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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?

Prevention is better than cure – maybe

[Part one- of many – probably]

The last few decades have seen medicine move inexorably towards the idea that its primary function is to prevent diseases from happening in the first place. Rather than trying to cure them after they have started. Which is a nice simple thought. It also seems an inarguably good thing. So presenting any case against preventative medicine can seem wilfully contrarian, and is often met with extreme anger….’do you want people to die!’

In truth, I do not want people to die – although I would have to add that we are all going to die anyway, whatever we do, so what would be your point exactly? No, what I want is for more people to understand that prevention is not a panacea. It can do more harm than good. Indeed, in certain cases, it can cause significant damage to health and general wellbeing.

It almost goes without saying that many preventative activities are a good thing. Clean water supply, surgeons washing their hands before operations, stopping smoking, taking exercise, and suchlike. But once you have got past such obviously useful activities, the benefit to harm ratio can rapidly become far less straightforward.

I spent some time recently reading a book by Peter Gotzsche called ‘Mammography Screening, Truth Lies and Controversy’. It helped to highlight many issues about cancer screening that have disturbed me for some time.

The first, and most important, is this. Many women have cancerous cells in their breasts. Around 40% of women in their forties, on autopsy, have detectable breast cancer(s). To balance this out, most men after forty, if you took out their prostate and sliced them open, would have detectable cancer cells present as well.

Although 40% of women have potentially detectable cancers, around 4% of women die of breast cancer.

This means that, the vast majority of breast cancers do not actually do anything very much. They sit there, and they sit there and…..presumably, many of them regress (shrink) back down to nothing at all. They cause no health problems, and a large proportion of women will die with, rather than of, breast cancer.

Increasingly, however, someone calls you in for mammography, and you have your scan, and they find a small suspicious lump. In an instant you turn from a happy healthy person, into someone with cancer – the deadly killer. At which point all hell breaks loose.

Now, if that cancer happened to be one that was going to grow and kill you, then all the crushing fear and despair, and biopsies, and operations, would be a small price to pay. But if that cancer was one of the 90% that was going to sit there doing nothing for the rest of your life, then you have paid an exceedingly heavy price indeed.

In addition to this downside, in many cases, the suspicious lump was not even cancerous at all. The mammography identified a possible cancer – and it wasn’t. In screening terms this is known as the false positive. In human terms it is known as, the most terrifying thing that has ever happened to me….. and you’re telling me it was a mistake!

There are those who take an absolutist position on this and say that ‘If even one life is saved, it is all worth it.’ Perhaps, but mammography exposes a women to a radiation dose that is around five hundred times that of a simple chest x-ray. Some estimates suggest that each mammography carries a one in two thousand risk of causing cancer.

If, over a lifetime of screening, you have ten mammograms, that represents  a one in two hundred chance that a procedure designed to pick up cancer, may actually cause it. Or maybe the risk is greater than is. Is the potential to cause cancer additive, or multiplicative? I can find no-one able to answer this particular question.

Then, of course, there is the risk that the mammogram is negative. You are reassured that you do not have cancer – but you do. So when you feel a lump you think. It’s OK, I’ve had a mammogram and I am clear. But you are not. You could have been treated, but you waited too long. This is known as the false negative.

I could go on into further downsides, but I hope to have made the general issue clear. Breast cancer screening sounds wonderful, it is presented as an absolute good, but it is not. There are significant. and not uncommon. harms. Yet such is the zealotry (I hesitated to use the word zealotry, but I can’t think of a better one) of those involved in breast cancer screening that no downsides at all are ever presented.

Screening is good, breast cancer screening is perfect….or not. Here is what Professor Michael Baum has to say on the matter:

‘After a systematic review of all websites on this subject, a recent paper in the British Medical Journal concluded that women are being coerced into screening by those organisations connected to the government or the screening industry. I am neither for nor against screening, but I am a passionate champion of informed choice for women. For an informed choice women should be treated as adults and provided with balanced information, not with propaganda.’ http://www.spiked-online.com/articles/0000000CA382.htm

Preventative medicine, and screening and scanning, has almost become a religion for those involved. Only the positives are ever mentioned, and those who dare criticise are subjected to ruthless attacks. As I will be for writing this.

