[A slight divergence of theme]

As an election looms in the United Kingdom of Great Britain, the National Health Service has become the usual political football. All political parties now claim to love it and want to hug it, and squeeze it, and spend eye watering sum of money on it. Because, for the next three weeks or so, they truly ‘care’. Sincerity, once you can fake that, you’ve got it made.

A UK politician, Nigel Lawson, once called the NHS “the nearest thing the English have to a religion”. This, of course, rather pissed off the Scots, Welsh and Northern Irish. Forgetting that England is not the only country in the United Kingdom is something English politicians just, unconsciously, do. They now wonder wonder why the Scots are all going to vote for the Scottish National Party in a few weeks time. ‘But how could anyone possibly dislike us?’ Oh well.

But what is the NHS? It is, to state the bleeding obvious, a National Health Service. It is paid for out of taxes which are gathered with the usual threats of punishment and fines. The Government then hands it out, well over a hundred billion pounds (~$150Bn), through a mind-bogglingly complicated bureaucratic system, losing vast chunks as it goes.

What pitiful sum finally remains is spent on the healthcare of the people of the United Kingdom (including Scotland, Northern Ireland and Wales). Although Scotland would claim it now has its own NHS, sort of. As would Wales, and Northern Ireland, sort of.

Whatever country you are in, the key underlying principle of the NHS is that it is free at the point of use. If you turn up at a GP, or accident and emergency, or hospital, whatever is wrong with you, you are charged, not a penny. Yes, it is free.

Actually this is not quite true. Dentistry used to be part of the NHS, but most people now pay for dentistry. Many people also pay for prescriptions, and it is eye-watering expensive to get a decent hearing aid. Also you cannot get medical equipment for free, e.g. a nebuliser. So the NHS is mainly free, but this concept is being sneakily eroded.

I know that many Americans believe the NHS to be some terrible ‘communist’ system where you queue forever, cannot get expensive treatments, and people wither and death in dimly lit hospital corridors whilst uncaring staff blow their noses on your sheets and cackle as they stride past in their jackboots. The NHS, at least as reported over here, seems to be held up as the poster child of an ‘evil’ system by those on the right wing of American politics.

I would just like to point out that it costs less than a half (as a percentage of GDP) of American healthcare. Yet, almost all measurable outcomes for health in the UK are better than in the US. Looking at the single most important outcome, which is overall life expectancy; people in the UK live longer than in the US. As do, it should be added, the French, Germans, Italians, Danish, Swedish, Spanish… Indeed, in virtually every way you choose to measure it, US healthcare comes last of all developed countries in the Western World. Just saying. So, the NHS may not be perfect, but please, please, let us not drift into US style healthcare provision.

However, having said all this, I still have a huge problem with the NHS. In that, it is no longer a ‘free at the point of access healthcare delivery system paid for out of taxes’. It has become ‘The NHS.’ Sounds of trumpets and a celestial choir. A kindly bearded figure sits on a throne in the clouds, beaming, surrounded by angels. Hallelujah, hallelujah.

Many years ago, the one thing that Margaret Thatcher said which, more than anything else, marked her out as an evil witch (in the eyes of many) was when she said that ‘there is no such thing as society.’ This is all that most people remember her saying, and they still hate her for it.

It marked her out as an uncaring monster, which is why they song ‘The witch is dead’, from the Wizard of Oz, got to number on in the UK charts shortly after she died. Not, perhaps, the UK’s finest hour.

In fact, the full quote was as follows:

“I think we’ve been through a period where too many people have been given to understand that if they have a problem, it’s the government’s job to cope with it. ‘I have a problem, I’ll get a grant.’ ‘I’m homeless, the government must house me.’ They’re casting their problem on society. And, you know, there is no such thing as society. There are individual men and women, and there are families. And no government can do anything except through people, and people must look to themselves first. It’s our duty to look after ourselves and then, also to look after our neighbour. People have got the entitlements too much in mind, without the obligations. There’s no such thing as entitlement, unless someone has first met an obligation.”

As for me, I don’t really believe that there is such a thing as ‘society’ either. But not, perhaps for exactly the same reason as Margaret Thatcher. My problem is when an abstract concept becomes a real thing which is a form of ‘magical thinking.’

For example, on the left we have those who believe in ‘society’ and ‘the NHS’. On the right we have those who believe in ‘the Market.’ As in, the market won’t like this, or the market won’t like that. When the EU tries to bail out Greece, we are told that the Markets will stop this from happening. This idea, I believe, derives mainly from Adam Smith’s ‘The invisible hand of the market.’

I say. ‘Can you please introduce me to the ‘the Market’. Could I have a word with the market to understand what it thinks?’ Oops, silly me. There is no ‘market’. There are just individual bankers and financial workers and economists. These, in turn, are just individual men and women, with a high percentage of psychopaths sprinkled in.

You see, Market does not exist, it purely an abstract concept. Yet we talk about it as if it were almost a person, an entity with powers beyond mere mortal man. God like, in fact. The ‘invisible and all-powerful hand.’ Kind of like the vision of Emmet in the Lego Movie when he saw ‘The hand’.

When Nigel Lawson called the NHS the nearest thing the English have to a religion, he was right. In that many people have also raised ‘the NHS’ to a status of an entity. A super-corporeal being, infused with special powers and goodness beyond our understanding. An ‘invisible’ hand that works in mysterious ways to improve the health of the nation.

However, until we can stop thinking of the NHS as some sort of deity, and start thinking about the most equitable way to fund and provide healthcare in a rational way, all discussions about healthcare will become bogged down in cant and emotion. People will continue to wave banners about emblazoned with ‘Save the NHS.’ Politicians will gaze at television cameras with that special, coached, excruciating limpid expression on their face talking about how much they care about ‘the NHS.’ Bleurrgghh!

Guys, there is no such thing as ‘the NHS.’ There are paramedics and porters and lab technicians and nurses and managers and doctors and some buildings and equipment. What is the best way to use these resources to provide the biggest bang for your bucks? End of.

Sorry, I shall start slagging off statins again next week.

Dead men don’t bleed

I think I have become a connoisseur of scientific double-think. Swilling the most ridiculous statements around my glass with relish, and enjoying the finest vintages. Last week, whilst I was on holiday, someone sent me a piece about statins and coronary artery calcification. I’m not sure what such people think I do on my holidays – but reading medical reports is not one of them.

However, the moment I read this article, it immediately brought to mind a story about a patient who had a fixed delusion that he was dead. The psychiatrist he was seeing had repeatedly tried, and failed, to get this patient to admit that he was deluded. One day a conversation took place

Psychiatrist:    ‘Would you accept that dead people do not bleed?’

Patient:            ‘Of course.’

Psychiatrist:    Pulling needle from pocket. ‘Would you allow me to prick your thumb to see if you do bleed?’

Patient:            ‘Go ahead doc, nothing will happen.’

Psychiatrist:    Pricks the thumb of the patient, which then bleeds. ‘Aha!’

Patient:          Looks down with interest. ‘Well what do you know, I guess dead people do bleed after all.’

For many years now it has become, almost a known fact, that a highly significant sign of Coronary Artery Disease (CAD) is calcification of the coronary arteries. The most widely accepted thinking is that calcification represents the final stage of atherosclerotic plaque development. It is a clear indication that your arteries have been developing atherosclerotic plaques over the years. Or, to quote Medscape on the issue:

‘First and foremost, calcium is a marker for a diseased artery1.’

The same article expands on this simple quote: “Coronary calcium is part of the development of atherosclerosis; …it occurs exclusively in atherosclerotic arteries and is absent in the normal vessel wall.” Simply put, the presence of calcification in the epicardial coronary arteries indicates that the patient has coronary atherosclerosis.’

This could not be more clear, and has been almost unquestioned. Lots of calcium in your arteries means lots of arterial disease. More = bad. Less = good. Sorry to labour the point, but I am doing it for a reason.

Sherlock:         ‘So, my dear Watson. If we find that one of our treatments for heart disease is increasing the amount of calcification in the arteries, it would seem strange. Would it not?’

Watson:           ‘Indeed.’

Sherlock:         ‘And what, pray, does this make you think?’

Watson:           ‘I’m not entirely sure that I know what you are getting at?’

Sherlock:         ‘Think my dear Watson. Think.’

Watson:           ‘Our ideas about heart disease are wrong?’

Sherlock:         ‘Precisely.’

Statins, as we know, reduce the LDL/cholesterol level in the bloodstream. They also reduce (albeit not by very much) the risk of dying of heart attacks – and strokes. The current thinking, as I am sure everyone knows, is that excess LDL/cholesterol in the blood causes atherosclerosis. Ergo, lowering the level will reduce the burden. If this model is correct then, as LDL/cholesterol levels go down, we should lower the risk of atherosclerosis… and therefore we should see less calcium in the arteries. I know, I am labouring the point again.

However – as I have known for some time – this is not what we see. If you take statins you will increase the amount of calcium in the arteries.

CLEVELAND, OH – ‘The results of a new study suggest that there is a paradoxical relationship between calcification of the coronary artery and atheroma volume among individuals treated with statin therapy. In the analysis, statins, specifically high-intensity statin therapy, actually promoted coronary calcification.2

So, there you have it. At this point, if you are a scientist, you have a few possible explanations that you could look at. (Assuming that this research is correct – and no-one seems to doubt that it is true). You could, for example, say that that statins do not work by lowering LDL/cholesterol, and therefore must provide benefits through another mechanism. How else could you reduce the risk of heart disease, whilst increasing the atherosclerotic burden?

However, if you have a fixed delusion, namely that raised LDL/cholesterol is the most important causal factor in heart disease, and that lowering it must be beneficial, you need to look down at your, now, bleeding thumb and switch the game through one hundred and eighty degrees.

So, what would you do? What explanation would you come up with?

Well, and here I paraphrase. Steven Nissen – one of the most powerful and inexhaustible supporters and promoters of LDL/cholesterol lowering – a man of great influence throughout the world of cardiology. This man looked down at his thumb and said.

‘I guess coronary artery calcification is a good thing after all.’

In truth his actual words were:

“We have some physicians—some, not a lot—advocating for serial calcium scans to determine whether or not patients are doing well,” he said. “If you give them a high-dose of a statin and their calcium goes up that might actually be a good thing. Instead of saying, ‘Oh my goodness, your coronary calcium is increasing,’ we might be able to tell patients, ‘Your coronary calcium is up, your plaques are stabilizing.’ “

Or, as George Orwell may have put it. ’Four legs good, two legs better.’ ‘The creatures outside looked from pig to man, and from man to pig, and from pig to man again; but already it was impossible to say which was which.”




A victory

Here is the title of a scientific paper that will make your eyes glaze over

‘Randomized Phase II Study of 5-Fluorouracil Hepatic Arterial Infusion with or without Antineoplastons as an Adjuvant Therapy after Hepatectomy for Liver Metastases from Colorectal Cancer.’

It was published in the Public Library of Science (PLOS) on the 19th of March, and I danced a little jig of happiness. For I helped these researchers get this paper published, a battle that has taken well over a year. Just to blow my trumpet a little, here are the Acknowledgements:

‘We thank all patients who consented to participate in this study and Dr SR Burzynski for free supply of antineoplastons for this study. We appreciate greatly the editorial assistance provided by Dr. Malcolm Kendrick, Central and Eastern Cheshire Primary Care Trust, UK.’

In truth, my wife did most of the heavy lifting in editing the paper, whilst I took all the credit. Oh well, such is life. I shall buy her a bunch of flowers from the local petrol station.

I realise that, at this point, you have not the slightest idea what I am talking about, so I shall step you back in time. Three years ago, or thereabouts, I was speaking to Pete Cohen. He is a life coach and health guru, and all round good guy. He told me about his partner who had developed a brain tumour, gliobastoma. I hasten to add I am not giving away patient confidentiality here, Pete has written about this, and blogged about it many times.

Hannah had received orthodox treatment in the UK, but the prognosis was still very poor. These tumours are very difficult to eradicate, and usually recur quite quickly. To quote a recent paper ‘Median survival times of all patients diagnosed in the 2000-2003 and 2005-2008 periods were 8.1 and 9.7 months.’ 1

An ‘average’ survival time of about nine months is a very depressing thought. (Although it tends to be a bit longer in younger patients). Pete then spent a great deal of time effort, and eventually money, trying to find an alternative treatment. An oncologist, who will never be named, suggested Pete looked at the results from Dr Burzynski’s clinic in Texas.

The results certainly looked impressive, and Pete’s partner started on infusions of antineoplastons, which Burzynski has been using for patients with glioblastomas for many years. Some of you may have heard of Burzynski, for he is regularly condemned as being a complete dangerous maverick. A man who plays on parent’s desperate need for someone to help their children suffering from terminal brain cancer etc.

