Rapid Response BMJ 29/05/2014

I would like to draw attention to the neurological effects of statins. Pfrieger and colleagues have drawn attention to the importance of cholesterol in neuron synapse activity in a series of reports (Science. 1997 Sep 12;277(5332):1684-7; Science. 2001 Nov 9;294(5545):1354-7.; Curr Opin Neurobiol. 2002 Oct;12(5):486-90) while Muldoon and colleagues have drawn attention to reduced memory effects (Am J Med.. 2000 May. 108(7):538-46; Am J Med. 2004 Dec. 117(11):823-9).

In particular the association between low cholesterol, Alzheimer’s (AD) and statin use concerns me. Lorin’s review published in his book “Alzheimer’s Solved” (an extensive review of some 3000+ references) associates low cholesterol with AD and statin use. The AD/PD 2009 conference raised the query – Are We Experiencing an Alzheimer’s Epidemic? Incidence Has Soared Enormously in the 85+ yr-old group from 2% in the 1960s to and expected 50% in the near future!
http://www.medscape.com/viewarticle/590106

The particular paper that raised queries was the report by Solomon and colleagues (Dement Geriatr Cogn Disord 2009;28:75–80). This study attempted to prove that high mid-life blood cholesterol levels were associated and causal for AD. It used data from a Kaiser Permanente cohort with updated follow-up information. The authors examined the full range of cholesterol values (not just high cholesterol, 240 mg/dl, ~6.0 mmol/L), to determine whether even moderate elevations may be associated with increased dementia risk. The data provided was extensive but excluded all data on treatment and subsequent cholesterol levels.

Patient records without treatment data? I find that very odd; ask yourself why such data was not presented or was it simply redacted to obtain acceptance for publication?

Tables 2-4 provide the data on which the study concludes that high mid-life cholesterol is associated with AD. However, if the row titles are replaced with guideline recommended treatment (which was not available), neither the numbers nor the statistics change but a very different interpretation can be made.

Returning to the original Table 2 cited above, the following analysis can be performed:

Table Showing 2 x 2 analysis (CSS) for combined AD and VaD and assuming TC values above 239 mg/dl as treated with statins. Given the official guidelines and the American paranoia regarding cholesterol this is almost certain. Added after submission to BMJ but covered in appended *pdf files in email correspondence

Cholesterol categories No dementia %age AD + VaD %age TOTAL %age

NO TREAT (239 mg/dl) 2932 50.31 215 3.69 3147 54.00

Totals 5477 93.98 351 6.02 5828 100
χ2= 7.92 p= 0.0049 i.e those patients with cholesterol level >239 mg/dl (>6 mmol/L), (and that would be treated with cholesterol lowering drugs, possibly for decades) are more likely to become demented (Alzheimer plus vascular dementia)!
V2 = 7.91 p= 0.0049
Phi2 = p = 0.0014

After all the vast majority of statin takers (80-90% or 99% according to some) do not suffer adverse reactions so would continue to take them for 2-3 decades.

This raises questions regarding the absence of subsequent cholesterol levels and therapeutic treatment during that 2-3 decades. Why was this data left out? Was it because Kaiser Permanente has to negotiate with Big Pharma on drug prices? Was it because Big Pharma would not be pleased at any association of statins with AD? The current controversy suggest that they would not.

The most interesting aspect of Solomon’s report is that many major UK NHS Trusts probably have sufficient data over the last couple of decades to repeat Solomon’s study.

This comment was sent to the BMJ Rapid Response on statin Adverse Reactions. It was REJECTED. I am not surprised; it confirms my belief that any comment relating to the neurological adverse reactions to statins (polyneuropathy, Parkinson’s, ALS, transient global amnesia (TGA) and Alzheimer’s) is rejected while flawed articles (missing critical data on therapy, cholesterol levels and the time-line) suggesting statin benefits are regularly accepted.