Prevention is better than cure?

Sometimes. Maybe.

The Joy of Coronary Arteries (The body ain’t that simple)

‘For every complex problem there is an answer that is clear, simple, and wrong.’ H.L Mencken

Of all the things that I find most frustrating about medicine, it is the power of the simple solution. Nothing, probably, does more damage than a fixed belief in a simple idea. The history of medicine is littered with examples. ‘You have a bad headache…..well then, let us relieve it by removing a large section of your skull.’

‘You have recurrent infection of the tonsils. Well, let us remove these two glands, designed to fight infection, and your problems with infection will be solved.’

‘You had a heart attack. Well, you must rest in bed and take all the strain off your heart for six weeks, at least.’ I have calculated that this action caused the premature death of more people than died in the first and second world wars, Stalin’s pogroms, and the holocaust, added together. No, this doesn’t happen anymore.

But many things still do.

One such thing is the obsession of the medical profession with attacking coronary arteries. The arteries that supply blood to the heart. In many people these arteries develop thickenings (plaques), which can gradually narrow the artery and reduce blood supply to the heart muscle.

This can lead to angina, and suchlike. People also believe this means that a sudden blood clot forming over a narrowing can completely block the blood supply and cause a myocardial infarction (heart attack). People think this, but it is not necessarily true. Arteries without narrowings can suddenly block too – and if they do, the outcomes are usually far worse. Oh yes, the counterintuitive world of human physiology.

Anyway. If you think that a narrow coronary artery is the equivalent of having a ticking time-bomb inside your chest, you will probably want to do something about it. In 1967, someone managed to do so:

 ‘In 1967, the Argentine surgeon Dr. René Favaloro, working at the Cleveland Clinic, successfully used a vein graft to bypass an obstructed coronary vessel. Like Edmund Hillary and Tenzig Norgay, the first climbers to reach the summit of Mount Everest, or Roger Bannister, the first to run a four-minute mile, Favaloro opened a terrain deemed beyond human reach. In coronary artery vascular surgery he sundered the barrier to the seemingly impossible. Within ten years 100,000 patients were subjected to coronary bypass operations in the U.S.; by 1990s the number had quadrupled.’ Essay by Bernard Lown.

I suppose everyone has heard of the Coronary Artery Bypass Graft (CABG), pronounced cabbage by most doctors. What a wonderful idea, you use a bit of vein (sometimes a bit of artery, if you can find one) to bypass the narrowing. Huzzah!

You would think that someone would have tried to find out if it did any good, or not. But no-one really wanted to know. This operation bypassed a narrow coronary artery, increasing blood supply to the heart. This is such a simple and straightforward idea that to question it was to question common sense itself.

Which is why we ended up with four hundred thousand people being operated on each year in the USA alone. Yet no-one had ever done a study to find out if it did any good.

The someone who did try mighty hard was Bernard Lown. He is a Nobel laureate, and he also invented the defibrillator. So he was not some unqualified nut case. However, he had become very worried about ever increasing number of interventions:

‘Dealing with the growing tide of interventions, most of which I regarded as unwarranted, was morally challenging. To remain silent was complicit. To speak out was to invite confrontation with a powerful and unforgiving establishment. One pressing question was, how could we identify the subset of coronary patients that did well without surgical treatment? To determine how to proceed entangled me in a welter of contradictory views and emotions. One thing was certain, something needed to be done.’

And so he set out to try and find out if CABGs did any good. This was very tricky as he found that the moment he did an angiogram (an x-ray test for looking at coronary arteries), anyone who had a narrowing wanted a CABG straight away. At first, could not recruit a single person into his ‘control’ arm.

Eventually, though, he did manage to study this area and he found that….

‘…we recruited 144 consecutive patients with advanced coronary artery disease. These were followed for an average period of nearly five years, during which time 11 patients died, for an annual rate of 1.4 percent. We referred only 9 patients for CABG (1.3 percent annually). These results were better than the best outcomes being reported for those undergoing CABG.’

