Statins

What do you guys think about the new recommendations for statins? Don’t the “alternative” findings of harm from these drugs bother you?
Just ran across this one today:
Expert Rev Clin Pharmacol. 2015 Feb 6:1-11. [Epub ahead of print]
Statins stimulate atherosclerosis and heart failure: pharmacological mechanisms.
Okuyama H1, Langsjoen PH, Hamazaki T, Ogushi Y, Hama R, Kobayashi T, Uchino H.
Author information
Abstract
In contrast to the current belief that cholesterol reduction with statins decreases atherosclerosis, we present a perspective that statins may be causative in coronary artery calcification and can function as mitochondrial toxins that impair muscle function in the heart and blood vessels through the depletion of coenzyme Q10 and ‘heme A’, and thereby ATP generation. Statins inhibit the synthesis of vitamin K2, the cofactor for matrix Gla-protein activation, which in turn protects arteries from calcification. Statins inhibit the biosynthesis of selenium containing proteins, one of which is glutathione peroxidase serving to suppress peroxidative stress. An impairment of selenoprotein biosynthesis may be a factor in congestive heart failure, reminiscent of the dilated cardiomyopathies seen with selenium deficiency. Thus, the epidemic of heart failure and atherosclerosis that plagues the modern world may paradoxically be aggravated by the pervasive use of statin drugs. We propose that current statin treatment guidelines be critically reevaluated.
KEYWORDS:
ATP generation; atherosclerosis; coenzyme Q10; heart failure; mitochondrial toxin; selenoprotein; statin; statin cardiomyopathy; vitamin K2

This is a good topic to go over. This is the longest post I’ve ever written so I apologize, but its an important topic.
For those on the forum who are not aware in Nov 2013 new guidelines were issued for the use of HMG CoA reductase inhibitors commonly known as “statins”.
This includes drugs like Mevacor ( lovastatin), Zocor ( simvastatin), Lipitor (atorvastatin) and several others. New guidelines were issued to address evolving research on the mechanisms of statins and to maximize the benefits and reduce risks. The current guidelines issued by the Amercian Heart Association and the American Cardiology Association are as follows:
Use of statin drugs should be considered for the following four groups of patients

  1. All diabetics
  2. All patients with a history of Coronary Artery Disease
  3. All patients with a cardiac risk of 7.5% or higher. You can find the calculator at www.heart.org/gglRisk/main_en_US.html
  4. Patients with an LDL of 190 or higher
    Using these new guidelines some patients will no longer be treated with statins who would have been under the old guidelines ( ie. patients with no other risk factors but an LDL of 140-189 will no longer be treated), while others will be treated who would not have been ( diabetics with an LDL under 130 or patients with normal LDL but a high cardiac risk)
    In order to explain the rationale behind this change I need to explain a little bit about how statins work because the story is not as simple as most people believe. Statin drugs were first introduced in the 1980’s when it was discovered that we could dramatically lower LDL ( bad cholesterol) by inhibiting an enzyme important to cholesterol production. This enzyme is HMG CoA Reductase. The first FDA commercially available drug in this class was Mevacor (lovastatin) but since that time many other statin drugs have been developed.
    Studies have shown that so called statin drugs can significantly reduce the risk of heart attacks. These studies are referenced below. To reduce the time involved in posting, the information at the bottom below the blue sentence is copied directly from"UpToDate"
    What has motivated the recent change in recommendations is the understanding that the beneficial effects of statins may be due to something other than their effects on LDL levels. This conclusion came about as a result of observations that other non-statin drugs which reduce cholesterol do not show any statistically significant effect on coronary events. It is now believed that the statin class of drugs has a second and previously unappreciated mechanism by which they reduce heart attacks through a reduction in arterial wall inflammation. It is thought that this may be the primary mechanism through which they reduce the risk of heart attacks. This is the motivation behind the change in recommendations.
    Three of the categories in the new recommendations address patients who are felt to be at high risk of arterial wall inflammation, diabetics, patients with a history of CAD, and patients with a CAD risk of 7.5% or higher using the Framingham data. LDL is still used as a criteria for treatment but only for patients with the highest LDL’s of 190 or greater. Based on current understanding of Athersclerotic disease these recommendations seem to be the most logical approach to maximize benefits, reduce disease, and minimize risk.
    In regards to the article referred to by TG I would say this. Understanding the biochemical pathways which are affected by drugs is important but its the beginning of understanding not the end. The body is an incredibly complex system of biochemical pathways that have evolved over millions, and in some cases billions of years. The complexity of these systems makes it very difficult to predict with any degree of certainty how the inhibition or stimulation of one component will affect the whole. Additionally all living systems have evolved to maximize homeostasis so that mechanisms often exist to buffer changes introduced into the system. For this reason we need to be very careful about predictions of harm or benefit or conclusions based solely on the effects of a drug on a single substance or biochemical pathway. Since we don’t have a comprehensive model of how the system (our bodies) work we must use knowledge of the basic biochemical or micro effects of a drug only as a guide to look for actual systemic or macro effects. Despite the micro effects which TG refers to, when we look at the whole patient statin drugs are seen to be relatively safe interventions.
    While there are many reported side effects linked to almost every drug ever created most of these are associations rather than true side effects.
    http://doctormelgar.com/blog/2013/10/09/why-did-your-doctor-give-you-a-drug-that-causes-hot-dog-fingers-how-to-sort-out-medication-side-effects
    The main side effects associated with statins are as follows.
    1) Hepatic ( liver) dysfunction - Although approximately 3% of patients can experience some elevation of liver enzymes while on statins this is not significantly higher than the the incidence of liver enz elevation seen in the general population where some studies have found such elevations in up to 9% of otherwise healthy individuals. More serious complications such as acute liver failure do not happen at any greater rate than in patients not on statins
    Am J Cardiol. 2006 Apr 17;97(8A):77C-81C. Epub 2006 Feb 3.
    An assessment of statin safety by hepatologists.
    Cohen DE1, Anania FA, Chalasani N; National Lipid Association Statin Safety Task Force Liver Expert Panel.

