Latest / Ageless and Timeless Podcast® / Ryan Smith is founder of TruDiagnsotic.

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Ryan Smith is founder of TruDiagnsotic. · Ageless and Timeless Podcast®

0:09
Good morning everyone. This is Michelle Hughes from Ageless and Timeless. Today I
0:15
have a very special guest, as I always say, I have always have
0:18
special guests, but his name is Ryan Smith, and Ryan is the founder,
0:24
one of the co founders, i should say, of a company called
0:27
True Diagnostics, which is the company that many people are turning to these days
0:34
to test their biological age, their DNA methylation and all the markers for anti
0:42
aging that are becoming the most compelling in the longevity field today. So we're
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going to learn a lot today about all the markers for biological aging and how
0:55
Ryan has spearheaded this effort. Is a very young man, but he has
1:00
been at the forefront of this whole field, and epigenetics is what the field
1:06
is kind of generally called. But we're going to talk a little bit more
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about that today. So Ran, welcome to our podcast this morning, and
1:15
thank you for taking the time to join us and help us to learn more
1:19
about what you do at True Diagnostics. I'm going to give it just a
1:25
little bit of a bio on you, but I want you to fill in
1:27
the blank, So just a brief one that Brian did start out going to
1:33
get his BS in chemistry, right, Brian biochemistry, Yeah, yeah,
1:40
and then and then he decided to go to medical school. But then during
1:42
medical school, he realized that he wanted to become more get more into the
1:49
pharmaceutical side, and the pharmaceutical side led him to the preventative medicine business,
1:55
and he started a company called Taylor Made. Yeah right, yeah, absolutely,
2:00
that company grew to eighty million. It was the company that focused on
2:07
basically peptides, right way before the time of peptides. So Ryan has already
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always been kind of ahead of his time. So he's going to tell us
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more about all of those those conquests that he's made by being there before everybody
2:22
else. But ran, when you started out, you obviously knew what you
2:28
wanted to do in the world of medicine, and then or you thought you
2:32
did, and then you realize that you had a calling that you needed to
2:37
follow your heart, follow your mind. So tell us who and what guided
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you to those changes, because those are pretty monumental changes to start medical school
2:47
and then drop out and then go into a whole different field that's related but
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not directly schooling. So can you give us a little bit of background on
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how you became the person that led the forefront in at Taylor made Yeah.
3:04
Certainly, um, you know, I hate to say it without varying the
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lead too much, but it was a lot of luck. Quite frankly,
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I wish I could say it was all, you know, intuitive design,
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but um, you know, I did my first two years in medical school,
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which is really most of the I would say schooling portion, but gotten
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to them that third year with the clinical portion and got really disillusioned, I
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think with healthcare. Um, you know, I didn't think that I was
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doing much of a difference. You know, in Kentucky, I was treating
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relatively I would say, chronic disease population and really just managing symptoms. And
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it was really I would say difficult because I didn't feel like, you know,
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treating the symptoms. I certainly applaud that as a as a career build,
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but for me, it wasn't preventive enough. I think that at that
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point we were just sort of seeing patients who were already in the sort of
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downstages of disease, and so so I knew I wanted to do something else,
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and um, and really just got lucky with this field of pharmaceutical peptide
3:58
development. A lot of my previous work in biochemistry had been in peptide and
4:00
protein biosynthesis, so I had worked a lot with creating new products both were
4:05
combatentum as well as some of those other pharmaceutical creation methods. And we saw
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an opportunity in the market and we were lucky enough to hit it. And
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I think that at that point a lot of people weren't familiar with even what
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peptides are for some of their applications, and the positions that we were working
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with introduced me to a whole new side of medicine where things were really working
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preventatively, where they were trying to prevent disease before they were happening, focusing
4:30
on optimization, and that shifted I think a lot of my concept of medicine
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and uh and I was lucky enough to have that experience. Well, you
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know, it's interesting because I think when you say the word pharmaceutical, immediately
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we'd think of all the you know, the the drug companies and all the
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alepathic approaches. And to have been at the forefront of the pharmaceutical industry in
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the in the peptide world, and also a course in the in the prevent
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medicine anti aging rather than alipapt it. So how did that? How did
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that happen? Yeah, So generally we were doing some of these medications that
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we were doing, uh, you know, peptides that people might be familiar
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with, things like BPC one five to seven pt one forty one. You
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know, none of these drugs were used or approved whenever we sort of we're
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taking into the market, and legally that was only able to be done in
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a pharmaceutical compounding environment and one that also I should also mention doesn't have any
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insurance based reimbursement because these drugs are not approved. And so we really were
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focused on a cash pay market, and the people who were doing most cash
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pay medicine are people who are really doing preventative medicine before people have diseases,
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because that's insurance companies unfortunately don't oftentimes reimburse for healthy people who were looking to
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optimize their health. And so it really this community was sort of a new
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community, but one that is very collaborative and very open to learning new in
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best techniques, very innovation UM and so they were very receptive of all the
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things that we were doing UM and UH and as you mentioned, a lot
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of them were tweating age as a primary outcome because age is such a big
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risk factor for all chronic disease and death. UM. And so it really
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had this preventative approach in a different philosophy of medicine. And now I think
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that was really exciting. So again, sort of got lucky because I didn't
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know this space of medicine even existed. I think if I had, I
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might have, you know, continued with the medical school experience. UM.
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But unfortunately I didn't, and I was really lucky to find it. So,
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Ryan, what or who influenced you the most in your journey? Yeah,
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I would say just a multitude of positions UM. As I was on
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boarding, you know, learning about all the ways that they approach preventative medicine.
