Tag Archives: cholesterol

You are a very black swan indeed

Here is Wikipedia on the wisdom of Karl Popper:

“The classical view of the philosophy of science is that it is the goal of science to prove hypotheses like “All swans are white” or to induce them from observational data. Popper argued that this would require the inference of a general rule from a number of individual cases, which is inadmissible in deductive logic. However, if one finds one single black swan, deductive logic admits the conclusion that the statement that all swans are white is false. Falsificationism thus strives for questioning, for falsification, of hypotheses instead of proving them.”

Sorry, although I am a great fan of Popper, his language is a bit, well, pedantic.  What he is saying here is that science starts with a hypothesis e.g. ‘all swans are white.’ If you find white swan after white swan, then you will mildly strengthen the hypothesis. However, once you find one black swan, the hypothesis is dead.  (Unless you decree that, as all swans are white, a black swan cannot – by definition – be a swan).

One of the great white swans of cardiology is that Familial Hypercholesterolaemia (FH) causes heart disease. When I give talks to other doctors informing them that the cholesterol hypothesis is bunk, one of the ‘facts’ that is triumphantly used to knock me down is that ‘People with Familial Hypercholesterolaemia die very young from heart disease.’ Case proven, raised cholesterol causes heart disease, now move on.

A little bit of context is needed here. Familial Hypercholesterolaemia (FH) affects about one in five hundred people. It is a genetic condition where those who have it (I refuse to use the words suffer from it) have very high Low Density Lipoprotein (LDL) levels. As everyone knows LDL is known as ‘bad’ cholesterol, which is considered to be the number one risk factor for heart disease. (Of course LDL is not cholesterol at all but, hey, why let scientific accuracy get in the way of…. Well, science).

Goldstein and Brown established that the cause of FH is a lack of LDL receptors on cells. LDL receptors are the things that bind on to LDL molecules and then remove them from the bloodstream. Cells manufacture LDL receptors when they are low on cholesterol and need more.

Once the receptor is made it is pushed out through the cell membrane to attract an LDL molecule. When an LDL molecule has been caught, by binding on to the receptor, the LDL and the attached receptor are pulled back into the cell and broken down. Because they function this way, LDL receptors only work once. If a cell wants more cholesterol, then it needs to manufacture more LDL receptors.

Clearly, if there are not enough LDL receptors being manufactured, the entry of LDL into cells is restricted. This means that blood levels of LDL rise, and you will be diagnosed with Familial Hypercholesterolemia. If, that is, you have a blood test.

Moving sideways for a moment I need to mention that most people with FH are heterozygotic, by which I mean they carry one gene for FH. Their LDL levels are therefore about double that of the surrounding population. However, those with homozygotic FH (carrying both genes) have LDL levels that can be twenty times ‘normal’.  More on this group in a later blog.

Back to FH. If you have a heart attack when young, by which I mean under about 55, and you have FH, doctors will nod sagely and that that ‘it was the FH that did it.’ (If you don’t have FH, they will say it was something else that did it).

Sometimes the relatives of those dying young of CHD with FH, are contacted. It is often found that there is a higher rate of FH and premature CHD in relatives. This type of evidence has been used as proof that FH causes CHD. Maybe. Maybe not. If someone dies young from CHD, and has FH, and other relatives have a higher rate of both FH and CHD, what have we actually proved? We have proved nothing – for certain.

All we have done is to establish that relatives of people with FH and premature CHD also have FH (as they must, as it is a dominant gene) and also have a higher rate of CHD. Now, it could be that the FH is the reason for their CHD. Or it might not. It could be that something else, genetic of behavioural, is causing their high rate of CHD.

Given this problem of inherent bias, how could you tell if the FH is causing the CHD or not? Or, better, how could you falsify the hypothesis that FH causes CHD? Can you find a black swan?

Well the best way to find a black swan in this ara is to turn your study inside out. Instead of looking at people with FH and premature CHD, then looking at their relatives to find FH and CHD, you need look for premature CHD first (knowing nothing of FH status), then see if FH is more prevalent in first degree relatives.

How do you do this? Well, firstly you ask hundreds thousands of students if their father had a heart attack, or died of heart attack before the age of 55. Then you measure the LDL level of those students to see if they have FH. At the same time you find age and sex matched control students to see if they have FH.

Now, if FH really were a major cause of premature CHD you would expect to find that FH was far, far, more prevalent amongst those students whose fathers suffered CHD before the age of 55.

Such a study was done once, in the Netherlands. The results were as follows:

In the EARS (European Atherosclerosis Research Society) studies, University students whose fathers had proven CHD before the age of 55 years, were recruited …Age and sex-matched controls were recruited from the same populations for each case.

  • 2 of 1089 students with family history of CHD had FH
  • 4 of 1727 controls had FH

Thus, the prevalence of FH in both groups was not significantly different at approximately 1 in 500, which is the estimated prevalence of the condition in the general population. The evidence that heterozygote FH is, of itself, a cause of atherosclerosis is unsatisfactory.


In short, when someone finally did a study on the association between premature CHD and FH, where selection bias was removed, they found that FH was no more common in those with, and without, a strong family history of CHD. This was the blackest of black swans.

However, there is a twist to this tale. Which is that this study was never published anywhere. The only reason that I know about it, is that I was reading the responses section in the British Medical Journal, and the lead investigator of the study wrote the above letter in reply to a discussion on FH. (Something more than easily missed).

I contacted him, and asked why the study had not been published. He did not provide any answer that made any sense to me. The end result of the lack of publication is that the blackest of black swans is not actually black. It is invisible. Until now, of course.

P.S. As for homozygotic FH, I shall deal with this later.

Bias, bias everywhere

For hundreds of years, medicine was driven by anecdote and personal beliefs, without the slightest supportive evidence. In the nineteen twenties the most common operation done was ‘removal of toxic colon.’ Toxic colons were believed to be responsible for almost any symptom you could think of.

  • Headache…..toxic colon
  • Anxiety…toxic colon
  • Stomach pain…toxic colon… obviously
  • Cramps…toxic colon, etc. etc.

Surgeons became blindingly wealthy cutting out significant lengths of the large bowel in those who could afford it. This operation, and the greed and stupidity that drove it, is outlined in the book ‘Doctors Dilemmas’, by George Bernard Shaw.  He went on to say that: ‘If you pay people to cut things out of you, then that it exactly what they are going to do.’

Not many people have their toxic colons removed nowadays, in fact no-one does, as the condition no longer even exists. But many people still have coronary artery bypass grafts done. Although there is not the slightest evidence that this does any good either. For more on this read Bernard Lown’s essay

Anyway, over time doctors began to recognise that if you were going to cut things out of people, or prescribe drugs, it would be nice to know if any of this activity actually did any good. And so began the dawning of the age of evidence based medicine (EBM). (Evidence based medicine is a far more recent movement than you might think, not really getting under way until the 1980s).

The individuals who really drove this forward e.g. Sackett, Cochrane, Muir-Gray were extremely hard working idealists. They were highly ethical and had the patient’s interest at heart. They taught EBM on wards with students, and looked for evidence wherever they could find it.

This was a much more difficult thing to do before the advent of the world wide web. I remember searching around for papers in medical libraries, taking literally hours to find the papers I was looking for. Something I can now do in seconds on the Internet.

In theory, of course, EBM should be a very good thing, and in some ways it has been. However, EBM relies entirely on the belief that the evidence you are using is accurate, or true, or believable, or unbiased, or whatever form of words you are most comfortable with. This may have been true once upon a time, but things have most certainly changed.

In the early days a great deal of research was carried out in major teaching Universities. Doctors and researchers would set up the trials, run them, and analyse the results. However, the turn of the millennium less than a third of drug related studies were being done in academic units.

To quote from the New York Times:

The removal of research from academic centres also gives pharmaceutical companies greater control over the design of studies, analysis of data, and publication of results.

The end result: among even the highest quality clinical research the odds are 5.3 times greater that commercially funded studies will support their sponsor’s products than non-commercially funded studies. The authors conclude, “Readers should carefully evaluate whether conclusions in randomized trials are supported by data.” Careful readers with enough time can sometimes spot discrepancies between data and conclusions in published studies. However, the drug companies typically retain control over the data from their sponsored trials so the majority of the researchers don’t have open access to the results from their own studies.’ Petersen M. ‘Madison Ave. has growing role in the business of drug research.’ New York Times, November, 2002.

In a similar, if less emotive vein, the most downloaded paper within recent medical scientific literature was written by John Lonnadis. It was entitled ‘Why most published research findings are false.’

The vast majority of people have never heard of this paper. The vast majority of those who have heard of it have never read it, and the vast majority of those who have read it, have clearly not understood the implications of what they have just read. Or, if they have…they are too frightened to do anything about it.

The shortest summary of his research is, as follows:

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

These words sound relatively mild, but the implications are explosive. Basically, many researchers are claiming that they have proved something to be true, but all they have actually done is to manipulate their research in order to confirm what they already ‘knew’ to be true.

In essence, medical research has become horribly biased, to the point where David Sackett (a hero of mine) has virtually withdrawn from the arena

According to the founder of Evidence Based Medicine experts are hindering the healthy advancement of science.

Writing in this week’s British Medical Journal (BMJ), Canadian-based researcher, David Sackett, said that he would “never again lecture, write, or referee anything to do with evidence based clinical practice”. Sackett is not doing this because he has ceased to believe in evidence based clinical practice but, as the BMJ comments, because he is worried about the power of experts in stifling new ideas and wants the retirement of experts to be made compulsory.

Sackett claims that the prestige of experts (including himself) gives their opinions far greater persuasive power than they deserve on scientific grounds alone.”Whether through deference, fear, or respect, others tend not to challenge them, and progress towards the truth is impaired in the presence of an expert,” he writes.

He also argues that expert bias against new ideas operates during the review of grant applications and manuscripts. “Reviewers face the unavoidable temptation to accept or reject new evidence and ideas, not on the basis of scientific merit, but on the extent to which they agree or disagree with the public positions taken by experts on these matters.” http://www.abc.net.au/science/news/health/HealthRepublish_124166.htm

When the man who virtually invented evidence based medicine states that research has become institutionally biased, where can we look? I am not sure. I will leave you with a thought from Professor Bruce Charlton

The decline of honesty in science

Anyone who has been a scientist for more than 20 years will realize that there has been a progressive decline in the honesty of communications between scientists, between scientists and their institutions, and between scientists and their institutions and the outside world.

Yet real science must be an arena where truth is the rule; or else the activity simply stops being science and becomes something else: Zombie science. Zombie science is a science that is dead, but is artificially kept moving by a continual infusion of funding. From a distance Zombie science look like the real thing, the surface features of a science are in place – white coats, laboratories, computer programming, PhDs, papers, conference, prizes, etc. But the Zombie is not interested in the pursuit of truth – its citations are externally-controlled and directed at non-scientific goals, and inside the Zombie everything is rotten…..

Scientists are usually too careful and clever to risk telling outright lies, but instead they push the envelope of exaggeration, selectivity and distortion as far as possible. And tolerance for this kind of untruthfulness has greatly increased over recent years. So it is now routine for scientists deliberately to ‘hype’ the significance of their status and performance and ‘spin’ the importance of their research.

Bruce Charlton: Professor of Theoretical Medicine

So, what can be done?

Salt intake – What of Nuns?

Excess salt intake is one of the great issues in preventative medicine. Last year I watched a bus go by, with an advert for reducing salt plastered all over the side. Some restaurants have taken salt cellars off their tables, to protect customers. Many foodstuffs now have their salt content clearly labelled, with high salt content given a red sticker.

Given all of this you would think, would you not, that the case for excess salt consumption causing cardiovascular disease had been made beyond even the slightest possibility of doubt. One of the arguments in support of the dangers of salt consumption (the one that I am looking at in this article), comes from the native peoples living in the Amazon

The Amazon is an extremely low salt environment, and the average salt consumption of those living there is at very low. Several studies have found that the tribes people living in the Amazon have very low blood pressure which does not increase with age. They also have very little in the way heart disease and strokes.

Primitive societies who ingest little or no salt have no hypertension1

Proof, the anti-salt lobby cry, that it is excess salt intake that causes our blood pressure to rise dangerously.

Or is it? When presented with ‘proof’ like this I tend to look for contradiction, rather than confirmation. Are there, I wondered, other populations that fail to demonstrate a rise in blood pressure with age, that do not have a low salt consumption. My attention was drawn to nuns, living in Italy.

‘The powerful effect of psychosocial and acculturating influences on population blood pressure trends seems to be confirmed, through longitudinal observations, in the nuns in a secluded order. After initial observations had been made on culture, body form, blood pressure, diet, and other variables in 144 nuns and 138 lay women, included as a control group, a 30-year follow-up study was undertaken. Most striking were opposite trends noted between the two groups in blood pressure trend. During the follow-up period, blood pressure remained remarkably stable among the nuns. None showed an increase in diastolic blood pressure over 90 mm Hg.’

So, nuns do not develop high blood pressure as they age. What happened to the control women in this study?

‘By contrast, the control women showed the expected increase in blood pressure with age. This resulted in a gradually greater difference (delta>30/15 mm Hg) in systolic and diastolic blood pressure between the two groups, which was statistically significant.’

