The hydra

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

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

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

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

Hydra, or blob.

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

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

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

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

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

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

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

A humiliating climb down – or a Machiavellian move?

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

From: colin.baigent@xxxxxxxxxxx

To: maryannedemasi@xxxxxxxxxxxx


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

Dear Maryanne

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

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

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

Colin Baigent.

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

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

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

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

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

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

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

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

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

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

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

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


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

Thinking about diabetes once more

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

What is the underlying factor linking depression and insulin resistance?

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

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

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

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

More on this topic soon(ish).







Thinking about diabetes again

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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


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

Thinking about obesity and diabetes

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

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

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

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

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

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

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

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

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

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

In short:

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

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

But, but.

But what?

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

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

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

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

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

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


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

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

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

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

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

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

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

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

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

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



Eskimos and nose bleeds part II

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

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

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

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

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

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

The process of arterial thickening/plaque development

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

A whole new process – and potentially causal factors

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

  1. Endothelial damage
  2. Thrombus formation
  3. Repair

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Now you know… possibly?




Are some diets ‘mass murder’

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

2: Cause millions upon millions of people to become diabetic

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

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

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

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

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



Doctoring Data

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

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

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

Eskimos and nose bleeds

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

What is T?

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

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

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

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

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

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

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

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

Now, let us imagine death.

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

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

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

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

Heart Protection Study

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

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

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


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

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

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

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

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

So, when someone says….

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

…they are talking nonsense.

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

Can we believe any medical research – at all?

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

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

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

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

The shortest summary of his paper is, as follows:

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

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

As Dogbert might say. Hahahahahahahahahahaha!

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Oh Joy.

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


My father

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

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

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

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

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

It’s the same the whole world over,

It’s the poor that get the blame,

It’s the rich that get the pleasure,

Ain’t it all a bloody shame

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

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

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

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

Silence was the stern reply

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

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

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


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

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

All the best,


I replied


Excellent letter.

The reply will be, as follows

Dear Mr Bailey,

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

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



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

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

Dear Sir Rory,

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Sincerely yours,

David Bailey

‘You are killing my patients’ – again

[Bring it on]

A few months ago I was part of a group that wrote a letter to the National Institute of Health and Care Excellence (NICE) criticising their proposed guidance on the use of statins in primary prevention. I drafted the letter and it was signed by such people as the President of the Royal College of Physicians, past president of the Royal College of Physicians etc. This was not, in short, a group of fringe lunatics.

It caused a bit of a stir, and generated a considerable amount of air time. After receiving the letter, NICE reviewed their guidance and decided that they had been perfectly correct to promote the use of statins in primary prevention in the UK after all. NICE, in effect, judged NICE, and found itself not guilty of anything. Well, that’s one of the benefits of being judge, jury and executioner all wrapped up together in one body.

This letter, and the dismissal of all its points, followed a nasty outbreak of hostilities in which Professor Abramson and Dr Malhotra had been attacked by Rory Collins for publishing separate, but related, papers in the BMJ. These papers suggested that adverse effects from statins were quite common. Professor Rory Collins demanded retraction of the articles and also attacked the editor of the BMJ very publically. Generating articles such as this one:

‘Professor Sir Rory Collins, from Oxford University, said he believes GPs and the public are being made unjustifiably suspicious of the drug, creating a situation that has echoes of the MMR vaccine controversy.

The academic, one of the country’s leading experts on the drug, is particularly unhappy with the British Medical Journal (BMJ), which has run well-publicised articles by two critics of statins that he argues are flawed and misleading.

“It is a serious disservice to British and international medicine,” he said, claiming that it was probably killing more people than had been harmed as a result of the paper on the MMR vaccine by Andrew Wakefield. “I would think the papers on statins are far worse in terms of the harm they have done.”’ 1

Stung by this attack, the BMJ brought together an independent panel in response to Rory Collins criticism. The result, as reported by Forbes, was as follows:

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

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

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

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

“The panel noted with concern that despite the Editor’s repeated requests that Rory Collins should put his criticisms in writing as a rapid response, a letter to the editor or as a stand-alone article, all his submissions were clearly marked ‘Not for Publication’. The panel considered this unlikely to promote open scientific dialogue in the tradition of the BMJ.””2

In short, Professor Sir Rory Collins was told that he was utterly wrong to demand retraction of the papers, and that by refusing to take part in an open discussion was trying to strangle scientific debate.

