I have high cholesterol: is it really dangerous, or is it true that people with high cholesterol live longer?

First: cholesterol is not a poison

Cholesterol is absolutely necessary for our body. It forms part of cell membranes, participates in the synthesis of steroid hormones, vitamin D and bile acids, and plays numerous biological functions.

Therefore, the goal of medicine has never been to 'eliminate cholesterol'. The problem is a different one.

When there is sufficiently high and prolonged exposure to ApoB-containing lipoproteins, particularly LDL, these particles can penetrate and become retained in the arterial wall, initiating and fuelling the atherosclerosis process. And here the scientific evidence is extraordinarily robust.

We must therefore avoid two extremes: neither demonising cholesterol, nor denying that an excess of atherogenic particles increases cardiovascular risk.

So why do studies exist in which older people with high cholesterol appear to live longer?

This is probably the most interesting part. Some observational studies conducted in elderly populations have found associations between low cholesterol levels and higher mortality. At first glance we might conclude: 'The more cholesterol, the longer we live.'

But here a very important epidemiological phenomenon appears: reverse causality. Imagine a person who develops cancer, a chronic inflammatory disease, advanced frailty or malnutrition. As a consequence of that illness, they may lose weight and see their cholesterol fall. They subsequently die.

If we look only at the data, we find: low cholesterol → higher mortality. But this does not prove that having low cholesterol caused their death. The opposite may have occurred: the disease caused the cholesterol to drop. This distinction is fundamental.

Survivor bias

There is also another very interesting phenomenon. Suppose we study 85-year-olds with elevated LDL. By definition, we are studying people who have managed to reach the age of 85.

Some may possess genetic, metabolic or environmental characteristics that have partially protected them from the cardiovascular consequences of that exposure. Meanwhile, some of the individuals who are particularly susceptible to significant hypercholesterolaemia may have suffered a heart attack, a stroke or another cardiovascular event decades earlier.

Therefore, when we study exclusively those who have reached very advanced ages, we may introduce what we call survival bias. It does not mean that all older people with elevated cholesterol are genetically protected; it means we must be very careful when extrapolating the associations found among survivors to the population as a whole.

Confounding bias also exists

Something else happens in older people. Those with low cholesterol may also be those with greater frailty, weight loss, chronic diseases, inflammation or malnutrition. Although studies try to adjust statistically for these factors, it is not always possible to eliminate them completely.

That is why observational studies must be interpreted within the broader body of scientific evidence. And when we combine epidemiology, genetics, Mendelian randomization studies, and clinical trials, the current conclusion is consistent: cumulative exposure to atherogenic LDL particles plays a causal role in atherosclerosis.

"But doctor, the brain needs cholesterol"

Correct. The brain needs a great deal of cholesterol. But here too we must contextualize the statement. The central nervous system has a largely autonomous cholesterol metabolism, and much of the brain's cholesterol is synthesized locally.

Therefore, simply saying 'if I lower my blood LDL, my brain will run out of cholesterol' does not accurately represent our physiology.

So, is looking at total cholesterol enough?

No. And this is where cardiovascular medicine has become much more interesting. Total cholesterol can provide information, but to properly assess a patient we need to know at least their lipid profile and, above all, interpret those results within the context of their overall cardiovascular risk.

LDL-C remains extremely important and continues to be one of our primary therapeutic targets. But there are other markers that, in certain patients, can provide us with additional information.

ApoB: how many atherogenic particles are circulating?

One of the measurements I find particularly interesting is apolipoprotein B, or ApoB. Each atherogenic particle — including LDL and other ApoB-containing lipoproteins — carries essentially one ApoB molecule. That is why its concentration gives us an estimate of the total number of circulating atherogenic particles.

This can be especially useful when there is a discordance between LDL-C and particle number, something we may observe, for example, in people with elevated triglycerides, diabetes, or certain metabolic disorders. In many cases, knowing ApoB provides more practically useful clinical information than obsessing over whether LDL particles are simply 'large' or 'small'.

Lipoprotein(a): a test we should know about

Lipoprotein(a), or Lp(a), deserves special attention. It is a lipoprotein whose level is largely genetically determined and constitutes an independent causal risk factor for cardiovascular disease. Current recommendations advise measuring it at least once in adult life.

Why? Because you may have an excellent diet, exercise regularly, not smoke, and yet have a very high Lp(a) due primarily to your genetics. Knowing it can change our interpretation of risk and lead us to be more stringent about controlling the remaining cardiovascular risk factors.

And what about triglycerides and HDL?

They also provide information. Elevated triglycerides can reflect metabolic disturbances and the presence of atherogenic remnant lipoproteins. Low HDL can accompany certain risk profiles, but today we know that the interpretation is far more complex than simply 'high HDL = good, high LDL = bad'. Current cardiovascular medicine should no longer be reduced to two numbers.

Metabolic health matters enormously

When I assess a person's cardiovascular risk, I don't want to know only their cholesterol. I also want to know: do they smoke? What is their blood pressure? Do they have diabetes or prediabetes? What are their glucose and glycated haemoglobin levels? Do they have abdominal obesity? What are their triglycerides? Is there kidney disease? Is there a family history of heart attack or early stroke? What is their Lp(a)? How much exercise do they do? How old are they? Have they already had a cardiovascular event?

Because an LDL of 150 mg/dL does not mean exactly the same thing in every person. The absolute risk of a healthy young person with no other risk factors is not identical to that of a 65-year-old with diabetes, hypertension, smoking and kidney disease. But that does not make the young person's LDL irrelevant either: cumulative exposure over decades matters too.

And we can go even further: looking directly at the arteries

In certain patients where there is uncertainty about risk or about the need to start treatment, we can use additional tools. One of the most interesting is the coronary artery calcium score (CAC) obtained by computed tomography.

In appropriately selected patients, it allows us to detect and quantify calcification in the coronary arteries and can help us reclassify cardiovascular risk. In other words, we move from estimating risk factors alone to obtaining information about the presence of subclinical atherosclerosis. It is not a test that everyone needs, but in the right patient it can be extraordinarily useful.

So, doctor, what should I do if my cholesterol is high?

The first thing is not to panic. But don't ignore it either because you have watched a video claiming that 'high cholesterol is protective'. The full context must be examined.

We should assess LDL-C, non-HDL cholesterol, triglycerides and HDL, and where indicated we can add ApoB and Lp(a). We must then integrate that data with age, blood pressure, smoking, diabetes, kidney function, family history, diet, physical activity and overall cardiovascular risk.

And in certain cases we can turn to the coronary artery calcium score to refine the decision even further. Only then do we decide whether lifestyle modification alone is sufficient or whether there is also an indication for pharmacological treatment.

Cholesterol is not our enemy. But some of the particles that carry it play a direct role in the development of atherosclerosis when we remain exposed to them in excessive amounts for long enough. That is why we must avoid falling into either the old oversimplification of thinking that 'all cholesterol is bad', or the new internet oversimplification of claiming that 'a high LDL doesn't matter'. Modern medicine means understanding what risk that specific person faces, how long they have been exposed, and what other factors are acting simultaneously. Because we are not treating a number on a lab report: we are treating a person and their cardiovascular risk across an entire lifetime.