Tag Archives: LDL

A little more on the trial

When the background information leading up to the libel trial was released to us, there was one trail of e-mails that struck me as very damning. It emerged that Barney Calman was very keen to find case histories where people had stopped taking statins and then suffered a catastrophic event, such as a heart attack or stroke, or dying. This ‘stopping statins and dying’ concept was pretty much central to the articles.

Barney Calman asked a Samantha Brick (no idea who she is) to find case histories. Real life stories are always considered to be very powerful by the mainstream media. Which they are. Barney also told her she could offer people money to people who came forward with tales to tell.

Unfortunately for him, the only two case histories she got hold of were people who had started taking statins, and then died. [I believe the information has been sufficiently anonymised so that no-one can work out who these two people were. Although they are already in the public domain, in the court documents bundle, so I am revealing nothing here that is not already open for scrutiny].

The first case concerns a young woman who was put on a statin. Then died from liver failure. Liver failure is a known, although relatively rare, serious adverse effect of statins1.  The second case is less clear cut, but also seems to point directly to a statin ‘caused’ death. [I have tidied up the e-mails a bit to make them easier to read but I have not changed any of the words used].

From: SAMANTHA BRICK [mailto:samantha.brick@btinternet.com]

Sent: 25 February 2019 18:29

To: Barney Calman <barney.calman@mailonsunday.co.uk>

Subject: possible statins case studies – both died after stopping them*

External Sender~~

Hi Barney,

These 2 replied to my £500 alert. I can probably reduce them to £200 each if you use them both. They are quite similar though in terms of what happened. I’m not sure if this is what you’re after? 39, married mum of two who lives in North London. She lost her sister 16 months ago.

She says:

My sister was 39 when she was prescribed statins. She was a mum of 4 and worked as a manager of a dairy company. When she was diagnosed with high cholesterol, she was advised to change her diet and exercise. Her Dr also told her to take Fluvastatin. She was reassured that even with her busy lifestyle it would lower her high cholesterol.

She took the tablet as prescribed for six months. She began to vomit a lot and had pain in her chest. On more than one occasion she called an ambulance. Each time she was admitted to hospital she was told there was nothing wrong with her heart.

The vomiting episodes began to increase. She was eventually diagnosed with a fatty liver. She stopped taking the statins on the doctor’s advice (a month before she died) and went to see her brother who lives in Berlin. There she was admitted to hospital. By now she still struggled to keep food down and was fed via a tube She was in hospital for a fortnight when she suffered a stroke and died.

This was 16 months ago. The whole family were devastated because her demise came out of the blue. She’d never had problems with her liver beforehand.

————————————————————————————————————————-

Lady 30, is married mum of one who lives in London (waiting on a picture of her with her dad).

She says:

My Dad died two years ago after he had stopped taking statins. (just waiting to find out exactly which ones he was taking) He’d had a heart by-pass in 1998 and was prescribed simvastatin afterwards. He’d been taking others since. He’d been taking them for over 16 years without – seemingly – any problems.

During that time, he’d call ambulance because of pain in his chest. But he was discharged each time without issues. He was also diabetic and taking medication for that. Three years ago, he was diagnosed with liver problems. Straightaway he told to stop taking the statins. At the time he was also throwing up and struggling to keep food down.

Mum would try to feed him jelly or mashed potato but he couldn’t keep it down eventually he was admitted to hospital and was fed via a tube.

While he was in hospital the focus was on the issue with his liver (need to confirm what this was –she thinks that they had to drain fluid from it – will know overnight). While the investigations into the liver problems were carried out, Dad had a heart attack and died.

He’d been on the tablets for years – was it stopping them that caused this. Or were they behind everything that snowballed. I’m worried because my mum also takes statins for her health too – she is on avastatin (I assume atorvastatin). They were married for 50 years mum is still grieving.

Samantha Brick

My book: “HeadOver Heels in France” is out now

Twitter: @samanthabrick

Instagram: Sammy brick

Facebook: Sam Brick

*this e-mail should have read. Both died after taking them.

In the first case I think it is clear cut that this young woman died as a direct result of statin induced liver toxicity. The second case is a little more confused, but the history of throwing up and struggling to keep food down is identical to that of the young woman. Loss of appetite, nausea and vomiting are well recognised symptoms of liver failure. It is also known that it can take months, or years, for statins to cause liver failure. [The final ‘event’ in liver failure is often a cardiovascular event].

