Scandalous Lies About Cholesterol

In short

Cholesterol is absolutely not unhealthy, but essential. Decreased blood-cholesterol level causes depressions and sleeplessness, as a warning signal.

The only bad cholesterol is cholesterol that has been oxidized due to the influence of heat.

To prevent vascular diseases, consume as little prepared food in general, and as little prepared animal food in particular. See diet suggestions

To prevent depressions and insomnia, and enable maintenance of brain-cells and other organs, consume sufficient fresh raw animal food (like sashimi or fresh raw egg yolk, requiring an hour rest to digest by the way!). Lots of fruits and some fresh raw animal food combined contain all nutrients you need.

In Detail

Essential Cholesterol

10 to 20% of the brain is composed of cholesterol. Thanks in part to cholesterol in animal food, humans are as intelligent as they are. Essential substances like the sex hormones and vitamin D are also constructed of cholesterol. Therefore it is absolutely not true that a low cholesterol level is healthier. Just as it isn't true that a low blood-glucose level is healthier. Both a low glucose- and a low cholesterol level are proof that your body lacks nutrients.

When cholesterol level is low, you will get ill sooner. (1)

When cholesterol level is low, it is bad for the liver and the brain. (2)

Adequate cholesterol is so essential that your body warns you with depressions if your cholesterol level is too low. The lower the cholesterol level, the deeper the depression (and the more aggressive). (3) Numerous scientific investigations have shown that the cholesterol level was clearly lower in people who attempted or succeeded in committing suicide. (4)

Serotonine makes you happy. (Prozac is based on the action of serotonine) Cholesterol-products like progesterone, estradiol and testosterone increase serotonine-receptor activity (17) ; a low cholesterol level therefore decreases serotonine-receptor activity. (16)




Cholesterol is essential. Just look at your cat; normally fed domestic cats that catch a mouse or bird, first (and sometimes only) bite of their heads, which is full of cholesterol.

Because it is that important, the body itself produces most of the required cholesterol. Would that be the case if cholesterol was unhealthy ?

Of course not. You can say nature is cruel or whatever, but no one can say nature is illogical. If you consume lots of cholesterol, the body just produces and also (re-)absorbs less ; One purpose of cholesterol for example, is to be transformed into bile acids, to decompose consumed fats. After digestion these bile acids are re-transformed into cholesterol, dependent on the need for cholesterol.

Logically, it is not a problem at all to consume a number of fresh egg yolks daily (5) ,unless.......

Unless much damaged cholesterol is absorbed.

Damaged Cholesteol

Due to the influence of heat, cholesterol in food is oxidized. Already at 100°C, cholesterol oxidizes 'spontaneously'. (19) Through oxidation, the cholesterol molecules gain or lose atoms, originating new cholesterol-like molecules.

Due to the influence of heat, approximately 30% of cholesterol oxidizes into oxy-cholesterols. About 6% of oxy-cholesterol is absorbed into the body. (20)


Due to heat cholesterol oxidizes into new molecules like 7keto-cholesterol, 7beta-cholesterol, 5beta, 6beta-epoxycholesterol and 5alpha, 6alpha-epoxycholesterol. (20)

Unnatural oxy-cholesterols impair cell-membrane permeability, the functioning of LDL-receptors (causing hypercholesteremia), division of cholesterol among different cell-types, the synthesis of prostaglandin, and cause arteriosclerosis. (13) Excessive 7keto-Cholesterol-, 4alpha- and / or 7beta-hydroxycholesterol can cause vascular diseases (21).





Cholesterol Synthesis

Oxy-cholesterols also originate in the cholesterol-bile acids cycle, but these natural oxy-cholesterols do inhibit synthesis of cholesterol by the body, to maintain the ideal cholesterol level. Oxy-cholesterols in prepared food, however, are mostly “strange” oxy-cholesterols, and are not 'recognized' by the body. Therefore, most oxy-cholesterols from prepared food do not inhibit cholesterols synthesis, increasing cholesterol level. (6)


Natural oxy-cholesterols, like 24,25(S)-Epoxy cholesterol and 24(S)-Hydroxycholesterol, inhibit production of cholesterol (through mavolanate = pro-cholesterol) (22)


Decomposition of Cholesterol

The combined level of natural (oxy-) cholesterol and unnatural oxy-cholesterols can be further increased by unnatural oxy-cholesterols blocking transformation of cholesterol into bile acids. (7) And most unnatural oxy-cholesterols cannot be transformed into bile acids at all.

