Last updated: April 9, 2026
November 4, 2025
Timestamps:
0:00 – Introduction
0:53 – Biomarker Competition: Crissman Loomis vs Bryan Johnson vs Siim Land
1:53 – Strength
13:37 – Body Composition
20:18 – Hormones
24:04 – Liver Function
28:40 – Kidney Function
35:53 – Inflammation
39:36 – Blood Counts
45:45 – Lipid Panel
1:00:18 – Metabolic Health
1:05:23 – Cardiovascular Fitness
1:15:08 – Biological Age Tests
1:24:47 – Effort And Investment
1:33:00 – 2026 Unaging Challenge
Transcript:
Mike: Hey everyone, today’s guest is channel regular Crissman Loomis. This is episode seven of our podcast series. So with that, welcome Criss, and let’s get into the outline. What do we have for today?
Criss: Great. So thanks for having me on again, Michael. So today we’re going to talk about topics. We’re going to cover a throwdown with Siim Land, Bryan Johnson, and myself, and with some helpful context and commentary from yourself to put it all in perspective for us. Then you’re going to talk about the supercentenarian case study. And some of the things, I guess, as I was previewing the notes, what are the real limits to immortality?
And then at the end, I’ll be talking about an opportunity for everyone as I start up the 2026 Unaging Challenge, following up on the 2025 Unaging Challenge that’s just wrapping up this year, and give people an opportunity to put into effect the habits that will give them the longest life possible.
Mike: Fantastic. All right, so we start with that head-to-head matchup that you lined up on your blog. You’ve seen Bryan.
Criss: Yes, so there’s a lot of gritty stuff in here.
I’ve, so it started out with Bryan Johnson saying: “I have the best biomarkers in the world. None can match them, living nor dead.” And Bryan is currently 48 years old, and Siim Land responded with: “Well, that’s ridiculous. Mean, biomarkers change as you age, and no one has, well, virtually no one has the biomarkers of someone who’s 20 years older. But I’m 31 and I’ll compare my biomarkers to yours, Bryan Johnson.” And did so.
And about 80 or 90%, if I remember right, if his biomarkers were better. But the comment is that Siim Land is about 17, 20, almost 20 years younger than Bryan Johnson. So yes, his biomarkers are better.
So I’m here to provide context and a different benchmark for that as someone who’s 55. And in the straight march up, well, let’s see how I compare to Bryan Johnson and Siim Land.
So we’re gonna group these by areas, and I’m looking forward to having some comment from you on whether we’ve hit the mark, overshot the mark, or whether we need to improve things.
So the first thing to do is just sort of like the raw strength comparison.
Grip strength is often considered one of the best indicators of overall health, especially in older people. Sometimes, as opposed to having them actually lift a bunch of weights, they’ll just have older subjects come in and compare their grip strength. Because it’s an indicator not only of the muscular strength of your hand, but also because of the vein requirements to be able to use your hand effectively, it can be a very strong indicator of your cardiovascular fitness as well.
And for this one, the three of us are all in quite a tight range.
I’m slightly stronger than Bryan Johnson with my one-hand grip strength of 60 kilograms. I can’t remember the units on this. Same is stronger than both of us, but he trains quite a bit more and has a good twenty years on us.
For the bench press, this is always a challenge for me.
My bench press is not where I wanted to be at nearly 98 kilograms, estimated one rep max, and both Bryan and Siim are quite a bit higher than. Siim’s got a very impressive 166 kilogram bench. I’m working on it.
But for the squat, one rep max. For that one, Bryan Johnson’s about 115. It doesn’t seem to be part of his daily exercise. Siim’s at about 160 grams for his one rep max. And it doesn’t seem like an exercise for him as well that’s part of his base routine. For me, this is an everyday thing. Well, actually every other week I alternate between squats and deadlifts. But 160 kilograms, estimated one rep max. I’m very comfortable with it.
These lifts aren’t increasing probably for any of the three of us at this point. It’s mostly maintenance once you’ve been training for more than five years. But I’m continuing to maintain at this level, and I’m quite happy with that.
Mike: Quick notes, Criss? All right, so I’m glad you mentioned that it’s kind of an unfair comparison to have Siim in there, or against Siim. My first thought is, first of all, he’s a beast, which in the most respectful way possible – lean, fit, dedicated to training his whole life. So it’s not a fair comparison because, like you said, he’s at least 17 years younger than Bryan and 24 years younger than you.
So the other thing is that, but then he’s the positive control, right? Potentially, and all of his biomarkers aren’t perfect, but he’s got pretty good biomarkers from what I’ve seen. So there are two other things, too. So one is single-time-point measurements, which are important, but when we’re talking about aging rate, I think a lot of people lose side of this is they’ll only measure like once, maybe once a year, once every couple of years, whenever, infrequently, right? So is one measurement representative of a full year average? Like for the sports players, if I’m a baseball player and I hit four home runs in one day and then no home runs the rest of the year, am I the world’s best baseball player or maybe just on that day, right? So at some point we’ve got to, as a field, to the, and I even thought about just showing, of recording all of my workouts, right? So people can see, oh, look, he did 13 pull-ups on this day in 2018.
Is he still doing 13 pull-ups or is he doing 13 pull-ups every workout, or is this just peak? And then what does the rest of the year look like, right? It’s kind of that, you know, bodybuilder in season, out of season mindset. Like, are you lean and fit all year round, or are you muscle beasts? You know, it’s what I call muscle beast city, right? Where they’re gigantic and big.
It’s easy to know, it’s easy to find something. I think the main for me is I’m so busy. It’s very fun to be in space and be able to chat with people. And I’m very excited to be talk people. So, I think it’s a great experience. So, I think that’s it for me in terms of my experience with the basic training that I’ve so far. And yes.
And then also, I guess I have three notes. So you guys differ in terms of body weight. So normalizing to body weight, know, strength per unit mass probably has some value if you’re really gonna do a head-to-head matchup, because I think, what’s your body weight?
Criss: I’m 71 kilograms.
Mike: Yeah, I think Siim’s in the same ballpark, but Bryan’s a bit smaller than that, maybe five kgs, but still in the same ballpark. But normalize the strength, normalize the body strength, normalize the body mass could be important. Actually,have one more one more thought. So the other thing too is, I believe all of you guys, you know, these are your one RMs actually have two more thoughts. My gosh, that the spigot, the spigot that is my mind, right. So which is the same thing.
So bench press, you know, there’s got to be standardized limits because I don’t know if you’ve ever seen like some of these people, they’ll post their TikToks and you know, the official Olympic lift is, you know, the bar has got to touch the chest, but then sometimes the person will arch their back tremendously. So they’re moving the bar this much, but that’s an efficient bench press, right? You know, some of the bench presses are to, you know, mock, but you know, but for something like a squat, someone doing a quarter rep versus a half rep versus as to grass, you know what I’m saying? So seeing it can be beneficial there.
And then the other thing I think to note, the last is my last thought on this one. So grip strength is pretty easy. You can’t mess that one up. And grip strength is, I’d argue grip strength may be the most important biomarker on this short list, not of all biomarkers when it comes to strength and function.
Is the training for longevity, is it bench press? Mean, if you bench press, all you’re gonna be good at is pushing stuff away from your body. And if you do a squat, all you’re gonna be good at is basically sitting. I mean, you’re lowering the weight to a seated position, right? What about, you could make the argument, picking stuff up off the floor, maybe a squat would help, right?
But, you know, and I’m on it with these compound movements. They’re part of my approach too. Know bench press, deadlift. You know, flexibility, know, being able to pick something up from the floor, being able to do a lunge, you know, split squat, you know. Things that are more functional movement-based, where flexibility and strength through a full range of motion, you know, so if someone’s got an outrageously high one-arm squat, but then can’t touch their toes.
And I’m not saying I know, your flexibility isn’t the greatest, but I’m not trying to pinpoint you. Mean, I think this is broader, you know, so for me, the training for longevity isn’t just about peak strength, maintaining peak strength, but also the ability to do functional movements. And I don’t know how we would measure that. Do we have a yoga or Pilates instructor come in and test us all? So anyway, just something to think about.
Criss: Well, one of the interesting things, actually, I mean, it’s funny, because that exact example you give of being able to touch your toes, but until I got my squat into proper form, it was doing full reps down to below the crease, I wasn’t able to touch my toes. But now that I’ve got full range of motion in my squats, now that flexibility has come. So, in some ways, these are brought together.
My latest challenge is not on this list because not many people are trying to do it. I’m trying to work on doing a muscle-up. I just started about two months ago. So muscle up is where you pull yourself up to the bar and then continue beyond that to do a dip to get fully above the bar. It’s a mixture of a lot of techniques, but the real thing is that there’s a whole range of muscles in there that you never exercise doing bench press, lat presses, or chin-ups in the gym.
So it requires you not only to be able to get to this motion, which I can do around 10 or 14 chin-ups. But then from there to get from that to moving down to this level, to getting to where you’re here is an exercise that’s really never done in normal exercise unless you’re a gymnast or something. So in some ways, it’s very challenging for me despite being able to 160 kilogram rep, do 14, 10 or 12 or 14 chin-ups.
I’m starting at zero, trying to do a muscle up because it’s a different range that I’ve never practiced before. But I’m finding that doing that is giving me a lot more ab, abdominal exercise and other things and a lot more functional range that I never had to touch before. So it is definitely interesting that it can be quite different for them. But I’m still, the feeling that basically you need to get the big stuff. And I generally feel that the physical exercise is more important than worrying about the flexibility. Although to the point though, I say that and yet I do my Tabata kind of exercise where I’m 30 seconds of high intensity, actually 20 seconds of high intensity exercise. But I’m always doing something very different for that, like jumping jacks or mountain climbers or burpees or something, which is then giving me that kind of a full body thing.
At one point as i got around fifty or so i started to get what they call in japan fifty year old shoulder which is the same because you haven’t been doing this motion very much your shoulder now is kind of lost some range of motion and went through some exercises I have a post on it in my blog if you want to hear more about it or if this is something that’s useful for you.
But it was a series of just exercises of a kind to bring that back into it, and then I did that for a period of a month or two, and then it just vanished, and I’ve been fine since. But I’ve continued to do those kinds of functional movements you will even though it’s only four minutes, a Tabata workout is only four minutes long, two or three times a week. And that’s had a huge difference in what I feel in my ability just to do whatever is required of me, so I can apply the strength that I have with my grip strength, and my bench press, and other things.
Mike: Yeah, nice. So just, just, push back on the flexibility. I’m not saying that we all need to be, you know, super uber flexible. It’s just, you know, flexible for functional activity of daily living, you know, things. So, and within that too, so I get what you’re saying that the burpees and squats and deadlifts, you’re going to have a greater flexibility than, than as if you never did that. But even training those movements like you, I’ve seen it where I’ve trained, you know, I worked as a fitness trainer, you know, 20 years ago, and I trained a 75-year-old couple, and they couldn’t bend. I mean, their range of motion to bend getting close to the floor was so terrible that I can’t, and getting out of bed, that makes getting out of bed hard. Forget picking stuff up off the floor, you know, so I’m not saying to train like an old person, but at the same point, you know, if we’re not trying to take, my perspective is if we’re not trying to, you know, optimize strength through a full range of motion for functional stuff in addition to the big stuff, you know, we’re shortchanging it.
