Censorship in Lipid Land

Stories from Australia and Britain reveal the dangers of telling the truth about statins

DRUG BUST by Alan Cassels

• The people’s briefing note on prescription drugs
Portrait of columnist Alan Cassels

When policy dooms you, start telling stories – stories so fabulous, so gripping, so spellbinding that the king forgets all about a lethal policy.

– Karl Rove (one of George W. Bush’s advisors)

Welcome to Lipid Land, ruled by our old friends Scandal, Deception and Deceit. After last month, it’s time to add Censorship to the list.

If you think this subject doesn’t affect you, think again. With one in five Canadians swallowing a daily cholesterol-lowering drug, or statin – which leaps to 50% of Canadians over 65 – and all of us consuming media about pharmaceuticals, this is a vital issue, even beyond the massive prescribing of drugs like Lipitor, Zocor or Crestor.

Many of my voyages into the absurdities of Lipid Land over the last decade have delivered stories of intrigue and scandal, yet I have to admit things have never been this weird. Statin fanaticism seems to have so clouded medicine’s thinking that now even some of the most cherished tenets of medicine – i.e, “First, let’s try not to kill the patient” – seem quaint and outdated.  The motto “He who dies with the lowest cholesterol wins” pretty much captures the immense hubris around using chemicals to tweak a substance essential to our health.

Two stories from the UK and Australia in the last month have confirmed the arguments around statin drugs – their benefits and harms – have become completely unanchored from reality and are threatening to sink in a sea of propaganda.

There are three generally irrefutable points you can summarize from the research on the effectiveness and safety of statins: 1.) statins ‘work’ primarily for a small subset of men who have heart disease;  2.) most people currently prescribed statins are unlikely to see any net health benefit; and 3.) all statin takers expose themselves to risks of harm. When I say ‘work,’ I don’t mean lowering your cholesterol, I mean preventing a heart attack or stroke.  The only ones who benefit from the drugs are men who have had heart disease or previously had a heart attack. They may see a 4-5% reduced risk of a heart attack or stroke over five years by swallowing a daily statin. There is a lack of evidence showing women, the elderly and ‘low risk’ men (i.e. most of us) will benefit from statins. What is disputable is the rate at which statin swallowers are harmed. The big manufacturer-funded statin trials show a very small level of adverse effects, yet other case studies or observational studies note perhaps as many as one in five statin users will experience adverse effects.

Last year, one of the most prestigious medical journals in the world, the British Medical Journal (BMJ), weighed into this controversy by publishing a report that said there is no benefit of taking statins for people who have a less than 20% risk of a heart attack over the next 10 years. It also said that, from observational studies of statins, about 18-20% of patients don’t tolerate the drug due to side effects. Those effects can include fatigue, muscle aches and pain, stomach complaints, short-term memory loss and erectile dysfunction, among other things.

A large, influential group in the UK – the Cholesterol Treatment Trialists’ Collaboration (CTT) – soaks in millions of pounds of drug money and emits some of the most egregious pro-statin propaganda on the planet. The head of the CTT, Sir Rory Collins at Oxford, was obviously outraged by the BMJ’s piece and in media interviews, including the UK’s Guardian, accused the BMJ report of killing people. He then went on to brow-beat the BMJ’s editor Fiona Godlee saying the BMJ got it wrong and the side effects weren’t 18-20%; they were less. The BMJ published a correction, indicating the true number might only be “9% of the study population having possibly discontinued statin therapy as a consequence of statin related events, rather than the 18% cited.”

End of story, right?  Not quite.  Seems the BMJ correction didn’t exactly satisfy the CTT people and Collins next asked the BMJ to retract the article saying patients would be scared off their valuable statins unless the BMJ relented.

This is medical-academic bullying of the finest kind. Some observers say the whole fiasco is a smokescreen put up by statin manufacturers and their agents who are known to hide statin adverse events data while insisting the drugs are safe enough to be added to the drinking water. Godlee has sent the issue to an independent panel, but the whole thing stinks to high heaven. The most awful stench is the rot of censorship where the manufacturers want to protect the image of cholesterol-lowering drugs and do so by attacking the integrity and independence of a medical journal. Stay tuned on this one.

