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Monday, July 21, 2014

FDA Approves Dangerous and Worthless Cholesterol Drug - Brownstein

FDA Approves Dangerous and Worthless Cholesterol Drug


by Dr. David Brownstein

On May 3, 2013, the FDA approved a Big Pharma Cartel founding member Merck drug Liptruzet.  Liptruzet is a combination drug of Zetia and Lipitor.  I wrote to you about the failure of Zetia in three separate blog posts.  They can all be found by clicking here:  http://blog.drbrownstein.com/?s=zetia.
Zetia is a failed drug.  It should never be prescribed and should have been pulled from the market years ago.  There is no excuse for any doctor prescribing Zetia for any condition.  Zetia works by blocking cholesterol absorption in the gut.  Conventional doctors believe that drug therapies that lower cholesterol levels reduce the risk of heart disease.  However, Zetia, which has been around for over 10 years, has never been shown to lower the risk of developing a heart attack or stroke.  Furthermore, Zetia has never been shown to prolong life.

Why the FDA would approve this combination of Zetia and Lipitor is beyond belief.  The previous combination of Zetia and Zocor, known as Vytorin, was proven to be a colossal failure in multiple studies—see my previous blog posts.

FDA’s action is a perfect example of why we spend more money on health care than any other people on the planet.  Liptruzet will cost $5.50 per pill.  This means a patient prescribed Liptruzet will spend over $2,000.00 per year on a worthless drug that will be associated with side effects such as muscle aches and pains, memory loss, and neurological disorders.  We take too many ineffective drugs that are too expensive.  Do all of these drugs translate into better healthcare outcomes?  Heck no.  As compared to every other wealthy Western country, we finish last or near the bottom on every single health indicator.  In Liptruzet’s case, there is no justifiable reason for the FDA to approve it.  This is another example, amongst many, of why the FDA should be disbanded.  The FDA gives false credibility to Big Pharma.

If you are on Zetia, I suggest talking to your doctor about stopping it.  Ask him/her for any studies showing a clinical benefit such as a significantly lowered risk for heart disease, heart attack, stroke, or increased longevity.  I can assure you that you won’t be getting any articles from your doctor since they don’t exist.   More information about cholesterol-lowering medications can be found in my book, Drugs That Don’t Work and Natural Therapies That Do
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Do statins prevent or promote cancer? - Current Oncology

Do statins prevent or promote cancer?

Mark R. Goldstein MD FACP, Medical Director, Fountain Medical Court, 9410 Fountain Medical Court, Suite
The Editor, Current Oncology December 24, 2007
 
In their commentary, Drs. Takahashi and Nishibori discuss putative antitumour effects of statins. However, prospective data suggest that statins actually increase cancer in certain segments of the population. Additionally, new findings regarding the immunomodulatory effects of statins may explain the mechanism by which that increase occurs.

Statins increase the number of regulatory T cells (Tregs) in vivo by inducing the transcription factor forkhead box P3. Although that increase may be beneficial in stabilizing atherosclerotic plaque by reducing the effector T-cell response within the atheroma, it might impair both the innate and adaptive host antitumour immune responses. Not surprisingly, the number of Tregs present in many solid tumours correlate inversely with patient survival.

Indeed, analysis of large randomized statin trials demonstrate a highly significant (p = 0.009) inverse association between achieved low-density lipoprotein cholesterol levels and cancer. Close inspection of statin trials reveal the specific populations at risk for the development of incident cancer with statin treatment. These include the elderly and people with a history of breast or prostate cancer,. Furthermore, statin-treated individuals undergoing immunotherapy for cancer may be at increased risk for worsening cancer.

The elderly are relatively immunosuppressed and are more likely to harbour occult cancers. In the prosper (Prospective Study of Pravastatin in the Elderly at Risk) trial, a 3.2-year prospective study of pravastatin for cardiovascular disease prevention in the elderly (mean age at trial entry: 75 years) at high risk for cardiovascular disease, cancer incidence was significantly increased in subjects randomized to pravastatin. In fact, the increase in cancer mortality equalled in magnitude the decrease in cardiovascular disease mortality in the statin-treated patients, leaving all-cause mortality unchanged. Likewise, post hoc analysis of the lipid study, a 6-year prospective trial of pravastatin in individuals with cardiovascular disease, revealed a significant increase in cancer incidence in the elderly subjects (age: 65–75 years) randomized to pravastatin. In a secondary analysis of the tnt (Treating to New Targets) study, elderly subjects randomized to high-dose atorvastatin (80 mg daily) versus low-dose atorvastatin (10 mg daily) demonstrated a trend toward increased death, largely from an increase in cancer mortality. Therefore, the increase in incident cancer in the elderly might be dose-related. It is highly plausible that the elderly are particularly sensitive to a statin-induced increase in Tregs, further impairing their immune response to cancer.

