I just read yet another article praising the new messiah of cardiology (Lipoprotein(a)) and urging every physician in America to start testing for it. The tone was familiar: solemn, scientific, and a little evangelical.
The message? “Measure Lp(a) once in every patient.”
The subtext? “Because we finally found the missing piece.”
If this feels like déjà vu, that’s because it is. We’ve been here before: first with total cholesterol, then LDL, then HDL (our “good” cholesterol that turned out not to be so good), and niacin, the vitamin-turned-savior-turned-villain. Every decade, cardiology anoints a new molecule to absolve the last one’s sins. Lp(a) is simply the next messiah in the lipid church, another target promising redemption without ever questioning the creed.
Genetic fatalism is not physiology.
Yes, Lp(a) is largely genetic. But so are freckles, hair color, and tone deafness. To declare something untreatable simply because it’s heritable is to confuse inheritance with inevitability. Lp(a) is not destiny; it’s a signal, and one that rises during inflammation, infection, and vascular injury.
That nuance was missing entirely from the praise piece I just read. The author framed Lp(a) as a static villain, not a dynamic participant in the body’s immune orchestra. It’s an acute-phase reactant, not an assassin.
“Test everyone once”: the new ritual
Calls for universal Lp(a) screening sound virtuous but functionally do nothing. What will we do with the result? Tell 20 percent of our patients that their Lp(a) is high and then what?
There’s no FDA-approved therapy that lowers Lp(a) and improves survival. We’ll just tell them they’re high-risk, intensify statins, and call it precision medicine. In reality, we’ve added another number to frighten patients without improving outcomes.
This is ritualistic medicine, not preventive care. Screening without a proven intervention is like taking attendance at the apocalypse.
Therapeutic nihilism disguised as progress
The Lp(a) gospel ends, as all lipid sermons do, with a biotech benediction: “New drugs are on the way.” We’ve heard that before.
Remember torcetrapib, dalcetrapib, and anacetrapib? They raised HDL spectacularly (up to 130 percent) and still failed to save a single life. AIM-HIGH niacin trials collapsed in similar fashion. Even PCSK9 inhibitors, which modestly lower Lp(a), have yet to show convincing all-cause mortality benefit.
We keep mistaking biochemical success for clinical salvation. That’s not science; it’s sacrament.
What the puff pieces never say
They never mention that Lp(a) may serve a repair function, binding to damaged endothelium the way biological duct tape seals leaks. They never mention that chronic infection and inflammation (not cholesterol alone) drive the vascular fire that recruits Lp(a) in the first place.
Drs. J. Thomas Grayston and Allan Shor showed Chlamydia pneumoniae hiding inside arterial plaques decades ago. But instead of following that lead, medicine buried it under LDL trials and marketing budgets.
Now we’re resurrecting another number to distract from the same unresolved question: Why is the artery inflamed in the first place?
The coming pharmacologic resurrection
Of course, pharma sees opportunity in faith. Antisense drugs like pelacarsen and olpasiran promise to “silence” Lp(a). Wall Street is thrilled. But until Lp(a)HORIZON or OCEAN(a)-Outcomes show actual event reduction (not just pretty graphs) this is marketing in a lab coat.
Abbott’s $3.7 billion niacin debacle should have cured us of blind devotion, but cardiology never met a biomarker it couldn’t worship.
The real heresy
Here’s the uncomfortable truth: if 20 percent of people have high Lp(a) yet 80 percent of heart attacks occur in people with normal levels, maybe Lp(a) isn’t the assassin, just another bystander at the crime scene.
We keep tracing chalk outlines around molecules while the real killer (chronic infection-driven inflammation) walks free.
Lp(a) may be the next big thing to measure, but measurement is not medicine. Until we understand why the endothelium calls for these lipoproteins (why repair turns to scar, why inflammation never resolves) we’ll keep baptizing biomarkers and wondering why the arteries keep burning.
A final confession
As a recovering lipidologist, I’m not dismissing Lp(a). I’m just declining to kneel before it.
Heart disease isn’t a lab value; it’s a biological response to injury.
And until cardiology faces that, it will keep searching for new messiahs while the real pathology (infection, inflammation, and immune dysregulation) continues its quiet crusade.
Larry Kaskel is an internist and “lipidologist in recovery” who has been practicing medicine for more than thirty-five years. He operates a concierge practice in the Chicago area and serves on the teaching faculty at the Northwestern University Feinberg School of Medicine. In addition, he is affiliated with Northwestern Lake Forest Hospital.
Before podcasts entered mainstream culture, Dr. Kaskel hosted Lipid Luminations on ReachMD, where he produced a library of more than four hundred programs featuring leading voices in cardiology, lipidology, and preventive medicine.
He is the author of Dr. Kaskel’s Living in Wellness, Volume One: Let Food Be Thy Medicine, works that combine evidence-based medical practice with accessible strategies for improving healthspan. His current projects focus on reevaluating the cholesterol hypothesis and investigating the infectious origins of atherosclerosis. More information is available at larrykaskel.com.