That, if you like sets the scene. A scene whereby anyone who dares to criticise statins, even a prestigious journal such as the BMJ itself, is subjected to vitriolic attacks and a demand for silence. Rory Collins tried to keep all correspondence with Fiona Godlee secret, which kind of backfired on him. Hoorah. Type ‘Rory Collins and Fiona Godlee e-mails’ into Google, and you can see for yourself.

Of course, things have not stopped here. The ‘statinators’ although briefly thwarted in their initial attack on Abramson, Malhotra and the BMJ – and less directly me – have switched track. The British Cardiovascular Society (which you will not have heard of), have decided to run a survey of their members. They are trying to gather information about the damaging impact of the articles, and the letter to NICE:

Here is an e-mail which was sent to all members:

The British Cardiovascular Society is keen to know of any potential adverse effect on cardiovascular disease prevention which may have resulted from recent media stories and articles such as those published in the BMJ (1,2) and in an open letter to NICE (3). 
We would be grateful if members would complete this short survey. Your response will be anonymous and the link below is unique to you allowing you to complete the survey once only. 
The survey closes on 30th September and results will be made available subsequently on the BCS Website and in the BCS newswire.


(1) Abramson JD, Rosenberg HG, Jewell N, Wright JM. Should people at low risk of cardiovascular disease take a statin? BMJ 2013; DOI:10.1136/bmj.f6123.
(2) Malhotra A. Saturated fat is not the major issue. BMJ 2013; DOI:10.1136/bmj.f6340

Now, why would they be doing this? I do not think it is that difficult to work it out. The BCS is trying to gather evidence that the articles by Abramson, Malhotra and the open letter to NICE have caused harm to patients. They will be asking their members if they know of people who have stopped taking statins, or who will not go on statins, because of what they have read in the BMJ and suchlike.

Once they have done this, they will then extrapolate the raw figures to the entire population of the UK, in order to claim that ‘Thousands have died.’ Abramson will be attacked, along with Malhotra and the BMJ. I will get a few attacks as well for drafting the letter to NICE. This is a very unsubtle variation of the ‘You’re killing my patients’ tactic which is regularly used to silence any who dares criticise currently medical opinion.

At this point you may be wondering what the British Cardiovascular Society (BCS) may be, and could it possibly have any conflicts of interest with the pharmaceutical industry? Well, of course it does. The BCS is heavily reliant on the industry for its very existence. I would say totally reliant, but such bodies do not reveal detailed financial information.

However, you can start looking at what they charge for sponsorship at their conference, and begin to multiply. For example, if you want an exhibition stand at said conference, here is what you pay for an Option 1 stand3.

Option 1 – £33,500 + VAT
To include:

  • Stand – 8mx8m (64msq) island site
  • Full Page Colour advert in Heart Journal
  • Table (10 guests) at BCS Annual Dinner (Tuesday 3 June)
  • 4 x Conference Badges (company name only so transferable)
  • 20 x Stand/Exhibition Badges
  • 50 word entry in the Conference Programme and on the website
  • Opportunity to purchase additional adverts in Heart Journal

with up to a 50% discount of card rate

The BCS helpfully explains the benefits of exhibiting:

Why Exhibit?

The BCS Annual Conference is the most highly attended and respected cardiovascular event in the UK. The Exhibition is a crucial component to the success of BCS event, enabling cardiologists, physicians, scientists, physiologists and nurses to keep up to date with innovative and developing technologies, pharmacology, diagnostic equipment, educational materials and more.

