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Rapid Responses: Rapid Responses published:
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Dutch cardiologists decline to discuss
- Uffe Ravnskov (23 March 2007)
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No debate - only threats
- Malcolm Kendrick (24 March 2007)
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The Cholesterol hypothesis débâcle
- Carlos Monteiro (25 March 2007)
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Why Is This Issue Not Being Debated?
- Paul J. Rosch (25 March 2007)
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Statins - public debate long overdue
- Eddie Vos (25 March 2007)
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Dutch Cardiologists should thank Dr De Groot
- Melchior Meijer (26 March 2007)
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Statins-A "Partial Remedy"-Do Not Treat Stress Dyslipidaemia
- ROBERT J PEERS (16 April 2007)
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Uffe Ravnskov, independent researcher Magle Stora Kyrkogata 9, 22350 Lund, Sweden
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The interview with me in Duth television where I questioned the science that allegedly support the cholesterol campaign led to much criticism from the health authorities, as described in your News report. As a result the director of the program has invited critical cardiologists to discuss the issue with me, but hitherto everyone has declined. Competing interests: None declared |
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Malcolm Kendrick, General Practitioner Brownley Green Health Cenre, Brownley Road, Wythenshaw
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I have been aware of the Radar programme for some weeks now, and the response of the 'authorities' is both predictable and depressing. Dr Ravnskov has been personally and professionally attacked. His co- presenter, and supporter, Dr de Groot has been described as a 'retired' cardiologist. Which is both irrelivent and ageist. Are retired people no longer allowed to express views of any value? Do we ignore people after the age of 60-65 as they know nothing? The programme itself was vilified for its attempt to achieve high ratings....unlike all other TV programmes which do their best to produce programmes that no-one will watch, presumably. No scientific arguments have been made by the programme's critics, and no-one promoting the current views on cholesterol lowering and statins is willing to debate with Dr Ravnskov on the programme. One can only ask why? If he is wrong, they should relish the opportunity to expose the weakness in his arguments. They should be like dogs straining at the leash, but they are not....why not? The answer is so obvious that it doesn't need to be stated. On top of this the authorities are now threatening new rules and regulations to stop TV companies in Holland from producing dangerous, inaccurate programmes. This is a direct threat. It is not even thinly veiled. This is also an attempt to suppress scientific debate, which should be fiercly rejected. Debate and discussion is the very lifeblood of science. When the 'powers that be' use their powers to threaten and crush dissent we should all be manning the barricades. As Voltaire said, "I may disagree with what you have to say, but I shall defend to the death your right to say it." Competing interests: I am a member of thincs, and my book The Great Cholesterol Con has recently been published |
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Carlos Monteiro, President Infarct Combat Project (01549-000)
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The cholesterol concept of atherogenesis born in 1913 from the classical investigations of Anitchkov and Chalatov still as the main theory to explain the atherosclerosis development, despite the weakness of scientific arguments as being shown by Uffe Ravsnkov and colleagues in many published papers and books. In fact, there is little scientific validation or correlation between lowering cholesterol and preventing or reversing heart disease. So, there is compelling justification for a critical look to other hypothesis that explain the formation of atheromas by repeated injury to the artery's wall, which may occur through various mechanisms. This could provide a solid scientific basis for therapies that are more logical, safer and clinically more effective than those based on cholesterol theory. As shown in many recent studies, the significant but low beneficial results through statins (in absolute risk reduction numbers) come from pleitropic effects not by lowering high cholesterol. One of the new hypothesis inside of the repeated injury concept is the Acidity Theory of Atherosclerosis, developed in 2006 at Infarct Combat