Prof Børge Nordestgaard is a clinician and scientist in the Department of Clinical Medicine at the University of Copenhagen, in Denmark.
He’s spent his career studying cholesterol and heart disease, and was awarded the 2020 Marie and August Krogh Prize in recognition of his research.
I’ve been fighting cholesterol for 40 years in the lab and in the clinic. As a young doctor in my own country, Denmark, and in the UK, I saw people die from cholesterol problems and heart disease all the time.
And while things have got better here, the wider problem hasn’t gone away.
Increased awareness of cholesterol problems has led to changes in Europe and the US, at least. In some Scandinavian countries, we’ve made efforts to cut down our saturated fat intake, for example, by reducing how much meat and dairy we eat.
In Denmark, we’ve even banned the harmful trans fats that are widespread in processed foods. Cholesterol – at the population level – has gone down, as it has in the US.
Worldwide, though, heart disease still kills more people than any other disease. And now it’s increasing in developing countries too, thanks to the adoption of Western diets.
In parts of Asia and Africa, infectious diseases used to be the main problem. Now, it’s non-infectious diseases like heart disease.
For the next few decades, we can count on seeing more of the same. The number one killer will be atherosclerotic cardiovascular diseases – in other words, heart attack and stroke.
So, despite 40 years in this research field, I feel there’s still a lot of work to do – but I’m determined to do it.
As someone who was brought up in the culture of the Lutheran faith that’s common in Denmark, I was taught not to focus on my own ego but to do something for society. And I still believe in that.
As well as my work as a researcher, that also means communicating with politicians and ordinary people. Because it’s so simple to prevent atherosclerotic cardiovascular diseases, but it’s not being done.
So, from my career studying cholesterol and treating heart disease, here’s what I think you need to know, in six simple lessons.
1. Stop thinking about cholesterol as 'good' and 'bad'
Cholesterol is just a normal fat. It’s what gives the colour to egg yolks. In the body, we use it for building membranes around cells, and it’s used to make steroid hormones like oestrogen and testosterone.
There’s also a lot of cholesterol in our brains. But we don’t need to get cholesterol from our diets because our own bodies make it, in our liver cells.
The problem with cholesterol is that we don’t have any enzymes in the body that can break it down. We can eat it and take it up, but if it gets into the artery wall, it gets stuck there.
That’s when you get what’s called ‘atherosclerosis’ – narrowing of your arteries caused by cholesterol and other substances blocking them.
The most important type of cholesterol – the one we all know about – is low-density lipoprotein (LDL) cholesterol. We often refer to LDL as ‘bad cholesterol’. But while LDL cholesterol is bad, I would say that there’s no such thing as ‘good’ cholesterol.
The whole concept that the smaller, high-density lipoprotein (HDL) cholesterol is ‘good’ is a misinterpretation of the data. In fact, HDL cholesterol is just neutral – it doesn’t harm us, but it doesn’t really help us either.
What most people don’t realise is that there are other types of cholesterol too. So, a better way to think about it is that if you discount HDL cholesterol, the other types are bad.
And if you have too much of these other types of cholesterol, it causes atherosclerosis and cardiovascular disease.
2. There's another category of cholesterol you've never heard of – and it might be the worst
Even up until a couple of decades ago, the focus was still on HDL and LDL cholesterol. We weren’t looking at what the rest of the cholesterol was like. But, in fact, there are a whole load of other particles – particles bigger than LDL.
In my own research, I call this ‘remnant cholesterol’, because it’s what remains after you take away HDL and LDL. And this remnant cholesterol could be even more harmful when it comes to atherosclerotic cardiovascular diseases.
The evidence now suggests that the cholesterol content of these remnant particles is higher than LDL. What’s more, besides cholesterol, they also contain triglycerides – another type of blood fat that raises your risk of heart disease.
Most people have the LDL problem. But if you become overweight and obese – something that affects more and more of us – then you certainly have the remnant cholesterol problem too.
Thankfully, we do have drugs that are now being tested specifically for reducing remnant cholesterol – including drugs like statins that are already widely used.
