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https://twitter.com/Mangan150/status/19229994312399629012/6 than large, fluffy LDL. sdLDL is more plaque-promoting because it’s easily oxidized and triggers inflammation. Macrophages engulf oxidized sdLDL, forming foam cells. Foam cells are a key driver in the development and progression of atherosclerosis. /3
https://twitter.com/KCJerry/status/19195314633446239082/7 LDL is vital for cell repair & hormones. When insulin & inflammation are low, LDL is protective. Oxidized LDL (oxLDL) from high insulin is the real culprit in heart disease.
https://twitter.com/Chrisherbert196/status/19192824683491537822/10 Trials like ASTEROID and ZEUS claim Statins and Ezetimibe “shrink plaque” and reduce Percent Atheroma Volume (PAV), but broader evidence shows Statins increase CAC. How can plaque volume decrease while calcification rises ? /3
https://twitter.com/75H884/status/19170361519339647602/7 high doses, drug interactions (e.g., with CYP3A4 inhibitors), or other underlying health conditions.
https://twitter.com/marilyn_ella/status/19116703671037299162/9 There’s no hard proof Trump’s doctors were influenced to inflate his heart health, but circumstantial factors, political pressure, selective reporting, and a history of shaped narratives make it a reasonable suspicion. Low triglycerides and “excellent” claims /3
https://twitter.com/dramerling/status/19078717966129688752/7 In osteoclasts. This disruption prevents the prenylation of these GTPases, which are necessary for cytoskeletal organization. As a result, osteoclasts become less active and can undergo cell death, leading to decreased bone resorption.
https://twitter.com/NBCDFW/status/19066596762021072732/14 Studies from the 1990s (e.g., Brown & Goldstein, Journal of Lipid Research, 1997) suggest Lp(a) accumulates at sites of endothelial damage, delivering cholesterol to REPAIR cell membranes or stabilize injured vessels. /3