You need a statin – now what was the question?

As many of you are aware the American College of Cardiology (ACC) and the American Heart Association (AHA) came out with new guidelines on cardiovascular disease prevention a few days ago. As part of this, they produce a risk calculator. Using this calculator, if your risk of heart attack or stroke is greater and 7.5% over the next 10 years, you should take a statin – for the rest of your life.

I downloaded this calculator, and I have been playing around with it. I think I would tend to agree with the headline in the NY times 18th November 2013:

Risk Calculator for Cholesterol Appears Flawed

To be frank you can fiddle around with the figures on this calculator for hours. I think my OCD is getting worse. (Maybe I should take a statin to cure my OCD). One of the questions I wanted to find an answer to was the following, at what age would a perfectly healthy man (with ‘optimal’ risk factors) have to take a statin for the rest of his life.

So, I fed in the figures, and use the ‘optimal’ figures for cholesterol and blood pressure on the risk calculator

THE PERFECTLY HEALTHY MAN

  • Male
  • Age 63
  • Race: WH (white)
  • Total cholesterol 170mg/dl [This is 4.4mmol/l in Europe i.e. very low]
  • HDL cholesterol 50md/dl [This is 1.3mmol/l in Europe]
  • Systolic blood pressure 110mmHg
  • Non-smoker
  • No treatment for high blood pressure
  • Non diabetic

CV risk over the next 10 years = 7.5%

So, there you are. You can do absolutely everything ‘right’ be as healthy as healthy can be – according to the AHA and ACC. Yet, by the age of sixty three you need to take a statin – for the rest of your life.

The next question I wanted to find the answer to was, at what age does a ‘normal’, very healthy man have to start using a statin? In the UK, the average total cholesterol for men is 5.0mmol/l. [this is 193mg/dl in the US]. The average blood pressure in the UK systolic is 129mmHg.  (To be frank, I think the average cholesterol level for men is higher than this, but the WHO says not).

Feed these figures in, and you would need to start taking a statin, for the rest of your life, by the age of fifty eight. Which means that very healthy men, with no real risk factors for cardiovascular disease – at all – have to start statins at fifty eight.

What of women. Well, they get another seven years of statin free life. A super healthy woman, with optimal risk factors, reaches the dreaded 7.5% risk aged 70. An ‘average’ healthy women, with average BP and cholesterol levels, would have to start a statin aged sixty three.

In summary, using this risk calculator, extremely healthy men will be starting statins at fifty eight, and very healthy women at sixty three. This, then, marks the age at which life becomes a statin deficient state. You can be as healthy as healthy can be. You can do everything right, have no risk factors at all for cardiovascular disease, and yet you still need to take medication to reduce the risk of cardiovascular disease.

Sorry, what was the question again?

European cardiovascular disease statistics can be found here.

They have now, officially, all gone mad?

The Mad Hatter: ‘Have I gone mad?’

Alice: ‘I’m afraid so, you’re completely bonkers, but let me tell you something, the best people usually are.’

Alice in Wonderland

I find myself quoting Alice in Wonderland more and more these days. I now think it was never a children’s book, it was an accurate scientific analysis of human behaviour.

As many of you are aware the American medical authorities have come up with the latest guidelines to reduce cardiovascular risk. A major part of the guidelines is now to inform us all that we should forget about lowering cholesterol (LDL) levels, and just take a statin…. no matter what¹.

This is how the New York Times put it:

First, the guidelines have moved away from achieving target cholesterol levels.
Americans have long been urged to focus on their laboratory numbers. Many people are obsessive about checking their cholesterol levels and pursuing even better numbers. Doctors have been told to focus on these numbers and, in some cases, the quality of their care was assessed by the percentage of their patients with low cholesterol levels.

Those days are over. The new guidelines recognize that for patients who have exhausted lifestyle efforts and are considering drug therapy, the question is not whether a drug makes your lab tests better, but whether it lowers your risk of heart disease and stroke. Studies over the past several years have shown that improving your lab profile with drugs is not equivalent to lowering your heart risks².

One of the most influential cardiologists in the world, Steven Nissen, had this to say:
“The evidence was never there” for the LDL targets, he said. Past committees “made them up out of thin air,” he added.

Past committees made them up out of thin air….. Let me try that statement again…. Past committees made them up out of thin air. Exactly. Ex-bleedingly-zactly.

So, ladies and gentlemen, you have been conned. Utterly, completely and barefacedly conned, for the last thirty years. Your cholesterol level has absolutely no impact on your risk of cardiovascular disease. You think not? Well, that is precisely what they are saying in these guidelines. If not in quite such plain words.

But, of course, I am not being entirely fair to them. The level of LDL may actually matter after all – according to the same guidelines. For, as the New York Times article goes on to say.
There’s one exception to the numbers rule. People with very high levels of the harmful cholesterol known as LDL still need to worry about targets. The new guidelines set that LDL level at 190 milligrams per deciliter – but the principle is that if people have very high cholesterol levels, then their cardiovascular risk is so high that it is likely that treatment to reduce the levels would offset any risks of the drug treatment.

So, your LDL level doesn’t matter in the slightest, unless it is a very high level. Then the level does matter a great deal. Please explain, oh great cardiologists, does LDL, or does it not, cause cardiovascular disease.

Well, it seems that it both does, and does not, simultaneously. Amazingly, we have achieved a quantum state with LDL. It simultaneously exists as a molecule that can both cause – and not cause – CVD. Which means, of course, that the levels must be both lowered, and not lowered. Yes, well, this makes perfect sense. At least it would to a lunatic.

Perhaps if we open the box with the ‘at risk cat’ in it, we will find that this new version of Schrodinger’s cat died of a heart attack caused by LDL. Alternatively, it did not. Before opening the box, it exists in both possible states. It is an interesting variation on a theme.
The most astonishing thing is not that these people are now talking the most complete gibberish. They have been doing this for years. The most astonishing thing is that the vast majority of the population will still listen to what they have to say – and follow their advice.
Well, good luck with that all you billions of mad people, following the advice of these mad scientists Good luck with that indeed. I salute you. Meanwhile I shall attempt to find the answer to a far more important question than what causes heart disease.

“Why is a raven like a writing desk?”

1: http://circ.ahajournals.org/content/early/2013/11/11/01.cir.0000437740.48606.d1
2: http://well.blogs.nytimes.com/2013/11/12/3-things-to-know-about-the-new-cholesterol-guidelines/

The backlash begins

(Catalyst under fire)

Those who read this blog will know that Maryanne Demasai, a journalist at the Australian Broadcasting Company (ABC), put together two programmes. One questioning the cholesterol hypothesis; the other very critical of the over-prescribing of statins. They can be seen here.

Heart of the Matter Part 1 – Dietary Villains

Heart of the Matter Part 2 – Cholesterol Drug War

Over several months I helped Maryanne to put together the scientific arguments, and I feel proud to have done so. I warned her, though, that she should expect a vicious backlash if the programmes ever went out. Of course, it has happened.

Also, exactly as I told her, the attacks are not on the data. They can’t be, as the science she presented is pretty much spot-on. They are personal attacks on everyone who took part. Those she interviewed are being accused of being “crack-pot quacks”, ‘into earthing’….and ‘snake oil salesman selling vitamins’ etc.

You can see the latest (evidence free attack) here. A programme by media watch, which includes such scientific observations as the fact that Maryanne did not smile when speaking to a conventional ‘expert.’ Off with her head, the biased hussy! http://www.abc.net.au/mediawatch/

Of course none of this surprises me. I knew exactly what would happen, and how it would happen. This is not because I am sort of a genius. It is that I have seen it all before, many times. Here follows a personal testimonial from a Dutch Journalist Melchior Meijer, who had the temerity to criticise statins in the past:

My name is Melchior Meijer. I’m medical reporter for several magazines and newspapers in The Netherlands. Reporting about the many obvious flaws in the cholesterol hypothesis, shedding light on the biologically plausible adverse consequences of statin therapy, is as close to 21st century blasphemy as a medical journalist can come.

