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Welcome to a special episode of the drive. This is an episode that is set up like an AMA where Nick is asking me questions. However, this will be an episode that is available to everyone where this differs from most amas. Is that in this episode? I haven't seen the questions beforehand and I come in kind of blind as such, whereas most amas, go, an inch wide and a mile deep.
Here we go. I would say a mile wide and a foot. Deep for this conversation, the team pulled, some of the most common questions that we are asked, including some that I traditionally can't stand answering. Of course, I have no choice here and therefore, we go through those in today's podcast wind up talking about why? I don't think people are currently going to be able to live to 120 150 or 180 some of the claims. You see out there all the time. We talk about what supplements, I take and why you shouldn't just blindly follow me by taking the same thing.
Talk about how to lower your apob with and without medications. Talk about how I think about taking statins over a long period of time. And what we know about other a SCV, demodulating drugs today or in the pipeline talk about why there's no such thing as good or bad cholesterol? Why nutrition research is so hard? How I think about the question of quote, what is the best diet? How I hit my protein targets throughout the day? What my current favorite wearable is and what the role for CGM is in non
On diabetics and much more. If you're not a subscriber, this episode will hopefully give you some insight into our amas. Although, as mentioned earlier, the format here is a little different without further delay. Please enjoy this special episode of the drive.
Peter, welcome to a special podcast, how you doing doing pretty good, good. So today's episode, we're going to do something a little different. It's going to be kind of like an AMA Style.
Or you're the one answering questions, but it's going to be an episode that's available to everyone. We've done this a few times in the past usually are strong convictions, Lucy held episode celebrating. The 100 200 episodes. Those are just received really good feedback. And so what we decided to do was do another type of those episodes, but instead, pull some of the most frequently asked questions that have come through the site. And so we organized them a little bit by various topics.
Yeah. But this is going to be an episode. That's kind of more old-school style where it's just question. Answer a lot of these questions you haven't seen before which is probably good because some of them you've always refused to talk about on a Mac such as what supplements do you take? I know it's not your favorite subject to go into those details so we're going to get into them today which I think will be good and I think it should just be a fun conversation where you're coming into this blind.
And it should be really interesting. I think for the listener and viewer. So with that said anything you want to add before we get
started, why do people care what supplements? I take,
we can save that for the question. We will get to it and I think people will find it enjoyable. The other thing I should say is, do you know why I'm also excited to have this conversation today of all days with, you know, as our friend Karla Brown, would say, based on some emails, weaves exchanged earlier, you
Kind of seem like you're in a spicy mood today. So, I think it's going to be kind of fun to go through these questions. What do you
think? I think I am in a very spicy mood.
So, for the listener and viewer, this should be a fun one all around. With that said, first question, when people think of longevity, a lot of times in the space they think of living to 120, 150, 200 years old.
I think anyone who's listened to your podcast, read the book listener. Views you've done. You're not really in that camp of very confident that we're going to live to 120. 150 years old, one of the common questions we get is just Why is that? Why do you think that's maybe not possible and the follow-up? Would be based on that. Why do you think it's important to act and live? Like we might only get to 90 years old.
This is a bit of a complicated question.
So why do I not have confidence in the biohacking, your way to 120, 150 180. I've heard all of these sorts of numbers because I don't think we have the tools to address the underlying aspects of the Aging of biology that are relentlessly pushing us towards the end of our Lives. Again, that's not a depressing statement. I think it's just an obvious reality, right? So,
There are things about us as we age that we have the capacity to reduce the rate of change on, we can slow them down, but I've seen no real evidence that we can reverse them in a meaningful way. Now, it's true that there are some people out there claiming they've got their aging clock, and it shows that even though their birth certificate says they're 60, they're really 35. We could put some time into explaining why, that's not correct. So
The long and short of it is, we don't have any evidence that we can take the diseases of aging and erase them or that we can take the underlying processes of everything from defects in mitochondrial function defects in protein, folding and misfolding changes in DNA, breaking and repair breakdown in nutrient sensing all of these Pathways. I haven't seen any evidence that we can undo that so then,
Would you have to believe? So if you're going to believe someone my age, IE someone who's 50 is going to be around in 70 years, you have to believe that in the next dozen years or so. Someone is going to come up with a way to completely halt aging and or reverse it. In other words, it's not going to do me any good if this happens 50 years from now because in 50 years, I probably won't be here. And I spend a lot of time looking at
This type of literature, I really do spend a lot of time. Looking at this technology, I haven't seen many examples where there's a bigger mismatch between what is actually happening scientifically and what is being talked about in the Press on social media on podcasts and that Chasm is enormous. In other words,
what's really happening is like nowhere near
the Sci-Fi? That's being portrayed, so, because of that and because I
Confidence that what's actually happening is more a representation of reality. I know that these things are not a decade away. That's why I take that point of view. Now, why does all of this matter? I think this matters because if you knew that this was as good as it was going to get and I don't think it is. By the way I do think there are incremental things that are going to make a difference even in the lives of people my age. But if you thought that look, this is directionally as good as it were going to get I
kit would motivate you to be more serious about using the tools that we have today for primary and secondary prevention of disease for optimizing and maximizing lifespan and healthspan if for no other reason you would do that as a hedge against the enormously long odds that something dramatic and miraculous is going to happen in the next decade or two
to double-click on a few things there when you were talking early on about diseases,
Were those diseases. What you call the four horsemen from your book? Is that what you're referring to? Yes,
you still have to have a strategy that says, how are you not going to die of a s cvd cancer, neurodegeneration dementia, and of all of those diseases the only one where I can see a pretty clear path to delay. It significantly would be a SCV D if you take really dramatic Steps early in life instead of
Talking about what we think of as primary prevention, think of ultra primary prevention, treating people in their 30s. Making sure a person never ever walks around with an APO, be over 30 or 40 milligrams per deciliter. Making sure a person doesn't even spend one year with mild hypertension. Making sure a person is always metabolically healthy. If you do that, I agree. You would not get atherosclerosis in a normal lifespan, but we don't have that
We have certainty for pushing off cancer indefinitely for pushing off, neurodegeneration indefinitely for pushing off dementia indefinitely. Nor do we have it by the way for pushing off, I think sarcopenia indefinitely are pushing off arthritis in. Definitely mean there's these other conditions that are not as interesting to think about because they don't rise to the level of the horsemen but they matter a lot. So physical Frailty is a really really really big one. If you manage to not die of heart disease
Disease cancer. Neurodegeneration dementia.
And you're willing to train really hard, like I really do think there's a path to be physically robust as a centenarian but I don't see a path to doing that at 120 or 150 unless there is a significant technological breakthrough. That would basically allow us to rewind and maybe this is a different discussion and maybe it's a longer discussion Nick and I don't know if we want to go into it because it's taking a little off topic but it really gets into. What does it mean to age at a cellular level?