If you look Burzynski up on the internet there is a complete diatribe of vitriol rains down upon him. Put him in the Andrew Wakefield camp. The BBC assassinated his character in a half hour programme a couple of years ago. To read what is written of him, you would think he is the sort of man who would happily pitchfork babies into the back of a lorry.

However, as someone who is regularly attacked for being a maverick myself, I consider attacks from mainstream medicine, and the media to be a badge of honour, and I pay little attention to such things. I like to look into things myself, and make my own mind up. Clearly some of those attacked for being dangerous mavericks are, indeed, dangerous mavericks. Others are not. Into which camp did Burzinski fall, I wondered?

The first thing about Burzynski’s treatment was that, in Hannah’s case, it seemed to be working. The tumour had gone. As least it was no longer detectable on MRI scans. It has still gone, and Hannah remains well. Will it remain in remission forever? I know not.

Of course a single case is not proof, never is, never will be. But recurrence free survival of several years is extremely uncommon in Gliobastoma, so a single case is rather more powerful evidence than in many other conditions. I then communicated with Burzynski and gained access to his many, many, case histories. Whilst many patients did die, a significant number were surviving longer than would be expected. In some cases patients were alive twenty years later.

I agreed to write up a number of his case histories and got some of them published here and there. It was always a battle do so, batting away objection after objection. Have no doubt that the ‘authorities’ know exactly who Burzinski is, and they do what they they can to stop anything he does being published, anywhere. Often there was just blank refusal to publish anything, once the name was seen.

I was then contacted by someone, who shall currently remain nameless, who told me that a group of Japanese researchers had done work on antineoplastons as adjuvant (add-one) therapy for patients with liver metastases following colorectal cancer. They did not know how, or where, to publish it. So I agreed to look at it, and try and get it published in a peer-reviewed journal.

They were turned down by Lancet Oncology (no surprise), and a couple of other journals. I suggested PLOS (Public Library of Science), which has a high impact and tends to be a bit more open to non-mainstream articles. So we sat down to write, rewrite, edit, alter and adapt.

To be honest, I have never, ever come across so many objections by the peer reviewers. Stuff that was so trivial, so difficult to answer. Re-write, re-write, re-write. Water down the conclusions. I thought by the end of it, nothing would be left, although the most important points did, just about, survive.

Of course this was not a study on gliobastoma, but it was a carefully controlled (not placebo controlled, as that would be impossible) study of high quality. Setting out to answer the question, can antineoplastons benefit patients suffering late stage cancer?

The answer is that they can. They work. They are not a miracle cure; they are not the answer to cancer. But they have clear and clinically significant benefits. So Burzinski is not a maverick… well, he is a maverick, but his (terribly named) antineoplastons significant effects in cancer. So he is the right sort of maverick, in that he is challenging the status quo – and he is right.

Will his work now be accepted, will Burzynski ever be allowed to treat patients again? Probably not. So, a victory, but probably a small one. Meanwhile, in the UK, Charles Saatchi’s efforts to allow ‘mavericks’ to try and treat cancer are being well and truly crushed. ‘We have enough innovation’ is the cry – by the establishment – that most innovative of groups.

I would counter-argue that innovation by large University departments, and pharmaceutical companies, is not really, innovation at all. They just plough the same old furrows, looking to unearth the occasional goody that was missed in the past.

Their most fervent wish is to cry ‘Eureka’ (I have found it – the thing that I knew was there). The true maverick, however, is on a restless quest for ‘that’s funny.’ For only in the ‘that’s funny’ moments does science truly progress.



Don’t bother me with facts, son. I’ve already made up my mind,” Foghorn Leghorn

NICE stands for the National Institute for Health and Care Excellence. It is a little known fact that it started life as the National Institute for Cost Effectiveness, before rapidly transforming into the National Institute for Clinical Effectiveness, then the National Institute for Clinical Excellence. As you can see it changed again, and now it should be NIHCE, but we do so like our acronyms also to be words. A life of simple puns is the life for me.

I was involved with NICE early on; I set up their first website for them, before being rather rudely elbowed aside. Naively, at the time, I thought the underlying concept of NICE was sound. An attempt to try to work out which medical interventions both worked, and also provided good value for money. This would bring rational thinking to the complex and difficult world where limited resources have to be rationed in some way.

Clearly, I knew that the Government of the time had basically set NICE up to act as a barrier to attacks by the public and a restless media. As everyone knows, the minute you refuse treatment to a young child for, say, cancer, the front pages of the newspapers light up in outrage. By getting NICE to say no, the Government could cower behind NICE’s decisions in relatively safety.

For, as we all know, even if a treatment costs two million, and the chances of success are one in a hundred, most people simply adopt the ‘pay anything, do anything, to save this child.’ mode. The counter argument, that I could use that two million to save fifty lives elsewhere rarely gets an airing. ‘A child is dying….’ Is an argument that usually shuts everyone else up pretty quickly. You can look a tad heartless, very rapidly.

In reality, the cowering didn’t last too long, for as some of you will know, the UK Government is now happy to pay almost unlimited monies into the cancer drugs fund. NICE says it is too expensive… don’t worry, ‘Our caring kind and compassionate Government is willing to pay anything for cancer drugs.’

Of course this rather destroys the entire point of NICE whose decisions are simply bypassed, and also makes it clear that people with cancer are considered far more valuable than anyone else. ‘Dying of motor neurone disease, or heart failure, or kidney disease…. Sorry mate, no money. We have spent it all on cancer drugs.’ The NHS, for a system so terrified of discrimination, against anyone, on the grounds of anything, it seems strange to positively discriminate in favour of people with one form of disease vs. another. Oxford entrance exam, discuss.

Don’t worry, it has long been clear that vote winning irrationality will crush evidence and judgement at every turn.

Anyway, I am getting far away from the point of why I set out to write this blog. NICE, like most organisations started out with a fairly clear aim. To look at medical interventions, then decide which ones provided enough benefit, at reasonable cost, to be funded. But it has grown and grown, or perhaps I could say that its role has metastasised.

It now has become – primarily – a guideline generating monster. Every couple of weeks NICE will drop six hundred pages of ‘how condition x must now be treated,’ onto the medical profession. Dense and verbose and boring and very, so very very, long, and then what?

Are they rules, must they be followed? This all becomes very opaque. Last year NICE decided (super short summary) that everyone with a risk of a cardiovascular event greater than 10%, over the next ten years, should be put on a statin. There was much debate, and the BMA (British Medical Association) voted – unanimously – that these guidelines should not be followed.

Did this make any difference? No. Did it make any difference that the Local Medical Committees (that represent all GPs) at their annual conference voted unanimously against these guideline? No. What are NICE doing about the fact that, at least, two thirds of GPs are completely ignoring these guidelines. Nothing…yet. No debate, no discussion. Nothing. They know that, over time, their guidelines will solidify into something that becomes, effectively, mandatory.

Our great and magnificent guidelines have been written, they shalt be distributed to the populace who shalt fall upon them with gratitude. This is the word of NICE.’ The huge stone gate to the citadel, that encloses the enclave of the wise men of NICE, then swings shut, until the next holy set of guidelines will be brought out, to magnificent fanfare. ‘All hail the NICE guidelines.’

Can you discuss anything with them? No, you cannot. A number of people, including me, wrote an open letter to NICE criticising the guidelines. NICE deigned to read our letter, they reviewed their own decision making, and they decreed that they could find no errors in what they had done. They were good enough to inform us of this fact citing the eminence of their ‘experts’ whose greatness and wisdom passes all mortal understanding.

Then what could we do? Nothing. NICE, you see, are both the prosecution and the defence council, the Judges and the Supreme Court all wrapped in one. There is no higher authority. There is no executive, no Ombudsman. The only authority that can review a NICE guideline is… NICE.

Which means that, for example, when a study comes out showing that long term statin use increases the risk of Parkinson’s disease by 230% (Relative Risk increase)1, NICE can feel free to totally ignore it. In fact, when confronted with this study they said it was ‘nonsense.’ An interesting response, I felt, before they had even seen it.

Ignoring NICE’s view that this study was nonsense, I did a little calculation based on this paper. It went something like this.

Parkinson’s disease affects about 1 in 250 people. It is not rare, but not that common. The NICE guidelines on statins mean that, at the very, very, least, 50% of people should take statins from the age of fifty, for the rest of their life [how many actually will is a moot point, but stay with me here].

If 50% of people take statins and the risk of Parkinson’s increases by 230% it follows that the 1/250 lifetime risk of developing Parkinson’s becomes an extra 2.3×1/250/2 = 0.0046.

IN short, the NICE guidelines will result in an extra 0.0046% of the population developing Parkinson’s. On the face of it, this may not seem like a massive problem. But the population of the UK is around sixty million, and if we multiply sixty million by 0.0046, we get 276,000. That is more than a quarter of a million people who will develop Parkinson’s disease who would not otherwise have done so.

Just from a purely economic basis, this would be hugely costly. Like all things in medicine, it is difficult to establish exactly how much it costs to look after a Parkinson’s patients, but in the UK it has been estimated as between £3,500 to £10,000 per year2. (Up to $100K in the US, I have read).

Multiply these two figures by 275,000 and we get a range of: £962,500,000 – £2,750,000,000/year ($1.443 – $4.12Bn/year)

Now you can argue these figures, and I am sure that NICE would – were they ever to engage in this debate. They will say that Parkinson’s is less common than this (I have seen both higher and lower estimates), they will argue the exact costs, they will bore you into submission with NPVs and suchlike.

You can argue all you like on the minutia, but if this paper is right, and I see no reason to suspect it is not, the NICE guidelines will inevitably result in hundreds of thousands of extra people developing Parkinson’s disease, at a cost of billions to the NHS. Leaving aside the added suffering and Disability Added Life Years (DALYs) this will bring.

Now this represents a massive and very major issue. If NICE were to take this research seriously, they would have to reconvene and review the evidence, and work out the ‘new’ costs and harms to patients, and perhaps they would have to reverse their guidance.

However, I know that they will not do this. They will just ignore this paper, and the implications thereof. I knew this would happen even before they started off by calling it nonsense, as you will remember they did that before they even read it. Even if they do actually read it, they will dismiss it as just one study to set against (my most hated of phrases) the ‘weight of evidence in favour of statins.’

The simple truth is that there is too much at stake here for NICE, and the entire spider’s web of interconnected reputations, and status, and opinion leaders, and money, for NICE to ever reconsider their guidance on statins. Facts and evidence are puny weapons in this battle.


Next week, dear reader, we shall examine the economic consequences of statins increasing the risk of type II diabetes by 46%. Get ready for some pretty gigantic figures. The zeros, they shall stretch as far as the eye can see.

1: Huang X et al: ‘Statins, Plasma cholesterol, and risk of Parkinson’s Disease. A Prospective study.’ J of Movement Disorders (epub ahead of print).


What does cause heart disease?

I have danced around this subject for a long time – as regular readers may have noticed. One of the problems in this area is that you have to start with definitions. Which is somewhat tedious, but also rather necessary? Last week, for example, I read someone argue that we should not use the word cancer, we should talk about cancers. Which is true. Multiple myeloma and pancreatic cancer are both usually called cancers, but they don’t have a great deal in common.

Heart disease is also a pretty meaningless term. Do you mean pericarditis, hypertrophic obstructive cardiomyopathy, aortic stenosis, coronary artery disease etc. et bleeding cetera. In fact, in 1948 the World Health Organisation, recognising the need for accurate definitions, made the first stab at creating an international disease classification (ICD) system. Prior to this, for example, Ischaemic heart disease did not exist. Which meant that you could die of a myocardial infarction in the US, but you could not do so in France – because the French had no term for such an event.

Issues such as this mean that trying to look back in time to ascertain death rates from specific diseases in different countries is a fairly pointless exercise. The French, just to pick on them again, did not accept the ICD system until 1968 – typical, you might say. Even when countries do accept the ICD system, it is difficult to be certain that people are using it in the same way. When I started in medicine a very common diagnosis at death, in the elderly, was bronchopneumonia. ‘The old man’s friend.’

Essentially, when an old person died, and you weren’t really sure what they died of, you put down bronchopneumonia. Try doing that today and the local coroner will be on the phone before you can say Harold Shipman. Now you have to die of something rather more specific – even if the patient is a hundred and two and have been going downhill for the last year.

‘I think they died of old age, Mr Coroner sir. But please sir can I write bronchopneumonia.’

‘Bronchopneumonia! You want more bronchopneumonia!’

In the UK we have now conquered bronchopneumonia. Today, the scourge that used to wipe out millions of elderly people, hardly kills anyone at all. Hooray, great celebrations, all around. My goodness it is a miracle of modern medicine… or not.

Yes, be very careful with medical definitions, and not just because they can often just follow the fashion of the day. Also, because, once you think you have defined something this can constrain your thinking to a painful degree.

