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The Cholesterol Times, Issue #003 -- Statins, Stroke, and Dementia
August 29, 2005
A Publication of Issue #003, August 29, 2005

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In this Issue:

Site Updates
  • The Synthesis of Steroids From Cholesterol
    Best of the 'Net
  • Not All Milk Is The Same
  • Craving the Cookie
    Research Watch
  • Statins Increase Dementia Risk
  • Statins Double Risk of Stroke
  • Oxidative Stress and Heart Disease
    Weston A. Price Foundation Conference
  • Conference Details
  • Hotel Reservations
  • Travel Accomodations
    Copyright and Disclaimer

    Site Updates

    The Synthesis of Steroid Hormones From Cholesterol

    All steroid hormones-- responsible for such functions as libido, fertility, building lean body mass, counteracting inflammation, regulating blood sugar, and more-- are synthesized from cholesterol. Cholesterol is also the precursor of bile acids, used for digesting fats, and vitamin D, used for regulating the uptake of calcium and maintaining its blood levels, and therefore important for building strong bones. This flow chart shows the biosynthesis of these compounds from cholesterol, and will soon be updated so that you will be able to click on each compound for a more in-depth explanation of its role in the body.

    This page is linked from The Synthesis of Cholesterol-- Flow Chart", which shows how cholesterol is synthesized, as well as why statin drugs not only interfere with cholesterol synthesis, but also with the synthesis of important compounds such as squalene and coenzyme Q10.

    Best of the 'Net

    Not All Milk is the Same

    Milk-- especially whole milk-- has been maligned as a fatty, disease-causing junk food by many. Yet some people who can't tolerate milk in America find that they can tolerate milk fine in other countries. This report summarizes the A1/A2 debate: many now believe that a genetic mutation in modern breeds of cows causes a specific variant of milk protein, A1 casein, to be an allergen and a disease-promoting protein, while the ancient form, A2 casein, is non-allergenic and does not promote disease. The above link leads to a .pdf document. You can either click on it, or download it onto your computer by right-clicking and selecting "save target as," in the drop-down menu, which might be preferable if your internet connection is slow.

    Craving the Cookie

    The allure of the Oreo-- and how it became addictive.

    "Documents made public through litigation against the tobacco industry show that in March 1991, the Philip Morris scientist who led studies on nicotine's impact on the brain met with neuroscientists at Kraft's sprawling research center in Glenview.

    "The scientist, Frank Gullotta, discussed with Andrade and others 'the possibility of collaborative studies in areas that would be of mutual interest' to Kraft and Philip Morris, according to a Philip Morris memo describing the visit."

    Click on the link above for the full story.

    Research Watch

    Statins Increase Dementia Risk

    A July, 2005 study by Rea et al., published in the Archives of Neurology reported that ever-use of statins, contrary to their hypothesis, was not associated with a lowering of the risk of Alzheimer's or other dementia.

    (As discussed in a two-part article on our website, the myth that cholesterol causes Alzheimer's disease has led to the investigation of using statins to lower the risk of Alzheimer's.)

    Actually, the interesting part of the study is not the effect of ever-use or current-use of statins on dementia risk, but the huge association of former use of statins with dementia risk.

    The report was an analysis of data from the Cardiovascular Health Cognition Study, which studied a subset of patients (numbering 2,798) from the Cardiovascular Health Study.

    After adjusting for some possible confounding factors, ever-use of statins was associated with an 8% increase of risk of all-cause dementia, a 21% increase in risk of Alzheimer's disease alone, a 13% decrease in risk of mixed Alzheimer's and vascular dementia, and a 36% increase in risk of vascular dementia alone, all at 95% confidence.

    Yet current use of statins showed a very mild association with reduced risk of all-cause dementia, and with reduced risk for all forms except vascular dementia, where it was associated with a 39% increase in risk. There was no dose-response effect between duration of statin use and decreased risk, meaning that a patient did not experience a greater reduction in risk when statins were used for a longer period of time. Dose-response analysis wasn't provided for dosage of statins or the cholesterol-lowering effect of the statins.

    Why the discrepancy between ever-use and current-use? Because former use was associated, after adjusting for confounding factors, with a whopping 88% increase in all-cause dementia, a 154% increase in Alzheimer's disease, and a 61% increase in mixed Alzheimer's and vascular dementia.

    Put another way, someone who uses statins currently is 92% as likely to develop Alzheimer's as someone who never used statins, yet someone who previously used statins and stopped statin therapy is 254% as likely to develop Alzheimer's disease than someone who never used statins.

    The authors suggested that stopping and starting statin therapy might somehow trigger the dementia process, but claimed it was more likely that former use is a marker for declining health, and "patients and physicians may be less inclined to maintain preventive treatments such as statin use as overall health deteriorates."

    Remarkably, the authors did not suggest the possibility that a decline in health may be caused by the statin therapy! After all, is it not more likely for a patient to discontinue statin therapy if memory loss, fatigue, or the widely reported problems with myopathy settle in?

    It seems less likely that the author's suggestion-- patients and physicians simply give up hope and don't bother with drugs if they see health declining-- would occur, especially if statin therapy had already been initiated. It would be much more likely that statin therapy would be terminated due to the widely experienced adverse effects.