I experienced this in 2004, when I wrote an article about statins in a national newspaper. In the article, several doctors and scientists expressed well founded doubts about the safety of statin therapy in the general population. I also presented a few `anecdotal’ cases of statin induced harm, which were extremely easy to find.

The medical establishment reacted in fury and started an aggressive media offensive. Carefully avoiding the arguments in my article, they used their authority to hang me out on TV as a liar, a potential mass murderer. They called for `official measures’ to prevent naive journalists from making similar `tragic mistakes’ in the future.

They also took me to the Press Court, but they didn’t reckon with the fact that the Press Court checks facts and figures. The Court did an investigation and decided that I had just done my job, observing and questioning. [As an aside: the chief of my newspaper, born into a family of influential physicians, was not happy with the Court’s decision. He had already apologized on television for `this tragic mistake’.]

After this statin users started calling and mailing to the media, always reporting the same symptoms: various degrees of (muscle pain) and loss of muscle mass, exhaustion, personality changes and amnesia. But my colleagues didn’t like to take up this serious issue. That is, until last March when the TV-colleagues of TROS Radar, a consumer programme with an average of 2 million watchers (we have 16 million inhabitants), took up the subject.

Dutch cardiologist Dr Paul de Groot expressed his doubts about cholesterol as a causal factor, and postulated that statins sometimes do more harm than good, especially in primary prevention. Dr Uffe Ravnskov, who by the way was honoured yesterday with the prestigious Leo Prize for independent science, pointed out the many flaws in the cholesterol hypothesis.

The programme also interviewed people who had experienced devastating side effects from statins, which quickly disappeared upon discontinuation – although sometimes they did not. I was on the programme to explain how Unilever had succeeded in keeping an unfavourable article about its cholesterol lowering spread Flora out of the press.

When the shit hits the fan…

My time is limited, so I will make it short. Radar was vigorously attacked from all directions. Professors Martijn Katan and John Kastelein used various media outlets to shamelessly fire irrelevant, slanderous attacks on Dr Ravnskov. As usual, they did not address any of the scientific arguments. Radar invited Katan and Kastelijn for a public debate with Drs Ravsnkov and Kendrick, but they declined.

The Dutch Cardiologists Association, together with the Healthcare Inspectorate – and this is critical – announced official guidelines for medical journalists who plan to cover `delicate medical matters.’

History, you see, does repeat itself, and so I can predict what now happens in Australia. There will be calls to bring in ‘official guideline for medical journalists who plan to cover ‘delicate medical matters.’ This is also known as press censorship. It has been popular in various dictatorships over the years. Currently, North Korea is the best place to see this in action.

Believing in impossible things – there is a trick to it

At times, all you can do it shake your head in amazement, and wonder at the ability of people who think of themselves as scientists to make statements that are impossible to reconcile with reality, or logic….or pretty much anything to do with science.

Yesterday, I was sent a copy of a paper called ‘High coronary plaque load: a heavy burden.’ Published in the European Heart Journal in August 2013. It looked at the use of statins to reduce the volume of plaque in arteries. I include three verbatim quotes from the paper:

  • Of particular interest, neither LDL cholesterol levels at baseline nor those after high dose statin treatment could independently predict major adverse cardiovascular events (MACEs)
  • One of the most striking results of this study is the fact that LDL levels at baseline or after statin treatment showed no predictive value for MACEs. This could lead to doubt about the beneficial effect of LDL-lowering therapy. However, as also discussed by the authors, there is overwhelming evidence for the beneficial effects of statin therapy on plaque progression and MACEs.
  • Currently statin therapy is so fundamentally established in clinical practice that its beneficial effect is beyond doubt. Even though it has been demonstrated that in patients receiving statin therapy LDL levels have no additional prognostic value, further lowering of LDL cholesterol levels with novel PCSK9 monoclonal antibodies could further reduce the residual risk in these patients1.

So, the researchers discovered that LDL (‘bad’ cholesterol) levels did not predict major coronary events:  angina, heart failure, heart attacks and suchlike. Neither did the degree of LDL lowering with statins have any correlation with coronary events. At this point, having very clearly established that their research flatly contradicts the cholesterol hypothesis, they finished off by remarking that when the new cholesterol agents arrive, which will lower LDL levels even more than statins, they will ‘further reduce the residual risk in these patients.’

I shall try to reduce this paper to its ineluctable essence.

  • We have found that LDL levels have nothing to do with cardiovascular disease
  • We have found that the degree of LDL lowering with statins does not correlate with cardiovascular events
  • We think we need to the lower the LDL more to prevent cardiovascular disease

‘Alice laughed. ‘There’s no use trying,’ she said. ‘One can’t believe impossible things.’

‘I daresay you haven’t had much practice,’ said the Queen. ‘When I was your age, I always did it for half-an-hour a day. Why, sometimes I’ve believed as many as six impossible things before breakfast. ‘Lewis Carroll – Alice in Wonderland.

I suppose it becomes easier to believe in impossible things if you have a few conflicts of interest to help you along the way…..smooth the pathway of belief, so to speak. Here follows the conflict of interest statement from the paper:

Conflict of interest:

J.W.J. receives research grants from and was a speaker at meetings sponsored by Astellas, AstraZeneca, Biotronic, Boston Scientific, Bristol-Myers Squibb, Cordis, Daiichi Sankyo, Eli Lilly and Company, Medtronic, Merck-Schering Plough, Pfizer, Orbus Neich, Novartis, Roche, Servier, the Netherlands Heart Foundation,the Interuniversity Cardiology Institute of the Netherlands, and the European Community Framework KP7 programme. M.A.dG. has no conflicts to declare. The Department of Cardiology received research grants from Biotronik, Medtronic, Boston Scientific

Corporation, St Jude Medical, Lantheus Medical Imaging, and GE Healthcare.

For those paying attention, you may have noticed the mention of PCSKP monoclonal antibodies earlier.  What are these, I hear you cry. These are the next monstrous regiment of cholesterol lowering agents that are waiting in the wings, engines running smoothly. If you thought statins were heavily promoted – you ain’t seen nothing yet.

You may not be astonished to learn that one or two of the companies listed in the conflict of interest statement of that paper are developing PCSK9 monoclonal antibodies. I wonder if that could have anything to do with the statement……’further lowering of LDL cholesterol levels with novel PCSK9 monoclonal antibodies could further reduce the residual risk in these patients.’

And if that thought depresses you, as it does me, here is a little poem by W.H. Auden to cheer you up:

‘Give me a doctor partridge-plump,
Short in the leg and broad in the rump,
An endomorph with gentle hands
Who’ll never make absurd demands
That I abandon all my vices
Nor pull a long face in a crisis,
But with a twinkle in his eye
Will tell me that I have to die.’

1: Michiel A. de Graaf and J.Wouter Jukema. ‘High coronary plaque load: a heavy burden.’ European Heart Journal (2013) 34, 3168–3170

If not cholesterol – what?

(Part 2 of an occasional series about what really causes heart disease)

One of the greatest strengths of the cholesterol hypothesis is that there is no obvious alternative to replace it with. Stress? Well I believe that, in fact, stress is the number on cause of premature cardiovascular disease (although there are many provisos attached to this statement).

But if stress does cause heart disease, how does it do this? With the cholesterol hypothesis you have the massive advantage of superficial simplicity

  • You eat too much cholesterol
  • The level of cholesterol in your blood rises
  • The excess cholesterol is deposited in the artery wall, causing narrowings/thickenings (plaques)
  • Eventually these block the circulation, causing heart attacks and strokes

Dead simple?

