It's a wrong way of thinking about vo2max.
The correct way is "if I train to increase vo2max, does this cause an increase in longevity compared to not training an increase in vo2max?"
That's the question we should all want answered.
I do research in genetics and have co authored some Mendelian Randomization studies.
This is looking at directo causal relationship between VO2max -> Longevity.
I don’t think nobody is surprised by this results. We just know that VO2max is a good quantitative metric of cardiovascular fitness, but nothing more.
I do research in causal inference (and publish a lot as well), unless I'm misunderstanding the method, it isn't accounting for confounders as I note in this thread. Open to discussion.
https://www.reddit.com/r/PeterAttia/s/NrTIozu2Ob
You “adjust” for cofounders using genetic variants (that’s why the Mendelian name), but you are right “adjusting” for cofounders is no the right statistical name. In this scenario it would be colliders bias adjustment.
To put it simple this paper states:
Exercise improve both VO2max and Longevity. (Think it as triangle).
What they found that is false is this statement.
Exercise increases VO2max and this higher VO2max improves longevity.
So this is a classic example of “when a metric becomes a goal it stops being a good metric.” VO2max is a good metric for cardiovascular health so people with higher VO2 max are more cardiovascularly healthy, but if you train for just that you’re missing the point?
Yeah pretty much. It is a good quantitative metric to measure cardiovascular fitness, and cardiovascular fitness helps with overall longevity.
I would say grip strength (and muscle mass) is probably the same stuff.
Honestly makes a lot of sense. It feels like so much of longevity research feels like over complication of Michael Pollan’s “eat food, mostly plants, not too much” along with general “do strength training and cardio a few times a week”
100%, I’m getting to the point where I want to leave the subreddit. Many folks here are too focused on the metric. While simultaneously forgetting the health-span =\= longevity.
Yes. There has been a lot of technical discussion about this. As this association might be due to population stratification and not actual real biological associations.
Sasha Gusev (professor at Harvard) is always criticizing this.
Exactly. And the answer seems to be "Yes", based on this study.
> MVMR showed independent causal effects of body fat percentage, appendicular lean mass, physical activity, and hematocrit on VO2max, as well as of body fat percentage and type 2 diabetes (T2D) on longevity. Genetically predicted VO2max showed no associations.
IIUC the implication is this: Take two people, one is born with genetically good v02 max, the other is born with genetically poor v02 max. Person 1 is sedentary, person 2 trains to the point where their actual v02 max is equal to person 1. Person 2 has increased their longevity.
Haha, still not answering the right question.
You Want to know if person 1 increases their longevity by increasing vo2max and if person 2 increases their longevity by increasing their vo2max.
The comparison between people is irrelevant.
Edit: just to unpack it and make it less confrontational. The study is interested in genetic aspects of vo2max, so it's a fine study design for looking at that. It just doesn't tell us about the average treatment effect of actually increasing vo2max on a person.
Good point, edited slightly. TL;DR Training to increase your V02Max is going to increase your longevity. If there was a magic pill to increase your v02max without training, that might not (but there isn't anyway).
If genetically predicted vo2max is not associated with mortality but actual vo2max is wouldn’t that prove that acquired vo2max is associated with longevity?
Not necessarily, too many unmeasured confounders going along with things that also increase VO2MAX and living longer (Healthcare access , socioeconomic status, geographic location, etc.)
I listed some, but in case there is genuine confusion, here's an example:
Scenario 1: Person decides to exercise to increase vo2max, reads reddit because it's free and they have limited expendable income. Gets ok advice and implements it in an ok way. Vo2max goes up some. Person gets cancer, because of low financial means, can't travel to research hospital for top level treatment, dies 1 year after onset.
Scenario 2: Person decides to exercise to increase vo2max, hires personal trainer or exercise physiologist. Vo2max goes up substantially. Person gets cancer, but because of high financial means, travels to research hospital for top level treatment, dies 5 year after onset.
Financial means is a strong unmeasured confounder to making the statement you want to make. In both cases, you will show a strong association between longevity and vo2max apart from genetics, but it's due to finances.
Thank you for taking the time. I promise I am not trolling. I agree. Acquired vo2max is a good, clear signal of healthy habits and is associated with longevity but ability to change genetically predicted vo2max is associated with having means. People whose actual vo2max worse than their genetically predicted ones may also be living in bad conditions, stressful jobs, other health issues and the people who can train may also have access to other things that can influence their longevity.
What happens if Person 2 has a heart attack or develops a disease? Will the training matter? The benefits of being in peak condition only last while you can maintain peak condition. If you get into an accident or have a heart attack or get sick, you might never reach peak condition again.
Of course life is better if you've been in peak condition for a long period of your life vs never reaching it. But I don't see how it offers any long term protection. There are people who have long COVID who never were the same and some people even die from diseases which strike randomly.
What's the difference? Control what you can control.
But if we're going to obsess, I'm not sure it's well studied. It's possible, event likely, training to have a higher V02 Max is protective even after its lost, relative to not doing so.
That's definitely true for strength training for things like bone strength.
