Feb 05 2008
The International Network of Cholesterol Skeptics
There is an organization that calls itself The International Network of Cholesterol Skeptics (THINCS). Its members “thinc” they are smarter than the average doctor. They “thinc” that cholesterol has nothing to do with cardiovascular disease and that we have been deluded into waging a “cholesterol campaign” for which the scientific evidence is non-existent. They say, “What we all oppose is that animal fat and high cholesterol play a role.” I find even the wording of this statement problematical: one does not usually hear scientists “opposing” matters of fact or non-fact. They go on to say, “The aim with this website is to inform our colleagues and the public that this idea is not supported by scientific evidence; in fact, for many years a huge number of scientific studies have directly contradicted it.”
They tell us about those contradicting studies; but they don’t tell us about the flaws in those studies, they misrepresent some of the results, and they don’t tell us about the many good studies that support the cholesterol/heart link. The issue is a complex one, and it is easy to find studies to support any claim. Good science is about weighing all the evidence pro and con before reaching a conclusion. As far as I can see, these folks have cherry-picked the literature to support an agenda. They seem to have a vendetta against statin drugs in particular.
The website solicits complaints of adverse effects from statin drugs. It features a petition to the WHO that you can sign requesting an investigation of statin side effects. It alleges that lowering cholesterol endangers the elderly. It provides “what the medical journals and newspapers won’t let you hear” – letters and papers that have been rejected for publication. It lists books, published papers and talks by its members. It solicits financial contributions to the cause.
This movement seems to have started with Uffe Ravnskov’s book The Cholesterol Myths, published in Swedish in 1991 and in English in 2000. That book has been severely criticized, for instance in The Skeptic’s Dictionary , where Bob Carroll points out some of the distortions and deceptive techniques found in the cholesterol skeptics’ arguments. A typical claim: “Cholesterol is highly protective against cancer, infection and atherosclerosis” and “high TC [total cholesterol] and LDL levels are beneficial at all ages.” These statements are not only false, they are potentially dangerous to the health of those who believe them.
I’ll admit there is a grain of truth in what they say. The public may falsely perceive cholesterol as some kind of “Great Satan” of heart disease, and diet has been overemphasized, and some doctors may be over-prescribing statins. But there is plenty of evidence from multiple avenues of research to show that high cholesterol is a risk factor for heart disease and that lowering it reduces risk. A Lancet article from December 2007 reviewed trials involving nearly a million people and found that “Total cholesterol was positively associated with IHD [ischemic heart disease] mortality in both middle and old age and at all blood pressure levels.”
Another Lancet meta-analysis of over 90.000 patients concluded “Statin therapy can safely reduce the 5-year incidence of major coronary events, coronary revascularisation, and stroke by about one fifth per mmol/L reduction in LDL cholesterol, largely irrespective of the initial lipid profile or other presenting characteristics. The absolute benefit relates chiefly to an individual’s absolute risk of such events and to the absolute reduction in LDL cholesterol achieved. These findings reinforce the need to consider prolonged statin treatment with substantial LDL cholesterol reductions in all patients at high risk of any type of major vascular event.”
Most doctors follow guidelines like those in a recent issue of American Family Physician. The article reviews the evidence, makes evidence-based practice recommendations for treating cholesterol abnormalities, and grades the quality of the evidence for each recommendation. It gives most of the recommendations the highest “A” rating.
Prevention is much more complex than just throwing statins at patients with high cholesterol. There are other ways to lower cholesterol, including weight loss. It makes a difference whether you are aiming for primary prevention (preventing disease in the first place) or secondary prevention (preventing further harm to someone who already has cardiovascular disease). A high LDL may not be as significant in a patient whose HDL (“good” cholesterol) is also high. Before prescribing, a good doctor looks at the whole patient: all the other risk factors, such as age, sex, weight, diet, exercise, family history, smoking, blood pressure, and past history. He looks at the risk/benefit ratio of statins in the patient’s particular situation. He considers the NNT (number needed to treat) to prevent one death or heart attack (which may vary from 5 to 333 depending on the situation). He looks at what other medications the patient is on, at the cost and convenience, at the patient’s personal philosophy and preferences. Ideally, the decision to use statins should be a joint decision of the patient and the doctor based on all the information available.
The cholesterol skeptics doubt that all-cause mortality can be reduced by statins. It clearly can for secondary prevention. In primary prevention, it at least reduces the rate of cardiovascular events. It’s not entirely clear whether the risk reduction with statins is due solely to the lowered cholesterol; statins may have other beneficial effects. But at least it appears that the degree of risk reduction can be measured by the degree of cholesterol lowering.
If you have the right genes, a high cholesterol level may not hurt you. And if you are at low risk, you can’t eat yourself into a heart attack just by overindulging in dietary fats and cholesterol. Some of the cholesterol skeptics’ objections are based on a misunderstanding of the relationship between dietary cholesterol and blood cholesterol levels. We used to recommend a low cholesterol diet, then a low fat diet, then a low saturated fat diet, and now we are concerned about trans-fats. We are refining our knowledge, and recommendations are changing accordingly. A reduced fat diet is still recommended for those with elevated blood cholesterol levels, but it may only lower the cholesterol level by 3 – 6%.
When I first went to the THINCS website, the first thing that popped up was a letter warning that statins caused cancer. When I checked the recent articles on “cancer” and “statins” in PubMed, most of the studies showed either no correlation with cancer or an apparent protective effect, especially for colorectal cancer and skin cancer. The NIH is studying statins for cancer prevention, and there is a plausible biologic rationale to support that concept (statins work against cellular functions that may help control tumor initiation, tumor growth and metastasis).
There are even suggestions that statins might benefit other diseases like Parkinson’s disease and Alzheimer’s.
The skeptics cite studies where elderly people with low cholesterol had worse outcomes, but the elderly often have confounding factors: in that age group low cholesterol can be a marker for inadequate diet and chronic disease. A 2008 study shows that “Statins reduce all-cause mortality in elderly patients and the magnitude of this effect is substantially larger than had been previously estimated.”
My impression is that the general trend of recent statin studies in the better journals has been to show even more efficacy and fewer side effects than previously thought. For instance, the 2007 West of Scotland Coronary Prevention Study, reported in the New England Journal of Medicine was very encouraging.
The cholesterol skeptics’ website rejects the consensus of medical science, saying that consensus is politics, not science. I beg to differ. Consensus based on opinion is politics. Consensus based on the evidence is an integral part of the scientific enterprise: when the evidence is convincing, the majority will be convinced.
Dissent, debate, and questioning the status quo are important in keeping science honest, but science doesn’t advance through activist groups like this. We didn’t need an “X-Ray Skeptics” group to realize that routine annual chest x-rays were a bad idea; we saw the evidence and stopped x-raying everybody.
We are still struggling to understand all the ins and outs of preventing cardiovascular disease. Current guidelines have been criticized because they are often based on extrapolations and on insufficient data about actual outcome. A letter to the editor of the American Family Physician compared guidelines in six different countries, and found that the American guidelines would save a few more lives but only at much greater expense: 198 patients treated at an expense of over $198,000 to prevent one death. I’m sure we’ve gotten some things wrong, and our present approach will surely be revised as we continue to learn. But to reject the cholesterol connection and statins entirely is to throw the baby out with the bathwater. In my opinion, THINCS is spreading misinformation that could lead patients to refuse treatment that might prolong their life or at least prevent heart attacks and strokes.
364 Responses to “The International Network of Cholesterol Skeptics”
This site has excellent writers. However, Harriet is my favorite; I always look forward to reading her pithy but easy-to-understand writings. Thank You.
While this is far from being an area I have any knowledge in, one thing did strike me about this organisation, THINCS – the fact that they call themselves skeptics. I do wish people who are determined to ignore compelling evidence would not describe themselves thus – it gives the rest of us a bad name. Just wrote a post on the subject, so thanks for the inspiration!
Thank you, Dr. Hall. I’ve never had heart disease, and I take a statin for mildly high LDL. I’m grateful for your summary of the research and for the links you provide.
Although I hadn’t heard of THINCS, I did read last week in the New York Times that there are doubts about the health effects of serum cholesterol and what benefits statins do or do not offer. The net lesson I take away is that although statins may not increase my life span, they may well improve my quality of life.
One quality-of-life issue I worry about is statins’ effect on muscle strength. I don’t have muscle pain, but as a weightlifter, I’ve seen a significant drop-off in my strength in the year or so I’ve been taking a statin. I wonder if there’s any evidence statins have that effect, short of the serious muscle disorder a few statin-takers suffer from.
There appears to be a strong reluctance among practitioners of medicine to overturn, or even to examine, the meme that lowering cholesterol by means of HMG-CoA inhibition is a desirable objective.
This notion refuses to die despite the shoddy science of Ancel Keys or the inability of the first 22 years of Framingham to find any relationship between dietary intake of cholesterol and in vivo cholesterol levels. That is also to say nothing about the collected works of Professor Bruce Ames, Drs Peter and Ali Langsjoen, Duane Graveline, Uffe Ravnskov, Malcolm Kendrick and many others.
It is never profitable to attempt to educate the unwilling so I will leave you with a patent application from Merck from 1990. You may read the application for yourselves but the synopsis is that the Merck were applying for a patent to combine CoQ10 with a statin for the purpose of “counteracting HMG-CoA reductase inhibitor-associated myopathy” (later referred to as skeletal muscle myopathy)
The case for iatrogenic harm is flimsy at best (if ever justifiable) and thoroughly incompetent medicine at worst. The evidence is provided that Merck knew with certainty that statins were harmful. Q.E.D
United States Patent 4,933,165
Brown June 12, 1990
Coenzyme Q.sub.10 with HMG-CoA reductase inhibitor
Abstract
A pharmaceutical composition and method of counteracting HMG-CoA reductase inhibitor-associated myopathy is disclosed. The method comprises the adjunct administration of an effective amount of a HMG-CoA reductase inhibitor and an effective amount of Coenzyme Q.sub.10.
Inventors: Brown; Michael S. (Dallas, TX)
Assignee: Merck & Co., Inc. (Rahway, NJ)
Appl. No.: 07/298,535
Filed: January 18, 1989
Current U.S. Class: 424/94.1 ; 514/415; 514/460; 514/510; 514/689; 514/922
Current International Class: A61K 31/20 (20060101); A61K 31/185 (20060101); A61K 31/35 (20060101); A61K 31/403 (20060101); A61K 31/405 (20060101); A61K 031/405 (); A61K 031/35 (); A61K 031/21 (); A61K 031/12 ()
Field of Search: 424/10,510 514/415,690,460,922,689
Other References
The New England Journal of Medicine, Scott M. Grundy 319 No. 1, pp. 24-33 Jul. 7, 1988. .
Folkers et al, Proc. Natl. Acad. Sci., 82, 901(1985). .
Folkers et al, Proc. Natl. Acad. Sci., 82, 4513(1985). .
M. S. Brown & J. Goldstein, J. Lipid Res., 21, 505 (1980). .
H. Mabuchi et al, N.E.J. Med., 478 (1981)..
Primary Examiner: Robinson; Douglas W.
Assistant Examiner: Henley, III; Raymond J.
Attorney, Agent or Firm: Winokur; Melvin DiPrima; Joseph F.
Claims
What is claimed is:
1. A pharmaceutical composition comprising a pharmaceutical carrier and an effective antihypercholesterolemic amount of an HMG-CoA reductase inhibitor and an amount of Coenzyme Q.sub.10 effective to counteract HMG-CoA reductase inhibitor-associated skeletal muscle myopathy.
2. A composition of claim 1 in which the HMG-CoA reductase inhibitor is selected from: lovastatin, simvastatin, pravastatin and sodium-3,5-dihydroxy-7-[3-(4-fluorophenyl)-1-(methylethyl)-1H-Indole-2yl]- hept-6-enoate.
3. A method of counteracting HMG-CoA reductase inhibitor-associated skeletal muscle myopathy in a subject in need of such treatment which comprises the adjunct administration of a therapeutically effective amount of an HMG-CoA reductase inhibitor and an effective amount of Coenzyme Q.sub.10 to counteract said myopathy.
4. A method of claim 3 in which the HMG-CoA reductase inhibitor is selected from the group consisting of: lovastatin, simvastatin, pravastatin and sodium-3,5-dihydroxy-7-[3-(4-fluorophenyl)-1-(methylethyl)-1H-Indole-2yl]- hept-6-enoate.
Description
BACKGROUND OF THE INVENTION
Coenzyme Q.sub.10 (2,3-dimethoxy-5-methyl-6-decaprenyl-1,4-benzoquinone) is a redox component in the respiratory chain and is found in all cells having mitochondria. It is thus an essential co-factor in the generation of metabolic energy and is particularly important in muscle function. For example, Folkers et al., Proc. Natl. Acad. Sci., 82: 901 (1985) have measured the levels of Coenzyme Q.sub.10 (CoQ.sub.10) in endomyocardial biopsy samples taken from patients with varying stages of cardiomyopathy. Folkers et al. states that these data show decreasing tissue levels of CoQ.sub.10 with increasing severity of the symptoms of cardiac disease. Folkers et al., Proc. Natl. Acad. Sci., 82: 4513 (1985) in a double-blind study have reported improved cardiac output for some patients upon receiving an oral administration of CoQ.sub.10.
HMG-CoA reductase inhibitors represent a new class of cholesterol-lowering drugs. Relatively low doses of these drugs effectively reduce plasma cholesterol levels. These drugs are believed to function by inhibiting the chemical transformation HMG-CoA to mevalonate, which is an early and rate-limiting step in the biosynthesis of cholesterol. A branch of the mevalonate cholesterol biosynthetic pathway in mammalian cells leads to the formation of CoQ.sub.10. [reviewed by Brown and Goldstein J. Lipid Res., 21, 505 (1980)]. Furthermore high levels of lovastatin can reduce CoQ.sub.10 in the liver (MK-803 NDA report) and compactin reduces LDL-bound CoQ.sub.10 at doses employed in humans [H. Mabuchi et al, N. E. J. Med., 478 (August 1981].
The Physician’s Desk Reference, 42d Ed., 1366 (1988) states that myalgia has been associated with lovastatin therapy. Tobert, N. E. J. Med., 48 (Jan. 7, 1988) states that in a very small number of patients (0.5 percent) myopathy appeared to be associated with lovastatin therapy. Concomitant therapy with immunosuppressant drugs, including cyclosporine, with gemfibrozil or niacin or a combination, appears to increase the risk of myopathy. (J. A. Tobert, Am. J. Cardiol. 1988, 62: 28J-34J). The myopathy is reversible upon discontinuance of lovastatin therapy.
Although cholesterol-lowering therapy through the use of HMG-CoA reductase inhibitors is generally free of side reactions, it would be of considerable benefit to counteract the myopathy observed in a small percent of patients. Since CoQ.sub.10 is of benefit in congestive heart failure patients the combination with HMG-CoA reductase inhibitors should be of value in such patients who also have the added risk of high cholesterol levels.
DETAILED DESCRIPTION OF THE INVENTION
The present invention relates to a method of counteracting HMG-CoA reductase inhibitor-associated myopathy in a patient receiving HMG-CoA reductase therapy which comprises the adjunct administration of an effective amount of an HMG-CoA reductase inhibitor and an effective amount of Coenzyme Q.sub.10. Included within the scope of the present invention is the treatment of those patients receiving HMG-CoA reductase therapy and who are also taking immunosuppressant drugs, gemfibrozil or niacin.
The HMG-CoA reductase inhibitor employed may be lovastatin, simvastatin, pravastatin, XU-62-320 (Sodium-3,5-dihydroxy-7-[3-(4-fluorophenyl)-1(methylethyl)-1H-Indole-2yl]- hept-6-enoate) or any other member of the class of compounds that inhibit HMG-CoA reductase. The preparation of lovastatin (U.S. Pat. No. 4,231,938), simvastatin (U.S. Pat. No. 4,444,784) and pravastatin (U.S. Pat. No. 4,346,227) have been described in the patent literature. The preparation of XU-62-320 is described in WIPO Pat. No. WO84/02131, published June 7, 1984. These methods of preparation are hereby incorporated by reference.
Coenzyme Q.sub.10 is manufactured by the Kanegafuchi Chemical Industry Co., Ltd. and is widely available.
In its application to the counteraction of myopathy the present invention is accordingly to be understood as providing for the avoidance of myopathy where this may otherwise occur as well as the amelioration of myopathy. The term counteracting is accordingly to be understood as connecting both a precautionary or prophylactic as well as curvative or treatmental function.
In accordance with the method of the present invention, an HMG-CoA reductase inhibitor and CoQ.sub.10 can be administered separately at different times during the course of therapy or concomitantly in divided or single combination forms. Thus treatment with CoQ.sub.10 can commence prior to, subsequent to or concurrent with the commencement of HMG-CoA reductase treatment. The present invention is to be understood as embracing all such regimes of treatment and the term “adjunct administration” is to be interpreted accordingly.
The compounds of the instant invention may be administered orally or parenterally in the form of a capsule, a tablet, an injectable preparation or the like. The general amounts of HMG-CoA reductase inhibitor will be of the same or similar order to that employed in HMG-CoA reductase therapy. In general, satisfactory results are obtained by administration of 0.10 to 80 mg/day of the HMG-CoA reductase inhibitor in a single or divided dose. Doses of CoQ.sub.10 may vary from 25 mg to 1 g day in a single or divided dose. Tablets or capsules may also be administered which contain both compounds in the dosage ranges indicated.
EXAMPLE 1
As a specific embodiment of a composition of this invention, 20 mg of lovastatin and 35 mg of Coenzyme Q.sub.10 are formulated with sufficient finely-divided lactose to provide a total amount of 580 to 590 mg to fill a size 0 hard-gelatin capsule. Optionally added are a excipient such as finely divided cellulose, a disintegrant such as Explotat and a lubricant such as magnesium stearate.
Jayemcee,
Why are you under the impression that medical professionals are unwilling to examine the idea that statins are effective/useful in the treatment of high cholesterol?
I don’t understand your point about the Merck application. Is it not useful to try to make effective drugs safer?
Linda
Wicked Lad,
This recent large study found no decrease in muscle strength with statins. http://www.medscape.com/viewarticle/555363_print
This doesn’t rule out the possibility of an effect in subgroups of the population. Further research is needed to really answer the question.
Jayemcee,
I thought what I had just done WAS to re-examine the meme that lowering cholesterol with statins was beneficial and I found clear evidence that it was, at least when statins are prescribed according to evidence-based guidelines.
You mention one individual who you say has done shoddy science. Whether or not that is true, there is a wealth of other good science done by large numbers of other researchers. And most importantly, there is coherence between different avenues of investigation.
I can’t understand why you mention the Framingham study’s failure to find an association between dietary cholesterol and cholesterol levels. You’re beating a dead horse. We now recognize that eliminating cholesterol from the diet has little effect. However, we know that blood cholesterol is a risk factor for cardiovascular disease and that lowering blood cholesterol reduces risk. A low fat (not just low cholesterol) diet, exercise, weight reduction and statins can all contribute to that goal.
Statins may lower CoQ10 levels, but it is not clear that this has clinical significance for the average patient, and it is not clear that supplementing with CoQ10 has clinical benefits. Research is in progress. We need not just lab studies, but POEMS – patient-oriented evidence that matters.
Merck knew that statins had side effects. Instead of trying to cover up the side effects, they were trying to be proactive about one side effect. Was the patent application approved? It was dated 1990. I don’t see any such product listed on Merck’s website today.
It is silly to say that Merck knew that statins were harmful. They knew that statins were beneficial but had side effects, like any other effective drug.
There’s a great 5-part history of the “cholesterol controversy,” written by Dan Steinberg, one of the major players, in J Lipid Research. All five parts are available for free online:
http://www.jlr.org/cgi/content/full/47/7/1339
(That’s the link to the 5th part, which cites the other 4 at the beginning of its references)
Darkwinter wrote:
I agree. Such people are not skeptics. They are denialists.
There is some preliminary evidence that taking CoQ10 may reduce the risk of muscle side effects from taking a statin. This notion has high plausibility, is relatively benign, and so far the evidence is pointing in that direction. But, we still need more definitive trials.
A number of cardiologists have starting using the CoQ despite current lack of evidence because of, as you said, the plausibility and lack of harm.
The evidence that statins lower risk of stroke and heart attack in many groups of patients, and that LDL-C and CRP serve as markers for this risk reduction is really unassailable at this point.
It is essentially malpractice not to give a statin to a patient with CAD (which costs maybe 4.00/mo at target). Studies have found the earlier the statin is started, the better.
Denialists can schrie about it all they want, but facts is facts.
Side-effects are much less prevalent than at first believed. Mild, subclinical elevations of liver enzymes happen, and very few people develop actual myopathy. Everyone will feel bad at some point with or without a statin…unfortunately, if they just started a statin, they may blame it.
I don’t know enough about cholesterol metabolism to understand how elevated cholesterol is causal in these problems, or what is causing the elevated cholesterol.
Statins do have other effects on physiology. They do raise NO levels, and I do know about NO physiology. Raising NO levels all by itself would be protective for all of the bad things associated with elevated cholesterol, and the NO level is elevated before cholesterol is lowered.
http://circres.ahajournals.org/cgi/content/full/97/12/1232
What bothers me about the TINCS site is that they don’t offer an alternative explanation for the data, all of the data. All they do is throw stones at cholesterol. That does make them denialists, not collaborative scientists.
NO is what regulates cytochrome P450 enzymes by inhibiting them. Inhibition of nitric oxide synthase increases blood cholesterol in rats.
http://www.ncbi.nlm.nih.gov/pubmed/8857518?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum
My suspicion would be via disinhibiting the cytochrome P450 enzymes that make cholesterol downstream of HMG-CoA reductase. If inhibiting nitric oxide synthase increases cholesterol, then HMG-CoA reductase is likely not the “rate limiting enzyme” in cholesterol synthesis.
Without looking up the details of cholesterol synthesis, cholesterol would seem to be far too important for the “rate limiting step” to be 5 steps before the final synthesis without multiple control points in between. Cholesterol is far too important as a substrate for steroid synthesis. I suspect that HMG-CoA reductase is called the “rate limiting step” because HMG-CoA reductase inhibitors (the statins) reduce cholesterol synthesis. But they might do so via NO physiology (which is why increased NO precedes cholesterol reductions).
@ fls:
Cholesterol is essential to all cellular life that respires and to the production of myelin. It has not been shown to be the cause of heart disease. The need for its reduction is unproven. One director of the Framingham study, Dr William B Kannel, gave an interview to the newspaper “The News, Framingham & Natick” and these statements appear on page 36 of the issue dated Friday-October 30th 1970.
Although there is no discernible relationship between reported diet intake and serum cholesterol levels in the Framingham Diet study group, “it is incorrect to interpret this finding to mean that diet has no connection with blood cholesterol” Dr William B Kannel, director of the Framingham heart study has stated.
“It has been repeatedly demonstrated that blood cholesterol levels can be altered by changes in diet; and dietary alteration is still the most acceptable form of medical management for persons with elevated blood lipids” Dr. Kannel said.
Which studies support the change of in vivo cholesterol levels that are attributed to diet? Dr Kannel stated “no discernable relationship” and the study commenced with the original cohort in 1948.
Dr Kannel was being interviewed in 1970, twenty two years after the study was started. His statement about it being incorrect to interpret the finding of no discernable relationship between dietary intake of cholesterol and serum cholesterol levels appears to be based on what he would rather have found rather than what he did find.
You may say (with the kindest possible interpretation) that Dr Kannel was being very cautious about the finding. I would say that after 22 years of intense expert study and analysis, that not believing the finding was a foolhardy act. I belabour this point because it is clear to me… following extensive dialogue with the department of health, that the UK system of cardiovascular healthcare (with regard to statins, heart disease and the cholesterol hypothesis) is still largely based upon Framingham.
It is settled ground that statin producers and prescribers are ‘certain of the rightness of reducing ‘bad cholesterol’ and thus the usefulness of statins. One lunatic has even gone as far as to suggest that statins ought to be put into our drinking water. (reminiscent of the proponents of the polypill for all)
The medical profession have been singularly blind to a raft of debilitating adverse reactions to statins and I personally know of many people who have and are still suffering. Many clinicians appear to think that statinisation has benefits that outweigh risks and medicating people for life is the chosen method to secure the supposed benefits of statin therapy.
Turning the populace into statin junkies, with the corollary of requiring medical attention for life, is a medical strategy for good health that is bereft of merit. The quality of life gained in exchange for a decade and a half of statinisation is vanishingly small. The disruption of vital processes (that have their genesis in the MMP) is far more serious than the relative risk of dying from a cardiac event that is supposedly caused by a surfeit of LDL cholesterol.
The so-called ‘opinion forming clinicians’ who apparently speak for the medical profession, despite there having been no election or such a position, are open about the myriad consultancies and research grants which tie them to pharmaceutical manufacturers. The clinical trials that are funded by pharmaceutical companies where the research workers are pressured to find desirable results.
The adverse reactions that always fall below the clinically significant level. The underreporting of adverse reactions. It was a recent NEJM study that indicated that a large proportion of their respondents were connected to pharmaceutical companies. In the UK the average GP earns an extra £121k on top of the normal salary. The payment is a bonus for meeting targets set by the government. The cardiac domain accounts for around £62k of the additional payments… all of this is stated in the government’s own figures.
The national policy on prescribing statins is decided by several bodies, among which there are drug company funded charities and the ludicrous position they find themselves in… of deciding the national policy for statinisation, when they are funded by statin producers to promulgate the viewpoint that statins are the saviour of everyone and the cholesterol/heart disease hypothesis is a real danger that will kill us all.
It has not escaped my notice that the use of statins appears to be ineffective in reducing cardiac events. How does one explain the statinised post CABG patients who go on to require several more CABG surgical episodes, for example?
The point of my inclusion of the Merck patent application… the drugs were marketed without the addition of CoQ10. Merck believed its addition would have counteracted the propensity of statins (if the patent application was an honest appraisal of the harm that could be caused by statins) to cause skeletal muscle myopathy.
What possible reason could there be for Merck not to have added any substance that would have lessened the impact of a very serious adverse reaction such as skeletal muscle myopathy? At the very least there would appear to have been some element of duplicity in marketing a drug that they knew was going to hurt people.
It only seems prudent, as a Statin side effect sufferer, for me to add a brief but undeniable counterpoint to the proposition that Statins are primarily beneficial, cancer preventing, minimally health threatening medications. At 60 I was healthy, robust and my appearance belied my age. After a small increase in my cholesterol levels (with favorable “good” cholesterol readings) I was placed on a Statin drug which was, in time, increased in dosage to 40 Mg. I won’t belabor my current, statin-related symptoms, but suffice to say I am a shell of my former self. With the aid of a host of OTC supplements I am trying to recover some semblance of my former health AND during my time on Statins I DEVELOPED heart muscle irregularities. One day the truth will out, and Statins will be labeled for what they truly are: an effective anti-inflammatory but otherwise, a HEME, Dolichol, and CoQ10 reducing poison to human physiology.
There is research showing associations between elevated cholesterol and heart disease.
There is research showing that statins lower cholesterol.
There is research showing that statins decrease the risk of heart disease.
So you might conclude that elevated cholesterol causes heart disease and that statins prevent heart disease by lowering cholesterol.
Or you might not.
Statins have an anti-inflammatory effect which might decrease the risk of heart disease.
The fact that statins lower cholesterol might be incidental.
The fact that elevated cholesterol and heart disease are associated says nothing about causation. Elevated cholesterol might be an effect, rather than cause, or it might be an irrelevant third variable.
Where is the research showing elevated cholesterol as a cause of heart disease?
Heart disease, and artery disease in general, might be an inflammatory process. The plaques that lead to clogged arteries might be the body’s attempt to patch up damaged blood vessels. If that is true — at least in some cases — then you would not prevent artery disease by keeping cholesterol levels down.
The idea that lowering cholesterol prevents heart disease might be a mistake arising from the fact that statins lower cholesterol AND ALSO decrease inflammation.
An additional source of confusion is the fact that some individuals may have a genetic defect resulting in extremely high cholesterol levels and early death from artery disease. In those individuals — a small percentage of all adults — cholesterol-lowering makes sense.
The cholesterol story might not be altogether true. And therefore, the effort to keep cholesterol levels very low might be ineffective and harmful.
Jayemcee,
I don’t think anyone is saying cholesterol causes heart disease. Cholesterol is one risk factor among many in a disease with multifactorial causes.
I don’t understand why you are quoting a 1970 statement about diet that is not pertinent to this discussion. I don’t think anything is “largely based on Framingham.” Scientific consensus is based on the totality of the evidence, never on one study. There are plenty of other good studies.
You give us no data to support your claims that statins cause poorer quality of life or disrupt vital processes. The evidence shows otherwise.
You mention debilitating reactions to statins but recent well-designed studies have found reactions to be few and mild. Are you citing testimonials, or do you have data from double-blind studies?
You persist in saying, “the use of statins appears to be ineffective in reducing cardiac events.” even after you have been shown incontrovertible evidence that they are effective.
You ask, “How does one explain the statinised post CABG patients who go on to require several more CABG surgical episodes, for example?” The same way one explains the patients who die from pneumonia despite antibiotics. The evidence shows that treatment reduces the rate of cardiovascular events, repeat surgeries, and death. It doesn’t guarantee a perfect outcome for every patient.
Your comments about financial influences fall under the “cui bono” fallacy unless you can support them with convincing evidence. In the US, there is no national policy on statins, just clinical guidelines developed by concerned independent physicians who have carefully reviewed the evidence.
As to why Merck didn’t add CoQ10, I can think of 3 probable reasons right off the bat: not every patient needed it, it was expensive, and until there was better research they couldn’t know that adding it would do more good than harm.
I’ll point out for a second time that it is disingenuous to say that Merck was marketing a drug that it knew was going to hurt people; it was marketing a drug that it knew was going to help a great many people but had side effects like any other effective drug. The benefits far outweigh the harms.
Your bias is showing. You are giving us unsupported opinions and innuendo. This is a science-based medicine blog: show us the scientific evidence.
Well put Dr Hall, and might I add that you have showed commendable restraint. I think that the controversy about statins is an excellent example of the difficulty in doing very large-scale population-based studies, and the need to be cautious about interpreting any individual study in isolation.
Jayemcee has made a number of gross misrepresentations and assertions without adducing any evidence to support them, and in particular I fail to see how paying UK doctors to reach their prevention targets (which are set by the Department of Health presumably in accord with Government policy) is evidence of anything apart from conscientious doctoring..
Actually, there is quite solid evidence that cholesterol (really LDL cholesterol) is involved in—not merely associated with, in the epidemiological sense—the formation of atherosclerotic plaques. “Cause and effect” evidence did not exist, however, prior to the publication of the NIH Coronary Primary Prevention Trial in 1984, in which the intervention was cholestyramine. Thus any statements about cholesterol and heart disease made in 1970 were not so unreasonable for their time, although the circumstantial evidence was building.
It was the advent of statins that clinched it, as described by Steinberg in the history that I previously cited:
because the statins decreased blood cholesterol so much more than any of the existing diet or drug treatments, it suddenly became much easier to demonstrate the decrease in coronary heart disease events and to do so in a statistically significant, unarguable way. For example, in the groundbreaking 1984 NIH Coronary Primary Prevention Trial, using the drug cholestyramine (39, 40), total blood cholesterol in the treated group decreased by only 10% and LDL cholesterol by 20%. This was enough to reduce the heart attack rate, but only by 20%. The result barely reached statistical significance. By contrast, in one of the first large-scale statin trials, total cholesterol was reduced by 25%, LDL cholesterol by 35%, and coronary heart disease deaths by 42%. This reduction was highly significant (P < 0.00001). This trial, the so-called 4S study (for Scandinavian Simvastatin Survival Study) in Scandinavia (41), was done using simvastatin, the second Merck statin, which was discovered while the company was assessing the safety of lovastatin. The 4S study showed, for the first time in any cholesterol-lowering trial, a significant decrease in all-cause mortality. A new era in the treatment of hypercholesterolemia and coronary heart disease had arrived.
A recent meta-analysis of 14 statin trials with an astonishing total of 90,056 individuals randomized (using lovastatin, simvastatin, pravastatin, fluvastatin, or atorvastatin) showed that the decrease in coronary events was best predicted by the absolute decrease in LDL levels. The incidence of major vascular events was reduced by 20% for each 1 mm/l (40 mg/dl) decrease in LDL cholesterol (42). Thus, an individual starting with an LDL of 280 mg/dl whose level decreased to 200 mg/dl on therapy (a 29% decrease) would be predicted to have a 40% decrease in risk over a 5 year period.
Dr Hall, I’ll start with your opening post. Your own words will appear between square brackets, thus: [quote] [unquote]
The tenor of your writing is needlessly and gratuitously offensive, in my considered opinion, especially when you deign to mock clinicians and scientists, from your own lofty vantage point, despite them being honourable clinicians and scientists who have taken great pains to make clear their position vis a vis the cholesterol/heart disease hypothesis.
[quote]There is an organization that calls itself The International Network of Cholesterol Skeptics (THINCS). Its members “thinc” they are smarter than the average doctor. They “thinc” that cholesterol has nothing to do with cardiovascular disease and that we have been deluded into waging a “cholesterol campaign” for which the scientific evidence is non-existent.[unquote]
I would doubt that any of the THINCS membership believe that they are smarter than the average doctor. You seem to “thinc” that they do believe that. Well, as this is supposed to be an evidence-based scientific website, please produce the evidence for this ersatz ‘fact’, that you have used to dress-up your unseemly diatribe. I would guess by your comment under the general head “cholesterol campaign” that you have avoided apprising yourself of anything that would impinge on your own worldview. more of this anon…
You appear, Dr Hall, to be in thrall to your own press. Nevertheless, you are one and the same Dr Hall that writes for eSkeptic and you appear not to want other people to exhibit any skepticism. Perhaps you will be good enough to provide the evidence for viewpoint that only you can be right in demanding proof of cause and effect and all other clinicians, whom you happen to disagree with, have no business telling you that they disagree with your well-researched viewpoint. It appears that you believe that everyone you feel is actually wrong (or leastways ought to be wrong according to your own dim lights) is in some way holding an inferior viewpoint to your finely honed mind.
I nearly forgot the evidence for my own assertion… try reading any of your own numerous diatribes (which I have recently had the misfortune to read) that pollute large amounts of the internet. You are a prolific writer and I see little evidence of any willingness, on your part, to see a point of view that you happen to disagree with. Your articles for eSkeptic and Quackwatch adequately demonstrate your hectoring tone, your belligerence and your intransigent stance, as you declaim to all and sundry from your pulpit. Albeit unintentionally, your writing reveals much about you, Dr Hall.
[quote]I find even the wording of this statement problematical: one does not usually hear scientists “opposing” matters of fact or non-fact. They go on to say, “The aim with this website is to inform our colleagues and the public that this idea is not supported by scientific evidence; in fact, for many years a huge number of scientific studies have directly contradicted it.”[unquote]
A matter of opinion, even your own opinion, Dr Hall, does not become a fact by dint of your wishes; no matter how many times you choose to repeat it.
[quote]They tell us about those contradicting studies; but they don’t tell us about the flaws in those studies, they misrepresent some of the results, and they don’t tell us about the many good studies that support the cholesterol/heart link.[unquote]
The studies used to support the notion that statins are good have always told the truth, have they? They have never mis-respresented the facts? They have never deliberately obfuscated the truth? They have never consigned viatl adverse reaction data to the realm of the clinically insignificacant? Atorvastatin/Torcetrapib cancelled study? Vytorin and the withholding ofinformation? I suppose that you wont be able to recall either of those studies. Given the relationship between the pharmaceutical industry and clinicians in the USA, as was recently revealed by the New England Journal of Medicine, I presume that there can be no possibility that any pro-statin clinical trials are using false information to promulgate a viewpoint that supports the meme?
[quote]As far as I can see, these folks have cherry-picked the literature to support an agenda. They seem to have a vendetta against statin drugs in particular.[unquote]
Clearly, you cannot see very far. Once again it is necessary to point out to you, Dr Hall, that the gratuitous addition of the emotionally loaded term, “vendetta” is evidence for your closed mind and your unwillingness to brook any opinion that is not your own. When I want you tell me what my opinion ought to be, you can be certain that you will be the first to know.
[quote]The website solicits complaints of adverse effects from statin drugs.[quote]
It is a great sadness that you appear unable to pass on information without putting your own little spin on it. (there is no case for allowing you one iota of journalistic licence, on a website that purports to promulgate facts) It is true that the THINCS website does ask people if they have complaints about statin side effects. Naturally enough, if one is concerned about the possibility of iatrogenic harm, one needs to assess the extent of it and the possibility of further harm. I would have expected that as the minimum response from any clinician worth the epithet.
Why did you hide the fact that the request was made on behalf of another agency that is interested in the side effects of statins?
from the THINCS website… [quote] Have you had side effects from cholesterol lowering (statin) treatment, in particular from the nervous system? Researchers from University of California, San Diego are studying side effects from statin treatment and are also interested in hearing from you [unquote]
I would have thought that an eminent clinician, such as yourself, who was keen to see the promotion of evidence-based medicine, would have known of the work being carried out by Dr Beatrice Golomb. She is a very well-published and prolific research scientist with a formidable CV. Indeed, she published her findings at an interim point in her study and I would find it hard to believe that you are unaware of the publication, given your expertise with, and your interest in, the promotion of statins.
You then move on to trashing the work of Dr Ravnskov. You referred to his book, entitled ‘The Cholesterol Myths’ in the same sentence as you mentioned that the book had been “That book has been severely criticized, for instance in The Skeptic’s Dictionary , where Bob Carroll points out some of the distortions and deceptive techniques found in the cholesterol skeptics’ arguments.”
I attempted to find the accreditation for the Skeptic’s Dictionary, from among the various medical databases. I was surprised to learn that the Skeptic’s Dictionary has no locus as a repository for medical knowledge. I had found the Bob Carroll to whom youy had referred. It appears that he is not a medical doctor and has no medical training of any description. As far as I can see he was not even a member of the domestic staff in a hospital. His credentials are that he was a teacher of philosophy and he has written a textbook entitled ‘Becoming a Critical Thinker’. He states that he has taught classes in Logic & Critical Reasoning, Law, Justice, & Punishment, Critical Thinking About the Paranormal, Introduction to Philosophy, History of Modern Philosophy, and World Religions.
Help me out here, Dr Hall. You claim to stand for science and evidence, and yet you refer to the criticism of a book (written by an eminent clinician) by a person bereft of medical training, who runs a sensationalist website that is redolent of the nonsense to be found in the National Enquirer. You are not seriously suggesting that the criticism of Dr Ravnskov’s book, by a person who could hardly have managed to be less qualified to analyse the content of that book, even if he arranged it personally, is evidence for the rejection of Dr Ravnskov’s work?
You stated…
[quote]But there is plenty of evidence from multiple avenues of research to show that high cholesterol is a risk factor for heart disease and that lowering it reduces risk. A Lancet article from December 2007 reviewed trials involving nearly a million people and found that “Total cholesterol was positively associated with IHD [ischemic heart disease] mortality in both middle and old age and at all blood pressure levels.”
Another Lancet meta-analysis of over 90.000 patients concluded “Statin therapy can safely reduce the 5-year incidence of major coronary events, coronary revascularisation, and stroke by about one fifth per mmol/L reduction in LDL cholesterol, largely irrespective of the initial lipid profile or other presenting characteristics. The absolute benefit relates chiefly to an individual’s absolute risk of such events and to the absolute reduction in LDL cholesterol achieved. These findings reinforce the need to consider prolonged statin treatment with substantial LDL cholesterol reductions in all patients at high risk of any type of major vascular event.[unquote]
I will refer you to issue 48 of Therapeutics Initiative, which was published for April to June 2003 (a Canadian Publication from the University of British Columbia) and it is a publication that is devoted to evidence-based drug therapy.
The question that was asked was ‘Do Statins Have A Role In Primary prevention.’ The meta-analysis encompassed PROSPER, ALLHAT-LLT, ASCOT-LLA, AFCAPS & WOSCOP. The conclusions were…
“If cardiovascular serious adverse events are viewed in isolation, 71 primary prevention patients with cardiovascular risk factors have to be treated with a statin for 3 to 5 years to prevent one myocardial infarction or stroke”.
“This cardiovascular benefit is not reflected in 2 measures of overall health impact, total mortality and total serious adverse events. Therefore, statins have not been shown to provide an overall health benefit in primary prevention trials”.
The URL follows… http://www.ti.ubc.ca/en/node/52
Of course, you may say that this was only one study and I will say that there are many studies that support the proposition that statins are only vaguely useful.
The explanation you give about NNT and the weighing of risk versus benefit are the supposed ideal. Once again the NEJM would suggest that in the USA, the truth may be somewhat removed from your rose-coloured view.
[quote]The cholesterol skeptics doubt that all-cause mortality can be reduced by statins. It clearly can for secondary prevention. In primary prevention, it at least reduces the rate of cardiovascular events. It’s not entirely clear whether the risk reduction with statins is due solely to the lowered cholesterol; statins may have other beneficial effects. But at least it appears that the degree of risk reduction can be measured by the degree of cholesterol lowering.[unquote]
It does not reduce the rate of cardiovascular events in primary prevention, according to the study to which I have referred you… immediately preceding this section. Having witnessed your predilection for managing the truth, within your writing, I would much rather accept the work of the University of British Columbia, in preference to your own viewpoint. unless you are prepared to be brutally honest about the current situation apropos statinisation and cholesterol and heart disease, then we cannot proceed any further with this conversation. I find it unacceptable to be lied to to for any reason. That any clinician would do so in order to further their own personal agenda, is truly shocking to me.
[quote]My impression is that the general trend of recent statin studies in the better journals has been to show even more efficacy and fewer side effects than previously thought[unquote]
Thus spake the avowed devotee of science and evidence-based medicine. ??? Science is not about your impressions and current trends and fashions and it is thoroughly dishonest of you to include a reference to your impressions in a supposedly scientific treatise (it was not) in an effort to give the impression that you have thoroughly researched your viewpoint. Our discussion ends here…
Harriet, you are a charlatan and your ‘science’ is nothing but a worthless simulacrum of scientific endeavour!
I’m flattered that my critic has run out of good arguments and has had to resort to ad hominem attacks and name-calling. To my mind, that is a sign that I have won the debate.
Just for the record, I have no personal agenda. I don’t take or prescribe statins, I don’t have any ties to Big Pharma, and if the evidence showed statins did more harm than good, caused cancer, or failed to improve cardiovascular risk, I would gladly follow the evidence.
It must be the TV writers’ strike: jayemcee is making a bid to replace a comedy writer. I laughed out loud at numerous places in his diatribe. Funny guy.
All the citations below exhibit:
* Statins decrease CoQ10 levels in humans
* Decreased levels of CoQ10 cause various side effects
* Statins can cause additional ADR’s not previously disclosed
The FDA does not acknowledge that statins deplete CoQ10 (Ubiquinone), but Canada and the UK do. They’ve undated their statins to reflect this documented fact.
Why are we in the USA kept in the dark? Why don’t our statins contain this warning?
My husband experienced all of the following from statins and even after stopping statins over 3 years ago, these symptoms persist: sleep disturbances, memory loss, sexual dysfunction, depression.
Our doctors completely denied any connection while the data has been there all along. At least give us the facts so we can make an informed decisions.
FDA’s MedWatch is a joke. Are our doctors reporting adverse effects to MedWatch each time they switch their patient from one statin to another? Or are they too busy writing a prescription for another statin? That’s the typical scenario… try all the statins, then the non-statins and last resort try the good old fibrates.
The main problem right now other than statins are over-prescribed is that doctors do not have a clue once things go terribly wrong. They want to try Aricept or Prednisone or anything else they can think of… stopping statins does not always resolve side effects and I’m living through that scenario right now. One day my husband is going to wake up and say, “Who the hell are you?” And that, my friends, was caused by Lipitor.