Access over 2,300 cardiovascular healthcare professionals face to face – including top cardiologists, physicians, scientists, physiologists and nurses

Promote and demonstrate products and services directly to key cardiovascular healthcare professionals and gain first-hand feedback

Associate your brand/company with the Society for Cardiovascular Care – the British Cardiovascular Society

Introduce new products/services and test the market

Opportunity to network with industry peers

Of course there are other sponsorship opportunities, such as Advertising in the BCS Conference Programme, which will set you back another £10K:

Advertising in BCS Conference Programme

A copy of the Conference Programme is given to each delegate upon arrival to the event. This is the perfect opportunity to reinforce your presence and support of the BCS Annual Conference 2014.

Inside Front Cover: £2,000 + vat (exclusive)

Inside Back Cover: £2,000 + vat (exclusive)

Outside Back Cover: £2,000 + vat (exclusive)

Double Page: £2,000 + vat

Single Page: £1,200 + vat

There are limited opportunities available

I could go on, but I think you get the general drift. The BCS are funded and supported by the pharmaceutical industry. An industry that is not, currently, that bothered about statins – as the patents have run out. But it is an industry that remains extremely interested in the whole idea of lowering cholesterol. Which remains THE multi-multi-billion dollar market.

Any attack on statins threatens the foundations of this market, one that has been painstakingly constructed over the last thirty years. Keeping the cholesterol lowering idea alive, vibrant, and expanding, will make it far simpler to sell the next generation of cholesterol lowering agents that are currently lurking in the wings, engines purring.

To cut a long story short, the forthcoming attack by the BCS can be considered, to all intents and purposes, an attack by the pharmaceutical industry on anyone who dares to suggest that drugs lowering cholesterol may not be such a brilliant idea. So when you see the headlines in the newspapers damning and rubbishing Aseem Malhotra, John Abramson, and me (and a few others), you now know exactly where this attack originated, and why. Knowledge is, as they say, power.





Reality control

“And if all others accepted the lie which the Party imposed – if all records told the same tale – then the lie passed into history and became truth. “Who controls the past,” ran the Party slogan, “controls the future: who controls the present controls the past.” And yet the past, though of its nature alterable, never had been altered. Whatever was true now was true from everlasting to everlasting. It was quite simple. All that was needed was an unending series of victories over your own memory. “Reality control,” they called it: in Newspeak, “doublethink.” 1984

In my first book, the Great Cholesterol Con, I included a passage about Ancel Keys by Henry Blackburn, a colleague and admirer of Keys. It points out that Ancel Keys was humiliated by George Pickering at a meeting of the WHO in Geneva 1954 discussing the new ‘epidemic’ of heart disease. The quote from Henry Blackburn finishes thus:

My theory is that Keys was so stung by this event that he left the Geneva meeting intent on gathering the definitive evidence to establish or refute the Diet-Heart theory. Out of this single, moving, personal experience – so my theory goes – came the challenge, the motivation, the implantation of the Seven Countries Study.’

As I wrote in the book. ‘So there you have it. As a result, Ancel Keys stormed off, put together a huge research budget, hired a staff of thousands, did his study and was the able – in objective ‘scientific speak,’ of course – to say ‘I told you so, I told you so. Nyah, nyah, nyah.’ Not, as I pointed out, the best possible motivation for a research project.

Of course you are going to have to take my word on the exact events described. For, shortly after my book was published, this passage was removed from the University website it was on, never to be seen again. Cause and effect, who can say? But it does raise an important issue. If there is no record of a thing happening – did it happen? If you control the historical record, what is truth?

In the age of the Internet you might think it is more difficult to hide the historical record, but in some ways it is easier. If something only exists on a server somewhere, all you need do is delete it and it is gone – forever. Unless you ensure that you archive it yourself – something I did not do with the Henry Blackburn quote.

At this point you may wonder where this is all going. Well, for some years, I have used statistics from the European Heart Survey which looks at data from nearly a million people. The latest version is here This is very impressive bit of research, and is full of good stuff. For a few years I have included statistics from this study to produce tables such as the one below (See table).