So also, the muscle up is great. Still, there too, you know, it’s like, want to do, part of me has that same mindset. I want to do these quote unquote fun, fancy things, but then I’m like, what do I care that I can do, you know, so even there too, it’s like, the technique of it, you you do the pull ups, so some people will do the pull up and then they kind of push their way up to do that, you know? But then there are the gymnast types, where it’s one consecutive movement, and it’s just like, they’re just like, they’re just like bouncing. It’s so fluid, but functionally, I don’t see the value. Like, so I don’t, I don’t spend the time, you know, to do, even though I should say as I’m doing my pull-ups, and I don’t know, maybe this is just, you know, we’re born from the same litter, the same generational litter. And we have a similar mindset for this. But lately, when I’ve been doing my pull-ups, I’ve been thinking about the muscles-up: it’s a real muscle-up, a full muscle-up, one consecutive movement, not a squirm-up. As I’m doing that first pull-up, I’m thinking about, right, I’m gonna make this one. So I don’t know, if I get there by accident, I get there, but if not, I’m content just to do high-quality reps.
Criss: Yeah, I know you’re totally right. The muscle up is going to help me do nothing except that I’m able to do a muscle up. It’s kind of bragging right. So yeah, I don’t think it’s functional, but it’s fun.
Mike: Yeah, at some point, at some point, you know, as I mentioned earlier, I think if we’re going to really compare strength and VO2 max and all this stuff, people have to post videos, not just one video, but like week after week, just like we can watch the baseball players every day and then assess this was the better player versus this one over a full year. You know, I think that’s the, and that’s kind of my general comment for the head-to-head matchup is, you know, I want to see more than just one test. Want to see the test consistency over time.
Criss: Well, let’s keep working through the one test that we’ve got for now. I can provide some context on the other measurements and things that I’ll add in.
So then now we start to get into some more, actually, this one started actually coming to the story of why I’m doing lifting or some of the health stuff that I’m doing at all when we talk about body composition.
So the first one I probably should have written this out is bone mineral density.
So BMD, and this is grams per centimeter squared. And I come in last place on this one and far last.
And this actually is a great story for me because I had a DEXA scan done, which you’ve done as well, where they do a scan and tell you what your body fat is, your muscle is, and also your bone density is. And when I did this, the answer was that my bone density was poor. It was on the borderline.
I think that would have been around when I was around 45 years old. And the conclusion at that time is, 45-year-old person, you are already on borderline osteopenia, which is the one step above osteoporosis, where you need to be careful you don’t break a hip or a bone or something. And at 45, that’s too early to be in that situation. I was there with my brother and he got flying grades on it his bone density was fine and the reason is he’d always been lifting weights and I never had.
So I did the research I mean it wasn’t just like okay he lifts weight I don’t, therefore I will. And lifting weights is one of the key determinants of what your bone mass density is, so I then changed from that, and that’s when I started lifting weights regularly every week. So I’m now no longer osteoporotic borderline. I’m now just below around 40 percentile or so but well within the green range.
I think both Siim and Bryan Johnson have been lifting from a younger age. Probably Siim had been doing the lifting but Bryan Johnson also was significantly larger before he decided to become healthy. He was quite overweight. And that is one of the things that carrying the extra weight is another way that you can have higher bone density. I’ve always been fairly lean.
So while I’m distant third on this one I’m happy to be third because I’m at least within the green zone on this one, which wasn’t where I was when I started.
Mike: Do you remember, Criss, do you remember what your bone BMD was at 45 versus now, the actual number?
Criss: No, I don’t remember what that one was. It was significantly less. This is like, even if they just look at age irrelevantly. So it actually increased significantly as I added free weights and other things, and put in serious gym time.
Mike: So for me, that’s a more important number, knowing that you’ve not only resisted age-related decline, or you could say, I don’t wanna say sedentary cause, but your lack of strength training or less strength training than, that you’ve reversed that, because BMD declines during aging. For me, that you’ve resisted that and actually improved it over the past 10 years when it should be getting worse, is potentially more valuable than people who have already been high. We don’t know if they started higher, and they’ve already come down, right? I mean, and probably not, but you know, so I wouldn’t, I wouldn’t look at this as, they’re killing me in BNB. It’s the other side of it; you’ve resisted age-related change. That’s a win in your own, you know, that, that, that’s kind of the reason I don’t, you know, and I know, I mentioned this where I was like, I don’t care about head-to-head matchups against other people. It’s me against me, against aging. So, yeah.
Criss: So pardon me, I’m looking this up. Of course, I have all of this online, so I can find out what it was at the very first one. Would have been 2014.
It was 1.128 at the time.
Not that much less, but the real important thing is that it’s now 11 years ago and my net bone mass density is much higher. You can also see it when you look at the picture of the actual DEXA scan, because they give you sort of like a here’s your density through your body, and I looked ghostly from the waist up, like my upper body had significantly lower bone mass density to it. And now I’ve evened that up and overall increased it on average so I’m quite proud of it. As I said, it’s pulled me off of what was borderline and like a few hundreds of a point on this make quite a bit of difference. So the right direction.
Mike: Yeah, and even if it was stable over 11 years, also a win, you know? Yeah, it doesn’t have to be the highest of the high. You don’t have to have a 400-pound bench press, but are you resisting age-related change and even making a small improvement? That’s a win.
Criss: On the visceral fat, on to the next one here as well, Siim has trained on this one quite specifically and deliberately. And as you say, he’s a bit of a beast. He’s in the gym longer than I would consider to be healthy. Actually, longer than he would consider to be healthy by his own book. At the same time, he’s 31 years old. It’s fine. He’s not going to fall over at this point, especially given all the other things that he does. But I have a little bit less visceral fat than Bryan Johnson, despite having a few years on him.
So then moving on to, go ahead.
Mike: So, wait, wait, wait, going back real quick. So I think this is an important point because most people, even if they’re focused on, so when you think about the eat real food and exercise approach, which is great, that’ll get most people to 85, 90, maybe even 95 and a few people beyond that. This is the silent aging right here: BMD, visceral fat, and muscle mass. The body weight may stay the same, but the body composition changes. Less muscle mass, fat and visceral fat, less bone density.
I see this as essential in the longevity testing hierarchy, top tier, DEXA, know, some measure, consistent measure of body composition. And visceral fat may not seem like a big deal. You know, you just lower overall body fat, you should have low visceral fat. But at least in rats, when you remove visceral fat, they live longer. And, you know, it’s like 20 % longer. So, visceral fat’s a big one.
Now, in terms of the absolute numbers for you guys, and again, know, seen being, you know, 17 to 24 years younger is fantastic, you know, fantastic for his visceral fat, and he purposely stays lean. Your data and Bryan’s data is far from terrible. Mean, values in 20 year olds is about where your data is, both of your data is, half a pound, so 200 or so grams. The other side of that though is, is having 200 grams of visceral fat worse than Siim only having a quarter kg you know 100 grams and one way to assess that is you know so visceral fat is going to impact things like uh liver health so if you have a lot of visceral fat around your liver fatty liver you’re going to have higher triglycerides, worse metabolic health including glucose and hba1c so if at yours and Bryan’s level for visceral fat if your triglycerides are less than 45 if your hba1c is five. It’s not bad, right? And so, even if it’s slightly on the higher side, I mean, both of your data is in the outstanding rate.
Criss: Yeah, I’m very happy, and we’ll get to all of those figures that you just talked about, actually.
Like, so the next one is, is to talk about the hormones.
Hormones, I think that it’s much overdiagnosed. It seems to be kind of like trendy right now to get testosterone supplementation. I don’t do any of that. Just work out of the gym and do the exercise stuff on these things I think i was generally in the middle of our testosterone was a little total was a little lower but free testosterone between Bryan Johnson and Siim.
Sex hormone binding globulin, not sure I’m getting that quite right, you can correct me on that then I’m the highest in that one considered like lowers considered to be better for that and then DHC am the middle of them
But I don’t, I think these are in a normal range. There’s no concern for me, but I don’t have too much to say about this. Comments?
Mike: Yeah, so total testosterone. So, you know, and this goes to my general point too, of age-related change. Less than 300 is associated with an increased alcohol’s mortality risk. How much above that is optimal is very debatable. I mean, I don’t know that 900 is better than 700, is better than 500 in terms of mortality risk. There isn’t any data on that. But resisting that age related change is huge, right? So was your data once 700, now it’s 500. I don’t know, right? That’s the big thing. Free testosterone.
Criss: Right, I don’t do the testing often enough to know whether that was just variation or whether that’s an age-related decline. Also, I can’t get this tested in Japan, where I live, so I’m always sort of jet-lagged to some degree. And testosterone varies a fair amount based on the time of day when you test it, highest in the morning and lower later on. So I’m always kind of like, okay, this is this a comparable number when I go back and maybe measure it the first day after I get back, and I’m very jet lagged from the States, because I can get this tested in the States, but not here so it’s yeah I actually, I definitely could use more data on this one to know where it’s going,
Mike: Yeah. Free testosterone is an interesting one because, you know, it should track with total testosterone. So if total T is low, free T will be low. Things like calorie restriction, lower androgens overall, including free testosterone. But there’s a lower limit there. Now you guys aren’t close to that lower limit. The lower limit is about five, five picograms per mill, being below that associated with an increased all-cause mortality risk. But knowing that calorie restriction lowers free testosterone. And knowing the calorie restriction is like the gold standard for longevity, at least in animal models. It raises that balance of is lower free T and even lower total T, not necessarily 500, but not below 300. Is that pathological, or is that a sign of pro-longevity? And to that point, SHBG, all of you guys are in quote unquote what I would consider normal, but calorie restriction dramatically increases SHBG to values greater than 100. So now that may not seem like a big deal, but SHBG binds to total testosterone, thereby reducing it in blood, which would then potentially lower a free T.
Now, in the caloric-restricted state, as I mentioned, I don’t know that that’s a big deal, but SHBG increases during aging. And higher SHBG during aging is associated with metabolic syndrome. So now you’ve got this dichotomy of okay, well, CR increases SHBG, but that’s a pro-longevity potential thing. And then you’ve got the average population where SHBG increases not on CR, and that’s associated with metabolic syndrome. So this isn’t as easy a story as I think most people put out there.
And then, in terms of DHEA, I don’t track that; I track its sulfated form, DHEA sulfate, which is a neurosteroid and declines during aging, just like testosterone. And that’s actually, you know, a biomarker of adrenal function. So that’s a big one to me that I’m tracking consistently.
Crissman: That’s a big one to be an importer. It’s just the name. All things are okay here. It’s hard to see where the big picture is on that.
But as we come to liver function, I’ve actually had more recent tests of these, and my results have improved further.
I’m not sure what the issue was at the time. For me, honestly, I don’t have that much to say about this. When they give me these tests, I also get an ultrasound as part of them, which lets them look for fatty liver directly. They can then actually see the fat content by the reflection, or something, not sure if it’s a reflection of what it is, but the ultrasound. My liver is healthy.
These, by the way, are some of the you talk about the history of it when i ran the marathon, I was training for the marathon I should say these were all disasters they were all like my AST, ALT and DTG, or I think it was my AST and ALT, were both of them over 70, which is significantly outside, like 50 or below is kind of where it’s considered to be normal. So they were very much affected by the overtraining and overexertion that were part of the marathon training. But within a month or so afterwards, I think they were back within the range that they should be.
