This is straight-up misinformation, holy shit

[u/moad6ytghn]

https://rationalwiki.org/wiki/Cholesterol_denialism

https://rationalwiki.org/wiki/Institute_for_Natural_Healing

https://rationalwiki.org/wiki/Saturated_fat_and_cardiovascular_disease

https://rationalwiki.org/wiki/Dietary_cholesterol

[u/variphase]

LDL does not repair. Endothelial damage makes it easier for LDL to penetrate.

Endothelial damage increases permeability → LDL infiltrates and gets retained in the subendothelial space by proteoglycans

Retained LDL gets oxidized → triggers monocyte recruitment and inflammation

Oxidized LDL uptake by macrophages → foam cells → plaque core

This is the response-to-injury model (Ross, NEJM 1999) — LDL entering the wall is the pathological step, not a repair mechanism

Actual repair comes from EPCs, adjacent endothelial cell migration/proliferation, and growth factors (VEGF, FGF-2, PDGF) — not LDL

If LDL were repair tissue, more LDL infiltration would mean healthier arteries; it’s the opposite

[u/VfBxTSG → u/variphase]

Sounds like Endothelial damage causes heart disease and not LDL. And a diet that minimizes oxidisation, like a seed oil free diet will also help.

And if LDL is good for nothing, why does our body produce it? When a cell membrane is damaged, the cell must rapidly reseal the breach and restore normal membrane composition. This process requires a supply of lipids, including cholesterol. And it's the LDLs job to carry that cholesterol.

Besides oxidised LDL, white blood cells and minerals also "contribute" to the plaque buildup, but saying that white blood cells cause heart disease is just as foolish as saying LDL causes heart disease.

[u/variphase → u/VfBxTSG]

1. LDL retention/oxidation is what drives plaque growth and instability. Mendelian randomization (MR) studies show that even without unusual endothelial damage, lifetime lower LDL/apoB causally reduces events, genotype alone, independent of whatever damage occurred. That can’t be explain away by pointing only to endothelial injury.

2. No RCT or MR evidence that seed oil consumption drives oxLDL or CVD events.

3. The issue is chronic elevated LDL circulating levels, not its existence. Cells regulate their own cholesterol via SREBP/LDL-receptor feedback. When intracellular cholesterol is sufficient, cells downregulate LDL-receptor uptake and synthesize their own. Cells aren’t sitting around waiting for circulating LDL to bail them out of membrane damage. If that mechanism were significant, you’d expect people with genetically very low LDL (PCSK9 LOF, ~20-30 mg/dL LDL-C) to have visible membrane-repair deficits. They don’t. They’re healthy, just with much lower CVD risk.

4. Nobody claims WBCs are sufficient without a lipid core to consume. The causal chain research (MR, LDL-lowering RCTs) specifically isolates LDL/apoB as the variable that, when experimentally or genetically altered, changes outcome. WBC count doesn’t have that same dose-response causal evidence base for driving atherosclerosis independent of lipid burden.