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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
https://twitter.com/LDLSkeptic/status/12802177030267904002/13 cholesterol needs. HMG-CoA reductase, the key enzyme in this pathway, converts HMG-CoA into Mevalonate, which is then used to produce cholesterol and other critical molecules like isoprenoids (e.g., for protein prenylation). Because LDL uptake is impaired in FH, cells /3
https://twitter.com/LDLSkeptic/status/19016384099882270752/11 and proline residues of collagen which get exposed in damaged arterial walls. Like LDL, it is a method of applying a sticking plaster to a damaged vascular endothelium. If you have lots of damage to your arteries you would expect your liver to make more Lipoprotein(a). /3
https://twitter.com/William63374757/status/19009127619928149622/8 statins since 2008. 16 yrs of relentless, frothing-at-the-mouth obsession. That’s not a casual fling; that’s a vendetta carved in blood & biochemistry. Your posts like that March 13, 2025 screed hit like a Molotov cocktail: mevalonate pathway choked out, CoQ10 stripped /3
https://twitter.com/HalCranmer/status/18965936183932603862/4 The brain relies on cholesterol—it is a key component of cell membranes, myelin (which insulates neurons), and helps with synapse formation. Memories are made of this. About 25% of the body’s cholesterol is in the brain. /3