I don’t want to be a cardiovascular disease (CVD) statistic eventually. And I’m sure neither do you, if you’re reading this.
The World Health Organization estimates that CVD claims 19.8 million lives per year worldwide, and it is the leading cause of death globally:
19.8 million people died from CVDs in 2022, representing approximately 32% of all global deaths. Of these deaths, 85% were due to heart attack and stroke.
Yes, we humans do have serious issues with CVD. 19.8 million deaths per year
Unfortunately, there are so many different factors for consideration within CVD, because of all the underlying factors involved in CVD. Even then, it would take multiple iterative presentations of the same factors for different people to be able to completely understand what is going on.
Today, I’ll focus on 4 major Cs involved in CVD — cholesterol, collagen, consumption and clotting.
Cholesterol
Cholesterol, on its own, isn’t the demon that many medical professionals make it out to be. Fight that demon squarely, and we’ll end up losing sight of the big picture. We may win the battle on managing cholesterol levels but still lose the war in maintaining our own heart health.
It Isn't Really Just The Cholesterol That Contributes To Heart Disease.
The cholesterol molecule is something that we have a problem with.
Because it’s not just about the cholesterol, but rather about the oxidation of the cholesterol-containing lipoproteins in our blood. Especially when we’ve accumulated enough cholesterol in our lipoproteins to turn it into low density lipoproteins (LDL).
The Problem With Cholesterol Accumulation In Our Body
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LDL has a long shelf life in our body and can therefore be “most vulnerable to oxidative modifications”.
When LDL gets oxidised (we’ll call that oxidised molecule oxLDL), an inflammation signal is raised for the immune system’s macrophages to gobble up all that oxLDL before they can cause further damage.
Unfortunately, as the macrophages gobble up the oxLDL, their production of the CD36 protein receptor is upregulated, which signals to them to gobble up even more oxLDL.
And these macrophages therefore go on this oxLDL binge-eating spree, until they become fat and bloated foam cells. They can’t really move much in the blood, and they’ll end up settling on the sides of our arteries, where they’ll eventually get entrapped in a “prison” matrix that comprises mainly collagen.
Collagen
We know of collagen as an important component in our joints for providing joint structure and support. Collagen is yet another protein that is implicated in the formation of atherosclerotic plaques, as it is used to seal off the accumulated communities of foam cells.
When that happens, an angiogram will reveal the presence of “blocked arteries”. All the foam cells and collagen materials end up occupying some of the cross sectional space of the artery where blood is supposed to be flowing through.
It’s a strong, supple material that ought to hold up, just that in the case of atherosclerosis, the foam cells are also able to produce matrix metalloproteinase (MMP) enzymes to digest their way out of the collagen matrix.
Much like how a prisoner tries to find ingenious ways to escape out of jail, a foam cell already has the means to escape. It’s just a matter of when the foam cells can produce a critical mass of MMPs to digest their way out of jail.
Now, Seriously, What's So Tricky About Cholesterol?
This article is the final part of a 3 part miniseries. The first 2 parts can be found at:
Consumption
The statistic that we’re looking at is the rate of collagen consumption, or how fast the collagen layers get decomposed. Because they will be decomposed to a point where they can no longer withstand the pressure from the “prisoners” entrapped within their jail cells.
The inflammatory conditions within the jail as some of the foam cells die and turn necrotic do aid in upregulating the production of MMPs, which means that there will be more attempts made to get out of jail.
When the foam cells eventually do get out of jail, they’ll rush back into the blood, and they will get engulfed in a clot almost instantaneously.
Clotting
So now, we’ve got a clot. In a major artery.
If the clot is sufficiently large enough to block blood flow to the heart by occluding the coronary artery, we’re looking at the heart losing its pumping function, and from there a heart attack will proceed.
If the clot ends up travelling to the brain and lodges in one of the arteries in the brain, we’ll see the development of a stroke.
If the clot ends up travelling down to the legs and blocks a vein coming back up the leg, we’ll see the development of deep vein thrombosis.
Hence, CVD patients are prescribed anti-clotting drugs such as aspirin or warfarin to reduce the effects of clotting for that very purpose, though the clotting mechanism is just one factor to work on:
Blood Clotting Is Necessary For Wound Healing But May Be Deadly In Heart Attacks
Our blood is a very unique fluid. It doesn’t just contain water. It contains a whole load of other dissolved substances such as proteins, electrolytes and vitamins, as well as other insoluble components such as the red blood cells.
While we do see the development of major medical techniques and drugs to control various C factors, they do focus on specific Cs and rarely the overall big picture.
Statins, for example, focus on limiting cholesterol synthesis in the body, but they don’t focus on helping to clear out existing excess cholesterol — that is the duty of the liver and the digestive system as we aim to dump it out via the toilet bowl in our daily poop runs.
Some people don’t even have the ability to do a daily poop, especially when statistics put constipation as affecting approximately 16% of the human population worldwide.
Aspirin focuses on clotting but does not have a hand in promoting the clearance of the foam cell plaques via efferocytosis.
Efferocytosis And Its Oft-Unstated Role In Artery Clogging.
The word “efferocytosis” isn’t one that is frequently thrown about these days. Most heart disease patients would not have heard of this word before, because rarely is it (if ever) discussed by their doctors.
We do need to focus on the biochemical pathways in our bodies with regards to maintaining proper dynamic equilibria to prevent ourselves from getting into a state where everything’s broken, because…
If it ain’t broke, why do we need to even bother about fixing it?
The problem is that many of us get so broke but we don’t even realise the state of brokenness in our own bodies!
Do feel free to refer to 10 Nutrients That Support A Healthy Heart to see how we can support those biochemical pathways in our bodies!
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