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The real story of cholesterol plaques, not the Hollywood version
The war on cholesterol, although laudable, is not going to “fix” atherosclerosis, because the blockage starts deep inside the blood vessel, the vasa vasorum is to blame
Cholesterol, or more specifically, atheromous plaques, which are primarily made up of immune cells jammed up with cholesterol, are blocking up your arteries !
This is not a contentious issue.
It is a fact.
But, where does the cholesterol come from ?
The war on cholesterol
Well from the blood of course.
This is why we go to war against those cholesterol carrying particles.
The more of them that are circulating, the more chance they have of slipping into big blood vessels. Prompting a frantic mop up, by hardworking macrophages…………..
The marcophages work like crazy – trying to save the day. And they do………… kind of.
They mop up all that cholesterol.
A suicidal mission
But it is a suicidal mission.
They transition from being macrophages to foam cells. From being active cleaner upper, to an engorged laggard, to dead beat bunging up the works. And then as they die…………….. they release the cholesterol they have so diligently squirreled away.
The cholesterol flood becomes another macrophages problem………..
And so it goes.
Initially this awful scenario plays out, deep inside the blood vessel.
Then the heart attack happens
At some point in time – the whole lots blows. The plaque ruptures, clumps of congealed up cholesterol spews forth……………
If the clump is big enough – and it often is.
It lodges in a blood vessel.
Starving the blood vessel of oxygen and YOU HAVE a problem.
But let’s go back to the beginning…….
Locating the block
The actual location of the problem is not on the edge of the blood vessel. The problem is layers and layers below. It is actually at the border between the little layer of muscles that whip the blood around and the edge of the border that separates the blood from “the body”.
These layers all have fancy latin names. The muscle layer is the tunica media and the border layer is the tunica intima. For the record, there is another layer after the muscle layer, this one is made of fibrous tissue and fat – it’s called the tunica adventia.
Here is a cross section through an actual tissue sample.
The arrows show the border between the tunica intima and the tunica media. The red staining shows where the lipids are located. © 2016 Vladimir Subbotin
The point………….. it is not a surface problem.
So what ?
LDL particles
Well have you “seen” what cholesterol travels in. It’s an enormous particle – made up of fats and protein AND cholesterol.
This BLOB of blobs, has to cross around thirty or more layers of cells-cum-matrix, to arrive at this point. The “crossing” must be fast and seamless …………
You’re on the border, then you’re on the other side. There is nothing in between.
Teleporting LDL particles !
Sounds a bit far fetched ?
LDL particles won’t teleport
But this is what we’re told happens in atherosclerosis.
Lipoprotein particles drifting around in the blood, going about their business of making deliveries. Specifically cholesterol deliveries, “spontaneously” move across the blood vessel border, drilling through 30 layers…………
And once here, they proceed to become damaged.
Necessitating a clean up by the immune system.
Which for the record, also dug their way through 30 layers of cell. Eish ! It doesn’t make sense.
This cannot be the full story.
The REAL story
Well let’s start at what these BIG blood vessels looks like when you’re little.
When you’re little, all three layers are there. But the inner layer is skinny, really skinny 1-2 layers thick. LDL particles would be able to cross in a jiffy. But they don’t. All sorts of protective layers keep them in their place.
As you grow bigger, so do your blood vessels. Specifically the intima tunica layer.
Tissue samples of blood vessels at different life stages. The I shows the location of the tunica intima and the M, shows the location of the tunica media. © 2016 Vladimir Subbotin
By the time you get to 15, it has thickened up to be about 10-15 layers thick.
You keep growing….. and your intima tunica, get’s thicker. So by the time you’re 30, it’s now about 30 layers thick.
Now 30 layers thick is the sweet spot.
Blood vessels thicken up
It is thick enough to do the job of ensuring blood moves around seamlessly, but NOT too thick that the cells at the bottom go hungry.
You continue aging and get bigger (hopefully not).
So by 40, it’s 40 layers thick, at 50 it is 50 layers thick. ……….
I’m joking.
Actually if all is on track, the layer should not get thicker. Unfortunately, if you’ve got BAD body chemistry, the layer has a tendency to expand. Now the fact that it get’s thicker is NOT in and of itself BAD.
The cells divide because they feel compelled too.
Tissue samples of blood vessels in someone who is healthy, compared to someone with metabolic problems. The I shows the location of the tunica intima and the M, shows the location of the tunica media. © 2016 Vladimir Subbotin
The impetus for their division is fixing damage.
Feeding the masses
The trouble is…………more cells need feeding.
So to keep the more cells going, a plan must be made.
The plan……………..involves growing new blood vessels.
But hooking up a direct line across the thirty plus layer of cells making up the tunica intima is fraught with difficulties. So, lines are sent from the other side – from the tunica media side.
It’s a quick an easy solution………..
The location of the blood vessels (known as the vasa vasorum) that are formed in response to bad body chemistry. © 2016 Vladimir Subbotin
But, a “dirty” solution.
Not designed for blood flow
You see the cells on the border where never designed to have blood vessels, they’re mean to be a-vascular i.e. blood vessel free. Being avascular, they’re not by their nature, very mindful of how clean and tidy their matrix is.
So dotted around are matrix proteins such as biglycan etc.
These matrix proteins are a magnet for LDL particles.
So, as these new blood vessels come on line to feed the additional layers, blood leaks have unintended consequences.
LDL particles begin to stick…….
Clean ups inside blood vessels
Macrophages “see” this “sticky’ situation – and intervene. Firing ROS tazzers at the stuck LDL particles, encouraging them to move on.
The trouble is………… being tazzered with ROS, causes the serious damage to the LDL particles.
Battered and bruised, things go from bad to worse.
Clean ups are required…..
Atherosclerosis
And before you can say, Bobs your Uncle, there is protrusion DEEP inside the blood vessel. It protrudes into the lumen……………
Interfering with blood flow.
And at some point in time – the whole lots blows.
The plaque ruptures, clumps of congealed up cholesterol spews forth……………
You know the rest of the story.
And it is a story YOU want to avoid…………
Cholesterol lowering
Which is why you’re doing what you can to avoid cholesterol.
But cholesterol wasn’t the cause of the trouble, per se.
So the war on cholesterol, although laudable, is not going to “fix” atherosclerosis. The fix is to manage the expansion of the tunica intima. A good place to start……
Rein in insulin
This will limit the expansion, decrease the ROS damage and maximize clean ups.
Need help getting started ? Download the free Willpower Report here.
Further reading
Blood vessels clog up when they become sticky
A special non-stick layer, known as the glycocalyx, prevents things from sticking to the sides of blood vessels. When it’s not there, atherosclerosis happens.
Deploying your body’s dustbin men will clean up your health
Your dustbin men sit tight, when you’re insulin resistant. So cleaning up barely happens. Wastes pile up and this has health consequences – diabetes, CVD, NASH
Putting high cholesterol in perspective
High cholesterol is seen as the kiss of death….. If your LDL level has crept up, a little – IT MUST BE BROUGHT DOWN. Well maybe, maybe not.