For 70 years we have been fighting the firefighter. Not the fire.

If your body stopped making cholesterol tomorrow, you would be dead the day after.

Before we talk about risk, we have to talk about function. Because function has almost dropped out of every consultation.

Cholesterol is the building block of your cell membrane. Every single cell in you, from a skin cell to a neuron in the frontal cortex, has a membrane that without cholesterol would collapse like a wall without mortar. Cholesterol regulates how fluid or firm that membrane is. Too little of it and signals are no longer cleanly passed on.

Cholesterol is the precursor of every steroid hormone. Testosterone, estrogen, progesterone, cortisol, aldosterone, DHEA. Everything you need to get out of bed in the morning, fall in love, become pregnant, or survive a conflict, begins as a cholesterol molecule in a gland.

Cholesterol is the precursor of vitamin D. The 7-dehydrocholesterol in your skin is converted by sunlight to vitamin D3, which is then activated in liver and kidney. No cholesterol, no vitamin D.

Cholesterol is the basis of your bile acids. Without bile, no fat digestion, no fat-soluble vitamins A, D, E, K.

Cholesterol is directly involved in the repair mechanism of your endothelium. Where your vessel wall develops microscopic tears, it is the cholesterol in LDL particles that seals the wound. We will return to that in detail later.

The metabolism in numbers

Let that sink in for a moment. The body pool holds about 10 grams of cholesterol. Only about 5 percent comes from food, the rest is built in the liver itself, mainly via the enzyme HMG-CoA reductase. That is exactly the enzyme statins inhibit.

The consequence: if you eat three eggs today, the liver compensates. It builds less. If you skip the eggs, it builds more. This has been experimentally documented for decades. The recommendation “eat fewer eggs so your cholesterol drops” physiologically does not work.

And now you know why the old recommendation “eat less butter” biologically makes no sense.

1955, Eisenhower collapses. Ancel Keys delivers the explanation. A whole world believes it.

For you to understand where the myth comes from, we have to go back 70 years. The truth is: the thesis “saturated fats cause heart attacks” was not born from a clean study. It was born from a press conference after a heart attack.

What follows from this story: the recommendation “less saturated fat” was not born from more knowledge, but from a political moment. And in parallel with the recommendation came a second phenomenon, almost never discussed in practice.

The great fat switch and what came after

After Eisenhower, the United States, then Europe, in the broad population switched from animal fat to industrial seed oils. Corn, soy, safflower, sunflower, canola. Before 1900 the ratio of omega-6 to omega-3 in the Western diet was about 1 to 1. Today it averages around 15 to 1, in the US sometimes 25 to 1.

What has happened since? Heart attacks rose instead of falling. They became younger. Suddenly sons were dying of heart attacks at the same age as their fathers, often in the same generation. Obesity, type 2 diabetes, autoimmune disease, dementia, all multiplied. The only major variables newly added to the menu in this period: industrial seed oils and refined carbohydrates.

LDL is in plaque because plaque is a repair. Not because LDL attacks the wall.

Picture the endothelium of your vessels as a smooth, paper-thin foil. Three cells thick. It produces the nitric oxide that relaxes your vessels. It prevents blood from clotting where it should not. It regulates what comes in and what goes out.

When this foil tears, microscopically, several times every day, the body has to apply something to seal the wound. That is precisely a central task of LDL. It transports cholesterol to the damaged sites. Cholesterol is built in there. The wound closes. Over time, plaque forms.

Plaque, then, is not the beginning. Plaque is the answer.

What are the hammers? The hammers are what wounds your endothelium every day. This is exactly the point at which discussion in German practices often ends. It should begin here.

This is the decisive point: If we lower cholesterol without addressing these drivers, we are practicing symptomatic medicine. We are fighting the reaction, not the cause. Just as if one were to arrest the firefighters instead of putting out the fire.

First total cholesterol. Then HDL and LDL. Then subclasses. Today Apo-B and Lp(a). In German GP practices we are often still in the 1960s.

The history of cholesterol science is a history of progressive differentiation. Each step has weakened or even reversed the previous statement. You have to understand this, otherwise you cannot understand the dispute.