The second tale from Lipid Land concerns an investigative report produced by the Australian Broadcasting Corporation. Journalist Maryanne Demasi’s two-part investigative program, The Heart of the Matter, was part of  ABC’s Catalyst program examining the health effects of diets (part 1) and statin drugs (part 2). (Go to www.youtube.com and search for Heart of the Matter, The Cholesterol Myth, Part 2.)

This two-part series was dynamite, probably one of the hardest hitting programs you’re likely to see on statins anywhere. Demasi interviewed a wide range of researchers and physicians, including some desperate defenders of the statin hypotheses and prominent non-conflicted statin researchers Drs. John Abramson, Rita Redberg and Beatrice Golomb. Uffe Ravnskov, a prominent cholesterol scientist from Denmark, has covered the misinterpretations and exaggerations around cholesterol for decades. He said, “As far as I know, this is the first TV program in the western world where critics of the cholesterol campaign have been allowed to present their view in detail.”

Instead of kudos for Demasi and her team, Australia’s National Heart Foundation and the drug companies immediately began their attack, forcing the ABC to convene their “Audience and Consumer Affairs” group to examine the critical comments. The 49-page judgment on the Catalyst program says the program generally did a very balanced job and 10 of 11 critical points were cleared of bias. Apparently, one part offended the sensibilities of the reviewers with the conclusion: “The program could have done a better job of teasing out the mainstream perspective to leave audiences better informed.” What the heck does that mean? We’re not sure.

The Director of Australia’s National Heart Foundation, an organization which lives off the avails of drug companies, came to defend statins by repeating the usual canard: “Statins reduce the risk of death or cardiovascular events in populations without a history of cardiovascular disease, irrespective of age and gender and across a wide range of cholesterol levels.”

Despite the program showing vital evidence of the very minor effects of statins for most people and the lack of any lifesaving benefit in women or in those without established heart disease, as well as an indeterminate number who suffer adverse events from the drug, guess what happened? ABC pulled the Heart of the Matter series off the air. Jaws were heard dropping around the world.

In the end, I’m fearful these kinds of bully tactics don’t just affect the officials at the Australian Broadcasting Corporation or the British Medical Journal; they also affect all journalists worldwide who we expect to expose these sorts of controversies so consumers can make informed healthcare decisions. Will these two episodes usher in a new era of self-censorship as future problems with pharmaceuticals are avoided by serious journalists or obscured or manipulated by the manufacturers and their sycophants?

I have to give the last word to French cardiologist and researcher Michel de Lorgeril. In his book, Cholesterol and Statins: Sham Science and Bad Medicine, he asks, “Why does challenging the cholesterol theory trigger such extreme reactions?” And further, “Why are the media afraid of revealing the greatest medical scandal in modern time?” All I can add is “Why indeed?”

Alan Cassels is a pharmaceutical policy researcher at the University of Victoria and the author of three books, each of which contain chapters on cholesterol-lowering. www.alancassels.com

10 thoughts on “Censorship in Lipid Land”

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  2. I used to think biochemistry was an impenetrable subject. There are rather too many biochemicals to contemplate, the majority of which may not have even been identified yet. Those that have been identified have been granted names that defy the will to remeber them.

    Then I realised two things, biochemistry runs in families, and glucose must be the the ultimate mother of all biochemicals. Glucose is the great founder of biodiversity as we can witness it to day. Take the acetyl and mevalonate pathway, for instance, this biological process of several steps spawns a biochemical called mevalonate while right at the beginning of the pathway the process begins with humble molecules of glucose.

    In turn mevalonate can spawn other wonderful off spring, again as a result of processes involving a number of steps. In humans mevalonate spawns cholesterol, and it spawns at least another five vital biochemicals that have been identified and named. This is true for all mammals, all vertebrates, and likely for anything we might term one of ‘gods creatures’.