An alarming increase in breast cancer incidence, some of which were recurrences, was seen in women randomized to pravastatin in the care trial Thereafter, cancer was an exclusion criterion in randomized statin trials. In clinical practice, however, it is not infrequent to find an association between recurrence of breast cancer and concurrent statin therapy. Long-term follow-up (10 years after trial completion) of woscops (West of Scotland Coronary Prevention Study), a 5-year prospective trial of pravastatin in hypercholesterolemic men, revealed an increase in prostate cancer in the men who were randomized to pravastatin therapy. That finding indicates that cancers may become evident a decade or more after treatment with statins. Treg increases have been associated with both breast and prostate cancers,, and therefore, it is highly plausible that the increase in cancers seen with statin therapy is related to a statin-induced increase in Tregs.

Statin therapy has been associated with tumour progression leading to radical cystectomy in patients treated for bladder cancer with bacille Calmette–Guérin immunotherapy. That association may be likewise due to a statin-induced increase in Tregs, resulting in impaired host antitumour immunity.
Statin trials have typically randomized subjects free of prevalent cancers and have been about 5 years in duration. Long-term follow-up data are limited, particularly for the development of cancer. Statins are now promoted for widespread use in adults of all ages and at high doses, potentially for decades. Importantly, they are used in individuals with other significant comorbidities such as cancer. Unfortunately, the post-market surveillance of drugs has been poor. Because cancer is highly prevalent in the population, particularly in the elderly, a statin-induced increase in cancer incidence will likely go unrecognized.

Long-term prospective data are needed on the feasibility of statin therapy in the very elderly, the immuno-suppressed, and those with prevalent cancer. Furthermore, long-term outcome data are needed in young individuals treated with statins for prolonged time periods. Perhaps a constant increase in Tregs over years, even in the young, will weaken host antitumour immune surveillance and increase the risk for various cancers.

In conclusion, we feel that there is ample evidence that statins may promote cancer in certain segments of the population. Currently, the indications for statin therapy are based on lipoprotein levels, prevalent cardiovascular disease, other vascular risk factors, and family history. Maybe it is time for a new paradigm that also includes age extremes, prevalent cancer, a past history of cancer, and overall immunocompetence.

