Cardiovascular disease is still the leading cause of death worldwide, decades after Western medicine built its entire prevention strategy around cutting saturated fat and dietary cholesterol. That strategy hasn’t worked. Dr. Rolandos Pavlou, a general practitioner and certified Nutrition Network practitioner specializing in metabolic health and cardiovascular disease has spent years questioning why and his answers point in a very different direction than the one most patients hear in a standard consultation.

Why the Coronary Arteries Take the Hit

Before getting into diet, it helps to understand why coronary arteries are so prone to blockage in the first place:

• They carry blood to the hardest working muscle in the body, so even a small drop in supply produces real symptoms
• They sit close to large vessels like the aorta, which exposes them to more mechanical stress from oscillatory blood flow
• And several of them branch off at acute angles, creating extra friction at exactly the points where plaque tends to form

Put those three factors together and you have a set of vessels that are mechanically primed for atherosclerotic damage well before diet even enters the picture.

The Diet That Actually Drives the Damage

Pavlou’s central argument is that the low-fat, low-cholesterol approach targeted the wrong villain. What’s actually driving cardiovascular deaths, in his view, is the combination of a high carbohydrate diet with a high intake of polyunsaturated vegetable oils, layered on top of poor sleep, chronic stress and inactivity. Linoleic acid, the dominant fatty acid in seed oils, doesn’t just sit passively in the body. It activates inflammatory receptors and gates directly, including PPAR, TLR and TRPV1, driving oxidative stress and disrupting insulin signaling. The effect most relevant to heart disease specifically is what it does to LDL particles: an LDL particle loaded with omega-6 fats oxidizes far more easily, and that oxidized particle is what actually kicks off the atherosclerotic cascade, not cholesterol on its own.

When Your Labs Look Great Except for One Number

Here’s a scenario Pavlou sees constantly. A patient’s triglycerides are normal, their HDL is excellent, and their LDL is high, so the doctor recommends a statin. His first response to a patient in this position is refreshingly simple: if most of your markers are improving and only one is moving the wrong way, something about the underlying assumption deserves a second look. Someone on a ketogenic diet typically sees triglycerides fall, HDL rise, HbA1c drop, CRP fall and liver enzymes improve as fat clears from the liver. Total cholesterol and LDL may climb at the same time. Rather than treating that one number as proof the diet is dangerous, Pavlou argues it’s worth asking whether LDL is even a reliable marker in this context, since large, well-designed studies have found no statistically significant link between it and cardiovascular risk once you account for particle oxidation and inflammation. He points to a study on one week of water fasting that produced a 66 percent rise in LDL and a 37 percent rise in total cholesterol, numbers that make no sense under the standard dietary-cholesterol model but fit neatly once you understand cholesterol as part of the body’s stress and repair response rather than a direct dietary readout.

His practical advice for patients facing this exact conversation with their doctor: ask for direct measurement of atherosclerosis itself, through a coronary artery calcium score or a carotid intima-media thickness scan, rather than relying on a single blood marker. Then repeat the test after six months or a year and track the actual change.

Doctors Are Slowly Coming Around, Driven by Their Patients

Pavlou is candid about how hard this shift has been within the profession. Many doctors, he says, rely on pharmaceutical-funded journals and rarely read past the abstract. But he’s seeing more physicians willing to listen and the pressure is coming from an unexpected direction: patients returning from a ketogenic diet reporting clearer thinking, more energy, resolved fatty liver and steadily improving numbers. Funding remains the deeper obstacle. No pharmaceutical company has an incentive to fund large trials on a dietary intervention that can’t be patented or sold.

Lipoprotein(a): Not the Villain It’s Made Out to Be

One of the more technical parts of the conversation covered lipoprotein(a), or Lp(a), a genetic variant that gets flagged as high risk almost automatically in conventional cardiology. Pavlou’s explanation reframes it. Lp(a) is an LDL particle with an extra protein, apolipoprotein(a), attached. That extra protein reduces the particle’s affinity for the liver’s LDL receptor, so it circulates longer and is exposed to oxidative and glycating damage for longer. It also has a stronger affinity for oxidized fats already in circulation and it competes with plasminogen for the same receptors, which affects clot resolution. In someone with chronic inflammation, all of this adds up to genuine risk. But in a metabolically healthy person, Pavlou points out, a higher Lp(a) can actually function as an advantage, supporting faster tissue repair. The real driver of harm isn’t the particle itself, it’s the inflammatory environment it’s circulating in.

Statins complicate this picture further. Because they work by upregulating the liver’s LDL receptor, and healthy native LDL particles bind that receptor more readily than Lp(a) does, statins end up clearing normal LDL faster than Lp(a), which means Lp(a) rises as a percentage of total LDL, by roughly 20 percent according to research from cardiologist Sotirios Tsimikas. For a patient with elevated Lp(a), a statin may be actively counterproductive.

Genetics set the ceiling on how much Lp(a) the liver produces, and Pavlou puts the hereditary contribution at roughly 80 percent, but he’s skeptical of how neatly modern medicine tries to separate genetic risk from environment. 

What the Calcium Score Can and Can’t Tell You

Coronary artery calcium scoring is a genuinely useful test, but Pavlou flags real limits. It works best in people over sixty, since younger patients can carry soft, non-calcified plaque that a calcium score misses entirely. For younger patients, he leans more on carotid intima-media thickness ultrasound, which can catch plaque even when the artery has remodeled outward and the vessel opening itself stays wide, a pattern that hides risk from a standard stenosis measurement. He also raises a finding from pathology studies that should reshape how anyone thinks about heart attacks: roughly two-thirds of infarctions occur at sites with less than 50 percent stenosis, undermining the simple model of a slowly narrowing artery finally clogging shut.

On cost, Pavlou is pragmatic. Advanced testing isn’t always necessary or affordable, and an experienced clinician can read a lot from triglycerides, HDL, liver enzymes, HbA1c, CRP and body composition alone. More often than not, it’s an anxious patient, not the doctor, pushing for the calcium score after hearing a frightening cholesterol number from elsewhere.

Getting Patients Past the Bread

Adherence is where a lot of good clinical intentions fall apart, and Pavlou’s approach here is worth borrowing regardless of specialty. Rather than arguing with a patient who’s bargaining over bread or a weekly beer, he offers a strict two-month trial. Long enough to produce real, felt results, short enough that it doesn’t feel like a life sentence. Patients who see the trial through and experience the shift in energy and lab markers rarely want to go back. Those who don’t get real results within two months, he notes, are the ones most likely to give up on low-carb eating entirely and wrongly conclude it doesn’t work for them.

The Mediterranean Diet, Reconsidered

Living and practicing in Greece puts Pavlou in an interesting position on the Mediterranean diet, which he describes as a marketing construct from the 1980s built substantially to support olive oil exports, with no consistent definition of what it actually includes. Comparative studies that pit the standard American diet, the Mediterranean diet and a very low carbohydrate diet against each other consistently find the low-carb approach comes out ahead, though he’s careful to note the right approach still depends on the individual’s specific health situation.

The One Thing to Remember

Asked what he’d want listeners to take away above everything else, Pavlou didn’t hesitate: outside of genetic disease, lifestyle is what determines cardiovascular risk, and metabolic health and cardiovascular health are close to the same thing. Reducing carbohydrate intake, cutting polyunsaturated fats, managing stress and quitting smoking will move the needle more than any single number on a lab report. Try it, he says, and check the results for yourself.