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UM. You know, there's too many to name, UM, but
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but I appreciate all the lessons and the mini diversity areas that they've helped me
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with. And I think that, you know, as we were going through
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all of these different paths Tide products, one of the things we realized was
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probably the biggest weakness was that a lot of them didn't have the data needed
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for FDA approval. And so one of the things we were always looking at
7:10
was one of the best ways to actually quantify some of these health traits and
7:14
health improvements in short timelines. And that really introduced me to this field of
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epigenetic methylation and these epigenetic clocks, and that really was what started, I
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would say, of my vision for this company, a True Diagnostic, to
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be able to really use some of those tools in a variety of different ways,
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but particularly to quantify aging. So what I think we're going to take
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a deep dive right now, So let's talk. Let's just define some terms.
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Okay, So let's start with aging. Yeah, what is aging?
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And how do you qualify aging in terms of what True Diagnostic does with aging?
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Yeah, So I think that you know, most people, if they
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had to answer that question, would probably say that age is your how long
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you've been alive, right, um, Yeah, from the moment that you've
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been born to now, that's age. However, I think that our philosophy
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of what age is is very different. Um. And I think that that's
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because of this concept of what we call phenotypic variation. And it might sound
8:16
complicated, but everyone knows this idea. It's whenever you find out someone's age
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and you're shocked. Right. You might say, you meet someone you think
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that they're you know, thirty five years of age, and you find out
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they're in their fifties, and you can be like, how is that possible?
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This person is looks and young, they're behaving young, they're physically functioning
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young, um, and then vice versa. The same people who you might
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see, uh, you know, and they say that they're you know,
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thirty five and you think that they're in their fifties. That difference, that
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theotypic difference, is really how we would what we would define as aging or
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um. And the reason for that is because aging from a chronological perspective,
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how many times you've been around the sun, for instance, is a relatively
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arbitrary number to what makes his difference in our health. But even that arbitrary
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number is still the greatest predictor the greatest risk factor of all other chronic disease
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risks. And so that is what we're really really trying to quantify. And
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we call those differences basically the difference of chronologic age versus biologic age, but
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that definition of biological age is much more complicated. M Well, that's what
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we want to dive into today part of it. So because that helps us
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to the baseline of what True Diagnostics is measuring and and why you are ahead
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of the pack in terms of everything that you do in that in that field.
9:33
So so okay, So if if we have the difference between chronological and
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biological aging, so would you dissect for us that difference in terms of what
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makes up the biological age of a person versus the how many times take been
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around the sun, which is the chronological age. We all know the aging.
9:54
The chronological age is just a number. That's what we all know.
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All of us say, but let's let's understand that a little better. So
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what is the What are the markers the biomarkers of biological aging that you use
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as part of your algorithm. Yeah, so so, UM, this is
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a very complicated question and one that I would say that there's not a lot
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of scientific consensus on. Um. You know, even when we started our
10:20
company True Diagnostics, most people recognize that there were nine big hallmarks of aging,
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things like epigenetic disregulation or nutrient snsing problems or telomere link shortening. Um.
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You know, those are a few, just just to name a few,
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but even now a few years later, only three years later since we
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first started true diagnostic there are even fourteen recognized hallmarks of aging. And so
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this definition of all the processes which tend to lose function as we get older
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can be what we call these hallmarks of aging. And this process is enormously
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complex. As we learn more and more about the body, we start to
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find more and more changes that relate to or so cated with our chronological age,
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but even more importantly, they're heavily associated with function. And this is
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why, for instance, we see people you know, in their sixties with
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the same bio markers as people in their thirties, but they have more diseases.
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Is because we tend to lose the physiological function that of optimal as our
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body ages. And so this is a really hard process to quantify because aging
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biology is just so complex. But with that being said, the way that
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we can always judge it is by how predictive are these ways of quantifying age
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to negative outcomes, And so, really, you know, the history of
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these epigenetic clocks is a great way to sort of tackle this conversation and to
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talk about it, and really, these epigenetic clocks really started in twenty thirteen
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by doctor Steve Porvath at UCLA, and at first they started to be used
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in a variety of ways, but really no health related ways. So they
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started to be using, for instance, to quantify DNA at a crime scene
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to see how old someone was if they left their DNA there. That way
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you could sort of narrow down your suspect list. They were used in European
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refugees, so for instance, in the Syrian refugee crisis, as people started
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going in large numbers to Europe, they started to use this testing to see
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if people were adults or miners, and if there were miners and they would
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be eligible for asylum. And so they started using in a lot of strange
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ways, but they were still at that point in time predicting chronological age.
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And the problem with that is that the better that those clocks got, the
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closer they got to just your birthday, which is something we could ask for.
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We don't need an expense a test form. And so really in twenty
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eighteen, these clocks started to be a little bit different and they started to
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be trained to biological phenotypes, so things like that we know change with age,
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like your insolence sensitivity, or your blood cholesterol markers, or even your
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telomere length for instance. In these clocks, we know are better because we
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know that they were more associated to aging outcomes. So if you're aging quicker
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than you're in your chronological age, so you're older than your chronological age of
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this testing, you're going to be more at risk for all negative outcomes.
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And if you're younger with this testing than your chronological age, you're going to
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be protected from all of those same negative outcomes. And so once it'sistic,
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I always like to use that was used in a presentation by Morgan Levine,
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another researcher who is very famous for these biological age clocks, is that if
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everyone in the world were to be seven years younger biologically than their chronological age,
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we would be able to cut disease in half. Fifty percent of people
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would no longer be sick. And that just gives you an idea of how
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much age plays a role into the development of these these outcomes for us.