REFERENCES

1. Takahashi HK, Nishibori M. The antitumour activities of statins. Curr Oncol. 2007;14:246–7. [PMC free article] [PubMed]
2. Mausner–Fainberg K, Luboshits G, Mor A, et al. The effect of hmg-coa reductase inhibitors on naturally occurring cd4+cd25+ T cells. Atherosclerosis. 2007 [Epub ahead of print] [PubMed]
3. Goronzy JJ, Weyand CM. Immunosuppression in atherosclerosis: mobilizing the opposition within. Circulation. 2006;114:1901–4. [PubMed]
4. Tiemessen MM, Jagger AL, Evans HG, van Herwijnen MJ, John S, Taams LS. cd4+cd25+Foxp3+ regulatory T cells induce alternative activation of human monocytes/macrophages. Proc Natl Acad Sci U S A. 2007;104:19446–51. [PMC free article] [PubMed]
5. Curiel TJ. Tregs and rethinking cancer immunotherapy. J Clin Invest. 2007;117:1167–74. [PMC free article] [PubMed]
6. Yakirevich E, Resnick MB. Regulatory T lymphocytes: pivotal components of the host antitumor response. J Clin Oncol. 2007;25:2506–8. [PubMed]
7. Alsheikh–Ali AA, Maddukuri PV, Han H, Karas RH. Effect of the magnitude of lipid lowering on risk of elevated liver enzymes, rhabdomyolysis, and cancer: insights from large randomized statin trials. J Am Coll Cardiol. 2007;50:409–18. [PubMed]
8. Shepherd J, Blauw GJ, Murphy MB, et al. on behalf of the prosper (Prospective Study of Pravastatin in the Elderly at Risk) study group. Pravastatin in elderly individuals at risk of vascular disease (prosper): a randomised controlled trial. Lancet. 2002;360:1623–30. [PubMed]
9. Hunt D, Young P, Simes J, et al. Benefits of pravastatin on cardiovascular events and mortality in older patients with coronary heart disease are equal to or exceed those seen in younger patients: results from the lipid trial. Ann Intern Med. 2001;134:931–40. [PubMed]
10. Wenger NK, Lewis SJ, Herrington DM, Bittner V, Welty FK. on behalf of the Treating to New Targets Study Steering Committee and Investigators. Outcomes of using high- or low-dose atorvastatin in patients 65 years of age or older with stable coronary heart disease. Ann Intern Med. 2007;147:1–9. [PubMed]
11. Sacks FM, Pfeffer MA, Moye LA, et al. The effect of pravastatin on coronary events after myocardial infarction in patients with average cholesterol levels. Cholesterol and Recurrent Events Trial investigators. N Engl J Med. 1996;335:1001–9. [PubMed]
12. Ford I, Murray H, Packard CJ, Shepherd J, Macfarlane PW, Cobbe SM. on behalf of the West of Scotland Coronary Prevention Study Group. Long-term follow-up of the West of Scotland Coronary Prevention Study. N Engl J Med. 2007;357:1477–86. [PubMed]
13. Hoffmann P, Roumeguère T, Schulman C, van Velthoven R. Use of statins and outcome of bcg treatment for bladder cancer. N Engl J Med. 2006;355:2705–7. [PubMed]
14. Gruver AL, Hudson LL, Sempowski GD. Immunosenescence of ageing. J Pathol. 2007;211:144–56. [PMC free article] [PubMed]
15. Winer EP, Harris JR, Smith BL, D’Alessandro HA, Brachtel EF. Case records of the Massachusetts General Hospital. Case 32-2007. A 62-year-old woman with a second breast cancer. N Engl J Med. 2007;357:1640–8. [PubMed]
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Read the complete article here.

Wednesday, July 9, 2014

Low Cholesterol Leads to an Early Death - FallonMorell

Low Cholesterol Leads to an Early Death: Evidence From 101 Scientific Papers

This book is a sequel to Cholesterol and Saturated Fat Prevent Heart Disease: Evidence from 101 Scientific Papers by the same author (and given a Thumbs Up review in Wise Traditions, Summer 2013). Evans provides studies in chronological order showing that the lower your cholesterol, the earlier you die; that high levels of both “good” and “bad” cholesterol help you to live longer; that high cholesterol does not cause cardiovascular disease; that low cholesterol leads to an early death in many diseases; and that low cholesterol leads to an increased prevalence of many diseases.
Some gems from Evans’ book: A 1992 study of over three hundred fifty thousand men, aged thirty-five to fifty-seven, followed for twelve years, found that higher cholesterol levels were associated with lower death rates; a five-year study published in 1989 found that low cholesterol increases the risk of death by at least 340 percent in elderly women; a twenty-year study published in 2001 found that those with the lowest cholesterol levels have a 35 percent increase in death rates compared to those with the highest cholesterol levels; and a 1998 study found that low cholesterol levels are associated with higher rates of many infectious diseases including hepatitis, appendicitis, digestive and liver infections, kidney and urinary tract infections, venereal disease and musculo-skeletal infections. None of these important studies got front-page billing in the media; meanwhile the anti-cholesterol juggernaut rolls on.

This book represents a great compilation of studies we never hear about and is enhanced by an amusing foreword by Tom Naughton, producer of the movie Fat Head. Thumbs up!
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Read the complete article here.

This book is available here.

Monday, July 7, 2014

Merck Uses Legal Threats To Stifle Negative Advice About Zetia And Vytorin

Merck Uses Legal Threats To Stifle Negative Advice About Zetia And Vytorin In Italy


In response to repeated legal threats, a public health doctor in Italy has withdrawn advice to curtail use of a controversial drug. The drug, ezetimibe, is a key ingredient in Zetia and Vytorin, which is manufactured by Merck Merck. The cholesterol-lowering drug has been the subject of fierce controversy because it has never been shown to improve clinical outcomes. Despite the controversy, in 2013 the drugs had combined sales of more than $2.6 billion.
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Read the complete article here.

