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At this point, it’s worth asking: if polyunsaturated seed oils and plant sterols disrupt red blood cells, fuel oxidation, promote inflammation, and crystallise in plaques — then why are they still recommended as “cardioprotective”?

Explore the physiological link between seed oils, linoleic acid, and oxidized LDL. Learn how high triglycerides and metabolic dysfunction turn LDL into "explosive cargo," leading to arterial inflammation and plaque formation. A deep dive into MPO, LOX, and the real cause of heart disease.

What’s actually most prone to oxidation in LDL is the fatty acid tail of the cholesteryl ester in the “oil barrel” (and the PUFA in the phospholipid shell). Cholesterol itself — the rigid steroid ring — is remarkably stable. Pure cholesterol won’t just oxidise easily in the body.

When the metabolic environment is calm — low inflammation, low oxidative stress, good insulin sensitivity — LDL particles circulate, deliver nutrients, and return to the liver without incident. But in an inflamed environment, those same particles can get trapped, oxidised, and turned into plaque.

The simple claim “saturated fat raises LDL, therefore causes heart attacks” is outdated. A more accurate view must consider biochemistry, particle quality, metabolic health, and dietary context.

Saturated fat became a convenient scapegoat, while the role of refined carbohydrates, ultra-processed foods, and chronic inflammation in driving heart disease was largely overlooked.