“High HDL cancels out the risk from high LDL.”
High HDL does not cancel out the risk from high LDL.
A high HDL number does not offset a high LDL number. Your LDL, along with your other risk factors, is what tells you and your doctor how much heart risk you carry.
At your next checkup, look at your LDL result on its own and ask your doctor what it means for your heart risk.
Safety note: Do not stop or skip a prescribed cholesterol medicine because your HDL is high.
Talk to a healthcare professional if: your LDL is high, even if your HDL looks good, or you are thinking about stopping a cholesterol medicine.
Genetic studies show that being born with higher HDL does not lower heart attack risk, while higher LDL clearly raises it, and drugs that raised HDL did not prevent heart attacks unless they also lowered LDL-type cholesterol. Confidence is strong because genetic studies, large drug trials and LDL-lowering trials all point the same way.
High HDL does not cancel out the risk from high LDL. LDL is a proven cause of heart disease, and genetic studies and drug trials show that higher HDL by itself does not protect against it.
People with high HDL do tend to have fewer heart attacks, which is where the idea comes from. But in a 2012 genetic study, people born with a gene variant that raises HDL had the same heart attack risk as everyone else, and a score of HDL-raising genes showed no protection, while a score of LDL-raising genes roughly doubled risk for each step up. In the AIM-HIGH trial of 3,414 heart patients already on statins, niacin raised HDL from 35 to 42 mg/dL but did not reduce heart events (16.4% vs 16.2%). In a trial of 30,449 heart patients, anacetrapib roughly doubled HDL and modestly lowered major coronary events (10.8% vs 11.8%), but it also lowered non-HDL cholesterol by 18%, and earlier drugs in the same class had neutral or harmful results. Lowering LDL with statins, by contrast, cut major heart and stroke events by about 21% for each 39 mg/dL drop, which meant about 11 fewer events per 1,000 people over five years even in people at low risk.
- Voight BF, Peloso GM, Orho-Melander M, et al. Plasma HDL cholesterol and risk of myocardial infarction: a mendelian randomisation study. Lancet. 2012;380(9841):572-580. DOI: 10.1016/S0140-6736(12)60312-2. PMID: 22607825. PMCID: PMC3419820
- AIM-HIGH Investigators; Boden WE, Probstfield JL, Anderson T, et al. Niacin in patients with low HDL cholesterol levels receiving intensive statin therapy. New England Journal of Medicine. 2011;365(24):2255-2267. DOI: 10.1056/NEJMoa1107579. PMID: 22085343
- HPS3/TIMI55-REVEAL Collaborative Group; Bowman L, Hopewell JC, Chen F, et al. Effects of Anacetrapib in Patients with Atherosclerotic Vascular Disease. New England Journal of Medicine. 2017;377(13):1217-1227. DOI: 10.1056/NEJMoa1706444. PMID: 28847206
- Ference BA, Ginsberg HN, Graham I, et al. Low-density lipoproteins cause atherosclerotic cardiovascular disease. 1. Evidence from genetic, epidemiologic, and clinical studies. A consensus statement from the European Atherosclerosis Society Consensus Panel. European Heart Journal. 2017;38(32):2459-2472. DOI: 10.1093/eurheartj/ehx144. PMID: 28444290. PMCID: PMC5837225
- Cholesterol Treatment Trialists' (CTT) Collaborators; Mihaylova B, Emberson J, Blackwell L, et al. The effects of lowering LDL cholesterol with statin therapy in people at low risk of vascular disease: meta-analysis of individual data from 27 randomised trials. Lancet. 2012;380(9841):581-590. DOI: 10.1016/S0140-6736(12)60367-5. PMID: 22607822. PMCID: PMC3437972