Project, where acidity has an important role in the mechanism generator of atherosclerotic lesions, giving a new perpective for the understanding of the etiology and pathogenesis of atherosclerosis. Moreover it reinforces the thoughts from Pollak placed in an article from 1952: "Certainly all tissues change with age. There is anatomic and chemical aging. The acidity of tissues increases with age; this favors the precipitation of cholesterol (1) The acidity theory of atherosclerosis concept arose from the demonstration by scientists in California that normal stretching/relaxing of an artery does not produce atherosclerosis, while stretching/relaxing in different directions simultaneously does (2). The sequence of events in Acidity Theory of Atherosclerosis: I. Sympathetic dominance by continuous stress plus II. Deficiency in production of endogenous digitalis-like compounds with alterations in Na(+), K(+)-ATPase activity results in III. Lowered pH (acidity) that leads to the generation of mechanical forces in blood flow which may cause atherosclerosis Carlos Monteiro secretary@infarctcombat.org http://www.infarctcombat.org References: 1. An Etiologic Concept of Atherosclerosis Based on Study of Intimal Alterations after Shock, O. J. Pollak, Circulation 1952;5;539-550 http://circ.ahajournals.org/cgi/reprint/5/4/539.pdf 2. Beyond Lipids: Understanding the Mechanics of Atherosclerosis. UCSD News, July 12, 2006, at http://tinyurl.com/llmdx 3. Regulation of stretch-induced JNK activation by stress fiber orientation, Kaunas R, Usami S, Chien S, Cellular Signalling, 2006 (Epub ahead the print) at http://tinyurl.com/na6pt 4. New Explanation for the Cause of Atherosclerosis: The Acidity Theory. Press release at Infarct Combat Project at http://www.infarctcombat.org/media/081006.html Competing interests: Carlos Monteiro has developed the Acidity Theory of Atherosclerosis |
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Paul J. Rosch, President, The American Institute of Stress, Clinical Professor of Medicine and Psychiatry, NYMC 124 Park Avenue, Yonkers, NY 10703
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As noted, the main issues in this controversy are whether high cholesterol is the major cause of coronary heart disease and if cholesterol and/or LDL should be lowered as much as possible by giving statins. Although the Framingham study is cited as support for the first claim, a 30-year follow up of this cohort showed "a direct association between falling cholesterol levels over the first 14 years and mortality over the following 18 years".1 In addition, most heart attacks occur in people who do not have an elevated cholesterol. With respect to statins, it is apparent that any alleged benefits are not related to lipid lowering since they are seen regardless of cholesterol or LDL levels and are more likely the result of anti-inflammatory, antithrombotic or other "pleiotropic" activities. As a result, current guidelines for statin therapy based on lowering LDL to a level that few can achieve will only result in increasing dosages for longer periods of time, both of which are associated with increased adverse side effects, many of which have been suppressed.2 No significant statin dose response relationship has ever been demonstrated, and like aspirin, anti-inflammatory benefits may be achieved with much smaller doses than those used for other indications.3,4 The public has a right to hear these and other views that oppose current dogma about diet and cholesterol as the cause of coronary disease. I suspect that the unwillingness to debate the above claims stems not only from vested statin interests but also manufacturers of low fat foods. There is mounting evidence that dietary fat is not the cause of high cholesterol or heart attacks and may actually have favorable lipid efects.5 References: 1.Anderson KM, Castelli WP, Levy D. Cholesterol and mortality. 30 years of follow-up from the Framingham study. JAMA 1987; 257: 2176-2180. 2.Rosch, PJ. Peripheral neuropathy, Lancet 2004; 364:1663-1664. 3.Rosch, PJ Guidelines for diagnosis and treatment of high cholesterol. JAMA 2001; 286:2400-2402. 4.Rosch PJ. Determining optimal statin dosage. Mayo Clin Proc. 2003 Mar;78(3):379, 381 5.Volek, J.S., Sharman, M.J., and Gomez A.L., et al., An isoenergetic very low carbohydrate diet improves serum HDL cholesterol and triacylglycerol concentrations, the total cholesterol to HDL cholesterol ratio and postprandial lipemic responses compared with a low fat diet in normal weight, normolipidemic women," J. Nutr. 2003; 133:2756-2761. Competing interests: None declared |
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Eddie Vos, maintains www.health-heart.org Sutton (Qc) Canada J0E 2K0
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The public debate over statins is long overdue.
