Why “normal cholesterol” doesn’t always mean low cardiovascular risk
A standard cholesterol test is an important starting point for assessing cardiovascular risk. But it does not tell the whole story.
Advanced lipid and genetic testing can look beyond a conventional cholesterol result by measuring apolipoprotein B (ApoB), Lipoprotein(a), or Lp(a), and, in selected people, a polygenic risk score for coronary artery disease.
These tests answer different questions. ApoB gives us a better measure of the number of potentially atherogenic particles circulating in the blood. Lp(a) identifies an important inherited risk factor that is not included in a standard lipid profile. A polygenic risk score can provide additional information about someone’s inherited susceptibility to coronary artery disease.
The important part is not simply obtaining another number. It is understanding whether that number meaningfully changes your cardiovascular risk, and whether it should change what you do about it.
About this service
I’m Dr Chris Critoph, Consultant Cardiologist in Bournemouth, with a particular interest in cardiovascular prevention, lipid management, inherited cardiac disease and more detailed assessment of cardiovascular risk.
I use tests such as ApoB, Lp(a) and, selectively, polygenic risk scoring when I think they can add useful information beyond conventional risk assessment.
My aim is not to perform every available test on everybody. It is to understand an individual’s risk as accurately as we reasonably can and then use that information to make proportionate decisions about prevention.
That might mean being more proactive with cholesterol treatment in somebody whose underlying risk has previously been underestimated. Equally, it can sometimes support a decision not to escalate treatment where the overall picture remains reassuring.
Why look beyond a standard cholesterol test?
A routine lipid profile usually includes:
- total cholesterol
- LDL cholesterol
- HDL cholesterol
- triglycerides
These measurements are genuinely useful and remain the right first-line tests for most people.
However, people with apparently similar LDL cholesterol levels do not necessarily have the same lifetime risk of developing coronary disease.
A conventional cholesterol test does not directly tell us:
- how many atherogenic lipoprotein particles are circulating in the blood
- whether you have a raised Lipoprotein(a), an important inherited cardiovascular risk factor
- how hundreds or thousands of inherited genetic variants combine to influence your lifetime susceptibility to coronary artery disease
ApoB, Lp(a) and polygenic risk scoring provide different pieces of that additional information.
A word about “good cholesterol” and “bad cholesterol”
I have never particularly liked the terms “good cholesterol” and “bad cholesterol”.
Cholesterol itself is neither good nor bad. It is an essential substance that we all need: among other things, it forms part of our cell membranes and is used to make steroid hormones and bile acids.
The issue is how cholesterol is transported around the bloodstream.
Because cholesterol cannot travel freely in blood, it is carried inside particles called lipoproteins. Some of these, particularly particles containing apolipoprotein B, including LDL particles, remnant particles and Lp(a), can enter and become retained within the artery wall, contributing to atherosclerotic plaque.
So when we talk about “LDL cholesterol”, we are really measuring the amount of cholesterol being carried inside LDL particles. It is not a special, inherently “bad” type of cholesterol.
Similarly, calling HDL “good cholesterol” is an oversimplification. Higher HDL cholesterol has been associated with lower cardiovascular risk in population studies, but simply raising HDL cholesterol does not necessarily reduce cardiovascular events.
The shorthand is easy to understand, but biologically it misses an important part of the story: the particles carrying cholesterol matter, not just the cholesterol itself.
Why does lowering LDL cholesterol matter?
There is exceptionally strong evidence that reducing exposure to atherogenic cholesterol lowers the risk of heart attack and stroke.
In a major analysis by the Cholesterol Treatment Trialists’ Collaboration involving approximately 170,000 people in 26 randomised statin trials, every 1 mmol/L reduction in LDL cholesterol was associated with around a 22% proportional reduction in major vascular events over approximately five years. Major coronary events fell by about 24% and stroke by around 16%.