No difference in diet or salt consumption, yet one population developed the ‘normal’ Western rate of hypertension whilst the other did not. What did the authors of this thirty yearlong study think was the reason for this finding?

‘In conclusion, it seems reasonable to attribute much of the difference in blood pressure and cardiovascular events, to the different burden in psychosocial factor and to the preserved peaceful lifestyle of the nuns2.’

Now I do not know for sure if those living in the Brazilian rain forests have managed to preserve a traditional peaceful lifestyle – but it seems a reasonable assumption to make.

However, the main point I am trying to make here is that you do not need a low salt diet in order to prevent hypertension. You can find populations with a normal salt diet who do not develop hypertension either.

What factor, or factors, appears to link these two populations? The factor appears to be living a preserved peaceful lifestyle. This would suggest that stress is the cause of hypertension and cardiovascular disease, and not salt. Whilst association cannot prove causation, a lack of association disproves it.

1: Freis ED. The role of salt in hypertension. Blood Pressure 1992; 1: 196-200.

2: Timio M, et al: ‘Blood pressure in nuns in a secluded order: A 30-year follow-up.’ Miner Electrolyte Metab. 1999 Jan-Apr;25(1-2):73-9

What does cause heart disease?

(Part one of an occasional series)

So what does cause heart disease then, if it is not cholesterol?  This is question I am often asked – with varying degrees of accusation – by other doctors. Usually after I’ve given a talk dismissing raised cholesterol as a risk factor.

The simplest answer is that the most important causal factor of cardiovascular disease aka the development of plaques (thickenings) in the arteries, is stress (sorry about that rather clumsy form of words). However, as with many simple answers, explaining how stress causes ‘heart disease’ is a bit more complicated.

Which means, gentle reader, that we must go back to the beginning of the whole story, and weave a number of interconnected strands together.

The first strand here is to explain what ‘stress’ may be. I must admit that this is not easy, because few people have an agreed definition of stress. Many concepts are bandied about, and everyone has their own ideas on the subject, but most of them are rather too vague to be of any real use.

I define stress as a measurable dysfunction in the Hypothalamic-Pituitary-Adrenal axis (HPA-axis). But that may be jumping ahead rather too fast, and it requires many steps to get to this point. The first step is to attempt to break stress down into its component parts.

To do this, we have to start by accepting that stress has two basic components. There is the Stressor – the thing causing stress, and the Stressee – the individual affected by the stressor. Without making this important distinction, we will constantly mix up two concepts that need to be kept separate.

For example, many people talk about having a stressful day. I would immediately ask. Does this mean you were impacted on by lots of different stressors e.g. a traffic jam, a tight work deadline, your children getting ill. Or that you found yourself unable to cope with stressors that you would normally be able to cope with. Or both. [To be truthful I would rarely ask this, as I don’t want people shuffling away from me at the dinner table. But I might think it].

By looking at stress as having a cause, or causes, (the stressor), and then looking at their impact upon an individual (the stressee) we can start to disentangle the things that cause stress, from their actual impact.

In addition to this important distinction, there is also a need to accept that different stressors can create positive or negative effects, depending on how the person reacts to them.  Without getting too tangled in this issue, I will attempt put these first ideas into their simplest possible form

Stress has four distinct components:

  • Stressor – positive
  • Stressor – negative
  • Stressee reaction – positive
  • Stressee reaction –negative

Positive stressors could be:

  • Exercise
  • Winning the lottery
  • Giving a well-accepted speech
  • Watching your children perform on stage

Negative stressors could be:

  • Using cocaine
  • A close relative dying
  • Severe criticism at work/being bullied
  • Getting hit by a bus
  • Watching your army comrades being blown to bits by an IED

Some negative stressors are very short acting and, as such, the human psyche and physiology can cope and restore homeostasis (unless the trauma is gigantic). The problems start to arise when negative stressors act hour after hour, day after day, week after week. For example, being repeatedly physically or sexually abused as a child. Or being bullied day after day at work.

Problems created by a constant battering of negative stressors are also made significantly worse if your coping mechanisms are poor. Being bullied at work is not so bad if you have a good social life, a supportive partner, and a loving family. It also helps significantly if you are physically, fit and free from significant chronic disease.

If, however, you have no friends, no supportive family, and you have a chronic illness that weakens you, it does not take too much else to tip your system over the edge.

Unfortunately, early life trauma, and abuse, can leave people with very poor coping mechanisms. In addition, people who have suffered repeated negative stressors through their childhood often find themselves in a cycle of repeating negative behaviour. They are also likely to have poor coping skills, and difficulty with interpersonal relationships.

Effectively, therefore, the same ‘stressor’ can have very different effects on people, depending on their resilience. This resilience can be both psychologically and physically determined, and is hugely important. A ‘strong’ person can cope with stressors that might seriously damage a ‘weak’ person.

Some people say that stress can be simplified into the flight or fight response being constantly activated and eventually ‘burning’ out. Whilst it is true that a constantly stimulated flight or fight response is key to understanding the physiological damage that ‘stress’ causes, it is not the only factor in play.

A lack of social support is not the same thing as the flight or fight response. However, it can create significant problems with production of stress hormones. Depression is not the flight of fight response going wrong. Not having human contact, or touch, can damage your hormonal and autonomic/unconscious nervous systems just as much as being bullied.

In short, stress is not just determined by external factors, such as perceived – or real – threat. A vastly important aspect of stress lies within the individual, their responses to life events, and their resilience. As social animals, loneliness is just as damaging, if not more so, than someone threatening to fire you.

In my world, therefore, being depressed is a form of ‘stress’, and it causes exactly the same type of physiological damage as, say, post-traumatic  stress disorder. This is why you cannot look at an event in someone’s life e.g.  losing their job, or getting divorced, or suffering a car crash and loss of a limb, and score this from one to ten on how stressful this is.

  • Loss of job =2
  • Moving house = 3
  • Getting divorced = 4

For some people losing a job may be a blessed relief. For other a terrible humiliating shame. Others may just shrug their shoulders and move on.

For some of us, an apparently trivial event can be devastating e.g. a passing comment on our appearance.  Others will just laugh it off. Some years ago I was told by a doctor that stress couldn’t be a cause of heart disease because he had seen a well-off lady living in rose covered cottage in the country who had just had a heart attack.

I just replied ‘How do you know she wasn’t stressed?’ The externally idyllic existence may, in reality, be a battleground. Perhaps her smiling, smart, well-off, magistrate husband got home and beat the living daylights out of her every weekend. If so, it wouldn’t be the first time – and most certainly would not be the last.

In short, there is no point in guessing if someone is stressed. Often, there is no point asking them either. Most of us play complex internal games with regard to stress. Where it is considered a badge of honour to be ‘stressed’ and working incredibly hard – people will tell you how stressed they are. – even if they are not. Equally, if you have had a terrible upbringing, you may be so desensitised to stress that you cannot even recognise that you are suffering.

At this point I should probably attempt to bring together what makes up the concept of ‘stress’

Stress consists of stressors, and the stressee. Stressors can be positive, or negative. They can be psychological, or physical.

The same stressor can have a completely different impact on the stressee depending on their resilience.

Resilience can be damaged by such factors as:

  • Abuse in childhood
  • Long-term illness
  • A lock of supportive relationships, friends, family, church

Resilience will be improved by

  • A loving upbringing
  • Good health
  • Supportive relationships
  • Good interpersonal skills

There is no point in guessing is someone is suffering the physiological consequences of stress. Equally, there is no point in asking someone if they are stressed – they may well not know. The only way to know if someone is actually suffering from the consequences of repeated negative stressors is to measure their biochemistry and physiology.

Part two: How to measure if a person is ‘stressed’.

A simple Question – that opens a can of worms

A day or so ago I received this e-mail from a doctor in London.

Dear Dr Kendrick,

I work as a GP in Wandsworth London and I read that you don’t
believe that much in cholesterol and CHD.

I do agree up to 50% of MI patients have normal cholesterol
but some say what’s normal for UK is actually high. Is this argument valid?

Best wishes

Define ‘normal.’ Does normal mean average? If we took the average height of everyone in the UK we would find (very nearly) that 50% of those dying of CHD (coronary heart disease) were above average height and 50% below. So average is clearly normal, but then again so is being tall, or short.

However, if we decided that average height of everyone living in the UK was above ‘normal’, and we then lowered the definition of ‘normal height’ by three inches, we would find that the vast majority of people dying of CHD were now above average height. At which point we could decree that being taller than normal was a risk factor for CHD.

This would obviously be a completely bonkers thing to do. Yet, you can do it with cholesterol levels and everyone nods in general agreement.

Aha, but the argument goes that our lives are completely different than the lives of our ancestors, which has caused our cholesterol levels to be unnaturally high.

An article in the Journal of the American College of Cardiology best summed up this line of thinking. Under the heading ‘Why average is not normal’, O’Keefe, the lead author, made the claim that: ‘Atherosclerosis is endemic in our population, in part because the average LDL (“bad” cholesterol) level is approximately twice the normal physiologic level.’ In short, according to O’Keefe, our cholesterol level should be about 2.5mmol/l, not 5.2mmol/l.

He based his argument, in part on looking at the cholesterol levels of various animals e.g. elephants, and boars, and suchlike. He also used the argument that very young babies (neonates) have cholesterol level of about 2.5mmol/l. Now, in my opinion, anyone proposing this argument should have their medication increased. We should base our cholesterol levels on those found in other animals species….yes, of course we should. You mean those animal species with an average life expectancy of ten years, for example.

However, this argument is now pretty widely accepted by the medical community. We are all, everyone, living in the West, living in such an ‘unhealthy’ way that our cholesterol levels are unnaturally high. The true normal cholesterol levels is 2.5mmol/l.

Fine, if we re-set normal at 2.5mmol/l we will find that 99% of people dying of heart disease do have a ‘high ‘cholesterol level. Problem sorted, average is no longer normal, and the hypothesis that a high cholesterol level is a risk factor for heart disease is now true.

Hold on, I’ve got an idea…

How medicine now works – or doesn’t.

It may surprise some of you that read this blog that, amongst other things, I still work as a doctor in the jolly old NHS. Yes, one can be a critic and still remain inside the system….although for how long, who knows. In fact, in some ways I am quite establishment, as I sit on the main BMA negotiation committee for GPs, the General Practitioners Committee (GPC). I am also on the Local medial committee (LMC) and local negotiation committee (LNC).

From within the NHS you can more clearly see how the world of medicine is gradually going completely bonkers.

In one of my jobs I do Out of Hours (OOH) General Practice work. That is working in the evenings and weekends. In East Cheshire, where I work, we had a system which was highly rated by patients and everyone who came into contact with it. However, in line with the rest of the country we were told we were now to be incorporated into the Government’s latest and currently stupidest idea, called NHS111. The 111 bit being the single telephone number for people to call for urgent – not 999 care.

NHS111 call handlers get about six weeks training, and are supposed to act as front line troops to direct patients to the correct urgent service. Before this we had nurse triage, with experience nurses dealing with local residents and their health issue. We now have non-medically trained staff given superficial advice on how to go through a treatment algorithm. First question:  ‘Are you alive or dead?’ Not quite, but nearly.

At the end of asking ten thousand questions, or so, the call handler reaches the end of the algorithm where it states ‘You must see a GP.’ Actually, not quite true.  If there is anything actually wrong,  then the call handler tells them to phone an ambulance immediately [Yes, ambulance calls under NHS11 have risen stratospherically]. In my opinion, these people are not doing triage, they are just appointment Clerks.

As we repeatedly warned the Government NHS111 rapidly went wrong.  In East Cheshire and many other areas, NHS111 immediately collapsed the moment it went live, and we had to take back all the call handling. Why, primarily because the private providers running the service had so badly underestimated demand that the system went into melt-down, and patients were left waiting for hours to be called back. (Oh the joys of competitive tendering. In order to get the contract you have to bid so low that you cannot actually provide the service).

Anyway, we still get some calls coming through from NHS111 (A system now running in parallel – at double cost – with the old system).  With the old system we used to get the key facts e.g. a rash, non-blanching, child floppy, temp 39oC, mother worried. Now we get the following (this is an actual transcript of a very, very  simple case, with any patient identifiable data taken out – by me).

