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Statins are back in favour

The lady from Oxford seemed very uncertain, very unimpressive....
 
Oldvatr said:
http://www.bbc.co.uk/news/health-37306736
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It's slightly concerning that the reviewers on this study are all part of the "Statin Industry" and thus, just like the controversial paper that suggested Statins are bad, this one also has to be taken with a pinch of salt.

Especially when you consider there's rather more evidence now that cholesterol volume is not what drives issues in relation to CVD and lack of cholesterol has severe consequences for the neural system...
 
I really want to see clarity on what evidence they looked at and how the study was done. I suppose we need to read the Lancet article.
 
I've just had a quick look. There is no section outlining what data or studies looked at. There's no mention of any additional data being examined beyond re-surveying existing RCTs - or even a clear statement of precisely which RCTs they looked at.

So it seems they didn't actually look at the controversial clinical trial reports that Ben Goldacre has been agitating to access, or any of the additional statins trial data that Rory Collins has private access to.

So, preliminarily, this seems to be a general and abstract argument in principle about what RCTs can be taken to show.

This impression is supported by this language at the end under Contributors:

"RC had the idea for this paper and wrote the initial drafts." And it's headlined as a Review.

So it seems to be a general theoretical argument about interpretation - not an examination of new data.

LSW
 
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LucySW said:
I've just had a quick look. There is no section outlining what data or studies looked at. There's no mention of any additional data being examined beyond re-surveying existing RCTs - or even a clear statement of precisely which RCTs they looked at.

So it seems they didn't actually look at the controversial clinical trial reports that Ben Goldacre has been agitating to access, or any of the additional statins trial data that Rory Collins has private access to.

So, preliminarily, this seems to be a general and abstract argument in principle about what RCTs can be taken to show.

This impression is supported by this language at the end uer Contributors:

"RC had the idea for this paper and wrote the initial drafts." And it's headlined as a Review.

So it seems to be a general theoretical argument about interpretation - not an examination of new data.

LSW
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RC interviewed just now on BBC. Apparently the study had 50,0000 taking statins, and 50,000 taking placebo. No difference between the two groups in terms of muscle pain. However, the trial is not identified, and we cannot se the trial data that he refers to. No idea who carried out this major study, or what group of people were being analysed/

I am more impressed by the study published last year based on post mortems in a hospital that showed that there was no correlation between LDL levels and mortality due to CVE.
 
Oldvatr said:
RC interviewed just now on BBC. Apparently the study had 50,0000 taking statins, and 50,000 taking placebo. No difference between the two groups in terms of muscle pain. However, the trial is not identified, and we cannot se the trial data that he refers to. No idea who carried out this major study, or what group of people were being analysed
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I heard him too. But I don't think, from scanning the article - have a look! - that there was *a* study, as in "the study". He must be talking about specific aspects or combinations of particular pre-existing studies. This article doesn't present any new data.
 
It's this section in that review which should give pause for thought:

Declaration of interests JA, CB, LB, RC, JE, RP, DP, and CR work in the Clinical Trial Service Unit & Epidemiological Studies Unit (CTSU) at the University of Oxford. The CTSU has received research grants from Abbott, AstraZeneca, Bayer, GlaxoSmithKline, Merck, Novartis, Pfi zer, Roche, Schering, and Solvay that are governed by University of Oxford contracts that protect its independence, and it has a staff policy of not taking personal payments from industry (with reimbursement sought only for the costs of travel and accommodation to attend scientifi c meetings). RC is co-inventor of a genetic test for statin-related myopathy risk, but receives no income from it. DP has participated in advisory meetings for Sanofi related to PCSK9 inhibitor therapy in his previous employment. The CTT Collaboration, which is coordinated by CTSU with colleagues from the University of Sydney, does not receive industry funding. JD has received research grants from, and served as a consultant to, Merck and Pfi zer. GDS has twice received travel and accommodation funding and honoraria from Merck; DD receives compensation for serving on data monitoring committees for clinical trials (including of statins) funded by Abbvie, Actelion, Amgen, AstraZeneca, Boehringer Ingelheim, GlaxoSmithKline, Merck, Sanofi , and Teva. NW and ML are inventors of a combination formulation for the prevention of cardiovascular disease that includes a statin, covered by patents licensed to Polypill in which they both hold shares and which owns the website polypill.com. SMac has received research grants for research on statins and polypill development from Bristol-Myers Squibb and BUPA. SMar is co-inventor on a pending patent for a LDL cholesterol estimation method, and has served as an advisor to Sanofi , Regeneron, Quest Diagnostics, Pressed Juicery, and Abbott Nutrition. NP has received research grants and honoraria for participating in advisory meetings and giving lectures from Amgen, Lilly, Menorini, and Merck. PR has received investigator-initiated research grants from Amgen, AstraZeneca, Kowa, Novartis, and Pfi zer. PSe has received research grants and honoraria for consultancies from Amgen and Pfi zer. LS has undertaken advisory work unrelated to statins for AstraZeneca and GlaxoSmithKline. SY has received a research grant from AstraZeneca through Hamilton Health Sciences. AR declares that George Health Enterprises, the social enterprise arm of The George Institute, has received investment to develop combination products containing statin, aspirin, and blood-pressure-lowering drugs. JS has received grants from the National Health and Medical Research Council, Australia; Bayer Pharmaceuticals; Roche; and Merck Serono. RB, SE, BN, IR, and PSa declare no competing interests.

Or in other words, there's rather a lot of people involved who have also been working with the developers/manufacturers of Statins.
 
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LucySW said:
I heard him too. But I don't think, from scanning the article - have a look! - that there was *a* study, as in "the study". He must be talking about specific aspects or combinations of particular pre-existing studies. This article doesn't present any new data.
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Interesting also that the 'study' is talking about statins reducing haemorrhagic strokes in particular. My simplistic understanding of LDL is that it supposedly leads to plaque buildup and through this blood clots, thrombosis, and occlusive strokes. Not sure about leaky plumbing being caused by LDL.
If the 'study' is using the RCT trials pre 2006 then those have been clearly shown to be using statistical analysis methods that have been discredited as being 'open to misinterpretation and bias' and the method has been banned for use since 2006. A new report that revisited the old statin trials shows that taking the max dose of Atorvastatin daily for a year may prolong life by around 1 day (for men) and NO EFFECT for women.

This is similar to the conclusion I made when I looked at the published trial data, whereas the official conclusion of the report claimed something like a 40% risk reduction/ It was obvious that the conclusion was not born out by the data it was supposedly based on.

EDIT to Add: Seems others agree with me on the haemorrhagic stroke aspect, Recent study http://www.ncbi.nlm.nih.gov/pubmed/23704101
Does not support the RC edtorial of today
 
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Prof Rory Collins is on the Jeremy Vine R2 show now.
 
My biggest issue with Statins is that they don't tie in with the physiological model for Cholesterol. HDL is good, sdLDL is bad, LDL of its own isn't bad. Statins indiscriminately remove everything. You die. (Okay that's a bit extreme, but you get my point).
 
tim2000s said:
My biggest issue with Statins is that they don't tie in with the physiological model for Cholesterol. HDL is good, sdLDL is bad, LDL of its own isn't bad. Statins indiscriminately remove everything. You die. (Okay that's a bit extreme, but you get my point).
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SdLDL is a relatively new concept that mainstream physicians have not yet been taught about. As we have seen recently the textbook 'bible' for endocrinologists does not mention it (2015 edition according to Luna51). So according to current belief systems used by HCP's and eminent professors is that LDL is the real killer, which must be exterminated. LDL is the White Van Man of the endocrine transport system.
 
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