These results were better than the best outcomes being reported for those undergoing CABG. Of course, the net effect of this was that the entire world applauded. Er, no

‘Our sense of achievement was short-lived. Leading medical journals refused to publish these findings.’

Of course, as is the way of such things, the world moved on. Instead of CABG, we now have angioplasty. This is a procedure where you open up the artery from the inside using a small balloon, or inserting a wire mesh (stent).

Angioplasty is now taking over from CABG as the intervention du jour and, guess what, it is less effective than CABG – which makes it less effective than doing something that is less effective than doing nothing. Which means that every day it grows in popularity.

Ah yes, the tyranny of the simple solution continues.

I am indebted to Paul Rosch for sending me the essay from Bernard Lown on this issue.

Does treating high blood pressure do any good?


Although I am most interested in the medical madness surrounding cholesterol lowering and statins, I have long been interested in the parallel ‘Looking Glass’ world of blood pressure lowering. During a recent on-line discussion, someone recently sent me a link to study from two or three years ago which re-ignited my interest in this area.

‘A new review has found that lowering blood pressure below the “standard” target of 140/90 mm Hg is not beneficial in terms of reducing mortality or morbidity1.’ July 2009

It confirmed, or re-confirmed, what I have long believed to be true. Unless the blood pressure is very high, lowering it seems to be an exercise in ‘sweeping a symptom under the carpet,’ rather than doing anything remotely useful. However, before discussing the management of raised blood pressure in more detail, I need to establish a little context.

The average blood pressure of an adult is around 120/70mmHg. The 120 ‘systolic’ figure represents the highest pressure reached. This happens just after the heart has finished contracting. The 70 ‘diastolic’ figure represents the lowest pressure, occurring just before the heart contracts again (there is no time for it to drop all the way down to zero).

There is no doubt that, if the pressure is very high, say 200/120, that this is associated with a greatly increased risk of stroke, heart failure and other form of cardiovascular disease. No-one disagrees with this, not even me.

There is also no argument that lowering an extremely high blood pressure can be lifesaving. But, or perhaps there are many different buts here. Things are far less straightforward when it comes to a moderately raised blood pressure.

The first question to ask is. What exactly are we ‘treating’ when we lower it? A raised blood pressure is not a disease. It is not even symptom of a disease; because a raised blood pressure does not cause any symptoms unless it is extremely high. A raised blood pressure is simply a sign, or a measurement.

What is it a sign of? It is a sign that your heart is pumping so hard that the blood pressure is raised above the ‘normal’ level. Why would the heart pump too hard? It is statement of the obvious to say that it cannot just happen for no reason at all.

In some cases, an underlying cause can be found. If you have a narrow renal (kidney) artery, for example, this reduces blood supply to the kidney. The kidney therefore believes that the blood pressure must be too low, and it releases hormones designed to raise the blood pressure. Cause and effect.

In a case like this, you can do an operation to widen the renal artery, the blood flow to the kidney increases, and the blood pressure normalises. In around five per cent of cases of high blood pressure a cause, such a renal artery stenosis, can be found. In the other ninety five per cent there is no obvious reason.

At which point, something very strange happens. Instead of calling this ‘a raised blood pressure where no cause can be found,’ the medical profession decided to turn a clinical sign into a disease. This disease is Essential Hypertension, which literally means ‘a raised blood pressure where no cause can be found.’ But you have to admit that essential hypertension sounds rather more impressive.

Once it became a de-facto disease, it can be ‘treated.’ And so it came to pass that, over time, a whole series of drugs were developed. Some reduce the blood volume, some relax the blood vessels, some block the production of hormones designed to raise blood pressure, and others prevent the heart pumping too hard.

They come by names such as thiazide diuretics, beta-blockers, alpha-blockers, angiotensin converting enzyme inhibitors, angiotensinogen II inhibitors etc. etc. After statins, these are the most prescribed type of medications. Around the world, hundreds of millions of people take them each and every day.