  • Symptoms: Cough
  • Case Summary
  • Disposition: The individual needs to contact the GP practice or other local service within 6 hours. If the practice is not open within this period they need to contact the out of hours service. Dx06
  • Selected care service: OOH – GP OOH Service (xxxx Base)
  • Pathways Assessment: Birth had not occurred within the last hour. An injury or health problem was the reason for the contact. The individual was breathing and conscious at the time of the assessment. Heavy bleeding had not occurred in the previous 30 minutes.
  • An illness or health problem was the main problem.
  • The individual was not fighting for breath.
  • A probable allergic reaction, a fit within the previous 12 hours or successful resuscitation were not the main reason for the assessment.
  • The child was not limp, floppy and/or unresponsive.
  • The skin on the torso felt normal, warm or hot.
  • Pathway selected – Cough
  • The individual had not coughed or vomited blood.
  • There was normal breathing between bouts of coughing.
  • Severe illness and a rash suggestive of septicaemia were not described.
  • There was no difficulty rousing.
  • There had been no episode of choking within the previous 24 hours.
  • There had been no inhalation of a hot or poisonous substance in the previous 24 hours.
  • There was no fever at the time of assessment or within the previous 12 hours.
  • There had been no previous diagnosis of heart disease, asthma or other lung disease.
  • There was not a problem for which medical advice must always be sought.
  • There were no severe coughing bouts with whooping, a red or blue face or vomiting after coughing.
  • The cough for had persisted for less than 3 weeks.
  • Instructions given were: The individual needs to be seen
  • by the GP practice or other local service within 6 hours.
  • If the practice is not open within this period they need to be seen by the out of hours service.
  • Directory of Services referral: OOH – GP OOH Service (xxxxxxx Base)
  • Advice given: Worsening
  • Advice given: If the condition gets worse, changes or if you have any other concerns, call us back.

As you can see, if you bothered to read it, 99% of this is just meaningless guff, stating irrelevant negative findings. But it does take a considerable amount of time to read. Some of it just made me despair. For example, the report states that: ‘An injury or health problem was the reason for the contact.’ Well really, how completely amazing. Someone calls a health line and they may have an injury or health problem.  Who’d a thunk?

This is followed later by…’ An illness or health problem was the main problem.’ Well at least they had narrowed it down from an injury or health problem to an illness or health problem. [So it now seems that illnesses are not health problem?]

What did I actually need to know? I needed to know that a child had a cough that was getting worse. Whilst it is possible to establish this from reading the report (just)  other key information was conspicuous by its absence. Past history of asthma, for instance (which this child had) or other respiratory problems? Any medications?  That type of thing.

As with most new initiatives in the health service I am now getting swamped with information – but the vast majority of it is completely and utterly useless, and just gets in the way of finding out what I want to know.

This, by the way, was a very small part of the report that the GP (in hours), will receive. They will get about ten more pages of other extraneous guff that they have to wade through. At some point my consultation (the only bit they are interested in) will appear so they will know what I found and what I did – and if they need to do anything. This will not be at the front of the report, no, it will be stuck in the middle, surrounded by information about when the call came in, how long it took to respond, what pathways were used etc. etc. etc. thud.

This, ladies and gentlemen, is the type of nightmare bureaucrat driven nonsense that is turning healthcare in the UK from something local, flexible, and responsive to patient needs, into a flabby form filling, algorithm following, arse-covering exercise. Millions of hours spent producing lengthy reports that have no value; they simply get in the way of providing useful information and de-skill, demotivate and de-professionalise everyone involved.

I imagine the UK is not alone in this. Somehow or another we need to fight back.

How Risky Is A Risk?


[I was contemplating risk the other day, when someone forwarded me an article I wrote a couple of years ago on risk. I think it is still highly relevant to what is happening today with the mangling of medical statistics]

I have only just recovered from the idea that everyone in the whole world over the age of fifty-five should spend the rest of their lives on six different medications, all stuck together in one great big pill. The following was headline from a study in the BMJ.

‘Polypill—A Statin plus 3 Blood Pressure Drugs plus Folic Acid plus Aspirin. Authors claim Polypill would reduce risk of dying from coronary heart disease by 80%. The authors of the polypill article in the BMJ made the claim that taking their polypill would reduce the risk of dying of coronary heart disease (CHD) by 80%.’

You may have seen the non-story about the, yet to be marketed polypill, peddled in the British Medical Journal (BMJ). I was stimulated to look again at the concept of risk.

Whether or not you believe their figures—and I don’t—I sense that this figure of 80% would be taken by most people to mean that eighty out of one hundred people would be saved from death if they took this magic tablet. But this figure, if true, could only possibly be a relative risk reduction. And a relative risk reduction means almost nothing, by itself.

However, because everyone’s eyes glaze over whenever you start talking about statistics, most researchers manage to get away with using relative risk reduction figures when, in reality, they should be shot for doing so. Now, here’s a challenge. The challenge to make a short article about statistics interesting. Okay, that’s not possible. But maybe a little bit interesting?

You must know the time period, and the absolute risk, for the relative risk to have any meaning

When you talk about a risk, you need to know the absolute risk of a thing happening. For example, the risk of getting struck by lightning. I don’t actually know what this risk is, but I would imagine it is about one in five million. But again, that figure means little unless you put a time scale on it. Is this a one in five million risk over a hundred years, or one year, or a day? If you don’t put a time scale in, you can claim pretty much anything you like.

For example an astronomer could attempt to shock you by stating that ‘The Earth will be hit by a big Asteroid. This is one hundred per-cent certain.’ – stunning announcement from A.N. Astronomer. Read all about it.  And of course, this is true. The Earth will be hit by a big Asteroid, sometime in the next three billion years or so. The odds ratio for this event is 1 = 100% certain. I am even willing to take a bet on it. What you probably want to know is however, is, what is the likelihood of this happening in my lifetime. Sorry, no idea.

Anyway, I hope this makes it clear that you must define risk in two ways, the possibility of the nasty thing happening, and the time period during which it is likely that the thing will happen. With lightening strikes, I would guess this is about a one in five million risk, over a five year period. Not high.

However, whilst the time factor is important, people don’t just bend statistics by ignoring the time factor. What also happens is that people inflate the risk by using relative instead of absolute risks.

For example, the chances of dying of lung cancer, for a non-smoker, are about 0.1% (lifetime risk). If, however, you live with a heavy smoker, your chances will increase to about 0.15%. (These figures are for illustration only, and are not completely accurate).

Now, you can report this in two ways. You can state that passive smoking can increase the risk of lung cancer by 0.05% – one in two thousand. Or, you can state that passive smoking increases the risk of lung cancer by fifty per cent (0.15% vs 0.1%). Both figures are correct. One is increase in absolute risk, the second the increase in relative risk.

If you are an anti-smoking zealot, then I would imagine you would prefer to highlight the second figure. The relative risk figure. And when it comes to reducing cardiovascular risk, exactly the same procedure is used (in reverse).

Let’s say that the chance of dying of CHD over the next five years, in a healthy fifty-five year-old, is 1%. By reducing this risk to 0.2%, you can claim to have reduced the relative risk of dying of CHD by 80%. The absolute risk reduction is 0.8%. Mangling statistics is easy when you know how. It’s even fun.

Anyway, now you know the difference between a relative risk and an absolute risk, and I hope this makes it easier for you to hack your way through the misinformation that spews forth from the great medical research machine.

By the way, I believe the Polypill will achieve a 0.00% absolute and relative risk reduction. But we shall see.



The Untainted Mind


A few weeks ago, a sixth year student at Westminster School sent me an essay she had written on cholesterol, and why it does not cause CHD. She wants to go to medical school. No one made her do any of this. She just looked at the evidence and made her mind up.  She wrote me this e-mail

Dear Dr Kendrick,

I am a final year student at Westminster School who intends to study medicine. I am extremely interested in your research and reading your book enthused my and led me to spend a large portion of my time researching studies which you and other authors on the same topic have referenced.  The Chief Medical officer came to speak to us today and after her talk I quizzed her about what I have read in your book as well as a large wealth of research I have done myself. (Attached, if you care to look, is a copy of an essay I wrote which won the top prize in school essay competition based on this research). She was extremely defensive of the cholesterol causes heart disease hypothesis and claimed that NICE had on a population level declared this to be the case. She said that the evidence did not add up on a small study level, but when studies were put together (I assume by NICE) that the conclusion is in favour of cholesterol causing CHD.

I would love to know your thoughts on this and where I can find this population based evidence.

Kind regards,

Francesca Greenstreet

I wrote back to her, to say that there was no population based evidence. Or, if there was, it very clearly demonstrated no link between cholesterol levels and heart disease. The Chief Medical Officer was just blustering – as most people do when confronted with someone who dares to question medical dogma.

I thought her essay was extremely well written and makes all the points that I have been making for years. It is just gratifying to see that the evidence on cholesterol and heart disease is clear to anyone with a brain.

In Defence of Cholesterol

The  American government, the British government and the NHS, three venerable bodies respected as sources of dietary advice, currently recommend a diet low in saturated fat and cholesterol.[1] The predominant  reason this advice is given is the accepted belief held within the scientific community that high serum cholesterol levels are linked causally with the accumulation and build up of atheromas which lead to atherosclerosis and Coronary Heart Disease (CHD).

The commonly accepted and taught theory which links cholesterol to heart disease, the Lipid Hypothesis, states that cholesterol is carried from the liver to the rest of the body’s cells in Low Density Lipoproteins (LDLs) and carried back from the rest of the body’s cells to the liver in High Density Lipoproteins (HDLs). After being transported back to the liver by HDLs, Cholesterol is broken down by the liver or passes out of the body as a waste product. The Lipid Hypothesis states that eating saturated fat raises LDL levels. The cholesterol from LDLs forms fatty deposits, atheromas, which build up beneath the endothelium of the arteries. The build up of atheromas narrows the arteries and pieces of the atheromas can break off and become lodged in narrower arteries .Clots can form in the narrowed arteries which prevent blood flow and can starve organs of oxygen and nutrients. When clots or blockages form in the coronary arteries, necrosis occurs. This leaves part of the heart muscle not contracting and relaxing and can lead to a myocardial infarction.[2]

Figure 1: Sudan-stained aorta of a rabbit fed 61 egg yolks over a 70-day period, showing lesions in red.

Figure 1: Sudan-stained aorta of a rabbit fed 61 egg yolks over a 70-day period, showing lesions in red.

The Lipid Hypothesis was brought to attention following a series of studies, the first of which was carried out by Anitschkow, a Russian scientist, in 1913. Anitschkow fed rabbits a diet of purified cholesterol dissolved in sunflower oil and examined the cells and the arteries of the rabbits after killing them. [3] Rabbits which were fed the purified cholesterol were found to have vascular lesions which bore a close resemblance to atheromas found in humans (Figure 1). Following Anitschkow’s study, Dr John Gofman led a team to similar findings and hypothesized that serum cholesterol was the cause of the lesions developing.[4] The similarity of the lesions to those found in humans suffering from CHD was catalytic in the formation of theories that a high cholesterol diet might be linked to CHD in humans.

The ideas behind the Lipid Hypothesis were formalised by Ancel Keys when, in a study in 1953, he used data from six countries to show a direct link between the percentage calories from fat in the average diet and the number of CHD deaths per 1000.[5] Furthermore, he found the incidence of CHD deaths in those six countries was best predicted by the intake of saturated fat.[6]

However, not all scientists and physicians are in agreement with the Lipid Hypothesis. Regarding Anitschkow’s rabbit study, it has been pointed out that cholesterol does not form part of the natural diet of a rabbit and thus it is possible that the rabbits had an allergic reaction to the high cholesterol diet, or that they were otherwise incapable of processing the chemical. It is significant to note that similar experiments carried out on dogs and rats showed that a rise in blood cholesterol did not lead to a rise in atherosclerosis.[7] This is potentially due to the fact that dogs and rats, unlike rabbits, consume cholesterol as part of their natural diet. The lack of cholesterol in a rabbit’s natural diet, combined with the failure to replicate the findings in dogs or rats, whose natural diets are much more similar to our own, is a significant flaw in the reasoning behind Anitschkow and Gofman’s conclusion: that a high cholesterol diet is linked to atherosclerosis in humans.

Figure 2: Keys’ (1953) selection to show relationship of fat intake to heart disease deaths of 55–59 yr. old men in 1951–53 (open circles left)and the 15 other available countries (closed circles). The relation of heart diseases to animal protein intake is on the right (Mann, 1993). (Adapted from WHO Ann. Epid. and Vital Statistics).

Figure 2: Keys’ (1953) selection to show relationship of fat intake to heart disease deaths of 55–59 yr. old men in 1951–53 (open circles left)and the 15 other available countries (closed circles). The relation of heart diseases to animal protein intake is on the right (Mann, 1993). (Adapted from WHO Ann. Epid. and Vital Statistics).

Another flaw in the Lipid Hypothesis is that Ancel Keys selected with purpose the countries for which he presented data in his study in 1953, rather than choosing them at random. “Yerushalmy and Hilleboe (1957) observed that Keys would have had available data from 22 countries, which would have given a much weaker correlation “(Figure 2).[8]

Figure 2 shows a very weak correlation between deaths per 1000 (from CHD) and percentage of calories from fat when all 22 countries are plotted on the same graph. It is interesting to note that the correlation between deaths per 1000 (from CHD) and percentage of calories from animal protein has a similar and even slightly stronger  correlation than between deaths per 1000 (from CHD) and percentage of calories from fat.  All of this data would have been available to Keys, so his focus on the link between percentage of calories from fat and the number of deaths per 1000 (from CHD) is curious.

The data sample presented by Keys gives a correlation of coefficient of +0.84, a strong positive correlation, whereas “in the simulation study by Wood (1981) on the consumption statistics of 21 countries a total of 116280 different samples of six countries were found, and the correlation between consumption of animal fat and CHD mortality varied from -0.9 to +0.9, the average being    -0.04.”[9] Such a difference in correlation coefficients between similar studies indicates some bias in Keys’ selection of the six countries or insufficient data, since Wood’s study uses many more countries and therefore is more likely to be accurate. As it is obvious that Keys had sufficient access to data from the 22 countries, it seems that his selection was biased.

