The country I live in vilifies saturated fats, especially of animals origins, for the well-known reasons (clogging arteries and raising cholesterol, duh). Recently, though, a new argument started to appear, and that is: during heating of meat, cholesterol gets oxidised, and leads to atherosclerosis. This is where is get confused and would like to ask for some support.
I understand that within atherosclerotic lesions, there is oxLDL, which is a lipoprotein built by our liver, and oxidised in vivo under unfavourable conditions. But would the oxidised cholesterol from the food we consume be part of those lesions as well? In other words, should we actually avoid exposing meat to temperatures above 150 Celsius / 302 Fahrenheit?
Couple of sources I found on this topic (mostly animal experiments):
Under what circumstances is cholesterol oxidised.
“The oxysterol diet did not result in elevation of the aortic cholesterol level or the lesion volume in the aortic valve. These present results indicate that exogenous oxysterols do not promote the development of atherosclerosis in ApoE-deficient mice.”
“Thus, alpha-epoxy cholesterol in the diet is incorporated into Chylomicron/Chylomicron Remnants fraction and then transferred to LDL and HDL contributing to lipoprotein oxidation. We hypothesize that diet-derived oxidized fatty acids in chylomicron remnants and oxidized cholesterol in remnants and LDL accelerate atherosclerosis by increasing oxidized lipid levels in circulating LDL and chylomicron remnants. This hypothesis is supported by our feeding experiments in animals. When rabbits were fed oxidized fatty acids or oxidized cholesterol, the fatty streak lesions in the aorta were increased by 100%. ”
“In mice fed the oxidized-cholesterol diets, the levels of oxidized cholesterol in sera were increased. At the end of the experiment, aortas were removed and atherosclerosis was assessed. We found that in LDLR-deficient mice, feeding of an oxidized-cholesterol diet resulted in a 32% increase in fatty streak lesions (15.93+/-1.59% versus 21.00+/-1.38%, P<0.03). Similarly, in apo E-deficient mice, feeding of an oxidized-cholesterol diet increased fatty streak lesions by 38% (15.01+/-0.92% versus 20. 70+/-0.86%, P<0.001). The results of the current study thus demonstrate that oxidized cholesterol in the diet accelerates fatty streak lesion formation in both LDLR- and apo E-deficient mice.”
“Oxysterols are produced during excessive frying of food; cholesterol gets converted into oxysterols during that process.” à external sources of oxidised cholesterol vs “The consumption of too much polyunsaturated fat can overtax the liver. The excess polyunsaturated fat trips the mechanism that turns cholesterol into oxysterols.”à internal oxidation.
Again, a rabbit study.
Mice study comparing oxysterols (oxidised cholesterol) and oxyphytosterols (oxidised plant sterols) in creation of CVD.
“An important question is whether in vivo formed oxysterols and oxyphytosterols have atherogenic potential the same as that of their diet-derived counterparts that we used in the present study. To what extent oxyphytosterols are formed, metabolised and excreted in the human body has not been studied.”
I need someone much smarter than me to explain this in layman terms
OldDog
(Gregory - You can teach an old dog new tricks.)
#5
It is pretty well established the cholesterol does not cause atherosclerosis. It shows up in atherosclerotic plaque because it is used to try repair the damage.
We also know there is little affect on serum cholesterol from dietary cholesterol.
The correlation between oxidized cholestorol and disease outcomes is most likely due to the confounders associated with an otherwise unhealthy diet.
Most of these studies are financed by drug companies, hoping to find some correlation to cholesterol and CVD so they can push the use of statins. The results of these studies never produce the dramatic results they are looking for, so they publish relative risk numbers that look far more compelling than they actually are.
Here is a good presentation about Drug company manipulation of study results.