Frankie
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
“Statins sold in Canada are required to carry on their labels a precautionary warning expressly stating that such CoQ10 depletion can lead to impaired cardiac functioning in patients with congestive heart failure. The US government requires no such warning, despite an emerging generation of “super-statins” (rosuvastatin, pitavastatin) that may further increase the risk and rate of CoQ10 depletion in patients taking the drugs.”
http://lefcms.lef.org/magazine/mag2004/aug2004_report_coq10_02.htm
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
MHRA – Drug Safety Update from the UK – February 2008
Statins: class effects identified
Keywords: atorvastatin, fluvastatin, lovastatin, pravastatin, rosuvastatin, simvastatin, statins, sleep disturbance, insomnia, nightmares, memory loss, sexual dysfunction, depression, interstitial lung disease, class effects
“Several additional side-effects—sleep disturbances, memory loss, sexual dysfunction, depression, and interstitial lung disease—have been recognised with statins. The product information for the class as a whole is being updated.”
New advice for healthcare professionals
• Patients should be made aware that treatment with any statin may sometimes be associated with depression, sleep disturbances, memory loss, and sexual dysfunction
• Statins may very rarely be associated with interstitial lung disease. Patients should seek help from their doctor if they develop presenting features of interstitial lung disease such as dyspnoea, non-productive cough, and deterioration in general health (eg, fatigue, weight loss, and fever)
Reporting of adverse events
Healthcare professionals and patients are encouraged to report any suspected adverse drug reactions with statin treatment to us via the Yellow Card scheme.
See http://www.mhra.gov.uk/mhra/drugsafetyupdate
See http://www.yellowcard.gov.uk/
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
“Cognitive impairment associated with atorvastatin and simvastatin.”
PMID: 14695047
http://www.ncbi.nlm.nih.gov/pubmed/14695047
“Clinicians should be aware of cognitive impairment and dementia as potential adverse effects associated with statin therapy.”
“Evidence of plasma CoQ10-lowering effect by HMG-CoA reductase inhibitors: a double-blind, placebo-controlled study.”
PMID: 8463436
http://www.ncbi.nlm.nih.gov/pubmed/8463436
“CoQ10 is essential for the production of energy and also has antioxidative properties. A diminution of CoQ10 availability may be the cause of membrane alteration with consequent cellular damage.”
“Lovastatin decreases coenzyme Q levels in humans.”
PMID: 2247468
http://www.ncbi.nlm.nih.gov/pubmed/2247468
“Oral administration of CoQ10 increased blood levels of CoQ10 and was generally accompanied by an improvement in cardiac function. Although a successful drug, lovastatin does have side effects, particularly including liver dysfunction, which presumably can be caused by the lovastatin-induced deficiency of CoQ10.”
“Metabolism and function of coenzyme Q.”
PMID: 14757233
http://www.ncbi.nlm.nih.gov/pubmed/14757233
“Coenzyme Q (CoQ) is present in all cells and membranes and in addition to be a member of the mitochondrial respiratory chain it has also several other functions of great importance for the cellular metabolism.”
“Atorvastatin decreases the coenzyme Q10 level in the blood of patients at risk for cardiovascular disease and stroke.”
PMID: 15210526
http://www.ncbi.nlm.nih.gov/pubmed/15210526
“CONCLUSIONS: Even brief exposure to atorvastatin causes a marked decrease in blood CoQ(10) concentration. Widespread inhibition of CoQ(10) synthesis could explain the most commonly reported adverse effects of statins, especially exercise intolerance, myalgia, and myoglobinuria.”
“Lipid-lowering drugs and mitochondrial function: effects of HMG-CoA reductase inhibitors on serum ubiquinone and blood lactate/pyruvate ratio.”
PMID: 8877024
http://www.ncbi.nlm.nih.gov/pubmed/8877024
“Statins inhibit synthesis of mevalonate, a precursor of ubiquinone that is a central compound of the mitochondrial respiratory chain. The main adverse effect of statins is a toxic myopathy possibly related to mitochondrial dysfunction.”
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
Dear precious Harriet,
You’ve won absolutely nothing and yet still you preen and flatter yourself. What colossal arrogance!
All you have managed to do is to underscore the maxim that there is no profit in trying to educate the wilfully ignorant.
Res ipsa loquitur
bye
I love it when people like jayemcee declare victory and then exit with a flourish of ad hominems. It amuses me to no end.
Of course, he’ll be back. They always come back.
I want to correct a glaring factual error in jayemecee’s email (he did squeeze in a couple factual claims amid the personal attacks).
He wrote: “It does not reduce the rate of cardiovascular events in primary prevention,”
This is clearly wrong, even from reading his own quoted articles. In the meta-analysis it did reduce cardiovascular events, just not total major adverse events (which includes things other than cardiovascular).
I also disagree with the articles conclusions from their own data. Treating 71 people for 3-5 years to prevent one MI or stroke sounds good to me. It’s probably even cost effective if you consider the total health care cost of a stroke or heart attack. These numbers are much better than the use of ASA or Plavix for stroke prevention – which is not controversial at all.
Regarding Frankie’s comments:
You should be wary of subjective assessments about what is “typical” for doctors to do. Unless you can reference data measuring practices.
I and other neurologists in the US already prescribe CoQ10 for neurological side effects of statins. Taking patients off statins is not a last resort – I often see it as a first resort when symptoms appear. Also I doubt that it is common practice to use dietary methods of cholesterol management only as a last resort, that is certainly NOT the standard of care.
I hope all the scientific experts here will tolerate a comment by an ordinary person.
First for Wicked Lad: You best educate yourself on statin adverse effects. Losing muscle strength is a big red flag.
To Harriet: The most telling comment in all your arguments is that you “don’t take statins.” Perhaps, in the name of science, you should give them a go.
Unfortunately, I DID take a statin. To make a very long story short, I will never have a life again. I have been told that damage to my muscles and nerves (yes statins can cause nerve damage) is permanent. I can only walk a few feet with the help of a cane, any farther I must use a wheelchair. I was in my early 40′s when my life was destroyed by statin therapy for a slightly elevated cholesterol level.
Lest you think I am one of the very “rare” examples of those that experience serious life changing problems after taking statins, I can assure you I have lots of unfortunate company. I have encountered perfect strangers, using canes and wheelchairs, that had no problems what so ever, prior to taking statins.
My own husband had major trouble with Lipitor, his personality changed drastically, he lost muscle mass, his memory was awful, and he could barely pick up a sack of groceries. Before starting Lipitor, he was a strong, athletic, healthy man in his 40′s. He has been extremely lucky to recover most of his abilities, although he will never be quite the same.
I have talked to many, many folks (in person) that have had statin problems. At least 80% of them have had problems severe enough to throw their statin in the garbage.
While I have done plenty of research, trying to find a way to get my life back, I’m not going to belabor repetitive scientific pro/con arguments.
I have a perfectly clear view from my wheelchair, every day of what statins can do. That’s all I need.
Interesting article, interesting debate in the comments. Thank you, Dr. Hall and Dr. Novella for the information you’ve provided in the comments regarding statins’ effects on muscles.
What a great blog you people have put together. It’s an instant success in my estimation.
Steven Novella writes:
“I also disagree with the articles conclusions from their own data. Treating 71 people for 3-5 years to prevent one MI or stroke sounds good to me. It’s probably even cost effective if you consider the total health care cost of a stroke or heart attack. These numbers are much better than the use of ASA or Plavix for stroke prevention – which is not controversial at all. ”
I understand there is some controversy about Plavix now. Anyway, whether it is good to treat 71 people for 5 years to prevent one nonfatal cardiac event depends less upon the financial cost than upon what the number needed to harm is. If you give 71 people statins for 5 years, will there be at least one extra case of clinically significant liver, muscle, or kidney damage, brain dysfunction, or cancer? (Yes, statin promoters would like us to believe statins prevent cancer, based on the same sort of evidence that said HRT prevented cancer. However, since statins cause cancer in animal studies, the elevated cancer rates in some of the RCTs are cause for concern.) It appears that the answer is yes, meaning that people given statins as primary prevention will experience just as many illnesses, but be poorer.
My father’s MD socked him on not only statins but one or two of the in-patent blood pressure drugs a few years ago (and talked about putting him on even more toxic drugs) as primary prevention, even though his cholesterol levels were already unusually low and his BP normal. He’s an obedient sort of patient who will not seek a second opinion, and suffered some months of muscle pain in silence before being diagnosed with rhabdomyolysis, whereupon he was graciously allowed to quit the statin. It seems like some of these promoters of “aggressive treatment” think an iatrogenic illness is more acceptable than a natural one, because they’ll do anything to prevent the latter, while refraining from doing something to prevent the former is not in their repertoire. “Primum non nocere” doesn’t seem to fit into American medicine anymore.
Of course the vast majority of patients are neither visibly harmed nor helped by the statin, but all of them can be persuaded that the MD may be “saving their lives” with every prescription written — and the MD can persuade himself of the same thing, which makes him feel good in a way that extends far beyond his bank account. If the MD does nothing, he cannot give himself credit for his patients’ health. There is therefore a psychological motive to overestimate the value of prophylactic treatment of the healthy.
Wicked Lad:
Regarding muscle issues with statins, this study should be of interest to you.
http://www.jci.org/117/12/3940?content_type=abstract
apteryx:
All I can say to your above post is: AMEN!
Not only did my insurance company pay for the initial statin costs, they also ended up with major bills to treat the side effects and all the tests I had to have done. I don’t have an exact total but I can say without hesitation it is in the tens of thousands of dollars.
Not to mention 2 medications I will need to be on for the long term, perhaps for life, for permanent side effects.
How cost effective is that?
To the poster who mentioned meta analysis of statin use, Please remember the meta analysis of HRT use in women and positive correlation to breast cancer and coronary heart disease reduction. Once a prospective study was completed, those meta analyses were proven to be completely incorrect. Meta analyses require further study….
Prior to lowering LDL to such levels, a few things to consider: Barres and Smith’s in vitro findings of importance of brain cholesterol (recalling that fat soluble statins cross the BBB) synopsis: http://www.sciencemag.org
Neurons need cholesterol secreted by glial cells to form and maintain functional synapses. In addition to synaptogenesis, cholesterol is probably responsible for production and transport of vesicles necessary for neurotransmission. If one accepts the concept of neuronal plasticity in the adult brain, then deliberately
suppressing cholesterol metabolism in the brain seems more than questionable.
Also consider Dr. Xuemei Huang’s findings of positive correlation btn low LDL and Parkinson’s (http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1906875), and her study proposal to determine if statins are linked to Parkinson’s.
and Ralph Edwards’ reporting excessive # of cases of ALS like syndrome reported by pts on statins from WHO drug safety data:
http://www.ncbi.nlm.nih.gov
“…The aim of this paper is to present the upper motor neurone lesion cases, with other evidence, as a signal of a relationship between statins and an amyotrophic lateral sclerosis (ALS)-like syndrome. The paper also presents some arguments for considering that a spectrum of severe neuromuscular damage may be associated with statin use, albeit rarely. ”
and.
In addition, report by Meske, etal.
tinyurl.com
” Experimental data suggest that manipulation of cholesterol levels may lead to changes in tau phosphorylation. These changes vary depending on how cholesterol metabolism is manipulated. ”
Increases in tau phosphorylation via statins is not considered an especially favorable response….granted, study involved rat neuronal cultures….
V. Meske, F. Albert, D. Richter, J. Schwarze, T. G. Ohm (2003)
Blockade of HMG-CoA reductase activity causes changes in microtubule-stabilizing protein tau via suppression of geranylgeranylpyrophosphate formation: implications for Alzheimer’s disease
Histopathologically, Alzheimer’s disease is characterized by plaques and tangles that develop progressively over time. Experimental data described a statin-induced decrease in β-amyloid production, a major constituent of the plaques. Others reported data on statin-mediated changes in neuronal survival and cytoskeleton, including the microtubule-associated protein tau, a major constituent of the tangles. However, these latter reports remain contradictory. To clarify and extend our knowledge on the effect of statin on the cytoskeleton, we challenged rat primary neuron cultures by lovastatin and determined the metabolite that is critical for structural integrity and survival of neurons. During the blockade of 3-hydroxy-3-methylglutaryl-coenzyme A reductase, the neuritic network was affected and eventually was completely destroyed. This process was not part of the execution phase of apoptosis and was marked by alterations in the microfilament and microtubule system. The distribution and phosphorylation of protein tau changed. Immunoblot analysis and indirect immunofluorescence revealed a transient increase in tau phosphorylation, which ceased during the execution of apoptosis. All of these effects could be linked to the lack of the geranylgeranylpyrophosphate intermediate. Inhibition of the geranylgeranylation of Rho family GTPases (geranylgeranyl-transferase I) evoked similar changes in neurons. These data and our findings that statin treatment reduced the membrane-bound fraction of RhoA-GTPase in neurons suggest that reduced levels of functional small G proteins are responsible for the observed effects. Our data demonstrate that lovastatin concentrations able to suppress not only cholesterol but also geranylgeranylpyrophosphate formation may evoke phosphorylation of tau reminiscent of preclinical early stages of Alzheimer’s disease and, when prolonged, apoptosis.
Data suggest statins are protective for middle aged men who have suffered a cardiac event; beyond that, there are no good data for use in other populations –ie men who have not suffered a cardiac event, women, men >age 65. Statins are powerful anti-inflammatory agents and increase perfusion everywhere initially. Over time, all the “pleiotropic effects” are of major concern–aptly summarized in the following:
Drugs Today 2005, 41(4): 267
Statin-associated neuromyotoxicity
Baker, S.K., Tarnopolsky, M.A.
The sequelae of cardiovascular disease contribute significantly to morbidity and mortality in developed nations. As a class, the statins have been shown to measurably reduce the burden of atherosclerotic illness. However, muscle- and, more recently, nerve-related toxicity have emerged as potential complications leading to treatment withdrawal. Generally, the myopathic signs and symptoms of tenderness, myalgias, cramping and elevated serum creatine kinase (CK) activity are fully reversible after drug discontinuation. Growing evidence suggests that latent or previously minimal symptomatic muscle disease may predispose to the development of myopathy. Less information is available regarding the natural history of the sensorimotor neuropathy, but it appears to be less reversible if large fiber function is clinically manifest. Pathophysiologic clues regarding the potential causes of statin myopathy with or without neuropathy are discussed with particular attention paid to the implications of disrupted mevalonate metabolism. For example, secondary defects in isoprenoid biosynthesis are expected to impair the production of a variety of intermediaries such as dolichols, which are crucial for N-linked glycosylation; geranylgeranyl pyrophosphate, which is necessary for coenzyme Q10 and G-protein synthesis; farnesyl-pyrophosphate, which facilitates the endoproteolytic cleavage and maturation of prelamin A and modifies B-type lamins and G-proteins; and isopentenylpyrophosphate, which is involved in a nucleoside modification of selenocysteinyl-tRNA and thus indirectly related to the synthesis of all selenoproteins (estimated at 35). The nature of statin neuromyotoxicity remains unresolved; however, investigating the cellular corollaries of deranged isoprenoid metabolism may uncover clues that lead to a more complete understanding of the elusive pathophysiology.
Just a review of selenoproteins function should give one pause…..not to mention review of N-linked glycosylation and isoprenoid metabolism……..and coenzyme Q10 function.
I have never taken statins or any cholesterol or blood pressure drugs (I try to avoid MDs as much as possible) but I have close relatives who have been on them for decades. As skeptical as I am, I trusted their MD’s decisions on this.
NOT ANY MORE. Since reading this blog my skepticism has increased, from moderately high to very high! I am going to warn my trusting relatives about statins and cholesterol-lowering drugs in general.
Oh by the way, these poor trusting patients have psychiatric problems, including depression and memory loss. No problem — their MDs just prescribed more drugs!
Apteryx wrote: “My father’s MD socked him on not only statins but one or two of the in-patent blood pressure drugs a few years ago (and talked about putting him on even more toxic drugs) as primary prevention, even though his cholesterol levels were already unusually low and his BP normal.”
This story is so unusual that either this is an anomalous incompetent doctor or the story is inaccurate. Either way it is irrelevant because is has nothing to do with the evidence -based standard of care or with common practice. It is an absurd straw man.
The discussion of all the benefits, risks, and statistics involving statin use is very constructive. It seems most commenters agree with the actual evidence that statins work as they are claimed to, but the real question is what are the benefit compared to the risks and in which populations? Can we maximize the benefit to risk ratio by optimizing the target population – primary vs secondary prevention, by cholesterol profile, by other vascular risk factors, by response to prior treatment with diet and exercise, etc. ?
I think the primary point of Harriet’s article is that these are all good questions and, guess what, doctors and medical scientists are actively and sincerely asking these questions. It is childishly naive to assume that they are not, that the medical profession is just simplistically and stupidly prescribing drugs when any lay person with a modicum of common sense can discuss the pros and cons at length. It’s just anti-establishment conspiracy mongering, and it’s insulting to one’s intelligence. It also bears no resemblance to medicine as it is actually practiced – its a paranoid straw man version of medicine.
Regarding cost effectiveness, the average cost of the first 90 of stroke management is $15,000 (http://www.theuniversityhospital.com/stroke/stats.htm) this does not include long term treatment and lost productivity. But the total cost of treatment vs non treatment is complex and more complete data is necessary to make any final conclusions, that’s why I said “may” be cost effective.
I am an 86 year old, badly damaged by statin use. 4 years of simvastatin left me very weak and with considerable muscle loss. My doctor, while sympathetic, put it all down to age and previous polio, and really had no alternative but to leave me to deteriorate. I scoured the internet to no avail, but eventually found clues to the causes of my problems from a small polio network which had done much research of the literature.
As previous contributors have mentioned, Merck knew very well that the reduction of coenzyme Q10 was the cause of statin side effects, but kept this knowledge away from general knowledge, so I was given a drug, without any warning that it could deplete of one of the most necessary factors in life, without which the Krebs cycle cannot be completed, and the production of Adenosine triphosphate (ATP), the whole body’s power supply, is damaged in the mitochondria of whatever part of the anatomy happens to fall foul of this shortfall. But Coenzyme Q10 appears to be a dirty word in medical circles, a leading medical journal’s web page once carried a remark from a doctor ” What does it matter if Q10 is reduced?” A Biology A-level biology student is expected to know the answer, and those whose heart has been adversely affected, as was mine, know only too well that heart failure symptoms arise, as insufficient energy is available for its needs. The use of Q10 to treat heart failure is well known in Japan, where it has 75% success rate, but the medical research bodies will not investigate that “dirty word” The answer probably lies in the fact that Merck knew all about the benefits of Q10 in 1990, but sold the rights off to Japan, sending them well away from the lucrative statin marketplace, and there are several reports of research folk being forbidden to research Q10.
As for THINCS, it was in place long before Uffe Ravenskov wrote his book, and for good reason, he is not the only one to write on this matter, there at least two other similar studies, very well researched.
I have read some of the so-called scientific evidence based trials on which cholesterol lowering is founded, I am extremely sceptical of the veracity of the final results published. In the first place, in UK, 70% of drug research funding comes from industry, so the research bodies, who have to get individual project funding. are virtually employees of Big Pharma, and must produce something of financial benefit to their employer.
The HPS trial, a very large one, and “gold standard RCT” may have theoretical correctness, but the depth of treatment, for such large expenditure, is little advanced from the old monk with his physic garden produce, trying it out on the locals. No attempt was made to look into the biology of possible side effects, and the level of CPK thought significant for mention was much too high. Then here was that “Run in” period, when drugs were taken, but any who dropped out in the first 3 months were not interrogated, the participants falling from 30.000 to 20.000 in this period. It is no wonder that the recorded side effects were so few, in my experience, many have problems very early in statin use, although, conversely, they can surface after many years.
Within the trial outcomes, events were observed with little variation in those with low, medium, or high cholesterol levels, and the improvement in the treatment was similarly distributed. By hopeful expectation rather than logic, the thought was that greater lowering would give greater benefit, but what is obvious to an unbiassed observer, is that it is the use of the statin, and not the cholesterol level reached, that give the only benefit from its use, and that this is by preventing inflammation in the endothelium. Dr McMully found that homocysteine was one of the major causes of inflammation, but his work went against the great cholesterol theory golden egg, and he was relieved of his post. It is now well recognised that homocysteine level is a much better predictor than cholesterol of heart problems, but trials such at the NORVIT had so many confounders that one could be forgiven for believing that it was designed to fail.
I know 3 patients who were given statins after heart attacks, with disastrous results and having given them up, have not had further heart problems, but have been left to rot in pain and many other problems because medicine has no answers, but the “dirty word Q10″ and carnitine yield great benefits for them.
These substances are named alternative medicine, they certainly are not drugs which interfere with vital functions, it seems to be a badge of honour for a drug that it must have side effects. How can the supplementation of a necessary body product be other than true science based medicine, is blood transfusion, insulin, iron sodium, potassium or calcium supply alternative medicine, Only in that it does not involve the use of expensive patented medications.
I know many of the contributors and some THINCS members, they are genuinely interested in truthful science based medicine, and I am grateful to some of them for giving the last 5 years of my life, snatched from the jaws of a very misguided and only supeficially researched mass medication regime, which will ruin many more lives before the real truth of its damaging potential is realised.
“what is obvious to an unbiassed observer, is that it is the use of the statin, and not the cholesterol level reached, that give the only benefit from its use, and that this is by preventing inflammation in the endothelium.”
That’s what I keep trying to tell them here, but they can’t hear it. I knew this decades ago from the Dr. Atkins radio show. He based his opinions on logic, rather than peer pressure, and was extremely informative.
Of course, Atkins is not my only source of CAM knowledge. But he was so logical and knowledgeable, a genuine skeptic — he understood the dangers of “syndrome X” and insulin resistance, and he understood that refined carbohydrates, not fat or cholesterol, is the major cause of heart disease in America.
The low fat diet craze has caused tremendous damage, and may have actually caused the current obesity epidemic.
Everyone is suffering except the medical industry and Big Drug.
Steven,
Looking back at this thread, I observe that there are statin-promoters and statin-skeptics who argue politely from logic, and statin-skeptics and statin-promoters who argue rudely using emotive language. The same is more generally true on other threads. My rationale for trying to stay in the former category is that I feel more likely to convince an open-minded reader by appealing to his intellect than by demeaning his intellectual ability if he initially does not embrace my views.
You could note that my story about my father is merely a single anecdote, but your insinuation that it maybe didn’t happen will not win you converts, since many readers of this thread seem to have seen or experienced side effects of statins given to healthy people. One thing I did not mention is that about 15 years previously, my father had experienced what might or might not have been a TIA (a brief period of hand numbness, not treated at the time), which his new doctor considered to place him in the high-risk category. However, he had had no similar problems in the intervening years, his heart was fine, and his cholesterol level was well below average. Statinization of people with already-good cholesterol levels may not be standard practice, but I doubt that it is so vanishingly rare as to make mere mention of the practice “irrelevant” or “absurd,” given that many doctors are trained to read “aggressive” as a complimentary term; my father’s doctor is no more an extremist than those folks who have publicly suggested putting statins in the water supply. I will certainly inform my father that someone online who considers himself to be a medical expert thinks that his care has been inappropriate, and once again urge him to get a second opinion.
At the risk of invoking more invective, I’d just like to say that testimonials and personal horror stories generate more heat than light. Statins may get the blame for things they didn’t do as well as things they did do. For instance, 3.5% of patients on Zocor reported headaches – but so did 5.1% of patients on placebo. The actual rate of severe reactions is very low. From the Merck website:
The incidence of
myopathy/rhabdomyolysis was <0.1% in patients treated with ZOCOR.All patients starting therapy with simvastatin or whose dose of simvastatin is being increased,
should be advised of the risk of myopathy and told to report promptly any unexplained muscle
pain, tenderness or weakness. Simvastatin therapy should be discontinued immediately if
myopathy is diagnosed or suspected. In most cases, muscle symptoms and CK increases resolved
when treatment was promptly discontinued. Periodic CK determinations may be considered in patients
starting therapy with simvastatin or whose dose is being increased, but there is no assurance that such
monitoring will prevent myopathy.
Many of the patients who have developed rhabdomyolysis on therapy with simvastatin have had
complicated medical histories, including renal insufficiency usually as a consequence of long-standing
diabetes mellitus. Such patients merit closer monitoring.
Thanks, Dr Hall. My husband takes a statin and I’m happy to know it’s doing what it’s supposed to.
I prefer scientific evidence to anecdotes. Silly me.
And I love the idea that lowfat diets are contributing to the obesity epidemic. Those cheeseburgers and fries, chips and ice cream, are totally irrelevant.
pec writes:
“[Atkins] understood that refined carbohydrates, not fat or cholesterol, is the major cause of heart disease in America.”
I am not a big fan of the Giant Slabs o’Meat diet (if you will forgive a little snarkiness) but the evidence that refined carbohydrates are a major contributer to the harm done by the Western diet seems to be building. A new study (Katcher et al. 2008, Am. J. Clin. Nutr. 87:79-90) gave a group of fat people dietary advice and told half to eat only refined grain, half to eat only whole grains. Over 12 weeks the two groups lost identical amounts of weight, but CRP in the whole-grain group decreased 38% in the whole-grain group, not at all in the refined-grain group. In other words, they may believe that weight loss is reducing their risk for heart disease, but biochemical markers of risk suggest that as long as they keep scarfing that Wonder bread, it won’t do any good.
What a great relief to read so many responses by statin-injured individuals. I suppose the proponents here of statin use still deny, even in the face of so many injured patients’ narratives, that any serious problem exists. Dr. Hall, They call it Ubiquinone because it’s need in human physiology is ubiquitous. I refer to a quote from one of your earlier posts:
“As to why Merck didn’t add CoQ10, I can think of 3 probable reasons right off the bat: not every patient needed it, it was expensive, and until there was better research they couldn’t know that adding it would do more good than harm.”
‘Not every patient needed it’?… I’m sure ubiquitous means the same in the King’s English as it does here in the US… please! It might do more harm than good’?… again… please! ‘It was expensive.?… ah, now there dr., I think you are in the proper arena; the money game. This manufacturer’s motives are and were entirely motivated by net profits, and we are left to pay price for their gluttony. Shame on you!
regarding statin anecdotes – don’t fault me for laying out all logical possibilities. In my experience whenever (almost 100% of the time) I hear a story about what some other doctor did, then I have an opportunity to compare the story to documentation, the story is inaccurate. This is true of positive and negative stories – human beings are notoriously bad historians, we alter the details to fit the theme and emotion of the story. This is one reason that anecdotes are so misleading.
As far as I can tell there are no statin promoters in these comments. The authors promote scientifically rational evidence-based standards of care. We can reasonably argue and disagree about what the evidence says those standards should be regarding statins. What I reject are the ad hominem logical fallacies against doctors, the medical profession, scientific researchers, etc. and the promotion of lone dissenters as if they were the second coming, just because they take a contrarion view. This is not a constructive approach.
It is also not constructive to present anecdotal accounts of aberrant clinical decision making as if it represents anything. That is the very definition of a straw man argument.
MDs who encouraged their patients to follow a low-fat diet did not always warn them about the dangers of a high-carbohydrate diet. Carbohydrates, especially if they are processed, can lead to elevated insulin levels. This is turn can cause hypoglycemia, which can lead to increased desire for carbohydrates. Some call this carbohydrate addiction, and it can lead to something called syndrome x, which in turn can lead to type 2 diabetes.
As we know diabetes 2 is now becoming an epidemic, even in young adults. Aside from cigarette smoking, it is the leading cause of heart disease and stroke.
If you want to lower your risk of artery disease, do not worry about cholesterol or natural fat (trans-fat is another story). Instead, worry about carbohydrate addiction and lack of physical exercise. And of course, do not smoke.
The extreme Atkins diet was for extreme cases of carbohydrate addiction, and its purpose was to break the addiction. Most people do not need to follow an extremely low-carb diet. Just be reasonable and avoid processed flour and sugar.
If you suspect you have hypoglycemia DO NOT eat frequent high-carb snacks. That leads to insulin spikes and carbohydrate addiction, and can result in obesity and diabetes 2, and then heart disease or stroke.
Unfortunately, MDs have NOT been warning their patients about any of this.
The food industry is still caught up in the low fat, high carb craze. I cannot find plain natural yogurt in the grocery store. It’s all low-fat and no-fat, and it’s all full of refined sugar.
“Unfortunately, MDs have NOT been warning their patients about any of this.”
Any evidence for this, or is this just blind prejudice?
Your claims are overstated. This should be a separate thread – and plan on a future article about this. But, our knowledge of fats and sugars have been increasing over the last few decades and our recommendations along with them. For heart health the evidence suggests that type of fat is more important than total fat – vegetable and legume based fats are good, animals fats are bad, and trans fats are very bad (but don’t tell this to the cholesterol “skeptics”). Likewise, total carbohydrates does not appear to be a problem for most people, but high glycemic index foods (simple sugars and refined starches) may be a problem, and are definitely a problem with those who are overweight or predisposed to problems with glucose metabolism.
None of this appears to matter significantly for weight control – total caloric intake and exercise are what appear to matter.
The problem with Atkins is that he didn’t ever do the research to support his claims – he just made his millions. Meanwhile nutrition research just moved past him.
But this topic really needs an article length discussion with references.
Sob stories are nice but none of them are convincing in the least.
One wonders why the Maasai and Inuit don’t all have heart attacks by the time they’re 30. I’m not suggesting that it’s ideal to live on cow blood or fish, but the relative health of some people following animal-heavy traditional diets shows that it is too simplistic to label all animal fats “bad.” Likewise, there is evidence that omega-6-laden plant oils are not something the Western diet needs more of. The tragic flaw of the reductionist approach to nutrition has always been to label certain molecules “good” and others “bad” (much like “good cholesterol” vs. “bad cholesterol,” itself necessary for brain function), which inspires gorging on the one hand and paranoid avoidance on the other. I really like Michael Pollan’s latest book, “In Defense of Food,” which cites historical flip-flopping and modern studies contradicting the fat-phobic paradigm to explain why the “nutritionist” emperor has no clothes.
Wow! I haven’t plowed through all the comments here, but farmgal, thank you for the link to that study:
http://www.jci.org/117/12/3940?content_type=abstract
It’s always useful to have good sources like that. I haven’t gotten through the whole thing yet, and I’m not sure how much I’ll understand, but the abstract and intro seem consistent with what Dr. Hall and Dr. Novella have been writing here.
Dr Hall
Anyone who believes the unbelievably low figure quoted by Merck for muscle problems is very naive, to say the least, and a very large pinch of salt is needed to swallow it. Studies elsewhere, not Pharma sponsored, put the figure near 20%, and although you would speak of personal horror stories, a website for statin damaged people in April 2006 had a forum enquiry asking for help for unbearable leg muscle pain. A reply was made to him, suggesting the beneficial effects of carnitine supplementation to alleviate his problem, which worked. In the ensuing 22 months, nearly 23,000 visits have been made to that individual thread, so not just a personal story, but one affecting a great many people who were frightened by an allegedly dangerous cholesterol figure into a statin regime because their life was said to be in danger. How many now curse their doctors for setting them on this so-called safe medication. I recently heard a radio doctor compare statin muscle pain to the odd ache he felt when getting up in the morning!!! If only it was so mild!! I know 2 men who had to give up work because of the severity of the problem. I read many cursing their doctors for setting them on this path, and telling them that “Statins don’t do that”
The UK Yellow card scheme for doctors to report events believed to be caused by drugs has 80 deaths total against the two most recommended statins in the current guidelines, atorvastatin and simvastatin, but the authorities either haven’t noticed or don’t care, so much for regulatory authorities.
Periphal neuropathy is now quite often seen, and is not relieved by Q10 or carnitine, often persisting for a very long time, possibly permanently, as are the deficiencies of Q10 and carnitine production, not measured in trials, but at least one THINCS member, and also the Mayo clinic are able to demonstrate the numerical value of Q10 level. Again, so much for the assumed superiority of “science based medicine”, which does not even acknowledge the existence of such vital substances, let alone quantify them. A large dose of humility is needed in high places in medicine, and a lot less of what one author recently named as “Eminence based medicine”
The many unbelievable uses to which statins have been thought to be useful prompted me to remark that they would be advising them for ingrowing toenails next, until I heard of a statin victim whose nails and hair stopped growing when taking them. The loss of Q10 was the probable cause of this cessation of a normal body function. There is virtually no body function which is exempt from damage due to statin depletion of Q10, but no pharmaco will fund research into this important area, which has little large profit prospect, and probable damage to the sales of the most profitable, but certainly not the safest, drug on earth.
I have no longer any trust in the pronouncements of much medical research, and believe that many of those who set Government guidelines are not serving the public, but their commercial paymasters.
And there you have it, from the proverbial horse’s mouth, the reason why no amount of evidence, logic, or reason will ever persuade raygee. His prejudice against “conventional” medicine and “big pharma” is such that he is clearly not persuadable.
“high glycemic index foods (simple sugars and refined starches) may be a problem”
MAY be a problem!!! I guess you have to wait for the formal research before you acknowledge the obvious.
Atkins was right — the current heart disease epidemic results from high insulin levels, caused by carbohydrates, not cholesterol or fat, but you refuse to admit it. He didn’t care what mainstream medicine said, he cared about what made sense.
I am not saying Atkins was god and knew everything. But I was impressed by his skeptical and scientific attitude. Most MDs are more interested in belonging and acceptance (peer pressure) than in science, but he didn’t care about that.
You very grudgingly admit there might be a problem with carbohydrates. You brush it aside because you don’t want to admit that the MOST IMPORTANT FACTOR, probably the biggest influence on health in America today, has been practically ignored by the medical industry.
I can’t help wondering why. Is it because you would rather sell statins?
Dr Novella said…
[quote]I also disagree with the articles conclusions from their own data. Treating 71 people for 3-5 years to prevent one MI or stroke sounds good to me. It’s probably even cost effective if you consider the total health care cost of a stroke or heart attack.[unquote]
Permit me to disagree with your support for the practice of initiating treatment in 70 people for a period of between 3 ~ 5 years, when it is known that the treatment will not have prevented a stroke or an heart attack, which is touted as the raison d’être for prescribing the medication in the first instance.
Furthermore there is evidence that links the administration of statins to adverse reactions that run a rather full gamut from mild to fatal. My question is to do with the risk/benefit equation… What possible justification can there be to needlessly expose 70 people to the risk of statin-mediated adverse reactions, when none of them will benefit from taking the statin?
Additionally, how many years must patients be dependent on both statins and their attending clinician, before they derive any of the benefits that statins allegedly bestow upon them?
[quote]These numbers are much better than the use of ASA or Plavix for stroke prevention – which is not controversial at all.[unquote]
Clopidogrel is most definitely not a statin. Is comparing one type of pharmaceutical with another type of medication, a valid method of determining the safety of a medication that is used differently and which belongs to another pharmaceutical group with different bio-availability characteristics, therapeutic range and a different mode of action?
While it may well be the case that the use of clopidogrel (as an agent to prevent strokes) may be uncontroversial among the neurology community, it cannot be right to extend that specific uncontroversial approval from the nuerologists to include the use of statins and then go on to assume that they are just as effective or as clopidogrel in stroke prevention, with the obvious corollary that statins are uncontroversial too.
As to the concept of stroke prevention… how can one know that the drug prescribed was the agent that prevented the stroke? When is the conclusion of ‘effective prevention’ made? Does the patient (for example) have to survive for ten years since treatment was first commenced, for a positive finding to be made; that effective stroke prevention was achieved?
What would the situation be if the patient were to suffer a stroke one day after the ten years were up? Would that happenstance presage a change in the finding of ‘effective prevention of stroke’ to a finding of ‘unable to prevent stroke’? Attributing the lack of a stroke to the initiation of a drug regime, sounds more than a little like superstition rather than the practice of clinical medicine, to me.
David
I no longer have faith in so much medical so-called research because it is so unbelievably unbalanced, negligible amounts of money are spent on what one might call Devil’s advocate views to counteract the might of the drug industry, which is often comparable with that of government.
I have been in a scientific career all my life, and some of the logic which I read in trials and studies, is not logic at all.
Having found the real reason for statin damage 5 years ago I have written to authorities from Prime Minister, to professors, consultants and anyone I could think of who might listen and take note, but I find that most do not even know the vital need for substances such as Q10, and I believe their personal status might be compromised if they even admitted to the existence of and need for such a substance, their financial backers might prejudice that position.
A very sorry state of affairs, I am not prejudiced, I have convinced my local medical personnel of the facts of statin damage, and only keep alive by taking quite large doses of the two substances depleted permanebntly by statins, Q10 and carnitine, any shortfall of the first, my heart complains and my blood pressure rises, of the second, my muscle wastage CK figure rises. All very scientific, but there is little doubt that money and not truthful science is at the heart of much of medicine today.
Particular specialties take possession of some problems and muddy the scene, eg post polio is in the territory of Neurology, whereas it is a metabolic problem, and ME/CFS belongs to Psychiatry, but a Pathologist has had success with prolonged anti biotic treatment. In the statin case, cardiology appears to reign supreme, leaving no room for the experts in bio energetics and those conversant with the real functions of the mevalonate pathway.
Perhaps one day truth will prevail and conventional medicine will catch up with the whole range of beneficial body necessities, and stop labelling them alternative medicine because they are not in the fortune makers for Big Pharma. in the meantime be aware that the once well respected name of medicine is not as unblemished as it was in days before business interests took over control of the finances. I have no time for complementary medicine, real scientific knowledge must always reign supreme.
jayemcee wrote: “Permit me to disagree with your support for the practice of initiating treatment in 70 people for a period of between 3 ~ 5 years, when it is known that the treatment will not have prevented a stroke or an heart attack, which is touted as the raison d’être for prescribing the medication in the first instance.”
This is a gross misunderstanding of the application of statistics in medicine. The “number needed to treat” is just a way to express risk vs benefit and cost effectiveness. You can’t know ahead of time who is going to benefit or not. It’s statistical. All preventive medicine is statistical.
Also – as I wrote previously, we need to identify those groups for whom the net benefit outweighs the net risk. Stop pretending like we are saying something else.
Jayemcee wrote: “Clopidogrel is most definitely not a statin. Is comparing one type of pharmaceutical with another type of medication, a valid method of determining the safety of a medication that is used differently and which belongs to another pharmaceutical group with different bio-availability characteristics, therapeutic range and a different mode of action?”
Complete non-sequitur. I made a very specific comparison – the number needed to treat over how long compared to the number of adverse events prevented. For clopidogrel estimates range from 50-125 people for 1 year (for secondary prevention) to prevent one vascular event (which can be a TIA or stroke). The number is higher for strokes alone. It’s lower if you include heart attacks as well.
Of course for any drug the NNTT has to be compared to adverse events. Most preventive treatments will be studied to look at all outcomes to measure a net risk/benefit.
I was not trying to extend any other analogy to statins. They have to stand on their own evidence.
Jayemcee wrote: “As to the concept of stroke prevention… how can one know that the drug prescribed was the agent that prevented the stroke? When is the conclusion of ‘effective prevention’ made? Does the patient (for example) have to survive for ten years since treatment was first commenced, for a positive finding to be made; that effective stroke prevention was achieved?”
These are good basic (first year medical student) questions, but I get the sense that Jayemcee is implying the medical community doesn’t ask such questions.
As I stated, preventive measures are always statistical. You never know in an individual patient what would have happened to them if they had not been given a specific preventive treatment. So what? Or are you arguing against all preventive medicine, or the application of all statistics in medicine? If not, then what (if anything) is your point?
Jayemcee wrote: “Attributing the lack of a stroke to the initiation of a drug regime, sounds more than a little like superstition rather than the practice of clinical medicine, to me.”
Then you should read a basic book on medical statistics.
pec wrote: “MAY be a problem!!! I guess you have to wait for the formal research before you acknowledge the obvious.”
Yes. The obvious is often wrong, formal research will tell.
pec wrote: “Atkins was right — the current heart disease epidemic results from high insulin levels, caused by carbohydrates, not cholesterol or fat, but you refuse to admit it. He didn’t care what mainstream medicine said, he cared about what made sense.”
What Atkins cared about was making millions. How can you say he cared about science when he never did any. If he cared about patients then why not conduction the research necessary to convince the scientific community he was right?
pec wrote: “I am not saying Atkins was god and knew everything. But I was impressed by his skeptical and scientific attitude. Most MDs are more interested in belonging and acceptance (peer pressure) than in science, but he didn’t care about that.”
You are easily impressed. What science did he do?
pec wrote: “You very grudgingly admit there might be a problem with carbohydrates. You brush it aside because you don’t want to admit that the MOST IMPORTANT FACTOR, probably the biggest influence on health in America today, has been practically ignored by the medical industry.
I can’t help wondering why. Is it because you would rather sell statins?”
You have an active imagination. How do you imagine I “grudgingly” admitted the problem or that I “brushed it aside?” Carbohydrates and insulin are part of the problem – but this varies in different people. It is also not the only problem, animal fat plays a role too.
What is your evidence (apart from your paranoid imagination) that any of this had been ignored by the medical profession?
Also – I don’t sell statins or any drugs. I am a salaried academic. I have no financial ties to any of this. But I guess it is beyond your narrow view of reality to consider that perhaps I have looked at the evidence and honestly came to a different conclusion than you.
Noticed the incidence of rhabdomyolysis was taken from Merck’s web site. Would be useful information if adverse events were reported in all the statins studies. Many of these studies do not include the actual #’s of serious adverse events. In fact, Two of the very large statin studies did not publish the total # of SAEs. ALLHAT-LLT did not publish the total serious adverse events, nor did the ASCOT-LLA study. It is difficult to determine one’s risk/benefit ratio when the true risk #’s are not published.
Concerning the individual with post polio syndrome, there has been published 4 case reports of individuals whose neuromuscular diseases were “unmasked” by statin use:
Jul 25 Lomasin.com
Statins May Unmask Underlying Neuromuscular Disease
NEW YORK (Reuters Health) Jul 26 – Patients with asymptomatic neuromuscular disorders may have their condition precipitated by statin use, according to investigators from the University of Athens Medical School…
Dr. Panagiota Manta and colleagues describe four such cases in the July 24th issue of the Archives of Internal Medicine…
… Statin-induced neuropathy is well recognized and reported more and more often, Dr. Manta’s group notes. These four cases show that statins can also trigger underlying neuromuscular conditions.
The investigators suggest that if neuromuscular symptoms persist after discontinuation of statin therapy, clinicians should “pursue further diagnostic evaluations for the detection of underlying neuromuscular disease.”
Arch Intern Med 2006;166:1519-1524.
Copyright © 2007 lomasin.com. All rights reserved.
A more recent report of atrogin-1 gene being turned on by statin use–
Discovery of gene responsible for statin-induced muscle pain.
Wed, 28 Nov, 2007
Statins, the popular class of drugs used to lower cholesterol, are among the most commonly prescribed medications in developed countries. But for some patients, accompanying side effects of muscle weakness and pain become chronic problems and, in rare cases, can escalate to debilitating and even life-threatening damage.
Now a study led by investigators at Beth Israel Deaconess Medical Center (BIDMC), helps explain the source of these problems. Published in the December 2007 issue of The Journal of Clinical Investigation, the findings offer the first evidence that a gene known as atrogin-1 plays a key role in statin-related muscle toxicity.
“Although it is not known exactly how many of the 500 million individuals who take statins experience muscle pain and weakness, muscle symptoms are generally considered the most common side effects of these medications,” explains co-senior author Vikas P. Sukhatme, MD, PhD, Vice Chair of Medicine for Interdepartmental and Translational Programs, Chief of the Division of Nephrology, and Chief of the Division of Interdisciplinary Medicine and Biotechnology at BIDMC.
“Statin users describe a wide spectrum of symptoms – at the most extreme end is a severe breakdown of skeletal muscle known as rhabdomyolysis,” says Sukhatme, who is also the Victor J. Aresty Professor of Medicine at Harvard Medical School (HMS). “At the other end is ‘grumbling muscles,’ milder, more diffuse muscle soreness and cramps. This kind of symptomatic muscle weakness and pain is quite frequent, but often difficult to quantitate.”
Known by such trade names as Lipitor, Zocor, Pavacol and Mevacor, statins lower cholesterol by inhibiting HMG-CoA reductase, a key enzyme in cholesterol synthesis.