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And so I think that this is something that is actually very freeing for most
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people because you do have the ability to control your biology to some degree,
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and by making improvements in the way that you function throughout the world. You
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can improve that biological aging process and prevent those outcomes. But in addition to
13:52
that been all these quality of life things that we tend to avoid in fear
13:56
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methods. Epigenetics is again to me, the biggest topic and the most exciting
14:39
topic here because the way I traditionally explain it to people is by saying that
14:43
most people are very familiar with genetics, right, your sequence of DNA that
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gives you the code of your body, and this has been around for a
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long time, but epigenetics is much newer. And so if every cell in
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your body has the same DNA like your lungs, your heart, your skin,
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the question is how do those have different behaviors? Right? How does
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your skin know how to behave like a skin cell and how does your heart
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know how to behave like a heart cell? And the way that it does
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that is by um sort of the instructions not just of the DNA, but
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what DNA is actually turned on or turned off. And those markers or those
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on or off switches are sort of what we call epigenetics in a really simplified
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way. And so in case of what we're measuring, we're measuring DNA methylation,
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which is a little bit of a basically a methyl group, a carbon
15:28
group which is attached to your DNA, which is sort of the off switch
15:31
for your DNA. So when you have an attached methyl group, you're you're
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basically not transcribing that DNA. Your DNA is not being produced to mRNA,
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which then creates proteins and peptides that make up the infrastructure of your body.
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And so what we're sort of measuring at each of the gene locations that we
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test is the percentage of methylation. What is the percentage of that off switch,
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And so we're doing that at right around a million locations in your genome.
15:56
UH and so that is really what we're measuring. And the good thing
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about that is it it can be changed by almost everything that you do in
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your life. So your methylation patterns can change in alt of your diet nutrition,
16:08
as a result of the supplements or medications that you take, as alt
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of your fitness activity, even your stress and your social interactions with individuals will
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change these patterns, and so we can start to read these patterns in a
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variety of ways, even beyond aging. So right now there are already algorithms
16:26
that we can use to tell you how much you've smoked across an entire lifetime,
16:29
how much you're currently drinking. For instance. We can even tell you
16:32
about pollution markers, how much pollution have you been exposed to you in your
16:34
DNA. We can even predict when you're going to die or and this is
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already actually being used by life insurance companies to quote you a premium on how
16:44
much they should be charging you. And so there's a lot of really cool
16:47
applications for this. You can track progression of cancer, detect cancer before any
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other method. Even so a lot of implications will affect a lot of different
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fields of medicine. In agriculture and really everything you can imagine, but we're
17:00
really focused on aging, and to do that, we create these epigenetic age
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clocks where we take that data, that percentage of methylation at each of the
17:08
locations on your genome, and we use it to try and predict outcomes.
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In this case, we really try and quantify your biological aging um by looking
17:17
at all of the different factors that we can and using computer learning and machine
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learning to interpret that data in ways that humans just haven't been able to in
17:26
the past. So when you when somebody does your test, can you actually
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pinpoint those lifestyle factors when you're trying when you're coming up with the DNA methylation
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outcome? Can you you know, the things that you've just mentioned. Are
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they possible to pinpoint with every individual person so that they get kind of a
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Taylor use me for saying, Taylor made U customized understanding of what they need
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to do to improve their epigenetic clock or their biological age. Yeah, certainly
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so. So we can certainly we already report on behaviors like smoking and drinking,
18:10
for instance, and one of the reasons is to get that One of
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the best things you can do to improve your biological age is reduce bad behaviors
18:17
or things that are going to hurt your aging process. And I think it's
18:19
pretty definitive now that things like smoking and drinking definitely hurt that process and are
18:25
generally not good for you. There was a time early in this type of
18:27
research where we thought maybe some drinking was good for you, but but now
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I think we've we've sort of switched that, so we can certainly quantify that.
18:33
We can also quantify things like your inflammatory markers, how inflamed is your
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body as a marker, which we know increases I would say aging across the
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board. And very soon we're going to be even start to add resolution into
18:45
the aging of different organ systems. So for instance, you know, how
18:51
is your brain aging versus your heart, versus your liver versus your skin or
18:55
your immune system. And so we're starting to get even much more resolution into
18:57
those aging signals to tell you what's really driving your own aging um and and
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for us, we always adopt a philosophy of you can't manage what you can't
19:06
measure, and so what we're really trying to do is to get the best
19:08
in class way to measure this process. Of biological aging so that people can
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really start to find out ways they can reverse it and what's working for them.
19:17
M So, um in your experience, how many patients have you so
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far treated for the biological age result? Yeah, we've tested over twenty five
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thousand patients. Now, which is the Does that make you the largest of
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the diagnostic testing for biological aging? Oh? Yeah, certainly we are the
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largest private epigenetic database in the world now. Um, and we've done it
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in just three years. It's been Uh, it's such a new field that
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but we also have tested a lot of scale. We test, as I
19:55
mentioned, almost a million different locations in the genome, which also helps we
20:00
improve resolution of these algorithms and find out even more patterns about what's connecting your
20:04
aging to these different behaviors. And we've started to do a lot of a
20:08
different analysis with that. We've done a lot of interventional trials, which I'm
20:11
sure we'll talk about about things that we can learn about how to reverse your
20:15
biological aging. We've also done things like looking at smoking and drinking or marijuana
20:21
used to figure out how it's changing some of those expression markers in your genomes.
20:25
What genes is it upregulating what geans is it down regulating We've been able
20:29
to quantify the immune system in really really amazing ways to look at how our
20:33
system is aging over time, and all of these have applications almost every area
20:37
of health. And so I think there's one big takeaway from anyone that's listening
20:41
now. It's certainly that I love to put emphasis on age as something that
20:45
you can have an impact on in your own health. But secondarily that I
20:48
think it's that epigenetics is a platform will be just as robust, if not
20:52
bigger than genetics because it's very, very informative, but it's also changeable.
20:59
And so instead of taking one at test once in a lifetime with your DNA,
21:02
which you can't change, you can actually measure your apogenetic expression, implement
21:07
solutions, and then retest to see if those solutions are actually helping or hurting.
