One Person Dies Of Cardiovascular Disease Every 36 Seconds. Will We Be The Next Statistic?

What we do need to know are the underlying factors that increase the probability of it happening.

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 statistical data provided by the American Heart Association mentioned that cardiovascular disease (CVD) kills someone in the US every 36 seconds, based on 2018 figures. The World Health Organization estimates that CVD claims 17.9 million lives per year worldwide, and it is the leading cause of death globally.

Yes, we humans do have serious issues with CVD.

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 Ain't Really Just The Cholesterol That Contributes To Heart Disease.

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

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.