Ischaemic heart disease would be what most people think of as heart disease. But just for starters, it is not a disease of the heart; it is a disease of the arteries supplying blood to the heart – through the coronary arteries. The ‘disease’ itself is atherosclerosis (thickening and narrowing of the arteries), and the condition underlying this atherosclerotic plaque development.

This is, sort of covered by ICD 414.0

414.0 Coronary atherosclerosis

Atherosclerotic heart disease

Coronary atheroma

Coronary (artery) sclerosis

But is 414.0 what actually kills you? You can have coronary arteries blocked up to 70:80:90 even 100% without having a heart attack a.k.a. a myocardial infarction:

‘We conclude that total occlusion of the major coronary artery occurs commonly in patients with chronic coronary disease, but is associated with myocardial infarction in only 65%.2

On the other hand you can find people with completely clear coronary arteries who have died of – what has been clearly diagnosed as – a myocardial infarction. Here is a paper from the European Heart Journal published last year, entitled: ‘Acute myocardial infarction with no obstructive coronary atherosclerosis: mechanisms and management.’

‘Myocardial infarction with no obstructive coronary atherosclerosis (MINOCA), a syndrome with several causes, is frequent in patients admitted with the diagnosis of M (myocardial infarction ‘heart attack’ my words). An accurate and systematic diagnostic work-up, is crucial for the identification of the cause of MINOCA in each individual patient, and then for risk stratification and for the implementation of the most appropriate forms of treatment. Yet, patients with MINOCA, in particular those with angiographically normal-coronary arteries, are frequently labelled as ‘non-cardiac patients’, thus missing the opportunity to appropriately treat patients with an outcome worse than previously believed.1

In this study they found that about 5 – 25% of those admitted with ‘infarctions’ had no coronary atherosclerosis. So ischaemic heart disease/MI can very frequently occur without the presence of any atherosclerotic plaques at all.

Unfortunately, the plot thickens even further. In many cases it can be found that a large blood clot (thrombus) can form in an artery days or weeks before the myocardial infarction actually occurs.

Here is an interesting little section from an article with a very boring title: ‘The temporal relationship and clinical significance of plaque substrate in healing coronary thrombi from sudden deaths attributed to rupture and erosion.’

‘Although the morphology of the culprit plaque has been extensively studied, especially rupture, relatively little is known about the temporal relationship between the onset of acute coronary events and thrombus maturation. The occurrence of nonlethal ruptures recognized by accumulated fibrous tissue at healed repair sites suggests that healing thrombi represent an episodic cycle of lesion progression. Moreover, thrombi from fatal plaques are in various stages of healing, further suggesting that death might not necessarily coincide with the initial onset of thrombus formation.3

Now, in English.

The thrombus ‘clot’ formation – the thing that is supposed to kill you within minutes of hours after forming – may well not actually occur shortly before you die. It can occur days or ever weeks earlier. Which mean that, in many cases the thrombus forms, the artery blocks, and nothing happens until – in some cases – weeks later.

This does not really fit with the current model of heart disease, which is very simple, and it goes something like this:

  • The coronary arteries gradually narrow and thicken.
  • At some point, a thrombus forms on top of one of the narrowest bits (the plaque),
  • This blocks the artery completely.
  • The heart muscle then rapidly runs out of oxygen and infarcts (dies).
  • In around 50% of cases you die as the heart stops beating, or goes into fibrillation – or suchlike

I call this the plumbing model of heart disease. Pump, pipes, blockage to the pipe in the pump …death. However, you can have final stage 100% occlusive atherosclerotic plaques without an MI. It is also perfectly possible have an MI without atherosclerosis. In addition, the formation of a thrombus does not necessarily correlate in any way, in timescale, with the MI – at all.

Because of all these problems with the current model, it would be perfectly possible to argue that we have the entire process of ‘heart disease’ the wrong way round. Indeed, I regularly communicate with a Brazilian called Carlos Monteiro, a researcher who proposes the myogenic theory of heart disease. He believes that the MI starts within the heart muscle itself, and the clot in the arteries comes afterwards.

His reasoning – following on from the work of his father in Law, the cardiologist Dr Mesquita is, as follows:

  • Clinical observations showing the absolute lack of efficacy of anticoagulants in the treatment of unstable angina pectoris. Unstable angina is considered to be a stage leading to myocardial infarction
  • The strong correlation of myocardial infarction with stress or unusual physical activity
  • Frequent coronary angiographies showing no obstructions in the presence of myocardial infarction
  • Many anatomic-pathological studies have demonstrated no relationship between thrombus and infarction, which led many authors since the 1940s to consider coronary thrombosis—the clot in the arteries—as a consequence of acute myocardial infarction, not its cause
  • The development of coronary thrombus after a heart attack, demonstrated experimentally4

True or false, right or wrong? Can the myogenic theory explain more of what we actually see? Yes, no, maybe. Personally, I don’t think his theory is correct in totality, although it has many correct bits in it. Causality is always a bugger, which way round do things go? This before that, or that before this? Are things actually related at all?

Sorry to say that I provide no further explanations. Or this blog would end up three hundred pages long, and I will not impose such a thing on anyone. What I hope to have made clear is that we have models and definitions of heart disease/IHD/MI that cannot be considered even remotely adequate. Whatever is going on, it is a far more complex and interesting thing than the plumbing model.

Which boils down to one simple thing. Namely that to ask the question, what causes heart disease, is easy. But in order to try and answer it we have to establish, as clearly as is possible, what the bloody hell is this disease? If find that you cannot find the answer to anything whilst sinking into a bog, or staring into the fog. Both of which seem the activities of choice of my cardiology colleagues.







The hydra

I was thinking about the astonishing resilience of the cholesterol hypothesis the other day – something I often do. As you may know the ‘authorities’ in the US have now decreed that cholesterol in the diet is no longer a dietary factor of concern, as it has no effect on cholesterol levels in the blood.

Well my, my, this was discovered sixty years ago by Ancel Keys. However, several decades later various US Departments seem to have noticed this astonishing fact. They have sprung into immediate action and proposed that cholesterol is removed from the guidelines – as a dietary substance to be avoided (well it hasn’t quite happened yet, but it will).

No doubt they will take about two hundred pages of verbose guff to state this, along with all the reasons why no-one was actually wrong, and no-one ever really said that cholesterol in the diet should be avoided in the first place blah blah de blah. I certainly would not expect that the words ‘we were wrong’ will be found anywhere in the document, at least not in that order.

Blimey though, sixty years to get rid of a recommendation with never a scrap of evidence to support it. Not a single scrap. Of course, cholesterol in the blood is still bad. At least bad cholesterol is still bad, whereas good cholesterol is still good. Even though neither thing is actually cholesterol at all. But why let science get in the way of a good scientific hypothesis.

Hydra, or blob.

I was thinking should I call this blog, the ‘hydra’ or the ‘blob’. Because, when it comes do the cholesterol/diet-heart, or the ‘whatever you now want to call it, because you can call it almost anything you like hypothesis’ we see both mechanisms, multiplication and growth/mutation.

From the hydra perspective, if you cut off the head, this hypothesis simply grows a couple more. We now know it is not cholesterol in the diet that is bad. But anyway that doesn’t matter, for another head grew years ago. It is the ‘saturated fat is bad head’. If you attack that, it is the ratio of saturated to polyunsaturated head that suddenly appears. And if you attack that, the monounsaturated head appears, or the odd-chain saturated fat head, or even chain, or short chain. Chop chop, more heads.

In the blood, it is not LDL ‘bad’ cholesterol that is the problem, it is the new head of the ratio of good to bad cholesterol. Or is it dyslipidaemia, or it is oxidised cholesterol, or particle numbers, or small dense ‘bad’ cholesterol, or light fluffy ‘good (and simultaneously) bad’ cholesterol. Chop, chop. OMG not more bloody heads.

However, there are also good reasons for calling the many headed cholesterol hypothesis the blob, as it just grows and grows bigger. Attack it with contradictory evidence and is also capable of engulfing it, using your evidence to grow bigger and stronger. ‘Run for your lives.’

The French have a high cholesterol diet, a high cholesterol level in the blood, and low rates of heart disease. ‘Ah yes, that it because they eat lightly cooked vegetables, eat lots of garlic and drink red wine.’ The blob, gentle readers shrugged, grew a few pseudopods and engulfed these contradictions, digesting them with a contented sigh.

Eventually the hypothesis became ‘multifactorial’ a state in which any attack on any part of it is doomed to fail amongst a forest of heads attached to a monstrous blancmange like organism. The cholesterol hypothesis has become so massive and shapeless that any attempt to attack it is doomed to failure. You will be simply turned to stone, or engulfed. It will be lot longer than another sixty years before this hypothesis will finally keel over and die – I fear.

After all, the fact that cholesterol in the diet has no effect on cholesterol levels in the blood has had not the slightest discernible effect on a hypothesis that began life as… the cholesterol hypothesis. Although I defy anyone to tell me what it has now become.

A humiliating climb down – or a Machiavellian move?

Some of you may have seen a headline in the Sunday Express Newspaper ‘Statin, new safety checks.’ The subheading was ‘Oxford professor who championed controversial drug to reassess evidence of side effects.’

Those of you who read this blog probably know that the professor in question is Sir Rory Collins. He, more than anyone, has championed the ever wider prescription of these drugs. He has also ruthlessly attacked anyone who dares make any criticism of them.

You may remember that last year he tried to get the BMJ to retract two articles claiming that statins had side effects (correctly called adverse effects, but I will call them side-effects to avoid confusion) of around 18 – 20%.

He stated that these articles were irresponsible, worse than Andrew Wakefield’s work on the MMR vaccine, and that thousands would die if they were scared off taking their statins by such articles. Ah yes, the old ‘thousands will die’ game. A game I have long since tired of.

Is this story ringing any bells yet? The truth was that both articles quoted a paper which stated that 17.4% of people suffered adverse effects. So, yes, a pedant would say that the 18 – 20% figure was wrong – although not very wrong. Certainly not worth a demand of instant retraction, and apology, which is a very drastic step indeed.

Anyway, below is a short description of the findings of an independent panel set up by Fiona Godlee, editor of the BMJ, regarding the Rory Collins attacks [This has appeared on my blog before]:

“As previously reported, Rory Collins, a prominent researcher and head of the Cholesterol Treatment Trialists’ (CTT) Collaboration, had demanded that The BMJ retract two articles that were highly critical of statins. Although The BMJ issued a correction for both papers for inaccurately citing an earlier publication and therefore overstating the incidence of adverse effects of statins, this response did not satisfy Collins. He repeatedly demanded that the journal issue a full retraction of the articles, prompting The BMJ’s editor-in-chief, Fiona Godlee, to convene an outside panel of experts to review the problem.

The report of the independent statins review panel exonerates The BMJ from wrong doing and said the controversial articles should not be retracted:

“The panel were unanimous in their decision that the two papers do not meet any of the criteria for retraction. The error did not compromise the principal arguments being made in either of the papers. These arguments involve interpretations of available evidence and were deemed to be within the range of reasonable opinion among those who are debating the appropriate use of statins.”

In fact, the panel was critical of Collins for refusing to submit a published response to the articles:

“The panel noted with concern that despite the Editor’s repeated requests that Rory Collins should put his criticisms in writing as a rapid response, a letter to the editor or as a stand-alone article, all his submissions were clearly marked ‘Not for Publication’. The panel considered this unlikely to promote open scientific dialogue in the tradition of the BMJ.””1

To provide a bit more context at this point, you should know that for a number of years, people have been trying to get Rory Collins to release the data he and his unit (the CTT), holds on statins. [The CTT was set up purely to get hold of and review all the data on statins, it has no other function].

He has stubbornly refused to let anyone see anything. He claims he signed non-disclosure contracts with pharmaceutical companies who send him the data, so he cannot allow anyone else access. Please remember that some of the trials he holds data on were done over thirty years ago, and the drugs are long off patent. So how the hell could any data still be ‘confidential’ or ‘commercially sensitive’ now?

[The concept that vital data on drug adverse effects can be considered confidential, and no-one is allowed to see it, is completely ridiculous anyway. But that is an argument for another day.]

Now, amazingly, after running the CTT for nearly twenty years, Collins claims that ‘he has not seen the full data on side-effects.’ In an e-mail to the Sunday Express he stated that ‘his team had assessed the effects of statins on heart disease and cancer but not other side effects such as muscle pain.

Let that statement percolate for a moment or two. Then try to make sense of it. So, they have got the data, but not bothered to look at it? Or they have not got it – which surely must be the case if he hasn’t even seen it. Give us a clue. Either way, Collins states he has not assessed it.