Washing your hands has impact too. But to say VO2Max is a metric I should track? I don't care what my VO2Max is. What I care about is how my blood tests look, and how I feel when I work out.
There is no evidence that VO2Max offers protection from a heart attack. You might be more likely to survive, but heart damage and heart failure aren't something anyone comes back from.
Yeah I think this sub gets obsessive over metrics and ignores the things actually stated in PA's podcast. IIRC he specifically says the value of V02 max is that you can't "cheat the test". If he has a patient he can't really tell how they feel after a workout, or trust that they're doing what they say, but if their V02 Max goes from 30 to 50 they're definitely doing the right stuff.
There’s almost no evidence that training ti maximize VO2 max is the optimal way to exercise for longevity. And as there are an infinite number of ways to train the cardiovascular system, the question you are asking is really not likely to be that important. PA’s focus on VO2 max is really misplaced. Wide varieties of consistent aerobic activity will move your V02 max about as far as it can go. The specific trainings that will get it the last half a percentage point are highly unlikely to be important for longevity.
The answer is probably not by much. If you get long COVID or have a heart attack your VO2Max will go down permanently, and no amount of training will recover you from that damage. If you are lucky enough not to have that happen to you then a higher VO2Max can convey a higher quality of life. Maybe your dick works for longer for instance.
This is showing that the normally omitted variables of genetics around metabolism and other things are causal to the outcome not vo2 max. One issue is vo2 max as a denominator takes in those very variables (body weight which includes fat which comes in part from genetics) which is going to boil off predictive power in this kind of study when you do tests around predictive power causal or otherwise. Also, physical activity is causal to longevity not vo2 max. Vo2 max is thus the measurement of that and body genetics, the things that make it a high number are apparently the things that are good for you.
Any true stats nerds able to do better? I’m not quite a stats nerd
I am genetic epidemiologist MD nerd. This type of studies called Mendelian Randomization look at direct causal relationship between any variables and outcome.
In this case, they are controlling for things that produce high VO2max, using genetic variants associated with these factors, and then you can measure this “direct” causal relationship of variants -> VO2max -> longevity.
In this paper they are showing that VO2max in itself does not produce longevity.
To put it simple:
ie: Exercise produce both higher VO2max and Longevity. -True
Exercise produce higher VO2max and this higher VO2max produce longevity -False
BTW I don’t think nobody is surprised by this finding.
Yeah, this doesn't actually even have much to do with the Mendelian approach. If an observational study had good data on exercise (and body composition), and set up the model the same way, the result would be very similar or even the same (there may be additional confounders in the observational data).
There are some things I don't get from the abstract though - they describe measuring vo2max in an exercise test, but the result section refers to "genetically predicted vo2max", which sounds like they are using MR for that. How do you think they used the measured vs gene-based vo2max here? I guess it will obvious when the full paper is available though..
You are 100% spot on.
MR is only good because it accounts for “hidden” cofounders. You can use any instrumental variable for that, but we already have so many GWAS… we might as well use them.
As for your questions. It looks like they used the genetic predisposition to higher VO2max independent of all these other factors (muscle mass, fat, diabetes, etc) to check if longevity was being driven by higher VO2max itself or by other factors associated with higher VO2max. They found that factors associated with higher VO2max drive longevity benefits but not VO2max on itself.
Exactly. This is why we should not care about VO2Max. We shouldn't try to become elite in that. We should just try to be our personal best or close to it, for as long as we can maintain, so as to maximize healthspan.
I like and follow Peter as he truly inspired me to restart strength training after his talk on the marginal decade but the guy is utterly obsessed over some details that are needless complicated to regular folks or their longevity per se
If the average person can get cardio and strength training in multiple times weekly, eat a plant based whole foods diet rich with protein and sleep 7-8 hours consistently uninterrupted a night, I'm not sure how much more life they would squeeze obsessing over or even measuring their VO2max or ApoB levels.
I agree completely, stick to the basic principles and wait for the evidence base on everything else. I’m glad he listens to the science but I have no interest in getting ahead of confirmatory science. I’m old enough to recall when it seemed like a glass of red wine every day was a good idea, so I did. It wasn’t. Years ago, he was pro-rapamycin, he may still be, but I wouldn’t do that. He was also into multi day fasting, and stopped doing that. Stick to the basics. Benefits on paper must always be weighed against real world risks.
Grip strength is another fun one… strength training and lean muscle mass? Hell yeah, but hacking for grip strength because some study showed that its a predictor or longevity… :/
> Grip strength is another fun one
I find this a really stupid thing for him to focus on. Grip strength has to be highly correlated with longevity...but greater grip strength can't be causing people to live longer. That sounds kinda insane.
Completely agree - I’ve had this argument with friends IRL and it stuns me that anyone would think that grip strength alone is anything more than a proxy for general strength and maybe functional mobility.
But he doesn’t mean VO2Max precisely, he just means that since it’s very hard to have a high vo2max, it means someone does heavy training, which brings benefits to someone’s longevity. Not sure if I can put links in this subreddit, but here’s a short video where I think he explains that. https://youtu.be/qgjAaD2M-JE?si=mQTC3bPIPmhhuqtc
Tbh I don't really think Peter is very guilty of this. For years he's been clear that there are big buckets that people need to put energy into before you start arguing in the margins.