Because unnatural oxy-cholesterols cause accumulation of (oxy-) cholesterols, there logically is much damaged cholesterol (8) and -fats (9) in arteriosclerotic plaque. Some of these directly harm arteries. (10)


The transformation of cholesterol into bile acids is regulated through LXRalpha- en LXRbeta-receptors in the liver, which are influenced by oxy-cholesterols like 22(R)-Hydroxycholesterol, 24(S)-Hydroxycholesterol and 24(S), 25-Epoxycholesterol. (23) 7beta-hydroxycholesterol and 3,5cholestane-7-dione strongly inhibit the transformation of cholesterol into bile acids. (7)

The LXR-receptors regulate 7alpha-hydroxylase- syntheses. This enzyme adds a hydrogen- and an oxygen-atom to cholesterol, originating 7alpha-hydroxycholesterol. Subsequently more substitutions take place where most unnatural oxy-cholesterols are damaged, blocking further adequate transformations, and causing accumulation of cholesterol and oxy-cholesterols. Crystallized cholesterol / oxy-cholesterols become bile stones.

Next through 7alpha-hydroxycholesterol, cholesterols are also transformed into bile acids through 27-hydroxycholesterol and 3beta-hydroxy-5-cholestenonic acid. (24) These transformations also require undamaged cholesterol.


Besides vitamin D and sex hormones, the body also composes some other very important substances of cholesterol. It synthesizes specific oxy-cholesterols (11) to regulate cell-growth. Specific oxy-cholesterols can both stimulate and inhibit growth of cancer-cells. (12)

Therefore, absorbing oxy-cholesterols from prepared food can cause cancer. (13) Oxysterols can also inhibit the synthesis of essential long-chain polyunsaturated fatty acids. (30) 

Fighting Oy-cholesterols

Increased cholesterol level, nor vascular diseases, nor cancer is caused by cholesterol.

Lowering cholesterol level is therefore as clever as cutting down all forests to prevent fires.

The only way to prevent oxy-cholesterols from causing diseases is to reduce the intake of oxy-cholesterols.

Foods containing most oxy-cholesterols are cholesterol-containing foods that have been heated and / or frozen a number of times ; products containing eggs (14), but especially -dried egg, -cheese and -milk powder, and meat products. (15)

Raw egg yolk and raw fish contain clean cholesterol. (if fed raw grains, and not processed food- and ‘other’ wastes)


Of course it is extremely important to consume sufficient (and as much as you like) 'clean' cholesterol, from raw egg yolk (you can add it to fruit shakes; don’t blend the yolk) or raw salmon.

Also consume sufficient fruits, containing vitamin C, E and ß-carotene, which prevent cholesterol-oxidation inside the body. Do not take vitamin supplements.


Why are there so many 'misunderstandings' about cholesterol ?


Because you can make big bucks by scaring people. Billions of dollars have been made by selling 'cholesterol-level-lowering' drugs and -margarines, and expensive HDL/LDL-assessments to scared people.

This deceit becomes even more malicious knowing that diet products in particular contain harmful trans-fatty acids, and 'cholesterol-lowering drugs' can cause severe 'side-effects', and not just because the body is deprived of essential cholesterol:

Some of these products increase pancreas cancer. (25) In tests, Clofibrate caused liver-tumors. (26) In some products cholesterol is artificially transformed into coprostanol (27) (a natural process in the body), but this extra coprostanol can cause cancer. (28) In another method cholesterol is transformed into ......oxy-cholesterols !!! (29)