Within the last year, we’ve seen studies being published on six different drugs that can bring down remnant cholesterol by at least half.
Partly through my own research, remnant cholesterol is now on the radar of many more researchers and clinicians. But in health guidelines, LDL and remnant cholesterol are often lumped together as ‘non-HDL cholesterol’.
It’s not as simple as that – everyone needs to understand that ‘bad’ isn’t just about LDL. There’s this whole different category that is equally, or even more, dangerous.
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3. Cholesterol isn't associated with heart disease – it causes it
As scientists, we’re always refining our understanding of cholesterol and its impacts, but we can’t – and shouldn’t – forget the basic fact that cholesterol causes heart disease.
The link between cholesterol and atherosclerosis (and heart disease) is extremely well-understood.
It all started with a Russian scientist called Prof Nikolai Anichkov, who conducted a study over 100 years ago where he fed cholesterol to rabbits and they got atherosclerosis, like humans.
We now know that when you have these particles – either LDL or remnants – they cannot penetrate the artery walls. They are too large, so they get stuck there.
And then, like if you get a thorn stuck in your skin, you get some inflammation around it. The same thing happens on the inside of your arteries.
Initially, immune cells called macrophages arrive and try to eat the cholesterol, but they can’t digest it or take it away. So they overeat and die at the scene.
As these atherosclerotic ‘plaques’ start to form, you can see these very fat, cholesterol-filled macrophages on the surface of the plaques.
Once formed, these plaques, which are mostly just cholesterol, can rupture and cause a blood clot. This is what stops the blood from going to the heart, or to the brain, and can cause a heart attack or a stroke.
These processes are so well-understood. But, of course, because heart disease is the disease that kills the most people, some researchers keep studying and refining our understanding of it.
One aspect that is still not so well-understood, for example, is the inflammation part. It’s thought that once people have severe atherosclerosis, they might also benefit from anti-inflammatory drugs.
But I’m more concerned with prevention, and I think we shouldn’t lose focus on cholesterol. After all, that’s what causes atherosclerosis in the first place.
Over the years, new findings from scientific trials have meant that cholesterol targets in health guidelines have also changed.
Today, there are different cut-off points for cholesterol levels depending on your heart disease risk. If you are otherwise healthy, then the cut-off is 3.0 mmol/L or 115 mg/dL.
However, if you already have heart disease, stroke or severe diabetes, then you should be worried if your LDL cholesterol is above 1.4 mmol/L or 55 mg/dL.
4. Eat as if you were trying to prevent global warming
There is a surefire way to reduce your cholesterol, and that’s to eat less saturated and trans fats. These fats affect your liver function and stop it from clearing cholesterol, so more stays in the blood.
On a day-to-day basis, what this means is that you need to think more about what’s in something before you eat it. If it’s from a plant, it won’t contain any saturated fat, so it’s safe to eat (most of the time). But if it’s from an animal, then you’d better investigate further.
Of course, it’s not always that straightforward. Not all plants are safe – coconut oil and palm oil, for example, are full of saturated fats. Besides, they’re both linked to deforestation to make space for their huge crops.
Generally speaking, though, you can eat as many wholefood plants as you like. And the bonus is that producing them puts less carbon in the atmosphere than farming animals.
In fact, the best advice I can give for bringing down cholesterol is to eat the way you would to prevent global warming.
It’s not about cutting out things altogether. If you do want to eat meat and fish, then South Asian-style meals are healthier – small strips mixed together with noodles or rice. But that’s not an excuse to leave out that extra serving of vegetables!
As for exercise, it doesn’t directly affect cholesterol. It does bring down triglycerides, and if you exercise a lot, you’ll likely become slim, meaning your remnant cholesterol will go down.
But it’s diet we need to focus on for reducing overall cholesterol levels and heart disease risk.
The basic principle is simple: everything in moderation. Personally, I’ve never smoked, I try to keep my weight down, and I eat healthily.
