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On this thread I will post passages from studies or abstracts of studies related to cholesterol, especially the dangers of oxidized cholesterol. Here are several that are worth considering:
Food Chem Toxicol. 1996 Feb;34(2):193-211.
Biological effects of oxysterols: current status.
Guardiola F, Codony R, Addis PB, Rafecas M, Boatella J.
A review of relevant literature on biological activities of oxysterols (OS) and cholesterol is presented. The data clearly demonstrate manifold biological activities, often detrimental, for OS compared with little or no such activity of a deleterious nature for cholesterol itself. Cholesterol is perhaps the single most important compound in animal tissue and, as such, it is difficult to imagine it as a toxin or hazard. In contrast, OS exhibit cytotoxicity to a wide variety of cells leading to angiotoxic and atherogenic effects; alter vascular permeability to albumin; alter prostaglandin synthesis and stimulate platelet aggregation, an important process facilitating atherosclerosis and thrombosis; alter the functionality of low density lipoprotein (LDL) receptors, possibly stimulating hypercholesterolaemia; modify cholesteryl ester accumulation in various cells, inducing foam cell formation; and enrich the LDL particle in cholesteryl esters, possibly increasing its atherogenicity. Furthermore, OS are mutagenic and carcinogenic, although some have been studied as antitumour agents based on their cytotoxic properties. Moreover, numerous studies have implicated OS in membrane and enzyme alterations that are interrelated with many of the foregoing effects. The authors find that OS deserve much more attention than cholesterol itself in terms of research activity but that unfortunately the reverse is true with regard to funding.
Metabolism. 2004 Jun;53(6):823-30
High intake of cholesterol results in less atherogenic low-density lipoprotein particles in men and women independent of response classification.
Herron KL, Lofgren IE, Sharman M, Volek JS, Fernandez ML.
"...these data indicate that the consumption of a high-cholesterol diet does not negatively influence the atherogenicity of the LDL particle."
Bioessays. 2006 Apr;28(4):387-98.
Cellular toxicity of oxycholesterols.
Wielkoszynski T, Gawron K, Strzelczyk J, Bodzek P, Zalewska-Ziob M, Trapp G, Srebniak M, Wiczkowski A.
Oxycholesterols (OS) are formed from cholesterol or its immediate precursors by enzymatic or free radical action in vivo, or they may be derived from food. OS exhibit a wide spectrum of biological activities. In OS cytotoxicity, several mechanisms seem to be involved: e.g. inhibition of HMG-CoA reductase activity, antiproliferative action, apoptosis induction, replacement of cholesterol by OS in membranes followed by changes in cellular membrane structure and functionality, and immune system functions alteration. Furthermore, OS may be mutagenic and carcinogenic and may serve as intracellular signaling or regulatory molecules. Here we review OS cellular activities with special attention to the cytotoxic action in vivo and in vitro using experimental models.
Bioessays. 1991 Nov;13(11):583-9.
Biological activities of oxygenated sterols: physiological and pathological implications.
Hwang PL.
Oxygenated derivatives of cholesterol (oxysterols) are widely distributed in nature, being found in the blood and tissues of animals and man as well as in foodstuff. They exhibit many biological activities which are of potential physiological, pathological or pharmacological importance. Many oxysterols have been found to be potent inhibitors of cholesterol biosynthesis and one or more oxysterols may play a role as the physiologic feedback regulator of cholesterol synthesis. Oxysterols also inhibit cell replication and have cytotoxic properties, effects which suggest that these sterols may participate in the regulation of cell proliferation and may be potentially useful as therapeutic agents for cancer. Furthermore, there is considerable evidence that oxysterols may be involved in the pathogenesis of atherosclerosis. Although the mechanism of action of oxysterols in all these instances is not well understood, the existence of cytosolic and microsomal proteins which bind oxysterols with high affinity and specificity suggests that this group of compounds may represent a family of intracellular regulatory molecules.
Int J Cardiol. 2006 Sep 25;
Effects of simvastatin on plasma antioxidant status and vitamins in hypercholesterolemic patients.
Shin, MJ, et al.
"These data indicate that simvastatin not only decreases blood lipids and circulating oxidized LDL but also increases lipid corrected levels of antioxidant vitamins and may improve plasma antioxidant status synergizing with the biological effects of antioxidants."
J Nutr. 1999 Dec;129(12):2177-83
Extra-virgin olive oil increases the resistance of LDL to oxidation more than refined olive oil in free-living men with peripheral vascular disease.
Ramirez-Tortosa MC, et al.
