Statement/observation around 27;20 is worth repeating... "Carb determines small LDL while saturated fat determines large LDL. The advice to avoid saturated fat effectively set up type B phenotype in the population over the last 50 years.
More accurately, "high sugar determines..." Study subjects on the "high carb diet" ate 75% of calories from carbohydrates, half of which were simple sugars.
You didn’t define your terms. Exactly what do you mean by “low” carbohydrate? Meat given as a percentage but what about in grams or ounces? In what context were the experiments performed? If a dietary daily intake in based on an appropriate number of balanced calories, such that the body is not overwhelmed with calories, do these conclusions still hold? What about an experiment that focuses on monounsaturated fat being higher than saturated fat? Etc. what about LpA?
I would rather ask: would it bring my risk down? My answer would be: there seems to be a strong link (apparently through a number of individual mechanisms) between chronically elevated insulin and atherosclerosis / CHD.
May be an LDL-receptor issue (i.e. ApoB containing Lipoprotein particles don't get removed from the blood stream by the liver). I don't know if that matters though...
Statement/observation around 27;20 is worth repeating...
"Carb determines small LDL while saturated fat determines large LDL.
The advice to avoid saturated fat effectively set up type B phenotype in the population over the last 50 years.
More accurately, "high sugar determines..." Study subjects on the "high carb diet" ate 75% of calories from carbohydrates, half of which were simple sugars.
These determinations hold in a population eating excessive amount of veg/seed oil. That is our data set.
You didn’t define your terms. Exactly what do you mean by “low” carbohydrate? Meat given as a percentage but what about in grams or ounces? In what context were the experiments performed? If a dietary daily intake in based on an appropriate number of balanced calories, such that the body is not overwhelmed with calories, do these conclusions still hold? What about an experiment that focuses on monounsaturated fat being higher than saturated fat? Etc. what about LpA?
Didn't know a lot about dairy to be funded by dairy.
I am ApoE3E4. My TG and LDL-p does much better without dairy especially cheese. Sorry. Diet is keto.
Bunch of correlation, no explanatory data of disease process.
If I can get my insulin low by eating carnivore will it bring down my APOb ? Total cholesterol 306. TG 90 HDL 49.
I would rather ask: would it bring my risk down?
My answer would be: there seems to be a strong link (apparently through a number of individual mechanisms) between chronically elevated insulin and atherosclerosis / CHD.
"Healthy phenotype" = non-diabetic or non-prediabetic.
I guess it just can't be said out loud in the medical establishment.
Why would VLDL be low 11 yet the LDL-P be very high over 2500. HDL 49 Tryglcerides 90.
May be an LDL-receptor issue (i.e. ApoB containing Lipoprotein particles don't get removed from the blood stream by the liver). I don't know if that matters though...
"Why would VLDL be low 11 yet the LDL-P be very high over 2500. "
Because your body is able to burn the fat rapidly.
If you are over 35 start getting CIMT or CAC scans. Plenty of things besides diet damage arteries.