The table makes it very clear that saturated fat intake has absolutely nothing to do with the rate of CHD deaths in any country in Europe. In fact, in general, the association is completely inverse i.e. the more saturated fat you eat, the lower the rate of coronary heart disease (CHD). Twenty times as low in France, as Georgia, despite the French eating three times as much saturated fat. This, of course, completely contradicts everything you have ever read about the impact of saturate fat on heart disease.

Jerome Burne, a friend and colleague, and medical journalist, wanted to use a couple of my tables for his blog. So I sent them over. He pointed out that my data was from the 2008 survey. In the latest 2012 survey – it take some time for the data to be published – the figures on saturated fat intake have simply gone. They are no longer published at all.

I hurriedly went back to the search the 2008 data to make sure that this had not been wiped from the record. They have not, although it is rather more difficult to find. I have now stored these data on my computer, and archived them. For I suspect that these data on saturated fat intake will gradually disappear from the historical record.

Of course, I am going to write to the researchers in charge of the European Heart Statistics and ask them why, of all the data, the data on saturated fat no longer features. Why have they done this? I strongly suspect I know the answer, and I suspect that you do to.

I am going to write although I already know the type of answer I will get. It will be some complete fudge, not answering the question but saying something along the lines of ‘Our panel of International Experts constantly review the data that we include and make decisions based on priorities that are determined by many different factors. For various reasons not all data are included, but we are always working to ensure that everything is done to provide the most useful and up to date information. Unfortunately, it is not possible to enter a discussion on specific issues.’ Beep, message ends.

It has long amused me the European Heart Statistics – if you look through them carefully – contradict almost everything we have ever been told about the causes of heart disease. Of course they are now somewhat less contradictory, because they have removed the data on saturated fat.

“Day by day and almost minute by minute the past was brought up to date. In this way every prediction made by the Party could be shown by documentary evidence to have been correct; nor was any item of news, or any expression of opinion, which conflicted with the needs of the moment, ever allowed to remain on record. All history was a palimpsest, scraped clean and reinscribed exactly as often as was necessary.” 1984

Watch this

Someone I have come to know recently is Dr David Newman, Director of Clinical Research in Mount Sinai University, New York. He has been a great thorn in the flesh of the ‘statinators’ recently. He runs a website called I recommend that everyone goes and has a look at it.

He is very concerned about providing information to the public that they can understand about various medical interventions. His work is excellent, he is clear, passionate and (nearly) 100% correct about everything.

He gave a talk called ‘The truth that lasts’ and you can catch it on you tube here.

For those of you, who have not had a heart attack or stroke, and are on statins, or are bullied into going onto statins, I suggest that you watch this. It is seventeen minutes long, and will be the most valuable seventeen minutes you have spent in your life.

Best wishes.

The planet Vulcan

I love reading about the history of science. In part, because I think you can learn so much about the process of thinking itself. Especially when it goes wrong. More especially when you are looking at the process of immunisation.

Immunisation is something that Karl Popper was particularly interested in. Popper was a scientific philosopher who is a bit of a hero of mine (when I can actually understand what he is saying). Amongst many other things, he was interested in the techniques used by scientists to protect favoured scientific hypotheses, which he called ‘immunisations’.

An immunisation is essentially a way of explaining why a fact, which appears to contradict a favoured hypothesis, does not actually contradict it at all. For example, when it was found that the orbit of the planet mercury could not be explained by classical Newtonian physics, a mathematician called Le Verrier postulated that there must be another, smaller, planet inside the orbit of Mercury that was affecting Mercury’s orbit. The planet Vulcan.

Vulcan was invisible – primarily because it did not exist. But for many years the invisible and non-existent planet served its purpose. It protected classical Newtonian physics from a potential contradiction, or refutation. Or, to be more blunt, of being simply wrong. In this case, scientists were quite happy to believe in invisible non-existent things, if the alternative was to cast aside a hallowed hypothesis.

