Your doctor runs a lipid panel, sees your LDL at 140, and reaches for the statin prescription. No conversation about particle size. No discussion of your triglyceride-to-HDL ratio, your fasting insulin, your inflammatory markers. Just LDL, a number that has been demonised for sixty years based on research that was flawed at its inception and has been selectively maintained by industry interests ever since.
Ancel Keys, the researcher behind the diet-heart hypothesis — the idea that dietary saturated fat raises LDL and LDL causes heart disease — conducted his famous Seven Countries Study by selecting seven countries from a dataset of twenty-two. The fifteen countries whose data contradicted his hypothesis were excluded. This is not conspiracy theory. It is documented scientific history.
This post covers what cholesterol actually does, why LDL particle size matters more than total LDL, which markers actually predict cardiovascular risk, and the nutritional levers that address the real drivers of heart disease.
What Cholesterol Actually Is
Cholesterol is not a poison delivered to your arteries by red meat. It is a structural and functional molecule that your body manufactures in the liver regardless of dietary intake — because it is essential. Every cell membrane in your body is composed primarily of cholesterol. Your brain is approximately 60% fat and cholesterol.
Cholesterol is the precursor to every steroid hormone in the human body: testosterone, oestrogen, progesterone, cortisol, and aldosterone. Low cholesterol is directly associated with low testosterone. Statin drugs — which block cholesterol synthesis — consistently reduce testosterone in male patients.
Cholesterol in the skin is the direct precursor to Vitamin D3 synthesis under UVB light. Blocked cholesterol synthesis impairs Vitamin D production — creating a cascade of downstream hormonal and immune deficiencies.
Bile acids — essential for fat digestion and fat-soluble vitamin absorption (A, D, E, K) — are synthesised from cholesterol. Low cholesterol means impaired fat digestion, which means impaired absorption of the fat-soluble vitamins that regulate nearly every hormonal and immune process in the body.
Ravnskov U (2009) — The Cholesterol Myths. New Trends Publishing.
LDL Particle Size: The Detail Nobody Discusses
Not all LDL particles are equal. Small, dense LDL particles (pattern B) are oxidised more easily, penetrate arterial walls more readily, and are the form associated with cardiovascular risk. Large, buoyant LDL particles (pattern A) are largely benign. A total LDL number tells you nothing about which pattern you have.
A diet high in refined carbohydrates and sugar shifts LDL toward the small, dense pattern B. A diet high in saturated fat from animal sources shifts LDL toward large, buoyant pattern A — while simultaneously raising HDL. The dietary intervention most likely to improve your cardiovascular risk profile is reducing refined carbohydrates, not saturated fat.
Krauss RM (2010) — Lipoprotein Subfractions and Cardiovascular Disease Risk. Current Opinion in Lipidology.
What to Measure Instead
If you want to understand your actual cardiovascular risk, the markers that matter are: fasting triglycerides (target under 100 mg/dL), triglyceride-to-HDL ratio (target below 2:1), fasting insulin (target under 5 mIU/L), ApoB (particle count), and high-sensitivity CRP (systemic inflammation).
- Request a full lipid panel with LDL particle size (NMR LipoProfile or similar)
- Request fasting insulin — most standard panels don't include it; insist
- Request hsCRP — the inflammation marker that actually predicts events
- Reduce refined carbohydrates and seed oils — these drive the dangerous LDL pattern
- Eat saturated fat from animal sources — grass-fed beef, eggs, raw dairy — and watch your triglycerides fall
The most dangerous nutritional intervention for your arteries isn't steak. It's the breakfast cereal that replaced it.
— Josh Button · @thatjiujiteiroThe Bottom Line
This didn't come from a textbook or a coach handing me a protocol. It came from years of training hard, getting injured, burning out, and rebuilding — smarter every time. Everything in this post is something I do, have done, or have researched deeply enough to stake my performance on.
Start with one thing. Implement it fully. Then add the next. The compounding effect of doing the basics with precision beats any biohack or supplement stack.
Hard to Kill isn't a slogan. It's the standard.
Stay Dangerous. Stay on the Mats. Hard to Kill in Midlife.