Level. What is the role of the epigenome in regulating our genetic code? I don't know if there are other questions about that topic, but we could certainly defer to
that on that topic, I know that's talked a little bit about in the episode with David sabatini, Mac came Berlin and so maybe we'll pull questions from there and do a future. Am a kind of diving into that a little deeper kind of what I'm hearing you say is you still think that we will succumb to the same diseases that will kill us?
Goal with medicine 3.0 and prevention is still to put that off as far as possible. But that doesn't mean you're going to put it off until your 120 years old. The goal is to really live as robustly as possible and avoid those as long as you can, but still more in the traditional lifespan opposed to the 150 year old lifespan.
I think that taking all of the steps that I talk about in the book and could seriously a decade to life, I don't doubt that you can live a
Decade a decade and a half, maybe two decades longer. I don't doubt that, but I don't think we're talking about adding 30 years or 50 Years to Life Span. What I think is more important is that whether you're adding five years seven years or ten years to your life span what I think is much more interesting and much more important is reducing or compressing the period of morbidity late in life.
What I think people should fixate on is how do I not be really, really frail, both physically and cognitively in the last decade of my life, what I call the marginal decade. I don't know if I'm going to live till I'm 85, or 90 or 80, or whatever. I mean, I don't feel like I have as much control over that. I think there are some elements of bad luck that factor into that. What I feel like I have much more control over is when I'm in my marginal decade, can I still go?
Go for a rock. Will I carry 80 pounds on said Rock? No way, but I might be able to carry 10 or 20. Will I be able to swim half a mile in a pool? Yeah. Will I be able to swim it as fast as I can? Now no chance. But I could still swim half a mile and get out of the pool under my own power, could I sit on the floor? You know, it's all those things that I talked about in the centenarian decathlon. Those are the things I think that we really want to relentlessly fixate on because I think most people would rather live to 90 and
Died of a heart attack while swimming in the ocean, but being otherwise in remarkable shape than live to 120 and spend the last 30 years of that unable to do much
earlier. You also mention there's incremental things, you think that could happen that will help someone even your age at 50 live longer. Do you want to just lightly touch on what a few of those things are that you are talking about? They're
one of the most interesting, and I talked about this on a recent podcast with David,
Sabatini and Matt K Berlin is, I still think we are really in early days of understanding what pharmacologic inhibition of mtor can do. There's really a lot of promise with this approach in virtually every other model species outside of humans. And that doesn't mean it will work in humans but it's very interesting. And I think if we had better biomarkers again, I think that's something that can happen in our lifetime. I think that's a very
In strategy and it's especially promising. When you consider that the animal models show that pharmacologic inhibition of mtor using rapamycin or its analogs even applied late in life. Still provided lifespan and healthspan Improvement and why that's interesting is very few other interventions that have shown to be Jarreau protective work when applied that late in life. So that to me is very promising.
Ting
last question on this aging, topic would be let's take someone who's listening maybe your age but they have a son, or a daughter. Who is 10 years old? How do you think that 40 year, timescale, differs, as you look at a 10 year olds potential life span today compared to your 50 year old lifespan today? That's
a good question. I don't know, look, I'm that guy, right? I mean, I have a six year old and a 9 year old to 15 year old and I often think about what's the difference.
Between me and them. In terms of their Runway versus mine vis-à-vis, the types of technological breakthroughs that were interested in. And again, the one that I'm most interested in is probably on selective and High Fidelity high-precision. Modulation of the epigenome, I don't know, the answer truthfully. I simply don't have a way to predict the pace of that type of innovation and of
Course, not to be a doomsday, ER, but even though they have a longer Horizon for good things to happen, they also have a long Horizon for bad things to happen and when I think about bad things that can happen to our kids, of course, you can't help but think about nuclear war, by the way, in order. How would I rank them? I don't know. Probably I would say biological terrorism would be the single greatest threat to our species simply based on the low barriers to entry.
The ease with, which there's proliferation. But again, you could sit here. And debate, what's the greater threat to our species? Is it nuclear war, is a climate change. Is it biological warfare? The point being here? They have just as much time to be exposed to really bad things that could obliterate our species as good things, that could extend the life of our species. So I just don't know how to handicap the pros and cons on
that that could be your next book. We could call it the fifth Horseman and it could be all about that.
That's a good intro into this next section, which gets into drugs and supplements and the most common questions we get asked there. But I think you mentioned one thing in the agent section that I think would be worth touching on real quick. I think it will affect what we talk about here which is we really don't have biomarkers for aging and you've been open about frustrations with that because when you look at your protective molecules and you look at if these things are working or not, we
I really don't know because we don't have those biomarkers. So do you maybe want to talk about that for just a minute to kind of set the stage? So when people hear your framing for everything else, I think it will make a little more sense. I think one of the
most important things to understand, when you're using some sort of intervention is, do you have a biomarker to know if you're doing it correctly? So think of like really basic things that most people don't even consider as interventions, like nutrition. How would you know?
So, if you're eating too much, do you have a biomarker
for it? Sure, there are lots,
one biomarker, might be your weight. Another biomarker might be your waist circumference. Another biomarker might be your insulin level, your glucose level, your average glucose. I mean, you get deeper and deeper down this and you start to realize that how much you eat. You have a way of getting feedback from the system that tells you do you need to correct.
This the same is true for exercise. The same is true for sleep, so there might not be a lab value, that is specific to sleep, but there are clearly ways to get feedback to know. If you're sleeping too much or not sleeping enough. If you think about it through the lens of taking exoticness molecules, you take a drug like lisinopril an Ace inhibitor for lowering blood pressure. How do you know if you're taking the right amount, you
Measure your blood pressure. Let's say, you get started on a dose of Lisinopril when you're starting blood. Pressure was 135 over 85 and all of a sudden it's 115 over 75, that says the drug is working, are you symptomatic? By the way, that's another biomarker in a sense. No, you're not lightheaded. Great, everybody wins the game. If your blood pressure goes too low and or your symptomatic, which is probably the bigger issue than you're taking too much, you have to dial the drug back. If your
King the drug and your blood pressure comes down, but doesn't come down enough. That's more feedback, dial the drugged up. So you have this sort of input output ability with every drug that we like to think of. Again, the same is true with drugs, for diabetes with drugs, for lipids with cancer drugs that you take, you would be able to look and study is the tumors shrinking is the tumor growing. So you have some, we're getting feedback. Well, the problem when it comes to gyro protection, this broad category where we are not targeting diseases specifically but instead
We're targeting the underlying mechanisms of Aging, as we can't measure it, we don't have a way to measure it. So we take a drug, we take a supplement that we believe is gyro protective and we don't know if it's working. Are we taking enough? Are we taking too much? Maybe if you're really lucky, you might find a side effect. That tells you you're taking too much. But do we really want to be in the game of pushing things to the point of seeing over at side effects. So that's
Why I believe as unsexy as the world of Diagnostics and biomarkers are and it is a very, very unsexy world. I mean, this is not a place where people like, investing money. This is not a place where there's an enormous amount of capital being thrown at the problem. It is a very important problem and it's going to be very important in humans. If we're interested in studying, gyro protection, probably the very first time I went on kind of a long day.
