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Peter Attia MD#07 – Deep Dive: Lp(a) — what every doctor, and the 10-20% of the population at risk, needs to know
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At a glance
WHAT IT’S REALLY ABOUT
Peter Attia Explains Lp(a): Risks, Testing, Treatments, and What's Coming
- Attia describes Lp(a) as an LDL particle with an additional apolipoprotein(a) attached to its ApoB by a disulfide bond, with a structure resembling plasminogen and a variable kringle IV type 2 repeat region.
- He says elevated Lp(a) drives three problems: enhanced atherosclerosis, aortic stenosis, and venous thrombosis, with atherosclerosis being the greatest population-level concern because it is so prevalent.
- Lp(a) is best measured as particle number in nanomoles per liter rather than mass or cholesterol, because mass varies with apo(a) size and molecular weight is unknown; Attia wants it below 50 nmol/L.
- Current options are limited: statins don't lower Lp(a), niacin lowers it but is contested, PCSK9 inhibitors lower it roughly 30-50% off-label, and antisense oligonucleotides in phase three trials aim to cut it dramatically.
- Lp(a) is largely unaffected by lifestyle, so Attia treats it by aggressively lowering LDL-P with statins and other tools, and he argues patients should demand testing and doctors should learn about it.
IDEAS WORTH REMEMBERING
5 ideasLp(a) is an LDL particle with an apo(a) tail attached to ApoB.
Every apo(a) sits on an LDL particle, but not every LDL carries one, and people differ in how many of their LDLs have it and in apo(a) size.
Particle number is the best Lp(a) measurement.
Mass is distorted by apo(a) size, so two people with equal mass can have different particle counts; Attia prefers under 50 nmol/L and worries above 100 to 125.
Atherosclerosis is the biggest Lp(a) risk despite a smaller hazard ratio.
Attia argues a roughly 1.6 hazard ratio on a condition that affects a third of people matters more than a 3x ratio on rarer events like venous thromboembolism.
Attia screens elevated-Lp(a) patients for aortic stenosis.
He says about two-thirds of aortic stenosis cases are explained by elevated Lp(a), and he uses echo or preferably cardiac MRI even in patients in their 30s.
Statins don't lower Lp(a) but still matter for these patients.
Statins and other treatments target LDL-P, and Attia says patients with elevated Lp(a) usually need a lower LDL-P target, at or below the 10th percentile.
WORDS WORTH SAVING
5 quotesSo a 60% increase in risk on something that is going to kill a third of people is a big effing problem, whereas a 3% es- risk on something that's gonna, you know, ding 1% of people, yeah, we'll manage it, but, um, that's not what we stay up late thinking about.
— Peter Attia
If you're listening to this as a patient, you should demand that your Lp be known. It's non-negotiable, especially if you have a family history of atherosclerotic disease.
— Peter Attia
I'm still shocked at how many doctors don't understand this.
— Peter Attia
Has my knowledge gone up in five years? Yeah, it's gone up tenfold. The problem is my appreciation for how much information is out there on this topic has gone up 50-fold, so my relative insight has actually gone down fivefold.
— Peter Attia
I don't want people to get the impression that if you have an elevated Lp you shouldn't be taking a statin. No, it's quite the opposite. You probably should be taking a statin, but just understand that the statin is there to control ApoB and not Lp.
— Peter Attia
High quality AI-generated summary created from speaker-labeled transcript.
