Talk:Statin/Archive 1

Archive 1

Archive 2

Archive 3

What's

What's your thinking on the use of the {{Statins}} template? It is currently only used on the Atorvastatin article, and does not even appear here. Is the thought generally that it should be used or should be avoided? If it should be avoided, should it be nominated for deletion?

Courtland 14:50, 2005 Mar 27 (UTC)

I think it's beautiful. Let's keep it. This means that links to these drugs in "see also" can disappear.

Perhaps you'd like to put the fibrates and the bile acid sequestrants in it as well! JFW | T@lk 19:08, 27 Mar 2005 (UTC)

I've added the template to all of the referenced articles.

Addition of the two additional items would require a change to the title, someting like "Hypercholesterolemia treatments". Do you really want to do that?

Courtland 19:38, 2005 Mar 27 (UTC)

---

The article currently reads:

Although statins inhibit endogenous cholesterol synthesis, their action goes further than that. By reducing intracellular cholesterol levels, liver cells upregulate expression of the LDL receptor, leading to increased clearance of Low-Density Lipoprotein from the bloodstream.

The second sentence states that liver cells reduce intracellular cholesterol levels, but I think what is meant is that statins reduce those levels, and liver cells react. AxelBoldt 00:14, 28 May 2005 (UTC)

You're right. JFW | T@lk 08:24, 29 May 2005 (UTC)

Axel, could you monitor when these statin/cancer results are published in a journal? I'm a bit allergic to New Scientist links when a peer-reviewed publication is available. JFW | T@lk 20:09, 30 May 2005 (UTC)

PPS -> statin myopathy

My source for this info is private communications with dozens of PPSers over the past three years. I have heard at least a dozen state that they experienced myopathic symptoms apparently due to statins, and have not so far encountered any who can say they've been on statins for more than a few months without experiencing myopathy.

Based on this, the probablility of statin myopathy in PPSers is probably in the 75-100% range, but I felt is best in the article to just say "higher than normal rate".

One could argue that the article should remain silent on this topic unless one can quote a published source, but PPS is receiving extraordinarily little research, and no researcher seems interested in the statin-PPS link. It seems unfair to the reader to omit this potentially important piece of information entirely.

• • Not sure who you are hanging out with..  ;-) Yes a small number of patients can't take them, but there are millions of patients on statins. I'm sure we'll find more minor problems with them in the future since they are so popular. I see patients everyday who are on statins (I don't prescribe) who have no complaints. Full disclosure: I myself (50y/o male) take Lipitor (so does my mom) 40 mg/d for about 5 years. Only change has been a 60% reduction in my LDL. For what it's worth, lots of doctors in the US take statins.EtherDoc (talk) 03:43, 27 January 2009 (UTC)

On a slightly different topic, it should also be noted that statins can induce significant myopathy without producing clear signs of rhabdomyolysis (elevated CK and/or myoglobinuria). Since rhabdo is supposedly "infrequent", Drs are unlikely to attribute muscle symptoms to rhabdo without clear lab signs, even though the physical symptoms are there. I think the existing wording of the article is a little biased in this regard, by not mentioning myopathy and therefore downplaying muscle symptoms considerably.

• • By definition, if you can't measure it, or find it on biopsy, then it isn't myopathy. Better term is myalgia.EtherDoc (talk) 04:20, 27 January 2009 (UTC)

(I want to note that I'm not a rabid anti-statin person. I understand the value of statins, and I'd be on them now if I could tolerate them, but I can't.) drh 14:27, 2 August 2005 (UTC)

See your talkpage, and please review this policy. JFW | T@lk 21:47, 2 August 2005 (UTC)

I've removed it for now. When you've published it, please let me know because it may well be worthy of inclusion. JFW | T@lk 01:08, 7 August 2005 (UTC)

With respect to ubiquinone comments that get deleted, there's ample testimony of Co-Q-10 users (ubiquinone) that benefit from supplementation, in terms of relieving CHF symptomatology and myalgias. References to follow with respect to CHF once I learn how to add them. There's a large multi-center Italian study for example. In the interim, you can call Dr. Peter Langsjoen in Tyler, Texas if you want to know more. Hubie59, 11-09-06

Hubie59, positive personal experience that has not been studied on a wider scale and not reported in a reliable source is classified as original research.The reason is very simple: many people have positive experiences with this, that or the other. But when the same remedy is studied on a larger scale, especially in a placebo-controlled context, one finds that it doesn't actually have any intrinsic benefit.

Of course Q10 supplements make sense, but we should not present it as "effective" until the trials have been reported. Statins took 8-9 years to become widely accepted, and then only because large studies such as the 4S showed a real statistical benefit. We should demand no less from Q10 supplementation. JFW | T@lk 20:49, 9 November 2006 (UTC)

Thank you for your comments, JFD. The Italian study had thousands of patients (4K? 5K?) and has corroboration with additional studies. (Elsewhere I mentioned Merck's patent re:ubiquinone in combination with statins). The drug companies and the FDA are quite the bedfellows. A multi-antigen vaccine--Pediarix--was approved by the FDA based on a study of less than 200 kids! "Large, placebo-controlled, double-blinded, well-designed studies" in a postmodern culture means whatever the holders of the purse strings intend it to mean. Statin users shouldn't hold their breath waiting for drug companies to study quality-formulated Co-Q-10 because, as you know, its unpatenable. With respect to the 4S study, (4444 men and women with a previous MI treated with simvastatin (Zocord®) or placebo. A 1994 study – Credited for ushering in the era of statins). There were 111 CHD deaths in treatment group and 189 CHD deaths in control group, which amounts to an absolute risk reduction of a paltry 3.5%. With respect to total deaths, there were 256 total deaths in placebo group and 182 total deaths in treatment group--an absolute risk-reduction of 3.3%! In other words, if 30 patients are treated for 5.4 years then 1 person will benefit. Moreover, the benefits were realized in men only; not women (25 women in the placebo group died (6%) and 27 died in the treatment group (6.6%). And with respect to cancer, there were 13 cases of skin cancer in treatment group and 6 cases in the control group. If this is one of their hallmark studies you can imagine how much the other studies weakened the case for statins. Hubie59 02:36, 12 November 2006 (UTC)

Which Italian study? Where did you make that comment about Q10 together with statins and would you care to repeat it? Simvastatin is now generic, and some clever company will no doubt combine it with Q10 for those people genuinely worried about this.

I dislike your conspiracy theory on a totally unrelated subject (a vaccine). Can we stick to the issue? I'm also not in the mood to do number crunching. What was the hazard ratio for skin cancer, and what was the 95% confidence interval? JFW | T@lk 17:27, 12 November 2006 (UTC)

Co-Q-10 with a statin? See Merck's patent #4,933,165. I suspect Merck's patent may block other companies from formulating a statin-Co-Q-10 combo product so we'll leave that to the attorneys to hash out.

Conspiracy theory? I mentioned the vaccine study only to point out the hypocrisy that surfaces occasionally with the "need more, larger studies" argument that's often put forth to thwart an opposing view. This is not too dissimilar from the "experts" that ignore non-mainstream "original" data solely because of alleged financial conflicts of interest. This should cut both ways. For example, when was the last time anyone said, "You can ignore the statin studies. Many of the study leaders appear to be lapdogs for the National Cholesterol Education Board (NCEB), as attested to by the fact they receive grants, consultant fees and honorarias from multiple drug companies. They just want the money." You don't hear that.

I too will leave the number crunching to the other statin and Co-Q-10 wiki-lurkers. I've left plenty of fodder (and have plenty more). Time is always in short supply. Hubie59 03:27, 13 November 2006 (UTC)

Your position is still not clear. Do you think statins are harmful pharmacological bombs designed to make money for drug companies? JFW | T@lk 21:04, 13 November 2006 (UTC)

Are statins "harmful pharmacological bombs?" If you take one and go amnesic or need Tylox to treat your myalgias you would be inclined to say "yes." If you have familial hypercholesterolemia with a LDL of 500 you would likely say "no." Are they designed to make money? That's what drug companies do isn't it? Seek to make a profit while providing a product that provides a benefit with acceptable risks. However, statin makers have effectively disqualified themselves as witnessed by the Merck patent, failure to grant equal footing to the pleiotropic effects, the spin spun into their commercials, etc. Hubie59 20:01, 17 November 2006 (UTC)

Amnesic? Your evidence, please.

Of course drug companies want to make money. They are not charitable foundations. Sorry. Even the Howard Hughes Medical Institute needs drug companies to effectively market drugs discovered by its scientists (see imatinib). That is not equivalent with the accusations you have been making.

Disqualified? In whose eyes? In yours? JFW | T@lk 21:57, 20 November 2006 (UTC)

Alzheimer

Someone has been inserting laboratory evidence of statin action on microglia in Alzheimer's models. This was, however, in a section on cardiovascular disease (Alzheimer's, while associated with atherosclerosis and low-grade inflammation, is not a cardiovascular disease). Furthermore, this was in an animal model, not in patients. Finally, the four points quoted are from Furberg's review (I will add the reference).