Unfortunately for him, the case histories Barney Calman received totally contradicted his argument. At this point you would think Barney may have taken stock. He had two case histories, and two deaths, both almost certainly caused by statins. And it gets worse.

It’s not as if he didn’t understand what he was reading. To use his own words. ‘We’ve had two quite dramatic stories of patients who have been taken off statins by their doctors because of developing serious liver problems, and then died.’ So, he can’t claim he didn’t see them Or, that he failed to understand what he was reading.

But the very next day, he took it away and redoubled his efforts.

From: Barney Calman

Sent: Tue, 26 Feb 2019 08:44:40 +0000From: “Barney Calman” To: “Fiona Fox” , “Rory Collins” , “Colin Baigent” , “samanin@bhf.org.uk” , “Sever, Peter S” ,

“Liam Smeeth” CC: “Greg Jones” Thread

To: Fiona Fox Rory Collins Colin Baigent samanin@bhf.org.uk Sever, Peter S Liam Smeeth

Cc: Greg Jones

Sensitivity: Normal

Dear all, thank you again for all your input into this article so far. I wanted to readdress the issue of finding a case study. One of the key factors in your collective argument is that criticism of statins discourages use amongst high-risk patients, and this is a public health threat.

Since putting calls out we have been inundated by stories of people who have stopped taking statins and felt far healthier (I put this comment in bold). We’ve had two quite dramatic stories of patients who have been taken off statins by their doctors because of developing serious liver problems, and then died. The families themselves both naturally question whether statins caused the problems. What we haven’t had is a single story which backs your thesis (I put this comment in bold) and obviously I’m concerned.

I think it makes us look rather weak to use a very historic story about Clinton [Bill Clinton stopped his statin then had a heart attack]. What I do not want this piece to be is simply another exercise in singing to the choir and I fear without a real-life example, we may be veering towards it all just seeming like scary theories and doctors saying ‘because I said so.’

What has struck me is that the reason Kendrick, Malhotra, Harcombe and their ilk have really struck a chord is because they are great, emotive communicators. What we’re offering is a chance for you all to be that too, and we are planning to devote an unprecedented amount of space to this.

Have any of you heard a real-life example of someone who has suffered a heart attack or stroke because they declined/quit statins because they thought they didn’t really work anyway, or similar? I really want us do everything we can to make this work. Please do ALL let me know asap today your thoughts about how to move forward. BC

_________________

Barney Calman

Health & Lifestyle Content Director

Mail on Sunday

As you can see, in addition to his two incompatible case histories, Barney was also ‘inundated’ with stories about people giving up statins then feeling far better. Concerns, he still had none.  He only had eyes on the prize.

And what of glorious professors, such as Professor Peter Sever, who had proven themselves so eager to assist Barney in putting together his libellous articles. Did he feel the slightest nagging doubt at this point. Nope, nothing of the sort. In fact, this is what Professor Peter Sever had to say

From: Sever, Peter S

Sent: Tue, 26 Feb 2019 09:20:05

To: Colin Baigent Barney Calman Fiona Fox Rory Collins samanin@bhf.org.uk Liam Smeeth

Cc: Greg Jones

Subject: Re:

Sensitivity: Normal

External Sender~~

I’m afraid I disagree [Professor Baigent had argued against using case histories, as they were not scientific].

We (my bold) are not trying to convince a scientific audience. This is a communication to the public and they are influenced by case reports and anecdotes whether we like it or not. This is precisely why our opponents* are so successful.

If we are to be successful in countering their claims I’m afraid we have to play by their rules. I’m all for scientific integrity as Colin and Rory opine but this doesn’t work when dealing with the public

Look how many scientific reports have countered the Wakefield claims with so little effect. May I remind you that we all use case reports to illustrate optimal treatment strategies when are teaching. Perhaps not a perfect analogy but not far off!

I support Barney’s point and think we should find a case report (or two!)

Barney what is the timeline?

