Discovering Your True Age with Epigenetics – Featuring Hannah Went of Tru Diagnostics

Episode Summary: In this episode, we dive deep into the fascinating world of epigenetics with Hannah Went, co-founder of Tru Diagnostics. Hannah shares her journey from the world of peptides to pioneering epigenetic testing. We explore how these tests, developed in collaboration with prestigious institutions like Harvard, can reveal your true biological age, offering insights into how your environment and lifestyle impact your genetic expression.

Key Topics Discussed:

  • Introduction to Epigenetics: What epigenetics is and how it affects your genes’ configuration (which ones are turned on or off).
  • Tru Diagnostics: The founding and mission of Tru Diagnostics, and their cutting-edge epigenetic testing.
  • Chronological Age vs. Biological Age: Understanding the difference and how Tru Diagnostics can help you determine your true age.
  • Impact of Environment on Epigenetics: How lifestyle, environment, and even ancestral factors (like your grandmother’s behavior during pregnancy) influence your epigenetics.
  • Peptides and GLP-1 Medications: Hannah’s background in peptides, the nature of GLP-1 medications, and ongoing research in this area.
  • Personal Experience with Tru Diagnostics: Host’s personal experience with Tru Diagnostics testing and the anticipation of retesting to track changes in biological age.

Guest Bio: Hannah Went is the co-founder of Tru Diagnostics, a company she started in 2020. With a background in peptides and a passion for understanding aging, Hannah has dedicated herself to developing innovative epigenetic testing that helps individuals understand their true biological age and how it can be influenced by various factors.

Resources Mentioned:

  • Tru Diagnostics
  • Epigenetic testing and its collaboration with Harvard
  • Information on GLP-1 medications and peptide research

Call to Action:

  • Check out Tru Diagnostics’ testing to discover your true biological age.
  • If you have questions for Hannah Went or want to learn more, visit the Tru Diagnostics website.
  • Don’t forget to retest to monitor changes in your biological age over time.

Connect with Us:

  • Visit our website for more episodes and information.
  • Follow us on social media for updates and health tips.
  • Subscribe to our podcast and leave a review!

Ready to dive in? Listen here.

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Hey everyone and welcome back to the Empower Nutrition Podcast. This episode was on my steal favorite topic, which is epigenetics. And if you don’t know what that is, we’re gonna talk all about it. But my guest is Hannah Went, who really blows my mind. She’s a low key genius who has, we’ll talk about her background quite a bit in the episode, but she started a company called True Diagnostics in 2020, and it’s really impressive what they’ve done. They basically make testing that uses epigenetic algorithms that are created and coordinate in combination with institutions like Harvard that basically translate the epigenetics, meaning the configuration of your genes, which ones are turned off on and off, and translates that into a report that is specifically around aging. So you probably heard people talk about, oh, this is my, I know sure my age by my birthday is X, but my true age is Y.
And that’s what this testing does, is it lets you see what your really internal or true age is, because we actually do age at different paces, but depending on, again, our epigenetics, which are largely impacted by our environment. But I really like how we talked about there is a limit to how much you can change your epigenetics. And some of it is a little bit more hardwired from really fascinating things like what your mother may have done when you were pre, when she was pregnant with you, or even your grandma did when she was pregnant with your mom. So it’s, it’s just like a really fascinating topic. And we also get a little bit into kind of how she got into this was from the world of peptides. And so we talked a little bit about GLP one medications, how they are peptides, and how they’re doing some research around GLP one medications. I can’t wait to see. So I hope you enjoy this episode with Hannah Went and, and really I recommend checking out true diagnostics testing I’ve done on myself, and I am actually ordering my retest today as well. So I can’t wait to see how my biological age is shifting over time. And I hope you enjoy hearing about this testing. And definitely if you have questions for her, check them out and we’ll put all the details in the show notes. Enjoy.
Hi Hannah. We’re so happy to have you on the Empowered Nutrition Podcast. Welcome.
Hey, Erin, thanks for having me. I’m excited to chat with you today.
Same, this is secretly my favorite topic. I am fascinated completely by epigenetics, which we’ll talk about what that even means. But before we get too crazy with that, maybe you can just share a little bit with our audience about your background and how you got into this space.
Yeah, definitely. So I’m excited for everyone who’s, who’s listening. I come from, you know, a background of biology entrepreneurship, which is kind of odd because no one in my family ever was, you know, they were all more like business oriented, which I guess that’s, you know, may align with the, the entrepreneur type of spirit. Yeah. But I’ve always been yeah. Interested in, you know, how the body works science. So I originally am from, from Ohio, came to University of Kentucky to do my undergrad and took a really interesting position afterwards, was gonna, you know, take a year off school and actually go back to, to grad school, but ended up really working at this pharmacy in the compounding space that specialized in unique peptide production. Mm. And that was a big turning point in my career just because that’s when I first realized there’s this entirely different health system out there, rather than the traditional one, which everyone who’s like in our space, Erin, I see you shaking your head, goes through this like, you know, moment in their career where they’re like, aha, you know, there’s more than just that sit care model.