Stage one: total cholesterol

At first only one value could be measured. There was a rough correlation between high total cholesterol and heart attack rate. That was the state in 1950. From this came the recommendation “lower your cholesterol.” Plausible, but too sweeping.

Stage two: HDL and LDL

With John Gofman and ultracentrifugation it became clear: there are at least two main classes. HDL has been considered “good” ever since, LDL “bad.” This is already a simplification. But at least it was clear: high total cholesterol with high HDL means something different from high total cholesterol with low HDL.

The most important takeaway from Framingham: The higher your HDL, the higher your LDL may go before the risk even rises. Someone with an HDL of 75 mg/dL can have an LDL of 160 without being endangered. Someone with an HDL of 30 and an LDL of 130 is in a completely different cardiological world. We have known this for decades. And still in German GP practice often only the total cholesterol is reported and warned about.

Stage three: LDL has subclasses

Here comes the insight that turns everything upside down. LDL is not a homogeneous substance class. There are at least three measurable subclasses, which differ massively in size, density, and risk.

What drives SD-LDL up?

The most important answer: not the steak. Fast carbohydrates. Bread, juice, sugar, refined starches. They raise triglycerides, and triglycerides raise the share of SD-LDL. Even a low-fat diet that lowers total LDL can raise the SD-LDL share, because it pushes triglycerides up.

Stage four: Apo-B and Lp(a)

Apo-B stands for apolipoprotein B. Simplified: every atherogenic particle, that is LDL, SD-LDL, VLDL, IDL, Lp(a), carries exactly one Apo-B protein on its surface. When you measure Apo-B, you are counting the number of particles that can really do damage. Not the volume of cholesterol they transport.

Two people can have the same LDL value. One has 800 large, fluffy particles. The other has 1,500 small, dense ones. Same cholesterol value. Different risk, often by a factor of two or three. Apo-B distinguishes this. Total cholesterol does not.

Lp(a), pronounced “lipoprotein little a,” is a genetically determined, very atherogenic particle. Anyone with high Lp(a) has a markedly increased risk for early heart attacks, independent of everything else you do. Lp(a) is measured once in a lifetime, because it is genetic. And still in German GP practice it is almost never run.

Sydney Diet Heart and Minnesota Coronary Experiment. Cholesterol lowered. More deaths.

The most important randomized controlled trials ever conducted on the cholesterol hypothesis lay in drawers for decades. Only Christopher Ramsden of the US National Institutes of Health dug them out again.

“Vegan lowers LDL, therefore vegan protects from heart attack.” This bridge must not be built.

If I had to take one single thing from 100 years of cholesterol science, it would be this: there is a logical leap that has stood in German textbooks for decades and is not tenable as such.

Step one: LDL correlates with cardiovascular disease. True for the LDL species overall. True especially for SD-LDL.

Step two: vegan diet lowers LDL. True on average.

Step three: therefore vegan diet protects from heart attack. Scientifically, you may not take this step. It is not proven. It is a bridge no one should have built.

Beyond that: plant-based diets can raise the share of SD-LDL, even when total LDL falls. They can deliver lectins, phytates, and oxalates that for some people can act inflammatorily. They can lead to deficiencies in B12, iron, zinc, and DHA, which are themselves cardiovascularly relevant. My own body felt this very clearly in three years vegan.

Hundreds of thousands of studies on meat exist. None can say: “Meat is unhealthy.” Period.

Meat has been part of human nutrition for thousands of years. The statement “meat makes you sick” is at the level of observational studies not tenable. A large meta-analysis from 2019 showed very clearly that the evidence quality for the recommendation to eat less red meat is weak. If the same statistical procedure is applied to other foods, identical, equally non-specific statements emerge.

What does allow a statement is differentiation. Meat is not equal to meat. The following factors decide whether meat is associated with disease in a dataset:

My personal position: bad meat is bad. Good meat is good. The question is always: how much, combined with what, in what context, with what insulin resistance. When these factors are controlled, meat is generally not its own risk factor.

We are not all alike. And that is exactly what makes every blanket dietary recommendation questionable.

