I saw these things. I prefer to eat soy as it’s low in saturated fat and cholesterol. Soy is SOOOOO good, I love to rub it all over my face and take baths in it…mmmmmmmm.
I saw something on tv last night where there was some sort of food festival and all these people were eating foods made from soy and were saying how good it tastes and that they couldn’t tell it wasn’t beef. All I could do was feel sorry for them.
Cesk Fysiol. 2003 Feb;52(1):34-41.
[Lipid metabolism in atherogenesis]
Bobkova D, Poledne R.
Laborator pro vyzkum aterosklerozy, Centrum experimentalniho vyzkumu chorob srdce a cev, IKEM, Praha.
Lipoprotein (LP) metabolism plays a pivotal role in atherogenesis. Breakdown of triglyceride (TG) rich lipoproteins, both of exogenous–chylomicrones and endogenous–very low density lipoproteiny (VLDL) produces remnant lipoproteins after repeated action of lipoprotein lipase (LPL). Atherogenity of remnant lipoprotein has been proved. Also atheroprotective high density lipoproteins (HDL) are produced from surface of TG rich lipoproteins during their lipolysis. Protective role of HDL particles in atherogenesis is manifested by reverse cholesterol transport from all extrahepatic cells to the liver including cells of the arterial wall. Plasma concentration of atherogenic low density lipoproteins (LPL) is regulated by the production rate of VLDL in the liver on the one hand and their utilization by selective LDL receptors (mainly in the liver) on the other hand. Number of functioning LDL receptors is regulated genetically (gene for own LDL receptor and gene for both ligands–apoprotein B and apoprotein E) and also by environmental factors. Diet low in saturated fat and cholesterol and rich in dietary fibres increases number of LDL receptors and consequently decreases LDL cholesterol concentration. Monocytes entering arterial wall when intravasal and then subendothelial concentration of LDL is increased absorb LDL and predominantly oxidized LDL by scavenger receptors. During this repeated process they are changed to macrophages, residual macrophages and foam cells. Production of foam cells represents a starting point in atherogenesis but their high presence is typical also for advanced vulnerable atherosclerotic lesions, which are prone to rupture producing clinical complication–myocardial infarction and stroke.
J Nutr. 1998 Feb;128(2 Suppl):444S-448S.
Dietary fatty acids and the regulation of plasma low density lipoprotein cholesterol concentrations.
Department of Internal Medicine, University of Texas Southwestern Medical Center at Dallas 75235-8887, USA.
Epidemiologic studies over the past 25 years have shown that the level of dietary fat intake is positively correlated with the average serum cholesterol value and mortality from coronary heart disease (CHD). A number of different investigators demonstrated that in addition to total fat, the fatty acid composition of diets influenced serum total cholesterol (TC) in humans. In general, saturated fatty acids were found to elevate the serum cholesterol concentration, and unsaturated fatty acids were found to decrease this value. The lipoprotein fraction most affected was the level of cholesterol carried in low density lipoprotein (LDL-C). It has now been demonstrated that the steady-state level of LDL-C is predominantly dictated by metabolic events in the liver. As the amount of dietary cholesterol entering the body is increased, there is expansion of the sterol pool in the liver cell and down regulation of LDL receptors (LDLR) that are primarily responsible for clearing LDL-C from the blood stream. When dietary cholesterol intake is kept constant, however, long-chain saturated fatty acids further suppress hepatic LDLR activity, whereas several unsaturated fatty acids have the opposite effect. These regulatory events depend upon the availability of the various fatty acids to shift intracellular cholesterol between a regulatory and storage pool of cholesterol, and this effect is mediated by the enzyme acyl-CoA:cholesterol acyltransferase (ACAT).