1: “Do we tell people it’s okay to smoke until they are 65 and then have them stop?” Peter Attia asks in his terrific book Outlive.
“Should we tell someone to stop smoking only after their ten-year risk of lung cancer reaches a certain threshold?” he asks.
Of course not. Much better to do everything we can to stop people from starting smoking.
“The sooner we cut the head off the snake,” Peter writes, “the lower the risk that it will bite us.”
2: Yet, when it comes to heart disease, we let the snake hang around. We feed it rather than kill it.
“Chronic diseases like heart disease, cancer, neurodegenerative disease, and type 2 diabetes build slowly over time,” Peter notes.
The problem?
“Once they become established,” he notes, “it is often too late.”
Which is what we do today, Peter believes. We start way too late.
He contrasts the current medical protocols, what he calls “Medicine 2.0,” with “Medicine 3.0,” where the goal is to “delay or prevent these conditions so that we can live longer without disease.
The problem with Medicine 2.0’s approach to heart disease is that “guidelines for managing cardiovascular risk are based on an overly short time horizon, compared to the timeline of the disease,” Peter observes.
Medicine 3.0 takes a much longer view, which changes our treatment strategy: “The only way to stop the disease is to remove the cause, and the best time to do that is now.”
3: We must do three things to reduce the risk of heart disease.
First, if we smoke, we need to stop.
Second, if we have high blood pressure, we must lower it.
“Smoking cessation and blood pressure control are thus non-negotiable first steps in reducing cardiovascular risk,” Peter writes.
Third, we must aggressively lower our “bad cholesterol,” the concentration of LDL-C or apoB particles in our blood.*
How low should our bad cholesterol be?
“The various treatment guidelines specify target ranges for LDL-C, typically 100 mg/dL for patients at normal risk, or 70 mg/dL for high-risk individuals,” Peter writes.
In Peter’s view, that is way too high.
“Simply put, I think we can’t lower apoB and LDL-C too much, provided there are no side effects from treatment,” he notes. We “want it as low as possible.”
Peter cites Peter Libby, one of the leading experts on cardiovascular disease, and his colleagues, who wrote in Nature Reviews in 2019, “Atherosclerosis probably would not occur in the absence of LDL-C concentrations in excess of physiological needs (on the order of 10 to 20 mg/dL).”
The study’s authors continue: “If the entire population maintained LDL concentrations akin to those of a neonate (or to those of adults of most other animal species), atherosclerosis might well be an orphan disease.”
Peter’s translation: “If we all maintained the [the LDL-C] and apoB levels we had when we were babies, there wouldn’t be enough heart disease on the planet for people to know what it was.”
How do we do that? That’s what we’ll cover in tomorrow’s RiseWithDrew.
More tomorrow.
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Reflection: What surprises me about Peter’s research regarding heart disease?
Action: Talk to my Primary Care Physician about Peter’s work.
*Peter writes: “When I look at a patient’s blood panel for the first time, my eyes immediately dart to two numbers: apoB and Lp(a).
“I look at the other numbers, too, but these two tell me the most when it comes to predicting their risk of ASCVD (Atherosclerotic Cardiovascular Disease).
“ApoB not only tells me the concentration of LDL particles (which is more predictive of disease than the concentration of cholesterol found within LDL particles, LDL-C), but it also captures the concentration of VLDL particles, which as members of the apoB family can also contribute to atherosclerosis.
“Furthermore, even someone whose apoB is low can still have a dangerously elevated Lp(a).”
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