So that’s where I really, you know, became interested in this all cash pay, integrative, functional, you know, anti-aging space, if you will. And we really then created my company now true diagnostic that specializes in, you know, epigenetic DNA methylation testing that we’ll get into, but on, on, on the entire premise that we needed more quantitative data behind how those peptide peptides really worked and really tested that with the biggest risk factor that we still know today being aging. Right? How can we measure aging and, and kind of slow that down and use those peptide and, and pharmacy products in order to do that. So, fast forward from 2019, you know, up until, you know, 20, 24 up until now, so that was five years ago. We, we sold the, the pharmacy Yeah. Back in, in 2019, and then solely started focusing on true diagnostic and creating these predictors really for overall health, which has been such a, a fun journey.
Yeah. I mean, it’s so impressive. I mean, especially because I feel like, I first heard about you a few years ago, and I think it was from like Mark Hyman at a, at the con at this conference I was at. So like somehow within a couple years you had Mark Hyman using your test. So good job.
Yeah. Thank you. Thank you. I know we’ve, we’ve known each other for, you know, quite some time. It, it seems like Erin and our past have have crossed, which is always a Yeah. Good. Nice to, to catch up. I think, wasn’t he at maybe the IHS conference?
It was that, yeah.
Yeah. We had a ton of people reach out afterwards like, oh, mark Hyman’s using the test and Yeah. Yeah. Not, not sponsored at all, all just again, I think, you know, stays on the cutting edge
Outcomes and you know, what’s available. And maybe believe that our testing fell within that realm at that point, which was awesome. Yeah. And he continues, yeah. Yeah. To I think be, be a big advocate just for, you know, aging longevity in general.
Yeah. I, and I had, I didn’t realize that you had kind of started in the world of peptides, which is makes sense because that can be one of the most powerful uses of peptides and as around aging. And we could even, I think it’s like people might not realize how much peptides have come to the center in the sense of GLP one medications. I think a lot of people don’t realize that those are peptides as well. And like we’re starting to see some signs that they may have, aside from obvious metabolic impacts, they might have a, they like definitely impact all over the brain. And there’s some early research around like dementia and, and GLP one medications and pain is another big thing I’m seeing. So peptides are really powerful, but I could see how if you’re in the world of peptides, it’s, it’s a little shady. It’s a little confusing, it’s a little unclear what to do. And so maybe that, tell me if I’m imagining this, but maybe that’s kind of where this part of where this idea came from of like, well, what if we had some tests that would kind of tell us like who needs peptides and potentially like what kind of peptide?
Yeah. You know, you’re exactly right. And that’s kind of why we got out of the space. We were actually the fastest healthcare grow healthcare company in the, in the no fastest healthcare Yeah. Company in the state of Kentucky, fourth fastest in the nation actually when we had that pharmacy. But it was a compounding pharmacy, right? So we were able to do things that were not FDA approved and got a lot of backlash for just how quickly we were growing and those who are still getting compounded peptides. There are a lot of different rules and regulations now.
Yeah. I think the FDA is really locking this down. Yeah,
Yeah, you’re right. Like Semaglutide is gonna be one of those peptides again, you know, that’s gonna be commercialized in a different way. So, so it’s interesting. I mean, regardless, and I think with everything you can make the argument, we just need more data, we need more tests, we need more information behind them. We do have a really cool clinical trial we’re doing right now. We did it, you know, kind of an, an internal trial with the GLP ones with some of our healthcare providers and how that’s affecting aging. But we’re doing a larger one even with Cornell University right now, with thousands, thousands of subjects to see how these markers we’re measuring and, you know, biological aging is actually changing with those GLP ones. So I’m really excited for that one.
Same. Yeah, same. I am too. Gosh, I’m so tempted to just really go deep on this, but I’m, I’m gonna, I’m gonna hold back because I think we need to take, tell people about your test. Let’s talk about maybe just overview, and I’m sure you have a whole spiel on it, but tell us about your test. Tell us about what, how, how, what the science is and, and how it looks at aging.
Yeah, absolutely. So, you know, even maybe backing up and talking about like biological aging versus chronological aging. I know that’s silly, but to define that, right? You have like how old you are, your birthdate, that only increases with age. But we know, like think of your, how old you are chronologically. You probably know people who look way older than you, right? Physiologically. Yeah. And then people who look way younger than you. So that’s what we’re looking at. There’s this idea that you’re actually aging at a cellular level and that’s gonna be your, you’re kind of biological age. So there’s all different ways to measure biological aging. The way we actually measure it is pretty unique. We’re looking at what’s called epigenetics, which Erin, you mentioned was your favorite topic. Obsessed. So EPI’s just a Greek prefix, it just means above or on top of we’re kind of looking, yeah.
What’s happening, you know, to the DNA itself, because you’re not gonna change your genetic sequence. Your genetic sequence is, you know, 20% of your health outcomes. It’s 50% from parent, one 50% from parent two. It’s that nature aspect. But then you have your epigenetics, which is gonna be more of that nurture. It’s about 80% of all of your health outcomes and what you do. And you’re really gonna be in control and be able to change your epigenetics. And for the most part, for the point of this conversation, they’re not necessarily all inherited from your parents. A very small fraction is, but for the most part they’re, they’re not gonna be inherited. So again, it goes back to you and like your health and puts the power in, in your hands because you’re no longer a Yeah. You, you’re no longer
A pre-coded defined destiny with your health. Like the way that exactly we thought in the nineties when we started really starting to map out the human genome, it was like, this is it. We’re gonna map out the genome, we’re gonna know everybody’s health future, and that’s gonna be the end of the story. And now we’ve learned it can be further from the truth. It’s more like that’s kind of just defines what the switchboard is. But the, the function of the switchboard depends completely on how the switches are flipped. And your environment is what flips these switches, not your pre-coded genes. And so what you’re looking at, it sounds like this is not a perfect analogy, but you are not looking at the genetics you inherited from your parents. You’re looking at how that switchboard, what’s the configuration of those switches and the impact that it has on health?
