Lab & Data — Pillar 1
“Your cholesterol is fine” is one of the most misleading things a doctor can say.
Total cholesterol tells you almost nothing meaningful.
Cardiovascular disease is the leading cause of death in the Western world — and yet the standard lipid panel used to assess risk has barely changed in 40 years. The “total cholesterol” number that most patients receive is a blunt instrument that routinely misclassifies both risk and safety. Modern lipid science has advanced considerably beyond it. Here’s what you should actually be measuring, what the numbers mean, and what the research shows about optimising each one.
What You’ll Learn
- Why total cholesterol is a poor cardiovascular risk predictor
- LDL, HDL, triglycerides, and non-HDL: what each marker actually indicates
- ApoB: the most important lipid marker most people have never heard of
- The triglyceride/HDL ratio as a proxy for insulin resistance
- Optimal vs clinical reference ranges — and why the gap matters
Why Total Cholesterol Is Misleading
Cholesterol is not inherently harmful — it’s an essential molecule. Every cell membrane in your body contains cholesterol; it’s the precursor for steroid hormones, bile acids, and vitamin D. The problem is not cholesterol per se, but where it is, in what form, and in what quantity.
Total cholesterol is the sum of all cholesterol-containing particles in the blood — LDL, HDL, VLDL, and others. Because HDL (the “protective” fraction) and LDL (the atherogenic fraction) are combined, a high HDL can mask high LDL in the total number, and a low HDL can make a normal total look deceptively safe. Total cholesterol is a poor predictor of cardiovascular events in multiple large population studies.
The markers that actually carry predictive weight are LDL (specifically LDL particle number or ApoB), HDL, triglycerides, and their ratios. Each tells a different part of the story.
The Core Lipid Markers
LDL Cholesterol — the primary atherogenic marker
Low-density lipoprotein carries cholesterol from the liver to peripheral tissues. LDL particles can infiltrate arterial walls and, when oxidised, trigger the inflammatory cascade that leads to atherosclerosis. Higher LDL-C is causally associated with cardiovascular disease — the evidence from genetics (Mendelian randomisation), statin trials, and PCSK9 inhibitor studies is robust.
| Range | Interpretation |
|---|---|
| <2.6 mmol/L (<100 mg/dL) | Optimal (low CV risk) |
| 2.6–3.4 mmol/L | Near optimal / above optimal |
| 3.4–4.1 mmol/L | Borderline high |
| >4.1 mmol/L | High — discuss with physician |
HDL Cholesterol — the protective fraction
High-density lipoprotein performs reverse cholesterol transport — returning excess cholesterol from tissues and arterial walls to the liver for processing. Higher HDL is consistently associated with lower cardiovascular risk in population studies. However, HDL is less straightforward than LDL: not all HDL particles are functionally equivalent, and attempts to raise HDL pharmacologically have not always translated into CV benefit — suggesting function matters as much as quantity.
| Range | Interpretation |
|---|---|
| <1.0 mmol/L (<40 mg/dL) | Low — significant CV risk factor |
| 1.0–1.5 mmol/L | Acceptable |
| >1.5 mmol/L (>60 mg/dL) | Protective — associated with lower CV risk |
Triglycerides — the dietary and metabolic mirror
Triglycerides are the primary form of stored fat and are transported in VLDL particles. Fasting triglycerides reflect the liver’s output of fat — driven primarily by dietary carbohydrate (particularly fructose and refined sugars), total caloric excess, insulin resistance, and alcohol. High triglycerides are an independent cardiovascular risk factor and, importantly, are one of the most rapidly modifiable lipid markers through diet. Cutting refined carbohydrates can lower triglycerides dramatically within weeks.