Approximately five years ago, the study’s co-senior author Stewart Lecker, MD, PhD, and colleagues in the HMS laboratory of Alfred Goldberg, MD, first discovered the atrogin-1 gene, so named for its role in muscle atrophy.
“We learned that atrogin-1 is rapidly turned on in wasting muscle,” explains Lecker, who is an investigator in the Division of Nephrology at BIDMC and Assistant Professor of Medicine at HMS. Muscle wasting occurs in a large number of disease states, including cancer, AIDS, and kidney disease and can also occur when muscles are underused due to injury or lack of exercise. “In the absence of atrogin-1 activation,” he adds, “muscle atrophy is diminished.”
Since this initial discovery, atrogin-1 has been found in every existing model of muscle wasting, prompting Lecker and Sukhatme to investigate whether cholesterol-lowering statins might also be “turning on” this gene.
“We reasoned that since atrogin-1 plays a key role in the development of wasting in skeletal muscle, it might also mediate part of [patients'] sensitivity to statins,” the authors write.
They proceeded to conduct three separate experiments to test this hypothesis. They first examined the expression of the atrogin-1 gene in biopsies of 19 human quadricep muscles from five control patients, six patients with muscle pain who were not being treated with statins and eight patients with muscle pain/damage who were using statins. Their results showed that atrogin-1 expression was significantly higher among the statin users.
Next, the scientists studied statins’ effects on cultured muscle cells treated with various concentrations of lovastatin. Compared with control samples, the lovastatin-treated cells became progressively thinner and more damaged. But remarkably, say the authors, the cells lacking the atrogin-1 gene were resistant to statins’ deleterious effects.
Finally, the authors tested the drug in zebrafish. And, they showed that just as in mammalian muscle cell culture, lovastatin led to muscle damage, even at low concentrations; as the concentration was increased, so too was the damage. And, once again, they observed that fish lacking the atrogin-1 gene were resistant to statin-induced damage.
“These three complementary experiments demonstrate that atrogin-1 has a fundamental role in statin-induced toxicity,” notes Lecker. “Future experiments will be aimed at understanding how statins turn on the atrogin-1 response in muscle, and in ascertaining what transpires in muscle following atrogin-1 activation that leads to muscle damage and atrophy. The hope is that eventually patients will be able to glean statins’ positive benefits to cholesterol metabolism and reduction of cardiovascular events while being spared accompanying muscle toxicities.”
http://www.bidmc.harvard.edu/
I don’t think the Merck website data on myopathy/rhabdomyolysis is significantly different from the data from the many, many statin trials and meta-analyses in the published literature. The risk was greater with the now-withdrawn cerivastatin than with the currently used drugs, it is greater with larger statin doses and with pre-existing conditions, it is greater with combined therapy than with monotherapy, and prompt recognition and discontinuance of the drug usually solves the problem.
This article estimates a NNH of 22,727 for rhabdomyolysis.
http://www.jr2.ox.ac.uk/bandolier/band131/b131-2.html
“Carbohydrates and insulin are part of the problem – but this varies in different people. It is also not the only problem, animal fat plays a role too.”
The syndrome that leads to diabetes 2 can also cause high blood pressure and high cholesterol.
Therefore your belief that high cholesterol, caused by dietary fat, is not carefully considered.
Conventional medicine is notorious for being reductionist and for failing to consider complex relationships between variables.
And how in the world can you claim to know what Atkins cared about? You probably don’t even know what he said, let alone his private thoughts. He was a famous CAM physician and you don’t like CAM, so you have no curiosity about his ideas.
Atkins’ ideas made more sense than the conventional approach to heart disease because he considered the whole system. Mainstream medicine frequently mistakes correlations for causative relationships, partly because of your habit of looking at variables in isolation.
Man, this blog makes me glad I don’t get many comments on my own. I don’t know how in the world I’d keep up with the trolls without making it a full-time job.
Just a couple of studies that are self explanatory. In short, the studies need to be reliable, and doctors need to pay better attention to complaints:
“Drug Safety. 30(8):669-675, 2007.
Golomb, Beatrice A 1 2; McGraw, John J 1 3; Evans, Marcella A 1; Dimsdale, Joel E 4
Abstract:
Objective: Using a patient targeted survey, we sought to assess patient representations of how physicians responded when patients presented with possible adverse drug reactions (ADRs). As a demonstration case, we took one widely prescribed drug class, the HMG-CoA reductase inhibitors (‘statins’). This information was used to assess whether a patient-targeted ADR surveillance approach may complement provider reporting, potentially fostering identification of additional patients with possible or probable ADRs.
Methods: A total of 650 adult patients taking statins with self-reported ADRs completed a survey. Depending on the problems reported, some patients completed additional surveys specific to the most commonly cited statin ADRs: muscle, cognitive or neuropathy related. Patients were asked to report drug, dose, ADR character, time course of onset with drug, recovery with discontinuation, recurrence with rechallenge, quality-of-life impact, and interactions with their physician in relation to the perceived ADR. This paper focuses on patients’ representation of the doctor-patient interaction and physicians’ attribution, when patients report perceived ADRs.
Results: Eighty-seven percent of patients reportedly spoke to their physician about the possible connection between statin use and their symptom. Patients reported that they and not the doctor most commonly initiated the discussion regarding the possible connection of drug to symptom (98% vs 2% cognition survey, 96% vs 4% neuropathy survey, 86% vs 14% muscle survey; p < 10-8 for each). Physicians were reportedly more likely to deny than affirm the possibility of a connection. Rejection of a possible connection was reported to occur even for symptoms with strong literature support for a drug connection, and even in patients for whom the symptom met presumptive literature-based criteria for probable or definite drug-adverse effect causality. Assuming that physicians would not likely report ADRs in these instances, these patient-submitted ADR reports suggest that targeting patients may boost the yield of ADR reporting systems.
Conclusions: Since low reporting rates are considered to contribute to delays in identification of ADRs, findings from this study suggest that additional putative cases may be identified by targeting patients as reporters, potentially speeding recognition of ADRs.”
AND THE OTHER STUDY:
Drug company funding of drug trials greatly influences outcome
In head-to-head trials of two drugs, the one deemed better appears to depend largely on who is funding the study, according to an analysis of nearly 200 statin-drug comparisons carried out between 1999 and 2005.
UCSF researchers examined 192 published results of trials comparing one cholesterol-lowering statin drug to another, or to a non-statin drug.
Their findings found that two links stood out. If the reported results favored the test drug, the trial was about 20 times more likely to be funded by the maker of the statin rather than the comparison drug company. Even more striking, they say, if the conclusions or interpretation of the drug trial – which reflect the impressions of the trial investigators — favored the test drug, the trial was about 35 times more likely to be funded by the maker of that drug rather than the comparison drug.
The results of the new analysis are reported in the June 7 online edition of the journal “PLoS Medicine.”
“Many people are concerned about the growing proportion of drug trials funded by the drug’s manufacturers,” says Lisa Bero, PhD, UCSF professor of clinical pharmacy and health policy studies. “Results of drug trials affect what drugs are covered by medical plans, and so what drugs physicians will prescribe. If drug trial outcomes are largely determined by who pays for the trial, we don’t really know what the best drug is.” Bero is senior author on the PLoS paper.
The UCSF study examined the links between reported outcomes of the statin trials and many factors, including study design, sample size, thoroughness and type of analysis, as well as funding source. They examined only published randomized controlled trials. The trials involved seven different statins overall, all studied in head-to-head drug comparisons.
The analysis found that about half of the trials were funded by industry, and about a third did not disclose any funding source. Among those declaring industry funding, about one fifth explained the role of the sponsor, such as data analysis, or writing and preparing the manuscript. Trials with no disclosed funding sources were less likely to have conclusions favoring the test drug, compared to trials with industry funding, the researchers report.
The researchers note that a number of factors can result in the drug trial results favoring the trial drug’s sponsor. Drug companies could selectively fund trials on drugs that are likely to produce a statistically significant result, the researchers explain. This can be accomplished, they say, by selecting non-equivalent doses of drugs for testing. Also, sponsors may choose not to report results that don’t favor the drugs they sell. Or, they may report positive results in more than one journal, skewing the number of positive articles about their drug.
In addition, almost half of the trials lacked adequate blinding – assuring that study scientists don’t know which drug the patients were taking until the end of the trial. Blinding is considered of paramount importance in clinical trials. The researchers found that those studies with adequate blinding were less likely to report results favoring the test drug. This finding was independent of who funded the study – in other words, funding source was a stronger predictor of outcome than blinding, but both had independent effects on outcome.
The most important weakness found in most of the trials was a lack of clinical measures of outcome, such as heart attacks or mortality — considered better indicators in trial design than less direct measures such as lipid levels.
“The lack of true clinical outcome measures in these direct head-to-head comparisons of drugs is disappointing because the studies don’t give us the best information we need to choose one statin over another,” Bero says.
The analysis is one of the first large studies examining the influence of funding source on the outcomes of head-to-head drug comparisons, rather than comparing the effectiveness of one statin with no drug at all. The market for statins is competitive, so it is important to have valid information to choose one statin versus another, Bero explained. For policy makers, the relevant choice is not to select a statin versus a placebo, but to select one statin compared to another.
The study also differed from most other assessments of influences on drug trials by examining 11 different factors, and how they may interact to affect trial results. Most previous studies examined the link of results to one factor alone, such as funding source. But this analysis adjusted for “confounders” – study aspects that can influence the results, such as study design, including randomization, blinding, sample size, even choice of comparison drug in the study.
Inclusion of the confounders still pointed to industry sponsorship as the most influential factor related to positive results and conclusions.
The study examined trials by all funding sources, as well as a subset of studies that were only industry funded. Favorable results and conclusions were associated not so much with industry sponsorship, but with the specific company that funded the study, Bero points out.
“The data available on choosing between statins based on head-to-head drug comparisons appears to be influenced by financial conflicts of interest,” Bero concludes. “So decision makers — those choosing drugs for a formulary or insurance plan — should be skeptical about these kinds of trials. We need to know if a newer, more expensive drug is really better compared to older, less expensive drugs.”
Co-authors of the study are Peter Bacchetti, PhD, professor of epidemiology, and Kirby Lee, PharmD, assistant professor of clinical pharmacy, both of UCSF; and Fieke Oostvogel, University of Leiden, Netherlands.
The research was funded by a California Tobacco Related Disease Research Program grant.
UCSF is a leading university that advances health worldwide by conducting advanced biomedical research, educating graduate students in the life sciences and health professions, and providing complex patient care.
Your point is?
This is one reason why I’m jaded:
http://www.nytimes.com/2008/02/07/business/media/07jarvik.html?_r=1&hp&oref=slogin
Plus, exercise should be the primary prescription and doctors who ask their patients to come in to get their cholesterol checked yearly or blood pressure routinely, should require patients to bring in their exercise diaries. Shame on docs who prescribe statins without doing what’s outlined below.
Studies show patients are far more likely to give up smoking if their doctor tells them to. They will more likely exercise if told by their doc.
Aspirin (25% reduction), exercise (42% reduction), 8 serving of fruits and veggies (30% reduction), beta blockers if necessary(33%) : ALL far less expensive and more beneficial in reducing risk.
Re: my (Frankie’s) post… “The main problem right now other than statins are over-prescribed is that doctors do not have a clue once things go terribly wrong. They want to try Aricept or Prednisone or anything else they can think of… stopping statins does not always resolve side effects…”
# Steven Novellaon 06 Feb 2008 at 8:21 am, stated…
Regarding Frankie’s comments: “You should be wary of subjective assessments about what is “typical” for doctors to do. Unless you can reference data measuring practices.
I and other neurologists in the US already prescribe CoQ10 for neurological side effects of statins. Taking patients off statins is not a last resort – I often see it as a first resort when symptoms appear.”
Hello Dr Novella,
From the over 800 correspondences with statin users experiencing side effects (not just my own experiences over the past 11 years with my husband’s Doctors) Physicians are not listening to their patients when they complain of the ‘known’ statin ADR’s much less the ‘rare’ side effects. Our Neurologist, when told I suspected my husband’s cognitive issues (TGA and short term memory loss) were from Lipitor, his only recommendation was to start Aricept and to RESUME Lipitor. Believe me, hubby’s cholesterol levels were the least of our worries, as he was experiencing numerous other side effects from Lipitor. When I asked our PCP, Cardiologist & Neurologist if it was possible to test to make sure he was getting enough CoQ10, I was told there was no such test. None of them suggested a CK/CPK (numerous muscle/joint pain complaints over the years) or to supplement with CoQ10. So if you and other Neurologists are prescribing CoQ10, I applaud you. My experience and that of others wish we had walked into your offices.
Yes, my over 800 correspondences are anecdotal, but they are what’s going on in the real world. And these are just the people that are looking for answers… most still have complete faith in their physicians and are also clueless that their sleep disturbances (one of the 1st signs of adverse effects), memory loss (which is usually observed by others long before the patient knows) and the more common side effects… they are just chalking them up to ‘something else’. I did too much yard work or exercised too hard at the gym.
My husband’s doctors told him he was trying to do too much ‘for his age’… good grief… he was in his 50′s… could hardly walk and finally forced to give up golf… initially due to the pain, then because he couldn’t keep track of his score. His buddies were no help, they insisted he was fudging his score.
Fact: albeit anecdotal ~ Statin side effects can be and for some are permanent. And some are maimed so much that their quality of life now ‘sucks’ to put it bluntly.
We are real people, not clinical trial, hand picked data producers. And there are many, not just the 1 or 2% quoted in clinical trials.
I’m glad some of them are starting to speak out. Why is no one listening…
Frankie
Dr. Novella,
I add my applause to Frankie. I too wish I had you for my doctor when the statin was attacking my body.
Please understand the anger many of us have toward the many doctors we saw looking for help, and got brushed off.
Just to see a neurologist “use” the phrase Co Q10 is refreshing.
The fact that you recognize statin damage is also wonderful.
I envy your future patients, how I wish you had been on my team when I needed you.
The first neurologist I saw confirmed muscle weakness, gave me a permanent handicapped permit for parking, and referred me to another neurologist.
At any rate, thanks for listening.
Dear mgl
Statins do not unmask an underlying neuromuscular disease in post polios, but create a greater deficiency of carnitine, already in short supply because of metabolic changes in muscle energy source needs, and cause muscle loss through simulated starvation conditions. I have written a (lay) paper on this and associated matters, it is available via Dr Graveline’s website http://www.spacedoc.net, medical journals said it was of too little general interest to publish, but there is far more interest now and need for more understanding of the factors involved.
Dr Hall
I see you are still hung up on trial outcome reports of problems from statins, as I explained earlier, at least 3 of the major trials had the notorious run-in period at the start, when those leaving trial medication were not included in reported results. From the experiences of those whom I know personally, side effects can occur after taking only 2 small dose statin tablets, and are often quickly apparent. Conversely, others find the sudden onset of problems years later.
The conditions of trial reporting rule out the inclusion of many people in these categories, and the reported results reflect little of life in the real world. Why are these problems written off as anecdotal, as if that meant they are only hearsay, is my near visit to nemesis to be thought of as irrevelant? I took the writer of a statin-praising article in the Lancet to task for having her head firmly in the statistical sand beneath Oxford’s gleaming spires, and being totally unaware of the scale of suffering outside affecting real living people. But then, epidemiologists only deal with statistical people, and have little direct knowledge of what each unit in their statistics represents in terms of human suffering.
The comments so far are divided between those who accept the scientific consensus and those who don’t. Those who dispute the scientific consensus have presented two kinds of evidence:
(1) studies that the scientific community is already aware of and that were not considered sufficient to change the consensus
(2) emotional testimonials and estimates based on personal experience.
This discussion has generated a great deal of heat, but also considerable light. I hope readers will not lose sight of my original point – that scientific consensus does not change through activism, but through convincing scientific evidence. The evidence is clear that statins can save lives and prevent cardiovascular events WHEN USED APPROPRIATELY. We recognize that not all providers are prescribing them appropriately, and the emphasis should be on getting those providers to follow evidence-based guidelines and to accumulate more long-term data about effectiveness and safety, especially in subgroups.
No one is disputing that statins, like any effective pharmaceutical, can produce side effects, and that sometimes those effects can be devastating. The dispute is only about how often that occurs. I suspect it happens more often than Merck would like us to believe but less often than some of the commenters would like us to believe. Even where we have reliable NNT and NNH numbers, individuals will make different decisions based on factors like their personal willingness to accept risks. Science should not presume to tell patients they “should” take statins – that is a value judgment. Science can only present the best available evidence so patients can make an informed decision for themselves.
Dr Novella stated:
[quote] This is a gross misunderstanding of the application of statistics in medicine. The “number needed to treat” is just a way to express risk vs benefit and cost effectiveness. You can’t know ahead of time who is going to benefit or not. It’s statistical. All preventive medicine is statistical. [unquote]
I agree that it is unknowable as to whom will be a beneficiary of any particular treatment. What concerns me about the statistician’s approach to prophylaxis is that the numbers can only reveal the cases which fall within closely proscribed limits.
In the case of the patient who has taken statins for 5 years and does not go on to suffer with a stroke or any other sort of cardiovascular system related malady, we can conclude that our preventative measure was successful, if it meets with our target time that the patient must be free from cardiovascular system related incidents.
Where the patient has developed Amyotrophic Lateral Sclerosis, and it was attributable to statinisation, the incident does not get recorded as a caution against statins, for the patient did not even suffer with a non-fatal stroke or heart attack. If you gave me the choice between having a non-fatal cardiovascular event and ALS or ALS-like condition that was apparently induced or mediated by statins, then I would rather suffer with the cardiovascular incident.
The joining of the relevant dots is apparently taking a very long time for the medical profession, en masse, to get to grips with. Meanwhile rather a lot of recipients of statin therapy have developed conditions that would appear to have been caused by statin toxicity. The toxicity of statins appears to be unrelated to either the duration or the dose of statin therapy and I can produce many accounts of people who have suffered within a short time of commencing taking statins.
Having any neurologist consider the possibility of profound statin-mediated damage to the neurological system is a new and an exciting step forward in the campaign to remove statins from the armamentarium of clinicians. ALS and ALS-like symptoms, peripheral neuropathy, CIDP, dysarthria, tinnitus, neuromata, parasthesia, neuralgia and neural damage have all been mentioned in association with statin use.
Neurology has, strictly speaking, little interest in the cardiovascular system other than on a gross level. I would hope that there would be less investment in expending huge amounts of energy in defending the preservation of the cholesterol heart disease hypothesis (by the neurology community) and far more professional interest (of neurologists) in discovering the aetiology of the multitude of neurological phenomena that have developed in the statinised patient.
[quote] Also – as I wrote previously, we need to identify those groups for whom the net benefit outweighs the net risk. Stop pretending like we are saying something else. [unquote]
No reasonable person would disagree with that which you have outlined above. I am not pretending anything and your imputation may have come about because you have misunderstood my position. My initial response on this forum was to Dr Hall. It was not the way I would have wished to open a discussion with anyone but her judgement on the position of Dr Ravnskov was both flawed and deeply offensive to me.
I have corresponded with Dr Ravnskov less than 10 times in my life and I am certain that I do not have to defend him. He happens to be an internationally known clinician and he is a research worker of high reknown. It was not appropriate to dismiss his work through the device of quoting the opinions of a non-medically qualified individual and his misguided opinions about the work of Dr Ravnskov.
I am belabouring this point with you because I want you to know that without that egregious inclusion in Dr Hall’s posting, I would have been considerably less combative. I would not want you to think that I don’t genuinely want answers here. I am committed to doing what I can to prevent any more patients from suffering needless harm from taking statins and that harm is ultimately iatrogenic harm so it is obviously the medical profession which needs to be addressed. this forum represents one means of doing this.
In return, I would prefer it if you could refrain from loading your words so that don’t I gather the notion that your interest in having a reasonable conversation with me is precisely none at all. Even if that was your intention, you should just say that was the case rather than comparing me with a first year medical student, which I most-assuredly am not. Trading insults is not the way forward. I hope that I have now made my position clear enough for there to be some forward motion in this debate.
[quote] Complete non-sequitur. I made a very specific comparison – the number needed to treat over how long compared to the number of adverse events prevented. For clopidogrel estimates range from 50-125 people for 1 year (for secondary prevention) to prevent one vascular event (which can be a TIA or stroke). The number is higher for strokes alone. It’s lower if you include heart attacks as well. [unquote]
This is a completely pointless game that I can play just as well as you can… I was not interested in making a point to be dissected to the nth degree for the purpose of dismissing the point. The idea was to demonstrate the general point inherent in the difficulty there was with discussing prevention. specifically, you had raised clopidogrel as a stroke prevention strategy and then followed it by stating that the treatment was uncontroversial.
I was attempting to clarify that statins in general (and as a treatment for stroke) are not uncontroversial and I was unwilling to let the reference pass, lest observers would believe that you were stating, by implication, that the use of statins for stroke prevention was also uncontroversial.
[quote] Of course for any drug the NNTT has to be compared to adverse events. Most preventive treatments will be studied to look at all outcomes to measure a net risk/benefit. I was not trying to extend any other analogy to statins. They have to stand on their own evidence. [unquote]
I accept what you say. The probability for statin mediated adverse reactions is that there appears to have been some general failure of the medical profession to log many adverse reactions as devolving from statin use.
General twinges and muscle aches with associated non-specific pains that would otherwise be unremarkable in any general practice, when a 60 year old person complains, take on an altogether different aspect when the patient is taking statins.
Many initial warnings of adverse reaction are likely to dismissed and may be accounted for simply because the patient is already aged to the degree where such complaints are common. CPK has been shown (in the literature) to be an unreliable indicator of early statin damage.
[quote] These are good basic (first year medical student) questions, but I get the sense that Jayemcee is implying the medical community doesn’t ask such questions. [unquote]
You have misunderstood my reason for asking such basic questions. Had the medical community asked (and answered) these questions it is probable that we would not need to have this discussion. Something has prevented the help, which is needed by statin-damaged patients, from being given. The rush to statinate large swathes of the populace (with the corollary that they will stay medicated and thus treated for life) appears to me to be the antithesis to good health.
We have all watched the acceptable level for total cholesterol levels fall and it continues to fall. The notion that cholesterol levels must fall is predicated on the cholesterol/heart disease hypothesis. The damage being done to the body at cellular level is profound. It is not a case of if the statinised patient will suffer statin-related damage, but when and how much damage will the patient sustain. To state anything else is to misinform the patient.
The mevalonate metabolic pathway is responsible for processes other than the biosynthesis of cholesterol. Statins inhibit cholesterol early on in the pathway without any regard for the fate of ubiquinone, prenylated proteins, dolichols and heme a.
The initiation of apoptosis may be linked to a reduction in heme a. Cell wall integrity may be harmed by the reduction in cholesterol. Myelin sheath may be affected by the reduction in cholesterol. On its face, one could possibly make out a case that statins are inimical to life itself.
[quote] As I stated, preventive measures are always statistical. You never know in an individual patient what would have happened to them if they had not been given a specific preventive treatment. So what? [unquote]
So perhaps the practice of the statistical measurement of the effectiveness of any specific preventative action ought to be deprecated. Statistical manipulation can be used to prove or disprove anything. It is not unknown for statistics to be used to obfuscate reality and prevent knowledge of poor performance from becoming widely known.
[quote] Or are you arguing against all preventive medicine, or the application of all statistics in medicine? If not, then what (if anything) is your point? [unquote]
Many statin studies have regarded the statin-damaged as clinically insignificant. It is possibly a dishonesty that is inherent in the tool of clinical study. More telling is that product maker involvement usually presages favourable findings for the product maker. The clever academic game of removing unpleasant findings from the final paper is a common and widely understood gambit, that is frequently used to curry favour with the sponsors.
I would want to see all clinical studies conducted because of a clear clinical need rather than having projects suggested by sponsors with goods to peddle in related clinical areas. I would remove the possibility of product suppliers having any input into which clinical studies are carried out. If they wished to sponsor genuine clinical advances, then the money should all go into a central pot.
Senior clinicians should be responsible for devising clinical research projects and they should be permitted to fund them from the central pot. They should be protected from interference from outside agencies and they should be encouraged to publish actual results. A requirement of all clinical research should be that a log of all outcomes is kept, even if they are not clinically significant.
All clinical research that is published, should be freely available from a central repository, so that members of the public could make truly informed choices about treatment options before being coerced, either by national policy or unscrupulous clinicians, into following any treatment regime. Such a step would require each publication to be summarised in lay language so that clarity of purpose would be assured.
[quote] Jayemcee wrote: “Attributing the lack of a stroke to the initiation of a drug regime, sounds more than a little like superstition rather than the practice of clinical medicine, to me.”
Then you should read a basic book on medical statistics. [unquote]
Done
Frankie, et al
I understand your frustration. No one is saying that the practice of medicine is perfect. But I find that frequently those criticizing the practice of medicine in extreme terms are describing something that I do not recognize from my daily practice and interaction with other physicians.
I admit my own experience is biased, but I am a neuromuscular specialist. This means I get patients referred to me every week with muscle symptoms. In almost every case, if they were on statins when their symptoms occurred the FIRST thing their doctor did was take them off the statins. (In addition to other routine stuff.) If their symptoms persisted, then they referred them to me.
Doctors are generally aware of the side effects of statins, and will stop them when appropriate. Of course, there are many doctors and many patients out there. The internet can now act as a filter to collect all the negative outcomes and frustrated patients. This creates a very distorted view of what is happening “in the real world”.
Hopefully we can use this blog to bridge the gap of communication. The situation is not as bad as it may seem – the best academic researchers and physicians are actually quite on top of things, asking the right questions, etc. They are not all blithering idiots or corrupt fiends, and some would have you believe.
jayemcee is halarious
“Where the patient has developed Amyotrophic Lateral Sclerosis, and it was attributable to statinisation, the incident does not get recorded as a caution against statins, for the patient did not even suffer with a non-fatal stroke or heart attack. If you gave me the choice between having a non-fatal cardiovascular event and ALS or ALS-like condition that was apparently induced or mediated by statins, then I would rather suffer with the cardiovascular incident.”
If you think that researchers haven’t looked at things like this you are seriously naieve. Give me a break man, you waste so many words with crap like this.
“The joining of the relevant dots is apparently taking a very long time for the medical profession, en masse, to get to grips with.”
Oh but you have the inside line on this! Connecting those relevant dots is but a cakewalk for one man – but the whole medical profession, en masse, just cant get it. Sure buddy. You are over reaching.
“I can produce many accounts of people who have suffered within a short time of commencing taking statins.”
Ahh so all you really have is stories. Nice way to eliminate bias there.
“Neurology has, strictly speaking, little interest in the cardiovascular system other than on a gross level. I would hope that there would be less investment in expending huge amounts of energy in defending the preservation of the cholesterol heart disease hypothesis (by the neurology community) and far more professional interest (of neurologists) in discovering the aetiology of the multitude of neurological phenomena that have developed in the statinised patient. ”
Not only an authority on Statins but on Neurology as well. Impressive.
“I was not interested in making a point to be dissected to the nth degree for the purpose of dismissing the point.”
If your point is a non-sequiter it’s invalid. Think of a better one. One that isn’t a logical fallacy.
“The probability for statin mediated adverse reactions is that there appears to have been some general failure of the medical profession to log many adverse reactions as devolving from statin use.”
Sounds like the words of a man talking out his ass! There “appears” to be some kind of “general failure” for you to “log many” facts that stand up to scrutiny. Evidence for your assertions should be forthcoming when making blanket statements conjured from the depth of limited reasoning.
“General twinges and muscle aches with associated non-specific pains that would otherwise be unremarkable in any general practice, when a 60 year old person complains, take on an altogether different aspect when the patient is taking statins.”
Did you get this from the stories you’ve been told as well?
The rest is just more of the same – anyone with a baloney detection kit can discover the cheap meat in your posts. I’m no professional but I think Steve adressed every point of all your posts, you just ignore and repeat the same ish over and over.
Just to echo Novella, I prescribe statins every day, and very rarely, but occasionally see myopathic side effects. I certainly monitor for them.
As you said, most doctors aren’t idiots (most). We actually did a bit of training to do this stuff. It wasn’t a day or two a “google university”.
Jayemcee mentions “a new and an exciting step forward in the campaign to remove statins from the armamentarium of clinicians.” A scientific mind doesn’t embark on “campaigns” to impose his own version of the truth but tries to keep an open mind and hone in on where the truth lies – which is usually somewhere between the extremes of opinion.
I was particularly amused by his comments on the Skeptic’s Dictionary critique of Ravnskov’s book. He protests that Bob Carroll is not a scientist, but a professor of logic and critical thinking. Yes, that is precisely the point: a non-scientist was able to point out serious logical flaws in Ravnskov’s arguments. Even if the evidence those arguments are based on is good science, his interpretation of that evidence is faulty. Carroll did not offer “opinions” but analyses of logical errors.
I have had a several-year ongoing e-mail discussion with another cholesterol skeptic that has remained polite and courteous on both sides. Neither of us felt any need to offer ad hominems or insults. Jayemcee’s personal attack on me was entirely unwarranted, inappropriate, and offensive. The language he used has no place in a respectlful scientific discussion. Fortunately, I was more amused than offended. When someone “loses his cool” that way, he has already lost the argument.
I have only seen such behavior in people who have been unable to defend their position with logical arguments and good data, and who have felt the need to strike out to defend themselves the only way they can. The last time it happened to me was on a chiropractic forum where I was “flamed” as an IGNORANT HO. That time, 3 forum members wrote me offlist to apologize for the behavior of their colleague and to tell me they couldn’t object to anything I had said.
Personally, I couldn’t care less, but I think perhaps Jayemcee owes an apology to the rest of you for violating the conventions of polite discourse.
We still have not heard an explanation here for the possible confound relating to the cholesterol hypothesis. Statins lower cholesterol and also have an anti-inflammatory effect. We know that artery disease is related to inflammation. Therefore, we don’t know if the effectiveness of statins results from their cholesterol-lowering effect or their anti-inflammatory effect, or both.
It’s possible that cholesterol-lowering is incidental to the effectiveness of statins. And in that case the cholesterol hypothesis might be wrong. And that would mean prescribing statins to people with high cholesterol but no health complaints would be a mistake.
I know people who have been on statins for many years. I would like to find out if cholesterol level is relevant or not. I suspect it is not, or that it is much less important than has been assumed.
I believe, and I think this is well accepted, that the major cause of heart disease, aside from cigarette smoke, is hyper-insulinism. High insulin may cause high cholesterol, and this is another possible confound in the hypothesis.
To summarize: high cholesterol may be an effect of cardiovascular disease, rather than a cause. The general metabolic imbalance sometimes known as syndrome x (which is caused by the American lifestyle) involves many complicated variables. This syndrome is known to be a major cause of heart disease. Therefore it is a mistake to focus on one variable, cholesterol levels, in isolation. It is a mistake to treat a complex syndrome by attacking one symptom, rather than searching for and treating the cause or causes.
No one at this blog has addressed this question, which I have brought up several times. Is there any research which tries to separate out various factors and determine directions of causality?
If high cholesterol predicts heart disease, we should not jump to the conclusion that high cholesterol is the cause. Something else might cause both the high cholesterol and the heart disease.
If lowering cholesterol with statins prevents heart disease, we should not jump to the conclusion that the effectiveness of statins depends on their ability to lower cholesterol. It might be the anti-inflammatory property of statins. And in that case, lowering cholesterol might be irrelevant to preventing heart disease.
How can we find out? Has anyone tried? Or are medical researchers entirely satisfied with their assumption that cholesterol is the culprit?
Dr. Novella,
I appreciate your reply to Frankie. Just to make my position clear, the folks I referenced as having statin problems are not anyone I encountered online.
They are people I know in real life, some family, some friends, and some strangers. The subject only comes up because of my cane, or wheelchair.
Over and over again, if they ask, “My goodness, what happened to you?” I tell them. Just a simple statement, “I took a statin drug for cholesterol, and it messed me up.” THAT is when I get feedback.
I originally assumed that I was just a very unlucky individual.
Then more and more, over the last 4 years, SO many folks have told me they too had problems, and chucked the statin in the garbage. Some had recovered, some have partially recovered, and some ended up like me. These are just chance encounters.
And yes, many of these folks are angry for ever being put on these drugs. VERY angry.
Two people I know have major heart disease problems and EVERY reason to take a statin. They ditched the stuff several years ago, and are still with us to tell about it. They haven’t dropped dead for lack of statins, and they are quite elderly.
I do think that doctors are more on the ball now, than back when I first started having problems in 2001. I am glad you are one of them.
According to a recent study date of 2007 (that I posted above), it appears that in not always the case:
“Results: Eighty-seven percent of patients reportedly spoke to their physician about the possible connection between statin use and their symptom. Patients reported that they and not the doctor most commonly initiated the discussion regarding the possible connection of drug to symptom (98% vs 2% cognition survey, 96% vs 4% neuropathy survey, 86% vs 14% muscle survey; p < 10-8 for each). Physicians were reportedly more likely to deny than affirm the possibility of a connection. Rejection of a possible connection was reported to occur even for symptoms with strong literature support for a drug connection, and even in patients for whom the symptom met presumptive literature-based criteria for probable or definite drug-adverse effect causality. Assuming that physicians would not likely report ADRs in these instances, these patient-submitted ADR reports suggest that targeting patients may boost the yield of ADR reporting systems.
Conclusions: Since low reporting rates are considered to contribute to delays in identification of ADRs, findings from this study suggest that additional putative cases may be identified by targeting patients as reporters, potentially speeding recognition of ADRs.”
That study, in addition to my own real life encounters of folks that have had a bad statin experience has formed my opinion regarding that class of drugs.
I accompanied a cardio patient to an appointment. The cardiologist told me he has seen “hardly any” adverse statin events. My answer to him, “Then you are not looking very hard, or something is obscuring your vision. Have you considered seeing a Proctologist?”
In defense of cardiologists, it was one that told me to ditch the statin. I wasn’t there because of actual heart problems, I was referred because my health had declined while on the statin to the point my primary said I had developed complete heart failure, and didn’t have long to live. My heart checked out amazingly fine, to the total surprise of the cardio clinic.
My primary has since told me he has seen “more and more” cases of statin problems, but most are recovering as he takes them off the drug immediately”….guess I was the canary in the mine.
I do realize what you are saying about bias of like minded folks that gather online with similar experiences.
But I’m here because of what I have observed in the real world.
You said you do advise Co Q10 for statin problems. Is there is anything else you recommend, for nerve and muscle damage? I hope it’s not inappropriate to ask, but the neurologists around here haven’t been much help.
pec,
You’re not paying attention. These issues have been fully addressed. Please go back and read more carefully. This is not the first time you have misunderstood or missed what was really said.
To quote from my article above, “It’s not entirely clear whether the risk reduction with statins is due solely to the lowered cholesterol; statins may have other beneficial effects. But at least it appears that the degree of risk reduction can be measured by the degree of cholesterol lowering.”
Of course medical researchers are not “entirely satisfied with their assumption that cholesterol is the culprit.” No one assumes that cholesterol is ‘the’ culprit, but it is definitely involved and it is perverse to deny that it has anything to do with heart disease as the cholesterol skeptics do. Research is ongoing. We know inflammation is involved. We are rapidly refining our knowledge.
Hyperinsulinism is not “the major cause of heart disease” – wherever did you get that idea? Have you been reading the pseudoscientific nonsense on Mercola’s website?
great to see a neurologist on this blog—am acquainted with 8 individuals diagnosed with Parkinson’s disease who all attribute their disease to lipophilic statin therapy. given the Phase IV studies of megadose coenzyme Q10 for early PD, would one not suspect lowering coq10 via statins is not a good idea?????
Admittedly I have not read every article in every journal (but i’ll go to medline in a minute), but I’ve never heard of Parkinson’s or Parkinsonism being caused by statin therapy. Ever. There’s not even a way to try to explain that.
Do you have any data to go with that, because it would be pretty earth-shattering.
PMID: 17177184 [PubMed - indexed for MEDLINE]
PMID: 15734664 [PubMed - indexed for MEDLINE]
http://www.bmj.com/cgi/eletters/325/7369/851
I would like to bring the discussion back to the original article, in which Harriet Hall gratuitously rubbishes THINCS as folk who set themselves up as being more smart than doctors. There are some members who have personally contributed greatly to the knowledge of what statins really do. Is disagreement with less than perfect research to become a subject for ridicule? Free speech is a vital ingredient of any walk of life.
Dr Langsjoen’s “Introduction to Coenzyme Q10″ is one of the few sources of information on this subject, his father was associated with Dr Karl Folkers, who when at Merck, first synthesised Q10 and discovered that statins reduced Q10 levels. The mainstream medical journals would not publish the papers, the dead hand of drug financial power lurks in the background, and Folkers spent the rest of his life touring Europe to get the message across unaided.
Dr Langsjoen is a cardiologist, specialising in non-invasive techniques, and has stated that he sees 2 or 3 new cases of statin induced cardiomyopathy each week. With others, he has done trials where the levels of Q10, heart ejection fraction, flow velocity and other important factors in affected patients before and after using Q10 have been carefully recorded. The benefits are indisputable. However, these are dismissed by his critics as having insufficient power compared with the expensive major statin trials. In my book, a handful of carefully made measurements is of far greater value as evidence than thousands of trial reports solely looking for symptoms, where no measurements had been made of Q10 or carnitine levels, which are the major factor in statin side effects. Even the CPK limit suggested in some trials (10x normal) is too high to show up incipient muscle wastage, mine was serious at twice normal, and far too low to denote rhabdomyolysis. I have been in contact with people with figures in the thousands.
I thank God for Dr Langsjoen, my life would have ended 5 years ago without his knowledge so published.
Then there is the remark which you made about Uffe Ravnskov mixing up dietary and serum cholesterol. In his book, he tells how he ate eggs each day, increasing the daily total until he got up to 8 eggs per day, meanwhile measuring his own cholesterol, which was actually lower on the highest egg consumption. He did this just to show the LACK of connection between dietary and serum cholesterol. I wonder how many professional researchers would undertake such a personal approach to their work.
I think you owe the THINCS members an apology for your offensive remarks about them, such treatment of a group of people who are doing their best to counter the excesses of medicine which HAS to be believed because of the intensity and so often repeated message “Statinate or die”
The failed ENHANCE trial, where cholesterol level lowering had some negative effects, should also give food for thought and encourage a wider vision of cardiovascular problems.
[Hyperinsulinism is not “the major cause of heart disease”]
Of course it is Harriet. Where have you been? Insulin resistance, in type 2 diabetes, results in high insulin levels. Type 2 diabetes is known to be the leading cause of cardiovascular disease, and it is not at all ridiculous to think that high levels of insulin in the bloodstream contribute.
And by the way, you call the cholesterol skeptics pseudoscientists and then admit they do have a point — the assumption that cholesterol causes heart disease is not supported by scientific evidence. So maybe they aren’t complete fools?
@ jaymcee
one reference is a letter, and not a great one.
One is a preliminary study with conflicting conclusions (“Thus, our data provide preliminary evidence that low LDL-C may be associated with higher occurrence of PD, and/or that statin use may lower PD occurrence, either of which finding warrants further investigation”)
The other was a negative study (“Statins although they may affect Co-enzyme Q10 levels in the body and the brain, do not worsen PD at least as assessed by stage, and prevalence of wearing-off, dyskinesia, and dementia.”)
@PalMD
Just a little to add to the point of PD
I have a friend who has Parkinsons, and has been taking Q10 in an attempt to stave off deterioration.
I take a lot of Q10 myself, but only the best Kaneka manufactured type in the capsules gives me certainty of satisfactory dosage, I have tried many different brands, with less success. I had bought 2 packs of 300 mg Q10, but found it was not working well. I did not wish to waste it, so I gave it to my friend to add to his dose, as the higher dose the better in his circumstances, according to trials which have been made.
He did this, and in just a week, his wife told me he went up the stairs without using the stairlift, and he has been able to swallow his food much better. I realise that this may only be a transient or “placebo” like effect, but if Q10 makes such a difference, is it not a corollary that reduction of Q10 through statin use could worsen the condition.
(As far as I am aware, he has not taken statins.)
@ PaIMD
[quote] but I’ve never heard of Parkinson’s or Parkinsonism being caused by statin therapy. Ever. There’s not even a way to try to explain that. [unquote]
[quote] one reference is a letter, and not a great one.
One is a preliminary study with conflicting conclusions (”Thus, our data provide preliminary evidence that low LDL-C may be associated with higher occurrence of PD, and/or that statin use may lower PD occurrence, either of which finding warrants further investigation”)
The other was a negative study (”Statins although they may affect Co-enzyme Q10 levels in the body and the brain, do not worsen PD at least as assessed by stage, and prevalence of wearing-off, dyskinesia, and dementia.”) [unquote]
I had provided a few links to articles that addressed the possibility of the association between statins and Parkinsonism. Now you have heard of it and you can choose to ignore it or to do your own research. Your complaints about the quality of the links provided, are irrelevant within the context I had provided them to you.
Harriet thinks the cholesterol skeptics should be ignored. She insists that cholesterol is involved in heart disease, but can’t tell us if it has an important role. She can’t admit that the cholesterol skeptics are doing everyone a great service by pointing out that the connection between heart disease and cholesterol is far from clear.
Harriet would like us to be trusting sheep and follow the medical industry’s recommendations. Since we do not have medical degrees, she thinks, we are incapable of thinking for ourselves. Trust the experts is her message.
I have a Ph.D. and, although it is not in medical research, I am capable of noticing confounds in medical research. Sometimes I can see it better than MDs, since most MDs are not Ph.D.s and have no direct experience with statistics and methodolgy.
But even if I had no direct research experience or advanced education, I would still be capable of reading and thinking. Sometimes non-MDs have more common sense than MDs because they have not gone through the subliminal brain-washing of medical school.
http://money.cnn.com/2008/02/04/technology/simons_cholesterol.fortune/index.htm
“Anti-cholesterol drugs are a $36 billion segment of the world’s second-most profitable legal industry behind Big Oil. Roughly, 19 million American adults take a cholesterol-lowering medicine of some kind. And according the most recent National Cholesterol Education guidelines – the suggestions most doctors adhere to – about 36 million Americans should be on some form of statin therapy.”
“The national guidelines state that use of a statin to reduce LDL cholesterol is recommended for people at high or moderately-high risk of heart disease. People in the high-risk group should aim for a LDL cholesterol count of less than 70 mg/dL, and those in the moderately high-risk group should have a count between 129 and 100 mg/dL.
The guidelines were published by the National Cholesterol Education Program (NCEP), a branch of NIH’s National Heart, Lung, and Blood Institute. Critics of the drug industry claim that the guidelines themselves are biased toward drug therapy because a majority of the medical experts who drew up those suggestions have financial relationships with drug companies.”
“As with so much health science, it may be years before doctors and patients receive more data on just how useful it is to reduce cholesterol – and even then it may not be definitive.”
BE SKEPTICAL NOW.
“I had provided a few links to articles that addressed the possibility of the association between statins and Parkinsonism. Now you have heard of it and you can choose to ignore it or to do your own research. Your complaints about the quality of the links provided, are irrelevant within the context I had provided them to you.”
Sorry. I was simply pointing out that the references cited, while containing the words “Parkinsons” and “statins” did not provide any evidence of a connection.
They did however provide me with a context to understand the earlier comments, which I appreciate.
http://www.businessweek.com/magazine/content/08_04/b4068052092994.htm?chan=search
“the statin trials of people without existing heart disease showed no reduction in deaths or serious health events, despite the small drop in heart attacks. “We should tell patients that the reduced cardiovascular risk will be replaced by other serious illnesses,” says Dr. John Abramson, clinical instructor at Harvard Medical School and author of Overdosed America.”
http://www.businessweek.com/magazine/content/08_04/b4068052092994_page_6.htm
Oh look Harriet — I’m not the only one saying that statins prevent heart attacks by decreasing inflammation, and cholesterol is irrelevant.
“current evidence supports ignoring LDL cholesterol altogether,”
I wish my med school profs had told me that business week was such a good source for all my medical information.
Ill make a note..
“I wish my med school profs had told me that business week was such a good source for all my medical information.
