We talk about cholesterol but do you really know what it is? Or what it isn’t? LDL, HDL, DHL (that one is actually a delivery service)— it’s important to understand this one word that has been a focal point, both good and bad, for the last few decades in the world of health. If there’s one association people make with the word “cholesterol”, we bet it’s “heart attack” that comes to mind, but there’s more to this term than meets the eye.
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#realfolks #truthshallsetyoufreeWhat is cholesterol anyway and should I hate it? Cholesterol is a fat-like steroid, a small molecule essential to life. It’s generally incorporated into cell membranes where it offers indispensable structural and functional stability. There are two main types of cholesterol: LDL (low-density lipoprotein) cholesterol and HDL (high-density lipoprotein) cholesterol. The former is often noted as the “bad” type of cholesterol and the latter as the “good,” but it’s important to note such labels are sweeping generalizations. Myelin, the insulation that surrounds nerve fibers, is rich in cholesterol. Hormones progesterone, estrogen(s), testosterone, cortisol and aldosterone depend on cholesterol for their existence. Without cholesterol, there can be no vitamin D made from sunshine or bile acid to aid digestion. If cholesterol were completely toxic, 90 percent of it wouldn’t be reabsorbed and recycled to the liver—it would all be flushed. If the liver thinks the ovaries, for example, need more cholesterol to produce estrogen, it makes more cholesterol and bundles it with a protein in the form of LDL and sends it on its way to the bloodstream. In transit, any cell that needs it can claim it. The liver can make more than a gram a day. Whatever is unused is wrapped in HDL, which collects stray LDL and takes it back to the liver. The system is striking, but imperfect. Some bodies are genetically better than others at self-regulating the manufacture of cholesterol, meaning their livers won’t produce too much if dietary intake is high. It’s possible, though, to stop eating cholesterol for the rest of your life and still have more than you need. Cholesterol is a waxy substance that looks like a yellowish-white candle. A lipid, cholesterol is oil-based. Blood, on the other hand, is water-based. The two don’t mix. If cholesterol were just plopped into the bloodstream, it would form an irregular glob, so the body packages it into lipoproteins, using apolipoprotein to hold it all together. The whole thing consists of cholesterol, triglycerides and phospholipids. Any food that contains carbon provides the raw material to make cholesterol. In the small intestine, free fatty acids are bundled, three at a time, to make triglycerides, which then are joined with cholesterol to make chylomicrons, which enter circulation along with fats and sugars to be used for energy. In the liver, LDL is released into the bloodstream in order to transport cholesterol to all the organs. The liver also makes HDL to carry cholesterol away from cells (and blood vessel walls) and return it to the liver for eventual excretion. In the event an energy source is not burned, it gets stored as fat. What do all these numbers mean? When your doctor looks at your lipid profile, they will pay attention to the numbers that are believed to predict cardiovascular issues. Those values seem to have changed over the years, maybe according to pharmaceutical sales goals. Total cholesterol numbers of 200 are no longer good enough to satisfy the traditional medical community. Now, they want 170 to be the maximum. Wanting HDL to LDL ratio to be greater than 0.3, however, is a reasonable goal. Putting it the other way, LDL to HDL is 3 to 1. LDL of 130 is iffy; 100 is nice. Saturated fats and trans fats should also be watched carefully as they influence lipid numbers more than dietary cholesterol. Surprisingly, high cholesterol levels aren’t always cause for alarm. As far as blood numbers go, after age 50, serum cholesterol levels appear to make little difference in mortality, while earlier in life they might (Anderson, 1987). In fact, in the aged population, high cholesterol levels are associated with increased lifespan (Weverling-Rijnsburger, 1997). In women, particularly, moderately elevated cholesterol is deemed not only harmless, but beneficial (Halfdan, 2012). A study performed years ago at a VA nursing home realized that cholesterol and hematocrit levels were the most informative predictors of mortality, with those whose cholesterol was lower than 156 mg/dL dying at many times the rate of those with values above the thresholds (Rudman, 1987). One study found that mortality in women is lowest at 270 mg/dL (Forette, 1989). Taking into account body measurements and biochemical factors, research in Italy discovered that cholesterol values lower than 189 md/dL created a