Diatribe on this was back. When I was really really obsessed with trying to understand the perfect routine for fasting. I'm sure you can recall this Orca, 2018 2019, 2020, I was very frustrated that as much as I was trying to study this in myself and doing every sort of blood analysis Under the Sun, I had no way of knowing if my fasting protocol of seven to ten days of water only once a quarter three days, once a month, was that too much was that
Little, was that doing anything? No idea to this day, I have no idea if that provided any benefit at all, I could certainly point to some negative things. It did write it cost me probably 20 pounds of muscle over six years, but maybe that was a worthwhile trade-off given some other benefits. But how would? I know, don't know what the benefits are. Don't know how to measure it. It's a very important problem and it's one that I hope more and more resources will be poured into because otherwise it's going to be very difficult for us to move.
Of further in understanding what works in
humans on that. I do actually have another framework question, which before we get to the list of supplements, which I know people are anxious to get to. You've often talked about your analogy of. Are you picking up a gold coin or a penny? Are you picking up in front of a train or a tricycle? And often times when I've heard you use this, it's a lot of times as it relates to interventions specifically drugs and supplements. Do you maybe want to quickly give people what that framework is because
think it is really important based on everything you said, which is a lot of this is kind of a guessing game and we don't really know. So we kind of need to Anchor it to another framework to try and figure out what are the risks and what are the potential rewards as we try and figure out what then ourselves. What are we willing to do and not do?
It's nothing more than a very simple Matrix of risk and reward which I'm sure anybody would easily be able to walk themselves through. All I do is just to make it easier.
To remember, I just put very obvious concrete examples in the corners of the Matrix, so it doesn't matter which axis is horizontal or vertical. But if you just say that the horizontal axis represents risk going from low to high and the vertical axis represents reward going from low to high you would say, okay at a, very extreme level low risk is bending down in front of an oncoming.
And as you move from left to right on that horizontal axis, it goes to jumping in front of a train track and grabbing something and then getting off the train track. So that's going from low risk to high risk. And in terms of reward, you would think of a penny being pretty low reward. And you'd think of a big fat juicy gold coin being very high reward. So as you go from higher risk, you would expect and demand higher.
Reward. So, I'll tell you a story. I'm embarrassed to say this because it speaks to just how stupid teenage boys are and how much of a miracle it is that our species still exists, with the utter lack of judgment that exists in the presence of young boys. So when I was in high school, one of our favorite games to play was when we would get off the train we would immediately jump under the train and see who could lay the most
Queens on the train track and then get out as quickly as possible. So that once the train started rolling, you could see how many coins got flattened. Just think about the abject stupidity of this game. Another game that was tragically very popular when I was young was playing Chicken in front of the subway, in Toronto who could be the last guy out and very sadly, the younger brother of one of my friends in high school did not make it.
Doubt he was killed by a Subway. Playing a stupid game of chicken. Talk about incredibly. High risk for no reward. So how do we apply that to interventions? I guess we're talking about this through the lens of supplements. Well, I think we have to acknowledge that there's a great uncertainty with many of these things and therefore we should ask ourselves. How can we handicap the risk based?
Human data, animal data, safety data, efficacy data, as far as reward and we're on that Matrix. Do we place this intervention? So if you're going to take, I don't know fill in the blank. Some fancy supplement. That's internet Guru is telling you like he's making with his own proprietary blend of crushed bird feathers, and testicular juice. Okay? I mean do you want to take that risk?
Because it's hard for me to imagine the reward is really there. So one of the things I will push my patients on is when they show me their laundry list of supplements, I walk them through a framework about thinking through it. And one of them is where are you on the risk-reward Matrix?
So with that said, let's get into Peter RTS list of supplements that he takes. You can pick whichever one you want to start with.
For some reason I hate talking about this only because I noticed that it tends to show up online and
How becomes like, well, if Peter does this, you should do this or something like that, and there's no context to it and therefore nobody understands the rationale, nobody understands the clinical history, and all those things. So, with that caveat, which I don't think matters. Cause I just at the end of the day, don't think people care. I think a lot of people just are sort of searching but I take EPA and DHA. So I take fish oil again, I'm happy to even State. The brands that I take of these
Things because I don't have any affiliation with any of these companies. And frankly, I like to give a shout out to companies that I think so good products. So, I use Carlson's EPA and DHA. I can't remember exactly which one I take, I can never remember their names their so convoluted, it's like super EPA or something. But it is the highest EPA version that they have. So by taking four of these capsules a day, I'm taking roughly 2 grams of EPA a day, and probably a gram and a half of d.
Jay, the reason I take that much is I'm treating to Dos. I'm treating to a red blood cell membrane concentration of EPA and DHA of about 12 percent. So, that's a blood test. You would do you have a biomarker that I can use to say? I'm taking too much. I'm taking two little. Here you go. I take vitamin D, I'm sorry that I'm blanking on the brand. I can see the bottle, but I'm blanking on the brand. I take 5000 IU of vitamin d. Y, largely,
Because this is one of those things where I think the risk is insanely low. I think this is really a tricycle and I'm not sure what I'm picking up. I think it's more than a penny, I definitely think it's less than a gold coin, it might be a five dollar bill but I'd pick up a fight. If I was walking down the street and there's a kid riding a tricycle towards me and is a five dollar bill, I would pick it up. I think that most of the studies on vitamin D have been very poorly done and we do need to do a podcast.
Just on this. Maybe this is something we could deep dive onto an AMA, so I won't get into it more now. But having looked very critically at the vitamin D literature, which is insanely underwhelming, I think it is almost assuredly. The result of very lousy studies that add no value to our understanding of the problem. So, the dosing has been wrong, the duration has been wrong. The compliance has been wrong, and the targeting has
I'm wrong. Everything has been blown and so, I would say, we truly have no idea, I take slow mag. That is a brand, and I take two or three of those every day. So that is a slowly and completely absorbed form of magnesium. All in all, I'm trying to get up to about a gram of total magnesium or Elemental magnesium in my system a day. And I get that through again through slow mag through magnesium, L3, and ate, and threw magnesium oxide. So I take all of those
Things. I take methylfolate and methyl B12. I use jarrow as a brand. Again, here we do have biomarkers. You can measure B12 levels, but more than anything, I'm measuring homocysteine levels. That's why I'm taking methylated versions of those. And basically, I take these to keep homocysteine below 9, that for me just means just taking one a day. So, I take the standard dose of that they do make it into strengths and I take the lower of the two.