I mean, aside from knowing where I fall between the three of us on these, cuz I looked it up, some of it with help from some of the reference ranges that you have, I don’t really know which of these is better or worse, so I’m open to comment on how these look.
Mike: Yeah, a couple of things.
One, that’s a great point about training impacting liver biomarkers. Before every test, I standardized on whether the last workout is before the blood test to minimize the potential impact of training or overtraining on biomarkers. So if the blood test is on a Monday, it’s a Friday workout, no later than a Friday workout. Monday or Tuesday test, Friday workout. So I’ve got three to four days because if training is gonna negatively impact the biomarkers, how can I see if other stuff, diets, supplements, et cetera, can move the needle? So I think that’s an important point.
In Bryan and Siim’s case, I mean, I don’t think they did a hard workout the day before testing, but for most people who are new to this, I’d recommend standardizing when their last workout was. And that may be some of the patterns in your data, especially when considering the ultrasound of your liver. And I think you’re gonna show triglyceride data, which also links to fatty liver. Your triglycerides are super low or low, which would suggest great liver health.
But in terms of what’s optimal, AST, ALT, CMN, Bryan would be closest, so high teens, low 20s. And when I say optimal, I mean in terms of all-cause mortality risk, based on a study of 16.6 million people. GGT is less than 12, and it also increases with age. Unfortunately, I mean, it’s probably training-related. I find it hard to believe you’d be that far out, but they’ve got you beat there. ALP less than 48. So they’re pretty close to that. Bryan, for whatever reason, is off the charts. Well, not off the charts, but he’s far away from that. And that’s based on a meta-analysis of about 9 million people.
Bill Rubin is an interesting one because it’s basically a biomarker of red blood cell degradation. So hemoglobin is degraded into heme, and then heme is degraded by a series of steps into bilirubin. So at younger ages, the data is where Bryan and Siim’s values are. But in centenarians, bilirubin is often one or around that or higher. So, that’s in association with, you know, longevity and reduced all-cause mortality risk.
On the one hand, you’ve got bilirubin relatively low levels is more likely to be found in youth, but there’s also something about bilirubin, whether it’s an antioxidant or it’s neuroprotective, whatever the mechanism may be where at advanced ages, having higher levels would be beneficial. I don’t think having values at one, though, at your age, would be a good thing. I’d be aiming for where Bryan and Siim’s values are. And then in terms of albumin, actually, I think your data is the best of the bunch. Mean, higher is generally better.
Here too, though, albumin declines during aging. And for those who don’t know, albumin may seem like an obscure biomarker relative to, like, glucose or triglycerides, but albumin’s concentration in blood is around where you guys have five grams per deciliter or 5,000 milligrams per deciliter. Glucose, at best, is 80 milligrams per deciliter. So albumin is 60 times more concentrated in blood. Even if you take cholesterol, 200 milligrams per deciliter, you know.
It’s 25 times more concentrated in the blood. So when we think about the biggest trees in the blood forest, albumin is a big tree in that forest and at least in terms of concentration. So, 4.5 to 4.8, or a bit higher, is my optimal range. You guys are all pretty close to that, but it declines during aging. So, you know, your data there would be the best of the bunch for comparing a single data point.
Criss: Oh, interesting. Right. Then on the kidney function, this one is always kind of a bit of a challenge for me. And a lot of it goes to what you’re talking about, about standardizing around your workout times.
In some of my old tests, for example, I’ve gone and done a big workout on Sunday and then gotten my blood tested on Monday.
I’m so easy if are as I’m sure you’re I know you know is basically very heavily influenced by the creatinen which can be produced by workout and often times my creatinine they’ll tell me that it’s too high I have sympathy here for Bryan Johnson at one point to one having a higher creatinine cuz he’s doing a kind of gym lifting pretty much everyday.
And then the EGFR which is your effective global fibrillation rate, then that’s calculated off your creatinine. So if you’re doing the lifting, then they’re going to say your kidneys are bad, which is not the case. So that’s why I have the cystatin C below that. And cystatin C is one, correct me it goes up in the goes down issue a trying it goes up as you age.
So my cystatin C, a little bit less than Bryan Johnson, the both of us are in the fine range. So Siim was saying that he thought that Bryan Johnson had kidney problems. I would say no. I think he is basically has higher creatinine because of the man of workout that he’s doing he probably didn’t take an appropriate break maybe before he did his blood test which will then give him a poor EGFR. But then the cystatin C, which is consistent with his age, may be slightly higher than you would want; it seems to be saying that his kidneys are fine. And then all of us are coming in with a reasonable bun rating, I would say.
Mike: Yeah, so I’d actually agree with Siim. So exercise could impact kidney function. I don’t know if Bryan’s supplementing with creatine, which could increase creatinine. So that could be a part of his creatinine being relatively high. That 1.21 is way too high. But again, I don’t know if that’s creatine on its own or, you know, and then creatinine is proportional to muscle mass. So creatinine can be higher, but if we use that metric, and Siim has probably got both you guys beat and me by far in terms of muscle mass and density, his creatinine should be off the charts, but it’s not. EGFR place no value because that algorithm, that equation is based on creatinine and H, chronological H.
So, if your creatinine is relatively high, EGFR is gonna be relatively low. And they have EGFR equations based on cystatin C also. Rather than using an equation that you could have low creatinine, and just because your chronological age is increasing, EGFR is gonna be decreasing. It place no value in EGFR. I want the actual data. Now, if we’re gonna assess Bryan’s kidney function, that cystatin C does provide more insight because Cystatin C is thought to be non-proportional to muscle mass, less influenced by muscle mass. In terms of what’s optimal there, less than 0.7. So lowest all-cause mortality risk, increases during aging. I don’t know where Bryan’s data was aside from this test, but when you put those two values together, the creatinine, even though it could be influenced by creatine and cystatin C, 0.87 is way too high.
Now, cystatin C can be impacted by diet. I know that because my cystatin C has trended upward from around 0.7 to closer to 0.8789. But then, making a dietary change, I’m able to bend it back down closer to 0.7. You know, it goes to this idea of,, should we, and I know Bryan has always said things like, my team and I designed this diet, and that’s why I’m eating X, Y, and Z. Well, your biomarkers are saying that stuff in your diet may be able to move the needle in directions to improve your biomarkers, are you looking into that? So I don’t know what it is in his case, because in my case, it’s for whatever reason, sat fat, coconut butter, cacao beans. I cut that out, and all of a sudden cystatin C reversed that five- or six-blood-test trend, .74, .75 back in that range—still a bit outside of optimal, that .7.
But cystatin C and creatinine would suggest that Bryan does have some optimal suboptimal kidney function, additionally. During aging, when kidney function declines, blood urea nitrogen or urea will increase. So urea and blood are derived exclusively from nitrogen-containing compounds, specifically amino acids coming from proteins. So even if your kidney function is normal, if your protein intake is too high or if your protein intake is high, you’ll have high bun. Just because of protein degradation, just not using all of it. So then you can say, well, maybe Bryan has a very high protein intake. Well, he doesn’t eat meat. I don’t know if he’s supplementing with pea protein or other vegan proteins, but I find it hard to believe that his protein intake is going to be so high and higher than Siim and yours that that would be a cause for a higher than expected BUN.
The other side of that is protein intake is probably a bit lower than you guys and his kidney function is probably a bit sub-optimal as the data suggests, thereby leading to a higher than expected bun. Now bun on its own may not seem like a big deal. So what it’s urea circulating in blood, but when considering that it increases during aging and also, and I don’t know what the value would be for everybody, but in cell culture, high levels of urea degrade tight junctions. So in the intestine, you have, you know, it’s a tube and then you have intestinal epithelial cells basically that make the inside of that tube. Those epithelial cells are connected by tight junctions.
So if you have high circulating levels of urea and blood, the intestine is, it gets a blood supply. Urea can degrade those tight junctions, making it easier for stuff inside the intestinal lumen, poop, microbes, microbial products, whatever it may be, to leak into the blood and activate the immune system. How high does the bun have to be to get there? Does it have to be 25? 30 is found in very old people. I don’t know, but on bun, I lean towards lower being better, values where you’ve got it 12 or a bit less. Now, just to add one more bit of context, bun can indeed be too low because it’s produced by the liver as part of the urea cycle. So for people who have liver disorders, bun can be very low, five, six milligrams per deciliter. This is a very rare case, though, where you’ve got to have extreme liver failure for that to be the case. 12 in your case is probably not liver failure or liver disease or whatever, but it’s just something to think about, my bun is seven. Well, okay, is that because you’re not making it because something’s going on with your liver, or is this just a very low protein intake?
So anyway, long story short, I would agree with Siim’s assessment on this that Bryan’s got some kidney-related issues going on, and it’s probably correctable by diet. It’s just a matter of figuring out which aspects to move around to get it going in the right direction.
Criss: His diet is quite atypical, I think, and so I wouldn’t be surprised if there’s something in there that was causing a bit of an issue, and like for all of these kidney function things, despite his being a bit younger than myself, he’s the worst on all four of these, so okay.
Right, so as we jump in then and look at inflammation, and this is one where I’m able to basically, my inflammation has never been measured, as in they’ve never been able to find it. We have high sensitivity CRP here, and they get down to 0.1 milligram per liter, and they basically always tell me we can’t detect any, it’s below that. And then Bryan has about 0.3, and then under the inflammation, I also put the white blood cell count. I felt that fit best here, but I’m not really that familiar with what these ranges mean, so I’ll leave it for you to comment.
Mike: Yeah. So HSCRP, all three of you guys, fantastic. It’s even more fantastic that your data is as close to zero as possible. Meta analysis shows that less than 0.3 may be optimal. So the lower, the better for HSCRP increases during aging, higher levels associated with increased all-cause mortality risk. Is there better, is it better for it to be 0.3 versus 0.05 milligrams per liter? I don’t know, but I’m avoiding that age-related change, and making sure that it stays relatively low essential.
Now for white blood cells, I find no value in looking at the absolute number because they’re not a homogeneous group of cells. In other words, up to about 97%, 95 % or more for white blood cells are neutrophils, monocytes, and lymphocytes. Neutrophils and monocytes increase during aging, lymphocytes decrease during aging. So your white blood cell counts could be stable, and you could have divergent things going on at the same time. So I find no value in looking at the absolute number of white blood cells, but if we did, 3.5 to six would be my optimal. So Bryan’s would be a bit too low, but then we could take it even a step further because people often say like, your optimal ranges are based on sick populations.
Well, first of all, I’m looking at the studies that have millions of people, if they exist, if not millions and thousands, hundreds of thousands of people, the biggest studies that exist, large population-based averages. Could you make a case that the less-than-my-quote-unquote-optimal range, 3.5 to 6, is optimal at the individual level for certain people? Yeah, potentially. So could Bryan’s 3.1 be optimal, even though it’s a bit lower than the 3.5? It could be, but you know, it goes back to this division of the neutrophils, monocytes, and lymphocytes.
