DNA epigenetic methylation clocks are becoming the gold standard in longevity for determining biological [as opposed to chronological] age. 

Today we speak with Dr Yelena Budovskaya, CEO of Trume Labs that makes a consumer DNA epigenetic methylation clock for $99. Yelena obtained her Ph.D. in Molecular Genetics at Ohio State University and then studied the genetics of aging at Stanford University, leading her own research program in aging and the effects of genetics, epigenetics, and microbiome on the aging process at The University of Amsterdam.

Health Longevity Secrets show listeners who wish to try The Trume DNA methylation clock on themselves can receive a 20% discount by entering the code DRLUFKIN at the https://trumelabs.com/ website.

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Robert Lufkin  0:00  
Welcome back to the health longevity Secret show with Dr. Robert Lufkin DNA epigenetic methylation clocks are becoming the gold standard in longevity for determining biological as opposed to chronological age. Today we are speaking with Dr. Elaina, Buda Skye, CEO of true mi labs that makes a consumer epigenetic methylation clock for $99. He Elena obtained her PhD in molecular genetics at Ohio State University and then studied the genetics of aging at Stanford University, leading her own research program in aging and the effects of genetics, epigenetics, and the microbiome on the aging process at the University of Amsterdam. Health longevity secrets show listeners who wish to try the true me DNA methylation clock on themselves can receive a 20% discount by entering the code. Dr. Lufkin all caps no space at the true me labs.com website and the link will be in the show notes. Now, please enjoy this interview with Dr. Elena Buda Skaia. Elena, welcome to the show.

Yelena Budovskaya  1:14  
Thank you so much for having me.

Robert Lufkin  1:16  
I can’t wait to dive into DNA epigenetic methylation clocks and and hear about all the work you’re doing and, and and the company as well. But before we do that, maybe you could take a moment and tell us a little bit about how you came to the so interested in this fascinating area?

Yelena Budovskaya  1:41  
Well, um, it’s actually did not start in very early, early age. Although I will start wondering about why do we age like, really, I guess, about age of 14 or so. And the main reason why was because my grandfather, at the moment passed away at the age of 65. And I was thinking, back then, my parents were about 30 Somethings a bit too. And it sounded like way too close. So, and, of course, as a young person, you always think your parents going to live forever, your grandma is always gonna be there. Your grandpa is always going to tell you stories and, and things like that. And that really shocked me. And I was wondering, like, why did he not entirely why he died by Why did his last maybe five years of his life was so miserable. And 65 was very young. And then I’ve learned that my other grandfather on my father’s side, actually died in the age of 55. And back then I grew up in Soviet Union. So nobody thought twice about this, because we want a big war. And a lot of men went to war and they came in injured and, and a lot of people just were happy to have as many years as they possibly can get from that generation. So to me, that was kind of shocking. And as I was interested in biology already, then I was wondering, like, why why do we have to eat? Why does it even have to start in the first place? And then why for such a developed country, and they always consider it to be developed country. We live so short, compared to other Western world world. And of course, at first, I didn’t think about diet, we were going through transition and all the kind of crash of Soviet Union and perestroika and everything. It was not about that it was just, I thought it was genetics. I honestly thought it was genetic program. So I went to university and studied biochemistry actually, in genetics quite. I get started doing my PhD, and I noticed that everybody’s looking at what’s cancer. So how to cure cancer, how to cure diseases. But indeed, aging is actually sort of a cause for most of the diseases that we’re trying to cure. So I thought maybe it’s worthwhile to look at the coast. So if we can cure aging, we can cure the diseases. So one, one bird with one shadow with the phrases. So that’s why I joined the NI actually purposefully when to study this process was Stuart came because he was doing at that time, he was one of the few people who was using genomics and studying aging. So I thought, I want to look at everything and how the whole process changes when the animal goes from young to old. And that’s Probably that’s kind of where the first interest started that. And the clocks in particular.

Robert Lufkin  5:06  
Yeah. Oh, interesting. So, clocks. Let’s talk about clocks. Clocks are becoming fundamental for longevity research. And can you tell us what is a clock? And why are they so important for for longevity research?

