I was conditioned to view heart disease as a plumbing issue. Cholesterol blocks the pipes, and statins remove the blockages. When LDL decreases, we celebrate together. But what if we have been targeting the wrong antagonist all this time?

A new [Japanese study](https://pubmed.ncbi.nlm.nih.gov/36176379/) examined 50 plaques taken out during coronary atherectomy. Each one of those plaques was found to be positive for Chlamydia pneumoniae via PCR or immunostaining. That’s not “a few,” or “most.” That’s a full 100 percent.

Should any other discovery appear in 100 percent of afflicted arteries, we would eagerly label it as causal. Yet, this received merely a polite acknowledgment.

This isn’t an isolated instance. Years of research have identified viral and bacterial DNA (herpes, CMV, Chlamydia pneumoniae) within unstable plaques. Moreover, the association isn’t coincidental: Infected plaques demonstrate greater inflammation, increased necrosis, and a higher likelihood of rupture. A systematic review and meta-analysis noted microorganisms in a remarkable percentage of [plaques across vascular beds](https://onlinelibrary.wiley.com/doi/10.1155/2022/8678967). Additional studies have indicated how viral antigen load correlates with [plaque instability](https://www.mdpi.com/2227-9059/10/10/2634) and how viral particles can disrupt endothelial function via [extracellular vesicles](https://www.mdpi.com/1422-0067/24/8/7567).

The conventional retort is: “Well, the antibiotic trials didn’t yield results.”

True. However, those trials focused on the incorrect patients, at improper timings, with medications that barely addressed the pathogen. Once the house is engulfed in flames, removing the match does little to solve the problem.

Here’s the larger notion:
– LDL may act as the accelerant.
– However, infection could be the source of ignition.
– And inflammation represents the smoke we have been addressing.

We have witnessed this narrative previously. Ulcers weren’t “caused” by stress or acidity; until H. pylori demonstrated otherwise. Cervical cancer wasn’t thought to be “infectious” either; until HPV transformed the understanding. Medicine has a long track record of overlooking microbes that are in plain sight.

Envision if we actually considered upstream factors:
– Profiling plaque “virome” as a component of risk evaluation.
– Employing antiviral or antimicrobial treatments alongside statins and anti-inflammatories.
– Conducting trials in early stages of disease, rather than post-damage.

We have dedicated 50 years to refining the lipid hypothesis. Perhaps it’s time to examine the pathogen in the plaque.

*Larry Kaskel is an internist and “lipidologist in recovery” with over thirty-five years of medical practice. He runs a concierge practice in the Chicago area and is part of the teaching faculty at the Northwestern University Feinberg School of Medicine. Furthermore, he is associated with Northwestern Lake Forest Hospital.*

*Prior to the rise of podcasts in popular culture, Dr. Kaskel hosted Lipid Luminations on [ReachMD](https://reachmd.com/programs/lipid-luminations/), creating a library of more than four hundred programs featuring prominent figures in cardiology, lipidology, and preventive medicine.*

*He is the author of [Dr. Kaskel’s Living in Wellness, Volume One: Let Food Be Thy Medicine](https://amzn.to/4n0CjWF), which blends evidence-based medical practice with accessible methods for enhancing healthspan. His ongoing projects concentrate on reassessing the cholesterol hypothesis and exploring the infectious roots of atherosclerosis. More details can be found at [larrykaskel.com](http://larrykaskel.com/).*