith: Yeah. One of my favorite peptides, I bring back to this mitochondrial conversation. My favorite probably of all peptides is a product called SS 31. And without getting too complex in the mechanism as we get older, our mitochondria get worse. And one of the reasons is that most people have seen a picture of mitochondria where they got that inner mitochondrial membrane, very curved, but like an old t shirt, the more we age, that inner membrane starts to slowly get broken.
This is not hyperbole. This is from a scientific study, which showed that this product, that’s necessarily one, one injection is the daily or the energy equivalent ATP equivalent of six months of daily [00:55:00] endurance training exercise. And again, it’s not hyperbole and by fixing the mitochondria, it’s been shown to help in a variety of things, everything from osteoarthritis to Parkinson’s.
To metabolic syndrome. I think it goes to show you the importance that mitochondria can have, but also how we might be getting close to some really great interventions that could have massive impacts on all of our health,
Dr Pedram Shojai: Thanks for doing the work that you’re doing. I will put links to all the resources that you talked about here. So our listeners can get involved and get going and yeah, true diagnostics. What’s the website so they could see it.
Ryan Smith: Yeah. So it’s true diagnostic. com that’s TRU and diagnostic is singular. But again, if anyone wants to reach out you can connect with us on LinkedIn Twitter or even reach out to us directly via email. My email is Ryan at true diagnostic. com and happy to answer any questions you might have.
Dr Pedram Shojai: Thank you so much.
Hope you enjoyed the show. , Ryan’s doing some great work. Check it out. True diagnostic.com. Get your biological age and then more importantly, figure out [00:56:00] what you can do. To game that number, to bring that number to a place where you are younger. We are at a time right now. In human history where we can start turning that dial.
We know a lot of these lifestyle measures work. We know sulforaphane works. We know a number of interventions are starting to show really, really powerful promise in doing this. I see it all the time with people in our community. People are actually moving the dial on this. Why? Because they’re getting involved. They’re taking away the things that accelerate aging and they are stacking the things that reverse aging and eventually. It starts to tilt the scales.
So what are you waiting for to get older? It’s harder when it is later down the road now is the best time to start doing this work. Check out the temple grounds in the urban monk academy, check out everything in the urban monk academy. Do this testing, do the stuff. That is being [00:57:00] recommended. As you start to join this side of the equation, you start pulling yourself out of the sick care model and you are more and more on the health and wellness side of the ledger.
It’s a much better place to live. We’ll see you there.