To in part because my MTHFR Gene most of us have variance of MTHFR. The variance I have are reasonable at methylation. This is actually an interesting change. I used to take 50 milligrams of B6 daily. I've now lowered that to three times a week. We have seen some people who when they take too much B6 can actually develop a sort of neuropathy as a result of it though, I've never experienced any symptoms from it a little further.
Getting has led me to realize we don't need nearly as much B6 as I thought we did. So I've lowered that to 50 milligrams three times a week and it helps with the homocysteine, you just have to be careful that you're not. Overdoing it I take a baby aspirin a day. I think the evidence for the use of baby aspirin in cardio protection is pretty weak. This is kind of a soft call. I don't think there's an evidence-based reason why I
I should take a baby aspirin and there's even some evidence to suggest that once you get significantly older unless your risk of cardiovascular disease is significantly High, the benefits of it, which are clear, there's no doubt. There are benefits of a baby aspirin. But there are outweighed by the bleeding risks, that are associated with aspirin. Use in particular. If you fall and hit your head, that becomes a bigger liability baby. Aspirin use Falls in and out of favor.
Over time, given that, I am very young relatively speaking to the study populations and not really at risk for bleeding injury. I think of this as picking up like a dollar or two dollars in front of a tricycle at this point. But again, I'm always happy to re-evaluate the use of this and any supplement for that matter, in the presence of new data, that might be it for daytime supplements in the night. I take ashwagandha, I take
100 milligrams of ashwagandha. I recently switched to the soul gar brand. I take two grams of glycine. I use the thorn brand. I take magnesium, L, 3 and 8, which I just mentioned, I use the mag teen brand. By the way, anytime you're buying, magnesium, L3, and eight, just make sure it has mag teen in it. So you could buy it from any different company, but they have to have
the mag team, proprietary combination, because they're the only people that have the license to make all three and eight, occasionally for travel. I will take Jerry Rose, phosphatidyl serine. It comes in 100 mg capsules or gel caps for some reason. I like the gel caps better. No idea if they're just more quickly absorbed. I truly have no idea and I'll take if I'm really going to the trouble of taking it, I'm presumably on a long flight where I'm trying to overcome a significant time zone.
I usually take about four hundred milligrams. That's a compound that's been tested. Readily up to 600 milligrams. It's possible, I'm forgetting something else but I think those are my supplements. Sorry, there's two others, I take but they're not in the cabinet and that's why. So I take athletic Greens in the morning disclosure. I am an investor in that company. I'm also an advisor to that company. So I take a G1 is a green drink in the morning and I take a probiotic called glucose. I think it's
glucose control by a company called pendulum. So I take two of those in the morning with my AG. That's kind of like the first thing. I consumed in the
morning with those, just on the whole just because you take them, not everyone should take them and you're looking at your medical history. What percent of that, let's say the same drugs, the same supplements in the same doses. Were you taking a year
ago? How is this changing? Yeah.
Yeah, so that way, if someone listening to this down the road here is it they don't
Matically. Just go do the same thing.
Yeah. So a year ago I was not taking the pendulum probiotic. That's something I've only been taking for a couple of months and I'm doing an experiment there which is looking at average blood glucose. So the reason I'm taking this particular probiotic, as I believe having looked at all of these probiotics. I think this is the most rigorously tested and validated probiotic out there and in a small but double blinded
Um, eyes clinical trial, it demonstrated a point, six percent, meaning .6, absolute percentage, Point reduction in hemoglobin A1c in people with type 2 diabetes. And that was only a 90 days, which is pretty interesting. It also was associated with, I would say more than associated with it. Demonstrated been caused about a 30% reduction in postprandial, glucose AUC area under the curve. So, meaning when you gave people a glucose Challenge, and then measured and
Plotted a graph of their glucose response and look at the area under that curve. The people who had been taking this pendulum glucose control, probiotic, had a 30% reduction in that meaning they had become more insulin sensitive. And I'm a couple weeks away from doing a blood test on myself to see if I've had any Improvement in glycemic markers in response to. That was not taking about a year ago. I was not taking ashwagandha a year ago. I had taken it a long time.
I'm earlier but just came back to it. Probably found a slightly more potent version of it. I was taking a different brand of fish oil before I had used Carlson's in the past had switched to Nordic Naturals. Now, I've switched back to this, I find it to be just a slightly more robust product, the Nordic Naturals ones for some reason, every third bottle had a broken capsule in it. And once a capsule breaks in the bottle, it just totally destroys the remaining of the capsules. It was just happening too frequently.
I was kind of aggravated by it. I don't think I was taking a baby aspirin a year ago I think again, that's something I've kind of done on and off over periods of time and probably the same with vitamin D. It's possible. I wasn't taking vitamin D A year ago.
Yeah. So it's not only the drugs of change but even like the B6 you mentioned the dosing has also changed, right? So then if we look at outside of supplements and we kind of look at drugs, the most common drug we had asked about would be rapamycin, followed by men.
Foreman and we won't get into those too much here because of that podcast with David and Matt and then also we won't get into too much on that form. And because you and Andrew did a journal club and you kind of focus on that foreman. And so just for time sake, well, kind of hunt those to those other resources, but outside of that, the question around drugs that we get asked. The most is kind of within the ascd. And you mentioned early. That's a disease that you
I think we have some chance to really stop it and to really delay the onset of it. If we take early interventions and one of the most common questions we get, is, how do you lower your apob and what's realistic with and without
pharmacology without pharmacology? So first of all, exercise has no meaningful impact on a scpd, risk factors through lipoproteins it does in other ways. But if you're just talking about managing lipoprotein risk, it really comes down to pharmacology hands.
Down the most potent way to do it and then nutrition. They far less potent but not insignificant way to do it on the nutrition front. You basically have two levers to pull, you can dramatically reduce carbohydrates which will lower triglycerides, and all things equal, the lower triglycerides, the lower, the apob burden, because you have to traffic fewer triglycerides with the cholesterol. The other way to do it is dramatically cut, saturated fat in a high saturated fat diet. What typically happens in addition to an increase in cholesterol synthesis
Is the liver through something called the sterol regulatory binding. Protein says, I don't need any more fat brought in. I don't need any more cholesterol brought in so it down regulates LDL receptors. So it pulls fewer LDL out of circulation and LDL will Skyrocket. So the reverse is true, if you cut saturated fat, the liver is going to want more LDL coming in. It will up regulate LDL receptors and pull more LDL out of circulation.