Despite this, he still managed a vicious attack on the BMJ for publishing articles, claiming statins had side effects of around 20%. This was an interesting stance to stake, as he now claims he has no idea what the rate of side effects are? In which case he should make a grovelling apology to Fiona Godlee immediately.

What is certain, and must be reiterated, is that Rory Collins has consistently refused to allow anyone to see the side effect data, or any other data, that that the CTT may, or may not, hold. See e-mail below from Professor Colin Baigent to the ABC producer MaryAnne Demasi (she was trying to get the CTT to confirm that they would not release data, Colin Baigent is deputy to Rory Collins)

From: colin.baigent@xxxxxxxxxxx

To: maryannedemasi@xxxxxxxxxxxx


Date: Tue, 24 Sep 2013 17:02:23 +0000

Dear Maryanne

The CTT secretariat has agreement with the principal investigators of the trials and, in those instances where trial data were provided directly by the drug manufacturers, with the companies themselves, that individual trial data will not be released to third parties. Such an agreement was necessary in order that analyses of the totality of the available trial data could be conducted by the CTT Collaboration: without such an agreement the trial data could not have been brought together for systematic analysis. Such analysis has allowed the CTT Collaboration to conduct and report all of the analyses on efficacy and safety that have been sought directly or indirectly by others (eg by Dr Redberg in her papers on the efficacy and safety of statins in primary prevention, and in questions raised by the Cochrane Collaboration). Hence, the CTT Collaboration has made available findings that would not otherwise have emerged.

I would be very happy to ring you at whatever time is convenient for you in order to help you to understand our approach, and then address in writing any residual concerns. It would be a shame if we were not able to speak as this would be the most effective way of explaining things.

Please let me know where and some times when I can reach you, and I will endeavour to telephone.

Colin Baigent.

I put the word safety in bold in this copied e-mail. You will note that Professor Colin Baigent does not say that that the CTT do not have these data on safety. He just says that the CTT won’t let anyone else see any data.

If they do have it, why have they not done this critically important review before, as they have had much of the data for over twenty years. If they don’t have it, how exactly is Rory Collins going to review it – as he states he is going to? Sorry to keep repeating this point, but I think it is absolutely critical.

Picture the scene in a lovely oak panelled office in Oxford, the city of the dreaming spires….

Professor Collins:   ‘Hey guys, you’re just not going to believe this, but a researcher just found a big box in the airing cupboard, and guess what, it has all the safety data in it….phew.’

Professor Baigent:  ‘Ahem… Why that’s lucky Professor Collins, now we can do the safety review.’

Professor Collins:   ‘Ahem… Indeed, Professor Baigent, we can. So, let’s get cracking shall we?’

And lo it has come to pass that after all these years Professor Collins has deigned to look at the safety data. This review shall, in Collins own words ‘be challenging.’ But you know what really don’t think they should bother, because we all know exactly what they are going to find….

That they were right all along, statins have no side effects. Hoorah, pip, pip. Nothing to see here, now move along.

A.N.Other Researcher:       ‘Please sir, can anyone else see these data that you hold, to ensure that you are being completely open and honest?’

Professor Collins:               ‘Don’t be ridiculous, these data are completely confidential.’

At this point I feel that I should ask how much do you, gentle readers, believe you can trust a review by Collins, on the data that Collins holds, on behalf of the pharmaceutical industry. Data that no-one else can ever see. [And the data from clinical trials on side effects is totally inadequate anyway].

Were I to be given the task of finding someone to review the safety data on statins, Professor Sir Rory Collins would not be the first person I would ask. He might even be the last.


P.S. Actually, he would be the last.

Thinking about diabetes once more

I suppose I should start this particular blog by stating that my interest in diabetes (type II) first came about as an extension of my interest in heart disease. This means that I approached diabetes in a different direction from most people. I was not looking at type II diabetes as an isolated condition; I was searching for the underlying links between heart disease and diabetes. This is probably why I have never thought about diabetes from the obesity, insulin resistance, perspective.

Instead, I was studying the impact of stress hormones, specifically cortisol, on various physiological systems. I knew that stress and cortisol levels were closely linked to cardiovascular disease. I also knew that type II diabetes increased the risk of cardiovascular disease – or perhaps vice-versa. Could both conditions be linked by abnormal cortisol levels?

Obviously I was aware that stress – however you define it – is a far more complex thing than simply raised blood cortisol levels. The stress response, or ‘flight or fight’ response or whatever you feel most comfortable with calling it is far more complex than that. It also involves a myriad of different mechanisms triggered by the sympathetic nervous system. Many other hormones are also involved, from glucagon to growth hormone, adrenaline and nor-adrenaline – and others too numerous to mention.

However, I decided to keep things simple and keep my attention focused on cortisol. I did this for two reasons. First, because I find that if you try to look at too many things at the same time you get dragged down into endless complexity. Second, I felt that cortisol may be the key hormone to study, because it is the primary ‘catabolic’ hormone. By which I mean that it triggers a whole series of ‘energy burning’ processes.

For example, a high cortisol level will convert glycogen in the liver into glucose – which is then released into the bloodstream, raising blood sugar levels. This is known as ‘glycogenolysis’. Cortisol also drives ketone synthesis in the liver. Furthermore, it breaks down fat and protein stores, releasing them for energy use. It also stimulates glucagon production in the alpha cells in the pancreas.

Looking at things from this perspective you could say that cortisol does the exact opposite of insulin. Insulin is the energy storage hormone; cortisol is the energy burning hormone. Therefore it seemed likely that people with high cortisol levels would develop insulin resistance and, in many cases, type II diabetes. I knew that stress raises cortisol levels and so here, perhaps, was an obvious link between stress, heart disease and type II diabetes.

This thought immediately led me to look at of people with Cushing’s disease (sometimes called Cushing’s syndrome). People with Cushing’s disease have a tumour on their adrenal glands which pumps out excess cortisol, in an uncontrolled fashion. This creates a whole series of metabolic problems:

‘Chronic cortisol hypersecretion causes central obesity, hypertension, insulin resistance, dyslipidemia, protrombotic state, manifestations which form a metabolic syndrome in all patients with Cushing’s syndrome. These associated abnormalities determine an increased cardiovascular risk not only during the active phase of the disease but also long after the “biomedical remission”’ 1

It is not exactly a state secret to announce that people with Cushing’s disease suffer from a wide, wide, spectrum of abnormalities, from increased visceral obesity to type II diabetes, high triglyceride levels, low HDL, raised blood pressure and on and on. They also have a very, very, high rate of death from heart disease. In some studies a 600% relative increase in risk. [Stick that in your pipe and smoke it…cholesterol].

Some of you may have looked at that list of abnormalities and thought. Hey, isn’t that also called the ‘Metabolic Syndrome.’ Why, yes, indeed, it is. Just to make research extra confusing, it is also called, at least, four other things:

  • Syndrome X
  • Reaven’s syndrome
  • Insulin resistance syndrome
  • Pre-diabetes

Anyway, leaving behind the terminological inexactitude in this area, it is beyond the slightest shadow of doubt that a high cortisol level can causes enormous and widespread metabolic disruption. Possibly this is all modulated by severe insulin resistance. Here is Wikipedia on the effects of Cushing’s syndrome (sometime called Cushing’s disease, sometimes called Cushing’s syndrome) on insulin resistance:

…Other signs include polyuria (and accompanying polydipsia), persistent hypertension (due to cortisol’s enhancement of epinephrine’s vasoconstrictive effect) and insulin resistance (especially common in ectopic ACTH production), leading to high blood sugar and insulin resistance which can lead to diabetes mellitus.’2

But is it definitely the raised cortisol that causes these problems? Could other things be going on in Cushing’s disease? To be absolutely certain that it cortisol was the culprit, I felt the need to double check.

So, I looked for people who are given high doses of cortisol. You may think that this would be a very strange thing to do. However, as some of you may be aware, cortisol is also known as a ‘corticosteroid’. Corticosteroids are group of hormones synthesized in the adrenal glands (all made from cholesterol, by the way). Just in case you are wondering, anabolic steroids are an artificial form of testosterone (another corticosteroid hormone), but one that builds up muscle, rather than breaking it down.

Synthetic corticosteroids based on cortisol are usually referred to as just, plain old steroids. Steroids are used in a very wide variety of diseases from asthma, to rheumatoid arthritis, Crohn’s disease, Systemic Lupus and Sarcoidosis. Essentially, they are used in any disease which has a significant ‘inflammatory’ component.

They are prescribed in these conditions because they are the most powerful anti-inflammatory agents known to man. There is no doubt that they are brilliant, and fantastic… however if used for too long… they can be deadly. I think of steroids as the bazooka of medical intervention. They blow up things ahead, but they also blow things up behind. So you need to be very careful what you point them at. And for how long… which is where my bazooka analogy rather fails.

Anyway, as you might expect, long-term use of steroids leads to exactly, and precisely, the same metabolic abnormalities that are seen with Cushing’s disease. Here is a short section of a paper looking at the impact of steroids on human metabolism:

‘Clinical-overt and experimental cortisol excess is associated with profound metabolic disturbances of intermediate metabolism resulting in abdominal obesity, insulin resistance, and low HDL-cholesterol levels, which can lead to diabetes.’3

None of this should be in the lease bit surprising, and I found that I was just confirming facts which, it seemed, had to be true. I knew that cortisol was a ‘stress’ hormone, and the key catabolic hormone (food burning/energy usage). I knew that Insulin was the key hormone directing energy storage. Frankly, I would have been amazed if raised cortisol did not cause insulin resistance and type II diabetes, and a whole serious of other problems from raised blood pressure to visceral obesity, low HDL levels, increased blood clotting etc. etc. All of the things associated with a high risk of heart disease.

In fact, when you look at heart disease and diabetes as two sides of the same coin, with stress/cortisol linking them together, things that may seem difficult, or impossible to connect, snap into place. Just to give one example here. Depression is known to be linked to a higher rate of death from heart disease. Here is a meta-analysis of nearly nine hundred thousand people

‘The results of our meta-analysis suggest that depression is independently associated with a significantly increased risk of CHD and MI, which may have implications for CHD etiological research and psychological medicine.’4

Depression can also increase the risk of insulin resistance and type II diabetes:

‘A positive association was found between depressive disorder and insulin resistance in this population-based sample of young adult men and women. The association seemed to be mediated partially by waist circumference.’ 5

What is the underlying factor linking depression and insulin resistance?

‘PMD (PMD is shorthand for depression – my words in bold) is associated with increased cortisol levels during the quiescent hours. Enhanced cortisol activity, particularly a higher nadir, was related to depression severity and the interaction of depressive and psychotic symptoms. This increase suggests a defect in the action of the circadian timing system and HPA axis, creating a hormonal milieu similarly seen in early Cushing’s syndrome and potentially an (im)balance of mineralocorticoid and glucocorticoid receptor activity.’6

Sorry about the jargon, but I wanted to make clear that severe depression mimics early Cushing’s syndrome… Interesting? At this point I could go deeper and start discussing the Hypothalamic Pituitary Adrenal axis (HPA-axis) and how you can link post-traumatic stress disorder, depression, fibromyalgia, childhood abuse, smoking and a lack of exercise to HPA-axis dysfunction, abnormal cortisol levels, central obesity the metabolic syndrome diabetes and heart disease together. But maybe that is for another day.

What I wanted to make clear here is that, when you look at things from a different perspective, type II diabetes becomes a much more interesting condition. It is not, and never was, a simple case of: you eat too much > you get fat > you become insulin resistance > you get type II diabetes.

But it seems that we are stuck with this ‘energy-centric’ model forever. All facts must orbit round excess energy consumption, and the role of other hormones in the body shalt be ignored. Glucagon…what’s that got to do with diabetes. Cortisol – do not look through that telescope young man. Depression causing visceral obesity heart disease and diabetes… nonsense. Oh well, dogma, dogma, dogma. It seems indestructible.

More on this topic soon(ish).







Thinking about diabetes again

When Banting and Macleod won the Nobel Prize for the discovery and purification of insulin in 1923, a very great thing had been achieved. Many, many lives have since been saved, and there is no doubt that the prize was justified. Even if Banting and Best did their furious best to write Macleod (A Scotsman, of course) out of the history books, and trash his reputation. Oh yes, how horrible people are to each other in the world of science.

However, as the same time as this great thing happened, something else, silently, took place. Insulin and sugar become so closely intertwined in the minds of everyone, that we got stuck. Thinking got stuck… into the following paradigm

  • When blood sugar goes up, insulin is released to bring it down.
  • Without insulin we develop diabetes
  • If the blood sugar drops too much, it is because there is too much insulin, and we get the patient to eat more sugar
  • You treat people with high sugar levels with insulin etc.