Put another way:
1 mmol/L lower LDL cholesterol → roughly 20–22% lower relative risk of a major cardiovascular event
A reduction of around 2 mmol/L is associated with approximately a 40% reduction in major vascular-event risk over a comparable treatment period.
These are relative, not absolute, reductions in risk.
That distinction matters. A 20% relative risk reduction is much more valuable to somebody whose underlying cardiovascular risk is high than to somebody whose risk is already extremely low.
This is precisely why I think careful risk assessment matters. The question is not simply:
“Is my cholesterol high?”
A better question is:
“Given my overall risk, how important is lowering my cholesterol for me?”
ApoB, Lp(a), family history, evidence of atherosclerosis and, in selected circumstances, genetic risk can all help answer that question.
The three advanced tests
1. What is ApoB?
Apolipoprotein B, or ApoB, provides a measure of the number of potentially atherogenic lipoprotein particles circulating in your blood.
Each LDL particle, remnant particle and Lp(a) particle carries one molecule of ApoB. Measuring ApoB therefore gives us a practical measure of the total concentration of these atherogenic particles, rather than simply measuring how much cholesterol happens to be carried inside them.
This matters because particles can contain differing amounts of cholesterol.
Two people can therefore have the same LDL cholesterol concentration but a different number of LDL and other ApoB-containing particles.
For many people, LDL cholesterol and ApoB tell broadly the same story. But sometimes they are discordant.
For example, somebody can have an apparently satisfactory LDL cholesterol level but a relatively large number of cholesterol-poor atherogenic particles. In that situation, ApoB may suggest that their lipid-related risk is higher than their LDL cholesterol alone implies.
Contemporary guidance recognises ApoB as a useful additional measure, particularly in people with raised triglycerides, diabetes, metabolic disease or established cardiovascular disease, and where residual lipid-related risk may be underestimated by a conventional lipid profile.
Is ApoB better than LDL cholesterol?
Not simply.
LDL cholesterol remains extremely useful, has an enormous evidence base behind it and remains central to cardiovascular prevention.
I tend to think of ApoB as additional information rather than a replacement for LDL cholesterol.
Where ApoB and LDL cholesterol agree, the additional test may not change very much. Where they disagree, ApoB can sometimes reveal a risk that the standard lipid profile has underestimated.
That is one reason I prefer to interpret these results as part of an overall risk assessment rather than viewing a laboratory “normal range” in isolation.
2. What is Lipoprotein(a), or Lp(a)?
Lipoprotein(a), usually abbreviated to Lp(a), is an inherited lipoprotein particle that can increase the risk of heart attack, stroke and other atherosclerotic cardiovascular disease.
It is not routinely included in a standard cholesterol profile.
Unlike LDL cholesterol, your Lp(a) concentration is determined predominantly by your genes. Diet, exercise and weight loss have relatively little effect on the level itself.
Around one in five people worldwide have a high Lp(a), yet most people do not know their level unless it has specifically been measured.
It is particularly important because somebody can:
- eat well
- exercise regularly
- have a reasonable LDL cholesterol
- have no obvious conventional cardiovascular risk factors
…and still have substantially increased inherited cardiovascular risk because of a high Lp(a).
Should everyone have Lp(a) measured?
Current cardiovascular guidelines increasingly say yes — at least once during adult life.
The 2025 European Society of Cardiology/European Atherosclerosis Society update recommends considering Lp(a) measurement at least once in every adult, and the 2026 American dyslipidaemia guideline recommends at least one measurement in all adults.
That is a significant change from the older approach of only measuring Lp(a) when somebody had premature heart disease or a striking family history.
Family history still makes the test particularly relevant, but you do not need a family history of heart disease to have an elevated Lp(a).
What is considered a high Lp(a)?
There is no absolute point at which risk suddenly switches from “normal” to “abnormal”. Cardiovascular risk rises progressively as Lp(a) increases.