So, if you were on a really low carbohydrate really low, saturated fat diet, you would indeed lower your apob. Would you lower it to the levels that I think are necessary to make a SC VD irrelevant? Most people probably not. And then would that be a diet that for most people is sustainable long-term. That's probably a very individual decision. So for someone like me, who has very low try,
Glycerides. I don't go out of my way to eat saturated fat, but I'm also not restricting it either. I'd say I probably am in line with where the average person is my a poby at a baseline. Would still be. I don't know. 90 to 100 milligrams per deciliter, which puts me out about the 50th percentile of the population. So that's my normal a poby that's far, far, too high for someone who a has genetic predisposition to a cvd and be just somebody who
Wants to take the one Horsemen that can be taken off the table and take it off the table. So my target for a probie is 30 to 40 milligrams per deciliter. Therefore that would require pharmacology and so I take three drugs to do that. I take a pcsk9, inhibitor called repatha, and I take a combo drug called Next Lisette which is Bumpin toeic acid. And is that a my combined into a single pill and the mechanism of action of is that a, my biz that well, not to get too technical but it blocks
Ox the niemann-pick, see one like one transporter, in both hepatocyte sand enterocytes, if the gut it prevents non-esterified cholesterol from coming back into the gut, after you've recirculated it through your liver and into bile. So it prevents you from reabsorbing, your cholesterol of the three drugs. I'm taking that's far and away the least potent bump in toeic acid is a prodrug, what that means is by itself, it is inactive. So when you ingest it, it goes to the liver.
It gets activated and there it is. A cholesterol synthesis inhibitor. It acts on a different enzyme from statins and what makes been pandemic acid. Special for lack of a better word is that it only inhibits cholesterol synthesis in the liver where as statins which are very potent Inhibitors of cholesterol synthesis. They do so throughout the body because they don't have this prodrug trick when the liver senses less cholesterol it increases
Cell receptor expression on its surface, and pulls more LDL out of circulation. So that's how both statins and epidemic acid work, that work. Indirectly. The difference is Peppa Doak acid is less potent than a Statin and more selective in that way. So the combination of those three drugs will keep my apob negligible. And equally importantly, there are no side effects associated with that, for me personally. And again, when it comes to lipid management, it's certainly one of my favorite topics. I always tell patients we have tools
Today that we couldn't even fathom 20 years ago, 20 years ago, if you needed to have your apob slammed. There's only one way to do it, which was megadose of statins. I don't believe any patient needs to be on a megadose of a Statin. Today, we just have too many other tools and I do have some concern about megadose of Statin because one, the efficacy curves show that statins, hit their maximum efficacy at about quarter dose. The curve, for the efficacy of a Statin looks like,
This for example, if you look at reservist at and you're getting 85 percent of its maximum, a poby reduction at five milligrams. Roughly 85% you hit the maximum and by the way, it's a drug that is typically dosed up to 40 milligrams. So once you hit 10 mg, there is no need to go any higher because all you're really doing is buying side effects and you're getting very little in the way of increased efficacy. So we're very quick to Pivot patients off.
Statins, if we can't get great efficacy with no side effects at low
dose on those drugs, including statins. Let's say, if you can get that fricassee, at the low dose often times, what people who are younger and their 30s 40s, 50s kind of reach out and say, do you have any concerns about taking those drugs for such a long period of time?
Yes. And no. I think it depends on the alternative. So I think that there are some people who kind of poo poo
The side effects of statins and say they're non-existent. Well, I think that's a ridiculous thing to say, there are well, documented side effects of statins. At least three, that shouldn't be ignored. One is muscle aches. The to is elevations of transaminases or liver function tests and the third is insulin resistance, all of these are relatively small but they're not zero. Two of the three are objectively. Measurable, why would we ignore that? So I really like when you have objectively measurable,
Side effects. So I would say that if a young person is in a situation where perhaps they can't afford been pathetic acid. Next Lisette pcsk9 Inhibitors because to be clear those drugs are expensive at this time and statins are not. Yeah your alternative might be. I'm going to be on a Statin at least go through the trouble of trying to find the right one that produces the fewer side effects again we think that probably Petrova, Statin or live a low
Reserve a Statin or Crestor, probably the best places to go but it's also so highly individualized that I think you just have to try a couple until you find. The ones that are doing the best without any collateral
damage. You've talked about PCS canines before, but do you think we're any closer to those being more widely available and by widely available, just meaning, add a potential lower cost to
individuals. I think so because we now have through a different mechanism. You have a shot that can be administered.
Once every six months. So I think that the twice-monthly shot that I take for pcsk9 inhibitor, which has already come down in price by more than 50% since that drug came out eight years ago, I think there will just be continued price pressure on these drugs as more and more other drugs become available.
Speaking of drugs, you mentioned before, you think for the future of LP, little a that there's a drug in the pipeline that you're pretty optimistic about being available for people who have a high,
LP little a which could be anywhere from 8 to 12 up to 20% of people and we've had podcasts on that before. And so just with the amount of people that have a high LP little, a often, they'll reach out because up until now, there's not really a drug that can lower that. So do you just made me want to talk a little bit more about what's on the future for LP. Little a medications
truthfully. I haven't been following anything for the last few months so I don't have anything new to say on this since I probably last spoke about it. But there is a drug being
By a company, I think in San Diego, that is an antisense oligonucleotides. So the drug disrupts the process of DNA. Making RNA to make a pole little a it interrupts the synthesis of the protein that turns an LDL, into an LP little, a the drug worked very well in Phase 2. So in Phase 2 studies which don't have clinical hard outcomes. The outcome is just is the biomarker improving. There was
complete obliteration of LP, little a and there were no side effects over the short haul. So what matters now is the phase 3 trial which is ongoing and that's testing. The more important question which is does eliminating LP little a via this mechanism reduce clinical events. Does it reduce major adverse cardiac events. So the answer to that question will determine whether or not this drug is approved and therefore becomes available.
But I will say this. It is unlikely for me to imagine that that drug will be approved to treat patients with primary prevention because the manner in which it's being tested understandably, is for secondary prevention. This is very common in drug development where you first test the drug, the clinical indication is in the highest risk patient. So you get the answer relatively quickly. So this is a trial that is looking at people who have already had major adverse cardiac events and it's basically seeing, can we prevent
Subsequent events. And if the answer is, yes, I believe. The drug gets approved. It gets approved for that use case, it would still be able to be used by anybody for primary prevention but it's not likely that an insurance company would pay for that yet.
Very interesting. What's a traditional timeline for drug development to go from that first use case, which is the most urgent to that primary prevention, is that usually years over a decade,
the rule of thumb
As one decade and 1 billion dollars for a drug to go from IND to FDA approval. And again, once a drug is approved by the FDA, anything can be done with it can be used off-label. In the case of statins, they were very quickly employed for primary prevention. Probably even before primary prevention trials were published because the drugs weren't that expensive. The only reason I think this is an issue here is I do not expect this drug to be
cheap. Got it. Anything else you want to say on the drug supplement category before we move?