There have also been many studies which investigate serum cholesterol level in relation to atherosclerosis and CHD in Humans rather than in animals. A notable example is the study led by Paterson  entitled: “Serum Cholesterol Levels in Human Atherosclerosis”. 800 patients who were permenantly confined to hospitals and 100 war veterans who were in hospital for dimiciliary care were given 2500-3000 calories a day in their daily diet, of which 25 to 35% was derived from fat. Serum cholesterol was determined annually or semi-annually and when any patients died, the severity of atherosclerosis was determined using six differnet criteria: crude morphological grading, measurement of the thickness of the largest plaque, determinations of the total lipid content, lipid concentration, total calcium content and calcium concentration. Figure 3 shows a graph showing the abscence of a correlation between Serum Cholesterol in mg.% and Total Lipid in Mg. This shows that for the criterium of total lipid content, there is no correlation in the age group of 60-69 years.

Figure 3: Total coronary artery lipid and serum cholesterol levels in patients 60-69 years. The open circles represent cases without complications of coronary atherosclerosis; the closed circles, cases with complications.

Figure 3: Total coronary artery lipid and serum cholesterol levels in patients 60-69 years. The open circles represent cases without complications of coronary atherosclerosis; the closed circles, cases with complications.

Similar findings were observed in the other age groups with a significant number of participants (70-79 and 80-89). The study concludes: “In the 58 cases in the age group 60-69 years, significant relationships between the serum cholesterol and the severity of the disease were found only once in 40 statistical analyses, and the complications of atherosclerosis were just as frequent in cases with low serum cholesterol levels (150-199 mg. %) as in cases with moderately high ones (250-299 mg. %).”[10]Considering the emphasis from the government and the NHS to reduce cholesterol and saturated fat intake because cholesterol causes heart attacks, this seems to be a remarkably weak correlation.

The Paterson study was not alone in its findings: Sigurd Nitter-Hauge and Ivar Enge published a study in The British Heart Journal in 1973 which reported: “No significant correlation was found when total coronary arterial score was correlated to serum cholesterol values or to triglycerides.”[11]

Not only is there strong evidence to show that serum cholesterol levels have no link to atherosclerosis, but there is also strong evidence to suggest that high cholesterol consumption does not raise blood cholesterol levels. The Framingham Heart Study, which set out to prove that eating more cholesterol in your diet increases your blood cholesterol levels, in fact showed that there was minimal difference in the blood cholesterol levels of the subjects despite subjects consuming cholesterol in widely varying amounts. [12] Scientists working on the Framingham Heart Study also studied the intake of saturated fats but eventually concluded: “There is, in short, no suggestion of any relation between diet and the subsequent development of CHD in the study group.”[13] It is difficult to stress the importance of this finding enough: there was no connection found whatsoever between diet and the development of CHD.

Further evidence that eating a diet high in saturated fat does not lead to CHD was published in The American Journal of Clinical Nutrition in 1981. The study compared the diets of two populations of Polynesians living on atolls near the equator. It also assesses the effect the diets have on the serum cholesterol levels in the populations. One of the populations, the Tokelauans, obtained a very high percentage of energy from coconut (high in saturated fat) compared to the Pukapukans, 63% compared with 34%. The Tokelauans had serum cholesterol levels 35-40mg higher than the Pukapukans. However , “vascular disease is uncommon in both populations and there is no evidence of the high saturated fat intake having a harmful effect in these populations.”[14]

Taking all these studies into account, it would appear that not only does having a high serum cholesterol level not have any connection to CHD, but that a diet high in cholesterol does not lead to high blood cholesterol levels and that a diet high in saturated fat does not have any link to CHD.

One final argument used to support the Lipid Hypothesis is the apparent effectiveness of statins in treating CHD. If, so the argument goes, statins reduce levels of serum cholesterol and they also reduce the risk of CHD, then reducing serum cholesterol levels must be the reason for the lower incidence of CHD. However, this reasoning contains two fallacies: firstly it assumes that statins have been shown to reduce the risk of CHD, and secondly it assumes that lowering serum cholesterol levels is the only effect of statins that could lower the incidence of CHD.

Both of these assumptions are false. A study was carried out by the University of British Columbia, part of the not-for-profit Cochrane collaboration, which concluded: “If cardiovascular serious adverse effects are viewd in isolation, 71 primary prevention patients have to be treated with a statin for 3 to 5 years to prevent one myocardial infarction or stroke.”[15] Small mortality benefits from statins have been shown for high-risk middle aged men.[16], [17] However, these trends are not seen in women and the elderly.15, 16 Even an advertisement for LIPITOR (atorvastatin calcium), one of the best-selling statins in America, has a disclaimer which includes: “LIPTOR has not been shown to prevent heart disease or heart attacks.”[18]

For the small minority of people who are protected  by statins, there is another explanation. Statins have been repeatedly shown to act as “potent anti-inflammatory” agents in patients with cardio vascular disease[19]. The reason for their effects in reducing incidence of CHD could be due to those effects rather than the reduction of serum cholesterol levels. This means that it is innappropriate to use the limited protection against CHD by statins as evidence for high serum cholesterol levels being a cause of CHD.

Gathering together the arguments made in this essay, we can conclude that it is very likely that there is absolutely no causal correlation between high cholesterol, either in the serum or in the diet, and CHD. Nor is there any causal correlation between a diet high in saturated fat and CHD. The emphasis placed on the Lipid Hypothesis by the government and other organisations concerned with public health is potentially due to the inital panic after the publication of Keys’ and Anitschkow’s studies. The feeling of urgency to act in order to prevent ever increasing numbers of deaths from CHD led to premature acceptance of the Lipid Hypothesis without sufficient evidence. The long term effect of this view has been the demonisation of diets high in saturated fat and cholesterol without sufficient justification from otherwise reputable organisations for the past thirty years.

Word count : 2431 words

(excluding title, name, biliograph and references)


“Trick and Treat” (Barry Grroves,2008)

“The Great Cholesterol Con” (Dr Malcolm Kendrick, 2007)

“The Cholesterol Myths” (Uffe Ravnskov, M.D., Ph.D., 2000)

“Seven Countries: A Multivariate Analysis of Death and Coronary Heart Disease” (Ancel Keys, 1980, Introduction, p. 1-17)

KIM CRAMER, SVEN PAULIN, LARS WORKÖ, 1966. Coronary Angiographic Findings in Correlation with Age, Body Weight, Blood Pressure, Serum Lipids, and Smoking Habits. Circulation; 33:888-900

U. RAVNSKOV, 2002. Is Atherosclerosis caused by high cholesterol?. Q J Med; 95:397-403

Prevention of Coronary Heart Disease. British Medical Journal , 21 September 1968; No. 5620, p.689

Sigurd Nitter-Hauge, Ivar Enge, 1973.  Relation between blood lipid levels and angiographically evaluated obstructions in coronary arteries British Heart Journal. 35, 791-795.

J. R. CROUSE, J. F. TOOLE, W. M. MCKINNEY, M. B. DIGNAN, G. HOWARD, F. R. KAHL, M. R. MCMAHN, G. H. HARPOLD, 1987. Risk factors for extracranial carotid atherosclerosis. Stroke; 18:990-996

Mukesh K. Jain, Paul M. Ridker, 2005. Anti-Inflammatory Effects of Statins: Clinical Evidence and Basic Mechanisms, Nature Reviews Drug Discovery 4. 977-987

Ian A. Prior, M.D., F.R.C.P., F.R.A.C.P., Flora Davidson, B.H.Sc., Clare E. Salmond, M.Sc., and Z. Czochanska, DIP.AG., 1981. Cholesterol, coconuts, and diet on Polynesian atolls: a natural experiment: the Pukapuka and Tokelau Island studies. The American Journal of Clinical Nutrition 34, p. 1552-1561.

Kannel WB, Gordon T., 1970.The Framingham Diet Study: diet and the regulations of serum cholesterol (Sect 24). Washington DC, Dept of Health, Education and Welfare.

J.C. PATERSON, M.D., LUCY DYER, M.Sc. and E.C. ARMSTRONG, M.D., London, Ont., 1960. Serum Cholesterol Levels in Human Atherosclerosis. Canad. M. A. J., 1960, vol. 82

Scandinavian Simvastatin Survival Study Group, 1994. Randomised trial of cholesterol lowering in 4444 patients with CHD: the Scandinavian Simvastatin Survival Study (4S). Lancet; 344: 1383-1389

Kalle Maijala, 2000. Cow milk and human development and well-being. Livestock Production Science 65 1–18

Daniel Steinberg, 2004. Review series: The Pathogenesis of Atherosclerosis. An interpretive history of the cholesterol controversy: part I, The Journal of Lipid Research, 45, 1583-1593.

GOFMAN, J.W.;LINDGREN, F.; ELLIOT, H.; MANTZ, W.; HEWITT, J.; STRISOWER,B.; HERRING, V.; LYON, T.P., 1950.The role of lipids and lipoproteins in atherosclerosis,  American Association for the Advancement of Science  Vol. 111pp. 166-171; 186

National Service Framework for Coronary Heart Disease – Modern Standards and Service Models, March 2000.




Figure 1: Daniel Steinberg, 2004. Review series: The Pathogenesis of Atherosclerosis. An interpretive history of the cholesterol controversy: part I, The Journal of Lipid Research, 45, 1583-1593.

Figure 2: Kalle Maijala, Cow milk and human development and well-being, Livestock Production Science 65 (2000) 1–18

Figure 3: J.C. PATERSON, M.D., LUCY DYER, M.Sc. and E.C. ARMSTRONG, M.D., London, Ont., 1960. Serum Cholesterol Levels in Human Atherosclerosis. Canad. M. A. J., 1960, vol. 82


[1] http://www.health.gov/dietaryguidelines/dga2000/document/choose.htm

[2] http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001224/

[3] Daniel Steinberg, 2004. Review series: The Pathogenesis of Atherosclerosis. An interpretive history of the cholesterol controversy: part I, The Journal of Lipid Research, 45, 1583-1593.

[4] GOFMAN, J.W.;LINDGREN, F.; ELLIOT, H.; MANTZ, W.; HEWITT, J.; STRISOWER,B.; HERRING, V.; LYON, T.P., 1950.The role of lipids and lipoproteins in atherosclerosis,  American Association for the Advancement of Science  Vol. 111pp. 166-171; 186

[5] “Trick and Treat” (Barry Groves, 2008, p.61-62)

[6] “The Cholesterol Myths” (Uffe Ravnskov, M.D., Ph.D., 2000, out of print – available at: http://www.ravnskov.nu/myth4.htm)

[7] “Trick and Treat” (Barry Groves, 2008, p.59)

[8] Kalle Maijala, Cow milk and human development and well-being, Livestock Production Science 65 (2000) 1–18

[9] Kalle Maijala, 2000. Cow milk and human development and well-being. Livestock Production Science 65 1–18

[10] J.C. PATERSON, M.D., LUCY DYER, M.Sc. and E.C. ARMSTRONG, M.D., London, Ont., 1960. Serum Cholesterol Levels in Human Atherosclerosis. Canad. M. A. J., 1960, vol. 82

[11] Sigurd Nitter-Hauge, Ivar Enge, 1973.  Relation between blood lipid levels and angiographically evaluated obstructions in coronary arteries British Heart Journal. 35, 791-795.

[12]“Trick and Treat” (Barry Groves, 2008, p.63)

[13] Kannel WB, Gordon T., 1970.The Framingham Diet Study: diet and the regulations of serum cholesterol (Sect 24). Washington DC, Dept of Health, Education and Welfare.

[14] Ian A. Prior, M.D., F.R.C.P., F.R.A.C.P., Flora Davidson, B.H.Sc., Clare E. Salmond, M.Sc., and Z. Czochanska, DIP.AG., 1981. Cholesterol, coconuts, and diet on Polynesian atolls: a natural experiment: the Pukapuka and Tokelau Island studies. The American Journal of Clinical Nutrition 34, pp. 1552-1561.

[15] “The Great Cholesterol Con” (Dr Malcolm Kendrick, 2007, p.164-165)

[16] “Trick and Treat (Barry Groves, 2008, p.52)

[17] Scandinavian Simvastatin Survival Study Group, 1994. Randomised trial of cholesterol lowering in 4444 patients with CHD: the Scandinavian Simvastatin Survival Study (4S). Lancet; 344: 1383-1389

[18] http://www.westonaprice.org/cardiovascular-disease/dangers-of-statin-drugs

[19] Mukesh K. Jain, Paul M. Ridker, 2005. Anti-Inflammatory Effects of Statins: Clinical Evidence and Basic Mechanisms, Nature Reviews Drug Discovery 4. 977-987

Potassium, your invisible friend

I recognise that I spent a lot of time telling people what does not cause heart disease, and what does not protect against heart disease. My sister told me… ‘well, what advice would you give people, then?’ I usually shrug my shoulders and reply ‘there is no shortage of advice around, I don’t think I need to add to the daily bombardment.