However, a level of approximately 50 mg/dL or above is widely regarded as clinically important. Guidelines using nmol/L commonly use thresholds in the region of 105–125 nmol/L, although mg/dL and nmol/L are not perfectly interchangeable and should not be converted using a simple fixed formula.
The 2026 American guideline estimates that an Lp(a) of at least 125 nmol/L/50 mg/dL is associated with roughly a 1.4-fold higher risk of atherosclerotic cardiovascular disease, while levels around 250 nmol/L are associated with approximately double the risk.
Those figures still need context. A high Lp(a) does not mean that you will inevitably have a heart attack.
It means that the background against which we assess your other risk factors has changed.
Can you lower Lp(a)?
Lifestyle measures have many cardiovascular benefits, but unfortunately they do not substantially lower an inherited Lp(a) level.
At the time of this page’s medical review, there was not yet a medication licensed specifically to lower Lp(a) with proven cardiovascular-outcome benefit, although several highly effective Lp(a)-lowering treatments are in late-stage clinical development.
That does not mean that knowing about a high Lp(a) is pointless.
It often makes the things we can change more important.
For example, if somebody has a significantly elevated Lp(a), I may be more inclined to treat their LDL cholesterol aggressively, pay particularly close attention to blood pressure, smoking, diabetes and weight, and consider whether further cardiovascular risk assessment is justified.
Knowledge of a raised Lp(a) may also be relevant to close relatives, because the level is strongly inherited.
3. What is a polygenic risk score for coronary artery disease?
Most inherited susceptibility to coronary artery disease is not caused by one single abnormal gene.
Instead, there are very large numbers of common genetic variants across our DNA, each of which may increase or decrease risk by a very small amount.
A polygenic risk score, or PRS, combines information from many of these variants to estimate how an individual’s inherited susceptibility to coronary artery disease compares with that of the wider population.
This is different from conventional genetic testing for a specific inherited disorder.
A PRS does not tell us:
“You have the gene for coronary disease.”
There is no single gene that works like that for most people.
Instead it asks:
“Taken together, does your genetic background put you towards the lower or higher end of inherited susceptibility to coronary artery disease?”
I offer this as a home saliva test analysed by an accredited UK laboratory, followed by a consultation in which the result is interpreted alongside cholesterol, blood pressure, family history, lifestyle and any previous cardiovascular investigations.
Is a polygenic risk score recommended for everyone?
No.
Polygenic risk scoring is an evolving area of cardiovascular prevention rather than a routine screening test that everybody should have.
The 2025 European Society of Cardiology consensus statement recognised potential clinical uses for cardiovascular polygenic risk scores. The more recent 2026 US dyslipidaemia guideline does recognise a high polygenic risk score, if it has been measured, as a cardiovascular risk-enhancing factor.
I therefore use PRS selectively rather than as a blanket test.
I find it most useful when the result has a realistic chance of changing a prevention decision — for example, in a younger person whose conventional 10-year risk looks low but where lifetime risk is more uncertain.
You can read more about polygenic risk scoring, the consent process and pricing on my Family History and Inherited Heart Risk page.
Who might benefit from more detailed lipid and genetic risk assessment?
A more detailed assessment may be worth considering if:
- Heart attacks or coronary disease run in your family, particularly at younger ages.
- You have been told that your cholesterol is “normal” or only mildly elevated, but your family history does not seem to fit with that reassurance.
- You have developed coronary artery disease or had a heart attack relatively young without the usual risk factors to explain it.
- You have diabetes, raised triglycerides, obesity or metabolic risk where ApoB may add information beyond LDL cholesterol.
- You are trying to decide how proactive to be with cholesterol-lowering treatment.
- Your calculated 10-year cardiovascular risk is low or intermediate but you are concerned that it may not capture your lifetime risk.
- You have already had ApoB, Lp(a) or genetic testing elsewhere and want to understand what the result actually means for you.