greater risk of death from all-cause mortality, holding low levels as a potential indicator of occult disease and declining health (Brescianini, 2003). In the United States, subsequent investigation found that the non-demented elderly of all races with cholesterol values in the lowest quartile were twice as likely to die as those in the highest quartile (Schupf, 2005). There’s more: low levels of cholesterol have been implicated in the onset of dementia, where poor performance on cognitive tasks is displayed. The renowned Framingham Heart Study looked at cholesterol levels of almost two thousand people over an 18 year period and found that participants with total cholesterol (TC) lower than the “desirable” 200 mg/dL fared terribly contrasted to those with TC in the borderline-high and high ranges (Elias, 2005). A decline in TC values over the 15 year period prior to the diagnosis of dementia indicates the importance of this molecule in maintaining mental acuity (Stewart, 2007). Such information is in direct contrast to what’s generally accepted as fact in the traditional medical community and begs further questioning (Martinez-Carpio, 2009). How to manage your cholesterol levels As with all facets of health, there must be an ideal level of cholesterol for each of us individually, not as a one-size-fits-all model. To find an ideal cholesterol level, we need look no further than to phosphatidylcholine (PC), the molecule that makes the cell membrane. Where modern medicine is satisfied to address and target the symptom, functional/integrative medicine doesn’t rest until the cause has been uprooted and alleviated. PC is an entity especially well-versed at supplanting the cause of sickness with the root of well being. Phospholipids, as PC, inhibit the absorption of dietary cholesterol in the small intestine, increasing high density lipoprotein (HDL) while enhancing the mechanism that carries cholesterol back to the liver for shipping and handling (Iwata, 1993) (Tchoua, 2010). Reduction in triglycerides may be realized and blood clots are thinned in the presence of PC (Brook, 1986). The hardening and narrowing of arteries (atherosclerosis), then, may be interrupted and the lipid profile made desirable (Juzwiak, 1996). Because they contain measurable amounts of PC, eggs are removed from the no-fly list and may be enjoyed without fear of cardiovascular repercussions (Fernendez, 2006, 2010) (Blesso, 2013). Management of high cholesterol includes willful attention to a few dietary guidelines. For the most part, this is all about balance. For instance, some saturated fat is needed for cell membrane health, but that doesn’t mean you should eat every ounce of it found on your steak. Additionally, adding more fiber to your daily intake helps to bring the entire lipid profile into focus, and eating the proper ratio of essential fatty acids guarantees the membrane fluidity that keeps the orchestra that is your body in tune. Barley and oats, for example, are great for correcting lipid imbalances. The fame garnered by high-dose vitamin B3 has considerable merit, but only with your doctor’s blessing. The long list of PC attributes exceeds the space available here, but its inclusion is undoubtedly one of the better choices we can ever make. PC is neither lecithin nor triple lecithin, but a phospholipid that escapes the digestive rendering perpetrated by the hostile environment of the upper GI system. As a liposome, authentic PC is able to make it through the intestinal wall and arrive at each cell membrane intact, ready to deliver heart-healthy benefits. PC directs the process of reverse cholesterol transport by empowering an enzyme known as lecithin cholesterol acyltransferase (LCAT). Its job is the removal of cholesterol from the blood and tissues through esterification, where cholesterol is packed into HDL particles. PC allows more cholesterol to fit into the HDL. Although intravenous PC works faster, the oral does work. In the U.S., neither is blessed by the powers that be, despite the track record for preventing and treating atherosclerosis (Brook, 1986). It’s your ball; you be the quarterback.
|Anderson KM, Castelli WP, Levy D. Cholesterol and mortality. 30 years of follow-up from the Framingham study. JAMA. 1987 Apr 24;257(16):2176-80. Nelson Arispe and Michael Doh. Plasma membrane cholesterol controls the cytotoxicity of Alzheimer’s disease. AP (1– 40) and (1– 42) peptides. FASEB J. 2002; 16: 1526-1536 Behar S, Graff E, Reicher-Reiss H, Boyko V, Benderly M, Shotan A, Brunner D. Bezafibrate Infarction Prevention (BIP) Study Group. Low total cholesterol is associated with high total mortality in patients with coronary heart disease. The Eur Heart J. 1997 Jan;18(1):52-9. Blesso CN, Andersen CJ, Barona J, Volek JS, Fernandez ML. Whole egg consumption improves lipoprotein profiles and insulin sensitivity to a greater extent than yolk-free egg substitute in individuals with metabolic syndrome. Metabolism. 