I’ll make a note..” PalMD
If you didn’t know about that, you shouldn’t be so flip. And don’t overlook People Magazine and the National Inquirer.
Can somebody tell us how to do the distinctive quotation here (the big, blue mark?
Sometimes it’s easier for outsiders to see that the emperor has not clothes. Besides, the article has plenty of expert testimony. You might try reading it.
Science… for anyone who may be interested
Statin-Associated Myopathy with Normal Creatine Kinase Levels
http://www.annals.org/cgi/content/abstract/137/7/581
Pfizer Stops All Torcetrapib Clinical Trials in Interest of Patient
http://www.fda.gov/bbs/topics/NEWS/2006/NEW01514.html
Cardiovascular risk estimation: important but may be inaccurate
http://www.bmj.com/cgi/content/full/332/7555/1422
Statins and risk of polyneuropathy: a case-control study.
http://www.ncbi.nlm.nih.gov/pubmed/12011277
Serious Adverse Event Analysis: Lipid-Lowering Therapy Revisited
http://www.ti.ubc.ca/node/58
Carcinogenicity of lipid lowering drugs
file:///Volumes/Cyclops%20II/files%20from%20Cyclops%20II/THINCS/Statins/Entrez%20PubMed4.webarchive
Heme deficiency selectively interrupts assembly of mitochondrial complex IV in human fibroblasts: Relevance to aging
http://www.jbc.org/cgi/content/abstract/M108362200v1
The Role of Heme and Iron-Sulfur Clusters in Mitochondrial Biogenesis, Maintenance, and Decay with Age
http://www.ncbi.nlm.nih.gov/pubmed/11795893?ordinalpos=10&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum
Heme deficiency may be a factor in the mitochondrial and neuronal decay of aging
http://www.pnas.org/cgi/content/abstract/99/23/14807?etoc
Heme, iron, and the mitochondrial decay of ageing
http://cat.inist.fr/?aModele=afficheN&cpsidt=15943712
I’ll try once more to make my point, although I fear that the emotions and biases of my critics will make it impossible for them to understand.
I have no agenda. I have no bias for or against cholesterol or statins. I have done my best to look at the evidence objectively, and I have found no support for the claims of THINCS that cholesterol has nothing to do with heart disease, that low cholesterol is harmful and high cholesterol desirable, or that statins cause cancer. It seems clear to me that THINCS is not considering the evidence objectively, and that there are logical flaws in their arguments. There is some truth in some of their arguments, and I have said that.
There are many unanswered questions about the heart disease/cholesterol/statin connection. The medical scientific establishment is doing a pretty good job of asking questions on its own, without any need for prompting from activist groups. I will continue to follow the evidence wherever it leads. I will try not be swayed by horror stories and testimonials or by opinions.
“I have found no support for the claims of THINCS that cholesterol has nothing to do with heart disease”
Right Harriet, you are absolutely correct, on the most literal of levels. If THINCS says that cholesterol has NOTHING TO DO WITH HEART DISEASE, they are wrong. It has something to do with heart disease. But it doesn’t cause it. And lowering cholesterol in many or most cases does not to prevent it.
You found something THINC is wrong about. Great for you! But you steadfastly ignore everything they are RIGHT about, and everything we have been deceived about.
You should be a public relations spokesperson. Have you considered working for the tobacco industry?
Hmm…someone clearly isn’t a fan of Haldol.
@ PaIMD
[quote] Hmm…someone clearly isn’t a fan of Haldol. [unquote]
An in joke if you are a medic (albeit rather tasteless) and an insult if you are not.
Was that really necessary?
“The growth of knowledge depends entirely on disagreement”
(Karl R. Popper, 1902-1994)
Despite a shaky start, I had thought it possible to make further progress. One could perhaps be forgiven for assuming that medics were; individuals who were worthy of the esteem that society holds them in and by and large that they are intelligent, compassionate beings.
You have already seen that I am rather swift to anger. I have been around the block more than once and have a very accurate BS meter. I have no problem with using the same literary coin as an adversary, especially when it emanates from ignorance.
In this case I will make an exception and refrain from replying in kind to your unkind comment to pec because there will be never be progress if you cannot keep this type of juvenile comment out of the discourse. In another life, I too could make smart-arsed remarks and think them funny… this is neither the time nor the place.
I would sincerely hope that is an end to it for further progress depends on consensus to abide by rules and a combative stance is the end of civil discussion. If you wish to withdraw from the debate then say it aloud so that we all can understand it. Don’t dress up your unwillingness to face the issues (that the opening post has raised) as puerile humour.
Excuse the ad hom, but there is no discourse when one of the parties has fixed, false beliefs.
Jayemcee says, ” there will be never be progress if you cannot keep this type of juvenile comment out of the discourse…
I would sincerely hope that is an end to it for further progress depends on consensus to abide by rules and a combative stance is the end of civil discussion.”
After the ad hominem insults he spouted at me (above) this is really rich! Talk about the pot calling the kettle black!
He has missed his calling as a comedian.
[quote] I’ll try once more to make my point, although I fear that the emotions and biases of my critics will make it impossible for them to understand. I have no agenda. I have no bias for or against cholesterol or statins. [unquote]
Your summary dismissal of Dr Ravnskov’s work would suggest that you do have an agenda and a bias, especially when combined with some of the content from some of your numerous blog entries.
[quote]I have done my best to look at the evidence objectively, and I have found no support for the claims of THINCS that cholesterol has nothing to do with heart disease, that low cholesterol is harmful and high cholesterol desirable, or that statins cause cancer.
[unquote]
The small list of scientific references which I have provided may point you towards some areas of special interest that you have not yet considered. The last 4 references are highly detailed technical papers, from the widely regarded Professor Bruce Ames and co-workers, about the impact on cellular life when there is disruption in the cycle of processes involving heme a.
The mevalonate metabolic pathway is where heme a is synthesised. This is the exact same pathway where cholesterol is inhibited by statins. Heme a is only found in the mitochondria and when it is depleted, apoptosis (programmed cell death) and premature aging appear to be the logical outcome.
Pfizer’s had stopped their phase 3 clinical trial of the compound atorvastatin/torcetrapib. Not because they had especially wanted to do so but because the independent monitor (DSMB) had noticed the number of deaths associated with the compound on trial and had informed Pfizer.
Luckily, the link to the FDA notice of the closure of the trial on December 3rd 2006 has never been removed, in contradistinction to the notice of cessation on Pfizer’s website, where a copy of the document (with similar wording to the FDA document) announcing the cessation of the trial had stayed visible for around 24 hours. One could say that Pfizer were burying bad news… literally as well as figuratively in this case.
[quote] It seems clear to me that THINCS is not considering the evidence objectively, and that there are logical flaws in their arguments. [unquote]
Here we will have to disagree. I have been in contact with many of the members of the THINCS group. I find them to be a caring group of people who have the best interests of patient at heart. I see that they want to halt the sheer madness that shouts ‘statins for life for everyone’, so as to prevent yet more terrifying cases of iatrogenic damage that is so ably demonstrated by the statinated populace.
[quote] There are many unanswered questions about the heart disease/cholesterol/statin connection. The medical scientific establishment is doing a pretty good job of asking questions on its own, without any need for prompting from activist groups. [unquote]
It don’t understand why a well paid group of clinicians would jeopardise their careers, face the misplaced opprobrium of the profession and lose their clinical friends through isolating themselves by taken a controversial stance on statins. The activist group would suggest that they are fringe clinicians with nothing to offer other than snake oil. why would they inhabit that uncomfortable space?
The answer may lie in the viewpoint that they are ashamed of the way the profession has been subsumed into the maw of the pharmaceutical manufacturers. Furthermore, that for a fat consultancy fee or the promise of a research grant, be willing to prostitute the profession and say what the drug company bosses want to hear.
When I was younger, systolic hypertension was calculated by the following formula… your age plus 100. Today anyone with a systolic reading of 130 is almost abnormal. Total cholesterol reading guidelines have also fallen… soon it is likely to be 4.0… more statins and lets have then put in our drinking water, courtesy of the the unfortunately named Dr John Reckless.
Is it any wonder that concerned clinicians should want to be anti-statin activists?
[quote]I will continue to follow the evidence wherever it leads. I will try not be swayed by horror stories and testimonials or by opinions. [unquote]
I guess that on its face you have espoused a truly laudable aim and it is certain that scientists will agree with you and applaud your position. The horror stories ought to sway you for they are the stories of the mounting pile of corpses and permanently statin-damaged people, who trusted their medical practitioner to care for their health and who will never be able to get your attention any other way. Ignore them at your peril.
Holding stubbornly to a suspicious view of statins (based on their proven side effects, high NNT, carcinogenicity in animal studies, and near-total lack of evidence of efficacy in women and the elderly) is not the same as holding, say, to a positive view of homeopathy (based on no facts at all). It’s more comparable to holding stubbornly to a rosy view of statins despite the abovementioned facts. Of course, I see in reading the homeopathy threads that believers in that practice are being called not just deranged and incapable of discourse but “psychopaths” and “bloodsuckers,” so perhaps jayemcee can console himself here with the thought that the attacks on his character have been pretty mild by quackbuster standards.
OTOH, jayemcee, if you don’t mind my pointing it out, you addressed Harriet Hall in similar tones above and called her belligerent (which she may be) and a charlatan, which reduces your ability to grouse about ad hominem attacks. I too have a good BS detector and a short temper, but let’s both try to maintain a higher rhetorical standard than is resorted to by some of the anti-CAM writers on this site. When you let them get your goat, it only makes them happy.
pec,
I wrote: “There is some truth in some of their arguments, and I have said that.”
You answered: “you steadfastly ignore everything they are RIGHT about”
Can you see any discrepancy there? I’m sure everyone else can.
Raygee:
“In his book, he tells how he ate eggs each day, increasing the daily total until he got up to 8 eggs per day, meanwhile measuring his own cholesterol, which was actually lower on the highest egg consumption. He did this just to show the LACK of connection between dietary and serum cholesterol. I wonder how many professional researchers would undertake such a personal approach to their work.”
Dietary cholesterol has little if any effect on blood cholesterol. Eggs are very low in saturated fat. Eggs are high in lecithin. Lecithin binds sterols in the gut, blocking absorption.
This is why the advice to cut down on egg consumption is wrong. The average Japanese eats 6 eggs per week and they avg. a total cholesterol of 135.
If I may, I suggest uncaged hens and eggs fed omega 3s.
@ Harriet Hall
Further back in the thread, you remarked that personal stories generated more heat than light.
Would you not expect someone whose life was permanently altered for the worse by statin use to be angry and have strong views on the cause of their downfall, and do all in their power to help others avoid falling into the same trap.
Surely it should be of the utmost concern for doctors to get to grips with methods of ameliorating the situation. Being medically qualified is assumed by many to mean that a doctor will have up to date knowledge of the operation and dangers of new drugs and their causes, for a universal medication programme like statination, one could be forgiven for believing that this is essential.
I spent my working life in telecommunications, one still had to wind the handle to call the operator when I started, but we obtained our qualifications in the appropriate branches of technical knowledge and went on our way. But technical progress was continuous, and career long study was necessary to keep abreast of current practice.
Is it not a little arrogant for doctors to presume that their qualifying knowledge is sufficient to cope with the problems set up by the many side effects of ever more system interfering drugs, with only the drug reps advice, as time goes on in their careers. Deeper understanding of the more molecular functions working within, as for the Krebs cycle, are needed when such basic processes are subject to interference from such things as statins and beta blockers, to name but two.
Should it not be a priority for them to take the lead in searching for answers, and not besmirch the names of those who really are trying to stem the tide of the multi billion dollar onslaught.
Why is it that an octogenarian such as I has to study the relevant portions of biologolical knowledge to point statin damage sufferers to hard-to-find information which can actually help them. why are there not hordes of doctors doing their utmost to help, instead of hiding behind totally irrelevant trial statements that such problems are extremely rare, and treating such patients as an embarassing statistical unit.
Is not Farmgal, consigned to a wheelchair at 40 to be allowed to have her voice heard, or myself, struck with great weakness just as my dear late wife became affected by Alzheimers, with only me to care for her. One has to accept naturally occurring problems, but to dealt such a blow by a “safe”medication purporting to preserve one against one risk, when the makers already knew how and why damage occurs but did not reveal it, and the moguls of medical research and regulation did not pick it up, in spite of Dr Karl Folkers’ message, is beyond belief in such an advamced society as we have today.
More individual efforts should be made to avoid continuing fresh dangers, and the efforts of those fighting against the brainwashed tide of profit motivated statin pedlars, should be applauded, and not trampled underfoot.
@ PaIMD
[quote] Excuse the ad hom, but there is no discourse when one of the parties has fixed, false beliefs. [unquote]
Excused.
Technically speaking, you are correct about the nature of discourse and fixed and unshakeable ideas may seem to be vexatious and underpinning vacuous notions but the opportunity to change them is ever present.
Belief is, on the other hand, a word that summons religion to my mind and when that way is followed then surely madness is the likely corollary.
Disagreement is healthy for it is the agency by which we can all learn. Perhaps wisdom is knowing when persistence is no longer a useful attribute.
@ Dr Hall
[quote] After the ad hominem insults he spouted at me (above) this is really rich! Talk about the pot calling the kettle black!
He has missed his calling as a comedian. [unquote]
Where I come from it is a perfectly reasonable act to highlight gratuitous vitriol. I did that by means of using the same methods as you. The difference between us is that you are not particularly talented in the use of the gratuitous insult.
Regardless of the bad start we had made, I still want to persist with moving the debate on the value of statins and the cholesterol/heart hypothesis forward. I had made my comment to PaIMD because the Haldol comment implied (at the least) that pec was suffering from schizophrenia, psychosis and delirium and possibly Tourettes. All patently false and all deeply insulting. The overall thrust of the comment was that pec was mad and had no insight into that fact.
Later, PaIMD asked for the comment to be excused, and I have done so because it was accepted as an unnecessary comment by PaIMD. It wont prevent me from addressing any points that are made about statinisation nor will it prevent me from responding to PaIMD if I am addressed. I don’t believe that PaIMD is Satan because of one moment of thoughtlessness. See! Progress.
You professing not to care then having another dig at me when a suitable moment presents itself, speaks loudly. I have stated that I had made a bad start and that I was not behaving well when I had responded to your first post… and the argument that “you started it” would not wash in any civilised circle. I was responding in an intemperate way because your casual dismissal of an earnest and highly regarded scientist was based in nothing but your personal prejudice.
you said…
1. “Its members “thinc” they are smarter than the average doctor.”
2. “They “thinc” that cholesterol has nothing to do with cardiovascular disease and that we have been deluded into waging a “cholesterol campaign” for which the scientific evidence is non-existent.”
3. “They tell us about those contradicting studies; but they don’t tell us about the flaws in those studies, they misrepresent some of the results, and they don’t tell us about the many good studies that support the cholesterol/heart link.”
4. “As far as I can see, these folks have cherry-picked the literature to support an agenda. They seem to have a vendetta against statin drugs in particular.”
5. “It provides “what the medical journals and newspapers won’t let you hear” – letters and papers that have been rejected for publication.”
6.”These statements are not only false, they are potentially dangerous to the health of those who believe them.”
The numbered clauses were written by you as evidence of your science. Any rational being would dismiss your commentary as emotional vitriol bereft of scientific merit.
The fact that they are gratuitously vitriolic comments with not one iota of scientific merit, is precisely what had raised my ire. That you had sought to tar all of the THINCS membership with the one brush you had chosen to wield (to execute Dr Ravnskov) was inexcusable.
If you want to address the science references which I have provided, I am more than willing to put our bad start behind us. If you wish to drop back into your mindless fishwife mode, just so you mete out whichever further punitive measures that you think I richly deserve, then do so, but please don’t be surprised if I refuse to tolerate your intemperate haridan personna.
Just to throw it out there, one of the points made by the “skeptics” seems to lead to a difficult contradiction.
We have always known that LDL levels are not the whole story, but at least a marker.
We know there are subsets of patients who benefit from statins regardless of LDL levels (those with DM or CAD).
So, I certainly agree that LDL is not the whole story (as would any physician), and we know that partly because there are patients who benefit from statins despite low LDL levels.
This, of course, seems to mock the basic idea of the “skeptics” that statin=bad and no evidence can show otherwise.
@ PaIMD
[quote] Just to throw it out there, one of the points made by the “skeptics” seems to lead to a difficult contradiction.
We have always known that LDL levels are not the whole story, but at least a marker. [unquote]
My thought is that a simple question and answer and the discussion anent the scientific support would clarify aspects of the debate. I may as well begin.
What are the mechanisms responsible for varying the serum levels of cholesterol in individuals?
PalMD
[quote] This, of course, seems to mock the basic idea of the “skeptics” that statin=bad and no evidence can show otherwise. [unquote]
Dr Malcolm Kendrick, who I believe is a member of THINCS, quite clearly states in his book, “The Great Cholesterol Con”, that if you have heart disease he strongly recommends you take a statin. So I do not think that the members of THINCS are totally against statins. What they are totally sceptical of is the cholesterol theory of heart disease. It would be dangerous of anyone to tell CAD sufferers to not take statins when we know there is a benefit to these people. (this benefit can be seen within days of starting the treatment. This strongly points to s statin effect totally unrelated to cholesterol lowering).
[quote] So, I certainly agree that LDL is not the whole story (as would any physician), and we know that partly because there are patients who benefit from statins despite low LDL levels [unquote]
I wish one of these physicians would speak to my cardiologist. As far as he’s concerned LDL is THE cause of heart disease.
On a slightly different issue, it seems to me that the scientific community is only interested in developing drugs that lower cholesterol and do not seem to be looking at anything else. I think we are all agreed here that cholesterol is only part of the story but this does not seem to be interesting the pharmaceutical companies. What worries me is that because of this stance the cure for heart disease might be further off than it needs to be.
That’s a great question…i’m going to wait and see if one of my betters answers it first, so that I won’t look too foolish…
@PalMD
I am concerned that you do not recognise the unpredictable nature of the occurence of statin side effects, the reduction of other essential products in the mevalonate pathway when cholesterol is reduced can cause problems at any age and early or late in the treatment process. The fact that essential factors in the production of ATP for energy are depleted means that whatever function’s mitochondria is starved of energy that is also unable to function. The multiplicity of cells performing the same duty means that the loss of the odd one might be tolerable for the time being, but should by chance a large proportion of the same function become deprived at the same time, disaster!!
The effects are more likely to occur in older patients, because their supply of Q10 is decreasing naturally, and so insufficiency will be felt sooner. I feel so strongly that this effect may occur anywhere, thyroid problems are mentioned on wustl university website, there is definitely an effect on diabetes, and the possibility of bringing forward macular degeneration has been noticed elsewhere, and has been passed to Cochrane to investigate.
Heart failure symptoms can arise, as in my case, not because the muscle is damaged, but because such a large quantity of ATP is needed to supply pumping energy, (1000+ mitochondria per muscle cell) and angina and raised Blood Pressure occur. Muscle problems can arise from carnitine supply damage, giving either muscle wastage, or severe pain due to the inabilty to take away the products of energy production, causing lactic acidosis.
Peripheral neuropathy is also fairly common, but also difficult to deal with, often persistent, and carpal tunnel type symptoms.
These problems are often thought to be natural occurences, and the usual treatment applied , without success.
I am afraid that the possible and actual effects are almost endless, but are so often seen in those asking for help on appropriate websites. The officially listed side effects are not the whole story, but fortunately, supplementary Q10 and/or carnitine may help, but are often a permanent necessity.
That’s all lovely, but the data doesn’t support your hypotheses
I’m thinking perhaps I was remiss in not giving specific examples of the kind of distortions promulgated by THINCS. I covered many of these in correspondence in Skeptic magazine and on the JREF forum.
THINCS member Kauffman said, “cholesterol is highly protective against cancer, infection and atherosclerosis.” His reference for this is not supportive data, but a speculative piece by Ravnskov entitled “High Cholesterol MAY protect against infections and atherosclerosis.” Cancer is mentioned nowhere in the referenced article.
He cites a plaque progression study as evidence against statins but neglects to mention that all patients in the study were already on statins because the authors recognized their efficacy.
He makes the J-LIT study sound like it shows low cholesterol to be a hazard, yet this study showed a clear relationship between higher LDL cholesterol levels and coronary events, and it did not recommend avoidance of statins, only close monitoring of those whose LDL levels drop very drastically with treatment.
He reports that another study showed statin use could be associated with an increase in mortality of 1% in 10 years; the study actually showed that statin use was beneficial in all but the lowest risk groups. The authors concluded that the risk outweighed the benefit only for the lowest risk groups, and they recommended statins for patients whose overall risk was greater than 13% in 10 years.
These are just a few examples. There are many more. My criticism of THINCS is based on their misrepresentations of evidence and gross errors in logic (which Bob Carroll addresses in Skeptic’s Dictionary). It is not based on my opinions.
While I deplored their thinking, I actually had a rather good opinion of the individuals in THINC after my prolonged polite interactions with Marshall Deutsch. Jayemcee is making me reconsider.
I’d like to throw out a thought for consideration. If we disregard the results of controlled studies in favor of individual reports of harm, aren’t we in danger of giving up a lot of useful treatments and harmless products? The horror stories promulgated by groups like the anti-vaccinationists and the anti-aspartame folks come to mind.
Individual reports are important. After-marketing surveillance is essential. Personal testimonials can point to areas where further research is needed. But sober scientists do not use them as a reason to ban a product until meaningful data can be collected in a controlled fashion.
@PalMD
But what data? There so many reasons, of which I have quoted a few, why the data is incomplete, run-in periods, failure to realise what is a statin side effect, and performance and recording of trials in the hands of researchers dependant on manufacturers finance. I have long observed in many walks of life that if the sponsor/ manager calls for good statistics, he will get them, but the extent to which people will go to produce those figures doesn’t bear thinking about.
There are also trials, as one mentioned by Harriet earlier, where the triallists are not aware of the mechanism by which things come about, it is of no value to examine muscle weakness and statins unless those individuals have been affected in that particular manner.
Letters in the BMJ note that trial results often show favourable outcomes for the drug being sponsored.
Until there is much more transparency in studies and research, or a completely independent body to carry them out and oversee them, they are often little more than sales promotion operations
@Harriet
I am in full favour of properly organised and in depth trials, and would support the outcomes if, and only if, they are carried out by organisations without reliance on the manufacturer for some of their income. In UK, a parliamentary select committee reported that 70% of drug research was financed by industry,. Now that might mean all institutions relied on getting 70%of their income that way, or at the other extreme, 70% of them relied 100% upon it. in the first instance, the use of their independant income for projects not in line with their major sponsor’s wishes, could jeopardise the larger part. There are many stories of the heavy hand being used or threatened, and there are large numbers of departments and careers which could be threatened.
I suppose the great ogre is the drug industry, with financial power enough to challenge governments. The Codex Alimentarius committee, reportedly made up of drug industry employees, has managed to get the WHO/WTO to try to force all nations to regulate or ban many non drug supplements, carnitine needed for statin damaged folk is only available on prescription in Canada. If that were the case here, my £10 per month supply would cost £700, and nemesis would once more loom.
Raygee,
I share your concern about biased researchers, but I don’t think it is fair to automatically dismiss studies just because they get some or all of their funding from pharmaceutical companies. Most scientists try hard to do good research because their reputations and future funding depend on it. I don’t think the drug companies could suppress important data for very long no matter how hard they tried. Remember Phen-Fen? – it didn’t take long for the information to get out and the drug to be taken off the market.
And there is coherence in the data from different sources and different lines of investigation. I’m keeping an open mind, but I’m not willling to throw out all the existing research unless we can find clear evidence of fraud.
BTW, this is the best blog EVER.
Hi Harriet,
I don’t think I can make the leap, “individual reports of harm” to “harmless products”. If they are in fact “harmless” where do individual reports of harm come from?
I have to tell you, I relied on the FDA and many statin studies that I read to be assured they were in fact, quite safe.
I was told that regular blood tests to monitor for any liver or muscle problems would add an extra layer of safety, so how could I go wrong taking it? I never had a single blood test that indicated a problem, and ended up in this mess anyway.
I even heard of doctors taking statins “off lable” cause they were such a great, wonderful, and SAFE drug.
Even with everything that happened to me personally via statin therapy, I would not be here, if I thought I was in fact a “RARE” case.
It is all the other accounts, in real life, that makes it quite obvious, statins are not “harmless” by any stretch of the imagination.
Most of the people I have spoken with about their statin experience did not stop taking them after just one negative outcome. They have been urged by their doctors to try again, some folks have been on every brand of statin available. In other words they have been “rechallenged” several times with the same results.
Some of us out here in lay person land, do rely on something called “common sense”. If it quacks like a duck, walks like a duck, and poops duck poo on my sidewalk, I don’t need a DNA study to call it a “duck”.
And I have to wonder, of those particpating in this discussion defending the statin class of drugs, how many are taking statins. For how long? At what dose?
And please, don’t say you don’t need a statin, because your cholesterol is fine. With the lower and lower cholesterol targets, it would be a rare individual indeed, that would be exempt from the statin recommendation.
I would hazard to say that those pointing to statin studies to tout how safe and beneficial statins are, have not ingested a single statin dose.
I have read some very good arguments and seen a lot of valid points being aired, what I cannot see is the reason for the Dr’s responding so harshly or treating what has been said as unimportant to what they have to say or want to hear.
Statins have been prescribed for many years now, if it wasn’t for people like the Doctors in Thincs or sites like Spacedoc.net and others bringing the problems out in the open, many people like myself would be much worse than we already are after years of statin therapy.
As far as Doctors knowing about the side effects of statins, you just do not know how wrong you are!
My doctor and other specialists I have seen have only just started to realise that there is a connection between statins and my problems and that is only because I mentioned what I had found online and one doctor looked into it.
Like other folk who have posted here about the effect that this “wonder drug” has had on them, I also know far too many other people that have had adverse effects from taking them. Q10 and Carnatine as mentioned elsewhere in this blog are a great help but can be expensive and it isn’t a cure.
To all of you Doctors,
maybe some of what has been mentioned is not 100% accurate but neither is any of the results that the drug trials state, instead of putting folk down why don’t you open your eyes to what is happening in the real world, maybe your patients would tell you what problems they may be having if you would only listen before dismissing what you do not want to know.
The people at Thincs may not have proven everything they said but at least they went out on a limb to help people to realise that there is a problem.
What have you done that will make a difference to so many real people?
farmgal,
You ask a legitimate question: where are the reports of harm coming from if they’re not due to the drug?
Please note that no one is saying statins are harmless. We all agree that they can harm. The question is how often, and the only way to answer that question is with good science.
Some of the reports are of actual harm from the drug; but some reports may falsely blame the drug for something that it did not do. One of the logical fallacies people are most prone to is the post hoc ergo propter hoc fallacy: I was taking drug X when I got symptom Y, therefore X must have caused Y. They don’t stop to consider that Y might have happened for other reasons. Correlation does not prove causation. If the sun comes up every time the rooster crows, that doesn’t mean the crow raised the sun.
There have been innumerable sad reports from parents of autistic children who are firmly convinced that because they noticed the autism after vaccination, the vaccines caused autism. This has been thoroughly refuted by good science, but the “victiims” refuse to accept the science because personal experience is so convincing.
There are people who are convinced they get headaches from aspartame, but double blind studies have shown that they don’t get headaches if they don’t know they are getting aspartame. People have blamed aspartame for all kinds of symptoms and diseases from insomnia to brain tumors. These symptoms would be occuring in some people today if aspartame had never been discovered. The evidence does not show that they occur any more frequently in people using aspartame than in people not using it.
I mentioned before that muscle pain is a commonly reported side effect of statins, but it may occur even more often in patients taking placebo! Look at any list of side effects of any medication compared to the side effects of the placebo control. If you assumed all reported symptoms were due to the drug without realizing how many might have happened anyway, you would be making a big mistake.
The bottom line is that counting people who have had symptoms after taking a drug is meaningless until you compare them to the numbers of people who have had similar symptoms but did not take the drug. I know this seems counterintuitive, but humans are very prone to misattribution, and the only way to avoid misattributions is the scientific method.
Harriet,
I totally understand and appreciate what you are saying. I am aware of the many issues that cloud the venture of obtaining solid answers.
For me, one thing I hear time and again, is that people have been repeatedly convinced to try another statin. In these cases, when symptoms return upon rechallenging, it become less likely that the statin is faultless.
I do agree with your rooster example. However with rechallenging, it is more like a light switch. ON…symptoms…OFF…no symptoms…ON more symptoms. In this case there is a direct cause and effect between the light switch and the light going on and off.
The best of science is full of peril and the unknown. Since we know more now than any time in history, we tend to deem ourselves pretty superior compared to the day of blood letting as a treatment. In the bigger picture, we are still taking baby steps in our knowledge.
It seems the ability to develop new drugs has outpaced the ability to understand the complex and unpredictable effects on the human body.
When you combine that with, for instance, the recent Vytorin case, it gets very worrisome. There are enough problems with good science, let alone drug companies that manipulate and hide negative results.
Add that to slick marketing, relative risk vs absolute risk, doctors that are blowing off complaints (see study I posted above), then I have to question how accurate the data is when sizing up any drug.
A very wise doctor once told me that “tests can’t think that is my job as your doctor”.
The same applies to study data. But first the data has to be accurate, complete and honest.
“One of the logical fallacies people are most prone to is the post hoc ergo propter hoc fallacy: I was taking drug X when I got symptom Y, therefore X must have caused Y. They don’t stop to consider that Y might have happened for other reasons.”
Medical researchers are just as prone to that fallacy as the rest of us. Statins lower cholesterol so you assumed that lowering cholesterol prevents heart disease. You didn’t stop to consider that statins might prevent heart disease for other reasons.
“It seems the ability to develop new drugs has outpaced the ability to understand the complex and unpredictable effects on the human body.”
That is so true farmgal. The new drugs are artificial substances and evolution has not prepared our bodies to deal with them. Statins interfere with intricate natural processes which are part of a complex network that is very poorly understood by science. When statins interfere with the production of cholesterol they also interfere with the production of other substances which the body needs. We cannot possibly predict how this will effect the body over years or decades.
The current philosophy in medicine is reductionist and often fails to look at the system as a whole. It also tends to focus on treating symptoms rather than searching for causes. And it often neglects to worry about long-term unforeseen consequences.
I do not think the drug companies intend to cause harm and most people who develop drugs probably believe they are serving humanity. But what Harriet does not see is that the natural human talent for self-deception is just as prevalent among medical researchers and MDs as it is among the general public.
Medical professionals and other scientists have a tendency to feel their education has raised them above the common level. They have the power to avoid logical fallacies and to zero in on truth.
But Harriet the sad fact is that all of us, highly educated or not, fall into logical fallacies every day. We all think we know much more than we really do. We are all nearly complete ignoramuses, no matter how we read and think and study. Most of nature is utterly beyond our ability to comprehend.
Yes sure our knowledge increases, but we go from .01 percent of infinity to .02 percent of infinity. Our ignorance is still infinite.
No one has a reason to look down their nose at the non-medical public with its common sense and its logical fallacies. You are an example — with all your medical experience, you still never noticed the logical fallacy of assuming, without evidence, that statins work by lowering cholesterol.
@ Dr Hall
[quote] I share your concern about biased researchers, but I don’t think it is fair to automatically dismiss studies just because they get some or all of their funding from pharmaceutical companies. [unquote]
It comes down to whether it is reasonable to try and serve more than one master. Many studies are completed and the data are taken away for examination and writing up by the pharmaceutical company that paid for the study. Under that sort of arrangement it is unlikely to be a study that is impartial in every aspect.
[quote] Most scientists try hard to do good research because their reputations and future funding depend on it. [unquote]
Finally! We agree on something. Of course, the term ‘good research’ is relative, and it is a variable that is only used by whomsoever is paying for the research. The future funding is also an important issue and will decide what gets left out and what gets included.
Proof? As if it were really required but try this on for size. This is taken directly from the document held by the National Cholesterol Education Program.
The URL is here…
http://www.nhlbi.nih.gov/guidelines/cholesterol/atp3upd04_disclose.htm
This document is a part of the third report of the expert panel on Detection, Evaluation and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III)
It cannot be right that the august expert panel of clinicians that decides what the national treatment guidelines will be are all receiving honoraria, research grants and have been paid consultants and hold stocks in the very drug companies that produce statins and bile acid sequestrants… can it?
Only one clinician had nothing to disclose.
How can these opinion forming clinicians be permitted to speak for the profession and decide on treatment policies when they are receiving pecuniary gains from their secondary paymasters? Just must not only be done but it must be seen to be done and I have no problem with clinicians making whatever sort of living they feel is appropriate.
The right to speak publicly (on matters which they have been paid by pharmaceutical companies to advise the company about) should be automatically withdrawn, as should the right to publish drug company research in any of the medical journals. Think of it as a career choice, where the clinician in question put large sums of drug company money and the elevated status that goes with huge research grants, before healing the sick. It appears to be a reasonable trade-off.
In my experience, senior clinicians are in the perfect position to ensure that the required findings are found.
[quote]I don’t think the drug companies could suppress important data for very long no matter how hard they tried. [unquote] Pfizer’s abandoned atorvastatin/torcetrapib trial in December 2006… that just so happened to kill too many guinea pigs? Please tell me where I can find the data about that trial.
Merck had filed the CoQ10 patent on January 18th 1989. How long has it taken to get the CoQ10 message out to prescribers? If care of humans was a part of their brief, January 18th 1989 would have seen Merck release a press communique telling the world about the value of CoQ10 combined with statins. As it stands, many clinicians have no clue about CoQ10 depletion or its dreadful sequelae.
Presumably plan B was for Merck to market their own combination as gravy train patents began to expire and generics were being permitted. Then an original patent holder (Merck) could have pointed to the inferior generics without the vital CoQ10 added, while holding yet another highly lucrative 20 year patent themselves. Tell me it isn’t so and I will demand my refund from my business 101 class.
[quote] Remember Phen-Fen? – it didn’t take long for the information to get out and the drug to be taken off the market. And there is coherence in the data from different sources and different lines of investigation. I’m keeping an open mind, but I’m not willling to throw out all the existing research unless we can find clear evidence of fraud. [unquote]
Clear evidence of fraud is the list of clinicians advising the NCEP and their disclosed list of ‘interests’. I don’t share your enthusiasm for the speedy withdrawal of faulty drugs as a given. Remember Thalidomide? It was sold during the 50s and 60s for around 4 years. It went under something like 40 different names and it was licenced for sale in something approaching 50 countries.
Yes, you are correct. We can all trust that the drug companies will act swiftly to save patients from harm and the medical profession will rapidly provide the coherent data. ONLY 10,000 children suffered with severe birth deformities. It was a disaster that prompted the US Congress to enact legislation that demanded safety testing before a drug could be prescribed during pregnancy.
@ PaIMD
[quote] That’s a great question…i’m going to wait and see if one of my betters answers it first, so that I won’t look too foolish… [unquote]
Since there has been no other response perhaps you would care to discuss it with me.
I promise not to laugh…
Your rider raises an interesting point. If the very clinicians who are prescribing statins are wary of discussing these issues, is there any way that a patient can make an informed consent to be statinated?
pec,
I am really, really getting fed up with your nonsense. Here you go again: “Medical researchers are just as prone to that fallacy as the rest of us. Statins lower cholesterol so you assumed that lowering cholesterol prevents heart disease. You didn’t stop to consider that statins might prevent heart disease for other reasons.”
I not only stopped to consider it, I have said so several times in my original article and in the comments. Statins have other effects besides lowering cholesterol, including antiinflammatory effects. When the LDL level is lowered with statins, cardiovascular risk decreases. You are free to attach whatever meaning you choose to that, and you may choose to think the lowered cholesterol is nothing but a marker for some other beneficial effect of statins. I wouldn’t argue with that. But the fact that the lower the cholesterol level, the lower the risk is indisputable.
You say, “But what Harriet does not see is that the natural human talent for self-deception is just as prevalent among medical researchers and MDs as it is among the general public.”
I do see it. I not only see it, I know that rigorous use of the scientific method is the only way we can hope to avoid fooling ourselves. In fact, that is the whole point of this blog. How could you miss that? What did you think the blog was for?
pec, I can’t believe you are incapable of reading and understanding simple English. I can only assume you are deliberately pretending to misunderstand and putting up straw men just to cause trouble. It really makes me angry when you say I don’t think something that I just got through saying I think. You have done this over and over. Please stop it.
The Thalidomide numbers were incomplete… must have fallen off the end of my post.
4 years sales is 1461 days
10,000 birth deformities is equivalent to approximately 7 children being born every day for 4 years.
Good job, Grünenthal
Inflammation and heart disease – some reading
Cutting Edge: T Cell Ig Mucin-3 Reduces Inflammatory Heart Disease by Increasing CTLA-4 during Innate Immunity
(from the year 2006)
http://www.jimmunol.org/cgi/content/full/176/11/6411
In search of the grail: the never-ending story of biomarkers for coronary risk prediction
(from the year 2004)
http://eurheartj.oxfordjournals.org/cgi/reprint/25/15/1271
Low grade inflammation and coronary heart disease: prospective study and updated meta-analyses
(from the year 2000)
http://www.bmj.com/cgi/content/full/321/7255/199
Band neutrophil count and the presence and severity of coronary atherosclerosis.
(from the year 1996)
http://pt.wkhealth.com/pt/re/amhj/abstract.00000406-199607000-00002.htm;jsessionid=HnLC3p4nQM9SSG0Tg2WZtLQg3G0GyyqP5BTH96RPTvjBYy2W3qJ1!-809317659!181195629!8091!-1
Thalidomide, like phen/fen, is an example of recognizing a problem and removing the drug from the market in a timely manner. It was a particularly interesting drug, because it was perfectly benign in most patients, and passed initial testing with flying colors. It was even sold over the counter in Europe. The connection to birth defects was not easy to detect, because it was only a danger when taken in a small window of a few days in early pregnancy – between days 20 and 36. Pregnant women could take it with impunity before and after those dates. It was a tragedy, but within a short time it was recognized and appropriate action taken. Teratogenicity studies sound like a good idea, but they’re fallible. A drug can be safe for one species and teratogenic in another. Aspirin is teratogenic in mice and would never have been approved for humans because they would never have learned that it isn’t teratogenic in humans. At any rate, we are now doing better testing, and thalidomide was never approved for marketing in the US, so for once our much-maligned FDA did something right.
I think the thalidomide story just reinforces my contention that if a drug has serious side effects that fact can’t remain unrecognized for long. In both the fen/phen and thalidomide cases, doctors noticed the problem, published reports, and then the drugs were off the market in short order. If there was some conspiracy to suppress the truth, it sure did’t work very well.
Dr Hall
I have recently been told that my cholesterol is high and have come across a multitude of conflicting views about what this means and what should be done about it. Can I just thank you for your sensible, rational approach. It has helped me enormously. Great blog.
I am deeply concerned that this discussion is developing into a bit of a slanging match. Can we try getting back to a factual discussion about Statins, heart disease and potential solutions?
I have CVD and am desperate for the medical world to come up with an answer to the problem. When I was diagnosed with CVD I had none of the risk factors. I was not overweight, my cholesterol was 4.87 (in UK currency) and there was no family history of heart attacks. My cardiologist said I had just been unlucky (not very helpful).
All of this makes me sceptical of the cholesterol theory of heart disease. My own investigations into the subject only raised more questions, rather than answered any. So let’s get back to a proper discussion.
To jayemcee I would like to say I know you have suffered at the hands of Statins (I am not completely enamoured with them either). I have read about your experiences on the spacedoc forum. However not everyone has suffered like you and the rest of the correspondents on that site. Statins, for some people, are their only hope of making it to old age to enjoy their retirement. Until something better comes along we are stuck with them. Also I have to object to this conspiracy theory stance you are taking. I admit there are some dodgy doctors and some unscrupulous companies (a view rather unfortunately borne out of the recent ENHANCE debacle) but on the whole these people are working hard to find solutions to very difficult questions. They do not always get it right (as I believe with the current cholesterol theory) but this does not make them bad people. Yes they need people to question their research and findings but they do not need to be hounded so vociferously.
I am a programmer by trade and so am quite accustomed to writing an application that works fine in my test environment but as soon as I start dishing it out to the customer things start going pear shaped. Some may argue I did not test it enough (and they might be right) but the bottom line is sometimes these things happen. Problems that appear in the real world do not materialise under test. So is the case with Thalidomide from the 60’s. I agree my application going wrong is nowhere near as serious as a drug going wrong, but it does not mean that the scientists and doctors did not do their jobs properly.
So let’s get back to a healthy, friendly discussion.
@ Dr Hall
[quote] It was a tragedy, but within a short time it was recognized and appropriate action taken. [unquote]
I understand what you have said.
The passage of 4 years would seem to be stretching the definition of ‘a short time’.
I accept that there was a small window of danger, with the likely corollary that an adverse reaction of teratogenicity was perhaps initially difficult to ascribe to the drug.
I don’t happen to believe that drug company executives sit around discussing their next scam to make money (well not quite in those terms anyway) but there seems to be a general reluctance to accept the mountains of anecdotal accounts of drug-induced harm that may well provide an earlier warning than current formal reporting systems permit.
In 100 self-reported accounts of statin adverse reactions, I had noticed 5 people complaining of ALS/ALS-like symptoms. This is not a self ascribed diagnosis. It is made by suitably qualified clinicians and it suggests that far more people than the expected number of 2 cases per 100,000 people are dealing with a tragedy.
We could await the advent of well-designed studies that ask and answer a single question and when all of the component parts of this conundrum have been examined and all of the relevant questions asked and answered, we may conclude that statins and their activity may be a pre-cursor of ALS.
How many good research projects and knowledgeable scientists will this take? What sort of time scale are we going to be looking at? How many people will be needlessly damaged by the delay? Instead of dismissing all reporters as cranks and non-scientists, it would behove the medical profession to call for the establishment of a short moratorium on prescribing, while the phenomenon is examined.
I know that there will be people who will claim that this approach may be harming people if we do not let them take statins. Of course, death certificates never say that the cause of death was that the person did not have sufficient statins in their body. It is far too easy (given the specialist knowledge that medics enjoy) to dismiss the words of lay-people.
Perhaps an approach that can respect what the patient says to the clinician would be better. If the patient is talking nonsense, it should be an easy matter to disprove it and to remove any anxieties that the patient may express. On the other hand, if the clinician cannot address the patient’s concerns with science (and be certain that they themselves understand the issues) then warning bells ought to be sounding in the head of the clinician, in my view.
UPDATED: In 300 self reported cases of stain adverse reactions, I have now come across 9 cases of ALS. However I dress it up, it would seem to be excessive. We can argue about RCTs and double-blind trials until we have blue faces. It is futile and it denies (the people who have made these reports) access to our most diligent efforts.
I have not specifically trawled for ALS sufferers and I have not offered any inducement for ALS sufferers to come forward. I am aware of the so-called viral effect of internet information but I don’t feel that is the sole reason why I am seeing what I have seen.
What if the patients are right? Who will prevent further iatrogenic harm. It wont be the drug companies that have only the one interest and that over-riding duty to their shareholders bank accounts. Only clinicians can stop this statin gravy train in its tracks. Dismissing the anecdotes of patients is far too easy.
I would also suggest that it is entirely wrong-headed.
Harriet,
I agree with you that the truth cannot be hidden for very long. I don’t believe in giant conspiracies to fool the public. The results of research eventually come out. And patients talking about their experiences, as on this blog, can also make a difference.
As I have said, I have nothing against science. But unlike you I also respect and consider personal experience. Clinical trials take a very long time and must be extremely expensive.
How many years did it take before they discovered the dangers of HRT for women, for example? Millions of women took their doctors’ advise and went on hormones. I didn’t, of course, because it was perfectly obvious to me that messing with nature has unforeseen consequences. If I were not so skeptical of the reductionist approach, I would have gone on HRT and found out years later that it may have been harmful.
So I agree with you that science is valuable (especially when it avoids reductionism) and I agree that all humans are limited and fallible and capable of self-deception. I do not agree, however, that science saves us from error. We have to use common sense most of the time, while years for research results.
