Cholesterol & Lipoproteins Explained: How Cholesterol Travels, What Lipoproteins Do, and What Truly Drives Cardiovascular Risk

Cholesterol has been made into one of the most misunderstood molecules in modern health.

Most people have been taught a simple story: cholesterol is bad, LDL is bad, HDL is good, and if your numbers are high, you’re heading for a heart attack. That story is easy to remember, but it’s not how biology actually works.

Cholesterol itself is not a toxin. It’s an essential building material.

Your body uses cholesterol to build cell membranes, produce steroid hormones, make bile acids so you can digest fats properly, and even make vitamin D. Every cell in your body needs cholesterol. Your brain is full of it. Your immune system uses it. Your endocrine system depends on it.

So the problem isn’t “cholesterol exists”.

The real question is: how is cholesterol being transported, what is happening to those transport particles over time, and what is the state of the artery wall they are travelling through?

Because cholesterol doesn’t float freely in the blood. It has to be packaged and transported. And that is where cardiovascular risk lives.

 

Why Cholesterol Needs Transport in the First Place

Blood is water-based. Cholesterol is fat-based.

So cholesterol cannot dissolve in blood any more than oil dissolves in water. If your body wants to move cholesterol around, it has to package it inside specialised transport particles.

Those particles are called lipoproteins.

A lipoprotein is basically a tiny spherical “delivery vehicle” made of fats (lipids) and proteins. The proteins on the surface are called apolipoproteins, and they act like identity tags and docking codes. They tell the body where the particle can go, how it should be handled, and how it should be cleared from circulation.

This matters because when we talk about “LDL cholesterol” or “HDL cholesterol”, we’re not talking about cholesterol itself in isolation. We’re talking about cholesterol inside certain types of particles.

And cardiovascular risk is far more tied to the particles than the cholesterol cargo.

 

The Main Lipoproteins: VLDL, LDL, and HDL (And What They’re Actually For)

The liver produces a particle called VLDL — very low density lipoprotein.

VLDL’s main job is to carry triglycerides, which are essentially packaged energy, out from the liver to tissues that can use them. You can think of VLDL as a delivery van loaded with fuel.

As VLDL travels around the body, it drops off triglycerides. When it has delivered most of its load, it shrinks and becomes a different particle — first IDL, and then LDL.

LDL is more cholesterol-rich. Its primary purpose is to deliver cholesterol to cells that need it for maintenance, repair, and hormone production.

So LDL is not a “mistake”. It’s a normal transport system.

HDL does the reverse job. HDL helps carry excess cholesterol away from tissues and back to the liver to be recycled or disposed of through bile.

So rather than thinking “LDL bad, HDL good”, it’s more accurate to think:

LDL is a delivery system.
HDL is part of the clean-up and recycling system.

But — and this is where it gets important — if you have too many delivery vehicles circulating for too long, and the road they’re travelling through (your arteries) is inflamed and irritated, the system stops being harmless.

 

LDL: Not the Villain — But the Main Opportunity for Trouble

LDL becomes a risk marker because it is the primary particle involved in plaque formation.

The key concept is exposure.

If you have more LDL particles in circulation, you have more chances for those particles to interact with the artery wall. Even if each individual particle isn’t particularly “dangerous”, the statistical chance of some particles entering the artery wall goes up as particle number rises.

Once LDL particles enter the artery wall, one thing determines whether they become a problem:

Do they become damaged and trigger an immune response?

If the artery wall is healthy, flexible, and not inflamed, LDL particles are less likely to get trapped, and less likely to become chemically modified.

But if the vessel lining is irritated — by high blood pressure, smoking, high blood sugar spikes, chronic inflammation, oxidative stress — then LDL particles are more likely to cross the lining, get stuck, and become oxidised.

And oxidised LDL is where the immune system steps in.

Your immune system does not react strongly to LDL because LDL exists. It reacts because LDL has been modified in a way that looks abnormal and threatening. That triggers immune cells to arrive, engulf the particles, and begin the early stages of plaque formation.

So the story isn’t “LDL is poison”. The story is:

More particles plus more arterial irritation equals more opportunity for inflammatory plaque biology.