There is a wealth of research into statins for all sorts of conditions, from Alzheimers to anaplastic thyroid carcinoma. I think we should be sensible and only include the major avenues of research here. I am not apposed to an Alzheimer paragraph, but preferably in keeping with the style of the rest of the article. JFW | T@lk 10:33, 19 August 2005 (UTC)

A lot has changed in a couple of years. I think a section on memory loss associated with Statins should be added to this article. Particularly since tests have been developed that can distinguish between memory loss due to Alzheimer's and memory loss due to statin use. --Jmcclare (talk) 15:41, 13 February 2008 (UTC)

To this day, the evidence in support of memory loss associated with statins is strong but anecdotal. I would wait until results of well designed trials are available. It's true that if what happened with Vytorin is an indication of the impartiality of pharmas, we may need to wait a long time to see those results. Still, a randomized controlled trial funded by NIH is currently analyzing the effect of low dose statins on thinking and other behavioral indicators ( http://statineffects.ucsd.edu/ ).AK Arakaki (talk) 23:45, 27 February 2008 (UTC)

Beatrice Golomb has been making noises for a very long time about cognitive effects of statins. The bottom line is that the Heart Protection Study did not find any changes on neurocognitive testing, and all negative reports are anecdotal (and therefore not "strongly associated"). Some studies have shown an improvement in Alzheimer's risk; I don't know whether ApoE phenotype has been factored into that equation. At the moment I continue to disagree with Jmcclare that we can say anything definitive on cognition and memory vs statins, and we might as well wait for some actual evidence. JFW | T@lk 00:54, 28 February 2008 (UTC)

JFW: I disagree with your calling "making noises" to Beatrice Alexandra Golomb's research on cognitive effects of statins. She definitely is a qualified researcher, Professor of Medicine @ U.C. San Diego, board certified MD with a PhD in neurobiology, and her research on statins and noncardiovascular endpoints is funded by a four million dollar NIH grant.

In my comment, I said "the EVIDENCE is strong but anecdotal", I think we all understand and agree with the "anecdotal" nature, by "strong evidence" I mean that there are several reported cases where: 1) patients on statins have severe concentration and/or memory problems, 2) that disappeared after stopping the statins and 3) reappear when they start the statins again. This is an very reasonable criterion for assessing causal association, i.e the adverse drug reaction abates with dechallenge and recurs with rechallenge (PMID 15148066). Anyway, I think we agree on waiting until results of well designed trials are available. AK Arakaki (talk) 16:40, 5 March 2008 (UTC)

In the UK there has been some strong publicity for the theory that statins prevent the development of Alzheimer's disease. The Guardian carried a PA article headed "Statins can cut risk of Alzheimer's, study shows" (29 July 2008) in the "News in Brief" section. A few days later, it was the front page headline in The Daily Mail. There is a more balanced headline in Medical news today online: "Statins Linked To Lower Dementia Risk" and cites the article giving rise to this enthusiastic journalistic response. It would be good to have a review of the evidence, giving sources, in the WP Statins article. 86.149.172.182 (talk) 18:06, 1 August 2008 (UTC)

• The references here may shed some light on this.Mevalonate_inhibition#Abnormal_Phosphorylation_of_Tau_protein80.189.7.5 (talk) 20:25, 11 June 2009 (UTC)

Disambiguation: rat liver protein

Apparently there is a protein called statin expressed in rat livers (PMID 2246273). Yes, this confused me for a bit too. Should there be a disambiguation page?

Courtland -- I remember you from my AZ days!

--Andrew Clegg 17:37, 6 November 2005 (UTC)

Cancer risk

JAMA this week: no benefit but also no risk of cancer[1]. JFW | T@lk 08:34, 5 January 2006 (UTC)

Yes, but the article which cited the rodent studies viz cancer stated that long term studies are needed, and that until they are done, statins are not recommended for anyone other than those in immediate risk of heart attack. The JAMA round-up is not a round-up of *long-term* studies. It is rather misleading to state "no benefit and no risk" instead of "no benefit and no risk based on cume of short-term studies, however due to rodent carcinogeneity, long term studies are needed before risk is justifiable for anyone not in immediate danger of heart attack."

Cindery 02:16, 29 July 2006 (UTC)

PMID 8531288

That article is ten years old and has been superseded by enormous series showing no increased cancer risk and indeed a decreased risk of particular malignancies. JFW | T@lk 17:27, 12 November 2006 (UTC)

Jfdwolff, regarding the meta-analysis of 23 statin studies, a p-value of 0.009 is statistically significant, but I removed the "highly" that may be subjective. Now, about the "requires further investigation" statement, why do you think that a statistically significant higher incidence of cancer does not deserves further investigation? I mentioned this article in the cholesterol discussion page, but I haven't seen any objection against it since last September, so I brought it to the statins page, where it seems to fit better. —Preceding unsigned comment added by AK Arakaki (talk • contribs) 15:53, 27 February 2008 (UTC) I just realized what you meant by '"meriting further study" is WP:NOR', I apologize for my lack of familiarity with WP policies. I read the "No original research" page and understand that "requires further investigation" can be considered my personal interpretation. In fact, that was a conclusion from the authors, so I'll rephrase to make that point clear.AK Arakaki (talk) 16:11, 27 February 2008 (UTC)

I was misinterpreting your comment, I thought you didn't consider a p value of 0.009 as statistically significant. I agree that "significant" can be interpreted in other ways other than "statistically significant", I'll make similar corrections in my contribution to the cholesterol page.AK Arakaki (talk) 22:31, 27 February 2008 (UTC)

You shouldn't leave these comments halfway the discussion page. I hadn't noticed them. I'm glad we can agree on the use of the term "significant". JFW | T@lk 00:54, 28 February 2008 (UTC)

Ethics

"The issue of large asymptomatic populations taking a powerful drug, that most likely won't impact the chance that they will contract heart disease, is rarely discussed by physicians who prescribe the drug. As an example, if a group of 100 people all having a 10% risk for a heart attack in the next ten years start taking statins (reducing the risk of a heart attack by 30%), only the cardiac outcome of three people will be modified! Is it ethical to subject such a population to the risks of the various side effects, some of them serious, when many of those who will suffer from them would not have had cardiac problems anyway?"

While a discussion of medical ethics is certainly not something to be ignored, a better place for such a discussion might be medical ethics. However, the author's implied assertion that use of statins for prevention of cardiovascular disease is unethical is based on some flawed assumptions, thus I removed the section above from the main page.

The author cites an example of a group of 100 people with a uniform 10 year MI risk of 10%. In reality, the hypothetical population group members receiving statin therapy each have a minimum of 10% risk. And indeed, in Australia for instance, an individual is not usually considered for statin therapy unless he/she has a minimimum 5 year risk of 10–15%. Hence, although it is difficult to quantify, the benefit is greater than the purported "three people" in a hypothetical sample of 100 people.

Since it is impossible to predict precisely which individuals will benefit, the choice to treat for prevention of cardiovascular risk is a public health issue. Prescribers must balance risks of adverse drug reactions with the expected benefits. In this instance statins are well-tolerated by the vast majority of patients, and therapy is normally ceased in the minority of patients that do experience adverse drug reactions. From a public health viewpoint, the actual prevention of adverse cardiovascular events in a proportion of the group does outweigh the much smaller risk of adverse drug reactions. Additionally, the prevention of adverse cardiovascular events results in fewer patients requiring hospitalisation, freeing-up health system resources for other patients.

-Techelf 06:47, 14 April 2006 (UTC)

The same logic applies to 100s of other drugs. It does not belong here, that paragraph. JFW | T@lk 07:11, 18 April 2006 (UTC)

I *strongly* disagree. First off, an ethics section should be included in every drug entry, in my opinion, with general warnings about the unrelibility of medical studies due to unethical practices by pharmaceutical companies. Consumers/Patients should exercise caveat emptor--and perhaps be explicitly warned, by law or ethical imperative of Hippocratic Oath--that pro-drug studies may not be reliable or impartial.

Second, there is *particular* concern where this class of drug is concerned, as the estimates I have seen seem awfully high for how many people should take this drug and for how long. The profit motive for drug companies to compel such a colossal number of people to take these drugs every day at--what length, excatly?--renders them particlarly subject to skepticism/warning of potential unethical drug company practices.

http://www.guardian.co.uk/medicine/story/0,11381,1101706,00.html Cindery 02:23, 29 July 2006 (UTC)

I disagree that every drug article needs an "ethics" section, unless there have been explicit ethical concerns about that drug in major information outlets. Statins are better studied than any other class of drugs. Those questioning the impartiality of the trials would question the impartiality of any trial not conducted by themselves. JFW | T@lk 07:05, 5 September 2006 (UTC)

I would offer the following alternative to the above closing proposition: Those questioning the impartiality of the trials would question the impartiality of any trial not conducted by an impartial party. Impartial means no benefits are to be extracted by any stakeholder involved in such investigation. In particular, when a popular drug group such as this enjoys a mass market uptake, there is an equally vast audience to whom the issue of possible drug trial partiality is directly relevant. Certain drug types are more than an a mere academic interest; they are highy familiar to, and even ingrained in modern health culture. The consumer must not to be excluded from such discussion via the suggestion that ethics are not relevant to for example this particular subject of mass market drugs and their surrounding issues. Acssm 12:59, 31 October 2006 (UTC)

Again, this applies to many other drugs and not just the statins. Take it elsewhere. JFW | T@lk 00:54, 28 February 2008 (UTC)

Edits by Yankeedoodle and Jfdwolff

I happened to be reading this page out of interest, and wikilinked a paragraph by User:Yankeedoodle which was subsequently reverted by User:Jfdwolff, with well-motivated reasons. This is not a subject I have studied to any great extent, and I hadn't noticed the material I was wikilinking was a very recent edit by a new editor. However, after I noticed the previous edit had been reverted I was curious and did a search on pubmed.org for statin "beta blockers" mevalonate which had one hit [PMID 15577180] that is possibly the research YankeeDoodle was attempting to incorporate. The abstract suggests statins do supress mevalonate, but does not explicitly say that beta blockers do. A second search for mevalonate "Coenzyme Q10" again came up with one hit (!) [PMID 16286544] which directly addresses Jfdwolff's question by measuring how statins affect Coenzyme Q10 levels in a controlled study, although more research seems to be needed. My limited knowledge of these issues do not make me inclined to incorporate this myself at present, but it seems to be relevant and worthy of consideration. My unqualified conclusion is that Coenzyme Q10 supplementation for statin users would be worth considering for this reason alone. Elroch 15:22, 17 May 2006 (UTC)