    The last step needed to complete the biosynthesis of mevalonate requires an enzyme, that enzyme is called HMG-CoA reductase. HMG-CoA reductase is the enzyme that cholesterol lowering drugs called statins target. By interfering with the action of HMG-CoA statins restrict the synthesis of mevalonate and thus restrict synthesis of its’ own further progeny. So less cholesterol is produced, but it appears less of each of the other five important biochemicals are produced too. It would be irrational not to anticipate complications.

    What nobody has bothered to inform anyone (until now) is that the acetyl and mevalonate pathway is fairly ubiquitous across biology. Even plants have one. Plants need to produce sterols of their own, and plants produce plant sterols from mevalonate.

    Sterols are a diverse family. They number about 200. Most are described as phytosterols because certain of them are found are found in certain plants. Just a few are termed zoosterols because they arise in animals. Cholesterol is the best known zoosterol ever. Generally zoosterols are not found in plants, and conversely phytosterols are not found in animals.

    That said phytosterols and derivative molecules (their own progeny) can account in part for the rudimentary physiology and responses we can witness in plants, and very much in parallel with this the zoosterols, cholesterol especially, can account for in part for the more sophisticated physiology and responses to circumstance that we can witness in animals. Cholesterol is essential to all life that has a beating heart, and so is another mevalonate derivative called CoQ10. Cholesterol is as essential to one half of the tree of life, that which eats and metabolises, as water is to the entire tree of life.

    I’ll bet nobody ever told you (until now that is) that cholesterol can spawn many offspring.

    Cholesterol is a potential ‘mother’ to 49 known alternate cholesterol oxides. Many of these behave in keeping with simple hormones and have legitimate biological and physiological function. 10 might not be so legitimate, or so well managed (biologically speaking), and of these 10 a smaller number have been investigated for their potentially deleterious effects.

    Cholestane triol, 25-hydroxycholesterol, and 7-ketocholesterol each have bearing upon the behaviour of certain cell types that is consistent with events that describe the advance and nature of atherosclerosis, to an extent. So these three oxides look like candidates for being atherogenic. Homocysteine is unrelated to cholesterol oxides (its an amino acid) but it too has been implicated in the business of atherogenicity. The way this might work is that homocysteine may incite (directly or indirectly) oxidation of cholesterol to form these most suspect cholesterol oxides. Cholesterol plays ‘mother’ to all the steriodal hormones (steroidal hormones account for gender, cycles and sexual activity) and is also ‘mother’ to vitamin D.

    Every biochemical has a place in a family tree, and while biochemistry is an involved subject that simple acknowledgement greatly assists how one navigate the topic. Having a sense of a map makes the subject no less involved but renders it far less impenetrable.

    Cholesterol is highly labile. that it can be reworked to form highly functional molecules is the upside. A downside is that not all amongst the family of cholesterol oxides can be deemed ‘good’.

    Experimental atherosclerosis is my term for what happens when you successfully recreate atherosclerosis (fatty plaques cholesterol is said to cause) in an experiment. Just so long as you are not too picky experimental atherosclerosis is easy to induce. Choose a species (rabbits were the first instance) and add cholesterol to their feed. Cholesterol-fed animals will develop atherosclerotic indications. However if you overlooked that going about this might also introduce cholesterol oxides into the experiment then you would draw the wrong conclusions. Permit yourself a wry smile. The very foundations of the cholesterol hypothesis rest upon this easy mistake.

    Take the necessary steps to introduce only pure cholesterol and you will not return positive indications of atherosclerosis in any species. Only the extracted contaminants be that as an isolated sample, or when present in impure cholesterol will return a positive indication. That finding reported by Imai et al in 1974 spawned renewed interest in cholesterol oxides.

    Let’s get back to mevalonate.

    Recall mevalonate is ubiquitous across plants and animals, yet each go on to use it differently. Also recall that mevalonate requires the action of specific enzyme to make it. That enzyme is HMG-CoA reductase. How old do you suppose mevalonate is? When did it make it’s first appearance in the long run of the evolution of life on Earth? I can inform without any doubt it will be more than 500 million years old, and I think it far more primal even than that.