Regards

Peter**

*note the use of the words our opponents. Yes, ‘our’ opponents. This e-mail was sent to Barney Calman, amongst others. So, whose side do you think Barney Calman is seen to be on? I also made the word ‘we’ bold in the text.  At one point during the hearing our barrister asked the question, ‘who is, or are, ‘we’ in this case? Yes, you can damn your defence without even realising you are doing so. It is difficult to claim you are writing a personal opinion piece when your collaborators are using terms such as ‘we’ and ‘our’. And they are including you. Whose opinion is it anyway?

**note how friendly they have all become

Of course I knew, or suspected, that discussions like this had been going on in the background. I did not know who all the collaborators were. However, Barney did let me know, on the 1st of March 2019 that a critical article was going to be published, naming me. I had less than 24 hours to respond. One part of my reply was – as follows.

‘Listen, we all know where this attack is coming from. The CTT* and Professor Rory Collins and Baigent et al. They attacked Aseem Malhotra and Professor Abramson, then the BMJ, for publishing articles by Aseem and Abramson suggesting statins caused adverse effects in around 20% of people. Collins attacks were severe, and the BMJ was require to hold an investigation, in which Collins attacks on these papers were judged to be unfounded.’

*The Cholesterol Treatment Triallists Collaboration in Oxford. Headed by Collins and Baigent, among others.

As it turns out, I was bang on the money. Which was not difficult. These two lash out at anyone, or anything, who dares criticize statins in any way. It was Collins who first came out with the ‘worse than Andrew Wakefield and the MMR scare’ meme. If he wasn’t the first, he sure uses it a lot. Be careful about the language you use, for it can come back to bite you on the backside.

Next time. Let me have a think. So much to choose from. And, oh, by the way. How are things going Rory and Colin? [I have been told that they read my blog – through gritted teeth].

1: https://www.ncbi.nlm.nih.gov/books/NBK548067/#:~:text=(Review%20of%20safety%20of%20statins,and%200.04%25%20with%20placebo).

Conflict of Interest at the CTT?

What is a conflict of interest? One definition is thus: ‘A conflict of interest is a set of circumstances that creates a risk that professional judgement or actions regarding a primary interest will be unduly influenced by a secondary interest.’

Or, in my simple world. ‘Someone pays you money. You then say or do things that you would not have said or done, if they hadn’t.’ The secondary interest doesn’t have to be directly monetary. It could be a promise of a promotion, or an invitation to be chairman of an important committee, or a chance to meet someone famous, or watch a world cup final, or suchlike.

However, for the sake of keeping things simple, we are talking about money here. We are talking about pharmaceutical companies paying money to medical ‘experts’, who may then say or do things that they would not otherwise have said or done.

The first problem is, thus. How do you know they would not have said or done it anyway? If the dairy industry paid me a million pounds to say ‘Dairy foods do not cause heart disease.’ This would be a bonus. Because it is what I believe, it is what I say already, and you really don’t need to pay me a million pounds to say it. [Although I am open to offers].

However, if I was paid a million pounds and I then said ‘dairy foods to do not cause heart disease’, and you discovered that the dairy industry had paid me a million pounds, what would you think? I know exactly what you would think. ‘I trusted him, now it turns out he is just lining his wallet, the same as everyone else.’ Some would state this more vehemently than others. However, any reputation that I have would never be the same again. There would always be that loss of trust. That doubt.

The people we admire and trust the most do not take backhanders. Pity.

For many years, pharmaceutical companies paid doctors ‘honoraria’, which is just a posh word for money. The doctors happily stuffed said honoraria into their bank balances, and no-one seemed much bothered. You did not need to declare any financial interests, and the only limitation on how much you got paid was your perceived value to the companies.

Your value was measured in a few different ways:

1. Ability to influence other doctors – your status as an ‘opinion leader’
2. Your quality as a speaker at meetings and/or ability to set up and run clinical trials
3. Your influence within the healthcare system i.e. do you advise Governments on treatment, do you sit on committees that advice NICE, or the Food and Drugs Administration (FDA)
4. Your position on Guideline committees. Can you play a key role in writing the guidelines that other doctors have to follow e.g. drug x a must be used first line in all patients with condition y.

These things are, of course, all linked. As an expert you start on rung one and two, and then move onto three and four. Your progress up this ladder requires very close links with the industry. You cannot influence other doctors if you haven’t done research, and it is very difficult to do research without industry funding. If not impossible.