21:12
When you talk about the genes, because you know a lot of people
21:18
have the misconception that you can change your genes. Your genetic expression is who
21:25
you are and that's what your parents give you and there's no way to change
21:27
that. And yet that does alter the premises of your business. If you
21:33
were to believe that. So how do you dispute the claim that you cannot
21:38
change your genes? And how do you prove that? Would would what you
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do? Yeah, so I would. I would agree you can't change your
21:47
genes, you know that's hard to do, but you can change the way
21:51
your genes are expressed. And that is what the important part is, because
21:56
you know, I always like to use the can't the example of some can't
22:00
related genes. UM. So, for instance, you have genes in your
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body which we call tumor suppressor genes. These are meant to suppress cancer UM
22:07
and when they're activated, they're doing their job. They're suppressing cancer from developing
22:12
UM and that's great. But if those will become deactivated, that would be
22:18
a problem because then you're not having the breaks on the system which is supposed
22:22
to prevent cancer and vice versa. UM. You know, sometimes we have
22:25
oncogenes or genes that are tend to proliferate cancers or growth UM. And in
22:30
some of those oncogenes you might want turned off more than usual UM. But
22:33
if they get turned on UM, then that can be a problem. And
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so UM. So gene expression absolutely matters the function of our body in our
22:41
cells UM and and how these this genetic information is used. UM Sometimes people
22:48
like in it too hardware versus software. But like a computer system, where
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the DNA is the hardware, it's your computer, it's how it's set up,
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it's you know, it's processing, it's random, it's it's you know,
22:57
how many gigabytes of storage. But the actual software which is choosing what
23:00
to use is the epigenetics, which is sort of saying this needs to be
23:06
turned on, this needs to be turned off. We're going to go in
23:07
this direction or that. And so although you might not be able to change
23:11
your genes, you might be able to mitigate some of the genetic risk that
23:15
you have through proper I would say treatment, and that that treatment could be
23:19
diet, lifestyle nutrition. And that's really what we're trying to answer. So
23:23
first we're creating a way to predict or measure the risk, and then we're
23:26
creating analysis to find out ways to reverse that risk. And so that's sort
23:32
of the whole process is first create the tool and then secondarily find the ways
23:36
to improve or to fix some of those deficiencies. So do you allow the
23:44
consumer to interact with your staff and to do the testing or must they come
23:49
true a medical professional to be able to take advantage of true diagnostics algorithms.
23:57
So, for you know, age is actually in a weird place medically because
24:03
you know, the FDA does not consider age's disease and and so as a
24:07
result, we are able to do a lot of this testing to consumers directly,
24:11
and that's great. We're able to quantify things like aging. However,
24:15
we're not able to do some of the really advanced things that we can do
24:18
on the back end with our positions, where we're able to predict things like
24:22
diabetes risk or you know, obesity risk, or cardiovascuer disease risk, or
24:26
immune system dysfunction. And so we always recommend going through a position because you
24:32
can get more data and it's also easier to analyze some of their experience.
24:36
The position experience in this area might be able to give you really good recommendations
24:41
on what to do, but it is also available as a consumer. And
24:44
even in our consumer testing, we really prioritize education among everything. Usually we
24:48
don't recommend any type of treatment unless it has studies that have been published on
24:53
it. And that's another thing I think that makes true diagnostic. Very unique
24:57
is that all of our algorithms are published UM and so this is really really
25:02
important because if someone doesn't have a published algorithm, it's a little bit like
25:06
going to a fortune teller. We sometimes say you can choose believe them,
25:10
but it's always better to have evidence and uh and and so all of our
25:12
algorithms are published. UM. We published papers all the time UM, not
25:18
only on interventional trials, but also on new algorithms we create UM and we
25:22
even published data on things that don't go the way we expect. We're about
25:26
to have a couple of publications coming out on interventions we thought would help but
25:30
actually ended up hurting. UM and and so we published both negative and positive
25:33
data. And so when when has that happened where you actually get data that
25:40
is not what you expect? What do you When has that happened? And
25:44
what was this? What were the specifics of that for? Yeah, so
25:47
we're gonna be releasing this paper in a few weeks. So I'm I'm bearing
25:51
the lead here just a little bit. But that's okay, I'm sorry,
25:55
it's final. I'm happy to share. But we did a pretty small trial
26:00
on what we call synalytic and for those of you who don't know, sometimes
26:06
as we get older, our cells go into this process we call senescence.
26:08
Some people call them zombie cells, but there's cells that sort of pause and
26:14
start secreating a lot of inflammation. Sometimes this inflammation is called inflammaging as a
26:18
process because it really encourages a lot of negative aging outcomes. But those cells
26:25
accumulate as we get older, and it's been highly linked to processes like osteoarthritis
26:30
or cardiovascular disease, and so a big anti aging treatment strategy has been to
26:36
clear these from the system. And you can do this in a variety of
26:40
ways. There are peptides, for instance, like boxo for dri people might
26:44
be familiar with, or there are other nutritional supplements like biasatin or golden rod
26:51
extract. But we actually chose for our study a combination of the satine but
26:55
which is a cancer drug that's been used off label to treat sinescence. And
26:59
we also use corsetin um, which probably many of people are familiar with as
27:03
a sort of a botanical ingredient um and we use that over the course of
27:10
a year and a half in some patients, tracked them over five different time
27:12
points and we recently saw that actually all their biological age markers got a little
27:18
bit worse. UM, their telomere link decreased, UM, their biological aging
27:22
increased by most of these really good algorithms, UM and UH. And we
27:27
were really really surprised by that. UM. We did see markers of sinescence
27:32
being reduced, so we knew it was acting like a synalytic, but by
27:34
somehow doing that, it was also increasing people's biological age. And so that
27:41
was definitely a surprise. So how do you deal with that when you get
27:45
that result and now you're faced with communicating they you know, the result,
27:52
to the consumer and to the medical world. What how do you deal with
27:56
it? Publication number one, We want the data to be widely available and
28:00
peer reviewed. We also, i would say, want to make sure that
28:04
we understand our restrictions and restraints. You know, I am not by any
28:10
means saying that people should never use the synalytic or think about using synalytics.