However, I shall break the habit of a lifetime and, with slight trepidation, announce that I strongly believe that Potassium is good for you.  If you consume more of it you will, most likely, live both longer and in better health.

How much should you consume? A couple of extra grams a day should do the trick. Having said this, I do recognise that most people will not have the faintest idea how much potassium they consume and, frankly, neither do I. But you are probably not consuming enough, and your kidneys will easily get rid of any excess.

For those who are not keen on bananas, spinach and broccoli, and other foods high in potassium, you could take it as a tablet. Potassium bicarbonate or potassium citrate appears to be the best formulation. Depending on which brand you decide to buy, it should cost about £15 – 20/year.

Why this sudden potassiumophilia? Well, there is a growing body of research which points to the fact that potassium is very good for you. The first time I became aware that it might be good for you was when I first looked at the Scottish Heart Health study. The researchers looked at twenty seven different ‘factors’ they thought might cause, or protect against, heart disease – and overall mortality.  The authors noted that:

“[There was] an unexpectedly powerful protective relation of dietary potassium to all-cause mortality,” the study concluded.

The paper showed that:

  • Men consuming an average of 5400 mg of potassium per day vs 1840 mg were 55% less likely to die during 7.6 year study (the highest one-fifth of men vs the lowest one-fifth of men)
  • Men consuming an average of 5400 mg of potassium per day vs 3350 mg were 22% less likely to die during 7.6 year study (the highest one-fifth of men vs the second highest one-fifth of men)
  • Women consuming an average of 4500 mg of potassium per day vs 1560 mg were 59% less likely to die during 7.6 year study (the highest one-fifth of women vs the lowest one-fifth of women)
  • Women consuming an average of 4500 mg of potassium per day vs 2700 mg were 15% less likely to die during 7.6 year study (the highest one-fifth of women vs the second highest one-fifth of women

The study can most easily be found here http://www.ncbi.nlm.nih.gov/pubmed/9314758

I immediately liked this finding. Mainly because it was almost completely unexpected, and unexpected findings are always far more likely to be correct than expected findings. Also, this was a very large effect indeed.  It turned out that increased potassium consumption was very nearly as protective as smoking was damaging.

Of course, this was an observational study, so I filed it under – most interesting – but did nothing much more about it. As the authors said themselves: ‘ Potassium excretion was very significantly related to risk of death from all causes, having a protective role, whereas its role in coronary events was weaker and that of sodium excretion weak and even paradoxical. These results are unifactorial, without correction other than for age and sex. Our findings need corroboration from elsewhere and more detailed analysis with more events from longer follow-up.’

Since then, a large number of other studies have followed up, and appear to have confirmed that potassium has considerable health benefits. Some of these studies were not just observational, they were interventional. Here is summary of the potential beneficial effects. Potassium:

  • lowers blood pressure
  • lowers the risk of arrhythmias
  • lowers the risk of cardiovascular disease
  • lowers the risk of stroke
  • lowers the risk of heart attacks
  • lowers the risk of cancer, and
  • lowers the risk of death

These benefits have been confirmed in a number of different studies.  However, as this is a blog, I am not going to turn it into a medical paper and provide references for every statement, so I will stick to a couple of referenced studies. (If enough people are interested I can point you at additional papers).

With regard to blood pressure, a study published in 1997 found that adding roughly 2 grams (2000 mg) of potassium per day lowered blood pressure in older people by 15/8 mm Hg. As good, if not better, than any antihypertensive drug1.  And with no side-effects at all.

When it comes to stroke, it has been found that having a low potassium level is a very potent risk factor for both bleeding (haemorrhagic) and clotting (ischaemic strokes). In an American study it was found that in those with low potassium levels the relative risk of ischaemic stroke increased by 206%. The relative risk increased by 329% for haemorrhagic stroke2.

Admittedly, these two studies were done in people with high blood pressure to start with, but these effects are also found in healthy people.  However, to my mind, the most important thing about potassium is that I cannot find any study, anywhere, which suggests that increasing potassium consumption may be harmful. In short, it seems to be something that does only good.

I do recognise that a lot of doctors will shudder at the thought of adding potassium to the diet, as they have all been taught that a high potassium level is something terribly dangerous. A condition  that needs immediate treatment, or else it will cause arrhythmias and death.

It is true that you need to be careful of adding potassium to the diet of patients taking medications that can raise potassium levels. These are mainly drugs used to lower blood pressure. However, even in this group the risk of overdosing on potassium is exceedingly small. For everyone else the risk seems to be zero. This is why I now recommend potassium supplementation as a good way to live a longer, healthier life.

My goodness, I think this is the first time I have ever recommended a dietary supplement. Must go and lie down.

1: ‘Long term potassium supplementation lowers blood pressure in elderly hypertensive subjects’ Fotherby M.D. et al: Int J Clin Practice 1997 41(4): 219 – 222)

2: Smith NL, et al: ‘Serum potassium and stroke risk among treated hypertensive adults.’ Am J Hypertens. 2003 Oct;16(10):806-13

I told you so (The Obesity Initiative)

Don’t trouble me with the facts my mind is made up.’ Foghorn Leghorn

So, now the great obesity initiative is to be rolled out across the UK, driven by the UK Academy of Medical Royal Colleges (AOMRC). Some time ago I wrote a blog in which I outlined exactly what they would say….and lo, they have said it. The main recommendations are:

  • Food-based standards to be mandatory in all UK hospitals
  • A ban on new fast food outlets being located close to schools and colleges
  • A duty on all sugary soft drinks, increasing the price by at least 20%, to be piloted
  • Traffic light food labelling to include calorie information for children and adolescents – with visible calorie indicators for restaurants, especially fast food outlets
  • £100m in each of the next three years to be spent on increasing provision of weight management services across the country
  • A ban on advertising of foods high in saturated fats, sugar and salt before 9pm
  • Existing mandatory food- and nutrient-based standards in England to be statutory in free schools and academies

There is more such stuff, mainly about taxing and banning. It was all wearyingly predictable. This is exactly what the ‘experts’ have been saying for the last thirty years – this time with an ‘amazing 50% added legislation’. If what you have been doing doesn’t work. Then redouble your efforts, with added punishments. That’ll work. Just like prohibition worked in the states.

Even if these were the right things to do, and had some chance of working, I would not support them. Social control through legislation absolutely must be the last resort of a democratic society. Making people do what is good for them….hmmm. Aldous Huxley had something to say on this matter. That, however, is a broader issue.

Looking specifically at some of the recommendation, starting with the concept of putting a duty on all sugary soft drinks. This will inevitably mean that people will drink more ‘diet’ drinks- without sugar in them. Will this be a good idea? Well, here is a study from the USA, and the conclusions thereof:

‘Findings from this cohort of adolescents yielded strong evidence for cross-sectional associations between diet soda consumption with weight status in both boys and girls. Specifically, youth who consumed diet soda were more likely to have a higher BMI and PBF (percentage body fat) compared to those who did not.’ http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3402912/

This is consistent with other studies which show that drinking ‘diet’ soda is strongly associated with a greater risk of obesity than drinking sugary soft drinks. Such evidence is not hard to find. It is rather more difficult to interpret, but that is – again – another issue.

As for trying to reduce saturated fat consumption. I can say here and now that there is not one molecule of evidence to suggest that saturated fat consumption causes obesity. Not one. As for impact on heart disease….again, nothing.

My favourite quote on this comes from the Framingham study. The single most influential study on heart disease in the world.

‘In Framingham, Massachusetts, the more saturated fat one ate, the more cholesterol one ate, the more calories on ate, the lower people’s serum cholesterol.’ Dr William Castelli, Director of the Framingham study. 1992

[Not that I think cholesterol has anything to do with heart disease, but for those of a conventional view point, lowering cholesterol is supposed to be a good thing].

As for salt….where did this come from? I have yet to see any evidence linking increased salt intake to obesity. And why would it. How could it? Salt has no calories in it; it has no impact on any metabolic parameters that I know of. And I would challenge anyone to show me any evidence from any controlled randomised study that salt restriction (in health adults) has any benefits on cardiovascular disease.

I could go on, and on. But the main point is that the ‘experts’ are trapped with a mind-set that they cannot and will not change. Like all the best zealots, they know what the causes of obesity are. To misquote from Terminator.

‘Listen, and understand. That obesity initiative is out there. It can’t be bargained with. It can’t be reasoned with. It doesn’t feel pity, or remorse, or fear. And it absolutely will not stop, ever, until you are dead.’

How Flora and The British Heart Foundation disproved the existence of the Higgs Boson – or maybe not


Energy cannot be created or destroyed, merely converted to a different form. And matter, as we all know, is a form of highly concentrated energy.

Looking up Wikipedia I discovered that one gram of matter contains 9.0×1013 joules. (Theoretical total mass-energy of 1 gram of matter). This is approximately the same energy yield as the fat man atomic bomb used in World War Two.

However according to Flora and the British Heart Foundation (who have joined forces to inform the world of the terrors of saturated fat, and cholesterol, and the benefits of Flora), ten grams of matter can easily be gained or lost on the average kitchen stove.

How so, you may wonder. Surely, losing ten grams of matter would create a serious risk of releasing enough energy to wipe out a major city, and all residents contained within. Not so, it seems that if you fry an egg, it weighs 60grams. However, if you boil an egg, it weighs 50grams. See the Flora BHF poster for further detail on this remarkable fact: http://www.flora.com/PDFAuth.aspx?redirectURL=/Resources/others/pdf/HCPPdf/Fat%20Swaps.pdf

Ten grams of matter can simply disappear when you boil an egg? Quite remarkable. I think we should ask CERN to close down the large hadron collider straight away. Their search for the Higgs Boson, the reason why mass exists, and naïve reliance the Unified Field Theory itself, are clearly misguided.

All you need do, to disprove the existence of the mass/energy equation is boil an egg, and ten grams of matter simply disappear. 900,000,000,000,000 joules of energy……just gone. How remarkable is that.

But the wonders of Flora and the BHF do not stop with disproving the existence of the Higgs Boson, and the uselessness of all theoretical physicists. They can also do maths which prove that you can alter the amount of matter contained within the egg as well.

According to this self-same remarkable British Heart Foundation/Flora poster, a fried egg contains 2.4 grams of ‘bad’ fat, and 4.5 grams of good fat.  On the other hand a boiled egg contains a mere 1.6 grams of ‘bad’ fat and 3.0 grams of good fat. So, eating a boiled egg means that you reduce intake of ‘bad’ fat by 0.8 grams. (Bad fat is saturated fat, by the way).

For those of you with a mathematical bent, you may have noticed that if  a fried egg weighs 60g, and boiled egg weighs 50g, it is 20% heavier. Yet it manages to contain 50% more bad fat (2.4g/1.6g = 1.5). Aha, you might be thinking, when you fry an egg good fat (polyunsaturated), is converted to saturated fat – or something of the sort.

Well, clearly not so (and biologically impossible). Because a fried egg also contains 4.5 grams of good fat, whilst a boiled egg contains 3.0 grams of good fat. So, the ratio of good fat in a fried egg and a boiled egg is also 1.5 (3.0/1.5 = 1.5). In other words, exactly the same ratio as in a fried egg.

So, not only do fried eggs weigh more – 20% more. They also contain significantly more good and bad fat – 50%, at the same time. Bringing all this information together we find that, according to the scientists at Flora and the BHF, a fried egg ends up 1.2 times as massive as boiled eggs and contains 1.5 times as much bad and good fat at the same time. Yes, of course.

My solution to all this is simple, sneak up on the eggs from behind, and damn well fry the ones that thought they were going to be boiled. In this way you can reduce bad fat in a fried egg from 2.4 grams to 1.6 grams. Hah! I bet the scientists in Flora never thought of that – did they.

I am so glad that the British Heart Foundation have brought keen scientific rigor to their partnership with Flora. If I wasn’t laughing, I’d be crying.

Real Life vs. Pharma Company Studies


At what point, exactly, does credibility snap? When does the difference between what we are told, and what we observe, reach such a state of dissonance that it is no longer possible to believe both. Sometimes it seems the answer is ….never.

Here is one example. The clinical trials on statins found that they have virtually no adverse effects. Or, to be a little more accurate, that adverse events were virtually identical to placebo. Here, for example, is part of the press release from the Heart Protection Study (HPS).This was the last major placebo controlled statin study done in people with already diagnosed cardiovascular disease.

As the benefits of statins are now thought so wonderful it would be considered unethical to do a placebo controlled study anymore. You would be withholding statins from people who need them. Which means that you are not going to get any more evidence in this area – ever again. The HPS results were published around ten years ago, and the press release contained the following

‘Although muscle pain was reported by the participants, this happened about as commonly among those allocated the active simvastatin as among those allocated the placebo tablets. Despite 20,536 randomised patients having been followed for an average of five years, blood tests among people reporting muscle symptoms found only 11 simvastatin-allocated patients and 6 placebo-allocated patients with a rise in the muscle enzyme creatine kinase (CK) to more than 10 times the upper limit of normal Of these, 14 met the definition for “myopathy” (i.e. muscle symptoms associated with such CK elevations) of whom 10 were in the simvastatin group and 4 in the placebo group.’


