On 21 May my blog featured calls by Professor Sir Rory Collins for the retraction of two articles that raised issues about the safety of statins. In both articles, evidence from a particular study was misrepresented and misquoted. The BMJ has withdrawn the comments and even featured them in an editorial. But Professor Sir Rory Collins is not satisfied: he wants both articles retracted. This, even though, he has not challenged the main thrusts of these articles which were (individually) that statins don’t do any good for people at low risk of cardiovascular disease and saturated fat doesn’t cause heart disease.
The editor has convened a committee headed by Dr Iona Heath to judge whether there are good grounds to retract the papers (or not).
The BMJ has a ‘rapid response’ service, where individuals can submit on-line responses to articles and people. The editorial about this issue has, at the time of writing, received 64 responses (that is a lot for the BMJ, and in fact, the article is currently by far the most commented on piece in the journal). Take a look at the responses and you will see that the vast majority of them are supportive of the BMJ and its editor (Fiona Godlee). Many people feel strongly that the articles should not be withdrawn.
I wrote a response in which I called into question the validity of the data so often used by Professor Sir Rory Collins (and people of his persuasion) to state that ‘statins are safe’. My position is that Professor Sir Rory Collins and others have misled us (wittingly or unwittingly) about the safety of statins and the trustworthiness of the data (potentially putting people at risk of health issues caused by statins). Readers can vote on rapid responses with an ‘up-vote’. There has clearly been some support for my position in that my response has over 850 up-votes (I have never seen such a high number for any response in the BMJ). Perhaps you voted. If you did – thank you!
Not everyone who has commented is supportive of the BMJ. One malcontent is Professor Peter Sever, who is a colleague of Rory Collins, and has run one big industry-funded trial that (among other things) tested the effectiveness of the statin atorvastatin (known as the ‘ASCOT’ trial, published in 2003).
Here’s a link to Professor Sever’s response , but to make it easy for you I’ve reproduced it below. Professor Sever rams home the point (with righteous indignation, I think) that the original papers misled us on the findings of the statin side-effect paper, and gives full backing to Professor Sir Rory Collins’ calls for retraction. Judge for yourself…
Dear Dr Heath,
In your role as chairman of the panel set up by the BMJ to consider the question of whether a full withdrawal of the Abramson and Malhotra papers, relating to side effects of statins, should be expedited, I write to you to provide my full support of the detailed case made by Rory Collins that these 2 papers are examples of bad science, in that the authors misrepresent the truth and sensationalise a variety of side effects claimed to be due to statins, the consequence of which, is that for the wrong reasons patients, whose future morbidity and mortality from cardiovascular disease would have benefited substantially from statin therapy, will be dissuaded from taking the drugs or discontinuing them if they are already receiving treatment.
The BMJ has taken a strong position on scientific integrity and its detailed review and condemnation of the Lancet’s publication of the Wakefield MMR scandal was well received. The same principles should apply over the critical reviews of these two statin papers and the misrepresented claims of Zhang et al, that statins were causally related to side effects in 20% of statin users.
As the Co-chief Investigator of ASCOT, a trial that was independently designed and lead, and where the executive committee held the data base, analysed the results and published the papers independent of the funder, Pfizer, I strongly refute the implications of authors of the 2 recent studies implying that trial sponsors could have influenced the results and downplayed the side effect profiles of the drugs.
In ASCOT, side effect profiles were identical on those taking placebo and statin.
Interestingly, in the blood pressure arm of ASCOT we detected drug related side effects of the ACE inhibitor (cough) and the calcium channel blocker (ankle oedema) with incident rates not dissimilar from those experienced in clinical practice. So if statins were to be causally related to myalgia/ myopathy, why did we not detect this in a trial of 10,000 subjects ?
I would like to remind you that in a recent study published in Archives, a rechallenge of patients previously withdrawn from statin because of muscular side effects, yielded the return of identical symptoms in 80% of patients. Problem was the rechallenge was a placebo !
We are dealing with a very serious issue here, and editors of major international journals have a duty to publish good science and not popularize bad science which is regrettably the prerogative of the lay press.