If, for example, his lymphocytes are less than 1,000, so that would be 1.0 of the 3.1, and then his neutrophils and monocytes are, say, 2,000, neutrophils and monocytes would be pretty close to optimal in that context, but his lymphocytes being 1,000 would be far away from optimal. And we could even, I know we talked about this a bit before, subdivide the lymphocytes into CD4 and CD8, which are what’s known as immune health grades.
1000 lymphocytes will be subdivided into T cells. And I know I’m gonna lose people here because it lost me. know, we get into the weeds, but this is where the beauty is. We’ve got to really understand the depths and the mechanism of our biomarkers. So the lymphocytes getting further subdivided into T cells, B cells, and K cells. If you don’t have enough of certain of those cell types to fight off infection, you’re gonna be more likely to get infections, stay infected for longer, increase your risk of death from infectious mortality, and all-cause mortality risk is a part of that story. So even if his neutrophils and monocytes were, quote-unquote, optimal, but lymphocytes were too low, leading to a worse immune health grade based on CD4, CD8, and 3.1, may not be optimal. So we would need more context to really properly evaluate whether that’s, quote-unquote, optimal. But in terms of the Luskardon definition of optimal, Siim, and your data would probably be closer to optimal than Bryan’s.
Criss: I think we have some more details on the red blood cells, but I don’t think we have that neutrophil kind of breakdown, unfortunately. okay. Right, I mean, here we are with some more of the blood counts. I mean, we have lymphocyte breakdown here.
For these, as well, I’m not quite sure how to read them. I do know that on the hemoglobin, more is better. I’m on the top of this one. For the RDW, the Red Blood Cell Distribution Width, if I remember correctly, this one is sort of like you want them to have them as regularly sized as possible. This one, mine, is slightly less regular than Siim and Bryan. Bryan, coming out number one on this one.
And then the platelets are the MCV and the platelets were all comparable these although I have a slightly higher platelets than the others, and then the lymphocyte percentage, which I have is the lowest of the three of us, and you said that was important so I know this is something you’ve been studying so what do you what do you make of this?
Mike: Yeah, so hemoglobin, 14 to 16 for men, quote unquote optimal, but 14 is not better than 15.9. Sorry, I should say 15.9. That’s the upper range. Once your 15.9 is right on that border, because once it’s above 16, that’s a bit too high. It’s associated with an increased risk of all-cause mortality. Bryan’s would be a reason for concern for me. First, it’s below 14 to 15.9, quote unquote, optimal range based on all-cause mortality risk. But then, as you mentioned, also declines during aging. And you know, this might be one reason why I think he mentioned something about HBOT. He’s been doing HBOT and HBOT has improved biomarkers. Well, hemoglobin carries oxygen. And if you have deficits, well, first of all, if you have deficits in red blood cells, red blood cell number, you’ll gonna have lower hemoglobin, because hemoglobin’s found in red blood cells, hemoglobin carries oxygen. Your tissues aren’t gonna be as properly oxygenated.
Actually in your cells aren’t gonna be as properly oxygenated as they should be. So HBOT, within that context, you’re essentially forcing oxygen into your body and potentially improving aerobic metabolism because now it has oxygen that it didn’t have before. So that might be part of the reason why he says things like, HBOT improves my biomarkers, maybe it’s because his hemoglobin is lower than it should be. That said, at his chronological age, his hemoglobin is, he’s gotta figure out how to reverse that.
That’s going in the wrong direction. Now for the RDW, your data is a bit too high. Optimal is either 11.4, 11.5 to 12.5. So, RDW there too increases during aging. Higher levels, I think, once it gets to 13.7, now we’re talking all-cause mortality, it starts to increase. So we’ve got that optimal that’s up to about 12.5 and then, 12.5 to 13.6, it’s not significantly different than that optimal range, but then once it goes above 13.7, now we’re talking higher risk. So RDW, just, for people who don’t know, it seems like an obscure biomarker. It’s the top predictor of Dr. Morgan Levine’s biological age, clock PhenoAge, or the biggest contributor to it. So if your RDW is relatively high, your quote-unquote biological age using that blood-based biomarker test is gonna come in higher than it should be.
That’s just one easy way to assess that it’s something to, it’s not just an obscure biomarker on a blood test report. MCV is the average volume of your red blood cells. So in youth, red blood cell volume is relatively small. And then red blood cells are all, as you mentioned, homogeneous in size or in volume. So they’re all pretty small, which that’s the youthful phenotype for red blood cells. But then during aging, that changes where the red blood cells volume starts to increase. MCV correspondingly starts to increase.
Here too, your and Bryan’s data would be too high. Siim is right on the money with this. My target is close to 90. And I should say not to make this about me and to interject my stuff here, but I’ve actually seen my MCV trending higher, too, with my latest data being around 96, way too high. Siim seems the champion on.
It’s just the published data, know, so platelets are a J or U-shaped curve with values around 200 being optimal. But if we look at what the all-cause mortality data is, 200 to 300 is the optimal lowest all-cause mortality risk. So, Siim would be best here, but you could make the argument that closest to 200 may be optimal based on the lowest portion of the J or U-shaped curve. So you could be actually closest to optimal.
165 would be too low, you know, so I put up a red flag on Bryan. MCH is the average hemoglobin found in red blood cells. I don’t track that. I don’t see the importance of, know, that’s not to say it’s not important, but I see other biomarkers. You know, so when we think about red blood cells, most people, you know, just to bring it back to glucose and cholesterol, right? They think of metabolic health as the most important biomarkers, but red blood cells are the most abundant cell type in the human body, human cell type, by far; it’s not even close. So tracking total red blood cell numbers, hemoglobin, which is found in red blood cells, as I mentioned, declines during aging, the MCV, their volume, and then the variability in their volume, the RDW, are the, for me, the four most important measures to be tracking with respect to red blood cells and overall red blood cell health and functionality, essentially.
So now, last step, lymphocyte percentage, I would have put that in the white blood cell, you know, potentially inflammation, but here we can kind of address that question of: is Bryan’s 3.1, is that potentially too low? Because his 38 % lymphocyte, so if you do 38.38 times 3.1, so now we’re looking at a total lymphocyte count that’s probably, so what is that, 1300, 1300 lymphocytes? So if we just look at CD4 and CD8, they should be about 800 and 400. But then that doesn’t include B cell or NK cells. So if your CD4s aren’t greater than 800, now you’re in immune health grade two, is immune health grade one is most likely to be found in young people, Siim’s age. So this would suggest his total lymphocytes are on the lower side and not a part of the youngest immune health grade.
Now, that for all of his tests? Is this just one test? You know, we’d have to get more data to find out.
Criss: I think you could say it’s a full-blisted instance, because it’s just one test. And a bit more data-infused. Hmm. Right, okay. So it does seem to track then. Hmm. Well, he’s living a quite ascetic life, so probably. Maybe. Okay.
Let’s see, in the Lipid panel, this one’s gonna be interesting, I think. My numbers are quite far out of range in several places, so we start with ApoB, which is sort of an LDL correlate. For this one, my numbers are basically a bit higher than the other two. I think I probably eat a messier diet, although I know Siim is not vegan, not vegetarian, he does eat meat from time to time. I have friends who love to do barbecue, and I love to eat barbecue. So I do have red meat from time to time, and also have milk with my coffee every day. Then, on APOA1, which is an HDL correlate, I’m off the charts on this one. So usually they’ll look at APOA1 and HDL and say, well, it should be high and over 40 or so for HDL is good. But I’m way at the 227. On the HDLC, you can see there that as opposed to being over 40, I’m 113.
And I mean, I think it actually is okay. I can go ahead and jump ahead to the next one.
There are three things that can raise your HDLs or your APOA-1. One is strength training. The second one is alcohol consumption. And the third one is walking and other exercises. And I do all three of those.
My strength training, I do it for about an hour or so a week, right within range, healthy range, not doing too much, not doing too little. For the alcohol consumption, I have exactly one drink of about 200 milliliters of wine at night every day. But two or three days a week, I’ll go out with friends and have three or four drinks. So that maybe is a little bit of an increase, but I don’t consider myself a heavy drinker.
But then on the walking, I am absolutely a heavy walker. So I have a walking desk. In some of our earlier videos, I walked throughout the entire video. I’ll walk 20,000, 30,000 steps a day without really noticing it. And there’s a chart here. I’ll jump ahead to this:
We can see that the more steps you walk, the higher your HDL is. And this is pretty much a linear correlation, right? So you can see here that basically my 20,000 steps a day are causing my high HDLs. So given that we know that more steps is actually, although there’s a diminishing return after about 10 or 12,000 steps where you’re not getting much more benefit from it, we know at least it doesn’t have a u-shaped curve or doesn’t become bad for you at any point that we’ve seen in the charts. So, I think my HDL is even though very high above the range, and in fact, I went to an HDL calculator to figure out what a healthy range is before. I plugged in 113 from HDL, it bounced right back at me with an error saying “invalid answer, please change your HDL value”, which is a little bit frustrating.
Still, I think that it’s fine given that I know the cause of it, which is the walking steps as opposed to having an alcohol problem or lifting more than an hour a week, which I think is the optimum level.
Total cholesterol, given the HDL, is then above what would be normal, but that is mostly the HDL content.
The triglycerides here, as you noted before, are quite low for me. In fact, my recent test, they came back as 38. So they’ve even dropped down from the 54 I had at the time.
And the Lp(A1), which you’ve talked about quite interestingly in some of your videos, is mostly genetic, although you’ve been able to move yours materially. I have good genetics for this one at 12.3, which gives me good hope that all of these are going to be fine.
Mike: Yeah, I guess, I wanna start at total cholesterol.
So, total cholesterol for me is kinda like the white blood cell story because total cholesterol is not homogeneous. You’ve got HDL going in one direction, cardioprotective versus the APO-B containing lipoproteins, LDL, lipoprotein A, VLDL going in the other. So I find no value in looking at total cholesterol. The individual lipoproteins and APO-B I find the most value. So that’s one.
Two, if you can go forward to the HDL, if you can go forward one slide. So if you look at extrapolation of the trend line, even up to 20,000 steps per day, that’s probably about 1.6 millimolar on average, right? So one millimolar is about 40 milligrams per deciliter, which means that if you’re walking 20,000 steps per day, the average expected HDL based on this plot, and you can even see the
The gray is the 95 % confidence interval. So at the highest, you’d expect to see HDL 65, 70. So I don’t know that this is the major factor in your case for higher HDL. It may be a part of that story, but based on this, your HDL would be 50 milligrams per deciliter lower. Now, can you go back? So, unfortunately, yep, go ahead. So I was.
Criss: I was just gonna say, yeah, so I have all three of those factors. So as you say, like that in and of itself is not enough to explain it. Although then I figured that if you add on top of that regular moderate alcohol consumption, and then on top of that, I do an hour of weightlifting, but as we’ve talked about before, it’s pretty hardcore. It’s full on squats and all the exercise, the entire exercise time is based on multi muscle movements.
Mike: Yeah, so weight lifting may be a part of the story where for whatever reason, you’re sensitive to producing more HDL within that context. But, and I’m not happy to say it, but, and I don’t know how much alcohol is contributing to it. But how would you know when HDL is indeed too high? So if you look at the all-cause mortality data, it’s a J or a U-shaped curve, actually probably closer to a U-shape, whereas you mentioned less than 40, higher risk. Then once you get above 70, also higher risk.