 

Particle Number Versus Cholesterol Amount: Why This Confuses People

Here’s a key point that helps people finally make sense of cholesterol tests.

You can have a normal LDL cholesterol reading, but still have a high number of LDL particles.

And you can have a high LDL cholesterol reading, but not necessarily have a very high particle number.

Why? Because “LDL cholesterol” is the amount of cholesterol being carried inside LDL particles. But each particle can carry more or less cholesterol depending on its size and composition.

Think of it like cars on a motorway.

LDL cholesterol is like measuring the total weight of cargo on the motorway.
Particle number is like counting how many cars are actually on the motorway.

From a traffic-risk perspective, the number of cars matters a lot.

This is why measurements like ApoB can be so helpful.

 

ApoB: The Most Useful Concept Most People Have Never Heard Of

Apolipoprotein B — ApoB — is found on every “atherogenic” particle: VLDL remnants, IDL, and LDL.

Crucially, each of these particles carries one ApoB molecule.

So ApoB is essentially a direct proxy for how many plaque-capable particles are circulating.

This is why someone can have “not-too-bad” LDL cholesterol but still have a high ApoB and a higher risk profile — particularly if they also have insulin resistance and high triglycerides.

It’s not about demonising any single number. It’s about understanding what that number is actually representing.

 

LDL Particle Size: Why “Small Dense LDL” Matters

LDL particles vary in size.

Small, dense LDL is more likely to slip into the artery wall and more likely to become oxidised. Larger LDL particles are generally less likely to do that.

But what creates small dense LDL?

This is where metabolism enters the conversation.

When triglycerides are high — often because the liver is overproducing VLDL — LDL particles tend to become smaller and denser as they’re remodelled in the bloodstream.

And what drives high triglycerides?

Most commonly: insulin resistance and excess carbohydrate energy being channelled through the liver.

So small dense LDL is not usually a standalone problem. It is a marker that the underlying metabolic environment is pushing lipoprotein patterns in a more atherogenic direction.

That’s why “fixing cholesterol” without addressing blood sugar and insulin is often a dead end.

 

HDL: Protective, But Only When It’s Functioning Well

HDL is often called “good cholesterol”, but HDL isn’t good simply because the number is high.

HDL has protective functions — it helps remove cholesterol from tissues, it has antioxidant and anti-inflammatory effects, and it supports endothelial function.

But in a state of chronic inflammation and insulin resistance, HDL can become dysfunctional — meaning it loses some of its protective capacity.

That’s why chasing HDL with gimmicks doesn’t work. What improves HDL function is improving the metabolic and inflammatory environment: better blood sugar control, lower triglycerides, more movement, better sleep, and less chronic inflammation.

Again, the theme repeats:

The biology matters more than the label.

 

How Plaque Actually Forms (The Bit Most People Never Get Told)

Atherosclerosis isn’t limescale in a pipe. It’s an immune process.

It begins with endothelial dysfunction — the inner lining of the artery becoming irritated, inflamed, and less able to regulate blood flow and immune activity.

Then LDL particles cross into the artery wall. If they become oxidised, the immune system sees them as abnormal. Macrophages engulf them and become foam cells. This creates a fatty streak. Over time, smooth muscle cells migrate and a fibrous cap forms over the growing plaque.

Here’s the most important part:

Heart attacks and strokes most often occur not because an artery slowly blocks up, but because an inflamed plaque becomes unstable and ruptures, triggering clot formation.

This is why inflammation and oxidative stress are not side issues. They are central to risk.

 

What Actually Raises Cardiovascular Risk in Real Life (And Why)

People need more than labels here — they need the “why”. So let’s make this human and clear.

If your blood sugar is swinging up and down all day, your blood vessels are being exposed to repeated oxidative stress. Glucose spikes create more reactive by-products and inflammation, and that irritates the endothelium — making it easier for LDL particles to enter the artery wall and become damaged.

If you are insulin resistant, your liver is often producing more triglycerides and more VLDL. That increases the total number of ApoB-containing particles and pushes LDL toward a smaller, denser pattern. It’s not that insulin resistance “makes cholesterol high” in a simplistic way — it changes the whole transport system.

