Cholesterol never travels alone: it is carried in particles, the lipoproteins, whose number and size matter as much as the amount of cholesterol they contain. A standard lipid panel measures this cholesterol (LDL, HDL, non-HDL); apolipoprotein B and nuclear magnetic resonance (NMR) count and classify the particles, which refines the estimate of cardiovascular risk.
What is a lipoprotein, and why do we talk about “good” and “bad” cholesterol?
A lipoprotein is a spherical particle made of a shell of phospholipids and proteins (the apolipoproteins) surrounding a core of fats: esterified cholesterol and triglycerides. Because fats do not dissolve in water, this packaging is the only way for the body to move them through the bloodstream. Cholesterol itself is not an enemy: as French National Health Insurance (Assurance Maladie) points out, it is a building block of cell membranes, hormones, bile salts and vitamin D.
Lipoproteins are distinguished by their density, hence their names: VLDL (very low density), IDL (intermediate density), LDL (low density) and HDL (high density). VLDL, made by the liver, mainly carry triglycerides to the tissues; as they unload them, they become IDL and then LDL, rich in cholesterol. HDL partly travel the opposite way: they collect cholesterol from the tissues and bring it back to the liver.
| Lipoprotein | Main origin | Dominant cargo | Role | Link with atherosclerosis |
|---|---|---|---|---|
| VLDL | Liver | Triglycerides | Distribute fats to the tissues | Particles and their remnants are atherogenic, especially when triglycerides are high |
| IDL | Conversion of VLDL | Triglycerides and cholesterol | Intermediate step toward LDL | Atherogenic |
| LDL | Conversion of IDL | Cholesterol | Deliver cholesterol to cells | Established cause of atherosclerosis (EAS consensus 2017) |
| HDL | Liver and intestine | Cholesterol, proteins | Bring cholesterol back to the liver | A low level is associated with higher risk; raising it with medication has not shown any benefit |
| Lp(a) | Liver, genetically determined | Cholesterol and apolipoprotein(a) | Poorly understood | Independent risk factor, to be measured at least once in a lifetime according to the ESC/EAS |
“Bad” cholesterol refers to the cholesterol carried by LDL, “good” cholesterol to that carried by HDL. These shortcuts contain some truth: Inserm (the French National Institute of Health and Medical Research) describes how LDL accumulate in the artery wall at areas of turbulent flow, undergo chemical modifications that trigger an inflammatory reaction, are taken up by macrophages and gradually form a plaque covered by a fibrous cap. But they have a limitation: it is not cholesterol that enters the artery wall, it is the particles that carry it.
What does a standard lipid panel include, and what do LDL, HDL, non-HDL and apoB mean?
The lipid panel prescribed in France, called exploration d’une anomalie lipidique (EAL), measures total cholesterol, HDL cholesterol, LDL cholesterol, non-HDL cholesterol and triglycerides, on a blood sample taken after a 12-hour fast (French National Health Insurance). In the absence of risk factors, French National Health Insurance recommends it from age 40 in men and age 50 in women, with a repeat test every 5 years if the result is normal, and earlier or more often when risk factors are present. The reference values it cites for a person without risk factors are LDL below 1.6 g/l and triglycerides below 1.5 g/l; they do not apply to everyone, as targets depend on the level of risk.
Four notions to distinguish:
- LDL cholesterol (LDL-C) is the mass of cholesterol contained in LDL particles.
- HDL cholesterol (HDL-C) is the mass of cholesterol carried by HDL.
- Non-HDL cholesterol is total cholesterol minus HDL: it combines the cholesterol of all potentially atherogenic particles (VLDL, IDL, LDL, Lp(a)). It is the lipid variable used by the European SCORE2 score published in 2021.
- Apolipoprotein B (apoB) is the structural protein present as a single copy on each VLDL, IDL, LDL and Lp(a) particle. Measuring it therefore amounts to counting the atherogenic particles, whatever their cholesterol load.
Why does the number of particles matter as much as the cholesterol they carry?
Because it is the particle, not the cholesterol, that crosses the artery wall and deposits there. Two people can have the same LDL-C with a very different number of particles: one carries a few large, cholesterol-rich LDL particles, the other many small, cholesterol-poor ones. The second person has a higher risk, which LDL-C alone does not show. This “discordance” is common when triglycerides are high, and in cases of abdominal obesity, metabolic syndrome or diabetes: these are the situations in which European guidelines suggest preferring apoB or non-HDL over LDL-C.
The European Atherosclerosis Society (EAS) consensus published in 2017 in the European Heart Journal reviewed more than 200 prospective cohorts, randomized trials and genetic studies, totaling more than 2 million participants. Its conclusion: the link between the arteries’ cumulative exposure to LDL and the risk of a cardiovascular event is “remarkably consistent, dose-dependent and log-linear,” and lowering the concentration of LDL particles reduces risk proportionally, whatever the means. Two lessons: what counts is cumulative exposure over decades, hence the value of acting early; and the number of particles is the quantity most directly linked to the mechanism.
What does NMR metabolomics add to the lipid panel?