The retraction of these two papers will go some way towards damage limitation, but do not underestimate the huge impact these publications will have had and the disastrous consequences for the vulnerable patient population who stand to benefit enormously from their statin treatment.
Peter Sever
Professor of Clinical Pharmacology
National Heart and Lung Institute
Imperial College London
May 24th 2014
Competing interests: Recipient of grants to Imperial College from Pfizer Inc for conduct of ASCOT Recipient of honoraria for speakers bureau- Pfizer Inc
Let me cut to the chase here and say that I believe Professor Sever’s response to be verging on hysterical, and actually a great example of misinformation and sensationalism. I think it employs the same ’eminence-based’ and bully-boy tactics I suspect Professor Sir Rory Collins deployed when he ‘forced’ a meeting with the BMJ’s editor without formally tabling his objections.
So, taken aback was I by Professor Sever’s response, that responded to him with a detailed analysis of his assertions, and several questions of my own (including questions about the reliability of his own research, as well as that of Professor Sir Rory Collins. Also, I respectively point out to Professor Sever that nothing in his response in anyway counters the central claims of the papers he wants retracted.
To see my response, click this link. Again, there’s an opportunity to lend your support for the arguments with an ‘up vote’.
ENDNOTE:
Yesterday, I emailed Professor Sever directly to alert him to my response. He declined the offer of posting again at the BMJ, saying that it “simply provides an opportunity for authors such as Abramson and Malhotra ( and indeed yourself ) to repeat the misleading claims relating to statin induced side effects”. He did, to his credit, address some of my questions and concerns. However, not to his credit is that fact that he. again, provided no evidence at all that would justify retraction of the papers. I’ll be posting about his latest response and my reaction to it next week.
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Nice reply. There is simply no justification for stopping trials early, especially without any cardiovascular mortality or total mortality benefit as seen in ASCOT, which is especially dubious in the face of conflicts of interest. To complicated matters, they even found potential interactions with the statin and the sponsor’s anti-hypertensive drug, claiming that the atorvastatin/amlodipine group had a 53% reduction in CHD events compared to a non-significant 16% reduction in the atorvastatin/atenolol group, a difference not explained by blood pressure or lipids. I think ASCOT should be retracted.
Well I don’t know why I came here tonight (transient global amnesia – that’ll be the statins)
I got the feeling that something ain’t right, (low blood pressure – that’ll be the statins)
I’m so scared in case I fall off my chair, (dizziness – that’ll be the statins)
And I’m wondering how I’ll get down the stairs, (Rhabdomyolysis – that’ll be the statins)
Clowns to the left of me,
Jokers to the right, here I am,
Stuck in the middle with you.
Yes I’m stuck in the middle with you, (chronic neuromuscular degeneration has got worse)
And I’m wondering what it is I should do, (serious cognitive impairment now apparent)
It’s so hard to keep this smile from my face, (personality change)
Losing control, yeah, I’m all over the place, (Polyneuropathy, increased mitochondrial DNA damage and mutation)
Clowns to the left of me, Jokers to the right,
Here I am, stuck in the middle with you.
LOL!
Enjoy this blast from the past with Stealers Wheel: http://vimeo.com/71960886
Hilarious and pertinent. Thanks for making me smile (and nod in agreement.
Hilarious, Mark, thank you!
Hi John,
“why won’t those calling for statin papers to be retracted use some science?”
I suppose it is just because there is nothing wrong on those papers, but those bullies surely know who gives them the “grants”. Have they “compiting interests” or have they just one interest in mind?
Logic says a healthy human body doesn’t need a drug to work properly. My father has been prescribed with statins “just in case”, although his cholesterol numbers are ok. Does that make any sense? Peter Sever may say my father is going to “benefit enormously from his statin treatment” but I see the treatment as a hazard for him and a benefit for others.
It is extraordinary that the statin lobby, which is clearly very well funded by the pharmaceutical industry, is so conspicuously strident in it’s efforts to keep the literature on-message.
It is very clear that Collins, whose research has selected out those who are intolerant to statins, is bullying the Editor in Chief of the BMJ to suppress the message that Statins may not be as safe as he claims.
We can but hope that the statin lobby’s behaviour will be its undoing.
‘Bullying’ is exactly the word I’d use too, John.
