Statins make the liver stop making so much cholesterol and also help the liver pull more bad cholesterol out of the blood.
Scientific Claim
Inhibition of hepatic HMG-CoA reductase reduces circulating LDL cholesterol by decreasing endogenous cholesterol synthesis and upregulating hepatic LDL receptor expression.
Original Statement
“Statins work by blocking an enzyme in your liver called HMG COA reductase. That enzyme is responsible for producing cholesterol. When you inhibit it, your liver makes less cholesterol. Simple enough. But the second effect is actually more important. When your liver detects that cholesterol levels are dropping, it upregulates LDL receptors on its surface. Those receptors pull more LDL cholesterol out of your bloodstream and into the liver for processing. The net result is that circulating LDL cholesterol goes down.”
Context Details
Domain
pharmacology
Population
human
Subject
HMG-CoA reductase inhibition
Action
reduces
Target
circulating LDL cholesterol
Intervention Details
Evidence from Studies
Supporting (1)
Reduction of LDL cholesterol by 25% to 60% in patients with primary hypercholesterolemia by atorvastatin, a new HMG-CoA reductase inhibitor.
This study gave people a drug that blocks a liver enzyme involved in making cholesterol, and their bad cholesterol (LDL) dropped a lot — exactly what scientists expect when you block that enzyme.
Contradicting (1)
Inhibition of HMG-CoA reductase by atorvastatin decreases both VLDL and LDL apolipoprotein B production in miniature pigs.
The study found that the drug lowered bad cholesterol by reducing how much cholesterol the liver makes and releases, not by making the liver better at removing it from the blood — which is the opposite of what the claim says about liver receptors.