So APOA1 tracks with the HDL story because APOA1 is found almost exclusively on HDL. It can be freely floating in plasma, but if it’s in blood, it’s almost exclusively coming from HDL. And I know that not just because of the published mechanism in that it’s found on HDL, but I’ve measured APOA1 and HDL, looked at the correlation over seven tests, and the correlation coefficient is greater than 0.9. So I actually stopped measuring APOA1, and just I’m only focused on HDL. There’s no need to measure them both.
So if you look at the quote-unquote optimal range for HDL, 50 to 69 men and women, this is a study of like 12 million people or more. I don’t remember the actual number. It was greater than 10 million.
So okay, let’s bypass that. Let’s look at APOA1. Well, in a small study, I think this study was about 300,000 people. All-cause mortality for APOA1 was lowest for 150 to 180 milligrams per deciliter. All right, what about greater than 180? Although lowest risk was that 150 to 180, all cause mortality risk went away at greater than 180. So you essentially lost the lowering of all-cause mortality risk at values greater than 180. So in your case, I’d say that’s the best-case scenario. I don’t think your HDL is gonna be associated with a higher all-cause mortality risk when considering 8.1, but there’s a factor to consider. So HDL, high HDL, know, cardio protective.
So then why, or within what context, with high HDL be potentially bad for health and or longevity? Well, we’re considering that as you mentioned, alcohol can raise it, and knowing that, and I’m not saying you’re an alcoholic by no means, I’m not saying that, I’m sure you’re not, moderate alcohol intake. But for people who are alcoholics, HDL is dramatically high. And within that context, they’ve got damage to liver enzymes, GGT is relatively high, AST, and ALT. So could that be a part of your story where maybe you wouldn’t die from cardiovascular disease, but maybe some liver-related issues? Could you clean up your liver-related issues with training, know, not blood testing the day before a hard workout, and now GGT is less than 12, AST, ALT closer to the, you know, low twenties. And then the HDL story doesn’t become a liver health story. It’s just, okay, well, it’s maybe it’s a bit too much wine, where I’m losing the lowering of all cause mortality risk just being outside of that 180. So that would be the context for that.
APO-B, less than 70. So it’s interesting because if you look at blood test reports, they’ll say, like, less than 80 for primary prevention. So these are people who have, or diagnosed CVD less than 80, less than 70 for primary prevention. They get really strict once people have pre-existing CVD. But if you look at studies in the general population, less than 76 lowest CHD mortality risk. And then all cause mortality data actually less than 70. So these are people who don’t have preexisting CVD. So the reference ranges are behind the times.
Now here too, this is a bit, know, Bryan’s a bit of juicing here. You know, he’s on some PDs where he’s taking a statin. So he’s 70, right at that quote unquote, Lustgarten optimal, he’s juicing, right? He’s taking a statin to lower it. Would that be as beneficial if he could do it naturally? I know Siim’s not on a statin, so I’d actually place the greatest value on Siim’s 58 relative to Bryan. You’d be a bit too high. Now, you could say, all right, if optimal is 70 and the slowest CVD progression is gonna be less than 70, what’s the CVD, what’s the atherosclerosis progression rate for someone at 80 or 90 versus 70? Is it 1 % per year, .1 % per year? But even at a very slow rate. You know, ideally we want it to be flat at the lowest, right? So trying to get it lower than 70 would be optimal. And it’s easy, you mentioned eating barbecue, and I think it’s probably full-fat dairy that’s going in that coffee. You know, it’s not, it’s low-fat.
Criss: It’s low-fat.
Mike: So April B is pretty easy to reduce for most people. Sat fat, higher sat fat will increase it. But then there are published RCTs where if you increase soluble fiber and total fiber intake super high, APLB comes down very fast within two weeks. So cutting fat and increasing fiber intake, how high people may need to go? Is that from 30 grams of fiber to 40 grams? Probably not, may have to double it or go even higher. But for people who are struggling with APLB, it’s a relatively easy biomarker to move the needle on.
Trugless rides, I mentioned less than 45. If you go by all cause mortality data, less than 90 would be optimal. The reference range has less than 150. But if you look at CHD mortality risk, it’s less than 45. Here too, is 55 materially worse than 45? Is that a 1%, 0.1 % over time increase for atherosclerosis progression? I don’t know, but my target is getting it to less than 45. I’m in the ballpark of where you and Bryan are, 55, 60. Depending on my diet composition, if it’s higher carb, I actually goes to 70. So I’m still working on the recipe to get it consistently less than 45. And like protein A, last but not least, even though it’s, as you mentioned, it’s a genetic marker and thought to be, you know, resistant to change. From my experience, as you mentioned, it’s definitely malleable. How low you can get is debatable though. I’ve never had values where Bryan being the high end of this range is.
In terms of what’s optimal there, although lower should be better, there are published studies where it’s just not associated with all-cause mortality risk. But on the other hand, there are studies showing that it’s six to seven times more atherogenic than LDL. And triglycerides are approximately two times more atherogenic than LDL. So the way I’m thinking about this now is, so ApoB consists of LDL, lipoprotein A, VLDL and IDL.
IDL is almost never measured; it’s a very small fraction, so we can essentially boil APLB down into those first three: LDL, lipoprotein A, and VLDL. So if your APLB is less than 70, quote-unquote, optimum, if the major fraction of that is coming from lipoprotein A and VLDL or triglycerides, so triglycerides divided by five is a very close approximation to VLDL. So if your APLB is coming almost exclusively from lipoprotein A and VLDL, and less from LDL, that’s actually gonna be a worse cardiovascular disease profile, even at very low APOB. So, making sure that it’s not just about low APOB, it’s making sure that lipoprotein A is as low as you can get it, VLDL is low as you can get it. And then within the context of low APOB, relatively higher LDL. So, easier said than done, my lipoprotein A is higher than it should be, actually, even higher than Bryan’s, because that’s in millimolar, my millimolar is like 80, 75, 80 consistently. So I’ve got to work on figuring out how to get that even lower.
But, all right, just to add a little more context, so, fortunately, there is stuff for people like me, and you guys aren’t in this boat, your Siim is the best of the bunch there. So even if someone’s got relatively high liver protein A, 75, 80 nanomolar or more, having HSCRP less than two milligrams per liter, not 0.2, that essentially the CHD mortality risk goes away. But if you’ve got high HSCRP, the risk increases based on, CHD risk based on lipoprotein A. And then also the waist-to-hip ratio. So when the waist-to-hip ratio is less than 0.93, it’s not associated with an increased risk of lipoprotein A-associated CVD outcomes. But for people who had a waist-to-hip ratio greater than one, and I’ve got a video commenting on, actually, I released it today, it’s on YouTube today.
But, so for people who have a waist to hip ratio greater than one, Libraprotein A higher than 50 milligrams per deciliter, which would be 125 nanomolar, way off the charts compared to the three of you guys. That’s associated with an increased CVD mortality outcomes risk, whereas people with Libraprotein A, less than 50 milligrams per deciliter and 125 nanomolar with a waist to hip ratio less than 0.93, no association with CVD mortality related outcomes. So there may be ways for people who have relatively high lipocortinase to modulate that risk by keeping inflammation low and waist-to-hip ratio low. But anyway, context.
Criss: Yeah, that’s interesting. I hadn’t thought of doing the sort of math to break down the cholesterol. I mean, the thing everyone sees is the LDL and the HDL and then breaking that into the LPA out of the LDL. Interesting.
Mike: Yeah, this is I get paid the big bucks, know, it’s higher levels of…
Criss: I guess, yeah, you get into the numbers deeper, deeper, and, you know, get more correlations. Okay.
So let’s see, continuing on sort of metabolic health.
So I find this one interesting, and this is actually one of my wishes for Levine’s age calculator, which you use very effectively. Unfortunately, my understanding is that the dataset he used to calculate his, make his calculator with, only had fasting glucose. didn’t have HbA1c available for all data points because HbA1c, as I’m sure you’re aware, is a longer-term indicator of your overall blood sugar level. So I’m quite happy with this one, although Bryan, Siim, and myself are all in quite a tight range around the pretty optimal level of 5.1%. Fasting glucose, 86 %, is kind of generally useful here, and some other people have done some interventions with vitamin B, if I remember correctly, to lower this. Honestly, I haven’t really tried to address this or do anything with it. So I’m kind of just let it as it is. I figured my LPA-1 and the other things that I had would be enough to protect from the CVD, which is understanding what this is the concern for.
And then for the uric acid, Siim and I are about the same. And this one, Bryan Johnson, although it’s not exactly clear whether blower is better on this one, I think it’s more of a range than anything else.
Mike: Alright, wait, so HBA1C, five to six percent based on the lowest all-cause mortality risk, but then lower is found in youth, increases during aging. So, as close to five as possible, so all three of you guys, pretty great. Even Siim’s 4.9, I’m not gonna nitpick over 4.9 versus 5.0, probably fantastic.
I see more value in HbA1c as you mentioned, just because it’s a longer-term marker up to about 120 days, and I say up to because that’s an average, right? Red blood cells can live shorter than 120 days and they can live longer which can affect HbA1c measurements. So I see that as a better measure than fasting glucose. So I’m not worried about Bryan’s 97 because his HbA1c is 5.1, optimal for glucose 80 to 94, being closer to 80 being optimal. So, you know. I see, yeah, Bryan’s 5.1 is probably okay within that 97 context.
Homocysteine, in your case, that’d be something I’d be trying to reduce. So even though, so the argument against homocysteine lowering is that, you know, whenever I raise it as a biomarker, people are like, well, look at primary prevention trials that try to lower homocysteine, it didn’t improve CVD related outcomes. And then my retort to that is, okay, yeah, in the short term, but CVD is a long-term process. You know, these intervention trials, maybe they’re six months, a year, two months at most? Are you really impacting CVD related outcomes if you’re reducing homocysteine for a, you know, up to a two year period, but it’s been elevated for 30 years when CVD has happened, right? So, so that’s one side of that story. The other is that it’s in vitro and cell in cell culture models, it’s neurotoxic, and it causes endothelial cell senescence. So this is a big one in my mind.
The question of how to reduce it is not, not so simple. Most people, every time I make a homocysteine video, I get comments like, “Try methylglycine, betaine”, know, that brings it down for me. And it could work, you know. But that’s not the only place to look, because there are many ways to lower homocysteine. In my case, I’ve supplemented with four or up to five grams per day. No dent on homocysteine. So figuring out where the weak link is in that methylation chain, it’s not just, it may not just be about B vitamins, it could be, you know, other methyl donors are lacking that are not donating that methyl group to homocysteine to convert it into methionine. So yeah, my target is actually closer to where Siim is at around five. And then uric acid, you mentioned, you know, not knowing if, I think you said something like that, what’s optimal there for longevity.
So there’s a study that was done on the odds of living to a hundred years in association with uric acid levels. And actually 4.2 was right at that cutoff. So if value’s less than 4.2 milligrams per deciliter were associated with about a two-fold higher odds. Now, granted, this was like 4 % versus 2 % of living to 100. But still, it’s people who had uric acid levels of less than 4.2 had a higher odds of living to 100. Now, this may actually be good news for Bryan because he’s got values of 4.2. Uric acid levels are inversely proportional to EGFR. So worse kidney function, uric acid should increase.