Rapid Response BMJ 29/05/2014

I would like to draw attention to the neurological effects of statins. Pfrieger and colleagues have drawn attention to the importance of cholesterol in neuron synapse activity in a series of reports (Science. 1997 Sep 12;277(5332):1684-7; Science. 2001 Nov 9;294(5545):1354-7.; Curr Opin Neurobiol. 2002 Oct;12(5):486-90) while Muldoon and colleagues have drawn attention to reduced memory effects (Am J Med.. 2000 May. 108(7):538-46; Am J Med. 2004 Dec. 117(11):823-9).

In particular the association between low cholesterol, Alzheimer’s (AD) and statin use concerns me. Lorin’s review published in his book “Alzheimer’s Solved” (an extensive review of some 3000+ references) associates low cholesterol with AD and statin use. The AD/PD 2009 conference raised the query – Are We Experiencing an Alzheimer’s Epidemic? Incidence Has Soared Enormously in the 85+ yr-old group from 2% in the 1960s to and expected 50% in the near future!
http://www.medscape.com/viewarticle/590106

The particular paper that raised queries was the report by Solomon and colleagues (Dement Geriatr Cogn Disord 2009;28:75–80). This study attempted to prove that high mid-life blood cholesterol levels were associated and causal for AD. It used data from a Kaiser Permanente cohort with updated follow-up information. The authors examined the full range of cholesterol values (not just high cholesterol, 240 mg/dl, ~6.0 mmol/L), to determine whether even moderate elevations may be associated with increased dementia risk. The data provided was extensive but excluded all data on treatment and subsequent cholesterol levels.

Patient records without treatment data? I find that very odd; ask yourself why such data was not presented or was it simply redacted to obtain acceptance for publication?

Tables 2-4 provide the data on which the study concludes that high mid-life cholesterol is associated with AD. However, if the row titles are replaced with guideline recommended treatment (which was not available), neither the numbers nor the statistics change but a very different interpretation can be made.

Returning to the original Table 2 cited above, the following analysis can be performed:

Table Showing 2 x 2 analysis (CSS) for combined AD and VaD and assuming TC values above 239 mg/dl as treated with statins. Given the official guidelines and the American paranoia regarding cholesterol this is almost certain. Added after submission to BMJ but covered in appended *pdf files in email correspondence

Cholesterol categories No dementia %age AD + VaD %age TOTAL %age

NO TREAT (239 mg/dl) 2932 50.31 215 3.69 3147 54.00

Totals 5477 93.98 351 6.02 5828 100
χ2= 7.92 p= 0.0049 i.e those patients with cholesterol level >239 mg/dl (>6 mmol/L), (and that would be treated with cholesterol lowering drugs, possibly for decades) are more likely to become demented (Alzheimer plus vascular dementia)!
V2 = 7.91 p= 0.0049
Phi2 = p = 0.0014

After all the vast majority of statin takers (80-90% or 99% according to some) do not suffer adverse reactions so would continue to take them for 2-3 decades.

This raises questions regarding the absence of subsequent cholesterol levels and therapeutic treatment during that 2-3 decades. Why was this data left out? Was it because Kaiser Permanente has to negotiate with Big Pharma on drug prices? Was it because Big Pharma would not be pleased at any association of statins with AD? The current controversy suggest that they would not.

The most interesting aspect of Solomon’s report is that many major UK NHS Trusts probably have sufficient data over the last couple of decades to repeat Solomon’s study.

Will it be done? I suspect not – too much money and statuses at stake!

In this article the under reporting of findings on statin major adverse effects is described as a “Scientific farce”.

Perhaps the most sinister and disturbing impact of these nasty drugs is the fact that the authors point out that statins are associated with triple the risk of coronary artery and aortic calcification.

As safe and as effective as some advocate old statins to be, I’ve sometimes wondered why then are they not allowed to be sold over the counter? Maybe they shouldn’t be prescribed. Let people buy them off the shelf. If that happened though, I wonder if the belief in statin’s would remain as high.

Does anybody know how long – the longest – study is?

Are there studies that, specifically,look at adverse effects?

Are there long-term studies on middle aged and older people, men and women?

Are there unbiased studies on these subjects?

.
My mother was put on simvastatin when she was over 80 (after a small heart attack).
This went on for a some years. She complained of muscle weakness, pain and cramps in her legs. She also had sleeping problems. Her doctor refused to see the connection. He was on the same kind of medication and,therefore ,my mother took that as a guarantee that the medication was beneficial and harmless.