    2) Muscle Inflammation (Also known as statin myopathy) - severe muscle injury is a known risk with statins but occurs in less than 0.1% of patients on these drugs
    Can statins cause chronic low-grade myopathy?
    Grundy SM Ann Intern Med. 2002;137(7):617)
    .
    Milder forms of muscle pain may occur in relation to stain use but since muscle aches are such a common complaint even among patients who don’t take statins it is not clear how many of these complaints are actually due to statins. Some studies have shown no difference in muscle complaints between groups of patients on statins and those on placebo.
    An interesting note to illustrate the point I made above about not making judgements based entirely on our knowledge of biochemical pathways. As mentioned in TG’s post, statins have been shown to reduce CoEnzyme Q10 and some have suggested that reduction of this important muscle enzyme is the mechanism by which muscle injury may occur. Some physicians have recommended that their patients take CoQ10 if they are on a statiin but there is no evidence from any studies that this supplement is beneficial or that it can reduce the incidence of this side effect.
    To answer the original question, I think the new guidelines are well thought out and the reasonable based on our current state of knowledge
    In contrast to the results seen with nonstatin hypolipidemic agents, a number of studies have demonstrated a benefit from lowering the serum cholesterol with statins in patients without clinical evidence of CVD:
    "The West of Scotland Coronary Prevention Study (WOSCOPS) showed that cholesterol lowering with pravastatin reduced both the number of nonfatal myocardial infarctions and CHD mortality in middle-aged men with a serum LDL-C concentration above 155 mg/dL (4.0 mmol/L) . There was a borderline statistically-significant 22 percent reduction in all-cause mortality. Long-term follow-up after completion of the trial found that these benefits were sustained and the reduction in mortality increased over five to ten years, despite equivalent post-trial use of statins between groups
    "These observations were extended in the Air Force/Texas Coronary Atherosclerosis Prevention Study (AFCAPS/TexCAPS), which showed that lovastatin reduced the incidence of a first major coronary event (unstable angina pectoris, fatal and non-fatal myocardial infarction, and sudden cardiac death) in low-risk men and women without clinical evidence of CVD and LDL-C levels near the average for the general population (150 mg/dL [3.9 mmol/L], range 130 to 190 mg/dL [3.4 to 4.9 mmol/L]). These patients also had HDL-cholesterol levels that were below average for an age and sex matched cohort. For every 1000 men and women treated with lovastatin for five years, 19 major coronary events, 12 myocardial infarctions, and 17 coronary revascularizations could be prevented. No effect was seen on all-cause mortality.
    "Similar results were seen in the ASCOT-LLA, which studied atorvastatin (10 mg) in men and women with relatively normal serum cholesterol levels but with hypertension and at least three additional cardiac risk factors, however there was a trend toward a reduction in all-cause mortality (hazard ratio 0.87, 95% CI 0.71-1.06) [18].
    "The JUPITER trial of rosuvastatin 20 mg daily in healthy adult men and women with elevated C-reactive protein levels and LDL-C levels below 130 mg/dL (3.4 mmol/L) found a marked reduction in the primary endpoint of first major cardiovascular events and for all-cause mortality (hazard ratios 0.56 and 0.80, respectively). The absolute benefit for the primary endpoint was 0.59 events per 100 person-years and for all-cause mortality was 0.25 deaths per 100 person-years. This trial was stopped early for benefit which may exaggerate the true level of benefit, particularly for the primary endpoint .

