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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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.

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).

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.

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)

Bibliography

“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.

http://www.nhs.uk/conditions/cholesterol/pages/introduction.aspx

http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001224/

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

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

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

‘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.’