Remnant Cholesterol: The Particle That May Be 4× Worse Than LDL
Researcher Elias Bjornson used genetic data from roughly half a million UK Biobank participants to compare remnant lipoproteins with LDL, particle for particle. Remnants came out roughly four times more atherogenic per particle — but they are also about ten times less abundant, so LDL still carries most of the risk for most people. Remnants move to centre stage when triglycerides are high or when LDL has already been brought far down.
Overview
Every lipoprotein that can drive plaque carries exactly one copy of a protein called ApoB, which makes it possible to count particles and compare them fairly. Three families matter: LDL, remnants (also called triglyceride-rich lipoproteins), and Lp(a). For decades it was unclear whether a remnant was as dangerous as an LDL particle, or worse. Bjornson's team used Mendelian randomization — treating inherited genetic variants as a kind of lifelong natural randomization — across more than a thousand variants in UK Biobank to separate the effect of remnants from the effect of LDL.
Per unit of cholesterol, remnants tracked with roughly two-and-a-half to three-and-a-half times more risk; per particle, roughly fourfold. The team spent 18 to 24 months trying to break the result with NMR particle counts, polygenic scores and purely observational analyses, and the picture held. Bjornson is emphatic that this does not overturn clinical practice: for an average person only about one particle in ten is a remnant, so LDL remains the dominant contributor.
The balance shifts for people with high triglycerides — around 3 mmol/L or roughly 250 mg/dL — and for people whose LDL has been lowered by medication, where remnants can account for the majority of remaining risk. The conversation closes on how to read a standard lipid panel with this in mind, and on the drug trials that could settle the question.
Key quotes
5For the same unit increase in ApoB you get a certain risk increase from LDL, but you get roughly a three or fourfold higher risk increase if you change remnant particle number by the same amount.
We tried really, really hard to kill the results, but no matter how we did the analysis the results came out pretty much the same.
They may be more atherogenic per particle, but LDLs are literally ten times as common in the bloodstream for an average person.
If you have a plasma triglyceride level of maybe 3 mmol/L or above, you really can't ignore the remnant risk — it becomes a major player.
It's all just a numbers game: how many particles you have, times how atherogenic they are.
Key ideas
9Three atherogenic families, one shared protein
Every particle that can lodge in the artery wall carries exactly one copy of ApoB: LDL, remnants, and Lp(a). Because the ratio is one-to-one, ApoB is effectively a particle count, which is what makes a fair per-particle comparison possible.
Lipoproteins are transport vehicles
Fat does not dissolve in an aqueous bloodstream, so the liver and intestine wrap lipids in a phospholipid shell — Bjornson likens them to tennis balls. They carry fat-soluble vitamins and cholesterol, and let the liver offload excess lipid.
Remnants are a continuum, not a tidy category
A freshly released VLDL loses triglyceride to lipases and shrinks: VLDL → IDL → LDL. Technically it becomes a remnant the moment the first triglyceride is stripped away, so the class labels are convenient markers on a continuous process.
Clearance pathway defines the particle
While a particle still holds enough triglyceride it is a substrate for lipoprotein lipase. Once enough has been removed, lipase loses interest and the LDL receptor takes over. The catabolic route, not just the size, marks the boundary.
Mendelian randomization as a lifelong natural trial
Some people inherit variants that nudge LDL or remnants up or down, effectively randomizing exposure at birth. The team screened over a thousand such variants in roughly half a million UK Biobank participants followed for more than a decade.
Roughly fourfold per particle
Per unit of cholesterol, remnants tracked with about two-and-a-half to three-and-a-half times the risk of LDL. Because remnants also carry more cholesterol per particle, the per-particle figure comes out at roughly four times.
Triangulated from every angle
The team repeated the analysis with NMR-measured particle counts, with ApoB-based estimates, with polygenic scores, and with purely observational data. Every route produced the same answer, which is why they eventually published.
Abundance still decides the total
For an average person only about one particle in ten is a remnant. Multiply potency by abundance and LDL still carries the clear majority of risk — Bjornson repeats this point deliberately, because the finding is easy to over-read.