Of course, when exposed to the harsh light of critical thought, each link in this neat and tidy causal chain crumbles to dust. But it is such a seductive hypothesis that the mind is drawn back to it again and again, like moths to candlelight. It seems so perfectly simple that it must be true.

On the other hand, as I write this, I am also studying the cover of a recent British Medical Journal (BMJ). The headline is ‘Cardiovascular Disease and Aircraft Noise.’ You may have heard about this research in the mainstream media. It seems that living near an airport raises the risk of stroke by 24%, and the risk of heart disease by 21%. It is suggested this is due to the noise pollution. Okay, nice idea, but how?

How can aircraft noise cause your arteries to thicken and narrow?

I believe that this can be explained, but only if you completely discard the cholesterol hypothesis of cardiovascular disease, and look afresh at what heart disease may actually be, and how it is caused.

Atherothrombosis

At this point I am going to introduce a relatively arcane term, ‘atherothrombosis’. No, I have not just made this word up. Nor is it recent. In fact, the basic idea has been kicking around for the last one hundred and sixty years. The concept of atherothrombosis was first proposed by Karl Von Rokitansky in 1852. He believed that thickenings in arteries, or plaques, were the end result of thrombosis (blood clots) forming on the arterial wall. Mainly because plaques looked exactly like blood clots, and seem to contain the same materials e.g. fibrin (a key ingredient of blood clots).

Virchow, another doctor and researcher, who lived during the same era, and who was significantly more influential, argued that this was nonsense. He had noted that plaques were to be found underneath the lining of the artery (endothelium). He argued that it was not possible for a clot to form within the artery wall itself. Frankly, a pretty good argument in the light of their knowledge at the time.

It was also Virchow who noted that plaques contained a lot of cholesterol, and so he hypothesised that cholesterol in the blood irritated the lining of the artery and then entered the arterial wall. Thus began the cholesterol hypothesis.

Although Virchow won the argument, the atherothrombosis hypothesis has sprung back into life at various point over the years, only to die back again. A fellow Scot called Duguid promoted the idea heavily around the second world war, and just after. Various other researchers have also supported the concept that heart disease is primarily due to blood clotting (thrombosis) – in some way.

Interestingly, at one point Pfizer also started to promote atherothrombosis as the cause of heart disease. For sentimental reasons I have kept hold of an educational booklet produced by Pfizer in 1992. On page four it states

Several features of mature plaques, such as their multi-layered pattern, suggest that the platelet aggregation and thrombus formation are key elements in the progression of atherosclerosis. Platelets are also known to provide a rich source of growth factors, which can stimulate plaque development.

Given the insidious nature of atherosclerosis, it is vital to consider the role of platelets and thrombosis in this process.’ [Well, quite]

There is little point in referencing this document, as I probably have the only copy left in existence. It is called ‘Pathologic triggers. New insights into cardiovascular risk.’ Produced by Medi Cine Inc. For Prizer Inc Copyright 1992, All rights reserved etc. etc.

It is interesting that when Pfizer did not have a statin, they were looking away from cholesterol as a cause of cardiovascular disease. It will come as no surprise to you that this was not through some altruistic attempt to discover the truth about the true cause of heart disease. It was to help market their drug doxazosin (a BP lowering drug) which had some additional anticoagulant properties.

Of course, as soon as atorvastatin arrived on the scene, no more was heard from Pfizer about the ridiculous concept of atherothrombosis. It was cholesterol, cholesterol, all the way, and fifty billion dollars in profit from atorvastatin.

Pity, really, because in my view, Pfizer had it right in 1992. C’est la vie.

Perhaps I am straying from the issue here. What is atherothrombosis? Or, what is the hypothesis of atherothrombosis?

It goes something like this:

  • The lining of the artery (endothelium) is damaged
  • A thrombus (blood clot) forms over the area of damage
  • After a very short time the blood clot stops growing – and stabilises
  • Blood cells called endothelial progenitor cells (EPCs) are attracted the surface of the clot
  • The EPCs grow bigger, join together at the edges, and form a new endothelial layer on top of the thrombus [so the thrombus is now present inside the artery wall]
  • Various repair systems go into action, to clear away the thrombus from within the artery wall

Rokitanksy did not know there were such things as EPCs, so he had no explanation as to how the thrombus could be found underneath the endothelium (single later of cells lining artery walls). The answer is, of course, that the endothelium was not there when the thrombus occurred. It reformed on top of the thrombus. Yes, simple when you know how.

Had Rokitansky known this, and won the argument, we would possibly never have heard of cholesterol ever again. Unfortunately, as he didn’t know that EPCs existed, Virchow kicked the idea of atherothrombosis into touch, and so cholesterol became the single molecule that has triggered more Nobel prize winning research than any other.

The role of endothelial Progenitor Cells

I recently asked a medical student who had the misfortune of being stuck with me for the day.

Me:  ‘What happens in you scratch your skin.
Medical student : ‘You bleed.’
Me: ‘Then what?’
Medical Student: ‘A scab forms.’
Me: ‘Then what?
Medical student:  ‘The scab falls off after your skin has healed.’
Me: ‘Good, so what happens if you scratch/damage the lining of your artery?’
Medical student: ‘A scab/thrombus forms.’
Me: ‘Then?’
Medical student: ‘Then it falls off…..’
Me: ‘Then what happens?’
Medical student: ‘It….’
Me: ‘It travels down the artery till the artery narrows, and the blood clot gets stuck somewhere?’
Medical student: ‘Ummmm….’
Me: ‘Ummmm, indeed.’

Clearly, you cannot have blood clots breaking off and travelling down arteries to get stuck further down. This would be horribly damaging.  Strangely, human physiology is a bit cleverer than that. Yes, if you scratch your skin the clot/thrombus falls off after the skin has healed. This causes no harm to anything. But a damaged blood vessel has to be able to get rid of the thrombus that forms without it breaking off and travelling to the nearest organ e.g. the brain, where it blocks a blood vessel and causes a stroke.

Also, the lining of the artery wall is nothing like the skin. The most superficial layer of the skin (the epidermis) is a single layer of cells. But this layer starts life deeper down, in the dermis. Cells formed in the dermis gradually move towards the surface where they then fall off.

However, the single layered of cells lining the artery walls do not start life deeper in the artery wall, and grow outwards (or inwards). These cells come from within the bloodstream itself. These are Endothelial Progenitor Cells (EPCs). They are formed in the bone marrow and float around in the bloodstream. They are attracted to areas of endothelial damage. They stick to these areas, grow into mature endothelial cells, and form a new layer of endothelium.

A neat and perfect system for ensuring that damage to blood vessels can be covered over, and the resulting thrombus does not end up jamming up the downstream blood vessels. Ask the average doctor about EPCs and I can guarantee they have never heard of them. Never, ever. Important little things though.

As you age, the production of EPCs falls. If you are stressed, the production of EPCs falls. If you take steroids the production of EPCs falls. If you have kidney disease, the production of EPCs falls. Guess what. All of these things are associated with a vastly greater risk of cardiovascular disease. Vastly greater.

For now just to look more closely at one of these risk factors, steroids. Steroids are used in a wide range of medical conditions such as asthma, rheumatoid arthritis, and inflammatory bowel disease. Essentially, they are the most potent anti-inflammatory agents known – and in any disease where inflammation is a major problem steroids work brilliantly (for a while at least).

Steroids can be more accurately called corticosteroids, because the basic building block of all steroids is cortisol. This is one of the natural steroid hormones made within the adrenal glands. It is a stress hormone, which will be produced in much greater amounts under a situation of threat/stress.

So, what happens if cortisol levels are chronically raised? Well, there is a condition called Cushing’s disease. The underlying problem in Cushing’s disease is excess production of cortisol, which can happen for various reasons….that I do not have the time to discuss here.

