Introduction 

You’ve probably heard people say dyslipidaemia is when there’s an imbalance between the good cholesterol and the bad cholesterol, and then suddenly blame cholesterol altogether. While that definition isn’t entirely wrong, it oversimplifies things. Some even say, “I have cholesterol”, making cholesterol out to be the villain. But that couldn’t be farther from the truth, because cholesterol isn’t the enemy, it’s a vital part of the body’s normal processes.

Having established that dyslipidaemia is not just a simple imbalance between good and bad cholesterol, what is dyslipidaemia? Dyslipidaemia is defined as an abnormal level of lipids (fat) in the bloodstream. Now, abnormal could mean:

• A higher level (above 100 mg/dL) of low-density lipoprotein (LDL), popularly known as bad cholesterol
• A higher level (above 150 mg/dL) of triglycerides
• A lower level of high-density lipoprotein (HDL), the good cholesterol, less than 50 mg/dL for people assigned female at birth (AFAB) and 40 mg/dL for people assigned male at birth (AMAB)
• Or even a total cholesterol level above 200 mg/dL

Dyslipidaemia can occur due to:

• Genetic causes (called primary dyslipidaemia)
• Lifestyle and environmental factors (called secondary dyslipidaemia) 

Either way, it increases the risk of atherosclerosis (plaque build up in the arteries) and other cardiovascular diseases.^1,2

Read on to understand the mechanism behind dyslipidaemia, because once you get how it works, managing it suddenly becomes a lot easier.

Why is cholesterol essential for your body?

Imagine a cell as a small water balloon: soft, round, and filled with vital materials. The outer layer of that balloon, known as the cell membrane, acts as a protective barrier. It needs to be just the right balance of firm and flexible to keep the cell stable while allowing nutrients and signals to pass through.

This is where cholesterol comes in. It is a lipid (type of fat) that fits between the fatty components of the cell membrane, helping it maintain the right level of fluidity. Without cholesterol, the membrane could become too soft and leaky, or too stiff to function properly.

In fact, your body depends on cholesterol to make several essential substances. Vitamin D, for example, is produced in the skin through a process that requires cholesterol. This vitamin is not just important for bone health, but also plays a role in regulating the immune system and even blood sugar levels. Cholesterol is also the building block for hormones and is equally vital in producing bile salts, which your body needs to properly digest and absorb fats.

So you see, cholesterol is absolutely essential for your body to function properly.³

What are lipoproteins?

Cholesterol and triglycerides do not dissolve in water, and since the body’s transport system (like blood) is water-based, they can’t just float around on their own. That’s why they need to bind to proteins to move around. These combinations are called lipoproteins.

What are triglycerides?

Triglycerides are the form in which fats are stored in your body. The body uses them for energy, and any excess is stored in fat cells for later.

Lipoproteins are complex particles with a hydrophobic (fat-loving) core that holds triglycerides and cholesterol esters. This core is surrounded by a hydrophilic (water-loving) outer membrane made up of phospholipids, free fatty acids, and apolipoproteins.⁴ It is this hydrophilic membrane that makes it possible for lipoproteins to move around the body.

Classes of lipoproteins

Depending on their size, content, and surface apolipoproteins, they are classified into seven types: Chylomicrons, Chylomicron Remnants, Very Low-Density Lipoprotein (VLDL), Intermediate-Density Lipoprotein (IDL), Low-Density Lipoprotein (LDL), High-Density Lipoprotein (HDL), and Lipoprotein(a).⁴

Chylomicrons

Chylomicrons are lipoprotein particles packed with triglycerides. They’re made by the intestines and are responsible for transporting dietary triglycerides and cholesterol to peripheral tissues. Basically, places like your muscles and fat stores where the body uses or stores fat, and the liver. They also transport fat-soluble vitamins like vitamins A, D, E and K.

Their size depends on how much fat you eat. The more fat in your meal, the larger the chylomicrons your body will make. In fasting states, their size tends to be much smaller.

Chylomicron remnants 

These are formed from chylomicrons after they have given off most of their triglycerides to peripheral tissues. What’s left is a smaller, cholesterol-rich particle that eventually travels to the liver.

Very low density lipoproteins (VLDL)

These are produced in the liver and are rich in triglycerides. Their main role is to transport these triglycerides to peripheral tissues.

Intermediate density lipoprotein (IDL)

After VLDL leaves the liver and gives off some of its triglycerides, it becomes IDL - a transitional form between VLDL and LDL.

Low-density lipoprotein (LDL)

LDL is enriched in cholesterol and carries the majority of the cholesterol found in circulation. Each LDL particle contains one molecule of Apo B-100, which is its primary protein. The size of LDL particles varies, but it’s the small, dense ones that cause concern. These smaller particles are more likely to stay in the bloodstream, undergo oxidation, and contribute to plaque build-up in arteries, making them proatherogenic (more likely to cause atherosclerosis).

High-density lipoprotein (HDL)

These are very important lipoproteins because they play a role in something called reverse cholesterol transport, that is, they help remove excess cholesterol from peripheral tissues and carry it back to the liver. This process is one possible reason HDL is considered protective against atherosclerosis.

But it doesn’t stop there. HDL also has anti-inflammatory, antioxidant, anti-thrombotic, and anti-apoptotic properties. All these work together to further inhibit the development of atherosclerosis.

Lipoprotein (a)

This is essentially an LDL particle with an added apolipoprotein (a) attached to it. Like small dense LDL, it is pro-atherogenic, meaning it promotes the development of atherosclerosis. Its size can vary between individuals, and higher levels are considered an independent risk factor for cardiovascular disease.⁴

Lipoprotein metabolism explained

There are two main pathways involved in how lipoproteins are formed and function in the body: the exogenous pathway and the endogenous pathway.