Friday, July 4, 2014

How do statin proponents deal with debate? They stifle it - Briffa

How do statin proponents deal with debate? They stifle it.

Last month, one of my blog posts featured a letter written by a group of doctors, expressing their concerns about the mooted expansion of statin therapy. The letter detailed six major objections to the plan, including the mass-medicalization of millions of healthy individuals, the unreliability of the evidence regarding the adverse effects of statins, and the facts that almost all the evidence is industry-funded and that multiple conflicts of interest exist on the ‘expert committee’ that is adjudicating on the statin issue. The letter received widespread coverage in the press and other media, and I think it did much to stoke the flaming debate that some have described as the ‘statin wars’.

Those strongly supportive of the plans to widen statin prescriptions are hardly going to go away without a fight, though. And this week six professors convened a press briefing at the Science Media Centre to put forward their arguments. The briefing was reported in the British Medical Journal this week [1].

Two of the ‘usual suspects’ were Professor Sir Rory Collins (head of the Cholesterol Treatment Trialists collaboration) and Professor Peter Weissberg (medical director of the British Heart Foundation).

One of Professor Collins’ gripes was, apparently, that “misrepresenting the evidence” will have a negative impact on people who are at high risk of cardiac events. He is quoted as saying: “It’s perfectly reasonable to debate whether patients at lower risk should get statins or not, but it’s inappropriate to misrepresent the evidence.”

He redoubled his assertion that rates of ‘myopathy’ are much lower than some people state. However, he is referring to the incidence of muscle problems where the threshold of ‘abnormal’ is when levels of the enzyme used to assess muscle damage (creatinine kinase) is at least 10 times the upper limit of normal. Professor Sir Rory Collins is apparently disinterested unless muscles are in near-meltdown. We can, I suppose, just ignore those poor unfortunates with less biochemical aberrations even though their symptoms are real and often debilitating. I think it’s clearly business as usual for Rory Collins, who makes claims that some are misleading the public while I think he, ahem, continues to mislead the public.

Professor Weissberg tells us that the “…the critics are wrong. They’ve retracted, they’re wrong.” Except, that the only thing that has been retracted were the misleading representations of statin side-effects as reported in one piece of research. All the major objections detailed in the original letter stand until someone properly disputes them.

With regard to these, Professor Weissberg calms any concerns about industry involvement in the evidence base, because drug companies only paid people to do the studies, rather than the drug companies doing the studies themselves. So, nothing to concern ourselves with here.

He adds that: “The biggest threat to good medicine is prejudice and anecdote.” I have some sympathy for this view, but boy would I like to see Professor Weissberg stay away from prejudice and anecdote myself. It was not so long ago that he made claims to support statins using data that did not support the use of statins at all.

And perhaps the most telling thing of all are the comments that come from Fiona Fox, director of the Science Media Centre. Apparently, only pro-statin experts were invited to the briefing. In defence of this tactic, Ms Fox tells us that the “vast majority” of cardiac and statin experts believed that the evidence was overwhelming, and that it was not the centre’s job to provide a platform to a minority who did not and thereby project a false image that the debate was in equipoise (when it was not).
First of all, I wouldn’t be too sure that the evidence is overwhelming or that the pro-statin camp is in the great majority.  And even if there things were true, is that a reason to stifle debate and allow no right of reply?

Do these tactics suggest that Professors Collins and Weissberg and the rest of their merry band of men have true confidence in their position? I personally doubt it, and believe that their attempt to shut down debate suggests they may be desperate not to have the weakness of the data and their arguments revealed in front of their very own eyes.

References:
1. Hawkes N, et al. Six professors back NICE guidance on extending use of statins. BMJ 2014;349:g4380
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Read the complete article here.

Wednesday, July 2, 2014

Statins & Increase Diabetes Risk

Higher-Dose Statins Linked to Moderate Increase in Diabetes Risk
      By Kelly Young
          Edited by Susan Sadoughi, MD , and Jaye Elizabeth Hefner, MD

 Higher doses of statins are associated with greater risk for incident diabetes than lower doses, according to a BMJ study.