Teasing these figures out a little more it seems that an extra six people taking simvastatin suffered muscle ‘problems’ than those taking the placebo. This is six people, out of more than ten thousand taking simvastatin. This represents in one thousand seven hundred and eight 1/1708 (over five years).

If this were true, then muscle problems should be exceedingly rare. The average GP with about two hundred of their fifteen hundred patients taking a statin should see a patient with muscle pains/problems about once every twenty five years. At this rate, you would not even know you had a problem.

Yet, wrapped around my copy of the BMJ last week was an advert for rosuvastatin [Crestor]. The strap line shouted out ‘Myalgia on his initial statin?’ [Myalgia is the medical word for muscle pain]. The main message the advert was… ‘If your patient was suffering muscle pains on their initial statin, they should switch to Crestor 5mg.’

Their ‘initial statin’ will almost certainly be Simvastatin 40mg. The drug, and the dose, used in the HPS study. The same drug, and the same dose recommended by the National Institute of Clinical Excellence (NICE).

Now, you do not run an expensive advertising campaign without doing a lot of market research first. What the market research must have told AstraZeneca – who make Crestor – is that a lot of people are suffering muscle pains on 40mg simvastatin.

Which means that simvastatin, which caused no discernible increase in muscle pains in the clinical study…… actually creates such a massive burden of muscle problems that a pharmaceutical campaign is running a major advertising campaign highlighting this, exact, adverse event.

What does this tell us, gentle reader? It tells us many things. Some of which would be considerable slanderous if I said them out loud. The most outstanding thing it tells me is that, although we have all been repeatedly informed that statins have no more side-effects than placebo, I now find that AstraZeneca encouraging doctors to switch statins due to the burden of side-effects.

F Scott Fitzgerald opined that …“The test of a first-rate intelligence is the ability to hold two opposed ideas in the mind at the same time, and still retain the ability to function.’

I would suggest that there comes a point where you have to decide between which idea is right, and which is wrong. With regard to statins, I did this many years ago when I recognised that they cause a gigantic burden of adverse effects, with muscle pain the single most outstanding. I knew that the clinical trials had somehow or another managed to bury this fact.

Yet, when I speak to most doctors they continue to tell me that statins have very few side-effects, as do most opinion leaders. This belief, whilst AstraZeneca starts up an advertising campaign based on side-effects reported by doctors. F Scott Fitzgerland would be impressed by all these first class intellects. I just despair of them.



Data Manipulation – Gosh Really


Now that Ben Goldacre’s book Bad Pharma has come out, exposing the fact that much medical research is controlled by, and manipulated by, the pharmaceutical industry, I thought I should revisit a short article I wrote six years ago:


Gosh, Really, You Don’t Say:

Sometimes you read something of such blinding obviousness (if that is actually a word), that you wonder why anyone even bothered writing it at all. You know the sort of thing – ‘constant criticism of children does not lead to a sense of self-worth.’ ‘A centralized command economy does not create wealth for citizens.’

But the blindingly obvious can be critically important depending on who says it. I can bang on and on about the fact that medical journals have basically turned themselves into advertorials for the pharmaceutical industry, and be readily dismissed as a fringe lunatic.

However when Richard Smith, editor of the British Medical Journal (BMJ) for many years who resigned last year, says it, then it would seem that even the cosy ‘establishment’ may be starting to feel the first cold fingers of doubt creeping in. Perhaps things really have started to go too far. So read and enjoy a short section from an article in the BMJ, 21st May 2005.

Medical journals are no more than ‘an extension of the marketing arm of pharmaceutical companies’ because a large proportion of their revenue comes from drug advertisements and reprints of company funded trials, claims former BMJ editor, Richard Smith.

“Dr. Smith argues that although medical journals make a sizeable income from drug advertisements this is the least of their ‘corrupting form of dependence’ on the industry, since the advertisements are ‘there for all to see and criticize’.

“Dr Smith’s strongest criticism is levelled at the fact that journals publish clinical trials that are funded by the industry. Unlike advertisements, trials are seen by readers as the highest form of evidence, he says. Trials funded by drug companies rarely produce unfavourable results and make up between two thirds and three quarters of the trials published in key journals.

“The potential profits from reprints of such a trial can run to $1m (£0.5m; €0.8m), says Dr Smith. And it is this potential income that can have the biggest corrupting influence on a journal because many editors are charged with ensuring their journal makes a profit.

“Editors may be confronted by ‘a frighteningly stark conflict of interest’, writes Dr Smith They may be forced to choose between publishing a trial that will bring $100,000 of profit or meet their end of year budget by making a member of staff redundant.”


Will this article in the BMJ change anything?….. You have GOT to be joking……

And you know what changed in the last six years. You got it. Nothing.

Silence was the stern reply

A friendly journalist asked me if I had seen the paper from Norway which looked at cholesterol levels heart disease and overall mortality. Amazingly, as I have sensitive antennae for such things, I had not heard of the HUNT 2 study. Not quite so amazingly, no-one else seems to have heard of it either.

Strange, in a world where the most ridiculous dietary studies are plastered across the front pages of the newspapers, and get top billing on the BBC. You know the type of thing…. Eating red meat regularly ‘dramatically increases the risk of death from heart disease’ A typical headline from the Daily Mail.

But when a ten year study looking at cholesterol levels, overall morality, and heart disease comes out….Silence. I wonder why? Perhaps it has something to do with the results. (See below) http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2753.2011.01767.x/pdf

A friendly journalist asked me if I had seen the paper from Norway which looked at cholesterol levels heart disease and overall mortality. Amazingly, as I have sensitive antennae for such things, I had not heard of the HUNT 2 study. Not quite so amazingly, no-one else seems to have heard of it either.

The graph on the left looks at overall mortality vs. cholesterol levels. The one on the right looks at ischaemic heart disease and cholesterol levels in both men and women.

As you can see, for women the story is very straightforward indeed. The higher the cholesterol level, the lower the risk of overall mortality. With regard to heart disease alone, the highest risk is at the lowest cholesterol level. For men there is more of a U shaped curve, but overall mortality is highest at the lowest cholesterol level.

This was a ten year study done in Norway, looking at fifty thousand people – with no pre-existing heart disease. So what we have here is five hundred and ten thousand years of observational data.

These findings do not surprise me in the least, for I have seen many other studies demonstrating exactly the same thing. The lower your cholesterol level, the shorter your life expectancy. Just to take one example. An Austrian study twice this size of this Norwegian one came to the following conclusions:

‘In men, across the entire age range, although of borderline significance under the age of 50, and in women from the age of 50 onward only, low cholesterol was significantly associated with all-cause mortality, showing significant associations with death through cancer, liver diseases, and mental diseases.’  http://www.ncbi.nlm.nih.gov/pubmed?term=adam%20%20eve%20cholesterol%20austria

Added together these studies looked at two hundred thousand people, with a total of two million years of observational data which is a pretty damned impressive amount of work and figures.

I am willing to bet that you have heard nothing about either of them. But how could you? The Austrian study passed by the mainstream media without a whisper, as did HUNT 2. The boy tried to shout that the Emperor had no clothes, but the crowd had stuck in ear plugs. For who wants to hear such an annoying message anyway?

Breast Screening – The Truth…

I am against over-medicalisation in all its forms. So, apart from being very skeptical about preventative medicine in the area of heart disease, I also worry about other forms of preventative medicine. Breast cancer screening is one area where the balance between benefit and harm may well slip towards harm. Yet, it is presented as an absolute good.

One man who is very critical of breast cancer screening  is Professor Peter Gotzsche, who is the clinical director fo the Nordic Cochrane Collaboration Centre, and has written a book called ‘Mammography Screening. Truth, lies and controversy.’ He outlines exactly what has been going on in this are, and makes it very clear that there are significant problems. Primarily with overdiagnosis (there are other problems, but no time for everything in one blog).

Overdiagnosis means finding ‘lumps’ of other suspcious things on mammography ‘lumps’ that would never have caused any problem.  How big is this problem. Well,  detailed pathological studies done in Australia found that in women who had died of other thngs (not breast cancer) had the following pathologies, any of which could lead to a ‘diagnosis’ of breast cancer if found on a biopsy :

Hyperplasia 12.6%
Carcinoma in situe 13%
Focal secretory changes 24.1%
Perilobular hemangioma 11.2%
Radial scars
(precursor of infiltrating ductal cancer)


In other words, a very high percentage of women have ‘cancerous’ lesions in their breasts. Yet, around 4% of women die of breast cancer.  In the words of the authors of this study…

‘….in any case, the high frequency of ductal hyperplasia and CIS (carcinoma in situ) 25.6% suggests that only a small proportion of these must ever progress to invasive carcinoma.’

If only a small proportion of ‘cancerous’ lesion actually progress to invasive carcinoma, then the majority of those found would never cause any harm to the woman. Thus overdiagnosis must be a very major problem indeed. Ironically, the more detailed an accurate screening beomces, the more overdiagnosis will occur.

Anyway, I was unsurprised to see the recent headline:

‘Breast cancer screening does ‘more good than harm’ http://www.bbc.co.uk/news/health-19571173

‘Breast cancer screening saves the lives of two women for every one patient who receives unnecessary treatment, according to a major European review. There has been a fierce debate about the use of screening, and policy is being reviewed in England.

The latest study, published in the Journal of Medical Screening, said at least seven lives were saved for every 1,000 women screened. Health charities say the findings will provide further clarity for women. Tens of thousands of women die from breast cancer across Europe each year. The effectiveness of screening programmes across the continent was evaluated in a series of studies.

It concluded that for every 1,000 women screened, between seven and nine lives were saved and four cases were over-diagnosed.. Mammograms spot dangerous tumours, increasing the chances of survival, but also detect lumps that are essentially harmless, exposing some women to undue anxiety and surgery.

Screening doesn’t just save lives today or tomorrow, it saves lives 10-20 years down the line” Prof Stephen Duffy Queen Mary, University of London.’

I know that there is no possible way that anyone can know that for every seven and nine lives ‘saved’ four cases were overdiagnosed. This is scientific nonsense. The reality is that more cases must have been overdiagnosed than future invasive cancers diagnosed.

I have asked someone to forward me the full studies on which this BBC story was based.  I have only one part of it so far, and it is a part that worries me greatly, for it makes the following statement.

‘What these papers tell us is that the time has come to move away from relying solely on the older randomized trials of mammographic screening for the evidence-base, and to use data regularly collected and monitored from service screening programmes, with proper statistical analyses in addition to the results from the randomized trials. The authors of these articles set a precedent for how this could be done effectively.’ http://xa.yimg.com/kq/groups/14947167/193204470/name/benefits%20and%20%20harms%20of%20mammograms%202012.pdf

The time has come to move away from relying on randomized trials!

Once you move away from randomized trials you are no longer doing science. You are doing dogma. At which point the truth can never, ever, be obtained. When someone tells me we should use data regularly collected and monitored from service screening programmes with ‘proper’ statistical analysis – I know that THE TRUTH is being buried.

So long science.


A sudden flash of truth


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

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

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

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

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

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

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

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

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


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

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

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

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

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

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

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

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

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

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

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


Statin Nation

If you would like to see a fascinating counterblast to the current statin promotion madness I recommend you have a look at the following film made by Justin Smith.
(A bit of self promotion here, as I am – of course – one of the stars).

I strongly recommend, and hope you can help to make it go viral. This message is needed more than ever.

How unwelcome research is discredited


I am grateful to Arie Brand for this, admittedly, rather long blog posting. He now lives in Australia, and shares my passion in medical research – and how it is often, far too often,  twisted for non-scientific reasons. He was stimulated to write this article in response to my blog on ‘losing faith’ with medical research.

For many years Arie has looked at the work of Linus Pauling – double Nobel  prize winner, and genius. In his later life Pauling turned his attention to vitamin C, and the benefits that it could have in heart disease and cancer.

I have written on the subject of Pauling’s many times, and feel that he,  and the infamous Matthias Rath, were well on the way to making some important discoveries. However, for various reasons, the mainstream research world turned on Pauling, and his work in this area.

Anyway, here is a tale of how Linus Pauling’s work was undermined, discredited and , eventually, dumped. I hope you like it. It is long, and it is packed with facts, but it represents a forensic attempt to get at the truth. Something which I completely support.

A lie gets halfway around the world before the truth has a chance to get its pants on.’ Winston Churchill


1. How to discredit unwelcome research

As far as losing faith in medical research is concerned I have got to tell a tale as well.

A few years ago a nephew of mine who is involved in cancer research in the Netherlands sent me a newspaper column by an eminent Dutch oncologist, an emeritus Professor Piet Borst, in which this worthy spoke in a rather scathing tone about Linus Pauling’s preoccupation with vitamin C, and particularly Vitamin C and cancer.

The general thrust of his little article was, yes, of course, this double Nobel laureate was a brilliant man but as far as vitamin C was concerned he had a screw loose. In the case of cancer, the professor thought that this had been proven through work done by ’ bona fide’ oncologists which appeared to contradict the results of Dr. Cameron. Dr Cameron had done some very positive studies on the use of vitamin C  in cancer in the Scottish Vale of Leven hospital – a treatment in which Linus Pauling had been Dr.Cameron’s intellectual ally.

