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LDL was never the problem

This is for you LDL (low density lipoprotein). The lonely lipid, vilified since the 90s as low-fat diets took the US by storm. Big Pharma and biased publications blamed you for all aspects of heart disease and called you “the bad cholesterol”. Statin drugs were aimed to eliminate and reduce you. There was an attempt to make the public, and even doctors, seem to think the ‘solution’ to heart disease was treating a “statin deficiency”.

It’s time to follow the science. To review the physiology. To realize you were never to blame.

Let’s first discuss LDL & heart attacks. See the image below.

One of the reasons health professionals freak out about your LDL level is because LDL is conventionally associated with atherosclerosis. This is the formation of fatty plaques on the blood vessel wall. If the plaques keep getting bigger then this causes a narrowing of the vessel where blood used to freely flow. If the blood flow is slowed, or eventually stopped all together, this can create an episode of ischemia. This is a lack of blood flow. If this happens to vessels supplying the heart this is a heart attack. If it happens in the brain it’s a type of stroke called an ischemic stroke.

Another possibility is that the plaque gets larger and unstable and breaks free of the vessel and this forms a clot. This can get stuck places… the legs, lungs, brain, etc. This is equally concerning as causing ischemia as discussed above.

BUT, here’s the kicker. Here’s why I’m defending the lonely lipid. LDL was just trying to help. The blood vessels were damaged and inflamed, so the stickiest LDL particles (better known as oxidized LDL) stuck themselves onto the damaged vessel in its own form of patchwork. Overtime in an inflamed body more and more LDL was layered on. And then we have the “clogged arteries” LDL is blamed for.

It’s the OXIDIZED LDL we need to be concerned about and the traditional lipid panel is not testing for this. You need to get your LDL pattern, as well as, measure oxidized LDL levels. LDL pattern A is the healthy structure of LDL, its big and soft and fluffy. LDL pattern B is the unhealthy structure that is small and dense and more likely to be oxidized and stick to your arteries.

What causes LDL to be oxidized? Inflammation, excess sugar driving inflammation, environmental toxicants (eg heavy metals, pesticides), stress/hormonal imbalance, and smoking.

And, the oxidized LDL was still just trying to help. It placed it’s sticky bandaid on the damaged vessel wall in an attempt to mask the damage and inflammation.

But what does all of this mean? How is it clinically applicable. The take home is that LDL on a lipid panel is virtually useless. It has to be taken within context. Particle pattern and oxidation status is important in understanding the degree of how LDL might contribute to plaque formation and, subsequently, heart disease.

Additionally, it’s expected that low-carbohydrate and high-fat diets will see an increase in LDL levels alongside total cholesterol and HDL. However, they often show improved TG:HDL ratios (see below) and better metabolic fitness (eg decreased inflammation and sugar levels). It’s normal and beneficial to see these changes.

Furthermore, the triglyceride-to-HDL is a better predictor of overall cardiovascular risk. The goal is to have a 2:1 or 1:1 ratio. Read more here and here.

It’s also important your doctor is testing inflammatory markers (eg hsCRP, ESR) to assess for systemic inflammation and inflammatory markers suggestive of cardiac inflammation. Testing for lipoprotein(a) is also an important biomarker commonly associated with heart disease and is not linked to overall cholesterol levels and has a strong genetic component. Lastly, B vitamin status, homocysteine, and genetic mutations are other potential contributing factors to heart disease.

It’s time to throw out the out-dated and unfounded beliefs that fats are bad and all LDL should be reduced. LDL - no longer the lonely lipid!


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