From this article on August 1 2014 at bloomberg.com:
Harvard Study Questioning Cholesterol Drugs in Low-Risk Cases Survives Oxford Challenge

The verdict is in on a bruising spat between big-name researchers at Harvard University and the University of Oxford over a paper questioning the value of prescribing cholesterol-lowering drugs to people at low risk of heart disease. The decision goes to Harvard—and that’s not great news for pharmaceutical companies that make the medications.
Error in the side-effect rate, but:
Abramson acknowledged the error in the side-effect rate but insisted his paper’s main point—that statins do not reduce the risk of overall mortality for people with less than a 20 percent risk of cardiovascular disease over the next decade—remained accurate.
Bold added by me. Debate over who should get statins:
The debate over who should get statins comes as sales of the drugs declined 11 percent last year, to $29 billion. Expanding the use of the drugs to healthier patients would be one way to offset declining sales.
Raw data from industry-sponsored clinical trials?
For his part, Abramson on Friday called on the CTT group led by Collins to make its raw data—assembled from industry-sponsored clinical trials—available to outside researchers.
Apparently, the link to the article is "blacklisted" by the CFI server. :cheese:
From this article on August 1 2014 at bloomberg.com: Harvard Study Questioning Cholesterol Drugs in Low-Risk Cases Survives Oxford Challenge
The verdict is in on a bruising spat between big-name researchers at Harvard University and the University of Oxford over a paper questioning the value of prescribing cholesterol-lowering drugs to people at low risk of heart disease. The decision goes to Harvard—and that’s not great news for pharmaceutical companies that make the medications.
Error in the side-effect rate, but:
Abramson acknowledged the error in the side-effect rate but insisted his paper’s main point—that statins do not reduce the risk of overall mortality for people with less than a 20 percent risk of cardiovascular disease over the next decade—remained accurate.
Bold added by me. Debate over who should get statins:
The debate over who should get statins comes as sales of the drugs declined 11 percent last year, to $29 billion. Expanding the use of the drugs to healthier patients would be one way to offset declining sales.
Raw data from industry-sponsored clinical trials?
For his part, Abramson on Friday called on the CTT group led by Collins to make its raw data—assembled from industry-sponsored clinical trials—available to outside researchers.
Apparently, the link to the article is "blacklisted" by the CFI server. :cheese:
Send it again, but first take out the http://. It isn't so much a blacklist as a glitch in the CFI program.
Send it again, but first take out the http://. It isn't so much a blacklist as a glitch in the CFI program.
Again. From the article here] It works. Thanks Loisl. However, in the case of this article, removing the http:// as follows: url=hms.harvard.edu/news/harvard-study-questioning-cholesterol-drugs-low-risk-cases-survives-oxford-challenge and using the brackets [.......] receives this response from the CFI server:
The form you submitted contained the following errors * Computer says your input might be spam, so it was discarded.
Is there also a workaround for this glitch?

This worked
www.bloomberg.com/bw/articles/2014-08-01/harvard-researcher-wins-round-in-brawl-with-oxford-peer-over-benefits-of-cholesterol-drugs
which is the full article which your link eventually links to

This worked www.bloomberg.com/bw/articles/2014-08-01/harvard-researcher-wins-round-in-brawl-with-oxford-peer-over-benefits-of-cholesterol-drugs which is the full article which your link eventually links to
It does work, but it is lengthy. Using to shorten the link to here only works if http:// is removed from the link as in my post 4.

Nice. The dollar is always right.
(Ahem, please pardon my cynicism).
I don’t purport to be an expert on statins but what I do see is people who think they have been harmed. I also read about industry shenanigans leading to corrupt science. We say we use science and evidence to make decisions, but who is guarding the science? Here’s a UK blog about the data-sculpting that has occurred there, including concealment of side effects, and a comparison that was not (as implied) between statin takers and placebo, but between the placebo group and the subset of statin-takers who lowered their cholesterol the most. Misleading “data” can cause entire populations to fall prey to poisonous side effects of the profit motive depersonalized.
Here’s the interesting blog post:
http://healthinsightuk.org/2015/02/19/keep-statin-supremo-away-from-the-missing-side-effect-data/
If you’ve been following this pharmacological soap, your response when you heard this was probably first amazed laughter, followed by outrage at the breath-taking hypocrisy and then, after a brief reflection, alarm at the implications.
and at the end of the article:
And finally…
Just after this post went up a paper was published showing yet another way statin researchers manipulate statistics to make very iffy trial results look really positive. The authors, David M. Diamond, a professor of psychology, molecular pharmacology and physiology at the University of South Florida, and Dr. Uffe Ravnskov, an independent health researcher and an expert in cholesterol and cardiovascular disease, show how the minimal actual benefit – one fewer heart attack among a 100 on statins – can be presented as a benefit of 30-50%. An explanation of the magic can be found here:
Diamond and Ravnskov conclude that while a a pill that promises a longer, heart attack-free life has great appeal, statins only have a small impact on heart disease while their adverse effects ‘are far more substantial than is generally known.’