Patients with peripheral vascular disease (Fontaine stage II) are characterized by ischemia of the lower extremities, atherosclerosis and alteration of blood coagulation and fibrinolysis. A randomized, two-period, crossover design was used to compare the effects of extra-virgin (VO) and refined olive (RO) oils on plasma lipids and lipoprotein composition and LDL oxidation susceptibility in free-living men with peripheral vascular disease. The oils differed in their antioxidant profile (alpha-tocopherol: 300 vs. 200 mg/kg; phenolic compounds 800 vs. 60) and concentration but not in their fatty acid composition. Subjects were randomly assigned to two groups. The first group (n = 12) received VO with which to freely cook all meals for 3 mo, followed by a 3-mo wash-out period; they then received RO for the final 3 mo. The second group (n = 12) consumed the oils in the opposite order. Energy, fat, polyunsaturated fatty acids (PUFA) and alpha-tocopherol intakes were not different when patients consumed the two oils. Profiles of the major fatty acids in plasma and LDL were not different after consumption of VO and RO. The slope of the line for LDL oxidation vs. the line for copper concentration was significantly higher after the intake of RO than after the intake of VO. Total LDL taken up by macrophages was significantly greater when the men consumed RO rather than VO. We suggest that antioxidants present in VO may protect LDL against oxidation more than does RO in men with peripheral vascular disease.
Nutr Hosp. 2005 Jul-Aug;20(4):293-6
[Cholesterol oxidation products in fresh and frozen shrimps, raw and grilled]
Echarte M, et al.
Cholesterol oxidation products (COPs) have been related to different toxic effects, being the atherosclerotic process one of the best known. The presence of cholesterol oxides in freshly and frozenly commercialised shrimps, both raw and grilled, was studied. The determination was made by gas chromatography-mass spectrometry (GCMS). Fresh shrimps showed significant amounts of all analysed COPs, except for 7alpha-hydroxycholesterol, accounting in total for 33.15 microg COPs/g fat. In contrast, in frozen commercialised shrimps only 7-ketocholesterol and 7beta-hydroxycholesterol were detected. These results point out the great effectiveness of the commercialisation of this type of products under freezing, in terms of to the minimisation of the COPs formation. The cooking method (grilling) increased the COPs content in both types of shrimps, reaching 55.43 microg COPs/g fat in fresh shrimps and only 13.06 microg COPs/g fat in frozen ones.
J Agric Food Chem. 2003 Sep 24;51(20):5941-5
Consequences of microwave heating and frying on the lipid fraction of chicken and beef patties.
Echarte M, Ansorena D, Astiasaran I
Two types of commercial meat patties were analyzed to evaluate the effect of two applied cooking methods on the lipid fraction and the cholesterol oxidation process during heating. Microwave heating hardly modified the fatty acid profiles of both chicken and beef patties, whereas frying in olive oil increased oleic and eicosapentaenoic acids and decreased linoleic and docosahexaenoic acids in both types of products. Frying improved the omega6/omega3 fatty acids ratio in beef patties from 10.67 (raw) to 5.37 (fried). Total cholesterol oxidation product (COP) increments were 5.3-6.1-fold with microwave heating and 1.5-2.6-fold with frying. Chicken patties, raw and cooked, had a COP content twice as high as the corresponding beef ones.
J Food Prot. 2003 May;66(5):840-6
Combined effect of cooking (grilling and roasting) and chilling storage (with and without air) on lipid and cholesterol oxidation in chicken breast.
Conchillo A, Ansorena D, Astiasaran I.
The oxidation of the lipid fraction and cholesterol in raw and cooked chicken breast samples stored for 0 and 6 days at 4 degrees C under aerobic conditions and in vacuum packaging was studied. The multivariate statistical analysis showed significant effects of both culinary process and storage conditions on the lipid and cholesterol oxidation process, with a significant interaction between the two variables. Aerobic storage increased thiobarbituric acid reactive substances (TBA) from 0.04 to 0.06 ppm for raw samples, from 0.21 to 1.20 ppm for grilled samples, and from 0.24 to 1.62 ppm for roasted samples. During vacuum storage, only roasted samples showed significant increases in TBA. Levels of total cholesterol oxidation products (COP) remained low (2.88 to 4.35 microg/g of lipid) for all raw samples. Cooking increased COP levels to 12.85 and 11.54 microg/ g of lipid for grilled and roasted samples, respectively. Total COP and all individual COP except for cholestanetriol were significantly correlated with TBA and the peroxide index. However, the most extensive effect was attributable to the aerobic storage of cooked samples, which led to COP levels of 92.35 and 88.60 microg/g of lipid in grilled and roasted samples, respectively. Vacuum packaging did not increase COP levels for cooked samples.
Asia Pac J Clin Nutr. 2002;11(1):72-8.
Cholesterol oxides: their occurrence and methods to prevent their generation in foods.
Savage GP, Dutta PC, Rodriguez-Estrada MT.
Eight cholesterol oxides are commonly found in foods with high cholesterol content, such as meat, egg yolk and full fat dairy products. Factors known to increase the production of cholesterol oxides in foods are heat, light, radiation, oxygen, moisture, low pH, certain pro-oxidising agents and the storage of food at room temperature. Processes, such as pre-cooking, freeze-drying, dehydration and irradiation, have all been reported to result in increased production of cholesterol oxides in meats. As prepared consumer foods are becoming increasingly popular, the consumption of higher levels of cholesterol oxides in foods is inevitable. An understanding of the mechanisms involved in the generation of cholesterol oxides may assist in their reduction in foods and possibly reduce the impact of these compounds on human health.