Vaughn only that I can't believe we wasted. How many ever minutes we wasted talking about that
as a reward. You get to talk about nutrition, we go from one positive to another. The first question is what set of words trigger you more when you are asked which diet is best or what is good, cholesterol and bad cholesterol.
I don't know. Those are those are the sir pretty upsetting questions.
Let's start with the second considering we just hit a s cvd. You made a YouTube video about this but I do think it's an important subject because not only is there a misunderstanding of this with patients, but also the amount of doctors out there who I think still use good, bad cholesterol. You just want to give a rundown why there is no such thing as
Bad cholesterol.
The term originates from the differentiation between low-density lipoprotein, LDL and high-density lipoprotein HDL. So let's start with where there's a grain of Truth here. So LDL or low density lipoprotein, which is not cholesterol. LDL is the carrier molecule, it's the low density lipoprotein. It's the boat or the submarine that carries cholesterol ldls are bad and
Gl's, high-density lipoproteins are good, but HDL and LDL are not laboratory measurements. There's no such thing as an LDL or an HDL that you can check at a lab, you can measure the content of cholesterol within the LDL that's called ldl-c. And similarly, you can measure the content of cholesterol within the HDL. That's called hdl-c. So when you have a basic lipid panel and it says your HDL is 50. Well, if you read the fine print, what it's actually saying is your HDL cholesterol.
Strong concentration is 50 milligrams per deciliter so don't say that your LDL is 120 say that your LDL cholesterol is 120 milligrams per deciliter, it's very important I think to be accurate in our nomenclature. So the reason that saying there's good cholesterol and bad cholesterol is nonsensical is because cholesterol is cholesterol is cholesterol the same molecule of cholesterol inside. The HDL is present inside. The LDL, what's bad about the LDL is that the LDL traffic's that cholesterol into
To the artery wall, where it will get retained and oxidized and lead to the process of atherosclerosis, whereas the HDL will not do that. That's the fundamental difference. We should really never say, good cholesterol and bad cholesterol because it's highly inaccurate and it only reflects a lack of understanding of what one is talking about which is why it certainly would be a red flag. If a doctor ever said that
and then moving to the nutrition side, do you maybe want to take a minute?
To talk about, why nutrition research is so flawed and so hard to do and then how because that's true, that kind of affects everything you look at within nutritional epidemiology and trying to understand that question of which diet is quote unquote, best.
Well, I mean we could spend an hour on that question, which I don't have the appetite for. I think it comes down to the complexity of the
Matt question, which is us and the complexity of the Intervention, which is eating. So it's really the worst of Both Worlds. We can study something as complicated as nutrition in a simple organism that can be put in a cage where you can control everything and where life span is short enough that you can actually measure how inputs affect outputs on a reasonable time scale. But for be clear, even studying the effects of nutrition in a confined environment, using more complicated organism.
And such as rhesus monkeys, as was the case in the Niña Wisconsin experiments from the 1980s, which began began in the late 80s. I believe that's an experiment that could never be replicated. I mean it took north of 20 years to do an experiment in rhesus monkeys where you could still have perfect control over what they ate and it's not entirely clear. What the answer was that was an experiment that sought to test. The question does caloric restriction extend life and the answer turns out to be. It depends if your monkey lives in Wisconsin or Bethesda.
Marilyn, of course, I'm being tongue-in-cheek. I think that study did answer the question. If you knew how to read the study, I won't get into that because I think I have a whole chapter devoted to that in the book. That's basically the long and short of why it's so difficult to study. So when you study it in humans you can do controlled experiments in a research setting but by definition they can't tell you anything about health in the long term sense because it would be almost impossible to confine humans for more than a month or so and control everything they ate.
So one can do those types of experiments to understand very precise mechanisms of action but those rarely translate to a clear understanding of Health if you want to understand what happens over the course of a year, three years, five years, ten years, by definition, you have to do that outside of a hospital and you have to do it with patients, being able to eat what they want. There are some historical exceptions to this rule. So, for example, the Minnesota coronary study was a seven-year study. That was
Well, I shouldn't say that I think the actual intervention was probably closer to three or four years. I could be wrong on that but it was done on patients in a nursing home. And there you have the interesting situation where you had patients, who are relatively old therefore at high risk for a SCV D but the investigators had complete control over what those patients 8 because every meal was being provided to them, that experiment was rather interesting and that it did not yield what the hypothesis suggested. I think there's lots of that could be learned from that potentially but
Net net. This is why nutrition in humans tends to rely heavily on epidemiology where you are looking for patterns without doing an experiment without randomization.
So with your patients then are you still continuing to try and manage their nutrition manage their diet, not to you put everyone on the same diet but more so what is that patient doing? And how do you get the best metabolic health for that patient?
Yeah, I mean we think
At the most important parameter for determining. Metabolic health is energy balance. So even the quote-unquote best diet if it's in excess of energy, balance will produce poor metabolic health. So regardless of what you think, the best diet is if you think it's a keto diet or a paleo diet or a low-carb diet, or a Mediterranean diet or a vegan diet, take any version of those and consume them to access to the point where you are no longer in energy balance and
and you were accumulating adipose tissue, that leaks out of the subcutaneous pays and gets into the liver, gets into the viscera, you're going to be unhealthy. So I always think people are majoring in the minor and minoring in the major on nutrition. When they start to fight in dietary tribes on this stuff, there are some general principles, like I do still think that clinically in my experience, patients, with profound insulin resistance, tend to respond better to carbohydrate restriction as the best tool to
Use total intake. You have to create a caloric deficit in those patients and in my experience, they respond better to carbohydrate restriction than they do Straight caloric, restriction or fat restriction. Ultimately it matters most that you can find something that is manageable and sustainable over the Long Haul. None of this matters. If you can adhere to the perfect diet for three months and then you can't, it's better to have a 7 out of 10 diet in terms of
Quality and Perfection that you can sustain indefinitely then a 10/10 diet that you can only sustain for 3 or 6 months.
Some other questions, we see, come through our questions where people are kind of confused on. Why should we not just look two populations with longer life? Span and attribute their longevity to their diet. So there's different populations around the world who will traditionally live longer. And so do you associate their longevity with their diet? Is that a mistake?
For people to do.
It's a complicated question because there are probably too many factors that factor into why these populations live a long time. So if you look at, for example, the Okinawa right? Everybody loves to talk about the Okinawa and Japan unquestionably. A very long-lived people. Although I've read recently not as long lived as the current generation of Okinawan, adopt a more Western lifestyle, inclusive of diet, by the way, a lot of those
things seem to go away. So it suggests that it might not just be the diet that is responsible for the benefits, that these cultures are bestowed with. So what are some of the other things that could factor into that? Well, we could certainly look at activity level exercise, level sleep stress, social connections, lack of other toxic elements in the environment. I think the same exercise is true. When you look across all of these populations,
The other reason that I think it's very difficult to say there's anyone. Perfect diet is when you look at these different populations and Pockets over the past hundred years that have popped up and have been studied who seemed to outlive others, even in relative proximity to them, their diets are actually quite diverse. So what does that tell us, right? So if you have people in Japan and people in Switzerland and people
In this part of Africa and people in this part of the Arctic or whatever, where you see reasonable pockets of longevity but their diets are relatively diverse. It might be interesting to look at what's missing from all of the diets or what do they have in common in their absence or what do they have in common in their presence. But to me at least it suggests that there's probably a pretty robust nature within the human to manage a variety of different dietary.