- You simply do not know your Lp(a). For this particular test, once-in-adulthood measurement is increasingly recommended even in people without a strong family history.
Who does not need a full advanced assessment?
I do not think everybody needs an extensive panel of specialist blood tests and genetic testing.
A standard lipid profile, blood pressure measurement, smoking history, assessment for diabetes and attention to diet, activity and weight remain the foundations of cardiovascular prevention.
Lp(a) is the exception: there is now a good argument for most adults having this measured once.
ApoB is more selectively useful, while polygenic risk scoring remains something I use when it can genuinely add to a particular clinical decision.
Testing for the sake of collecting numbers is rarely helpful.
Testing is useful when the result can change our understanding of risk or what we do about it.
Advanced testing versus mail-order cholesterol and genetic tests
Direct-to-consumer blood and genetic testing has made ApoB, Lp(a) and polygenic risk much more visible over recent years. In many ways, that increased awareness is positive. However there is an important distinction between obtaining a result and understanding what that result means clinically.
An ApoB of a particular value, a high Lp(a), or a genetic risk percentile cannot sensibly be interpreted without knowing the person’s age, blood pressure, conventional cholesterol results, smoking status, family history, medical conditions, medication and, sometimes, previous investigations.
The same result may reasonably lead to very different decisions in two different people.
I also have a little personal caution about point-of-care testing.
I once had a finger-prick cholesterol and diabetes screen myself and obtained results that were surprisingly different from a conventional laboratory test performed a few months previously. I therefore repeated the tests using a venous sample in the laboratory the following week, and the finger-prick results proved to have been substantially inaccurate.
That does not mean that every home or finger-prick test is inaccurate. It does mean that if a result is going to influence an important medical decision, I prefer it to have been measured using an appropriate accredited laboratory method, and I will sometimes confirm an unexpected result before acting on it.
For me, the value of advanced risk testing lies less in generating another set of numbers and more in turning those numbers into a sensible plan.
What happens if my ApoB, Lp(a) or genetic risk is high?
A high result does not automatically mean medication, a scan or another investigation. First, we put the result back into context. Depending on the overall picture, the next step might include:
- no immediate change other than continuing healthy lifestyle measures
- more intensive attention to diet, weight, exercise, smoking or blood pressure
- starting or intensifying cholesterol-lowering medication
- reconsidering what LDL cholesterol level is appropriate for you
- further cardiovascular assessment, where genuinely indicated
- discussing testing with close relatives
- reviewing risk again over time
The aim is a proportionate prevention strategy, rather than treating a laboratory result in isolation.
What is involved?
ApoB and Lp(a)
ApoB and Lp(a) are straightforward venous blood tests and can usually be taken alongside a conventional lipid profile and other blood tests.
Polygenic risk score
The coronary artery disease polygenic risk score uses a saliva sample collected at home and returned to an accredited UK laboratory.
Results are usually available in approximately five weeks and are then discussed in a dedicated consultation.
Interpretation
Whichever tests are performed, I review them in the context of your overall cardiovascular risk rather than simply returning a laboratory report marked high, normal or low.
How much do ApoB and Lp(a) tests cost?
ApoB and Lp(a) are relatively inexpensive compared with most specialist cardiac investigations.
Laboratory charges for individual advanced lipid tests at the hospitals I use are typically in the region of £50–£100 per test.
Exact laboratory charges can change, so I prefer not to publish a fixed figure that may subsequently become out of date. The current cost will always be confirmed before testing.
Polygenic risk scoring is a more involved test and has separate pricing, detailed on my Family History and Inherited Heart Risk page.
Frequently asked questions
My LDL cholesterol is normal. Can I still have increased cardiovascular risk?
Yes. LDL cholesterol is extremely useful, but it is only one part of cardiovascular risk. A person can have an apparently satisfactory LDL cholesterol while having a high ApoB particle concentration, a significantly elevated Lp(a), a strong family history or high inherited polygenic susceptibility. Equally, having one of these risk factors does not mean that heart disease is inevitable. The purpose of testing is to improve the estimate of risk and make better prevention decisions.