Biol Res. 2003;36(3-4):291-302
Cholesterol oxidation: health hazard and the role of antioxidants in prevention.
Valenzuela A, Sanhueza J, Nieto S.
Cholesterol is a molecule with a double bond in its structure and is therefore susceptible to oxidation leading to the formation of oxysterols. These oxidation products are found in many commonly-consumed foods and are formed during their manufacture and/or processing. Concern about oxysterols consumption arises from the potential cytotoxic, mutagenic, atherogenic, and possibly carcinogenic effects of some oxysterols. Eggs and egg-derived products are the main dietary sources of oxysterols. Thermally-processed milk and milk-derived products are another source of oxysterols in our diet. Foods fried in vegetable/animal oil, such as meats and French-fried potatoes, are major sources of oxysterols in the Western diet. Efforts to prevent or to reduce cholesterol oxidation are directed to the use of antioxidants of either synthetic or natural origin. Antioxidants are not only able to inhibit triglyceride oxidation, some of them can also inhibit cholesterol oxidation. Among synthetic antioxidants 2,6-ditertiarybutyl-4-methylphenol (BHT), and tertiary butylhydroquinone (TBHQ) can efficiently inhibit the thermal-induced oxidation of cholesterol. Some natural antioxidants, such as alpha- and gamma-tocopherol, rosemary oleoresin extract, and the flavonoid quercetin, show strong inhibitory action against cholesterol oxidation.
Prog Food Nutr Sci. 1989;13(1):17-44
Atherogenic effect of oxidized products of cholesterol.
Hubbard RW, Ono Y, Sanchez A
Cholesterol under certain in vitro and possibly in vivo conditions may be oxidized to oxysterols, which are suspected of being initiators of atherosclerotic plaques. Oxysterols inhibit HMG-CoA reductase activity resulting in a decreased cholesterol concentration in the cell membrane, which leads to endothelial membrane injury and probable premature cell death. Exogenous oxidation of cholesterol in human tissues under certain unusual conditions is highly probable. Dietary oxysterols are absorbed in the gastrointestinal tract and are selectively transported by the athrogenic lipoproteins LDL and VLDL. The oxysterols cholestanetriol and 25-OH cholesterol have been shown to be atherogenic. Oxysterols are commonly found in dried egg products, powdered milk, cheeses and in a variety of high temperature dried animal products.
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And here's a new report, entitled:
"Higher Occurrence Of Parkinson's Linked To Low LDL Cholesterol."
QUOTE: People with low levels of LDL cholesterol are more likely to have Parkinson's disease than people with high LDL levels, according to University of North Carolina at Chapel Hill researchers... UNQUOTE.
Source: http://www.sciencedaily.com/releases/2006/12/061219121727.htm |
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The opinion about cholesterol is starting to change ...
source: http://tinyurl.com/2kqydz
Have we been conned about cholesterol?
by MALCOLM KENDRICK
Conventional medical wisdom about cholesterol �?and the role of statins �?is now being challenged by a small, but growing number of health professionals. Among them is Dr Malcolm Kendrick. A GP for 25 years, he has also worked with the European Society of Cardiology, and writes for leading medical magazines.
When it comes to heart disease, we have been sold a pup. A rather large pup.
Actually, it's more of a full-grown blue whale. We've all been conned.
If you've got a raised risk of heart disease, the standard medical advice is to take a cholesterol-lowering statin drug to cut your chances of having a heart attack �?because, as we all know, cholesterol is a killer.
Indeed, many of you already believe that you should take statins for the rest of your natural lifespan.
Nearly everybody is in agreement about the need to lower your cholesterol level. The NHS spends nearly £1 billion a year on prescriptions for statins and possibly the same amount administering the cholesterol tests, surgery visits and the rest.
But is it all worth it? According to an article being published in the medical journal The Lancet this week, the answer is probably no.
A leading researcher at Harvard Medical School has found that women don't benefit from taking statins at all, nor do men over 69 who haven't already had a heart attack.
There is a very faint benefit if you are a younger man who also hasn't had a heart attack - out of 50 men who take the drug for five years, one will benefit.
Nor is this the first study to suggest that fighting cholesterol with statins is bunk. Indeed, there are hundreds of doctors and researchers who agree that the cholesterol hypothesis itself is nonsense.
What their work shows, and what your doctor should be saying, is the following:
�?A high diet, saturated or otherwise, does not affect blood cholesterol levels.
�?High cholesterol levels don't cause heart disease.
�?Statins do not protect against heart disease by lowering cholesterol - when they do work, they do so in another way.
�?The protection provided by statins is so small as to be not worth bothering about for most people (and all women). The reality is that the benefits have been hyped beyond belief.
�?Statins have many more unpleasant side effects than has been admitted, while experts in this area should be treated with healthy scepticism because they are almost universally paid large sums by statin manufacturers to sing loudly from their hymn sheet.
So how can I say saturated fat doesn't matter when everyone knows it is a killer? Could all those millions who have been putting skinless chicken and one per cent fat yoghurts into their trolleys really have been wasting their time?
The experts are so busy urging you to consume less fat and more statins that you are never warned about the contradictions and lack of evidence behind the cholesterol con.
