Your cholesterol is high: do you really need to start a statin right away?

Let's start with something fundamental: cholesterol is not a poison

We have so strongly associated the word 'cholesterol' with cardiovascular disease that many people think of it as a toxic substance the body should ideally get rid of. That is wrong. We need cholesterol to live.

It contributes to the structure of our cell membranes, plays a role in the synthesis of steroid hormones, is necessary for the production of bile acids, participates indirectly in the vitamin D synthesis pathway, and plays a particularly important role in the nervous system. Our body actually produces it on its own, and the liver is at the centre of its synthesis, recycling and elimination.

From this, a first essential idea: having cholesterol is normal. The cardiovascular problem is not the existence of cholesterol, but above all the quantity and the duration of our arteries' exposure to certain particles that carry it.

Because cholesterol does not travel alone

Cholesterol is a lipid molecule: it cannot circulate freely in blood, which is essentially composed of water. To transport lipids, the body uses specialised particles called lipoproteins. You probably know two of them: LDL and HDL.

But saying 'I have good and bad cholesterol' is an oversimplification. LDL is not a cholesterol molecule: it is a particle that, among other things, carries cholesterol. And when too large a number of atherogenic particles — those containing a protein called ApoB — circulate for years, some can penetrate the arterial wall. That is where an essential part of the atherosclerosis process begins.

Atherosclerosis does not begin on the day of your heart attack

It can progress silently for decades. ApoB-containing particles penetrate the arterial wall and become trapped there; a local inflammatory response develops; and gradually an atherosclerotic plaque forms, which can grow for years without causing the slightest symptom.

Then, under certain circumstances, a plaque becomes unstable, ruptures and triggers the formation of a clot. If this occurs in a coronary artery, it is a myocardial infarction; in certain cerebral arteries, it is a stroke.

This is why we take LDL and other atherogenic lipoproteins seriously. Not because cholesterol is a waste product, but because cumulative exposure to these particles directly contributes to cardiovascular disease.

So why is your LDL elevated?

An excellent question. And the answer is not always 'you eat too much fat'. Several mechanisms are possible, and they often combine.

Genetics, first

It is extremely important. Some people naturally have much higher LDL concentrations. In familial hypercholesterolaemia, for example, the system responsible for removing LDL particles from the circulation works less efficiently, and LDL can be very high from a very young age. In this context, diet and exercise remain essential… but they are not always enough.

Diet, next

Saturated fats raise LDL in many people, even though the response varies greatly from one individual to another; soluble fibre, on the other hand, can help bring it down. But diet also influences triglycerides, insulin sensitivity, visceral fat, weight, blood pressure, and ultimately the overall cardiovascular risk. That is why I refuse to reduce nutrition to 'eat less cholesterol': the physiology is far more complex than that.

And insulin?

This is where the narrative you may have heard on social media deserves some nuance. Insulin resistance can profoundly alter lipid metabolism: we frequently observe a profile of elevated triglycerides, low HDL, an increase in triglyceride-rich lipoproteins, and often changes in LDL particles. This profile often accompanies abdominal obesity, metabolic fatty liver disease, prediabetes, and type 2 diabetes.

But this does not mean that 'high LDL = high insulin'. A lean, athletic person who is insulin-sensitive can have high LDL for predominantly genetic reasons; and another person may present with significant insulin resistance and an LDL that, on paper, does not appear impressive. Once again: you have to look at the whole picture.

And the liver?

The liver is at the centre of lipid metabolism: it produces, transforms, recycles, and eliminates many lipids and lipoproteins. Metabolic fatty liver disease can therefore be accompanied by abnormalities in the lipid panel. But beware of the oversimplification: a high cholesterol level does not mean your liver is 'overloaded', and not every patient with high LDL automatically needs a liver ultrasound.

On the other hand, in the presence of abdominal overweight, elevated triglycerides, diabetes or prediabetes, abnormal liver enzymes, significant alcohol consumption, or other risk factors, assessing liver health can become particularly relevant.

Before treating a number, let us look at the patient

This is probably the message I feel most strongly about. Two people can have exactly the same LDL and not face the same cardiovascular risk.

Imagine an LDL of 150 mg/dL in two people. The first is 35 years old, does not smoke, has normal blood pressure, is not diabetic, and has no family history of early cardiovascular disease. The second is 62 years old, smokes, has hypertension, is diabetic, and their father had a heart attack at 48. The number is identical. The risk, absolutely not. That is why the decision to treat must never rest solely on total cholesterol.

What should we look at in a modern lipid risk assessment?

The standard panel includes total cholesterol, LDL cholesterol, HDL cholesterol, and triglycerides. But in certain situations, we can go further.

ApoB: how many atherogenic particles are actually circulating?

Apolipoprotein B, or ApoB, is particularly interesting because each atherogenic particle contains one molecule of it. Measuring it therefore gives us a good approximation of the number of atherogenic particles in circulation. Why is this useful? Because two people can have a similar amount of LDL cholesterol but a different particle count — and in certain metabolic situations, particularly when triglycerides are elevated, this information can change everything.

What about lipoprotein(a)?

Here is a parameter we still talk about far too little. Lp(a) is a particle determined primarily by genetics: some people have very little of it, others a great deal, and an elevated concentration represents an independent cardiovascular risk factor.

What is striking is that diet and exercise modify it relatively little. You can therefore have an excellent lifestyle and still have an elevated Lp(a). This is precisely why current guidelines increasingly insist on measuring it at least once in adult life. Sometimes, knowing your risk begins with knowing your lipid genetics.

And triglycerides?

They provide yet another piece of information. Elevated triglycerides can be linked to excess caloric intake, alcohol, a diet high in refined carbohydrates, insulin resistance, poorly controlled diabetes, abdominal excess weight, certain medical conditions, or certain medications. That is why I always look at the lipid panel as a whole: LDL, HDL, triglycerides, non-HDL cholesterol, and — when it genuinely adds something — ApoB and Lp(a).