One single PubMed hit for each? Boy, I'm underwhelmed. We need quite a few more. JFW | T@lk 19:27, 28 May 2006 (UTC)

Specifically: the Taguchi article is in Japanese, and the abstract does not indicate in which way β-blockade could possibly influence Q10 levels. As for Lamperti et al, the sample size was too small to say anything meaningful. There was no statistical difference in Q10 levels, and the statistical outliers could well have been the result of selection bias (a genetic propensity to low Q10, predisposing them to statin myopathy). When it comes to suggesting Q10 supplementation, I really doubt there are scientific grounds for recommending this to anyone. Does it even survive the gastric pH, or are you suggesting it is administered parenterally (intermuscularily, for example :-) JFW | T@lk 20:46, 28 May 2006 (UTC)

I am glad to be able to answer your last question from what I recall about CoQ10. Typically about half the daily requirement for CoQ10 comes from the diet and CoQ10 is a widely used supplement which is clinically proved to be have measurable benefits against several of the diseases of aging. Therefore I infer that it survives the stomach in substantial quantities. More information (supporting supplementation with CoQ10 in the elderly for several reasons) is given in CoQ10 at NIH, which seems relatively cautious about potential benefits. Elroch 11:02, 30 May 2006 (UTC)

The statement that Coenzyme Q10 is lowered by beta blockers (although not relevant here) is in the wikipedia article and although, as you and I agreed, a paper I referred to above said nothing about any effect, other research does say that the original statement was justified (for some beta blockers). [2][3] Elroch 00:10, 2 June 2006 (UTC)

Statins blocking the production of ubiquinone is well-established. Merck even got a patent combining statins with ubiquinone in the 80s-- patent #4,933,165. A cardiologist by the name of Peter Langsjoen of Tyler, Texas has had good results treating CHF patients with ubiquinone, inclusively. A large, multi-centered study done in Italy revealed a benefit in treating CHF with ubiquinone. I'll dig out the citation later. There are other favorable studies too.Hubie59 01:47, 12 November 2006 (UTC)

Please provide data before making further claims. You have already made significant representations of Langsjoen's view. JFW | T@lk 17:27, 12 November 2006 (UTC)

I'll not drop Langsjoen name anymore apart from citing specific references as requested. But if there's going to be consistency I suggest the statins wiki entry be rewritten so as to not falsely elevate the "importance" of lowering cholesterol, until more proof is available as to the influence of the pleiotropic effects. The article clearly imparts a greater importance on the lowering of cholesterol that is inconsistent with the available studies. Perhaps the drug companies trumpeting relative-risk reduction statistics is to blame here. Hubie59 03:44, 13 November 2006 (UTC)

In a world where absolute risk reduction is a rare commodity, statins are good at doing at least something. If all teenagers decided to stop smoking overnight, never to pick up again, more health effects would be achieved in the future than all the statins in the world could ever achieve, whether as primary or secondary prevention.

If this page presents lipid lowering in an overly effusive tone it does so in commission. A simple look at large guideline sites, or timi.org, will show that modern medicine seems to like lipid lowering and prefers to use statins. I agree that there are some issues (e.g. degree of lipid lowering seems to be subordinate to simply "being on a statin"). If you present papers that genuinely review the evidence (rather than just shouting "Merck and the FDA are bad") we can have an open discussion and try to make the article neutral and balanced. JFW | T@lk 21:04, 13 November 2006 (UTC)

Reviewing studies must take into account the integrity of multiple parties--the study leaders, whomever funds the things, past history of parties associated with the studies, etc.--this is nothing new to most. When you think about the travesty of pumping infants with thimerosal in the late 90s via vaccines, the Vioxx fiasco, the silence over the SV40 found in polio vaccines, the burial of the Merck patent combining statins with ubiqinone--and that 's a start--there's ample reason to emphasize Merck's motivation and the FDA may be share holder-driven more than anything else. Hubie59 01:04, 20 November 2006 (UTC)

I detect the agenda of a conspirationalist. "Pumping infants with thimerosal?" Please don't be so obvious, man. It hurts your credibility. JFW | T@lk 21:57, 20 November 2006 (UTC)

Safety

Bellosta S, Paoletti R, Corsini A: Safety of statins: focus on clinical pharmacokinetics and drug interactions. Circulation 109 (Suppl. III):50–57, 2004. I have no access to the fulltext. JFW | T@lk 19:27, 28 May 2006 (UTC)

The Italian study in support of ubiquinone (Co-Q-10) supplementation for improving one's congestive heart failure (CHF) status is entitled Italian Multicenter Study on the Safety and Efficacy of Coenzyme Q10 as Adjunctive Therapy in Heart Failure. It's in the Molec Aspects Med journal, volume 15 (supplement), pp. s287-s294, 1994. 0098-2997(94)00039-5. Hubie59 20:06, 17 November 2006 (UTC)

You mean PMID 7752841. Has it been replicated? Why are you relying on a trial >10 years old when there is good recent evidence for much more evidence-based treatments, such as ACE inhibition (SOLVD and many subsequent trials), beta blockade (BEST), spironolactone (RALES trial)... Why is Q10 holy and are drugs with clearly proven efficacy evil? JFW | T@lk 21:57, 20 November 2006 (UTC)

Mental effects

From the article:

Small studies have also raised the possibility of an effect on personality, according to articles published in QJM: the International Journal of Medicine and The Annals of Internal Medicine. Another article in Clinical Cardiology suggested the possibility of an effect on daytime performance. A review published in Pharmacotherapy noted a small number of reported cases of memory loss, recommending only that "Until causality is assessed in more rigorous studies, awareness of this issue may help clinicians better counsel patients and improve monitoring of adverse events."

162.119.64.111 (talk · contribs) keeps on insisting we cover material on the mental effects of statins. The above material is a collection of papers that address the subject. However, most of these are not notable to be included in a general scope article for the lay reader. For example, the QJM article covers six patients, as contrasted to the >20,000 in the heart protection study in which no neuropsychiatric deterioration was found. The Clin Cardiol article was about various sleep problems, something 162.119.64.111 grouped incorrectly under "personality".

It would be much better if we had a single systematic review that we could quote when it comes to neurological side-effects of statins. The stuff we've had so far is anecdotal.

162.119.64.111 is also advised to familiarise him/herself with WP:CITE. URLs are not acceptable for peer-reviewed journal articles. This article uses cite.php for the references, and it shouldn't be too hard to adhere to this. JFW | T@lk 20:49, 20 June 2006 (UTC)

162.119.64.111 responds: "It would be much better if we had a single systematic review that we could quote when it comes to neurological side-effects of statins."

I agree. In March I wrote that the statin entry "should at least mention research about the effect of statins on memory - even if it's only to point out it hasn't been proven. I added a placeholder line; feel free to polish as necessary." Instead the topic disappeared altogether. Let's work together to find an unintrusive way to mention this....

I understand that the benefits of statins may widely outweigh the disadvantages, but it bothers me that this article contains no mention whatsoever of any of these concerns. (The MRC's heart protection study wasn't specifically looking at memory or cognition; it was studying the effect on mortality and major morbidity.)

I appreciate the feedback; I'm new to Wikipedia. Please be patient with me. (I think the Clinical Cardiology article I cited was in fact about both "nighttime sleep and daytime performance," and was correctly placed in a separate sentence from the personality problems.) Again: let's work together. Unsigned by anon

There are several reports of cognitive dysfunction with statin usage. Dr. Duane Graveline wrote a book on this very subject. Even if the percentage of statin patients coming down with amnesia is small it's still worthy of inclusion in wikipedia. Chloramphenicol rarely caused aplastic anemia when it was in vogue but every good practitioner knew it could. How many statin users weren't told about statins and the possibility of amnesia after filling their prescriptions? For those interested, Graveline's book is entitled, Lipitor: Thief of Memory, Statin Drugs and the Misguided War on Cholesterol. Hubie59 02:00, 12 November 2006 (UTC)

Hmm, that's interesting. From the title of the book it seems that the book is more than just about cognitive dysfunction. What measures of cognitive dysfunction does he employ (MMSE, specific neuropsychological scales)? How large are his case series and why couldn't he publish his findings in a serious publication? I strongly doubt this should be included in Wikipedia, as I dispute the claim that Graveline's book is a reliable source (in view of his clear conflict of interest). JFW | T@lk 17:27, 12 November 2006 (UTC)

Why doesn't Dr. Graveline publish in a serious publication? I haven't met him but I imagine he recognizes the clear conflict of interest the major journal editors have (per the huge sums of monies they receive from runng drug ads) and has chosen to go the book route because of that. To elaborate, I suspect Pfizer, Astra-Zeneca and Merck wouldn't take kindly to journal editors publishing studies on patients going amnesic while taking statins, even if the percentage is quite low. Speaking of "clear conflict of interest," when you play that card against "non-serious publications" you discredit yourself by ignoring the same dilemma inherent with "prestigious journals." Will you be addressing ghost writers in the near future, or the amount of money that flows from the statin makers into the hands of the members of the National Cholesterol Education Board? Hubie59 01:06, 20 November 2006 (UTC)

Complot theories everywhere, huh? Now it's ghost writers! JFW | T@lk 21:57, 20 November 2006 (UTC)

Jfdwolff: I can't speak to the availability of peer-reviewed studies, but given that a lawsuit has been filed against Pfizer on behalf of two patients who claim to have suffered memory loss as a result of statin use [4], I think it's unequivocally worth including as "news" if nothing else. Also see this article [5] in Geriatric Times, and this story [6] from CBS News. All of this suggests that it's being discussed sufficiently to merit inclusion, which really should be the main criterion IMHO.