People with Cushing’s disease develop a range of metabolic problems: high blood sugar levels/type II diabetes, high levels of clotting factors, raised triglycerides, low HDL, high blood pressure, central obesity etc. Production of EPCs also falls. This abnormal metabolic pattern is also seen in those who take a high dose of steroids over a long period of time, where production of EPCs also falls.

Of greatest interest is the fact that people with Cushing’s disease suffer a greatly increased rate of heart disease. Relative risk increased by around 600% – 700% (Or more). People who take steroids long-term have a ~400% increased risk of dying of CHD.

These are not small increases in risk. They are far greater than any of the standard accepted risk factors for cardiovascular disease. In fact, we are talking molehills next to Mount Everest here.

For now, taking the discussion back to those who live near to airports. It is known from a great deal of research that people who suffer long-term negative stress exhibit abnormal cortisol production.  Although it won’t be nearly as extreme as those with Cushing’s, or those taking steroids. They also have an increased risk of dying of heart disease and stroke.

It is known that noise pollution creates long-term negative stress. It is now known that people living next to airports suffer a high level of strokes and heart disease.

Try and use the cholesterol hypothesis to explain the increased risk, and you can’t. Try and use the atherothrombosis hypothesis to explain this phenomenon and, it all fits together without any trouble at all. So, who wins this argument? Virchow, or Rokitansky?

Of course it is not nearly as simple as: stress > increased cortisol secretion > reduce EPC production > atherothrombosis…… But it is one important link in the chain.

More on this, at some point.

The Cholesterol Myth [video] Part 2

Heart of the Matter | The Cholesterol Myth: Dietary Villains and Cholesterol Drug War.
Thursday, 31 October 2013 on ABC 1 (Australia)

Is the role of cholesterol in heart disease really one of the biggest myths in the history of medicine?

For the last four decades we’ve been told that saturated fat clogs our arteries and high cholesterol causes heart disease. It has spawned a multi-billion dollar drug and food industry of “cholesterol free” products promising to lower our cholesterol and decrease our risk of heart disease.

But what if it all isn’t true? What if it’s never been proven that saturated fat causes heart disease?

And what if the majority of patients taking cholesterol lowering drugs won’t benefit from taking these pills?

In a special two part edition of Catalyst, Dr Maryanne Demasi investigates the science behind the claims that saturated fat causes heart disease by raising cholesterol.

A new blog that I hope you will support

HealthInsightUK.org gives progressive doctors and health experts a platform to make a science-based case for changes in the treatment and prevention of disease.
Edited by award-winning health journalist Jerome Burne, HealthInsightUK explains, without bias, why drugs are not the only – and may not be the best way to cut the risk of the big 3 killers: cancer, heart disease and diabetes, as well as the major debilitators: obesity and Alzheimer’s.
The team sets out the science behind ‘alternative’ regimes, which your doctor may not have the time or inclination to discuss – and which drug companies have no financial reason to research.
HealthInsightUK will be, Jerome Burne says, “an independent and reliable source of information about drug risks and side effects, as well as providing scientific evidence for non-patentable treatments.”

The launch version which goes live today leads, with an article by Jerome Burne about why a very low carb diet could be a new treatment for cancer.

Integrated medicine practitioner and nutrition specialist Dr John Briffa GP describes the British Heart Foundation’s promotion of a risky treatment; statin-sceptic Dr Malcolm Kendrick explains why statin’s side-effects outweigh the benefits and Dr Des Spence, a columnist for the BMJ, asks: if diabetes is a lifestyle disease why do we spend 600 million treating it with drugs?

The Cholesterol Myth [video] Part 1

The Cholesterol Myth: Dietary Villains and Cholesterol Drug War.
Thursday 24 October on ABC 1 (Australia)

Is the role of cholesterol in heart disease really one of the biggest myths in the history of medicine?

For the last four decades we’ve been told that saturated fat clogs our arteries and high cholesterol causes heart disease. It has spawned a multi-billion dollar drug and food industry of “cholesterol free” products promising to lower our cholesterol and decrease our risk of heart disease.

But what if it all isn’t true? What if it’s never been proven that saturated fat causes heart disease?

And what if the majority of patients taking cholesterol lowering drugs won’t benefit from taking these pills?

In a special two part edition of Catalyst, Dr Maryanne Demasi investigates the science behind the claims that saturated fat causes heart disease by raising cholesterol.

Sweden gets it right

I sometimes think that I should go and live in a Scandinavian country. They get so many things right about how to run healthy, equitable, societies. In addition, the people who live there seem more balanced and, well, frankly, more grown up. So it comes as no surprise to me that if a nation was to turn round and begin the process of rejecting the absolute nonsense that a high fat diet is bad for you, then it would be a country in Scandinavia.

That Scandinavian country is Sweden1.

Now, I have been aware that there has been a movement towards a high fat low carb diet (HFLC) going on in Sweden for some years. This has been led recently by the heroic Dr Annika Dahlqvist, a General Practitioner who had been advising her diabetic patients to eat a low carb high fat diet (LCHF).

She was, of course, attacked by the idiots…sorry experts:

‘In 2007, the controversy began when two dieticians pointed out to Sweden’s National Board of Health and Welfare that LCHF dietary advice recommended to diabetic patients by general practitioner Dr Annika Dahlqvist was not compatible with either scientific evidence or conventional practice. However, following a report by diabetologist Dr Christian Berne, Dahlqvist was cleared.’

Cleared of what, exactly? Advising diabetic patients not to eat sugar. The mere fact that anyone could be dragged in front of the authorities for advising this just shows had completely mad the world of dietary advice has become. How entrenched the idiotic anti-fat dogma now is. How utterly divorced from reality and science.

As I have pointed out many times on this blog, and elsewhere, carbohydrates, at least all the carbohydrates humans can digest, are converted to sugar(s) in the GI system. They must be, because all that carbohydrates consist of are different number of sugar molecules bonded together in different ways. When you break them to bits in the digestive system, they become simple sugars.

As we all know, people with diabetes have problems with high blood sugar levels. So, dum de dum….let me think. Should diabetics eat carbohydrates/sugar, or should they eat fats. Yes, you are right, they should eat fats. This is a complete no brainer.

But, of course, the argument goes that diabetics are more likely to die of cardiovascular disease and eating fat increases cholesterol levels, and this increases your risk of cardiovascular disease. Well, this could obviously be a problem if any part of that causal chain were true. But it is all nonsense. As the latest Swedish report from the SBU (Swedish Council on Health Technology Assessment) makes clear (after reviewing 13,000 studies), a low carb diet leads to the terrible dangers of

‘…a greater increase in HDL cholesterol (“the good cholesterol”) without having any adverse effects on LDL cholesterol (“the bad cholesterol”). This applies to both the moderate low-carbohydrate intake of less than 40 percent of the total energy intake, as well as to the stricter low-carbohydrate diet, where carbohydrate intake is less than 20 percent of the total energy intake. In addition, the stricter low-carbohydrate diet will lead to improved glucose levels for individuals with obesity and diabetes, and to marginally decreased levels of triglycerides.’2

In short, when they looked at all the evidence, they found that low carb/high fat diets raise HDL cholesterol (the so-called ‘good’ cholesterol). They have no effect on LDL levels; they also lower blood sugar levels and triglyceride (VLDL) levels. All good and healthy, and all of which bascially means that insulin resistance has been reduced – the underlying cause of diabetes.

In reality all that the Swedes really ‘discovered’ is the quite astonishing fact that eating a high carbohydrate diet is bad for you, and worse for you if you are a diabetic. Well, blow me down with a feather. They have found exactly what a working knowledge of human biology/physiology would tell you would happen.

But we live in a wold controlled by entrenched stupidity, dogma, and the financial interests of massive companies who are making billions selling tasteless low fat mush. These companies know that the only way you can make low fat food, e.g. low fat yoghurt, taste like anything half palatable is to stuff it with sugar. Cheap, nasty, and damaging to health – also driving the ever increasing weight gain and diabetes in the Western World.