This is a paradigm with only two variables. Blood sugar*, and insulin. Type I diabetes is due to a lack of insulin, Type II is due to a relative lack of insulin caused by ‘insulin resistance’ whereby enough insulin is produced, but its effects are blocked. Insulin sugar, sugar insulin. End of.

I think of this as the super-simplistic model of diabetes. Of course insulin and blood sugar are connected, but this model is inadequate. A violin with only one string, playing a hopelessly restricted tune. For those who did watch Professor Unger’s YouTube lecture, you will be aware that this ‘insulino-centric’ model of diabetes is, in many ways, just plain wrong.

He has, for example, done experiments on mice whereby he completely destroyed the beta cells in the pancreas, conducted a glucose tolerance test, and found that the resulting glucose levels followed almost exactly the same pattern as in mice with intact beta cells. In short, insulin is not required to keep blood sugar levels under control after a glucose meal.

For those who have watched the video, you will be aware that this statement is true, but I have left out something rather critical. However, the main part of the statement is still correct. Despite what we are repeatedly told, you don’t need insulin to keep your blood sugar levels under control – the body can do this almost as well using other systems. Shock, horror, the body does not need insulin to absorb and store sugar.

This even trumps a statement that I have made repeatedly in other writing. Namely, keeping blood sugar under control is probably the least important thing that insulin does. You may just think that I am talking nonsense at this point. Without insulin, you die. That is what happened to all type 1 diabetics before insulin was discovered, isn’t it. So, why are you trying to tell me that insulin is not hugely important?

Well it is, but it is only important in that, without insulin, we do not control glucagon levels. Ah yes, glucagon, something most doctors heard about in the second year of medical school, then forgot that it ever existed. Except that, if a diabetic gets very low blood sugars levels you can inject glucagon and the sugar level bounces right back up.

However, despite that fact that most people have never heard of it, and most doctors have forgotten that it exists, glucagon is critical, and the interplay between insulin and glucagon is hugely, hugely, important. It is not a lack of insulin that causes catastrophically high sugar levels in type I diabetes. It is the overdrive of glucagon that does this. Equally, if you do not produce glucagon, you cannot get high blood sugar levels. End of.

Ah yes, so we have another player in the game of diabetes. Insulin, sugar… glucagon. And this, ladies and gentlemen is merely the start. Now, just as a teaser, I will introduce you to the critical importance of visceral fat in diabetes. Here is a little snippet from a study on mice:

‘In the present study, DIO [diet induced obesity – my comment] and diabetes mellitus were achieved in 100% of the mice after 8 weeks of treatment. At this point, some animals were submitted to visceral fat removal and the metabolic and molecular consequences of this procedure were evaluated. First, we observed that, 8 days after the surgical procedure, the mice were no longer diabetic

…Thus, we conclude that, in an animal model of DIO and diabetes mellitus, the removal of visceral fat is effective for rapidly reducing the blood levels of glucose. This is accompanied by improved in vivo and molecular actions of insulin and is paralleled by a favorable modulation of the levels of adipokines.1

Remove visceral fat and diabetes is gone. So, here is another massive variable in the old obesity, diabetes, insulin model. This variable is visceral fat, not be confused with subcutaneous fat – the type that Sumo wrestlers have tons of. Indeed, visceral fat is so different, metabolically, to subcutaneous fat that we shouldn’t really call it fat. It is something else entirely, a different organ.

Visceral fat is also another vitally important player in type II diabetes. As is, of course, adipokine production… which you will be no doubt glad to hear I shall talk no more about for the moment. As you may have guessed, I am not providing any answers in this blog about type II (insulin resistant) diabetes – or indeed type I. I am just trying to make it very clear that the model containing two players, insulin and sugar, is a complete barrier to understanding what is going on. You must remove it from your mind.

I will also state that I have most certainly not got it all figured out, fully. So, you are not going to get a definitive answer here – although perhaps some better answer. I keep thinking I have got all the pieces in place, then another bit of information appears and my carefully constructed model splinters apart. Try, for example, looking up the effect of insulin and cortisol on visceral fat, and see if you can make sense of what the hell is going on there. If you do, please let me know.

No, the reason for writing this blog is to continue with my endless theme. Please think for yourselves, and do NOT accept what you are told. This is most especially true in the area of obesity and diabetes.


*I use the word sugar to mean, mostly, glucose

Thinking about obesity and diabetes

Outside of heart disease and statins, another area I have been studying for many years is diabetes. Not type I diabetes (caused by destruction of beta-cells in the pancreas and a lack of insulin), but type II diabetes. Type II diabetes has nothing to do with a lack of insulin, it is generally considered to be caused by insulin resistance i.e. enough insulin is produced, but there is ‘resistance’ to its effects.

This resistance firstly drives up the insulin levels. However, as it worsens, the raised insulin levels are no longer sufficient, so the blood sugar levels rise anyway. At first the fasting sugar levels may be normal, but the response to a sugar ‘test’ shows an abnormally high level about an hour later. This is why a glucose tolerance test (GTT) used to be the way of diagnosing early stage type II diabetes.

This has been superseded by the HbA1c test. This test, essentially, looks at the amount of glucose that has stuck to your red blood cells over the last month. Which gives an idea of what the ‘average’ sugar level has been over a longer time period. It is a better measure.

Anyway, without getting too bogged down in technical details, the model that is used to explain type II diabetes is very simple.

  • You eat too much
  • You become obese
  • As you become more and more obese you become more and more insulin resistant
  • Your insulin level rises to overcome this resistance
  • At some point the resistance become too much
  • You develop raised blood sugar levels aka type II diabetes

I call this the ‘blowing up a balloon’ model of diabetes. As the balloon expands, you need to blow harder to get more air in.

This model (or variations thereof) is almost universally agreed, by almost everyone. It should come as no surprise, therefore, that I do not agree with it. Yes, there is not the slightest doubt that diabetes and obesity are related. In fact, there is no doubt that obesity; insulin resistance and type II diabetes are closely related.

Equally, there is no doubt that if people lose weight, their diabetes can go into reverse, and ‘reversibility’ is one of the most powerful pieces of evidence possible in proving causality. So where exactly, you may think, is my problem?

My problems first started with the recognition that you can find far too many direct contradictions to this model. Just to look at two examples. First we can look at the least obese people in the world. Those unfortunates who have a condition called ‘Beradinelli-Siep generalised lipodystrophy’. In this condition you have no fat cells – at all. So, of course, the rate of type II diabetes in these people would be zero…right? Wrong, the rate of type II diabetes is 100%.

Then we have Sumo wrestlers, the single most obese group of people on earth. So, they all have severe insulin resistance and type II diabetes right…? Wrong, whilst in training, none of them have type II diabetes.

In short:

  • Thinnest group of people in the word, 100% diabetes
  • Fattest group of people in the world 0% diabetes

Or to put this another way round, it is clear that obesity is neither necessary, nor sufficient to cause type II diabetes. If you were a follower of Bradford Hill, or Koch, of Popper this, effectively, writes off obesity as a possible causal factor for type II diabetes.

But, but.

But what?

To move sideways for a moment or two. When you first read about type I diabetes, one of the things that stands out is that those diagnosed with type I (at least in the past) lost weight very rapidly. They grew thinner and thinner, becoming almost like skeletons – before they all died. Why?

Why, is because insulin is the energy storage hormone. It does not just affect blood sugar levels. In fact, the almost obsessive focus on the interplay between insulin and blood sugar has blinded almost everyone to the fact that insulin does far more than just lower sugar levels. It affects fat, protein and sugar metabolism. It interacts with many different pathways in adipose tissue, muscle cells and the liver. Lowering blood sugar may be, in some ways, the least important thing that it does.

The reason why you die in type I diabetes has little to do with blood sugar levels. You die because, without insulin, fats escape from adipose tissue and travels to the liver as free fatty acids. In the liver these fatty acids are automatically converted into ketone bodies (which the body uses for energy in a fasting state).

The ketone bodies are, in turn, acidic, and in a high concentration they cause ‘acidosis’. This acidity overwhelms the alkali buffering systems, and you die in a keto-acidotic coma. To reiterate, it is not the high sugar that kills you in type I diabetes, it is the uncontrolled release of fats. This has nothing to do with sugar at all – except indirectly. Which, although you may not think it, returns us to the matter in hand. Namely, what is the association between obesity and diabetes?

As we have seen, without insulin, fats escape from fat cells at a high rate, so you lose weight. If we turn this though one hundred and eighty degrees, it should be clear that, if you have too much insulin in your bloodstream, fat can no longer escape from fat cells, and you will get fatter and fatter.

Essentially, insulin is obesogenic. A fancy way of saying that if you produce too much insulin you will become obese. An amazing fact ‘discovered’ in August 2014


“DALLAS – August 25, 2014 – UT Southwestern Medical Center researchers have identified a crucial link between high levels of insulin and pathways that lead to obesity, a finding that may have important implications when treating diabetes.”[1]

Yes chaps, well done. You made a breakthrough discovery of the absolute bleeding obvious. You mean, insulin makes you fat? Well who’d a thunk? Well, lots and lots of people actually. At which point, let me introduce you to the Pima Indians of North America. This race has an almost unbelievably high rate of type II diabetes. It is greater than 50%. Perhaps more. Are they obese, yes? Of course. However, of greater interest is that Pima Indians, long before they become obese and/or diabetic, produce far, far, more insulin than any other race [2]:

‘The normal and prediabetic Indians had fasting and stimulated insulin levels during all the tests two-to-threefold greater than the Caucasians. Differences in insulin levels between the two races could not be explained by differences in glucose level, age, or obesity.’

Interesting… It is clear that the model with the Pima Indians is, as follows:

  • You produce too much insulin
  • You become obese
  • You become insulin resistant
  • You develop type II diabetes

Of course, it is not just the Pima Indians where this happens. This causal chain works for us all. It contains most of the same ‘factors’ as the blowing up a balloon model of diabetes (although you will notice it does not contain the ‘you eat too much’ factor). However, as you can also see, the facts are in a different order. I like to call this, the correct order.

In short, yes, obesity, insulin resistance and diabetes are closely associated. But not quite in the way that everyone believes.

Moving on. What, you might think, would cause people to produce too much insulin. Well, what foodstuffs cause the greatest rise in insulin levels? Why, let me think… Yes, carbohydrates would cause the greatest rise in insulin levels. So if you eat lots of carbohydrates, you will produce lots of insulin. Insulin forces fats into fat cells and stops it escaping. Insulin is obesogenic… Join those dots ladies and gentlemen.

P.S. Pop quiz. What do you think happens if you try to force blood sugar levels down in type II diabetes by prescribing insulin?

P.P.S. So why does everyone with Beradinelli-Siep syndrome have type II diabetes? Answers on a postcard please.



Eskimos and nose bleeds part II

When I first realised that the conventional ideas about heart disease were, to put it kindly, flawed, I decided to try and start again with a blank sheet of paper and see if it was possible to work out what was really going on. Nothing was ruled in, nothing was ruled out. At first, like almost everyone else, I began to look for alternative potential ‘causal’ factors’ e.g. potassium, or stress, or fibrinogen, or other things in the diet.

However – as I have written before – I came to realise that this was a fool’s quest. There was so much noise, so many apparent contradictions, so many possible interactions and confounding variables that you could pick and choose your evidence to support almost any factor, or set of factors, that you wanted. Gradually I began to realise that if I truly wanted to understand heart disease, I had to start looking at the underlying processes.

In order to do this, I had to try and define exactly what ‘heart disease’ might be. I already knew that that heart disease is not really a disease of the heart. It is a disease of the arteries supplying blood to the heart (the coronary arteries). It is also a disease of other arteries around the body, the arteries supplying blood to the brain (coronary arteries), the kidneys (renal arteries) etc.

What we usually call heart disease is really arterial disease, where the arterial walls are thickened with atherosclerotic plaques, which eventually narrows the lumen, or central channel of the artery, causing angina and suchlike. In the arteries around the heart these plaques can finally ‘rupture’ causing a large blood clot to form on top of the plaque leading to a heart attack or, perhaps to be more ‘accurate’, a myocardial infarction.

In the carotid arteries in the neck, blood clots can also form on top of the plaques. The clot can then break off, travels into the brain, and block an artery. This leads to a stroke or a cerebral infarction. [There are other forms of stroke, but this is the most common].

Whilst this is a relatively simplistic model, I shall use it for the purpose of this blog, because it provides a close enough description of what happens. I shall also continue to use the term heart disease to mean the development of atherosclerotic plaques and formation of clots. Using this as the definition of ‘heart disease’, what processes can explain it?

The process of arterial thickening/plaque development

Moving backwards for a moment, I believe that the main reason why the cholesterol hypothesis has proven so resilient to all contradictory evidence is that the process seemed seductively simple. You eat too much cholesterol, the cholesterol level in the blood goes up and this excess cholesterol is then deposited on the artery walls… thickening and narrowing them. I once saw an episode of The Simpsons, demonstrating this exact thing happening in Homer’s blood vessels. Once something appears on The Simpsons you know you have a meme on your hands.

