Atorvastatin reduces cholesterol by blocking the enzyme that the liver uses to make cholesterol from scratch, then lowering cholesterol levels in the blood.
It blocks cholesterol production in the liver by inhibiting HMG‑CoA reductase
Atorvastatin is a statin. Its key mechanism is inhibition of HMG‑CoA reductase, the rate-limiting enzyme in the mevalonate pathway of cholesterol synthesis. When this enzyme is blocked, the liver produces less cholesterol internally [1].
Lower liver cholesterol increases LDL receptor activity and clears LDL from blood
Because liver cells make less cholesterol, they compensate by pulling more cholesterol out of the bloodstream. They do this by increasing LDL receptor expression on their surface. More LDL receptors means more LDL particles are taken up from the blood and removed, which lowers circulating LDL cholesterol [1].
It shifts cholesterol balance toward lower LDL without needing dietary cholesterol to change first
Even before diet changes, the drug’s two-step effect (less cholesterol synthesis in the liver, followed by increased clearance of LDL) reduces the amount of atherogenic cholesterol circulating in the blood [1].
How this translates to lipid numbers people usually track
The net result of the mechanism is typically a reduction in LDL cholesterol and total cholesterol, along with effects on triglycerides and HDL that vary by patient and baseline lipids [1].
Sources
- https://www.ncbi.nlm.nih.gov/books/ (Search: “statins inhibit HMG-CoA reductase increase LDL receptor clearance”)