The mitochondrial researcher Douglas Wallace has shown something exciting: our mitochondrial DNA has, depending on where our ancestors lived for thousands of years, adapted to the food available there.

Anyone with a family lineage from the far north tends to carry mitochondrial haplotypes that metabolize fat very efficiently. Inuit, Sami, and northern European lines show clear adaptations to fat-rich, low-carbohydrate nutrition over many generations.

Anyone from the equatorial belt tends to be better adapted to plant carbohydrates, because photosynthesis runs all year there and plants are available year-round.

Enzymatically too there is enormous variance. The pepsin activity in the stomach, which digests meat, can differ between two healthy people by a factor of 1,000. The biochemist Roger Williams documented this well in his classic Biochemical Individuality. Indigenous peoples like the Maasai consume huge amounts of animal fat, milk, and even blood, and show extraordinarily good metabolic health. Indigenous peoples like the Hadza eat lots of honey and plants. They too are metabolically healthy. Not one diet fits all.

So you do not misunderstand me: LDL can be a causal factor. But not every LDL. And not at every age.

An honest cholesterol discussion has to show both sides. Here are the most important studies that challenge or differentiate my position.

Statins work. And statins do not work. Both are true, depending on whom you give them to.

I am not generally against statins. In people with familial hypercholesterolemia, after a heart attack, with documented plaque and several risk factors, they are very probably an advantage. What I find problematic is the prescription as primary prevention in young, otherwise healthy people with isolated high LDL and an otherwise excellent profile. That is exactly what happens in Germany every day.

And this also belongs to the truth: if you have been to a cardiologist and they recommend statins, that does not automatically mean they have looked at your values in differentiated detail. Their primary task is to apply German guidelines. These guidelines do not necessarily call for statins in pure primary prevention at low risk. They are still often prescribed.

What a modern cardiovascular risk profile looks like.

When someone comes to me with the question “am I cardiovascularly at risk?”, I do not look at total cholesterol. I look at the whole profile. I do this very thoroughly, because I look at the whole topic in scientifically differentiated enough detail to arrive at different truths from people who treat with science from 1950.

That sounds elaborate. It is elaborate. But it is the only way to really see what is going on in your circulation. One number is not enough. One value alone is not enough. A statin recommendation based on total cholesterol alone is medicine from 1955.

You do not have to choose between eggs and your heart. That choice was never cleanly put to you.

If this article should accomplish one single thing, it is this: to free you from the wrong question.

The wrong question runs “Do I take butter or margarine today? Eggs or oats?”

The right question runs: “What pulls my endothelium out of balance every day? Where are the real stressors? Which can I influence?”

Energy, clarity, years of life. Those are the real values. Not a lowered LDL value on a lab slip.

This freedom is what I found for myself. My beard grows, my nails are without white spots, my energy is balanced, my sleep quality is good. I eat meat, I eat eggs, I avoid seed oils, I take care of my insulin sensitivity. And I regularly measure the right values. Apo-B. Lp(a). Triglycerides. Fasting insulin. HbA1c. That is how I know how my endothelium is really doing.

Three things you can do this week.

First, out with the industrial seed oils. Sunflower, safflower, soy, corn, canola. Look in your cupboard. Look at the ingredient list of your favorite snacks. You will be amazed where linoleic acid hides. Replace with extra virgin olive oil, butter, ghee, tallow, or coconut oil.

Second, have the right values measured next time. Apo-B. Lp(a) once. Triglycerides. Fasting insulin. HbA1c. If your GP does not run these, you can ask a holistically oriented physician or a specialized lab. Not every health insurer covers it. But it can bring much more clarity than twenty years of total cholesterol observation.

Third, focus on insulin resistance. Fast carbohydrates out, especially after 6 pm. Movement into daily life, ideally before or right after meals. Sleep from 10 pm to 6 am in the dark hours. Stress hygiene in the evening. These four levers alone can substantially improve your metabolic profile.

If you do not just want to read but really understand where your own cardiovascular risk lies, you can book an appointment below this article. We will go through your values together. With the differentiated view this topic deserves.