A recent article from the Washington Post highlights the importance of earlier identification of atherosclerosis and promotes a shift from an “ischemia-centric” to an “atheroma-centric” approach. Nonetheless, this viewpoint misses a vital aspect: plaque is not the primary cause but a manifestation of a more complex problem.

For many years, the medical profession has concentrated on the cholesterol hypothesis, fostering a trillion-dollar sector around treatments like statins, PCSK9 inhibitors, ezetimibe, inclisiran, and Lp(a) drugs. While LDL cholesterol is recognized as a contributing factor, it acts more like an accelerant than the root cause.

Research indicates that a potential infectious agent may be involved. This theory is not recent; it traces back to the 1990s when Dr. J. Thomas Grayston and Dr. Allan Shor detected Chlamydia pneumoniae within atheromas using electron microscopy. Numerous studies have supported these conclusions, including a recent study from Japan that found C. pneumoniae DNA and antigens in all analyzed atheroma samples.

Even with this evidence, medical treatments continue to concentrate mainly on cholesterol, overlooking the infectious pathogen linked to the progress of atherosclerosis.

To effectively tackle the leading cause of mortality in the United States, it is essential to initiate a trial that should have been conducted years ago:

• Adopt a triple-therapy antibiotic regimen akin to those for TB, leprosy, and HIV targeting all life phases of C. pneumoniae.
• Target younger demographics (20-40 years) where the condition may arise without symptoms.
• Employ coronary CT angiography as a noninvasive, economical, real-time assessment method.

The need for another statin-centered study is minimal. What is required is a TACTIC trial aimed at addressing the underlying infectious origins.

This situation is reminiscent of historical cases: peptic ulcers caused by H. pylori, syphilis, TB, and cervical cancer linked to HPV. Many times, established medical narratives persisted until the infection was effectively managed.

Why should atherosclerosis be approached any differently?

A call to action for NIH and cardiology leaders

It’s time to invest in this crucial trial. Regardless of whether it supports or contradicts the hypothesis, the inquiry must be undertaken. It’s time to move beyond solely cholesterol-centric theories. The infectious pathogen is clearly present, and we have no further rationale for disregarding it.

Larry Kaskel is an internist and “lipidologist in recovery” with more than thirty-five years of medical practice experience. He runs a concierge practice in Chicago and is affiliated with the teaching faculty at the Northwestern University Feinberg School of Medicine. He also has connections with Northwestern Lake Forest Hospital.

Prior to the rise of podcasts, Dr. Kaskel hosted Lipid Luminations on ReachMD, producing over 400 programs with prominent figures in cardiology, lipidology, and preventive medicine.

He authored Dr. Kaskel’s Living in Wellness, Volume One: Let Food Be Thy Medicine, merging evidence-based medical practices with accessible health strategies for patients. His ongoing work includes re-evaluating the cholesterol hypothesis and investigating the infectious sources of atherosclerosis. Further information can be found at larrykaskel.com.