For cell membranes to work, they MUST HAVE cholesterol – how much, depends on what else you’re eating….the more your eat, the easier it is, to get what’s needed
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No need to panic if your cholesterol level is high on a high fat diet
In many people, not all, a diet rich in saturated fat, does increase total and LDL cholesterol. In the short term at least. And increased total and LDL cholesterol is typically associated with cardiovascular disease.
The assumption is…………
Saturated fat causes cardiovascular disease.
So eating less of it, solves THE PROBLEM !
The cholesterol myth
We’ve “grown up” with, this myth, but the science to support it, is iffy at best, many, me included, would say, it doesn’t exist.
It is a case of two wrongs don’t make a right !
So what is wrong with the idea ?
Well the first point of contention…. is MANY people. but NOT ALL. There is a huge amount of inter-individual difference, in how people respond to dietary cholesterol. These differences have been attributed to
- And habitual diet.
The dietary load
It’s the last point, that prompted a group of researchers, based in Norway, to put their thinking caps on and come up with a plausible explanation. They’ve called it the homeoviscuous adaption to dietary lipids model or HADL for short.
In my opinion………… they’ve nailed it.
Of course, in the process, they have opened up a can of worms, but if you’ve decided to throw, convention to the wind and tuck into meat, eggs and butter, for dinner, this will explain, why it doesn’t make you a heart attack waiting to happen.
And, rather than hurt, helps you function BETTER.
Cholesterol is a resource
We have somewhere between 100 to 140 grams of total body cholesterol, which is divvied up, as follows
- A small fraction of it is circulating in the blood – being transported about, in lipoproteins (LDL, HDL and VLDL particles)
- A chunk of it, is whirling around in the form of bile
- The rest, which is the vast majority of the cholesterol, is in cell membranes
It comes from one of two sources…….
You eat it or you make it.
The cholesterol supply is diet dependent
And related to what type of cells, you’re eating.
When, you’re eating animal protein, you’re eating animal cells. Now if you remember from high school biology……….. the big feature of animal cells, is they DON’T HAVE A CELL WALL.
Contrast this with plant based foods. A big strong cell wall made of cellulose, is a key attribute of plant cells.
Without a big strong cell wall to hold things up, animal cells need a plan B.
Cholesterol is the plan B
Actually it’s more like plan A – the cholesterol stabilizes the membranes of animal cells, providing the “strength”, with flexibility ! Those thick cell walls made of cellulose, limit mobility. On the plus side, they can be challenging to digest.
More cholesterol less fiber
We humans, don’t have the equipment to digest cellulose, but no worries, the residents of our colon, help out.
So a diet, high in plant cells, is low in cholesterol and high in fiber.
Of course, processed foods have no cells in them, so they’re…low in cholesterol and fiber , while being high in omega-6 PUFAs. Plus a host, of other nasties.
But this story is about cholesterol…
By hook or by crook
Interestingly enough, if you eat a PUFA rich diet, your body, pumps up cholesterol production, because it’s a REQUIRED resource.
If you don’t eat it, you make it.
And for the record, it’s anything but easy to make, to go from acetyl co-A to a newly minted molecule of cholesterol, takes more than 30 chemicals steps and lots of energy.
Required for what ?
Half a dozen hormones start out as cholesterol, plus it maintains membrane fluidity….
Put another way, it makes sure the membranes are strong enough, to allow the transporters, channels and receptors, embedded in them…….to do their thing.
Nothing would work properly, if it was constantly flopping about, in a weak membrane.
The cholesterol straight jacket
Cholesterol is wedged alongside the lipid tails, that make the phospholipid bilayer.
Now how much is wedged, depends on what the tails look like.
Basically there are two types of tails
- Straight ones , which are derived from saturated fatty acids
- Bendy ones, which are derived from unsaturated fatty acids
Anytime a tail is unsaturated, it has more flexibility, so it is not quite as “stiff”, to compensate for this…… cholesterol molecules are popped in the spaces, so the membrane is stiff enough, to do its job.
Membrane stiffness is actively monitored
The fluidity is always being adjusted, to ensure, the membrane stiffness, is just “right”……… this is done, by moving cholesterol around.
What you diet looks, has a big impact on the situation…..
High PUFA diet
If you are eating, a high PUFA diet…… more of the phospholipids, forming the membranes, are going to have unsaturated fatty acids, in their tails. Since by definition PUFAs, are poly unsaturated – poly means many, so they have many kinks.
Lots of kinks, makes the membranes more fluid.
This is why, polyunsaturated fats, like sunflower oil, are liquid at room temperature.
To compensate for this increased flow, cells must pop more cholesterol into the membrane. The cholesterol comes from somewhere. The easiest place to source the cholesterol from, is a passing LDL particle. Cells upgrade the number of LDL receptors, on their surface…….and get them some cholesterol.
This means, total cholesterol and LDL cholesterol falls.
High saturated fat diet
If you’re eating a high saturated fat diet the phospholipids, forming the membranes, are more than likely, going to be saturated fats. Plus, many of these fats come, with cholesterol. Remember it’s built into, animal cells to give them strength.
Saturated are straight laced, and a little bit, inflexible.
This is why coconut oil and butter, are solid, at room temperature.
So the membrane does not need much stiffening, this allows the cells to say, “No thanks”, to the circulating cholesterol. LDL receptors are buried, resulting in less cholesterol, being taken up.
This means, the total cholesterol and LDL cholesterol rises.
Cholesterol production is toned down
When cells on board cholesterol, most of the cholesterol is shipped, straight to the outer membrane, with the view to meet the demands of this membrane. But, if there is cholesterol to spare, it travels into a structure, known as the endoplasmic reticulum. Cholesterol levels inside this structure, dictate, how much cholesterol should be produced, in house.
The signalling happens via SREBP2.
Excess cholesterol, triggers the off switch.
NOTE : Cells do not waste resources, producing things that are not needed.
But, too much of a good thing, can be a bad thing – excess cholesterol is potentially toxic.
HDL cholesterol rises too
So, spare cholesterol, prompts an increase in the production of ABCA1 transporters. These transporters, pack the “extra” cholesterol onto passing HDL particles. The HDL particles, then take the cholesterol, back to the liver.
From here it can be used, as needed.
Don’t worry, be HAPPY
The rise in cholesterol, that is sometimes seen, when people switch to a diet, higher in saturated fat, is due to a redistribution of the cholesterol, already present.
The redistribution is happening, to maintain optimal cell function.
It’s NOT a pathology, it’s good resource management.
Unfortunately, if the environment the cholesterol is travelling in, is UNPLEASANT, things can go wrong, HORRIBLY WRONG.
Cholesterol is not the problem, BAD BODY CHEMISTRY IS !
HMG co-reductase, the enzyme responsible for cholesterol production, should knock off, at night. Find out why he doesn’t knockoff…and how to safely boot him out.
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
A cell lining a blood vessel suffers a catastrophic event AND IS NOT REPLACED, because you’re short of EPCs – cholesterol then fills the leaking pipe, and so it begins.