The tip of my perception got here on a fall evening in 2011. I used to be driving to a suburban restaurant to offer a paid dinner discuss on Niaspan for Abbott Labs. It was a typical evening for a doctor speaker—slide deck polished, HDL-cholesterol optimism intact. Then the outcomes of the AIM-HIGH trial came visiting public radio. Niacin, when added to a statin, had no cardiovascular profit. My world cracked. I by no means gave that discuss.
That was the evening the HDL speculation died for me.
I had been a believer—no, an evangelist. HDL was the “good ldl cholesterol.” In the event you raised it, you saved lives. That perception wasn’t simply mine; it was baked into persevering with medical training, pharmaceutical advertising, and cardiology dogma. Kos Prescribed drugs constructed a billion-dollar niacin enterprise on it, just for Abbott to purchase in—simply in time to look at it collapse.
However the HDL dream didn’t die with niacin. Torcetrapib, dalcetrapib, anacetrapib—every drug raised HDL sky-high and nonetheless failed to cut back occasions. Billions had been spent chasing a biomarker. None of it helped sufferers. We had been measuring the mistaken factor. Worse, we had been treating the mistaken trigger.
Round this time, I rediscovered one thing I had learn 25 years earlier: The silent killer in your blood, a small guide by South African heart specialist Dr. Allan Shor. He had photographed Chlamydia pneumoniae dwelling inside arterial plaque utilizing electron microscopy. It wasn’t a principle. It was visible proof.
I dug deeper. Dr. J. Thomas Grayston, former dean of the College of Washington College of Public Well being, had additionally discovered C. pneumoniae within the coronary arteries of sufferers who died from coronary heart assaults. He ran trials utilizing azithromycin and different antibiotics. However the research had been flawed—brief length, aged sufferers, no effort to match drug timing to the micro organism’s advanced life cycle. Once they failed, the infectious principle of atherosclerosis was dismissed.
However historical past tells us: Infectious causes of persistent illnesses are sometimes ignored—till they aren’t. Ulcers weren’t from stress; they had been from H. pylori. Cervical most cancers isn’t simply unhealthy luck; it’s HPV. Syphilis prompted insanity, and TB lived in bones. We missed these for many years as a result of we had been locked into outdated frameworks. Why ought to atherosclerosis be any completely different?
We now know that:
- Half of all coronary heart assaults happen in sufferers with regular LDL.
- Stents don’t forestall coronary heart assaults.
- The identical organism, C. pneumoniae, causes persistent respiratory infections and has the flexibility to persist intracellularly in a “stealth” kind—similar to TB or leprosy.
Regardless of this, the ldl cholesterol speculation reigns supreme. The cash path explains why. Cardiovascular care is a $500 billion trade. Stents, statins, PCSK9 inhibitors, CT scanners, cardiac cath labs—none of it questions the underlying mannequin. An infectious trigger threatens your complete system.
It’s time to launch a brand new type of trial: One which checks triple antibiotic remedy focusing on C. pneumoniae’s full life cycle (elementary physique, reticulate physique, and protracted kind), modeled after mixture therapy in TB and HIV. We should always deal with youthful sufferers—these with excessive coronary calcium however no superior illness. Use coronary CT angiography as an final result measure. Title it TACTIC: Concentrating on Atherosclerosis By way of Chlamydia-Knowledgeable Care.
I’m a lipidologist in restoration. That is my confession. And my name to motion.
Larry Kaskel is an inner medication doctor and lipidologist.