I think that his content and this sub have overlap with the biohacking crowd who are often guilty of making small details look like huge deals.
I've literally seen people ask questions about how to improve grip strength or something, even when Peter has said in no uncertain terms that the correlation is likely just a proxy for other variables.
Grip strength is another fun one… strength training and lean muscle mass? Hell yeah, but hacking for grip strength because some study showed that its a predictor or longevity… :/
I find it hard to interpret the findings of this study, in terms of its relevance to whether exercise is effective for increasing lifespan. The reason is that the genes impacting VO2max could impact it in very different ways, such as 1) how the muscles and cardiorespiratory system are constructed, and 2) innate motivation to exercise. These may have different implications for the impacts of voluntary exercise on lifespan.
That said, I do think Peter Attia doesn't pay enough attention to potential residual confounders in the observational studies he cites on the association between physical fitness measures and mortality risk. These could greatly impact the strength of the relationships.
Nevertheless, I still think getting abundant physical activity is a smart gamble for those of us who care about health and physical function as we age.
No causal effect, but Vo2max is associated with longevity - so it's a good marker of healthy habits.
So, no reason to be anal about increasing Vo2max as the be all and end all (same goes for grip strength btw).
Peter has a bad habit of throwing most of his eggs in the basket which he has chosen for the time being. For things he likes - like Vo2max - one study is enough. But for something like plant protein superiority, 20 association studies wont be enough (because of 'healthy user bias' as if that doesnt apply to vo2max).
It’s interesting how you selectively choose which non-causal variables to care about and disregard. oxLDL, HDL, and small LDL particle count are variables I frequently see you disregard on the basis of not being causal, yet they are clearly associated with poor health outcomes and risk factors. Here is a variable that is not causal, but I think you take the reasonable stance of saying we should be concerned about it due to its association with favorable health outcomes.
Yes - oxLDL is absolutely useless. Show me one cardiology body guideline which uses oxLDL as a marker. As a bonus, here is lipidologist Dr. Tom Dayspring crapping on oxLDL blood tests.
https://youtube.com/shorts/E6KPJ-j6mTA?si=_JZpB4Lxxm0MJTlD
HDLc is not causal to heart disease- it didn't work either in mendelian randomized studies nor in HDL raising drugs. Just like vo2max it's a marker, not a cause. You would know this is you heard Attia podcasts with HDLc experts.
Small LDL count is not more predictive of Atherosclerosis than ApoB. All ApoB particles are equally atherogenic (except lp(a) and one more rare case concerning chylomicrons). If you have heard anything about Attia's discussion with Dayspring or Dr Allan Sniderman, you would know that ApoB is what matters, not sdLDL.
I will repeat, being in 3rd vs 4th quartile of vo2max will have no effect on longevity on its own. You don't need to be the world best athlete to live long. But you do need to be on a diet and exercise regimen which helps avoid chronic disease.
In the process of getting defensive, you missed my point, in which you selectively care about variables that are and are not causally associated with an outcome. I do not disagree with any of the points you made. It was just interesting to hear you make a statement about VO2 max that could easily be applied to other variables you often dismiss.
Both HDL and small LDL particle counts are measurements of “healthy habits,” as you also acknowledge with VO2max.
Whether or not a variable is causal doesn’t change the fact that it can provide useful insight regarding someone’s day to day decisions and health.
A practical example is inflammation measured by CRP. There are countless instances where CRP is not causally associated with a disease, yet it is a powerful piece of information regarding one’s health. To dismiss it on the basis of a lack of causality is shortsighted, in my opinion.
>Both HDL and small LDL particle counts are measurements of “healthy habits,”
No, HDL is not. All these crazy ketoers and carnivores with crazy high 200 mg/dl ApoBs have high HDL. Absolutely is not a measure of healthy habits. Plus, HDL temporarily falls during active weight loss in moderate fat diets, while the patient is objectively becoming healthier. So no, HDL is not a good marker of health.
No-one needs to track sdLDL. Only ApoB should be tracked as it supercedes sdLDL in every way. If one is prediabetic, they should know it from glucose hba1c and insulin test, not via sdLDL.
Vo2max is a good unified number of fitness, unless there are better markers it is at least a decent metric to track.
Eta: you added in CRP. HsCRP is the best objective number to measure systemic inflammation, and it also includes autoimmune diseases, infection etc. so its a good number to track, and does not belong in this conversion since it's not specific to heart disease. Hdl and sdLDL are 3rd rate measures of heart disease risk. ApoB is causal and easy to track.
Tldr: hsCrp and vo2max are best markers in their category even if not causal, so good to track.
ApoB is causal, so fantastic.
OxLDL, HDLc and sdLDL neither causal nor best markers in category. Basically I have good reason to crap on these markers.
If HDL is not a relevant metric of metabolic health, then please help me to understand why it is included as a criteria of metabolic syndrome according to the World Health Organization and all other medical organizations.
