Lipid-lowering agents, also sometimes referred to as hypolipidemic agents, cholesterol-lowering drugs, or antihyperlipidemic agents are a diverse group of
pharmaceuticals that are used to lower the level of lipids and lipoproteins, such as cholesterol, in the blood (
hyperlipidemia). The American Heart Association recommends the descriptor 'lipid lowering agent' be used for this class of drugs rather than the term 'hypolipidemic'.
Classes
The several classes of lipid lowering drugs may differ in both their impact on the cholesterol profile and adverse effects. For example, some may lower
low density lipoprotein (LDL) levels more so than others, while others may preferentially increase
high density lipoprotein (HDL). Clinically, the choice of an agent depends on the patient's
cholesterol profile,
cardiovascular risk, and the
liver and
kidney functions of the patient, evaluated against the balancing of risks and benefits of the medications. In the United States, this is guided by the
evidence-based guideline most recently updated in 2018 by the
American College of Cardiology &
American Heart Association.[1]
Established
Statins (HMG-CoA reductase inhibitors) are particularly well suited for lowering LDL, the cholesterol with the strongest links to vascular diseases. In studies using standard doses, statins have been found to lower LDL-C by 18% to 55%, depending on the specific statin being used. A risk exists of muscle damage (
myopathy and
rhabdomyolysis) with statins. Hypercholesterolemia is not a risk factor for mortality in persons older than 70 years and risks from statin drugs are more increased after age 85.[2]
Fibrates are indicated for
hypertriglyceridemia. Fibrates typically lower triglycerides by 20% to 50%. Level of the good cholesterol HDL is also increased. Fibrates may decrease LDL, though generally to a lesser degree than statins. Similar to statins, the risk of muscle damage exists.
Niacin, like fibrates, is also well suited for lowering triglycerides by 20–50%. It may also lower LDL by 5–25% and increase HDL by 15–35%. Niacin may cause
hyperglycemia and may also cause
liver damage. The niacin derivative
acipimox is also associated with a modest decrease in LDL.
Bile acid sequestrants (resins, e.g. cholestyramine) are particularly effective for lowering LDL-C by sequestering the cholesterol-containing bile acids released into the intestine and preventing their reabsorption from the intestine. It decreases LDL by 15–30% and raises HDL by 3–5%, with little effect on triglycerides, but can cause a slight increase. Bile acid sequestrants may cause gastrointestinal problems and may also reduce the absorption of other drugs and vitamins from the gut.
Ezetimibe is a selective inhibitor of dietary cholesterol absorption.
Lecithin has been shown to effectively decrease cholesterol concentration by 33%, lower LDL by 38% and increase HDL by 46%.[5][non-primary source needed]
Phytosterols may be found naturally in plants. Similar to ezetimibe, phytosterols reduce the absorption of cholesterol in the gut, so they are most effective when consumed with meals. However, their precise mechanism of action differs from ezetimibe.
Omega-3 supplements taken at high doses can reduce levels of triglycerides.[6] They are associated with a very modest increase in LDL (~5%).
Red yeast rice[10] is the natural source from which statins were discovered, but the FDA currently disallows any RYR with significant amounts of statin to be sold as a dietary supplement [11]
CETP inhibitors (cholesteryl ester transfer protein), 1 candidate is in trials. (
Anacetrapib) It is expected that these drugs will mainly increase HDL while lowering LDL