Yeah, I love that. Yeah. You took the words right outta my mouth. I was, I was looking for say that for something there. I think I was gonna say Yeah. Victim of, you know, your, your genetic makeup, right. So it’s, it’s pretty powerful and I’ve never actually heard anyone compare it to like a switchboard like that, but I like that. I usually do like the light bulb or the light switch. Yeah. But I like the switchboard because, you know, it’s definitely more complicated than just a light switch because it’s everything. So yeah, it’s, it’s, you know, super unique kind of a personal story I use as, as well, I just gave a, a lecture at, at a conference in London and, and kind of used a story for the first time and, and felt like it was explained rather good. But you know, my grandmother passed away from Alzheimer’s and it was awful. Yeah, right. Like everyone, you know, someone who has a neurodegenerative disease. So that’s why like I bring up this example, it’s just so common. And like that was when I was a senior in in high school and I went and I got my genome run like right away. I’m like freaking out. You know, I had no idea what epigenetics was at the time. And I have one of the A POE epsilon
Variance. Yeah. So I’m three four. So I have one of the, you know, copies, well it’s kind of the second like to worst, it’s the second worst kind of combination to have.
Yeah. Because you’re not I your head around. Yeah, yeah.
So you know, increased two to three more ti two to three times more likely than like the average person to get diagnosed and then earlier as well. But there are actually studies that have come out more recently talking about things you can do from an interventional standpoint, lifestyle supplement medication, procedural things to change the DNA at methylation or you know, epigenetics of that functionality of that gene and then reduce your overall risk. So it throws it again, back in your own hands, which I didn’t know that when I was, you know, in high school I was so scared. But that’s what’s so cool about this field.
Very cool. That’s amazing. So it sounds like, and, and then tell me a little bit about how the algorithm works. So you just in general maybe go from there on it, so you are somehow looking at Yeah. Epigenetics and I think specifically methyl groups probably. Yeah, yeah,
Yeah. The DNA methylation I just hinted at too. So there are a ton of kind of like epigenetic modifications we call them. We look at the DNA methylation and if something’s methylated, it means that gene’s turned off, it’s not functioning. But if it’s unmethylated, then that gene’s turned on and you’re kind of going through that central dog one ending up with that phenotypic outwards expression. So you’re exactly right, Aaron, we’re looking at just a CH three group, A carbon in three hydrogens. Yeah, that’s what I mean by by methylated. And again, flipping that, that switch or, or going back to that switchboard example. So at true diagnostic, what we do more specifically is we measure about 1.2 million of those DNA methylation methods. Wow. So it’s a lot. And what we can get from that data is pretty incredible. We can tell you, I’ll just give a a couple examples, but we can tell you how much you’ve smoked across your entire lifetime, which is more accurate than self-reported smoking status. Oh,
We can tell you your zip code where you are based on your environment. Wow. And those exposures kind of, you know, the toxics of the, the air pollutants and, and your specific location down on the zip code. Wow. Now this is more of a real world example and it’s a weird one, but I have a reason for giving the example, it’s neurosyphilis diagnosis. So we’re actually working on this. So it’s really kind of rare diagnosis, but what you do is you basically compare, you know, people who have neuro neurosyphilis, people who do not, you can see the pattern, what we call your fingerprint of those DNA methylation markers and people who have neuro neurosyphilis people who do not. Now I use this example because with our testing, you just test with a blood spot card, it’s really easy. If you wanted to see, if you were diagnosed with neurosyphilis, you’d have to go into the office, you have to pay about five to $10,000 out of pocket and you’d have to get an extremely invasive lumbar pine or spine puncture. So that’s again how this testing can really like help people. Right. So everything I’m describing, it’s like a fingerprint. You’re just looking at patterns and you’re comparing them Yeah. Throughout the body with a blood spot card with a couple drops of blood. That’s all you need to look at these patterns.
So fascinating. Yeah, I love that. That’s so cool. And, and to be honest, I’ve taken your test, so I like, it was awesome and there’s a lot of really cool things that come out on it, but I think the, the keystone of it is you really see, as you said, I guess you could call it almost like an internal age or like a true age and it’s gonna be a different, it could be a different age than your biological age of like what it says on your
License. Right. So I guess like one thing that I like about that is that when you’re, like you said in the sort of like sick care model and you’re seeing like, oh, your cholesterol is high or your blood sugar is high, those are indirectly related to a future risk of a true problem. Like you don’t actually feel a blood sugar of 120 is a problem, but you feel like a late stage diabetic foot amputation, like in one extreme example, right? So, or you feel a heart attack for sure. So it’s a very in, in exact sort of like imperfect thing that we’re doing with the sit care model of seeing, okay, well because you have these elevations, there’s a, there’s more future risk, but we don’t really know how you’re doing. And so I like how this is showing like, okay, let’s say that I do have concerning things about my health and I implement some changes.