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(1) Weverling-Rijnsburger, A.W. et al, Total cholesterol and risk of mortality in the oldest old. Lancet 1997 / 350 (9085) / 1119-1123. , Forette ,B. et al, Cholesterol as risk factor for mortality in elderly women. Lancet 1989 / 1 (8643) / 868-870. , Isles, C.G. et al, Plasma cholesterol, coronary heart disease, and cancer in the Renfrew and Paisley survey. Brit. Med. J. 1989 / 298 (6678) / 920-924. , Rose, G. & M.J. Shipley, Plasma lipids and mortality : a source of error. Lancet 1980 / 1 (8167) / 523-526.
(2) Xu, G. et al, Relationship between abnormal cholesterol synthesis and retarded learning in rats. Metabolism 1998 / 47 (7) / 878-882. , Schoknecht, P.A. et al, Dietary cholesterol supplementation improves growth and behavioural response of pigs selected for genetically high and low serum cholesterol. Nutr.1994 / 124 (2) / pag.305-314. , Hague, Z.U. et al, Importance of dietary cholesterol for the maturation of mouse brain myelin. Biosc. Biotech. Biochem. 1992 / 56 (8) / 1351-1354.
(3) Golomb BA, et al, Low cholesterol and violent crime. J Psychiatr Res 2000 Jul-Oct;34(4-5):301-9. , Hillbrand M, et al, Serum cholesterol concentrations and mood states in violent psychiatric patients: an experience sampling study. J. Behav. Med. 2000 / 23 (6) / 519-529. , Rozzini, R. et al, Low serum cholesterol and serotonin metabolism. Risk of depression is higher in elderly patients with lowest cholesterol values. Brittish Medical Journal 1996 / 312 (7041) / 1298-1299. , Delva, N.J. et al, Brain serotonin (5-HT) neuroendocrine function in patients taking cholesterol- lowering drugs. Biol. Psychiatry 1996 / 39 (2) / 100-106. , Guggenheim, C.B. & H.G. Foster Jr., Serum cholesterol and perception of anger and sadness. Psychol. Rep. 1995 / 77 (3 pt 2) / 1343-1345. , Kaplan J. et al, The effects of fat and cholesterol on aggressive behaviour in monkeys. Psychosom. Med 1990 / 52 / 226-227. , Kaplan J. et al, Demonstration of an association among dietary cholesterol, central serotonergic activity, and social behaviour in monkeys. Psychosom. Med. 1994 / 56 / 479-484.
(4) Sarchiapone M, et al, Cholesterol and serotonin indices in depressed and suicidal patients. J. Affect. Disord. 2001 / 62 (3) / 217-219. , Papassotiropoulos, A. et al, The risk of acute suicidality in psychiatric inpatients increases with low plasma cholesterol. Pharmacopsychiatry 1999 / 32 (1) / 1-4. , Kunugi, H. et al, Low serum cholesterol in suicide attempers. Biol. Psychiatry 1997 / 42 (2) / 196-200. , Kaplan, J.R. et al, Assessing the observed relationship between low cholesterol and violence related mortality. Implications for suicide risk. Ann. N.Y. Acad. Sci. 1997 / 836 / 57-80. , Zureik, M. et al, Serum cholesterol concentration and death from suicide in men : Paris prospective study 1. Brit. Med. J. 1996 / 313 (7058) / 649-651. , Gallerini, M. et al, Serum cholesterol concentrations in parasuicide. Br. Med. J. 1995 / 310 (6995) / 1632-1636. , Gier, JA et al, Low serum cholesterol level and attempted suicide. Am. J. Psychiatry 1995 / 152 (3) / 419-423. , Engelberg, H. ,Low serum cholesterol and suicide. Lancet 1992 / 339 (8795) / 727-729.
(5) Vorster, H.H. et al, Egg intake does not change plasma lipoprotein and coagulation profile. Am. J. Clin. Nutr., 1992 / 55 (2) / 400. , Kern, F. Jr. et al, Normal plasma cholesterol in an 88-year-old man who eats 25 eggs a day. Mechanisms of adaption. N. Engl. J. Med. 1991 / 324 (13) / 896-899. , Faidley, T.D. et al, Effect of dietary fat source on lipoprotein composition and plasma lipid concentration in pigs. J. Nutr.1990 / 120 (10) / 1126-1133.