Of course, this is just one of thousands of examples whereby unwelcome facts have been simply swatted aside, or immunised against. It is not just the Catholic Church that refuses to look through telescopes.

Vulcan, although just one example, does provide a good case study of a widely used form of immunisation tactic, the ‘ad-hoc’ hypothesis. An ad-hoc hypothesis is a secondary hypothesis that is bolted on to the side of the main hypothesis in order to defend it, or protect it. A more recent example of this can be seen in the Global warming debate.

It has been noted that global temperatures have not increased by much, if at all, in the last 15 years. This, however, is not viewed as a contradiction to the hypothesis of man-made global warming. Why not? Because it is argued that the oceans are taking in the excess heat, and trapping it. This process has held back the degree of global warming that had been predicted by the experts.

I am not going to debate whether or not this is true. I am just using it as a more recent example of an ‘ad-hoc’ hypothesis which came into existence to protect the central hypothesis. I would further add that ad-hoc hypothesis are not always wrong. They can very often be right. Le Verrier, prior to inventing the planet Vulcan, had predicted the presence of the plant Neptune due to irregularities in the orbit of Uranus.

However, if you read his works, you will know that Popper was not a fan of ad-hoc hypotheses. He felt that a good hypothesis should be fully predictive of future ‘events’ without the need for additional explanations, adaptations, or suchlike.

He did not state how many ad-hoc hypotheses it took before you had to admit defeat. One, ten, a hundred, a thousand? No-one can give you a clear cut figure, but the more of them there are, the less likely it is your central hypothesis was correct in the first place. The phenomenon of adaptation/immunisation had been recognised many years before Popper.

‘A nice adaptation of conditions will make almost any hypothesis agree with the phenomenon. This will please the imagination, but does not advance our knowledge.’ J Black 1803

I have recently been pondering the ad-hoc hypothesis once more in relation to heart disease. For I suspect that never in the history of science has a central hypothesis had so many ad-hoc hypotheses bolted on to it. Indeed, we have now reached the point where ad-hoc hypotheses have had ad-hoc hypotheses bolted onto them, to protect the ad-hoc hypotheses themselves from being refuted.

Just to look at one example. There are a number of drugs that have been developed to raise High Density Lipoproteins (HDL), the supposed ‘good’ cholesterol. A few of them also lower LDL ‘bad’ cholesterol at the same time. Billions have been spend on this class of drugs known as ‘trapibs’ . The first of these was Torcetrapib.

At this point I should probably remind you that the ‘good’ cholesterol hypothesis was only created as an ad-hoc hypothesis to explain why some/many people with high total cholesterol levels do not suffer from heart disease. ‘It’s because they have a high HDL level.’

The logic here was obvious, if horribly facile. Raise the HDL and reduce the risk of heart disease. Anyway, ignore the chasms of logic, along came the ‘trapibs’, which were going to take over from statins:

‘Hailed as a potential blockbuster that could take Lipitor’s place, torcetrapib was a cholesteryl-ester transfer protein inhibitor (CEP-T inhibitor) designed to increase good cholesterol and lower bad cholesterol. Development of the drug began in 1990 with clinical trials starting nine years later. But it wasn’t until 2006 that Pfizer got close to submitting the drug to the FDA. The company touted torcetrapib as the answer to its near-term pipeline woes, predicting the potential blockbuster could make up for billions of dollars in lost Lipitor sales when that drug went off patent in 2011.’

Well, torcetrapib certain raised HDL by about 50%, and lowered LDL by about 10%. So, what could possibly go wrong?

‘What went wrong: In late 2006, the walls came crashing down around the company. Pfizer announced in December that it was halting development of it’s prized Phase III asset. The decision came after an independent Data Safety Monitoring Board recommended terminating the study because of an imbalance of mortality and cardiovascular events. Results from a 15,000-person trial showed that patients taking torcetrapib with Lipitor experienced excess deaths than those taking Lipitor alone. Not long after torcetrapib demise, Pfizer announced that it was cutting 10,000 jobs. The company spent $800 million developing the drug.’