We can’t get all our questions answered by research because many of our questions are not asked, and many others will take years to answer.
Harriet,
I agree with you that the truth cannot be hidden for very long. I don’t believe in giant conspiracies to fool the public. The results of research eventually come out. And patients talking about their experiences, as on this blog, can also make a difference.
As I have said, I have nothing against science. But unlike you I also respect and consider personal experience. Clinical trials take a very long time and must be extremely expensive.
How many years did it take before they discovered the dangers of HRT for women, for example? Millions of women took their doctors’ advise and went on hormones. I didn’t, of course, because it was perfectly obvious to me that messing with nature has unforeseen consequences. If I were not so skeptical of the reductionist approach, I would have gone on HRT and found out years later that it may have been harmful.
So I agree with you that science is valuable (especially when it avoids reductionism) and I agree that all humans are limited and fallible and capable of self-deception. I do not agree, however, that science saves us from error. We have to use common sense most of the time, while waiting years for research results.
We can’t get all our questions answered by research because many of our questions are not asked, and many others will take years to answer.
Again, I’d like to see cardiologists and internists take at least some time driving home the importance of lifestyle change. They should hire a nurse or assistant to do this if they don’t because of time constraints.
And, we’re talking minimal lifestyle change giving one the same results as one can get from statins.
Here’s an example from one physician who couldn’t take statins:
http://health.usnews.com/articles/health/heart/2008/02/06/lowering-ldl-cholesterol-without-drugs.html
Perhaps, Jay, given that your collection of anecdotes has never been investigated by a professional, as far as you or I know, and that millions of cases have been monitored, and hundreds of studies have been done…given that, perhaps your anecdotes are not the best evidence.
The plural of anecdote is not “data”. Modern medical decision making is impossible without statistics.
jay, I have looked and can’t find any evidence to support any association between ALS and statin use. The incidence of ALS hasn’t changed much over the time that statin use became common.
http://www.ncbi.nlm.nih.gov/pubmed/15990445?ordinalpos=187&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum
If the incidence of ALS didn’t change when statins were introduced, than statins are not a cause of ALS.
Given that so many people are taking statins, it is likely that some of them will get ALS. But if there is no increase in the incidence of ALS when statins are used, then statins are not causing ALS.
9 cases of ALS in 300 self-reports of statin adverse reactions? What does that even mean?
If those 9 people had reported auto accidents instead of ALS, would you conclude that statins caused auto accidents? Would you stop to ask how many people have auto accidents when they are not on statins? Would you stop to think that statin takers might have the same incidence of auto accidents but might be falsely attributing them to statins?
It is a gross calumny to suggest that doctors are dismissing patient’s anecdotes. We take them very seriously, but we try to understand what they really mean rather than jumping to conclusions or panicking.
I think we’re all in favor of better post-marketing surveillance programs. But few would agree that unexamined anecdotal horror stories are enough to justify a moratorium on prescribing a drug that is known to save lives.
Responding to above, I prescribe statins based on evidence based guidelines. My biochem is not up to date, but because of my education and background, I can catch up very quickly when needed.
The fact that I don’t keep the minutiae of cholesterol metabolism memorized hardly disqualifies me from prescribing statins, any more than not being an electrophysiologist prevents me from prescribing metoprolol and warfarin for atrial fib.
I’m sorry but the comment was (ad hom warning) idiotic.
@PaIMD
[quote] Perhaps, Jay, given that your collection of anecdotes has never been investigated by a professional, as far as you or I know, and that millions of cases have been monitored, and hundreds of studies have been done…given that, perhaps your anecdotes are not the best evidence.
The plural of anecdote is not “data”. Modern medical decision making is impossible without statistics. [unquote]
I agree that anecdotes don’t constitute data, for they are two different animals. All clinical care is based on the anecdote discussed by the patient, where they are conscious and capable of giving the relevant history of their complaint.
Time and experience may permit the clinician to arrive at a working diagnosis in cases of say… the gross deformity attending a bimalleolar fracture. In such cases the history provides corroboration of the clinicians suspicions. Subtle clinical signs, if unusual, may also alert the well-read clinician to possibilities that would be missed by junior clinicians.
Would, for example, angor (if associated with precordial tightness/pain) direct your mind to the possibility of myocardial infarction, absent a 12 lead ecg reading? A positive apprehension test, when dealing with an account of a presenting complaint history that sounds like a possible dislocation of the patella, would alert a clinician to the veracity of the account.
Taking the patient’s anecdote at face value is unlikely to blind an alert clinician to the underlying problem. I am not sure that I can support the idea that patients will deliberately lie (with notable exceptions that have pecuniary gain, secondary benefits of illness and abuse of drugs) when trying to get a clinician to understand what is happening to them. If people feel unwell, then they would usually want to feel ‘better’ as soon as practicable.
People spontaneously claiming they have developed ALS would seem an odd way to get enjoyment out of life. It is undoubtedly not data but the numbers suggest that something may be happening, that we are just starting to learn about. I wont gainsay it because the possibility of neurological damage being caused by the biochemical action of statin therapy is a very distinct possibility.
The 4 papers that I had referenced earlier deal with cellular destruction that is well within the ambit of statins to create. I have seen no evidence to refute the role of heme a, as laid down by Professor Ames. My crie de coeur is that some system of hearing the patients, that does not rely on the yellow card system or the FDA, is required in addition to the pre-existing systems.
I consider it interesting that statinated patients are complaining of the development of ALS, in what appears to be greater numbers than the incidence rate generally accepted. Hearing that peripheral neuropathy, total global amnesia and ‘foggy’ cognition are all complained about by patients who have been taking statins, it should not be so difficult to consider the small step to thinking about the possibility of catastrophic disruption of the neurological system.
I would stress that this not wish fullfilment on my part and I desperately want to be shown that I am as wrong as it is possible to be… for the alternative is far too horrible to contemplate. The research required is expensive and time consuming and the funding of such an enterprise is unlikely to be easy.
Whither the patients who develop ALS post statinisation and if there is a link, who will protect the patients who will be statinated? The lack of data has these people falling below the clinically significant line, just as in studies that were not looking for whatever malady carried the trial patient off. I can do no more than sound the cautionary bell.
You have created a non sequitur. The point is not that patients are untruthful…Of course, every day medicine is individual encounters, informed by evidence based medicine.
The point is, if I were to use each patients experience to try to form evidence based decisions, I would be doing bad science and bad medicine. EBM informs decisions that you make for individuals and their situations. Individual anecdotes do not, conversely, form data.
Jayemcee repeats his claim that “statinated patients are complaining of the development of ALS, in what appears to be greater numbers than the incidence rate generally accepted” but he has offered no information that would support that claim. Daedalus has offered evidence that would tend to refute it.
No one has suggested patients are lying about ALS. We don’t question that they have ALS; we question whether ALS is more common among patients taking statins.
Just as the “anecdote” of reported symptoms is the beginning of the diagnostic process for individual patients, multiple anecdotes of symptoms in patients taking statins must be the beginning of a diagnostic process to determine whether those symptoms are due to the drug.
jay, the “cause” of ALS remains unknown. The incidence hasn’t changed much during the time that prescriptions of statins went from zero to many millions. If statins were a significant cause of ALS, the rate of ALS would have gone up. It hasn’t gone up, therefore statins are not a significant cause of ALS. No matter how much the symptoms of statin induced muscle damage mimic those of ALS, if there is no change in the incidence of ALS, statins are not causing it.
@ jayemcee,
I have read all of your posts up to the present in this Blog and I am pleased to see someone who is in touch with the real world and what actually is happening to this day when it comes to statins.
The medical profession have had around 20 years to sort out my particular poison and yet here we are today and we are still being made to look foolish by DRs who obviously have not seen past what is selectively laid out for them to read.
Why on earth in that length of time are doctors still unaware of the severity and frequency of side effects and blindly prescribing this rubbish to unsuspecting patients.
When I have read on other sites, the very same symptoms that I have mentioned to my own doctors over the years and seen that the poster’s were also made to believe that it was nothing or you are just getting older etc it makes me very angry.
Most of the papers written from trials for statins and other drugs contradict themselves or have been poorly set out and even interpreted to give a false or rather enhanced outcome.
Remember in years to come when people say can you remember that Doctor who wrote about ????, what a plonker he/she was, always trying to be clever and talking utter rubbish well I think a few of the names I will remember are in this Blog.
My excuse for being sceptical are 1 MI 12 years of Zocor-Simvastatin and a triple bypass and most of the symptoms that come with taking statins (the ones doctors don’t know exist for some reason).
If anyone needs any information about false or misleading results, all you have to do is Google “statin side effects” and plenty of newspapers, TV and Radio reports as well as many sites there for your selection. You will also have access to many Medical sites where the written papers are published.
Even youtube has a Talk given by Dr Malcolm Kendrick and a few others. There are links at THINCS for Dr Malcolm Kendricks meeting of the Leeds branch of the Briish Medical Association
If anyone has not actually looked at the THINCS site and read what is there then you are really missing a lot of good and valid material. Whether you are a supporter of statins or a disbeliever it is a pretty darn good site to see what has gone on in reality and not someone trying and failing to be a critic of any notability.
I hope readers will follow the advice of UK-Bloke to read what is on the THINCS website. I hope they will seek out the original sources that the THINCS folks quote and be able to recognize how THINCS misrepresents those findings by quoting out of context, selective quotation, and putting their own spin on the way they report the studies. I hope they will also seek out the studies that THINCS does not mention, the many studies that refute THINCS’ claims. I hope they will also read what the Skeptic’s Dictionary says about the logical errors of THINCS, and I hope they will consult other independent sources such as The Medical Letter and Wikipedia, which mentions THINCS only briefly as dissenters to what Wikipedia accepts as based on good evidence. http://en.wikipedia.org/wiki/Statins
UK-Bloke’s opinion is obviously colored by his personal experience. Others who don’t share his prejudices will be better able to see that some of what THINCS says is true and some of it is fallacious.
If you are determined to dispute the scientific consensus, THINCS will give you plenty of ammunition (albeit of poor quality). If you are objectively looking for the truth based on the best available evidence, you will almost certainly find some of the THINCS’ claims as ridiculous as I did.
I was criicized for expressing an “opinion” of THINCS, but it’s curious that after I responded by giving specific examples of “facts” demonstrating how THINCS distorted the truth, no one has even tried to refute those facts.
And we’re still being classified as “supporters of statins” or “disbelievers” when most of us are neither. We realize there are both risks and benefits, and we’re only trying to better define the risk/benefit ratio, which is clearly different in different populations of different risk levels.
@ daedelus2u
[quote] jay, I have looked and can’t find any evidence to support any association between ALS and statin use. The incidence of ALS hasn’t changed much over the time that statin use became common.
http://www.ncbi.nlm.nih.gov/pubmed/15990445?ordinalpos=187&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum
If the incidence of ALS didn’t change when statins were introduced, than statins are not a cause of ALS.
Given that so many people are taking statins, it is likely that some of them will get ALS. But if there is no increase in the incidence of ALS when statins are used, then statins are not causing ALS. [unquote]
I don’t believe that the incidence rate is currently keeping up with reality. The reluctance to ascribe any ill to the taking of statins may be one reason. I have seen the term ‘ALS-like symptoms’ being used to describe what for the patient is effectively ALS, with the same devastating outcome. The death certificate does not record ALS and the likelihood is that the death is recorded as “possible neuro-degenerative disorder of unknown aetiology”. That sort of approach will add nothing to the ALS database.
Despite any appearances that I may be giving to the contrary, I am not a complete fool. Not a single scientific reference which I have provided to this site has been questioned. For what it is worth, I will provide a few more…
The issue of neuro-degenerative conditions such as ALS, potentially being induced by statins (as yet another aetiological pathway rather than a sole causal mechanism) has been addressed in part by the references provided.
NEJM 353:93-96, 2005
Central nervous system and limb anomalies in case reports.
Edison R and Muenke M.
Eur J Neurosci. 2003 Jan;17(1):93-102.
Blockade of HMG-CoA reductase activity causes changes in microtubule-stabilizing protein tau via suppression of geranylgeranylpyrophosphate formation: implications for Alzheimer’s disease.
Meske V, Albert F, Richter D, Schwarze J, Ohm TG
(abnormal tau protein phosphorylation induced by a statin drug)
Molecular and Cellular Biology, January 2005, p. 278-293, Vol. 25, No. 1
Increased tau Phosphorylation on Mitogen-Activated Protein Kinase Consensus Sites and Cognitive Decline in Transgenic Models for Alzheimer’s Disease and FTDP-17: Evidence for Distinct Molecular Processes Underlying tau Abnormalities
Sarah L. Lambourne, Lynda A. Sellers, Toby G. Bush, Shewly K. Choudhury, Piers C. Emson Yoo-Hun Suh and Lawrence S. Wilkinson
Lancet 363:892-94, 2004
Selenoprotein synthesis and side effects of statins.
Mooseman B and Behl C
Pharmacotherapy 23(7) 871-880, 2003
Statin associated memory loss: analysis of 60 case reports and review of the literature.
Wagstaff L, et al
It would be a real pleasure to have any of the references that I have provided to this site addressed rather than being shown how unscientific I am being because I choose to use a common language to describe my thoughts.
I don’t want to waste my time trying to produce a fully referenced academic breakdown of my thought processes, that would meet with the approval of Lancet’s finest minds and editors. I would respectfully suggest that all of the references I have provided, to press, are read and understood before fruitful debate can begin. To complain about my words without reading what lies behind them, is an act that is unlikely to provide fertile ground for further debate.
Cellular disruption, and neurological effects that are likely to have devolved from statin use have been well documented. I could point to a wealth of scientific documentation that underscores the position that the cholesterol/heart disease hypothesis is nonsensical. I don’t see the point, when even a simple question cannot be addressed. The question that PaIMD described as a great question, yet it has languished unanswered while I have been told repeatedly how poor my science is.
To ignore the provided scientific papers and then point to my ‘written speech’ as evidence of my anecdotal approach to science, is not the way that one would expect a site that purports to devote itself to evidence-based medicine to conduct its affairs. The least one would expect is that an interested scientist would read the supplied material for it may contain something novel and interesting.
References related to ALS don’t mean a darn thing unless those references show that the rate of ALS is higher in patients taking statins.
Sure you can “point to a wealth of scientific documentation that underscores the position that the cholesterol/heart disease hypothesis is nonsensical.” But the scientific consensus has been formed by looking at all that documentation plus an even greater wealth of documentation that underscores the position that lowering elevated LDL cholesterol reduces the risk of heart disease. It’s not what you can cite, it’s the total weight and quality of the evidence that matters.
@ Dr Hall
[quote] References related to ALS don’t mean a darn thing unless those references show that the rate of ALS is higher in patients taking statins.
Sure you can “point to a wealth of scientific documentation that underscores the position that the cholesterol/heart disease hypothesis is nonsensical.” But the scientific consensus has been formed by looking at all that documentation plus an even greater wealth of documentation that underscores the position that lowering elevated LDL cholesterol reduces the risk of heart disease. It’s not what you can cite, it’s the total weight and quality of the evidence that matters. [quote]
A hypothesis is a provisional idea that requires evaluation. To be considered as useful, the hypothesis would, ideally, be capable of predicting the behaviour of variables that have been described and included as a part of the hypothesis.
When the hypothesis fails to predict the behaviour of the variables, the hypothesis must be considered to be false. This is elementary knowledge and there are many documented examples of the cholesterol heart disease hypothesis being unable to predict the outcome of the various studies, where the hypothesis broke down.
Only one failure of the hypothesis to predict the outcome of the variables is sufficient to negate the hypothesis and the sheer number of positive reports cannot outweigh a single negative falsifying report… that is science. I suspect that is the bit that you are having having a problem with so I will paraphrase and repeat it.
10 million supporting cases for the hypothesis will be negated by one single case that can falsify the hypothesis. The cholesterol heart disease hypothesis has failed to support the outcome of many studies. To continue to think that it remains a good hypothesis and that it is suitable for incorporation into theoretical medicine, betrays a poor understanding of the meaning of the terms ‘science’ and ‘evidence-based medicine’.
I don’t believe I can serve any useful purpose in writing any more…
I’m done with this.
jay, are you saying that “The reluctance to ascribe any ill to the taking of statins” is causing physicians to not diagnose cases of ALS? That if the patient ever took a statin they misdiagnose ALS as something else?
ALS is rare enough that a primary care physician will only see a few cases. They will then diagnose those cases not from their own experience, but by reading diagnostic criteria. Unless the ALS diagnostic criteria include an exclusion for statin use, a physician would have no reason to exclude patients who used statins from an ALS diagnosis (if that is what they had).
If there was such an exclusion, then the diagnosis would be “statin caused neuro-degenerative disorder”.
If there is no such exclusion, then you are saying that in addition to the ~5,000 cases of ALS that are diagnosed each year there are additional cases that are misdiagnosed because the patient took a statin?
In the absence of any data, that idea doesn’t make sense to me. That thousands of physicians would independently misdiagnose ALS because the patient took a statin. There would have to be a vast conspiracy with complete buy-in of every physician.
Referring back to the disbelief of doctors that statins are the cause of a multitude of ills, I am reminded of a saying of my father, many years ago :”There are none as blind as those who won’t see”
Harriet talks of the need for RIGOROUS trials, but one can hardly say that trials that just dish out pills and note the symptoms resulting, (overlooking some because they sometimes occur without the pill in question), and leaving it there. are rigorous. Especially so when the reason for serious side effects was demonstrated 18 years ago. It is hard to imagine any research authority ignoring these failings, and continuing their work without real investigation of the fundamentals of the working of the statin. There is no evidence of any such work being carried out after Dr Karl Folkers’ studies, the reverse appears to have happenned, and Q10 has been marginalised and subject to a taboo in mainstream quarters.
Where any Q10 trials were done, in such as heart failure cases, the trials failed, because far too small doses were administered, eg 100mg Q10, whereas my daily dosage needs to be 900mg. The other weapon used against Q10 has been to name it as Alternative medicine and try to show it in the same category as homeopathyand such.
In May 2007, the Annals of pharmacy published a study of the effects of Q10 on blood pressure, it was under the section Alternative Medicine, and those who carried it out were either totally ignorant of the function of Q10 in the body, or had some ulterior motive, the trial used men in their 20s, and measured BP at intervals before and after taking Q10.
Now Q10 is known to be at its maximum level at about 20 years of age, diminishing slowly through life, so adding Q10 is a rough equivalent of testing the power output of an engine, whose fuel tank is nearly full, and filling that tank to overflowing to see if that altered matters.
They recorded virtually no change in BP, pharmacists are used to BP drugs which drag BP down, but Q10 works in older people by giving the heart access to more ATP for its energy, and normalising matters.
I feel certain that we will read references to this trial noting the lack of effect of Q10 on Blood pressure, but it will be totally misleading.
As Q10 is at its maximum level at age 20, and falls to 50% at 80, in rough terms, that works out at 8% per decade, probably it falls exponentially, but for simplicity, we will just consider it to be linear. Statins lowered my cholesterol by 20%. It is fair to assume that all other products in the mevalonate pathway were simillarly affected. and thus Q10 falls by 20%, a loss of energy production capability of 20%, equivalent to the loss of some 24 years. It is not surprising that often seen problems of age occur much earlier in statin users, it does not bode favourably on the chances of younger patients to have a problem free old age after many years of statin Q10 attenuation.
Statins should really be named Alternative or herbal medicine, being little more than cleaned up versions of Red Yeast Rice, the old Chinese herbal, made on sufficient different bases to permit separate patents for the various drug companies to have their own share.
In all my experiencce at the time of statination, my own GP was very supportive, but he had no more to go on than I had, and predicted the worst, but continued to take great interest in the saving factors which I later managed to unearth
To PalMD, I remember a quote from a beloved professor “you can’t find a fever if you do not take a temperature”. thus, the thrust of the problem with statins–. May I suggest, anyone with a clinical practice that includes PD patients, drug histories be scrutinized for statin use–esp those pts with “atypical PD” or who are somewhat “sinemet resistant”?
In answer to your question regarding case reports in the literature, there have been 3 case studies published. One case report appears in a German Medical Journal–a translated copy of the article appears at end of this posting. the other 2 case reports appear in
Ann Neurol 1995: 37:685-686
Parkinsonism unmasked by lovastatin.
Muller T, Kuhn W, Pohlau D, P
Blocking the mevalonate pathway to isoprenylated proteins by statins interferes with the production of selenoproteins (specificially selenoprotein N) and glutathione synthase(major antioxidants within the brain–deficits theorized to result in increased ROS–definition of oxidative stress) as well as a myraid of other compounds.There is scientific evidence that use of statins lowers muscle, platelet and serum coq10.
Statins interefere with production of dolichols, necesary for N-glycosylation of proteins, and interestingly, dolichols constitute the largest % of fats that make up the substantia nigra. What effect does that have on the function of the SN? No one has looked at this, I suppose hoping specificity of the drug for cholesterol lowering predominates –but over a life time of taking the drug???Glutathione and coenzyme q10 are found to be depleted in PD pts irregardless of their previous/present statin status. Mt dysfunction and oxidative stress are theorized to be etiopathologic in PD. Seems counterintuitive to give a drug that further depeltes glutathione and CoQ10 to pts with a disease where these compounds are already deficient. Given the recent in vitro studies determining cholesterol and APOe4 as the principal components in synaptogenesis and neurotransmission, if you believe the theory of brain plasticity, statin use seems even more than questionable. Also, critical levels of brain cholesterol may not be reached with statins for >5yrs, given that brain cholesterol is thought to have a half life of ~5 yrs. Consequently, temporal association btn the initiation of statin therapy and symptoms of neurodegenerative diseases may not exist.
You are probably aware of the article authored by clifford Shults, et al published in annals of neurology, 2002, showing a decrease in progression of disease in early stage PD patients who received 1200 mgm/day of coenzyme Q10. this was a small study (80 patients total),thus multiple center studies are underway using megadose coq10 in PD, ALS and mt cytopathy. (recent published data from these studies concluded that use of megadose coq10 was “safe and tolerable”.)
I assume one of the studies you noted was Dr. Lieberman’s small study looking at progression rates of 2 different groups of PD patients–one group on a statin, the other group not taking statins. His conclusion after following these 2 groups for a period of 2 yrs was that their rates of progression were “similar”. Included in this study was a small paragraph noting that of the original group who were not taking a statin, 5 patients were started on a statin during the trial period (from the report, one would assume that only 5 individuals were started on a statin during the study period). Important (to me anyway) was the fact that all five patients experienced an increase in severity of their symptoms within 3 months of beginning a statin. I know that is a very small #, but that’s 100% of all the patients who were started on a statin during the trial period. The statin was stopped for a “washing out” period and when the symptoms did not revert, the drug was re-started. (I assume the possibility that whatever statin damage occurred could be permanent was not considered)
. Dr. Paul Phillips, interventional cardiologist from san diego who has been studying statins, maintains that tissue half life of statins is more important than serum half life in reference to “wash-out” period of this class of drugs, and that this # is unknown–could be months to years..
Statins interfere with Lipid rafts (excerpted from a chapter which appears in the following book: AXON GROWTH AND GUIDANCE)
Carmine Guirland and James Q. Zheng
The plasma membrane of cells contains a variety of lipid and protein molecules that are often segregated and heterogeneously distributed in microdomains. Lipid rafts represent a generalized concept of membrane microdomains that are enriched in cholesterol and sphingolipids and, characteristically, resistant to cold detergent extraction. Lipid rafts have recently received considerable attention because they are thought to be involved in many cellular functions, in particular, signal transduction for extracellular stimuli. Many of these functions are also intimately related to the processes involved in neural development, including neurotrophic factor signaling and synaptic plasticity. Recent studies from our lab and others have indicated an important role for lipid rafts in axonal growth and guidance. Specifically, our data show that lipid rafts on the plasma membrane provide platforms for spatial and temporal control of guidance signaling by extracellular cues. In addition, lipid rafts may also function in other aspects of axonal growth and guidance, including spatial and temporal regulation of adhesion, cytoskeletal dynamics, and growth cone motility. Further elucidating how membrane rafts are involved in guided axonal growth would provide important insights into the intricate signaling mechanisms underlying neuronal wiring, which is fundamental for normal brain development and functional recovery after injury and diseases.
Statins interfere with geranylgeranlypyrophosphate synthesis:
Journal of Neurochemistry
Volume 89 Page 24 – April 2004
doi:10.1046/j.1471-4159.2003.02305.x
Volume 89 Issue 1
HMG-CoA reductase inhibition causes neurite loss by interfering with geranylgeranylpyrophosphate synthesis
Joachim G. Schulz, Julian Bösel, Magali Stoeckel, Dirk Megow, Ulrich Dirnagl and Matthias Endres
Abstract
To determine whether neurite outgrowth depends upon the mevalonate pathway, we blocked mevalonate synthesis in nerve growth factor-treated PC12 cells or primary cortical neurones with atorvastatin, a 3-hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase inhibitor, and substituted different intermediates of the mevalonate pathway. We show that HMG-CoA reductase inhibition causes a profound reduction of neurite length, neurite loss and ultimatively cell death in undifferentiated and pre-differentiated PC12 cells and also in rat primary cortical neurones. Geranylgeranylpyrophosphate, but not farnesylpyrophosphate, squalene or cholesterol, completely compensated for the lack of mevalonate. Our data indicate that, under HMG-CoA reductase inhibition, geranylgeranylpyrophosphate rather than farnesylpyrophosphate or cholesterol is critical for neurite outgrowth and/or maintenance. Loss of neurites is an early manifestation of various neurodegenerative disorders, and dysfunction of isoprenylation might play a role in their pathogenesis.
Letter with case report:
Der Nervenarzt
Issue: Volume 74, Number 2
Date: February 2003
pages 115-122
Letter in response with case study of
statin-unmasked Parkinsons
“To the excellent review about the development
of myopathies following long-term medication of
cholesterol level decreasing fibrates and statins, there
should be considered additional differential diagnostic
possibilities.
Because of the similar clinical symptomatology
with muscle aches and increased stiffness, the
diagnosis of statin-> induced aggravated
Parkinson Disease Syndrome should be
discussed. The development of such muscular
side effects is seen more with statins than with
fibrates.
The case report in Table 1 indicates the
history of a 60 year old patient with statin-induced
Parkinson Syndrome occurring over a long time.
On the other hand, with central effective
statins, a possible neuro-protective effect in
neuro-degenerative diseases has been considered,
especially in dementia. But long term use of statins,
especially Lovastatin, leads to the reduction of
coenzyme Q10 and can cause damage of the
mitochondrial breathing chain. Co Q-10 is an electron
receptor in the mitochondrial complexes 1 and 2 and
very effective absorber of radicals. This antigen
substance increases the complex 1 activity.
Co-Q10 shows a certain therapeutic effect with
encephalomyopathy where there is a lack of
various enzyme functions of the breathing chain.
Dysfunction of various parts of the mitochondrial
breathing chain is also considered in the
pathophysiological mechaism of idiopathic
Parkinson’s disease.
Treatment with Co-Q10 in patients who are not
treated with Dopamine for Parkinson patients,
caused less disease symptomatology and
progression than patients treated with
placebo, though placebo treatment can cause
stimulation of dopaminergic neurotransmission.
Therefore, the long-term treatment with Co-Q10
possibly is neuroprotective in idiopathic morbid
Parkinson, though new evidence shows it
appears to cause mild symptomatic effect.
Under these circumstances treatment with
prophylactic medication of Co-Q10 which has
been well tolerated in doses up to 1200mgm in
patients with neurodegenerative diseases should
be considered for statin myopathy or statin-
induced Parkinson syndrome in addition to
discontinuation of the cholesterol decreasing
medication.
The Table 1 summarizes a patient with Parkinson
syndrome.
1995: start of therapy with Fluvastatin 40 mg.
1997: increasing weakness with shoulder and hip
pain on the right
1999: diagnosis of right sided Parkinson
syndrome of akinetic dominance type.
Careful induction of Pergolid with daily doses
of 3 mg and Salagen 7.5 mgm
2000: complaints about increasing edema
development in legs, loss of hair, start of a
potas.sium sparing diuretic and increasing
of Pergolid medication from 4.5 mg
in June 2000 to 6 mgm in December.
March 2001: discontinuation of Fluvastatin,
continuation of Pergolid 6 mg
June 2001: reduction of Pergolid to 4 mgm
Sept 2001 Pergolid 3 mgm. Improvement of edema
December 2001 discontinuation of Pergolid and
diuretics
March, 2002 discontinuation of Salagen”
Dr. Th. T. Muller
I need to stop now–have not even touched on effects of statins upon GTPases and TNF-a, nor the gene expression with exercise for those on statins, or the decrease in cellular membrane fluidity and membrane electrical potential.
Perhaps these 8 instances are due to genetic variation interacting with an environmental agent–in this case a lipophilic statin–to produce disease. Given the millions of individuals who are taking statins, even if this genetic variation is very low, the numbers affected could be very high indeed. So incidence of Alzheimer’s and PD are both increasing; are we certain it is all attributable to aging baby boomers and not to ubiquitous use of statins?
http://www.ncbi.nlm.nih.gov/sites/entrezSaeedm AM, Siddique, N,et al: Paraoxonase Cluster Polymorphisms are Associated With Sporadic ALS
1: Neurology. 2006 Sep 12;67(5):771-6. Epub 2006 Jul 5.
Genetic variations in three enzymes that detoxify insecticides and nerve gas agents as well as metabolize cholesterol-lowering statin drugs may be a risk factor for developing sporadic amyotrophic lateral sclerosis , and possibly responsible for a reported twofold increased risk of ALS in Gulf War veterans.PON gene cluster variants have previously been associated with other neurodegenerative and vascular disorders, including Alzheimer’s disease, Parkinson’s disease, coronary artery disease and stroke.
The genes for human paraoxanases (PON 1, PON 2 and PON 3), which are located on chromosome 7q21.3, code for the production of detoxifying enzymes involved in the metabolism of a variety of drugs including statins, organophosphate insecticides, such as parathion, diazinon and chlorpyrifos, and nerve gas agents such as sarin.
The mavelonate pathway blocked by HMG CoA Reductase Inhibitors is the pathway to many biolgical substances. Why block production of selenoproteins, Coenzyme Q10, Dolichols, GTPases, TNF-a, Lipid rafts in an attempt to reduce cholesterol, which may or may not be the principal substance in the etiopathology of CAD? Statins impact more than cholesterol….
“To PalMD, I remember a quote from a beloved professor “you can’t find a fever if you do not take a temperature”. ”
It’s hard to take seriously anything that comes afte a quote from “House of God”.
Had no idea the quote is from House of God–(never read the book–never had time)I heard the quote (among many others)years before House of God was even thought of. Though your response is quite a good one–ridicule of a quote unrelated to the science works when you are unable to refute any of the science. (I suspect you did not read any of the rest of the post)
if memory serves, the author trained at the Beth Israel, a well respected institution back in the late 60′s early 70′s anyway.
I am much dismayed at the response–i truly thought you were curious about a link btn statins and neurodegenerative ds. Disregard for all the biological functions of the products of the mevalonate pathway, esp those functions within the neuro system is what has gotten us here. Seems you are satisfied with the status quo…..
This blog is censored. If you bring up a serious objection that they can’t answer, they will first try ridicule and, if that fails, they just won’t publish your comment.
pec,
The nonsense you have been spouting is bad enough, but this is a gross calumny.
This blog is not censored. If it were censored, you would have been the first to go.
Would that that were true in your case at least.
Look, I know I’m snarky—that’s just me. But really, I did read your entire post…it just happens that it adds nothing new to the discussion.
The discussion has preceded thusly:
1) Presentation of evidence for cholesterol/statin use in clinical medicine based on vast preponderance of evidence.
2) Individuals presenting case reports, published or otherwise, claiming some specific harms of statins.
3) The rest of us trying to explain why it is not sufficient evidence to prove anything.
So, the snarkiness comes from your basic inability to grasp the nature of how science works.
I posted comments that were not published, because you didn’t like them. We have no way of knowing how many other comments, including patients’ experiences, were deleted because you had no logical answer.
I have nothing at all against evidence-based medicine. I think it’s great, and I think the scientific method is great. But it is not an all-knowing infallible oracle. It can easily be distorted to serve propaganda and business interests.
It is wrong to discount people’s experiences just because there does not happen to be a controlled study to support them. As this blog has acknowledged, research is imperfect and we often require many studies in order to reach a conclusion. And most things have not been addressed by research yet. And furthermore, general research conclusions may not apply to individuals — some people are highly sensitive to unnatural substances.
I have also tried to point out that there are important limitations in the reductionist approach to medicine, and to science in general. Biological systems are unimaginably complex and it is naive and/or arrogant to think you can change any variable you like without unexpected and long-term consequences.
Most people like to think they have the answers, or the means to find the answers. This applies in science, religion, politics; all areas of life. The desire to know and to be right tends to overshadow skepticism and prevents us from acknowledging that our ignorance is, and will always be, infinite. This is especially true for experts and professionals whose reputations and careers depend on having answers and inspiring trust.
The medical profession has probably inspired more trust than any other. But it has taken advantage of that trust, in certain things. My mother trusts her MD like a god — this is typical of her generation. Her MD is not careful enough about what he puts into her body. He follows the current trends and seems to believe the drug commercials.
Things are getting out of hand and patients are suffering. I do not mean that the medical industry is evil or worthless. Just that, like any powerful institution, it needs to be controlled. It needs to be watched and questioned by outsiders.
“1) Presentation of evidence for cholesterol/statin use in clinical medicine based on vast preponderance of evidence.
… your basic inability to grasp the nature of how science works.”
Oh I understand how science works, maybe better than you. At least I know enough to look for confounds. I tried hard to explain — but you apparently did not get it — that the heart disease – cholesterol association may be incidental. The cholesterol skeptics obviously are not right about everything, but they have some valid criticisms.
The crusade to get everyone’s cholesterol below a certain number may turn out to be harmful.
If I question the conclusions of medical science you accuse me of not understanding how science works. But questioning and doubting is supposed to be the essence of science. Science is not supposed to be a religion or a club, but that is what it’s becoming. Anyone who doubts the consensus on any topic is ostracized and ridiculed.
“I do not mean that the medical industry is evil or worthless. Just that, like any powerful institution, it needs to be controlled. It needs to be watched and questioned by outsiders.”
The thing is, there is no “medical industry”. From the level of the individual doctor, no one “controls” how we practice.
If I were a quack, the only thing controlling my practice is basically law suits and maybe, just maybe, my state medical board.
It is a common fallacy to believe that there is some body that regulates or controls how physcians practice, but that just isn’t the case.
somehow I remember PaImd asking for any case reports in the literature linking PD and statins. I did not say it was science–I listed the case reports as per the request. ALso requested was any science to explain how there could possibly be a relationship btn statin and PD–I listed several mechanisms for which statins could trigger or unmask neurodegenerative diseases. Obviously disregarded/dismissed. The personal “anecdote” concerning 8 individuals with whom I am acquainted who developed PD which they all attribute to having taken a lipophilic statin was not presented as science.
They delete anything they are not able to ridicule. They say I don’t understand science, and when I post a comment that shows I obviously do understand science, they delete it.
I should have said — they delete SOME of my comments that show I obviously understand science. They delete whatever is most difficult to dismiss or ridicule.
pec – you are lying. We have not censored your posts.
pec, you are correct when you say that physiology is extremely complex. Physiology is inherently non-linear and coupled and comprises many thousands if not more parameters. Such systems are inherently chaotic. Such systems cannot be modeled beyond certain levels of precision.
When you say “things are getting out of hand”, I think they are better than they have ever been. Treatments now are a lot better than they used to be. 75 years ago the “standard of care” for neurosyphilis was to give the patient malaria, let them go through about 10 cycles of fever (about 40 days) then cure the malaria with quinine. It was called “fever therapy”, and the man who developed it won the Nobel Prize. His treatment cured many thousands of people who would have otherwise died. I discuss it on my blog in the context of resolution of autism symptoms with fever. I think both effects are due to NO from iNOS. Fever therapy was a desperate treatment for a desperate condition. It had serious side effects. The side effects were considered acceptable because they were worse than the disease (for those who didn’t die).
Physiology is not getting more complex but some of us are beginning to understand some of just how complex it is. It is scientists and medical professionals who are doing the research that is leading to that understanding. There are plenty of individuals who are trying to hold us back. The authors of this blog are not among them.
It is extremely difficult to keep up with even a tiny fraction of the scientific literature. Even the literature that directly intersects with your field of research. I know because I am trying to do that in the NO field. PubMed now lists 86,000 citations under “nitric oxide”. NO regulates ATP levels via sGC. There are 112,000 citations for ATP. NO controls O2 consumption by cytochromes. There are 110,000 for cytochrome and 326,000 citations for oxygen. Cholesterol has 167,000. Statins only have 18,000. Cardiovascular disease has 1.4 million. A tremendous amount of effort has gone into doing the research that is documented in those papers.
There is a lot of material in the literature that is wrong. Not because people are evil, or greedy, or not paying attention to details, but because science is really difficult to figure out and sometimes people don’t get it exactly right. There are some frauds, but those are rare in the scientific literature. Virtually all of the error comes from people who are trying to get it right, but don’t despite their best attempts to do so. In most cases of error the data is ok, but it is the interpretation of the data that is wrong.
I know how frustrating it is to have insight which is ignored because it doesn’t fit with preconceived notions that are wrong. Even when that insight fits the actual data in the literature better than the preconceived wrong notions. Virtually all researchers don’t have the time to read enough of the literature to get enough perspective on it and sort out what is wrong. They are unable to evaluate claims because they don’t have enough background. They are still caught up in scientific paradigms that are wrong, but don’t have the time or the inclination to evaluate them. These wrong paradigms hurt real people. The recent ACCORD trial testing tighter control of blood glucose was stopped because more people were dying in the treatment arm.
http://whitecoatunderground.com/2008/02/07/diabetes-more-questions/
The reason people more people were dying when their blood sugar was controlled more precisely is because the “real” problem with diabetes type 2 isn’t too much glucose in the blood, the “real” problem is not enough glucose reaching the peripheral tissues (which is where it really matters). Those tissues “need” more glucose because they don’t have enough mitochondria and so “need” to make more ATP via glycolysis. The only way to deliver more glucose is via raising blood sugar, and if that is blocked (by “better” control), then the peripheral tissues don’t get “enough”, they can’t make enough ATP, and so they go down the low ATP death spiral.
An interesting article showing the difference between blood glucose and the glucose level in the peripheral tissues (at a single site, perhaps not representative or accurate (the dialysis sampler was much larger than the actual sites for glucose utilization)).
http://www.minervamedica.it/index2.t?show=R02Y2005N11A0711
How did they figure out what glucose level to try and reach in the ACCORD trial? Via the (wrong) paradigm of “homeostasis”. They simply assumed that “normal” blood glucose (the level in people without diabetes type 2) was the “best” blood glucose to have. Too high a blood glucose is bad, but too low a blood glucose is worse. The optimum level depends on how many mitochondria you have (and in what tissues), and how much glycolysis those tissues need to do (and how much glucogenesis your liver can sustain). A “better” treatment would be to increase the number of mitochondria which greatly reduces the need for glycolysis.
But still, 100 years ago the treatment for diabetes type 1 was inanition, gradually starving oneself to death. Treatments are a lot better now. Treatments have gotten better because the scientists and health care professionals have discovered better treatments with fewer side effects. Improvements have not come from outsiders exerting control.
@ Harriet Hall
You wrote:
“I hope readers will follow the advice of UK-Bloke to read what is on the THINCS website. I hope they will seek out the original sources that the THINCS folks quote and be able to recognize how THINCS misrepresents those findings by quoting out of context, selective quotation, and putting their own spin on the way they report the studies. I hope they will also seek out the studies that THINCS does not mention, the many studies that refute THINCS’ claims. I hope they will also read what the Skeptic’s Dictionary says about the logical errors of THINCS, and I hope they will consult other independent sources such as The Medical Letter and Wikipedia, which mentions THINCS only briefly as dissenters to what Wikipedia accepts as based on good evidence”. http://en.wikipedia.org/wiki/Statins
The Wikipedia reference you mention is pasted below and link 19 is a good paper with plenty of references, however I am unable to get very far with link 20.
Some scientists take a skeptical view of the need for many people to require statin treatment. The International Network of Cholesterol Skeptics is a group that has questioned the “lipid hypothesis” that supports cholesterol lowering as a preventive measure for heart disease, and has argued that statins – especially at higher doses – may not be as beneficial or safe as suggested.[19] Similarly, some authors argue that recommendations for the expanded use of statins to stave off cardiovascular disease are not supported by evidence.[20]
This is 19
http://www.bmj.com/cgi/content/full/332/7553/1330 Read this and its Rapid response before commenting
This is 20 (I am unable to access this information).
Abramson J, Wright J (2007). “Are lipid-lowering guidelines evidence-based?”. Lancet 369 (9557): 168-9. doi:10.1016/S0140-6736(07)60084-1. PMID 17240267.
Sorry to see that you have such a hard time in believing what THINCS and the people who have actually taken this rubbish and experienced what it can do, as scientific proof. I can offer no explanation as to why you so strongly think everyone else’s experience with this medication does not matter. I have no doubt that I am biased against statins as you previously mentioned, if you actually know what they do to your body and your ability to think and function like a human being then you would not be doubting everyone the way you do. The proof/evidence of what happens when people take statins is all around, if you choose to ignore it then, what can anyone say except “well we did try to tell you!”
In another post you wrote:
“I think we’re all in favor of better post-marketing surveillance programs. But few would agree that unexamined anecdotal horror stories are enough to justify a moratorium on prescribing a drug that is known to save lives.”
Talking about good science, where is the proof that taking Statins actual does save lives, I have not seen or heard of any proven results that supports this as a FACT, isn’t this just a theory and could you tell me the name of the person or persons that would have died if they had not been taking this medication?
All that I see is the very same selective cherry picking going on that you accuse THINCS of but without the actual referenced material to back up your claims, not really scientific proof. I also did have a previous post that mentioned among other things that THINCS didn’t always get it right but at least they brought the matter to our attention, this post didn’t actually appear in this blog so I can only assume it was deleted.
People are giving you the insight to make a difference, instead of trying to disprove all they are saying, why not take advantage of the situation and any newly gained knowledge and put it to good use.
You must also take into consideration that the doses of statins over the last few years have increased in size dramatically, I know when my dose was changed from 10mg straight up to 40mg (Zocor-Simvastatin) things went downhill even faster but I was at the time unaware what the cause was.
“pec – you are lying. We have not censored your posts.”
Then how do YOU define “censor?” According to my definition, if you delete some of my comments, those comments have been censored.
Your readers should be aware that not everything everyone says here actually appears.
And by the way Dr. Novella, I think I understand why you have no problem with tossing arbitrary combinations of synthetic chemicals into patients’ brains. You wrote at neurologica that the brain is a product of “messy evolution.”
That explains your attitude towards the new drugs, and it explains the current medical approach in general. Evolution has produced a mess. It’s a wonder we are alive at all. We need those drugs.
But the reality is that evolution has produced systems that are far beyond the comprehension of modern science. Your understanding of how the brain works is minimal, yet feel you can judge the quality of its design.
PalMD, since the references I quoted “added nothing to the discussion”, I am quite impressed that you were aware of the various metabolic substrates blocked by statins and their functions. Is it your opinion the blockage of these products are of no consequence?
pec- we have not deleted your posts. This is simply wrong. You are making false accusations and drawing insulting, self-serving, and paranoid conclusions.
Your interpretation of the significance of “messy evolution” is an absurd straw man.
UK-Bloke said
“I also did have a previous post that mentioned among other things that THINCS didn’t always get it right but at least they brought the matter to our attention, this post didn’t actually appear in this blog so I can only assume it was deleted.”
You mean this one on the 9th Feb at 5.38pm where you said
“The people at Thincs may not have proven everything they said but at least they went out on a limb to help people to realise that there is a problem.”
It’s been there on the blog all the time (as a UK-person, I remembered).
I’m a bit wary of trusting anything you say if you can’t even find your own posts on the blog.
@kathleen,
you are quite right, I refreshed the page after posting that comment and found it to be there.