| Range | Interpretation |
|---|---|
| <1.1 mmol/L (<100 mg/dL) | Optimal |
| 1.1–1.7 mmol/L | Normal |
| 1.7–5.6 mmol/L | Borderline to high — dietary review warranted |
| >5.6 mmol/L | Very high — pancreatitis risk, medical review |
Apolipoprotein B — the most important marker you’re not measuring
Every atherogenic lipoprotein particle — LDL, VLDL, IDL, Lp(a) — carries exactly one ApoB molecule. ApoB therefore directly counts the number of potentially atherogenic particles, regardless of how much cholesterol each one carries. This is the key limitation of LDL-C: two people can have identical LDL-C values but very different particle numbers — and particle number is what drives arterial damage. A person with many small, cholesterol-depleted LDL particles will have a normal or near-normal LDL-C but a high ApoB — and significantly higher cardiovascular risk than their LDL-C number suggests. ApoB is now considered by many cardiologists to be the single best lipid predictor of atherosclerotic cardiovascular disease.
| ApoB level | Interpretation |
|---|---|
| <0.65 g/L | Optimal |
| 0.65–0.9 g/L | Acceptable |
| 0.9–1.1 g/L | Borderline elevated |
| >1.1 g/L | Elevated — significant atherogenic particle burden |
Foodimus Lab Testen
Meet je volledige lipidenspectrum — inclusief ApoB — thuis.
Onze at-home bloedtest geeft je LDL, HDL, triglyceriden én ApoB — de markers die samen een volledig cardiovasculair risicoprofiel geven.
The Triglyceride/HDL Ratio: A Proxy for Insulin Resistance
The ratio of fasting triglycerides to HDL-C is one of the most useful — and most underused — numbers in a standard lipid panel. It correlates strongly with LDL particle size and insulin resistance: high triglycerides and low HDL are both downstream consequences of impaired insulin signalling, and together they predict the presence of small, dense LDL particles (the most atherogenic phenotype) more accurately than LDL-C alone.
| TG/HDL Ratio (mmol/L) | Interpretation |
|---|---|
| <1.0 | Optimal — likely large, buoyant LDL, low IR |
| 1.0–1.8 | Acceptable |
| 1.8–3.0 | Borderline — possible insulin resistance, small dense LDL |
| >3.0 | High — significant IR likely, atherogenic lipid pattern |
What Actually Moves These Numbers
To lower LDL and ApoB: Reduce saturated fat (particularly from processed sources), increase soluble fibre (oats, legumes, psyllium — which binds bile acids and forces the liver to use cholesterol for replacement), maintain healthy weight, and exercise. Statins are the most potent pharmacological intervention when lifestyle changes are insufficient.
To raise HDL: Exercise (particularly aerobic) is the most reliable lifestyle intervention. Omega-3 fatty acids and niacin have modest effects. Smoking cessation raises HDL significantly. Alcohol raises HDL but the net health effect is negative at amounts that would meaningfully raise it.
To lower triglycerides: Reduce refined carbohydrate and sugar intake (the most powerful lever), reduce alcohol, lose weight if overweight, increase omega-3 fatty acids. Triglycerides are one of the most diet-responsive of all lipid markers — changes can be dramatic within 4–6 weeks of dietary modification.
The Bottom Line
Stop relying on total cholesterol. The markers that matter are LDL-C (ideally below 2.6 mmol/L), HDL-C (above 1.5 mmol/L), fasting triglycerides (below 1.1 mmol/L), ApoB (below 0.65 g/L), and the TG/HDL ratio (below 1.0). ApoB in particular is the most informative single marker and should be requested routinely. If your triglycerides are high and HDL is low, the most impactful intervention is reducing refined carbohydrate — changes can be visible on a retest within weeks.
Foodimus Lab Testen
Weet precies hoe jouw lipidenspectrum eruitziet
Meet LDL, HDL, triglyceriden en ApoB met een at-home bloedtest — geen verwijzing, geen wachttijden. Resultaten binnen dagen.
This article is for informational purposes only and does not constitute medical advice. Lipid management decisions should be made in consultation with a qualified healthcare professional, particularly if you have existing cardiovascular disease or are considering medication.
