I have been assessing for several decades cholesterol risk was built around a plain idea: lower “bad” cholesterol, reduce the risk of heart attack. The test underlying this approach measures the amount of low-density lipoprotein, or LDL cholesterol, circulating in part of the blood. It has shaped everything from clinical guidelines to the widespread employ of statins, the LDL-lowering drugs.
It works. Lowering LDL cholesterol reduces the risk of heart attacks, strokes and premature death. But that doesn’t tell the whole story.
An LDL cholesterol test measures the amount of cholesterol inside low-density lipoprotein particles circulating in the bloodstream. Cholesterol-containing LDL particles can become trapped in the walls of arteries, forming plaques that can ultimately block blood flow. Because the test measures the amount of cholesterol transferred rather than the number of LDL particles themselves, two people can have the same LDL cholesterol level but very different particle numbers and therefore different levels of risk.
This gap has pushed researchers toward a different way of measuring risk. Apolipoprotein B, or apoB, reflects the total number of cholesterol-carrying particles in the blood, not the amount of cholesterol they contain. A growing body of research suggests that this is a more correct way of determining who is at risk and who is not.
In March 2026, this was recognized by the American Heart Association and the American College of Cardiology. The updated cholesterol guidelines recognize apoB as a potentially more precise marker, in line with previous European recommendations. However, they have stopped recommending apoB as the primary testing method.
“They are reviewing the evidence and declaring apoB is better, but the actual road traffic regulations still prioritize LDL,” says Allan Sniderman, a cardiologist at McGill University.
Sniderman was the author of, among others, JAMA Modeling 2026 study that analyzed the lifetime outcomes of approximately 250,000 American adults eligible for statin treatment. By comparing LDL cholesterol, non-HDL cholesterol and apoB, the study showed that using apoB to make treatment decisions would prevent more heart attacks and strokes compared to current approaches, while remaining cost-effective.
ApoB testing can be done with standard blood tests. So why hasn’t this been included in routine care? Even in Europe, where guidelines have been reflecting their usefulness for years.
Part of the answer is inertia. For decades, LDL cholesterol has been both a scientific breakthrough and a public health success story. It is plain, broadly understood and directly related to effective treatments.
“For 50 years, LDL cholesterol has been an amazing discovery,” Sniderman says. “It’s not that it’s not a good marker. It’s a good marker.”
Børge Nordestgaard, president of the European Atherosclerosis Society, agrees that LDL cholesterol remains crucial for a reason. “The evidence is overwhelming and beyond dispute,” he says. “Statins reduce the risk of heart attacks, strokes and premature death by lowering LDL cholesterol levels.”
This success has helped shape a powerful narrative: LDL is “bad cholesterol” and lowering it saves lives. But this simplicity also limits how we understand risk.
“As a result, patients and physicians know little or nothing about apoB,” Sniderman says.
More recent research suggests that the cholesterol picture is more elaborate, especially in people already taking statins. Previous research led by Nordestgaard found that in treated patients, high levels of apolipoprotein B and non-HDL cholesterol were still associated with an increased risk of heart attack and mortality, while LDL cholesterol was not. In particular, ApoB proved to be the most correct marker.
For Kausik Ray, a cardiologist at Imperial College London, the challenge is not choosing one marker over another, but understanding what each one records and what it misses.
“We’re not interested in cholesterol per se,” Ray says. “We’re trying to prevent heart attacks and strokes.”