Yelena Budovskaya  5:30  
Well, before clocks, maybe I can do two sentences about why we even started searching and digging that area. So if you think about any disease, any processes studying, you always need a marker that to measure. So if you go to the physical exam, the doctors measure glucose level to list rights. And it’s kind of like a picture of your physiology, right? Do you have diabetes? Do you have high cholesterol? Do you have inflammation? They might measure CRP, so and then they can correct it. We cannot correct it unless we measure. And for a long time, the only measurement of LGBT was how long would you live your maximum median lifespan, which we have to pretty much let you live and and wait until you die. So the human population, one experiment would be a lifetime of one individual right? So you will never put more than one experiment and you probably will not end you have to guess how to split the group. Which one is a healthy aging cohorts and which one is not a healthy aging cohort. So it was clear to me if I ever want to do experiment, human, I need a biomarker of aging. And then we learned about all the biomarkers and blood. So the same story we counted all this red blood cells, white blood cells, every kind of some markers for liver function, kidney function, and we have this physiological clock that you can do like I think you can put finger age measures like 10 biomarkers, and based on that predicts biological age.

Robert Lufkin  7:25  
Oh, excuse me, that’s that’s Finn LH from Morgan Levine. Right? Yeah, they will put a link to that in in our show notes for for our audience, and they can enter those values. And and, you know, ah,

Yelena Budovskaya  7:39  
yeah, it’s actually available online, this will be like, I think it’s interesting. A lot of all customers do that. And just sort of compare it side by side. And of course, in developing that, we, like the first person kind of pioneered all this was Steven horbat, who great mathematician just took all kinds of methylation datasets, and start looking through how different tissues are aging. And if he can predict the biological age, or chronological age based on this methylation profiles, and I think a lot of scientists these days use that clock to in their experiments. And I really like this two lines of work, like measuring biological age based on blood biomarkers, and the DNA methylation, they provide kind of two different pictures on the same process. And because DNA methylation is so tightly kind of bound into our physiology, because a lot of what we eat, what we do, how we exercise, what lifestyle do we lead is actually reflected in our basic metabolism and basic metabolism influences DNA methylation. And DNA methylation is sort of like a really quick and dirty mechanism for the for the cell to regulate its activity. So all the material groups that get produced it’s like markers that cells very easily can put in the right places and right time quickly regulating up or down gene expression and therefore regulating this physiology. So

Robert Lufkin  9:16  
is it fair to say then, the the genetic suite, our genetic code we get from our our parents and our ancestors, but our epigenetic modifications through DNA methylation is one of the three types we get from our lifetime experiences our lifestyle choices that that and we can we could change that through our lifestyle

Yelena Budovskaya  9:45  
in the way in the way Yes, I believe we can. I think a lot of even didn’t even methylation in part would do inherit, because it’s does write down like the body. kind of already have an information For example, what your mom were doing during pregnancy or what’s your ancestors did in the previous and previous generations. But I think that it’s changes. It’s much more fluid than genetics. Genetics is kind of a blueprint of your of your life, if I may use this analogy. And epigenetics is something like add ons that you putting in by living your life, even healthy way or not to healthy way or if you’re doing right things, so not right, not so right things, I guess. And I think we can manipulate our epigenetics and we can hopefully, we can learn more and more about it. So it’s very young field. It’s, I would say we know, very little we don’t know more than we know. But we started building this new biomarker said this, like with AP genetics clocks is one of them. But there are also panels for detecting diseases and looking at a different metabolic and physiological states. I think it’s, it’s just way in the beginning before like, we really use it in a full capacity, I would say.

Robert Lufkin  11:23  
Yeah, and the the methylation being affected by the grandparents we just had Judah Finlayson is on the program who is written a book with a great title of you are what your grandparents ate, but it basically deals with epigenetic modifications in utero passed on essentially two generations. They’re the the, the DNA methylation that we’re talking about, how does that compare to other types of clocks for aging, such as telomeres? We hear about protein omics glycan ation what what are those measuring? And how do they compare with DNA methylation?