Using healthcare databases from Canada, the UK, and the US, researchers identified 137,000 patients who were prescribed statins after hospitalization for a major cardiovascular event. At 2 years, patients prescribed a higher-dose statin (rosuvastatin, 10 mg and up; atorvastatin, 20 mg and up; simvastatin, 40 mg and up) had a 15% higher rate of new diabetes diagnoses than lower-dose statin users. Incidence rates were highest in the first 4 months.

The authors conclude: "Clinicians should consider our study results when choosing between lower potency and higher potency statins in secondary prevention patients, perhaps bearing in mind that head-to-head randomized trials of higher potency versus lower potency statins have not shown a reduction in all-cause mortality or serious adverse events in secondary prevention patients with stable disease."


- See more at: http://www.jwatch.org/fw108892/2014/06/02/higher-dose-statins-linked-moderate-increase-diabetes#sthash.pAKrtJTt.dpuf


and

http://www.bmj.com/content/348/bmj.g3244

Saturday, June 28, 2014

The burden of proof in science always lies with those who propose a theory - Curtis

Evidence Against Cholesterol Causing Atherosclerosis

ernest_curtis_145by Ernest N. Curtis M.D. (Internal Medicine and Cardiology)


The burden of proof in science always lies with those who propose a theory. In this case the claim is that cholesterol is one of the chief causative agents for atherosclerosis.

Since the burden of proof is on those making the claim, we need only rebut their arguments. We don’t have to prove anything or advance an alternative theory.
The claim that cholesterol causes atherosclerosis can be rebutted on many levels. I don’t give much credence to epidemiologic evidence, but even that doesn’t pass scientific muster when it comes to cholesterol.

The correlations between cholesterol and heart attacks (the chief complication of atherosclerosis) cited in the medical literature are not even high enough to suggest an association between the two, much less a significant correlation. Even a high degree of correlation would not prove causation but the figures are nowhere near that level.

Another fly in the epidemiological soup is the fact that the incidence of heart attacks is fairly evenly distributed throughout the entire range of blood cholesterol levels. In fact more than half occur in those with cholesterol levels in the low normal range.

Many people with very high cholesterol levels live long healthy lives with no signs of complications from atherosclerosis. Conversely, many people with relatively low levels of cholesterol suffer from severe atherosclerosis and its complications. Add to that the fact that women have, on average, significantly higher cholesterol levels than men yet suffer far fewer heart attacks and I think we can conclude that the so-called evidence from epidemiology is nonexistent.

Many proponents of the cholesterol theory cite some of the statin drug trials as proof of the significance of cholesterol as an important factor by showing that reduction of its blood level provides a small degree of protection against heart attacks.

But these studies all showed a lack of normal response/exposure. There was a total disconnection between the small degree of outcome improvement and both the initial cholesterol level and the degree of cholesterol lowering attained. That is, the same small amount of benefit (which was so small as to be of no practical significance) was seen in subjects whose cholesterol declined only slightly and those in whom it declined a lot.

The benefit was also the same for those with low initial cholesterol levels and those with high initial levels. In scientific studies, this disconnection means that the factor being studied is not a cause of the outcome in question and that some other factor is at work. In this case it is possible that the anti-thrombotic action of the drug is the cause since the degree of protection against heart attack was almost identical to that seen in similar studies using aspirin or other anti-platelet drugs.

On the pathophysiologic level there are many reasons to doubt that cholesterol plays a causative role. Researchers have shown that some of the initial signs of atherosclerosis can be seen in the arteries of infants. These changes are seen in the same areas of the arteries where atherosclerotic lesions tend to occur later in life and consist of subintimal thickening with no sign of cholesterol infiltration or inflammatory reaction.

While the significance of these early changes can be debated, it is hard to deny the significance of the fact that atherosclerosis is a very focal disease process. It is found in the large and medium sized arteries and almost never in the smaller arterioles, capillaries, and veins.

Moreover, within the large and medium sized arteries there is a marked predilection for lesions to occur at branching points and along the lesser curvatures of arteries. These are areas of maximum shear stress on the arterial wall. Often one side of an arterial segment may be severely affected while the opposite wall shows no evidence of atherosclerosis whatsoever.