In fact, what many major studies show is that as far as protecting your heart goes, cutting back on saturated fats makes no difference and, in fact, is more likely to do harm.
So how did fat and cholesterol get such a bad name? It all began about 100 years ago, when a researcher found feeding rabbits (vegetarians) a high cholesterol carnivore diet blocked their arteries with plaque.
But it took off in the Fifties with the Seven Countries study by Ancel Keys, which showed that the higher the saturated fat intake in a country, the higher the cholesterol levels and the higher the rate of heart disease.
The countries he chose included Italy, Greece, the USA and the Netherlands. But why these particular ones?
Recently I did my own 14 countries study using figures from the World Health Organisation, and found the opposite.
Countries with the highest saturated fat consumption �?Austria, France, Finland and Belgium �?had the lowest rate of deaths from heart disease, while those with the lowest consumption �?Georgia, Ukraine and Croatia �?had the highest mortality rate from heart disease.
Added to this, the biggest ever trial on dietary modification put 50 million people on a low saturated fat diet for 14 years.
Sausages, eggs, cheese, bacon and milk were restricted. Fruit and fish, however, were freely available. I’m talking about rationing in Britain during and after World War Two. In that time, deaths from heart disease more than doubled.
Even more damning is what happened in 1988. The Surgeon General's office in the US decided to gather all evidence linking saturated fat to heart disease, silencing any nay-sayers for ever.
Eleven years later, however, the project was killed. The letter announcing this stated that the office "did not anticipate fully the magnitude of the additional expertise and staff resources that would be needed".
After eleven years, they needed additional expertise and staff resources? What had they been doing? If they'd found a scrap of evidence, you would never have heard the last of it.
Major trials since have been no more successful. One involved nearly 30,000 middle-aged men and women in Sweden, followed for six years.
The conclusion? "Saturated fat showed no relationship with cardiovascular disease in men. Among the women, cardiovascular mortality showed a downward trend with increasing saturated fat intake." (In other words, the more saturated fat, the less chance of dying from heart disease).
Even stronger evidence of the benefits of increased fat and cholesterol in the diet comes from Japan. Between 1958 and 1999, the Japanese doubled their protein intake, ate 400 per cent more fat and their cholesterol levels went up by 20 per cent.
Did they drop like flies? No. Their stroke rate, which had been the highest in the world, was seven times lower, while deaths from heart attacks, already low, fell by 50 per cent.
It's a bit of a paradox, isn’t it? That's one of the features of the dietary hypothesis - it involves a lot of paradoxes.
The most famous is the French Paradox. They eat more saturated fat than we do in Britain; they smoke more, take less exercise, have the same cholesterol/LDL levels, they also have the same average blood pressure and the same rate of obesity.
And you know what? They have one quarter the rate of heart disease we do.
The official explanation is that the French are protected from heart disease by drinking red wine, eating lightly cooked vegetables and eating garlic.
But there is no evidence that any of these three factors are actually protective. None. By evidence, I mean a randomised, controlled clinical study.
Every time a population is found that doesn't fit the saturated fat/cholestrol hypothesis - the Masai living on blood and milk with no heart disease, the Inuit living on blubber with low heart disease - something is always found to explain it.
One research paper published more than 20 years ago found 246 factors that could protect against heart disease or promote it. By now there must be more than a thousand.
The closer you look the more you find that the cholestrol hypothesis is an amazing beast. It is in a process of constant adaptation in order to encompass all contradictory data without keeling over and expiring.
But you don't need to look at foreign countries to find paradoxes - the biggest one is right here at home. Women are about 300 per cent less likely to suffer heart disease than men, even though on average they have higher cholesterol levels.
For years there was an ad hoc hypothesis to explain this apparent contradiction - women were protected by female sex hormones.
In fact, there has never been a study showing that these hormones protect against heart disease in humans.
But by the Nineties, millions of women were being prescribed HRT to stave off heart disease.
Then came the HERS trial to test the notion. It found HRT increased the risk of heart disease.
So what to do? Put them on statins; bring their cholesterol level down �?below 5.0 mmol is the official advice.
But, as The Lancet article emphasises, women do not benefit from statins. The phrase "Statins do not save lives in women" should be hung in every doctor's surgery.
But it's not just hugely wasteful handing out statins to women and men who are never going to benefit; it also exposes them to the risk of totally unnecessary side effects.
These include muscle weakness (myopathy) and mental and neurological problems such as severe irritability and memory loss.
How common are they? Very rare, say experts, but one trial found that 90 per cent of those on statins complained of side effects, half of them serious.
Only last week, a study reported a link between low LDL cholesterol and developing Parkinson's disease.
Statins are designed to lower LDL. In the face of anticholesterol propaganda, it is easy to forget cholesterol is vital for our bodies to function.
Why do you think an egg yolk is full of cholesterol? Because it takes a lot of cholesterol to build a healthy chicken.
It also takes a hell of a lot to build and maintain a healthy human being.
In fact, cholesterol is so vital that almost all cells can manufacture cholesterol; one of the key functions of the liver is to synthesise cholesterol.