In the US the question is still “when” to use statins instead of “if”. The vast majority of people are unaware of how the science is manipulated and sculpted into a promotion for Big Pharma. They do know however that they can’t trust the government to police big business, and so they are leery of recommendations that come from anyone who could be corrupted by the money stream. Skepticism is warranted.

TG you do not seem to be making any real arguments here except that science has been corrupted and that money plays too big of a roll. There is some truth to both of these statements but your solutions are not logically consistent.

  1. The solution to manipulated science is better science NOT less science. Naturopahty is the replacement of science with a belief in magic
  2. Medicine is to some degree corrupted by money. Ever human endeavor is corrupted by money because humans are involved and humans are corruptible. That’s not to say this is acceptable. Those of us who would like to see this corrected are always working to shed light o this problem and correct it where possible. In fact the reason you know about any of these issues is largely due to our own efforts to bring them to everyone’s attention. The solution however is not to turn away from a profession that has literally saved billions of lives in the past 100 years to one (naturpoathy) that has saved few if any and which is more corrupt (charging money for unproven, ineffective, and at times dangerous treatments).

From this article here]
Safety And Life-saving Efficacy of Statins Have Been Exaggerated, Says USF Scientist

Tampa, Florida (Feb. 20, 2015) - Hailed as miracle drugs when they hit the market two decades ago, statins, the cholesterol-lowering drugs prescribed to prevent heart attacks, are not as effective nor as safe as we have been led to believe, say Dr. David M. Diamond, a professor of psychology, molecular pharmacology and physiology at the University of South Florida, and Dr. Uffe Ravnskov, an independent health researcher and an expert in cholesterol and cardiovascular disease.
Absolute risk versus relative risk:
The effect of the drugs on the population is called the 'absolute risk,' which has shown that statins benefit only about 1% of the population. This means that only one out of 100 people treated with a statin will have one less heart attack. Statin researchers, however, don't present the 1% effect to the public. Instead they transform the 1% effect using another statistic, called the "relative risk," which creates the appearance that statins benefit 30-50% of the population.
Bold added by me. Adverse effects:
"The adverse effects suffered by people taking statins are more common than reported in the media and at medical conferences" explains Diamond and Ravnskov. According to the authors, "Increased rates of cancer, cataracts, diabetes, cognitive impairments and musculoskeletal disorders more than offset the modest cardiovascular benefits of statin treatment." The authors emphasized that low cholesterol levels related to statin use have frequently been associated with an increased risk of cancer. They also noted that most statin trials are terminated within two to five years, a period too short to see most cancers develop. Nevertheless, studies have shown a greater incidence of cancer in people who take statins, and one long-term study demonstrated a dramatic increase in the incidence of breast cancer among women who had used statins for more than 10 years.
Bold added by me. It is scary, but all my friends and relatives invariably followed the advice of their doctors to take statins with hypertension medication as "insurance" for years, notwithstanding the adverse effects of statins. Ironically, they will not stop taking the statins as they are worried that if they were to do so, they will die prematurely of a heart attack or a cerebral hemorrhage by only taking the hypertension medication.

Kkwan these comments are meaningless without data to back them up. Show me the data.

In temrs of evidence, here’s a systematic review looking at statin side-effects. It confirms that despite individual anecdotes, they are quite rare. And one of the authors, I would point out, is Ben Goldacre, author of Bad Pharma and a strong critic of the pharmaceutical industry’s attempts to withhold relevant data about their products.
I agree with mcgyver that while we must certainly identify and acknowledge the problems with healthcare and health research, we also need to consider the alternatives. DO we help more patients by recognizing the bad behavior of corporate entities in medicine and regulating them more effectively, or by giving up on science and using other kinds of evidence (anecdote, personal experience, historical tradition, etc.) to make healthcare decisions? Cynicism is not productive, and criticism of the status quo is only useful if it is followed by constructive, and effective suggestions for improvement.