So if Bryan does have some amount of poor kidney function, I’d expect higher than expected uric acid levels. The other side of that is uric acid levels can increase with a high meat diet, even alcohol, which I know are not a part of Bryan’s diet, which may suggest that maybe limiting the dietary precursors for uric acid are helping him keep it low, even within the context of suboptimal kidney function. But, yeah, 5.2, 5.1 is far from terrible. mean, it’s associated with lowest alcohols mortality risk, but less than 4.2 is my target based on the centenarian data.
Criss: Okay, yeah, I’m not sure how to move this one. I’m quite happy with the HP one. That’s one of my key metrics along with the HSCRP the overall information the HbA1c is the metabolic health I think these are fundamental.
Then, in the sort of once again taking a step away from the direct blood tests on the VO2 max, all three of us are quite exceptional on these things.
Siim at 66 although he’s a younger chap, younger lad. I’m mine is currently 5848 the last time I checked it which was when I just was having a trip back to the states where there’s good machines they’re available for testing it although when I was training for the marathon it was sixty one point five so when I’m in full on giving it all I’ve got it’s quite a bit higher than this it’s not necessary I’m quite happy with the day to day of 58.
My blood pressure at 121 over 78 is a little higher than I’d like it to be. I’ve been working with taking potassium to lower this because I don’t want to eat vegetables and fruits all day long.
Resting heart rate, all of us are quite low. Heart rate variability at the time was 50. Since I did this test now, it’s more like around the 60, 70 rate as it sort of increased. I don’t know, just as I’ve been tuning my overall fitness and reducing the number of days that I work out. You know, this is quite responsive to whether you’re overloaded in your training or not. Comments?
Mike: Yeah. So most of this is great news. so VO two max, you know, I get it’s important, you know, the clients during aging, but here too, when you think about what we’re actually looking at, it’s your maximum ability to consume oxygen under physiologic stress. I just don’t know how functionally related that is to just everyday life. Right? Sure. Sure. If you’re trying to run for hours or run for miles important, but you know, we’re not operating at VO2 max.
Now you could say, all right, it declines during aging. If you live long enough, your VO2 max will decline to the point where just not very good.
Criss: (01:15:56.301)
You can’t breathe and you can’t make any energy. Yep. Okay.
Mike: Yeah, so sure. But if you look at all cause mortality data, it’s like greater than, anything greater than 50 is the lowest risk. Is having a VO2 max of 65 better than 50? Maybe. But even the groups, you know, that were close to 50, 40 to 50, you know, all cause mortality risk was still dramatically reduced relative to someone who’s sedentary. So I think here too, just like the, you know, bench press and other strength measures, the absolute number, as long as you’re above 40, 40ish, not that important in my opinion, but resisting age-related change, a big part of that story.
Also too, you know, what VO2max doesn’t really capture is, you know, like sprinting or reaction time. Mean, granted, you’d expect someone with a high VO2max to be able to, you know, sprint relatively fast, but they’re not necessarily similar because, you know, the marathon runners are not in the meter dash, right? It’s two different types of athlete and even body types. Sprinting may not seem like a big deal, but if you’re walking down the street and your reaction time is poor because of old age and you can’t move out of the way. So anyway, I see value in, in not just VO2 max, but other aspects of anaerobic fitness too. BP 120 over 80 is associated with lowest risk. There is.
Obviously data in younger people where average blood pressure is 100 over 60. But here too, avoiding age-related change is important, which goes beyond one test measurement. Was your data 115 over 75? And now it’s 120 over 80, right? mean, that’s a big one. And blood pressure is, measuring it, I’ve measured it the last three days in a row. I’m measuring it at least 10 times a month. I really have to increase my, 10 times a month may not seem like a lot, or it may seem like a lot to some people, but, my dad is 83 and he just started blood pressure meds. So I may have some genetic predisposition to, and my averages have been about 120 over 80 more recently. So this is a big one, and most people aren’t thinking about it in terms of CVD risk. They’re thinking about lipo proteins and insulin sensitivity, but people who have…
There’s a study I haven’t made a video about yet, but BP is on that list for, you know, most likely related to having a CVD event, is having relatively high blood pressure. And it doesn’t have to be 150 over a hundred. It can be 130 over 80 increases risk. So BP is a big one, and it’s easy to measure. It’s, get that it’s time consuming and it sucks to have to sit there for 30 minutes, relax for 10 minutes, measure every couple of minutes to take an average. But I mean, it’s an easy biomarker to measure.
Criss: Yeah, I can’t, like I just find it too boring. I do like a five-minute waiting thing and then take my blood pressure, wait a minute, and take it again. Although one of the things that I’ve talked about on my blog, I mean, I think there’s a definite cheat code for blood pressure. It’s about three times as effective to increase your potassium as it is to decrease salt. And they’ve been saying decrease salt for blood pressure for decades, ever since the DASH study came out, which if you follow the literature, the DASH study was a huge outlier in the effectiveness they had of that. That was not able to be replicated in the amount of reduction in salt they had versus the blood pressure results. But I find it to be much more effective to increase the potassium intake, which you can do. Natural sources would be like bananas and other things, but also you can get a powder that you can just take in dosage that then be gets you to the few grams or so that you would need a day to reduce it and i found that takes down my blood pressure by about five off of the the systolic number in two or so off the diastolic. And my blood pressure is already good range i think those effect would be greater if you had a higher blood pressure to start with.
So carry on, you’re about to talk about how resting heart rate?
Mike: No, wait, so that’s a great point. So increasing potassium and lowering sodium is probably the lowest-hanging fruit. So just along those lines, though, note that my average potassium intake, because my diet is abundant in vegetables, especially potassium-containing vegetables, right?
Criss: I know when I’m talking about, like, I don’t want to spend my whole day eating fruits and vegetables. Wait a minute, that’s what Mike does every day.
Mike: I don’t get triggered, but I’m on 7,000 milligrams on average, about 7,000 milligrams of potassium per day. The AHA, American Heart Association, their recommendation is like 4,800 milligrams per day. And I’ve actually been a lot higher for potassium, and that’s on the context of around 2,200 milligrams of sodium per day. So I’m at AHA or better targets, and yet blood pressure is not 100 over 60. So there may be.
So that would always be the first place to start. Increased potassium, lower sodium. And if you look at the published studies, it’s right in line with what you said of higher sodium diets, even very high, five, six grams per day. If you cut that down to the lowest end of the sodium intake range, it’s only about a 5 mmHg difference for very high versus very low. So it’s right in line with what you’re saying. Some people may get a bigger impact than that, but there, too, I’ve been playing with my sodium intake because I’ve gone a bit higher intentionally, 2,700. Now I’m cutting it back down to 22; I may go back down to 1,800 because sodium is part of the stress response, including norepinephrine. So if your sodium intakes are actually too low, like 1,300 per day, norepinephrine can be higher. And why that’s important is because norepinephrine is a marker of chronic stress.
Norepinephrine negatively impacts the next two values on the list, resting heart rate and heart rate variability. So then it raises the question of how much sodium intake is optimal for lowering systemic levels of norepinephrine and potentially allowing for highest heart rate variability and lower resting heart rate, but without messing up blood pressure. So I’ve been doing that experiment, my blood pressure, I’d rather have the blood pressure improvements and keep it on the lower side.
So, okay, so wrestling heart rate’s an interesting one because inverse U during aging, relatively low in youth and older ages, it couldn’t be hard to discern with a peak at midlife. So heart rate variability breaks that tie. So HRV is very high in youth, and then it declines pretty steadily over lifespan. So at older ages, you’d expect to see a relatively low wrestling heart rate, but a low HRV. Whereas at younger ages and fit people, very high HRV, very low resting heart rate. Siim’s data is a perfect example of that.
Now, people then often say, oh, it’s genetic, my HRV is terrible, it’s always been terrible, it can be improved, can you get your HRV from 50 to 90? I mean, I know you saw changes during marathon training, and as you mentioned, balancing activity versus rest, goes up. For me, it’s not so much, the absolute numbers are important, high HRV, low resting heart rate, it’s important. But moving it within one’s own genetic maximum.
So if you’re starting off with an HRV of 35, if you can get that to 60, maybe you can’t get it to 100 within the context of a low wrestling heart rate, but figuring out that recipe to get it there, and then also avoiding the age-related change. So lowering your wrestling heart rate over time, but improving your HRV, getting it closest to that more youthful profile. And I know we’ve talked about this in previous pods, but the idea of how it is that exercise is good for average but not maximal lifespan? And I think chronic overtraining is a part of that phenotype, or getting the exercise prescription slightly wrong. Because when you think about function predicting health span, which should predict longevity, if you’re overdoing exercise by a bit and you’ve got chronically, you’re chronically stressed, whether through norepinephrine or lower HRV and higher arresting heart rate, I’d imagine that’s gonna be bad for some measure of lifespan is that a one or two year change is that a ten year change? I don’t know. But if we can keep HRV high and wrestling heart rate low, function as high as possible.
My bet is that there’s no published date on this. Nobody’s done a study on it. This is my speculation is that we’d be able to push the longevity, promoting effects of exercise from just an increase in average to closer to the maximum. So I look at HRV, wrestling heart rate is essential in this equation.
Criss: I think that’s a perfect segue here as we look at sort of the here we go to the aging biomarkers.
So afterwards we’ll talk about the exercise but before we get to that this is something that I honestly don’t put a whole lot of weight on although the fenu age reduction which you’re doing outstanding at is at the bottom of this.
The Dunedin pace, mean, Siim also has kind of cast some shade on this, and I have to agree with him on this is that it’s kind of a manufactured benchmark that then they measure against. And the people who make the Dunedin pace themselves say that we find no benefit of doing exercise or eating a healthy diet on our own metric. So that for me, I’m like, okay, those are the most powerful things that we have. If you say that your metric shows them to be of no use, I have no use for your metric.
And it’s quite expensive. It’s around like, I don’t know, several hundred dollars to take. I’ve done it twice. The first time I was at 0.8, I was like, okay, well, the second time was at 0.98. I don’t know why there seems to be a lot of variability in it. Bryan Johnson takes this a lot. He puts quite a bit of he’s got the Olympics and stuff that he competes on.
Telomere length, I don’t know. No, mean, it’s supposed to be more is supposed to be better, but mine is quite low. But that’s supposed to be a cancer prevention marker or something that goes down as you age for sure. But I don’t know.
The phenoage reduction. This then is tracking back into some of things I think are quite important like the I mean, not the HbA1c like I would prefer, but the glucose, the CRP, which is the inflammation marker, the albumin, which you mentioned the red blood cell distribution with and other things. So I think it’s useful. Although many of the things that I’ve talked about here would not be affected or reflected in that at all. And I think they are quite important, like the VO2 max, grip strength, and other things.
Mike: Yeah, so the epigenetics, that’s an interesting one, right? Because when you think about genetics, genetics is the prediction for what can happen, right? Epigenetics is one step above that: you’re not looking at genetics; you’re looking at methylation marks on your genome, which then determine whether genes are turned on or off. So there too, it’s a prediction. It’s not a measure of what’s actually happening. In terms of what’s actually happening, how they derive the algorithm.