It's vital for the proper functioning of the brain and it's the building bock for most sex hormones.
So it should not be such a surprise to learn that lowering cholesterol can increase death rates.
Woman with a cholesterol level of five or even six have a lower risk of dying than those with a level below four.
The Lancet reported that statins didn't benefit anyone over 69, not even men; in fact, there's good evidence that they may hasten your death.
The Framingham study in the US found that people whose cholesterol levels fell were at a 14 per cent increased risk of death from heart disease for every 1mg/dl.
Set up in 1948, the study screened the whole population of Framingham near Boston for factors that might be involved in heart disease and then followed them to see what happened to them.
It is still going today, making it the longest running and most often quoted study in heart-disease research.
A massive long-term study that looked specifically at cholesterol levels and mortality in older people in Honolulu, published in The Lancet, found that having low cholesterol concentration for a long time increases the risk of death.
This may be because cholesterol is needed to fight off infections or there may be other reasons �?but many other studies have found exactly the same thing.
Low cholesterol levels greatly increase your risk of dying younger. So the cholesterol hypothesis looks something like this:
There is no evidence that saturated fat is bad - and there are lots of 'paradoxes' where countries with a high cholesterol intake don't have a higher death rate from heart disease.
But there is an even more fundamental problem. The theory claims fat and cholesterol do things in the body that just don't make sense.
To begin with, saturated fat and cholesterol are talked of as if they are strongly connected. A low-fat diet lowers cholesterol; a high-fat diet raises it.
What is never explained is how this works. This isn't surprising because saturated fat doesn't raise cholesterol. There is no biochemical connection between the two substances, which may explain all those negative findings.
It's true that foods containing cholesterol also tend to contain saturated fats because both usually come from animals.
It's also true that neither dissolve in water, so in order to travel along the bloodstream they have to be transported in a type of molecule known as a lipoprotein - such as LDLs (low-density lipoproteins) and HDLs (high-density lipoproteins).
But being travelling companions is as close as fats and cholesterol get. Once in the body, most fat from our diet is transported to the fat cells in a lipoprotein called a chylomicron.
Meanwhile, cholesterol is produced in the liver by way of an incredibly complicated 13-step process; the one that statins interfere with.
No biochemist has been able to explain to me why eating saturated fat should have any impact on this cholesterol production line in the liver.
On the other hand, the liver does make fat - lots of it. All the excess carbohydrate that we eat is turned first into glucose and then into fat in the liver.
And what sort of fat does the liver make? Saturated fat; obviously the body doesn't regard it as harmful at all.
Recently, attention has been shifting from the dangers of saturated fat and LDL "bad" cholesterol to the benefits of HDL "good" cholesterol, and new drugs that are going to boost it.
But the idea that more HDLs are going to fight off heart disease is built on equally shaky foundations.
These lipoproteins seem to be cholesterol "scavengers", sucking up the cholesterol that is released when a cell dies and then passing it on to other lipoproteins, which return it to the liver.
Interestingly, the "bad" LDL lipoproteins are involved in the relay. The idea seems to be that HDLs can also get the cholesterol out of the plaques that are blocking arteries.
However, there is a huge difference between absorbing free-floating cholesterol and sucking it out of an atherosclerotic plaque which is covered by an impermeable cap. |
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| I've read this kind of thing before, and what I tell people is that you have to be careful. "Meat" is generally not healthy, particularly because of the way it is cooked (I'm assuming it is fresh, which is often not the case). Also, I still hear people say "saturated fat," and then mention lard as a "saturated fat," though it is only about 40% saturated fatty acids. This makes no sense on a basic common sense level, but then when you see the evidence, some of which goes back decades (such as Houssay's work), that shows how much of a difference there can be between lard and coconut oil, you have to ask why this information is not in every nutrition textbook. My sense is most of the people who give nutritional advice and write textbooks are very selective in how they review the relevant studies, ignoring or misinterpreting anything that does not fit into their preconceived notions. And don't forget about how much money is made from cholesterol-lowering drugs these days. There are powerful interests at work, for example, on the US evening news programs on the major networks, there are almost always commercials for cholesterol-lowering drugs. Yet despite the fact that a spokesman for the AHA (Dr. Richard Stein) said over a year ago that only oxidized cholesterol is dangerous, there has never been a story on any major TV news program about this, as far as I know. |