Doctors and patients should realize that statins do not extend lives in women or elderly, and the results in men are all but clear. The
bad news first:
Atorvastatin, Lipitor[tm], for example, has shown (versus placebo) not to reduce infarct in women [ASCOT] or fatal myocardial infarct in men [SPARCL], not to reduce mortality in anyone, not to slow calcification [Medline 16415377 and 15944423] and to cause the ubiquinone [CoQ10] lowering detriment [mitochondrial function, myalgia] a mevalonate production reducer is expected to cause [it takes 10 mevalonate molecules to make CoQ10, 6 to make cholesterol]. Top-dose atorvastatin lowers both blood CoQ10 and LDL-cholesterol levels by 50% [Medline 15210526]. The good news is that one can consider atorvastatin as mild antiinflammatory, or as a 'nitroglycerin mimic' [promoting the NO-synthase pathway and thus arterial compliance] with a 40% reduction in angina [ASCOT]. However, just like the pain reduction from a COX-2 inhibitor would keep people away from a knee surgeon, a reduction in angina pain would be expected to keep patients away from cath-labs, explaining fewer 'interventions' in some combined-endpoint 'event' studies. Atorvastatin reduces angioplasty incidence but so does going to a non-cathlab hospital FIRST after acute coronary syndrome and when the chances to eventually wind up with a balloon or by-pass intervention are both reduced by 90% -- while the chance of being alive at 6 months was found to be not less but in fact 14% greater [Medline 1566006]. Atorvastatin lowers 'interventions' by possibly 40%, your choice of first hospital by 90%. The lack of any mortality benefit from atorvastatin suggests that we are treating and affecting symptoms, not the fundamental cause of arterial decline and deaths. A mevalonate synthesis inhibitor lowers the amount of LDL since it takes ~48% cholesterol to create a stable LDL particle but it does not alter LDL composition (quality) for the better -that could be effected by reducing homocysteine, by lowering trans-fat intake and by healthy levels of carotenoids, tocopherols, CoQ10 and omega-3 content of the LDL particles, avenues that need urgent exploration. The simplified picture and the core of the debate is here: http://www.health-heart.org/LipitorNowWeKnow2006.gif eddie{at}vos.health-heart.org Competing interests: None declared |
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Melchior Meijer, Medical Journalist Zoutkamp, 9974 RR The Netherlands
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The Dutch Cardiology Society and the Dutch Healthcare Inspectorate seek an official tool to control how Dutch journalists treat 'delicate' medical isues. This is a serious an unprecedented threat and should alert (medical) journalists and doctors all over the world. The TV program Radar observed and broadcasted the fact that many medical scientists have grave and well founded reasons to doubt the causal role of lipoproteins in the pathogenesis of coronary disease. This is perfectly legal. It then asked if the severe side effects reported by many statin users - which often miraculously disappear following discontinuation of the medicine - are indeed mostly in the heads of these patients, as the majority of physicians will tell them. There is mounting evidence that suppressing HMG Co A-reductase, and thus cutting a whole tree of mitochondrial nutrients, may lead to a plethora of hitherto not understood adverse effects in a substantial amount of people (Beatrice Golomb, MD, PhD, leader of the 'Statin Study', personal communication). The statin may turn a not known sub clinical mitochondrial dysfunction into a manifest mitochondrial dysfunction. This should be studied in depth. Based on the information provided by the colleagues from Radar, EU MP Dr Dorette Corbey has demanded an independent investigation into the effects of statin treatment in the 'wild' population. All Dutch physicians, especially those united in the Dutch Cardiology Society, should thank Dr De Groot and the colleagues from Radar for their courage and welcome this study. Competing interests: Have defended myself successfully in fornt of the Council for Journalism after writing critically about statins in 2004. |
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ROBERT J PEERS, GP Melbourne, Australia
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1. In general practice, I strongly recommend low fat diet and exercise, to lower cholesterol, and rarely need to initiate statin therapy. I believe in reversing the cause. Prof R J Barnard, at UCLA, and cardiologist Dr Dean Ornish, in San Francisco, showed many years ago that a rigorous low-fat diet, increased grains and legumes, and regular exercise would lower both total cholesterol and LDL, by 23%--as good as any statin; and also lowered "trigs" by 33%--better than any statin. 2. If it is true that most cardiac deaths and infarcts occur in people with only mild cholesterol elevation, we need to define this at- risk group. I suspect that these people have so-called "diabetic dyslipidaemia" (low HDL, small dense LDL, raised trigs), which stress expert Geoge Chrousos maintains is actually stress hormone-related. Statins have limitations, apart from reducing relative risk by a measly 25-30%: one hears that total mortality seems no better, while sudden cardiac death marches on, and 40% of acute coronary unit admissions --even with statins?--show raised trigs. 