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The Cholesterol Times, Issue #002 -- Statins, Dioxin, and Vision
August 20, 2005
A Publication of Issue #002, August 20, 2005

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If you have recently signed up for The Cholesterol Times and missed the first issue, you can view it here. It contains stunning information about corruption in Alzheimer's research and the complicity of major, prestigious scientific journals, the surreptitious passage of cholesterol and blood pressure guidelines timed with the release of related drugs, cholesterol-lowering drugs used as food additives, and more.

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In this Issue:

Site Updates
  • The Doctor's Heart Cure
  • Biosynthesis of Cholesterol
  • Coenzyme Q10
  • Squalene
    Best of the 'Net
  • Dr. Duane "Space Doc" Graveline, MD
    Research Watch
  • Statins and Dioxin
  • Statins and Vision
    Weston A. Price Foundation Conference
  • Conference Details
  • Hotel Reservations
  • Travel Accomodations
    Copyright and Disclaimer

    Site Updates

    Review of The Doctor's Heart Cure

    If you've read The Cholesterol Myths you know that cholesterol doesn't cause heart disease. But what does cause heart disease? Dr. Al Sears' The Doctor's Heart Cure picks up where Dr. Ravnskov left off, and gives us-- at least some of-- the answers to that question.

    The Biosynthesis of Cholesterol

    This flow chart traces the synthesis of cholesterol from acetyl CoA, a substance derived from the metabolism of any source of energy. It shows where statins (HMG CoA reductase-inhibitors) interfere with cholesterol synthesis, and how they also interfere with the synthesis of squalene and coenzyme Q10. Coenzyme Q10's synthetic pathway is also shown, where it deviates from that of cholesterol.

    The flow chart allows you to click on important end-products such as squalene and coenzyme Q10 to read further about their important functions in the body.

    Best of the 'Net

    Duane Graveline, MD

    Former NASA astonaut, Dr. Duane Graveline has compiled personal stories and articles about the negative effects of statin drugs. He has also published a new book, accessible from the site, on the same subject.

    Research Watch

    Statins May Increase Vulnerability to Dioxins

    Dioxins are a class of molecules with endocrine-disrupting, toxic, and carcinogenic properties. Recent research has been showing that various dietary factors are potent inhibitors of the toxicity of dioxins, meaning that actual dioxin exposure is only one small part of the equation.

    A study by Alsharif et al., found that vitamins A and E had between 57% and 70% reduction in various measures of dioxin toxicity in mice!

    What does this have to do with statins? Two indications are given that statins could play a role in increasing one's susceptiblity to dioxin.

    The first is that this study attributed vitamin A's effects to its ability to protect the integrity of cell membranes, which it cited ubiquinone, or coenzyme Q10, as possessing a similar role. Secondly, coenzyme Q10, apart from its independent membrane-protective and anti-oxidant status, also is required for the proper function of vitamin E, which passes its free radical on to coenzyme Q10, causing its regeneration.

    Statins directly inhibit the synthesis of coenzyme Q10, and can reduce coenzyme Q10 status up to 40% in humans. This translates to a compromise of vitamin E function and an abolition of coenzyme Q10's independent protective role. This highly suggests, then, that statins would increase one's vulnerability to dioxin.

    A Medline search for "ubiquinone dioxin" turns up four studies, none of which tested the effects of coenzyme Q10 supplementation on tolerance to dioxin exposure. A Medline search for "statin dioxin" turns up zero results.

    Scientists should study both the effects of intervening with coenzyme Q10 supplementation on toxicity in response to dioxin exposure, and the effect of statins on the same phenomenon.

    Statins Inhibit Synthesis of Compounds Important to Retinal Function

    Statin drugs are generally referred to as "cholesterol-lowering" drugs, but their actions also include the inhibition of the synthesis of a class of molecules called "isoprenes." Isoprenes are continuous chains of a recurring subunit of varying lengths. The 15-carbon version, farnesyl, is a precursor to cholesterol. The 50-carbon isoprene makes up the isoprene side-chain of coenzyme Q10. Isoprenes are also found as side-chains in fat-soluble vitamins that we obtain dietarily, such as carotenes, and vitamins A, E,and K.

    A study published two days ago in Neuron by Kassai, et al., investigated the effects that changing the isoprene subunit of certain retinal proteins had on visual function in mice.

    The gamma-subunit of the essential retinal protein retinal transducin ordinarily contains a farnesyl chain, which is the 15-carbon isoprene. This study genetically modified mice to express an identical transducin protein with a geranylgeranyl chain in place of the farnesyl, which is the 20-carbon isoprene. The study found that the two isoprenes were interchangeable in some respects, but that the geranylgeranyl isoprene inhibited the translocation of transducin away from the surface of rod cells in response to light. This impairs the visual response to changing light patterns.

    Although a wide variety of proteins in the retina involve isoprene side-chains, this study was the first study to modify these chains without modifying the structure of the protein with it, thus unequivocally showing the specific effects of changing isoprene side-chains.

    What is interesting with respect to statins is that both farnesyl and geranylgeranyl are inhibited by statin drugs, which cut off the synthesis of all isoprenes. How many functions in the retina are dependent on isoprene side-chains, and what is the critical limit of isoprene sythesis inhibition, beyond which visual function may become impaired?