This mass pharmacological assault happened before anyone had actually established that lowering blood pressure was actually beneficial. There had been a couple of short term studies on people with very high blood pressure. These did show benefit.

However, when it came to moderately raised blood pressure, there were absolutely no studies at all. Yes, you did read that right. No studies. It was not until the 1970s that anyone actually set out to answer this rather fundamental question by setting up a major study. The UK Medical Research Council (MRC) study.

Recruitment started in 1973. Seven hundred thousand people were contacted, and half a million people accepted an invitation to participate.  As is the way with such things, this enormous initial number was whittled down to just under eighteen thousand people who had a diastolic blood pressure between 90 – 109, and a systolic pressure below 200.

The eagerly awaited results were released in 1985. I remember the year well, as I was at a cardiovascular conference at the time. Everyone was convinced that that there would be major benefits.

And what were the results? Well, if you get down to the most important outcome of all, which is overall mortality, there were 248 deaths in the treated group and 253in the placebo group2. Or to put this another way: 248 out of 9000 died in the treatment arm died, and 253 out of 9000 died in the placebo arm:

Overall mortality: 248/9000 = 2.75% (treatment group)

Overall mortality: 253/9000 = 2.81% (placebo)

The total difference in deaths was seven. The absolute percentage difference in deaths was 0.06% over five years. There was no difference in the death rate from heart disease.

I remember thinking at the time. ‘Blimey that should throw the cat amongst the pigeons. We are going to have to re-think this area.’ How wrong could one man be? Because the result of the MRC study was that absolutely nothing changed. There was no re-think, no fundamental review, nothing.

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

Actually, it is not entirely true to say that nothing happened. Within the world of anti-hypertensive therapy a subtle, but critically important, change did take place. Whilst there was no benefit on heart disease, or life expectancy, there was a small, but statistically significant, effect on stroke. One stroke delayed for around nine hundred years of treatment.

At this point, the research community started to combine stroke and heart disease under the heading ‘cardiovascular disease’. It was then reported that blood pressure treatment reduced total deaths from cardiovascular disease. Which is true. The fact that there was no impact on Coronary Heart Disease and/or overall mortality was gradually pushed into the background

Nowadays, when people report on blood pressure lowering, the discussion is almost entirely focussed on cardiovascular mortality (which basically means stroke).

In a parallel move, researchers started to move away from outcome data e.g. death from stroke and heart disease, and began to use a mathematical model (the log-linear model) to define the success of lowering blood pressure3.

Once you decide that the lower you get the blood pressure the better this is, you no longer need measure death from heart disease and stroke and suchlike. You just measure the blood pressure reduction, feed these data into the log-linear model, then you can establish the clinical benefit you must have had.

There is just one slight problem. This model doesn’t actually work in practice. Twenty years ago Ancel Keys – the man who created the diet-heart hypothesis – concluded that the linear model was useless. Twelve years ago, a group of medical statisticians re-analysed the original data which underpinned the log-linear model and they concluded the following:

‘Shockingly, we have found that the Framingham data in no way supported the current paradigm to which they gave birth. In fact…. The paradigm MUST be false4.’

They went on to make the following statement:

‘No randomised trial has ever demonstrated any reduction of risk either overall, or cardiovascular death by reducing systolic blood pressure to below 140mmHg.’

The effect of their analysis was, as you may expect, a deafening silence. This was despite the fact that these researchers had just proved that everything that everybody believed about lowering blood pressure was wrong. The log linear model rules, lowering blood pressure is beneficial.

Nine years later, another analysis appeared. The one mentioned at the start of this article. It exactly the same thing…. again:

‘A new review has found that lowering blood pressure below the “standard” target of 140/90 mm Hg is not beneficial in terms of reducing mortality or morbidity1.’ July 2009

During that twelve year period between these two studies, the thresholds for ‘treating’ blood pressure became lower and lower. For diabetics, essential hypertension has now fallen to a systolic of 115mmHg. This definition was created from combined end-point cardiovascular data, and the log-linear model. The one that has been proved ‘shockingly’ to be false. I wasn’t that shocked.