3. There is an entirely new way of treating this lethal lipid pattern, that does not require fibrate drugs. "Low HDL/raised trigs" pattern is seen in the offspring of fat-fed pregnant rat dams (L Poston), and is actually part of the Metabolic Syndrome (Met Synd). Lifelong anxiety, as shown by sympathoadrenal and stress axis activation, is a common--and easily missed--component of Met Synd, the origins of which can be traced to fatty maternal diet in pregnancy. Fatty diet promotes pre-diabetic or diabetic metabolism in pregnancy, which may weaken the placental barrier to maternal cortisol. Cortisol can programme lifelong anxiety in the fetal brain, anxiety which--accompanied by Met Synd--affects 20-35% of people in "high-fat" societies. 4. All the described features of anxiety and Met Syndrome, including the stress hormone-induced lipid pattern, may be reversible with the simple glucose isomer Inositol, which is abundant in seeds, nuts, grains and legumes. Inositol, first shown by J Levine to be anxiolytic, has been shown (by J Nestler) to lower glucose and insulin levels, trigs (by 43%), blood pressure and weight; and to raise HDL (S Gerli). 5. Here, then, is a major step forward in lipidology--available to any clinician who bothers to ask about shyness in childhood! At least half of GP patients are chronically anxious, so are likely to have Met Synd-- especially if eating a fatty diet as well. Low-fat grain-and legume-rich diet, already known to prevent Type 2 Diabetes, will provide 2-3 g/day of Inositol, a useful anxiolytic dose, while also curbing binge-eating. 6. Inositol strategically inhibits Serotonin 2A receptors (C Brink), blocking the anxious brain's Corticotropin Releasing Factor-driven activation of a. the fear centres b. the HPA axis c. the Sympathetic. I see quite large falls in blood pressure in my anxious hypertensives, and am collecting data on lipid effects. 7. Statins may improve underlying atherosclerosis: but so do whole grains--Alice Lichtenstein has shown that higher grain consumption led to the least coronary stenosis progression over 3 years, in female IHD cases. 8. For an encore, the Inositol Hexaphosphate (IP6) found in all seeds, nuts, pollens and spores, is a potent iron-chelating antioxidant, with related anti-cancer and anti-ageing properties. I dare say the antioxidant function would be at least as strong as what is claimed for statins. References Barnard R J (1991). Effects Of Lifestyle Modification On Serum Lipids. Arch Intern Med 151: 1389-94 [Potent effects of very low-fat diet, whole grains and legumes, and exercise--a study well ahead of its time] Chrousos G P and Gold P W (1998). A Healthy Body In A Healthy Mind--And Vice Versa--The Damaging Power Of "Uncontrollable " Stress. J Clin Endocrinol Metab 83:1842-45 [Chrousos--a stress "guru"--claims that anxiety disorder can cause all the features of Metabolic Syndrome X, including "dyslipidaemia", via cortisol and noradrenaline] Ghosh P et al.(2001). Abnormal Aortic Fatty Acid Composition And Small Artery Function In Offspring Of Rats Fed A High Fat Diet In Pregnancy. J Physiol 533: 815-22 [offspring also had low HDL and raised triglycerides--a landmark finding] Welberg L A et al.(2000). Inhibition Of 11 Beta-Hydroxysteroid Dehydrogenase, The Foeto-Placental Barrier To Maternal Glucocorticoids, Permanently Programmes Amygdala GR mRNA Expression And Anxiety-Like Behaviour In The Offspring. Eur J Neurosci 12: 1047-54 [converging evidence suggests that fatty maternal diet lets maternal glucocorticoids leak across the placenta, to programme fetal anxiety] Levine J (1997). Controlled Trials Of Inositol In Psychiatry. Eur Neuropsychopharmacol 7: 147-55 [Myo-inositol improves anxiety-linked disorders] Iuorno M J et al.(2002). Effects Of D-Chiro-Inositol In Lean Women With The Polycystic Ovary Syndrome. Endocr Practice 8: 417-23 [BP and trigs fell] Nestler J E et al.(1999). Ovulatory And Metabolic Effects Of D-Chiro-Inositol In The Polycystic Ovary Syndrome. N Engl J Med 340: 1314-20 [Large fall in trigs--43%] Gerli S et al.(2003). Effects Of Inositol On Ovarian Function And Metabolic Factors In Women With Polycystic Ovary Syndrome: A Randomized Double-Blind Placebo-Controlled Study. Eur Rev Med Pharmacol Sci 7:151-9 [HDL rose; wt. fell] Brink C B et al.(2004). Effects Of Myo-Inositol Versus Fluoxetine And Imipramine Pre-treatments On Serotonin 5HT-2A Receptors And Muscarinic Acetylcholine Receptors In Human Neuroblastoma Cells. Metab Brain Dis 19: 51-70 [Irish psycho-pharmacologist B E Leonard states that 5HT-2A receptor inhibition should block anxiety pathways: Brink shows that Inositol does the required job, and does it better than fluoxetine, the first SSRI] Erkkila A T et al.(2005). Cereal Fibre And Whole-Grain Intake Are Associated With Reduced Progression Of Coronary Artery Atherosclerosis In Postmenopausal Women With Coronary Artery Disease. Am Heart J 150: 94-101 [Benefits on artery diameter ? due to strong antioxidant effects of Inositol Hexaphosphate, +/- anti-anxiety effects from derived Inositol] Venn B J, Mann J I (2004). Cereal Grains, Legumes And Diabetes. Eur J Clin Nutr 58: 1443-51 [Regular seed consumption lowers diabetes risk by 20-30%] Graf E et al.(1987). Phytic Acid. A Natural Antioxidant. J Biol Chem 262: 11647-50 [Pioneering--but neglected--study, by US food scientist, of potent iron-chelating antioxidant properties of Inositol Hexaphosphate in seeds, with immediate relevance to seed longevity, cancer prevention and treatment, and human life extension] Competing interests: None declared |
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