You commented on high values of HDL. I am referring to a low HDL, which is strongly associated with insulin resistance and systemic inflammation, among many other risk factors and non-cardiovascular diseases.
Lol, you were talking about oxLDL, sdLDL and HDL - clearly in context of heart disease.
Now you made a bait and switch to metabolic syndrome. Anyway, large waistline, high BP and high glucose is enough to diagnose metabolic syndrome.
Hdl measurement is not a requirement to know one is a fat and unhealthy, or diabetic and unhealthy.
You seem to be super slow and obtuse. A test has sensitivity and specificity.
A high HDL in the context of a super high fat diet with high ApoB, for example, is not a marker of health or habit. So, a high HDL is a false positive in this case.
A low HDL on the other hand, can indicate insulin resistance and diabetes; but also can be genetic or due to exogenous testosterone. It can also be due to a low fat diet or ongoing weight loss. If it is because of those last 3 things or some other reason which is not metabolic syndrome, it has no bearing on risk. low HDL is a false negative in these cases.
On the other hand, ApoB is clear. High ApoB is more risky, less ApoB is less risky in terms of causality towards heart disease. Genetic or not is immaterial.
If you want to know whether you are fat, have high BP, or are diabetic - HDLc is not the test for these lol.
There will be no or minimal difference between 3rd or 4th quartile of vo2max in either 'healthspan' or 'lifespan'.
One does not need to be an ultra elite athlete to life a healthy and long life.
Everyone should try to avoid being in the lower 2 quartiles though.
Watch this discussion https://youtu.be/IkxHBUUVhnw?si=04zO9QpZzcUEdKmE
And that's my point. Some people are just genetically gifted and we shouldn't be comparing ourselves to them ever. We should just compare ourselves to our younger selves and trying to maintain as long as we can.
Mendelian randomization tries to answer the question by looking at people with genetic factors that result in (in this case) a higher VO2Max. That allows you to control for basically every behavioral difference.
I haven’t done this type of research myself, but it is viewed as a high quality test of an hypothesis.
However our knowledge of the genome is incomplete.
I think of VO2max as being a surrogate for cardio vascular conditioning. If mind is high because I exercise, there are advantages. If it’s high because of genetics it doesn’t mean anything.
I also haven’t read the paper and it’s possible they tried to control for all of this.
I would not dismiss the paper, but it’s one piece of the puzzle.
Well I think this is what the expected outcome would be. High vo2 max means you have done the work, you have trained in your life. That seems to matter. The vo2 level itself is not thought to be causally related to longevity, the work you did to get to that figure might.
More people drown when ice cream sales go up, not because of the ice cream but because of the underlying factors - heat.
I believe the work is the predictor. VO2 shows you’ve put in a lot of work and stayed active. Just like grip strength, muscle mass, etc. Those things are probably indirectly tied to longevity because they are the result of not being sedentary.
VO2Max does not predict when you could get COVID which cuts your VO2Max in half permanently (long COVID). It does not predict if you'll have a heart attack which could cut your VO2Max permanently. I think the VO2Max metric is mostly survivor bias. The people who survive, who didn't get sick, or have a heart attack, preserved their VO2Max. But to act like VO2Max offers any protection is naive in my opinion. I don't see that it does.
Youth offers protection.
>VO2Max does not predict when you could get COVID which cuts your VO2Max in half permanently (long COVID).
It does though, higher cardiorespiratory fitness is associated with a lower chance of long covid.
Show me a study? And associated with does not mean casual. It doesn't mean high VO2Max is the reason for lower chance of long Covid. Age seems much more of a factor.
There are very few solid causal approaches in covid yet, as challenge RCTs are kinda challenging, especially if you'd want enough sample size to study long covid. But here is an observational study that did control for age and found vo2max still had an effect https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9335466/
This is on people who did not have a severe initial infection. A severe initial infection makes long covid more likely, and there are plenty of studies showing better cardiorespiratory fitness makes a severe initial infection less likely, so this study is on people who already had passed the first hurdle (but even then, CRF matters).
Age is a much bigger factor for sure, but cardiorespiratory fitness still has an effect.
Attila’s logic for espousing vo2 max as a causal factor in longevity has always been weak. Every time I’ve heard him explain it, it’s purely correlational - the higher the vo2 max, the better the health outcomes. This ignores the obvious fact that as people become less healthy and more sick, their vo2 max will decline, but their poor health is not caused by declining vo2 max.
It's a wrong way of thinking about vo2max. The correct way is "if I train to increase vo2max, does this cause an increase in longevity compared to not training an increase in vo2max?" That's the question we should all want answered.
I do research in genetics and have co authored some Mendelian Randomization studies. This is looking at directo causal relationship between VO2max -> Longevity. I don’t think nobody is surprised by this results. We just know that VO2max is a good quantitative metric of cardiovascular fitness, but nothing more.
I do research in causal inference (and publish a lot as well), unless I'm misunderstanding the method, it isn't accounting for confounders as I note in this thread. Open to discussion. https://www.reddit.com/r/PeterAttia/s/NrTIozu2Ob
You “adjust” for cofounders using genetic variants (that’s why the Mendelian name), but you are right “adjusting” for cofounders is no the right statistical name. In this scenario it would be colliders bias adjustment. To put it simple this paper states: Exercise improve both VO2max and Longevity. (Think it as triangle). What they found that is false is this statement. Exercise increases VO2max and this higher VO2max improves longevity.