I think you’re right on the ‘undoing’ as well. I think whatever credibility Collins (and those of a similar mindset and persuasion) had is being quickly eroded by the taking of a position that is so obviously biased, misleading, conflicted, stupid or all these things.
I think his ‘shock and awe’ tactics have spectacularly backfired.
Extraordinary how many diseases that Statins can give protection against: melanomas, prostate cancers, hepatocellular carcinomas, gastric cancers, colorectal carcinomas, breast cancer recurrence and venous thromboembolisms[1].
It’s a panacea. Is it really possible that one treatment can prevent so many diseases?
1. http://www.bmj.com/content/348/bmj.g3306/rr/699067
Can they unblock the kitchen sink as well?
Or stop the tap dripping?
‘On the money’, John D! Made me smile.
I wrote a letter to the Indy in 2008 (!) which of course they did NOT publish. Might as well publish it here 🙂 Quote:
Sir,
Statins ability to ‘halve’ the risk of dementia? (Independent, Tues. 29 July)
And a subsequent10-minute Internet search finds additional claims to:
moderate an influenza pandemic, prevent onset of Alzheimer’s, prevent Parkinsons, reduce the incidence of cardiovascular events, reduce the risk of stroke, reduce the risk of flu death, aid recovery after pneumonia, assist secondary prevention medication, reduce risk of sepsis, assist periodontitis patients, cure one of the most common forms of learning disability, cure acne and associated skin conditions, reduce the risk of lung cancer, prevent lung cancer, fight colon cancer, alleviate erectile dysfunction in men, lower cholesterol in children and infants, help treat Hep.C. and, as if all this healing power wasn’t enough, statins have now been ‘shown’ also to stop depression.
Now pull the other one!
M. Peralta
I discovered this very rarely cited report.
Dement Geriatr Cogn Disord 2009;28:75–80
DOI: 10.1159/000231980 Can be downloaded in full.
Midlife Serum Cholesterol and Increased Risk of Alzheimer’s and Vascular Dementia Three Decades Later
Alina Solomon et al.
I came across this paper first on the WebMD site in 2009. Not properly referenced therein and I enquired from
both WebMD and WebMD-BOOTS (UK version) about this use of statins and my comments Both declined to
answer.
From the full paper, the following extracts are very pertinent:
Extract from Introduction:
“Thus, the best approach implies not only early diagnosis and treatment, but also emphasizes prevention.
However, chronic diseases with a long preclinical phase (such as AD) pose inherent difficulties in the
identification of their risk factors. Since disease onset cannot be pinpointed, the chances are that true risk
relationships (factors increasing the probability of getting the disease) and reverse causality (the effects of
the disease itself on various factors) get confused.”
Comment: Indeed and three decades use of drugs, with an acknowledged adverse reaction of polyneuropathy
and other neurological adverse reactions is ignored as a factor in the development of Alzheimer’s. Now that takes some bias.
Extract from Strengths and Limitations of the Study
Information on lipid lowering treatments, which have been suggested to decrease dementia risk , was not available for this study.
Comment: The patient records were available for many possible factors such as age, sex, race, education and other medical conditions (Table 1) but not the therapeutic records. This is unbelievable; patient records without treatment details im plies either gross incompetence or negligence or that the records were withheld DELIBERATELY for the purpose of obfuscation and protection of Big Pharma profits.
I therefore did a quick 2×2 Chi-square test using Table 2 of the paper using both the combined and separately the AD and VaD numbers using guidelines on therapy, i.e. cholesterol blood levels over 200 and over 239 mg/dl should be treated with statins while cholesterol levels less than 200 mg/dl would not usually be treated. The results are shown below in the table. As the results were significant it is quite clear why the data on therapy was NOT available; Big Pharma would certainly not approve of results that implicated statins as a possible cause of Alzheimer’s and VaD
PMID: 168669 14 [PubM ed – indexed for MEDLINE]
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 guidelines this is almost certain.
The table below will have to be copied to a word processor and columns aligned manually. Columns delineated by “|” Tabs do not copy.