Why is everyone in the Western World becoming obese? Because we are replacing fat with sugar in many foodstuffs. The obesity ‘epidemic’ started at exactly the same time as the idiots, sorry experts, decreed that a healthy diet was a diet full of carbs. Which was, and remains, the exact and complete opposite of the truth.

However, anyone who dares to stand up and state the truth, gets dragged in from of organisations such as the National Board of health and Welfare. Eventually, however, the truth does emerge, as it must. Because the truth never dies. It can be stomped on, squashed, concreted over and napalmed. However, it lives on, taunting those who do everything in their power to deny its existence.

The truth is that all of the dietary advice we have been bombarded with for the last forty years about the dangers of fat consumption has been utterly and completely and damagingly wrong. Of course there will be a backlash against the Swedish report – there always is. Various powerful idiots, sorry experts, will be pushed in front of cameras to make various denunciations of the Swedes and their damaging and dangerous conclusions. The strings of these idiots will be jerked in unison by faceless marketers in companies that promote low fat spreads, and the like. Yes, you know who you are.

And yes, this stuff does make me angry. It is killing people prematurely, millions of people, all around the world.

1: http://coconutoil.com/sweden-becomes-first-western-nation-to-reject-low-fat-diet-dogma-in-favor-of-low-carb-high-fat-nutrition/

2: http://www.dietdoctor.com/swedish-expert-committee-low-carb-diet-effective-weight-loss

P.S:

Question:            ‘What do you call five hundred dieticians lying at the bottom of the ocean?’
Answer:               ‘A good start.’

So much for scientific debate

I thank Ted Hutchinson for pointing me at this article in the Irish Independent. It appeared on the 5th of October, and I reprint it in full, here.

A LEADING vascular surgeon, whose research review concluded cholesterol-lowering medicines may do more harm than good for many otherwise healthy people, has been gagged by the Health Service Executive.

Sherif Sultan, a senior medic at University College Hospital, Galway, reviewed a range of studies of statins and found a lack of evidence to show they should be given as a means of prevention to healthy people with high cholesterol but no heart disease.

Mr Sultan and his surgeon colleague Niamh Hynes said lifestyle changes to reduce cholesterol were better because this allowed people to avoid the risk of statins’ side effects.

However, in a statement last night, Dr Pat Nash, a cardiologist and the group clinical director in University College Hospital said the recently published views of his colleagues were “not representative” of those in Galway or neighbouring hospitals.

“As group clinical director of the West/North West Hospitals Group, and a working cardiologist, I wish to reassure patients that statins are safe,” said Dr Nash.

“These are very important, well-validated drugs for the treatment of elevated cholesterol. We have extensive evidence to show their benefit and to show that they improve outcomes for patients with heart disease and stroke and that they have a role in preventing heart disease and stroke.

“As always, if patients have any concerns, they should not discontinue their medication without discussing with their GP or consultant.”

Asked to comment, Mr Sultan said: “I have received an official warning from the HSE and have been instructed not to liaise directly with the press in my capacity as a HSE consultant.” However, he said he could continue to comment as a consultant vascular surgeon at the Galway Clinic, where he has a private practice.

The HSE declined to comment on the reasons for ordering Mr Sultan not to speak as a public consultant. He said he stood by his analysis of the role of statins in otherwise healthy patients with high cholesterol. He pointed to another recently published review on exercise versus drug therapy in the management of pre-diabetes and cardiovascular disease.

“That ‘British Medical Journal’ analysis showed the superiority of exercise over drug therapy extends even to secondary prevention (where patients have developed disease)1.

This story has been rumbling on for a while. A report on the research paper can be found in the Irish Medical Times from a couple of weeks before.

The under-reporting of findings on major adverse effects of statin therapy and the way in which they had been withheld from the public, and even concealed, is a scientific farce, claims new Irish research.

Mr Sherif Sultan, Consultant Vascular and Endovascular Surgeon, and Niamh Hynes, Clinical Lecturer In Vascular and Endovascular Surgery, claimed their study, just published in the Journal of Endocrine and Metabolic Diseases (2013, 3, 179-185) highlights the major side-effects and dangers of statins.

They said there is a categorical lack of clinical evidence to support the use of statin therapy in primary prevention. They are both based in the Western Vascular Institute at University College Hospital Galway and the Galway Clinic. “Odds are greater than 100-to-1 that if you’re taking a statin, you don’t really need it2..

I was sent the original paper by Sherif Sultan a couple of months ago, and it is very scathing about statins….. very scathing indeed. It even suggests, perish the very thought, that pharmaceutical companies may have been trying to present statins in the best light possible. I find such a suggestion almost impossible to believe. Knowing how completely ethical these companies are.

Anyway, I suppose the key phrase in all of this sorry episode is the following:

The HSE declined to comment on the reasons for ordering Mr Sultan not to speak as a public consultant.”

If the Health Service Executive were to comment, what could they say to justify their actions?

The hell with scientific debate. He should just damned will shut up and say what we want him to say?”

“How dare anyone criticise the sainted statins which work in mysterious ways their wonders to perform.”

We expect utter loyalty from those who work in the glorious Irish Health Service. Those who do not support us can expect serious sanctions……”

On balance, declining to comment is probably the best policy for the HSE. Because if you start trying to justify why you are gagging a researcher for trying to tell the truth then, well, you will end up having to justify state censorship of scientific debate. Which never looks that good on the printed page, I find.

I feel I should sign off this blog with a quote from George Orwell, taken from 1984. “Being in a minority, even in a minority of one, did not make you mad. There was truth and there was untruth, and if you clung to the truth even against the whole world, you were not mad.”

1: http://www.independent.ie/irish-news/hse-gags-surgeon-after-cholesterol-drug-claims-29636095.html

2: http://www.imt.ie/news/latest-news/2013/09/study-claims-to-highlight-the-ugly-side-of-statins.html

Statins do not help you live longer – or do anything much else for that matter

Sometimes you read a thing quickly, and then you have to read it again to make sure you read it right. Yesterday I was sent a copy of a ‘Patient page’ from the Journal of the American Medical Association (JAMA).  The page was from the April 3rd 2013 edition, pp 1419. It is stamped ‘JAMA – copy for your patients’. JAMA is one of the highest impact medical journals in the world.

This patient page states that:

‘One question involves disagreement about whether the statin side effects are merely uncomfortable or actually pose significant health risks. The other question is whether reducing bad cholesterol will actually help you live longer than you otherwise would. Some of this disagreement involves how physicians interpret the results of studies. However, a 2010 analysis combined the results of 11 studies and found that taking statins did not lower the death rate for people who did not have heart disease. If your physician recommends taking a statin, talk to him or her about the risks and benefits for your individual situation.’

For many years I have been ridiculed by colleagues for saying that, if you do not already have established heart disease, statins do not increase your life expectancy. By which I mean that they don’t’ actually work. ‘Don’t be ridiculous.’ Is what they exclaim to me. I usually reply that the evidence is pretty clear, and always has been. But I know that they don’t believe me.

Recently, without warning, one of the most influential medical journals in the world turned round and confirmed it. JAMA has stated in black and white that if you do not have established heart disease e.g. angina, previous heart attack, you will not live any longer if you take a statin.

Frankly, I think JAMA will now come under ever increasing bombardment from the ‘experts’ and will end up retracting this statement. In fact, I am willing to bet that they will – having now seen some of the outraged letters sent in. However from time to time the truth – like a small grass shoot growing through a concrete pavement – will emerge. As it did in April.

(I should add, at this point, that around 95% of people who take statins do not have established heart disease.)

