How to Make Sense of Cholesterol Tests—and What Actually Drives Cardiovascular Risk
ApoB, LDL, and Lipid Subfractions Explained
This is Part 3 of sour series on ASCVD.
If you’ve ever looked at a cholesterol panel and felt confused, you’re not alone. Terms like LDL, HDL, triglycerides, particle size, and “subfractions” are often presented as if they each tell a different story about heart disease risk. In reality, they are all attempts to describe pieces of the same underlying biology.
At Ikigai, our goal is not to overwhelm patients with numbers—but to help you understand which markers truly drive atherosclerosis, which ones add useful context, and which ones tend to create more confusion than clarity.
This article builds on our recent Ikigai Insights exploring atherosclerotic cardiovascular disease (ASCVD), including What Drives Atherosclerosis, Part 1 and Part 2, and a recent study examining why a zero calcium score doesn’t always tell the full story—especially in younger adults. We recommend reviewing those pieces for deeper background, but this article is written to stand on its own.
A Quick Step Back: What Is Atherosclerosis—and How Does It Start?
Atherosclerosis is the gradual buildup of plaque inside the walls of arteries—the blood vessels that supply the heart, brain, and rest of the body. Over time, this process can lead to heart attacks, strokes, and other forms of cardiovascular disease.
Atherosclerosis does not begin with symptoms or sudden events. It begins quietly, often decades earlier, with subtle injury to the inner lining of the artery.
In earlier Ikigai Insights, we explored how:
Damage to the artery’s inner lining and its protective surface layer makes the vessel more vulnerable
Cholesterol-carrying particles can slip beneath the surface of the artery wall
The immune system responds, leading to inflammation and plaque formation
Early plaque can exist long before it becomes visible on a calcium score
The key takeaway from this biology is simple:
Atherosclerosis only develops when cholesterol is carried into the artery wall by specific particles—and the number of those particles matters.
That brings us to apoB.
ApoB: The Most Important Number Most People Have Never Heard Of
Cholesterol does not float freely in your bloodstream. It is transported inside particles called lipoproteins. Every particle capable of contributing to atherosclerosis carries a protein on its surface called apolipoprotein B, or apoB.
You can think of apoB as a count of cholesterol-carrying particles that are capable of entering the artery wall.
Each of the following particles contains exactly one apoB molecule:
LDL
VLDL
IDL
Lipoprotein(a), or Lp(a)
As these particles circulate and deliver triglycerides to tissues, they change in size and composition; their remnant forms remain apoB-containing and atherogenic, reinforcing why total apoB particle burden—not just LDL cholesterol—drives cardiovascular risk.
For completeness: there are two forms of apolipoprotein B. ApoB-48 is produced in the intestine and is found on short-lived particles that transport dietary fat after meals. ApoB-100 is produced by the liver and is found on LDL, VLDL, IDL, and lipoprotein(a)—the particles that circulate in the bloodstream and can enter the artery wall. When we refer to “apoB” in this article, we are referring to apoB-100.
Cholesterol Is Essential—Excess ApoB Particles Are Not
This distinction is important.
Cholesterol itself is a vital molecule. It is a key building block of cell membranes, a precursor for steroid hormones and vitamin D, and essential for many normal biological functions. Every cell in the body is capable of making the cholesterol it needs.
ApoB-containing particles are not delivering a scarce or essential nutrient. Instead, they exist to transport excess lipid energy through the bloodstream. When too many of these particles circulate for too long, they increase the likelihood of entering the artery wall and being retained there—where they can drive inflammation and plaque formation.
In this way, apoB-containing particles represent a form of biologically unnecessary exposure when present in excess.
This is why apoB-containing particles are necessary for atherosclerosis to occur, but not beneficial in high numbers. Without them, plaque does not form. With increasing particle burden over time, risk rises.
This is why apoB is best understood as a causal marker of risk, not a reflection of cholesterol itself being harmful.
Where LDL Cholesterol Fits In—and Where It Falls Short
LDL cholesterol (LDL-C) is the number most people are familiar with. It measures the amount of cholesterol inside LDL particles, not how many particles are present.
This distinction matters.
A simple analogy:
LDL-C tells you how full the buckets are
ApoB tells you how many buckets are being carried into the artery wall
You can have:
A small number of cholesterol-rich particles
Or a large number of cholesterol-poor particles
Both situations can produce the same LDL-C value, but the second exposes the arteries to far more particle traffic and greater opportunity for retention.
This mismatch—called discordance—is especially common in insulin resistance, metabolic dysfunction, obesity, and elevated triglycerides. In these settings, LDL-C can appear unremarkable while apoB particle burden remains high.
LDL-C is not “wrong”—it simply answers a different question than the one most relevant to plaque formation.
Why ApoB Explains What Calcium Scores and LDL Sometimes Miss
In our recent review of a large Danish study, researchers found that many individuals with a calcium score of zero still had early, non-calcified plaque visible on advanced imaging. Higher LDL-C correlated with this hidden plaque, particularly in younger adults.
What matters here is not the cholesterol number itself, but what it reflects: cumulative exposure to apoB-containing particles over time.
Early plaque is:
Soft
Non-calcified
Biologically active
Invisible to calcium scoring
ApoB helps explain risk during this earlier, quieter phase—before plaque hardens and becomes visible on traditional scans.
What About Lipid Subfractions and Particle Size?
Lipid subfraction tests attempt to further categorize lipoproteins by size, density, or particle type.
While these measurements can add descriptive detail, they often distract from the central issue. Regardless of size or subclass, any apoB-containing particle has the potential to enter the artery wall.
Small particles are not harmful because they are small. Large particles are not protective because they are large. What matters is how many atherogenic particles are circulating and for how long.
For this reason, lipid subfractions are best viewed as secondary tools. When apoB is known, they rarely change the overall understanding of risk.
“Good” and “Bad” Cholesterol—and What We Really Mean
Cholesterol itself is not “good” or “bad.” The cholesterol carried inside HDL particles is chemically identical to the cholesterol carried inside apoB-containing particles. What differs is the particle carrying it—where it travels, how long it circulates, and whether it can enter the artery wall.
The labels “good” and “bad” cholesterol grew out of early population studies, but they oversimplify the biology and often create confusion. In this article, we focus on apoB-containing particles because they are the ones that can enter the artery wall and drive plaque formation.
In our next Ikigai Insights article, we’ll take a deeper look at HDL—why it earned the label “good cholesterol,” why that terminology is misleading, and what HDL actually tells us about cardiovascular and metabolic health.
Putting It All Together: How We Think About Lipids at Ikigai
When assessing cardiovascular risk, we focus on:
ApoB particle burden
Duration of exposure over time
Factors that influence whether particles enter and are retained in the artery wall
Imaging, when appropriate, to understand plaque presence and behavior
LDL-C, triglycerides, HDL, and lipid subfractions all provide context—but apoB anchors the biology.
Key Takeaways
Cholesterol is an essential molecule, not a toxin
Atherosclerosis is driven by excess apoB-containing particles entering and being retained in the artery wall
ApoB reflects particle burden, not cholesterol chemistry
LDL-C can underestimate risk when particle number is high
Lipid subfractions add description but rarely change the core story
Understanding your lipid profile should empower you—not confuse you. The goal is not to fear cholesterol, but to reduce unnecessary exposure to the particles that drive plaque formation over time.
That is how we protect long-term heart health.
To more deeply understand your personal risk and how to prevent plaque formation, please schedule a call to learn more about Ikigai Health Institute.
