Cholesterol: What You Need to Know

Disclaimer: Not Medical Advice. Opinions are my own.

In partnership with Momentous

Cholesterol.

Everyone knows the word, but I would argue there's a lot of confusion.

Many are taught good vs. bad cholesterol, but this level of simplicity misses the mark.

My goal is that after you read today's newsletter, you will better understand cholesterol, what biomarkers you need to know, and have broad ideas about how to approach the future.

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What is Cholesterol?

Let's start by answering this question.

Cholesterol is a lipid. Lipids are hydrophobic, meaning they are not water-soluble.

Every cell in the human body makes cholesterol.

Cholesterol is necessary for cell production and is the foundation of our cells' membrane structure. It allows for:

• Stability: Maintains the integrity of the membrane.

• Fluidity: Keeps the membrane flexible and functional.

• Permeability: Regulates the movement of substances in and out of cells.

No cholesterol = no cells = no life.

Cholesterol is also the precursor of synthesis or the building blocks of life, such as Vitamin D, hormones (testosterone, progesterone, cortisol, etc.), and Bile Acid, which allows us to digest and absorb nutrients from food.

Great.

By now, we can agree that cholesterol is crucial.

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Cholesterol Transportation

Quick science lesson. Stick with me.

As we discussed, every cell in the body needs cholesterol. However, not every cell is capable of making enough cholesterol.

The liver produces much more cholesterol than it needs, and it has enough to share with the cells that need it.

The problem is that cholesterol is a hydrophobic lipid that repels water, so transporting its lipids through the blood wouldn't work.

Introducing lipoproteins. Lipid (cholesterol) + protein.

Proteins are much easier to transport because they are water-soluble.

Lipoprotein uses the protein as the outer layer, and the lipid is packaged inside.

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'Good' vs. 'Bad' Cholesterol

The type of protein (apolipoproteins) around the lipid defines which family of lipoproteins it is. For example: Apolipoprotein A (ApoA), Apolipoprotein B (ApoB), etc.

ApoA is the main protein component of High-Density Lipoprotein (HDL).

ApoB is the main protein component of Low-Density Lipoprotein (LDL) and other lipoproteins (like VLDL and IDL).

The technical difference between the two is density.

LDL carries more lipids relative to protein, and HDL carries more protein relative to lipids.

For simplicity, HDL and LDL cholesterol have been labeled "good" vs. "bad" cholesterol.

Is the cholesterol in LDL different than the cholesterol in HDL? Answer: No!

However, LDL, as a lipoprotein (not cholesterol), is the culprit because of its function. LDL is more prone to getting stuck in the arterial walls, sparking the process of atherosclerosis.

Furthermore, HDL, as a lipoprotein, is helpful because it helps remove excess cholesterol and transport it back to the liver.

Why does this distinction matter?

Every lipoprotein that contributes to atherosclerosis carries the apoB protein.

Cholesterol Biomarkers

How can we utilize this information?

Instead of solely focusing on LDL, we have established that proteins (apolipoproteins)—specifically apoB — are responsible for catalyzing atherosclerosis.

Testing for apoB will paint a much better picture of the total atherogenic (leads to atherosclerosis) lipoproteins.

You will see the total count of the blend below:

1. Low-Density Lipoprotein (LDL)

2. Very Low-Density Lipoprotein (VLDL)

3. Intermediate-Density Lipoprotein (IDL)

4. Lipoprotein(a) [Lp(a)]

5. Chylomicron Remnants

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How to Lower Your ApoB

When it comes to lowering ApoB, you can take two routes.

First, dietary intervention. Second, pharmacologic intervention.

I want to stress that everyone has their own instruction manual, and different interventions will produce individualized results.
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Let's tackle the dietary intervention.

If you are insulin-resistant (type 2 diabetic or pre-diabetic), the first plan of action is to address this. I recommend checking out continuous glucose monitoring to understand your glucose levels fully. I use the Levels app to follow mine (Note: Levels is a sponsor of the newsletter).

Insulin resistance is more often than not linked to elevated triglycerides, which can result in higher ApoB.
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How can you lower triglycerides?

1. Caloric deficit - burning more calories than consumed.

2. Lowering refined/starchy carbohydrates

3. Limit refined and added sugars

In summary, improving insulin sensitivity and lowering triglycerides can lower ApoB levels.

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Finally, let's touch on pharmacologic intervention.

Depending on your ApoB's magnitude, I recommend starting with nutrition modifications before administering medication.

The significant players in lowering ApoB are:

1. Statins

2. Ezetimibe

3. PCSK9 Inhibitors

I won't go into much detail on the medications in this newsletter, but if there is interest, I will dedicate a complete newsletter to them.

Discuss the above medications with your qualified healthcare physician to see if one might be a fit for you.
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(Bonus) Does Dietary Cholesterol Increase Your ApoB?

Despite the demonization of eating cholesterol-dense foods such as eggs - dietary cholesterol has been proven to have minimal to zero effect on ApoB and increasing LDL.

However, food sources packed with saturated fats will generally raise your LDL cholesterol.

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What Now?

I know this newsletter was more technical, but for good reason.

Hopefully, you better understand cholesterol and, more importantly, which lipoproteins to keep an eye on to monitor your risk of CVD.
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If you haven't already, I urge you to get an in-depth lipid panel done to determine your ApoB levels.

Understanding your risk profile will help you make meaningful lifestyle decisions to improve your healthspan and lifespan.

Only the best,
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Jeremy London, MD