Eur J Prev Cardiol. 2014 Apr;21(4):464-74. doi: 10.1177/2047487314525531. Epub 2014 Mar 12. What proportion of symptomatic side effects in patients taking statins are genuinely caused by the drug? Systematic review of randomized placebo-controlled trials to aid individual patient choice. Finegold JA1, Manisty CH, Goldacre B, Barron AJ, Francis DP. Author information Abstract OBJECTIVE: Discussions about statin efficacy in cardiovascular prevention are always based on data from blinded randomized controlled trials (RCTs) comparing statin to placebo; however, discussion of side effects is not. Clinicians often assume symptoms occurring with statins are caused by statins, encouraging discontinuation. We test this assumption and calculate an evidence-based estimate of the probability of a symptom being genuinely attributable to the statin itself. METHODS: We identified RCTs comparing statin to placebo for cardiovascular prevention that reported side effects separately in the two arms. RESULTS: Among 14 primary prevention trials (46,262 participants), statin therapy increased diabetes by absolute risk of 0.5% (95% CI 0.1-1%, p = 0.012), meanwhile reducing death by a similar extent: -0.5% (-0.9 to -0.2%, p = 0.003). In the 15 secondary prevention RCTs (37,618 participants), statins decreased death by 1.4% (-2.1 to -0.7%, p < 0.001). There were no other statin-attributable symptoms, although asymptomatic liver transaminase elevation was 0.4% more frequent with statins across all trials. Serious adverse events and withdrawals were similar in both arms. CONCLUSIONS: Only a small minority of symptoms reported on statins are genuinely due to the statins: almost all would occur just as frequently on placebo. Only development of new-onset diabetes mellitus was significantly higher on statins than placebo; nevertheless only 1 in 5 of new cases were actually caused by statins. Higher statin doses produce a detectable effect, but even still the proportion attributable to statins is variable: for asymptomatic liver enzyme elevation, the majority are attributable to the higher dose; in contrast for muscle aches, the majority are not.
Kkwan these comments are meaningless without data to back them up. Show me the data.
They are observations on the most recent unbiased findings on statins and not merely "meaningless" comments. FYI, the onus is not on me to show you the data because I am not the scientist/researcher. However, if you do require data, from the same article cited in my post 9:
Their critique of the exaggerated claims regarding statins' ability to prevent strokes, heart attacks and heart disease-related deaths on a large scale has been published in the medical journal "Expert Review of Clinical Pharmacology" at http://informahealthcare.com/ .
And:
The exaggeration of beneficial effects of statin treatment was illustrated in their analysis of a subset of statin studies, including the Jupiter Trial (Crestor), the Anglo-Scandinavian Cardiac Outcomes Trial Lipid Lowering Arm (ASCOT-LLA), and the British Heart Protection Study. "In the Jupiter trial, the public and healthcare workers were informed of a 54 percent reduction in heart attacks, when the actual effect in reduction of coronary events was less than 1 percentage point," said Ravnskov and Diamond, who is also a Career Research Scientist with the Medical Research Service at the James A. Haley Veterans Hospital in Tampa, Florida. "In the ASCOT-LLA study, which was terminated early because it was considered to have such outstanding results, there were heart attacks and deaths in 3% of the placebo (no treatment) group as compared to 1.9% in the Lipitor group. The improvement in outcome with Lipitor treatment was only 1.1 percentage point, but when this study was presented to the public, the advertisements used the inflated (relative risk) statistic, which transformed the 1.1% effect into a 36% reduction in heart attack risk.
Also:
Diamond and Ravnskov's paper is particularly relevant at this time as reports out of Britain have revealed that leaders in health care and research, including the editor in chief of the British Medical Journal, Fiona Godlee, and the chair of Britain's Commons Health Select Committee, Sarah Wollaston, have called for drug companies to release all of their records involving undisclosed adverse effects of statins in their clinical trials.
Bold added by me. FWIW, clinical pharmacologists know more about drugs and their adverse effects than doctors who do mean well but do not keep up with the latest unbiased research/findings on drugs. We must keep in mind that drugs are useful poisons, from the chapter on how drugs act in a clinical pharmacology textbook which I read.
FYI, the onus is not on me to show you the data because I am not the scientist/researcher. However, if you do require data, from the same article cited in my post 9:
Their critique of the exaggerated claims regarding statins' ability to prevent strokes, heart attacks and heart disease-related deaths on a large scale has been published in the medical journal "Expert Review of Clinical Pharmacology" at http://informahealthcare.com/ .
FWIW, clinical pharmacologists know more about drugs and their adverse effects than doctors who do mean well but do not keep up with the latest unbiased research/findings on drugs. We must keep in mind that drugs are useful poisons, from the chapter on how drugs act in a clinical pharmacology textbook which I read.
The onus is always on the person making a claim and since you made the claim the onus IS on you. Referring me to an a site to search for support for your point of view does not meet this requirement any more than it would if I were to refer someone to pubmed to support a claim that I was making In addition your claim that clinical pharmacologists know more about drugs than physicians is a gross generalization and factually incorrect. Physicians have extensive academic training in clinical pharmacology and far more practical experience in most cases. There are no doubt some pharmacologists who know more than the average physician as well as some physicians who know far more than the average pharmacologist. You should restrict your comments to something you can actually defend with data. Finally the "drugs are useful poisons" quote may be poetic but it creates an unnecessary fear of drugs and its not accurate. The term "drug" refers to an enormously wide class of molecules that work in so many different ways that I can not possibly catalog them all here. Many drugs are substances that our own body makes ( cortisol, thyroid hormone, insulin), others are elements ( potassium,magnesium, calcium) which are essential in the correct amounts. Most drugs like antibiotics and antivirals have been designed to affects proteins and enzymes that are unique to their targets and generally have little to no affect on our cells and systems. Others are receptor antagonists or agonists while others inhibit certain enzymes and that is only a partial list. To label them all as useful poisons was probably meant to instill a level of respect for drugs but it is simplistic and somewhat misleading if taken literally. You would have to also label water, air, and food as useful poisons.
The onus is always on the person making a claim and since you made the claim the onus IS on you. Referring me to an a site to search for support for your point of view does not meet this requirement any more than it would if I were to refer someone to pubmed to support a claim that I was making
You have misconstrued what I wrote. It is not I who made those claims wrt statins. It is:
Dr. David M. Diamond, a professor of psychology, molecular pharmacology and physiology at the University of South Florida, and Dr. Uffe Ravnskov, an independent health researcher and an expert in cholesterol and cardiovascular disease.
Hence, the reference to their paper in my last post.
In addition your claim that clinical pharmacologists know more about drugs than physicians is a gross generalization and factually incorrect. Physicians have extensive academic training in clinical pharmacology and far more practical experience in most cases. There are no doubt some pharmacologists who know more than the average physician as well as some physicians who know far more than the average pharmacologist. You should restrict your comments to something you can actually defend with data.
It is not a claim. It is my opinion based on my personal experience of many doctors who are either ignorant, unreceptive or dismissive of critique when prescribing drugs (even when the latest research/findings of clinical pharmacology are presented to them). From the wiki on clinical pharmacology here]
Clinical pharmacology is the science of drugs and their clinical use. It is underpinned by the basic science of pharmacology, with added focus on the application of pharmacological principles and methods in the real world. It has a broad scope, from the discovery of new target molecules, to the effects of drug usage in whole populations. Clinical pharmacology connects the gap between medical practice and laboratory science. The main objective is to promote the safety of prescription, maximise the drug effects and minimise the side effects.
Bold added by me. Also, this is CFI, not a medical/scientific forum and it is not expected here that an opinion must be defended with "data" (whatever that means). The same applies to your opinion on the knowledge of drugs by some doctors. FWIW, I stand by my opinion and all you can say is, we agree to differ.
Finally the "drugs are useful poisons" quote may be poetic but it creates an unnecessary fear of drugs and its not accurate. The term "drug" refers to an enormously wide class of molecules that work in so many different ways that I can not possibly catalog them all here. Many drugs are substances that our own body makes ( cortisol, thyroid hormone, insulin), others are elements ( potassium,magnesium, calcium) which are essential in the correct amounts. Most drugs like antibiotics and antivirals have been designed to affects proteins and enzymes that are unique to their targets and generally have little to no affect on our cells and systems. Others are receptor antagonists or agonists while others inhibit certain enzymes and that is only a partial list. To label them all as useful poisons was probably meant to instill a level of respect for drugs but it is simplistic and somewhat misleading if taken literally. You would have to also label water, air, and food as useful poisons.
Is a statin not a drug? OTOH, to label water, air and food as drugs and "useful poisons" is clearly ludicrous. From the wiki on drug here]
A drug is, in the broadest of terms, a chemical substance that has known biological effects on humans or other animals. Foods are generally excluded from this definition, in spite of their physiological effects on animal species. In pharmacology, a drug is "a chemical substance used in the treatment, cure, prevention, or diagnosis of disease or used to otherwise enhance physical or mental well-being."
Bold added by me.

