Animal Fats and Cholesterol Genes: Danger or Redemption?

by Laurent Glatz – for Athletic Carnivore

We still hear this question:
“Where does cholesterol fit into all this?”
As if increasing animal fats in a carnivore diet would inevitably trigger a heart attack. But behind this collective fear lies a more nuanced, personal reality: your reaction to fats depends on your genes. And perhaps what you call “high cholesterol” is simply your biology expressing itself.

Cholesterol: poison or regeneration tool?

Cholesterol is a vital molecule.
It composes your cell membranes, your sex hormones, your vitamin D, your bile, your myelin.
And 80% of the cholesterol in your body is produced… by your own liver. Not by what you eat.

But when you increase saturated animal fats, you change how this cholesterol circulates. In some people, it rises. In others, it reorganizes: triglycerides drop, HDL rises, LDL changes.

And this is where your SNPs come into play.

APOE: the genetic filter of fat

The APOE gene codes for a protein that transports cholesterol in the blood.
There are three main versions: E2, E3, E4.

APOE3/3, the norm: good tolerance to saturated fats.

APOE2: rather protective, tends to lower LDL.

APOE4: ancestral, conserved, but less efficient at recycling cholesterol.

If you carry APOE4, heterozygous or homozygous, you may see your LDL soar on a fat-rich carnivore diet. But is this dangerous?
Not necessarily. It depends on your baseline inflammation, CRP levels, your triglycerides—which should remain low—your insulin sensitivity or resistance, and especially the size of your LDL particles: large = less harmful; small = inflammatory.

LDL: the real issue is not quantity, but form

LDL is not “bad cholesterol.”
It transports energy, in the form of triglycerides, to tissues.
But if it becomes small, dense, and oxidized, it turns inflammatory. And that is not caused by meat, but by refined carbohydrates, oxidized vegetable oils, unstable blood sugar, and an inflammatory environment.

In a carnivore protocol rich in stable fats and low in carbs, LDL can rise… without becoming dangerous. It’s a shift in energy strategy, not a disease marker.

Liver genes: ABCG5, LDL-R, PCSK9…

Certain SNPs also influence your liver’s ability to recycle or eliminate cholesterol.

LDL-R, the LDL receptor: if this gene is underexpressed, your liver poorly recycles LDL, which remains elevated in the blood.

PCSK9: regulates degradation of LDL-R. Some profiles have exaggerated activity, keeping LDL circulating.

ABCG5/8: controls cholesterol excretion into bile. Mutations cause cholesterol accumulation.

These genetic profiles alter your lipid panels… without a direct or automatic link to cardiovascular risk if the environment is low carb, anti-inflammatory, and free of hyperinsulinism.

Could this be metabolic redemption?

In former obese, prediabetic, insulin-resistant individuals, the carnivore diet can raise cholesterol… while reversing the pathology.

Why? Because HDL rises. Triglycerides plummet. Insulin normalizes. The liver regains function. Lipid transport adapts to the new energy demand.

What some doctors call “keto-adaptive hypercholesterolemia” is not necessarily pathology. It’s remodeling.

Danger or adaptation signal?

Cholesterol is not what you should monitor.
It’s inflammation.
It’s oxidation.
It’s insulin.
And above all: it’s your genetic terrain.

Because what is dangerous in one person—APOE4 + oxidized LDL + unstable blood sugar—can be a perfect metabolic solution in another—APOE3 + low triglycerides + stable ketosis.

Animal fat is fuel. Cholesterol is a messenger.
And your genes are the map.

The question is whether you read it well.