I just read the new Cleveland Clinic Journal of Medicine introduction by its editor-in-chief, and it’s laying out the usual playbook: demonize lipoprotein(a) (Lp(a)), list all the terrible things it does, and hint that salvation is around the corner, pending results of a major pharmaceutical trial, of course.

It’s a neat narrative arc.

But it’s incomplete.

What’s missing is the one question almost no cardiology article seems willing to ask:

Why does Lp(a) exist …

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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 …

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As an internist and lipidologist, I’ve spent decades parsing data on statins, ezetimibe, PCSK9 inhibitors, and the endless parade of “LDL-lowering breakthroughs.” Yet the most potent, and perhaps the most underappreciated, intervention to prevent heart attacks each winter doesn’t come from a cardiology journal or a pharmaceutical rep. It comes from your local pharmacy fridge. For years, I’ve told my patients that getting a flu shot may prevent a heart …

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Tonight, my lab quietly changed what it considers a “normal” ApoB. On Monday, my patient’s ApoB of 98 mg/dL was comfortably green. On Tuesday, that same number was flagged high, a 30-point swing in the normal range overnight. No new evidence. No new trial. No public health crisis. Just a reference-range recalibration. And with that one quiet adjustment, millions of people who went to bed “normal” may wake up “abnormal.”

Reference …

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When most people hear nicotine, they picture stained lungs, cigarette ads, or sweet-flavored vapes. But nicotine isn’t tar, benzene, or formaldehyde. It’s a potent nicotinic acetylcholine receptor agonist with real neurochemical effects, and in carefully selected patients, it can help. I’ve been using nicotine gum and lozenges for years in patients with fatigue, mild depression, and ADHD, not as a miracle cure but as a targeted cognitive and mood-enhancing tool. …

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I was trained to treat heart disease like a plumbing problem. Cholesterol clogs the pipes, statins clear them out. LDL goes down, we high-five each other. But what if we’ve been chasing the wrong culprit all along?

A recent Japanese study looked at 50 plaques removed during coronary atherectomy. Every single one of those plaques tested positive for Chlamydia pneumoniae by PCR or immunostaining. That’s not “some,” or “most.” That’s …

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A recent Washington Post article called for earlier detection of atherosclerosis and a shift from “ischemia-centric” thinking to an “atheroma-centric” model. That’s progress, but it’s still missing the most important piece: Plaque isn’t the root cause.

For 50 years, we’ve built a trillion-dollar cardiology machine around the cholesterol hypothesis. Statins, PCSK9 inhibitors, ezetimibe, inclisiran, Lp(a) drugs, all circling the same biochemical drain. LDL plays a role, yes. But LDL is …

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