(6) Vine, D.F. et al, Dietary oxysterols are incorporated in plasma triglyceride-rich lipoproteins, increase their suspectibility to oxydation and increase aortic cholesterol concentration of rabbits. J. Lipids Res. 1998 / 39 (10) / 1995-2004.
(7) Novikov, D.K. et al, Study of HDL-2 dependent synthesis of bile acids in culture of rabbit hypotocytes : Effects of oxidized cholesterol derivates. (in Russian) Biull. Eksp. Biol. Med. 1990 / 110 (9) / 267-269.
(8) Brown, A.J. et al, Oxysterols and atherosclerosis. Atherosclerosis 1999 / 142 (1) / 1-28. , Brown, A.J. et al, 7-hydroperoxycholesterol and human atherosclerotic plaque. J. Lipid Res. 1997 / 38 (9) / 1730-1745. , Breuer, O. et al, The oxysterols cholest-5-ene-3beta,4alpha-diol, cholest-5-ene-3beta,4beta-diol and cholestane-3beta, 5aplha, 6alpha-triol are formed during in vitro oxidation of low density lipoprotein, and are present in human atherosclerotic plagues. Biochem. Biophys. Acta. 1996 / 1302 (2) / 145-152.
(9) Guiwotta, C. et al, Prostaglandin F2-like compounds, F2 isoprostanes, are present in increased amounts in human atherosclerostic lesions. Atheroscler. Thromb. Vasc. Biol. 1997 / 17 (11) / 3236-3241.
(10) Miyashita, Y. et al, Cytotoxicity of some oxysterols on human vascular smooth muscle cells was mediated by apoptosis. J. Atheroscler. Thromb. 1997 / 4 (2) / 73-78. , Zhou, Q. et al, Cytotoxicity of oxysterols on cultured smooth muscle cells from human umbilical arteries. Proc. Soc. Exp. Biol. Med. 1993 / 202 (1) / 75-80.
(11) Edwards, P.A. & J. Ericsson, Signaling molecules derived from the cholesterol biosynthetic pathway : mechanismes of action and possible roles in human disease. Curr. Opin. Lipidol. 1998 / 9 (5) / 433-440.
(12) Adamczyk, M et al, Inhibition of p42/p44 mitogen-activated protein kinase by oxysterols in rat astrocyte primary cultures and C6 glioma cell lines. J. Neurosci. Res. 1998 / 53 (1)/ 38-50. , Harada-Shida, M. et al, Oxidized low density lipoprotein induces apoptosis in cultured human umbilical vein endothelial cells by common and unique mechanisms. J. Biol. Chem. 1998 / 273 (16) / 9681-9687. , Lizard, G et al, Induction of apoptosis and of interleukin-1 beta secretion by 7beta-hydroxycholesterol and 7-ketocholesterol : partial inhibitin by Bcl-2 overexpression. FEBS Lett. 1997 / 419 (2-3) / 276-280. , Johnson, B.H. et al, Glucocorticoid / oxysterol-induced DNA-lysis in human leukemic cells J steroid Biochem. Mol. Biol. 1997 / 61 (1-2) / 35-45. , Ayala-Torres, S. et al, Characteristics of 25-hydroxycholesterol-induced apoptosis in the human leukemic cell line CEM. Exp. Cell. Res. 1997 / 235 (1) / 35-47.
(13) Guardiola, F. et al, Biological effects of oxysterols : Current status. Food Chem. toxicol. 1996 / 34 (2) / 193-211.
(14) Zunin, P. et al, Cholesterol oxidation in baked foods containing fresh and powdered eggs. Journal of Food Science 1995 / 60 / 913-916.
(15) Addis, P.B. ,Occurrence of lipid oxidation products in foods. Food Chem. Toxicol. 1986 / 24 (10-11) / 1021-1030. , Guardiola, F. et al, Biological effects of oxysterols : Current status. Food Chem. toxicol. 1996 / 34 (2) / 193-211. , Hubbard, R.W. et al, Atherogenic effect of oxidized products of cholesterol. Prog. Food Nutr. Sci. 1989 / 13 (1) / 17-44.