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)
CHI2 = 7.92 p= 0.0049
V2 = 7.91 p= 0.0049
Phi2 = p = 0.0014
This is highly significant and the fact that the actual therapies used were “unavailable” suggests doubtful, if not corrupt, practice and bias.
The Relative Rate (RR – much loved by medical statisticians) is a
58% INCREASE associated with the recommended prescription for statins. (Based on US guidelines
http://www.nhlbi.nih.gov/guidelines/cholesterol/atp3xsum.pdf)
Total Cholesterol
240 mg/dl = ~6.2 mmol/L High )
Using the combined AD and VaD figures from Table 2 for cholesterol levels >200 mg/dl (5.2 nmol/L) is shown below. Again the results are highly significant but suggest that the treatment of lower levels of
cholesterol may have been less aggressive.
Cholesterol categories | No dementia (%age)| AD & VaD (%age)| TOTAL (%age)
NO TREAT (200 mg/dl) | 6703 (68.09) | 460 (4.67) | 7163 (72.77)
Totals | 9248 (93.95) | 596 (6.05) | 9844 (100)
Chi2 = 6.24 p= 0.0124
V2 = 6.24 p= 0.0124
Phi2 = p = 0.0006
CONCLUSION: No wonder that details of therapy were “not available”. This is emphasised by the acknowledged “unavailabilty” of treatment data on the medical records. We are asked to believe that the
medical records did not include treatment records. I find that this is incredible; it is clear that the treatment records were deliberately withheld to obfuscate the real result of this study.
” Is it really possible that one treatment can prevent so many diseases? ”
Yes, of course it’s possible.
If you die from the first illness you don’t get the others.
Just not the desired way to prevent illnesses.
Doesn’t this just smack of man-made Climate Change and the University of East Anglia all over again?
Perhaps you should start referring to these people as Prox. X, sponsored by [name of company here]. If it was good enough for the Speaking Clock ….
What, we must ask, are the likes of Collins and Sever really afraid of? The logical answer is ‘the science.’
So the point put forward by many nutritionists is that saturated fat raises cholesterol and therefore CVD. However, if saturated fat does not (so reported) lead to CVD then does this not invalidate, to some degree, the argument for statins?
Am I being stupid on this one?
Actually, Bill, there is some doubt about the ‘cholesterol-raising’ effects of sat fat.
Also, though, there are lines of evidence that suggest that whatever benefits statins may (or may not) have, this is not really to do with their cholesterol-reducing effects (but other effects including anti-inflammatory and blood-thinning actions).
Hi,
The reason I mention this is that during a TV “discussion” between Dr Maholtra (spelling?) and a state registered nutritionist (extremely arrogant and pompous at that) who said there were many studies showing that saturated fat elevated cholesterol and I assumed their argument then was that this caused CVD.
Yes I have heard the anti-inflammatory argument.
As a side note my LDL figure was 4.2 and a nurse suggested that it be medicated. No mention whatsoever of my good hdl, low tri’s, low crp and good Hba1c and reasonable blood pressure. I was going to argue and discuss the failings of the calculation method of ldl and particle size etc but no point.
Thanks,
Bill.
More than likely the studies were in the context of a high carb diet..
My understanding of the history is that the [saturated] fat causes CVD argument arose during the 1970s from research conducted in the 1960s and 1970s that did not control for smoking status.
Saturated fat was a proxy for smoking.
The informed person doesn’t have to take the statins. However, for a ‘quiet life’, we have to allow the doctor to prescribe them. What worries me more is the breath of a rumour I heard that the Government are considering putting statins in our water supply, as they do with fluoride. I hope I can rely on my water-filter to get rid of it!
I beg slightly to differ.
To accept the script and not take the meds is potentially wasteful but also unassertive.
We all have a right to withhold consent to treatment and if we don’t consider the treatement to comply with our values or if we judge the risk is not acceptable the GP needs the feedback.
Some medics do get grumpy or even aggressive when you withhold consent to treatment. That perhaps tells us something.
I am most definitely with you on this one, John.
Firstly, here in the UK, the General Medical Council tells we doctors that we must respect our patients’ wishes.
But also, not uncommonly, patients are actually more up on the research than their doctor, and this is becoming increasingly common, I think. So, in addition to refusing treatment, if they like, I encourage individuals to tell their doctor precisely why.