Now Pauling (according to the journal New Scientist one of the ten greatest scientists who ever lived) has been rather a hero of mine for many years.  Starting when I managed to cope with the rather rough climate at Aberdeen  many years ago, thanks to his advice on vitamin C (or so I thought). Coincidentally, I had been appointed at Dr.Kendrick’s alma mater, Aberdeen University. Because of my personal interest in Pauling’s work, I went a bit deeper into the matter.

The essence of research in the natural sciences, including medicine, is to come up with results that can be replicated. But what if this replication is a sham designed to discredit the original inquiry? I have the feeling that this is what happened with Dr.Cameron’s (and Pauling’s) results.

There is a short summary of Dr.Cameron’s research here:


After achieving his rather remarkable results naturally he, and even more so Pauling, looked for a bona fide replication of the Vale of Leven tests by a seemingly independent research institute. It took Pauling a lot of effort to persuade the American National Cancer Institute to arrange for this (he even managed to involve President Carter). The arrangement was finally made, through the Mayo clinic. However, it is clear there never was genuine replication.

The article I have linked to quotes part of Pauling’s and Cameron’s own opinion on why this was the case. But this does not provide the whole story. In particular, it does not address the question whether one can justifiably suspect that the Mayo Institute, never intended to come up with a genuine replication in the first place.

2 The first Mayo test

Before the Mayo test started its chief investigator, the late Dr.Charles Moertel, had an exchange of letters with Pauling, in which the former claimed that he would try to replicate Dr.Cameron’s tests as exactly as possible. Pauling wrote him in reply on the 9th August 1978: “In my last letter to you I pointed out to you that the patients studied by Dr.Cameron had not received chemotherapy. The cytotoxic drugs damaged the body’s protective mechanisms, and vitamin C probably functions largely by potentiating these mechanisms. Accordingly, if you hope, as you stated in your letter, to repeat the work of Cameron as closely as possible, you should be careful to use only patients who have not received chemotherapy… On page 2 (of your letter) there is no mention of earlier chemotherapeutic treatment as a contraindication for patient eligibility.’

 I think that this question might be important however, and I recommend that you be sure that there are a sufficient number of patients enrolled who have not received chemotherapy. Otherwise the trial cannot be described as repeating the work of Cameron.”

Moertel answered to this: “Certainly in any presentation of this (sic) data I can assure you we will call attention to the fact that the majority of our patients had had prior chemotherapy, whereas in the study conducted by you and Dr.Cameron it was clearly stated that none of the patients had had prior chemotherapy.” 1

In the first report on their research Moertel and his associates do indeed clearly indicate this (New England Journal of Medicine 1979 Vol 301 No 13). They wrote: “It should be noted, however, that only nine out of our 123 patients had not previously received chemotherapy or radiation therapy.

It is therefore impossible to draw any conclusions about the possible effectiveness of vitamin C in previously untreated patients. In Cameron and Campbell’s report of a 10 per cent regression rate in 50 patients with widely disseminated cancer, none had received definitive prior treatment and presumably were more immunocompetent than our patients.”

At this point, one can justifiably ask the question why Moertel and his associates started on this bit of research in the first place because the supposed intention was that they would replicate Cameron’s tests. So, understandably, Pauling protested against the title of their report in the New England Journal, which was “Failure of high-dose vitamin C (ascorbic acid) therapy to benefit patients with advanced cancer”. They should have indicated more clearly, he thought, that the researchers had been dealing here mainly with patients who had already undergone chemotherapy.

There was, however, another marked difference with the original tests by Cameron. In the Vale of Leven hospital the patients involved in his test received their vitamin C dose intravenously during the first ten days. This did not happen in the Mayo-test.

So it was clear, as Moertel himself acknowledged, that the Vale of Leven tests had not been replicated. Pauling kept urging therefore for a second test that was finally done, years later.  But this only made matters worse. Not only was Cameron’s test again not replicated but also there were now grounds, given Moertel’s research design and his various statements and actions, to entertain doubt about his good faith.

3. The second Mayo test – Again no replication

At this point I will attempt to answer three questions:

  • Were the second Mayo tests an exact replication of the Vale of Leven tests?
  • Was the research strategy followed by Mayo in this second test “methodologically sound”- as sound as claimed in a guest editorial in the relevant issue of the NEJM by a certain Dr.Robert Wittes, then Associate Director of the Cancer Therapy Evaluation Program of the NCI
  • Are there reasons for doubting the good faith of Dr.Moertel and his associates?

Replication of the Vale of Leven tests?

Pauling and Cameron had never claimed that vitamin C could cure cancer. Their claim was far more modest. They claimed, and thought they had proved, that it could lengthen the survival time of patients deemed incurable, and enhance whatever remained of their quality of life.

Neither did Pauling and Cameron claim that vitamin C could stop the growth of the tumor, only that it could possibly delay it.  For these reasons Cameron gave vitamin C to his patients until the very end (or in some cases cure).

Though they had made this very clear in the articles they published about it in the Proceedings of the National Academy of Sciences, the Mayo team followed a different strategy. It gave patients vitamin C until these were no longer able to take this orally, or until it became clear that the cancerous tumor kept growing. So they dealt with vitamin C as if it were a cytotoxic drug that should no longer be administered after it became clear that it was not preventing tumour growth, rather than an ordinary nutritient that has no dangerous side effects even at high doses. Pauling objected to this.

The Mayo team’s haste in stopping with vitamin C was strange for another reason. They wrote in their 1985 article in the NEJM:

For this trial we elected to study patients with advanced cancer of the large bowel because this was the most frequent tumor type in the study of Cameron and Pauling and one for which they claimed a striking improvement in survival with vitamin C therapy. We felt ethically justified in studying this group of patients without first offering cytotoxic drugs because in our opinion there is no known form of chemotherapy for colorectal cancer that has been demonstrated to produce substantive palliative benefit or extension of survival.”

So why then this haste to stop administering a relatively innocuous nutritional element. They had, on their own testimony, no other effective medication to use. There was, moreover, a strange contrast with their first test. In their 1979 NEJM article about this test they wrote:

 “Treatment was continued until death or until the patient was no longer able to take medications by mouth.”

It is true that they were dealing here with patients who had already undergone chemotherapy but in reality this didn’t make any difference – for their new test group chemotherapy had been deemed to be useless anyway. So either way there was no alternative course of action for which vitamin C had to be stopped.

Once again, Cameron’s test was not replicated.

 4. Sub B. Mayo’s methodology – Double Blind?

Moertel et al’s article 1985 NEJM article about the second test is only five pages long. However, we are assured exactly nine times by the use of one or all of the following adjectives that we are dealing here with a “prospective randomized double blind” study – a fact designed to impress us with the great methodological superiority of their research strategy above that of Cameron and Pauling (who took as their control group cases that matched from the files).

But I have my doubts about that “double blind” character, and also about the way the control group was controlled – or rather not controlled. Here was a group of patients that, in all likelihood, was told that chemotherapy offered no hope in their situation. They were also told explicitly that there would be a test with vitamin C. Moertel et al. wrote:

 “The nature and purpose of the study was fully discussed with each patient, with specific emphasis on the fact that they would receive either vitamin C or an inert placebo on the basis of random assignment.”

So, patients whose hope for any other treatment had disappeared were told here that there would be a test with a potential medicine that can be easily obtained by anyone, and that could be easily self-administered because in the test that would only be done orally anyway.

They also knew that they would either be in the test- or in the placebo group (which stops the test from being double blind). Wouldn’t at least some of those people think, to insure myself against the chance of merely being in the placebo group I will get hold of that stuff myself.


That at least some of them would think so would seem fairly obvious. Which meant that strict monitoring of the control/placebo group have been a prime requirement. There were only about fifty people in this group, so control should not have been a major task.  But the test was deficient on this point as well.

Moertel et al. wrote:

To further ensure compliance, 11 consecutive patients were selected during the course of our study for urinary assays of ascorbate … Patient selection was made at an arbitrarily chosen time in our study and without knowledge of the drug assignment of individual patients. The laboratory was also blinded as to drug assignment. Patients were not told the purpose of the urine collection; they were simply asked to submit a 24-hour specimen. Five patients who were later determined to have been assigned vitamin C all had high urine levels of ascorbate (more than 2 g per 24 hours.). Of the six assigned to placebo, five had negligible levels that were within the range of normal controls for our assay method (less than 0.55 g per 24 hours). A single patient had an intermediate value between these two ranges.”

I conclude from this that this test was only done once, and that it was done on urine (whereas Dr.Cameron directly measured the serum level of vitamin C). There was also a patient in the control group who was above the (arbitrarily chosen) upper limit of more than 0.55 g.vitamin C per hour whereas another patient in that small test group of 11 people was at that upper limit. No further information has been provided about measurements among the others.

5. Sub B. (contin.)  No effective control of the control group

The figures clearly demonstrate that at least part of the control group were self-administrating vitamin C, as any one with common sense could have expected. Unless they were taking extra vitamin C, cancer patients should not have more than 0-10 mg in their urine (Richards). But here the upper limit for non-administration was supposed to be 550 mg.

Wikipedia provides (or provided) the following substantive criticism:

 “ … the dose given was oral, not intravenous (uptake of vitamin C from oral dosage is very low), of short duration (averaging 72 days rather than lifelong, roughly 2 years more) stopped the vitamin C abruptly (generally bad) after which death rates rose, used a different oral form (dry AA caps vs neutralized AA-DHA-sorbitol solution) and … the Mayo patients died after stoppage of vitamin C usually on or after chemotherapy.

The ascorbate monitoring was poor and compliance controls of outpatient treatment were flawed, despite Ewan Cameron’s specific request to Moertel for better monitoring….] Moertel (1985) tested only 6 of 49 placebo patients for a very high threshold of urinary residuals of ascorbate spillage, over 550 mg/day. This urinary threshold might roughly correspond to 2g-4g/day in healthy patients or about 8+g/day in less severe cancer cases vs ~0.06g/day intake (RDA then) assumed with a placebo. Still one of only six placebo “controls” measured higher than this threshold, belatedly dismissed as only a potential measurement interference. In one of Klenner’s rare comments on cancer, intravenous administration of 17g/day ascorbate for 92 days yielded no measurable urinary residual in a severe cancer case. The Moertel (1985) tests were poorly analyzed in terms of radically changing test conditions (initial delays, brief vitamin C; abrupt stop & repeated chemo) and quality of life improvements …”

So this whole exercise was problematic: “a proportion of the controls was clearly medicating with the substance under evaluation” and this whereas Dr.Cameron had urged effective monitoring of this control group.

This was even obvious to the guest editorialist Dr. Robert Wittes, who was, as we saw, was keen to give this study his imprimatur as a “prospective randomized double blind study”. He wrote that, if even more patients had been controlled “surreptitious ingestion of this easily obtainable vitamin among the control patients might have been excluded with somewhat more confidence”.

All the above returns us to the question as to whether one was dealing here with fools rather than knaves. Honest errors, as Dr. Cameron was inclined to think, or rather with a deliberate effort to make this test fail, as Linus Pauling was inclined to think. An opinion Dr.Cameron eventually shared. Was Pauling’s suspicion about the lack of good faith here justified? That is the question I will deal with next

6. Good faith?

Moertel et al wrote a propos of their second test:

 “We had previously attempted to validate the results of Cameron and Pauling in a prospective randomized trial that was double blinded to prevent any inadvertent bias. We selected patients for study according to the published criteria of Cameron and Pauling: i.e.all the patients had proven terminal cancer and “all were treated initially in a perfectly conventional manner by operation, use of radiation therapy, and administration of hormones and cytotoxic substances” “.

The bit between quotation marks is supposed to come from Pauling’s and Cameron’s first article (1976) in the Proceedings of the National Academy of Sciences. But let us look again at what Moertel wrote to Pauling a propos of his and Cameron’s 1976 article:

 “Certainly in any presentation of this (sic) data I can assure you we will call attention to the fact that the majority of our patients had had prior chemotherapy, whereas in the study conducted by you and Dr.Cameron it was clearly stated that none of the patients had had prior chemotherapy.”

And in their 1979 – NEJM artikel Moertel et al. wrote as I quoted earlier:

 “In Cameron and Campbell’s report of a 10 per cent regression rate in 50 patients with widely disseminated cancer, none had received prior treatment and presumably were more immunocompetent than our patients”

It is therefore rather strange, to put it mildly, that six years later they asserted that in that earlier test they had included people who had already received chemotherapy in the group to be tested. And that this had been guided by the “published criteria of Cameron and Pauling”.

Had they forgotten their earlier statements,  or did they not believe that anybody would go back to the earlier issue of the NEJM to check up (no articles online then).

Moreover there is a snake hidden in the grass of that alleged quote from Cameron and Pauling. We saw that Moertel quoted them as follows:  ”all were treated initially in a perfectly conventional manner by operation, use of radiation therapy and administration of hormones AND cytotoxic substances.” (emphasis added AB)

The suggestion is here that that “conventional manner” of Cameron always included the use of cytotoxic substances (= chemotherapy). However, Cameron and Pauling had written “OR cytotoxic substances”. Is this replacement of “OR’ by “AND” due to a simple oversight? Perhaps.