(16) Golomb, B.A., Cholesterol and violence : is there a connection ? Ann. Intern. Med. 1998 / 128 (6) / 478-487. , Diebold, K. et al, Are psychoactive-drug-induced changes in plasma lipid and and lipoprotein levels of significance for clinical remission in psychiatric disorders ? Pharmacopsychiatry 1998 / 31 (2) / 60-67. , Terao, T. et al, Effect of serum cholesterol levels on metachlorophenylpiperazine-evoked neuroendocrine responses in healthy subjects. Biol. Psychiatry 1997 / 41 (9) / 974-978.
(17) Cyr, M. et al, Gonadal hormones modulate 5-hydroxytryptamine 2A receptors : emphasis on the rat frontal cortex. Neuroscience 1998 / 83 ( 3) / 829-836. , Wetzel, C.H. et al, Functional antagonism of gonadal steroids at the 5-hydroxytryptamine type 3 receptor. Mol. Endocrinol. 1998 / 12 (9) / 1441-1451. , Frankfurt ,M. et al, Effect of 5,7-dihydroxytryptamine, ovariectomy and gonadal steroids on serotonin receptor binding in rat brain. Neuroendocrinology 1994 / 59 (3) / 245-250.
(19) Bascoul, J. et al, Preparation of autoxidized cholesterol from (4-14C) cholesterol and cholesterol fatty acid esters. J. Steroid Biochem. 1983 / 19 (6) / 1779-1782.
(20) Vine, D.F. et al, Absorption of dietary cholesterol oxidation products and incorporation into rat lymph chylomicrons. Lipids 1997 / 32 (8) / 887-893.
(21) Lemaire, S. et al, Different patterns of IL-1 beta secretion, adhesion molecule expression and apoptosis induction in human endothelial cells treated with 7alpha-, 7beta-hydroxycholesterol, or 7-ketocholesterol. FEBS Lett. 1998 / 440 (3) / 434-439.
(22) Accad, M. and R.V.Farese, Cholesterol Homeostasis : A role for oxysterols. Current Biology 1998 / 8 / 32-41. , Pinkerton, F.D. et al, Differing effects of three oxysterols on low density lipoprotein metabolism in HcpG2 sells. Biochem. Biophys. Res. Commun. 1993 / 193 (3) / 1091-1097.
(23) Janowsky, B.A. et al, Structural requirements of ligands for the oxysterol liver X receptors LXRalpha and LXRbeta. Proc. Natl. Acad. Sci. USA 1999 / 96 (1) / 266-271. , Lehmann, J.M. et al, Activation of the nuclear receptor LXR by oxysterols defines a new hormone response pathway. J. Biol. Chem. 1997 / 272 (6) / 3137-3140.
(24) Diczfalusyk, K. et al, Novel pathways for elimination of cholesterol by extrahepatic formation of side-chain oxidized oxysterols. Scand. J. Clin. Lab. Invest. Suppl. 1996 / 226 / 9-17. , Axelson, M. & O. Larsson, Low density lipoprotein (LDL) cholesterol is converted to 27-hydroxycholesterol in human fibroblasts. Evidence that 27-hydroxycholesterol can be an important intracellular mediator between LDL and the surpression of cholesterol products. J. Biol. Chem. 1995 / 270 (25) / 15102-15110.
(25) Manson ,J. et al, The primary prevention of myocardial infarction. N. Eng. J. Med. 1992 / 326 (21) / 1406-1416.
(26) Kim, S.C. et al, Formation of 8-oxodioxyguanosine in liver DNA and hepatic injury by peroxisome proliferator clofibrate and perfluorodecanoic acid in rats. J. Toxicol. Sci. 1998 / 23 (2) / 113-119. , Sepulveda-Saavedra ,J. et al, Quantative analasys of liver peroxisomes in rats intoxicated with peroxisomicine-A. Toxicol. Lett. 1998 / 98 (1-2) / 71-75.
(27) Iowa State Research Foundation : Method of converting cholesterol in food to coprostanol, US-patent nr. 4.921.710 / 1-5-1990.
(28) Pfeiffer, E.H. The carcinogenity of coprosterol, an intestinal reduction product of cholesterol (in German). Naturwissenschaften 1973 / 60 (11) / 525-526.
(29) Christodoulou,S. et al, Enzymic Degradation of Egg Yolk Cholesterol, Journal of Food Protection 1994 / 57 / 908-912.
(30) Rise P, et al, Regulation of PUFA metabolism: pharmacological and toxicological aspects. Prostaglandins Leukot Essent Fatty Acids 2002 Aug;67(2-3):85.