Of course, this initially simple process has altered and adapted and fragmented and shape-shifted so many times that it is now almost impossible to describe what it is. It has become something like this: you eat too much ‘unhealthy food’ (which may or may not include cholesterol and/or saturated fat), this raises LDL/cholesterol levels/or particle numbers and/or size, or other things, or lowers HDL, or raises triglycerides, or all three… which causes inflammation/oxidised LDL levels to go up, leading to development of plaques/thickenings in the arterial wall…

Sorry for the vagueness of it all, but I defy you try to get anyone to give you a more accurate summary of the current bad diet/heart hypothesis. I can’t. However, despite the fact that the cholesterol hypothesis has fragmented into a more and more confused mess, people still cling to the central process of ‘eating something > blood levels of something going up > narrowing of arteries.’ Primarily, I think, because it seems so simple. A leads to B, B leads to C, C leads to D…eath.

More than twenty years ago I realised that this model was bunk. It just could not explain heart disease. But what other process, or processes, could take its place?

In order to try and answer this I decided not to begin at the very beginning. Instead, I started at the very end, with the final event in heart disease. Essentially, this is when a blood clot or thrombus forms over a plaque, fully blocking an artery in the heart. [Most strokes (ischaemic) are also caused by a blood clot blocking an artery in the brain, although the process is not the same, it is very similar.]

Clearly, therefore, blood clotting (thrombus formation) is the terminal event in almost all heart attacks, and most strokes. This is widely accepted. Indeed, almost all forms of treatment for heart attacks, and strokes, involve the use of anticoagulants of different types: clot busters, aspirin, clopidogrel… or inserting stents to prize open the blockage caused by the blood clot etc. Acute cardiology intervention could, in many ways, best be defined as thrombus management.

The importance of blood clotting in heart disease death can be further highlighted if we look at people with Hughes Syndrome. This is a condition where the blood is dangerously more likely to clot – thrombophilia. People with this syndrome are far, far more likely to have strokes and heart attacks – often at a very young age – sometimes before the age of twenty. (Mainly strokes, actually). The condition is managed with various anticoagulants.

I could continue on this theme for some time, but the role of blood clots in causing death from heart disease, and strokes, is not in the slightest controversial. What is somewhat more controversial is to suggest that the earlier process of heart disease, atherosclerotic plaque development, could also be due to abnormalities/ dysfunction, with the system of blood clotting/repair.

At present, although I have never seen it stated clearly, it seems that everyone is happy to accept that atherosclerotic plaque development is due to one set of risk factors. Then the final event, the deadly blood clot, happens…coincidentally? Due to a completely different set of risk factors? This remains unexplained.

I was never comfortable with the idea that the creation of atherosclerotic plaques has one set of ‘causes’ whilst the final event, the blood clot, has another set of, potentially, unrelated causes. This seems clumsy, and always did – two diseases welded together to make one disease? I thought it was much better to see if a blood clot/thrombosis hypothesis could explain the entire process from start to finish. This could just be me trying to make things neat and tidy, but I don’t think so.

Firstly I tried to articulate what the unified ‘clotting’ hypothesis might look like. Whilst it does not have the elegant simplicity of the cholesterol hypothesis, I hope that it is clear:

Step One:              Various factors damage the artery wall (endothelial damage)

Step Two:              A thrombus or clot forms on top the area of damage

Step Three:          Once the thrombus has stopped growing/stabilised, endothelial cells re-grow over the top of it

Step four:              As a result of step three the thrombus becomes, effectively, incorporated within the arterial wall

Step five:               Various repair processes break it down and clear it up – but often not fully

Step Six:                 The area of ‘damage/repair’ becomes a focus for further damage/thrombus formation

Step Seven:         The thrombus/plaque grows through repeated episodes of thrombus deposition/repair

Step Eight:            A final thrombus forms over a large plaque that completely blocks the artery leading to a heart attack

Many parts of this are far from new. For those who have read my previous book, and blog, you will know that Karl Von Rokitansky proposed that plaques in arteries were really thrombi, over one hundred and fifty years ago. The problem that lead to his ideas being dismissed was, essentially, step three.

Whilst he recognised that arterial plaques looked very like thrombi, and contained everything you find in a thrombus, he could not explain how a thrombus could possibly come to be inside the arterial wall, covered by endothelium (the single layer of cells that line arteries). Virchow attacked his hypothesis simply by asking how this could occur – well, obviously, it cannot. Bong!

However, if Rokitansky had known what is now known, his hypothesis may well have won the battle of ideas, and the entire direction of research into heart disease would have gone off in a completely different direction.

The answer to the Rokitansky conundrum is, of course, very simple. If you damage the endothelium, and a thrombus forms over the area of damage (this will always occur), replacement endothelial cells do not come from within the artery wall (as happens if you scratch your skin). They come from the blood itself.

New endothelial cells develop mainly in the bone marrow, they float about in the bloodstream, and they are known in this state as Endothelial Progenitor Cells (EPCs). EPCs are attracted to areas where the endothelium is missing – where a thrombus has formed. Once there, they stick to the top of the thrombus and develop into mature endothelial cells. Hey presto, the thrombus becomes covered by a new layer of fresh endothelial cells and is now, effectively, within the arterial wall itself.

Of course, if you think about it, this has to be what happens. If a thrombus forms on your artery wall, it cannot simply fall off once the artery has ‘healed’ beneath, as would a scab on your skin. If this were to take place, the thrombus would just travel a bit further down the artery until it jammed. As you can imagine, jamming arteries with thrombi is generally pretty catastrophic. See under ischaemic stroke.

Which means that the repair system for thrombi that form on the walls of arteries has to involve covering them up – then clearing the debris away from within the artery wall itself. I would like to say that I hypothesized that EPCs must exist, before I found out that they did. But you only have my word for that.

A whole new process – and potentially causal factors

At this point, I would like you to look afresh at heart disease/plaque development as containing three interconnected processes:

  1. Endothelial damage
  2. Thrombus formation
  3. Repair

Viewing things in this way, you can see that factors that damage the endothelium e.g. high blood sugar levels, turbulent blood flow, stress, will cause more thrombi to form; the more thrombi that form, the more that plaques will develop. Factors that make the blood more likely to clot – and also create bigger and more difficult to shift thrombi – will accelerate plaque growth, and increase the risk of the final event occurring. Factors that interfere with repair process are likely to make plaques become bigger, and more damaging.

If these are the processes, then ‘factors’ which truly are causes (rather than associations), should fit easily within this model – and indeed they do. At this point you can play a game – if you are as sad as I am! It is one that I play when sitting quietly in a train, or driving, or half watching the television. It is called, think of a risk factor and see if it has a damaging effect on any of these three processes. The other half of this game is to think of something that ‘protects’ against heart disease and see if benefits any of these three process i.e. does it protect the endothelium, reduce blood clotting, or enhance repair.

Now to let you play this game yourself. Hit Google or Pubmed, and see what you come up with. Try endothelial damage, diabetes and CVD. Or smoking, EPCs and thrombus formation. Or try, effects of insulin resistance on EPCs and thrombus formation. Try exercise, nitric oxide and endothelial function. Or yoga and endothelial health, or smoking and blood clotting, EPCs and endothelial health.

Stick in any significant risk factor for heart disease, or stick in any factor known to reduce the risk of heart disease, and you will always find that they have a major impact on one of the three key processes: Endothelial damage, thrombus formation, or repair. Usually all three… This is not a coincidence.

In the light of this, I think it is interesting to review statins. Now I am a great critic of statins, as I believe their downsides greatly outweigh their benefits. However, they do reduce the risk of death from heart disease and strokes – if not by a great amount. At present this is generally attributed to to their impact on lowering cholesterol levels.

But I thought it was interesting to ask another question. Do they also have a significant effect on any of the three processes? Why, yes they do. Firstly, to look at their effect on the key repair system of EPCs. Here is a paper called:

Increase in circulating endothelial progenitor cells by statin therapy in patients with stable coronary artery disease1.

‘Statin treatment of patients with stable CAD was associated with an approximately 1.5-fold increase in the number of circulating EPCs by 1 week after initiation of treatment; this was followed by sustained increased levels to approximately 3-fold throughout the 4-week study period.’

In short, statins increase the number of EPCs which are essential to repair areas of damage to artery walls. Well, who’d a thunk? Well, me, actually.

Now to look at another critically important effect of statins. Before doing this I have an admission to make. It is something I have known about for many, many, years. It is this. Familial Hypercholesterolemia does increase the risk of heart disease. Something that I have tended to gloss over, for obvious reasons.

In my defence I have always known that this increased risk had nothing to do with the LDL/Cholesterol hypothesis. It was something else. The something else is that that Familial Hypercholesterolaemia causes (for a number of reasons, and not in everyone) increased thrombus formation. Or, to put it another way, it makes your blood much more likely to clot.

Here is a paper from the Journal Circulation called ‘Hyperlipidemia and Coronary Disease. Correction of the Increased Thrombogenic Potential With Cholesterol Reduction2.’ It is nearly twenty years old:

‘Background: Hypercholesterolemia is a risk factor for coronary disease, and platelet reactivity is increased with hypercholesterolemia, suggesting a prethrombotic risk. The aim of this study was to measure mural platelet thrombus formation on an injured arterial wall in a model simulating vessel stenosis and plaque rupture in hypercholesterolemic coronary disease patients before and after cholesterol reduction.’

‘Conclusions: Thus, hypercholesterolemia is associated with an enhanced platelet thrombus formation on an injured artery, increasing the propensity for acute thrombosis…cholesterol lowering may therefore reduce the risk of acute coronary events in part by reducing the thrombogenic risk…’

Yes, gentle reader, statins do work to reduce the risk of heart disease, but not directly by lowering LDL/Cholesterol. Instead they work a bit like aspirin, by stopping platelets stick together over areas of damaged endothelium. They also work a bit like Clopidogrel – which does much the same thing. They also work a bit like omega-3 fatty acids (which the Eskimos eat a lot of), and causes them to have nose bleeds.

What statins do not do is to mimic the action of warfarin. Warfarin has little or no impact on platelet thrombus formation, caused by endothelial damage, it works in a very different way. Once you know this, you can, as I promised, understand the conundrum I left in the last article on this topic. Namely, why does warfarin protect against strokes, but does not protect against heart attacks. Whereas aspirin, which is also an anticoagulant, primarily protects against heart disease.

Now you know… possibly?




Are some diets ‘mass murder’

Yes, hallelujah, the headline on a paper in the BMJ by Richard Smith, the previous editor of the journal. He has finally, if belatedly, come to realise that the dietary advice that has dominated western medicine for the last fifty years, or so, is complete nonsense.

This damascene conversion is mainly due to the fact that he read Nina Teicholz’s book ‘The Big Fat Surprise.’ As he states:

‘…the forensic demolition of the hypothesis that saturated fat is the cause of cardiovascular disease is impressive. Indeed, the book is deeply disturbing in showing how overenthusiastic scientists, massive conflicts of interest, and politically driven policy makers can make deeply damaging mistakes. Over 40 years I’ve come to recognise which I might have known from the beginning – that science is a human activity with the error, self-deception, grandiosity, bias, self-interest, cruelty, fraud, and theft that is inherent in all human activities (together with some saintliness), but this book shook me.’

The amazing thing, to me, is not the Richard Smith has finally realised the diet-heart hypothesis is a complete crock. The amazing thing is that it still holds sway, despite the fact that it was never based on anything other than the propaganda of a power-mad egotist (Ancel Keys). Any evidence that saturated fat, or any other fat consumption, causes heart disease has always been weak at best, more usually non-existent, or just flatly contradictory.

Many years ago Dr George Mann (who was running the Framingham Study at the time) stated that:

‘The diet-heart idea – the notion that saturated fats and cholesterol cause heart disease – is the greatest scientific deception of our times…The public is being deceived by the greatest health scam of the century,’

And what effect did this comment have? Well, none. In 2008 the Food and Agricultural Organisation concluded the “there is no probable or convincing evidence” that a high level of fat in the diet causes heart disease. A 2012 Cochrane review found no benefit from total fat reduction and no effect on cardiovascular or total mortality. ”More recently we have the Women’s Health Initiative, which enrolled fifty thousand women in the randomised trials of the low fat diet and cost £460m. To quote Richard Smith again:

‘The women were followed for 10 years, and those in the low fat arm successfully reduced their total fat consumption from 37% to 29.5% of energy intake and their saturated fat from 12.4% to 9.5%. But there was no reduction in heart disease or stroke, and nor did the women lose more weight than the controls.’

