There’s No Such Thing As ‘Good Cholesterol’ Says Pivotal New Study

There’s No Such Thing As ‘Good Cholesterol’ Says Pivotal New Study

A surprising new genetic study shows that some people with naturally high levels of HDL cholesterol — the supposedly good kind of cholesterol — are at increased risk of a heart attack. Doctors are now further questioning the use of drugs to boost HDL levels while looking to new therapies to reduce heart risk. For decades we’ve been told to avoid foods high in LDL cholesterol (such as butter, bacon, lard and palm oil) and to eat foods that raise HDL cholesterol (such as nuts, fish, olive oil and avocados). The truth, it now seems, is far more complicated than that. A Cambridge University study published in Science shows that, for a certain segment of the population, the good kind of cholesterol actually increases their risk of coronary heart disease.

This new study can be added to the mounting pile of scientific evidence showing that the causal link between heart disease and cholesterol — a waxy, fat-like substance that performs literally thousands of bodily functions — is a weak one, and there are other important health factors to consider. What’s more, this finding could further dissuade researchers from using HDL-raising drugs (such as Torcetrapib) to treat heart disease. As clinical trials have repeatedly shown, these drugs simply don’t work as prescribed.

For the study, the researchers studied nearly a thousand individuals with a mutation in a gene called SCARB1. This genetic glitch affects about one in every 1700 individuals, and it actually raises their levels of good cholesterol. So in theory these folks should be naturally well-equipped to stave off heart disease. But according to the new research, they actually had an 80 per cent increased risk of heart disease. That’s the same kind of heart risk associated with smoking!

“We found that people carrying a rare genetic mutation causing higher levels of the so-called ‘good’ HDL-cholesterol are, unexpectedly, at greater risk of heart disease,” noted lead researcher Adam Butterworth in a statement. Speaking to the BBC, he said this discovery “challenges our conventional wisdom about whether ‘good’ cholesterol is protecting people from heart disease or not”.

Coronary heart disease is the single leading cause of death in Australia, killing 54 Australians every day. It’s caused by the buildup of fatty material, or plaque, in the coronary artery walls. When enough of this plaque accumulates in the vessel walls, it restricts blood flow to the heart, increasing risk of a heart attack.

Butterworth says these new findings suggest that the way in which HDL is handled in the body is more important than determining the risk of a heart attack based on HDL levels in the blood. At the same time, he says the new discovery “could lead to new drugs that improve the processing of HDL-C to prevent devastating heart attacks”.

For some doctors, including University of Sheffield cardiologist Tim Chico (who wasn’t involved in the study), this new research doesn’t come as a surprise.

“Although there are drugs that can increase HDL levels, these do not reduce the risk of heart disease. These drugs are niacin, which is rarely used, and CETP inhibitors which have only been used in experimental studies and are not used in routine practice,” he said. “Statins reduced ‘bad’ cholesterol, and are clearly beneficial in people with existing or high risk of heart disease.”

Importantly, Chico says that the current study doesn’t alter any of the recommendations for who should receive treatment with statins or other drugs, and that exercise both increases HDL and reduces risk of heart disease.

So while doctors are questioning the practice of boosting levels of HDL cholesterol, they still feel it’s an important measure for predicting heart attack risk. And as for the claim that there’s such a thing as “good cholesterol”, this term would now appear to be destined for the dustbins of medical history.


Salmon and avocados raise “good levels” of cholesterol. Image: Alpha/Flickr/CC BY-2.0