(Perhaps I'm a bit biased, in that my mother, father, and one of my closest friends have all reported dramatic cognitive/memory dysfunction whose onset and remission seemed directly linked to statin use and discontinuation. I appreciate your caution around Dr. Graveline, et al., but I really think this one's legit.) Goldenband 23:43, 26 April 2007 (UTC)

I agree we should say something about the cognitive effects of statins, if for no other reason than the fact that it has been the subject of a lot of popular press coverage. The two best peer-reviewed trials I'm aware of (PMID 10806282, PMID 15589485) both found small decreases in cognitive performance with statins, although the small size of the decrease was of questionable significance. Of course, those findings represent an average - it's possible that most people show no effect, but a small percentage who are susceptible have significant cognitive side-effects. There's also this (PMID 17253908), although it used a low dose (10 mg/day of atorvastatin), which is less than most folks get in practice. It's been awhile since I prescribed a statin, but my practice was to ask about cognitive side-effects and seriously consider stopping the drug if a person could relate problems to the drug. Other thoughts? MastCell ^Talk 01:57, 27 April 2007 (UTC)

Interestingly, there are trials underway to determine whether satins can be used to treat cognitive dysfunction, as in neurofibromatosis [7] (under cognitive disorders). See also pub med PMID: 16271875. 69.248.150.59 (talk) 14:50, 10 February 2008 (UTC)

Cataract

Incidence of nuclear cataract (the most common form) is reduced by a quarter in patients on statins[8]. JFW | T@lk 21:54, 20 June 2006 (UTC)

Cancer risk

I will chase fulltext for this JAMA meta-analysis (PMID 16391219), which addresses cancer risk in statin use. Effects seem to be neutral, with no benefit or risk for particular tumour types. JFW | T@lk 21:59, 20 June 2006 (UTC)

Leave me a message if you want me to send it to you as pdf. --WS 00:21, 21 June 2006 (UTC)

Statins don't cause cancer? Are we sure? There were 13 cases of skin cancer in the 4S treatment group and only 6 cases in the control group. In the CARE trial (Mevacor studied) there were 12 cases of breast cancer in the treatment group and just 1 case in the control group. Statins block squalene which has anti-cancer actions. In the ASCOT, PROSPER, WOSCOPS and LIPID trials non-melanoma statistics were either not tabulated or not reported.

Patients with a prior history of malignancy were excluded from the HPS trial (funded by Merck). Also in the HPS trial, there were 243 cases of skin cancer in simvastatin group; 202 cases in control group (20% increased risk of skin cancer [in terms of relative risk])

Statins haven't been around that long. Cancer can take time before its detected. Statin users under the impression these drugs may reduce their risk for cancer are misinformed. Hubie59 02:11, 12 November 2006 (UTC)

You have already cited the 4S skin cancer risk. HPS was indeed funded by Merck but performed by an extremely reliable research group that includes some of the UK's most eminent epidemiologists; don't you think it's rather cheap to discredit a study in this way? Again, could you also give us the hazard ratio and 95% confidence interval? Raw numbers without statistical measures are quite meaningless and just serve to inflame this discussion (as is obvious from the tenor of your responses). JFW | T@lk 17:27, 12 November 2006 (UTC)

A research group excludes prospective study patients with a prior history of malignancy in a srug that inhibits production of squalene and you refer to them as an "extremely reliable research group." Did these reliable researchers have any clear conflicts of interests? Hubie59 19:59, 17 November 2006 (UTC)

I've heard that canard before, and replied to it in the BMJ when Ravnskov and his buddies played their tape again. Every reasonable intervention trial excludes cancer patients because they confound the results. This is not in any way to be seen as discrediting either the trials or the researchers. Why is squalene so important in cancer? And why are you going on about conflicts of interest? JFW | T@lk 21:57, 20 November 2006 (UTC)

Borderline relevance

I removed the following two paragraphs:

1. In May 2005, results of an observational study of half a million U.S. veterans showed that people taking statins had a 50% reduced risk of developing any of several types of cancer. The authors state that this does not suggest that statins had a causal role in reducing cancer risk, as patients receiving statins possibly may also have benefited from unrelated health-related advice, such as stopping smoking.[9]
   • This study has still not been published in a peer-reviewed journal, and I strongly doubt we should take a news article as a reliable source in a research area that is otherwise known for its emphasis on methodology.
2. In July 2006, a study was published in Hepatology which indicated that statins may inhibit hepatitis C virus (HCV) replication in vitro (PMID 16799963). Peculiarly, the anti-HCV effect is variable among the statins, with fluvastatin having the strongest effect and pravastatin having no effect. Hence, the anti-HCV effect is not associated with the statins' inhibition of HMG-CoA reductase.
   • This is a laboratory study which has not been replicated in clinical practice. Yes, I'm aware some Australian outfit uses anti-cholesterol drugs for the treatment of HCV, but that's bezafibrate and not a statin. This should not be included against the much stronger clinical trials in humans that are available for citing.

If there is any disagreement we can always move this back, but for the moment it's all very nonstandard. JFW | T@lk 08:43, 20 July 2006 (UTC)

Critical voices

This article presently does not mention a small but noisy lobby that disputes the benefits of statins. Given that these people get their work published in mainstream journals (I even had a little exchange in the BMJ with Dr Ravnskov) they are probably notable, but I'd like to include a reliable source that sums up their views without dramatics. Is such a source available? Is it a source that is not just someone's website (both Uffe and Eddie Vos have big websites), and does it give a point-by-point summary of how they see the relationship between cholesterol and atherosclerosis, the risks and benefits of cholesterol lowering, and obvious problems with their approach (such as premature atherosclerosis in patients with LDL receptor mutations).

Anyone willing to provide such a source, preferable a bird's eye view by a non-committed observer? JFW | T@lk 10:20, 20 July 2006 (UTC)

A non-committed observer? Medically aware professionals spend their whole lives committing themselves to medicine. It sounds like you're making a suggestion that commitment to a cause automatically discredits one's position. In a world where people tend to either have great faith in the advice of their doctor, failing which little faith in the advice of their doctor, finding sources which are apathetic to both expert medical consensus and alternative perspectives to it might be a difficult thing. Acssm 13:50, 31 October 2006 (UTC)

That's not what I meant at all. I'd like to have a source that gives this "cholesterol critics" group a fair but informative treatment. Just relying on their own publications may not reveal the true picture. JFW | T@lk 17:27, 12 November 2006 (UTC)

Maybe not exactly what your looking for but there is a recent Lancet paper . I'm in favor of a section that provides a critical response on the topic. —The preceding unsigned comment was added by 68.96.201.36 (talk) 02:34, 28 February 2007 (UTC).

I added a link to ask a patient.com which addresses some of the above concerns. Unfiltered, it gives voice to end consumers of all drugs. None of the statins are as highly rated as one might expect from the medical community's positive spin. I submit this as there is quite a contrast between patient experience with myalgia, in particular--it does not appear to be "rare," as reported by consumers. —Preceding unsigned comment added by 75.39.249.173 (talk) 16:21, 29 July 2009 (UTC)

"fungalbiotics"

hi, i reverted that because this is an article about statins, not about high cholesterol, per se. an experimental/minority view of the etiology of high cholesterol might have a place elsewhere, but please keep in mind that it is a minority view (i.e., probably doesn't need a whole paragraph) and that "fungalbiotics" is a neologism... Cindery 02:02, 5 September 2006 (UTC)

I agree, Cindery. I think this is a highly speculative theory with little support from anyone. Statins have been studied better than any other medical intervention in literally 100s of well-designed clinical trials. If we now come along with a poorly studied, unstudied and highly speculative theory, this completely degrades the article. Which fungi are we talking about anyway? Not Candida spp. I hope? JFW | T@lk 06:51, 5 September 2006 (UTC)

In response to "Cindery" below (comment moved here by JFW | T@lk): I have been adding the properties statins have as an antifungal, which is one of the reasons why they work. And people keep deleting it. Keep in mind that EVERYTHING is a minority view at one point or another. The world does not "wake up" one day and have a majority view. Either way - you can have your "majority" view. 71.204.83.198 (talk · contribs)

Welcome to Wikipedia, 71.204.83.198. Unfortunately we are not a crystal ball, and cannot predict which presently non-notable theory will become notable in the future when everyone has woken up.

Could you provide peer-reviewed studies into the properties of statins as antifungals? Are there any trials? What are the endpoints? Have fungi been demonstrated in atherosclerotic lesions in the same way as Chlamydia spp.? One needs to remember that all big trials looking at antibiotics for atherosclerosis have not shown any benefits. JFW | T@lk 06:59, 5 September 2006 (UTC)

One of the things that makes Wikipedia so great is: the ability for people to disseminate information which is relevant - even if some people don't agree. One of the biggest problems with Wikipedia is: the ability for people to delete information which they think is not relevant – even if some people disagree.

The mechanisms by which cholesterol works in the body is (as is all medicine) a constantly changing "science.” The best medical practice today is tomorrow’s joke, as it is with virtually all professions in a growing civilized society.

My information about the relationship between cholesterol, mycotoxins and statins may be a minority view but one supported by studies of the mycotoxin cyclosporin, cholesterol and statins. I added this reference because I thought I would get your attention or at least give a moment of pause before my contribution was summarily deleted as unverifiable - not just truth (a requirement of wikipedia) – I was wrong.

If you don’t agree with something that you think is wrong – but cannot prove it is wrong – the best course of action is to edit the page and move it to a different section marked “minority view” or something similar. This would serve all our interests and note the contributions of others to this endeavor called Wikipedia - and possibly enlighten readers as to verifiable alternatives. Unless, of course, somebody here is on the pharmaceutical payroll. This is also a problem with Wikipedia.