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J. Biol. Chem., Vol. 278, Issue 40, 38829-38839, October 3, 2003 Cellular Cholesterol Depletion Triggers Shedding of the Human Interleukin-6 Receptor by ADAM10 and ADAM17 (TACE)*, </NOBR><NOBR>Vance Matthews</NOBR>, <NOBR>Björn Schuster</NOBR>, <NOBR>Stefan Schütze  </NOBR>, <NOBR>Ingo Bussmeyer</NOBR>, <NOBR>Andreas Ludwig</NOBR>, <NOBR>Christian Hundhausen</NOBR>, <NOBR>Thorsten Sadowski</NOBR>, <NOBR>Paul Saftig</NOBR>, <NOBR>Dieter Hartmann  </NOBR>, <NOBR>Karl-Josef Kallen ¶</NOBR> and <NOBR>Stefan Rose-John ¶ ||</NOBR> Interleukin-6 (IL-6) activates cells by binding to the membrane-bound IL-6 receptor (IL-6R) and subsequent formation of a glycoprotein 130 homodimer. Cells that express glycoprotein 130, but not the IL-6R, can be activated by IL-6 and the soluble IL-6R which is generated by shedding from the cell surface or by alternative splicing. Here we show that cholesterol depletion of cells with methyl- -cyclodextrin increases IL-6R shedding independent of protein kinase C activation and thus differs from phorbol ester-induced shedding. Contrary to cholesterol depletion, cholesterol enrichment did not increase IL-6R shedding. Shedding of the IL-6R because of cholesterol depletion is highly dependent on the metalloproteinase ADAM17 (tumor necrosis factor- -converting enzyme), and the related ADAM10, which is identified here for the first time as an enzyme involved in constitutive and induced shedding of the human IL-6R. When combined with protein kinase C inhibition by staurosporine or rottlerin, breakdown of plasma membrane sphingomyelin or enrichment of the plasma membrane with ceramide also increased IL-6R shedding. The effect of cholesterol depletion was confirmed in human THP-1 and Hep3B cells and in primary human peripheral blood monocytes, which naturally express the IL-6R. For decades, high cholesterol levels have been considered harmful. This study indicates that low cholesterol levels may play a role in shedding of the membrane-bound IL-6R and thereby in the immunopathogenesis of human diseases. On the internet: http://www.jbc.org/cgi/content/abstract/278/40/38829 This is important because, as these and other researchers point out, IL-6 is generally "bad news," for example: QUOTE: IL-6 activates and enhances HHV-8 and HIV replication, Song and coauthors found. The researchers used a BCBL tumor cell line to examine the effect of IL-6 on HHV-8 activity. Exposing these cells to IL-6 triggered the expression of viral genes needed for replication, they reported. The effects of IL-6 on HIV replication, noted in previous studies, were also investigated by Song and coauthors. They confirmed that an HHV-8-encoded cytokine homologue stimulated HIV replication in chronically infected cells, and enhanced human IL-6 secretion by T-lymphoblastoid cells, according to the report. These effects appeared to be mediated by the signaling molecule gp130 (Human interleukin-6 induces human herpesvirus-8 replication in a body cavity-based lymphoma cell line. J Med Virol 2002 Nov;68(3):404-11. "These data suggest the possible existence of interaction between HIV and HHV-8 via IL-6," Song and colleagues concluded, "and that the blockade of IL-6 signal by anti-IL-6R antibody or anti-gp130 antibody can constitute a strategy to treat HIV/HHV-8 dually infected patients." The corresponding author for this report is Norihiro Nishimoto, Department of Medical Science I, School of Health and Sport Sciences, Osaka University, 2-1 Yamada-oka, Suita-city, Osaka, 565-0871, Japan. E-mail: [email protected]. Key points reported in this study include: -
Interleukin (IL)-6 may play a key role in the development of several AIDS-related malignancies, including Kaposi sarcoma (KS) -
IL-6 activates and enhances human herpesvirus-8 (HHV-8) replication, the causative agent of KS and other AIDS-associated cancers -
HIV replication is also augmented by IL-6. UNQUOTE. Source: http://www.aegis.com/pubs/aidswkly/2002/AW021202.html As Anthony Fauci himself has said: "...So what is it about the human body, the host, that helps drive virus replication, and what is it that tries to block virus replication? And because of our work and work from other labs on various cytokines, like TNF-α and IL-6 and IL-1 beta, as well as the discovery the previous year of certain chemokines to suppress HIV replication, it looked like there was this delicate balance between stimulatory and inhibitory effects of host factors, particularly endogenous cytokines, on HIV replication. It was not just the virus operating in a vacuum. There was an important and complicated interaction with these host factors..." Source: http://www.esi-topics.com/hiv-aids/interviews/AnthonyFauci.html Where I differ with some of these kinds of "experts" is in the notion that a "germ" is the cause. Instead, interpretation of the evidence as whole (that means including nutritional studies, molecular-level studies not supposedly directly related to "infectious disease," etc.) leads me to believe that it is much more likely that "germs" are just microscopic vultures, taking advantage of conditions that allow them to reproduce faster. I am much more concerned about low cholesterol levels and oxidized cholesterol, whereas "experts" like Fauci think that the "germs" (assuming they exist, which is unlikely in the case of "HIV," which appears to be effect rather than cause) more or less will affect healthy, adult humans equally. The "HIV/AIDS" idea is the worst, because healthy people are told that a "germ" will kill them within a dozen or so years, and that is if they endure highly toxic "medicines." I don't see any evidence whatsoever that any "virus" could do this to a person, let alone a few "retroviral" particles that are just effects of cellular-level stress. However, a person with low cholesterol and perhaps other unhealthy characteristics may indeed face a number of health crises (as I did). If such a person is then given highly toxic "medicines," it is no wonder that they only live several more years. In the wrong place and in a certain amount, a "germ" can basically speed up the damage (which occurs due to a dangerous "inflammatory" response) that one can get from low cholesterol over a longer period of time, but one would become very ill very quickly - it would not take several years to see severe symptoms. |
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I just came across a report that is one you might hear about in the "mainstream media:"
QUOTE: People who have high cholesterol levels may be much more susceptible to a particular disease transmitted by the bites of ticks, a new study in mice suggests... UNQUOTE.
