 What could help explain severe coronary disease? And someone considered to be at low cardiovascular disease risk with a healthy lifestyle. Young man ends up in the ER with a heart attack, ultimately found to have severe coronary artery disease, yet given his age, blood pressure, and cholesterol, his 10-year risk of a heart attack should only be like 2%. But what he did have was a high lipoprotein A-level, also known as LP-lital A. Markedly high at 80, which may help explain it. You can see the same thing with women, 27-year-old, with the heart attack, with a high LP-lital A. What is this LP-lital A, and what can we do about it? LP-lital A is an underestimated cardiovascular risk factor. It causes coronary artery disease, heart attack strokes, peripheral artery disease, calcified aortic valve disease, and heart failure. And these can occur even in people without high cholesterol. Because it is cholesterol, it's basically an LDL cholesterol molecule linked to another protein, which, like LDL, transferred cholesterol into the lining of arteries contributing to the inflammation in atherosclerotic plaques. But it has yet to gain recognition by practicing physicians, and the main reason for the limited clinical use of LP-lital A is a traditional lack of effective and specific therapies to lower it. LP-lital A concentrations are approximately 90% genetically determined. So, I mean, the conventional thinking has been that, look, you're just kind of born with higher or lower levels, and there's not much you can do about it. Even if that were the case, I mean, you still might want to know about it, since if we were high, then, I mean, that would be all the more reason to make sure all your other risk factors that you do have more control over are absolutely as good as possible. Like, you know, maybe help you quit smoking, and do everything you can to lower your LDL cholesterol as much as possible. LP-lital A levels in the blood can vary a thousandfold between individuals from less than 0.1 mg per deciliter to 100 or more. Here's the graph of odds of heart disease at different levels. Less than 20 is probably optimal, with greater than 30 to 50 considered elevated. Even when the more conservative threshold of greater than 50 is used, that describes like 10 to 30% of the global population, and that's made 1.4 billion people. So if we're like the one in five people with elevated levels, what can we do about it? The way we know that LP-lital A causes atherosclerosis is that we can put it to the ultimate test. There's something called aphoresis, which is basically like a dialysis machine where they can take out your blood, wash out some of the LP-lital A, and then give your blood back to you. And when you do that, you can reverse the progression of disease. Atherosclerosis continues to get worse in the control group, but better in the aphoresis group. I mean, this is great for proving the role of LP-lital A, but has limited clinical application given the cost, accessibility, and the time commitment required for bi-weekly sessions of two to four hours each. It causes a big drop in blood levels, but they quickly creep back up, so you have to keep going in. Costing more than $50,000 a year, there has to be a better way. And we'll explore the role diet can play next.