The standard panel tells you how much cholesterol is circulating. It cannot tell you whether that cholesterol is dangerous. Six markers that can, and the ranges to read them against.
01 of 09
The problem with total cholesterol
The standard lipid panel was designed in 1972. It measures how much cholesterol is circulating. It does not tell you whether that cholesterol is dangerous.
Cholesterol is a building block. Your body makes it on purpose. It repairs cell membranes with it, builds hormones from it and produces bile acids out of it.
What your body builds from cholesterol
Hormones
Testosterone, estrogen, progesterone, cortisol and vitamin D.
Cell membranes
Structural repair and integrity of every cell in the body.
Bile acids
Produced to digest fats and absorb fat-soluble nutrients.
The question was never how much cholesterol you have. The question is whether your cholesterol is being oxidised and deposited into arterial walls, and a standard lipid panel cannot answer that. That is the gap this guide closes.
02 of 09
What makes cholesterol dangerous
the particle only becomes a problem once it oxidises
Cholesterol becomes a problem when it is oxidised. Oxidised LDL penetrates the arterial wall, triggers an inflammatory response and initiates plaque formation.
Four things drive LDL oxidation
Insulin resistance
Drives overproduction of small dense LDL, the most oxidation-vulnerable type.
Seed oils
Linoleic acid integrates into LDL particles and makes them oxidation-prone.
Systemic inflammation
Inflammatory cytokines accelerate oxidative damage to particles.
High blood sugar
Glycation damages the LDL particle surface with chronic elevation.
The number is not the risk
Someone with high LDL-C but low inflammation, low insulin and no seed oil exposure may carry almost no cardiovascular risk. Someone with normal LDL-C but high insulin, high inflammation and small dense particles may be building plaque right now. The metabolic environment is the risk.
03 of 09
The six markers that actually predict risk
Marker
What it tells you
TG:HDL ratio
Proxy for LDL particle size and insulin resistance. The single most accessible predictor on a standard panel.
Fasting insulin
Direct measure of insulin resistance, the metabolic driver behind small dense LDL production and triglyceride elevation.
hs-CRP
High-sensitivity C-reactive protein. Systemic inflammation is what makes cholesterol dangerous.
LDL particle number
How many LDL particles you actually have. More particles means more opportunities for arterial wall penetration.
ApoB
One molecule per atherogenic particle, so it counts every particle that can cause plaque. Many clinicians now consider this the single best predictor.
Lp(a)
Genetic risk factor. Does not change with diet or exercise. The strongest inherited predictor of cardiovascular disease.
Most of these are not on a standard panel
If your doctor does not order them, we do. We have direct access to comprehensive lipid testing for clients across North America and the EU. No referral needed.
04 of 09
Functional optimal ranges
This is the page to screenshot. These are the ranges we interpret every client's panel against, not the standard lab reference ranges.
Under 1.0 mg/L. Between 1.0 and 3.0 is active vascular inflammation called normal.
Total cholesterol
Under 200
Context-dependent. Alone it predicts almost nothing. Interpret with particle data.
LDL-C
Under 100
Meaningless without particle size. 130 large buoyant is lower risk than 100 small dense.
HDL
Above 40 men / 50 women
Above 55 men / 65 women. Higher is generally better.
Triglycerides
Under 150
Under 80. Above 100 with HDL below 50 almost always means insulin resistance.
LDL-P
Not standard
Under 1000 nmol/L. Above 1300 is elevated regardless of LDL-C.
ApoB
Not standard
Under 80 mg/dL. Above 100 is elevated.
Lp(a)
Not standard
Under 30 nmol/L, or under 14 mg/dL. Genetic, so test once.
05 of 09
The TG:HDL walkthrough
This is the one marker you can calculate right now from a standard panel. Take your triglycerides and divide by your HDL.
three panels, three very different pictures
Ratio
The numbers
What it means
1.15
Triglycerides 75, HDL 65
Mostly large buoyant LDL. Low cardiovascular risk.
2.1
Triglycerides 110, HDL 52
Borderline. Warrants deeper testing to see particle distribution.
