Let's stop talking about "good" and "bad" cholesterol!

It’s not that we were “wrong,” but things change, and we must follow the science even if it challenges some of our certainties; it’s always been that way, and “good cholesterol” isn’t always good!
This marks the end of a myth: we need to stop talking about “good cholesterol.”
For years, HDL cholesterol was labeled “good cholesterol,” and we were told that the higher the HDL cholesterol, the better.

A simple and reassuring idea:
HDL cholesterol has long reassured both doctors and patients
The higher it was, the more protected we thought we were. Today, science is clear:
this view is not only outdated, but potentially misleading.
Here’s why the “good cholesterol” dogma is crumbling, as it has been widely challenged by scientific data.

What recent studies show:
Increasing HDL cholesterol does not protect:
If HDL cholesterol were truly protective, increasing it with medication should reduce heart attacks. Yet in studies where HDL cholesterol levels were raised with medications—fibrates and cholesterol ester transfer protein (CETP) inhibitors (the latter resulting in a 100% increase, or double the level)—this did not reduce cardiovascular events.
All failed to demonstrate a benefit, even in diabetic patients.
Even the injection of a specific HDL cholesterol has not proven effective.
HDL cholesterol is a marker, not necessarily an effective therapeutic target.

Why, then, was it believed that HDL could be “good cholesterol”?
This stems from the initial epidemiological studies, which were actually highly flawed (they used statistical tests that we now know increase the likelihood of observing a so-called “significant” result).
The first and most famous is the Framingham study (a town in the northeastern United States) published in 1977, which served as a benchmark for decades. It analyzed data from only 2,815 patients, whom it divided into 14 subgroups based on their initial HDL cholesterol levels, and recorded only 142 coronary events.
In its findings, it did not account for other clinical events.
Due to the small population included in this cohort, there were very few patients with very high cholesterol, and thus the number of clinical events in this subgroup was also very low.
In 2016, the results of the CANHEART study were published, which involved nearly 60,000 people. The number of patients with HDL cholesterol levels above 0.9 g/L was 17,944—more than six times the number of patients analyzed in the Framingham study in this subgroup alone. Similarly, there were a total of 17,952 deaths, including 4,658 from cardiovascular causes. When plotting a graph of HDL cholesterol levels against cardiovascular events, a U-shaped relationship is observed: low HDL cholesterol values correspond to an increased risk, but so do high values. HDL cholesterol levels > 0.8 g/L were associated with an increase in cardiovascular and overall mortality. These results thus formally contradict the notion that high HDL cholesterol levels guarantee cardiovascular protection. It has, however, been demonstrated—and this has never been questioned—that low HDL cholesterol levels are linked to an increased cardiovascular risk.
In reality, there are several categories or subtypes of HDL cholesterol, and certain small particles resemble LDL cholesterol in their function, and above all increase overall cardiovascular risk.

We can no longer feel reassured by high HDL cholesterol:
Contrary to popular belief, very high levels are associated with increased overall mortality, cardiovascular mortality, and even the risk of cancer or dementia.
On the other hand, a decrease in HDL cholesterol remains an indisputable risk factor.
We must now view the issue from a different perspective and interpret the values as follows:
Low HDL cholesterol: < 0.4 g/L: Increased cardiovascular risk
Moderate HDL cholesterol: 0.4 to 0.6 g/L: Minimal risk zone.
High HDL cholesterol: > 0.8 g/L: High cardiovascular risk
What this means in practice:
We can no longer rejoice in a very high HDL cholesterol level, thinking that it “offsets” elevated LDL cholesterol. This very high level does not provide protection.
Statin treatment should not be reduced simply because HDL cholesterol is high.
When faced with low HDL cholesterol, the priority remains drastically lowering LDL cholesterol.
Very high HDL cholesterol should be considered an indicator of potential risk, often linked to other factors (genetics, sedentary lifestyle, alcohol consumption).
It is necessary to examine LDL cholesterol, assess all risk factors, and evaluate the level of risk that determines the target LDL value in order to tailor treatment to the individual.

In conclusion
The term "good cholesterol" is an oversimplification that we must abandon.
The priority remains the management of LDL cholesterol and overall risk.