What can I say Aren’t Statins great!
pec persists in demonstrating his defects for all to view. He has lied, repeatedly. He has also contradicted himself, set up straw men, responded to things he imagined people wrote that they didn’t, and committed frequent errors of logic.
Fortunately, he has also done some good by serving as a bad example. One of his comments was used on episode 131 of the podcast Skeptic’s Guide to the Universe, in the segment “name that logical fallacy.” http://www.theskepticsguide.org/archive.asp
UK-bloke apparently can’t read very well. He asks “where is the proof that taking Statins actual does save lives, I have not seen or heard of any proven results that supports this as a FACT, isn’t this just a theory and could you tell me the name of the person or persons that would have died if they had not been taking this medication?”
If he had read my article carefully and followed the links, or if he had bothered to enter a clinical query on PubMed, he would have had no trouble finding the evidence that shows statins save lives – in high risk groups, when prescribed appropriately.
And he is demonstrating his ignorance of science when he asks for names of individuals. Statistics can tell us that hundreds of thousands of smokers die prematurely, but it can’t name names. That’s not the point. Analogously, when people take antibiotics and survive pneumonia, we can’t name which ones would have survived anyway.
@Harriet Hall,
once again where is the evidence?
Your statement is speculative at best, I followed the Wikipedia reference about THINKS and found that you obviously had not read what you are saying so why would I just use PubMed when there are so many other sources to choose from.
Please add the document source to verify your claims about how these drugs are proven to save lives because I would really like to read it.
Oh yes I think after a MI and years of taking statins then needing a triple bypass, that I may just fit the “high risk group”, this stuff almost killed me.
Why not take a look at this site and see all the people who had a great time with statins!
http://www.askapatient.com/viewrating.asp?drug=19766&name=ZOCOR
When Harriet can’t answer our objections with logic she resorts to insults and ridicule.
It is rational to be skeptical of the cholesterol hypothesis. It is rational to question the recklessness of some MDs in prescribing combinations of synthetic drugs.
Many patients are on several drugs, each prescribed by a different specialist. I doubt that clinical trials have tested all likely combinations.
When we express sensible and rational doubts, Harriet, and some others, respond with condescension and insults. It’s easier to call us ignorant or crazy than to address our very sensible concerns.
And when Steve Novella calls the brain a “messy” product of evolution, that does tell us something about his approach to medicine, and about the current approach in general. One reason CAM is gaining acceptance is that is does not see the products of evolution as “messy” or random. When you perceive a system as intricate, efficient and complex, you are less likely to treat it carelessly.
The complexity of living systems is far beyond the understanding of modern science, and it is arrogant to forget this. Yes, you can toss in artificial chemicals and observe that the system continues to function. But that is because these amazing natural machines are extremely intelligent, flexible and adaptable, and can therefore take a lot of abuse.
CAM is more likely to respect natural systems and try to work with them to encourage healing. This is NOT to say most CAM treatments have value — that is a question for scientific research. But it IS true that the general CAM philosophy makes more sense to a lot of people.
Modern medicine is highly effective in certain limited scenarios — when emergency surgery or antibiotics are required, for example. But success in some areas does not warrant applying the same philosophy in all areas.
The over-use of the new synthetic drugs is an example of a good thing gone haywire.
pec, which is the more reckless strategy, allowing people with known risk factors for heart disease to die because of nebulous “unknowns”? Or to treat them with drugs that have been shown in clinical trials to be safe and effective? Your reservation of “skepticism” for only what is considered mainstream science is telling. Why don’t you have this degree of skepticism about homeopathy? And I can’t see why you think the idea of water holding some kind of electromagnetic information is so absurd. How would that defy your established laws? (http://www.sciencebasedmedicine.org/?p=35#comment-723) Your notion that there is something credible about an electromagnetic memory effect in water only illustrates your ignorance of electromagnetism, the properties of water, and your ignorance of your own ignorance. There will always be unknowns about physiology. Physiology is vastly more complicated than can be understood mechanistically. Each person’s physiology is unique due to genetic and epigenetic factors. None of those factors are completely understood for even a single person. Putting off all medical treatments until everything about that treatment is completely understood for all individuals is to put it off forever.
@pec
“When Harriet can’t answer our objections with logic she resorts to insults and ridicule.”
I had noticed that on just about all the posts she has replied to. It is a shame though because a lot of the information that yourself and many others have provided is mainly high quality documentation.
I have also come across at least one person that has posted here who has an appearance in the BMJ and has had his papers published elsewhere.
Anyone who has knowledge good or bad about cholesterol should be able to pass on that information to help others make a constructive choice about what is best for them, they should also know what to look out for if they are amongst the people that are not suitable for statin drugs.
The facts and choices were not available to me and a heck of a lot more people in the past (including doctors) there is no excuse now though for pretending if I close my eyes and can’t see it then it doesn’t exist.
@daedalus2u
your comment about allowing people with known risk factors for heart disease to die because of nebulous “unknowns”? Or to treat them with drugs that have been shown in clinical trials to be safe and effective? in a perfect world this would be right. The problem is that what happens in selected individuals who are screened before trials are started, does not always cover what happens when someone outside this controlled selection has to take the medication in real life. Q10 deficiancy and Carnitine are just part of the problems that statins cause, also heart failure, brain fog, exhaustion, pain etc all of which as you know were not passed on to doctors and patients.
I do know about this as I am one of many who have found out the hard way, thankfully in the UK the multitude of tests that you have to go through are free. However the very same tests in America cost $1000s and if you have no insurance you are dammed to say the least, I have friends in America.
This is not a jab at you but it should be pointed out that not only do you pay for what may make you ill, but you will have to also pay a fortune to survive sometimes a low quality of life.
@kathleen
not a dig at you but before you make your mind up about treatment for your high cholesterol have a quick look at this site, I did post you a better note but it didn’t seem to go anywhere so if another note to you appears just ignore it ok.
http://www.askapatient.com/viewrating.asp?drug=19766&name=ZOCOR
“Why don’t you have this degree of skepticism about homeopathy?”
I am completely skeptical about homeopathy, and I have expressed that here. I have no idea if homeopathy works ever, or sometimes, or never. I said that I do not think homeopathy is necessarily impossible. I think more research is needed.
I am just as skeptical about CAM therapies as I am about mainstream therapies. However I do have serious objections to the philosophy behind some maintream treatments. Throwing arbitrary combinations of synthetic chemicals into a system as complex and poorly understood as the brain, or other organs for that matter, is madness.
Evolution has done an amazing job of building these systems, and they are not messy or haphazard. They are incredibly resilient and flexible and able to withstand years of abuse. But why abuse them? Why not stop the madness?
I’m sure there are cases where statins can save a patient’s life so he or she can go one to make radical lifestyle changes and recover. I’m sure the same is true of many other drugs.
But these drugs are being used with reckless abandon and unconcern. Biological systems are seen as piles of haphazard junk that need improvement.
I will not be commenting any more on this thread. Those who can read carefully and are not blinded by emotions will fully understand why and will only wonder why I didn’t quit long ago.
It’s frustrating to provide links to high qualilty evidence and then to be told I haven’t presented any evidence. It’s very frustrating to keep saying X is green and be answered by “You said X is blue and it isn’t.” It’s also frustrating to hear lies repeated (“This blog is censored”) even after they have been exposed as lies.
UK-Bloke
I did have a very good look at the site you posted (thank you) but I do have a lot of problems taking such a site as being any kind of evidence for or against taking a particular drug. For a start, I think that you would find that it is often people who have had a problem with a drug who post to such a site. Those who are happy with their medication don’t necessarily do so. I did also search the site for drugs that I have taken (with great success) in the past and for drugs that my husband is currently taking (again successfully and with no side effects). Yes, they had lots of negative comments too. It also seems to me that people tend to become ill from all sorts of causes, during the time that they are taking a particular drug and are likely to blame the drug, particularly if they are hearing lots of negative publicity about it.
In fact I think such sites are pretty scary. I found one comment, and I quote, “I took 20 mg. of zocor for about four yearswith only minimal side effects like neckaches, anxiety, and hair thinning. Now, I have developed tingling in both arms, hands and fingers. My first though was angina, but after reading all the comments here, I am pretty certain that zocor is the cause. Will stop the drug tonight.”
Why did this lady immediately put her symptoms down to the drug? To me, this just shows how much sites like this can influence gullible people.
In fact, I have been told that I don’t need treatment for my high cholesterol. Both my GP and cardiologist are happy for me to reduce it with diet and exercise. I have been recently investigated for cardiovascular disease and have been told that my heart is fine. But having weighed up the evidence I can assure you that if I had been told that I had CVD I would have jumped at the chance to take statins.
[...] (for all cause mortality) of 20%. Some of the most effective interventions appeared to have been statin medications and blood pressure medications, followed by [...]
Hiya kathleen,
I agree some people do jump to conclusions and can blame their ailments on the wrong thing.
Most people like me though who have had heart problems have been putting up with a lot of nasty problems for years and the doctors have just put it down to getting older or your memory problems have nothing to do with anything you are taking and all the time you are getting worse.
A lot of people including myself were ok for a year or two, then slowly things started to happen like getting tired more easily and forgetting names and what you were doing or even how to do things. You might think that some of those posts are extreme but the reality of what happens in real life is very much what has been written there.
I only recently found out after many years of taking Zocor what the cause of my problems were and that was by trying to find out why I was always so very tired all the time and unable to think properly, I can assure you that what I have put up with over the years is much the same as what those posters have written.
The truth is that I wished I had never taken a statin, it is almost a year since I had the last one and I am on long term incapacity benefit now, I cycled miles to work for over 18 years and now I find it hard to cycle 100 yards, My thinking ability is just starting to improve and I would hate to see anyone else go through this nightmare for the sake of a little excercise and possible diet change.
All the best,
UK-Bloke (I am really pleased you don’t need them).
@kathleen
I took zocor for 4 years, getting progressively weaker, with muscle wastage, and heart weakness with no-one attributing it to the statin, until I saw a newspaper article which pointed out that statins cause these effects. I later found out that Merck knew this in 1990 when they filed patents to add Coenzyme Q10 to statins to try to overcome the problem, but failed to publish this information.
The problems are very real, and lifelong supplementation of Q10 and carnitine, whose production may be permanently damaged, as in my case, will often be necessary.
I have a friend who was given statins after a heart attack, they had to be ceased because his CK (muscle wastage) figure rose to 9 times normal, only falling to 5 times normal when the statin was ceased by the hospital.(mine was just over twice normal, and I had severe muscle loss) He was in severe pain and unable to work over the next 4 years, with no solution but very strong pain treatment from his doctors, until he found the Q10 information, unknown to doctors generally, Merck seems to have had a hand in that. All is not sweetness and light in the world of cholesterol treatment, as Harret’s stone walling treatment so clearly shows
Keep away from statins if you possibly can, the trials show very little, if any, benefit for women. I will never take another one, ever.
“Throwing arbitrary combinations of synthetic chemicals into a system as complex and poorly understood as the brain, or other organs for that matter, is madness.”
Another glaring example of ignorance in the form of a strawman. Please try to understand what you are talking about before you write, it makes you look less dumb.
Raygee – so over 4 years of muscle wastage and you didn’t try to do some simple weight lifting or exercise? I hear resistance training will increase muscle mass and bone density – even in people who are nearly 90 years old. The story about your friend is nice but testimonies have a tendency to amount to a lot of white noise and bs. I don’t believe you.
“Throwing arbitrary combinations of synthetic chemicals into a system as complex and poorly understood as the brain, or other organs for that matter, is madness.”
“Another glaring example of ignorance in the form of a strawman.”
I realize that individual drugs are not arbitrary combinations of chemicals, obviously. You intentionally misinterpreted my statement. We know that it is also obvious that each patient may be taking several drugs prescribed by different specialists. And that combination is often arbitrary. The various specialists do not necessarily investigate to find out what other drugs each of their patients is taking. You cannot possibly think that all of these possible combinations are tested in clinical trials.
And besides, even if we were just talking about one drug, you must admit that you do not know exactly how the system as a whole is effected by a statin, for example. Especially over long periods of time, and in genetically varied individual patients.
Since the acrimony seems to have died down, I’d like to interject a related, but tangential request. While I have no problem with the correlation between cholesterol and heart disease, there is one “risk factor” I don’t yet believe: salt. I’d like to see a discussion here about it. The shoddy research (or reporting on the research as the case may be) on salt is a personal pet peeve of mine.
I recently (well, in the last year) saw a news article on a scientific study (yes, I know, but I am not a physician, and don’t have ready access to journals) that follow high risk heart patients for 10 years and those who did not lower their salt intake died at a very significantly higher rate. What it did not say is whether other dietary changes were made or taken into account. People with high blood pressure typically have poor diets and typically consume lots of saturated fat and simple carbohydrates along with their salt. If the salt was reduced, then the overall diet was probably changed as well. I mean, they don’t sell low-sodium Big Macs or Whoppers.
Then on the CSPI web site, there was a report on a study that compared similar (identical?) diets with varying salt intake. Finally?! Something that settles the issue? No. The reduction in blood pressure was quite modest, and reflected, in my opinion, what you would expect from having lower levels of salt (any salt) in solution.
I still am not convinced by what I’ve seen that it’s bad, and it seems that things such as arteriosclerosis and hypertension play a much bigger role than the modest reductions in osmotic pressure gained from a low-salt diet. It seems to me that the low-salt craze has come out of the same paradigm that brought us the low-fat craze. That is, simplistic notions and little science to back them up.
I’m going to admit my biases though. I hate bland food. I season food properly. I find that my taste for salt is on par with most chefs, as I have no problem with the salt content at most “good” restaurants. I don’t particularly like over-salted snacks, but I will not eat bland food, and it’s bland without salt, no matter how many herbs and spices you put in it. I just want to know whether I’m in the same league with THINCS or whether my skepticism is justified.
I know this thread is not the forum for this particular discussion, but having come over here from the JREF website, I was disappointed not to find an article on this so far. So here’s a prod.
You guys are much more knowledgeable than I am in this area. I simply know how science is done, and am not happy with the research (reporting?) that I’ve seen.
@Synaptix
I have just seen the posting that you left for pec and Raygee.
the comment to pec was a pretty stupid thing to come out with and when you commented about Raygee and weight lifting it just goes to show that your reference to ignorance is a reflection of your knowledge of this subject.
Statins are known to cause muscle wastage and exercise intolerence, excercising the muscles tend to make them break down at a faster pace and raise the cpk levels in the blood.
Please look up mevalonate pathway.
Please look up Coenzyme Q10 deficiency.
Please look up Excercise Intolerence.
I could go on to give you a full account of the process but everything you should really be aware of is available at http://www.spacedoc.net/ and various sites ie PubMed BMJ and many others and they do have the referenced papers pointed out.
—————————————————–
“Throwing arbitrary combinations of synthetic chemicals into a system as complex and poorly understood as the brain, or other organs for that matter, is madness.”
Another glaring example of ignorance in the form of a strawman. Please try to understand what you are talking about before you write, it makes you look less dumb.
Raygee – so over 4 years of muscle wastage and you didn’t try to do some simple weight lifting or exercise? I hear resistance training will increase muscle mass and bone density – even in people who are nearly 90 years old. The story about your friend is nice but testimonies have a tendency to amount to a lot of white noise and bs. I don’t believe you.
@synaptics
Disbelief of the truth in the sufferings of others is a simple way to bolster up your own false ideas. I had polio 50 years ago, and my back has had insufficient strength to think of weight lifting. The statin damage added to the carnitine deficiency which post polios experience, and energetic exercise can only use up the carnitine stocks in the body, so that muscles have to metabolise their own protein to produce that energy need, and so waste away.
I am now only a few years off 90, and can only just manage to keep my independence, my back strength is virtually nil, so no snide remarks about weight lifting, that may be ok for undamaged folk. I have lived an active life, I still fume at my inability to do the physical tasks I always did, I have no lack of determination, hence my persistence in trying to find the truth about statin damage and spread that truth around the world.
I resent being called a liar, the stories are not white, pink, or any other form of noise, they are truthful and backed up by hospital tests and figures. if you cannot believe them, you are deceiving yourself and burying your head in the sand. I had to care for my late wife with Alzheimers when at my weakest
The Washington University of St Louis, neuromuscular, on its website speaks of lipid lowering myopathies and statin toxicity, and gives treatment requirements, are they not to be given some credence? or are their findings, which are in line with those of thousands who suffer, to be dismissed in a totally irrational and illogical manner by one who believes in hearsay, and will not try to understand what is really going on. I believe the title Science Based Medicine is a misnomer for this site, something more like Biassed Status Quo Medicine might be more apt, there are so many blind spots apparent.
pec, I completely don’t understand how you arrive at your positions.
On the one hand you say physiology is so complex and scientific methods so limited and physicians don’t know enough to be able to prescribe pure compounds which have known effects via known mechanisms that have been tested in the lab, tested on animals and tested on humans, with these compounds being administered by physicians who have studied physiology, have been tested on that understanding and are licensed under conditions which require maintaining their knowledge base.
On the other hand you seem to have some confidence in CAM modalities which were arrived at via unknown or non-scientific methods and which (at best) are very complex and variable mixtures of nothing or of unknown herbal compounds, which have no known effects via no known mechanisms and which have not been tested in the lab, on animals or on humans, were developed and are being promoted by individuals who have either zero understanding of physiology or what they believe about physiology is actually wrong.
I understand you are dissatisfied with EBM because it doesn’t accomplish what you want it to accomplish. But the reasoning by which dissatisfaction with EBM leads to confidence in CAM is completely beyond me.
@daedalus2u
I realise that you trust EBM, but do not seem to be aware of the blinkered nature and lack of breadth of that evidence, for example, there is true evidence, false evidence, and being “economical with the truth” The suppression of the known fact that statins damaged Q10 and thereby caused myopathy and other damaging effects should have set alarm bells ringing, and the naming of the most necessary product to manufacture ATP for all kinds of energy needs in all animal species, especially our own, as alternative medicine beggars belief.
Has biological knowledge become subserviant to the wishes of drug manufacturers wealth creation schemes? I am as eager as the next man to know the real answer to CVD, but some research, and trials beyond the influence of the western world should not be ridiculed because they had no enormous funding available, and homocysteine levels are still an insufficiently researched factor, I am hedging my bets by taking a folic acid/Bvits pill every day, since statins nearly led to my demise.
I am not anti conventional medicine, but I see many treatments where drug interference can be made much less necessary if more trials were to be made into the use of supplementing essential, but not hugely profit making substances, such as Blood pressure reduction, and heart failure treatment with Q10, and the realisation that carnitine deficiency is not only found in newborns and dialysis patients, but in post operatives, penicillin derivative users, and post polios. These are well founded matters, but somehow they have not reached mainstream medicine.
“the low-salt craze has come out of the same paradigm that brought us the low-fat craze.”
Egaeus,
Yes I completely agree. The low-salt and low-fat crazes were not based on good scientific evidence. Salt may have important benefits. It’s really too bad because so many Americans are depriving themselves of good-tasting food, while still getting sicker. The main culprit is probably refined carbohydrates. And trans-fats.
daedalus2u,
You simply missed the point of everything I said. Mainstream medical science focuses on one variable at a time, such as cholesterol, and seldom worries about the system as a whole. Alternative medicine tends to be holistic, and that is why I prefer its general approach. That does NOT mean I believe every treatment that calls itself holistic is worthwhile.
Contemporary medical science has evolved into an extremely reductionist approach. This approach works well in certain situations — emergency surgery is the best example. In many other situations the reductionist approach can harm more than it helps.
It’s true that MDs have at last acknowledged the role of lifestyle factors. This is great but should be taken farther. We need more skepticism regarding drugs such as statins and more emphasis on lifestyle changes. Many patients think it’s much easier to take a pill than to exercise or avoid junk food. They believe the pill is keeping them healthy in the same way that lifestyle changes would — and this is completely untrue.
Holistic medicine makes much more sense because it understands that when you change one variable many others may change in unexpected ways.
Again, this does NOT mean I think every hare-brained idea that calls itself holistic must be a good idea. Holistic medicine doesn’t have the answers, any more than mainstream medicine. But there has been much less research funding for holistic medicine. Hopefully, that is changing and the holistic approach will make progress.
The authors of this blog want to do exactly the opposite — they want to prevent progress in holistic medicine by depriving it of funding. I think this is only because they do not understand holistic philosophy. They really should try to learn something about the science of complex systems.
pec and ray, let me paraphrase what you are saying to see if I actually understand it.
EBM looks at only a few variables at a time and attempts to control for variables that are known to interact and uses systems such as double-blind trials to eliminate bias. Results are published in peer reviewed journals which require disclosure of conflicts. Therefore EBM can’t possibly address the complexity of physiology.
“Holistic medicine” looks at dozens or hundreds of variables at a time none of which are measured, none of which are understood, none of which are characterized in advance, none of which are controlled for, none of which are kept constant, using trials that are not blinded and the results of which are not published in journals but collected as anecdotes usually by those who derive their income from sales of these “treatments”. Therefore “holistic medicine” will work better because physiology is complex.
It seems to me that every complaint you have of EBM is actually worse in “holistic medicine”, but with no safeguards to try and mitigate those complaints. Every drug in EBM has been tested and has been shown (in some cases) to be safe and effective. That is not true of any CAM based treatment. If it were true of a CAM based treatment then the treatment isn’t CAM any more, it becomes an EBM based treatment.
No daedalus2u you deliberately misinterpreted everything I said. You don’t get it.
In studying complex systems we WANT to isolate variables. But in treating a malfunctioning complex system we DO NOT WANT to change variables in isolation, without concern for the overall system.
I’m sure you will find a way to misunderstand that.
So how do you treat a complex system while being concerned for the overall system without knowing the details of that overall system?
raygee: I apologize for any insult to you about your condition. In terms of this arguement though, anecdotes hold no water. I was just trying to highlight this fact. Though it seems I became frustrated after hearing more and more of them.
UKguy – I’m not argueing with the fact that Statins can cause the problems brought up here. I just completely disagree that the “truth” is being somehow suppressed – the science is being done to adress these issues and the medical community does it’s best to make it so that people can get treatment. No system is perfect, people are going to have bad side effects – to misrepresent and what the authors of this blog are trying to accomplish helpes no one.
I had muscle and joint pain (I’d call it 7 or 8 on a 10 scale starting about two weeks after taking Lipitor. So I stopped taking it and within a week felt better. So I started taking it again. Within three weeks I had the same pains again. Again I stopped taking the medicine and again the pain went away. I’ve tried all the others too, with the same result. No surprise, my 82 year old mother recently was given Lipitor and began complaining of severe arthritis pain. I recounted my experience, she stopped taking it and within 3 days felt better.
One of the reasons we do large outcomes studies, such as 4S, is that we don’t know all the variables. This allows us to see the effect of statin use on important outcomes, regardless of mechanism, etc.
“So how do you treat a complex system while being concerned for the overall system without knowing the details of that overall system?”
Obviously we can’t know all the details of a system like the human body. But we can recognize that we don’t know, and use caution and restraint.
The medical industry has not been using caution or restraint in prescribing certain kinds of drugs in recent years.
CAM treatments are much less likely to be toxic, because the philosophy respects the intricacy of natural systems. That is NOT to say CAM treatments work. Many probably don’t, some might. But I am talking about the underlying philosophy, not the efficacy of treatments. There may be less potential for harm with CAM — unless of course a patient rejects a needed mainstream treatment in favor of a useless CAM treatment. If you fall off the roof, you need surgery not accupuncture.
I am not expressing any opinion on any particular CAM treatment right now. Effectiveness of CAM treatments should be studied scientifically.
In the mean time, our knowledge of what works or not for heart disease, for example, is very limited. I think we should refrain from ingesting synthetic chemicals unless we are very sure they are necessary, and lifestyle changes should always come first.
And we do not always have to wait for the results of clinical trials before making health decisions. If you take a statin and get a pain, and you stop the statin and the pain stops, and you repeat this with the same results, that should be good enough for the time being.
Similarly, if every time you eat a strawberry you get an asthma attack, you don’t need a clinical trial to tell you to stop eating strawberries.
We all do informal experiments all the time, and it would be irrational not to. If I sleep only 4 hours I feel tired the next day. Do I need a formal study to tell me how much sleep I need? There is nothing wrong with formal research, but it’s silly to doubt everything that has not been confirmed by big, expensive controlled experiments.
And the research results are often confusing and misinterpreted. The statin research was interpreted as showing that high cholesterol causes heart disease, but that conclusion does not follow from the evidence.
We have to think. We cannot expect scientific research to replace common sense.
“CAM treatments are much less likely to be toxic, because the philosophy respects the intricacy of natural systems.”
That statement is, prima facie, ridiculous. No, this isn’t an ad hom statement, simply an observation.
This argument just goes round and round, I have long known that doctors are as fallible as the rest of us, although most have the best interests of patients at heart.
I believe that you must have financial interests or career positions that make it inconceivable to you that the problems are real, true, and making many lives miserable for the foreseeable future through statin use.
If all these reports are anecdotal, then those reported in trials have also been treated as anecdotal, unless of such a proportion that they would not go away, so whenever does a report get on to an outcomes report. The variables do not see the light of day, and we get such terms as “nocebo” invented to ridicule those whom they affect.
Large studies have little merit unless there is a desire to address all sides of the situation, and the fullest and latest knowledge of the matter under trial is taken into account. the trial must proceed with TOTAL reporting of problems, with no recourse to such subterfuges as the run-in period, when initial problems get swept under the mat. Thoroughness, not size, is the keynote, power of the outcome should rest on the integrity of those involved, and a totally independent body should oversee those where huge markets are likely to be involved. Woe betide a researcher who allows a dent to appear in the billions of dollars flowing from statin use. A real effort should be made to work out the mechanisms by which the drug works and try to foresee what other problems these could cause. This most certainly has not been done for statins, or perhaps the damage to energy supply ATP to all systems in the anatomy would have been foreseen, or maybe it was foreseen and ignored for financial reasons.
But all these huge trials leave important substances which cannot be patented out in the cold, and research passes them by as insignificant, and the side effects of the popular drugs need more drugs to control them, a vicious circle.
In all this, the individual patient’s welfare assume less importance than the report of success of the final criteria, the individual is not believed, or he/she is somehow blamed for being intolerant of the potentially toxic statins. I know the feeling only too well.
One can only bang one’s head against a brick wall for so long, and I am unwilling to endanger my blood pressure in carrying on the fight in this arena, I am certain others will be opening up all the time in other places, I have made my mark in plenty of them, and will continue to do so as long as it is necessary and I am able.
“Science-based medicine” that title is, prima facie, ridiculous given that not even one single piece of evidence provided, has been discussed by the resident medics of this site; within 200 posts.
simply an observation
pec wrote “We have to think. We cannot expect scientific research to replace common sense.”
As you have amply demonstrated, “common sense” is not very common. That is ad hom, and I am proud of it.
The scientific method was developed because we discovered that we easily fool ourselves without it. Scientific medicine has brought us sanitation, vaccination, antibiotics, cancer cures, insulin, (somebody stop me!). Nothing in CAM has produced a demonstrable improvement in health care.
“CAM treatments are much less likely to be toxic, because the philosophy respects the intricacy of natural systems.”
“That statement is, prima facie, ridiculous. No, this isn’t an ad hom statement, simply an observation.”
Your brain has been well-washed if you don’t think the currently popular cancer and AIDS drugs are toxic.
Wow…a whole new level of teh stupid. “Philosophy” has nothing to do with it.
Of course cancer and HIV therapy can be toxic…they also happen to save and improve more lives than any harm they cause. The real test will come when you or a loved one gets a serious disease….I hope very much that never happens.
pec wrote “We have to think. We cannot expect scientific research to replace common sense.”
That is one the most arrogant and ridiculous statements I have ever heard.
Common sense – “My grandmother smoked a pack a day and lived to be 90. Therefore smoking does not cause cancer”
Science – “Large scale epidemiological studies indicate smoking causes cancer and here are some biochemical mechanisms of how it happens”
Common sense – “The sun goes around the earth. The earth does not move”
Really what you are saying is “when scientific research with control groups, placebo arms and large samples contradicts my limited personal experience or what I wish was true I will ignore it.
By the way – a couple of days I ran into a guy who has had brain cancer since before I met him (6 years ago). He looked as healthy and happy as I ever seen him (a little over a year ago he could barely walk). The chemo was toxic – but it has kept him alive.
@PalMD
Everyone knows that a doctor is “licensed” to administer potentially poisonous drugs to overcome a greater evil. But does that same implied authority extend to giving a potential poison to attempt to prevent an event, for which the possibility is only implied by reference to a rather arbitrary formula in which cholesterol plays a dubious role, only forecast to affect 2 out of every10 of those selected, and tackling cholesterol level, one of the least of the risk factors. The Qrisk study showed that the “formula” overestimates the risk by 30% for UK populations, so that nearly 9 out of every 10 patients treated will not need the benefit of such treatment, but will attract the risks of statin side effects. Not the most accurate of scientific forecasting, when the more accurate forecasting tool of CVD is Homocysteine level, which gets no mention at all.
I know you will say where is the data, but a disdainful attitude to real life problems, not recorded in trial reports, possibly for the same reasons that you disbelieve what today’s patients are saying, can hardly be described as medicine in the best interest of the patient. I have many friends who find problems with statins, locally and on line, can they all coincidentally have onsets of muscle and joint pains, peripheral neuropathy, confusion etc, etc, when starting with a statin, that is an awfully large number of improbalities for a logical mind to accept.
@ Synaptix
“UKguy – I’m not argueing with the fact that Statins can cause the problems brought up here. I just completely disagree that the “truth” is being somehow suppressed – the science is being done to adress these issues and the medical community does it’s best to make it so that people can get treatment. No system is perfect, people are going to have bad side effects – to misrepresent and what the authors of this blog are trying to accomplish helpes no one.”
Please take a look at this article from ABC News and read the comments left by real people who have had experience and maybe you can see what happens while all around the people who are pushing this rubbish totally ignore its existence.
http://abcnews.go.com/Health/HeartDiseaseCenter/story?id=4281162&page=1
The above link was found on http://www.spacedoc.net/board/ the folk that are in the forum as well as the site owner are all victims of this “wonder drug”.
Please look at the statement you wrote – {to misrepresent and what the authors of this blog are trying to accomplish helpes no one} – the authors of this blog went all guns blazing to ridicule anything that has been in a negative way about the effects statins have in the real world.
Initially while blogs like this keep trying to make the suffering of thousands of statin users seem to be insignificant and keep talking about how they are saving x amount of lives and that they would have died if they had not taken them and as in the link above {Doctors have largely discredited an anecdotal link between the popular cholesterol drug Lipitor and memory loss.} you have to ask where is the science in this?
If you have read the readers comments, you will see reality in the raw, no glorified puppet who is getting paid a fortune to say this rubbish is the best thing since sliced bread or whatever the catch phrase is that suits the moment. In the meantime doctors and patients are being told or mislead about the effects that Statins actually ARE causing. Too many people are being told “Statins don’t do that” and they are so very very wrong.
Anyone who has experienced the side effects of a Statin and reads what has been written by professionally trained medical practitioners is bound to get annoyed at the lack of knowledge on the subject that they the professionals are trying to prove or disprove.
Thank goodness for sites like spacedoc’s and the ability to access places like THINCS as well as being able to read online most of the major medical journals and published reports and references to other papers.
You may care to read the article here but even more so the comments that have been left by readers ok.
http://www.businessweek.com/magazine/content/08_04/b4068052092994.htm?chan=magazine+channel_top+stories
@ Synaptix
my previous effort could have been worded much better but I am actually tired and it is the best I can do for now. Unless you experience or have seen what these drugs are capable of doing to people with your own eyes, you will not be able to comprehend the true severity of the situation.
It is good that people like youself actually ask questions or raise doubts about different aspects, apart from sometimes being annoying it does get thing brought out into the open, this is not the impression that I got from the author of this blog. A healthy debate is better than a one sided conversation and I thank you and everyone else for taking the time to ask and listen to what has been argued.
I personally know that statins cause considerable damage to many people but it is up to yourself whether or not you think that if the millions of people taking statins were actually made aware of what they are capable of doing, would still be taking them at all.
The reality is that doctors were not made aware of the problems these drugs can cause, if a doctor was aware or had doubts about them they would surely have asked about a possible link via the sales reps or manufacturer etc.
You will also see that the old and vulnerable have had to take this medication because scientists and the medical profession believed that it was so wonderful. The amount of pain and suffering they have inflicted on those poor souls is unthinkable.
I am just waiting for them to add it to petrol so that cars will last longer or something equally as stupid to keep sales going.
I will leave this for now, but I think you already know what is going on from your own observations and from what you have also just read from the 2 links I mentioned in the last post, no one can see what they do not want to see but I think maybe you are better than that, either way everything is there to be seen for those who open their eyes.
Nothing is True unless it has been demonstrated by research funded by big drug companies.
Nothing is True unless your MD tells you it is True.
Your own experiences are not True, unless they agee with what your MD and the big drug companies say is True.
Now be good little sheep and get back in your herd.
@ pec
I am pleased I know you wrote this comment tongue in cheek and I know you expected someone is bound to say:-
“it’s flock and not herd”
and you they are right, BUT DO NOT SAY IT FAST!
“Now be good little sheep and get back in your herd.”
another report was descussed here:-
http://forums.wsj.com/viewtopic.php?t=1351
UK-Bloke,
I must disagree with you on this point. Sheep can belong to either a flock or a herd. We know this because we speak of herding sheep.
Now repeat after me:
Bahhhhh. Everything my MD tells me is true.
Bahhhhh. Research funded by big drug companies is never biased.
Bahhhhh. We must never have an opinion on anything unless it has been demonstrated by big science, preferably funded by big drug.
Bahhhhh. My MD is all-knowing and must never be questioned.
Now go back to your herd (or flock).
@raygee
You have no idea what you are talking about.
The data that supports statin use is not just aimed at cholesterol levels, but, as I and every other actual professional has mentioned, at real life outcomes.
Primary and secondary prevention ARE legitimate reasons to prescribe a medication.
I would suggest you look the terms primary and secondary prevention up.
pec, are you taking statins? If not, then I definitely will continue taking mine.
@ pec
Bahhhhh humbug EWE got me there I say rather sheepishly
Someone else talking about statins had similar comments about people being treated like sheep and came out with the name Sheeple ie those who are easily led and was very apt for the context of which they wrote at the time. I don’t have a problem with that but the first time I see a jar of mint sauce on my doctors desk I think I will make a hasty exit (unless he pulls the wool over my eyes), I will also start worrying if he comes to work wearing wellington boots and says hey ewe, come here my little lamb hehe
I can’t blame any medication for my warped sense of humour but after visualising my doctor in green wellington boots, I think I am starting to like the idea
Help!
@ PalMD
I know that primary prevention efforts with statins have 80 deaths recorded against them in UK Yellow Cards, and thousands of varied other problems, varied because the damaging suppression of Coenzyme Q10 and other mevalonate products prevents ATP being made in the mitochondria wherever in the body that deficiency happens to occur, it is not controllable. Those with a good supply of Q10 may not notice the death or cessation to operate of a few cells in a particular function, but others, particularly those in the second half of life, cannot afford any loss, and problems are almost inevitable.What price is primary pevention prepared to pay, and could everyone be told the full extent of the risks attached to it?
As for secondary prevention, those whom I know who have had MIs and been given statins have had such severe side effects that they had to give up the statins, still experiencing the side effects, but their hearts keep working OK. The same has been reported in trials by clinicians trialling the use of Q10 in such cases. Note: medical personnel appear to have no idea how to treat those severe side effects, some food for thought there.
Primary prevention must be essentially risk free, extension of life at the expense of quality of life is a very doubtful advantage, and the medical press has questioned if attempting to prevent CVD in the elderly is not likely to make the eventual cause of death something much more sinister and unbearable.
If the data that supports statin use is not aimed at cholesterol, why use a cholesterol lowering drug, and not fully investigate the real reasons why statins save some lives, for example prevention of inflammation, reduction of homocysteine, or Nitric Oxide support.
The influence of commerce has been much greater than that of science in the cholesterol field, commencing with Ancel Keys’ assertion that saturated fat and cholesterol were linked, only publishing the minority of studies that agreed with his theory, and ignoring the others. The Food Industry has made a great pile out of Lite products, and the drug industry much more. Lipitor is said by its manufacturer to be the most researched of drugs, but trials are not research, mainly they are market preparation. True research is necessary in much narrower and deeper biological fields, to ensure that the whole of the area of influence of the drug is known.
I am sure you will not let me convince you in all this, but the days of the paternalistic doctor, believed to know everything, are long past, and patients have access to more information with which to choose and make up their own minds on the course of action to take. I have studied this subject for several years now, I would have been dead long ago if I had not done so, and I have found that the big organisation is by no means the only fount of knowledge. Dedicated individuals and groups, interested in finding real answers to particular problems, find things that help, without having to try to invent mass market goods.
@ raygee
raygee, It is futile to address the authors and residents of this so-called science-based medicine blog. Clearly, they are all either unwilling, or incapable, of examining the scientific literature in a manner that does not support their personal prejudices.
It is absolutely disgraceful conduct to deflect anything with which they collectively disagree. It means this erudite site is little more than a mutual masturbation society.
I would have expected something more from people with the elevated and trusted role of the family medical practitioner. Nevertheless, the statin gravy train is finally coming off the rails. It follows that there will not be another social milieu that automatically lauds medics and places them on a pedestal, after this egregious display of quackery.
As for big pharma… the attitudes on this blog have obviously been bought and paid for by the drug overlords (to judge from the obfuscation and the reluctance to address a single point made in opposition to the prevailing one that is favoured by the residents of this blog) and it is a concrete example of the belief that drug companies, and their medically qualified stooges, can be left to act in an untrammelled manner because they have pots of gold to dispense to the hard of thinking.
“It means this erudite site is little more than a mutual masturbation society.”
Hmm…when groups of scientists agree about something, it’s usually called “consensus” rather than “masturbation”. Your idea does sound more fun, though.
If I recall correctly there was the PROVE IT study that compared low dose Pravachol to high dose Lipitor to see if something other than cholesterol lowering played a role. The study was run by the makers of Pravachol, who were hoping that a pleiotropic effect would be shown for their drug. Unfortunately their competitor drug came out on top showing that the amount of cholesterol lowering was what was important in preventing recurrent coronary events. Not everyone can benefit from a statin. They are safe as long as you monitor for side effects. There are people who have intolerable side effects from them and unfortunately there is little that can be offered them other than TLC and they die sooner. Others are too stupid to listen to their doctors and listen to CAM quacks and don’t benefit from them either and they also die sooner. Everybody does die, sooner or later. Some have a choice, some don’t.
@ weing,
That was a pretty decent post right up to the point about :-
*Others are too stupid to listen to their doctors and listen to CAM quacks and don’t benefit from them either and they also die sooner. Everybody does die, sooner or later. Some have a choice, some don’t.*
I think you will find that most of the victims have listened to their doctors telling them that statins don’t do that or you are just getting older and even that you will die if you stop taking them. We believed in what our doctors tell us, it is a disgrace when we find out that a patient has more knowledge about statins than the person who prescribed them, this is fact and not a fairy story.
You may not realise that most doctors did not even know about the side effects that statins cause, there are still doctors as on the ABC News article I mentioned in an earlier post claiming they have nothing to do with memory problems.
I have put the link here to save you searching, read the comments that have been left by ordinary people who have been affected by something that has been kept away from the doctors prescribing this stuff and the people who have taken it.
http://abcnews.go.com/Health/HeartDiseaseCenter/story?id=4281162&page=1
also a PDF copy of some interest:-
Primary and secondary prevention
http://www.dustri.com/ze/cp/samplecopy/cp12567.pdf
I am very much aware of the effects and side effects of statins. Have been prescribing them to patients and using them personally since my own MI in 1994. I have always carefully monitored my patients and have not forced anyone to stay on them. There are patients who do not tolerate them and we stop them. I would not take a medicine if it was making my life miserable and would not expect a patient to do what I wouldn’t. (Unless it was for a brief period. Unfortunately that is not the case with statins.) There are other medications that we try, unfortunately they are not as good as the statins, but we do our best. Even then, patients may not tolerate them either. There are no medications without side effects. Statins are only part of the treatment of the patient and lifestyle modifications are essential. My approach to patients is not a one size fits all, and therapy is individualized for everyone based on risk factor analysis (to determine risk of cardiac event over the next 10 years) for primary prevention and goals of treatment, risks and benefits are discussed, and the patient then decides on what he wants to accomplish.
The Steinberg article was very informative. Thanks for the link.
(It’s worth pointing out that he ends the article with a few unreferenced, and I’d have to assume relatively unproven, claims about statin benefits in women and the elderly, in an otherwise rigorously referenced historical account.)
@weing
PROVE-IT – 4,162 patients following an MI, or unstable angina. Half were given atorvastatin and half were given pravastatin. LDL was shown to have been reduced more with atorvastatin than with pravastatin. The principal finding was a 16% reduction in the ***relative risk*** of dying from a cardiovascular event.
All-cause mortality, for patients taking atorvastatin, fell by one percent from 3.2% to 2.2% in two years thus equating to one half of a percent reduction in absolute risk for each year. Not quite the stunning 16% reduction in cardiovascular events that reading the PROVE-IT study had suggested.
The PROVE-IT study exhibited a basic error in using two variables and the startling 16% reduction in relative risk was found in patients taking a different drug to that which was under scrutiny. The trial proof should have been derived from a single drug… not two different drugs; which did provide for one uncontrolled variable.
Deriving meaning from PROVE IT would have required that there was an identical mode of action from both drugs used. All PROVE IT managed to ‘prove’ was that atorvastatin appeared to offer more protection that pravastatin. It may have had little or nothing to do with any assumed effect on LDL. Hardly earth-shattering news and not really a scientific study either.
J-LIT studied more than 30,000 patients and the drug, simvastatin, was given at a single 5mg dose OD to all participants. That study demonstrated that there was NO CORRELATION between the amount of LDL reduction and the mortality rate.
@ PaIMD
[quote] Hmm…when groups of scientists agree about something, it’s usually called “consensus” rather than “masturbation”. Your idea does sound more fun, though. [unquote]
Methinks thou dost protest too much.
To qualify for the appellation ‘groups of scientists’ it is a given that science is the mutual glue that binds them into a group. Rubbishing anything that runs counter to the current religion or that is just disagreed with, from a position that is neither inviolate (practising clinicians) nor unassailable, is not the practice of science.
This site is inhabited by clinicians, who appear to be bent on refusing to look at any of the scientifically derived evidence proffered, from appropriately conducted clinical trials and collectively could never be considered to be a ‘group of scientists’.
It will be clear, to any half-sensate human being, that unless the clinicians on this site get around to answering any of the scientifically founded criticisms against statinisation, they are doomed to remain a random collection of individuals, whose sole purpose appears to be the tedious promulgation of unfounded personal opinions.
@ weing,
I am pleased to hear that you are amongst the enlightened doctors who are aware of side effects and treat your patients with care and monitor their progress closely. Without going into too much detail, the myriad of both mental and physical (memory problems, tiredness and pain sites etc) seem at first to be unrelated until it was observed that the statins depleted other vital resources in its blocking of cholesterol.
Unfortunately this information has not been passed on to so many doctors and their patients where it could and really would have made such a vast difference to the way treatment was carried out.
There are so many people who are exhausted all the time and have problems with names, stringing a sentence together and often in pain. When you go to see your doctor and try to explain your symptoms to him, all you end up doing is looking like a hypochondriac, even more so when nearly all tests come back negative unless the blood CK level becomes elevated etc.
If doctors were made aware about side effects and the depletion problem, I dare say that a lot of people would not have been made so miserable for so long and for some, that pain and misery could be permanent.
Most doctors do the right thing with the knowledge they have by getting blood tests, x-rays of joints, MR scans of the brain etc and get you to see a neurologist and rhumatoligist as well as cardiologist and all the tests entailed. The shame of it all is not one of them may know about statin side effects either!
For a doctor to do make the right decision, he/she should have vital information about side effects and symptoms passed on to them, Statins have been in use for around 20 years or so. Why are doctors still in the dark about the side effects and still unaware about the depletion issue?
