At the recent ECTRIMS Congress in Barcelona, researchers presented data that should make every specialist pause. In a claims analysis of nearly 70,000 patients with multiple sclerosis (MS), 98 percent of infections were first detected not in neurology clinics, but in primary care and other non-neurology practices. Even “serious” infections requiring hospitalization were almost entirely picked up elsewhere. The message was clear: Specialists, by design, often miss the forest for the trees.

Now shift the lens to cardiology. For decades, the dominant framework has been that atherosclerosis is a problem of cholesterol and lipids. Yet, like neurologists missing infections in MS, cardiologists may be missing the true first signs of the disease: infectious triggers smoldering silently in the vessel wall. We have compelling evidence:

• Electron microscopy has shown Chlamydia pneumoniae inside arterial plaques.
• Epidemiology has linked the same organism to coronary disease, much as H. pylori was eventually proven to cause ulcers.
• Korean War autopsies revealed advanced atherosclerosis in young, otherwise healthy soldiers, decades before fast food, vaping, or today’s obesity epidemic.
• And most recently, a Japanese pathology study detected C. pneumoniae DNA in 100 percent of arterial plaques sampled.

Here’s the uncomfortable possibility: The same infectious inciting events that complicate MS may also be the true drivers of atherosclerosis. In MS, infections may spark immune dysregulation. In atherosclerosis, those same pathogens may linger in arterial walls, fueling chronic inflammation and plaque formation. Different specialties, different outcomes, but perhaps a shared origin story.

Just as neurologists are rarely the first to see infection in MS, cardiologists may not be positioned or incentivized to recognize infection in heart disease. Lipids are easy to measure and manipulate. Microbial persistence is not. But ignoring it has led to decades of failed “HDL-raising” drugs, and now billions are being funneled into Lp(a)-lowering trials without asking the more fundamental question: What if the real culprit isn’t a particle, but a pathogen? The MS data remind us that what seems outside a specialty’s domain may be central to patient outcomes. For cardiology, it is time to look beyond LDL, HDL, and Lp(a). Atherosclerosis may be less about numbers in a lab and more about microbes in our arteries.

Until we test that hypothesis with the same rigor we devote to lipid targets, we risk repeating neurology’s blind spot: failing to see the infection hiding in plain sight.

Larry Kaskel is an internist and “lipidologist in recovery” who has been practicing medicine for more than thirty-five years. He operates a concierge practice in the Chicago area and serves on the teaching faculty at the Northwestern University Feinberg School of Medicine. In addition, he is affiliated with Northwestern Lake Forest Hospital.

Before podcasts entered mainstream culture, Dr. Kaskel hosted Lipid Luminations on ReachMD, where he produced a library of more than four hundred programs featuring leading voices in cardiology, lipidology, and preventive medicine.

He is the author of Dr. Kaskel’s Living in Wellness, Volume One: Let Food Be Thy Medicine, works that combine evidence-based medical practice with accessible strategies for improving healthspan. His current projects focus on reevaluating the cholesterol hypothesis and investigating the infectious origins of atherosclerosis. More information is available at larrykaskel.com.