Well the truth is it, it is how do you quantify of like how well that’s working out for you if you, with your tests, I like how it’s like, okay, then you can get like a less expensive repeat test over and over again. You can do it like to check in on okay, like how, how’s that actually working out for you? Because ’cause lifestyle change is hard for people to stick to, especially if they’re not getting feedback like, is it really worth skipping my favorite cinnamon bun every day or not because I can’t tell. But if you act, I think I find feel like it could be very rewarding to see that, oh, okay, I was aging faster than I should and now I can see that my age is, my internal age is actually reversing and you can even have it be younger than your true age. That’s more of an indication I think of like health outcomes than something that’s like less exact, but I dunno what you think.
Yeah, no, absolutely. And again, I think it all comes down to, yeah, what’s, what’s the one thing you can test that is kind of like the end all be all
Like all encompassing. Yeah, yeah.
All encompassing. And I think again, it’s, it’s not new aging has always been the number one risk factor for all cause mortality, morbidity. So even if you look at, I usually show really like pretty there, there’s really pretty graphic and I can send it to you afterwards if you had to like put it in the short or something. But if you look at the top three killers in 2020 in the US you have your heart disease, you have COVID, 19, you have cancer. All three. All three of those. If you look at the risk factors, I mean people think of like, you know, male versus female, they think of, oh, are you a smoker? Are you a drinker? Hypertension, you know, there are a couple other risk factors in there as well. But if you actually line them all up in a bar chart and graph aging, it just skyrockets.
I mean, as a risk factor, trumps and dwarfs all of those other risk factors, which is just crazy because, you know, I still almost can’t believe it that aging is even a risk factor. Right. But it sits at the center and the core of every single disease, we become disease because we get older. And if we actually are able to have a test that quantifies that number one risk factor, so the biological age, yeah, you can get it. Like you mentioned, you look at it, it’s tangible. You’re like, oh wow, you know, I’m aging faster, I’m aging slower. And then again, because it’s based on epigenetics and the DNA methylation, those, those on and off switches the switchboard, you can do things to slow it down. So it’s very actionable as well is the key. Now another key of this testing and something I’m again revisiting and starting to realize just how important that is, is the retesting you have to retest, right? Just like you would with your CBC panel or your, you know, hormone values every, you know, six to 12 months or so, or even a little bit sooner. That’s where the value comes in. Because like you mentioned, yes, should I be doing that cinnamon bun? Oh, cinnamon bun makes my age go up, but what if I did, I don’t know, carrot cake, right? Yeah.
That makes it go down. It won’t make it go down, but healthier dessert. Right? Stupid example. But you get the point.
Totally. Yeah. It’s because there’s a lot of controversy in the health space. So we get patients who are convinced they should be on a carnivore diet, and then we get patients who are convinced they should be on a vegan diet and everything in between. It’s like, well how do you really decide after six to 12 months of doing that how well it’s working for you? Right? Yeah. This is, I think, better than a more like single point thing because it’s more true to like the actual endpoint goal that you have, which is wellness and health and longevity. Nobody actually cares what their cholesterol level is. They care about not dying young from heart disease. Right?
Yeah. Yeah. So
It’s an interesting way to put it too. And, and yeah, I think, you know, the biological aging, to be again, completely transparent and honest may get, you know, it’s something fun, it’s flashy, it’s sexy when you hear about it. I think if you’re really thinking of it as a biomarker and something you’re taking seriously, a lot of people go, well, so what, you know, who cares about biologic age? Right? It’s just a trend. It’s not here to say, not here to stay. Well, the argument there is, you know, you’re right, right? We have to validate them. Just like at one point C-R-P-I-L six, triglycerides, hba one C, you know, fast glucose was all validated. So, you know, there are questions we ask ourselves, is it true? Meaning does it have analytical validity? Is it meaningful? Does it have clinical validity? And is it useful? Does it have clinical utility?
I think that last part isn’t useful. You know, there are certain things there, like you could argue these, what these things are, but maybe a list of like five to 10 almost checkpoints for the outcomes that you can kind of ask yourself or, or go through. And we’re seeing a lot of improvements in those checkpoints in the last couple of years with the, the biological aging and kind of these algorithms, the machine learning, the AI we’re using, where they keep getting better and better and better. So I think the biological age clocks I do as of right now, I mean it can always change, are here to stay, you know, point being they’re predictive of outcomes, right? Long-term health outcomes with our new biological age clock, we just created with Harvard, what we call OIC M age, based on kind of this idea of the, the multi, the different layers you have in the body can predict death with, you know, a 92% accuracy rate, which is crazy. We don’t report out on that, but
It’s getting closer and closer. And just to give a comparison again, you’re probably like, well, yeah, what does that mean? Could, to give a comparison, you can predict death with just chronological age alone, but that’s only a 72% accuracy rate. So again, if we’re looking more at these underlying biological markers that have more significance, you know, we’re, we’re getting better at predicting outcomes and that’s really the key.
That’s so cool. And, and what makes me think about too is I wonder if people might be wondering, okay, you know, methylation, you’re looking at how the switchboard switches are flipped, but how do you, how do you translate that into the age? So tell me more about how the algorithm is derived, like what type of data goes into that? Like is it, go ahead.