Yelena Budovskaya  12:19  
So I guess the most seamless one is, of course, telomeres, just because they’ve been around for so long. And it’s been shown like long time ago that telomeres are shortening as we grow old. And that was one of the hypotheses that when telomere shortening, become very critical, that the whole, it triggers the process of the whole body kind of decomposition in some way or the kind of destruction. However, it’s been shown that say is, it does correlate for sure. But at the same time, there was the processes that we clearly think that define aging process do not lead to telomere shortening. And one of them, I think, I read an article somewhere that some processes like diabetes, for example, we know that people with diabetes really, like they need to control their sugar and level insulin levels and everything. And a lot of them are measuring their telomere length. And telomere length was not predictive of the accelerated aging process, like for example. So I think the potential there was great, and it might be also depending on like, what tissue you measure. So a lot of times the telomeres are measured in leukocytes and blood. And a lot of and maybe that’s the problem, maybe leukocytes, telomere shortening is not really, as conducted, like, as doesn’t demonstrate that widely, how fast or how slow the aging. But I think the major problem here was and this is why I’m not really criticizing it too much. And I really would like to actually compare it side by side. I believe that every time we develop a new clock, we don’t do that comparative studies against all the other clocks that already exist. And I would really love to see that happening because I feel like every clock has their own space in the field. Like for example, telomere shortening might show some aspect of cell aging. And then Stanford was developed. As you mentioned, the biological clock based on a protein proteomics when they took the blood from healthy individuals and into of different and ages, and then we’re trying to predict the biological age. So again, it requires a lot of work of mass spectrometry to identify all the proteins, but it looks very promising, because it’s based on exactly like composition, it’s kind of downstream of your genome genetics, it’s what actually been produced or proteins been produced, in, in which form they exist in your body. And then another clock was based on microbiome, which recalled another the second brain of our bodies, and actually microbes do outnumber us tend to 10 to one. So it would be foolish to to exclude them from the clocks. And there is a different companies deploy longevity, as well as VIOME develop their own biological clocks based on microbiome. And they also can predict biological age for ascribe a prediction based on what your microbial composition of your gut and of course, biological clocks based on DNA methylation, so we have Fenner age that just talked about, then there is a Horvath clock that some companies actually offering to their customers. So they’re looking at about 356 sites on your DNA for methylation. There is a illicium health just thrown out there. Panel, it’s based on back Levine’s clock that I was just talking about, it’s FNH. Also, the look at DNA methylation of over 1000 fragments. And of course, science went even further becoming reybold and trying to predict your mortality, and also the day kind of time to death with this creamy chicken. Yes, yes.

And I apologize if I did not mention some other clots here. But as many of them so I think consumers and and scientists these days have great variety of clocks to work with and see which one is best, but I would really love like to actually compare them all against each other and see the strong and weak points of each of them. So we can actually have a very good make a very good decision of which one to use, and which experiments and, and how.

Robert Lufkin  17:31  
So each of the clocks that we have available. And we have many different types of many different technologies seem to look at a different aspect of aging, and that they may reflect upstream effects or downstream effects of the aging. And that’s going to be important when we apply them to ourselves or to research. Now, sort of focusing on DNA methylation clocks, in particular, the DNA methylation is is a process which when I first when I first began learning about it, I thought of it just as kind of aging, it’s sort of like rusting metal, acquiring more and more of these, but as I understand it, now, it’s much more much more nuanced in the sense that met methylation doesn’t necessarily change with aging, but rather just the locations of the methylation. So it’s not that methylation per se is bad, but it’s the particularly the location are bad, but I mean, associated with increased age, but it’s rather the the specific locations of the methyl groups and the methylation that occurs on the DNA is Zack, correct?

Yelena Budovskaya  18:48  
Yes, it’s absolutely correct. Actually, methylation is very good for you. It’s super useful. And we inherited through our ancestors, a lot of this sites where a lot of methylation happen. And those sites have very repetitive sequences. And it’s actually they have to be protected by methylation from recombination or from the a lot of transposable elements sitting there. So the jump out and start modifying a genome that was shown to be causing like a lot of age related diseases like cancers. So you should not be thinking about a global methylation as a bad thing. Absolutely not. Yeah,