So this is a classic example of “when a metric becomes a goal it stops being a good metric.” VO2max is a good metric for cardiovascular health so people with higher VO2 max are more cardiovascularly healthy, but if you train for just that you’re missing the point?
Yeah pretty much. It is a good quantitative metric to measure cardiovascular fitness, and cardiovascular fitness helps with overall longevity. I would say grip strength (and muscle mass) is probably the same stuff.
Honestly makes a lot of sense. It feels like so much of longevity research feels like over complication of Michael Pollan’s “eat food, mostly plants, not too much” along with general “do strength training and cardio a few times a week”
Michael Pollen forgot about the elk jerky and blood thinners though
100%, I’m getting to the point where I want to leave the subreddit. Many folks here are too focused on the metric. While simultaneously forgetting the health-span =\= longevity.
Just want to come here to say how much I love the dialogue between two researchers!
So you're adjusting for income and financial means via their genetics? That seems dodgy IMO.
Yes. There has been a lot of technical discussion about this. As this association might be due to population stratification and not actual real biological associations. Sasha Gusev (professor at Harvard) is always criticizing this.
Exactly. And the answer seems to be "Yes", based on this study. > MVMR showed independent causal effects of body fat percentage, appendicular lean mass, physical activity, and hematocrit on VO2max, as well as of body fat percentage and type 2 diabetes (T2D) on longevity. Genetically predicted VO2max showed no associations. IIUC the implication is this: Take two people, one is born with genetically good v02 max, the other is born with genetically poor v02 max. Person 1 is sedentary, person 2 trains to the point where their actual v02 max is equal to person 1. Person 2 has increased their longevity.
Haha, still not answering the right question. You Want to know if person 1 increases their longevity by increasing vo2max and if person 2 increases their longevity by increasing their vo2max. The comparison between people is irrelevant. Edit: just to unpack it and make it less confrontational. The study is interested in genetic aspects of vo2max, so it's a fine study design for looking at that. It just doesn't tell us about the average treatment effect of actually increasing vo2max on a person.
Good point, edited slightly. TL;DR Training to increase your V02Max is going to increase your longevity. If there was a magic pill to increase your v02max without training, that might not (but there isn't anyway).
If genetically predicted vo2max is not associated with mortality but actual vo2max is wouldn’t that prove that acquired vo2max is associated with longevity?
Not necessarily, too many unmeasured confounders going along with things that also increase VO2MAX and living longer (Healthcare access , socioeconomic status, geographic location, etc.)
I am not aware of any cofounders that increase vo2max.
I listed some, but in case there is genuine confusion, here's an example: Scenario 1: Person decides to exercise to increase vo2max, reads reddit because it's free and they have limited expendable income. Gets ok advice and implements it in an ok way. Vo2max goes up some. Person gets cancer, because of low financial means, can't travel to research hospital for top level treatment, dies 1 year after onset. Scenario 2: Person decides to exercise to increase vo2max, hires personal trainer or exercise physiologist. Vo2max goes up substantially. Person gets cancer, but because of high financial means, travels to research hospital for top level treatment, dies 5 year after onset. Financial means is a strong unmeasured confounder to making the statement you want to make. In both cases, you will show a strong association between longevity and vo2max apart from genetics, but it's due to finances.
Thank you for taking the time. I promise I am not trolling. I agree. Acquired vo2max is a good, clear signal of healthy habits and is associated with longevity but ability to change genetically predicted vo2max is associated with having means. People whose actual vo2max worse than their genetically predicted ones may also be living in bad conditions, stressful jobs, other health issues and the people who can train may also have access to other things that can influence their longevity.
Yeah and I personally think that training to increase vo2max increases longevity... But I'm just not sure there are of true causal evidence on it.
At the very least couldn’t acquired vo2max (regardless of the methods) be a leading indicator of increased longevity.
What happens if Person 2 has a heart attack or develops a disease? Will the training matter? The benefits of being in peak condition only last while you can maintain peak condition. If you get into an accident or have a heart attack or get sick, you might never reach peak condition again. Of course life is better if you've been in peak condition for a long period of your life vs never reaching it. But I don't see how it offers any long term protection. There are people who have long COVID who never were the same and some people even die from diseases which strike randomly.
What's the difference? Control what you can control. But if we're going to obsess, I'm not sure it's well studied. It's possible, event likely, training to have a higher V02 Max is protective even after its lost, relative to not doing so. That's definitely true for strength training for things like bone strength.
Washing your hands has impact too. But to say VO2Max is a metric I should track? I don't care what my VO2Max is. What I care about is how my blood tests look, and how I feel when I work out. There is no evidence that VO2Max offers protection from a heart attack. You might be more likely to survive, but heart damage and heart failure aren't something anyone comes back from.