    I have yet to pin the evolutionary age of mevalonate down with precisions but I think the order of 2 billion years old stands as a reasonably well informed best guess. Biology indicates that HMG-CoA reductase has likely been around for as long, or almost as long.

    Two billion years is a long time, even in evolutionary terms. Many species have come and gone within that period, yet the acetyl and mevalonate pathway not only endures but it is largely ubiquitous. This observation stands as context as opposed to hard evidence, but what do you suppose it informs? I’d say it says we have mevalonate and we have the enzyme HMG-CoA reductase and we have cholesterol because we jolly well need them; and that’s what it should inform anybody bar a complete bloody idiot.

    Cholesterols contribution to biology and physiology is overwhelmingly positive, and only a complete absence of evidence contributes to the common perception to the contrary. Mevalonates contribution to biology is overwhelmingly positive, too, and furthermore its contribution ranges far further in terms of diversity of context. HMG-CoA reductases contribution to biochemistry is overwhelmingly positive, every bit as great and as positive as is mevalonates. Only a fool would insist otherwise. Only those easily besotted by dogma could think it good sense to target HMG-CoA reductase with a drug that inhibits its action.

    The time is long overdue to inform statin pedlars this is where they get should get off and how. Two words, seven letters, three of which are ‘f’s.
    Hope you like, y’all.

    cjp.321.321 .. @ .. .. gmail.com

  3. Very enjoyable blog. I was made aware of it by a Canadian statin skeptic. I have spent rather too much of my life attacking the diet/heart cholesterol hypothesis, and the ridiculous overprescribing of statins. I helped Maryanne put together her programs, and had a role in the saga of Professor Sir Rory Collins (chief banana), vs. the BMJ. We are certainly seeing a rather dark and dangerous pattern of behavior emerging where any with a contradictory point of view is sought out for public destruction, normally using the ‘you are killing my patients,’ strategy. Keep up the good work at exposing this behavior for what it is. Vicious bullying, usually by those with a lot to lose financially.

  4. Hi,
    You write “There are three generally irrefutable points you can summarize from the research on the effectiveness and safety of statins: 1.) statins ‘work’ primarily for a small subset of men who have heart disease etc. ”
    Well this is a refutable one.
    This belief that is propagated with so much success and absence of questioning is based upon flawed, deeply flawed or spun studies (for those that were published)and cannot be supported. See this book :

  5. An Excellent article.

    Maryanne Demasi is no stranger to controversy, and is a very courageous scientist. She presented an ABC programme on the cause and treatment of Multiple Sclerosis, which was immediately reviled by the neurological contingent.

    The same stifling occurs. Cambridge MS research is bankrolled by the makers of Alemtuzumab. Charles Stratton and I sent a letter to the Lancet. It was rejected. Here is its text:

    Might Alemtuzumab pose risks were Multiple Sclerosis to have an infective input?

    Charles W Stratton MD Department of Pathology, Vanderbilt University Medical Center, Nashville, TN 37232, USA

    David B Wheldon MB FRCPath Department of Medical Microbiology, Bedford Hospital, Bedford, MK42 9DJ, UK

    11th November 2012

    The effectiveness of alemtuzumab in reducing the incidence of relapse in the relapsing-remitting form of multiple sclerosis is remarkable1. But how will this drug affect the long-term outcome of the disease? Therapy aimed at disabling a component of the immune system presupposes a primary auto-immune aetiology. This may not be the case 2. Indeed, the inflammation associated with the clearance of damaged myelin may be a secondary ‘housekeeping’ process: the sudden, orderly, local mass-death of oligodendrocytes is the first visible event in the MS relapse 3.

