LDL's are Not the Cause of Heart DiseaseMay 22, 2022
LDLs are Not The Key Driving Problem in Artery Disease
We are obsessed with cholesterol in our modern medical system. Don't get me wrong! 50% of us die of vascular disease in one way or another, so this is an overwhelming epidemic. But we won't cure the epidemic if we don't get to the root cause. The root cause is right before our eyes if we but see it. The science is there. We are just bucking the huge inertia of a massive pharmo-medical-industrial complex with a lot of money behind it. So, let's give it a try.
First of all, we must acknowledge the plain known fact that cholesterol above or below 200 is nonsense. There is unequivocal evidence that people live longer with cholesterol between 210-240. That 200 number was just put there as an arbitrary marketing tool to sell more statins. You want a cholesterol of 230. Just get over it and be happy when you get there.
Second of all, what is cholesterol and why is it in the blood? Cholesterol is a rigid membrane lipid that is useful for cells to make an outer membrane. Its rigidity allows cells to build firm outer walls that hold together (imagine bricks around the outer wall of a house). That way a liver cell looks like a liver cell. A heart cell looks like a heart cell. Only a few proteins can be embedded in the wall to allow just the right things to get in and out. You make cholesterol in your liver and deliver it to your cells with little pickup trucks called LDLs. If your cells are unhealthy and need a lot of cholesterol, your blood level will be lower. If you have plenty, the level will be high. That's what LDLs do, They deliver cholesterol to the cell.
Well then, how does cholesterol end up being in your arteries and causing heart attacks and narrowed blood vessels? Aha! The $ 64 billion dollar question.
Here are the steps. LDLs don't cause trouble until they get sticky. They don't stick to the blood vessel wall until they become oxidized and get sticky. The key to that happening is you have to be insulin resistant, which 88% of Americans are. When you are insulin resistant, the proteins on the surface of your cells become sticky, like velcro. With insulin resistance, you produce a protein called Apolipoprotein Apo-C-III that induces that stickiness. ApoC-III equals LDL velcro. With insulin resistance, your blood glucose is higher and more glucose sticks to various proteins, like Apo-C-III. Then, you are off to the races. The little tiny oxidized, glycated, LDLs can stick to the vessel wall and start being transported into the vessel. The LDL particle actually can turn on innate immune system inflammation.
Why does stickiness and damage start in artery walls? Why not in veins? Same blood level of LDLs in both places. Only the arteries get damaged. And when you make bypass surgery grafts with veins, they become clogged with plaque all too quickly too. Why did the artery get damaged, and not the veins? Because of high blood pressure and increased friction on the wall of the artery from the force of that pressure. We now know that high blood pressure and glucose resistance are all part of a continuum.
The LDLs are just there delivering cholesterol to the artery walls, just like to every other cell in your body. But now they are at the scene of the crime. They get sticky and get gobbled up by white cells trying to help repair the damage. Cholesterol pools begin to develop. Just like firemen at the scene of a fire, the LDLs are not the cause. The cause was the friction-based damage to the wall of the artery caused by higher blood pressure, stickier LDLs particles that have glucose on their surface, which signals white cells to attack them and try to remove them from the scene of the crime.
How to reverse all that? How to reverse glycation comes down to reversing insulin resistance. That's weight loss and moving to an ecosystem with less free glucose in it. White flour and sugar are the key enemies. Any food that makes lots of free glucose in your blood: potatoes, rice, and grains are problems. The instant you become overweight, the slope gets more slippery. Insulin resistance climbs. The cardiovascular surgeon with his home on Pine Lake is waiting for you.
How can you tell or measure your insulin resistance? Lab tests: Insulin level below 5. Fasting glucose below 85. A1c below 5.6. Labcorp's new Diabetes Risk Assessment Test level below 50 (men), 40(women).
www.What will Work for me. I'm on my own experiment with this as my HDLs have always been low and I have family history of heart disease. My A1c wants to drift up to 5.8 if I'm not vigilant and my fasting blood glucose stubbornly remains at 102. I've been wearing a continuous glucose monitor now for 4 months and have discovered the foods that make my glucose shoot up. I can see the change with just 5 raisins. My blood glucose will rise 15-20 points. One spoonful of chocolate ice cream will give me a 100 point rise. That indicates insulin resistance. If I do a 5 day fast mimicking diet, my insulin will be 2. But otherwise, 10. I'm there on the cusp, just like the 88% of Americans. I want to explore Lab Corps new Diabetes Risk Assessment Test. Next Week.
References: BMC, Biochem Biophys Acta, Diabetologica, Current Opin Lipidology, Wikipedia, Nature,
1. What is the real engine that drives heart disease? Answer: insulin resistance that leads to stickier LDLs, stickier artery walls and more damage to artery walls from higher blood pressure. Yes, 125/85 is worse than 1115/65.
2. What is the function of LDLs? Answer: To deliver cholesterol to every cell in the body to help build its outer membrane.
3. What has to be added to LDLs to make them sticky? Answer: Apo-C III
4. How can you raise your ApoC-III level? Answer: Easy, peasy. A trip to a fast food joint with a Big Gulp soda, nice refined bun and a shake on the side. Lots of refined sugar and flour.
5. Is heart disease reversible? Answer: Yes. One step at a time. Fix your insulin resistance. Then we will get to ketones.