Yeah I think this sub gets obsessive over metrics and ignores the things actually stated in PA's podcast. IIRC he specifically says the value of V02 max is that you can't "cheat the test". If he has a patient he can't really tell how they feel after a workout, or trust that they're doing what they say, but if their V02 Max goes from 30 to 50 they're definitely doing the right stuff.
There’s almost no evidence that training ti maximize VO2 max is the optimal way to exercise for longevity. And as there are an infinite number of ways to train the cardiovascular system, the question you are asking is really not likely to be that important. PA’s focus on VO2 max is really misplaced. Wide varieties of consistent aerobic activity will move your V02 max about as far as it can go. The specific trainings that will get it the last half a percentage point are highly unlikely to be important for longevity.
The answer is probably not by much. If you get long COVID or have a heart attack your VO2Max will go down permanently, and no amount of training will recover you from that damage. If you are lucky enough not to have that happen to you then a higher VO2Max can convey a higher quality of life. Maybe your dick works for longer for instance.
This is showing that the normally omitted variables of genetics around metabolism and other things are causal to the outcome not vo2 max. One issue is vo2 max as a denominator takes in those very variables (body weight which includes fat which comes in part from genetics) which is going to boil off predictive power in this kind of study when you do tests around predictive power causal or otherwise. Also, physical activity is causal to longevity not vo2 max. Vo2 max is thus the measurement of that and body genetics, the things that make it a high number are apparently the things that are good for you. Any true stats nerds able to do better? I’m not quite a stats nerd
I am genetic epidemiologist MD nerd. This type of studies called Mendelian Randomization look at direct causal relationship between any variables and outcome. In this case, they are controlling for things that produce high VO2max, using genetic variants associated with these factors, and then you can measure this “direct” causal relationship of variants -> VO2max -> longevity. In this paper they are showing that VO2max in itself does not produce longevity. To put it simple: ie: Exercise produce both higher VO2max and Longevity. -True Exercise produce higher VO2max and this higher VO2max produce longevity -False BTW I don’t think nobody is surprised by this finding.
Yeah, this doesn't actually even have much to do with the Mendelian approach. If an observational study had good data on exercise (and body composition), and set up the model the same way, the result would be very similar or even the same (there may be additional confounders in the observational data). There are some things I don't get from the abstract though - they describe measuring vo2max in an exercise test, but the result section refers to "genetically predicted vo2max", which sounds like they are using MR for that. How do you think they used the measured vs gene-based vo2max here? I guess it will obvious when the full paper is available though..
You are 100% spot on. MR is only good because it accounts for “hidden” cofounders. You can use any instrumental variable for that, but we already have so many GWAS… we might as well use them. As for your questions. It looks like they used the genetic predisposition to higher VO2max independent of all these other factors (muscle mass, fat, diabetes, etc) to check if longevity was being driven by higher VO2max itself or by other factors associated with higher VO2max. They found that factors associated with higher VO2max drive longevity benefits but not VO2max on itself.
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Good prognostic tool =! Causal. Cigarettes in your pocket is for sure a good prognostic factor of lung cancer. MR studies measure direct effect.
Exactly. This is why we should not care about VO2Max. We shouldn't try to become elite in that. We should just try to be our personal best or close to it, for as long as we can maintain, so as to maximize healthspan.
It almost seems like diet, exercise, and sleeping well are important keys to health 🤔
I like and follow Peter as he truly inspired me to restart strength training after his talk on the marginal decade but the guy is utterly obsessed over some details that are needless complicated to regular folks or their longevity per se If the average person can get cardio and strength training in multiple times weekly, eat a plant based whole foods diet rich with protein and sleep 7-8 hours consistently uninterrupted a night, I'm not sure how much more life they would squeeze obsessing over or even measuring their VO2max or ApoB levels.
I agree completely, stick to the basic principles and wait for the evidence base on everything else. I’m glad he listens to the science but I have no interest in getting ahead of confirmatory science. I’m old enough to recall when it seemed like a glass of red wine every day was a good idea, so I did. It wasn’t. Years ago, he was pro-rapamycin, he may still be, but I wouldn’t do that. He was also into multi day fasting, and stopped doing that. Stick to the basics. Benefits on paper must always be weighed against real world risks.
You sir take my upvote. Sorry to hear about the red wine situation many people got caught in that even today.
Grip strength is another fun one… strength training and lean muscle mass? Hell yeah, but hacking for grip strength because some study showed that its a predictor or longevity… :/
> Grip strength is another fun one I find this a really stupid thing for him to focus on. Grip strength has to be highly correlated with longevity...but greater grip strength can't be causing people to live longer. That sounds kinda insane.
Completely agree - I’ve had this argument with friends IRL and it stuns me that anyone would think that grip strength alone is anything more than a proxy for general strength and maybe functional mobility.
also, very few things in health are truly 100% causal speaking confidently about any one metric is laughable at best
But he doesn’t mean VO2Max precisely, he just means that since it’s very hard to have a high vo2max, it means someone does heavy training, which brings benefits to someone’s longevity. Not sure if I can put links in this subreddit, but here’s a short video where I think he explains that. https://youtu.be/qgjAaD2M-JE?si=mQTC3bPIPmhhuqtc
Tbh I don't really think Peter is very guilty of this. For years he's been clear that there are big buckets that people need to put energy into before you start arguing in the margins. I think that his content and this sub have overlap with the biohacking crowd who are often guilty of making small details look like huge deals. I've literally seen people ask questions about how to improve grip strength or something, even when Peter has said in no uncertain terms that the correlation is likely just a proxy for other variables.