Patients are increasingly in a position to educate their doctors, and we doctors are going to have to get used to this.
There are further good reasons actively to refuse medication rather than just to lie:
1) If a doctor assumes you are taking some medication, then you may be denied some other treatment from which you may benefit which is counter-indicated in conjunction with that medication.
2) You are presenting your doctor with a false medical history, which is unfair to them and to you, and can lead to misdiagnoses and worse.
3) If you do not take the medication, and thus do not suffer any side-effects, then you could falsely be used as statistics to prove the relative benignity of the drug! Let us imagine that, say, 10% of those prescribed statins quietly flushed their drugs down the toilet. That’d make the drug look up to 10% less likely to cause side-effects!
“Let us imagine that, say, 10% of those prescribed statins quietly flushed their drugs down the toilet. That’d make the drug look up to 10% less likely to cause side-effects!”
Not to mention, it could also put those 10% of prescribed statins into the water table, inadvertently exposing people to the effects of statins. Seems like that could also skew the side effect profile. After all, if people (supposedly) not exposed to the drug experienced some of the same muscle aches, it could bolster the arguments of those who claim these aches and pains are just a placebo effect.
I’m not sayin’ … I’m just sayin’ …
I recently visited my GP on a minor matter. On looking at her PC screen she commented that I had stopped taking statins [some 21 months ago, actually]. She went on to say that the guidelines for statin prescription ‘kept being changed’ and that because my triglycerides were ‘healthy’, and because my raised cholesterol levels were inherited, they would not re-prescribe statins [not that I would take them] unless my levels exceeded 7. This is amazing considering that they were only 6.9 when originally prescribed 2.5 years ago and that the target figure was 4.2 or some other arbitrary low figure. This illustrates the mess that NICE have got themselves into.
I would interpret changing guidelines as a positive thing. All prescribing or health policy is a sort of extended experiment. Trials and research give an initial approach, and then with experience in a larger population, more information becomes available, which should lead to some modifications if the science is working properly.
The problem seems to be how difficult it is for people to retreat from a previously strongly held opinion, especially when in the public realm. Maybe Dr Briffa could lead the way with a section “Things I Got Wrong”?
Pete
Change in and of itself it not a ‘positive thing’. The mooted change will (according to the evidence) help virtually no-one, and could leave considerable numbers suffering from adverse effects (some debilitating).
Yes, I’ve undoubtedly got things wrong, so here’s 3 to kick off:
1. the belief that experts know what they’re talking about
2. the belief that when someone states something as fact, it must be true
3. the belief that people commenting on health always have people’s best interests as their top priority
How naive I was.
Dr Briffa, how terrible that some Professionals find it easier to stand by and
deny a mistake even though it can cause Death.
Is it loss of Face or loss of Wealth I wonder.
Thank you for what you do.
I read somewhere that when they were looking for the reason for heart attacks etc, they found cholesterol and put two and two together. Duh – because of course we cant live without cholesterol!
In the last 24 hours the BMJ web-server appears to have developed ‘issues’. (?)
Sorry there seems to have been a problem in copying.
From Sever’s reply:
“the authors misrepresent the truth and sensationalise a variety of side effects claimed to be due to statins, the consequence of which, is that for the wrong reasons patients, whose future morbidity and mortality from cardiovascular disease would have benefited substantially from statin therapy, will be dissuaded from taking the drugs or discontinuing them if they are already receiving treatment”.
Let us look at “misrepresent the truth” first.
Collins HPS study went to great trouble to EXCLUDE all statin intolerants, potential intolerants, non-compliants etc. to ensure that the incidence of adverse reactions was low. Indeed, the process was highhly successful, BUT HIS ATTEMPT TO EXTRAPOLATE THIS RESULT TO THE GENERAL POPULATION IS GROSS BAD SCIENCE.
In fact, the whole study and its use to support the general medication of the population is grossly flawed. As I have pointed out to NICE, the HPS study with its highly selected test sample (merely ~30% of the initial sample) is only valid with respect to patients that would meet the exclusion/inclusion criteria of the study. Thus, the promotion of the study for the general population is grossly flawed, if not deliberately fraudulent.