28:15
I'm just saying that in our trial, these sinescent protocols were associated with increases
28:21
in these clocks, and so whether how that impacts people clinically is still a
28:26
question to be determined. There are many studies which have shown that synalytics improve
28:30
health span and lifespan and improve certain disease traits. We just got complict in
28:34
data in this one instance, and so I think you never want to overreact
28:38
too much, but hopefully more data is better, and as people start making
28:42
the decisions about what to do in their own health, or as physicians start
28:47
deciding how to treat their patients, this can be another piece of evidence which
28:49
they can weigh in their decision making process. Well, I certainly applaud you
28:53
for being so honest with people that are most dependent on your testing and you
29:03
in your research that you know this would be something that possibly could be hidden
29:11
if you were a pharmaceutical company. I'm not going to I'm not going to
29:15
denigrate directly, but I think a lot of these studies that we read about
29:19
in that world, in the elopathic world, very often there are studies that
29:25
are being done by people who have a bias, and that would certainly be
29:29
said of you. But yet you're telling the truth. So congratulations for being
29:33
so honest. Well, I think that's another important point as well, is
29:37
that we make an effort not to sell any products to fix this process.
29:42
Um. You know, we really want to focus on the best way to
29:45
measure the process of biological ating and other epigenetic ways to interpret data for health
29:52
outcomes. We don't ever want to turn it into a way to sell more
29:55
of our own products. UM and I think that we're probably the only epogenetic
30:02
age company out there that takes that approach. Most people will usually pair it
30:04
with supplements or UM and why I don't think that that necessarily is a badging
30:10
of itself. It does breed some of that conflict of interest that you mentioned.
30:15
Well, you know, they say truth will set you free, right,
30:17
so so truth and everything is always the best course. But so talk
30:22
to me in us our viewers today about aging and that aging really does matter.
30:30
Let's there's a few statements that you know have been certainly well publicized that
30:38
all aging starts in the cells, and that aging is a disease. So
30:45
could you take those two statements and define what true diagnostic perception is of those
30:52
two generalized statements that are out in the media. Yeah, So, you
30:56
know, I think I'll first I'll tackle aging is a disease because you know,
31:00
as I mentioned a little bit earlier, I think that you know,
31:03
the the FDA and the US government has not necessarily um you know, labeled
31:07
it as a disease, but they still give a lot of funding to age
31:10
related conditions. So for instance, the National Institute of Health has a division
31:15
called the National Institute of Aging, which is meant to help solve some of
31:18
these issues that increases we age UM and so I think that they're certainly recognizing
31:22
it as an issue, um, even though they're not quite sure how to
31:26
define it yet. Even groups like the Word Health Organization now have added DIAGNOSEDI
31:30
codes UM, where now someone can be diagnosed with a certain disease that is
31:34
a result of aging, so for instance, diabetes as a result of aging.
31:38
UM. And so I think that that we're starting to both just socially
31:44
and even in our political systems, start to even realize the impact of aging
31:48
on a much wider level UM. And that's great, And I think that
31:52
definitely is more consistent with what we think, which is that, you know,
31:56
aging is a process which can certainly be mitigated and improved um and and
32:01
so we certainly think that, you know, I also think that um,
32:05
you know, as aging help is on the cellular level, I think that
32:08
that is sort of what we're measuring, is we're measuring the DNA withinside the
32:12
cells, and we know that that correlates to outcomes UM, and so I
32:15
certainly think that that is also comparable. And so I would say that,
32:20
again, it's a wide debate is whether aging is a disease, but I
32:22
think that the answer would be, in my opinion, yes, UM.
32:24
And it's because it's something that we can mitigate and improve as we get older,
32:30
and we can quantify that process. Whether or not we can have a
32:32
reverse aging one hundred percent, whether we can live forever, I don't know.
32:37
I don't think at all at any time soon. But that doesn't mean
32:40
we shouldn't try. We shouldn't try and find what ways we can improve that
32:44
process. You know, there are some people who talk about something called the
32:46
longevity escape velocity. This is where our ability to sort of treat aging is
32:52
going to exceed our aging rate UM, so that we can might be able
32:57
to live, you know, two hundred years or more essentially forever with improved
33:02
biological processes. And I think we're a long way from that. But there
33:06
are amazing things that are happening in the field of aging that I think people
33:09
should be aware of. One of these things is called cellular reprogramming, and
33:15
for people who are not familiar with this, this is where they use technology
33:19
they want to know about Prize in twenty twelve called Yamenaca factors and the Jaminaka
33:24
factors are able to actually reset these epigeneta clocks to zero. They're actually able
33:29
to reverse these epigeneta clocks entirely. And there have been several studies, including
33:34
one notable one at Harvard, where they've been able to use these reprogramming growth
33:37
factors to reset these epigena clocks and in doing so restore vision to mice who
33:42
had been blind due to age related vision problems. And so we're getting to
33:47
where even we can make some amazing changes restore blindness, restore vision, i
33:52
should say, from blind mice, which is really really cool. And so
33:58
this field of aging biology is a very hot time topic, I think,
34:00
in in the zeitgeist, but also in the medical research field. There is
34:07
so much emphasis now on this is a technology and a way we can improve
34:10
health because aging is such a big part of the disease. And I know
34:14
we've talked about this previously, but I don't want to emphasize it again.
34:16
It is the biggest risk factor for every chronic disease and death. And so
34:22
if there's one thing, if you're a healthy person and you want to have
34:24
the best impact on your health, try and treat your aging as a primary
34:28
outcome because it's probably the best thing that you can do. And this dwarfs
34:31
even things that we know are really bad, like smoking and obesity. Most
34:36
people know this, things are very bad for you. But you know,
34:38
aging is you know, five times or six times a relative risk and even
34:43
some of those conditions, that's so important what you're talking about. And you
34:47
know those are controllable factors too that everybody can take responsibility for their own choices,
34:53
and those choices are going to affect the outcome. And you know you
34:59
mentioned the sinest since factor the synalytics and the fact that the cells do age,
35:04
but they age with influences. It's not just an absolute number, it's
35:09
it's it's an influenced by what you choose to do in everyday life. So
35:15
what are those factors you mentioned, smoking, drinking, alcohol, diet,
35:22
stress, what are some others that you would put in that list. Yeah,
35:29
so it's so really everything plays an impact and what these epigenet the clocks
35:32
have been able to tell us very early on are quite frankly not too surprising.
