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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The simple claim “saturated fat raises LDL, therefore causes heart attacks” is outdated.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.

Endogenous triglycerides are synthesized by the liver, primarily from excess dietary carbohydrates, and to a lesser extent from protein/fats

The majority of cholesterol in circulation is synthesized by the liver (from excess carbohydrates for the most part) and other cells.

The liver converts excess carbohydrates and proteins into triglycerides, which are exported as very low-density lipoproteins (VLDL)