2013 Mar;62(3):400-10. Boston PF, Dursun SM, Reveley MA. Cholesterol and mental disorder. Br J Psychiatry. 1996 Dec;169(6):682-9. Brescianini S, Maggi S, Farchi G, Mariotti S, Di Carlo A, Baldereschi M, Inzitari D; ILSA Group. Low total cholesterol and increased risk of dying: are low levels clinical warning signs in the elderly? Results from the Italian Longitudinal Study on Aging. J Am Geriatr Soc. 2003 Jul;51(7):991-6. Brook JG, Linn S, Aviram M. Dietary soya lecithin decreases plasma triglyceride levels and inhibits collagen- and ADP-induced platelet aggregation. Biochem Med Metab Biol. 1986 Feb;35(1):31-9. Elias PK, Elias MF, D'Agostino RB, Sullivan LM, Wolf PA. Serum cholesterol and cognitive performance in the Framingham Heart Study. Psychosom Med. 2005 Jan-Feb;67(1):24-30. Jacques Fantini, Francisco J. Barrantes. Sphingolipid/cholesterol regulation of neurotransmitter receptor conformation and function. Biochimica et Biophysica Acta (BBA) - Biomembranes.Nov 2009; 1788(11): 2345–2361 Fernandez ML. Dietary cholesterol provided by eggs and plasma lipoproteins in healthy populations. Curr Opin Clin Nutr Metab Care. 2006 Jan;9(1):8-12. Fernandez ML. Effects of eggs on plasma lipoproteins in healthy populations. Food Funct. 2010 Nov;1(2):156-60. Forette B, Tortrat D, Wolmark Y. Cholesterol as risk factor for mortality in elderly women. Lancet. 1989 Apr 22;1(8643):868-70. Fryirs M, Barter PJ, Rye KA. Cholesterol metabolism and pancreatic beta-cell function. Curr Opin Lipidol. 2009 Jun;20(3):159-64. Halfdan Petursson MD, Johann A. Sigurdsson MD Dr med, Calle Bengtsson MD Dr med, Tom I. L. Nilsen Dr Philos and Linn Getz MD PhD. Is the use of cholesterol in mortality risk algorithms in clinical guidelines valid? Ten years prospective data from the Norwegian HUNT 2 study. Journal of Evaluation in Clinical Practice 18 (2012) 159–168 Iwata T, Kimura Y, Tsutsumi K, Furukawa Y, Kimura S. The effect of various phospholipids on plasma lipoproteins and liver lipids in hypercholesterolemic rats. J Nutr Sci Vitaminol (Tokyo). 1993 Feb;39(1):63-71. Juźwiak S, Wójcicki J, Machoy-Mokrzyńska A, Samochowiec L, Biaecka M, Juzyszyn Z, Barcew-Wiszniewska B, Skowron J, Rózewicka L, Kadlubowska D. Effect of lecithin on the development of experimental atherosclerosis in rabbits. Phytomedicine. 1996 Jan;2(3):199-204. Klimov AN, Konstantinov VO, Lipovetsky BM, Kuznetsov AS, Lozovsky VT, Trufanov VF, Plavinsky SL, Gundermann KJ, Schumacher R. "Essential" phospholipids versus nicotinic acid in the treatment of patients with type IIb hyperlipoproteinemia and ischemic heart disease. Cardiovasc Drugs Ther. 1995 Dec;9(6):779-84. Kozarevic D, McGee D, Vojvodic N, Gordon T, Racic Z, Zukel W, Dawber T. Serum cholesterol and mortality: the Yugoslavia Cardiovascular Disease Study. Am J Epidemiol. 1981 Jul;114(1):21-8. Krumholz HM, Seeman TE, Merrill SS, Mendes de Leon CF, Vaccarino V, Silverman DI, Tsukahara R, Ostfeld AM, Berkman LF. Lack of association between cholesterol and coronary heart disease mortality and morbidity and all-cause mortality in persons older than 70 years. JAMA. 1994 Nov 2;272(17):1335-40. Kunugi H, Takei N, Aoki H, Nanko S. Low serum cholesterol in suicide attempters. Biol Psychiatry. 1997 Jan 15;41(2):196-200. Langhi C, Cariou B. Cholesterol metabolism and beta-cell function. Med Sci (Paris). 2010 Apr;26(4):385-90. Martínez-Carpio PA, Barba J, Bedoya-Del Campillo A. Relation between cholesterol levels and neuropsychiatric disorders. Rev Neurol. 2009 Mar 1-15;48(5):261-4. Mutungi G, Waters D, Ratliff J, Puglisi M, Clark RM, Volek JS, Fernandez ML. Eggs distinctly modulate plasma carotenoid and lipoprotein subclasses in adult men following a carbohydrate-restricted diet. J Nutr Biochem. 2010 Apr;21(4):261-7. Nago N, Ishikawa S, Goto T, Kayaba K. Low cholesterol is associated with mortality from stroke, heart disease, and cancer: the Jichi Medical School Cohort Study. J Epidemiol. 2011;21(1):67-74. Rudman D, Mattson DE, Nagraj HS, Caindec N, Rudman IW, Jackson DL. Antecedents of death in the men of a Veterans Administration nursing home. J Am Geriatr Soc. 1987 Jun;35(6):496-502. Schupf N, Costa R, Luchsinger J, Tang MX, Lee JH, Mayeux R. Relationship between plasma lipids and all-cause mortality in nondemented elderly. J Am Geriatr Soc. 2005 Feb;53(2):219-26. Stewart R, White LR, Xue QL, Launer LJ. Twenty-six-year change in total cholesterol levels and incident dementia: the Honolulu-Asia Aging Study. Arch Neurol. 2007 Jan;64(1):103-7. Tchoua U, Gillard BK, Pownall HJ. HDL superphospholipidation enhances key steps in reverse cholesterol transport. Atherosclerosis. 2010 Apr;209(2):430-5. Weverling-Rijnsburger AW, Blauw GJ, Lagaay AM, Knook DL, Meinders AE, Westendorp RG. Total cholesterol and risk of mortality in the oldest old. Lancet. 1997 Oct 18;350(9085):1119-23.|