35:37
There are things that we already know, m so. And again,
35:42
I don't think that that's a bad thing. I think it's a good thing
35:44
because it's not conflicting with all the data that we already know. It's beneficially
35:47
affecting health span. Um so. So again thinks some things that this has
35:51
told us is obviously things like smoking and drinking are bad. Most people would
35:53
probably know that. It's also, you know, shown us that physical activity
35:59
is very good for us, you know, staying active as we get older.
36:02
It's even showed us, I would say, things that are a little
36:05
bit harder to quantify, like there are relationships, and the quality of our
36:08
relationships play a massive impact. Even you know, we've even seen in our
36:13
internal data set correlations to sexual sexual activity and sexual satisfaction improving some of these
36:19
markers or being correlated with some of these markers. And so there's a whole
36:22
host of things that depend on this, and that's really what this tool allows
36:25
us to do is to really quantify those in a measurable passion so we can
36:30
say, if you're going to do one thing, it is to stop smoking.
36:32
That's the biggest priority. Or hey, you know the next big thing
36:36
you want to do after that is to improve insulin sensitivity, improve your metabolic
36:39
health. And so we can sort of set priorities on what everyone should do.
36:44
And so we're finding out a lot of these things, and sometimes we
36:46
have some prising information that we wouldn't expect, as I mentioned with the synalytics,
36:51
that's a good example. We also have found that in our really really
36:54
good athletes, like our olympians or our professional athletes, sometimes they actually have
37:00
worse aging than some of their counterparts because it maybe ages they're exercising too much
37:06
and putting a bides under a little bit too much stress sometimes. And so
37:10
it's really fun to see these types of associations. A lot of the early
37:15
work has not been too surprising, but we're starting to find a lot of
37:17
things that now as we get more detailed, like the synalytics, which are
37:22
becoming really exciting. We have another study that's coming out very soon with standfed,
37:28
which is looking at vegan diets versus omnivore diets in sort of comparing which
37:32
one is better. Here they looked at twins. So they took a pair
37:36
of twins, identical twins, they put one twin on omnivore diet, one
37:39
twin on a vegan diet, and compared to their aging rates over the course
37:44
of eight weeks. And we didn't think that we would see a ton of
37:46
difference at all because it was only an eight week trial intervention, but still
37:51
across multiple epigenetic clocks to find not only by us, but other individuals all
37:55
showed that the vegan diets had a slight preferential benefit um in aging compared to
38:00
the omnivore counterparts, and so um that was surprising for us. And again
38:06
that's a that's a big one. Yeah. A lot of people would dispute
38:09
that because they you know, they're omnivores, right, so they don't believe
38:13
that that. I mean, they believe that their diet is the best as
38:17
long as you're eating grass fed and organic. But you're you know, getting
38:24
your B twelve and protein for so, you know, to think that a
38:30
vegan diet could actually be superior, yeah, definitely. If you break that
38:37
down, Ryan, what would be the reason that a vegan diet would be
38:40
superior? Yeah, so that's the next question we're trying to answer, UM,
38:45
is the why of it? Um And and quite frankly, the study.
38:49
You know, studies like this should always be taken in context. UM.
38:52
And you know, I think studies like this the one that we did
38:53
in particular, UM, we're surprising, but they also have left limitations which
38:58
maybe impact it's application to every individual m. For instance, some of the
39:01
twins we had in this study were at relatively younger middle age, and so
39:07
whether or not these this vegan diet would hold out to older age groups,
39:12
maybe in their seventies or eighties, where they might be experiencing more muscle loss
39:15
and less protein UM for instance, that might not be the same case.
39:21
And so every study has limitations. But I think that UM, you know,
39:25
these trends are starting to accumulate evidence, and as they start to accumulate
39:29
more and more evidence, they can push us in the right direction. UM.
39:31
And so I think that one of the reasons that we were speculating that
39:35
this vegan diet had a beneficial change was probably because of some of the micronutrients
39:39
or the microbiome changes that were involved with some of these diets. But eight
39:44
weeks is a very short intervention time as well. You know, most people
39:47
wouldn't say that eight weeks of anything could drastically change their health behaviors. And
39:52
so again it's worth taking with with you know, some of those caveats.
39:58
But I think that as this data grows, we're going to be able to
40:00
pull on those threads a little bit more. So we can sort of ask
40:02
the questions exactly like you did, What part of this is most beneficial to
40:07
this agent penotype? Yeah, because everyone is every body is different, their
40:12
biochemistry is different. So it's really hard to u customize well to generalize about
40:19
which diet approach is best because it is different. People have different biochemistry that
40:24
would be responsive in different ways. So I think that would be a really
40:29
difficult conclusion to come to. So so Ryan, if you wanted to access
40:36
to diagnostic algorithm, you know, become a client, a user, what
40:43
is the what is the what are the steps? I mean, how do
40:45
you do it is? What is the method by which you measure? How
40:49
does the patient or the client get you what you need in order to diagnose
40:55
what they need? Yeah, so this is also another important point which makes
41:00
us a little bit different than some other companies in the space is because we
41:05
only use blood as a tissue method. And this is a important because every
41:09
cell is different and it's epigenetic expression, as we've already talked about right,
41:14
epigenetically, your heart's expressing a lot of different genes than your skin. And
41:17
so with that being said, you know, tissue type is important, and
41:22
most of these algorithms have been created off of one tissue type, which is
41:25
blood. And so we only use blood in our analysis to make sure that
41:30
it's consistent with the studies and the published data. So for us, we
41:35
asked for a blood sample. But with that being said, our blood sample
41:37
collection is very very easy. If someone wanted to do this testing, we
41:40
could order it on our website. We could send it to them and then
41:44
they would just prick their finger for a couple drops of blood and put it
41:47
on a dry blood spot card. I actually have one here. I'm taking
41:50
my sample this morning. They have one right there. This is what it
41:53
looks like, one of the purples filled with blood. That's not enough blood.