In fact, only one thing shocks me. It is fact that you cannot get anyone to change their minds in this area. A raised blood pressure is bad, and must be lowered, full stop. Whilst I would agree that a raised blood pressure is ‘bad’ in that it is associated with and increased risk of premature death. I cannot find evidence that lowering the blood pressure does any good, no matter what the level.

The simple fact is that when blood pressure is raised, it is raised for a reason. The reason is an underlying ‘disease’. And just because you cannot find it, does not mean that it doesn’t’ exist.

Lowering the blood pressure will certainly get rid of an annoyingly high measurement, but it cannot (unless by complete coincidence), have any impact on the underlying disease…… the thing causing you to die. So, unless it is startlingly high, what good can lowering blood pressure actually do?

The answer my friend, is not blowin in the wind. The answer is ‘no good at all.’

1: http://www.medscape.com/viewarticle/705670?src=mp&spon=2&uac=97302DZ

2: MRC trial of treatment of mild hypertension: principal results. Medical Research Council Working Party: BMJ 1985;291(6488):97

3: Stamler J. Blood pressure and high blood pressure, aspects of risk. Hypertension 1991; 18(Suppl I): I–95 – I – 107

4: Port S, Garfinkel A, Boyle N:  There is a non-linear relationship between mortality and blood pressure. EHJ (2000) 21 p 1635-1638

Do Low Cholesterol Levels Cause Cancer?

We live in a world where a high cholesterol is now considered to be virtually the most terrible and dangerous thing known to man. Everything possible must be done to bring the level down, or else you are going to die of a stroke or heart attack.

The anti-cholesterol propaganda has been so successful that six million people in the UK now take statins each and every day to reduce their risk of heart disease. Something which, I strongly believe, future generations will look back on in amazement. ‘Did they not know that cholesterol is essential for human health….what on earth did they think they were doing?’

Can it really be true that a chemical compound, so important that the liver synthesises at least five times as much as you consume in food, can be disastrous to our health. All cell membranes need it, our brains need it, almost all of our hormones are made out of it, and it is used to make vitamin D in our skin. It has always seemed to me that having too little cholesterol is just as likely to be damaging as having too much – probably more so.

One area I have particular concerns about is cancer. For many years it has been noticed that people with low cholesterol levels are more likely to die of cancer. This has been a consistent finding, for many years, from studies done all around the world1-9.

The statin ‘zealots,’ as I shall call them, are well aware of the association between low cholesterol and cancer, and they have gone out of their way to dismiss the possibility that low cholesterol may cause cancer.

The primary argument they have used is known as reverse causality. This ‘reverse-causality’ hypothesis suggests that depressed LDL-cholesterol levels are the result of subclinical cancer (not the other way round). This idea has been put forward with absolutely no evidence to support it. Despite this, it has been accepted without question.

It is true that if you have advanced cancer, your cholesterol levels fall. This happens for a number of interconnected reasons, including the fact that large tumours use a lot of cholesterol to divide and grow.

However, the idea that a cancer so small, that it cannot not yet be detected, is using up so much cholesterol that it lowers the total cholesterol level throughout the body, is stretching the boundaries of possibility. I would say breaking the bounds of possibility.

The second argument put forward, which is not really an argument, is the ‘how can a low cholesterol level cause cancer anyway.’ It should always be remembered that a great deal of medical research consists of bumping into effects, without understanding how it could happen in the first place – see under penicillin. See more recently under aspirin protecting against cancer. A finding as yet, without any clearly defined mechanism of action.

In short, just because you can’t easily see a mechanism of action, does not mean that it doesn’t exist.  In fact, several possible ways that cholesterol, or to be more accurate lipoproteins, could protect against cancer have been researched in some detail10.