The exogenous pathway

This begins after eating fatty foods. Once these fats reach the intestine, they undergo a series of digestive processes and are eventually packaged into lipoprotein particles called chylomicrons.

As chylomicrons enter circulation, they are acted upon by an enzyme called lipoprotein lipase, which helps them release a large portion of their triglyceride content. These triglycerides are then either used for energy or stored in tissues like muscle and fat.

What remains of the chylomicron after this process is called a chylomicron remnant, which goes into the liver.⁴

The endogenous pathway

This begins in the liver, which produces very low-density lipoproteins (VLDL). These particles are rich in triglycerides. As VLDL circulates, lipoprotein lipase acts again, metabolising the triglycerides. The VLDL is processed into intermediate-density lipoproteins (IDL), which can be further processed into low-density lipoproteins (LDL).

LDL particles deliver cholesterol to various tissues, including the liver, via LDL receptors.⁴

Reverse cholesterol transport

This is the body’s way of clearing out excess cholesterol from tissues. It starts with the liver and intestine forming small, immature HDL particles known as nascent HDL. These particles gradually acquire cholesterol from peripheral tissues to form mature HDL.

The mature HDL can return cholesterol directly to the liver or transfer it to other lipoproteins like VLDL or LDL, which then carry it back to the liver.⁴

This whole system is a carefully balanced network responsible not just for cholesterol transport, but also for the distribution of fats and even fat-soluble vitamins. HDL plays a protective role by helping to remove excess cholesterol, while other lipoproteins help distribute it where needed.

The problem arises when this balance is disturbed. For example, when LDL becomes excessive or HDL is too low, leading to disorders like dyslipidaemia and increasing the risk of atherosclerosis and cardiovascular disease.

Lipoprotein disorders and the development of dyslipidaemia

Behind the body’s use of cholesterol and fat is a well-organised system of carriers like LDL, HDL, and VLDL. They each have roles. LDL takes cholesterol to where it’s needed, HDL brings back the excess to the liver for disposal, and VLDL handles triglycerides. A problem arises when this transport system is interrupted. That’s what we see in dyslipidaemia, an imbalance in the levels of these lipoproteins.

There are two major types: familial and lifestyle-related.⁴

Familial dyslipidaemia

This one is inherited i.e., it is passed down through genes. The problem could be in the production, transport, or breakdown of lipids. There are different forms, but let’s take familial hypercholesterolaemia for example.

In this disease, there’s a mutation in the LDL receptor gene. These receptors are like doors that allow LDL to deliver cholesterol into cells. But in this condition, the doors are faulty or missing. So LDL can’t offload cholesterol where it’s needed. It keeps circulating in the blood, leading to high levels of LDL.

Over time, these excess LDL particles begin to lodge themselves in the inner lining of blood vessels (the sub-endothelial space). There, they undergo oxidation and attract immune cells, forming foam cells. These foam cells are the early signs of plaque and that’s how dyslipidaemia starts to take shape.⁴

Lifestyle dyslipidaemia

Now, this one is more common and happens over time. It could be due to diet, inactivity, or conditions like diabetes. It’s kind of similar in that LDL levels still go up, but the cause is different.

Let’s say someone eats a lot of fatty and sugary foods. The liver starts producing more VLDL (which carries triglycerides). At the same time, if the person has insulin resistance or diabetes, the removal of LDL by the liver is reduced. So again, LDL stays longer in the blood than it should.

That prolonged presence gives LDL time to undergo changes, i.e., it gets oxidised, enters the vessel wall, and forms foam cells too, just like in familial cases. And on top of that, HDL is usually low in lifestyle dyslipidaemia. That means there’s no one to clean up the excess cholesterol.

So whether it’s from genes or lifestyle, the story is the same: excess LDL in the blood, foam cell formation, and the beginning of what could later become atherosclerosis.⁴

How dyslipidaemia leads to atherosclerosis

One important reason dyslipidaemia increases the risk of atherosclerosis is the rise in small dense LDL (sdLDL) particles. These are mostly seen in lifestyle-related dyslipidaemia, especially when triglyceride levels are high. This can happen with excess calorie intake, lack of physical activity, or insulin resistance.⁵ The more triglycerides you have, the more sdLDL is produced.⁶

Now, sdLDLs are not your regular LDLs. They’re smaller, denser, and more dangerous. They stay longer in the bloodstream because they don’t easily bind to LDL receptors. This gives them more time to squeeze into tiny blood vessels where they don’t belong. They’re also more prone to oxidation, and oxidised LDL is a known trigger for plaque formation.⁷

What’s more, all these atherogenic particles i.e., sdLDL, LDL, VLDL, carry apolipoprotein B (apoB). ApoB acts like a tag that helps these particles enter the walls of arteries. Once inside, they attract immune cells, get trapped, and form foam cells, which is how plaque starts building up. Over time, this clogs and stiffens the arteries, leading to atherosclerosis.⁸

Summary

Cholesterol isn’t the problem, an overwhelmed system is. When too many atherogenic lipoproteins like sdLDL and apoB-carrying particles pile up, they sneak into your arteries, get stuck, and spark inflammation. That’s how dyslipidaemia quietly sets the stage for atherosclerosis. Understanding this helps you take control, because knowing the “how” makes managing the “what next” a lot easier. And the good news is, once you know what’s really happening beneath the surface, you can make choices that ease the pressure on your system, whether that’s through diet, movement, sleep, or sometimes medication. It’s not about fearing cholesterol; it’s about creating balance, lowering the burden on your arteries, and giving your body the chance to heal and protect itself.