Robert Lufkin  19:41  
and in fact, removing methylation or winding back epigenetic effects like using like Yamanaka factors, or something to do that will actually return this the cells to a stem cell state which is something we’ll differentiate the cells in which is something we necessarily don’t want to do. Although David Sinclair’s doing some interesting work with the with the mouse model that he just published with a vision loss and then the Oh SK Yamanaka factors. But that’s a whole nother area there. Yeah. So I’ve heard methylation clocks are referred to as like Steve Horvath clock, his initial one as a sort of a first generation clock that was very analogous to chronological age, which, while it may have a lot of applications in forensics, for example, it’s not really that valuable necessarily on longevity, because chronological age, you can just get from your driver’s license by looking at your birthday. But but the but then the second generation clocks, we’re seeing now sort of like grim age from from his group also, and others are, are more valuable because they they reflect biological markers of aging, and then more closely respond to interventions and everything as well. How does the clock your that you developed, fit into this whole thing? And how was it developed with your with your company?

Yelena Budovskaya  21:23  
Yeah. So when we started, they said, looking at the biological clocks, we had three main ideas in mind. So I did want to do biological clock of being very robust, and predict your healthy age, let’s put it this way, as accurately as possible, it should not be an should be an expensive to do, because we’ve been pretty much two scientists starting up the company with pretty much zero money. So we wanted to make sure that we can do it ourselves and managed to process samples accurately. And it has to be very easy to collect the painless for the customers to, to submit a sample. So saliva was an obvious choice from the beginning. Because I didn’t know you being a doctor, you probably I don’t know how much attention to pictures, but I know I’m on my friends, they dreading to go give blood tests.

Robert Lufkin  22:37  
So needles to

Yelena Budovskaya  22:39  
they don’t like needles. And for me, this test in the beginning, I did not think about this. No, I wanted to be as serious as possible. But I did not want people to go through stress of giving blood because they knew they will not retest. And that was the point of following up your aging process throughout your life, like every four to six months, you re measure your biological clock, to see how well you’re doing when you’re changing diet, or you start new supplements that somebody recommended to you or things like that. So the first thing we looked at, as I pulled all the datasets that were associated with aging process, so there are gene expression that changes during normal aging. And we try to look as many markers as we possibly can and genes as possible, again, just to see if we can get some kind of tissue, you know, like crosswave, the same sets that are reacting similar across multiple tissues. So that presented a little bit of a problem. But we managed to, to settle on from publications, just calm a lot of publications and and found about 400 Something genes that we settled on. And then of course, there was a lot of methylation studies published by that day. So again, we pulled all the publicly available datasets, and now I was a target in mind. I thought that if the methylation side would be relevant, we put in another constraint. So that

Robert Lufkin  24:29  
those excuse me, were those 400 sites similar to the the I guess, I think it was around 300 sites for Steve Horvath initial clock.

Yelena Budovskaya  24:39  
I wasn’t looking at that at the time. Oh, actually, because we wanted to be sort of independent and the reason for that, why not looking. So at that time was started. I started seeing a lot of publications come in saying that The sites would still be used, he is very on. Control not controlled. I’m looking for the word here, sort of mathematically. He approached it from mathematical point of view, he just looked at everything and revised his model. And a lot of sites, and I heard it from scientists who use this clock, a lot of sites lended in the dark areas of genome. So it’s, it’s intergenic region that we do not know if they’re associated with some genes or not. But they seem to be weighing in and his clock and predicting your age. So I want it to be more biologically significant process. So that’s why we started with age regulated genes. And I didn’t map it to his clock on purpose, like I thought, okay, let’s just go through this exercise and see what we found. Just so we put a constraint. So of course, every gene has multiple methylation side multiple, we call this CPG islands where the methylation actually happen and already been mapped. So we only selected those that were in the promoter region, because we wanted to see if it’s actually regulating this gene expression, or might be regulating gene expression. And I think on the first path, we also did, maybe first axon, because sometimes regulatory elements within like when, within the first kind of part of the gene, when the very beginning shown to be the most important one. But that was a little stretch, we wanted to stay in the promoters, but we kind of lacked just include bigger dataset. And then we look through a lot of published data just to see if those sites which of those sites change the most across different population. And we had studies from all over the world. So we had a Korean study published, like we pulled in, and several study from Great Britain that they had also, different nationalities of people submitted their samples. And that was the first kind of pass where we identified about 29 sites that we wanted to pursue further. And very quickly, we realized that 29 was not doable for a bootstrap company. So we settled on nine, that was really huge, like, very doable for us at the moment, and we thought, we’re gonna, and we picked nine that were that shown the biggest effect. So we thought, okay, we’ll start with nine, tested on healthy population tested, and then roll it out as a first kind of minimal viable product, see how people do how they test. And we’ll iterate, adjust, and then slowly introduce the rest of the clocks back in. So first, we tested on the published again, published data, it’s looked pretty promising. So we had our variation from chronological age of healthy individual. That was from published data that was recruited through the hospitals. So we assume that those were seen by the doctors and declared healthy was about 4.6 4.5 4.6 years deviation. So we’re like, okay, that’s less looks good. And then we start just calling friends and family, everybody who can spit in the tube, and, and give us a sample. So we got grown. About first, but 200 data points we got like that.