I had my own MI in 1995 and statins soon started after that, I also had a triple bypass December 2004. My Zocor – Simvastatin was raised from 10mg to 40mg prior to the operation and my health issues rapidly got worse from there on in. Everyone including myself thought it was because of the need for bypass surgery, all I can say about that is we were all so very wrong.
You obviously know what to look for in your patients who are receiving statin therapy, I do hope that you will pass on your knowledge to your colleagues as it really could save a lot of people from coming to harm even with the very best intentions.
jayemcee
Project much?
@ daedulus2u
I suggest that you try a little harder to find a credible scientific argument for the use of statins; rather than attacking the messengers arriving with bad news.
Oh wait… you don’t have one.
jayemcee,
“PROVE-IT – 4,162 patients following an MI, or unstable angina. Half were given atorvastatin and half were given pravastatin. LDL was shown to have been reduced more with atorvastatin than with pravastatin. The principal finding was a 16% reduction in the ***relative risk*** of dying from a cardiovascular event.
All-cause mortality, for patients taking atorvastatin, fell by one percent from 3.2% to 2.2% in two years thus equating to one half of a percent reduction in absolute risk for each year. Not quite the stunning 16% reduction in cardiovascular events that reading the PROVE-IT study had suggested.”
The above is a beautiful example of a straw man argument.
“The principal finding was a 16% reduction in the ***relative risk*** of dying from a cardiovascular event.” is not true and need not be defended.
“All-cause mortality, for patients taking atorvastatin, fell by one percent from 3.2% to 2.2% in two years” is true. So what?
“Not quite the stunning 16% reduction in cardiovascular events that reading the PROVE-IT study had suggested.” is false.
UK Bloke posted a link that was pretty compelling in favor of statins.
http://www.dustri.com/ze/cp/samplecopy/cp12567.pdf
So what is “wrong” with this study? Other than it doesn’t show that statins are the death substances you believe/want/need them to be?
“All-cause mortality, for patients taking atorvastatin, fell by one percent from 3.2% to 2.2% in two years” is true. So what?
I take statins myself but I have to say that if raised LDL is the main cause of heart disease, and statins lower this substance by such a big margin, I would hope for a much larger reduction in all-cause mortality than an absolute 1% or a relative 16%.
@ weing
translation… I don’t believe what you have said so I will ignore it.
Yet another demonstration that the clinicians writing on and for this web site eschew scientific evidence in toto and are completely unwilling to address peer-reviewed evidence against statins.
Your (lack of) argument relies on this web site’s common currency of claiming ‘logical fallacy’ or ‘strawman argument’ in every instance where some point is made that does not fit with your worldview. It is precisely the sort of Google logic 101 nonsense that is typical of protagonists with nothing to say. A little training in symbolic logic would possibly serve you better.
Care to try turning your hand to dismissing J-Lit?
pc,
All-cause mortality is one thing, a cardiac event is another. You don’t really expect a statin to prevent you from being shot or hit by a car and many other causes of death do you? Not all cardiac events are fatal too. And here, you are talking about only 2 years. Unfortunately, the best that statins can do is to decrease coronary heart disease risk by 30% max.
jayemcee,
I would not try to convince you of anything. I am just pointing out that you are using fallacious logic which results in wrong conclusions. There is no need for belief.
Regarding J-Lit:
Let’s imagine you have a country where the people are starving. Food that will save them costs 40 cents. They have no money. Some kind people decide to see if they can help them by giving them money. They allocate 5 cents to each starving person. They end up starving to death. The kind people deduce that money does not prevent starvation and stop wasting their efforts in this direction.
the date from J-Lit is not imaginary
Apart from the typo (date instead of data) what possible relevance does imagining anything have to with the data gathered from Japan which is not considered to be a country where the people are starving.
This is another example of the consistent failure of members of the pro-statin lobby, to address any factual evidence. On its face, one may easily conclude it was myopia. A little further consideration reveals the mass hysteria of clinicians who refuse to deal with facts.
Not a single factual piece of evidence (provided by the anti-statin lobby) has been addressed in a scientific manner since the beginning of this thread!
I see my analogy was totally lost on you. That explains why you misrepresented the findings in PROVE-IT. You simply are unable to understand it. You do not have to take statins, you may or may not need them. I have no way of knowing that. Anyone that needs to take them ,and who you convince not to use, will only feed the medical-industrial complex with heart attacks, strokes, peripheral vascular disease that will keep the cardiologists, cardiac and vascular surgeons, neurologists, and medical device makers, busy and making lots of money for a long time.
weing
“All-cause mortality is one thing, a cardiac event is another. You don’t really expect a statin to prevent you from being shot or hit by a car and many other causes of death do you? Not all cardiac events are fatal too. And here, you are talking about only 2 years. Unfortunately, the best that statins can do is to decrease coronary heart disease risk by 30% max.”
I take your point and whilst I agree with what you are saying, you simply cannot ignore all-cause mortality rates. Yes, the drug could be doing a good job at reducing cardiac events (and statins do, thats why I am taking them), but wiping you out in another way (heart failure, cancer etc). If the positive effects of the drug are totally negated by other means that have nothing to do with cardiac events then the drug is useless. I believe this is one of the points that the THINCS lot (Dr Malcolm Kendrick in particular) are trying to get across. I understand that in tests on rats with statins, there was a statistically significant increase in cancer. If this effect translates into humans there are going to be a lot of upset people!!
You say Japan is not a country where people are starving. You are correct. What is the prevalence of coronary disease in Japan? What is the prevalence in the US and European countries? Compare the risk of an MI of an average 40 year old man in Japan to that of the average 40 year old in the US. If the risk of MI is high, statins will help if the risk is low statins will not be of benefit. That is why individualize treatment. I would not prescribe statins to anyone whose risk of MI is low, there is no benefit and all you’ll get is side effects.
pc,
Fortunately for you and me, they have not been shown to cause cancer. I keep wondering though, if you were supposed to get cancer at 80 but an MI killed you at 40 or 50 or 60 or 70, would you say the MI prevented cancer? Now suppose you took a statin that prevented the MI from killing you and you reached 80, would you say the statin caused cancer?
weing
Yes, I understand from my cardiologist that a cancer link in humans has not yet been proven. As you say it would be hard to prove a definite connection using simple statistical analysis, mainly because a large proportion of the people given statins are the elderly (who are at increased risk of cancer anyway). Besides, being a fact based man, I would want someone to be able to explain the mechanism by which statins cause cancer rather than just relying on a set of numbers pointing to a possible link. However, I am still wary of taking statins having had several friends have such a bad time with them (one was off work for 5 months due to statin side effects. The doctors simply would not believe it was the atorvastatin, until he eventually saw a neurologist who decided the nerve damage he was seeing had to be statins. 4 weeks after coming off them he was back at work).
Dr Hall and others,
Thanks for taking the time to explore this subject so thoroughly. This discussion will inform my decision if my doctor were to prescribe statins for me (not that it seems likely in the near future.)
My very naive question for those who are more focused on statins’ risks than their benefits: If you feel that taking statins would be harmful to you, why not just say no? Medicine is a collaboration between doctor and patient. There are multiple ways to treat any disease; if you wish to avoid certain treatments you should work out other options with your doctor. And if the doctor refuses to be flexible, you should find another doctor.
@ Dacks,
your question is a valid one and if either the doctors or the patient had been made aware of all the problems that can and do occur to a great many people, then there is no way on earth that most people with a hint of common sense would take such a vast risk of letting themselves come to harm.
The answer to peoples choice in this matter is that they were not made aware of the dangers and were told that this medication is safe other than a very few people had liver problems with it (hence the blood work).
To top it all, there are still doctors proclaiming the virtues of this wonderful medication and denying that there is a problem. (ABC News report etc)
I am not going to get on my soap box and try to persuade you either way, everything you need to know IS coming to light now, but it was not a few years ago and people like those at THINCS and Spacedoc.net have helped so many people come to terms with there symptoms that they should be praised for it and not ridiculed by someone who really should know better.
The problem is, for those of us who have heart disease, there is no other proven medication that has the efficacy of statins. I tend to agree with Dr Malcolm Kendrick on the use of statins. That is, if you have heart disease then I would strongly advise you to at least try them. If you have not got this particular risk then I wouldn’t bother. I would concentrate on diet and exercise.
@ Dacks
[quote] My very naive question for those who are more focused on statins’ risks than their benefits: If you feel that taking statins would be harmful to you, why not just say no? [unquote]
People who have tried to just say no are frequently considered mad by their medical practitioner and in the UK, they are left without a doctor when the practice has them removed as awkward patients.
(you may not realise that the UK assigns the medical practitioner to the patient and rarely is there any choice… unless you are a private patient)
[quote] Medicine is a collaboration between doctor and patient. [unquote]
Nonsense. When does a medic accept the patient’s own view about a proposed course of treatment? ANY questioning of a clinical opinion by a lay person is met with incredulity.
Read above and note the sneering tone inherent in the following enlightened statement… [quote] It wasn’t a day or two at “google university”[unquote] from PaIMD, whom one would assume is an enlightened medic who would accept your statement in its entirety.
[quote] There are multiple ways to treat any disease; if you wish to avoid certain treatments you should work out other options with your doctor. And if the doctor refuses to be flexible, you should find another doctor. [unquote]
As indicated, you cannot transfer easily between assigned medical practitioners. There is an issue of informed consent. I happen to believe that the patient has a right (the clinician has the obligation) to be informed about any proposed treatment. It is the clinician’s role to make explicit the likely outcomes and the risks involved in pursuing any particular form of treatment.
Given the unwillingness of the medics (a large number of whom accept pharmaceutical company funding) to consider the possibility that statins may be harmful and furthermore, given the lamentable state of knowledge about basic biochemistry demonstrated by clinicians, it is clear that the patient cannot be informed appropriately before agreeing to take statins.
Statins aside, the cholesterol heart disease hypothesis has been demonstrated to be untrue on many occasions. Patients are being coerced into lowering the substance that their body needs. People with low cholesterol levels have been shown to die earlier than people with high cholesterol levels.
Explain to me why aboriginal Australians with very low cholesterol, get a lot of heart disease and then explain to me why the Swiss, with very high cholesterol levels do not get a lot of heart disease. Explain also why the other products of the body that are inhibited by statins within the mevalonate metabolic pathway, somehow become unwanted by the body just because statins are lowering cholesterol.
You original question was why not just say no. I do but I am concerned for the large numbers of people who believe that their doctor will never get it wrong nor do them any harm. I am happy to devote my time and my energy to preventing people from taking statins. An instructive phrase that has been attributed to Edmund Burke follows…
“All that is necessary for evil to succeed is for good men to do nothing.”
Take statins if you must but permit me to try to prevent that act.
“Take statins if you must but permit me to try to prevent that act.”
I’ll permit you, if you permit my family to sue you for everything you have and garnish your wages should I subsequently get a heart attack.
The problem you describe with physicians discharging patients like you from their practices is coming to the US as physicians are increasingly being paid on the basis of performance. If my patients have less heart attacks, I will make more money and I’ll be penalized if they have more cardiac events.
[quote] I’ll permit you, if you permit my family to sue you for everything you have and garnish your wages should I subsequently get a heart attack. [unquote]
This pre-supposes too much. To whit, that statins prevent MI (they don’t) and that heart disease will never occur when statins have been given (it does) Furthermore, people do not die through lack of statins. they have died over the aeons because from a myriad of causes… non of which statins address. Your family, as well as you, need to understand the damage done to the ability of cells to derive energy from food via, heme a, before rushing off to a lawyer.
[quote] The problem you describe with physicians discharging patients like you from their practices is coming to the US as physicians are increasingly being paid on the basis of performance. If my patients have less heart attacks, I will make more money and I’ll be penalized if they have more cardiac events. [unquote]
It is ridiculous to penalise you for not prevent an MI when there is no prevention available. Take away stress inducing factors and inflammatory causes before you remove anything else and you may be in with a fighting chance. until then, it would be unjust to make you suffer because of a poorly understood multi-factorial event taking place on your watch.
There is a shocking unwillingness to acknowledge that none of us (clinicians especially) are infallible. I object to large amounts of support being given by drug companies to medics who push their products but there is no case for penalising a medic doing his best for a patient, who may not even be compliant.
weing –
“Fortunately for you and me, they have not been shown to cause cancer.”
This is not strictly true. Go to pub med and. search on this:
“Effect of the magnitude of lipid lowering on risk of elevated liver enzymes, rhabdomyolysis, and cancer: insights from large randomized statin trials.”
Alsheikh-Ali AA, Maddukuri PV, Han H, Karas RH state in the conclusion:
“Furthermore, the cardiovascular benefits of low achieved levels of LDL-C may in part be offset by an increased risk of cancer.”
By no means evidence but a worrying finding nevertheless.
jayemcee,
Sorry to burst your bubble but those types of wrongful death lawsuits are a reality for physicians. They should also be a reality for cranks but they are not, so you need not worry. Just because you chose to ignore research and say statins don’t prevent MIs does not make your assertion true. As I posted previously, you cannot prevent coronary events 100%. 30% is about the maximum reduction in coronary disease that has been shown. I know, I’m disappointed too.
pc,
Definitely needs more studying. The association that they found does not imply causality. There are confounding factors. It is well known that cancer will lower your cholesterol level and low levels are an indicator or effect of the disease. This association was found in patients with lower baseline levels of cholesterol which would support that hypothesis. But definitely needs more studying and will be studied. In the meantime, I’ll keep my fingers crossed and continue to take my statin.
@ weing
[quote] jayemcee,
Sorry to burst your bubble but those types of wrongful death lawsuits are a reality for physicians. [unquote]
No bubble to burst. My recall is that it was the clinicians, themselves, who had invited lawyers to advertise in emergency rooms throughout the UK because of some additional sponsorship for equipment and FREE appointment cards with the law firm’s details printed on them.
When you give houseroom to a viper, you can hardly be surprised if it should choose to bite you.
[quote]
They should also be a reality for cranks but they are not, so you need not worry. [unquote]
pfft.
[quote] Just because you chose to ignore research and say statins don’t prevent MIs does not make your assertion true. [unquote]
I have not ignored any of the relevant research. I happened to choose to read a little more research concerning cholesterol, heart disease and the biochemistry of cells. I don’t object to you having a disagreement if you would support it with some references.
In fact, I accept what you say is true and statins do prevent MI. Just explain to me how statins manage to do that (the mechanism by which taking statins prevents a heart attack) and then cite some appropriate references… if there are any.
[quote] As I posted previously, you cannot prevent coronary events 100%. 30% is about the maximum reduction in coronary disease that has been shown. [unquote]
So for every 100 people taking a statin, 70 are taking the drug needlessly? Or is this a very selective 30% and we can all reduce our relative risk of a cardiovascular event by 30% if we all take a statin?
[quote]I know, I’m disappointed too. [unquote]
What disappoints me is the large number of people who have been damaged by statin therapies. The possibility of preventing any more cases of iatrogenic damage is precisely why I admit to being the crank to whom you would ascribe that epithet.
The damage to the body, caused by statins, is profound and incapacitating. Should you feel like discussing the why and the how, I will be around.
jayemcee,
You can look up how statins prevent a heart attack in any standard cardiology or pathophysiology textbook.
If you had a 50% chance of having an MI in the next 10 years, then by taking a statin you will lower your risk of an MI to a 35% chance.
What disappoints me is that you can’t lower it to 0% chance.
Damage caused by statins is real, easily recognized and dealt with.
There are no drugs without any risk of damage. Medicine is constantly learning and evolving. Remember cerivastatin? It got pulled from the market because of excess rhabdomyolysis.
I remember when I was a resident and people were using Quinidine for atrial fibrillation and palpitations. It worked great. Studies showed that it worked true enough, but people treated with the drug died faster. It didn’t take long to find out either. Guess what happened? We stopped using it. The statins have been in use since the late 1980s and no such studies have been forthcoming, in fact the opposite is true.
[quote]You can look up how statins prevent a heart attack in any standard cardiology or pathophysiology textbook.[unquote]
I have. I wanted to learn about the current theoretical basis for statins preventing cardiovascular events. If things work in a standard way, then the standard studies (double-blind RCTs) should be available to support the proposition.
My request was for you to provide those scientific references because this site arrogates the title Science-Based Medicine to itself and anecdotes are, presumably, not required here.
[quote] If you had a 50% chance of having an MI in the next 10 years, then by taking a statin you will lower your risk of an MI to a 35% chance. [unquote]
So you say but where is your evidence for adopting this position?
[quote] What disappoints me is that you can’t lower it to 0% chance. Damage caused by statins is real, easily recognized and dealt with. [unquote]
Agreed, although I don’t support the notion that the damage is easily recognised because so many people appear to be damaged and the clinician not only did not recognise the damage but refused to believe that such damage could devolve from the use of statins.
[quote] There are no drugs without any risk of damage. [unquote]
A fine example of a tautology.
[quote] Medicine is constantly learning and evolving. Remember cerivastatin? It got pulled from the market because of excess rhabdomyolysis. [unquote]
Would that were really true. Medicine ought to be constantly learning and evolving but the profession has ceded much of its professional responsibility to administrators, governments and pharmaceutical companies. Cerivastatin was rightly pulled.
I believe that a later examination had revealed rather more people were killed than Bayer had initially owned up to. Pfizer were informed of an increased death rate for the compound atorvastatin/torcetrapib and that study was pulled in December 2006. ENHANCE appears to have been pulling the wool over rather too many sets of eyes.
Merck not including CoQ10 with their original product shows the pharmaceutical companies’ willingness to betray the medical profession, governments and the people who will be buying and using their products.
[quote] I remember when I was a resident and people were using Quinidine for atrial fibrillation and palpitations. It worked great. [unquote]
Quinidine was not the treatment of choice in say… re-entrant paroxysmal SVT when I was working in an ER environment 3 decades ago. We used either carotid sinus massage, attempted to get the patient to carry out a Valsalva manouvre or we tried to harness the vestigial diving reflex and splashed ice cold water on the face of the patient. If these methods failed then treatment progressed to cardioversion and finally the drug verapamil were used.
[quote] Studies showed that it worked true enough, but people treated with the drug died faster. It didn’t take long to find out either. Guess what happened? We stopped using it. [unquote]
It was the only rational course of action, to stop using quinidine, when it was seen to be killing people faster than if they were not treated with it.
[quote] The statins have been in use since the late 1980s and no such studies have been forthcoming, in fact the opposite is true. [unquote]
Are you saying that statins are not harming people and that there are no studies to demonstrate such a happening?
No, I am saying that the studies show that high risk patients taking statins are less likely to have MIs and strokes than those not taking them. If you are one of the unlucky few, who experience disabling side effects from them, you will unfortunately, not be able to benefit from them.
You seem to be saying that high risk people should not use statins because they may experience disabling side effects from them. They should therefore not benefit from them because of your worry of side effects.
That’s very paternalistic of you.
Back to the cholesterol heart disease hypothesis. It has been falsified on more than one occasion and the hypothesis does not stand up to scrutiny. It does not hold true for every single study and black swans abound.
Given the facts, why should anyone be attempting to lower cholesterol in the first instance? Why should anyone have to be undergoing cholesterol reduction through the use of toxic drugs that are inimical to cellular life?
Yes, I know it is really paternalistic of me… not to want to see more people being harmed by a supine medical profession, that successfully gives the impression of being universally happy to take drug company largesse and carry out large scale research projects for the reflected glory that they can bask in while collecting industry sponsored accolades. You may have missed the NEJM study of that particular situation.
It is an utter disgrace that the medical profession still tolerates the fraud of highly paid (by the drug companies) clinicians, who have been permitted to make public pronouncements that uncritically recommend the products of their paymasters, in the face of evidence to the contrary.
It is no more paternalistic of me to want to see an end to the unsupported and falsified hypothesis, that cholesterol is the causative villain of the piece in heart disease, than an equally paternalistic medical profession… desiring to medicate large numbers of people for life (with everything that presages) with a deeply toxic preparation, without a proven clinical need.
The world is now redolent of ‘Alice Through The Looking Glass’ where everything is turned upside down and patients are only healthy if they take drugs (needlessly) for life and visit the medical practitioner every three months for vital sign monitoring, LFT’s and heck knows what else… to no other purpose than to sell more drugs and collect more fees for service from patients and drug companies alike.
I will remind you that it was the well-named Dr Reckless, who had advised government bodies, when they were deciding national health policies, that statins should be put into the water supply! Not just paternalistic but an indiscriminate blunderbuss approach to cardiovascular health.
It was a sad testament to the times we live in, that Reckless felt able to publicly declare his support for a clinical policy so obviously bereft of common sense. In the halcyon days of clinical practice, he would have had his future clinical career destroyed by declaiming his support for such nonsense.
Ward and Law had wanted to medicate everyone for life, with a polypill that they had the prescience and presence of mind to patent, BEFORE, they had published their life-saving stratagem for the developed world, in an execrable article that had graced the pages of a once august BMJ. The howls of protest to the BMJ did nothing to embarrass those fools.
Yes, I am paternalistic and advocating for the patient (who cannot advocate for themselves) is a paternalistic act that is to be deprecated. [/sarcasm]
Wow, you appear to have knowledge that has eluded all the researchers of the medical profession. I am sure the cardiologists, drug and medical device makers and surgeons will be grateful to you for giving them business. Are you sure you aren’t working for them?
Wait a minute, you are in the UK where they have socialized medicine. Maybe there is a conspiracy and you are working for the government trying to kill people off early in order to save them money?
I’m done with you now and your poor excuse for scientific debate.
Not one single scientific paper presented as proof of the need to take statins. It is just some universal truth that we are supposed to absorb by osmosis and accept as correct
Not a single reference refuted. No interest in examining evidence against the cholesterol hypothesis.
Whichever drug company pays for this site, they sure got their money’s worth.
bye
I gave you one study and you showed yourself incapable of understanding it whether deliberately or otherwise. Why should anyone waste their time giving you more studies to misinterpret. Learn first to analyze and interpret them. Take a course.
Cholesterol lowering trials have repeatedly been shown to be complet failures for reducing CHD mortality and incidence.
The Lipid Research Clinics Coronary Primary Prevention TRial
Out of 3,806 Using cholestyramine a NON statin
30 CHD deaths TREATMENT vs 38 CHD deaths CONTROLS
0.04 % ABSOLUTE CHD mortality risk reduction
How is this supportive of the Cholesterol Theory?
There are 18 clinical dietary intervention trials to date NONE fo which show any support to the false idea that saturate fat increases CHD mortality or incidence.
ANTHONY COLPO exposses all of this
Did YOU know Ancel Keys started this crap by OMITTING natiosn that ate alot of saturated fat and had VERY little CHD and nations that ate low saturated fat and had MUCH CHD
Ancel Keus study had no scientific validity at all.
The ENHANCE trial 58 % reduction in LDL (far more than ANY statin trial ever produced) and the result?
An INCREASE in atherosclerotic plaque at ALMOST DOUBLE the rate of those taking Zocor alone.
And if YOU want the NALYSIS of the J-LIT trial YOU can read here by ANTHONY COLPO
http://www.lowcarbmuscle.com/forums/showthread.php?t=162
NONE of YOU doctors on here have the intellect of ANTHONY COLPO.
ANTHONY COLPO has an OPEN CHALLENGE to ANYONE to SHOW THE TIGHTLOY CONTROLLED CLINICAL TRIAL SHOWING SATURATED FAT AND /OR CHOLESTEROL TO BE CAUSAL OF CORONARY HEART DISEASE
I KNOW NONE of you doctors on here can do it – because the evidence does NOT exist.
re ENHANCE, you are lying and totally misrepresenting the study. You are another one who can’t read and understand a study. Why don’t you read it to try to really understand it and not search for anything in it that titillates you to believe you have found the proof for your inanities. It really is a crime that you are not liable for adverse outcomes that any moron, that needs these meds, would sustain by falling for your nonsense and discontinuing them.
cuz he haz gramer ishues
I suspect it’s a parody.
Linda
Hey “Doctors”
Your merit badges mean NOTHING.
Arguments from “authority” carry little weight – because there are NO AUTHORITIES IN SCIENCE.
HOW has Anthony Colpo misinterpreted ANYTHING?
To the ‘doctors” on here:
Anthony Colpo OPEN CHALLENGE
PROVIDE the evidence from a tighly controlled clinical trials showing saturated fat and or cholesterol to be CAUSAL of coronary heart disease – OR SHUT IT !!!!!!!!
You biult your careers on NONSENSE.
Having elevated FASTING BLOOD SUGAR is a predictor of future coronary events NOT cholesterol.
STRESS and elevated blood sugar are DIRECTLY causal of coronary heart disease.
AGAIN GET FAMILIAR with the research. Thgere are EXCATLY 18 clinical dietary intervention trials to date NONE fo which support the Cholesterol Theory of CHD.
The Women’s Health Initiative 2006 being the latest.
AD HOMINEN attacks Anthony Colpo are A SURE SIGN OF SOMEONE WITH NO SCIENTIFIC ARGUMENT and they KNOW IT so they ATTACK THE PERSON PERSONALLY.
READ COLPO AND LEARN
‘
Think HDL is protective?
http://www.lowcarbmuscle.com/forums/showthread.php?t=1657
THINK LDL causes CHD?
http://www.jpands.org/vol10no3/colpo.pdf
Bad Cholesterol OR BAD SCIENCE?
YOu “doctors” have MUCH to learn from Anthony Colpo.
He puts YOU to SHAME. You KNOW it.
Think the Lyon Diet Heart Study supports the Cholesterol Theory of CHD “doctors”?
THINK AGAIN – Anthony Colpo explains
http://www.lowcarbmuscle.com/forums/showthread.php?t=111
THINK The Anti Coronary Club 1966 supports the Cholesterol Theory of CHD? THINK AGAIN
There were 8 deaths from CHD in those randomized to polyunsaturated vegetable oils DESPITE HAVING A CHOLESTEROL LEVEL OF 225 mg/dl COMPARED TO 260 mg/dl in animal fat crowd NO CHD DEATHS FROM PERSONS RANDOMIZED TO SATURATED FAT
You ONLY would see this in a throw away line in the FULL TEXT of the study.
At least they died with a low cholesterol level I am sure that was of great comfort to loved ones.
Did YOU know DESPITE the fraud of Ancel Keys upon further examination NO RELATIONSHIP was found between saturated fat and CHD mortality WITHIN, WITHIN nations
CHD varied 2-6 WITHIN NATIONS such as Italy and Greece and more.
COLPO EXPLAINS
AGAIN Cholesterol lowering trials have REPEATEDLY SHOWN cholesterol lowering is USELESS for lowering CHD mortality and incidence and potentially harmful.
Look up the A to Z trial, J-LIT, ENHANCE LRC-CPPT.
J-LIT for instance LOWER CVD risk at higher LDL and total cholesterol levels !!!!!!!!
http://www.lowcarbmuscle.com/forums/showthread.php?t=162
I HOPE I offended you Cholesterol Theory proponent doctors YOU have built YOUR careers on a bunch of scientifically untenable NONSENSE and I am NOT shy about telling YOU.
Anthony Colpo and Dr. Uffe Ravnskov EXPOSE YOU
Are you this Colpos’ butt boy? You mean he showed you the truth and you don’t think for yourself? Try reading the studies yourself to figure them out. A dictionary should be enough to help you. Don’t believe what anyone tells you about them. You might just learn something. Then again, you might not. Do you dare?
I’d be careful about citing articles published in the Journal of American Physicians and Scientists (JPANDS). JPANDS is about as poor a source as any I have ever seen. It’s antivaccinationist, pushing the discredited claim that vaccines cause autism; it’s published some truly dreadful, ideologically driven “research” (and I do use the term loosely) that claims, against all evidence contrary, that abortion leads to breast cancer; in short, it’s a crank journal, and I do not say that lightly.
That Colpo publishes in JPANDS tells me much about him, and what it tells me is not good.
Statins can SLIGHTLY reduce CHD mortality rates. They do this via ANTI INFLAMMATORY, INCREASED NITRIC OXIDE SYNTHESIS, REDUCED FIBRINOGEN CONCENTRATIONS, REDUCED BLOOD VISCOUSITY ANTI SPASM qualities to name a few.
The ENHANCE trial only FURTHER CONFIRMS THIS amoung mountains of other trials.
Statins have worked whether cholesterol was lowered a little or alot
Cholesterol lowering druge BEFORE statins which did NOT have statins 11 other effects WERE COMPLETE FAILURES FOR LOWERING CHD MORTALITY
See Dr. Malcolm Kendrick’s video on statins here
http://www.youtube.com/watch?v=jE_RIQY53ys
You are big on insults to THINCS short on refutation with FACTS
The ad hominen attack a classic sign of someone with NO ARGUMENT and can NOT refute with research.
Also I did NOT misrepresent the ENHANCE trial at all
You hero Dr. Nissen even said ” This is as bad of an outcome as you could have ”
58 % reduction in LDL INCREASE in atherosclerotic plaque.
Dr. Nissen ADMITS Zetia is USELESS. Recommends AGAINST IT
hHe just hasn’t come to the obviouos conclusion that numerous cholesterol lowering trials have found – cholesterol lowering is USELESS for lowering CHD mortality or incidence.
Perhaps if Dr. Nissen REVIEWED the research like DR KENDRICK DID he would admit this TOO
You are still missing the point and you are lying regarding the ENHANCE results showing increase in plaque. Read the studies yourself and come to your own conclusions instead of listening to some charlatan. To me the study is useless as the patients were not brought to meaningful cholesterol levels. From the little data that is available, the lowest LDL achieved in the study was 139. The average LDL of a patient with an MI is around 135. If the study showed any significant benefit from Zetia, it would argue for an effect on something other than cholesterol.
Please describe how Dr. Uffe Ravnskov and Anthony Colo are charlatans?
How has he misrepresented the literature?
See here:
http://www.opinions3.com/Uffe_Ravnskov_Report.htm
[...] post by Harriet Hall delivered by Medtrials and [...]
Why don’t describe how they are not charlatans. Give us their qualifications etc.
I have challenged YOUR falsely held beliefs and you ahet me for it.
The classic “appeal to authority” argument.
Dr. Ravnskov is a REAL DOCTOR.
Anthony Colo is a researcher.
There are exactly 18 randomized clinical dietary intervention trials conducted to date examining the claim that saturated fat restriction lowers CHD mortality and incidence.
NONE of these trials show saturated fat restriction to lower CHD mortality or incidence. In fact many just the opposite.
The Women’s Health Initiative 2006 being the most recent.
See Ancel Keys lies here:
http://www.fathead-movie.com
This movie is coming out soon exposing it all to the public.
See the video proof of Dr. Robert Olson begging Senator McGovern for ” MORE RESEARCH ON THE MATTER” before recommending low saturated fat diets.
That’s right, the low saturated fat diet was invented by a fraudulent scientists and pushed by a CONGRESSIONAL COMMITTEEE headed by Senator McGovern
How about their CVs?
The only dietary intervention that I remember showing something was the Dean Ornish diet along with all sorts of lifestyle modifications.
@ Razwell,
you are wasting your time trying to get any sense out of the donkeys on this site, OOOP’s I mean doctors, oh no I was right the first time.
They-ought, They-ought, They-ought to know better really!
I am very pleased to know that most doctors would not act in such a stupid farcical fashion as this bunch of know nothings.
weing writes:
“Fortunately for you and me, they have not been shown to cause cancer. I keep wondering though, if you were supposed to get cancer at 80 but an MI killed you at 40 or 50 or 60 or 70, would you say the MI prevented cancer? Now suppose you took a statin that prevented the MI from killing you and you reached 80, would you say the statin caused cancer?”
Nationwide disease rates, uncorrected for age, are in no way the basis for the concern that statins cause cancer. As far as I can tell, there are three major reasons for that concern: 1. They do cause cancer in lab animals. 2. People with low cholesterol have higher cancer risk; you note that cancer may cause low cholesterol but low cholesterol also seems to correlate with future cancer. 3. In a couple of large statin studies, statins had a definite cardioprotective effect (in males under 65), yet there was no reduction in overall morbidity and mortality in the treatment group, because that group – within the same time period – had a countervailing increase in other problems. Notably, cancer.
Also, accidental and violent death. You remark elsewhere:
“All-cause mortality is one thing, a cardiac event is another. You don’t really expect a statin to prevent you from being shot or hit by a car and many other causes of death do you? Not all cardiac events are fatal too. ”
No, I don’t, but strangely enough, it seems possible that a statin could cause me to be shot or hit by a car, as rates of such misadventures have been seen to increase when cholesterol is lowered. If statinization subtly impairs mental function, it is plausible that that impairment could have negative health consequences.
Given that for women and the elderly there is little evidence of cardiovascular benefit, the chances that total morbidity and mortality would be much improved for those people, especially in primary prevention, seem very low. Personally, I’d rather have a heart attack than cancer. As you admit, it might not kill me, and if it does, I won’t live long enough to be sold chemo in my last miserable weeks. You are vehemently hostile to the suggestion of patients’ forgoing statins, even if they might be trading a 3% extra cancer and misadventure risk with statins for a 3% extra heart attack risk without. Is the assumption that cancer is “better” than heart disease? The media are now reporting that aromatase inhibitors, though better than tamoxifen at preventing the recurrence of breast cancer (which already will not happen in most women), cause significantly more heart damage. Would you agree that women should consider avoiding these drugs because of the heart risk? If not, it starts to look like the unacceptable disease to you is the natural one, and the acceptable risk is the iatrogenic disease, no matter which is which.
apteryx,
re Tamoxifen, you have to weigh the risks and benefits and then make the decision. I agree that sometimes it is like a Sophie’s Choice. Regarding the cancer risk from statins, I definitely think it merits studying. If they cause cancer I want to know. But what have we got thus far? We have a proven benefit of statins of 30% risk reduction of cardiac events. We have speculation about a possible increase in cancer risk. For me the choice is easy. I’ll go with the devil that’s known. You may chose otherwise, again that is your choice, and as long as you are aware of these facts, I have no problem with your decision. My view regarding the relationship between cancer and cholesterol is that a low cholesterol is an effect of cancer and not a cause. Often its level will drop before the cancer is discovered. That is my hypothesis and I may be wrong, and that is why I think it merits further studying. I’m taking a statin myself since 1994 after an MI. My aim is to reverse my disease and I have kept my LDL below 60-70 from the beginning. I have been fortunate in being able to tolerate it without side effects and have had no recurrence of my disease since. As a matter of fact, a recent CIMT showed my vascular age to be about 20 years younger thant my biological age. I don’t want to have an invasive angiogram just to satisfy my curiosity. Do I want to be taking a medication all my life? Of course not. I am even considering a drug holiday, and maybe taking the medication one year on and one year off, but so far I am too chicken.
One more thing. Life is a fatal condition, and we will all eventually die, so I do not expect a decrease in all cause mortality. Now, if something else comes around and changes that fact…… I can guarantee it won’t be a statin.
But the statin studies that have shown no decrease in all-cause mortality aren’t looking at patients for a lifetime, until they die, and saying “yep, the death rate in each arm is 100%”! They are looking at deaths during a limited study period. If the statin reduced users’ chance of having a fatal heart attack during the next five years by an absolute 2%, say, and did not simultaneously increase their chance of dying from something else, then I certainly would expect a decrease in all-cause mortality during that period. People say that an observed decrease in mostly non-fatal heart attacks is very significant, but if the same study shows equal total mortality they say that this is speculative and not worth worrying about. Which number better reflects what patients really care about?
That is not true. Check out the study published by Afilalo et al in JACC from its first issue this year. They showed a 22% decrease in all cause mortality besides decrease in CHD mortality, nonfatal MI, stroke, and need revascularization.
You cannot claim it is “not true” that in certain statin trials all-cause mortality has been unchanged; this is a simple fact. Afilalo et al is not a clinical trial, it is a meta-analysis of published and unpublished data from elderly subgroups in selected clinical trials, using “hierarchical Bayesian modeling.” The results are far more favorable to statins than are seen in at least one of the included trials, the PROSPER trial, which apparently provided almost 30% of the data. PROSPER showed lowered CV risk but unaffected stroke risk, significantly increased cancer risk, and apparently no benefit for total mortality. Those results themselves are more favorable than seen in elderly subgroups of certain other studies (for which I don’t have citations handy at the moment). Afilalo et al are asserting significantly lowered stroke risk and are not mentioning cancer in their abstract. Now, in other contexts on this blog people have been very hostile to the idea of taking a bunch of studies and doing a meta-analysis to get a result that looks better than you would conclude from just looking at the raw results of many of the original studies. I’m no statistician and have no prejudice against meta-analyses per se, but “hierarchical Bayesian modeling” sounds like something rather more complicated than just counting up the numbers of heart attacks in the statin group vs. the placebo group.
What trials have specifically looked for all cause mortality?
Let’s see,
Ulf Stenestrand et al in JAMA, January 24, 2001. Damn it. 9.3% mortality in one year in the no statin group, 4% mortality in the statin group. I guess that’s not good enough. The fact is, there are plenty.
That would be an astonishing death rate for a primary prevention trial. Upon looking up the abstract, I discover that this deals with people who had just suffered a heart attack for which they were hospitalized. Here’s the address of the abstract.
http://www.ncbi.nlm.nih.gov/pubmed/11242427?ordinalpos=95&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum
It is not quite accurate to speak of “groups” as you do. This was a cohort study from a patient registry, not a randomized trial. When the figures were corrected for confounding factors, the relative risk of mortality in the statin users was 0.75, or a 25% reduction, rather than the 57% reduction you portray. “Damn it.” Still, good enough to warrant taking a statin if you have just had a heart attack.
But that’s not what we are talking about; we are talking about putting people who have never had a heart attack on drugs for life. For those trials, you ask which have “specifically” looked at all cause mortality. I should jolly well hope they all did, since that is what matters to patients. In at least some of the primary prevention studies, all cause mortality was not affected. (In certain others, the available abstracts don’t specify, leaving me to suspect that results were not impressive.) Examples:
ALLHAT, a trial often pushed as evidence of the benefit of statins, had no mortality difference; CV risks were lowered, but for the most part not significantly so. A later publication by Geraci and Geraci indicated that black statin users had lowered coronary events but more strokes.
PROSPER was partly secondary prevention, meaning that the underlying CV risk was much higher. The statin users had a relative risk of 0.85 (p=.014) for the primary CV risk endpoint, but a relative cancer risk of 1.25 (p-0.02). I recall reading that the total mortality was not lowered, and I suspect that is so, or the abstract would have boasted of it. I can try to dig up further information, but don’t have it handy.
AFCAPS/TexCAPS, touted as the first primary prevention statin trial in people with normal LDL levels, had a relative death risk of 1.04 for the statin users (1.21 RR for non-CV deaths, which were a large majority of the total, and 1.41 for cancer deaths in particular [p=.13, but suggestive]).
ALERT (a study with kidney transplant recipients) and ASCOT-LLA (with hypertensive patients) did not have significantly lowered total mortality. WOSCOPS initially did not have, but a follow-up publication did find significantly lower mortality.
See how the statin trials were manipulated with numbers in the ABSTRACTS That is why it is so important to read the FULL TEXT and CAREFULLY of all trials .
Dr. Uffe Ravnskov analyzes the statin trials here:
http://www.ravnskov.nu/myth5.htm
http://www.ravnskov.nu/myth6.htm
See how the statin trials are manipulated by using “relative risk ”
http://www.opinions3.com/Uffe_Ravnskov_Report.htm
[...] The International Network of Cholesterol SkepticsA Lancet article from December 2007 reviewed trials involving nearly a million people and found that “Total cholesterol was positively associated with IHD [ischemic heart disease] mortality in both middle and old age and at all blood … [...]
Having read this discussion on and off for a while now it is becoming obvious that the medical profession will not be swayed from their cholesterol theory of heart disease. Even when evidence points to the contrary, they simply will not accept it. This reminds me of the story of the 2 Australian scientists (Robin Warren and Barry Marshall ) who hypothesised that most stomach ulcers were caused by the bacteria H. pylori.
Even when they presented their evidence for this theory, they were ridiculed by their fellow scientists and doctors. In fact one American doctor said they should be put against the wall and shot for proposing such a stupid theory. Fortunately for us, despite all this abuse, these scientists persisted until eventually, after some 15-20 years of trying; they eventually got the medical fraternity to accept it. Bacteria caused stomach ulcers, not lifestyle (sound familiar?). Just think of all the people who needlessly suffered because of this. I wonder how many people will have to suffer heart disease and all of its debilitating (even fatal) effects before the medical world decide to take notice of descenters like THINCS. Then maybe, just maybe, the ultimate cure for this disease will be found.
THINCS is not really at all like the scientists who proposed H. pylori as a cause of stomach ulcers, the reason being that they are not proposing a theory of causation for heart disease, at least not as a group (some of them may have their own individual theories). So far as I know, the only thing that unites the members of THINCS is that they do not believe that “cholesterol,” by which they presumably mean LDL-C, is a cause for heart disease. (I do not know their views on HDL.)
I have had encounters with a couple of THINCS members, namely Malcolm Kendrick, Uffe Ravsnkov and Eddie something (can’t recall his last name). Kendrick and Ravsnkov are physicians, Eddie isn’t. In many cases when one encounters THINCS members, they do not say anything about their THINCS affiliation. Rather they post messages (on blogs, usenet, etc.) criticizing the use of statins for women or for primary prevention on the grounds that (according to them) statins have not been shown to lower total mortality in clinical trials for those patient groups. They also assert that any efficacy shown by statins is due not to LDL-lowering, but to pleiotropic effects. They tend to cherry pick which evidence they cite, ignoring anything that doesn’t match their positions. They also talk a lot about statin side effects (never about benefits of statins).
My 14-year-old daughter has heterozygous familial hypercholesterolemia (heFH). Even the members of THINCS admit that there is a higher incidence of heart disease in people with heFH, although they assert that the incidence is not as high as many people think. Ravsnkov told me in an e-mail that the higher rate of heart disease in heFH is due not to high LDL, but to a tendency toward blood clotting in some patients.
It is true that the incidence of heart disease in heFH is sometimes overstated, due to the fact that study populations have in many cases been drawn from lipid clinics. People who are referred to lipid clinics tend to already have heart disease, or a strong family history of heart disease, and may suffer from other risk factors. They are not a random sample of people with heFH, obviously. However, that doesn’t help us too much because even though we know that some people with heFH would live a normal lifespan even without treatment (or with less intensive treatment), we do not know how to predict who those people will be. So currently, everyone with heFH must be treated.
It is also true that statins have pleiotropic effects, but it seems unlikely that none of the benefits of statins are due to LDL-lowering, since a number of other interventions that lowered LDL have reduced the risk of cardiovascular events.
The bottom line for me is that my daughter, if untreated, could have a heart attack very early for a woman (say, late 40s, early 50s). She has male relatives who died of heart attacks at 35 and 40 (women with heFH develop heart disease about 9-10 years later than men, on average). My husband has also been told that he is at risk. I wish these THINCS people were right, but I just don’t believe them.
Marilyn
“Recent studies have shown that large reductions in the cholesterol levels of people with Familial Hypercholesterolemia were NOT followed by reductions in their vascular obstructions.”
A quote from The Cholesterol Myths” and Dr. Ravnskov gives some references.
I was not proposing that the THINCS members were equivalent to Robin Warren and Barry Marshall. This pair of scientists did have some evidence as to another cause of stomach ulcers; something that the THINCS, as a collective, do not have regarding heart disease. My point was that the medical fraternity, when faced with dissenting voices regarding the status quo get very defensive and at times damn right nasty against the dissenters. This appears to be the case with the THINCS. They might not be right in their ideas, but they do present some good data to backup their concerns regarding the current heart disease theories and as such should be given a respectful listen.
Whilst there has been some pure LDL lowering investigations that have yielded a positive outcome, there also some that have not. The jury is still out on the absolute benefit of LDL lowering alone. Nobody, as far as I am aware, has been able to accurately document scientifically, with data, the process by which any form of LDL causes heart disease. Any process that has been documented is purely theoretical. This is very surprising given the number of years this has been investigated.