However, wrapped up in this issue, is an inevitable argument. I know this argument well, for I have heard it a thousand times. ‘Ah, but it is not just death we are talking about here…. statins prevent non-fatal heart attacks and non-fatal strokes and suchlike. These are terrible things that damage the quality of your life. Medicine is not only about getting people to live longer, it is also about quality of life. Preventing a non-fatal stroke is extremely important, and statins do this.’ In other words, statins don’t make you live longer, but they do provide other, very significant benefits, by preventing Serious Adverse Events (SEAs).

This is a good argument. At least it would be if it were true. However, we have no idea about whether it is true or not. For the simple reasons that the data on SEAs is almost entirely hidden from view. Data on SEAs are considered so commercially sensitive that, in most jurisdictions, pharmaceutical companies won’t release them (and don’t have to release them), even if you ask nicely*.

Before moving onto that issue, I know that I need to explain I am talking about here in a little more detail, and clear up a bit of confusion with the nomenclature. For in the area of adverse events/effects, we have two terms that sound very similar, but mean very different things.

Firstly, there are drug related adverse effects. These are often called ‘side-effects’. But side effects can be good, or bad. For example Viagra was developed as an angina drug but it was found to create enhanced erections, as a side-effect. [You can decide if this is a beneficial side-effect or not]. Viagra also causes headaches. This is also a side-effect, but it would be more accurate to call it a drug related adverse effect.

Drug related adverse effects = negative/unpleasant ‘side-effects’ of a drug

A Serious Adverse Event (SEA) may sound similar to a drug related adverse effect, but it means something completely different. An SEA is a significantly bad thing that a drug might prevent e.g. non-fatal heart attack. Or, it could be something that the drug causes e.g. rhabodmyolysis (muscle breakdown), followed by kidney failure. Which is something that is known to be caused by statins.

SEAs can therefore be good, or bad. Depending on whether they are caused by, or prevented by, the drug. This means that there is absolutely no point in presenting figures on SEAs prevented by statins, without knowing if they caused an equal number of SEAs at the same time.

Completely unsurprisingly, whilst we are bombarded with statistics about how many SEAs are prevented by statins, we have very little idea about how many SEAs are caused by statins. Because in most countries, these data are not released. Its’ commercially sensitive dontcha know. [Damned right it’s commercially sensitive. If the public saw these data they would stop taking half their meds overnight.]

There have, however, been glimpses of SEAs with statins – when the data escaped from the clutches of the pharmaceutical companies. When the Cochrane collaboration fist looked at primary prevention studies, two of the five major studies did report ‘negative’ SEAs (although they did not say what the SEAs were, and still won’t). In these two trials AFCPAS and PROSPER, the SEAs were:

Statin arm:      44.2%
Placebo arm:  43.9%

‘In the 2 trials where serious adverse events are reported, the 1.8% absolute reduction in myocardial infarction and stroke should be reflected by a similar absolute reduction in total serious adverse events; myocardial infarction and stroke are, by definition, serious adverse events. However, this is not the case; serious adverse events are similar in the statin group, 44.2%, and the control group, 43.9% This is consistent with the possibility that unrecognized serious adverse events are increased by statin therapy and that the magnitude of the increase is similar to the magnitude of the reduction in cardiovascular serious adverse events in these populations.’  (read more…)

In short there were slightly more SEAs in those taking statins than in those taking placebo. Slightly more harm than good.

So what do we now know? We know that if you do not have established heart disease, and you take a statin, you will:

  • not live any longer
  • not avoid major Serious Adverse Events

Which means that there is no possible improvement in either the quality, or the quantity, of life. On the other hand there is a good chance that you will suffer from significant adverse effects e.g. muscle pain, joint pain, impotence, stomach upset, rashes etc. etc. On balance therefore we can state that, if you do not have established heart disease, statins provide no benefits on any important outcome. All they can do is to give you adverse effects. ‘Oh boy, that sounds like a great deal doc. Can’t wait, can’t wait, can I get them now?’

*Please see petition that I just put up on my blog. This petition arrived coincidentally as I was writing this article. At present the European Medicines Agency (EMA), will provide SEA data if requested (with huge persistence). The UK authorities will not release these data, nor will the FDA in the states. A recent move by the pharmaceutical industry is now threatening that the EMA will be forced to hide SEAs. ‘Six months ago two US pharmaceutical companies AbbVie and InterMune took a legal action against EMA that has closed down access to all trial data for all drugs for all doctors and researchers anywhere in the world.’

Closed down all access to all trial data for all drugs for all doctors and researchers anywhere in the world.

That statement is worth repeating. Be afraid, be very afraid indeed. And sign the petition please. Oh, and write to your MEP, as I am now doing.

Please sign – most important issue

I received this post and felt the immediate need to post it on my blog, to allow as many people as possible to sign a petition to stop pharmaceutical companies hiding adverse event data on their drug FOREVER. This is a hugely important issue for humanity.

See below…

Sorry for the Mass Posting here but we have just posted a Swedish translation of the RxISK petition calling for Access to Clinical Trial Data.

Some of you will have signed this but even if you have read on because we have a mission for you.

Two years ago, the European Ombudsman ruled that the European Medicines Agency should open up access to Clinical Trial Data for anyone who applied from anywhere in the world.

Six months ago two US pharmaceutical companies AbbVie and InterMune took a legal action against EMA that has closed down access to all trial data for all drugs for all doctors and researchers anywhere in the world…

Some of you may not have heard of AbbVie. Until recently they were Abbott Laboratories, one of the biggest pharmaceutical companies in the world.

They make Humira, a monoclonal antibody used for Rheumatoid Arthritis, Crohn’s Disease, Psoriasis and other conditions. It is the best selling drug in the world today, and projected to be the best selling drug of all time.

This is one of the most important legal actions in Healthcare ever. At a recent meeting in Bruxelles AbbVie made it clear that a main reason to keep clinical trial data confidential was to hide adverse event data, although there may be other issues like a Trade War with China.

You can read about this and see the whole video here

Essentially AbbVie are asking the Courts to grant their Corporation the privacy rights of an individual – a very powerful wealthy individual.

But the key help is this. If this legal action succeeds Adverse Event data will be hidden for ever.

So we’d love you and anyone you know to sign a petition calling on AbbVie to drop their legal action against the EMA’s policy of open access to clinical trial data. The petition is here or in Swedish as above

This petition is as much for anyone who may be prescribed drugs as for those prescribing them – so we are hoping to spread word about it generally.

In addition to signing, we are trying to get every country in the world to sign.

We have 72 of the 187 countries in the world signed up but would love to have all.  If any of you have contacts in any Eastern European, African or South East Asian countries that you could get to sign this it would be really excellent

Thanks, David

David Healy
Professor of Psychiatry, Hergest Unit,
Bangor, Wales LL57 2PW, UK

david.healy54@googlemail.com
davidhealy.org

Too much medicine – dementia

I am, in general, distinctly sceptical about mass screening programmes. Politicians, however, just love them. They use the complex scientific principle of ‘A stitch in time, save nine.’ Or else the concept of pure logical reasoning known as ‘Better to be safe than sorry.’

On a very superficial level screening is obviously a good thing. You pick up a disease early, then you ‘treat’ it, then it is gone. Huzzah! Pink ribbon anyone? Indeed, how could anyone possibly argue with such an obviously sensible thing to do? So sensible that we are drawn to this idea like moths to a flame. We flutter around it, unable to break free from its mesmerising power.

I am not suggesting that all forms of screening are useless. My favourite screening test is to take someone’s pulse. You can tell within about twenty seconds, or less, if someone has atrial fibrillation (AF). If they do, this is a condition that can be effectively managed, reducing the risk of stroke by nearly a half.