Again, we’ll look to a nice, so we thought, okay, maybe we should roll it out right now as a kitten, and see how it will behave with the wider population when we don’t know whether or not they’ve been healthy or sick or anything. And, and plan to kind of adjust accordingly as we go. So that’s where we kind of how we started. So now our test is nine sites is by some saliva, actually, by last count. Our division was 3.8 years. So we improved our algorithm. Yeah. And now hopefully, we can. I’m very excited to see if we can start testing the rest of the site soon. And incorporating our clock.

Robert Lufkin  29:41  
Yeah. Are there are how many other sites would you like to leave? Would you like to incorporate ideally, or what would the rest of the sites look like? How many more is that?

Yelena Budovskaya  29:52  
So it’s, it’s about I think it’s about 10 regions. And altogether, the whole set would be about 32 sites. And so did you methylation sites? So hopefully it’s, yeah, hopefully it’s going to be easy to roll out. But we’ll, we’ll have to change our platform, we will probably go more next generation sequencing, because that will not be able to accommodate that many people.

Robert Lufkin  30:29  
What’s the timeframe for that area? Is that how soon do you think?

Yelena Budovskaya  30:36  
Well, we hopefully will start testing, hopefully, by the New Year. And then as soon as we have a decent validation report, so I, I want to say spring, but I don’t want to rush into it. I’ve wanted to be solid before we roll it out.

Robert Lufkin  31:00  
Just to be clear, the the system is currently in use i I’ve actually tried it myself. Here’s the package it’s it’s it’s something that you just provide saliva actually onto the paper, you don’t it’s not even a tube and you mail that in it’s very convenient to use for that. Of the of the sites you’re looking at now, are they more or less sensitive to any particular diseases or groups of diseases? Or is it just sort of overall overall longevity?

Yelena Budovskaya  31:35  
No, it’s overall longevity. Some of the, like, I can tell you, like one of the regions that we’re looking at is associated with integrants proteins and integrants are apparently we haven’t looked at gene expression a level yet. So we’re planning on doing that. But integrins are a key part of our skin structure kind of proteins them involved in wound healing and, and wrinkling our skin and tied up in the whole like biological matrix kind of skin village comedic has functions. So we have the fact that one of our sites is actually my be regulating a skin aging is looked promising, especially after we tried to be as unbiased and selection of the sides as possible. So that’s, like, I cannot disclose without the lawyers being after me. Exactly. All the sites but yet, but hopefully, hopefully soon. But yeah, we we did they have all the regions and all the sites are very much biologically active, relevant. They’re not associated, as far as I know, with any diseases, although they might. I know, for the fact that they do change the expression in different diseases, like we briefly tested the set on, again, published data from cancer patients. And we did see like increase in biological agents for some cancers, not within test and fall, so I cannot claim everything yet. And I know that some of the patients did disclose that they have macular sclerosis. So I know that biological biologically, they’re much older that they should be although they’ve been doing it pretty well. So it’s kind of we’re really hopeful that it will work well, and if we’re expended, they will work even better. So, but again, we don’t try to predict the disease. We’re just trying to predict how well your body’s doing at the moment.

Robert Lufkin  34:03  
So now we have we have clocks. We have a variety of clocks. In particular, we have epigenetic DNA methylation clocks, and we have a a low cost consumer version that’s that’s accessible to people. Do you think that these these DNA methylation clocks will be is it possible to reverse or lower the biological age as measured by these clocks through things like lifestyle interventions and such?

