Today we are going to review my cholesterol test from a couple of years ago. Just so you understand, I will not interpret the values. Instead, I will simply use the results as an opportunity to explain general principals relating to cholesterol panels.
Today we will examine:
· Total cholesterol.
· LDL/ bad cholesterol.
· Direct-current of HDL/ good cholesterol.
· Triglycerides.
· Non-HDL cholesterol- that’s where you add up the total cholesterol and subtract the HDL from it.
· Apolipoprotein A, and Apolipoprotein B. Apo A being the best of the HDL particles, and Apo B being worst of the LDL particles.
· Look at the Apo B/Apo A ratio.
· Small dense LDL.
· LP(a).
Let’s review what the previously mentioned terms, and what they mean.
LIPOPROTEINS
We will start with lipoproteins. Essentially, they are proteins that the body uses to make cholesterol go into small particles. See a video on this here
Now, imagine this- a plastic bottle of water and some olive oil. When you pour the olive oil into water, you will get big blobs; this represents how lipoproteins move inside the bloodstream. What if you eat a burger? It has fat in it. If you drink a milkshake or something healthy, like a salad with good olive oil, it forms big blobs.
Well, that’s the last thing that you want to happen to you. And it is the last thing that will happen to you because a big blob of oil like, if not handled appropriately by the body, will kill you. It’s called a fat embolus. Embolus means clot. Interestingly, fat emboli can happen during trauma.
For instance, if you drive your car into a brick wall. You may break multiple bones. The fat inside your bones can come out and flow into the bloodstream. Long story short, the big clots can kill you. Here’s a video with more information.
Let’s back-track. Imagine shaking that bottle of oil and water. Naturally, you get tiny fat particles. These small particles merge again to form that big particle, the “embolus”.
How does our body keep that from happening? Lipoproteins, form circles around very small particles of fat. Here is another video to help you understand.
HIGH DENSITY LIPOPROTEIN
Next, is HDL. That said, HDL, or high-density-lipoprotein, is a good lipoprotein. As you can see by the name, it is high-density. That VS LDL, which is low density.
The difference between HDL and LDL is the amount of protein particles the body produces. These proteins form what we call polar components on the outside.
To explain, the external polar capsule of HDL contains protein. The fat, or non-polar ingredient, is in the middle. You can see a visual here
Source: https://commons.wikimedia.org/wiki/File:LipoproteineTipi.png.
FYI, a significant difference between HDL and LDL is that LDL has less protein and a lot more fat- 25% or less protein to be precise. Also, there is 50% or more protein in HDL.
Why is HDL good and LDL bad?
· HDL is “good” because it’s denser protein. That means the liver can pull it out of the blood easier.
· LDL continues to float around in the blood.
Below there is another image of LDL. A protein that’s located on the polar surface; the core is fats, and the polar surfaces are of a substance called phospholipids. It’s part of the pro, what the protein assembles to keep the particle in that formation.
Source: https://www.revolutionhealth.org/ldl-p/
Here is another interpretation of the interaction between LDL and HDL.
Source:https://www.hartwijzer.nl/ldl-cholesterol.
TG/HDL RATIO
Now let’s talk about triglyceride over HDL ratio. With high blood sugar and high insulin states, insulin stops you from forming triglycerides. It burns triglycerides, so your triglycerides continue to increase. With these high values, and high-fat values, your HDL sees more of these fats. When the HDL picks up a lot of triglycerides or fats, it is no longer HDL.
In a high insulin state, and high glucose state, you have burning of your HDL and an increase of triglycerides because you’re not burning triglycerides.
Considering all that, you get a high triglyceride over HDL ratio. It’s one of the important tip-offs for insulin resistance.
Above, you see an old image from Berkeley Health Labs. It helps us understand. We think of LDL as large and fluffy; therefore, that’s what’s causing the problem. This is not necessarily the case. It’s these small dense LDLs that cause the problem. They can go through the endothelium’s cracks- the intima.
LP (A)
Next is LP(a), also known as LP little a.
In the image below, a little hook-like thing hangs off the LP(a). The hook is thought to be the mechanism for LP(a) causing more atherogenesis, or sticking to the endothelial wall, and platelet coagulation. Also, LP(a) is a higher-risk form of LDL protein.