At a certain point in the process, you become exceedingly important to the industry. In fact there are companies who support the pharmaceutical industry whose entire raison d’etre is to manage Key Opinion Leaders (KOLs).

According to Dan Mintze, senior director, heartbeat experts, “The management of KOLs needs to be broader than identifying, segmenting, influence mapping and working with clinicians in order for products to gain clinical approval. Rather a comprehensive KOL solution which includes the identification and appropriate engagement of KOLs who impact market access decisions e.g. KOLs who serve as Government or payer advisory board members (see figure 3) should be adopted.” Such pharma-KOL engagement will lead to the development of value messages that can help pharma to access the market faster, gain quicker product adoption, and increase bottom line performance.’ [my words in bold]  Original PDF here

The more you increase bottom line performance, the more you are worth, and the more you get paid. Strangely, some left-wing commies a.k.a ‘people’ began to object to this cosy relationship. A bit too much potential for the situation whereby… a primary interest will be unduly influenced by a secondary interest.

Luckily this problem was instantly solved, amid scenes of wild rejoicing, by ensuring that doctors who did major studies, or wrote articles and suchlike, must disclose their conflicts of interest. Once this had been done there was nothing to worry about, ever again. [joke]
Although, what we are supposed to do with a disclosure of interest has never really been explained. As a Swedish doctor wrote to me:

‘While we are at this: I have often wanted to ask the purpose of revealing possible/probable conflicts of interest. Just what are we supposed to do with that editorial caveat? Does it mean the data might be suspect? If the editors want us to know it is suspect then why do they publish it?

If it means we should interpret the data with caution, can someone tell me how one is to be cautious. Does it mean one believes none of it or does one believe some of it? If the latter then which part do we believe and/or which do we not believe. Just how are we supposed to judge these things, after having been warned to beware?

Indeed, what are we supposed to do? The other problem is that, whilst doctors are meant to declare their conflicts, quite often they do not. Here is an addendum taken from the Journal of the American Medical Association.

It was in response to an article which was written by a number of authors, who did not see to need report any of their conflicts. Some eagle eyed readers wrote in to complain, and the journal responded thus [I put in bold those companies who would have benefitted financially from the original paper]:

Unreported Financial Disclosures in: ‘Association of LDL Cholesterol, Non–HDL Cholesterol, and Apolipoprotein B Levels With Risk of Cardiovascular Events Among Patients Treated With Statins: A Meta-analysis.’

….the following disclosures should have been reported: “Dr Mora reports receipt of travel accommodations/meeting expenses from Pfizer; Dr Durrington reports provision of consulting services to Hoffman-La Roche, delivering lectures or serving on the speakers bureau for Pfizer, and receipt of royalties from Hodder Arnold Health Press; Dr Hitman reports receipt of lecture fees and travel expenses from Pfizer, provision of consulting services on advisory panels to GlaxoSmithKline, Merck Sharp & Dohme, Eli Lilly, and Novo Nordisk, receipt of a grant from Eli Lilly, and delivering lectures or serving on the speakers bureau for GlaxoSmithKline, Takeda, and Merck Sharp & Dohme; Dr Welch reports receipt of a grant, consulting fees, travel support, payment for writing or manuscript review, and provision of writing assistance, medicines, equipment, or administrative support from Pfizer, and provision of consultancy services to Edwards, MAP, and NuPathe; Dr Demicco reports having stock/stock options with Pfizer; Dr Clearfield reports provision of consulting services on advisory committees to Merck Sharp & Dohme and AstraZeneca; Dr Tonkin reports provision of consulting services to Pfizer, delivering lectures or serving on the speakers bureau for Novartis and Roche, and having stock/stock options with CSL and Sonic Health Care; and Dr Ridker reports board membership with Merck Sharp & Dohme and receipt of a grant or pending grant to his institution from Amgen. (original JAMA correction here.)

As you can see, Paul Ridker had board membership with Merck Sharp and Dohme, and simply forgot the mention it. The authors’ collective punishment? Well, you have just seen it. Essentially, there is no punishment. A bit of momentary embarrassment, soon forgotten. [Although not by everybody, guys].