As for citing studies – I might do that when I get the impression somebody will listen. No offense taken.

I need not be introduced to the virtues of Wikipedia. I also agree that not everything should be deleted, and I even agree that science is constantly changing. But your contributions were inconsistent with two key policies that determine Wikipedia content: WP:NOR and WP:NPOV. NOR determines that original research should be published elsewhere before it merits inclusion; perhaps adding a reliable source would have avoided that problem. NPOV determines that the encyclopedia should be neutral in summarising different views, and makes a provision for those views that are simply not significant (yet). I also quoted WP:NOT, which states quite clearly that "Wikipedia is not a crystal ball" - there is no way of knowing whether your theory will stand the test of time.

I will happily review whatever source you provide on this talkpage and see if the revised material meets the requirements outlined above. JFW | T@lk 20:41, 10 September 2006 (UTC)

May want to reference this

Medscape article: Systematic Review of Statin Safety

http://www.medscape.com/viewarticle/550619

(I don't know if it can be referenced without a Medscape registration, but the registration is free.) drh 02:21, 25 January 2007 (UTC)

"Natural" vs. synthetic

I removed a statement to the effect that natural (fermentation-derived) statins are more effective at LDL-lowering than synthetic statins. First, it wasn't supported by the reference provided; second, it's just not correct. Atorvastatin, a synthetic statin, is one of the most potent in terms of LDL-lowering. Interestingly, this article (PMID 11583643) cites the same editorial I removed as supporting the fact that natural and synthetic statins are equivalent. So I removed the statement. MastCell 23:56, 9 February 2007 (UTC)

Perversion of the Healthcare system

(based on the Jan 20 Lancet article) Current guidlines call for 39 million americans to be treated; this wll cost billions of dollars, and many of these people will be taking statins for decades. Given this, it would seem a priority for the national health care system to establish that statins actually do good; yet the lancet article suggests that for many people there is NO BENEFIT, ie, statins cause as much harm as good. One could argue that this belongs in a seperte article, on how the profit motive distorts the health care system in the US, or something like that, but since statins are the lead example of this phenomenon, I think it should be part of the statin article. —The preceding unsigned comment was added by Cinnamon colbert (talk • contribs).

The Lancet article is already cited. An article describing "how the profit motive distorts the health care system" would be an opinion piece, and probably suitable for many venues, but not Wikipedia. Discussion about lipid treatment guidelines and attributable opinions on them is probably best dealt with in depth at cholesterol, coronary artery disease, primary prevention of heart attacks, hyperlipidemia, etc. MastCell 00:54, 11 March 2007 (UTC)

Furberg reference

In reading this article, I found a citation that had no information in it. Looking at the text, it was listed as <ref name=Furberg/>. There was no earlier reference to any work by Furberg. I found the following article by Furberg, which seemed to provide the information cited. I added this to the citation.

Furberg, Curt D. (1999). "Natural Statins and Stroke Risk". Circulation. 99. American Heart Association: 185–188. Retrieved 2007-03-04.

Please correct/revert me if this is incorrect. — ERcheck (talk) 15:13, 4 March 2007 (UTC)

That is correct. I originally added this reference. I wonder how it got removed. JFW | T@lk 23:48, 7 March 2007 (UTC)

SIM-ETL

Posting by Jtclemens removed by himself JFW | T@lk 14:18, 25 March 2007 (UTC)

You are deliberately misrepresenting my viewpoints. This is not just a single paper - this is a review by a celebrated USA pharmacologist whose overview of statin research is widely recognised.

The material you are trying to insert is disproportionate. Please post the relevant points here on the talkpage, and see whether other editors agree that they should be included in the article.

You have an obvious agenda and probably a WP:COI. JFW | T@lk 21:54, 21 March 2007 (UTC)

Posting by Jtclemens removed by himself JFW | T@lk 14:18, 25 March 2007 (UTC)

Bon appetit. JFW | T@lk

Posting by Jtclemens removed by himself JFW | T@lk 14:18, 25 March 2007 (UTC)

I've just googled your diagnostic entity, SIM-ETL. Sadly, nothing comes up. That makes it original research, for which Wikipedia is not a forum. The side-effects profile is still really benign compared to many other drugs (including simple antibiotics). Not every one of those 3% who cannot tolerate commonly-used statins develop the clinical picture you are describing. Citing advertisements of one particular manufacturer is a form of bias. JFW | T@lk 14:37, 22 March 2007 (UTC)

Posting by Jtclemens removed by himself JFW | T@lk 14:18, 25 March 2007 (UTC)

The formatting and length of your post makes it very difficult to follow. Please just provide a PubMed ID or brief identifying information for the sources you're referring to. For example: the incidence of true myositis or rhabdomyolysis is low (see PMID 15572716, PMID 16490577, and PMID 12639201 - note this is not Pfizer's data). However, muscle pain with a normal CK level does occur in somewhere between 1-10% of patients, sometimes leading to discontinuation of the drug - this is reversible when the drug is stopped (see PMID 12353945, PMID 12672737, PMID 16891287, etc). Statins are generally believed to modestly lower triglycerides (see PMID 8531308, PMID 9185636 for instance). Can you briefly explain what you'd like to see in the article, and point to some references (pubmed id preferred, please don't cut-and-paste them) to support claims like "muscle weakness is so great in many patients that they can not either stand or walk", or to increases in triglycerides with statin use? MastCell ^Talk 22:09, 22 March 2007 (UTC)

Jtclemens:

• Your first reference (PMID 12353945) concerns four patients. Not a very large group, given that there are 1000s of people on statins. I think Scott Grundy (PMID 12353951) makes most relevant points in his commentary.
• You totally misunderstand my use of Google. If Google does not link to a term, that term is not to be found on the internet (effectively). It even searches subscription-only links or sites. If SIM-ETL exists, why can't I find a single reference to it on any webpage? Or is it a term you've coined?
• If you are so het up about atorvastatin causing this symptom, what are you doing on this page? Or will you accept that it is a class effect and that you shouldn't be implicating the manufacturer in all evils of mankind? JFW | T@lk 22:34, 22 March 2007 (UTC)

Posting by Jtclemens removed by himself JFW | T@lk 14:18, 25 March 2007 (UTC)

Let's be civil. Obviously, Jfdwolff is literate. Even if you strongly disagree with someone, in your interactions on Wikipedia personal or ad-hominem attacks are frowned upon. For better or worse, credentials or who you are in real life doesn't mean much on Wikipedia. Partly, this is a function of anonymity; if I say I'm a physician, it may be true, or I may be a tenured professor of theology or a college dropout or who knows what. People's input here is generally evaluated separate from such context. Even if Stephen Hawking came to Wikipedia, he'd probably face a bunch of anonymous editors telling him how black holes really work, and if he resorted to personal attacks instead of debate his arguments would be discounted. It can be frustrating when you feel you're not being paid the respect you deserve, but that's just how Wikipedia is. Take your time with the references, but please avoid attacking other editors; it will be counterproductive in the long run. Jfdwolff is quite reasonable and responsible, and not a statin-pusher by any means; let's try to find common ground instead of going toe-to-toe. MastCell ^Talk 05:06, 23 March 2007 (UTC)

Jtclemens, I am not responding to your posts until you withdraw your personal attacks. I did not Google "J T Clemens" because this is not about you (or me for that matter). The combination gets 560 hits. So what? JFW | T@lk 12:16, 23 March 2007 (UTC)

Withdrawn

To MASTCELL and Jfwolff - I have withdrawn every major posting I have ever made on Wiki. Jtclemens 04:07, 24 March 2007 (UTC)

That was not the point of our discussion. You are free to return when you're ready to have a rational discussion about this issue. JFW | T@lk 14:18, 25 March 2007 (UTC)

I think that Mastcell and Jfdwolff may now be interested in reading the official Lipitor Web Page, published by Pfizer Inc. Look in the section that is for physicians and then look at the section on adverse side effects. There you will find the following:

Nervous System - peripheral neuropathy, ...

Musculoskeletal System - Arthritis (>2%), ...

and finally

Metabolic and Nutritional Disorders - hyperglycemia, ...

Both of you have failed the Wiki Pillar of Neutrality. Dr Paul S. Phillips reported on these effects in journals, which were referenced in this discussion page and you were aware of. Both of you were biased in your handling of the material. You allowed statements about researchers theorizing on possible mechanisms, but you discounted real proven, published scientific data. You have also failed in your promise to rewrite the Statin article, a promise that you made to me. Your conduct is really unprofessional. Wiseoldowl (talk) 23:59, 1 June 2008 (UTC)

Barring the personal attacks, could you explain what we ought to be reporting? And what's stopping you from making unbiased edits to this article, instead of ranting at others on this talkpage? And do you have a source for the information you are quoting, rather than sending us on a search? JFW | T@lk 08:53, 2 June 2008 (UTC)

First, you should really read the official drug manufacturers web pages before you make statements and then you should go back and read the whole discussion that you had with user Jtclemens. You do your research by reading Pubmed abstracts and using Google. If you don't have the time to read the research literature, then consider abstaining from deciding what published data should or should not be included. I watched in silence as you ridiculed him and refused to recognize/respect/include his references. He was way ahead of you in knowing the research literature. And I am aware of the conversations and discussions that you had with Mastcell about rewriting the Statin article. At this point in life you should understand that drug companies greatly manipulate the trials they run, the data that is published and the bias that they infuse into physicians and the entire medical and political community. You should also be aware of the work of Dr. Breatrice Goloumb on statins and the findings that physicians disregard the input of their patients. You should also be aware of the work of Dr. Phillips, who was the first one to show that the standard CPK test was not a universally valid marker for statin induced myopathy. Lastly, this is not a personal attack. It is a statement of your lack of neutrality, you stated that " you were underwhelmed" by a paper that carefully studied four patients. Those are your words - remember? That statement was a personal biased judgement, and a judgement of published data. In science one either repeats the observation for verification, or demonstrates that it can't be repeated, thereby bringing it into question. "Underwhelmed" is a personal, emotional word and it was you who used it with respect to the work of Dr. Phillips. Wiseoldowl (talk) 14:41, 2 June 2008 (UTC)

Sepsis in CKD

Statin use is inversely associated with hospitalisation for sepsis in patients with chronic kidney disease. JFW | T@lk 20:24, 5 April 2007 (UTC)

Are we really allowed to add positive information about statins? I thought the point of this article was to emphasize that statins are POISON! OK, enough sarcasm. MastCell ^Talk 21:01, 5 April 2007 (UTC)

Pancreatitis

MastCell rightly removed a lecture on underreporting of acute pancreatitis in statin use. This has been reported... in about 12 patients (PMID 16503723). These case studies are notoriously unreliable sources of actual AE ratios, which is why we have regulatory agencies that classify reactions between likely and unlikely. At least 40% of acute pancreatitis has no known cause, so there is a reasonable chance that those cases attributed to statins were in fact unrelated.

