The end of my belief came on a fall night in 2011. I was driving to a suburban restaurant to give a paid dinner talk on Niaspan for Abbott Labs. It was a typical night for a physician speaker—slide deck polished, HDL-cholesterol optimism intact. Then the results of the AIM-HIGH trial came over public radio. Niacin, when added to a statin, had no cardiovascular benefit. My world cracked. I never gave that talk.

That was the night the HDL hypothesis died for me.

I had been a believer—no, an evangelist. HDL was the “good cholesterol.” If you raised it, you saved lives. That belief wasn’t just mine; it was baked into continuing medical education, pharmaceutical marketing, and cardiology dogma. Kos Pharmaceuticals built a billion-dollar niacin business on it, only for Abbott to buy in—just in time to watch it collapse.

But the HDL dream didn’t die with niacin. Torcetrapib, dalcetrapib, anacetrapib—each drug raised HDL sky-high and still failed to reduce events. Billions were spent chasing a biomarker. None of it helped patients. We were measuring the wrong thing. Worse, we were treating the wrong cause.

Around this time, I rediscovered something I had read 25 years earlier: The silent killer in your blood, a small book by South African cardiologist Dr. Allan Shor. He had photographed Chlamydia pneumoniae living inside arterial plaque using electron microscopy. It wasn’t a theory. It was visual proof.

I dug deeper. Dr. J. Thomas Grayston, former dean of the University of Washington School of Public Health, had also found C. pneumoniae in the coronary arteries of patients who died from heart attacks. He ran trials using azithromycin and other antibiotics. But the studies were flawed—short duration, elderly patients, no effort to match drug timing to the bacteria’s complex life cycle. When they failed, the infectious theory of atherosclerosis was dismissed.

But history tells us: Infectious causes of chronic diseases are often overlooked—until they aren’t. Ulcers weren’t from stress; they were from H. pylori. Cervical cancer isn’t just bad luck; it’s HPV. Syphilis caused madness, and TB lived in bones. We missed these for decades because we were locked into old frameworks. Why should atherosclerosis be any different?

We now know that:

• Half of all heart attacks occur in patients with normal LDL.
• Stents don’t prevent heart attacks.
• The same organism, C. pneumoniae, causes chronic respiratory infections and has the ability to persist intracellularly in a “stealth” form—just like TB or leprosy.

Despite this, the cholesterol hypothesis reigns supreme. The money trail explains why. Cardiovascular care is a $500 billion industry. Stents, statins, PCSK9 inhibitors, CT scanners, cardiac cath labs—none of it questions the underlying model. An infectious cause threatens the entire system.

It’s time to launch a new kind of trial: One that tests triple antibiotic therapy targeting C. pneumoniae’s full life cycle (elementary body, reticulate body, and persistent form), modeled after combination treatment in TB and HIV. We should focus on younger patients—those with high coronary calcium but no advanced disease. Use coronary CT angiography as an outcome measure. Name it TACTIC: Targeting Atherosclerosis Through Chlamydia-Informed Care.

I’m a lipidologist in recovery. This is my confession. And my call to action.

Larry Kaskel is an internal medicine physician and lipidologist.