However, the steady pressure for doctors to provide disclosures of interest has had one major impact. It has made it a bloody site more difficult to know where the conflicts of interest might actually lie.

For it has been decreed….I don’t know who decreed, or agreed it, that if you are paid money directly by a pharmaceutical company, or say a PR company working for the industry, you have a financial conflict of interest that you must/should declare.

However, if you work for an organisation such as the Cleveland Clinic, or the Clinical Trials Research Unit (CTSU) in Oxford things are different. The clinic is paid money by the industry, and then the clinic pays you. This means that you are not conflicted in any way. You need not declare anything. Why?

I don’t know who stated that this is acceptable. As with most things in this area we are in a shadow world full of ghostly apparitions that elude your grasp. ‘They said it was fine.’ And who, exactly, are they. There is no oversight committee here, no investigations carried out, no rulebook, no punishment. Just a very woolly gentlemen’s agreement amongst the great and the good of medical research.

However, because it has been agreed, in some mysterious way, that ‘second hand’ payments are fine, it means that those working at the Cleveland Clinic, the CTSU, and suchlike, feel able to state that they have no financial conflicts – at all. Even if the organisation they work for earns hundreds of millions, or billions, in industry funding.

If those working at the CTSU do, somehow, find themselves working directly with the industry, they now give any money they might have eared to charity. To quote their rules on the matter:

Guidelines for CTSU staff with respect to honoraria and any
other payments offered and share ownership

——-

d: If an honorarium is declined, the intended CTSU recipient can still mention that a
corresponding amount might be donated to a specific charity.

A corresponding amount to a specific charity. What charity?

‘I guess if I had any advice for reporters, I would say, ask your local university if they’ve set up any associated [non-profit organizations]; many universities have an associated charity or foundation through which they solicit donations from corporate sponsors to support medical research. Find out about who those corporate sponsors are. Unfortunately, many universities set up these associated charities and foundations in such a way that they don’t have to disclose much publicly – ask about that, you know, try to push.’  (original article here)

Push away, but I don’t expect you will get very far.

Anyway, we are now supposed to believe that highly qualified and very influential KOLs, who work at the CTSU in Oxford, carry out work on behalf pharmaceutical companies for no payment, whatsoever. This is just charity work. Helping impoverished pharmaceutical companies is the same, really, as helping starving orphans in Africa.

Strangely, it appears that the CTSU doesn’t mind in the least that their staff are spending large chunks of their professional life helping pharmaceutical companies – out of the goodness of their hearts. The CTSU gets nothing; the pharmaceutical companies get nothing, other than a warm glow in their hearts. Meanwhile a ‘specific charity’ is doing rather well. Whatever that specific charity may be?

Of course the CTSU itself does rather well from the industry. Just for carrying out one of their many studies, REVERSE, they received £96million ($155million) from Merck Sharp and Dohme.

Yet, despite the huge sums of industry money sloshing about in the CTSU there are absolutely no conflicts of interest going on here. We are told this by none other than the CTSU itself. No-one is paid money directly by the industry in any way. So that is fine.
As Robbie Burns said: ‘O, wad some Power the giftie gie us to see oursels as others see us. It wad frae monie a blunder free us.’

As a sort of footnote to this blog, you may be interested to know that the Cholesterol Treatment Triallists Collaboration (CTT) in Oxford is probably the most influential organisation in directing the management of CV disease around the world.
The ACC/AHA guidelines launched last year in the US are based on the latest CTT meta-analysis; as are the latest NICE guidelines in the UK. The Cochrane Collaboration, which is also highly influential world-wide, changed their guidance on the use of statins in primary prevention, based on the CTT meta-analysis.

In short, if you want to identify a group of KOLs who can truly increase ‘bottom line performance’, you will not find any organisation more powerful than this. Best of all, CTT have absolutely no conflicts of interest with the pharmaceutical industry either. If you want to contact the CTT about any of this, you can e-mail them at: CTT@ctsu.ox.ac.uk

Believing in impossible things – there is a trick to it

At times, all you can do it shake your head in amazement, and wonder at the ability of people who think of themselves as scientists to make statements that are impossible to reconcile with reality, or logic….or pretty much anything to do with science.