Let us also look at the title which included the phrases “Heart protection” and “cholesterol lowering”. The report does absolutely nothing to support this contention. The data must include the cholesterol levels in various sub-groups of both treatment groups. The ones I am most interested in are the “no-event patients”, the “non-fatal event patients” and the “dead patients”. These groups are identifiable. If the cholesterol hypothesis is correct, then the cholesterol levels for each sub group should be:
[no-event patients]<[non-fatal event patients]300. This, not surprisingly, is the same as that found in Collins HPS trial (estimate 156 saved / 10269). Why was this basic result confused by introducing 3 million?
Another feature of misdirection and result hiding lies in the fact that 781 died despite treatment in the stain group. This is a massive 83% of the expected death rate based on the placebo death rate (781/937*100) leaving a paltry 17% efficacy rate. Why was this not reported as a basic result of study? More obfuscation perhaps?
Finally, there is no mention of the fact that statins are multi-actioned.
.
The Sever study (http://image.thelancet.com/extras/03art3046web.pdf) is similarly flawed. There was no significant difference in all cause mortality (Table 2 All-cause mortality Atorvastatin dead=185 (36%) Placebo dead= 212 (41%); p = 0.1649); ie., no life extension.
Much more interesting is the cardiovascular death rate from Table 2. (Cardiovascular mortality Atorvastatin dead= 74 (14); Placebo dead=82 (16); p = 05066) No benefit for cardiovascular death rate.
Need I say more. This is EMINENCE BASED EVIDENCE OF THE WORST KIND
Heh. Your final sentence makes me think that when Collins et al talk about “evidence-based medicine”, they really mean “eminence-based medicine”: the man who waves about his biggest pharma-funded lab wins!
Excellent new post at the BMJ.
I wonder how people like Professor Sever sleep at night when they they make claims that there is no evidence for adverse effects in a study which as part of the study design eliminated anyone who experienced adverse effects from the drug under study.
Appeal to authority need to be eliminated from the discourse in science. Rational assessment of the facts needs to be continuously promoted.
It is gratifying to see you taking the bull by the horns on this issue and running hard with it.
What never appears to be mentioned by the pro-statin brigade is that hypothyroidism causes high cholesterol; treat the underlying illness and the cholesterol levels go down.
Since the introduction of TSH tests in the seventies, many patients have either had their thyroid medications reduced or they are not treated, regardless of numerous signs and symptoms of an underactive thyroid, including high blood pressure, high cholesterol, weight gain etc, etc.
Why is the medical profession not looking for the basic cause of high cholesterol levels?
Also, as a lay person, as far as I can see, homocysteine levels should be questioned in relation to heart disease. If I am wrong, l please correct me.
You are right PL. Because of the reigning dogma of the TSH test (another stellar
example of Junk Science) thousands of people with Thyroid disease are every week
sent home with a prescription for antidepressants, and told to get some exercise,
The guy is now trying to defend his ASCOT trial by citing post-hoc observational follow-ups with incomplete data, but is concerned about the “popularisation of Bad Science”. Unbelievable!!!
Again, there is simply no excuse for stopping a trial early based on non-fatal events. He created bad science, and is now trying to defend bad science. He also brings up the typical excuse that the trial was underpowered to detect a reduction in mortality. When there are almost 400 deaths in a study and you fail to lower mortality, the trial is not underpowered, it’s just that the treatment sucks.
On top of this, we are supposed to believe that the sponsor’s lipid lowering drug was remarkably effective in combination with the sponsor’s hypertensive drug, but was essentially ineffective with the competitor’s hypertensive drug. Sounds like a bunch of BS to me.
Also, it is important to consider the ASCOT trial in the light of the negative ALLHAT trial, which was non-truncated, used total mortality as the primary endpoint, and had minimal conflicts of interest.
There is an interesting WHO view on cholesterol levels and disease at:
http://highsteaks.com/cholesterol/
Why is it that the “experts” never look at contradictory data; when I trained at the LSH&TM for research it was considered essential to consider all the data, not just the bits that suit a particular view.