You did not post a link to “paper”/study or even a clinical review. You posted a link to layman’s story about the subject which contains no data, only opinion.
Also, you don’t absolve yourself of the responsibility to support your position simply because it was originally proposed by someone else. If instead of doing your own research you want to defer to authority then I suggest you consult more than one authority. There are many who would disagree with the comments of the individual you cite.
Whether this is a medical forum or not this IS a skeptical forum and if you are going to take a position here you will be challenged to provide evidence to support that position. Since other people read our comments, as a physician I see it as my responsibility to make sure there is a rational evidence based debate when controversial views are presented.
In regards to the definition of a “drug”. There is no one authority on the definition and although foods may “generally” be excluded from this definition that does not mean they are not drugs. That is simply a convention just as we don’t conventionally refer to cigarettes as a drug delivery system even though they clearly are. It does not mean that foods and other substances are not drugs just because we don’t include them as a matter of convenience or convention. This is the same argument we have all the time about supplements and herbs. Just because we don’t cal them drugs does not mean they aren’t drugs.
If the motive for calling things drugs is to create a convenient method for us to distinguish between things which are potentially harmful and those which are not it fails completely. Every substance which is put in the body with resultant biochemical effects deserves respect and caution. However, rather than applying a blanket caution to all of these substance we need to examine each one for its risks and benefits. Oxygen and water can both be exceptionally toxic (poisonous) under the right circumstances and there are drugs that are completely harmless even when taken amounts that are ten times the approved dose. For this reason it is counterproductive to artificially define some bioactive substances as drugs and others as not drugs if the motive is to help the public decide which things they need to be wary of and which they don’t.

