@ScathachHerself@Jikkyleaks We have high quality mechanistic data for how vaccines work. Scrutinizing seeming glitches in outcome data is not a valid approach and constitutes abject incompetence. An intelligent vax skeptic will scrutinize the mechanism. Clearly none exist.
@BobKnezevic@anonemus349832@newstart_2024 there's actually zero evidence of mrna induced myocarditis and any paper you link regarding it will say "no causal link", which somehow you missed.
@grok@Kansanparantaja@dylanarmbruste3@anonemus349832@BioLayne sdldl has easier penetration but less cholesterol content, large ldl can also penetrate and has greater cholesterol content, so the effect is net neutral or too small a difference to be clinically relevant.
@Kansanparantaja@anonemus349832@dylanarmbruste3@grok@BioLayne and LDL sticks in the sub-endothelial layer to the proteoglycans due to electrostatic interactions, because it is grease. The same reasons grease sticks to a pipe. No endothelial dysfunction has occurred yet at this point. High cholesterol concentrations alone does this.
@Kansanparantaja@anonemus349832@dylanarmbruste3@grok@BioLayne You have the order of events backwards. Endothelial dysfunction occurs in late stage disease. Transcytosis is proportional to LDL concentrations. LDL is transported into the sub-endothelial faster than it can be cleared and sticks there.
@Kansanparantaja@anonemus349832@dylanarmbruste3@grok@BioLayne Grease sticks to pipes due to electrostatic interactions. Cholesterol likewise sticks to the subendothelial the same. High LDL concentrations overwhelm endothelial clearance mechanisms (e.g., scavenger receptors like SR-B1), leading to lipid accumulation in endothelial cells.
@Kansanparantaja@anonemus349832@dylanarmbruste3@grok@BioLayne No it sticks because the artery has no teflon-like coating, just like grease sticks to anything. The artery is not a non-stick substance. Once it has stuck, then the lipids decay and macrophages eat it, bringing it further into the artery wall.
@Kansanparantaja@anonemus349832@dylanarmbruste3@grok@BioLayne Cholesterol is a greasy viscous substance. Are you claiming that the human artery is coated with a teflon-like substance? That it should be resistant to grease? What chemical lines the arteries do you suppose that has teflon-like qualities?
@Kansanparantaja@anonemus349832@dylanarmbruste3@grok@BioLayne and no your "humans aren't kitchen sinks lol" isn't a rebuttal. Grease clogs pipes of both organic and inorganic builds. What is it about the human artery that should be resistant to grease buildup? Despite that what we see in a diseased artery is grease buildup?
@Kansanparantaja@anonemus349832@dylanarmbruste3@grok@BioLayne This is not a data issue. It's a mechanistic one. That's your main problem, you don't even understand what you're arguing against. You need to furnish a rebuttal disproving the mechanism -- grease clogging the pipe.
Why can no one do that? Should be easy right?
@Kansanparantaja@anonemus349832@dylanarmbruste3@grok@BioLayne The current opinion is a claim of causality. "Low density lipoproteins cause atherosclerosis".
You might not like the opinion, but you have no rebuttal against it, and so you are just noise, not actually contributing to the discourse.
@Kansanparantaja@anonemus349832@dylanarmbruste3@grok@BioLayne There's scientific consensus on the issue and I have given you the basic tenets of it. So if you want to challenge the consensus, you need to rebuttal the basic tenets in the proper forum. Why is that not a single skeptic such as yourself able to do that? Not even one?
@Kansanparantaja@anonemus349832@dylanarmbruste3@grok@BioLayne Dave feldman has no formal education and doesn't know what he's talking about. He's confusing a sub-clinical myocardial infarction for plaque regression. Heart attacks are caused by plaque moving around and if you're Feldman you'll think that's keto healing or some shit.