Is ApoB just another cholesterol test?
Not quite. LDL cholesterol tells us approximately how much cholesterol is being transported inside LDL particles. ApoB gives us a measure of the number of atherogenic particles carrying cholesterol and other lipids around the circulation. The two often correlate closely, but where they do not, ApoB can sometimes add clinically important information.
Is ApoB better than LDL cholesterol?
I would not describe one as simply “better”. LDL cholesterol remains central to cardiovascular risk assessment and treatment. ApoB can add useful information, particularly when triglycerides are raised, in diabetes or metabolic disease, or where LDL cholesterol may underestimate the total number of atherogenic particles.
Should I have an Lp(a) test even without a family history?
Probably yes, at least once in adulthood. Current European and American cardiovascular guidance increasingly supports once-in-adulthood testing because a high Lp(a) is common, predominantly inherited and usually causes no symptoms. A family history of premature cardiovascular disease makes knowing your Lp(a) particularly useful, but it is not a prerequisite for testing.
If my Lp(a) is high, does that mean I will have a heart attack?
No. It means your risk is higher than it would have been if your Lp(a) were lower. Your actual probability of developing cardiovascular disease still depends on your age, blood pressure, LDL cholesterol and ApoB exposure, smoking, diabetes, family history and many other factors. That is why Lp(a) should be used to refine a cardiovascular risk assessment rather than treated as a diagnosis in its own right.
Can diet and exercise lower Lp(a)?
Not substantially. Lp(a) is predominantly genetically determined. However, diet, exercise, not smoking, maintaining a healthy weight, controlling blood pressure and managing LDL cholesterol remain extremely important because they reduce the other components of cardiovascular risk around an inherited high Lp(a).
Do I need to repeat these tests?
Lp(a): usually only once, because the level is largely genetically determined and relatively stable during adult life. Polygenic risk score: once only. Your DNA does not change. ApoB: this can change with diet, weight, metabolic health and lipid-lowering treatment, so it may be worth repeating when monitoring treatment or a change in circumstances.
Does advanced testing replace my GP’s cholesterol monitoring?
No. It complements standard cardiovascular assessment rather than replacing it. Routine cholesterol testing, blood pressure measurement, diabetes screening and lifestyle assessment remain fundamental. The purpose of these additional tests is to answer particular questions that a conventional assessment does not.
Where I see patients
Consultations are available at Nuffield Health Bournemouth and Dorset Heart Clinic.
I can also provide phone or video consultations for suitable patients throughout the UK.
Ready to find out more?
If you would like to understand your cholesterol, Lp(a), ApoB or inherited cardiovascular risk in more detail, you can arrange a consultation to discuss which — if any — of these tests would genuinely be useful for you.
Call: 01202 084550
Email: info@coastalcardiology.co.uk
Evidence and guidelines
This page reflects evidence and guidance including:
- Cholesterol Treatment Trialists’ Collaboration: meta-analysis of approximately 170,000 participants examining cardiovascular-event reduction with LDL cholesterol lowering.
- 2025 ESC/EAS Focused Update on dyslipidaemias: including contemporary recommendations on Lp(a) measurement and cardiovascular risk.
- 2026 ACC/AHA Guideline on the Management of Dyslipidemia: including recommendations on ApoB, once-in-adulthood Lp(a) testing and cardiovascular risk enhancers.
- 2025 European Society of Cardiology Clinical Consensus Statement on polygenic risk scores and cardiovascular disease.
- European Atherosclerosis Society consensus on Lipoprotein(a).
Written and medically reviewed by Dr Chris Critoph, Consultant Cardiologist.
Last medically reviewed: September 2026.
The information on this page is general medical information and is not a substitute for individual medical advice.