I try to eat a lot of plant food, but I’m not a vegetarian – I eat fish too. I also walk whenever I can and cycle to work every day.
5. If you're recommended statins, take them
Nothing that we can do to prevent diseases in adulthood works as well as statins. They bring down LDL cholesterol. They reduce heart attacks and strokes. And, ultimately, they help people live longer.
Scientifically, the benefits of statins are beyond doubt. By now, the mechanism behind these benefits is very well-understood.
I’ve been taking the maximum dosage myself since I turned 50, and I plan to take them for the rest of my life. It’s the best gift you can give yourself when you get to a certain age – 50 for men and 55 for women.
You might have heard that statins have side effects. But as someone who is used to looking at medical literature, there’s no drug I’ve ever read about that has fewer side effects than statins – despite what’s been (wrongly) claimed by some journalists.
Unfortunately, some media outlets realised that, because so many people take statins (in Denmark, the figure is around 15 per cent of those above 40), it’s easy enough to find one person to say they have side effects.
And, if you put that on the front page of a newspaper, then a lot of people will buy it. These kinds of headlines were written simply for commercial reasons, and they’re nothing but fake news.
In fact, statins have far fewer side effects than the drugs we previously prescribed. Back when I worked in cholesterol clinics, we didn’t have statins. So, in consultations with patients who had cholesterol problems, we were always having to discuss side effects and how to avoid them.
And then along came statins. We stopped giving people the other drugs and put everyone on statins, and then nobody talked about side effects anymore.
That doesn’t mean that when a patient comes to me and claims they have side effects that I don’t take them seriously. But I do explain to them that it might just be their perception from what they’ve read in the newspapers.
We have good evidence showing that only around 15 in 10,000 people get muscle aches (myalgia) or feel a little tired. And far fewer, perhaps 1 in 100,000, get serious problems. Severe side effects from statins are extremely rare.
6. High cholesterol can be genetic
Poor diet is not the only reason for high cholesterol. Some people have a genetic cause, which makes it harder for them to keep their cholesterol levels low and can lead to early heart attack and stroke.
Familial ‘hypercholesterolemia’ (FH) – meaning, literally, high cholesterol – is one such genetic cause. FH affects about 1 in 250 people, and it’s due to a genetic fault that makes your liver less able to remove cholesterol from your blood.
High lipoprotein(a), known as Lp(a), is even more common – it affects 1 in 5 people. Lp(a) is a fourth type of particle containing cholesterol – so in addition to HDL, LDL and remnant cholesterol, you have Lp(a).
Although we don’t know everything about Lp(a) yet, we know that humans aren’t the only animals that have it. Hedgehogs do too, which suggests it developed twice during evolution and means it probably has some useful function, like stopping bleeding during childbirth.
For those with atherosclerosis, however, it’s likely involved in making blood clots bigger.
Both FH and Lp(a) need to be diagnosed and treated. Thankfully, that’s now becoming easier.
In the EU, there’s now a full plan – the Safe Hearts Plan published in December 2025 – saying that we should screen for both of these genetic cholesterol conditions early in life.
That’s very sensible – and what’s more, the European Commission is aiming to provide specific advice about how to implement it in all countries.
Screening costs very little, and some countries are doing this already.
Slovenia, for example, does childhood screening for FH. The Netherlands and Norway have been very good at finding people with FH too. And in Denmark, I was part of convincing politicians to give money to find FH.
If these programmes are successful, within 10 years we should have found everyone with FH. Next, we need to find all those with high Lp(a).
Once a genetic condition is identified, we can offer advice on healthy lifestyles, but also treatment with statins or other drugs.
Right now, there are at least five different randomised trials with Lp(a) drugs underway. And there are already ‘gene-silencing’ drugs that we know are capable of reducing Lp(a) by up to 98 per cent.
So big things are happening. It’s fantastic that politicians in some countries are now taking the cholesterol problem more seriously, and I’m glad to be part of influencing some of that.
But as long as heart disease remains our biggest killer, there will always be more work to do. And we’ve got to keep the focus on what’s causing it – cholesterol.
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