And what justifies such an extraordinary claim? They fed a group of genetically-modified mice a cholesterol-rich diet, and found that:
QUOTE: ...Scientists infected mice with Anaplasma phagocytophilum, the bacterium that causes human granulocytic anaplasmosis (HGA), a disease with flu-like symptoms. Bacteria levels were 10 times greater in mice that were genetically predisposed to high cholesterol levels and that were also fed a high-cholesterol diet. A. phagocytophilum depends on its host's cholesterol stores for its survival.
The implication is that the higher a person's cholesterol levels, the more susceptible that person may be to developing a severe case of HGA... UNQUOTE.
Obviously, they are making assumptions here and these are not mice in the wild, eating a "natural" diet, but the most likely explanation is that much of the cholesterol they were fed was oxidized. This makes the biochemistry of the mouse much more likely to make the bacteria "clingly," and then prompt an inflammatory response. It's not much of leap to speculate that the researchers here are simply unaware of the most recent evidence about how "infectious disease" actually occurs, and how one can make oneself much more resistant. It seems as though the author of the report felt no need to caution against avoiding cholesterol-rich foods, since few question the "cholesterol is bad" mantra that exists in nations like the USA today, despite the clear evidence that non-oxidized cholesterol is very important and not dangerous.
Source of the quoted passages: http://www.sciencedaily.com/releases/2007/07/070703172515.htm |
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I came across this study, which is interesting because cholesterol was raised when the animals were fed a diet with added soybean oil and a strong antioxidant, which lowered cholesterol if the soybean oil was not added. This is the abstract:
QUOTE: he efficacy of roselle as a functional food has been revealed lately, especially for its antioxidant bioactivity. In this study, the benefits of roselle were further studied in vivo using the model of male Sprague Dawley rats fed with normal diets (C), 2.5 percent roselle (R), 2.5 percent roselle with 15 percent soybean oil (RO) and 15 percent soybean oil (O) for 25 weeks. The results demonstrated that supplementation of roselle in the diets significantly (p < 0.05) reduced the gross body weight and increased the high-density lipoproteins cholesterol (HDL-C) compared to the rats fed with normal diets and oil diets, and reduced the level of triglycerides in the serum. Serum total cholesterol of R group decreased compared to C but increased in RO compared to O group. Significant increase (p < 0.05) of serum uric acid was observed in R group at week 15 and 20. Addition of roselle in oil diet significantly decreased (p < 0.05) the malondialdehyde formation at week 20 and 25 but there was no significant effect of roselle on the catalase activity among the treatments at all time points. Suggests that roselle might play a role in the prevention of atherosclerosis and obesity. UNQUOTE.
Source: Journal: Nutrition & Food Science
ISSN: 0034-6659
Year: 2002 Volume: 32 Issue: 5 Page: 190 - 196
DOI: 10.1108/00346650210445758
Publisher: MCB UP Ltd
On the internet: http://www.emeraldinsight.com/Insight/viewContentItem.do?contentType=
Article&hdAction=lnkhtml&contentId=866180 |
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A new report entitled "Low Cholesterol Levels Associated With Cancer, Study Finds" came out today. It's funny how old news gets "recycled" so often in scientific fields, and this is undeniably old news. See the book, "Heart Failure," by Thomas J. Moore, for example:
QUOTE: ...The researchers did not expect to find the increased cancer risk... from low LDL levels, and additional studies have already begun to investigate this potential risk further... UNQUOTE.
Source: http://www.sciencedaily.com/releases/2007/07/070724114057.htm |
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QUOTE: ...Around 1971, someone noticed that the commercial cholesterol being used in feeding experiments was oxidized, that is, it wasn't really cholesterol. Comparing carefully prepared, unoxidized cholesterol with the oxidized degraded material, it was found that dietary cholesterol wasn't necessarily atherogenic (Vine, et al., 1998)... UNQUOTE.
Source: http://raypeat.com/articles/articles/cholesterol-longevity.shtml
And here are those references:
J Lipid Res. 1998 Oct;39(10):1995-2004. Dietary oxysterols are incorporated in plasma triglyceride-rich lipoproteins, increase their susceptibility to oxidation and increase aortic cholesterol concentration of rabbits. Vine DF, Mamo CL, Beilin LJ, Mori TA, Croft KD.
Arkh Patol. 1971;33(6):51-5. [Changes in the arterial wall in rabbits following their prolonged ingestion of native and oxidized fat (a non-cholesterol model of arteriosclerosis)] Voskresenskii ON, Vitt VV. |
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On the other hand, one still encounters reports that demonstrate how ignorant many researchers are. Not only are they ignorant of things outside of their field of speciality, but they also appear to be ignorant of things they presumably should be familiar with:
http://www.sciencedaily.com/releases/2007/09/070918100608.htm
One claim is: "Using an animal model, Chun-Lin Chen, a senior graduate student on Dr. Huang's research team, found that cholesterol limits the activity of a key protective protein called transforming growth factor-beta (TGF-beta)..."
