Is it logical to think that our bodies would manufacture a substance in order to give us a disease? Of course not. Yet many of us are worried about our cholesterol levels, something our body manufactures regularly. Cholesterol is a waxy substance that is the precursor to many of our hormones, including testosterone, estrogen, progesterone, cortisol, pregnenalone and DHEA. Cholesterol is an antioxidant, sopping up free radicals, and is also a very important part of cell membranes, so as our cells die (blood cells, skin cells, bone cells, muscle cells etc.), cholesterol is needed to make the membranes of the replacement cells. Considering we
replace about 2 million blood cells each second, it becomes obvious that cholesterol is vitally important, and we would not survive without it. If tissue is damaged, more cholesterol is needed to repair and replace the damaged cells with healthy ones. No wonder it is so important that our liver can easily manufacture cholesterol.
So, if LDL and HDL are not cholesterol, what are they? They are proteins that act as transportation vehicles that carry the cholesterol to the various locations in the body, just like a bus carries people to wherever they want to go. Cholesterol is fatty, and needs to travel in a watery medium (blood), so protein carriers are necessary to make the cholesterol water soluble. The passenger is the same (cholesterol), but the bus (protein) is different, depending on the direction the cholesterol is traveling. Would we call Harry and John "bad people" when they happened to be traveling in a mini-van shuttle, and "good people" when they happened to be traveling on a large bus? The idea is absurd. Yet, this is what we do to cholesterol. LDL proteins (so called “bad cholesterol”) carry the cholesterol from the liver out to the tissues, and HDL proteins (so called “good cholesterol”) carry the cholesterol from the tissues back to the liver. Contrary to popular belief, HDL proteins do not rid the body of the cholesterol at all - they simply return it to the liver for recycling, so it can make its next trip out on the LDL bus.
The difference between High Density Lipoproteins (HDL) and Low Density Lipoproteins (LDL) is the size and density of the molecule, with HDL molecules being larger. The smaller the molecule, the more likely it will get stuck or caught in the gap junctions between arterial cells etc., where they then oxidize, causing inflammation, which begins the artery-narrowing process. Our bodies also make VLDL (Very Low Density Lipoproteins) which also carry cholesterol but in lesser amounts per molecule due to the much much smaller size, and these molecules are far more likely to get caught along the walls of the arteries than LDL. If the LDL molecules are of normal size, they don’t get stuck. They just do their job as they should. People are rarely tested for their VLDL levels, yet this along with triglyceride levels are much more predictive of cardiovascular disease than total cholesterol. So, it is not the cholesterol that is the problem, but the size of the protein carrier.
Can you do anything to control the size of the protein carrier? Yes. Diet is very important. And do you think it is lowering saturated fat and cholesterol intake that will make the difference? No. As it turns out, the higher the easily digestible carbohydrate intake (sugar, flour, processed grains - no, rice cakes are NOT healthy!), the more the VLDL proteins made (the smaller ones that are more likely to get stuck) which greatly increase one's risk of cardiovascular disease. Sugar and flour products also increase glycation and Advanced Glycation Endproducts (AGEs), which causes arterial inflammation, also known to increase cardiovascular disease risk, and sugar and flour increase insulin secretion, which increases sympathetic load, increasing blood pressure, another risk factor for heart disease. There is simply nothing healthy at all about quickly digested carbohydrates like processed sugar, flour and processed grains (puffed wheat etc.), and until we stop eating them, the scourge of modern degenerative diseases won't abate.
High Cholesterol does NOT cause heart disease
Cholesterol, heart-disease mortality, and cholesterol-lowering drugs
Another “healthy-heart guide” that got it wrong
Dealing with inflammation and inflammatory conditions
Sugar, the disease generator
How we become over-fat
Obesity, Type 2 diabetes and heart disease - what does history tell us?
Taubes, Gary Good Calories, Bad Calories, Challenging the Conventional Wisdom on Diet, Weight Control, and Disease Alfred A. Knopf, New York, 2007.
Rosedale, Ron MD The Cholesterol Lie: What your doctor doesn’t know. YouTube Video
Gardner CD et al. Comparison of the Atkins, Zone, Ornish, and LEARN diets for change in weight and related risk factors among overweight premenopausal women: the A TO Z Weight Loss Study: a randomized trial. JAMA. 2007 Mar 7;297(9):969-77.
Kraus R.M. Atherogenic lipoprotein phenotype and diet-gene interactions. J Nutr. 2001 Feb;131(2):340S-3S.
Dreon DM, Fernstrom HA, Williams PT, Krauss RM. Reduced LDL particle size in children consuming a very-low-fat diet is related to parental LDL-subclass patterns. Am J Clin Nutr. 2000 Jun;71(6):1611-6.
Dreon DM, Fernstrom HA, Williams PT, Krauss RM. LDL subclass patterns and lipoprotein response to a low-fat, high-carbohydrate diet in women. Arterioscler Thromb Vasc Biol. 1997 Apr;17(4):707-14.
Dreon DM, Fernstrom HA, Williams PT, Krauss RM. A very low-fat diet is not associated with improved lipoprotein profiles in men with a predominance of large, low-density lipoproteins. Am J Clin Nutr. 1999 Mar;69(3):411-8.
Samaha FF, Foster GD, Makris AP. Low-carbohydrate diets, obesity, and metabolic risk factors for cardiovascular disease. Curr Atheroscler Rep. 2007 Dec;9(6):441-7.
Sharman MJ, Gómez AL, Kraemer WJ, Volek JS. Very low-carbohydrate and low-fat diets affect fasting lipids and postprandial lipemia differently in overweight men. J Nutr. 2004 Apr;134(4):880-5.
Copyright 2008 Vreni Gurd
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