Yesterday, I was sent a copy of a paper called ‘High coronary plaque load: a heavy burden.’ Published in the European Heart Journal in August 2013. It looked at the use of statins to reduce the volume of plaque in arteries. I include three verbatim quotes from the paper:

  • Of particular interest, neither LDL cholesterol levels at baseline nor those after high dose statin treatment could independently predict major adverse cardiovascular events (MACEs)
  • One of the most striking results of this study is the fact that LDL levels at baseline or after statin treatment showed no predictive value for MACEs. This could lead to doubt about the beneficial effect of LDL-lowering therapy. However, as also discussed by the authors, there is overwhelming evidence for the beneficial effects of statin therapy on plaque progression and MACEs.
  • Currently statin therapy is so fundamentally established in clinical practice that its beneficial effect is beyond doubt. Even though it has been demonstrated that in patients receiving statin therapy LDL levels have no additional prognostic value, further lowering of LDL cholesterol levels with novel PCSK9 monoclonal antibodies could further reduce the residual risk in these patients1.

So, the researchers discovered that LDL (‘bad’ cholesterol) levels did not predict major coronary events:  angina, heart failure, heart attacks and suchlike. Neither did the degree of LDL lowering with statins have any correlation with coronary events. At this point, having very clearly established that their research flatly contradicts the cholesterol hypothesis, they finished off by remarking that when the new cholesterol agents arrive, which will lower LDL levels even more than statins, they will ‘further reduce the residual risk in these patients.’

I shall try to reduce this paper to its ineluctable essence.

  • We have found that LDL levels have nothing to do with cardiovascular disease
  • We have found that the degree of LDL lowering with statins does not correlate with cardiovascular events
  • We think we need to the lower the LDL more to prevent cardiovascular disease

‘Alice laughed. ‘There’s no use trying,’ she said. ‘One can’t believe impossible things.’

‘I daresay you haven’t had much practice,’ said the Queen. ‘When I was your age, I always did it for half-an-hour a day. Why, sometimes I’ve believed as many as six impossible things before breakfast. ‘Lewis Carroll – Alice in Wonderland.

I suppose it becomes easier to believe in impossible things if you have a few conflicts of interest to help you along the way…..smooth the pathway of belief, so to speak. Here follows the conflict of interest statement from the paper:

Conflict of interest:

J.W.J. receives research grants from and was a speaker at meetings sponsored by Astellas, AstraZeneca, Biotronic, Boston Scientific, Bristol-Myers Squibb, Cordis, Daiichi Sankyo, Eli Lilly and Company, Medtronic, Merck-Schering Plough, Pfizer, Orbus Neich, Novartis, Roche, Servier, the Netherlands Heart Foundation,the Interuniversity Cardiology Institute of the Netherlands, and the European Community Framework KP7 programme. M.A.dG. has no conflicts to declare. The Department of Cardiology received research grants from Biotronik, Medtronic, Boston Scientific

Corporation, St Jude Medical, Lantheus Medical Imaging, and GE Healthcare.

For those paying attention, you may have noticed the mention of PCSKP monoclonal antibodies earlier.  What are these, I hear you cry. These are the next monstrous regiment of cholesterol lowering agents that are waiting in the wings, engines running smoothly. If you thought statins were heavily promoted – you ain’t seen nothing yet.

You may not be astonished to learn that one or two of the companies listed in the conflict of interest statement of that paper are developing PCSK9 monoclonal antibodies. I wonder if that could have anything to do with the statement……’further lowering of LDL cholesterol levels with novel PCSK9 monoclonal antibodies could further reduce the residual risk in these patients.’

And if that thought depresses you, as it does me, here is a little poem by W.H. Auden to cheer you up:

‘Give me a doctor partridge-plump,
Short in the leg and broad in the rump,
An endomorph with gentle hands
Who’ll never make absurd demands
That I abandon all my vices
Nor pull a long face in a crisis,
But with a twinkle in his eye
Will tell me that I have to die.’

1: Michiel A. de Graaf and J.Wouter Jukema. ‘High coronary plaque load: a heavy burden.’ European Heart Journal (2013) 34, 3168–3170

A sudden flash of truth

 

 ‘Men occasionally stumble over the truth, but most of them pick themselves up and hurry off as if nothing had happened.’ Winston Churchill

Anyone reading this blog will know that I do not believe a raised LDL/Cholesterol causes heart disease. I am not going to bore you with my reasoning here. Suffice to say that it is a completely non-scientific theory that rapidly dissolves on contact with critical thought, or the evidence.