You did not post a link to "paper"/study or even a clinical review. You posted a link to layman's story about the subject which contains no data, only opinion.
Did I not do so? Again, from the article I cited:
Their critique of the exaggerated claims regarding statins' ability to prevent strokes, heart attacks and heart disease-related deaths on a large scale has been published in the medical journal "Expert Review of Clinical Pharmacology" at http://informahealthcare.com/ .
The paper is available here]
How statistical deception created the appearance that statins are safe and effective in primary and secondary prevention of cardiovascular disease David M Diamond, Uffe Ravnskov Expert Review of Clinical Pharmacology Mar 2015, Vol. 8, No. 2: 201–210.
It is not available if you are not a subscribing member of Informa Healthcare.
Whether this is a medical forum or not this IS a skeptical forum and if you are going to take a position here you will be challenged to provide evidence to support that position. Since other people read our comments, as a physician I see it as my responsibility to make sure there is a rational evidence based debate when controversial views are presented.
I am not taking a position and as such is not required to "provide evidence". I am merely informing CFI about the latest findings on statins. Whoever read our posts are at liberty to decide what to believe or disbelieve.
In regards to the definition of a "drug". There is no one authority on the definition and although foods may "generally" be excluded from this definition that does not mean they are not drugs. That is simply a convention just as we don't conventionally refer to cigarettes as a drug delivery system even though they clearly are. It does not mean that foods and other substances are not drugs just because we don't include them as a matter of convenience or convention. This is the same argument we have all the time about supplements and herbs. Just because we don't cal them drugs does not mean they aren't drugs. If the motive for calling things drugs is to create a convenient method for us to distinguish between things which are potentially harmful and those which are not it fails completely. Every substance which is put in the body with resultant biochemical effects deserves respect and caution. However, rather than applying a blanket caution to all of these substance we need to examine each one for its risks and benefits. Oxygen and water can both be exceptionally toxic (poisonous) under the right circumstances and there are drugs that are completely harmless even when taken amounts that are ten times the approved dose. For this reason it is counterproductive to artificially define some bioactive substances as drugs and others as not drugs if the motive is to help the public decide which things they need to be wary of and which they don't.
It is obvious to most people what a drug is and a statin is a drug, not a placebo.

This 2013 open access paper is available here]

The Ugly Side of Statins. Systemic Appraisal of the Contemporary Un-Known Unknowns Sherif Sultan1,2#, Niamh Hynes1,2 Department of Vascular and Endovascular Surgery, Western Vascular Institute, University College Hospital Galway, Galway, Ireland Department of Vascular and Endovascular Surgery, Galway Clinic, Galway, Ireland
From 3. Review of The Statin Saga: What cholesterol is for:
Cholesterol is crucial for energy, immunity, fat metabolism, leptin, thyroid hormone activity, liver related synthesis, stress intolerance, adrenal function, sex hormone syntheses and brain function. When prescribing HMGCoA reductase inhibitors one needs to be cognisant of the fact that the body had increased its’ cholesterol as a compensatory mechanism and investigate accordingly.
The consequences of inhibiting the production of cholesterol by the liver with statins:
The statin industry, with all of its spin-off, is a 20-billion-a-year industry. We are observing the revealing of the utmost medical tragedy of all times. It is unprecedented that the healthcare industry has inadvertently induced life-threatening nutrient deficiency in millions of otherwise healthy people. What is even more disparaging is that not only has there been a failure to report on these negative side-effects of statins, there has actually been active discouragement to publish any negative studies on statins.
Bold added by me. From the conclusions:
There is increased risk of Diabetes Mellitus, Cataract formation, and Erectile Dysfunction in young statin users, all of which are Alarming. Furthermore there is a significant increase in the risk of cancer and neurodegenerative disorders in the elderly plus an enhanced risk of a myriad of infectious diseases.
Have statins opened Pandora's Box?