    The protective effects of current use were mild, and the authors noted that confounding factors could have been involved and that "additional investigation is needed to determine whether and for whom statin use may affect dementia risk."

    But the harmful effects of former use are very pronounced, leading to an almost doubling of the risk of all-cause dementia and an even more massive increase in Alzheimer's, by a factor of 2.54.

    It may be that the extremely modest 10% reduction in all-cause dementia of current statin users simply indicates that those who have the most resilient health can tolerate the negative effects of statin (lowering brain cholesterol, vitamin E, and coeznyme Q10 levels, for example), while those who are vulnerable to these effects have their mental health utterly ravaged, nearly doubling their risk of dementia.

    For more information on the myth that cholesterol causes Alzheimer's disease, please see our article, Myth: Cholesterol Causes Alzheimer's Disease as well as Part II: The Real Causes of Alzheimer's.

    Statins Double Risk of Stroke

    Another July study in the New England Journal of Medicine by Wanner et al., found that atorvastatin had no statistically significant (meaning the liklihood the correlation was due to chance was less than 5%) effect on total mortality in Type 2 diabetes patients undergoing hemodialysis, but more than doubled the risk of stroke.

    The study was a multicenter, randomized, double-blind prospective study of 1255 subjects. The data were monitored, collected, and held by Pfizer-supported organizations, but the data were analyzed by independent, academic scientists.

    The increase in risk of stroke was the only statistically significant effect on any individual endpoint that was considered, but when all cardiac events were grouped together, there was a significant 18% reduction in all cardiac events.

    The study did not provide information about the dose-reponse relationship between cholesterol levels and endpoints, but they note that the assumed relationship between cholesterol levels and heart disease indicates a risk reduction of 30% or more for cardiac events, whereas the risk reduction achieved was only 18%. Since statins have some benefits (as well as major risks) that would be expected to lower heart disease independent of cholesterol, this suggests that the reduction in heart disease was not due to cholesterol-lowering.

    The authors, in fact, noted that this risk reduction was "driven mainly by differences in the rates of coronary-artery bypass grafting and percutaneous transluminal coronary angioplasty,"-- not cholesterol levels.

    The reduction in cardiac events was compensated for by a more than doubling of fatal stroke. Risk of fatal stroke was increased by atorvastatin by a factor of 2.03.

    While there was a 7% reduction in mortality among the atorvastatin group (totaling a difference of 23 individual deaths), it did not even approach statistical significance, with a 33% liklihood of being due to chance. Additionally, patients in the atorvastatin group were 68% more likely to discontinue the drug because of complications, which alone totals an excess of 21 individual patients, which emphasizes the meaninglessness of the reduction of total mortality, and the liklihood of confounding factors.

    What this study found is:

  • supporting evidence that reduction in heart disease fatality with statins is not due to their cholesterol-lowering activity
  • statins offer a chance to trade dying of heart disease for dying of stroke

    Since there is evidence that statins cause cancer, and, as noted above, that statins cause dementia, it may be that statins offer much, much more in the risk department than the benefit department.

    One must wonder how many patients would accept statin treatment if it were described as a way to die of stroke rather than heart disease.

    Oxidative Stress and Heart Disease

    A third study from last month, published in the New England Journal of Medicine by Tsimikas et al., found that, in people under the age of 60, it is oxidized phospholipids within LDLs, not the cholesterol, nor the mere presence of LDLs, that contribute to obstructive coronary artery disease.

    Oxidative damage occurs when oxidizing agents (induced by smoking, exercise, normal metabolism, pollutants, etc) exceeds the protective effects of antioxidants (which includes many vitamins and other compounds found in unrefined foods of both animal and plant origin).

    In those younger than 60, the percentage of phospholipids associated with lipoproteins that were oxidized was a better predictor (52% increase per doubling) of obstructed arteries than LDL (46% per doubling), but male sex was the most important variable, increasing one's chance of obstructed arteries by 340%.

    When combined with hypercholesterolemia, the predictive value of oxidized phospholipids was enhanced roughly by a factor of 4. This, of course, is an indication of the absolute amount of oxidized phospholipids. For a constant percentage of LDL-associated phospholipids that are oxidized, the more LDL there is, the more oxidized phospholipids there are.

    The proportion of oxidized phospholipids was strongly correlated with lipoprotein A, or Lp(a). The authors cite evidence that Lp(a) is involved in wound healing and preventing tumor growth, and that its levels are elevated in centenarians, and suggest that it is involved in "cleaning out" oxidized phospholipids from the body.

    They also speculate that at chronic, high levels it could be proatherogenic (meaning it causes atherosclerosis), but that it is levels of oxidative stress that are the root cause of this phenomenon.

    In patients over the age of 60, on the other hand, there was a very weak negative correlation between the proportion of oxidized phospholipids and coronary artery obstruction, but it was not statistically significant. The association of obstructed arteries and LDL also became very weak and not statistically significant above age 60.

    It should be remembered that most heart attakcs occur above the age of 60 when we consider the importance of these findings.

    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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