What went wrong was the Torcetrapib increased cardiovascular deaths about around 50% (relative increase in risk). Several other ‘trapibs’ have since come, failed, and slunk from the playing field, taking many billions down the drain with them. Yes, I know, you have never heard of them. At the risk of sounding rather big-headed, I predicted their total and abject failure long before the results of the clinical trials came out.

Now, there are those of us i.e. me who would suggest that this blows a hole in the entire good, bad, cholesterol hypothesis. But no. Why not? Because it was found that torcetrapib raised the blood pressure, and lowered potassium levels. This, it seems, was enough to explain the massive rise in CV mortality. Well, quite reasonable, you might say. Yes, but the rise in BP was minute, and the drop in potassium was equally minute. This could explain, perhaps, a 5% rise (at most) in CV mortality. Which should have been overwhelmed by the massive rise in HDL, and drop in LDL.

But no-one was going to look too closely into the figures themselves. An ad-hoc hypothesis had been found. The ‘experts’, rather than questioning the central good/bad cholesterol hypothesis simply bolted on the ‘BP rise, potassium falls’ ad-hoc immunisation device and moved on.

So, here we have an ad-hoc hypothesis, bolted onto an ad-hoc hypothesis, bolted onto the central hypothesis. We have another planet inside the invisible planet Vulcan, to explain why it is so difficult to find the planet Vulcan.

As you can see, the games played to protect the cholesterol hypothesis are, literally, endless. I am not sure when the games end? Perhaps they never do. Very clever people, given enough time and money can, it seems, twist reality round and round, inside out and upside down forever. I would call the process vulcanisation, but I think that has something to do with rubber.

What is a conflict of interest anyway?

Whilst away on my holidays I have been watching the battle between the BMJ and Professor Sir Rory Collins. A couple of years ago I watched the battle between Professor Sir Rory Collins and the Cochrane Collaboration. A month ago I was taking part in the battle between various professors and cardiologists and Professor Sir Rory Collins.

He, as you probably know, thinks statins are wonder drugs that should be prescribed to almost everyone. Actually, that is not entirely true. He doesn’t believe they should be prescribed to almost everyone. He believes that they should be prescribed to everyone.

He thinks statins have no adverse effects at all. In fact, they actually make people feel better when they take them. He viciously attacks anyone who might dare to suggest otherwise, and has accused them of killing people by frightening them off taking these uniquely lifesaving medications. This has been the basis of his attacks over the last couple of years.

Now, he might really believe all this to be true. In fact, I think he probably does. Of course, he might not believe it to be true, but he is just saying it anyway. One of the great frustrations of life is that you can never know what another person is really thinking. You can guess all you like, but it is only ever a guess.

The problem that we have here is that Professor Sir Rory Collins runs a unit called the Clinical Trials Service Unit at Oxford. This unit has received nearly £300m ($500m) in funding from pharmaceutical companies over the years. Without this funding, his unit would be very much smaller. It probably would not exist at all.

Now, you could say that this makes Professor Sir Rory Collins utterly dependent on pharmaceutical company funding, and therefore you should not believe a single word that he has to say about anything to do with statins, and other such drugs. He is completely corrupted.

You could counter argue that this is a ridiculous stance to take. His is a highly motivated and ethical researcher who works with the industry, purely in order to develop effective medicines that will help humanity. After all he is both a Sir and a Professor.

You could say that his Knighthood and professorship are completely irrelevant, and simply ask the following question. Why does he say he has no conflicts of interest to declare. Why does he state that he receives no money from industry. Why has he never admitted to the association between himself, the CTSU, of which he is a director, and £300m in drug company funding? Why does he never disclose these financial interests? Why not, indeed?

His argument, I believe, is the following. If the pharmaceutical industry pay the CTSU, who then pay him, he is not actually being paid any money directly by the pharmaceutical industry. So he has no conflicts of interest to declare. Discuss. [Shouldn’t take long].