This test costs nothing, requires no great skill, is non-invasive, and…… of course it is not on any screening programme anywhere in the world (as far as I know).  Strange, as it fulfils virtually all of the criteria of a successful screening test. As outlined by the WHO as far back as 1968

World Health Organization guidelines on assessing the value of a screening test

  • The condition should be an important health problem.
  • There should be a treatment for the condition.
  • Facilities for diagnosis and treatment should be available.
  • There should be a latent stage of the disease.
  • There should be a test or examination for the condition.
  • The test should be acceptable to the population.
  • The natural history of the disease should be adequately understood.
  • There should be an agreed policy on whom to treat.
  • The total cost of finding a case should be economically balanced in relation to medical expenditure as a whole.
  • Case-finding should be a continuous process, not just a “once and for all” project

Instead, we have vastly expensive, poorly sensitive tests for diseases where our treatments are poor, and our knowledge of the natural history of the disease is virtually non-existent. I am not discussing cancer screening here as that is a far more nuanced area.

What I am talking about here, specifically, is dementia screening. Which is the latest bonkers, poorly thought though, damaging bit of stupidity that the UK Govt is now intent forcing on General Practitioners in the UK – and the US. And that was the polite version of my real views.

Here is what the BMJ has to say about dementia screening:

‘Conclusions—Current policy is rolling out untested and uncontrolled experiments in the frailest people in society without a rigorous evaluation of its benefits and harms to individuals, families, service settings, and professionals.

In fact, the entire article is a paean of common sense, and I would recommend anyone to try and get hold of it, and read it. But journals place themselves behind pay for view barriers nowadays, so you probably can’t.

However on of my favourite passages is the following

What will be the effect of encouraging more widespread and earlier diagnosis of dementia? A meta-analysis of the diagnostic accuracy of clinical tools used by general practitioners, including 15 studies on dementia, estimated that if, a clinician saw 100 consecutive community based patients with a prevalence of dementia of 6%, using current criteria he or she would correctly identify four of the six but would incorrectly identify dementia in a further 23 people.

In short, if there were six out of a hundred patients in the community with early stage dementia. The average clinical would miss two of them, and state that twenty three without the condition had it. My, how fantastically accurate.

A good screening test needs to pick up (or not miss) well over ninety five per-cent of people who have the condition, and not misdiagnose more than one – or two – in a hundred.  A misdiagnosis (false positive), is not a trivial thing. ‘I am sorry to tell you Mrs Smith, that you have dementia.’ The effects of being told this can be utterly devastating.

Finances, family planning, the sense of despair that you are going to end up unable to recognise your close family. Dribbling to yourself in a nursing home, doubly incontinent.  These are all the things that flash through people’s minds when told they have dementia.

But don’t worry, we haven’t got any effective treatment for it either….. you will be glad to know….’ The doctors shall then happily inform the three out of four people that they have MISDIAGNOSED. Whilst thirty per cent of those with dementia wander off happily, reassured that they don’t have dementia – when they have actually got it.

There are times, when I look at the direction of travel in medicine, that I almost give in to despair. There is not enough money to pay for many proven and effective treatments. We are closing hospital beds and making nurses redundant. Our psychiatric services are virtually exterminated due to lack of funding, with severely distressed people unable to access any support.

Yet we can find money – it seems- to fund a completely useless. Sorry, not completely useless. Dementia screening is far more that completely useless – it is actively damaging. We have money to pour into an actively damaging, vastly expensive screening programme to pick up a disease that we cannot actually treat in any meaningful way. Gasp…thud. Noise of head hitting desk.

Luckily, there is always malt whisky to dull the pain.

’Political drive to screen for pre-dementia:
not evidence based and ignores the harms of diagnosis.’

Deadly Medicines and Organised Crime: How big pharma has corrupted healthcare

Deadly Medicines and Organised Crime: How big pharma has corrupted healthcareA bold title for a blog indeed, but not mine (I almost hasten to add). This is the title of a new book by Professor Peter Gotzsche.  I have ordered it, and started to read it. Gotzsche does not hold back. As the introduction states:

We take so many drugs is that drug companies don’t sell drugs, they sell lies about drugs. This is what makes drugs so different from anything else in life…Virtually everything we know about drugs is what the companies have chosen to tell us and our doctors…the reason patients trust their medicine is that they extrapolate the trust they have in their doctors into the medicines they prescribe. The patients don’t realise that, although their doctors may know a lot about diseases and human physiology and psychology, they know very, very little about drugs that hasn’t been carefully concocted and dressed up by the drug industry…If you don’t think the system is out of control, then please email me and explain why drugs are the third leading cause of death…If such a hugely lethal epidemic had been caused by a new bacterium or a virus, or even one hundredth of it, we would have done everything we could to get it under control.

This is a short blog. The only reason I have written it is to make you aware that this book exists, and to urge you to buy it, and read it.

Disclosure of Interest (D.O.I). I have absolutely no financial interest in this book. I know Peter Gotzsche through e-mail conversations.

What is your blood pressure (BP)?

Central arterial blood pressure

(What is it, don’t like it. Pay attention it could save your life)

It is a pressure that is measured, almost exclusively, by placing a cuff around one arm – usually the left. The cuff is then inflated to a point whereby all blood flow is stopped. If you have placed a stethoscope over the brachial artery (artery in the arm) you will hear nothing at this point. Because there is no blood flow, and nothing to hear.

As the pressure in the cuff is lowered, a noise will be heard as the blood first starts to squeeze through. This is defined as the systolic blood pressure i.e. the point of highest arterial pressure, just after the heart contracts. A sharp tapping noise would be the best description.

As you lower the pressure in the cuff, the noise changes and muffles. Eventually, there will come a point where the blood is flowing through the brachial artery all the time …the point of ‘lowest’ blood pressure. Once this pressure is reached, the noises in the brachial artery cease. This is defined as the diastolic blood pressure. (The pressure does not reach zero, because the heart pumps once again to boost the pressure again).

All of this means that your blood pressure is presented as two figures. The highest recorded pressure (systolic) over the lowest (diastolic).

Historically, blood pressure measured in millimetres of mercury. Because, in the good old days, blood pressure meant how many millimetres of mercury could be pushed up a tube by the force of the cuff being inflated round the arm. If you used water in the tube, instead of mercury, we would measure in metres, not millimetres.

Despite the fact that mercury has nothing to do with the process any more, the measurement is still called mmHg (millimetres of mercury that can be pushed up a narrow tube). A normal blood pressure is around 120/70. If you are an Olympic weightlifter, the blood pressure can reach over 300mmHg during a lift. Which is pretty high.

In a nutshell that is what your blood pressure is…. but what does it mean? The pressure in your arm is certainly not the same as the pressure in your finger, or your brain. The pressure will be different in the right and left arms, as the blood has further to go before it reaches your right arm. It will be different if the cuff is put in a slightly different place on the arm. It will also be different if you are stressed, if the cuff is a bit small – or slightly too big.

In short, your blood pressure can be all over the place. Which is why a single measurement is not used to define high blood pressure. You need at least three. In fact, this is not nearly enough either. To diagnose someone with high blood pressure you really need to monitor the blood pressure over a twenty four hour period – using ambulatory monitoring. This helps to get rid of ‘white coat’ hypertension (high blood pressure). A phenomenon whereby the act of a healthcare professional wrapping a cuff round your arm sends your blood pressure sky high.

Because of the difficulties of measuring the blood pressure, it is estimated that around twenty five per cent of people diagnosed as having hypertension – do not actually have high blood pressure at all. Which means that they are taking drugs that they do not need. Costing the NHS at least a billion a year, and a great deal more around the world (yes, this truly is an international blog).

The other major problem with measuring the blood pressure at the arm is that it may not reflect the blood pressure just after the blood leaves the heart. The central arterial pressure. This is important, because this is the most critical pressure of all. There are a number of reasons why this is so.