A 23% cut in saturated fat intake, and no impact on anything. What effect has this had? Well, none. Evidence has never had the slightest effect on this hypothesis. As of today, you can still order posters and other information from the British Hear Foundation which announce, in bold, ‘I cut the Saturated Fat.’ The blurb underneath states1:

‘Find out how to reduce the amount of saturated fat you eat using our A2-sized wallchart. It includes information on the different types of fat in food and advice on the healthiest options to choose both when cooking and eating out.’

So, saturated fat still demonised. And the BHF are still saying that:

‘At the crux of this debate is the role of saturated fat in our diet. Diets that are high in saturated fat have been shown to increase cholesterol. A high cholesterol level is linked to an increased risk of cardiovascular disease, so that’s why current recommendations emphasise the importance of reducing the saturated fat in our diets2.’

I suppose one could laugh at all this. Because, the BHF also states (in the same article) the following

‘Last week saturated fat came back to the top of the news agenda because research we’d helped to fund suggested there isn’t enough evidence to support current guidelines on which types of fat to eat. While the latest study didn’t show saturated fat is associated with cardiovascular disease, it also didn’t show that eating more of it is better for your heart health2.’

In short, the British Heart Foundation states that they funded a study which shows there is no evidence that saturated fat is bad for the heart. However, they also state that diets high in saturated fat have been shown to increase cholesterol and a high cholesterol level is linked to an increased risk of cardiovascular disease.

Be careful guys. If saturated fat does raise cholesterol, yet a high saturated fat diet does not cause heart disease then. Logically, you are stating that cholesterol does not cause heart disease/cardiovascular disease. In fact, this is exactly what they are stating. There is no escape from logic my friends.

This is just one example of the knots that people tie themselves into when they try to defend the indefensible. Luckily, for them, no-one seems able to draw the obvious conclusion from their incomprensible gibberish. Either the diet/heart (saturated fat) hypothesis is wrong, or the cholesterol hypothesis is wrong, or both. [The correct answer is, or course, both].

Of all the stupid scientific hypotheses of the twentieth century the idea that fat/saturated fat causes heart disease – or any other disease – is by all possible measures the most stupid. It is the most stupid because it has driven dietary advice to eat more and more carbohydrates a.k.a ‘sugars.’ Anyone who understood anything about human biochemistry and physiology could tell you what this would do

1: Cause millions upon millions of people to get fatter and fatter

2: Cause millions upon millions of people to become diabetic

3: Cause millions upon millions of diabetics to completely lose control of their sugar and fat metabolism, get even fatter and die prematurely

All of these things have happened, exactly as could have been predicted. Yet, our esteemed experts still propagate the dangerous myth that saturated fat is bad for us and we should stuff ourselves with carbohydrates instead.

Yes, some diets are ‘mass murder’. To quote Richard Smith for the last time:

‘Jean Mayer, one of the “greats” of nutritional science, said in 1965, in the colourful language that has characterised arguments over diet, that prescribing a diet restricted in carbohydrates to the public was “the equivalent of mass murder.” Having ploughed my way through five books on diet and some of the key studies to write this article, I’m left with the impression that the same accusation of “mass murder” could be directed at many players in the great diet game. In short, bold policies have been based on fragile science, and the long term results may be terrible.’

Richard, there is no may about it. The long term results have been terrible. So, to those ‘experts’ who continue to propagate the idea that saturated fat causes cardiovascular disease. Merry Xmas – you dangerous idiots. As it is the festive season, I shall refrain from calling them mass murderers.



Doctoring Data

I am pleased to announce that my book is finally written and edited and available to buy, on-line at

The full, formal launch will not be until next year. But for those who cannot wait (hopefully several hundred million people), you can pre-order it now on a restricted print run. First come, first served as they say.

It has been a mighty effort to write, and I hope that people can both enjoy reading it, and feel that they have learned something by so doing. I am but your humble servant.

Eskimos and nose bleeds

I have been studying heart disease for many, many, years now and I have read hundreds of different hypotheses as to what causes it. When I say heart disease, I mean the build-up of atherosclerotic plaques (narrowings) in the arteries. This can happen in the heart, the blood vessels leading to the brain, the aorta, the femoral arteries etc. etc. Usually followed by the formation of a blood clot over the plaque – leading to death.

I have read a hundred theories as to why this happens. From infective agents, to lack of micronutrients, to stress, copper deficiency and on and on. I have read theories suggesting that plaques are actually healthy adaptations, that heart attacks happen before the blood clot blocks arteries, causing the heart attack. That atherosclerosis has nothing to do with dying of heart disease – the Japanese, with a very low rate of heart disease, are just as likely to have atherosclerosis as anyone else.

In amongst this cacophony I have searched for the one factor that is consistent, and I have found nothing. Yes, mainstream medicine is still fixated on the LDL/cholesterol hypothesis. But it is perfectly simple to find population with low LDL/cholesterol levels and stratospheric rates of heart disease. Russians and Australian aboriginals spring to mind. Equally you can find populations with high LDL/cholesterol levels and very low rates of heart disease e.g. the Swiss or the French.

This leads us to the concept of necessary and/or sufficient. By this I mean a factor may be necessary for a disease to develop. Yet that factor cannot cause the disease alone. Koch demonstrated this by drinking water full of the cholera bacillus. He did not get cholera, because he was otherwise fit and healthy. He stated that a healthy person could fight off cholera, but if you were unhealthy it could kill you.

Thus, the cholera bacillus is ‘necessary’ to get cholera, but not ‘sufficient’ – on its own. The host needs to be compromised in some way.

So, are there even any ‘necessary’ if not ‘sufficient’ factors for heart disease that have been identified? The answer is quite clearly no. Many people have died of heart disease without a single identified risk factor. In short, there is no single factor that is necessary, or sufficient, to cause heart disease.

This is why heart disease is now considered ‘multifactorial.’ It has many different causes that all, sort of, act together – in some yet to be fully defined way. Whilst this must be true, to a certain extent, the concept of multifactorial allows anyone to say virtually anything, and nothing can either be proved, or disproved.

A skeptic:        ‘Here is a population with a low LDL/cholesterol level and a high rate of heart disease.’

An expert:       ‘Ah, that is because they have a low HDL level, they lightly cook their vegetables, they have a Mediterranean diet, they drink red wine, they [insert any one of three hundred different factors here].’

This type of discussion becomes utterly pointless after a while. You cannot, ever, get anywhere. It is like attacking the Hydra. Chop one head off and another two grow. Which is why we now have, just to look at blood lipids: good cholesterol, bad cholesterol, small and dense bad cholesterol, lightly and fluffy bad cholesterol, the good/bad cholesterol ratio, ‘dyslipidaemia’, high triglycerides, LDL particle number, and on and on. Try pinning anything down and it simply fragments in front of your eyes. Currently you cannot disprove the LDL/cholesterol hypothesis as it has become the perfect shape shifter.

Which means that I decided many years ago not to waste my time on attempting to argue against the LDL/cholesterol hypothesis too often, and pointlessly. Instead I searched for the factor that is necessary to cause heart disease. The factor that is consistent, where there are no contradictions. No need for adaptations, additions, sub-theories, sub-sub-theories.

I have to report that I never found one. Yes, it is true. There is no single factor that is either necessary, or sufficient, to cause heart disease. None. Or at least none yet identified. In truth, I do not think that such a factor ever will be found. Actually I am certain that this will be so.

The reality is that you have to move away from causal factors and start thinking about processes. Here, I believe, is where the answers lie. When you start thinking about process, you can understand why the Eskimos suffer a lot of nose bleeds, and had (when eating their traditional diets), a rate of heart disease that was….zero.

You can also understand why warfarin – an anticoagulant – protects against strokes, but does not protect against heart attacks. Whereas aspirin, which is also an anticoagulant, primarily protects against heart disease.

Yes, Eskimos, nosebleeds and heart disease. And yes, I do know that they are now called Inuit. But I still like Eskimo as it conjures up positive images in my brain.

P.S. A small prize for anyone who can correctly answer the warfarin/aspirin conundrum.

What is T?

Some questions puzzle me, and I search for the answer. For a number of years I am trying to establish. ‘What is T?’ My wife helpfully remarked that it is a drink with jam and bread. Ho, ho.

Moving swiftly on. My question relates to the concept of Number Needed to Treat (NNT). The NNT is a figure widely used in medicine as an outcome measure. It means how many people do you need to treat ‘T’ to achieve a benefit of some kind. The benefit can be many different things, for example: pain relief, curing a chest infection, improving pain and mobility following a hip replacement.

In these cases the ‘T’ is pretty clear cut. You have a medical problem and you intervene in some way to make it better, or cure it. But what is the ‘T’ when you are in the world of preventative medicine? If you are trying to stop something happening e.g. a heart attack, stroke, pulmonary embolism, or death, can you call preventing such things a form of ‘treatment?’

In reality, in preventative medicine, the ‘T’ turns into something else. It has become ‘P’, as in prevent. But treating and preventing are not the same thing, and you can’t use them interchangeably.

If you have a chest infection and I give you antibiotics then I have, in most cases, treated the infection. On the other hand, if you have a high blood pressure and I ‘treat’ it, all I have done is the lower the blood pressure. I have not immediately done anything else. A high blood pressure causes no symptoms, and there is nothing to be treated – other than future risk.

In fact, if lowering the blood pressure were a form of treatment, the NNT would be very nearly one, in that I will lower the blood pressure in almost every case where I prescribe a drug. But the NNT does not refer to the effect on blood pressure lowering; it refers to the number of people you need to treat to prevent, say, a stroke, by lowering the blood pressure.

As I hope is clear, in preventative medicine, the NNT should really be the NNP.

So what, you may think. Everyone working in this area knows that the NNT is really an NNP. You just need to know that when we use the term NNT, we are really talking about the number needed to treat to ‘prevent’ an event. Yes, this is true. However, the underlying problem with nomenclature does not disappear if we change NNT to NNP. The focus simply shifts to the word prevent itself. To prevent something means to stop it happening – forever.

Now, let us imagine death.

Can we prevent death? No, clearly we cannot. We do not make people immortal by lowering their blood pressure. All we can do, the very best we can possibly do, is to increase life expectancy – by some amount. Which means that prevention does not actually mean prevention. When we look at death as an outcome, prevention can only mean life extension. Or, turning this the other way round, the amount of time by which we delay something from happening.

At this point, I hope it has become clear that ‘T’ in preventative medicine has almost nothing to do with ‘treating.’ We treat nothing, we prevent nothing, we simply delay. At least that is all we can do with death. It is possible that we may prevent things such as non-fatal strokes, although we don’t really know, because we do not usually follow people up for long enough to be certain.

Why is this important? It is important for the following reason. When many clinical trials finish, and there is a difference in the number of deaths between the treatment and placebo arm, it is claimed that the difference represents lives that have ‘been saved.’ Which is another way of saying that death has been prevented which is, in turn, a different way of saying that death has been treated. NNT.

To give an example of how this work in real life I shall switch to statins and the Heart Protection Study (HPS)

Heart Protection Study

This graph shows the ‘mortality’ curves for the statin and placebo arms. At the start of the trial everyone is alive, 100% in both groups. Five years later, the end of the study, 92.6% of those in the statin arm were still alive, and 90.8% of those in the placebo arm were still alive. A difference of 1.8%.

This was presented, in the HPS press-release, as follows:

‘In this trial, 10 thousand people were on a statin. If now, an extra 10 million high-risk people worldwide go onto statin treatment, this would save about 50,000 lives each year – that’s a thousand a week.’
This is a very clear statement. Treat ten million people, and you will save 50,000 lives per week. But are these lives actually saved. No, of course not. Below, I have re-drawn the graph and extended both ‘survival’ lines by a year. We now have a year six.


As I hope is clear, by year six, if we assume the lines continue along their previous trajectory, every single extra person who was alive in the statin arm, compared to the placebo arm, is now dead. Thus 1.8% of people did not have their lives ‘saved’. In fact, the average increase in survival time for these 1.8% was approximately six months. [Half of the 1.8% would have died after six months, which give you the mean/average].

So what is ‘T’ in this case. It is certainly not treatment, prevention, or number needed to treat to prevent death. Nor is it 1.8% of lives saved. It is a life extension of six months, for 1.8%.

Or, to put this another way. If you treat one hundred people at very high risk of heart disease (secondary prevention) with statins, what you are achieving is the following:

• 1.8 will live, on average, an extra 6 months.
• 98.2 will gain no benefit

What is ‘T?’ What indeed. Not perhaps what you first thought. T, at present, is taken to mean treatment. With preventative medicine treatment is taken to mean prevention, and prevention is taken to mean lives saved. But you cannot save a life, all you can do is extend life.

So, when someone says….