Yeah, yeah. So I think it depends on all of the algorithms. Oh, or I should say all of the algorithms are gonna be different. So I’ll kind of give that one that I just mentioned with Harvard. If we, if we wanna kind of like say yeah, the same path, we can go into any of the others too. So I think this is one of the best clocks. And, you know, why do I think it’s one of the best clocks? Well, because it’s number one predictive of outcomes, like I just mentioned. It’s published in a peer reviewed journal. It’s predictive of, of, again, those, those other outcomes. It’s correlated with quality of life-based metrics, health span and lifespan. It’s very precise. It responds to interventions. We know beneficially affect the biology of aging and even explains why you’re aging as well. So that’s why I said I think it’s the best.
But let me answer your question directly and tell you how we created it. So what we did for this specific clock is we looked in this, the study took about three years. We took 5,000 patients from Harvard’s Biobank cohort. So we partnered with Harvard because they have this awesome cohort where we can look at outcome data with the samples, right? We can look at someone’s DNA methylation markers and then at, at one point in their life and say, oh wait, that person actually developed a disease later. What did their fingerprint look like? Right? So we took about 5,000 patients, we measured 27,000 un-targeted proteins on them, 8,500 different metabolites, 61 clinical lab variables, and a million of those DNA methylation markers. Wow. So we’re measuring all sorts of things. So you’re probably thinking, well, why are you measuring other things besides methylation? Right? Well, the more biomarkers you’re able to measure, the better the algorithm you’re able to create because you’re just fueling it with, with more information, right?
Yeah. So what we’re able to actually do then after we, we train the algorithm with, you know, machine learning AI is we can tell you what you need to work on to lower your biological age within the algorithm. So we set a threshold and said, Hey, you know, we asked kind of the model which clinical lab values metabolites and proteins are the most statistically significant and correlated with aging. So, you know, say your results come back, you get a a score, you get a biological age, you compare it to your chronological age, but I can actually say, I’ll just pick on you, Erin, Hey, your blood cell distribution width is super high. We want to lower that because we know lowering that is associated with slower aging. And to lower that we may make nutritional recommendations. So increasing iron B row,
Vitamin C for iron absorption, you can do that through diet, right? Meat, leafy greens, liver peppers, citrus fruits, tomatoes for, for the, the sea to help absorption. Or you could supplement with it, right? You take an easier route out or supplement if you need more. So that’s what’s really cool also about the omic mh and, and how we created it is because we’re actually able to tell you why you’re aging that way and give you specific recommendations on what to do about it. So that is a very different distinct algorithm. Hopefully that was a little bit of a preview on how we created it. I know it can be a little bit difficult when you get into like more of the, the machine learning and, and the modeling, but
No, that’s great. The inputs are, it sounds like specific health cases where okay, we’ve got the biomarkers, we’ve got the, the epigenetics that were measured, and then over time we saw the health outcomes that these people had. And then when you get enough of those data points, you can build out an algorithm of like, okay, this, the, the UI allows you to translate the, the epigenetic results into the health prediction.
Yeah, you’re exactly right. And to be more maybe specific on what I’m talking about, the red blood cell distribution with example that I gave you, that would be an EBP, it’s a new term, it’s an epigenetic biomarker proxy. So we created the term, we coined it, which is really cool, I think. But basically that means because of how we trained it with all of those biomarkers, we can only take a blood spot card test your epigenetics and report out almost anything, right? That’s Wow. Like the clinical lab value, like the metabolites, like the proteins, like the neurosyphilis diagnosis, right? Yeah. So it’s kind of, it’s, it speaks for itself, you know, eeb P but it’s just, yeah, the idea that we’re using DNA methylation as a proxy, kind of the input and like you mentioned something else as the output.
Wow, that’s so neat. And, and, and I think it sounds like that clock would be on your like panels that you already offer. Is that true?
Correct. Yes. Yeah. So the, not the neurosyphilis. Yeah. Yeah. I’m just kidding. Just to be clear, yeah. That’s not something we, we offer, it’s still in research development, but you know, there, but yeah, that’s something we, we offer. So we give you the age, right? We give you the omic M age, we tell you if you’re older than y, you know, younger according to where you’re at in our, our population and, and how that kind of looks and then say, Hey, you know, this is what came up as being significant. It held a high weight in you and you need to work on this. You know, in the future, what we’re working on right now is kind of some pretty cool reporting, what we’ll call it, maybe like true eval or, you know, kind of like a, a vitamin type of of test, right? Really any type of clinical lab value, any type of metabolite or protein where we can report out almost 4,000 of those EBPs with a one-to-one ratio, you know, our correlation values of above 0.9 as well. So it’s really cool research, again, for a fraction of the cost, which is key, just a blood spot card, which is still technically an invasive sample because you’re, you know, getting blood. Okay,
And then keeping, yeah, you know, all of those results kind of in, in one place locally.
So tell me if I understood that correctly, you’re saying that you could take the blood sample and just by looking at the epigenetics and that blood sample, you can report on what you can predict that what that person’s lab marker, a bunch of their different lab markers would be with like a 0.9 correlation?
Yeah, absolutely. Try. Absolutely. Yeah. Yeah. So it’s coming, yeah, it’s definitely almost, almost here. So that’s still, I would say in, in research phase, but it’s absolutely coming and getting really close as well. So yeah, it’s gonna cause it a major, major, I think, you know, paradigm shift in, in our traditional testing and what we’re doing today.