After having read a book by Uffe Ravnskov (his first) and listened to some patient stories that I translated from English to Swedish, she stopped.
She will soon be 94 and enjoys life.

I think it`s terrible how the pharmaceutical companies, medical staff and authorites have brainwashed people.

I hear statin-stories every day because I am interested (I am retired and have no connection to health care).

When I ask if their problems have been reported as suspected adverse effects, the all say – no. They look very surprised. It`s as if they have never heard of such a thing.
It`s unfortunate that our authorities don´t inform them (on TV, in newspapers, magasines etc). If you ask them – they tell you – it`s on their website!

I am sure there are more adverse effects, and they are more common, than what`s recoreded in the package insert.

The number of salient points runs to 39. Some reveal the lie in the fat/cholesterol hypothesis. Some show the folly in the delivery of retrospective censorship applied under the duress of ‘pressure from eminence. One pertains to Keys abuse of data on saturated fat and mortality exposed by Yerushalmy and Hilleboe. One pertains to the confounding error present in the work of Anitschkov & Chalatov as exposed by Hideshige Imai et in 1976. The presence of oxidised cholesterol better accounts for the development of atheromas in cholesterol-fed rabbits than does the cholesterol itself. Together they leave little doubt that consensus can be derived badly and without suitable editorial standards being applied (that how lies become established as consensus) and some of their number direct that if a consensus can be derived badly then the right to attempt to express dissent and yet fall short of perfection ought to be upheld and defended. Where the consensus is so (bloody) wrong dissent should not have to be so perfect.

I very much doubt that Sir Rory Collins preparation for his meeting ran to assimilating all these 39 facts or to sharing them with Fiona Godlee, In fact I doubt he’s considered the pertinence of even just one amongst their number.

I am about to write to Fiona Godlee and In the letter I will request that I am accorded the same rights to her time as Sir Rory Collins. I will say plainly it would be remiss of a person in her position if she were to deny herself the opportunity to be presented with 39 facts Sir Rory Collins would have no incentive, nor no interest, in bringing to her attention.

Abramson et als dissenting voices were justified, even if mistakes crept in or not all salient points or findings were recalled. The case being made for lipid modification (the policy on statins) is underpinned only by an almost total absence of evidence but a a heavyweight presence of eminence. Lowering the threshold makes no sense whatever.

No. 19 on my list reads along these lines .. Aseem Malhotras piece (Saturated fat is not the major issue – BMJ) fell wide of certain pivotal facts by a country mile, but it was essentially correct in its broad assertions. It indicated (I’m sure I recall) that risks of oxidation and oxidative stress or ‘inflammation rise with overconsumption of certain PUFAs (and not with saturated fats) – which is a direction I would not challenge, and overall it was a breath of fresh air in an atmosphere otherwise polluted by rank delusion.

I heard Sir Magdi Yacoub speak on last Saturday’s “Today” programme on Radio 4. I got the impression that he had been wheeled on as a “big gun” for the pro statin side as he was very dogmatic and not a particularly convincing speaker.
As Fiona Godlee says the independent panel investigating retraction will consist of people with “No dog in this fight”.
Incidentally, does Sir Magdi still do heart transplants at the age of 76.

I was put on 20 mg of Simvastatin way back when I was 30 because my cholesterol was too high… the statins didn’t reduce the levels at all, but some 20 years later I’d developed full blown T2 Diabetes… dropped the statins when I found my memory was becoming fuzzy and unreliable… switched to LCHF diet when I discovered that the official NHS eatwell plate diet for diabetes wasn’t working after purchasing my own blood glucose meter…

The “escape the diet trap” book confirmed everything the NHS was pushing on me was wrong.

my T2 diabetes was NOT my fault at all…

Shelley

Don’t think he understands the literature, otherwise I think he’d have to acknowledge just how ineffective statins are for the vast majority of people. With all due respect, I think Sir Magdi should probably stick to surgery.

http://www.telegraph.co.uk/health/10838558/magdi-yacoub-statins-british-medical-journal.html