The article you site is not a study. Its a review which is fine but I disagree with their conclusions and in fact most of the medical community would.
To address just a few points.
“There is a categorical lack of clinical evidence to support the use of statin therapy in primary prevention.”
This is “categorically” wrong. If you read my original post in this thread I give a number of citations which provide evidence to the contrary
“Furthermore statins are associated with triple the risk of coronary artery and aortic artery calcification”
This is irrelevant. Unless you can show that it leads to an increase in disease it doesn’t matter
“Cardiovascular primary prevention and regeneration programmes, through life style changes and abstaining from tobacco use have enhanced clinical efficacy and quality of life over any pharmaceutical or other conventional intervention”
Physicians would be extremely happy if this were true but in the real world it just isn’t. Its not because these things don;t work but because people have a difficult time complying with these recommendations. I spend a good part of my day encouraging and educating y patients on lifestyle changes to improve everything from hypertension to diabetes and heart disease but the sad fact is that its difficult to change habits that have been developed over a lifetime and despite our best efforts most of us will fail. For the author to suggest that this is an alternative is an insult to the medical community. We all work to encourage our patients to improve their habits but when that doesn’t work we need other tools like medications.
It must be noted that many of the reports of side effects associated with statins are not well supported by the trials.
For example, muscle pain is the most common side effect attributed to statins and probably the most frequent reason the drug is stopped. It is rarely a serious side effect and usually resolves as soon as the medicine is discontinued. Of note though, some studies have shown no real difference between the rate of muscle complaints in patients on statins compared to those on placebo. Other studies have looked at patients on statins and compared them to patients not on statins but these studies are flawed by observer bias and the nocebo effect. Many patients have heard that Statins can cause muscle pain so if you put them on a statin they are more likely to notice pains they did not pay attention to previously.
Other studies linking things such as renal failure, diabetes, and erectile dysfinction to statin use need to be viewed with caution because patients with elevated cholesterol levels are at greater risk of these problems even if not treated with statins. Since most of these studies which look at NNH ( number needed to harm) are not randomized trials and are often post hoc analysis its difficult to know how reliable such data is.
Some of the data is highly suspect. One of the statements made is that one would expect 74 cases of liver failure in every 10,000 patients treated yet I have been in practice for over 24 years and easily treated 2,000 patients with statins yet never had a single case of liver failure.
Then there is the blatant “cherry picking” and complete lack of objectivity in the article. The authors state that statins have been associated with an increase in cancer but fail to point out that one of the articles they cite in support of this comment states that there were increases in some cancers but a decrease in others.
Quote “For haematological malignancies there was a significant reduced risk associated with any statin use… Prolonged (more than 4 years) use of statins was associated with a significantly increased risk of colorectal cancer, bladder cancer "
“Exposure to Statins and Risk of Common Cancers: A Series of Nested Case-Control Studies,” BMC Cancer, Vol. 11, No. 1, 2011, p. 409. doi:10.1186/1471-2407-11-409
and again they fail to point out that these are not randomized control trials and as such the increase in cancer may have more to do with lifestyle factors that lead to the statin use (obesity, high fat diets, lack of exercise, insufficient fiber intake) in the first place and may not be attributable to the drug. We don’t know. These are associations. There is no evidence for causation.
There is also this comment which is biologically naive and of course self serving.
“When prescribing HMGCoA reductase inhibitors one needs to be cognisant of the fact that the body had increased its’ cholesterol as a compensatory mechanism and investigate accordingly”
Not every condition is a matter of beneficial compensation by the body. High blood sugar in diabetic patients is not due to compensation by our bodies endocrine system. Its due to failure of that system. We have no evidence that the spectrum of cholesterol levels we see throughout the population are a compensatory mechanism. more likely its a manifestation of our genetic variability which at its extremes may be harmful to the organism. A scientific article should not be making such unscientific statements as this one.
Given the wealth of data on this subject as well as my own experience which is in stark contrast to the claims of these authors I can’t help but come to the conclusion that they had a preconceived notion of what they wanted to find and say before they even started looking at the evidence. For a less biased opinion on this subject you may want to look at this statement from the Cochrane review.
http://www.cochrane.org/CD004816/VASC_statins-for-the-primary-prevention-of-cardiovascular-disease

I’m happy to see that you guys are going at it. And sad to say that I don’t have time to read all that is posted: must work! So just a brief note to say that I do not mean by my scant comments that we should stop doing science, far from it, rather that we need more science. We need more government funded and institutional science, to balance out Big Pharm. We need to keep collecting as much Big Data as we can so that later on, when we figure out what questions we want to ask of that data, we have it. We also need some way to ensure that pharmaceutical interests aren’t able to bury damning data, and that is tricky. The FDA is supposed to require hard data to approve a drug, but they have no way of accessing any data not actually submitted, and therein lies the problem. We don’t know what was in the studies that didn’t come to light, other than a guess that the data probably wouldn’t convince you to give a statin to your mother, hence the need to hide that data to protect sales.
The thing about cholesterol and cardiovascular disease that bugs me is the fact that the standards for acceptable cholesterol levels are arbitrary. It’s just like the 40 years of governmental advice telling us not to eat bacon and eggs: when statins have long gone out the window, what will we argue about next? Governments make mistakes. Doctors make mistakes. The trick is to be flexible enough in our thinking to admit it when we have made one, and to reverse course. I am interested in ALTERNATIVES to statins for gaining and maintaining low cardiovascular risk. There are many. Drugs, foods, supplements, nutrients, herbs, whatever you want to use, there are many ways to skin this cat. It is amusing to me to see how many people use red rice yeast thinking that they are avoiding the trouble with statins, when in fact they are taking a substance that works by the same mechanism and would have the same side effects if they were able to get the same dose. It is hopeful to me that many conventional doctors are prescribing CoQ10 to their patients who are on statins. Eventually we’ll arrive at some agreement about the best approach because the evidence will be overwhelming. Until then, we fight against overwhelm.
Water can be lethal in the wrong dose. =-]