Most physicians order what he considers the wrong test to gauge heart disease risk: a standard cholesterol readout, which may indicate levels of low-density lipoprotein or non-high density lipoprotein cholesterol.
“Many lines of evidence say there’s not a lot more predictive power of apoB over LDL cholesterol,” says cholesterol researcher Scott Grundy of the University of Texas Southwestern Medical Center in Dallas, who has helped craft several sets of cardiology care guidelines.
Total cholesterol level was the first widely used indicator of this risk, but after researchers discovered that one form of cholesterol, HDL, may be protective, LDL cholesterol became the benchmark.
Now, some physicians favor non-HDL cholesterol, which encompasses multiple cholesterol types, including LDL and VLDL. All of these measures reveal the amount of lipid in the blood, rather than the number of cholesterol-hauling particles.
At the same time, some people taking drugs for what seem to be dangerously high LDL cholesterol levels may not need treatment, Sniderman says.
In a study in The Journal of the American Medical Association in September, he and his colleagues dissected the impact of variants of two genes involved in cholesterol metabolism: CETP and HMGCR. Using data from more than 100,000 patients, the researchers found that people with sluggish versions of the enzyme encoded by CETP showed equivalent reductions in apoB and LDL cholesterol levels and were less likely than people with vigorous versions of the enzyme to suffer cardiovascular crises such as heart attacks or strokes.
LDL cholesterol is deeply entrenched in medical routines, and “It’s not going to change any time soon,” Rader says.