What Moertel et al. were, however, also silent about is that, immediately following that passage about that conventional treatment, Cameron and Pauling gave a few examples that make clear that virtually nobody in their test group had undergone chemotherapy. They wrote:

 “For example, all of 11 breast-cancer patients in the ascorbate-treated group, with the exception of one who first presented in a grossly advanced state, had already had mastectomy and radiotherapy and all, including the exception, had been given hormones, sometimes with considerable benefit; but all had relapsed by the time ascorbate supplementation was commenced, and it seemed clear that their tumors were escaping from hormonal control. Similarly, all of the seven bladder-cancer patients in the ascorbate-treated group, with one exception because of her frailty, had received megavoltage irradiation and several had had a partial cystectomy (one total) before ascorbate treatment was commenced when it seemed that these standard procedures had failed.”

Thus none of the patients referred to here had undergone chemotherapy. Chemotherapy in the treatment of cancer patients was apparently then comparatively rare in Scotland – compare Richard’s remark about the vitamin C strategy:

“ Its therapeutic promise, as Cameron and Pauling initially represented it, was that it would not replace or threaten conventional treatments but actually improve their efficacy by strengthening the intrinsic defence mechanisms of the patient and containing the spread of the tumour … This strategy, however, while appropriate to the context of conventional Scottish methods of cancer treatment where surgery and radiotherapy were the established therapies, did not, as we shall see, translate readily to the American medical context, where cytotoxic chemotherapy had become the norm in conventional cancer treatment”

Moertel et al. do mention that Pauling had mentioned in the retrospective discussion that only four persons in their test group had undergone chemotherapy, but they only did so after they had suggested misleadingly that they, in their choice of persons for the test group, had been led by the “published criteria” of  Pauling and Cameron.

7. More dishonesty

We are dealing with another example of dishonesty when Moertel et al: emphasize the virtues of their “prospective randomized double blinded”  test. They wrote in their 1985- NEJM article:

“Randomization and double blinding served to protect against any possible conscious or unconscious bias on the part of the investigators as patients were selected for treatment assignment and as their results were evaluated. There was no such protection against bias for Cameron and Pauling as they selected and then reselected the patients they decided to evaluate for their first and second reports” (emphasis added by author).

It is however quite clear from Cameron and Pauling’s 1976-PNAS article that their criterion for inclusion in the experimental group was “terminal” cancer – that is cancer incurable with the conventional therapies then found in Scotland. Whether patients had indeed reached this terminal stage was decided by ”at least two independent clinicians”. Cameron and Pauling wrote:

 “Fifty of the treated subjects are those described in ref.4 and the other 50 were obtained by random selection from the alphabetical index of ascorbate treated patients in Vale of Leven District General Hospital …”

Unfortunately ref.4 refers to an earlier article of these authors that I haven’t been able to track down.

The control group of one thousand patients was obtained by “a random search of the case record index” in the hospital of similar patients – similar in terms of sex, of approximate age, cancer in the same organ and histological type of tumor. The services of a medico who had no further involvement in the research was obtained to establish survival time since the patients had been declared to be “terminal”.

Thus when Moertel et al. wrote “they” in the quote I gave above they falsely suggested that only Cameron and Pauling were involved in this selection. And what is also conspicuous here is that Moertel et al.go on, from their high horse, about their own excellent “randomized sample” but in their report on how this randomization had taken place they do not get any further than saying:

 “All the patients selected for study had histological proof of advanced adenocarcinoma established as having originated in the colon or rectum. All were beyond any reasonable hope of potentially curative surgery or radiation therapy. All were ambulatory and capable of taking oral medication. None had received any chemotherapy.”

But who actually established that these patients were “beyond any reasonable hope”? And if the total number of such patients was greater than the ultimate vitamin C and placebo group (it is not very likely that their number was exactly one hundred) how then took the selection from this larger number place? Moertel et al. keep up a discrete silence about such questions.

Let us see whether there are more reasons to doubt the good faith of these researchers. Pauling asked Moertel in writing to be sent the manuscript with the report on the second Mayo test a few weeks before publication so that he could prepare himself for questions by the media. What actually happened was according to the academic historian of science Richards the following. She writes in her book:

 “ On 30 November Moertel confirmed in a letter to Pauling that the paper had indeed been submitted to the New England Journal of Medicine. He undertook to make certain that a true copy of the manuscript would be in Pauling’s hands a short time before publication date. But it was the press who got the pre-publication copies first, three days before Pauling received his on the actual date of publication – 17 january 1985.”

Feelings ran high at the Institute, with Pauling and Cameron besieged by reporters. Pauling was outraged by what he construed (and denounced in the media) as Moertel’s unprofessional conduct in deliberately withholding the paper from him and making it impossible for him to comment on a study he had not seen. By the time Cameron managed to obtain a copy from a United Press International reporter (on 16 January), the news was already going stale. Moertel had appeared on all major TV networks to denounce vitamin C as “worthless” in cancer treatment and the Pauling-Cameron studies as biased.” Pauling wrote letters with questions to all of the six authors – nobody answered him. Subsequently he wrote to the editor of the NEJM asking information about the way this article had been accepted by the journal. That letter also remained unanswered 2.

 Moertel can no longer be called to account. He died in 1994 – in the same year as Pauling and just like Pauling from cancer. But Pauling was 93 when he died and Moertel 66. Pauling’s cancer was, moreover, in the prostate, an organ in which almost any man can get cancer if only he gets old enough.

1: see Pauling’s letter in the New England Journal of Medicine 1980 Vol.302 No.12.

2: Richards, Vitamin C and cancer – medicine or politics?, 1991:142


Losing Faith


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

Recently, I have taken to looking at the headlines of various medical studies are groaning. You may have seen the hype surrounding a ‘low carb’ diet study in the BMJ. One headline, plucked from many, stated that ‘Heart disease linked to low-carb diets.’

Perhaps I should take such studies more seriously. After all, the BMJ is one of the most respected and highly ranked medical journals in the world. It is not the Fortean Times or the National Enquirer. So, one would hope that it prints things that should be serious and taken seriously.  I wish.

Instead, my first thought was. This is bollocks. I know that this is rubbish. But, frankly, can I be bothered to read the damn thing myself, to prove to myself it is rubbish. I immediately knew it was rubbish because I have been studying nutrition and health for nearly thirty years, and if there were anything inherently unhealthy about a low carb, high protein diet, I would know it. And I don’t.

I also know the context of such studies. Mainstream medical thinking has been high carb, low everything else for the past thirty years. It is unshakable dogma, maintained in the face of a relentless bombardment of evidence. When anyone, such as Atkins, dares to take on this established dogma, they are ruthlessly attacked, personal, professionally and scientifically.

On the other hand, when anyone produces a paper supporting the high carb, low everything else, dogma, it will be uncritically supported, waved through peer-review, then published. ‘See, we were right all along. Low carb diets kill you. Nyah, nyah, nyah…..you’re not singing any more etc.’ Such is the world of medical research today.

The decline of honesty in science

Anyone who has been a scientist for more than 20 years will realize that there has been a progressive decline in the honesty of communications between scientists, between scientists and their institutions, and between scientists and their institutions and the outside world.

Yet real science must be an arena where truth is the rule; or else the activity simply stops being science and becomes something else: Zombie science. Zombie science is a science that is dead, but is artificially kept moving by a continual infusion of funding. From a distance Zombie science look like the real thing, the surface features of a science are in place – white coats, laboratories, computer programming, PhDs, papers, conference, prizes, etc. But the Zombie is not interested in the pursuit of truth – its citations are externally-controlled and directed at non-scientific goals, and inside the Zombie everything is rotten…..

Scientists are usually too careful and clever to risk telling outright lies, but instead they push the envelope of exaggeration, selectivity and distortion as far as possible. And tolerance for this kind of untruthfulness has greatly increased over recent years. So it is now routine for scientists deliberately to ‘hype’ the significance of their status and performance and ‘spin’ the importance of their research.

Bruce Charlton: Professor of Theoretical Medicine

Getting back to the study, I did read it, it was rubbish. Luckily, others too read it, and there has pretty much been a barrage of criticism (none of which will ever reach the media, of course). Here is what  Dr Yoni Freehof had to say on the New England Journal of Medicine discussion forum. http://www.cardioexchange.org/voices/what-reading-that-low-carb-gives-you-heart-disease-paper-actually-told-me/

‘…..So, to review: The authors of this paper are  basing their 15-years-worth of conclusions off of a single, solitary — and clearly inaccurate — baseline food-frequency questionnaire; they didn’t control for clearly known smack-you-in-the-face dietary confounders; they found just a miniscule absolute increase in risk; and the diet they are reporting on can’t even be fairly referred to as a low-carbohydrate diet.

Useful?  Conclusive?  Press worthy?

It gets worse.

The BMJ didn’t just publish a completely useless paper, they gave this very clear, yet completely non-evidence-based, advice to clinicians in their accompanying editorial:

Despite the popularity of these diets, clinicians should probably advise against their use for long-term control of body weight.

Worse still, highly reputable, socially networked curators of medical information tweeted the resultant media stories as relevant, and even Physician’s First Watch — a news alert from Journal Watch and the publishers of the New England Journal of Medicine — reported it as valuable to scores of physician subscribers who trust JW to keep them abreast of the latest important journal studies.’

He didn’t like. I didn’t like it. No-one who knows anything about this area liked it. It was Zombie Science, to go along with an ever-increasing pile of Zombie Science. I am losing faith in medical research.

The UK Obesity Initiative (Failure guaranteed from the start)

Insanity: doing the same thing over and over again and expecting different results.’ A. Einstein

Perhaps one should applaud the recent initiative by the UK Academy of Medical Royal Colleges (AOMRC), in their attempts to tackle the obesity epidemic. This is a very esteemed group indeed of the great and good. In their own words:

The Academy Obesity Steering Group has been established to carry out a project on tackling obesity on behalf of the medical Royal Colleges and Faculties.

Its main responsibilities are to:

  • Produce a strategy on the most effective and coherent way to tackle obesity
  • Produce a recommendation report to form part of a wider Obesity campaign by the last quarter of 2012.

They are looking for evidence from those with expertise in the area of obesity. They are asking various question, including:

  1. What do you believe are actions and/or strategy that actually work in preventing or reducing obesity?
  2. What is the evidence either from practical experience or relevant literature you have that these actions are effective?

My first response would be that anyone with ‘expertise’ in the area of obesity should be instantly dismissed from all discussions. Never have there been more ‘experts’ in weight loss and obesity than there are now. Never have more books been written on the subject. Never have there been more ‘celebrities’ getting in on the act. (Including Jamie Oliver who proudly claims never to have read a book.)

Never have there been more obese people than there are now.

Conclusion: none of the experts have the faintest idea what they are talking about, and whatever it is they have been doing has made the problem far worse. Ergo, get rid of them all.

Of course, this will not happen. All the experts know that that what people must do, to prevent obesity, is the following: Eat less, exercise, more and eat less fat – and junk food. This has been a pretty constant message over the last twenty years or so. We should all be very familiar with it by now; it gets repeated over and over, whilst people get fatter and fatter.

Rather than suggest the possibility that this message is utterly useless, and clearly not working, the Royal Colleges are doing what people usually do when their favoured strategy is not working. They redouble their efforts and do exactly the same thing, with extra added vigour.

I know they this is exactly what they are going to do, because I looked back to see what the main message of the Royal Colleges was likely to be in this area. Lo and behold, and to no great surprise, they have already been demanding the following:

The academy, an umbrella organisation for the medical royal colleges and their 200,000 members, demands:

  • A ban on firms such as McDonald’s and Coca-Cola from sponsoring major sports events such as the Olympics.
  • A safe area around schools where fast-food outlets are not allowed.
  • A prohibition on the use of celebrities or cartoon figures to sell unhealthy food and drink to children.
  • A legal obligation on all food and drink manufacturers to publish on their products clear guidelines about the amount of calories, sugar, fat and salt.
  • Consideration of “fat taxes” similar to those being implemented in Scandinavia, designed to penalise the buyers of food and drink high in salt, sugar and fat.

Stephenson said the academy was speaking out as it launched an investigation into what can be done to curb the rise in obesity. It will spend six months researching the causes and effects of obesity, and in the autumn will produce a report that will contain far-reaching recommendations for action.  http://www.guardian.co.uk/society/2012/apr/14/obesity-crisis-doctors-fastfood-deals-ban

As expected, although the Royal Colleges appear to be asking for advice and information, they have already pretty much stated exactly what it is they are going to propose. Banning, prohibiting, taxing, and introducing new laws. All the usual knee jerk responses that are employed by authoritarian figures over the years….. ‘Why won’t people just do what we damned well tell them to do? As they will not, we will make them.’ Sigh.

I have been involved in sending in a few different submissions to the AOMRC. They have all pointed out that the obesity epidemic started around the early nineteen eighties. At almost exactly the same time that that UK and US nutritional guidelines came out telling everyone that they must stop eating fat, and start eating carbohydrates. Advice which has been, mainly, followed.

Do you think it is a coincidence that the obesity epidemic took off at this time?