Anyway, as I have always known must happen, the ‘reverse causality’ hypothesis has finally been laid to rest.  A recent analysis of the longest running heart disease research project in the world (the Framingham Study) has shown that low cholesterol levels predate cancer diagnosis by many, many, years. And, to quote:

“Based on these data, it would suggest that lower cholesterol predated the development of cancer by quite a long time. Now, that doesn’t necessarily speak to [low cholesterol] causing the cancer; it could have been related to something else altogether, but it’s not supportive of the hypothesis that cancer caused the low levels of LDL cholesterol. We don’t know why it predates cancer, but it would be premature to attribute it to the cancer itself.” 11

In short, it must now be accepted that cancer doesn’t cause low cholesterol levels. Which leaves the possibility that low cholesterol levels might cause cancer. This, inevitably, leads to the next question. If low levels of cholesterol precede cancer, can statins cause cancer?

The evidence is not conclusive, and I would not claim that it was. But there have been some significant warning signs from statin studies. Just to mention three. In the CARE trial12, twelve women in the statin group had breast cancer at follow up, compared on only one in the placebo group. In the PROSPER study13 there were forty six more cases of cancer in the statin group than the placebo group.

Possibly the most worrying figures come from a Japanese study which looked at nearly fifty thousand people taking statins over six years. They found that the number of cancer deaths was more than three times higher in patients whose total cholesterol was less than 4.0mmol/l at follow-up, compared with those whose cholesterol was normal or high:

The patients with an exceptionally low TC (total cholesterol) concentration, the so-called ‘hyper-responders’ to simvastatin, had a higher relative risk of death from malignancy than in the other patient groups.’

The authors then went on to warn:

Malignancy was the most prevalent cause of death. The health of patients should be monitored closely when there is a remarkable decrease in TC (cholesterol) and LDL-C (Low Density Lipoprotein ‘bad cholesterol’) concentrations with low-dose statin.’14
This is not proof of causation, but these are warning signs. Armed with the Framingham data, I believe that the medical profession has to face up to the painful reality that low cholesterol levels could be a cause of cancer, and this needs to be properly researched. We must remember that it took Richard Peto more than thirty years to prove that smoking caused lung cancer, and no statin trial has lasted longer than six.

1. Williams RR, Sorlie PD, Feinleib M, McNamara PM, Kannel WB, Dawber TR. Cancer incidence by levels of cholesterol. JAMA 1981; 245:247–52.

2. Salmond CE, Beaglehole R, Prior IA. Are low cholesterol lvalues associated with excess mortality? BMJ 1985;290:422–4.

3. Schatzkin A, Hoover RN, Taylor PR, Ziegler RG, Carter CL,Larson DB, et al. Serum cholesterol and cancer inthe NHANES I epidemiologic followup study. NationalHealth and Nutrition Examination Survey. Lancet 1987;2:298–301.

4. To¨rnberg SA, Holm LE, Carstensen JM, Eklund GA. Cancer

incidence and cancer mortality in relation to serum cholesterol. J Natl Cancer Inst 1989; 81:1917–21.

5. Isles CG, Hole DJ, Gillis CR, Hawthorne VM, Lever AF.Plasma cholesterol, coronary heart disease, and cancer inthe Renfrew and Paisley survey. BMJ 1989; 298:920–4.

6. Kreger BE, Anderson KM, Schatzkin A, Splansky GL. Serum cholesterol level, body mass index, and the risk of coloncancer. The Framingham Study. Cancer 1992; 70:1038–43.

7. Schuit AJ, Van Dijk CE, Dekker JM, Schouten EG, Kok FJ.Inverse association between serum total cholesterol andcancer mortality in Dutch civil servants. Am J Epidemiol1993; 137:966–76.

8. Chang AK, Barrett-Connor E, Edelstein S. Low plasma cholesterol predicts an increased risk of lung cancer in elderlywomen. Prev Med 1995; 24:557–62.