41:58
You need a little bit more than that. But then they can send
42:01
it back to us and we get an analysis within three weeks. And the
42:07
other beautiful thing about I would say our platform is that as our ability to
42:10
analyze this data becomes more robust, we actually update data that has been taken
42:16
even from three years ago. So right now we're adding new algorithms to our
42:22
platform to quantify physical performance things like your VOTWO max or your grip strength or
42:27
your walking speed, and we'll be updated mapp for anyone who's done a test
42:30
with us over the past three years. And so I think that for anyone
42:35
wants to do the test, it's a relatively simple process. A few drops
42:37
of blood and then you send that back to us in a simple envelope and
42:42
we do the analysis. Well, I know that when I did mine,
42:47
which I am really excited to hear the results in another week or two.
42:53
But when I did that, I had trouble filling up that circle. I
42:59
dive at a lab with a bottom a show that I could make sure that
43:04
I got it right, but he had trouble. So what if you don't
43:07
have enough the blood doesn't fill up that circle, can you still do the
43:12
test? Well, so we need enough DNA to do the analysis, and
43:15
if we don't have enough DNA, we might have to recollect, but we
43:19
do have other methods to collect DNA or for blood UM that are sometimes easier.
43:24
They tend to be maybe a little bit more expensive, but we have
43:28
ways that are painless. Collection devices you can even just slap onto your arm.
43:31
I have a few of them behind me um but uh, and it
43:36
collects enough blood that you can send back to us very easily. I think
43:38
they're an additional thirty dollars, but they're very easy to do. You just
43:43
press one button stick on your arm, press one button and it collects enough
43:45
blood if you if you if you are also are to prick your finger,
43:51
these can be a really good method as well because they're they're virtually paying.
43:57
So our website is trudiagnostic dot com. That's tru Diagnostic, nos On Diagnostic,
44:05
so true diagnostic dot com. You can also email me directly if you
44:08
have any questions at Ryan at trudiagnostic dot com, or you can reach our
44:13
support team. They might be a little bit quicker at getting back to you
44:15
at at support at trudiagnostic dot com. We're happy to answer any of your
44:21
questions, provide you documentation or answer. I would say anything within the process.
44:25
And and Michelle, I know that one of the things we really wanted
44:29
to do for anyone listening on this podcast was to offer a way to even
44:34
discount some of this testing, and so we did create a twenty percent off
44:37
code. If someone goes onto a website and uses the promo code Michelle twenty,
44:43
they'll be able to get an additional twenty percent off as well. That
44:45
is so sweet of you and generous, and we really do appreciate that because
44:50
we want people to be aware that well, I think the test is what
44:54
for ninety nine if you're just coming in directly and if you to come in
45:00
through the Michelle twenty code that Ryan has so generously offered for the first time
45:07
users, you get a twenty percent off of that five hundred dollars price.
45:13
So that's that's one hundred dollars savings right definitely, And we'll keep that open,
45:19
I think, for for a couple of months in case anyone wants to
45:22
use it. UM. You know, we we do recommend always retesting as
45:25
well. UM. Oftentimes people will always ask us what's the frequency we recommend
45:30
that testing, and we say no more frequently than every six months. Uh,
45:34
you know, we really like enough time to go buy UM in that
45:37
testing to make sure that we're actually seeing real biological change instead of just noise
45:43
and in the measurement UM and so we say at least six months UM and
45:47
we'll keep that that that code open for six months or so just in case
45:52
anyone would ever want to retest as well. So what are some of the
45:55
interventions that you would recommend and to people if to basically get that seven year
46:02
biological age events a target number for everyone to start with reductions? I mean,
46:08
so that they have a biological age seven years younger than their chronologically age.
46:14
That's kind of the target number that you mentioned. So what are what
46:17
are some of your favorites for improving your biological age? Yeah, certainly,
46:24
I think UM, you know, and really easy to get into to perform
46:31
UM. The number one of which would be chloric restriction. UM. I
46:36
know it's not a fun topic, but but eating less calories than you're burning
46:42
is one of the most well validated interventions across multiple species for health span and
46:46
lifespan extension UM and UH. And there was actually a study published by some
46:52
of our collaborators who created one of our algorithms that you need in pace algorithm
46:58
UM that they showed over the course of a two year color restriction study right
47:02
around eleven percent. So these people were, you know, taking the amount
47:07
of calories they burned per day UM and basically multiplying at times point nine and
47:12
that's how many calories they were eating per day UM. And over the course
47:15
that two years, they had reductions in their biological age. And so that
47:19
is a tried and trough method that we say would work for everyone, and
47:22
it's actually not expensive. It's just actually less expensive than your current behavior.
47:28
And so it's yeah, exactly, so what will would you say, intermittent
47:32
fasting has in your protocol? Yeah, So the unfortunately we don't know yet.
47:37
Muh. What we do know is that what we have measured in that
47:42
particular study was just the overall amount of calories. In terms of when and
47:46
you're consuming those calories, we're not quite sure UM. And so I think
47:51
that's still we need more work to be done there UM. But with that
47:55
being said, I think that we're really excited to see where that goes.
48:00
UM. One other intervention that I would say everyone could benefit from UM and
48:06
it plays a major impact in some of these algorithms, is UM is stress
48:10
production. This is something that I can even relate to that has helped me.
