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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When I tell colleagues that I offer Valtrex (valacyclovir) and low-dose lithium orotate to patients worried about developing Alzheimer’s, the silence in the room thickens. Someone always asks, “Where’s the randomized controlled trial?” That’s exactly the problem. We keep waiting for perfect evidence while the disease eats away at people’s brains.

I’m an internist and lipidologist who’s spent years watching the medical establishment chase the wrong villains, like cholesterol, salt, …

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When the FOURIER trial was published in 2017, cardiologists and lipidologists everywhere hailed it as proof that lowering LDL with PCSK9 inhibitors “saves lives.” But when you actually read the data, not the press releases, it’s hard not to shake your head.

Over a median of 2.2 years, evolocumab (Repatha) reduced nonfatal heart attacks by about 0.9 percent and had no significant impact on death. The absolute risk reduction for all-cause …

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A brilliant, like-minded cardiologist recently shared with me “A Reappraisal of the Lipid Hypothesis” by Dr. Robert DuBroff, published in The American Journal of Medicine. It should be required reading for every physician who has ever written “continue statin” without a second thought.

DuBroff’s analysis reviewed 29 randomized controlled trials of cholesterol-lowering therapy conducted after modern trial regulations were adopted. The results were quietly devastating:

• Only two of 29 trials …

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I thought of this while watching the Cincinnati Open tennis today. Between games, a sports drink ad flashed on screen claiming it “hydrates better than water.” The players kept chugging neon bottles, and the announcer repeated the tagline like gospel.

That is when it hit me: For recovery, I would still reach for milk.

Hydration is more than water replacement.

Hydration is not just about replacing fluids; it is about keeping them in …

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I’m not a financial advisor. But after 35 years in internal medicine and lipidology, I’ve realized that physicians are essentially wellth managers, stewards of human energy, rhythm, and resilience.

We help people diversify their time, protect their emotional capital, and build habits that generate compound interest in the form of years, vitality, and peace. In a way, our patients are portfolios: living, breathing balance sheets of choices and consequences.

It’s not money …

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I have written here before about my growing conviction that coronary artery disease is not just about LDL, inflammation, or bad luck. It is time to talk about what might be the elephant in the cath lab: infection.

A recent pathology study out of Japan looked at coronary plaque samples from patients with symptomatic CAD. Using both immunohistochemistry and PCR, they found Chlamydia pneumoniae in every single sample. All fifty plaques …

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For decades, neurology has told us that Alzheimer’s disease is caused by toxic proteins (amyloid plaques and tau tangles) that clog the brain. Pharmaceutical companies have poured billions into anti-amyloid drugs designed to wash them away. The results? Repeated failures, high-profile disappointments, and a handful of marginal approvals with no meaningful improvement in patients’ lives. Sound familiar? In cardiology, we’ve built an entire industry on lowering LDL cholesterol. Statins move …

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We have all been told the story: High cholesterol leads to heart disease, and statins are the magic bullet. The JUPITER trial, published in The New England Journal of Medicine in 2008, became one of the most heavily publicized pieces of “proof” supporting that belief. It claimed that rosuvastatin significantly reduced heart attacks, strokes, and cardiovascular events, even in people with normal LDL cholesterol levels.

But what if I told you …

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He literally rolls into my office every three months, shoes still clipped to his carbon-fiber lifestyle. Lycra damp, Apple Watch buzzing, resting heart rate of 42. He is fit, smart, and tightly wound.

“Doc,” he begins, eyes wide, “I read that morning workouts burn more fat and lower clotting factors. Should I move my rides earlier? Or maybe late evening is better for heart rate variability?”

This is a man who, when …

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