Where remnants take over: residual risk
In someone with high triglycerides whose LDL has been lowered by medication, remnants can account for 60–70% of remaining atherogenic risk. Statins do lower remnant cholesterol too — roughly 25% when LDL cholesterol drops 50% — but less efficiently than they lower LDL.
Practical takeaways
6- 1
Your standard panel already contains it 1:12:30
Remnant cholesterol can be estimated as total cholesterol minus HDL cholesterol minus LDL cholesterol — no special test needed. Worth knowing as one more lens on your lipid picture.
- 2
Check whether LDL was measured or calculated 1:14:00
If LDL cholesterol came from the Friedewald formula, the subtraction just reproduces your triglycerides. The calculation only carries new information when LDL was measured directly — most panels state which.
- 3
Keep a second eye on triglycerides 1:16:00
Bjornson prefers triglycerides below 1 mmol/L. As the number climbs toward 2.5–3 mmol/L, non-HDL cholesterol starts to under-read total risk because the mix has shifted toward remnants.
- 4
ApoB or non-HDL — both are solid 1:17:30
Two opposing effects nearly cancel out, and Bjornson calls the choice almost a wash. Tracking both and keeping them in a healthy range is the pragmatic answer for most people.
- 5
Low LDL is not the whole story 1:04:00
Residual risk is what remains once the LDL fraction is handled — remnants and Lp(a) being the usual candidates. A very low LDL alongside very high triglycerides is worth a closer look with your clinician.
- 6
Triglycerides are the practical lever 1:19:30
Since remnant load tracks closely with triglycerides, lifestyle approaches that bring triglycerides down are the accessible route for most people. Nothing here replaces personalised medical guidance.
Topics & chapters
15The particle nobody talks about
Beyond LDL there is a second atherogenic family that may be four times worse, particle for particle. Setting up the conversation with Elias Bjornson.
Three ApoB-carrying families
LDL, remnants (VLDL/IDL, also called triglyceride-rich lipoproteins) and Lp(a) — all carrying exactly one ApoB, and why the relative danger of remnants was never settled.
Lipoprotein school: what they are and why
How fat travels through water-based blood, where these particles are made and cleared, and how they end up in the artery wall.
Naming the family: remnants, TRLs, IDLs
Why researchers say remnants in conversation and triglyceride-rich lipoproteins in print, and how the particles shrink along a continuum.
What makes a particle distinct
Composition, surface proteins and clearance pathway all shift as a particle shrinks — the categories are arbitrary at the edges but not meaningless.
Mendelian randomization explained
Genetic variants as nature's randomized trial, and how UK Biobank made it possible to isolate variants that move remnants without moving LDL.
The headline result
Per unit of ApoB, remnants tracked with roughly three to four times the risk increase of LDL — the finding that gives the video its title.
From lipids to particle numbers
How the team bridged cholesterol measurements to particle counts, and the honest limits: Mendelian randomization speaks about average particles, not individual composition.
Trying to kill the result
NMR particle counts, polygenic scores and observational analyses, run over 18–24 months. Every approach gave the same answer.
The Sniderman counterpoint
Allan Sniderman's editorial pushback, and Bjornson's agreement that all available evidence has to be triangulated rather than cherry-picked.
Why LDL is still the main event
Remnants are roughly ten times less abundant, so for the average person LDL carries around 70–75% of ApoB-related risk.
Who this actually matters for
High triglycerides around 3 mmol/L, the top decile of the population, and people with type 2 diabetes — the groups where remnant risk approaches or exceeds LDL risk.
Residual risk on medication
When LDL has been lowered, what remains is disproportionately remnant- and Lp(a)-driven. Statins do lower remnants, just less efficiently.
The 25–30% threshold and non-HDL
Where the risk gradient becomes statistically visible, why most people sit below it, and what that does and does not imply clinically.
ApoB vs non-HDL, and what comes next
The opposing forces that make the two markers nearly equivalent, the PROMINENT trial puzzle, ApoC3-targeting drugs on the horizon, and the closing recap.