First of all, are un-natural amounts of cholesterol being used? And secondly, is the choelsterol largely oxidized is it non-oxidized? Then there is:
"...the findings also suggest answers to questions about other diseases associated with high blood cholesterol levels, including cancer..."
There is a lot more evidence that low cholesterol leads to cancer, not "high cholesterol." And, more generally, the approach of these researchers is focused on molecules that are over-expressed or under-expressed. Once that is determined, they can try to make drugs to inhibit or enhance the production of these molecules, though long-term effects in humans won't be known for years. They usually fail to even consider that something not natural (such as a huge amount of free radical activity) might be causing the over or under-expression in the first place, and that prevention might be very simple. |
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Here are two posts I wrote up on a thread I started on another newsgroup:
Compared to the "studies" you hear about in the mainstream media, this
one is excellent:
QUOTE: ...LDL vitamin E levels were highest in rabbits fed corn oil
with added cholesterol. The significant elevations in linoleic acid
[18:2(n-6)] in serum and LDL may partially explain the high
oxidizability of LDL in rabbits fed corn oil. LDL isolated from
animals fed corn oil, lard or milk fat had significantly greater
albumin transfer across cultured endothelial monolayers compared with
those of the low fat diet group. Their oxidative modification further
contributed to endothelial barrier dysfunction. Dietary cholesterol
supplementation to the corn oil diet decreased oxidizability of LDL
and partially protected the oxidized LDL-mediated endothelial cell
dysfunction as compared with the corn oil diet group... UNQUOTE.
They found that beef and chicken fat were best, but they did not test
any of the highly saturated fat sources, like butter or even better,
coconut oil. This is an on-point study because it focuses on LDL
oxidation, which begins the heart disease process. Rabbits are more
susceptible than people, but the underlying biochemical mechanisms
appear to be the same (and there is no alternative to it).
Source: J Nutr. 1995 Aug;125(8):2045-54.Click here to read
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView...
Moreover, this study is consistent with other molecular-level
evidence, for example:
"Cholesterol protects the phospholipid bilayer from oxidative damage."
Source: Free Radic Biol Med. 1995 Oct;19(4):511-6.
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView...
Just keep in mind that you should not eat foods with a rancid taste,
and there is no reason to use high-heat cooking. Boiling eggs is a
much better idea than frying, for example. Cholesterol can be
oxidized before it gets to your mouth, but if you take precautions,
it's unlikely that this will be a problem for you.
Some studies find that highly polyunsaturated oils lower cholesterol,
or LDL levels, but if LDL is not oxidized, it's not a problem, and non-
oxidized cholesterol, as we've seen, is protective. However, in some
of these kinds of studies, the researchers find some disturbing
aspects to corn oil-rich diets, such as the following:
"...In contrast [to animals fed lard or palm kernel oil], animals fed
the CO [corn oil] diet exhibited a shift of more buoyant to denser LDL
particles..."
This is due to oxidative processes, though the authors do not talk
about them in the abstract.
Source: Arterioscler Thromb. 1993 Oct;13(10):1418-28.
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView...
Now for those unwilling or unable to understand the evidence (such as
"Ron Peterson," apparently), you have my sympathies, though I do wish
you sould stop misleading others. |
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Interesting site on cholesterol:
http://www.thincs.org/ |
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Here's a study that found that LDL and HDL inhibit AA metabolization, which is likely at least one factor in the findings that lowering cholesterol leads to higher cancer risk:
QUOTE: ...plasma from hypercholesterolaemic and control rabbits, when added to the incubation mixture, significantly inhibited platelet aggregation and eicosanoid production. 3. High- and low-density lipoprotein (HDL and LDL, respectively) concentrations increased several-fold in plasma with cholesterol feeding. When added directly to the incubation mixture, both HDL and LDL inhibited platelet aggregation, as well as AA metabolism. 4. Haptoglobin, albumin and Cohn's fraction IV, but not globulins, exhibited antiplatelet and anti-AA metabolism activities. Their concentrations in plasma were not affected by cholesterol feeding. 5. We conclude that LDL and HDL account for at least some of the inhibition of AA metabolism produced by plasma. UNQUOTE.
Source: Clin Exp Pharmacol Physiol. 2008 Jan 21 [Epub ahead of print]. |
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Is there a danger of oxidised cholesterol with butter which smelts on a warm toast or is that danger negligible ?
Thanks.
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| I don't think that is a problem, but I do think it's wise to trim the yellowed sides off of a butter stick. Also, consider eating antioxidant-rich foods, like berries, when you eat food that is fat-rich. Only coconut oil and palm kernel oil are totally safe to eat without eating antioxidant-rich foods at the same time, just make sure it has a "fresh" (not rancid) taste/smell (or no taste/smell, which is acceptable). |
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