I just came across yet another write-up extolling the new savior of cardiology (Lipoprotein(a)) and imploring every physician in the United States to begin testing for it. The tone was recognizable: grave, scientific, and somewhat zealous.

The takeaway? “Measure Lp(a) in every patient.”

The underlying message? “Because we have finally discovered the missing element.”

If this resembles déjà vu, it’s because it is. We’ve experienced this before: first with total cholesterol, then LDL, then HDL (our “good” cholesterol that turned out not to be as good), and niacin, the vitamin-turned-savior-turned-enemy. Each decade, cardiology elevates a new molecule to cleanse the previous one’s failings. Lp(a) is merely the next savior in the lipid doctrine, another target promising salvation without ever questioning the established belief.

Genetic determinism is not physiology.

Indeed, Lp(a) is largely influenced by genetics. But so are freckles, hair color, and musical tone-deafness. To label something as untreatable solely because it is hereditary is to conflate inheritance with inevitability. Lp(a) is not fate; it’s an indicator, one that increases during inflammation, infection, and vascular damage.

That subtlety was entirely absent from the commendation piece I just perused. The writer depicted Lp(a) as a constant antagonist, rather than a fluctuating participant in the body’s immune ensemble. It’s an acute-phase reactant, not a killer.

“Screen everyone once”: the new custom

Calls for universal Lp(a) screening appear noble but accomplish next to nothing. What will we do with the results? Inform 20 percent of our patients that their Lp(a) levels are elevated and then what?

There’s no FDA-approved treatment that reduces Lp(a) and improves survival. We’ll just inform them they are at high risk, intensify statins, and label it precision medicine. In truth, we’ve only introduced another figure to instill fear in patients without enhancing outcomes.

This is ritualistic medicine, not preventive healthcare. Screening without a validated intervention is akin to taking attendance during the apocalypse.

Therapeutic nihilism masquerading as advancement

The Lp(a) mantra concludes, as all lipid discourses do, with a biotech blessing: “New medications are on their way.” We’ve heard this before.

Recall torcetrapib, dalcetrapib, and anacetrapib? They significantly elevated HDL (up to 130 percent) yet failed to save any lives. AIM-HIGH niacin trials similarly crumbled. Even PCSK9 inhibitors, which reduce Lp(a) modestly, have not yet demonstrated any substantial benefit for all-cause mortality.

We continually confuse biochemical achievements for clinical salvation. That’s not science; it’s ritual.

What the fluff articles fail to mention

They neglect to point out that Lp(a) may play a reparative role, adhering to damaged endothelium like biological duct tape mending leaks. They fail to mention that chronic infection and inflammation (and not cholesterol alone) ignite the vascular fire that draws Lp(a) into the mix.

Drs. J. Thomas Grayston and Allan Shor discovered Chlamydia pneumoniae lurking within arterial plaques decades ago. However, rather than pursuing that avenue, medicine buried it beneath LDL trials and marketing initiatives.

Now we are reviving another number to divert attention from the same unresolved question: Why is there inflammation in the artery to begin with?

The impending pharmacological revival

Naturally, pharmaceutical companies perceive a chance in belief. Antisense drugs like pelacarsen and olpasiran pledge to “silence” Lp(a). Wall Street is ecstatic. But until Lp(a)HORIZON or OCEAN(a)-Outcomes yield actual event reduction (not merely attractive graphs), this is marketing in a lab coat.

Abbott’s $3.7 billion niacin failure should have cured us of blind faith, yet cardiology has never encountered a biomarker it couldn’t venerate.

The true heresy

Here’s the harsh truth: if 20 percent of individuals possess high Lp(a) yet 80 percent of heart attacks happen in those with normal levels, perhaps Lp(a) isn’t the murderer, but just another spectator at the crime scene.

We continue tracing chalk outlines around molecules while the actual perpetrator (chronic infection-driven inflammation) roams free.

Lp(a) may be the next significant entity to measure, but measurement is not medicine. Until we grasp why the endothelium summons these lipoproteins (why repair turns into scar, why inflammation persists), we’ll keep sanctifying biomarkers and questioning why the arteries remain inflamed.

A final admission

As a rehabilitated lipidologist, I’m not dismissing Lp(a). I’m merely choosing not to bow before it.

Heart disease isn’t merely a lab value; it is a biological reaction to injury.

And until cardiology confronts this, it