Dr. Magryta: Cholesterol Part 2
The hypothesis: cholesterol and lipoproteins like LDL are inherently good and necessary unless they become unbalanced either through genetics or lifestyle choices.
From last week: It turns out that the carrier lipoproteins like LDL (bad) and HDL cholesterol are an ancient part of our innate immune system that have an important function in fighting infection. We have always used these lipoprotein to clear infectious material before they can do damage. The evidence to follow will show how the Kaiser Permanente study makes sense.
The carrier lipoproteins are known as chylomicrons, VLDL, IDL, LDL, and HDL. They have a primary role to carry fats around the body. While they serve the fat carrying primary role dutifully, these same lipoproteins are like little cars that float around in your blood stream looking for disturbed particles or pathogens to throw in their trunk in order to eliminate them at the liver.
There is a large body of science that now proves that these lipoproteins play a critical role in defending us against infection. In effect, these particles play a large part in our ancient rapid reaction force called the innate immune system.
These metaphorical cars can bind to and eliminate viruses, bacterial cell wall debris and parasites. If you remember back to the previous articles about the gut micro biome and LPS/lipopolysaccharides, we know that the bacterial cell wall debris from a dysfunctional intestinal micro biome can translocate into the bloodstream and circulate around the body causing inflammation. The lipoprotein cars have binding sites, “trunks”, to grab the LPS and other pathogenic bacterial endotoxins and transport them back to the liver for excretion in bile. This is a very advantageous mechanism for survival.
It turns out that the “good” HDL cholesterol gets used up trying to clear the acute inflammation and infection. As the HDL level drops the “bad” LDL cholesterol and triglyceride level rises as the next line of defense. As the infection clears, we would expect the HDL and LDL levels to flip flop back to normal.
Let us say that we have two sets of rats and infect them both with a deadly dose of a bacteria called E. coli while simultaneously giving one group an infusion of these protective lipoproteins. In the end, you will have most of the lipoprotein infused group relaxed and alive while the other group has died from the infection.
Let’s pause here.
The mammalian system was set up to provide a particle with multiple roles that would already be floating all around the body to engage a pathogen immediately. Let us imagine a warrior in the middle ages getting cut by a dirty sword. The availability of these lipoproteins to grab viral or bacterial particles and remove them rapidly is lifesaving and is a thing of beauty.
It would therefore be nice to have the genetic ability to have more of these lipoproteins floating around and protecting us against infectious disease.
Scientifically, it would make sense then that if you had an elevated cholesterol level, you may be suffering from an infection causing the body to mobilize more cholesterol to clear the systemic pathogens. The big question now is: is this an acute or a chronic problem?
Let us look at the acute scenario. There is a deadly disease called bacterial meningococcal sepsis that is fatal for many infected patents. As a pediatrician, this disease scares me because it kills quickly. When researchers evaluated the death rate in relation to the cholesterol level, they found an inverse relationship. In other words, at the time of infection, if you have higher levels of lipoproteins, you had a higher survival rate! The deceased group had much lower levels of LDL.
A chronic gut dysbiosis infection or abnormal micro biome that does not kill you would be expected to force the body to mobilize lipoproteins to clear the translocated bacterial LPS endotoxin. The increased levels would be a response to infection and not the cause of disease. This is exactly what we believe happens.
Based on the data as provided, it is clear to me that an elevated cholesterol is not the main issue with coronary artery disease. Now that we understand the immune function of cholesterol, it is likely a marker of underlying chronic infection in the gut and oral cavity.
We know that artery wall plaques that can cause a heart attack have walled off bacterial biofilms that come from our oral and gut bacteria. These bacteria have translocated to the heart and walled themselves off causing a local artery inflammatory process that is ground zero for a potential heart attack.
The fact that most if not all heart attack patients have signs of unchecked inflammation while many have normal cholesterol levels is the proof that we are barking up the wrong tree and need to focus more on bacterial pathogenesis of coronary artery damage and other genetic risk factors like lipoprotein receptor defects and apolipoprotein genotypes.
Things are never as simple as 1+1=2 in medicine. What we know is that God had a plan and every molecule in our body has it’s role or roles to play to keep us alive and healthy.
Next up: what to do to improve your heart attack risk.
Dr. Chris Magryta is a physician at Salisbury Pediatric Associates. Contact him at firstname.lastname@example.org