All change now with Professors being VERY SELECTIVE AND BIASED in supporting a view (can’t call it a theory or hypothesis – does not warrant such elevation)
I often wonder why they think Statins are a good thing and that low cholesterol is a thing worth having? It would seem to me that if every part of your body uses cholesterol and your body is producing a lot then does that not mean your body needs the cholesterol it is making? Why would you want to interrupt that natural process. Why would you not look for the reason your body is producing cholesterol in great amounts? Who determines what is low, average & high to begin with? And why do people have to fall into one category or another. The know we are all individual, no one has the same finger prints, or ear structure just to name 2 things that nature does not replicate so why would we all have to have the same cholesterol reading? How do they judge if my cholesterol is high by comparing it to someone else’s? What if we all are supposed to have different readings? The same goes for blood pressure. And surely if cholesterol is needed by the body for its various and numerous functions then lowering it must have a bad effect on every single part of the body. I wonder if those who get serious side effects from statins are supposed to have higher cholesterol readings because that is just how their body works and by lowering it’s perfectly natural levels causes the memory loss or the muscle wastage or the cancer?? Does any one even ask these questions let alone research them???
I think your body knows best not some randomly selected and decided upon numerical value put out as “NORMAL” by people who want to increase their profit margin.
Scanning the comments on the BMJ, I was chilled by the one written by Vasiliy Vlassov. As a Russian, he is well aware of state suppression, and notes that in this case the suppression is backed by pharma, as they cannot be seen to be fallible.
THE BIRTH OF THE DIET–HEART HYPOTHESIS
It’s hard to imagine that this theory was radical given how widespread
its acceptance is today, but at the time the prevailing wisdom was that
diet had little to do with heart disease. But Keys felt he was on to something.
Previous research by Russian scientists had shown that when you
fed rabbits large amounts of cholesterol and then dissected them later
on, their arteries were filled with cholesterol-containing plaque and
looked suspiciously like the arteries of people who died of heart disease.
Never mind the inconvenient fact that rabbits are herbivores.
The amount of cholesterol they normally get in their diets is pretty
close to zero. Other animals, such as rats and baboons, do not react in
the same way as rabbits to a high-cholesterol diet, and they metabolize
cholesterol very differently. Even Keys himself understood that cholesterol
in the diet was of no importance. In 1997, he stated, “There’s no
connection whatsoever between cholesterol in food and cholesterol in
blood. And we’ve known that all along. Cholesterol in the diet doesn’t
matter at all unless you happen to be a chicken or a rabbit.”
Yet the admonition to eat “no more than 300 mg of cholesterol” a
day remains the advice of every major health organization to this day,
despite the fact that even the scientist most responsible for popularizing
the diet–heart hypothesis thought it was ridiculous…
— The Great Cholesterol Myth
On it’s own ‘oxidative stress’ does not explain precisely what’s involved, in much the same way ‘obesogenic environment’ is a bit feeble for not highlighting what actually matters.
‘Oxidative stress’ is a bit more demanding of the intellect than is the fat/cholesterol hypothesis but if I could figure the outline and then understand what others have written then almost anybody should be able – cos I am bit ordinary and thick.
Oxidative stress is brought on by compromised capacity for detoxification by the detoxicant process of methylation (and perhaps compounded by compromise to detoxification by transulfuration, too). Methyl groups (CH3) are passed from donor to recipient and they zap the recipient which is likely a reactive oxygen species or ‘free-radical’. The process is essential to every cell and takes place billions of times per second.
Oxidative stress invokes ‘inflammation’, which is actually incidental and not causal to the process. So don’t let anyone convince you inflammation ’causes’ CVD, it does not. ‘Inflammation’ is much like a two-bar heater in that inflammation; ‘heat’ arises when current meets with resistance. One difference is that we might have to envisage ions as conveyors of current, but that is exactly what ions do, so let’s accept this and move on swiftly.
Adequate methylation and transulfuration (and other processes too) are essential to maintain wellness. Conversely inadequate methylation capacity hastens ageing and onset of chronic illness. Methylation is the front-line of detoxification. Thing is elevated levels of the excito-hormones that form the basis of the fright, flight, or fight responses driven by the hypothalamic – pituitary – adrenal axis (HPA-axis) elevate the level of competition for would-be methyl donors — which is often indicated by rising levels of homocysteine (Hcy), btw.
