Cholesterol is not your enemy — your liver makes most of it regardless of what you eat
The relationship between dietary cholesterol, blood cholesterol and cardiovascular risk is far more nuanced than four decades of public health messaging suggested.
science
is a structural molecule — not a toxin, not a fuel, not a waste product. Every cell membrane in your body contains it. Your brain is roughly 25% by dry weight. It is the raw material from which your body makes vitamin D, cortisol, testosterone, oestrogen and progesterone. Without it, none of those things exist.
The liver produces roughly 75 to 80% of the in your bloodstream. The remaining 20 to 25% comes from food. What most people don't know is that when you eat more dietary the liver compensates by producing less. When you eat less, it produces more. This feedback loop — mediated by the LDL receptor and an enzyme called HMG-CoA reductase — means that for the majority of people, dietary has a surprisingly modest effect on blood levels.
LDL and HDL are not — they are lipoproteins, protein-fat carriers that transport through the bloodstream. LDL carries to tissues. HDL carries it back to the liver for recycling or excretion. The problem isn't the itself but the behaviour of the particle carrying it
A 2024 study identified a gut-derived hormone called Cholesin that, when released in response to dietary intake, signals the liver to reduce its own synthesis — a previously unknown feedback mechanism that helps explain why dietary often has little net effect on blood levels in healthy individuals
Roughly 25% of people are 'hyper-responders' — their LDL rises meaningfully in response to dietary However, in many of these individuals, HDL rises proportionally, meaning the ratio of total to HDL remains stable, and the cardiovascular risk increase is smaller than the raw LDL number suggests
Dietary saturated fat raises LDL more reliably than dietary does — by reducing the liver's expression of LDL receptors, which slows the clearance of LDL from circulation. This is the more significant dietary driver for most people
Fructose has a separate and more direct effect on blood — it stimulates hepatic lipogenesis and increases VLDL production in ways that does not, explaining why high-sugar diets often worsen the and HDL picture independently of fat intake
The shift in scientific consensus over the past decade has been significant. Dietary was removed as a 'nutrient of concern' from US dietary guidelines in 2015, after decades of egg-restriction advice that the evidence never clearly supported. Eggs, shellfish and liver — all previously vilified for their content — are now understood to be among the most nutrient-dense whole foods available.
What actually predicts cardiovascular risk more reliably than total LDL is the number of LDL particles (LDL-P), the size and density of those particles, levels, insulin sensitivity and chronic inflammation. These are shaped far more by refined intake, sedentary behaviour, poor sleep and oxidative stress than by the content of whole foods.