9. Steenland K, Nowlin S, Palu S. Cancer incidencein the National Health and Nutrition Survey I. Follow-updata: diabetes, cholesterol, pulse and physical activity.Cancer Epidemiol Biomarkers Prev 1995; 4:807–11

10: http://qjmed.oxfordjournals.org/content/early/2011/12/08/qjmed.hcr243.full.pdf?keytype=ref&ijkey=kZGZxqVjYWEOtoc

11: http://www.theheart.org/article/1375049.do?utm_campaign=newsletter&utm_medium=email&utm_source=20120325_ACC_dimanche_2

12: Sacks FM, Pfeffer MA, Moye LA, Rouleau JL, Rutherford JD,Cole TG, et al. Effect of pravastatin on cardiovascular eventsin women after myocardial infarction: the cholesterol and recurrent events (CARE) trial. N Engl J Med 1996;335:1001–9

13: Shepherd J, Blauw GJ, Murphy MB, Bollen EL, Buckley BM,Cobbe SM, et al. Pravastatin in elderly individuals at risk ofvascular disease (PROSPER): a randomised controlled trial.Lancet 2002; 360:1623–30.

14: . Matsuzaki M, Kita T, Mabuchi H, Matsuzawa Y, Nakaya N,Oikawa S, et al. Japan Lipid Intervention Trial. Large scalecohort study of the relationship between serum cholesterol lconcentration and coronary events with low-dose simvastatin therapy in Japanese patients with hypercholesterolemia. Circ J 2002; 66:1087–95.


Association does not mean causation

Of all the things you should bear in mind when looking at health stories, this is probably the single most important. Association does not mean causation. The reason why this is so important is that studies that have only found associations make up the vast bulk of scare stories in the media:

Here is a typical recent headline, which you may have seen:

Eating red meat regularly ‘dramatically increases the risk of death from heart disease’

It is true that this newspaper headline does not actually state that eating red meat causes heart disease. Not quite, but very nearly, and you could be forgiven for thinking that it does. Read it again, and you will not see the word cause anywhere. It is just very implied very strongly

However, as you get into the article itself, any distinction between association and causation fades almost to nothing:

‘Senior author Professor Frank Hu, from Harvard School of Public Health in Boston, US, said: ‘This study provides clear evidence that regular consumption of red meat, especially processed meat, contributes substantially to premature death.

‘On the other hand, choosing more healthful sources of protein in place of red meat can confer significant health benefits by reducing chronic disease morbidity (illness) and mortality.’

The study found that cutting red meat out of the diet led to significant benefits. Replacing one serving of red meat with an equivalent serving of fish reduced mortality risk by 7 per cent.’

At this point we are heading into the territory of Bill Clinton in his impeachment trial where the meaning of words it being stretched to their very limit. ‘But what is, is?’

I defy anyone to read those paragraphs and not conclude the following:

1: These researchers proved that eating red meat causes premature death

2: The researchers further proved that cutting out red meat and replacing with fish reduced mortality risk by 7 per cent.

I don’t think you could be blamed for thinking these two things. Because that appears to be exactly what was said. Or was it? Were you just being fooled by a complex conjuring trick made up of carefully chosen words designed to bewilder.

Here are the actual conclusions of the paper:

Red meat consumption is associated with an increased risk of total, CVD, and cancer mortality.’

Note the word associated. Where is the word cause? It isn’t there, because this study could never, ever, prove causality. Why not? Because it was an observational study (actually it was a review of two other observational studies).

In an observational study you do not do anything active. You just study that things that people do, or eat, and see if any associations emerge. When you find an association the next question you have to ask is the following. Are you looking at yellow fingers, or smoking.

It is certainly true that yellow fingers are associated with a higher rate of heart disease Does it follow that yellow fingers cause heart disease? No, of course not, what it means is that people with yellow fingers are usually people who smoke. And smoking vastly increases the risk of dying of heart disease.

In this case the distinction between the cause and the association is blatantly obvious – or at it has become so after fifty years of research made it clear Indeed, if I were now to try and claim that having yellow fingers causes heart disease, you would look at me as though I were an idiot – and I would be.

Yet, when a study finds that eating red meat is associated with a higher risk of heart disease, we seem to rush headlong into the conclusion that eating red meat consumption almost certainly causes heart disease. But red meat could well just be the equivalent of yellow fingers.

You think not? In that case you are probably thinking that red meat contains saturated fat, and saturated fat raises cholesterol levels, and raised cholesterol levels cause heart disease. If you played this little causal chain in your mind, you would most certainly not be alone in doing so.