Atherosclerosis is often found in the arteries of the lower extremities but rarely in the arteries of the upper extremities. Atherosclerosis is never found in the veins of the body. However, veins that are subjected to arterial pressures when used as bypass grafts or arterovenous fistulas constructed for dialysis shunts often show rapid development of atherosclerosis.

These and other facts would seem to negate the possibility that atherosclerosis was caused by a chemical circulating in the blood since that should bring about a more generalized and/or random distribution of atherosclerotic lesions.

The blood flow through the larger arteries where atherosclerosis is typically found is much more rapid and laminar than it is in the smaller blood vessels. One would think that a slower flow would allow a noxious chemical to do more damage rather than less if it were a causative agent.
Einstein said that an elegant theory could be completely refuted by one inconvenient contradictory fact. In the case of cholesterol and atherosclerosis, there is a cornucopia of such facts.
Dr. Ernest N. Curtis, M.D
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Saturday, June 21, 2014

Peripheral Neuropathy from Statin Use - Graveline

Peripheral Neuropathy from Statin Use
dr_duane_graveline_m.d._134By Duane Graveline, MD, MPH







Neuropathy, short for peripheral neuropathy, simply means a malfunction of the peripheral nervous system that occurs without any inflammation of the nerves. There are many longstanding causes of neuropathy including diabetes, kidney problems and alcoholism.

Being placed on statin drugs is another more recent cause of peripheral neuropathy. Thousands of neuropathy cases have been reported to me over the past decade and in 2012, FDA's Medwatch finally warned about peripheral neuropathy as a major adverse reaction to all types of statins.

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Read the complete article here.

Tuesday, June 10, 2014

Statins linked to lower physical activity - Clinical Endocrinology

Statins linked to lower physical activity

By: MARY ANN MOON, Clinical Endocrinology News Digital Network - Jun 9, 2014

FROM JAMA INTERNAL MEDICINE
Vitals
 
Key clinical point: Statin use in older men may have the consequence of reducing their physical activity.
 
Major finding: Statin users engaged in 9.6% fewer minutes of moderate physical activity and 9.0% fewer minutes of vigorous activity per day than did nonusers, as well as 1% more minutes per day of sedentary behavior, than men who didn’t use statins. This equates to a mean decrease of approximately 151 minutes/week of walking and 37.8 minutes/week of more vigorous exercise, and an increase of 21.8 hours/week in sedentariness, for the statin users.
 
Data source: An observational study with both cross-sectional and longitudinal components, involving 4,137 U.S. men aged 65 years and older, of whom about one-fourth used statins throughout the 7-year study period.
 
Disclosures: This study was funded by the Medical Research Foundation of Oregon; the MrOS study was supported by the National Institutes of Health. Dr. Lee and his associates reported no potential financial conflicts of interest.
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Initiating statin therapy in older men was associated with a modest but significant drop in physical activity, according findings from a large, observational study published online June 9 in JAMA Internal Medicine.
 
In addition, older men who used statins showed lower activity levels and higher levels of sedentariness than did nonusers, for as long as they took the drugs. Although results of an observational study such as theirs cannot prove causality, it is likely that the statins’ well-known adverse effects of inducing muscle pain, myopathy, and muscular fatigue account for these differences, said David S.H. Lee, Pharm.D., Ph.D., of Oregon State University/Oregon Health and Science University, Portland, and his associates.
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Wednesday, May 21, 2014

Dr John Briffa's response to the BMJ's withdrawal of comments.

My reaction to the BMJ’s withdrawal of statements relating to the safety of statins

You may have noticed that there’s a bit of a ‘fight’ going on over the cholesterol-reducing class of drugs known as ‘statins’. I am simplifying here, but there are essentially two opposing camps. In one corner, there are those doctors and researchers who hold the view that the statins should be given to pretty much all adults from middle-age, and there is little to be concerned with regarding their safety. In the other corner, there are those who believe that statins do no good at all for the vast majority of people who take them, and that the side-effects are more common that ‘official statistics’ suggest.
The fight went up a notch last week when the editor of the British Medical Journal announced that remarks made in two BMJ articles about the side-effects of statins had been withdrawn [1]. One of the articles was written by Dr John Abramson from Harvard Medical School and colleagues, and principally questioned whether extending statin use to those at lower risk (as has been suggested by the National Institute of Health and Care Excellence) will save lives [2].  According to their analysis, it won’t. The other piece was written by UK cardiologist Dr Aseem Malhotra, and principally questioned the role of saturated fat in heart disease [3].