    There appear to be two distinct neuropathologies in MS. The more obvious is the sudden destruction of myelin resulting in acute relapse. Less obvious, and more insidious, is the gradual reduction of brain mass4. Application of Occam’s Razor to these disparate pathologies suggests a chronic underlying infection periodically but ineffectively targeted by the immune system. Chlamydia (Chlamydophila) pneumoniae is a good candidate. This intracellular pathogen is associated with vasculitic phenomena5. Vasculitis was shown to precede neural damage in the 19th century 6. The organism (which is difficult to grow) was first detected in the CSF of persons with MS in 19997. A prospective study revealed a new respiratory infection with this organism prior to MS relapse 8. A statistically significant elevation of antibodies to Chl pneumoniae was seen as relapsing-remitting disease became progressive 9. In a limited pilot study, antimicrobial therapy directed against Chl pneumoniae reduced the loss of brain mass10. We and others have reviewed the evidence for Chl pneumoniae infection in MS11,12.

    What would be the likely outcome of therapy targeting the immune-system were an underlying infection present? A reduction in visible relapse seems likely. But we would expect the continuation of a more insidious pathology. The barking guard-dogs might have been silenced but the burglars may still be making off with the silver. Alemtuzumab alone may not prevent the onset of progression: it was found ineffective in treating secondary progressive MS despite favourable MRI appearances13. We shall have to await ultimate outcomes.

    1. Coles AJ, Twyman CL, Arnold DL et al. Alemtuzumab for patients with relapsing multiple sclerosis after disease-modifying therapy: a randomised controlled phase 3 trial Lancet online 2012 doi:10.1016/S0140-6736(12)61768-1
    2 Chaudhuri A, Behan PO. Multiple sclerosis: looking beyond autoimmunity. J Roy Soc Med 2005; 98: 303-306.
    3 Barnett MH, Prineas JW. Relapsing and remitting multiple sclerosis: pathology of the newly forming lesion. Ann Neurol. 2004; 55(4): 458-68.]
    4 Rovaris M, Judica E, Gallo A et al. Grey matter damage predicts the evolution of primary progressive multiple sclerosis at 5 years.Brain. 2006 Oct;129(Pt 10):2628-34.

    5 Thibault PK. Multiple sclerosis: a chronic infective cerebrospinal venulitis? Phlebology 2012; 5: 207-18. doi: 10.1258/phleb.2011.011068.

    6 Rindfleisch E. Histologisches detail zu der grauen degeneration und Ruckenmarks. Arch Pathol Anat Physiol Klin Med 1863;26:474

    7 Sriram S, Stratton CW, Yao S, Tharp A, Ding L, Bannan JD, Mitchell WM. Chlamydia pneumoniae infection of the central nervous system in multiple sclerosis. Ann Neurol. 1999 Jul;46(1):6-14.

    8 Buljevac D, Verkooyen RP, Jacobs BC et al. Chlamydia pneumoniae and the risk for exacerbation in multiple sclerosis patients. Ann Neurol. 2003 Dec;54(6):828-31.

    9 Munger KL, Peeling RW, Hernán MA et al. Infection with Chlamydia pneumoniae and risk of multiple sclerosis.Epidemiology 2003 14:2 141-147

    10 Sriram S, Yao SY, Stratton CW, Moses H, Narayana PA, Wolinsky JS. Pilot study to examine the effect of antibiotic therapy on MRI outcomes in RRMS. J Neurol Sci. 2005 Jul 15;234(1-2):87-91.
    11 Stratton CW, Wheldon DB. Multiple sclerosis: an infectious syndrome involving Chlamydophila pneumoniae. Trends Microbiol. 2006 Nov;14(11):474-9.
    12 Contini C, Seraceni S, Cultrera R, Castellazzi M, Granieri E, Fainardi E. Chlamydophila pneumoniae infection and its role in neurological disorders. Interdiscip Perspect Infect Dis. 2010 doi:10.1155/2010/273573

    13 Coles AJ, Cox A, Le Page E et al. The window of therapeutic opportunity in multiple sclerosis: evidence from monoclonal antibody therapy J Neurol. 2006 Jan;253(1):98-108.


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