I don't think we should report side-effects that are not in the product literature, unless a major study reports these for the first time. JFW | T@lk 06:28, 7 August 2007 (UTC)

Yes. I've seen one case of pancreatitis which was possibly attributable to statins, but there were other possible causes as well, and as Jfdwolff points out, pancreatitis is often idiopathic. I agree that we shouldn't play up extremely rare side effects beyond what reliable sources indicate, nor should we speculate on underreporting without a source specifically addressing that issue. Pancreatitis is equally (or more) likely to be overreported, since so many cases lack a clear inciting cause and it's always tempting to finger a medication as the culprit. So there's my WP:OR. MastCell ^Talk 18:33, 7 August 2007 (UTC)

Consider

Rasmussen JN, Chong A, Alter DA (2007). "Relationship between adherence to evidence-based pharmacotherapy and long-term mortality after acute myocardial infarction". JAMA. 297 (2): 177–86. doi:10.1001/jama.297.2.177. PMID 17213401.{{cite journal}}: CS1 maint: multiple names: authors list (link)

JFW | T@lk 15:16, 7 August 2007 (UTC)

Good source. Care to add it, or should I? MastCell ^Talk 18:34, 7 August 2007 (UTC)

Colorectal cancer

doi:10.1053/j.gastro.2007.05.023 casts doubt on the effect of statins on colorectal cancer risk. JFW | T@lk 08:53, 12 August 2007 (UTC)

More on safety

Armitage:

Armitage J (2007). "The safety of statins in clinical practice". Lancet. 370 (9601): 1781–90. doi:10.1016/S0140-6736(07)60716-8. PMID 17559928.

Whopping meta-analysis:

Baigent C, Keech A, Kearney PM; et al. (2005). "Efficacy and safety of cholesterol-lowering treatment: prospective meta-analysis of data from 90,056 participants in 14 randomised trials of statins". Lancet. 366 (9493): 1267–78. doi:10.1016/S0140-6736(05)67394-1. PMID 16214597. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)

With no access to the Lancet from home I cannot say that I've read both, but their conclusions indicate that they might be worthy of mention. JFW | T@lk 19:53, 2 December 2007 (UTC)

Myopathy

PMID 17606177 - a MCO-based study of risk of myopathy in statin use. JFW | T@lk 22:00, 22 January 2008 (UTC)

Benefits of statins are overstated

Interesting story in BusinessWeek magazine, which could be incorporated to the Wikipedia page: Do Cholesterol Drugs Do Any Good? --71.112.107.119 (talk) 19:04, 27 January 2008 (UTC)mckoder

Cytochrom P450 must be corrected

The article states: 217.236.242.22 (talk) 20:04, 17 February 2008 (UTC)Consumption of grapefruit or grapefruit juice inhibits the metabolism of statins—furanocoumarins in grapefruit juice inhibit the cytochrome P450 enzyme CYP3A4, which is involved in the metabolism of most statins (however it is a major inhibitor of only atorvastatin, lovastatin and simvastatin) and some other medications[15] 217.236.242.22 (talk) 20:04, 17 February 2008 (UTC)

CYP 3A4 is not an inhibitor of above statins but involved in metabolizing them. These drugs increase in blood level if inhibitors are consumed - that's what's said in [15]

Mechanism of statin myopathy

An interesting paper was published last week in Nature Biotechnology, that may shed some light on the mechanisms behind the increased risk of myopathy exhibited by some statins. The authors find that a combination of the beta blocker propranolol and fluvastatin (Lescolsold), lovastatin (Mevacor) or simvastatin (Zocor), produces a strong decrease in cellular ATP levels and mitochondrial activity, while atorvastatin (Lipitor), pravastatin (Pravachol) and rosuvastatin (Crestor) showed little effect. However, the results are based on analysis of cultured murine myoblasts, still too preliminary for inclusion in the 'Drug interactions' section of the statin article, I think.AK Arakaki (talk) 20:51, 27 February 2008 (UTC)

I agree. The news agencies have responded well the the institution's excited press release. JFW | T@lk 21:08, 27 February 2008 (UTC)

Why hasn't anyone referenced the article in the Online version of the New England Journal of Medicine that shows that a large percentage of the population that experence myopathy to statins have a specific gene mutation. And why are these studies being done if the rates of myopathy are so low?04:48, 27 August 2008 (UTC)

Hi Wiseoldowl, good to hear from you again. But never let facts stand in the way of some well held prejudices. For your information, the study you are referring to was added by myself on 19 August.[10] JFW | T@lk 21:55, 27 August 2008 (UTC)

More cancer data

Take high-dose lipophilic statin, get reduced cancer risk: a pharmacoepidemiological study from Canada. I wonder how they assessed for confounders. http://www.amjmed.com/article/S0002-9343%2808%2900074-0/abstract JFW | T@lk 10:05, 28 March 2008 (UTC)

Business week deletion

Business week is a reliable source. There is no rule that only peer revue journals have to be added, is there. If there is a rule, please show me. This is an encyclopedia for the general reader, not just the scientist, and I dont see that data covered by other sources. --Richard Arthur Norton (1958- ) (talk) 16:57, 31 March 2008 (UTC)

This addition is under discussion on Talk:Number needed to treat. I would suggest that you await the outcome of that discussion before reattempting to insert it here.

The problem is that the Business Week article refers to the results of uncited scientific research. It is a typical piece of journalism with "expert vs expert" swordfight. This makes it very hard for the general reader to understand the origins and the limitations of the data. Contrary to your view, I believe the NNT=100 figure can be traced to the data; in that case, we should cite the data and not a piece of journalism. JFW | T@lk 17:19, 31 March 2008 (UTC)

Statins help but not by lowering cholesterol

The Enhance trial showed that two bestselling cholesterol drugs may have no benefit. Not because the drugs did not lower cholesterol, but because lowering cholesterol did not have the expected benefit. BusinessWeek is now reporting that statins may help prevent heart attacks but not because they lower cholesterol. See Heart Disease: Not About Cholesterol? --71.112.31.9 (talk) 04:14, 20 April 2008 (UTC)gp

That is a misinterpretation of the results of the ENHANCE trial. The use of statins in secondary prevention, and primary prevention in men, is not controversial. It is the use of ezetimibe that came out worse in a surrogate endpoint. Please do not reinsert the ENHANCE trial into this article unless you have explained why it would improve this article. And I dispute that Business Week is a reliable source for this kind of information - the "experts" quoted don't cite their sources, making it very hard to judge their sweeping statements at face value. JFW | T@lk 07:08, 25 April 2008 (UTC)

The question raised by the ENHANCE trial is not whether statins prevent heart attacks. The question is regarding the mode of action of statins. If the primary mode of action of statins is lowering LDL cholesterol then any other means of lowering LDL cholesterol should have produced benefits similar to that of statins. But it didn't. The reliable source here is The New England Journal of Medicine. From the preceding, it should be obvious how inserting the ENHANCE trial would improve the article. The Controversy section already mentions how some people believe cholesterol has not been adequately linked to heart disease. The ENHANCE trial provides data to back up this belief, and intensifies the controversy. As you noted, national and international guidelines still very much subscribe to LDL as a prime player in atherogenesis. That's the reason the new information belongs in the controversy section. Hopefully I have addressed all of your objections. --71.112.31.9 (talk) 13:01, 25 April 2008 (UTC) gp

There's a bit of a danger in selectively quoting the medical literature. The ENHANCE trial looked at whether the addition of ezetimibe (vs. placebo) to a statin would produce an additive benefit in patients with familial hypercholesterolemia. The surrogate endpoint was not heart attacks, stroke, or death, but change in thickness of the carotid-artery wall. ENHANCE found that the addition of ezetimibe to a statin lowered LDL further, but did not have an additive benefit on carotid-wall thickness.

There are a number of possible explanations. One, seized upon by the "cholesterol skeptics", is that LDL lowering doesn't affect cardiovascular disease, and that the benefit from statins is due to their pleiotropic, or non-LDL-based, properties. ENHANCE might be read as supporting this concept. However, it ignores other studies which have shown that LDL lowering by means other than statins has a similar clinical benefit (e.g. PMID 9625405, which used an actual clinical endpoint - mortality - rather than carotid-wall thickness). It also ignores recent analyses which have attributed much or all of statins' benefits to their LDL-lowering effects (PMID 16286171, PMID 17512355).