‘In this trial, 10 thousand people were on a statin. If now, an extra 10 million high-risk people worldwide go onto statin treatment, this would save about 50,000 lives each year – that’s a thousand a week.’

…they are talking nonsense.

In very short summary. NNT is a widely used treatment outcome, and it guides both clinical and economic decisions on what drugs should be used, or not used. It is a pity that in preventative medicine, NNT is meaningless, because ‘T’ has no value attached to it. Indeed, it might as well be a drink with jam and bread.

Can we believe any medical research – at all?

I have now finished my book, to be called ‘Doctoring Data.’ It has taken a long time to write, mainly because I had to bring together hundreds of different strands of thinking and research. Each strand seemed to get longer and longer as I attempted to pursue them to the end. In many cases I never really found the end.

Some ideas just keep stretching away forever and I had to give up, or else the book would have become a million pages long. And I was told three hundred and ten was to be my limit – or something like that. As if my genius could be contained to a mere hundred thousand words, or so.

Anyway, the main purpose of the book was to look at medical research and data, and try to make some sense of it for those who are interested in looking beyond a medical headline. The book was, at least in part, inspired by a paper written by John Ionnadis.

It was entitled ‘Why most published research findings are false.’ You can easily find it on the internet by searching the title. It is currently the most downloaded paper in recent medical scientific literature

The shortest summary of his paper is, as follows:

Moreover, for many current scientific fields, claimed research findings may often be simply accurate measures of the prevailing bias.’ J Ionnadis.

How can it be, you may think, that most published research is false? Surely research is the one area of human endeavour where bias and dogma are ruthlessly hunted down and destroyed. A scientific finding is a scientific finding….is it not? Did Francis Bacon die in vain?

As Dogbert might say. Hahahahahahahahahahaha!

Or you might be best to pay attention to the quote from Friedrich Nietzsche. ‘There are no facts, only interpretations.’ Of course, he was a bit bonkers, but there is an awful lot of truth to what he said. Especially in medical research. Facts are the most tricky little blighters to get hold of. Interpretation, however, that is stated as fact all over the place

Surely, though, we have ways to ensure that research is pure and objective, such as peer-review. A system of using respected ‘experts’ to check and approve papers before publication. This will weed out papers that are flawed, will it not. Well, here is what Richard Horton (editor of the Lancet) has to say on peer-review:

The mistake, of course, is to have thought that peer review was any more than a crude means of discovering the acceptability — not the validity — of a new finding. Editors and scientists alike insist on the pivotal importance of peer review. We portray peer review to the public as a quasi-sacred process that helps to make science our most objective truth teller. But we know that the system of peer review is biased, unjust, unaccountable, incomplete, easily fixed, often insulting, usually ignorant, occasionally foolish, and frequently wrong.’

There we are, nice and reassuring to know that peer-review is such a fabulous system. As for the quality of published research itself, here is one of my favourite quotes by Drummond Rennie, at the time the Deputy Editor of the Journal of the American Medical Association.:

‘There seems to be no study too fragmented, no hypothesis too trivial, no literature citation too biased or too egotistical, no design too warped, no methodology too bungled, no presentation of results too inaccurate, too obscure, and too contradictory, no analysis too selfserving, no argument too circular, no conclusions too trifling or too unjustified, and no grammar and syntax too offensive for a paper to end up in print.’

A view supported from a slightly different angle by Dr Marcia Agnell, who was the editor of the New England Journal of Medicine for two decades. This was, and remains, the single most powerful and influential medical journal in the world. At least it is, when it comes to citations and impact factor:

“It is simply no longer possible to believe much of the clinical research that is published, or to rely on the judgment of trusted physicians or authoritative medical guidelines. I take no pleasure in this conclusion, which I reached slowly and reluctantly over my two decades as an editor of The New England Journal of Medicine.” Dr Marcia Agnell

Here is a further view on the issue by Richard Smith, editor of the BMJ for many years. He wrote this in his blog:

Twenty years ago this week the statistician Doug Altman published an editorial in the BMJ arguing that much medical research was of poor quality and misleading. In his editorial entitled, “The Scandal of Poor Medical Research,” Altman wrote that much research was “seriously flawed through the use of inappropriate designs, unrepresentative samples, small samples, incorrect methods of analysis, and faulty interpretation.” Twenty years later I fear that things are not better but worse…

…The poor quality of much medical research is widely acknowledged,” wrote Altman, “yet disturbingly the leaders of the medical profession seem only minimally concerned about the problem and make no apparent efforts to find a solution.”

Altman’s conclusion was: “We need less research, better research, and research done for the right reasons. Abandoning using the number of publications as a measure of ability would be a start.”

Sadly, the BMJ could publish this editorial almost unchanged again this week. Small changes might be that ethics committees are now better equipped to detect scientific weakness and more journals employ statisticians. These quality assurance methods don’t, however, seem to be working as much of what is published continues to be misleading and of low quality. Indeed, we now understand that the problem doesn’t arise from amateurs dabbling in research but rather from career researchers.’

So, Ionnadis states that most research findings may often be simply accurate measures of the prevailing bias. Current and past editors of the three most respected and powerful medical journals in the world confirm that medical research is warped, biased and flawed and, in many cases simply not believable.

Would this be very evidence used by NICE* to tell us which drugs to use – for example. Why, yes it would be. So be afraid, be very afraid. For an idiotic politician (sorry for the tautology) recently made this announcement1.

‘A Labour government could reduce variation in access to drugs and procedures by making it mandatory for commissioners to follow national clinical guidelines, Andy Burnham has revealed.’ Andy Burnham was, at one time Secretary of State for Health. His is now shadow secretary of state for health. So, if the UK votes for Labour, it will mandatory for all doctors to follow the guidelines based on the evidence that comes from clinical trials.

Oh Joy.

*NICE stands for the National Institute for Care and Health Excellence. It is supposed to review all evidence for various healthcare areas and decree what is best practice. What NICE says tends to get taken up in many, many, other countries as their views are widely respected and acted upon.


My father

My father died recently, so I have been rather busy with other things. I wrote a short eulogy to him and I thought I would share it, and my memories of him, on my blog. I am not certain that this is the ‘done’ thing, but I am doing it anyway. I sort of feel the need to share it with those who are kind enough to read my blog.

My father was not a man who suffered fools gladly. In fact his favourite expression was BF, as in, bloody fool. We were all, at times, BFs. I am sure I was referred to as a BF on more occasions than I ever knew. Politicians were most certainly all BFs.

But beneath the façade of referring to everyone and most of their actions as those of a BF was a man who would, after he had finished his obligatory two minute rant, then do all that he possibly could to help someone out.

Crashed your car….you BF….then he would fix it. Needing help… he would invite foreign students into his house for the night. At heart he was, basically, a big softie. A velvet fist in a steel glove. He would forgive anyone anything – in the end.

I remember he used to sing a little song at times. At the time I never knew where it came from. Some of you may recognise it. It is incredibly rude, and incredibly sad. This is the chorus – which is the only bit I heard him sing.

It’s the same the whole world over,

It’s the poor that get the blame,

It’s the rich that get the pleasure,

Ain’t it all a bloody shame

This never seemed, to me, to be a favourite song of a man who did not care deeply about the world, and who would like to see it become a better place.

Yes he could be irascible – we all know that. Yes, he could be difficult and argumentative… and we all most certainly all know that. Yes, he too, he was a fully functioning BF at times, with bells and whistles, and there were most certainly moments when he drove me – and everyone else – completely mad. But my thoughts and memories now are almost entirely positive. As I think are those of everyone else gathered here.

As we know he did many, many things. A man of great energy and boundless enthusiasm for life. Whilst I was thinking about writing this short eulogy I remember a quote about Winston Churchill that I think best sums up my father.

When you first meet him, you see all his faults. It takes a lifetime to appreciate his virtues.

Silence was the stern reply

I thought I should share with you, a letter written to Professor Sir Rory Collins by a reader of my blog. Mr David Bailey. Of course I have ensured that I have his permission to re-print this here.

He sent the letter to me some time after he wrote to Professor Sir Rory Collins. I told I thought it was very well written and interesting. But then, as a confirmed statin/cholesterol geek, I think everything about statins is interesting [More meds please nurse].

Anyway, David Bailey wrote the letter, with the following cover note to me:


I followed your GOOGLE link in your latest blog, and of course I found Sir Rory’s email address! I sent him the following letter, but I didn’t explicitly CC you, because I thought he might be less likely to take me seriously!

I hope perhaps a few of your other readers will do the same, but I don’t intend to suggest this on your blog – I don’t want this to seem organised.

All the best,


I replied


Excellent letter.

The reply will be, as follows

Dear Mr Bailey,

Thank you for you letter. Professor Sir Rory Collins is unable to respond to personal issues of this type. Message ends….

Still a good letter though. Could I put it on my blog in a couple of weeks, once you fail to gain any response at all?



That is the background, here is the letter. It is typical of many hundreds that I receive from people suffering severe and significant statin related adverse effects. In virtually every case their doctor has dismissed the adverse effects as even existing.

When, rarely, their doctor has accepted they are having adverse effects they have NEVER, according to those who write to me, made any attempt to inform the authorities that their patient has suffered a statin related adverse effect. Medwatch in the US, the Yellow Card system in the UK…

Dear Sir Rory,

I am not a medical doctor, though I have a PhD in chemistry, but I am writing to tell you of my experiences taking Simvastatin.

As I understand it, you are of the opinion that statin side effects are rare, and not important when weighed against the chance to avoid cardiovascular events.

I took Simvastatin for 3 years, and for most of that time I suffered no obvious side effects. I felt extremely positive towards this drug, because although I have not had a stroke or heart attack, anything that reduced the risk seemed like a good idea.

The side effects started rather suddenly – with extreme cramps in my right leg, which was weakened by polio when I was a child. I naturally thought I was getting Post Polio Syndrome (PPS) – a problem that I understand has no specific test. Because there was some delay before I could see a specialist, and I was struggling as my symptoms got worse, I decided to stop my Simvastatin as a precaution because I remembered that it could cause ‘muscle pains’. By that time my leg was extremely painful in the muscles and the knee joint, and it had weakened further so that my right foot would drop as I walked – potentially causing me to trip on it.

By the time I saw a polio specialist, I was not diagnosed with PPS because the symptoms were receding – I got no specific diagnosis. As I continued to improve, I decided to restart my Simvastatin, assuming that it had had nothing to do with my problems, and within a week I could feel the symptoms returning.

All in all, I stopped Simvastatin 3 times, and each time the symptoms started to reduce after a delay of about a week, and returned after I restarted the drug!

Had I not realised that Simvastatin might be causing my problems; I think I might have ended up confined to a wheelchair in considerable pain, still taking the drug! As it was, once I gave up on Simvastatin, I recovered completely over a period of about 9 months.

Of course, my situation was a bit special, but I discovered from informal discussions with others in their late 50’s and 60’s that maybe half had had problems with statins, or knew someone else who had! Some had simply discarded their tablets without discussing it with their GP, others had been given prescriptions for a succession of different statins, and had trouble with all!  One man had suffered muscle cramps and severe memory problems – both reversed after he stopped taking statins.  These were personal contacts, but of course, the internet is overflowing with stories of statin side-effects. I realise that the internet may encourage such stories, but when I combine them with my own experience and those of others I know, I am very concerned that you are so ready to endorse an even wider use of statins in people who are currently well.

I would particularly like to draw your attention to the following aspects of my case:

1)           My side effects took 3 years to manifest themselves – making it less obvious what was happening.

2)          Only my polio leg was affected, which suggests that statin side effects may start in a part of the body already damaged in some other way. This must give particular concern because it suggests that there are people out these suffering statin side effects and still taking the drug!

3)          Because I was very positive about the value of Simvastatin, it is hard to attribute what happened to me as a nocebo effect. Furthermore, the fact that I tried stopping the drug several times and observed the symptoms recede each time, means that I can be essentially certain that my troubles were indeed caused by Simvastatin!

After this experience, I have read around the entire subject of statins, cholesterol levels, and saturated fats. What I read disturbs me greatly.

1)            The evidence against saturated fats is weak except for one graph by Ancel Keys, who cherry picked his data to ‘prove’ the result he wanted!

2)           Cholesterol in the blood (or LDL/HDL) seems far less well correlated with heart attacks than I would have expected.

3)           Even though statins also block the synthesis of Co-Enzyme Q10, doctors do not seem to be warned to combine statin treatment with this supplement.

4)           Many medical researchers are concerned by the consequences of taking statins – some even suggest that statin induced muscle damage may be responsible for a rise in the incidence of heart failure in recent years!

We live in an age of openness, and I really think it would help if you debated your views with medical critics – verbally or in written form. Simply repeating that statins are safe and good for you (I paraphrase slightly) doesn’t seem to be sufficient.

Sincerely yours,

David Bailey