48:14
Um. You know, stress pays a major impact in some of these
48:17
these different conditions, and in just mitigating your stress can play a major impact.
48:22
So just cortisol measurement come up in your DNA methylation results, so people
48:30
know what their stress level is. So it hasn't yet. But actually it's
48:35
funny you mentioned that, is we just create a predictor of cortisol um UH
48:38
in some of our cohorts, and so we hope we might be able to
48:42
add it soon. UM. But we do know that a lot of those
48:45
cortical signaling genes play an impact. And actually, um, you know,
48:49
even things like ptsd, UM and UH depression all show high associations with increased
48:54
biological aging UM and and so mitigating some of those high stress sort of bad
49:01
neurological environments even can play a major impact in improving your biological age. And
49:07
again, those are things that everyone can do. I think. Beyond that,
49:10
there are a couple other things like supplements that are very accessible, like
49:15
vitamin D for instance, have been sharing multiple studies to improve biological aging.
49:22
We also see a really good trend with other things like DHA for instance,
49:25
sort of one of those hormone metabolites or precursors that tends to diminish as we
49:30
get older, but with supplementation shows some improvements of biological age. And so
49:37
those are some other I would say tried and trude methods that really really work.
49:40
What would you say is the optimum level in your blood of DHA and
49:45
vitamin D twenty five? Yeah, So, unfortunately with the biological age studies,
49:51
we didn't directly quantify the measure in blood. What we did is we
49:54
actually took patients who supplemented with these protocols and then measured there before an after
50:00
change, and both for the DHA as well as the vitamin D, they
50:02
saw improvements. So we're not quite sure what the optimal level is within your
50:07
blood. That would certainly be a study we'd love to do and they're actually
50:09
working on. But at the moment, we do know that the generally supplementation
50:15
tends to help m So what about peptides. I know you started in that
50:20
world, and of course the peptides have gone to another whole level of complexity,
50:27
particularly as we had doctor Bill Laurance on and I know you work together
50:32
last week, and he talked about the peptide bioregulators, which is, you
50:37
know, a different subcategory of the peptides in that they are amino acid.
50:44
It's not synthetic. And I know you started out with you know, the
50:49
BPC one fifty seven, the PC one forty one, all of those are
50:52
all well and good and much more established. How do you feel about the
50:57
peptide bioregulators out of Russia as a protocol that you would recommend to people.
51:04
Yeah, so it's unfortunately we don't have a lot of data yet. But
51:07
as you mentioned, Bill Lawrence is doing amazing work there generating such a robust
51:13
data set with so much great data that I'm really excited to do some of
51:17
these big meta analysis with him and hopefully we publish and in the very near
51:21
future. But at the moment we're sort of blinded to some of that data.
51:24
So this is so new that anybody who wants to jump in is getting
51:29
into a field that you a true diagnostic where a lot of this data data
51:35
is assembled and diagnosed and deciphered for the outcome, for the best benefits for
51:44
biological age reduction. So you're still in the you know, the research phase
51:50
of that in terms, but you are interested in obviously finding some answers because
51:54
this is you know, in Russia they've been using these for forty years.
51:59
Yeah, definitely, and I think the US we're just getting becoming aware of
52:02
them. But you can't go on the internet now without having at least five
52:08
or six podcasts and other means of communication on this field of peptide bioregulators.
52:17
So thanks to Bill Lrons and Phil Mickens in London with Aging Matters, and
52:25
he's been a guest on our podcast as well. So actually you you becoming
52:30
a guest on our podcast was the result of those two people, and also
52:35
doctor Graham Simpson, who has been one of your huge fans and advocates.
52:40
So yeah, so we're very very happy that you've come today to give us
52:46
the beginnings of an awareness of something that will be basically be a tool.
52:52
You know, if you want a tool chest, look at True Diagnostics as
52:55
a way to begin your process of understanding how to control your understand first what
53:02
your aging is and then once you have the parameters, know how to deal
53:09
with the improvement. So Ryan, thank you so much. We run out
53:15
of time. I'm really happy that We've finally got this talk with you,
53:20
and what I'd like to suggest is as you get further along in some of
53:23
these studies, that you keep in touch with me and that we have you
53:28
back on so we can update people on some of the results and have another
53:32
go at this. Because this is a very fast growing and and very it's
53:37
complex, but it can be simplified by people like you so that people the
53:43
consumer can understand what they need to do. So I really appreciate all your
53:46
efforts in this very, very exciting field of anti aging. So thank you
53:54
again for coming today. Is there anything that you would like to say just
53:58
to sign off today and to our viewers, Well, I just want to
54:02
say thank you Michelle for having me. It's been wonderful to be on UM
54:06
and you can't wait to be back. I think with more information as we
54:08
start to uncover it, and I hope that everyone really takes away the message
54:14
that you know, aging is important and you can impact your own aging progress
54:17
UM. So hopefully we'll talk against them certainly if if they one orders wants
54:21
to reach out to us directly, you can reach us at support at True
54:23
Diagnostic, that's tru Diagnostic, Okay, yeah, and if you'd like to
54:30
order a test, you can go on to our website, UM and use
54:31
the promo cold Michelle twenty um and that gets one L and Michelle, yes,
54:37
thank you for saying that. Forgot about that definitely, but in for
54:42
twenty three percent off and uh and if you have any other questions about the
54:45
test, don't hesitate to reach out. Yeah, and if they want to
54:47
reach you to ask any questions, you're so available. So it's Ryan at
54:52
True Tru Diagnostic without thes dot com. That's correct. Hey, Ryan,
55:00
Well, thank you again and we'll be talking to you as we go along
55:02
here the next few months. We want to keep peep up with what you're
55:07
doing. So thank you for being with us. Yeah, thank you so
55:09
much, Michelle, appreciate you. Okay, take care, everybody, have
55:12
a beautiful day. This is Michelle Hughes signing off.