Another possibility is that LDL lowering beyond a certain threshold confers no additional benefit - that is, 80 mg of a statin maxes out the clinical benefit from LDL lowering, and a bit more LDL lowering with ezetimibe doesn't add meaningfully, at least not in terms of carotid-wall thickness. It's also worth keeping in mind that a) carotid-wall thickness is a surrogate endpoint, albeit a reasonably validated one, for heart attack, stroke, and death, and b) patients with familial hypercholesterolemia may have different biology from the average "wild-type" individual with high LDL cholesterol.

Bottom line is that while ENHANCE raises some questions, it's not we suddenly discovered that the sun revolves around the Earth or something. It's certainly worth noting the speculation that the benefit from statins may occur through mechanisms other than LDL lowering alone, but we should probably be a bit circumspect about overreading one study here. MastCell ^Talk 21:58, 25 April 2008 (UTC)

• A freely-available 2005 AHA article says in its abstract that "the regulation of eNOS by Rho GTPases, therefore, may be an important mechanism underlying the cardiovascular protective effect of statins". II | (t - c) 18:53, 26 March 2009 (UTC)

Controversy section is out dated

The controversy section does not include recent data such as the results of the ENHANCE trial. See this article in New York Times and this page on About.com. "Cholesterol scepticism" is now mainstream science. Excerpts from NY Times story: "Because the link between excessive LDL cholesterol and cardiovascular disease has been so widely accepted, the Food and Drug Administration generally has not required drug companies to prove that cholesterol medicines actually reduce heart attacks before approval. So far, proof that a drug lowers LDL cholesterol has generally been enough to lead to approval. Doctors generally believe that the amount by which cholesterol is lowered, not the method of lowering it, is what matters. In the last 13 months, however, the failures of two important clinical trials have thrown that hypothesis into question. ... For the second time in just over a year, a clinical trial found that LDL reduction did not translate into measurable medical benefits." —Preceding unsigned comment added by 71.112.31.9 (talk) 16:28, 22 April 2008 (UTC)

See my reply above. National and international guidelines still very much subscribe to LDL as a prime player in atherogenesis, and some trials do not displace this consensus. Please do not use newspaper articles as indicators of scientific consensus; journalists have the incorrigible habit of putting mavericks on a pedestal. JFW | T@lk 07:08, 25 April 2008 (UTC)

I would say that any group suggesting that statin therapy is controversial would be on the side of needing the burden of proof themselves. Internationally, case studies have replicated the result of a marked decrease in mortality associated with the proper use of statins. If you want to argue that they are not effective, then you need to produce sources. The articles showing the efficacy of statins are very numerous indeed. There could be arguments directed only at more versus less effective statins and when to properly use them, but not against them as a whole. [notice this one study]--Mrdeath5493 (talk) 08:15, 24 February 2009 (UTC)

CTT

We should be covering the two meta-analyses by the Cholesterol Treatment Triallists: http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=%22Cholesterol+Treatment+Trialists%27+(CTT)+Collaborators%22[Corporate+Author]. JFW | T@lk 00:10, 24 July 2008 (UTC)

Cholesterol is made not only by liver cells

The article implies that cholesterol is only made by liver cells. This is not correct. LDL is made by liver cells, but cholesterol is made internally in many (most?) tissues. —Preceding unsigned comment added by 130.208.183.230 (talk) 20:07, 29 January 2009 (UTC)

Mevalonate Inhibition - Redirect and Merge Debate

This is now under discussion at Talk:Statin#Mevalonate_Inhibition__-_Redirect_and_Merge__Debate —Preceding unsigned comment added by 80.189.14.166 (talk) 10:44, 8 June 2009 (UTC)

Based on the definition of statins as HMG CoA reductase inhibitors a Mevalonate inhibition page was set up to analyse the broader effects of statins in terms of the various mevalonate pathway products affected i.e terpenoids products like (CoQ10 dolichols and steroids like cholesterol, endocrine steroids and vitamin D. I personally want to develop the topic separately in terms of the biochemistry, although I have much empathy with the need to simplify it and connect it to the medical topics.Glynwiki (talk) 04:20, 8 June 2009 (UTC)

The merge should ideally result in a few lines about the biochemical changes that might result from statin treatment. I would limit this to the most definitive abnormalities (have you got direct evidence that dolichol is decreased?) and limit the sources to reviews in high-impact journals. JFW | T@lk 17:10, 9 June 2009 (UTC)

The dolichols we are reviewing for another paper as part of the the long-term changes (dolichols lose the terpenoid anchors which are mevalonate dependent). This effect is a slow one to emerge so it can await publication of another review. The classification of long-term statin effects by mevalonate product class was implicit in biochemistry but not picked up in medicine. I can only speculate why and this is a current review activity. Perhaps Dolichols is step too far until our review is ready.Glynwiki (talk) 06:44, 10 June 2009 (UTC)

Long-term CoQ10 and cholesterol depletion are the very high medical impact ones. Right from the start CoQ10 supplementation on statins and associated patents were available and is well documented, although the current advice to doctors and patients on this seems to be lamentable. The early work of Ikonen had suggested that the cholesterol homeostatic pool mechanisms would replace cholesterol in critical functions. But the current papers are beginning to describe problems with loss of new synthesis for the ER and Golgi for the lipid-wrap operations in granulation/exo/endocytosis mechanisms. The key things we are picking up in review work are the non-cardio impacts and the fact that no one is looking over their shoulders at this one which is a slow but powerful effect. I think a few lines to alert students and researchers as to the need to look at long-term Quality and Disability issues. In a healthy cohort (prevention) this could cause serious legal backlash (like Vioxx) once long term trends become obvious to a wider audience. The current NNT focus is purely cardiovascular. It took me by surprise when I first noticed it! So it would be remiss not to alert people to the broader picture that has emerged in publications across the disciplines. Glynwiki (talk) 06:44, 10 June 2009 (UTC)

You haven't really answered my question. Your claims may have an experimental basis but what is the real impact of dolichol and Q10 decrease, and how would you propose to separate it from other phenomena?

Could I attract your attention to WP:MEDRS (reliability of sources guideline)? You should certainly not be making contributions based on unpublished evidence. JFW | T@lk 17:33, 11 June 2009 (UTC)

That is a very good question - the clinical side is tricky because (funding apart) it is very hard to isolate the effects. Apart from evidence in Framingham the best sources are Beatrice Golomb's study unit at UCLA and here review summarises the Mitochondrial/CoQ10 knowledge. To understand dolichols I recommend this page on Glycoproteins [11]. Here you can begin to understand the ER Golgi inhibition of the mevalonate for the anchors (polyprenols/terpenoid) and the impact of the glycoproteins. Your question highlights why I wanted to distinguish the biochemistry of hmg coa reductase inhibition in a separate topic from the clinical discussion of statins. They topics could then be linked as clinical research and laboratory research becomes expressly connected. Merging the perspectives in one topic seems a risky strategy - but I am relatively new to Wiki? Glynwiki (talk) 05:39, 15 June 2009 (UTC)

I know that dolichol is required for N-glycosylation and membrane anchoring. I also know about Beatrice Golomb's work, which has been hyped a lot despite no results being available yet. What I actually wanted to know was: (1) which clinical conditions might be caused by dolichol deficiency? (2) has dolichol been measured in particular clinical scenarios, and is there a statistically significant link?

The average reader is not going to be very interested in suspected chemical alterations if these no definite functional correllate. So far you have not been able to convince me that an extensive discussion on terpenoid chemistry is going to be relevant here, apart perhaps from Q10 which has some clinical data (e.g. the narrative review in this week's Ann Intern Med). JFW | T@lk 15:53, 16 June 2009 (UTC)

the clinical effects are still very speculative because the long-term statin user survival data is not available or even collected. We only have the laboratory and pathway evidence. CoQ10 and cholesterol-depleted lipid rafts are far more significant issues clinically. Consequently dolichol depletion research is not currently getting the funding/attention - but it has to be a factor for anyone interested in mevalonate derived membrane-products under hmg coA reductase inhibition. Glynwiki (talk) 18:59, 23 June 2009 (UTC)

So you've conceded that most of these concepts are still essentially speculative. Do you agree that you wouldn't open an encyclopedia to read speculation but rather undisputed fact? JFW | T@lk 20:31, 24 June 2009 (UTC)

He is saying the clinical stuff is speculative and not saying the science is speculative, Encyclopedias aare about science and not about clinical opinions. Maybe we need more science in clinical trials and less associative speculation?91.125.112.67 (talk) 13:17, 4 July 2009 (UTC)

Who are you? Shall we let Glyn speak for himself? He wasn't in fact saying anything about associative speculation. At any rate, I think the science is speculative as well. I have still not seen a reference to a report that unequivocally shows a decrease in dolichol and terpenoids, let alone any consequences from such a decrease. JFW | T@lk 12:45, 5 July 2009 (UTC)

Merged

After a suitable period for debate, Mevalonate Inhibition being a definition of HMG CoA reductase inhibition - the action of statins - has been merged with the statin article and a redirection placed on the original page. There is also new information available on the cholesterol depletion page about NA+ leakage and membrane potential issues when cholesterol synthesis is inhibited. The work of biochemist Tom Haines on this effect has been updated and presented recently at a conference in Germany. Glynwiki (talk) 17:27, 30 August 2009 (UTC)

You seem to know a lot about cholesterol, mevalonate and lots of papers related to these subjects, but the new content does not explain why these alterations might be relevant. Some claims are just extrapolated from basic research without specifically looking at the effects of statins, and you simply cannot cite a patent application as this is not peer-reviewed and hence not a WP:MEDRS.

Instead of causing scares ("statins deplete this or that" - this is exactly what you're doing), why can't you address the obvious benefit exhibited by statins in large numbers of clinical trials with hard endpoints? It is impossible to grind this down with far fetched theories about mitochondria.

