| VLDL is worse than regular LDL but high LDL in general is an issue. The science here isn't "If your LDL is denser everything is just peachy and you can be fine with 100 LDL," it's "You might be anywhere between significantly worse and marginally better than your numbers suggest" If your LDL is in the 80s, you are almost certainly progressing plaque buildup regardless of all other factors. It won't be particularly fast in most people, maybe not even enough to matter over your lifespan unless you have other risk factors. If everything is favorable, you might see a halt or slow regression in the 70s, but this is like perfect storm levels of factors. Most people need to be below 60 to start see soft plaque begin to retreat, with under 55 being the general target for high-risk individuals that need regression. Your endo is right that basically no one gets there without some form of medication. It sucks, but it's also reality. > my dentist, who also has a bit of a fixation on cholesterol on a personal level and is educated on the matter, has said that a heart calcium scan is the best way to determine what someone's target cholesterol number should actually be, and that it should not be the same from person to person. Your dentist is an idiot and very much obviously not educated on the matter and should stick to teeth. CAC is a huge trailing indicator because it shows only calcified plaque. Plaque exists and blocks arteries long before it is calcified. 5+ years. People regularly have massive arterial soft plaque buildup with minimal or 0 calcium scores. And soft plaque is almost always the part that ruptures and breaks away and you throw a clot resulting in a heart attack or stroke. A CCTA will let you see soft plaque which could potentially help give you a better understanding of just how aggressive you need to be... But the problem there is that the target for everyone should still be keeping their LDL as lower than we have been targeting for years. And if they have other atherogenic particle load, like high Lp(a), then that numbers needs to be commensurately lower to account for the combined load. I'm not telling you to go on statins. I'm not your doctor. I'm not a doctor at all. But I do have risk factors that require I pay careful attention to this sort of thing, and I spend a lot of time reading research here because I like being alive and want to stay alive in a generally healthy state for as long as I can. And if you are the same, then, well, I would suggest listening to your doctors. They're telling you to get your LDL to that level because they think it will improve your health outcomes, and the vast, huge, overwhelming majority of research over the past decades points towards lowering LDL as being hugely important for improving ASCVD outcomes in at-risk populations across a wide variety of study types, including MR genetic studies looking at health outcomes in people that effectively do not produce LDL in their liver (in fact these studies are what really inspired the class of medicine in the article to begin with) and they basically just don't die of ASCVD. You have other options besides statins, too. Ezetimibe. These new inhibitors - hopefully the small molecule version will be more accessible than the MAB version. |