Yeah. Well it is super dumb question, but is it that the biomarker, let’s say that you’re talking about like a blood glucose, is it that that blood glucose alters the epigenetics, like high blood sugar changes your, your switchboard switches? Or is it the opposite that like your switchboard configuration impacts your blood sugar and that? I think
That’s the million dollar question.
Yeah, we probably, we still don’t know, right? Yeah. What’s happening first, like
You just know there’s tight correlation between the two.
Exactly. Like, yeah. Are you becoming diseased because you know, your DNA methylation markers are changing or,
Or, or maybe they’re not even causing each other. It’s like the external thing, the cinnamon bun is impacting both it’s causing high blood sugar and it’s causing epigene shifts, but they’re, it’s not that the two things are, one of them is causing the other, it’s, there’s this, the third external, like the environmental thing is like doing the shift on both of them.
Yeah, exactly. I think there, there are so many options right there, there are so many ways can kind of go there. So yeah, it’s like what is, what is really happening right on, on kind of that cellular level and then Yeah. What’s kind of causing it. And it’s probably a mixture of, I would say all three of them, right? If we, we had to guess, I don’t think it Yeah. Might be a hundred percent one thing, you know, 0% another, but definitely yeah, a combination of them. So it’s, yeah, it’s, you know, a really cool field to be in just pond even pondering that question, right? Like you could study that question for the rest of your life and you know, maybe, you know, just give the, the tip of the iceberg with all of everything else still underneath. Yeah. So yeah, we’re just scratching the surface.
It’s fascinating that those correlate so highly. That’s really wild.
Not all of them do, right? All
Of them. Yeah.
Yes, they do. And obviously the better we train them, the the more correlated they’ll be. But right now, even to give another example, you know, we could do, we could report out your VO two max, your FEV one, your, your gate speed. Yeah. All of them. No, yeah. In the same exact way, right? So it’s still an EBP where we train them with the actual physical outcomes and then we’re able to just give you that outcome through the epigenetics and the DNA methylation.
Wow. So, or another thing that makes me, this makes me think about, because it’s like, oh, okay, well, like, okay, I could see how exercise would cause e epigenetic impacts obviously, or on different genes or flipped over certain ways and it’s gonna, cause let’s, let’s call it, not even just exercise, like we’ll call it like high intensity exercise. Yeah. It’s gonna cause the epigenetic shifts and the increase in invo two max. So that’s like the third thing we talked about where it’s like the external thing causes these two shifts and they’re gonna correlate with each other where one can predict the other. And it kind of makes me think about like, wow, you could even, it, it’s fast. One of the fascinating things that epigenes with me is the way that like the switchboard configuration is inheritable to some degree from like one generation to the next, such that like say like studies, you know, no more than me, but like where when a mom is under like a lot of stress when she’s pregnant, it can literally impact the epigenetics of like her offspring, like in a significant way. And like, it’s kind of fascinating to think about like, could you use this almost like, okay, you get like a blood sample from like a baby and say, okay, yeah, this baby has like much increased risk of anxiety or like depression. Not that I necessarily know what you would do with that information, but it’s like a while to think about like, oh, like so much of their, their health futures is like, is like already right there in their blood and you could potentially like find it.
Yeah. Yeah. That’s one of my favorite things to talk about. I haven’t talked about in a while actually, but what you’re describing, it’s a mouthful, but it’s transgenerational epigenetic inheritance. Yeah. So it’s really cool. There’s, you know, someone from Washington University named Dr. Michael Skinner, he just studies it in animal models. I heard him speak at a conference when I was still kind of early to epigenetics, but a couple years ago and when he spoke I was like, we’re all screwed, we’re all good. Encouraging. Oh my gosh. And like, and, and you’re too late like yet, like there’s nothing we can do about it really. Like yeah,
There are some that are passed Yes. From older generations. Like if you’re, you know, if your grandmother, great-grandmother smoked, you know, when she was, you know, pregnant and, and things like that, which is really common, you know, back in the day. Yeah. Super common. My grandmother smoked when Yeah. She was pregnant with my mom, which is something I just found out recently. So I’m digging, I’m, you know, excited. I’m, I’m like digging into that a little bit more too. So yes, some, I mean, yes, epigenes is changeable. Some of those are gonna be malleable, but in the way that it’s passed on, some of them are not. And that’s where at, at the beginning, like some of the markers are gonna be pretty stable and, and you’re not gonna be able to affect them. But for the most part, yeah, the epigenes is gonna be changeable. So Michael Skinner, he studies it in animal models and he’s gone back like 10 to 15 plus generations and he can actually track it through mice and wrap models. It’s just harder to do human studies obviously because it’s such a new science and you know, we might not have the, the DNA from like our parents or grandparents or great grandparents. So you’re not, you know, there’ll be more studies coming out in the future on that.
Yeah. It’s so good. I mean, I guess there’s two sides to every coin, but on the, I think what I’m hearing you say is it’s like, okay, you’ve got this switchboard with your switches a certain way, and then like some of the switches can be like massively impacted by your decisions and your environment that you put yourself in, but some of them are kind of stuck, like they’re just kind of not movable. And some of those configurations might be problematic in the long term for your health, which can be upsetting. But on the other hand, I feel like I guess in clinical work it’s, it’s, it can be kind of heartbreaking to see so many people that are working so hard on their health and they’re doing so much more than other people and yet they’re not, they’re not doing as well. And I guess the silver lining of knowing that is just that, like, I think that that’s, that’s a lot of what’s happening with, with a lot of these patients.