I don't think Wikipedia needs the endorsement of the gentlemen you've mentioned. Graveline is not a major voice here (yes, he's written a couple of books and he used to be an astronaut) and I couldn't locate Bennett on Google - did you get his name right? JFW | T@lk 18:51, 30 August 2009 (UTC)

Glynwiki (talk) 07:22, 2 September 2009 (UTC)

Could I ask that we limit personal speculation and opinion, and focus on identifying appropriate sources and presenting them in an encyclopedic fashion? Specifically, Wikipedia is perhaps not the venue for what you hope to accomplish. The talk page guidelines enjoin us from using these pages as a platform for our personal opinions about a topic. Our content policies on sourcing, original synthesis of published material, and appropriate weighting of various viewpoints guide the content of the article, and I think your proposed text runs afoul of most if not all of these. That's not to say it's incorrect or poorly researched, only to say that it may not be appropriate for this particular venue. MastCell ^Talk 21:07, 1 September 2009 (UTC)

I have removed the opinion to my talk page. Than you for the guidanceGlynwiki (talk) 07:22, 2 September 2009 (UTC)

Book

ISBN 0-19532-357-2 is all about statins. Not read it yet. JFW | T@lk 23:45, 13 August 2009 (UTC)

There's a free preview on Google Book Search. The available chapter makes for some pretty interesting reading (also includes brief histories of epinephrine, phenytoin, chloramphenicol, oral contraceptives, and gemfibrozil). Fvasconcellos (t·c) 23:52, 13 August 2009 (UTC)

Mevalonate inhibition section

I've moved the section on "Mevalonate inhibition" here, from the article. This section needs extensive cleanup to be article-ready. There's a lot of duplication, a lot of material that needs to be more clearly sourced (i.e. the refs need to match up with specific statements), and a lot of material that should be integrated into the existing article rather than dumped in a new, partially redundant section. Since the section isn't quite ready for prime-time, I'd propose we work on cleaning it up here. MastCell ^Talk 22:29, 3 September 2009 (UTC)

Mevalonate inhibition section

Mevalonate Inhibition The biochemical definition of a statin is based upon its ability to inhibit HMG-CoA reductase enzyme inhibitor; the enzyme which produces mevalonate in the mevalonate pathway. "Mevalonate Inhibition" is often used in literature to describe the effects of long-term restriction of mevalonate production in cell membranes by the inhibition of the membrane attached enzyme HMG-CoA reductase. Such inhibitors are also known as the statins. They exert their effect at the very beginning of the mevalonate pathway, the location of this key reductase step, and thereby reduce the de-novo availability of a range of terpenoid and steroid products in cell membrane. The consequences of long-term statin use are classified below according to the depletion of a mevalonate product, e.g. de novo membrane cholesterol. and Co-enzyme Q10 There are also less direct impacts from mevalonate product depletions e.g. those affecting the synthesis of Tau proteins and Rho family of GTPases to consider here. Cholesterol depletion in cholesterol-rich lipid rafts Cholesterol produced and found in the membranes of eukaryotic cells where it is facilitates their form and function. A key example is the is glial cell cholesterol synthesis in our brains vital for memory function and cognition. Cholesterol also is the substrate for our most important hormones: aldosterone, cortisone, estrogen, progesterone and testosterone as well as the quasi-hormone, vitamin D (calciferol). Cholesterol's vital role in eukaryote biomembrane structure and function and lipid raft formation, makes it of critical importance in vesicle formation, exocytosis , endocytosis, lipid trafficking cell signalling, cell communication and immune defense. Potential adverse effects of glial cell inhibition of de novo cholesterol synthesis include amnesia, forgetfulness, confusion, disorientation and increased senility. . CoQ10 (ubiquinone) synthesis inhibition Coenzyme Q10 (CoQ10) also known ubiquinone is an isoprenoid made from mevalonate units and found primarily in the miochondria. It is depleted by inhibiting the supply of mevalonate. This leads to depleted anti-oxidant activity as well as its important role in Electron transfer phosphorylation in the respiration. Golomb et al. have extensively reviewed and documented the role of statin side effects and very strongly associated them with CoQ10 depletion. A direct causative biochemical link has been in the long term use HMG-CoA reductase and the depletion of the mevalonate required for the biosynthesis of mitochondrial CoQ10. Dolichol inhibition Dolichols are vital to the process of Glycoprotein formation in the endoplasmic reticulum of cells. In this capacity it is critical to the formation of the Glycoproteins involved in neuropeptides, cell identification, cell messaging and Immunodefence. Reduced bioavailability of dolichols can affect every cellular process in the body. Abnormal phosphorylation of tau protein Meske V et al. have shown that when normal phosphorylation is interfered with by mevalonate blockade, our cells increase the production of Tau protein. Tau is the protein substance of the Neurofibrillary tangles common to Alzheimers and other neurodegenerative diseases. Abnormal tau phosphorylation and deposition in neurones and glial cells is one of the major features in taupathies. The tauopathies are a group of neurodegenerative disorders characterized by the presence of filamentous deposits, consisting of hyperphosphorylated tau protein, in neurons and glia. Major neurodegenerative tauopathies includes sporadic and hereditary neurodegenerative diseases characterized by filamentous tau deposits in brain and spinal cord. In prototypical tauopathies, glial and neuronal tau inclusions are the sole or predominant CNS lesions. They includes amyotrophic lateral sclerosis/parkinsonism-dementia complex (ALS-FTDP) argyrophilic grain dementia diffuse neurofibrillary tangles with calcification frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17) corticobasal degeneration (CBD) Pick disease Progressive supranuclear palsy (PSP) Progressive Subcortical Gliosis (PSG) (Subcortical dementia) Tangle only dementia Section References: Selenoprotein Only recently have selenoproteins been discovered and the effects of statin use to blockade of the mevalonate pathway on their role in human physiology are just emerging. Deficiency of selenoproteins has been proven to result in various types of Myopathies formerly seen only in Selenium deficiency - ( a Trace element). Additionally some forms of cognitive dysfunction are associated with Selenium deficiency. Nuclear factor-kappa B NF-kB The benefit of statin drugs in cardiovascular disease control is in their ability to inhibit this vital transcriptase. The anti-inflammatory and immunomodulation effect of statins might be mediated by such statin inhibition of Nuclear factor-kappa B (NF-kB). Repoerted improvement in atherosclerosis may result from such inhibition of the key inflammatory elements: smooth muscle migration. lymphocyte adhesion, macrophage attraction and platelet activation has been associated with inhibition of NF-kB. The immunodefense system is also keyed to NF-kB, possibly explaining associative connections with changing patterns of certain infections and cancers. References

Beyond good and evil

I've restored the parenthetical descriptions of LDL and HDL as "bad" and "good" cholesterol, respectively. These are commonly used laypersons' terms, and presumably help the reader contextualize the subject even without a knowledge of lipid biology. The meaning is straightforward and well-supported by the medical literature: LDL is "bad" in that high levels are a risk factor for cardiovascular disease. HDL is "good" in that higher levels may offer some protection against cardiovascular disease. Perhaps I'm not fully understanding the IP's rationale here, so I would welcome further discussion. MastCell ^Talk 22:53, 12 November 2009 (UTC)

Doc News, MEDRS, and doctors' dismissal of complaints

This edit was interesting: User:Jfdwolff removed a secondary article published by a journal of the American Diabetes Association which discussed a published survey of patients (ref 1 in the article). The article has a very nice interview with Golomb, who wrote a nice 2008 review of statins' adverse effects. The reasoning was that something did not, apparently, live up to MEDRS. However, it's not clear what the problem is. Please try to use edit summaries which do not employ circular reasoning (X is X because Y, rather than just X is X). I'm interested in hearing what makes Doc News not allowed, particularly since previously this article was citing a Reuters article and a WashPost is also currently included. Reuters, which is much less scholarly than Doc News, was apparently fine when it was saying that "statins are well-tolerated". II | (t - c) 04:45, 30 November 2009 (UTC)

Ah yes, Beatrice Golomb again. The "statins are bad" lady. Very nice indeed. When I talk about secondary sources, I expect them to be peer-reviewed and not take the format of a news item, as in Doc News. I know about your very personal theories about peer review, and don't expect me to chew the cud again. JFW | T@lk 23:38, 7 December 2009 (UTC)

The article summarizes a peer-reviewed survey, and Doc News was a medical journal. Golomb recently published a nice 2008 review of the side effects (PMID 19159124). There's no reason to think the information is false, and it certainly seems like a notable piece of information. Seeing no real objections, I will reinsert the statement. II | (t - c) 00:12, 8 December 2009 (UTC)

Nice or not nice, you should be awaiting consensus rather than edit warring. I think MastCell's opinion may be relevant here. JFW | T@lk 00:41, 8 December 2009 (UTC)

Er... I don't feel that strongly one way or the other. If we mention it, I would prefer we point to the actual journal article because I think that's a better citation than the Doc News piece (which could conceivably be linked from the citation using the laysummary parameter). I don't think it ruins the article to include it, and I don't think its exclusion would ruin the article either, so call me agnostic on the underlying issue. MastCell ^Talk 00:50, 8 December 2009 (UTC)

• Since MastCell has no position, should I take this to WP:RS/N? These discussion threads tend to get few commentators; this could be hanging here for months before we get another outside opinion. Or can we come to a compromise? Personally, if we're going to include it I think the Doc News article is necessary as a lay summary link - it's freely-available and discusses the entire phenomenon of how physicians tend to view statins. I'll point out, as Golomb does in her review (and as multiple other reviews state) that case studies are considered important in the pharmacovigilance. The common perspective of primary care providers (that cases are next to useless) is not shared by the experts. II | (t - c) 00:59, 8 December 2009 (UTC)

I'd say RSN, provided you link WP:MEDRS as the guiding policy here. JFW | T@lk 01:45, 8 December 2009 (UTC)

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