Whether or not you think his is conflicted (and I do), this discussion leads into a rather more complicated area. What is the purpose of declaring that you have a conflict of interest in the first place? What does it matter if you are paid money by someone else who has a vested interest in making sure that certain things are said, and done.

Now, you may think the answer is simple. If Professor Sir Rory Collins states he has a conflict of interest e.g. the unit he runs is paid £300m by the industry, we can then….. We can then…..We can then what?

Believe nothing that he says about statins. Believe everything that he says. Believe most of what he says. Believe a bit of what he says. The problem is that there are only two rational positions here.

  • Believe everything
  • Believe nothing

How can you believe most, or a bit, of what Professor Sir Rory Collins says? Which bits could you ignore, which bits could you pay attention to? How could you possibly know? The answer is that you cannot.

Which then leads onto the next question. Why do medical journals, and suchlike, demand that researchers, lecturers and authors declare their conflicts of interest? What does this achieve? If having a conflict means that the author/researcher is biased, then surely the article cannot be published – as the journal is accepting a biased piece of work. Believe me, properly done, bias is impossible to spot. It’s like hearing the dog that didn’t bark.

On the other hand, if conflicts of interests mean nothing. In that you can have financial conflicts of interest, but this makes no difference to anything you say or do – why bother demanding that the conflicts of interests are declared.

In short, I cannot see what declaring a conflict of interest achieves.

Man on the Street 1: ‘Oh, I see Professor Sir Rory Collins unit has received £300m in funding from the pharmaceutical industry. Most interesting. However, this clearly makes no difference to anything he has to say on the matter.’

Man on the Street 2: ‘Oh, I see that Professor Sir Rory Collins unit has received £300m in funding from the pharmaceutical industry. Clearly he is corrupt and biased and I shall pay no attention to any he has to say.’

Man on the Street 3: …. ‘I shall believe 82% of what he has to say.’

Man on the Street 4: …..’I shall believe 23% of what he has to say.’

Which of the men on the street has the right idea? There is no way to tell, without becoming a mind reader. At present, when it comes to conflicts of interest, we just have a gigantic fudge. So long as people declare their conflicts they are then free, it seems, to do anything they like. Carry out research, write papers, sit on guideline committees, advise the Government and NICE. Declaring the interest…what? Makes the possibility of bias disappear?

But what should really happen. My view is relatively simple. I have said it before, and will say it again. If you get paid money by the pharmaceutical industry then, fine. I have no problem with that. Good for you. Buy that luxury ski chalet in the Alps if you want. Indoor swimming pools are lovely things to have. Have both – you will certainly be able to afford it.

However, once you have taken the money, directly or indirectly, you should not be allowed to sit on guidelines committees e.g NICE. Nor should you be allowed to educate your fellow doctors on best forms of drug treatment, or act as a Government advisor on healthcare matters – or suchlike. Because you are, even if you don’t think you are – and get very angry with anyone who suggests that you might be – biased.

This nettle needs to be grasped, and it needs to be grasped soon. I am not a great believer in absolutist positions, as they tend to block the compromises that are necessary for things to work in life. However, when it comes to conflicts of interest I think that the only possible position to take is absolutist. If you are paid money by the pharmaceutical industry, you cannot be appointed to a position that allows you to influence how drugs are used. End of.

Immovable Object

I have not been blogging much recently. One of the reasons is that I have been involved with a group of doctors and professors who have been fighting against the latest guidelines on primary prevention of cardiovascular disease which were due to be announced in July. We have had, as I knew, precisely no effect.

Here is the latest NICE guidance that was announced, today 18th July 2014. The committee having ignored any and all criticism:

Taking further steps to tackle the risk from heart attacks and strokes

NICE has today published its final updated guidance on the steps needed to prevent thousands of people from becoming ill and dying prematurely from heart attacks, strokes and peripheral arterial disease. NICE says doctors should consider many more people to be at risk of cardiovascular disease (CVD) which causes 1 in 3 deaths in the UK (180,000 each year).