It is something that our brains seem hard-wired to do…

‘….our brains and nervous systems constitute a belief-generating machine, an engine that produces beliefs without any particular respect for what is real or true and what is not. This belief engine selects information from the environment, shapes it, combines it with information from memory, and produces beliefs that are generally consistent with beliefs already held. This system is as capable of generating fallacious beliefs as it is of generating beliefs that are in line with truth.http://www.csicop.org/SI/show/belief_engine/

We cannot seem to help ourselves from linking things together to create causal chains, or beliefs, that certain things cause other things to happen. This is emotional, it is exceedingly powerful, and deconstructing such beliefs is the work of Hercules.

In this particular case, though, you would be hard pressed to use this belief as an explanation. How do I know this? I know that because the Harvard team found that those who at the most red meat actually had the lowest cholesterol levels. This table (figures taken from the paper itself) divides people into five groups/quintiles. Those in quintile 1 ate the least red meat, those in quintile 5 the most.

Total Red Meat Intake Quintile, Servings per Day









% with high







Pan A; Sun Qi;, ScD;  Bernstein A; et al: ‘Red Meat Consumption and Mortality:Results From 2 Prospective Cohort Studies.’ Arch Intern. Med.Published online March 12, 2012.doi:10.1001/archinternmed.2011.228

The authors chose not to make any comment at all on this finding. Although you might have thought it worth a quick mention. Had they found rising cholesterol levels with increased meat consumption you can be absolutely certain they would have presented this as a clear cut causal chain. So how did eating read meat cause an increase in the rate of heart disease? Because it just did….through some mechanism unknown to medical science? The evil power of redness.

What is far more relevant is that they also found that those who ate the most red meat also smoked the most, exercised the least, ate far more calories in total, and were more likely to have diabetes. But it was the red meat that killed them from heart disease….you think? Even if red med included pork, and unprocessed red meat included hamburgers.

This study demonstrated, as if any further demonstration were required, that a whole bunch of unhealthy lifestyle factors: smoking, taking no exercise, drinking, eating fast food are all linked together. But I think we knew this already.

To preventative medicine and beyond!

Preventative medicine has gone completely mad and it is only going to get worse. One of the most depressing articles I have read recently (and there was plenty of competition for this particular accolade) was in the Journal of Palliative medicine. It was entitled:

Statins in the last six months of life: A recognizable, life-limiting condition does not decrease their use.’

Statins, as you probably know, are used to reduce the risk of dying of heart disease, strokes and suchlike. Now, I am not exactly a fan of these drugs, to put it (very) mildly. But I thought that even the most fanatical ‘statinator’ might feel that if a patient is dying of terminal cancer, then there is little point in continuing with a drug designed to reduce the risk of heart disease.

Wrong. It seems that patients with terminal cancer are prescribed statins up until they draw their final breath on this Earth. What exactly are their doctors trying to prevent here? Well, at least they didn’t die of a heart attack first? Thank God for that.

I have had personal experience with this particular madness. I was visiting a lady of one hundred and one years old in a nursing home. The nursing staff asked me if I could change her statin from a tablet to a liquid form, as she was no longer able to swallow tablets. This lady was so severely demented that she could not speak, was unable to remotely recognise any of her relatives, and was lying immobile in her bed – doubly incontinent.

I felt that, in the circumstances, it was probably best just to stop the statin, especially as they are one hundred times more expensive in liquid than tablet form. So it all seemed like an expensive action in futility. For this action I was severely criticised by the nursing home, and another doctor involved in her care. I believe I was, at one point, accused of being ‘ageist.’ Well, I didn’t really know how to respond. I wondered where we drew the line with preventative medicine, and it appears we no longer draw the line, anywhere.

We carry on forever. We give drugs to the terminally ill, the extremely old and severely demented. Once started we never, ever, stop, no matter what, until the patient is dead. Perhaps at that point I should scatter statins on their ashes, just to make absolutely and completely certain that I am not missing a trick. After all, I would hate be thought of as ‘deadist’.