Yes they serve different functions which suggests their propensity to promote atherosclerosis is related to active processes and not merely passive diffusion based on size, density and count. If it was mainly due to count and density like grains of sand getting into machinery then HDL particles which are much smaller, denser and vastly more numerous than LDL ought to be causing most of the damage instead of being associated with better outcomes. I further suspect the active processes whereby LDL contributes to atherosclerosis are due to degradation such as by oxidation and particle counts as an indicator of risk are only relevant when damaged particle counts are correlated to total particle counts. I predict we will find that LMHRs can have ridiculously high particle counts without progression of CVD so long as there is very little degradation of the lipoproteins.
Found a low carb doctor
I suspect the reasons why HDL goes up or down is what matters rather than the level of HDL. HDL can go up for reasons such as alcoholism which are associated with increased risk of CVD. HDL can go down for reasons such as metabolic syndrome associated with increased risk of CVD. I expect we will eventually have tests far more meaningful than the ones we use today.
I cannot resist, sorry in advance.
Ah hem, Might want to use
E^2=m^2 c^4 + p^2 c^2 with your statement.
E=mc^2 is the simplified version of a stationary particle with mass, the formula I put in was for a moving particle or photon. Meaning the correct form (unless my memory is failing me)
The phrase âpropensity to promote atherosclerosisâ is what bothers me here. It is based on an assumption that these particles cause cardiovascular disease, which I donât believe has actually been solidly demonstrated. There is no doubt that cholesterol is part of arterial plaque, but there is actually a fair amount of evidence to suggest that it is there as part of the bodyâs healing response, and not as the cause of the original damage.
Question for extra credit: fire engines are generally seen at fires. Would restricting the number of available fire engines reduce the number of fires?
That is my thinking, as well.
I think as long as repair >= damage, you should be OK. (Letâs ignore people with FH, which might have more coagulation.)
I donât think particle count, level of LDL, Lp(a), any of that matters as long as repair >= damage. Because if it did, people with high particle count and LDL and Lp(a), but with low levels of atherosclerosis, wouldnât exist But they do.
About half of them do have more coagulation (variants of fibrinogen and clotting factor VIII, primarily), and those are the ones who develop cardiovascular problems and die young. The other half are fine.
And this has been known since the 1960âs BTW.
I think endothelial damage is the fire starting spark set off by LPS and other highly toxic insults. LDL binds and neutralizes LPS initially providing protection. Think of LDL as structural wood and much like hard dense large timbers of a log cabin can be very fire resistant but when LDL is sufficiently degraded by oxidation like those logs it can fuel the flames of a raging fire. Statins are like using termites to reduce the fuel burden of a house made of wood.