The world of cholesterol testing is evolving, and it's time to take a step back and reevaluate our approach. For decades, we've relied on measuring low-density lipoprotein (LDL) cholesterol, known as the 'bad' cholesterol, as the primary indicator of heart attack risk. But is this the whole story? Personally, I think it's time to explore a more nuanced understanding of cholesterol and its role in our health. The LDL cholesterol test has been a cornerstone of cardiovascular medicine, and its simplicity has made it widely adopted. Lowering LDL cholesterol has proven effective in reducing heart attacks, strokes, and early death, which is why it has shaped clinical guidelines and the widespread use of statins. However, what many people don't realize is that LDL cholesterol doesn't tell the entire story. The test measures the amount of cholesterol carried by LDL particles in the bloodstream, but it doesn't account for the fact that two people can have the same LDL cholesterol level but very different numbers of particles, and therefore different levels of risk. This is where apolipoprotein B (apoB) comes in. ApoB reflects the total number of cholesterol-carrying particles in the blood, providing a more accurate way of identifying risk. In March 2026, the American Heart Association and American College of Cardiology recognized this, acknowledging apoB as a potentially more precise marker. But they stopped short of recommending apoB as the primary method for testing. What makes this particularly fascinating is that apoB testing can be done through standard blood tests, yet it hasn't filtered into routine care. Part of the reason is inertia. LDL cholesterol has been a scientific and public health success story for 50 years, and it's simple, widely understood, and directly linked to treatments that work. Børge Nordestgaard, president of the European Atherosclerosis Society, agrees that LDL cholesterol remains central for a reason. The evidence is immense, and statins reduce heart attacks, strokes, and early death through LDL cholesterol lowering. However, recent research suggests that the cholesterol picture is more complex, especially in people already taking statins. High levels of apoB and non-HDL cholesterol remain associated with increased risk of heart attacks and mortality, while LDL cholesterol does not. This raises a deeper question: if we're not interested in cholesterol for its own sake, but rather to prevent heart attacks and strokes, what should we be measuring? Cholesterol enters artery walls through apoB-containing particles, but these particles are not all the same. LDL makes up most of them, but lipoprotein(a) and triglyceride-rich particles also play a role. ApoB captures the total number, but not their source. This is where nuance comes in. ApoB may be a better overall signal of risk, but clinicians still need to understand what is driving it. Because then you can personalize it. That need for a more detailed picture is already pushing cholesterol testing beyond a single number. Lipoprotein(a), a genetically determined form of cholesterol that is rarely measured but can significantly increase risk, is one example. We've got a huge problem in the UK with less than 5 percent of the population being tested, but you only need to measure lipoprotein(a) once in your lifetime. Nordestgaard argues that if lipid testing were designed from scratch today, it would not center on a single measure at all. You would test your LDL cholesterol, your remnant cholesterol, and your lipoprotein(a). You would make three parallel tests. The shift is not just about better markers, but earlier detection. Cardiovascular risk builds silently over decades, yet testing often begins only once symptoms or clear risk factors appear, such as being male and over 60. If you don't look, you don't know. Typically, people in their twenties, thirties, and forties are often not going to have things checked, because they feel fine. Instead, care is often reactive, which has consequences for prevention. Beyond apoB, researchers are beginning to explore even more granular ways of measuring risk. Large-scale examining the chemical molecules produced by the body's metabolism, alongside genetic data, suggests that cardiovascular risk is shaped by a complex interplay of biological pathways, not a single biomarker. One analysis found that combining metabolic and genetic information can improve risk prediction beyond traditional cholesterol measures, helping to explain why people with similar profiles can have very different outcomes. The challenge is translating that complexity into clinical practice. More detailed testing brings higher costs, greater analytical burden, and the need for new evidence to guide treatment decisions. For researchers, the direction of travel is clear. Medicine must move away from single-number diagnostics toward more layered, data-driven assessments of risk. For now, apoB sits at the center of that transition: a better population-level measure than LDL cholesterol alone, but still only part of a broader picture. This whole concept of normal - we've got to get rid of that and explain to people there's a continuum for all of these things. There isn't a black-and-white answer, unfortunately.