It’s an epigenetic prediction of 19 clinical chemistry biomarkers, including HSCRP, HbA1c, Apo B, waist-to-hip ratio, oral health. But it’s still a prediction of actual biomarkers. So I measured Donita Pace, I used True Diagnostics, and I love their company, I love their leadership. It’s not a knock on them. I got tired of looking the prediction of real stuff and I’m just focused on the real stuff. So I added HbA1c into the approach for basically the same cost, I added the actual biomarkers.
Now in your case, so in terms of how good or not that it is, so Matt Kaberline and Siim have kinda poo-pooed on epigenetic testing as a whole, but it’s important to know that all epigenetic tests are not the same. There are many epigenetic tests that exist that are not based in published literature that are just giving you a biological age. And this isn’t just epigenetic clocks, it’s other clocks too that companies are using, and they’ll say, even whoop, your biological age is X. Well, what is that based on? Show me your algorithm, publish the data, let’s see how good it is. Because if someone’s epigenetic or any biological age test is not significantly correlated with chronological age, for example, Dunedin-Pace’s correlation with chronological age is only like 0.3, very weak, whereas PhenoAage, which includes nine clinical chemistry biomarkers, its correlation is like 0.94 to 0.96.
So, now the other side of that equation is, is your biological age test associated with the risk of death for all causes? For Dunedin Pace, and PhenoAge, this is true. But then even there, there’s a scale. If you take all of the biological age tests, how strongly or not do they correlate with all-cause mortality risk and or chronological age?
So for something like Horvath, Horvath’s methylation clocks. strongly correlate and are the strongest correlates of chronological age, but they are weakly correlated with all-cause mortality risk. Dunedin-Pace is consistently strongly correlated or relatively higher, has a higher effect size for all-cause mortality risk relative to Horvath, but Grimmage, which I’m sure most people don’t know anything about, it sounds like an obscure name.
Also, an epigenetic test is consistently in head-to-head matchups versus Dunedin-Pace and even against pheno-age, the clinical chemistry blood biomarker-based test that I always talk about, GrimAge is better than them all. So, but PhenoAge is in the same ballpark and actually Dunedin-Pace is probably top three. If we’re gonna make a top three biological age test for all cause mortality risk, those three are in the boat, but GrimAge is far and beyond consistently the best. Now, then that raises the question.
All right. We know what the biomarkers are in PhenoAge, and I’m measuring it, you’re measuring it. We know what the biomarkers are in Danina paste and you’re measuring most of them. What are the biomarkers in GrimAge? So most of those are not on a clinical chemistry blood-based biomarker test, except for Cystatin C. So if we look at the seven, or actually it’s now nine biomarkers that are in GrimAge. So GrimAge has a version one and version two. Version two now includes HSCRP and HbA1c, so we’re covering that base, but for the six of the seven other biomarkers, not including cystatin C, they’re not stuff you find on a standard blood chemistry panel. And then, of the seven biomarkers, six contribute more or less strongly to the overall GrimAge algorithm. In other words, just like the RDW is a major predictor of pheno-age, which in your case is bringing your data down and making it look older than it is. Some of GrimAge’s biomarkers are actually more strongly correlated with the overall Grimm-Age algorithm. And this goes just to the idea of can we measure the actual biomarkers relative to the predicted.
So, long story short there, cystatin C is a strong contributor to the GrimAge algorithm. essential in my mind, essential biomarker for tracking quote unquote longevity and overall health. But there’s another I’m tracking regularly: beta-2 microglobulin. That’s another one of the nine Grimm-Age version 2.0 biomarkers that has a correlation of greater than 0.8 as a predictor of the overall GrimAge algorithm. It includes other proteins that are less strongly related. There is one that I wish I could measure, which is GDF 15, which is like 0.9, not commercially available. But when it comes to the epigenetic tests, I agree mostly with Matt Cablellion’s assessment, especially the ones he went over in his video, for most epigenetic tests being rubbish because the ones he covered in that test were pretty much rubbish.
But there is a difference between all epigenetic tests. In terms of telomere length, that’s also a methylation-based estimation of telomere length. For that, I wouldn’t worry about the absolute number, but avoiding age-related change for whatever that metric is measuring, because it’s still a prediction, epigenetic prediction of an actual number. But for the PhenoAge, this is an important one, because, know, and I hate to say it, but for someone like Bryan, who says he’s got the best biomarkers in the world, bro, you gotta do better. Your phenolate is terrible and his RDW is fantastic, so it’s not an RDW problem. And it’s not a hard one and I get you’re in the same boat as him, but your RDW is a bit high right now. But you don’t proclaim to have the best biomarkers in the world, aside from this video. He’s been saying it for a while. And there is a Longevity World Cup, and I don’t wanna say I’m currently leading it, but once I got in that game,
Criss: You’re currently leading it though.
Mike: Yeah, I am currently leading it though. And if you rank my data every year going back years, I still be top 10. So here too, it’s not just about the absolute number. This is a composite of nine actual biomarkers. If you’re resisting age-related change for all of those nine, I’m more interested in the overall number over time. Where is your quote unquote, PhenoAge 7, 10 years later, compared to where you started?
Mike: And if it’s the same, well, you’ve potentially slowed aging rate for at least those biomarkers, right? Does that translate into better health? Well, having a younger phenyl age is associated with a lower risk of death for all causes. So that’s a positive. That clock will increase by 0.9 years for every one year of chronological age. So if you fast forward 10 years, you should be nine years older. But if you’ve minimized that where there’s no age-related increase, well, you’ve increased your biomarkers and potentially slowed aging rates.
I’m more interested in long-term trends, and I have a video, I just posted it on Patreon yesterday, that won’t make it to YouTube for about, maybe about a month, where I show that data, seven years of PhenoAge, how am I doing in resisting age-related change, or not, how well am I doing? So it’s not just about the one test, it’s about long-term trends, right? A true pace of aging, not one test.
Criss: Right. Yeah, it’s been it’s been an interesting one. That was one of the ones that I started with was the PhenoAge and then punching into there actually because you provided online and immediately put in my data on that one.
Yeah, I have these as deltas in here as I think they should be, because as you mentioned, it sort of just will go up with your age because it’s part of the formula. ahead.
Mike: Yeah. So, a quick note, Criss, that I, my adding the free Excel spreadsheet, is now outdated because I guess if you just go to Grok on X and you type in, calculate my PhenoAge done easy. Don’t have to do it. Yeah. Yep.
Criss: Nice. Huh? Cool. mean, hmm. I’m gonna do that now next.
Mike: Yeah. Well, you’ve got to ask it for the corrected version because there was an error in the, you know, we’ve got the, maybe we’re not outdated. The Excel version has the updated algorithm. There was confusion about the algorithm for better or worse, but, yeah, you’ve got to, you know, with all things, LLMs, you’ve got to give it the right question, you know, and ask, it to have the corrected version. Definitely.
Criss: Okay, and check it. Yep. So this is the next one here I think is the key for me at least.
Well, as you mentioned, my numbers haven’t been the best, especially given the amount of effort I put into it. And this is what I optimize for. I’m quite happy with it. So as far as the weekly workout hours,
Both Bryan Johnson and Siim spend about six hours a week working out. Bryan literally works out for an hour every day except for Sunday. And then Siim, when I added the times together, came out to about six hours as well. And my whole intent behind this is I go to the gym once a week for about 40 minutes, do one HIIT workout for about 20 minutes, and one run for about 30 minutes. And as far as my straight up workout time, that’s all that I do for the entire week. So the payoff I think has been fantastic for this amount of effort.
On the daily steps, this is where I bring up the, bring the thunder, because with my walking desk and other things, and I think this is one of most important things. The benefit that you can get for it, I think this is one of the reasons why my CRP, my inflammation is so low, is because of the amount of walking that I do. I’m able to do it while I’m computer stuff, working on my computer.
Daily supplements as well. I mentioned the only thing I’m taking really is potassium, which is quite a mild, simple vitamin that you could get with any bananas or anything. Whereas Siem’s taking about 15 of them. He has a number of them. Glycine, taurine, creatine, other things. And then Bryan Johnson has over a hundred of them and many of which he actually sells in pills that you can buy I don’t think that the evidence is conclusive on these drugs and i think that the majority of the benefit is available from the exercise in the diet stuff similarly in the monthly cost Bryan brags about spending two million dollars year on his health coming to a hundred seventy thousand dollars per month.
Siim i think is paying more than i want to add up to the estimated cost for supplements this is my estimate for his number not his own he has a publicist numbers and for myself i have a sixty dollar jim membership which enables me to do those squats and bench press that I do and potassium is basically a wash so there’s virtually no expense put on my health.
Mike: Couldn’t you technically add the steps, so that’s about seven-ish hours of walking? Wouldn’t you technically add that to your weekly workout hours?
Criss: So it’s a workout, and it’s not aerobic or anything for me. That is one of the things that I kind of slide under the table, if you will. But I haven’t added that for the other people either. Although I think Siim does a certain amount of walking, maybe around 8,000 to 10,000 steps. Bryan Johnson, as far as I can tell from reading his stuff, doesn’t walk any appreciable amount over the average American’s 4,000 to 6,000 steps.
He does things like climbing a mountain on the weekend, but that’s clearly aerobic. He’s doing it with brooking and with heavy weights, and he’s going up at speed, which isn’t really the point of walking. You can’t speed run the walking to get the benefits out of it. The benefits of walking is the long time. It’s about an hour and a half to two hours of walking a day just to get 10,000 to 12,000 steps. So you’re right. If I include those daily steps into the work out hours then I am the worst of this because that’s two hours per day, it’s going to be around 15 to 18 hours of walking per week. But for me that’s time on my computer when I can be writing emails responding to emails reading things as well reading studies so I don’t consider it to be extra time.
Mike: Yeah, so, and I think walking is great exercise, don’t get me wrong, you know, it’s, there are other ways to get that cardiovascular stimulus that are not, that are lost because they’re not technically taking steps for example.
Criss: It’s not cardiovascular, though. I make a distinction between it. Mean it’s low physical activity, low intensity physical activity, but you shouldn’t be out of breath at all. I mean, it depends. For some people, if walking is a cardiovascular activity, I’m usually thinking of people for whom it is no longer, there’s no effort to do so.
Mike: But even if your resting heart rate is 50 or 60, and if you’re going for a walk, your heart rate during that walk is gonna increase. Maybe it’s up to, if you’re highly fit, perhaps it goes to 75, 85, 90. That’s a cardiovascular stimulus. You’re not doing a hard quote-unquote workout, but there is gonna be a benefit for high-volume, low-intensity walking. But anyway, my point around that is, the one reason I don’t focus on steps is that there are other, low-to-moderate intensity exercises that are beneficial for cardiovascular health that don’t have to be walking. Like, you know, my workouts are right now 75 minutes circuit training-based. I’m getting, you know, my average heart rate, which is an underestimate by WHOOP is around 120 beats per minute. It may be a bit higher, 130, because WHOOP is known to underestimate heart rate during workouts. So I’m getting a 75 minute cardiovascular stimulus. mean, which is pretty much, if you translate 75 minutes, whole body,
elevated heart rate for that time. That’s an eight mile run if we, or so, if we tracked it over at worst, that’s a slow pace, right? So if I track steps, I would never get that because I’m not walking anywhere. I’m just moving, I’m distributing it everywhere. Another thing also is like, if we put my steps on this list, I’d probably be just as low as Bryan. Walking is a part of my approach, don’t get me wrong, but for example, for the past two days, I’ve been doing some chainsawing. You know, cutting down tree. I mean, yeah, it’s for me, it’s exercise is a nice workout, but I’m not going anywhere. And I am getting a cardiovascular stimulus. When I look at the data, it’s a stress trace that looks like I’m doing, and I have to be careful to modulate that. Otherwise it’ll start to negatively impact my HRV arresting heart rate recovery.