Yelena Budovskaya  34:38  
Apparently, you can, um, I, I we have so few very early adopters of this of this technology. So I want to mention this when we first launched it. We were proposing it to Well, it was a direct to consumer product. And we wanted to go direct to consumers, right. But we also did make a bid for a couple of companies that sell either supplements or some kind of nutritional products that’s supposed to help you healthy aging. And we had a very difficult sell to the companies in the beginning, because the, the whole point of this was us selling a supplement I want. Everybody admits that there is no shoe that fits everybody, right. So there is some treatment will fit one person in less than other treatment will not fit another person. So we offering your customers a kind of a window into their health is this working or not working so they can give it a time tested. And then if it doesn’t work for them, quit and go, and maybe change the supplementation, change their lifestyle, do something else about their health. And it didn’t go with the pharmacy supplement companies, it didn’t go very well in the beginning. And then we did made a very, like probably the best partnership ever responsibly on health. And they were rolling out the supplement Coleridge wanted calcium, Alpha ketoglutarate supplement. And they were really interested to actually offer the there was so confident in their product that they were really interested in their the customers to get the steps. And at first answer a question I actually did warn them I said, I think in the best case scenario, we should expect not to see lifespan extension, or reversal biological age, I think in the best, what we will do, we will see a slowing down aging clock and your customers will not age at all. So they agreed to that, that we’ll take that. And we rolled out the program. And surprisingly, so now it’s been two years since we’re partnering. And I can see that I do see the if the customers respond very well to their supplementation, we do see reversal of their biological clock. So we do see that. And they did test by other biomarkers. So they did measure their blood, some blood biomarkers. And they do see the improvements in overall health when they taking alpha ketoglutarate. So that was at least a I can see that the clock is working. So we’re predicting their biological age and the starts. And it looks like the biological clock does correlate with some other blood biomarkers in the in the in at least those customers. And we also did like comparison with Horvath clock with other company that selling it more expensive clock. Unfortunately, we can only afford like 10 samples. But we’ve got to like pretty well with another clocks as well. So we usually predict a little older than Holloway clog does. But I’m actually in right now and our couple of our current customers do measure using our clocks and Horvath clocks. And they see that trend is similar. So it makes me feel better that we’re in agreement with with kind of a gold standards out there. So yeah, and I think since Honestly, all the more and more companies are enrolling in this program, and I’m actually very excited about that, because I think they’re providing great value for their customers. By showing that look, we are actually not just sell your product, we’re actually genuinely thinking that you should know how well you’re doing by taking it and and and find your best therapy for an eye for aging.

Robert Lufkin  39:16  
Yeah, it’s exciting that that you’re finding you can slow down the biological clock with these interventions or even some people even reporting reversing it. Over the two years did you notice did the effects slow down at all? Because obviously when you get to reversing your biological clock, you know, I’ll reverse it to you know, you know, I you don’t want to reverse it too far. You know, I’ll take 40 I’ll take 30 I’ll take 20 I don’t necessarily want to go back to 15. Or that’s really possible but But it’s interesting when you talk about reversing biological age. Does it slow down if you notice it to your period, did you were you able to see that effect at all? And?

Yelena Budovskaya  40:03  
Yes, it does. The customers that are taking, I don’t know, if they disappointed us, as much as I see, like, initially, they start doing something, if it works, it drops very fast. Let’s say buy five, six, sometimes over 10 years, and then it stays there. And I know some of them try to even lower it further. And it doesn’t work. And it’s again, it’s, I think it’s super interesting. Why not? Why if you lower your biological age to, let’s say, 46? You cannot get any younger than that. So is it your limit? Or? Or maybe it’s like this healthy steady state, that we should be focusing on maintaining rather than continuing lowing down a biological clock.

Robert Lufkin  40:57  
So that’s yeah, that’s That’s it. I agree, thought the idea of sort of a steady state that we return to, but doesn’t necessarily we don’t, ideally roll it back continually. And then like you touched on, very key question, if we reverse the clock, or slow down the clock, does that truly affect any underlying aging process because I’m, I’m broadcasting here from Southern California where people have been reversing their biological phenotypical clocks, many years, I mean, many, many times and things like you know, dyeing their hair, their gray hair, black, makes them look younger by that clock, or Botox injections for wrinkles, makes their skin look younger. But at a fundamental level, it doesn’t really change anything, but it appears there’s growing evidence, or there’s evidence accumulating that that reversing these DNA methylation and other physiological clocks can actually reflect significant things about a effects on longevity.