Grip strength is another fun one… strength training and lean muscle mass? Hell yeah, but hacking for grip strength because some study showed that its a predictor or longevity… :/
Or how about trying to increase VO2max just to go faster? 🤔
I find it hard to interpret the findings of this study, in terms of its relevance to whether exercise is effective for increasing lifespan. The reason is that the genes impacting VO2max could impact it in very different ways, such as 1) how the muscles and cardiorespiratory system are constructed, and 2) innate motivation to exercise. These may have different implications for the impacts of voluntary exercise on lifespan. That said, I do think Peter Attia doesn't pay enough attention to potential residual confounders in the observational studies he cites on the association between physical fitness measures and mortality risk. These could greatly impact the strength of the relationships. Nevertheless, I still think getting abundant physical activity is a smart gamble for those of us who care about health and physical function as we age.
No causal effect, but Vo2max is associated with longevity - so it's a good marker of healthy habits. So, no reason to be anal about increasing Vo2max as the be all and end all (same goes for grip strength btw). Peter has a bad habit of throwing most of his eggs in the basket which he has chosen for the time being. For things he likes - like Vo2max - one study is enough. But for something like plant protein superiority, 20 association studies wont be enough (because of 'healthy user bias' as if that doesnt apply to vo2max).
It’s interesting how you selectively choose which non-causal variables to care about and disregard. oxLDL, HDL, and small LDL particle count are variables I frequently see you disregard on the basis of not being causal, yet they are clearly associated with poor health outcomes and risk factors. Here is a variable that is not causal, but I think you take the reasonable stance of saying we should be concerned about it due to its association with favorable health outcomes.
People with high VO2Max can have a heart attack, suffer damage, and now have low VO2Max for life. It's not a useful metric.
Yes - oxLDL is absolutely useless. Show me one cardiology body guideline which uses oxLDL as a marker. As a bonus, here is lipidologist Dr. Tom Dayspring crapping on oxLDL blood tests. https://youtube.com/shorts/E6KPJ-j6mTA?si=_JZpB4Lxxm0MJTlD HDLc is not causal to heart disease- it didn't work either in mendelian randomized studies nor in HDL raising drugs. Just like vo2max it's a marker, not a cause. You would know this is you heard Attia podcasts with HDLc experts. Small LDL count is not more predictive of Atherosclerosis than ApoB. All ApoB particles are equally atherogenic (except lp(a) and one more rare case concerning chylomicrons). If you have heard anything about Attia's discussion with Dayspring or Dr Allan Sniderman, you would know that ApoB is what matters, not sdLDL. I will repeat, being in 3rd vs 4th quartile of vo2max will have no effect on longevity on its own. You don't need to be the world best athlete to live long. But you do need to be on a diet and exercise regimen which helps avoid chronic disease.
In the process of getting defensive, you missed my point, in which you selectively care about variables that are and are not causally associated with an outcome. I do not disagree with any of the points you made. It was just interesting to hear you make a statement about VO2 max that could easily be applied to other variables you often dismiss. Both HDL and small LDL particle counts are measurements of “healthy habits,” as you also acknowledge with VO2max. Whether or not a variable is causal doesn’t change the fact that it can provide useful insight regarding someone’s day to day decisions and health. A practical example is inflammation measured by CRP. There are countless instances where CRP is not causally associated with a disease, yet it is a powerful piece of information regarding one’s health. To dismiss it on the basis of a lack of causality is shortsighted, in my opinion.
>Both HDL and small LDL particle counts are measurements of “healthy habits,” No, HDL is not. All these crazy ketoers and carnivores with crazy high 200 mg/dl ApoBs have high HDL. Absolutely is not a measure of healthy habits. Plus, HDL temporarily falls during active weight loss in moderate fat diets, while the patient is objectively becoming healthier. So no, HDL is not a good marker of health. No-one needs to track sdLDL. Only ApoB should be tracked as it supercedes sdLDL in every way. If one is prediabetic, they should know it from glucose hba1c and insulin test, not via sdLDL. Vo2max is a good unified number of fitness, unless there are better markers it is at least a decent metric to track. Eta: you added in CRP. HsCRP is the best objective number to measure systemic inflammation, and it also includes autoimmune diseases, infection etc. so its a good number to track, and does not belong in this conversion since it's not specific to heart disease. Hdl and sdLDL are 3rd rate measures of heart disease risk. ApoB is causal and easy to track. Tldr: hsCrp and vo2max are best markers in their category even if not causal, so good to track. ApoB is causal, so fantastic. OxLDL, HDLc and sdLDL neither causal nor best markers in category. Basically I have good reason to crap on these markers.