It’s like your, your switchboard configuration is not optimal and, and, and you can change it to some degree, but it’s almost maybe validating to, to say like, but you can’t fully get the switchboard of whatever, insert your favorite athlete here or whatever, but like, or superstar, whatever, but you can’t, you can’t just eat the right food because I feel like social media especially puts that kind of thinking in people’s head of like, just tell me the right smoothie to make and the right fasting routine and the right workout, and I’m gonna, the clouds are gonna part, my health is gonna be like perfect. And they’ll try like so many things and like so many practitioners and so many aggressive diets and supplements and they’re just kind of flailing around looking for that thing. But it’s like, in the end, I agree with you, I just, working with so many people, I, I’m just confirmed that like there’s, there’s really only so far that people seem to be able to get.
Yeah. Yeah. I think one, one comment back to that is yeah, there’s always the question of what should I do to lower my biological age? Like, Hannah, what works, what can I do to, yeah. And like I can tell you two things and neither are probably gonna be super helpful. Number one, here’s what the studies say, right? They’re still large population studies, right. We’re not a, as an individual, we’re not a population. We’re a very unique, you know Yeah. We have a very unique makeup in that sense. So yes, you can still follow that and that that’s probably a good place to start, right? If it works for you, retest and actually do the testing yourself, but it doesn’t mean it’s gonna be successful. The second thing I can tell you is this is what works for me. And the reason I can tell you that is because I’ve do been doing this longitudinal testing for a while now, right. And can push those boundaries and can push those limits. Again, I think it comes back to, hey, if you don’t know, or if you are interested, and you mentioned this at the beginning a a little bit is, hey, do the, the cheaper kit, right? Retest your pace of aging every two to three months or so to get feedback on that number one risk factor Yeah. In that magical smoothie that you’re seeing from that influencer. Yeah. Like probably has a ton of sugar and probably has a ton of carbs in it and like, you know,
Is, you know, worsening your biological age when you dive into it at the end of the day
Yeah. Recheck on it. Exactly. And like you said, I think it’s, depending on what your specific challeng areas are, it’s gonna be different things for different people.
Yeah. Yeah. So
I I, I think the way you’re testing the way I, I’m obviously they able to spend less time marinating on thoughts on this, but the way I think to use it is, is not necessarily that you use it to come up with some like paradigm shifting idea of what someone’s health plan should be. It’s more a better way to tell them if it’s necessary to change their health habits, first of all, like are you aging quickly compared to your the calendar and then if, and then if you do implement some type of health plan, that’s just the evidence-based thing that we would’ve done anyway. Basically. Yeah. For you as an n equals one person, how well is that actually moving the needle on your health as a way of kind of calibrating it, deciding if it’s effective, deciding if it needs to shift and actually seeing a quantifiable result from it, which can be both analytically helpful, but also I think the like, like helpful in terms of just like buy-in Yeah. Motivation to continue. Yeah, I think you, yeah, I think
That’s the point is yeah, hey, this is quantifiable, right? We can actually yeah. Get something a little bit tangible, right? That you can go back and, and kind of look through and, and start to track over time. So yeah, I think it’s hard to make lifestyle changes, right? People get caught up in their ways, you know, they’re, they don’t realize that, you know, how much they’re, they’re drinking or I don’t know, you know, traveling right. Or having these external stressors and kind of the impact that like that can have on you in biology. So Yeah. Yeah. It’s, it’s I think useful in, in that sense and way
I’m fascinated and excited that you’re doing a study on GLP ones because I think, I, I could be wrong. I mean it, this, it might not go down this way, but my bet is that we are gonna see within the decade that like half, at least half of the US population taking this medications and there’s just so much we don’t know. I’m not saying that I’m against ’em, but there’s that it is true that there’s a lot we don’t know. And so I can’t wait to see that because I don’t want to get too off topic and controversial. Yeah. But I, I, I think there’s just so much weird thinking around people’s weight and around obesity that is really frankly like biased and poorly informed. And so I think people that don’t understand the disease of obesity well and what people contend with that have obesity, they’re, they kind of think of this as like an unhealthy, dangerous, irresponsible thing that people are doing that they, that is like incomprehensible, but, and done well.
I think it’s, it’s life changing. And if there’s, and I think there we will see that more data on that in a, from a lot of different places in terms of like the obvious things, increased mortality or decreased mortality risk from, from just taking it, decreased risk of diabetes, complications, heart disease risk. We’re already seeing that data, but I’m curious to see too, like where, where it lands on your, on your data, it sounds like, are you, tell me more about it if you can, of like, is it basically like the patient’s taking the medication anyway and then they at certain intervals take a true diagnostic test?
Yeah. Yeah. They, they would, to be honest, I actually am not as familiar with like in the details. Yeah.