    A Google search for "statin vision" or "statin vision loss" reveals claims that statins can both cause vision loss and prevent it. A Medline search for either phrase does not turn up any results.


    The use of statin drugs to lower cholesterol is founded upon a fundamental misunderstanding of cholesterol's role in heart disease.

    The unsystematic and inconsistent association of high cholesterol with heart disease is first simplified into a mythical consistent, systematic association. A second error is made in pointing to the presence of cholesterol in atherosclerotic lesions as indicating biological plausibility for a causal role of cholesterol in this association.

    Yet, as Dr. Ravnskov points out in The Cholesterol Myths, if high blood cholesterol was responsible for the accumulation of cholesterol in those plaques, then cholesterol would accumulate most in those plaques when its level is the highest. On the contrary, what we see is that cholesterol is absent from atherosclerotic plaques until after the middle-age peak in cholesterol levels, where it begins accumulating when blood cholesterol begins declining.

    In The Doctor's Heart Cure, Dr. Al Sears discusses how injuries to the blood vessels from homocysteine, bacterial toxins, components of cigarette smoke, and other abrasive materials, recruit the immune-repair response of LDL cholesterol and white blood cells, which results in a rough patchwork that can cause obstruction of blood vessels down the road.

    Many positive behaviors have what is considered a "positive effect" on blood cholesterol levels. For example, quitting smoking, losing weight, and exercising will all cause a "favorable" change in LDL to HDL ratios.

    Yet where is the value? If one lowers homocysteine by increasing B vitamins, and thereby lowers the need for LDL cholesterol's repair activity in blood vessels, does the body rejoice at the lack of LDL? Or does it rejoice at the absence of abrasive injuries to its blood vessels?

    If one makes a favorable change in lipoprotein ratios by exercising, does the body rejoice at the cholesterol levels? Or do the cholesterol levels simply reflect the body's rejoicing in response to the positive effects of exercise?

    The idea of using statins or herbal agents to lower cholesterol misses the point. There are two kinds of lowering cholesterol. One can lower cholesterol by decreasing the body's need for cholesterol (e.g. exercise, quitting smoking, losing weight, increasing nutrient intake) or one can decrease the cholesterol level directly (e.g. statins, red yeast rice, various "natural" therapies).

    The two are fundamentally different. The former assumes cholesterol levels to reflect other positive and negative processes in the body. The latter assumes cholesterol levels in and of themselves to be the causative agents in health-damaging processes.

    These two understandings can make the difference between helping and harming the body.

    If cholesterol is needed, for example, to manufacture hormones involved in stress adaptation such as cortisol, and therfore cholesterol levels rise along with harmful chronic stress, removing the stressors and learning to master relaxation will lower cholesterol at the same time as lowering cortisol and the harmful stress that elicits those compounds.

    On the other hand, if those stressors remain in place, and the body's need for cortisol and need for cholesterol remains intact, what harm could result in sabotaging the body's ability to meet that need with "cholesterol-lowering" drugs?

    Of course, it is a misnomer to refer to statins as "cholesterol-lowering." Statins have other independent effects, such as anti-inflammatory effects. But statins do not directly inhibit cholesterol synthesis. They inhibit the precursor to all isoprenes, mevalonate. They should be called isoprene-lowering drugs, which means that they equally attack cholesterol, squalene, coenzyme Q10, and the very many proteins that utilize varying isoprene side-chains for many different functions.

    It will be a long time before we find out fully what the true effects of statins are, although as Dr. Ravnskov has pointed out, evidence already indicates they cause some forms of cancer.

    If their value is in their anti-inflammatory action, would it not be safer to pursue the many natural therapies such as nutritional supplementation that can more safely inhibit inflammation? It makes sense to start with the basics and begin reincorporating some of the substances found naturally in human diets-- such as small amounts of DHA and EPA-- that are missing in standard modern diets, before we begin popping expensive pills that disrupt a plethora of important biological systems within our bodies.

    Weston A. Price Foundation Annual Conference

    Conference Details

    Friday, November 11, through Sunday, November 13, The Weston A. Price Foundation will be holding its Sixth Annual Wise Traditions Conference.

    Conferences in the past have featured Dr. Uffe Ravnskov's presentation of his hypothesis that cholesterol protects against infectious diseases, Dr. Kilmer McCully discussing his revolutionary work on homocysteine, Dr. Russel Blaylock's presentation of his work on excitotoxins, and many other excellent presentations.

    This year's conference will feature social activities, workshops on fertility awareness and fermentation of beverages, 2 main tracks on heart disease and cancer, and a long list of featured speakers, including Dr. John Cannell, President of the Vitamin D Council, and Dr. Noel Solomons, Director of the CeSSIAM International Nutrition Foundation.

    For more information on the conference, click here.

    Travel and Lodging.

    You can get a conference-related discount at the Westfield Marriot where the conference is being held of $139/night for double, triple, and quadruple occupancy by making reservations here.

    If you need to make travel arrangements, we encourage you to use Price Line, with which you can search for the cheapest price according to your own specifications.

    You can also use PriceLine for hotel accomodations if those at the West Marriot are too pricey. Plus, you'll help by using the link below:


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    Copyright and Disclaimer

    Please take notice that the contents of this newsletter and are copyright of Chris Masterjohn, 2005, and that this information is not to be construed or understood as any form of advice. Please visit our disclaimer page here.

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