Dr. Peter Attia
speaker
5,258 appearances
36 recordings
6 series
first heard Jan 2024
last heard Jun 2025
Dr. Peter Attia’s voice in public audio — every appearance, attributed to the second.
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That is not the case. I want to be clear. It might be that, and it likely is, in fact, it almost undoubtedly is, that smoking tobacco is a much higher level of risk. But I want to make sure people understand that if your nicotine is tobacco derived as opposed to synthetic, you are still probably assuming risk.
So the level of these compounds depends on the processing technique and the tobacco variety, of course. So they're found in the highest concentrations in products that actually still look like tobacco. So I think that's kind of a nice way to think about it. Everybody can imagine what a cigarette looks like. If you take tobacco chewing leaves, people chew tobacco,
that's going to have a lot of the negative properties. So the more closely you are to tobacco, the worse things are. So obviously if you're sticking it in a cigarette or a cigar or a pipe, yep, you're getting plenty of it there. If you're chewing it or taking it in snooze, also a big problem. So this is why I don't think I fully appreciated this four years ago.
When you take nicotine out of tobacco directly, you're still assuming some of that risk that comes in curing and fermentation of the tobacco itself.
Yeah, boy, that's okay. This is a philosophical issue. But as some people listening to this podcast know, I am an enormous fan of Formula One. And that goes way back for a long period of time. And up until 2005, tobacco was a major sponsor of Formula One. In fact, the largest sponsor would have been Marlboro. And they were in the early 2000s all over the Ferraris.
And in the era that is my favorite era of Formula One in the 1980s and the early 90s, they were all over the McLaren car. And so you are correct. From time to time, you will see me wearing something or memorabilia that I have that is a throwback to that era of Formula One. And I believe in the original livery of those vehicles.
In other words, I believe in era appropriate nods to things that we pay attention to. And so, yes, if you're looking at a hat or a shirt or a car that is a replica or pays homage to something of that era, you're going to see the livery of the sponsors of the time. And that would have been Hugo Boss, Nacional, Marlboro.
Anyway, there's nothing else I can say about it other than it has nothing to do with a tacit or otherwise approval of these products. I want to be unambiguously clear. I think smoking is an absolute error, arguably the single biggest unforced error you can make with respect to your health. And fortunately, Big Tobacco does not sponsor motorsport anymore, and I think they're better for it. Perfect.
Well, we're going to go into this in some detail, but I would say that clearly the biggest risk of pure nicotine, and now I'm just talking about it through the lens of synthetically acquired nicotine, so you're getting rid of all the tobacco-related processing, is in its addictive nature. And make no mistake about it, nicotine is highly addictive.
There are some other areas where, depending on the dose, there may actually be a harm. Again, I think this is very important to understand. There are some mechanistic insights that suggest a negative impact on the endothelium. And it's certainly plausible that anything that negatively impacts the endothelium could increase the risk of cardiovascular disease. But these are not large studies.
These are not studies that have been done in humans. And these are extrapolations typically from other animal models. So I guess we should probably just maybe spend a minute kind of talking about nicotine again. If people want more detail on this, I think it's covered four years ago.
But nicotine activates, so nicotine is a molecule, and it activates something called the nicotinic acetylcholine receptor. Now, these receptors are not just in the brain where we most frequently talk about them, but they can actually exist throughout the body.
And if you look at certain mouse models and rodent models, such as other rodents like rats, it's been demonstrated that high doses of nicotine can actually increase tumor growth and even foster metastases, in addition to increasing atherosclerotic plaques. Now, that sounds pretty devastating.
I just want to always point out, whenever we're talking about these rodent models, there's lots of daylight typically between what happens in that model and what happens in humans. And I think it's important to look at other ways to triangulate upon the answer. So we'll link to those studies in the show notes. But the closest thing that we could find in humans was a 2024 Mendelian randomization.
I know we talk about these a lot, but I always think it's worth explaining what an MR is. So a Mendelian randomization says, let's look at genes in the population, which we can assume are randomly assorted. That's the randomization part. And let's ask the question, will these genes be a proxy
for a behavior that I want to study or something that I want to study where I can now use effectively observational tools to see if there's a difference. One example is Mendelian randomization consistently shows that LDL cholesterol is causally associated with heart disease. Why?
Because LDL cholesterol is highly genetic, and you can look across a population and see different levels of LDL, even in people who are otherwise healthy, and you can examine the cardiovascular outcomes of these people, which would be the dependent variable, and that's how you can infer causality. By extension, by the way, HDL cholesterol turns out to be not causally related in the inverse.
So if you look at this Mendelian randomization, they wanted to look at the relationship of nicotine by itself on compromised lung function, lung cancer, COPD, CH, ASCVD, etc. Okay, I want to be clear. I don't think this was the world's best MR. I think it was clever, though. What did they look at?
Because like what genes would you try to parse out to understand how much tobacco someone is consuming, which is what you actually want to be able to do? So what they looked at was they looked at genes that spoke to nicotine metabolism. And so just as caffeine, we've talked about this in the past, caffeine metabolism is highly genetic.
So people like me are wickedly fast at metabolizing caffeine, and therefore I seem to be able to drink it later in the day without a negative impact. Someone who's a very slow metabolizer is going to feel it more. Similarly with nicotine, you have high and low levels of nicotine metabolism.
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