Dr. Peter Attia

And what the authors of this study postulated was people who are faster nicotine metabolizers are going to have lower levels of circulating nicotine and therefore less nicotine exposure. Now, technically, you could also argue that maybe someone who's a faster nicotine metabolizer would smoke more or consume more nicotine. So put that aside for the moment.

And what the authors of this study postulated was people who are faster nicotine metabolizers are going to have lower levels of circulating nicotine and therefore less nicotine exposure. Now, technically, you could also argue that maybe someone who's a faster nicotine metabolizer would smoke more or consume more nicotine. So put that aside for the moment.

But nevertheless, the authors used these genetic variants associated with nicotine metabolism to adjust for basically smoking heaviness. And again, we're not interested in the role of smoking. We're interested in the role of nicotine. Okay. Disease risk was increased with slower nicotine metabolism, but the added risk was abolished when adjusted for smoking heaviness.

But nevertheless, the authors used these genetic variants associated with nicotine metabolism to adjust for basically smoking heaviness. And again, we're not interested in the role of smoking. We're interested in the role of nicotine. Okay. Disease risk was increased with slower nicotine metabolism, but the added risk was abolished when adjusted for smoking heaviness.

Because of course, if you do this, you have to adjust for smoking. indicating that the main drivers of the outcomes are the non-nicotinic components of cigarette smoke. Let me state that again. This is a complicated MR, but it is the closest thing I think we have to looking at humans.

Because of course, if you do this, you have to adjust for smoking. indicating that the main drivers of the outcomes are the non-nicotinic components of cigarette smoke. Let me state that again. This is a complicated MR, but it is the closest thing I think we have to looking at humans.

And it's looking at how much people smoked, how quickly they metabolized nicotine, trying to do an overlay of that to appreciate the nicotine exposure. And it came away basically saying that the harm of smoking is due to the tobacco and tobacco-related products, not due to the nicotine. I want to be clear, this is way, way far away from what you would want to be able to say is level one evidence.

And it's looking at how much people smoked, how quickly they metabolized nicotine, trying to do an overlay of that to appreciate the nicotine exposure. And it came away basically saying that the harm of smoking is due to the tobacco and tobacco-related products, not due to the nicotine. I want to be clear, this is way, way far away from what you would want to be able to say is level one evidence.

If you wanted to do this in a level one fashion, you would actually have to randomize people to a whole bunch of different tobacco-free nicotine products and study the outcomes of interest. Now, of course, nobody's going to do that for hard outcomes like mortality, but I certainly think people could do that for softer outcomes. And my hope is that somewhere along there, people do that.

If you wanted to do this in a level one fashion, you would actually have to randomize people to a whole bunch of different tobacco-free nicotine products and study the outcomes of interest. Now, of course, nobody's going to do that for hard outcomes like mortality, but I certainly think people could do that for softer outcomes. And my hope is that somewhere along there, people do that.

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