Lp(a) is a family of proteins forming lipoproteins. Some of us have a high Lp(a), and others don’t. The hook of kringle repeats that hang off the particle and seems to cause the problem.
Source: https://www.researchgate.net/figure/Lipoproteina-Lpa-structure-Lpa-is-composed-of-two-parts-one-part-is-low-density_fig2_348831210
APO A & B
Moving on, let’s talk briefly about Apo A and Apo B.
Apo A is the main protein in HDL, while Apo B is the main protein of LDL. You can see that in the image below. Also, Apo A1 is the most protective in terms of HDL lipoproteins. It is important to note, apo A1/Apo B is a predictive ratio in terms of risk.
Source:https://www.researchgate.net/figure/The-structure-of-a-high-density-lipoprotein-particle-Apo-apolipoprotein_fig1_341541586
As you see, the lipid core, cholesterol, triglycerides, and the protein going through here hold the phospholipids together. On the HDL, you get Apo A1. Over here on the LDL, you have Apo B.
You also have Apo E. Apo E is one of these types of proteins, too. You can see Apo E 2,3, or 4.
Source: https://www.dietvsdisease.org/apoe4-diet-alzheimers-disease/
Those of us with one copy of Apo E4 have a significantly higher risk for dementia, heart attack, and stroke- but mostly dementia. With two copies of Apo E4, there’s a much higher risk for dementia.
We mentioned small, dense LDL and why they are dangerous
https://www.youtube.com/watch?v=ckkpnuqDyLA.
https://www.sciencedirect.com/topics/medicine-and-dentistry/atherosclerosis
Here’s where they get dangerous. Above, you see a diagram of the artery. In the artery wall, you have blood flow. There is an intima, and media layer of the vessel. This is where plaque gets laid down.
How does plaque get laid down exactly? When you have increased glucose or inflammation you get some breakage of these endothelial cells, or inner vessel walls. When they become inflamed and broken, the small dense LDL flows through, stops, then forms a plaque. That plaque attracts white cells, cytokines, and other inflammatory processes. Essentially, they can become inflamed, dangerous plaque.
However, new information is trending and considering LDL more a firefighter, a biomarker indicating something is wrong rather than the culprit causing plaque and heart attacks.
SUMMARY
Considering everything previously mentioned, here’s a quicky recap.
LDL:
· We talked about different versions of LDL, including small dense LDL.
· We talked about HDL and how LDL deposits fat.
· HDL cleans things up.
Triglycerides:
· A component of the core, along with cholesterol.
· Triglycerides don’t get burned when we have a high insulin state associated with insulin resistance or hyperglycemia.
· HDL does get burned up quickly as it pulls fat deposits out of the artery walls
· A high triglyceride/HDL ratio is a significant warning sign for insulin resistance.
Apolipoprotein A:
· Apolipoprotein is the protein within the lipoprotein.
· It is in the HDL family and more cardioprotective than Apo B.
Apolipoprotein B:
· It is within the LDL family
· Ratio of Apo B/low Apo A ratio indicates possible health consequences.
Anyway, you can see that I have relatively low Apo A1 because I have insulin resistance. My Apo B is over 800. The ratio is low because I have a reasonably low Apo B.
Small dense LDL- you remember they are another way, like Apo B, of looking at the most dangerous population. The smaller, denser LDL population can break the endothelium’s cracks.
With all that said, knowing the elements of a cholesterol panel can help you understand what your lab tests may be telling you. I hope this helps clear some things up.
If you found this article helpful and want to start taking steps toward reversing your chronic disease, Dr. Brewer and the PrevMed staff are currently accepting patients for a limited time. Book an appointment here: https://prevmedhealth.com/
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REFERENCES:
https://prevmedhealth.com/stopping-statins-is-it-safe-after-an-ischemic-stroke-part-1
https://prevmedhealth.com/fish-oils-omega-3s-do-they-work/
https://prevmedhealth.com/inflammation-not-cholesterol-is-the-bigger-heart-disease-risk/
https://prevmedhealth.com/how-john-reversed-calcium-score-by-59-in-16-months/
https://prevmedhealth.com/cardiovascular-inflammation-and-plaque-formation/