Yelena Budovskaya  42:09  
Yeah, yeah, I heard. Well, of course, the growing number of published data showing that also, people recently, for example, was a paper published that a certain diets, like for example, reaching polyphenols, people went on their diets, start exercising start changing something in their general lifestyle and behavior. And they did get biological, younger, biologically younger, but they also provided some other biomarkers where they’re measuring other aspects of their aging. And they also saw an improvement. So this is actually where we going. Hopefully, we will go next. And I’d really like to do more like sort of clinical trial study, like whether or not if we take so for example, in a cohort that we already have, when we take a person who self reported poor, general health, start doing some intervention, whether or not the ticking artifact was a good rate, or they went for a diet diet, or they did intermediate fasting, or something else. And they saw a dramatic improvement, and we look at their biological clock dropped down more than 12 years, actually, we do have even policy or we automatically retest you if you test too young or too old, just to make sure that we actually showing you the Ergotron biological age. And and then this, this person over sudden reports that they feeling good. I know it’s it’s subjective. I understand that. It’s just their feeling how they evaluate their biological health, right. It’s one of the metrics and I feel like, of course, there is an effect of placebo. It could not get away from it. But I think of the person really feels better. That’s a good indication that something might be working in the right direction. Yes,

Robert Lufkin  44:19  
yes. Yes. And we interviewed on this program. Dr. Lucia, Ronica, from Stanford, who is working with low carb diets and and some type of fasting to show reversal of DNA methylation, epigenetic clocks, and also another clinician on the East Coast. Kara Fitzgerald is enrolled patients in her study and involved dietary changes typically, ketogenic diets or low carb diets and then fasting as well as her program had exercise and some sleep things too. But she showed three over three years reversal of epigenetic age as measured by the clock they use. They were using a grim age type clock. But but that was only after eight weeks of intervention in their patients. And that was a randomized controlled trial is the pilot study of only only 40 patients, I believe, but but at least it it shows the possibilities of what this what this technology can do. Okay, so it’s it’s particularly great that now individuals can get access to DNA methylation clocks through companies like yours for you know, affordable prices, if they want to begin following their own their own lifestyle there. And speaking of lifestyle, now with all your your expertise in in DNA methylation and genetics and epigenetics, and how has this informed your own personal lifestyle choices, Elena for how you live your life?

Yelena Budovskaya  46:11  
I’m actually quite a bit surprisingly, because, well, I’m going to full disclosure, I guess, I am, I have been struggling all my life with obesity, and it’s genetic. Sort of I’m going against my genes here. And I have to say that, at some point, you do buy into all this diet and hype, I guess. And when we developed the test, this was the first thing I was I decided to test. So I recruited several my friends who are in different, very different kind of body composition. And we decided to test the ketogenic diet, I was determined that seeing all this people not just slimming down and losing weight, but also claiming to improve conditions that chronic conditions that they developed, I thought it must work. It’s like, look at this, this is such a great body of evidence like I should try. And again, I have to say like I’m, clinically, I’m absolutely healthy person, so decided to go anyway, and then died. So obesity being the only issue here. And I measured my biological age before and after an after about actual 12 weeks first measurement for us. And so in the beginning, I was about two years older than my biological age. And I was like, well make sense. Well, probably I’m as old as I am. So obesity did not affect my age quite yet. So when in 12 weeks diet measured again, and I become seven years older. And I started thinking about, I didn’t quit the diet quite yet. I thought, okay, I lost so much weight, and it must be doing in my probably ignited some stress response, sir. So digging into what other biomarkers, I could measure to see if my biological age was, indeed much older. So I actually turned out to be in that point in my life, I was also very much interested in microbiome, and I still am, but then I actually worked for a company that were doing microbiome testing. So I decided to test my microbiome. And my diversity went down quite a bit. And I tested with a different company. And that point was very young company. While right now they’re probably one of the best in the market, and I use them a lot. And the same story, they showed me that my diversity and micro micro flora goes down dramatically. So I tried ketogenic plant based diet, I become even two years older than that. And diversity improved a little bit but again, it was not as good as it was before. So I quit that nonsense and and when back to like more plant based diet and practice, intermediate started doing intermediate fasting. Well, probably not fast, long enough to pack my weight as much. But my definitely my health improved quite a bit and my diversity of my microbiome improved a lot. And I’m right now actually, five years younger than my biological age, surprisingly,