Conditions. Again, it comes down to provided energy balances met and I think provided that a person stays metabolically healthy. So they're active. They're sleeping. Well, cortisol levels are not through the roof. All of this is to say, I think our diets are problematic in this country, but I don't think that changing the way people eat alone will turn us into quote-unquote a Blue Zone.
You hinted at this earlier question we get asked a lot which is our
Are you still doing your longer fast? And if not, why is that
I'm not? And I think there are several reasons I'm not. But truthfully perhaps one of the most logistically relevant ones is just I don't travel anymore. I used to only do my long fast when I was traveling when I was away from home and it was just so much easier to be fasting when I was in New York, then being at the time in San Diego, but now I never travel. So it would mean
That if I wanted to do long fasts, I'd be doing them at home and I just don't feel like doing it and I don't have a better answer than that. I think it also speaks to the fact that I don't have a clear sense of what the benefit is. This is one of those things where I'm going to reserve the right to completely change my mind. If I had some biomarker that could convince me that a seven-day fast, even once a year had a meaningful rewrite on some negative processes in my body. I mean, I would happily make that sacrifice again, but in the absence of knowing
That the cost is a bit high right
now.
Another thing on the nutrition side that you talk about a lot is the importance of protein, we just did up premium email that kind of looked at the pros and cons of protein because when you look at protein in aging it does seem like it's a bit controversial and sense of what people will recommend. And so the question that came through and comes through off and as if someone's under 50. So let's say you're 30 or 40, do you think it's important that they are on the side of
Caution and eat less protein based on the research, or do you still think, no matter what age you are, protein is so important and that everyone should be getting as much as possible of it.
I think it depends on how much muscle mass that person has. So if you have an individual, who's over nourished and adequately muscled. So they're overweight, but they actually have a sufficient amount of muscle mass and they need to go into a caloric deficit.
It's certainly tolerate also a little bit of a protein deficit in that individual, not because I think it's necessary, but because I think it's easier to hit caloric targets. If you are able to relax your protein Targets, in other words, if you say you need to be in a caloric deficit and hold one gram of protein per pound of body weight, that becomes really challenging. If you say look you could be at Point 6, to point seven grams of protein per pound of body weight and critical or deficit is much easier.
Conversely. If a person is over nourished in under muscled, I think we do have to tow that fine line of keeping protein High because that person needs to be putting on muscle as they're losing fat. The truth of it is, I don't find the data for people below 50, having an increase in mortality with high protein being at all convincing. I think that is easily attributed to caloric excess as opposed to protein excess. And I think that there are enough other confounders there, that it's really a proxy for poor health than
Is a proxy for high protein. Furthermore, the absolute mortality in people below. 50 is so low in terms of absolute amounts, that even a slight increase in the relative amount is Trivial. Finally, it's very important when people are still able to put on muscle that they put on as much as possible. Because once you're in the over 50 category, your kind of clawing on for dear life, and trying to keep as much of that muscle as possible. So I don't really want people entering
In middle age with a muscle deficit, this kind of goes back to our original question. Like even if someone comes up with the solution for cancer and Alzheimer's disease, and all of these other things, you still have to Ward against Frailty. You still have to make sure that you enter that marginal decade, physically robust and most people don't come close to it. They're really, really under muscled late in
life. Another question we get asked a lot is, how do you eat so much protein in a day as we're kind of going through?
Peter, protocols, once you just run us through your protein per day and what that looks like,
again I have the luxury of being at home. So I have more control over what I eat than if I was back on the road. But I got a lot of it through venison. So now, inui, again, disclosure I'm an investor in that company, they make a really, really good venison jerky stick and I love it because it has no garbage in it. It's literally just got some natural flavors in it. I absolutely love the taste of it. So that makes life.
Easy and each stick 8, the peppered ones has like nine point nine grams of protein in it. It's funny. The USDA makes you around. If it's the USDA or whichever governing body determines food, labeling, you have to round down. So it says nine grams of protein on the stick, but it's actually nine point. Nine grams is what it measures. So, I actually think of each stick is having 10 grams of protein, so I will easily throw down five to ten of those sticks a day. And that would represent.
Sent one versus two, high protein snacks, and then the rest of it, I'm kind of getting in my food basically lately. I haven't really been doing much on the protein shake front because the jerky sticks are just quicker and easier for me than making a shake. But I would also use a high-quality whey protein, shake if necessary. So it's not that hard for me to kind of hit my goals throughout the course of a day. And by the way, what am I targeting somewhere between 150 and 180 grams of protein per
day?
And how often is that spread out between?
Typically like four
hits. Yeah, I've been in planning meetings with you, where you'll walk in with just a handful of jerky sticks. Drop them on the table. You'll be like anyone else want one? And then within 15 minutes they're all gone and all the rappers are right in front of you so I can attest that I've seen you do that protocol for sure. Anything else on the nutrition front you want to talk about before I move on.
No. Alright next section wearables. What is your current favorite wearable? Or just a device that tracks things for you so maybe doesn't have to be something that is like on your body at all times. But just what's your favorite device for tracking? And it can be tracking anything.
I've been using something called Morpheus lately. It's got to heart rate monitors, it's got a chest strap, and a wrist strap, not a wrist or forearm strap. It's got an app that
In the morning, you lay down and put the heart rate monitor on and you answer four questions. How long did you sleep last night? So I checked my eight sleep for how long I slept and then, how well did you sleep? So I look at my eighth sleep score and get a sense of with a quality of my sleep and then I enter that. And then how do I feel and house, or am I? So a task, these four questions and then I do a two-minute lay down with the heart rate monitor on and it measures my heart rate.
And my respiratory rate and my heart rate variability and then it spits out a Readiness score and it provides training zones via heart rate for the day. So, for the past six months, I've been doing an experiment where, every time I do a Zone to work out, I'm using the heart rate that it predicts. I'm riding to my rpe, and then I compared the lactate at the end of that ride.
To the predicted heart rate from Morpheus to the rpe heart rate. And I will say that it tracks pretty darn. Well better than I would have expected. And the reason I'm doing this is to see if this could be a good tool for our patients to use, who might not be as clued in to their own rpe and who clearly don't want to check their lactate levels
and are you using Morpheus for anything? Do you use any of that data for anything outside of
Zone 2. Are you using it for how hard you push that day? Lifting anything like that?
