Cholesterol: do you have all the information? (Spoiler: probably not, and don’t wait too long to find out!)

Do you know what your Apo B level is? Has anyone checked your Lp(a)? What is your lifetime risk of ASCVD?

If you don’t know the answer to these questions then you haven’t adequately assessed your risk of having a heart attack or stroke and may be missing a massive opportunity to avoid one. This article is quite long and gets a bit technical, but I strongly recommend pushing on through because there is one simple thing we need to do which will inform a range of titbits of advice we can provide, tangible and achievable changes adapted to you and your lifestyle, which will help prevent you having a heart attack.

Heart attacks are the number one cause of death in Western Society but we could all be reducing our risk in simple ways as long as we start thinking about it soon enough.

A Proactive Approach to ASCVD Risk: Beyond Traditional Cholesterol Testing

Atherosclerotic cardiovascular disease (ASCVD), a well-known and extensively researched disease process, causes arteries to narrow, leading to heart attacks and strokes. Tragically, these are the leading causes of death in Western society. The greater tragedy is that much of this risk is modifiable, yet the majority of first ASCVD presentations are massive, fatal heart attacks, often in a person's early fifties.

As General Practitioners, had we been able to perform a simple blood test 10 or 20 years earlier on these people, we could have identified and addressed their risk. Unfortunately, as a nation, we often wait until it’s too late to test things like cholesterol. Other countries are more proactive. For instance, in the Netherlands, where the genetic risk for Familial Hypercholesterolaemia (inherited high cholesterol) is particularly high, cholesterol testing is done in childhood, with statins starting early if necessary—a practice almost unheard of in the UK.

Understanding Cholesterol: a short science lesson

Cholesterol is a fat and does not dissolve in the bloodstream (which is essentially water). To transport this vital substance—essential for many bodily functions—it is packaged into water-soluble 'envelopes' called lipoproteins. The different types of these are commonly, but inaccurately, referred to as 'good' and 'bad' cholesterol.

The so-called 'bad cholesterol' refers to low density lipoproteins (LDL) that transport cholesterol from the gut and liver to the rest of the body. It is these particles that deposit cholesterol, causing arteries to 'fur up' around organs, particularly the heart. This process, however, is systemic, also contributing to erectile dysfunction, strokes/mini-strokes, kidney disease, and poor circulation.

Conversely, the so-called 'good cholesterol' particles are packed full of cholesterol creating high density lipoproteins (HDL) to bring cholesterol back from these areas to the liver for processing and beneficial use, such as tissue repair. Interestingly, 'good cholesterol' levels often rise in intensive care patients as the body attempts widespread repair - the liver is retrieving cholesterol from elsewhere to convert into useful things.

The Limitations of Traditional Testing

The 'bad cholesterol' group is what we really want to know about. Unfortunately it includes lots of different subtypes based on density, such as LDL (Low-Density Lipoproteins), VLDL (Very Low-Density Lipoproteins), chylomicrons, and Lipoprotein(a) (more on these shortly) and several others. If you measured all of these individually you’d end up with a highly complex set of numbers that was very difficult to interpret for all but the most eminent of biochemists.

Traditional and widespread cholesterol measures instead go for a single figure to cover all of them. They measure Total Cholesterol and HDL (High-Density Lipoprotein, the 'good' type), subtract HDL from the total to get Non-HDL Cholesterol. This Non-HDL figure represents all the rest and is an approximation of the bad cholesterol volume. While a breakthrough when introduced, science has advanced.

The Power of Apo B

We can now quantify 'bad cholesterol' much more accurately. Every harmful cholesterol particle, regardless of subtype, has a single marker on its surface called apolipoprotein B (Apo B). By measuring your Apo B, you get a highly accurate particle count of the elements that cause ASCVD, as opposed to a deduced volume which could be made up of all sorts of different proportions of particles. This is superior because different particles carry different risk levels. As I often say to patients, if you and I both have the same LDL volume, but yours is made up of 1000 particles and mine is made up of 10,000 particles, I am in much more trouble than you are because mine is everywhere and yours isn’t (this is an oversimplification, but a concept that works). 

Why is this not being done on the NHS? Unfortunately one has to suspect cost is a large part of it - although for an individual test the cost is not huge, to roll that out to all the cholesterol tests done daily would very quickly present the NHS with even greater problems than it already has. 

Lipoprotein A: The Genetic Wildcard

As a subtype of 'bad cholesterol', Lipoprotein A, often referred to as “LP little a”, abbreviated to Lp(a), is typically a small proportion but is disproportionately damaging, probably 10 times as damaging to the system as any of the others. This is why a separate measurement is essential.

The bad news is that if Lp(a) is high, there is little that can be done to lower it, as it is genetically determined, and statins are ineffective (though an expensive injectable drug exists and the search is on for others).

The crucial implication of a high Lp(a) is that you must take all your other risk factors extremely seriously. This means aggressively suppressing your Apo B levels with all available tools, maintaining the right exercise regimen, optimising your blood pressure, and generally looking after yourself—a topic for a separate, comprehensive article.

Conversely, a low Lp(a) is a bit of a genetic ‘win’: it can be a positive factor and may inform discussions on the necessity of statins, particularly for those with side effects or an aversion to daily medication.

Risk Scores: A Population Tool, Not an Individual Guarantee

Any discussion of risk would be incomplete without addressing risk scores. Almost all widely used scores, such as QRisk, calculate a 10-year risk. The primary factor influencing this outcome is age—something we sadly cannot modify yet (although when that science emerges we can apparently look forward to Walt Disney being defrosted to provide us with some more animated delectations, or is that a myth?).

For any 35-year-old, the score will be incredibly low, offering a falsely reassuring result, even if they smoke, take no exercise, are obese and have been orphaned at a young age by the death of their entire family from heart attacks. However, this is precisely the demographic that would benefit most from aggressive cardiovascular risk management, potentially avoiding becoming an 'early fifties' statistic.

You can try the online QRisk 3 calculator. You will quickly see that adjusting factors like smoking, family history, or diabetes makes a marginal difference compared to adjusting the age. Furthermore, these models are grossly imperfect because, in the next 10 years, you either will or will not have a heart attack—you won't have 20% of one. While valuable for public health screening, they are less helpful for individual decision-making.

The Good News: Taking Control of Your Future

It's time for some optimism. We can easily test both Apo B and Lp(a). Combined with a review of your lifestyle, a blood pressure check, and a deep dive into your medical history, we can generate a very accurate picture of your true cardiovascular risk.

The earlier you explore this with us, the greater our chance of making a substantial difference to your lifespan and helping you live a long, healthy life.

If we start a 35-year-old on statins and they reach 60 feeling fine, we will never know if we averted a heart attack. However, I would much rather be wondering about that answer at 60 than regretting a lack of proactivity 25 years earlier.

For the sake of a quick blood test and a conversation, it truly is better to know your risk. The best part is: it is never too late to start making changes. Any positive step you take, even if you feel you've left it late, will bring immediate benefits. Come and see us to discuss this. Please!