If triglycerides are high, it’s usually a sign that the liver is under metabolic load, exporting excess energy as fat. High triglycerides also tend to travel alongside lower HDL and smaller denser LDL, and that combination is strongly associated with risk.

If you carry more visceral fat, that tissue behaves like an inflammatory organ. It releases cytokines that worsen insulin sensitivity and increase vascular inflammation. So visceral fat increases risk even when someone’s weight isn’t extreme, because the biology of that fat depot is inflammatory.

If inflammation is chronically elevated, plaques are more likely to form and more likely to become unstable. Inflammation makes immune cells more reactive inside the artery wall. It also makes LDL oxidation more likely. In other words, inflammation turns cholesterol transport from neutral into risky.

If blood pressure is elevated, you have more mechanical stress on the artery wall, which accelerates endothelial dysfunction. More stress equals more irritation equals more inflammatory signalling inside vessels.

If someone smokes, it directly damages the endothelium and massively increases oxidative stress. It’s one of the most potent drivers of plaque instability.

If sleep is poor, insulin sensitivity worsens, cortisol rises, inflammation increases, appetite hormones shift, and blood pressure regulation becomes less stable. Poor sleep quietly amplifies almost every risk pathway we’ve discussed.

If you’re sedentary, you lose muscle mass, glucose handling worsens, triglycerides rise, endothelial function declines, and inflammation increases. Regular movement is not just about burning calories — it is a vascular and metabolic medicine.

This is why cardiovascular risk is rarely “one number”. It’s a network.

 

What Actually Improves Lipoprotein Health (And Why It Works)

The most powerful way to improve lipoprotein risk isn’t to obsess over cholesterol alone. It’s to change the physiological environment in which lipoproteins operate.

When blood sugar is stable, you reduce oxidative stress, you calm endothelial irritation, you lower insulin demand, and triglyceride production tends to fall. That often shifts LDL patterns toward larger particles and reduces particle number over time.

When insulin sensitivity improves, the liver stops behaving like an overworked factory exporting excess energy as VLDL. Triglycerides drop. HDL function improves. ApoB often decreases.

Resistance training is one of the best interventions because it increases muscle glucose uptake, improves insulin sensitivity, lowers visceral fat over time, and improves vascular function. It’s not “exercise for weight loss”. It’s exercise as metabolic regulation.

Higher fibre intake, especially from whole plant foods, increases bile acid binding and cholesterol excretion. The liver then pulls more cholesterol out of circulation to make new bile acids. Fibre also improves blood sugar responses and supports the gut microbiome, which influences inflammation.

Omega-3 intake can reduce triglyceride synthesis in the liver and supports anti-inflammatory signalling. It doesn’t replace the fundamentals, but it improves the inflammatory and lipid environment.

Sleep improvement is a genuine cardiovascular intervention. Better sleep improves insulin sensitivity, lowers inflammation, and improves blood pressure regulation. If sleep is broken, you can do everything else right and still struggle to shift metabolic markers.

Stress management matters for similar reasons — cortisol drives glucose production, worsens insulin sensitivity, promotes visceral fat storage, and increases blood pressure. You cannot separate heart risk from stress physiology.

The consistent theme is this:

You reduce risk by making the artery wall calmer and the lipoprotein system less overloaded.

 

Closing

Cholesterol is not the enemy. It’s an essential molecule your body needs.

The true story is about lipoproteins — the transport particles that carry cholesterol — and whether those particles are being produced in excessive numbers, circulating in a pro-oxidative environment, and interacting with an inflamed artery wall.

Atherosclerosis is not just “fat clogging arteries”. It is an inflammatory immune process that develops when LDL particles become trapped, damaged, and trigger immune activation over time.

When metabolic stability improves — through stable blood sugar, better insulin sensitivity, lower triglycerides, improved sleep, reduced inflammation, and stronger vascular function — lipoprotein behaviour improves, plaques become less likely to form, and cardiovascular risk falls.

Not through fear of cholesterol.

Through understanding the biology and restoring balance.