Nuclear magnetic resonance measures, from a single sample, the concentration and composition of 14 lipoprotein subclasses classified by size, as well as apolipoproteins B and A1 and the average particle diameter. The Nightingale Health panel applied to 118,461 UK Biobank participants (Julkunen et al., Nature Communications, 2023) includes 249 measurements, of which 168 are absolute concentrations and 81 are ratios; for each subclass, it reports the amount of triglycerides, phospholipids, cholesterol and total lipids. The 14 subclasses range from extremely large VLDL to small HDL, including IDL and several sizes of LDL.
| Standard lipid panel (EAL) | NMR metabolomic panel | |
|---|---|---|
| What is measured | Total cholesterol, HDL, LDL (often calculated), non-HDL, triglycerides | 14 lipoprotein subclasses (particle concentration, size, lipid content), apoB, apoA1, plus fatty acids, glycolysis, amino acids, GlycA |
| Number of measurements | 5 | 249, including 81 ratios |
| Particle number | No, unless apoB is added on prescription | Yes, by subclass |
| Setting | Routine prescription, reimbursed, basis of risk scores | Research and personalized prevention; medical interpretation essential |
| What it enables | Screening for and monitoring dyslipidemia, calculating SCORE2 | Documenting the profile behind an “average” LDL, tracking the response to lifestyle changes |
In the Women’s Health Study (27,673 women followed for 11 years, 1,015 events), NMR measurements of particle number and size were associated with risk comparably to standard lipids and apolipoproteins, without outperforming them, and adding them to a full model reclassified few people (Mora et al., Circulation, 2009). The value of NMR is therefore not to replace the standard lipid panel: it is to describe the full profile behind a single LDL number, to spot discordances and to measure, from one sample to the next, the effect of changes in habits on each family of particles. We explain the technique in our article on NMR metabolomics and the place of lipids among other blood biomarkers.
What is the link between lipoproteins and 10-year cardiovascular risk?
The SCORE2 score, published in 2021 by the European Society of Cardiology, estimates the probability of a fatal or non-fatal cardiovascular event within 10 years in people aged 40 to 69 from five variables: age, sex, smoking, systolic blood pressure and non-HDL cholesterol. Only one lipid variable is included, and it is the one that combines all atherogenic particles. France is classified as a low-risk region, which determines the charts to use.
The result, expressed in risk categories, adjusts the intensity of prevention and the LDL targets, which are lower the higher the risk; these targets are discussed with your doctor and we do not put figures on them here. People who already have cardiovascular disease, diabetes, chronic kidney disease or familial hypercholesterolemia are classified directly as high or very high risk, without going through the calculation. Details of the score, its limitations and what metabolomics can add to it are in our article on 10-year cardiovascular risk; it is also one of the topics of the prevention check-up at ages 45–50.
What are the levers for improving your lipid profile?
The proven levers concern diet, physical activity, weight and smoking; medications come in when these measures are not enough, or from the outset when the risk is high, by medical decision. None of these levers should be chosen alone in response to a result: what follows describes what the literature shows, not a prescription.
Replace saturated fats with unsaturated fats. The American Heart Association presidential advisory published in 2017 in Circulation concludes that, in randomized trials, replacing saturated fats with polyunsaturated vegetable oils reduced cardiovascular events by about 30%, whereas replacing them with refined carbohydrates and sugars provides no benefit. The World Health Organization recommends limiting saturated fats to less than 10% of total energy intake and trans fatty acids to less than 1% (“Healthy diet” fact sheet, January 2026). We explain these guidelines in detail in diet and nutrition in prevention and the role of fatty acids and omega-3s.
Move more, lose weight if needed, quit smoking. Regular physical activity and weight loss lower triglycerides and raise HDL; smoking lowers HDL and accelerates atherosclerosis.
Medications, when indicated. As Inserm summarizes it: statins and other treatments are prescribed when lifestyle changes are insufficient, particularly in secondary prevention. The 2017 EAS consensus points out that the benefit is proportional to the reduction achieved and its duration. The decision belongs to the doctor and the patient, informed of the overall risk, of which chronic inflammation is a component: see our article on GlycA and low-grade inflammation. For an overview of modifiable factors, see cardiovascular prevention within our personalized health section.
Key takeaways
- Cholesterol travels in lipoproteins (VLDL, IDL, LDL, HDL); it is the apoB-carrying particles, not cholesterol itself, that enter the artery wall.
- The standard lipid panel (EAL) measures total cholesterol, HDL, LDL, non-HDL and triglycerides; apoB counts the atherogenic particles, while non-HDL summarizes them and is included in SCORE2.
- LDL are an established cause of atherosclerosis (EAS consensus 2017); cumulative exposure over decades matters, hence the value of acting early.
- NMR details 14 lipoprotein subclasses by size and composition; it describes the profile behind a single number without replacing the reference lipid panel.
- Diet, physical activity, weight and smoking are the first-line levers; treatment is decided with the doctor based on overall risk.
What Sokrate lets you do
The Sokrate service prepares your prevention check-up online using an adaptive self-assessment questionnaire, then a doctor writes and signs a Personalized Prevention Plan, which is sent to your regular doctor (médecin traitant) unless you object. As an option, an NMR metabolomic analysis of 249 biomarkers, performed on the Nightingale Health platform, reports your lipoprotein profile by subclass, your apoB and your non-HDL, interpreted by a doctor in the context of your overall risk. A coordination nurse provides follow-up. You can start your check-up or find out how the pathway works.