The 'response to injury' hypothesis suggests atherosclerosis begins with physical damage to the artery wall, which is a credible alternative to the purely lipid-centric model.

A lean mass hyper-responder is specifically defined by having an LDL cholesterol of 200 or higher, HDL of 80 or higher, and triglycerides of 70 or lower.

The development of atherosclerosis may be less about the initial damage to arteries and more about the inhibition of the body's powerful repair mechanisms by factors like constant eating or over-exercising.

An initial analysis of the lean mass hyper-responder study found no statistically significant difference in arterial plaque compared to a healthy control group, despite an average LDL of 272 mg/dL.

Genetic variants that cause lifelong low LDL reduce heart disease but have not been shown to lower all-cause mortality, suggesting a potential health trade-off.

In a self-experiment, hyper-caloric consumption on a ketogenic diet caused LDL cholesterol to plummet, suggesting LDL particles were being consumed for structural purposes by fat cells.

A controversial theory proposes that APOB lipoproteins are part of the innate immune response in the artery wall, providing structural components for immune cells to grow.

Lean mass hyper-responders might transport more LDL particles across their artery walls than others, but for beneficial structural needs rather than for pathological reasons.