But they would, you know, I don’t believe it’s, it’s, I don’t believe it’s healthy people like taking the GLP ones, right? It’s people who meet the actual criteria. Yeah. You know? Yeah, of course. Type two diabetes, you know, need to lose, lose weight for x, y, Z reasons metabolic disease. So what’s really cool about these studies and what gets me excited is that, you know, the biological h clocks should validate everything that you just said, right? If the biological h clocks are right, you know, increasing with age, and we have all of this data that says, you know, it decreases risk then like something’s wrong with the biological age clock you would say, right? Yeah. So they act as almost like validation based studies to prove that what we’re capturing is, is really correct. So I’m excited about the results, you know, always, always a little bit nervous with like this larger kind of clinical trial. Yeah,
Yeah, I bet
We’re going through, but then you, you know, if something does look a little off or it doesn’t align with the hypothesis because yeah, we’ll all be, you know, blinded to the, to the groups and, and we won’t know who belongs where until after it’s, it’s published in the data analysis is, is complete, which again, is a really nice, nice thing to do when you’re doing kind of these cross-sectional analysis studies with, with larger groups. Yeah. Then you can dig into the findings a little bit more and, and understand maybe what’s really changing and you’ll, you’ll understand more of the mechanism of action of the clock and how it’s working.
Yes, yes. And the maybe of the GLP one med.
We don’t fully understand them, to be honest. They, they, there’s receptor sites all over the body for that hormone, so.
Exactly. Yeah.
So fascinating. Oh, I can’t wait to see that paper. I know it’s probably years out, but I can’t wait.
Yeah, well, timeline should be hopefully yeah, sooner than a couple years. I’m I’ll, I’ll push for it harder. Yeah.
Okay, great. Good. I’m here for it. Well, Hannah, your testing is truly incredible. I, I’m gonna get my act together. I’ve been meaning to get a pa a pace, I think you called the pa the second one, the, the pace. So I’m gonna do it and, and it’s just going up on my list to do. So tell me if people are interested in learning their intrinsic age or how can they learn more about your testing?
Yeah, so anyone who’s interested, they can go ahead and reach out, you know, to me first and foremost, hannah tru diagnostic.com. I’m always happy to answer questions. You can go directly the website though and you know, purchase the kid. It’s TRU and then D-I-A-G-N-O-S-T-I-C. So it’s, it’s singular not plural.com. And yeah, I recommend doing the complete kit to start and follow up where it best fits and aligns with, with your regimen.
A awesome, yeah, it’s just, I think of it as, I mean, just such a valuable thing. There’s nothing else like it and better now than later to get it because I think we’re always changing and our environment’s always changing and we’re always doing different things. And so I’m, I’m kind of thankful that I had a baseline, a, a little a like a lot’s changed for me in the past year or so, so I’m like, oh, that’s so exciting that now I can compare. I like how you can compare it across time. So yeah, I, we’ll put the, the website true diagnostic in the, in the show notes and thank you Hannah, for offering to answer questions for people as well. And yeah, very grateful. That’s so generous of you.
We’ll, we’ll get you retested, Erin, and then we’ll, you know, have to hop on a call and look at the, the changes if, if you want to,
It sounds so dumb, but it’s just like literally getting over the hump of like, how do I order the test? I just need, I put my credit card, I just need to do it. We’ll
Get you set up. No worries. Okay, sounds
Good. Thank
You so much. I appreciate it. Thank you, Hannah,
You’re, you’re incredible. You’re, you’re a genius when it comes to this, and thanks for making something that’s just so valuable as a clinician and for the, for the people that can use it.
Of course. Thanks, Erin.
You too. Talk to you later.
Hi there, Erin here. One of the things that I really wish people knew is how often it is that people have a damaged metabolism and it’s not their fault. It’s, this is really a feature of the food environment that we live in and that we’ve even been raised in. And the reason why I wish people knew that is that a damaged metabolism, I find really impacts people’s health and is connected to most of the, the health goals that I see people usually have. So things like weight loss, weight loss resistance, high blood sugar, problems with cholesterol and blood pressure hormone imbalances. So PCOS, infertility, loss of, of sex drive, all relate to metabolic health problems and inflammation. Mental health, for example, is another one where the anxiety and depression can be connected to inflammation and metabolic health really profoundly. So I wish that people knew the power of healing their metabolism and how common it is that people need an improvement of their metabolic health to really achieve the health and wellness goals that they have.
This topic is so important that I developed a full program to help people heal their metabolism, and the name of that program is Lean for Life. And now I’m thrilled to announce that Lean for Life is available via app, both in the App store and on Android. Via the Lean For Life app, you can access all three, four week phases of the program. Phase one is all about the pattern of eating and what to eat to have a healthy metabolism. Phase two is all about the timing of eating. So we talk about concepts around intermittent fasting, time restricted feeding, fasting mimicking diets, and how to optimize that. And then in phase three, we learn about the cyclical pattern of macronutrients that I recommend to keep your metabolism healthy and fine tuned over time so that you can achieve your health goals without restricting, without having to stay on the diet cycle, without having to continuously be on a either diet restrict versus binge cycle and basically break breaking free from Diet culture.
If you’d love to check out the Lean For Life program again, you can go ahead and get the app either on the Apple iStore or on Android, and you can check out the link for the app in our show notes. I’d love to hear what you think. It comes with a free trial of the first phase. Feel free to get in touch with us if you have any questions or feedback on the Lean For Life app and our contact details are in the show notes as well. Good luck on your health journey and best of best of luck to you in healing your metabolism. Thank you so much for taking the time to listen to the Empower Nutrition podcast. We love offering insight to help you optimize your wellness. If you enjoy this episode, feel free to leave us a rating on whichever platform you’ve stream from and consider subscribing. Also, you can learn more about our practice@www.empowernutrition.health, and that link is also in your show notes. Take care and talk to you soon.

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