“It is also true that statins have pleiotropic effects, but it seems unlikely that none of the benefits of statins are due to LDL-lowering, since a number of other interventions that lowered LDL have reduced the risk of cardiovascular events.”
This may be true. But going back to my stomach ulcer example, the antacids given to the ulcer sufferers offered some reduction in ulcer discomfort and a reduction in the formation of further ulcers. However this was achieved by treating a facet of the problem and not the root cause. Could this not be the case with statins?
“Recent studies have shown that large reductions in the cholesterol levels of people with Familial Hypercholesterolemia were NOT followed by reductions in their vascular obstructions.”
I do not know what studies he is referring to. Why don’t you cite them for us?
I’m not sure what he means by “vascular obstructions,” but if he is talking about atherosclerosis, as measured by say carotid IMT, he is incorrect. Read this paper, for instance:
Pernette R. W. de Sauvage Nolting, MD, PhD; Eric de Groot, MD, PhD; Aeilko H. Zwinderman, PhD; Rudolf J. A. Buirma, MD; Mieke D. Trip, MD, PhD; John J. P. Kastelein, MD, PhD, Regression of Carotid and Femoral Artery Intima-Media Thickness in Familial Hypercholesterolemia: Treatment With Simvastatin, Arch Intern Med. 2003;163:1837-1841.
If by “reductions in their vascular obstructions” he means that all the accumulated atherosclerosis built up over a lifetime did not just magically melt away, that’s true, but so what? That doesn’t prove the point he’s trying to make.
“But going back to my stomach ulcer example, the antacids given to the ulcer sufferers offered some reduction in ulcer discomfort and a reduction in the formation of further ulcers. However this was achieved by treating a facet of the problem and not the root cause. Could this not be the case with statins?”
Look, no one is saying elevated LDL is the only cause of heart disease. There are many other causes as well. But if LDL is not a cause of atherosclerosis and ultimately heart attacks, how do you explain why children with familial hypercholesterolemia, who generally do not have any risk factors other than very high LDL (except for family history of heart disease in some cases, and male gender in the case of boys), have endothelial dysfunction and accelerated atherosclerosis (as compared to normal children).
The full story on how statins work is not known. In any case, even if statins did not work partly through lowering LDL, that would not mean we should not use them. The thing we’re trying to accomplish is not to lower LDL (or raise HDL, or lower blood sugar, etc.), but to prevent heart attacks, strokes and death.
There are people who carry mutations that cause lower LDL from birth, the opposite of FH. These people have much lower rates of heart disease than you would expect given their other risk factors. How do explain that?
Jonathan C. Cohen, Ph.D., Eric Boerwinkle, Ph.D., Thomas H. Mosley, Jr., Ph.D., and Helen H. Hobbs, M.D., Sequence Variations in PCSK9, Low LDL, and Protection against Coronary Heart Disease, NEJM;354:1264-1272.
I’m done with this thread.
Marilyn
“Look, no one is saying elevated LDL is the only cause of heart disease”
If this is true why were statins invented. Certainly not for their pleiotropic effects because they were unknown at the time of development. They were only invented to lower LDL. My doctor/cardiologist is only interested in 2 measurements; cholesterol and blood pressure. I totally agree that LDL is a factor but is not THE factor which is certainly how it is touted by the medical profession. Are they now turning their backs on the LDL theory of theory?
However you have not understood my reasoning. By treating stomach acid they reduced the problems of stomach ulcers. By reducing the level of LDL they reduve the incidence of heart disease. In the first case they were only treating one facet of the ulcer problem and not the cause. I believe the same is true with LDL. I simply do not know what you find wrong with my statement because it is effectively backing up your conclusions.
I totally agree with you that LDL it is one factor of many. For people with Familial Hypercholesterolaemia their cholesterol is not just high but mega high. Maybe 5 times the normal levels. I do not know of many substances that would not harm the human body when 5 times higher than normal!
Hello Harriet Hall.
I am the dreaded Dr Malcolm Kendrick MBChB MRCGP, peer-reviewer for the BMJ etc. I am also a thincer, who thincs quite a lot about CHD. I presume you have read my book ‘The Great Cholesterol Con,’ prior to dismissing my (and others within thincs) views.
Pulling apart clinical trials in all directions is mildly interesting – if rather dispiriting. Rather than get dragged into this particular quagmire, the question I will pose to you is this.
If a raised LDL causes atherosclerotic plaques to develop then can you explain to your readers HOW it does so. In this area I went back to the very basics to try and find the answer to this question. I found nothing.
I ask four other things of your explanation
1: Explain why atherosclerotic plaques only form in arteries, not in veins – their structure is identical (other than the fact that veins are thinnner).
2: Explain why all artery walls, everwhere, do not fill up with LDL – if atherosclerosis is caused by LDL ‘leaking’ into the artery wall, why does this not happen in all artery walls.
3: Explain how LDL passes through the endothelium into the artery wall behind. (The healthy endothelium is a barrier to LDL).
4: Explain how you know that it is LDL that is found in plaques, and not Lp(a).
If you can explain these facts, with clear supporting information, then I shall publically disown my skepticism of the LDL/Cholesterol hypothesis. I give you until the end of 2008 as I accept that this stuff is hugely complex and will taken many months to get to grips with.
Regards
Dr Malcolm Kendrick
“There are people who carry mutations that cause lower LDL from birth, the opposite of FH. These people have much lower rates of heart disease than you would expect given their other risk factors. How do explain that?”
I take it you are talking about SLOS (Smith-Lemli-Opitz Syndrome). If you are, then your statement is not strictly correct because the list of health problems associated with this condition include congenital heart disease. Infact SLOS is far more deadly than FH. Thus indicating when substances in the body are mega high OR mega low when compared to the norm, can cause catastrophic illnesses. However I would not dream of using SLOS as a way of arguing that moderately low cholesterol levels are deadly. Likewise you cannot conclude that because FH causes heart disease, means that people with moderately high cholesterol will also get heart disease.
pc
I was referring to PCSK9 mutations, not SLOS. See the paper I cited in my post.
There are 2 types of FH, homozygous and heterozygous. Someone whose LDL was 5 times normal would presumably have the homozygous version (very rare). My daughter has heterozygous FH; her LDL when not on medication is in the mid-200s, a little over 2 times normal.
I agree that statins were invented to lower LDL and that their pleiotropic effects only became known later. I also agree that LDL as a cause of heart disease is sometimes overemphasized. However, I was under the impression that you were questioning whether LDL was a cause at all.
Statins are beneficial for people at high cardiovascular risk regardless of baseline LDL levels. What matters is the person’s overall risk. After all, many people who have heart attacks do not have particularly high LDL.
Dr Kendrick
Nice of you to join in. Alas, I think you might be too late as I have not seen any response from Harriet for many days.
I also suspect that you would not get any definitive answers to your questions either. I have spoken to my cardiologist about your opinions (having read your book) and he seemed most unimpressed by them. Infact he used the word “misguided” to describe your ideas. I suspect thats the feeling from the medical profession represented on this thread as well.
I have been following this discussion with interest but I am not a doctor and am learning as I go along.
Dr Kendrick posed some questions that would seem to me (possibly in my ignorance) to have some very basic answers.
I would very much appreciate further guidance from the medics reading this as to whether I am on the right track here
Dr Kendrick asked
1: Explain why atherosclerotic plaques only form in arteries, not in veins – their structure is identical (other than the fact that veins are thinnner).
But arteries and veins contain blood moving at very different pressures. Arteries have a pulse for instance – isn’t that a major difference that could account for minor damage to the endothelium?
2: Explain why all artery walls, everwhere, do not fill up with LDL – if atherosclerosis is caused by LDL ‘leaking’ into the artery wall, why does this not happen in all artery walls.
I thought it could. Atherosclerosis can occur in vessels apart from the coronary arteries. Isn’t this what peripheral arterial disease is?
3: Explain how LDL passes through the endothelium into the artery wall behind. (The healthy endothelium is a barrier to LDL).
The healthy endothelium might be but doesn’t the build up of fatty streaks occur due to minor damage to the vessel wall? Hence why it occurs in arteries with higher blood pressure or more often in branches or curves of the arteries which are under increased stress?
Don’t know enough about number 4 to hazard a guess, sorry
I would be interested in comments.
kathleen
I would say your responses to the good doctors questions are perfectly logical. However the current cholesterol theory states that it is the LDL that causes the damage. You are saying that the artery gets damaged first. If this is true then the current theory is wrong which is precisely what Dr Kendrick is arguing. However I have to agree about PAD. Atherosclerosis can occur in arteries in the leg etc.
Nice try, Dr. Kendrick.
I exited this discussion a long time ago because commenters were not responding to what I said but to what they wanted to think I said.
You have done the same.
I have no reason to prove to you how LDL “causes” plaques, because I never claimed it did. I only said that LDL is a risk factor, that lowering it lowers risk, and that statins can reduce the risk of heart attack and death when prescribed appropriately. Those are incontrovertible facts, supported by the weight of evidence and by the references I provided via links.
In my comment on 9 Feb, I pointed out a few specific examples of the distortions and logical fallacies of THINCS. You have just provided another good example. You tried to set up a straw man and divert attention from what I actually wrote.
Any (slight) reduction in CHD mortality statins have had is completely due to their 11 other effects. The recent ENHANCE Trial PROVES THIS EVEN FURTHER.
There is NO DOSE RESPONSE. Hear Dr. Uffe Ravnskov here in his Sydney talk
http://www.informyourself.com.au/The%20Cholesterol%20Myths.html
Read this article by Anthony Colpo the ULTIMATE Cholesterol Theory Myth Dispeller
http://www.lowcarbmuscle.com/forums/showthread.php?t=162
There is not a book around that is as thorough at completely dismantling the Cholesterol Theory to the point that any doctor who reads it could not look possibly spew anymore anti -cholesterol hyperbole to you.
pc wrote:
“Even when evidence points to the contrary, they simply will not accept it…the 2 Australian scientists (Robin Warren and Barry Marshall ) who hypothesised that most stomach ulcers were caused by the bacteria H. pylori…were ridiculed by their fellow scientists and doctors…despite all this abuse, these scientists persisted until eventually, after some 15-20 years of trying…”
Wrong.
“…the antacids given to the ulcer sufferers offered some reduction in ulcer discomfort and a reduction in the formation of further ulcers.”
Wrong again.
See http://csicop.org/si/2004-11/bacteria.html
pc wrote:
“Even when evidence points to the contrary, they simply will not accept it…the 2 Australian scientists (Robin Warren and Barry Marshall ) who hypothesised that most stomach ulcers were caused by the bacteria H. pylori…were ridiculed by their fellow scientists and doctors…despite all this abuse, these scientists persisted until eventually, after some 15-20 years of trying…”
Wrong.
Thats not the way the New Scientist described it in 2005
http://www.newscientist.com/article.ns?id=dn8088
To quote from the article: “The pair’s claims provoked a fierce backlash from the medical establishment, which held to the dogma that ulcers were brought on by stress and lifestyle, and could not be cured.”
“…the antacids given to the ulcer sufferers offered some reduction in ulcer discomfort and a reduction in the formation of further ulcers.”
Wrong again.
Sorry confused here. Are you saying that the medication of the day (Gaviscon, zantac etc) did nothing?
pc, read the article, which explains both the history of the H. pylori hypothesis and the therapeutic effects of antacids in peptic ulcer disease. The New Scientist article, which offered no documentation for its claims, was wrong. Its author also failed to do his or her homework.
pc, I got caught in the H. pylori trap too. It seems there was some “embellishment” of how much opposition there actually was. Once they published data on it the actual acceptance was quite rapid, a few years at most. No doubt it seemed like a long time to them, but from the outside it doesn’t seem that long.
In terms of how LDL “causes” atherosclerosis, the vasculature is in a constant state of flux (as are all tissues, except perhaps the brain, but even in the brain there is remodeling). That is, cells are dying and being cleared, cells are multiplying, cells are being replaced.
With tissues being continuously remodeled, a slight shift in the “remodeling control parameters” can/will eventually lead to dysfunction. This was what Judah Folkman did research on, the regulation of the balance between angiogenesis and the opposite of angiogenesis (vascular ablation) (see the earlier blog on him
http://www.sciencebasedmedicine.org/?p=23).
There are many pathways that regulate vascular health, so there are many ways for the regulation of vascular health to “go bad”.
I suspect that a little bit of cholesterol deposition might be protective under some circumstances and might be one of the normally adaptive stress pathways. Cholesterol deposits do tend to form in the largest arteries down stream of flow disturbances. That might be something that “protects” against free hemoglobin from hemolysis due to turbulence (wild speculation). Free hemoglobin is rapidly tied up by haptoglobin and so would be less of a problem farther down stream.
http://jama.ama-assn.org/cgi/content/full/293/13/1653
There are 2 major effects of free hemoglobin, the destruction of NO, and the formation of ROS. A layer of lipid or cholesterol on the lining of an artery might (conceivably) protect from both of these conditions. NO is ~9x more soluble in lipid than in aqueous, so NO could penetrate any lipid layer, but superoxide is blocked, as is hydroxyl radical.
Mental stress and epinephrine infusion do cause high plasma lipids. Stress (during evolutionary times) is most likely going to be associated with high aerobic activity (the “running from a bear” example is one I like), where blood flow and blood velocity will be at high, perhaps maximal levels, where turbulence induced hemolysis will be maximized. Deposition of very modest amounts of cholesterol during such periods might be quite protective against vascular damage from turbulence induced hemolysis. Maybe from myoglobin released during muscle damage too.
Atherosclerosis from elevated blood cholesterol may be an adaptive mechanism. Lower blood cholesterol and you lower atherosclerosis. Of course how you lower it is going to matter. I suspect raising NO is better, but that is what I always suspect.
The use of acid reducing medications to treat ulcers is seriously misunderstood by pc etc.
The whole point of the H pylori discovery is that simple acid blockade is not enough in HP pos. disease. Microbiological eradication via antibiotics PLUS acid blockade is necessary.
“The use of acid reducing medications to treat ulcers is seriously misunderstood by pc etc. ”
My explanation of the use of acid reducing effects on ulcers was intentionally curtailed because I was not trying to explain how peptic ulcers are treated, but to make a point regrading how difficult it is for the medical profession to have their mindset changed when somebody challenges the status quo.
Also as the son of a parent who suffered from stomach ulcers since she was 15 and had to have most of her stomach removed back in the 70′s because of it, Iam well aware of the ins and outs of peptic ulcers (even though I admit I am not a mdixal person)
sorry a mistype. mdixal should read medical. Apologies.
“I was not trying to explain how peptic ulcers are treated, but to make a point regrading how difficult it is for the medical profession to have their mindset changed when somebody challenges the status quo.”
Nevertheless, you failed to make that point. The H. pylori story is an example of the opposite of what the “Galileo gambit” claims. It shows just how quickly the status quo can be overthrown when real evidence is presented.
Nevertheless, you failed to make that point. The H. pylori story is an example of the opposite of what the “Galileo gambit” claims. It shows just how quickly the status quo can be overthrown when real evidence is presented.
I only failed to make the point because I was reliant on supposedly valid sources being accurate in their reporting (New Scientist). I accept that from the evidence that you have presented that my point has now no real gravitas. There is no need to be so terse about it though. Discussions like this are the only places that ordinary joes like me can have to speak to scientists and doctors. I certainly know that none of my doctors have the time to have any detailed discussions like those we are enjoying here.
pc’s example of unreliability in the literature is characteristic of all literature. Even peer reviewed literature needs to be viewed skeptically. That something is peer reviewed, all that means is that people the editors considered reliable scientific peers have reviewed it and think that it should be published. The editor may have biases, the peers may have biases too. Usually the bias will be in the direction of the status quo, but which status quo is a good question. For example as David Gorski mentions above “Journal of American Physicians and Scientists (JPANDS). JPANDS is about as poor a source as any I have ever seen.”
Usually data is ok and not clouded by these biases, particularly if the data in question is not a central part of the hypothesis that the authors are trying to “prove”. There may still be error, but non-systematic error is a lot easier to deal with than is systematic bias.
pc,
I apologize for the impatient tone of my comments. I wrote the article debunking the myth of H. pylori ostracism because I had heard it many times and knew it to be false. It was also too facile, in a cheap, Hollywoodish struggle-and-eventual-redemption-of-the-underdog-against-all-odds kind of way. That should have made anyone suspicious, even those without specific knowledge of medicine or bacteriology. Now, more than 3 years later, it’s even more frustrating to continue hearing the myth because there’s no longer any excuse: anyone with a connection to the Internet can quickly learn the real story.
Nevertheless, I understand your having been misled by New Scientist, which has a greater obligation to seek the truth and to document its claims than do you, a comparative underdog
. New Scientist oughtta know better.
Those who write for public consumption should document, document, document; those who read something that isn’t adequately documented should be skeptical.
@daedalus2u
I agree with your comments on peer review. About 5 years ago when I first discovered the need for Q10 and carnitine supplementation, after statin damage, I submitted an article on the subject to none less than The Lancet. It was not accepted, but a short time later, I received a letter saying that my name had been added to the list of peer reviewers. I wondered who were my peers, octogenarians who had damage from statin treatment?
I have never been asked to peer review anything.
Under criticism that its ads are misleading, Pfizer said Monday it would cancel a long-running advertising campaign using the artificial heart pioneer Dr. Robert Jarvik as a spokesman for its cholesterol drug Lipitor.
http://www.nytimes.com/2008/02/25/business/25cnd-pfizer.html?em&ex=1204174800&en=46f62e7cf0f9683d&ei=5087
I wish I could answer all of Dr Kendrick’s questions, then I could go to Sweden and collect my prize. I would even add, what causes the atherosclerotic plaque to rupture and cause a stroke or MI? I believe the answers will be found through systems biology as the development of atherosclerosis is multifactorial. LDL will probably be found to play a role. No specialist I know claims LDL is the sole cause of atherosclerosis. Numerous studies have shown that by lowering LDL you will reduce the risk of CHD by about only 20-30%. There are studies showing combinations with Niaspan to raise HDL that show reductions of 70-90%. Also there is no denying that statins have side effects. We are always looking for new drugs and approaches. My approach is more empirical, if it works and doesn’t hurt, knowing how it works can wait. I for one have not seen any good studies the CoQ is beneficial in treating or preventing statin myopathy. I am aware of the theoretical basis for its use, I just haven’t seen good studies proving it. Regarding Pfizer and Dr Jarvis. The misleading referred to the fact that Dr Jarvis is not a medical doctor.
Harriet
From the ULTIMATE Cholesterol Theory DISPELLER ANTHONY COLPO
“UNTIL ONE CAN PROVE that the slight benefit of statins are INDEED BE OWED to their LDL lowering actions and not their MULTITUDE of PLEOTROPIC actions , THEN ONE HAS NO BUSINESS whatsoever CLAIMING that LDL is indeed the causal factor…… UNLESS of course, one has a pet theory to DEFEND IS ISN’T TOO FUSSED ABOUT IGNORING INCONVENIENT FACTS THAT CONTRADICT this pet theory”
http://www.lowcarbmuscle.com/forums/showthread.php?t=162
There is NOTHING Harriet can say that Anthony Colpo can’t tear apart.
Razwell,
Let me simply repeat what I said in my last comment: “I have no reason to prove to you how LDL “causes” plaques, because I never claimed it did. I only said that LDL is a risk factor, that lowering it lowers risk, and that statins can reduce the risk of heart attack and death when prescribed appropriately. Those are incontrovertible facts, supported by the weight of evidence and by the references I provided via links.”
Your quotation from Colpo “tears apart” something I never said.
It is useless to try to argue with someone who can’t read.
No Harriet it is YOU who can’t read.
The ONLY thing that is “incontrovertible evidence” is that
Statins have (SLIGHTLY) reduced CHD mortality in middle aged males WITH CHD .
You can NOT say lowering LDL does this even though statins do this too
This is especially true .In light of the facts statins have 11 OTHER effects .
Cholesterol – lowering trials BEFORE statins were COMPLETE FAILURES.
There is NO DOSE RESPONSE with statins. They have wroked REGARDLESS of resultant LDL levels.
THAT is your mistake.
Again the ONLY “incontrovertible fact” is that STATINS reduce CHD mortality
Cholesterol – lowering itself does NOT. You really ought to look up the FULL TEXT of the LRC-CPPT trial
Out of 3,086 patients
Treatment 30 CHD deaths vs Controls 38 CHD deaths
STATINS is the important word here.
Colpo rules and YOU know it. Why don’t you debate him? I know the reason – you’d be torn apart publicly.
Colpo does NOTread misleading abstracts, he reads the FULL TEXT of studies AND VERY CAREFULLY
Should you place your hands round someone’s neck, apply pressure, strangle him, and remove the source of his body’s energy supply totally, that would be termed MURDER.
But if you give him an insufficiently researched statin, saying it will help extend his life span, and it then depletes essential components for energy manufacture in mitochondria in virtually all parts of his body, so “strangling” them cell by cell and causing (often severe) damage, then that is termed SCIENCE BASED MEDICINE
Razwell,
The degree of LDL reduction is an indicator of the degree of risk reduction. The evidence clearly shows benefit to other groups besides middle-aged men with CHD. I provided links to evidence that fully supports what I said. I’m not going to bother saying it again. It is useless to argue with someone who can’t read. I shouldn’t have bothered replying to you in the first place, and I won’t do so again.
Harriet
You have obviously NOT read the Colpo link OR his book
PROVE-IT didn’t prove diddly
TNT also failed
Hey Harriet
is that why virtually all of the major statin trials have shown NO RELATIONSHIP between the degree of LDL reduction and degree of cardiovascular risk reduction
READ THE LINK and Colpo’s book beofore opening your SEVERELY MISINFORMED MOUTH
ANTHONY COLPO EXPOSES YOUR B.S.
Here it is AGAIN ALL REFERENCED BY THE TRUE EXPERT COLPO
READ ALL OF IT CAREFULLY
http://www.lowcarbmuscle.com/forums/showthread.php?t=162
ALSO LISTEN HERE CAREFULLY
http://www.informyourself.com.au/The%20Cholesterol%20Myths.html
AUDIO OF DR UFFE RAVNSKOV EXPLAINING THERE IS NO DOSE REPOSNSE WITH STATINS
You are an MD and Colpo would tear you apart.
I really wish more patients had the guts to challenge doctors like YOU and your ilk face to face with Colpo’s and Ravnskov’s book in hand
I really wish you would use your brain and learn that MANY cultures around the workld eat a diet rich in saturated fat and have VERY LOW RATES OF CHD
The Maasai Dinkas Samburu Tokeluans Inuits
Would you like to tell uis how the Tokeluans walk around with cholesterol levels of 240-300 mg.dl and have NO CHD?
Documented by scientists
Look up Prior I A et al Cholesterol coconuts and diets on Polynesian atolls
Like the main post, you, Harriet, seem ignorant of what the argument is really about. If you people had done your homework, you would know THINC’s don’t dispute that statins lower CVD-risk. Yet you make it sound like they dispute this fact. That is called building a straw man argument. I find it strange that after so much effort is spent building this straw man argument, it is admitted “It’s not entirely clear whether the risk reduction with statins is due solely to the lowered cholesterol; statins may have other beneficial effects.”.
What the THINC’s dispute is that the lowering of CVD-risk has anything to do with the lowering of LDL – exactly what the above citation says. As Razwell has pointed out, statins have at least 10 other mechanisms which could explain why they lower CVD-risk.
Why is that so difficult to understand? It’s a simple enough argument.
The recent Ezetrol ‘Enhance’ trial lends support to that theory. Google and learn.
It seems none of the critics against THINC has really read what they have to say. I suggest picking up a copy of the books of either Ravnskov, Kendrick or Colpo. I also find it funny that this whole article tries to debunk THINC’s yet provides no references for the arguments put forward.
This is to Kimball:
Your mention of the Lipid Research Clinics Coronary Primary prevention Trial is quite amusing.
YOU obviously did NOT read the FULL TEXT of it and VERY CAREFULLY. You ONLY read the ABSTRACT.
ABSTRACTS ARE MISLEADING. They quote relative risk reduction NOT absolute numbers. This is a favorite tool of cholesterol proponents looking to amplify the results of an uninspiring trial
So let me educate you. The LRC-CPPT trial did NOT show any support at all to the idea that cholesterol – lowering lowers CHD mortality .
Out of 3,086 patients there were 30 CHD deaths in the treatment group using the drug cholestyramine.
There were 38 CHD deaths in the controls A miniscule difference of only 0.04 %.
Again
Treatment 30 CHD deaths (1.6% ) vs Controls 38 CHD deaths (2.0 %) THESE ARE THE REAL ABSOLUTE FIGURES.
Treatment 30 CHD deaths vs Controls 38 CHD deaths
Treatment (1.6 %) vs Controls (2.0 % )
NO SUPPORT AT ALL TOP THE FARCICAL CHOLESTEROL THEORY OF CHD
You quote a MANIPULATION of numbers using ‘relative risk’ used in the ABSTRACT to make it SOUND supportive.
The 24 % relative risk reduction you quote is a MANIPULATION of numbers to AMPLIFY the results of the trial to make it APPEAR supportive.
Relative risk is the percentage that 0.04 % comprises of 2 % the death rate in the control group ) This is a clever MANIPULATION OF NUMBERS TO SOUND IMPRESSIVE
ABSTRACTS ARE NOT RTELIABLE Kimball
The reality is that the NHLBI had spent yet ANOTHER outrageous sum of money on a trial that COMPLETELY FAOILED to support the FARCICAL Cholesterol Theory of CHD.
BTW, when TOTAL MORTALITY figures were calculated in the LRC-CPPT trial
Death rates from non CHD causes were HIGHER in the cholestyramine group
OVERALL DEATH RATES BETWEEN THE TWO GROUPS WERE ALMOST IDENTICAL 68 (3.6 %) died in the treatment group vs 71 (3.7 %) in the controls.
ANTHONY COLPO’S RESEARCH EXPOSES YOU Kimball
I can go ALL DAY.
Was the difference in CHD deaths statistically significant?
The upward trend in non-cardiac deaths sounds like a good reason to stay away from bile acid sequestrants but I don’t see how that says anything about whether lowering LDL can prevent heart disease.
Bile acid sequestrants upregulate HMG-CoA reductase. It is possible that this has harmful effects, just as inhibition of HMG-CoA reductase by statins has beneficial effects unrelated to LDL-lowering.
Relative risk reduction can be misleading to the average consumer. Drug companies like to use it when the absolute reduction in risk is unimpressive. But it is not misleading to people who actually know the difference.
Marilyn
If you have ever tried using cholestyramine, you would understand why the results were like that. It wasn’t until the statin trials that showed much earlier diversion of the curves for control and treatment groups.
These people seem to think that lowering LDL has no role in lowering CVD and appear to be on a religious mission to reverse lowering of LDL. Interestingly enough the 2 studies that come to mind that tried to show that something other than LDL lowering was important, PROVE-IT and ENHANCE, did not show it.
We know that LDL is not the only factor in CVD development.
Anthony Colpo’s “The Great Cholesterol CON” You would do well to read it.
http://www.lowcarbmuscle.com/forums/showthread.php?t=162
“Dr. ” Harriet would do well to read The Oxford European Heart Journal where they review the available evidence from clinical dietary intervention trials.
The Oxford European Heart Journal ADMITS the anti saturated fat paradigm is NOT scientifically supported .
See here:
http://eurheartj.oxfordjournals.org/reprint/18/1/18.pdf
Perhaps YOU , “Dr.” Harriet ought to get familiar with the research to date before spouting off your mouth against THINCS and
Perhaps YOU Dr Hariet ought to get familiar with The Minnesota Coronary Survey 1969 , National Diet Heart Study 1968, Lyon Diet Heart Study `1994, Women’s Health Initiative 2006
NO support to the FARCICAL , SECOND HAND Cholesterol PROPAGANDA from doctors, the media, and “health” authorities”
Anthony Colpo puts you to SHAME “Dr” Harriet
Here is the link again that works
http://eurheartj.oxfordjournals.org/cgi/reprint/18/1/18.pdf
Now take these references from the results of CLINICAL DIETARY INTERVENTION TRIALS , (there are 18 in all to date, 6 are mentioned in this article ) and READ THEM FULL TEXT and VERY CAREFULLY
Minnesota Coronary Survey and National Diet Heart Study were ALSO DOUBLE BLINDED
Hopefully “DR.” Harriet will actually do this before criticizing THINCS again.
Her ignornace on this is absolutely laughable
I am sure it thoroughly embarrasses her that Anthony Colpo , someone who is technically not a doctor), is FAR MORE KNOWLEDGEABLE and FAR BRIGHTER.
Dr. Hall,
A friend of mine (who, unfortunately, never saw an alternative treatment she didn’t like) has now told me that I needn’t worry about eating coconut milk: coconut oil is really healthy! She gave me a reference to a website coconutoil.com where Dr. Mary Eng holds forth about how saturated fat, cholesterol, animal fats are really good for you and vegetable fats cause cancer. Wikipedia indicates that Dr. Eng is on the fringes of nutritional science, but most of the citations I find when Googling her refer to her book, which rails against the “diet dictocrats.” My friend is impressed by all the footnotes on the website, but I am more (unfavorably) impressed by their lack of quality references, straw-man arguments, and name-calling. What do you think of Dr. Eng and her claims? They seem to support the “cholesterol is healthy, statins are bad” claims you refute in this article. Can I really start enjoying Thai curries on more than an occasional basis again? Right now, I eat them only as a rare treat, since I know they are loaded with saturated fat… and that’s bad for me, isn’t it?
Mary Enig is a member of the International Network of Cholesterol Skeptics. She rejects the current scientific consensus and cherrypicks the literature to support her opinions.
Trans fats are more to be avoided than saturated fats, and saturated fats are not as “bad for you” as common opinion thinks. As I tried to point out in my article, the effect of diet is small. What is important is your overall risk status. For some people, avoiding saturated fats may contribute a small amount towards lowering risk; other people can eat all the fat they want with no danger to their health.
The relatively small impact of diet should be weighed against the quality of life. I’m with Dean Edell: “Eat, Drink, and Be Merry.” You only live once, and if Thai curries contribute to your enjoyment of life, that’s important too.
Harriet Hall wrote:
However, per Sandy Szwarc over at Junkfood Science:
If what Sandy wrote is true, this is a very serious limitation of all statin studies.
Apples and oranges. She’s talking about recent studies for approval of new statin drugs. All the early studies were done with placebo controls.
It is common practice to test new drugs in a class against older, proven drugs in the same class. We know penicillin works for pneumonia: a new, slightly altered penicillin molecule could be tested against the old penicillin, and it would be unethical to use a placebo control because we know that without antibiotics some people will die.
Szwarc also criticizes using LDL lowering as a surrogate marker, and ideally it would be better to use a clincal endpoint rather than a lab value, but since the degree of LDL lowering has been shown in previous studies to correlate to the amount of reduction in risk of cardiac events and death, it is not unreasonable to use it as a rough measure of the effectiveness of a new drug in the same class.
Statins have been shown to work better than placebo.
Statins have been shown to reduce the incidence of cardiovascular events and to reduce overall mortality. The benefit varies with the risk status of the patient and with whether it is being used for primary or secondary prevention. I explained all this above.
Wow, it just keeps going and going and…
The overall mortality issue was argued around Feb. 20-21, above. I spent some time searching PubMed and, aside from a later-published followup to WOSCOPS, was not able to identify a single primary prevention study in which all-cause mortality was shown to be reduced by statins. That only seems to happen in secondary prevention trials, when the pre-existing heart risks are quite high.
Dr. Hall:Thank you for your original post and for taking the time to respond to me and other commentators. I am a newbie regarding this issue and have much to learn. Your original post has engendered a quite useful dialectic for further edification.It is unfortunate that all applicable Cochrane Reviews are still in the protocol stage but this gives all of us something to look forward to:
Statins for preventing cardiovascular disease
Statins for acute coronary syndrome
Lipid lowering efficacy of atorvastatin for hyperlipidaemia
Statins for primary hypercholesterolemia
Statins for familial hypercholesterolemia in children
“…but since the degree of LDL lowering has been shown in previous studies to correlate to the amount of reduction in risk of cardiac events and death…”
Does the meta analysis that showed this take into account all the pleiotropic effects of statins. Looking at the 2007 Lancet article It seems they did take into account blood pressure levels but not any other effects like the anti inflammatory effect of statins. Also it is interesting to note that the study says that although statins improved stroke rates there is no correlation between cholesterol levels and stroke.
I was a little bothered by this paragraph
‘The skeptics cite studies where elderly people with low cholesterol had worse outcomes, but the elderly often have confounding factors: in that age group low cholesterol can be a marker for inadequate diet and chronic disease. A 2008 study shows that “Statins reduce all-cause mortality in elderly patients and the magnitude of this effect is substantially larger than had been previously estimated.”’
Yes, in the elderly low cholesterol “could” be a marker but it also might not be; this is far from proven. And the cited study is about elderly patients who already have coronary heart disease, not about the elderly in general. So the cited study in the second sentence doesn’t actually disprove the skeptics claims in the first sentence.
This seemed a little bit unbalanced to me and like using the same approach that the cholesterol skeptics are being criticized for using. It could be that in the elderly cholesterol is much less of a risk factor than it is in younger people, for instance.
apteryx,
Isn’t that what I said?
pc,
Yes, statins have an anti-inflammatory effect. We don’t know how much of their success is due to lowering cholesterol and how much is due to anti-inflammatory and/or other effects. I tried to make the point that however they work, they do work, and the degree by which they lower cholesterol serves as a rough measure of how well they work to prevent cardiovascular disease.
CarolynS,
I don’t think you’ve fully understood the subtleties here. Low cholesterol IS associated with inadequate diet and chronic disease. The studies citing a worse outcome for low cholesterol are flawed and did not control for all the variables. All other things being equal, I don’t think there is any evidence that a healthy elderly person is more at risk if his cholesterol is low; in fact, there is evidence that risk rises with cholesterol level at all ages, although the degree of risk does vary with age.
The evidence shows that elderly patients with cardiovascular disease benefit from secondary prevention with statins. The elderly who do not have cardiovascular disease probably will not see any reduction in overall mortality with statins, although they may have fewer events. We don’t automatically recommend statins for the elderly for primary prevention. Treatment decisions should be based on an analysis of the ALL the individual’s risk factors (including age), the NNT for his particular risk group, and other considerations.
The claims of the cholesterol skeptics that low LDL cholesterol is bad and high LDL cholesterol is good are simply not compatible with the evidence.
To all of you: I thought I had already made these points clear. I’m wondering how carefully you read what I wrote.
“…but since the degree of LDL lowering has been shown in previous studies to correlate to the amount of reduction in risk of cardiac events and death, it is not unreasonable to use it as a rough measure of the effectiveness of a new drug in the same class.”
I am sorry but it is unreasonable. Statins lower cholesterol in a totally different way to Zetia. It could be the method of lowering that is effective rather than the ldl lowering alone. Statins have pleotropic effects that Zetia does not have and we are not sure how much of the cholesterol lowering effects of statins make up its efficacy. On top of that no one is totally sure how LDL causes heart disease (if at all). I suspect the FDA will probably not allow a drug to be released simply on its cholesterol lowering again, but will have to have proof of its clinical effectiveness.
Statins are the gold standard. The studies also show that the lower the cholesterol the better. I don’t think new drugs will necessarily be approved only by showing clinical effectiveness. That would be ideal, but impractical. Also it would be unethical to deny a control group a statin. That is the reason for surrogate markers like CIMT, and IVUS. I am not sure I feel totally comfortable with that. The recent study with zetia used CIMT as a surrogate marker and found no difference. It was not a clinical endpoint study.
Nobody denies anti-inflammatory effects of statins but that can’t be all of it. Why don’t anti-inflammatory drugs like Vioxx have a protective effect?
We do have a good idea of how LDL leads to atherosclerosis and plaque rupture but we clearly don’t have all the answers. If you wish, you can pick up a good pathology text and see what the current hypotheses are or check a vascular biology journal out. It truly is fascinating.
pc misread what I wrote. I said “it is not unreasonable to use it as a rough measure of the effectiveness of a new drug in the same class.” Pc missed the words “in the same class,” and responded with an argument about Zetia, which is in a different class. Since old statins have already been tested against placebo for clinical endpoints, it is not unreasonable to test a new statin using cholesterol lowering as a surrogate endpoint. Zetia works similarly to other drugs that reduce cholesterol absorption; the earlier bile acid sequestrants are in that same general class and have been tested with clinical endpoints, so it would not be unreasonable to test Zetia for its ability to lower LDL cholesterol.
As for the relative importance of the pleiotropic effects, see http://www.ncbi.nlm.nih.gov/pubmed/18441323?ordinalpos=9&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum
It concludes “Lipid lowering is more important than pleiotropic effects of statins for improvement in endothelial function and inflammatory markers in patients with dysglycaemia and CAD.” Not definitive, and not a clinical endpoint, but it is of interest.
I would love to see every new cholesterol-lowering drug tested in enough patients and followed long enough to determine all the side effects and the long-term effect on cardiovascular events and on overall mortality. In all age groups, both sexes, and various risk stratifications. I would love to have a reliable crystal ball, too!
Unfortunately, bringing new drugs to market involves a trade-off between ideal science and practical realities. If we don’t demand enough evidence, we license drugs that may harm people; if we demand too much evidence, we deny patients drugs that might have saved their lives. It’s a constant dilemma.
Like Weing, I don’t feel very comfortable with surrogate markers. I’d much rather see studies with clinical endpoints and POEMS – patient-oriented evidence that matters. We can write letters to the FDA. Meanwhile, we must take what we can get and try to do the best we can for our patients.
Dr. Harriet
I sincerely apologize for insulting you. You are far smarter than Anthony Colpo.
Anthony Colpo is just in it to sell books and is not qualified to interpret anything.
I can see that now. He misrepresents , misinterprets and takes out of context the data
The results of the links doctors have sent me to the literature he and what he claims do not match up .
I was stupid for listening to him without looking in to it
Sincerely,
Razwell
Razwell,
Apology accepted. Congratulations on your integrity and your ability to think for yourself. It’s not everyone who can really look at an opposing view objectively, change his mind, and admit it.
Razwell
Are you the “Razzi” from Colpo’s “low carb muscle website?
You are not the first person to be taken in by people like Colpo. They generally start off with good intentions but end up distorting the truth to prove their point. Take a look at Linus Pauling. An intelligent Nobel prize winning chemist, who got interested in Vitamin C and by the end of his time was basically proclaiming it could cure anything (and he still has his followers).
There is nothing wrong with questioning the status quo, but it has to be done methodically and with good quality data to back you up. I know, because I too have fallen in to the same traps. Even Dr Kendrick appears to have fallen for some of the Colpo effect. (if you read his book he quotes some of the same material as Colpo).
pc,
Your point about questioning the status quo is well taken, and I mentioned it in my article. The status quo doesn’t change because people join organizations like THINCS and write books. It changes when scientists submit their evidence to peer review and debate. Things get thrashed out and the best evidence always wins in the long run.
People like THINCS seem to forget that we all have access to the studies they quote. The status quo developed through consideration of those studies as well as other studies THINCS neglects to quote. And the status quo is constantly changing as new evidence comes in.
A good rule of thumb when reading a status quo-challenging book is to ask “Who disagrees with this and why?” and not to accept it until you have fully understood the opposing point of view.
Much of this discussion understandably focused just on cholesterol. Even the strongest proponents of the cholesterol hypothesis recognize that it prevents only a small percentage of heart attacks, whether through primary or secondary prevention. Most of the RCT’s also show that the benefits of cholesterol lowering are most clear in middle aged men with demonstrated heart disease, and not in women or the very elderly.
To me a thorough MD would spend the time with each patient – which time may or may not be reimbursable! – to systematically review all of the known risk factors for cardiovascular disease and then come up with a comprehensive treatment plan.
Among the very significant but largely ignored risk factors include:
sleep apnea
elevated lead levels (http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1892138)
gum disease
recent infection
in addition to of course a sedentary lifestyle, social isolation, obesity, processed food, high blood sugar and insulin levels, etc.
Some of these risk factors may well elevate cholesterol, others may be independent factors, or some combination.
A treatment plan would then be developed that would start with the least toxic interventions, and then over time if those interventions – weight loss, dental treatment, sleep appliances, as well as largely harmless natural substances with a some backing in research – such as Vitamin C and D garlic, plant sterols, and pomegranite (which preliminary studies show regresses plaque!) did not improve the biomarkers then and only then would a statin – at the lowest possible dose (see http://www.medicationsense.com/over_dose.html) be prescribed.
oderb,
When you say “not in women or the elderly” that is only true if you mean “not as significant,” and even then it should be qualified. See above.
You might want to re-read what I wrote. Most of what you say simply repeats points that I have already made.
Then you go beyond good science to suggest treatments that are supported only by preliminary or poor quality evidence.
To say the least, your article is arrogant. In fact, their is overwhelming medical evidence that statins can and do cause harm. I would encourage you to go to http://www.medications.com to read approximately 2000 patient complaints/adverse reaction experiences with statins.
Also, over 6 years ago the following Petition was filled with the FDA.(http://www.fda.gov/OHRMS/DOCKETS/dailys/02/May02/052902/02p-0244-cp00001-01-vol1.pdf)
CITIZEN PETITION TO CHANGE THE LABELING FOR
ALL STATIN DRUGS (MEVACOR, LESCOL, PRAVACHOL, ZOCOR, LIPITOR, AND ADVICOR) RECOMMENDING USE OF
100-200mg PER DAY OF SUPPLEMENTAL CO-ENZYME Q10 TO REDUCE THE RISK OF STATIN-INDUCED MYOPATHIES (INCLUDING
CARDIOMYOPATHY AND CONGESTIVE HEART FAILURE).
May 24, 2002
Petitioner:
Dr. Julian M. Whitaker, M.D.
This Petition is based in part on the clinical findings of Dr Peter H. Langsjoen, MD, FAAC stating:
“As the potency of statin drugs increases and as the target LDL cholesterol level decreases, the potential for statin-induced cardiomyopathy must be seriously considered and must be prevented with the concomitant administration of with all statin medications. In addition, since CoQl 0 is not obtainable fiom daily dietary sources sufficient to bolster flagging levels of statin-induced10 deficiencies,the aforementioned concomitant administration must be in specific supplement form and within 100-200 mg.” And, should contain a Black Box Warning to this effect.
More recently (2006), his safety concerns caused him to state the following:
“In my practice of 17 years in Tyler, Texas, I have seen a frightening increase in heart failure secondary to statin usage, “statin cardiomyopathy”. Over the past five years, statins have become more potent, are being prescribed in higher doses, and are being used with reckless abandon in the elderly and in patients with “normal” cholesterol levels. We are in the midst of a CHF epidemic in the US with a dramatic increase over the past decade. Are we causing this epidemic through our zealous use of statins? In large part I think the answer is yes. We are now in a position to witness the unfolding of the greatest medical tragedy of all time – never before in history has the medical establishment knowingly (Merck & Co., Inc. has two 1990 patents combining CoQ10 with statins to prevent CoQ10 depletion and attendant side effects) created a life threatening nutrient deficiency in millions of otherwise healthy people, only to then sit back with arrogance and horrific irresponsibility and watch to see what happens – as I see two to three new statin cardiomyopathies per week in my practice, I cannot help but view my once great profession with a mixture of sorrow and contempt.”
In closing a final question,
Are you responsible for the clinical treatment of patients?
drmike said,
“their is overwhelming medical evidence that statins can and do cause harm”
There was nothing in my article that suggested statins can’t or don’t cause harm. Every effective drug causes side effects. I tried to make it clear that statins should not be over-prescribed and that the risk/benefit ratio should be carefully considered for each individual patient.
Science doesn’t progress through lists of testimonials and public petitions, or through alarmist rhetoric.
Your question about whether I am responsible for the treatment of patients is irrelevant, but I will answer it anyway: I’m retired. You could have figured that out yourself by reading “About the Authors.” Before I retired, I practiced family medicine and I prescribed statins – selectively.
It’s funny that you should ask that, because THINCS is full of people who aren’t doctors and who don’t treat patients. I did not mention that in my article because it is irrelevant to the truth of untruth of their claims.
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