Cholesterol: Why It’s Not Just the Number That Matters

Patients often ask me what their cholesterol numbers really mean. My answer? It depends. The number alone doesn’t tell the full story—you need the whole picture to know what it means for your health.

Here’s why.

Cholesterol doesn’t act alone. It’s part of a complex system that can either protect or harm your arteries, depending on the environment inside your body. If you could zoom in on the inside of an artery wall, you’d see cholesterol working alongside (and sometimes against) other major players:

• Inflammation – damages your artery’s protective lining (the endothelium)

• Oxidation – changes cholesterol particles, making them sticky and harmful

• Genetics – can raise particle numbers or make them more dangerous

• Insulin resistance – floods the blood with excess lipoproteins

The truth? Cholesterol is just one part of a much bigger, interconnected story. If you want to protect your heart, you have to understand—and address—the whole system.

Cholesterol 101: The Essential Molecule

Cholesterol isn’t inherently bad—in fact, without it, you couldn’t survive. Your body makes about 80% of it in the liver, regardless of how much you eat, because it’s essential for:

• Forming and repairing cell membranes in every tissue

• Producing steroid hormones such as estrogen, testosterone, and cortisol

• Manufacturing vitamin D from sunlight exposure

• Creating bile acids to digest and absorb dietary fats

• Supporting brain and nerve function, including memory and mood

The problem isn’t that cholesterol exists—it’s when there’s too much of the wrong type, in the wrong form, in the wrong environment. That’s when it becomes a key suspect in plaque formation and cardiovascular disease.

Lipoproteins, ApoB, and Particle Count

Cholesterol can’t travel through the bloodstream on its own, so it’s packaged with proteins and fats into lipoproteins. The most important for heart risk are those that contain Apolipoprotein B (ApoB)—a structural protein found on LDL, VLDL, and Lp(a).

The higher your ApoB, the more atherogenic particles are circulating. It’s not just about how much cholesterol is inside each particle, but how many particles are present to penetrate the artery wall. That’s why Apo B is proving to be important to test and monitor.

When Inflammation Gets Involved

Your arteries are lined with a smooth, protective layer called the endothelium. Inflammation—from poor diet, toxins, infections, autoimmune symptoms, elevated blood sugar, high blood pressure, or oxidative stress—damages this lining, making it more permeable and “stickier.”

Damaged endothelium allows ApoB-containing particles to slip inside the artery wall. If those particles are oxidized, they trigger an immune response that recruits white blood cells, increases inflammation, and sets off the cascade that leads to plaque buildup.

In other words: inflammation changes cholesterol from a neutral building block into a dangerous irritant.

The Genetics Layer

Some people are genetically wired for higher cardiovascular risk, no matter how healthy their lifestyle.

• Familial Hypercholesterolemia (FH): Causes very high LDL from birth; without treatment, it can dramatically increase early heart disease risk.

• Lipoprotein(a) [Lp(a)]: A genetically determined LDL-like particle with an added apolipoprotein(a) tail that promotes clotting and inflammation. Diet has little effect (usually).

• ApoE Genotype: Influences cholesterol transport and response to dietary fat. Certain variants may increase risk. (We’ll cover this in depth in a future post.)

• Other genetics – such as 9p21 gene, that increases risk of coronary heart disease.

Genetic testing helps identify these risks early so prevention strategies can be personalized.

The Metabolic Connection

Insulin resistance often shows up alongside high cholesterol and inflammation. It happens when your cells stop responding well to insulin, and it sets off a chain reaction in your blood fats (lipids):

1. The liver turns extra sugar into triglycerides (a type of fat).

2. VLDL (a particle that carries triglycerides) increases, straining the system.

3. LDL particles become smaller and denser, which makes them more likely to get into artery walls and oxidize.

4. HDL (“good cholesterol”) drops, so less cholesterol is cleared away.

5. The liver’s LDL receptors don’t work as well, so more LDL stays in circulation.

A pattern of high triglycerides, low HDL, and fatty liver often points to insulin resistance as the underlying problem.

Looking Directly at the Arteries

Numbers tell part of the story—but sometimes the most powerful insight comes from actually seeing what’s happening inside your arteries. Imaging can reveal whether plaque is already forming, how stable it is, and what your real-time risk looks like.

Common tools include:

• Coronary CT angiography (CTA) – Visualizes both calcified and soft plaque in coronary arteries

• Calcium CT scan – Measures your coronary artery calcium (CAC) score to assess plaque burden

• Carotid Intima-Media Thickness (CIMT) ultrasound – Evaluates plaque and arterial wall thickness in the carotid arteries

This information helps connect the dots between lab numbers, genetics, lifestyle, and actual arterial health—so you can create the most accurate, personalized plan possible. In my practice, I work with my patients to help determine which image is most useful to assess and monitor CV risk and vascular health.

Fixing the Whole System

Lowering cholesterol is about more than removing it from your plate—it’s about:

• Reducing ApoB particle count (especially small, dense LDL and high Lp(a) levels)

• Calming inflammation so artery walls stay smooth and healthy

• Preventing oxidation of cholesterol particles

• Supporting endothelial repair and resilience

• Correcting insulin resistance to normalize lipid metabolism

That means:

• Nutrition: High-fiber, antioxidant-rich, plant-forward eating, avoiding glucose spikes and reducing saturated fat.

• Exercise: Both aerobic and resistance training are important.

• Stress & Sleep: Foundational for lowering inflammation. Prioritize these daily.

• Root cause testing – evaluate for hidden triggers of heart disease and address them as needed.

• Targeted therapies: Supplements and medications when indicated, with special

  approaches for high Lp(a) or FH.

• Testing: ApoB, Lp(a), inflammatory markers, genetic screening, and advanced lipid

  panels to guide strategy as indicated.

The Takeaway & Call to Action

Looking at a cholesterol number alone isn’t enough—it’s part of a bigger network involving inflammation, oxidation, metabolic dysfunction, and even genetics. Lowering your risk means addressing all of them, not just chasing a number on your lab report.

The good news is we can take charge of it.

Don’t guess—test.

Knowing your ApoB, Lp(a), inflammatory markers, and genetic profile can change your prevention plan—and your future.

It’s important to get the full picture and create a plan tailored to your biology. Being proactive

and knowledgeable allows you to uncover your unique risk factors and build a strategy to keep

your arteries healthy for decades to come. Your heart health is more than a number—it’s the

story of your choices, your genes, and your care. Write it well.

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