In both articles, the authors referred to a study [4] that found that 17.4 per cent of people taking statins had adverse effects as a result attributed to statins. In the articles this figure was expressed as 18 per cent or ‘about 20 per cent’ which, apparently, was the first error. However, other issues, according the BMJ, was that the authors claimed that the 17.4 figure related to the percentage of people who stopped statins (at least temporarily) due to side-effects – this is not correct (it represented the percentage of people who had adverse effects). Also, the study in question was ‘observational’ in nature, which means that we don’t know if the adverse effects are due to statins or are the result of the ‘nocebo’ effect (like a placebo effect, only with negative effects rather than positive). The Editor of the BMJ, Fiona Godlee, tells us in her editorial that the caveats concerning the observational nature of these findings should have been made.

Both the articles made it through the peer-review process, so how did these errors come to be picked up? Well, apparently, they were brought to the attention of Fiona Godlee by Professor Sir Rory Collins, who heads up what is known as the Cholesterol Treatment Trialists (CTT) collaboration based in Oxford, UK. The CTT holds data on statin studies and periodically assesses it to tell us that statins are safe and very effective.

However, the CTT has in the past made grand claims about the effectiveness of statins that are based on the extrapolation of data (rather than actual data). Plus, as some have pointed out, the CTT refuses to release its data for independent inspection. The CTT can basically say what it likes about the effectiveness and safety of statins, but no-one can challenge what it says because no-one else has access to its data.

Apparently, Professor Sir Collins was invited by Fiona Godlee to put his concerns in writing for publication but he refused. He and Fiona Godlee met, and this set the ball rolling which culminated in the withdrawal detailed above. However, apparently this is not enough for Professor Sir Collins: he is demanding retraction of both articles, even though he has not challenged the main points raised in the articles. Fiona Godlee has set up an investigation to determine whether or not the articles should be retracted.

I have written to the BMJ in the form of an online ‘rapid response’ that was posted yesterday. You can read my response here.

In my response I accept that errors were made, but ask if a simple correction might have done.
Professor Sir Collins bases his assertions regarding the safety of statins on data from randomised controlled trials, like the ones analysed by the CTT. However, there are many reasons why randomised controlled trials may not adequately identify and report adverse effects from statins. Fiona Godlee acknowledges this herself and lists some of the issues, and I add to that list in my response. In all, there are about a dozen reasons why randomised trials stand to ‘miss’ adverse effects.

I also raise the issue of a recent study which appeared to confirm the safety of statins [5]. The study also detailed many reasons why results from clinical trials are an unreliable assessor of side effects. The study was reported in the BMJ [6], but the report included none of the caveats listed in the paper (or any other ones). As I explain to the Editor, these omissions may lull individuals into a false sense of security, and put people at unnecessary risk of adverse effects of statins, some of which can be serious.

One might argue that the ‘crime’ committed by the BMJ is roughly equivocal to the ones perpetrated by Drs Abramson and Malhotra. I point this out to Fiona Godlee in my response, and request a meeting with Fiona Godlee to discuss my concerns. After all, why should I not be afforded similar privileges as Professor Sir Collins”

You can read the response in full here. If you agree with the sentiments expressed in it, please click on the ‘thumbs up’ symbol to the right of the response to log your agreement.

References:
1.    Godlee F. Adverse effects of statins. BMJ 2014;348:g3306
2.    Abramson JD, Rosenberg HD, Jewell N, Wright JM. Should people at low risk of
cardiovascular disease take a statin? BMJ2013;347:f6123

3.    Malhotra A. Saturated fat is not the major issue. BMJ2013;347:f6340
4.   Zhang H, et al. Discontinuation of statins in routine care settings. Ann Intern Med 2013;158:526-34
4.    Finegold JA, et al. What proportion of symptomatic side effects in patients taking statins are genuinely caused by the drug? Systematic review of randomized placebo-controlled trials to aid individual patient choice. European Journal of Preventive Cardiology 2014;21(4):464-74
5.    Wise J. Statins may have fewer side effects than is claimed, meta-analysis finds BMJ 2014; 348:g2151
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