I recognise that this flies in the face of conventional thinking. Indeed, almost every day there is a new headline about the wonders of cholesterol lowering using statins. Recently Professor Sir Rory Collins re-iterated his wish that all adults over the age of the fifty should take statins. http://www.dailymail.co.uk/health/article-2194892/All-50s-statins-regardless-health-history-says-Oxford-professor.html

Just around about exactly the same time someone sent me a link to an article about the effect of statins on coronary artery calcification in diabetics. For those who don’t know, calcification of the arteries is a very powerful indicator that you have serious atherosclerosis in the arteries in your heart. The basic underlying cause of coronary heart disease.

To quote from WebMD on an article in the Journal of the American Medical Association (JAMA):

“A test that measures calcium deposits in the walls of the blood vessels supplying the heart is better than other tests for identifying patients at risk for heart attack and stroke. Coronary artery calcium score (CAC) was found to be the most accurate predictor of whether people would suffer one of these events, in a study published today in the Journal of the American Medical Association.

The test is increasingly used by heart doctors to identify heart disease, says cardiologist Gordon Tomaselli, MD, of Johns Hopkins University Medical Center. He was not involved with the study. “Someone who has calcium in their coronary arteries is no longer at risk for developing heart disease — they have heart disease,” he tells WebMD. “That is why more and more cardiologists are using this test.” (WebMD Health NewsAug. 21, 2012)

So you would expect, would you not, that statins would reduce the amount of coronary artery calcification. Or at least the progression of calcification. Furthermore, you would expect that this effect would be especially pronounced in people with diabetes as their risk of heart disease is around three to five times as great as in the rest of population.

Much my great lack of surprise, the study I was sent found the following (just read the conclusion if you like):

ABSTRACT:

Objective: to determine the effect of statin use on progression of vascular calcification in type 2 diabetes (T2DM).

Research and Design methods: Progression of coronary artery calcification (CAC) and abdominal aortic artery calcification (AAC) was assessed according to the frequency of statin use in 197 participants with T2DM.

Results: After adjustment for baseline CAC and other confounders, progression of CAC was significantly higher in more frequent statin users than in less frequent users (mean ± SE, 8.2 ± 0.5 mm(3) vs. 4.2 ± 1.1 mm(3); P < 0.01). AAC progression was in general not significantly increased with more frequent statin use; in a subgroup of participants initially not receiving statins, however, progression of both CAC and AAC was significantly increased in frequent statin users.

Conclusions: More frequent statin use is associated with accelerated coronary artery calcification in T2DM patients with advanced atherosclerosis.

[Saremi A, Bahn G, Reaven PD:  ‘Progression of Vascular Calcification Is Increased with statin Use in the Veterans Affairs Diabetes Trial (VADT)’ .Diabetes 2012 Aug 8.  [Epub ahead of print]]

So, there you go. Statins, which protect against heart disease (a bit), accelerate coronary artery calcification. Explain that one.

My explanation is simple. Statins do not work by lowering cholesterol levels. In fact, lower cholesterol levels lead to more rapid development of atherosclerosis. Any beneficial effect of statins is due to anti-coagulant effect – amongst other non-lipid effects.

Would a supporter of the cholesterol hypothesis care to come up with another explanation that fits the facts?

Anyway, here was a sudden flash of truth. Like supernova they light up the sky for a bit, then fade. Then the world will carry on believing in the cholesterol hypothesis, pretty much as before. Facts cannot destroy belief.

To quote Daniel Kahneman, Nobel prize winner in economics, on the irrationality of the financial system, and how people come to believe in things. He makes many interesting points. For example:

The way scientists try to convince people is hopeless because they present evidence, figures, tables, arguments, and so on. But that’s not how to convince people. People aren’t convinced by arguments, they don’t believe conclusions because they believe in the arguments that they read in favour of them. They’re convinced because they read or hear the conclusions from people they trust. You trust someone and you believe what they say. That’s how ideas are communicated. The arguments come later.’