That Hcy might oxidise cholesterol and thence cholesterol converts to oxycholesterol and oxycholesterol drives necrosis of certain cells (not cholesterol) leading to arterial disease (atherosclerosis) is now where my curiosities are focussed.
Of course stress has long been a well-received risk-factor for cardiovascular disease of the kind that involves and follows from atherosclerosis (plaques forming and consequential narrowing). But stress is an epi-physiological risk-factor that must commute through some stepwise physiological events to feed into whatever physiological developments actually cause atheromas to form. Increasingly I feel competition for methyl donating antioxidants, which increases for several reasons, not least a rise in the levels of the fright, flight, or fight hormones raises that level of competition.
I kinda figured this, very sketchily, for myself and then landed on an essay by Stan Field and written in 2006. As a consequence of figuring and then landing on some measure of confirmation, I can tell you, I half scared myself to death.
It isn’t just that the fat/cholesterol hypothesis is under attack, it is crumbling, and with some hope the house of statin secrets whose head is Lord Statin of Oxford, the head of CTT collaboration, Professor Sir Rory Collins, is to crumble too, Because it should be inadmissible to claim benefits arising in data you hold secret and deny open access to. Waht the fat-headed cholesterol faithful do not realise is that the much needed (and likely) successor to the fat/cholesterol hypothesis is already out there, its being developed, and more attentive and interested parties are contemplating its merits.
The biggest merit this methylation, homocysteine, oxidation, oxidised cholesterol theory has going for it is that risk factors like stress, and smoking, and obesity, can be linked either to the endocrinological aspects or to the oxidation sides of this delicate balance. In other words, for the first time risk factors can be discussed intelligently, epi-physiological risk factors (smoking, stress, etc.) can be logical split from those that are more physiological, and the nature of convergence to some physiological process in common can be explained. Smoking introduces a whole cocktail of toxins that add greatly to the workload of methylation.
So, when faced by a GP who si about to prescribe a statin inquire what thought he/she has given to ‘convergence’, ‘methylation’, and how on earth an HMG-CoA reductase inhibitor can prevent oxidation of cholesterol. If they were connected to the bp monitor, we could see their bp and bpm rising, for sure, for a patient with level of understanding would scare them half to death; I give you my word.
Link to Stan Fields essay ; http://www.svhi.com/lateschmart/methylmagic.pdf
Clowns to the left, joker to the right, lets drive that wedge between em, baby!
How Statins Really Work Explains Why They Don’t Really Work.
by Stephanie Seneff
http://people.csail.mit.edu/seneff/why_statins_dont_really_work.html
‘Every individual gets at most only one chance to grow old. When you experience your body falling apart, it is easy to imagine that this is just due to the fact that you are advancing in age. I think the best way to characterize statin therapy is that it makes you grow older faster. Mobility is a great miracle that cholesterol has enabled in all animals. By suppressing cholesterol synthesis, statin drugs can destroy that mobility. No study has shown that statins improve all-cause mortality statistics. But there can be no doubt that statins will make your remaining days on earth a lot less pleasant than they would otherwise be.
To optimize the quality of your life, increase your life expectancy, and avoid heart disease, my advice is simple: spend significant time outdoors; eat healthy, cholesterol-enriched, animal-based foods like eggs, liver, and oysters; eat fermented foods like yogurt and sour cream; eat foods rich in sulfur like onions and garlic. And finally, say “no, thank-you” to your doctor when he recommends statin therapy. ‘
I don’t know if I can buy the theory that dietary cholesterol has on impact on your lipid profile. I took lipitor for many years and ate loiw fat vegetarian diet food decades. My total cholesterol was 120 to 145. But my hdl was 23 and trigs were 200.
Thee I got religion and started eating 4 to 6 eggs in a day. Salmon and chicken rerplacerd wheat and ri e. My hdl is 55 and trigs are 50 to 60. I am off stations and my total cholesterol is 180.
Can somebody comment what they make of it? I know hdl is said to be a proxy for sat fat intake. Is increased fat intake correlated with higher cholestrol ?