NICE advises that the threshold for starting preventive treatment of these conditions should be halved from a 20% risk of developing CVD over 10 years to a 10% risk. Prevention includes stopping smoking, reducing alcohol consumption, taking exercise and eating a healthy diet. Once these factors have been addressed, the guidance says high intensity statin therapy should be offered.

People can be at risk from CVD because of factors they cannot change including their age, sex, ethnicity, and family history. The guidance recommends that risk factors which can be addressed should be managed.

Professor Mark Baker, Director of the Centre for Clinical Practice at NICE, says: “To make progress in the battle against heart disease and stroke, we must encourage exercise, improve our diets still further, stop smoking, and where appropriate offer statins to people at risk.

“Doctors have been giving statins to ‘well people’ since NICE first produced guidance on this in 2006. We are now recommending the threshold is reduced further. The overwhelming body of evidence supports their use, even in people at low risk of cardiovascular disease. The effectiveness of these medicines is now well proven and their cost has fallen.

“The weight of evidence clearly shows statins are safe and clinically and cost effective for use in people with a 10% risk of CVD over 10 years. “We’re not saying that everyone with a 10% or greater risk of CVD within 10 years needs to take a statin. The guideline recognises the importance of choice in preventing CVD and that this should be guided by information on the trade-off between benefits and risks.”

By recommending a systematic approach to identifying those at risk of CVD, the guideline will enable people to access treatments to address that risk by reducing their cholesterol levels. It will also provide further clarity for practitioners in primary and secondary care about how to manage patients both with and without pre-existing cardiovascular disease.

NICE recommends that people are assessed (using the QRISK2 calculator) for their risk of developing cardiovascular disease using measurements including whether or not they smoke, their cholesterol levels, blood pressure, and body mass index. The calculator then provides a percentage risk of developing CVD in the next 10 years. “This new guideline complements the NHS Health checks programme in helping to identify people at future risk of developing cardiovascular disease at a stage at which lifestyle modification can make a significant difference “says Guideline Development Group Chair Dr Anthony Wierzbicki. “It updates and simplifies treatment protocols for people with established CVD, with diabetes or kidney disease so that these people can derive maximum benefit from lipid-lowering therapies.”Liz Clark, a lay member of the Guideline Development Group, said:

“One of the key challenges is how to convince people who feel well that they need to make substantial lifestyle changes or that they benefit from lifelong drug treatment. This requires high quality information and communication on the benefits and risks of these therapies and this is reflected in the guideline.

“The guideline therefore places patients centrally in any decision making about their management and it emphasises the need to address all CVD risk factors in combination. “It highlights the need for doctors to encourage people to participate in reducing their CVD risk. For example, it recommends that doctors assess a person’s readiness and confidence to make changes to their diet, level of physical activity and smoking and alcohol consumption, as well as taking long-term medication. It also recommends that people are involved in developing a shared management plan.”

So, up to 17 million people in the UK will now be taking statins for the rest of their lives. Well, of course, we will never get anywhere near this number. After about a year 50% of people stop taking their statins – I wonder why. A lot of people will refuse to take them in the first place. But millions and millions will take these drugs for many years.

This is clearly, and absolutely, nuts. My major fear, as I tell anyone, is not that statins have a lot of adverse effects – which they do. You can always stop taking them and the adverse effects go away. If, that is, the effects are not permanent.

I have heard enough testimony from patients, and people who e-mail me, and reviewing FDA Medwatch (the system for picking up drug related adverse effects in America) to believe, one hundred per cent, that many people have been left permanently disabled from taking statins.

My personal belief is that the true burden of damage that will be caused by millions of people taking statins, forever, is very heavy. Every individual case of irreversible neuropathy, or muscle wasting, or degenerative neurological condition, or suchlike, is dismissed as anecdote by the great and the good – and the NICE. ‘Statins don’t do that.’ Is what I hear.

Well, part of me hopes that statins really don’t do that. But, frankly, I don’t believe it. I believe that mass statination of the entire adult population is an absolute medical disaster. I shall continue the fight.