But there are other things we can do activity-wise. It doesn’t just have to be steps, you know, it can be in a variety of ways to get that cardiovascular stimulus. All right. I have one more note about this is the monthly cost.
Bryan’s is dramatically under because if you just factor in, I think he took 26 Dunedin Pace tests in a year or some outrageous number, because he’s trying to get his lowest number ever, right? So he’s taking the test as many times as he can, and it’s a 200-plus dollar test. So that’s at least twice per month, that’s $400 a month just on Dunedin test. Now I get you got it for supplements, but we can add at least $400 to that cost plus.
What about the cost of having your own HBOT and doing all the stem cell therapies and all the other therapies? Mean, the cost is off the charts. Also, the point I wanna make is with all those supplements, that PhenoAge is still not great, right? So, know, and I like Bryan, I appreciate him. You know, I’m not the type to ruin someone’s spotlight to shade them for their spotlight. I’m not that guy, but constructive criticism.
You know, for someone who claims to have a team, we do this for this reason and this for this reason, well, what are those hundreds of supplements doing? You know, are you actually moving the needle on more things than not? I’d like to see some correlations, you know, between, you know, supplements and biomarkers and, you know, planned approach. He did, he’s been doing that for psilocybin. Mean, he has heavily documented that. I’m awaiting the blood test, you know, data, and I’m sure that there are going to be some over exaggerations based on pre and post because you would need to do that experiment five times. Show me some five, at least five tests baseline and five tests with, without psilocybin. But yeah, I mean, for a hundred supplements, it’s a lot to be taking to have a nine-year younger PhenoAge. And that just shows you can’t biohack your way to having, quote-unquote, optimal biomarkers for at least those nine. So, you know.
Criss: Not not with the supplements those are gonna have a very indirect, if like, yeah, it doe.s I don’t think though well he chose the path doesn’t really get that way.
Mike: It could, it could, it could, but you know, it’s maybe that they’re just not targeting the right supplements or some supplements are just, you know, doing more harm than good in some cases. So, and which would those be?
Criss: Okay. Hmm. Well, that brings us to the end of this one.
So we’re gonna jump straight into the unaging challenge now. So I’ve talked about this a few times on your podcast.
It’s been an exciting journey. We’re just wrapping up now. We’re in the last month of the 2025 Unaging Challenge. We started with about 130 people who registered for the challenge. It’s a free challenge, and I’ve been watching it go steadily through, and I must say the numbers have dropped significantly. So I would say that it’s living up to the challenge name. It’s not easy to do the things, although the time, as I’ve mentioned, is not that significant. Is not that much of your week it’s about an hour and a half of exercise time per week and that’s not including the walking don’t spoil that. But the actual gym time is only about an hour and a half, and in return for that, you get about an estimated extra twenty years of life, taking you to nearly the centenarian level on average, according to the actuarial tables in the observational tables.
There’s no guarantee that you won’t get any money back. It’s not going to cure cancer, but it will give you a significant health increase at the end of it. We already still have around 10 or 20 people continuing the challenge, and we’ve made some improvements to it in terms of clarity, the emails, and the support structure we set up. So we’re doing the 2026 challenge.
So, to talk about some of the things that they did in the challenge last year.
So people had about a 65% increase in overall strength. This is a very blended figure. So some of these people were beginners and had doubled or more. It’s hard to say because they’re just starting to lift weights. But even the experienced people, myself, when I did it with the early adopters, I grew in about 10 % strength from doing more intensive stuff, as well as taking the creatine, which I don’t take regularly. But for special occasions and for really building bulk, it’s a great way to do it in a shorter period of time.
But the way I like to think of it, though, is you put all the people together who did the strength challenge part of the unaging challenge, and all the weight they lifted in kilograms was enough, actually, to lift a fully loaded semi between all of us.
So this is our joint effort in moving heavy objects, picking them off the floor or pushing them away from the bench.
And through the challenge, we go through it and let people customize and work out the best way to do an exercise for you, and make sure they’re doing it at the level that’s appropriate for them. It’s for beginners or trainers who can learn ways to treat their own routines and weightlifting routines to get the most effective ones for the least amount of time.
So then, after that, we go through a walking challenge and see how far people can walk and get closer to that 12,000 steps, which I think is ideal per day.
And between the entire team, we walked 11 million steps over a period of three months, which is enough to have walked from Anchorage, Alaska, down to Miami, Florida, and enjoy the beautiful beaches down there.
So we’ll continue to do these things. Part of the whole idea of the Unaging Challenge is not only that you learn to do some things yourself and you track it, so it’s a challenge, just make sure that you’re doing it. But we put people into groups together, teams that are then visible on a semi-private level, so you can see what the other people are doing. Not only are you accountable to yourself for doing the challenge and doing the steps or the weightlifting, but also other people will be able to see, and you can compare, trade notes, we have a Discord that we set up to do for it, and weekly emails that go with these are the goals for the week. Best of luck, here’s how things are going.
And sort of in that line, here’s the group of people who were the early adopters for the unaging challenge. These are friends of mine from around Tokyo who did it.
We had around 25 people who did it in the very first batch. And I can tell you, it’s one of the most rewarding things to have worked with the people I know and to have worked through the program and had actually seen the transformation.
My birthday is around September. And so, when I had a birthday party and had a bunch of people come over, it was very apparent that these people were in better shape than they had been at the beginning of the year.
So enrollment is free. It’s open now on my website at unaging.com. If you’d like to participate in the 2026 Unaging Challenge, welcome. You can come by yourself, or you can come with other people.
There’s a place in the form if you’d like to be placed with another group of people. I had some people from my high school, several who have continued all the way through to the end, who’ve done it with me or with my other friends or with a group of other people; all is welcome. And make 2026 the year that you achieve your health goals.
Anything you want to add or say about that, Michael? No, I think it’s great. I think it’s great.
Mike: No, I think it’s great. I think it’s great that 25 people is a lot, you know, and anything intended on improving people’s health through lifestyle, it’s great. Like, we don’t have to wait for published trials. Mean, you recruited a big enough group to potentially positively impact, you know, a lot of people. So I think it’s great. I think in an earlier, one of the earlier unaging challenges, you showed some biomarker data, maybe HRV or something like that, so are there plans to include at least HRV resting heart rate and or maybe even like, know, blood tests, because that would be really interesting to see, you know, blood pressure function, even blood pressure, if you have everyone come in for a blood pressure reading, you know, a couple days in a row before starting and then, you know, a month in two months in and really, you know, looking at something that would change over time to show that it’s not just fitness, it’s also the stuff on the inside that’s potentially improving, I think.
I don’t know, are there any plans to do some of that?
Criss: So the only device that we regularly ask for is the HRV, the resting heart rate, and also the VO2 max as measured by a wearable. And we leave that to people to determine for themselves what they want to use for the wearable. We had one person who said, I’m not sure about the walking thing. I don’t have a pedometer. I’m not sure I can do this. And then she’s like, wait, my phone counts my step. It’s fine. I got this. So we want to be as free for people to pick their own thing.
Many people have done exactly what you said where they’ve tested it, but we haven’t recorded all of that data. One is that I don’t want that much personal data. Although we do go through with the amount of weightlifting that’s been done and the resting heart rate and the other things, we can see the benefit over time. And some of the things have been surprising. Like some people have said that they’ve had the best sleep from the resting from the aging challenge that they’ve had in years specifically the walking seems to have a huge help with that one of the other people in it said that they’re able to sleep in the same room with her wife again because their snoring has greatly been reduced by doing the on aging challenge.
It’s not a weight loss program there are other things for that it’s more on overall health and longevity although several of the people on it have found that they’ve been losing weight if they’ve just kind of taken a different focus for it.
The last quarter of the challenges of call the unaging plate challenge where then we take a look at diet and just see what it would be to take a simple framework that give you the steps that you need to make sure that you’re getting a healthy diet to take out put in the big winners and take out the big losers so that you can have a healthier life and we track all of the meticulously on if you eat this food it cost you this many minutes of life or gain to this many minutes of life.
So it’s very much numbers based, but it’s more so about the team and coming through together and doing the best thing to improve for yourself. We don’t have a leaderboard on it because the leaderboard is what we achieve together and how much life we save on it. So I’m very happy with it, very proud of it, and I hope that more people participate in it this year.
Mike: Nice. Then, so is the intention to have it relatively small because what happens, what happens at some point, because I’m going to be doing this forever, or as long as my forever is. You too, I’m sure, in terms of health and, know, longevity optimization. So I can only imagine that. So in 20, in this year, were there more people for this version of the unaiding aging challenge, weren’t there more people in the last time?
Criss: We’ve operationalized it and the teams are always small. So the teams are around 10 to 20 or people so per team for a couple of reasons. Just one thing is to keep sort of the information a little bit tighter and so that it’s a group of people that you could say, okay, you sort of recognize, but we can scale up to a larger number of teams. With my initial early adopters group, we had just one team of about 20 people or so.
But then we did the challenge we started out with fourteen different teams of people actually I think we had about fourteen different teams so we’ll continue to increase the number of teams were also looking at the input mechanism to see if we can make it a little simpler and make it a little bit more intuitive eventually probably will make it into an app if it continues to be popular and we continue to increase the numbers on them that will give us a lot more ability to sort of pull some that data stuff to make it perhaps more rigorous on the reporting side.
Mike: So it could be a global movement, right? At some point, if it gets big enough, know I’m, you know, this is a delusional grand or grander, right?
Criss: That’s the goal. Yep.
Mike: Right. But you never know with these things. So, the intention is good. The intention is to do, you know, to improve people’s health. So, so do people have to be in Japan? Is this a Japan local only, or it can be a…
Criss: Nope. Not at all. We have someone doing it right now in Antarctica. So no, you can be wherever you are. It works with the materials that you have at hand. For the weightlifting portion of it, you do need to find a place where you can lift heavy objects. But many people have done that in their own houses, or with their own home gyms, or with straps and other things. So no, there’s no geographic requirement for it. Open to all.
Mike: Nice. I guess the Antarctica we can find out about the alien bases, right?
Criss: Exactly. He’s digging it up now. Sending messages.
Mike: I’m joking. I’m joking. Yeah. I’m like, I’m like 99 % joking. There are these internet memes of, you know, there are aliens in Antarctica and the US studying this and that. Anyway….
Criss: Okay, I can’t comment on that, but okay, good.
Mike: Yeah, well, thanks, Criss. This is great. I appreciate having you on. You’re always great to, we could go for hours. So yeah, this has been great, and thanks for being on today.
Criss: Yeah, great. Thank you so much for the opportunity and all the feedback on the biomarkers and things. Lots of stuff to think about. Always a pleasure, Michael.
