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Discussion in 'Book and Product Reviews' started by KevinPotts, Jul 4, 2016.
I'll summarise his conclusions re control later on today
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Selye, identified within each organism a sort of "life battery". His two poles of the battery were Good Oils and Proteins. Oils rich in EFAs, and sulphur rich proteins: oils containing many slightly negatively charged cis-double bonds and proteins containing many slightly positively charged sulphydryl groups. Between the two life poles runs our life currents, produced by the metabolism of carbohydrates and other molecules, flow when the circuit of essential nutrients is complete.
More stress requires more oils and proteins (as well as minerals and vitamins); less stress requires less. Whenever the demand by our body for good oils, protein and cofactors exceeds that supplied by our foods, our body begins to run down, and we slowly develop deficiency as reserves are used up. Deficiency leads to weakness, then sickness. The severity of the sickness depends on the severity of the deficiency. We then need rest, time to replenish our resources, and good nutrition for the low supplies.
So, Proteins and Good Oils are the two most abundant substances in our cells, we find them together in cell membranes, in lipoproteins that carry fats and cholesterol in our blood and in membranes of sub cellular organelles. They form the main structures and functional components of our entire body and so are the key biochemical armoury to deal with stress, and specially negative stress on a day to day basis.
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Another Rhonda Patrick interview, this time with one of the most respected lipid researchers in the US, Dr Ron Krauss. Rhonda's precis of the interview follows:
"In this conversation, Ron and I discuss...
Changes in the availability of funding for good nutritional research.
"It's a fact that NIH, which is the major funder of biomedical research in the world, has basically pulled the plug on clinical research support as a general area of emphasis. The infrastructure for doing good nutritional studies, in particular, has relied on a mechanism that is now being withdrawn." - Dr. Ronald M Krauss
The important difference between consumption of dietary cholesterol, which has a negligible influence on heart disease risk, and cholesterol produced endogenously in the body (which can be a marker of risk, depending on a complete profile).
The good, bad and the ugly of LDL-lowering drugs known as statins and much more.
What differentiates fructose from fruit versus fructose as an added sugar, namely: speed of absorption, presence or absence of other beneficial compounds (fiber, micronutrients, polyphenols, etc.), and differences in dose.
How LDL (low-density lipoprotein), and particularly the ApoB protein inside of LDL, is needed to transport cholesterol, triglycerides, and fatty acids throughout the bloodstream in order to deliver them to other tissues in the body that may need them.
What small, dense LDL particles are, how they form, what effect eating saturated fat versus refined carbohydrates have on LDL particle size and heart disease risk and more generally what the main risk factors for heart disease are.
The functional difference between large, buoyant LDL particles and small, dense LDL particles and introduces us to the traits of what he terms "atherogenic dyslipidemia." These traits consist of:
1. High levels of small, dense LDL cholesterol.
2. Low levels of HDL cholesterol.
3. High levels of triglyceride-rich lipoproteins (very-low-density lipoproteins or "VLDL") and their remnants.
How small, dense LDL particles increase the risk of atherosclerosis. There is only one ApoB protein per LDL particle, which is what enables ApoB to be a surrogate blood biomarker for LDL particle number.
How access to the ApoB protein can become obscured due to conformation changes in the small, dense LDL particles. As the size of the particle decreases, this conformation change reduces the ability for the particle to bind to the LDL receptor and be recycled by the liver.
How VLDL particles, the precursor to LDL, demonstrate an interaction with LPS (also known as endotoxin, a component of bacterial cell membranes), and how it's possible that some of the negative associations with this particle size may be a result of their simply being in the blood stream longer: this gives them a greater opportunity to undergo inflammatory transformations.
This part is especially exciting to me because it may be an interesting link by which gut health (where much of the bacteria and immune cells in the body are located) and the importance of controlling inflammation to cardiovascular health.
How saturated fat appears to increase the larger, more buoyant LDL particles, which do not have the same robust correlation to heart disease risk that the smaller, more dense particles do. Dr. Krauss also takes the stance that consumption of saturated fat does not have as strong of a link to heart disease risk as previously suggested by others, and may be less relevant except in the case of what he termed "hyper-responders." These "hyper-responders" have gene polymorphisms that cause them to respond differently to saturated fat.
How increased carbohydrate consumption, especially simple sugars may have been an unintended consequence of the push for low-fat diets, and how this increased traits associated with atherogenic dyslipidemia: namely, a shift from the larger, more buoyant LDL particles to the smaller, more dense LDL particles.
Broadly, the differences between the various types of lipoprotein particles, including very-low-density lipoproteins (VLDL), and high-density lipoprotein (HDL) and what their roles are in the body."
@KevinPotts thanks for your many chapter summaries that resulted in interesting conversations here. I'm coping with a cold at the moment, and this was a nice distraction tonight.