4.7
Triglycerides 180, HDL 38
Dominated by small dense LDL. High risk regardless of total cholesterol.
Above 2.0
If your ratio is above 2.0 and you want to know what is driving it, that is the first thing we look at on intake. We run a full panel, identify the upstream driver and build the protocol around it.
06 of 09
The insulin connection
Insulin resistance is the engine behind most lipid dysfunction. Here is the cascade, and fasting insulin sits upstream of all of it.
Insulin overproduces VLDL. Chronically elevated insulin drives the liver to overproduce triglyceride-rich VLDL particles.
LDL becomes small and dense. VLDL exchanges triglycerides for cholesterol with LDL via CETP, making the particles smaller and denser.
Particles penetrate the arterial wall. Small dense LDL is more easily oxidised and more likely to cross into the wall.
The panel still reads normal. Triglycerides rise, HDL falls, particle count climbs, and LDL-C may not move at all. The environment is atherogenic while the printout looks fine.
Address the engine, not the exhaust
We run fasting insulin on every intake panel and most providers skip it. If insulin resistance is driving your lipid profile, no amount of dietary cholesterol reduction will fix it.
07 of 09
Lp(a) and genetic risk
Lp(a) is a modified LDL particle with an extra protein attached. It promotes clotting and it is pro-inflammatory.
90%+
genetically set
Diet, exercise and most medications do not meaningfully change it.
~20%
of people carry it high
Most have never been tested for it.
1x
test once
It does not fluctuate, so a single result gives you a permanent answer.
Elevated does not mean inevitable
If Lp(a) is elevated it does not mean cardiovascular disease is coming. It means your margin for error on every other risk factor is smaller. Insulin sensitivity, inflammation, particle size and oxidative stress all matter more for you, not less.
08 of 09
The CAC score
CAC stands for coronary artery calcium. It is a low-dose CT scan of the heart that directly measures calcified plaque in your coronary arteries. Ten minutes, no contrast dye, and in most places no referral needed.
Score
What it means
Zero
No detectable calcified plaque. The single strongest data point for ruling out significant coronary artery disease, regardless of your cholesterol numbers.
Above zero
Plaque is present. This gives you a concrete baseline to track against over time and monitor progression.
Measure the disease, not the risk factor
The CAC score measures the actual disease rather than a risk factor for it. That distinction matters, and a score of zero is the most powerful piece of evidence against a statin prescribed on total cholesterol alone.
09 of 09
What to remove, what to add
Remove
Seed oils · highest impact
Canola, soybean, sunflower, safflower, corn, cottonseed, grapeseed and generic vegetable oil. Linoleic acid from these integrates into LDL particles and makes them more susceptible to oxidation. This is the single highest-impact dietary change for lipid health.
Refined sugar and processed carbohydrate
These spike insulin, which drives the VLDL to triglyceride to small dense LDL cascade. Reducing them lowers triglycerides and improves particle size, often within four to six weeks.
Highly processed food
Most contain both seed oils and refined carbohydrate. If the ingredient list runs longer than five items it is likely contributing.
Add
Omega-3 fatty acids
Wild salmon, sardines, mackerel, anchovies, two to three servings a week minimum. Omega-3s lower triglycerides, improve HDL function, reduce hs-CRP and shift particle size toward large buoyant. If you do not eat fish regularly, a high-quality fish oil at a minimum of 2 g combined EPA and DHA fills the gap.
Olive oil
Extra virgin, high in oleic acid and polyphenols. Replacing seed oils with it for cooking and dressings is a direct, high-leverage swap.
Pastured eggs
Whole eggs. The yolk carries choline, critical for liver function and VLDL metabolism, plus fat-soluble vitamins A, D, E and K2.
It is not the egg
Dietary cholesterol, eggs, shellfish and organ meats do not meaningfully raise serum cholesterol in most people. The thing raising your cholesterol is not the egg. It is the oil it was cooked in.
Ready to read your own panel like a clinician?
We run comprehensive lipid testing, interpret every marker against these functional ranges, and build a protocol around your actual biology rather than a template. No referral needed.