Should we also look at blood glucose?

In many patients, yes, because cardiovascular risk and metabolic health are intimately linked. Depending on the context, we may look at fasting blood glucose, HbA1c, and sometimes other metabolic parameters when they are clinically justified. But here again, there is no list of twenty tests that everyone should order: medicine is about choosing the investigations that answer a real clinical question.

And now, let's talk about statins

Statins are arguably among the most criticized medications on the internet. And yet, they are also among the most thoroughly studied cardiovascular drugs. How do they work? They inhibit a liver enzyme, HMG-CoA reductase, which is involved in cholesterol synthesis.

But the story does not stop there. In response, the liver increases the number of receptors capable of retrieving LDL particles present in the blood. The result: circulating LDL decreases. And most importantly, in people who need them, reducing exposure to atherogenic particles reduces the risk of cardiovascular events.

So, are statins bad?

No. But they should not be prescribed mechanically either, without assessing the context. In a person who has already had a heart attack or a stroke of atherosclerotic origin, or whose risk is very high, bringing LDL down significantly can be decisive. And in some people with severe or familial hypercholesterolaemia, waiting solely for the effects of diet can unnecessarily expose the arteries for years. In these situations, medication does not replace prevention: it is part of it.

But a statin should never become an excuse to neglect everything else

And that is where I agree with part of the prevailing discourse. If you are taking a statin but you smoke, sleep five hours a night, are completely sedentary, have visceral obesity, uncontrolled hypertension, drink a lot of alcohol, have poorly managed diabetes and eat mainly ultra-processed foods… your LDL may look wonderful on the blood test, but your cardiovascular risk has certainly not disappeared. A statin addresses part of the risk; on its own, it does not transform a diseased metabolism into a healthy one.

Do statins have side effects?

Yes, like all medications. Muscle symptoms are among the most frequently reported: pain, cramps or a feeling of weakness. Serious muscle complications, however, are much rarer. There is also a slight increase in the risk of developing diabetes in certain predisposed individuals, especially with the most intensive treatments — but this must be weighed against the expected cardiovascular benefit.

What about memory?

The available data do not show that statins, overall, cause cognitive decline or dementia. We must therefore not turn an effect reported by one isolated individual into a general rule.

If you experience side effects, do not stop your treatment on your own

This is very important, because several options exist: adjusting the dose, switching to a different statin, modifying the dosing schedule in certain situations, looking for another cause of the symptoms, or using other lipid-lowering treatments when necessary. An intolerance to one statin does not mean there are no solutions. But the decision is made with your doctor, not on your own.

And what about diet in all of this?

It remains fundamental, with or without medication. I favour a diet rich in vegetables, whole fruits, legumes, soluble fibre, fish, nuts, olive oil and minimally processed foods. Soluble fibre is particularly valuable because it helps eliminate bile acids, which can contribute to lowering LDL.

Regular physical activity is equally fundamental: strength training, daily walking, blood pressure control, sleep, smoking cessation and reduction of excess visceral fat where it exists.

Should sugar, fructose and carbohydrates be eliminated completely?

No, and I would not give that advice universally. Fruit naturally contains fructose and can perfectly well be part of a cardioprotective diet; legumes and whole grains contain carbohydrates. The real problem is excess: sugary drinks, added sugars, ultra-processed foods, refined carbohydrates and liquid calories. Alcohol also deserves particular attention, especially when triglycerides are elevated or in the presence of hepatic steatosis. Once again: the quality of the diet matters far more than waging war on a single isolated nutrient.

Can we try three months of lifestyle changes before a statin?

Sometimes yes, sometimes no. And that is precisely why the subject cannot be squeezed into a thirty-second video. In a low-risk person with no cardiovascular disease and a moderate LDL elevation, an intensive lifestyle intervention followed by reassessment can be perfectly reasonable. In a high-risk patient who already has cardiovascular disease, severe hypercholesterolaemia, or certain specific situations, waiting can on the contrary be a poor strategy. Treatment depends on risk, not on the number alone.

What if we are still undecided?

In certain primary prevention situations where the decision remains uncertain, other tools exist. One of them is the coronary calcium score, performed by CT scan: it detects and quantifies calcium in the coronary arteries, a marker of already-present atherosclerosis. It is not necessary for everyone, but in carefully selected patients it can help both the physician and the patient reach a more personalised decision. This too is modern medicine: not treating a blood test result, but estimating the real risk of the person sitting in front of us.

Key takeaways

Cholesterol is not a waste product: it is essential to life. But that does not mean that a high level of LDL particles is without consequence. Both things are true at the same time: we need cholesterol, and prolonged excessive exposure to ApoB-containing particles promotes atherosclerosis.

So, when faced with an abnormal lipid panel, I want to understand the full picture: what are your LDL, triglycerides, HDL, and non-HDL cholesterol levels? Would an ApoB measurement add anything? Do we know your Lp(a)? Do you smoke? What is your blood pressure? Are you diabetic? Is there insulin resistance or hepatic steatosis when suspected? What is your family history, your diet, your physical activity? And above all: what is your overall cardiovascular risk?

Only then does the question of treatment arise. Sometimes lifestyle measures will be front and centre; sometimes medication will be necessary; and very often, we will need both.

I am Dr Florian Vallecillo, and if I could leave you with a single idea today, it would be this: never treat a number in isolation, but never dismiss a risk factor simply because there is a metabolic explanation behind it. Good medicine does not pit medications against lifestyle: it looks for root causes, assesses risk, corrects the underlying terrain, and uses treatments that have demonstrated real patient protection when those treatments are needed.