I don't certainly that's how they would suggest you use it. I don't wear it outside of my zone 2 or VO2 max training so I don't wear it when I'm in the weight room. I don't wear it rocking in large part because I hate wearing heart rate monitors in general if I don't find them comfortable, I can sort of tolerate it when I'm on a bike but I don't want to be rocking with one. I don't want to be lifting with one. It's probably the case that it would be an even better predictor of my training. If
Could see me across the day. If it could see me trained in every workout, it would probably be an even more effective tool because it would understand where I am in terms of
overload. Another wearable we get asked a lot. You've talked a lot about this and I believe you still use it with a lot of patience is see GM's, is that something you're still using a lot with your patients?
We do? Yeah, we use CGM a lot. It's a great tool. When we have questions, it provides answers. We can sit here and look at a person's ogt.
Tea and some cases, it's just a slam dunk. Like, this person isn't super metabolically dialed in, in other cases, it's a complete slam dunk. This person has Type 2, Diabetes, by ogt criteria, even if not by A1C criteria, but there are a lot of people in the middle and this is a great way that we can glean more information and really dial in our treatment for
them. And so there were some controversy way back when on if CGI.
Were still valuable. Still useful for people. Who are non diabetics. Have you changed your opinion on that at all? Not one bit, do you maybe? Just kind of want to walk through people? What you look for with see GM's and ultimately what people have someone's wearing one? Because it seems like it is more widely available for non-diabetics now and so you see a lot more of them around. So if someone gets one, what are some of the things you like to see within patients? What are some of the things you love?
Look at. How do you use it?
I mean, we still look for the same things, I think average blood glucose is still the most important metric we care about, because that's the one for which we have the most data. In other words, we know all, cause mortality data, is it relates to hemoglobin A1c hemoglobin A1c is a measurement that's used to impute average blood glucose. So this is a very, very close proxy when we can see average blood glucose on CGM, even though it's not the same as measuring A1C, it's very difficult to
Argue that knowing your average blood glucose on CGM and knowing your A1C aren't highly comparable and therefore by proxy the lower your average blood glucose on CGM. The lower your all-cause mortality because it is abundantly clear that the lower your hemoglobin A1c, even outside of the diabetic range, the lower your all-cause mortality. So first and foremost, that's the metric. We care about the other metrics. We look at, of course our what's the standard deviation. So all things equal. Do you have less variability
Leti in your glucose then more and then finally and the least important, I think is how big are the spikes you're seeing now in truth that becomes less important. If the first two are reasonable, if a person's average, blood glucose is ninety eight milligrams. Per deciliter with a standard deviation of 16 milligrams per deciliter, it doesn't really matter what kind of spikes they have because they're clearly not going to be too many unless they're using insulin, you could obviously arrive at those numbers the wrong way.
I would say that fixating on average blood glucose and standard deviation are probably the most important thing
from when you would wear one. Do you recall what caused the biggest Spike you ever saw? No, I don't
recall. A buddy of mine took me to this vegan restaurant in New York. Once I think it was called, like, Candle 79 or something really, really close to my apartment. And it was great, it was amazing food, but obviously by definition, like it's just basically all carbs and I
Member the dessert was so incredible and I remember looking at my CGM after it was like a 180 and I feel like that's about the highest I've ever
seen funny. Do you think we're any closer to continuous blood pressure? Monitors.
Absolutely you do? Oh, yeah.
How far out? Do you think that is? Because I know in the past, with Ethan Weiss the a man blood pressure. You've talked about how important that is as a
device.
I think we have it so I think the actia device works at least it works as well as an automated cuff works. So this is a device that is not yet FDA approved, but it is approved by this similar, governing bodies in Europe. So this is a device that's already on the market in Europe. It's a bracelet that you wear that optically, measures a signal in your wrist, and you calibrate it against an automated cuff and every two hours, it gives you your average.
Courage blood pressure so over the course of a day you'll get 12 blood pressure readings. I would say even though automated Cuffs in general, are nearly as good as manual. Cuffs for an automated cuff, I don't see any difference between this and pick your favorite automated cuff. So I really hope that this device gets approved in the u.s. because will certainly have every one of our patients wearing this and it would do away with ambulatory blood pressure, cuffs which are cumbersome and difficult.
Use and low compliance, and part
official interesting. So, any listener viewer in Europe would have access to this? That's right. And then, what do you think the rough time frame for people in the u.s.? Is it years? A decade. How does that process? Typically work,
it's entirely dependent on the FDA, it's possible. It doesn't get approved at all. If the FDA is difficult to work with, on this
Unfortunately, I hope that's not the case.
So if anyone listening watching works for the FDA something to internally push on then. Yep. Any other wearables that you're excited about whether they're close to being here or even in the long term like ten plus years.
I would always welcome continuous lactate monitoring during exercise. That would really, really make Zone to training enjoyable for me,
just as opposed to, having to do the finger,
Pricks all the time or just knowing where it's
at to me, it's the most accurate way to really understand what's happening. I mean, even heart rate and our PE are just approximations for what you're really interested in. So I think, yeah, just being able to monitor lactate levels while you're exercising, especially doing cardio training. I'd also love to be able to do my vo2max workouts, with a lactate M, continuous, lactate M. So I could actually watch lactate rise and clearance on each subsequent set. As I'm fatiguing, am I really just
Breaking down metabolically as much as anything
else. So Peter I think that was the majority of the questions we wanted to get through as we kind of said. At the outset, those are questions that come through often. So we compiled them here. But any closing words you want to tell people, you know
what episode number? Are we at roughly
while at the time of this recording to 67. So this will be in the
70s creeping up on 300 but also at the time of this recording hit five years as a last month, which is crazy because that's what I was fun to have. David 17, IAM at cable and back on is because they were not only the first 10 episodes, but if I remember correctly, I think that was you. And Bob, interviewing them and recording it for the book that we then turned into a podcast. Which one shows that
We didn't even think about the podcast that time into it shows how freaking long you wrote that book for. That's
right. I remember those interviews I went up to Boston with Bob in the summer of 2017, to interview David and then Matt came to New York and I interviewed him a month later and that's like a year before the podcast came out. So yes that was literally just done for the book. Pretty funny.
Yeah. It's kind of crazy to see how far
Thanks came along not only with the podcast, but also now seeing the book out the reception from that, which is great because We've joked about it before. But I think we can both seriously. Say there was a lot of periods of time or we didn't think that book was ever going to get
released. Yeah. Right up until a couple months before.
Yeah. Yeah. All the way up until 2023. So awesome. Well, hopefully people enjoyed this, kind of, a little different of a style. But until next time, Peter have a good
one. You tunic. Thanks man. Thank you for.
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