Robert Lufkin  49:56  
fasting not not yet i per se just controlling when you eat, not what you eat, is it right,

Yelena Budovskaya  50:03  
I do not eat that much of red meat. Although it’s, it’s hard for me, I guess I’m also this is another thing, a lot of people just jump into which terian kind of lifestyle. Again, measuring your biomarkers, you can find out you cannot like I cannot be utilitarian. I cannot, for some reason absorb iron from anything but red meat. But eating red meat maybe once a month is more than sufficient for me to keep my healthier iron levels. But yeah, I’m trying to be more like Mediterranean type of diet. So more fish, vegetables, less meat. But yeah, I try not to stress too much what I eat, just eat good food cook as much as I can at home. And then I just practice intermediate fasting. So that’s kind of what I do

Robert Lufkin  51:04  
any, any particular supplements or drugs that you recommend?

Yelena Budovskaya  51:10  
Um, so I do. Again, I tried to satisfy my second brain. So I do follow right now all the recommendation that VIOME give me just test it out and see how it works. I experiment all the time, actually on on that. And I do take alpha ketoglutarate. So I do I start taking that as well. Just because I wanted to we see such a great results that I wanted to test it on myself. So that’s the only two things I’m doing

Robert Lufkin  51:48  
with your interest in longevity, so so no, na D supplements or it’s very trawl or Metformin or rapamycin. No, it sounds like what you’re doing is working for you as it is. That’s That’s great. Yeah, what what has been any any? What’s the most impactful thing you’ve done? Do you think to improve your, your your health, overall with your lifestyle?

Yelena Budovskaya  52:15  
Well, this is was this surprising that this combination of looking after your kind of second brain and looking after ending intermediate fasting, so far, it’s been really impactful, I still had need to measure the the effect of alpha ketoglutarate And my help, like it’s still coming up. I just, I did it before but I recently kind of introduced it again and to my regimen. I feel that same positive, also having an exciting life. And like for me it was developing something new and kind of using my brain also to kind of develop a new tests, or new ways of where we going with this empowering people. I think it’s kind of gives me purpose in life and also satisfying my social circle and social interaction. I feel like we maybe focus sometimes a little bit too much on what to what to do to extend our healthy years. And with pharmaceuticals, I think we should more like listen to your body, listen to our body and kind of listen to what it tells you and go with that. So that’s what I’m I don’t know, I think that’s when I stopped worrying too much about, like excessive stress at work or something like that, and just do what I enjoy. I think my lifestyle improved quite a bit.

Robert Lufkin  54:01  
That’s That’s great advice. How can people follow you on social media? Or can you give us the website of your company?

Yelena Budovskaya  54:11  
So yes, the website is to me labs.com And without www in the beginning, just dreamy labs.com. And we also have a true me labs group on Facebook and Instagram, where we’re trying to find the gist right now published you things that we find that our customers sharing with us and what’s affecting aging, and how well they feel or maybe current studies trying to report on that as well. We should be more I should be more active on social media so for sure, but we’re very responsive. So if you have any questions, we will answer any questions you got either through our website or through social media channels. So, yeah, and hopefully more will come soon. So we just growing our team. And I hope that as a scientist will grow more products and go to the next level, the marketing team would actually be reporting on that and keeping our customers up to date.

Robert Lufkin  55:25  
Thank you so much, Elena. It was great to be able to spend an hour with you here today and hear about the exciting work you’re doing and and the work that you’re doing with your company as well. And I look forward to staying in touch and and hearing about the new developments coming in the in the new year. Just Yes,

Yelena Budovskaya  55:47  
yes, absolutely. Thank you so much for inviting me it was very nice to do glad to

Unknown Speaker  55:53  
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