This is nothing new. Read some of my posts. Search this group for
montygram. Even AHA spokesman are saying now that oxidized cholesterol
is the problem, and PUFAs can oxidize cholesterol, but saturated fatty
acids cannot. However, there is a big difference between lard and
coconut oil, though both are called "saturated fat." Coconut oil is
92% saturated, and so is very healthy. Lard is at least 60%
unsaturated, and so should be avoided (it also has no antioxidant
protection). Do not cook any food with cholesterol in it while exposed
to air (boiling is okay). Avoid baked goods that contain eggs, cheese,
milk, etc. - this is very bad stuff. Here are a couple of many studies
making this point:
Oxidized LDL contains inflammatory PAF-like phospholipids.
Trends Cardiovasc Med 2001 Apr-May;11(3-4):139-42
Marathe GK, Prescott SM, Zimmerman GA, McIntyre TM.
Department of Pathology, University of Utah, Salt Lake City, Utah, USA.
Atherosclerosis has an underlying inflammatory component. Oxidation of
low-density lipoprotein (LDL) particles to modified forms promotes
atherogenesis by supplying cholesterol and through the oxidative
generation of agents that activate macrophages, smooth muscle and
endothelial cells. A primary target of oxidizing compounds, derived
from cigarette smoke, dietary sources, exuberant inflammatory cell
responses and normal cellular metabolism among other sources, are the
esterified polyunsaturated fatty acids in the phospholipid shell that
surrounds the insoluble lipids of the lipoprotein core. One type of
phospholipid oxidation product mimics the structure of the potent
inflammatory mediator platelet-activating factor (PAF), and these
oxidation products activate the PAF receptor found on platelets,
monocytes and leukocytes. Production of such PAF mimetics is, in
contrast to the physiologic generation of PAF, uncontrolled. PAF
mimetics and other phospholipid oxidation products are found in
atherosclerotic lesions or even in blood after exposure to cigarette
smoke. Here we summarize our data describing the structure, activity
and metabolism of the PAF-like lipids found in atherogenic LDL
particles.
Ital Heart J 2001 Dec;2(12):867-72
Low-density lipoprotein oxidation.
Iuliano L, Micheletta F, Violi F.
Istituto di I Clinica Medica Universita degli Studi La Sapienza
Policlinico Umberto I Viale del Policlinico, 155 00161 Roma.
Free radical mediated oxidation of low-density lipoproteins (LDL),
which has been extensively studied in the last two decades, plays a
central role in the development of the atherosclerotic plaque.
Oxidation involves the lipid moiety of LDL in a chain reaction
mechanism. In the initial phase, free radicals preferentially attack
highly oxidizable polyunsaturated fatty acids. Subsequent recruitment
of other molecules includes cholesterol and phospholipids. The process
of oxidation is counteracted by antioxidants present in LDL.
By-products formed during oxidation of LDL lipids, which may have
biological activity, react with amino acid residues of the LDL protein
backbone with the consequent modification of chemical and immunological
properties responsible for cellular receptor shift. Oxidation-altered
apolipoprotein B of oxidized LDL is, in fact, recognized by the
macrophage scavenger receptor responsible for foam cell formation. The
mechanism of LDL oxidation and the impact on atherogenesis are
discussed.