If HDL is not a relevant metric of metabolic health, then please help me to understand why it is included as a criteria of metabolic syndrome according to the World Health Organization and all other medical organizations. You commented on high values of HDL. I am referring to a low HDL, which is strongly associated with insulin resistance and systemic inflammation, among many other risk factors and non-cardiovascular diseases.
Lol, you were talking about oxLDL, sdLDL and HDL - clearly in context of heart disease. Now you made a bait and switch to metabolic syndrome. Anyway, large waistline, high BP and high glucose is enough to diagnose metabolic syndrome. Hdl measurement is not a requirement to know one is a fat and unhealthy, or diabetic and unhealthy.
This is not a bait and switch, but a response to your comment that I quote verbatim, “HDL is not a good marker of health.”
You seem to be super slow and obtuse. A test has sensitivity and specificity. A high HDL in the context of a super high fat diet with high ApoB, for example, is not a marker of health or habit. So, a high HDL is a false positive in this case. A low HDL on the other hand, can indicate insulin resistance and diabetes; but also can be genetic or due to exogenous testosterone. It can also be due to a low fat diet or ongoing weight loss. If it is because of those last 3 things or some other reason which is not metabolic syndrome, it has no bearing on risk. low HDL is a false negative in these cases. On the other hand, ApoB is clear. High ApoB is more risky, less ApoB is less risky in terms of causality towards heart disease. Genetic or not is immaterial. If you want to know whether you are fat, have high BP, or are diabetic - HDLc is not the test for these lol.
Healthspan is what VO2max is linked to not longevity. How long you're healthy. A lot of people live a long time in a very unhealthy state.
There will be no or minimal difference between 3rd or 4th quartile of vo2max in either 'healthspan' or 'lifespan'. One does not need to be an ultra elite athlete to life a healthy and long life. Everyone should try to avoid being in the lower 2 quartiles though. Watch this discussion https://youtu.be/IkxHBUUVhnw?si=04zO9QpZzcUEdKmE
And that's my point. Some people are just genetically gifted and we shouldn't be comparing ourselves to them ever. We should just compare ourselves to our younger selves and trying to maintain as long as we can.
Agree with that
See Oura Ring haha
Mendelian randomization tries to answer the question by looking at people with genetic factors that result in (in this case) a higher VO2Max. That allows you to control for basically every behavioral difference. I haven’t done this type of research myself, but it is viewed as a high quality test of an hypothesis. However our knowledge of the genome is incomplete. I think of VO2max as being a surrogate for cardio vascular conditioning. If mind is high because I exercise, there are advantages. If it’s high because of genetics it doesn’t mean anything. I also haven’t read the paper and it’s possible they tried to control for all of this. I would not dismiss the paper, but it’s one piece of the puzzle.
PA going to boeing these guys that did this study.
I don’t really care, increasing my Vo2 max has improved my quality of life so much, I can’t imagine not working to maintain it as I age.
So the higher your VO2 max, the longer you live - isn't true? :-(
It’s rather - the higher your VO2 max, the better you live as you get older
Doesn’t matter.. I’d still want higher vo2 max…
Well I think this is what the expected outcome would be. High vo2 max means you have done the work, you have trained in your life. That seems to matter. The vo2 level itself is not thought to be causally related to longevity, the work you did to get to that figure might. More people drown when ice cream sales go up, not because of the ice cream but because of the underlying factors - heat.
I believe the work is the predictor. VO2 shows you’ve put in a lot of work and stayed active. Just like grip strength, muscle mass, etc. Those things are probably indirectly tied to longevity because they are the result of not being sedentary.
VO2Max does not predict when you could get COVID which cuts your VO2Max in half permanently (long COVID). It does not predict if you'll have a heart attack which could cut your VO2Max permanently. I think the VO2Max metric is mostly survivor bias. The people who survive, who didn't get sick, or have a heart attack, preserved their VO2Max. But to act like VO2Max offers any protection is naive in my opinion. I don't see that it does. Youth offers protection.
>VO2Max does not predict when you could get COVID which cuts your VO2Max in half permanently (long COVID). It does though, higher cardiorespiratory fitness is associated with a lower chance of long covid.
Show me a study? And associated with does not mean casual. It doesn't mean high VO2Max is the reason for lower chance of long Covid. Age seems much more of a factor.
After he shows you the study will you tell him about your experience?
Depending on the study it might trump my experience. but he didn't offer any study.
There are very few solid causal approaches in covid yet, as challenge RCTs are kinda challenging, especially if you'd want enough sample size to study long covid. But here is an observational study that did control for age and found vo2max still had an effect https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9335466/ This is on people who did not have a severe initial infection. A severe initial infection makes long covid more likely, and there are plenty of studies showing better cardiorespiratory fitness makes a severe initial infection less likely, so this study is on people who already had passed the first hurdle (but even then, CRF matters). Age is a much bigger factor for sure, but cardiorespiratory fitness still has an effect.
Attila’s logic for espousing vo2 max as a causal factor in longevity has always been weak. Every time I’ve heard him explain it, it’s purely correlational - the higher the vo2 max, the better the health outcomes. This ignores the obvious fact that as people become less healthy and more sick, their vo2 max will decline, but their poor health is not caused by declining vo2 max.