Total cholesterol and all-cause mortality – a study among 13M adults
Cholesterol / lipid science is a mess. First it was LDL-C that was bad, then that doesn’t actually correlate, then it’s LDL-P, oh wait, then it’s LDL size, and then it’s ApoB that’s going to “clog your arteries”. Once you dive into the “hard” science like pathology of atherosclerosis, you’ll find that the lipid hypothesis makes no sense.<p>We have drugs (PKCS9 inhibitors: <a href="https://www.nejm.org/doi/full/10.1056/NEJMoa1615664" rel="nofollow">https://www.nejm.org/doi/full/10.1056/NEJMoa1615664</a>, bile acid sequesterants, CETP Inhibitors: <a href="https://www.nejm.org/doi/full/10.1056/NEJMoa1609581" rel="nofollow">https://www.nejm.org/doi/full/10.1056/NEJMoa1609581</a>) that can lower LDL to 10-20mg/dL — the later even increased HDL. No impact on cardiovascular mortality. The studies all use composite endpoints.<p>What might cause Atherosclerosis?<p>- Bacteria<p>- Bacterial lipid byproducts<p>- Endothelial damage from toxins (lead, mecury, etc)<p>- Endothelial glycation from high blood sugar (Diabetics have a lot of CVD)<p>- Bad genetics resulting in excess hemodynamic stress at coronary branch points (fun fact: CVD only develops in a few specific spots)<p>- Autoimmune conditions (higher rates of CVD in this population)<p>What most of these things have in common is they trigger the activation of the immune system.