Firstly, the central arterial pressure is the pressure in the aortic arch (the U bend in the aorta (biggest artery in the body)). This represents the pressure that sends blood straight up the carotid arteries and into the brain, which is clearly important with regard to stroke risk. [This where two, critically important, small BP sensing organs sit]

It is also the pressure that has the greatest impact on the kidneys. The renal arteries branch directly from the aorta itself. Therefore the central arterial pressure is closely monitored by the kidneys, which are the primary organs of blood pressure control. In addition, the central pressure has the greatest impact on the aorta itself. A relatively common cause of death is a ‘ballooning’ of the aorta (aortic aneurysm).  Such aneurysms can burst, with obviously catastrophic results.

Now, there is no doubt that the pressure at the arm is related to the central arterial pressure. It must be – to a certain degree. And for most people measuring at the arm is probably a good enough estimate of the ‘true’ blood pressure.

However, if your blood pressure measurement is high, or low, or you are on blood pressure medication….then the pressure measured in the arm becomes increasingly unreliable. It can even become misleading i.e. your pressure seems to be going down in the arm – but it is not going down as much centrally1. (It may even be going up.)

‘The results of the Conduit Artery Functional Endpoint (CAFE) study also suggest that the central aortic blood pressure may be more predictive of cardiovascular events, such as stroke and heart attack, than traditional peripheral (brachial) blood pressure measurements. CAFE was the first study to repeatedly measure central aortic pressure in a major clinical outcomes trial and the first to show that central aortic pressure is a plausible mechanism to explain the better clinical outcomes seen in patients treated with amlodipine-based therapy in ASCOT.’

Of course, central arterial blood pressure is somewhat difficult to measure. Up till fairly recently you had to insert a catheter, with a measuring device, into to the femoral artery, and push it up to the aortic arch. This would not be highly practical during a consultation with a GP. So central BP is very rarely measured. But it would be best if it could…

The anomalies of blood pressure trials

Now to introduce another thread to this discussion. Which is the fact that, if you choose to look at the clinical trials on blood pressure lowering with an objective eye, there is almost no correlation between the amount the blood pressure is lowered (at the arm) – and any clinical outcomes. By which I mean that the rate of heart attacks and strokes do not relate to the degree of blood pressure lowering.

To quote a series of bullet point in the European Journal of Cardiology entitled ‘There is a non-linear relationship between mortality and blood pressure’:

  • Drugs that lower the blood pressure by about the same amount have very different effects on outcomes
  • Cardiovascular benefits of ACE-inhibitors (Angiotensin Converting Enzyme – Inhibitors), independent of blood pressure, are not observed with calcium antagonists, despite the latter having more pronounced effects on blood pressure.
  • HOPE (Heart Outcomes Prevention Evaluation study) demonstrated that ACE inhibitors provided diverse and profound cardiovascular benefits, with only trivial differences in blood pressure between the treatment and control groups
  • ALLHAT (Antihypertensive and Lipid Lowering treatment to prevent Heart Attack Trial) showed a dramatic difference in cardiovascular risk between alpha blockers and diuretics, with essentially no difference in their effect on blood pressure. The investigators of ALLHAT concluded ‘blood pressure lowering is an inadequate surrogate marker for health benefits in hypertension.

This is extremely important, because for many years, most of the ‘evidence’ on blood pressure treatment has been based on a statistical model known as the ‘log-linear’ model. This model states that ‘the relation of blood pressure to risk of death is continuous, graded, and strong, and there is no evidence of a threshold.’ (Stamler). The model itself, and that statement, were almost entirely based on evidence from the Framingham Heart Study. The study that your doctors will use to calculate your risk of dying of heart disease.

Essentially, according the log-linear model, the lower your blood pressure (measured at your arm), the better. And the more that drugs lower it, the better. At least this is the thinking that is currently used.

However, thirty years ago Ancel Keys (yes, him) concluded that the linear model, in terms of the relationship of overall and coronary heart disease death to blood pressure was ‘unjustified’. Ten years ago, the authors of the article ‘There is a non-linear relationship between mortality and blood pressure’ further concluded (after reviewing the Framingham data – the data upon which your doctor will determine your future risk of dying of CVD)…the following:

‘Shockingly, we have found that the Framingham data in no way supported the current paradigm to which they gave birth. In fact, these data actually statistically rejected the linear model. This fact has major consequences. Statistical theory now tells us that the paradigm MUST be false ….’ (Their italics and capital letters).

In short, the blood pressure model that is used worldwide is simply, plain damned wrong. The reality is that the amount the blood pressure is lowered in the arm bears little, or no, relationship to any benefit on heart attacks and stroke.  How can this be? Well, there are two major reasons for this. One of which I am covering in this article. The other, later. Now to introduce another thread.

How do blood pressure lowering drugs work?

I am going to avoid being too technical here – which is tricky. I am also, only focussing on the four most commonly used blood pressure lowering agents/classes.

1: Diuretics. These drugs make you pass more urine, by blocking sodium re-absorption by nephrons in the kidney. This means that you pass a lot of urine (diuresis). This puts you into a state of mild dehydration, thus reducing blood volume. Exactly why this lowers your blood pressure is a moot point. (You may think you know. However, it is almost certainly far more complicated that what you are thinking – I certainly don’t understand it)

2: Beta-blockers: These, effectively, slow your heart rate and also decrease the pumping force of your heart. An unwanted effect is that they also cause peripheral blood vessel constriction.

3: Calcium channel blockers: These reduce the force of contraction of the heart, dilate blood vessels (arteries not veins), and slow the heart rate at bit. All of which lowers the blood pressure.

4: ACE-inhibitors: (a bit more explanation is required to explain how they work). The kidneys are the primary organs that control blood pressure. If they pick up that the BP is too low, they release a substance called renin. Renin triggers a whole series of other hormones into action. Ending up with increased angiotensin II levels.

This hormone has multiple effects. It reduces urine production, by increasing sodium absorption. It causes constriction of arteries, and stimulates the pituitary gland to produce anti-diuretic hormone (ADH) – thus reducing urine output.  It does several  other things too, all of which result in the blood pressure going up.

As is the complex way of the body, the kidney doesn’t actually produce angiotensinogen II  when the blood pressure drops(which would seem logical). The kidney produces renin, the liver produces angiotensinogen. When these two hormones met, angiotensinogen is converted into angiotensin I. Then angiotensin I is further converted to angiotensin II by an enzyme called Angiotensin Converting Enzyme (ACE). (There will be an exam later)

All of this means that angiotensin II is the main, active, substance. Once it has been produced, angiotensin II goes off to do all its blood pressure raising things. If, however, you give an ACE-inhibiting drug (ACE-inhibitor), angiotensin II production is blocked, and the blood pressure will fall.

Anyway, as I hope has now become clear, the blood pressure lowering classes of drugs all work though very different mechanism. They all lower the blood pressure at the arm, but what else are they doing?

Beta blockers tend to constrict peripheral blood vessels. Calcium channel blockers and ACE-inhibitors tend to dilate them. Diuretics are mainly neutral on blood vessel diameter.  ACE-inhibitors also do something else that is extremely important. They stimulate Nitric Oxide synthesis in the blood vessels themselves, which both dilates arteries, and increases blood vessel flexibility.

In short, the effect on central and peripheral blood pressure of various BP lowering medications will be very different.

Bringing these thoughts together

You may think, why now? Why is he quoting articles, and research, from many years ago? Well, you have to bear in mind that it is a long time since anyone did a placebo controlled blood pressure lowering study. It would be considered unethical to do so now (such are the alleged enormous benefits of BP lowering). So, there isn’t really any fresh information. Just the monitoring of one drug vs. another, and assuming benefit based on the degree of BP lowering – using the log-linear scale.

However, it has now become possible to measure central blood pressure by simply using a cuff placed round the arm. I have had this process explained to me many times, and cannot really understand how it is done. But the results are repeatable, and accurately reflect central blood pressure. Which is all that really matters.

When you do this, you can also measure the velocity of the pulse wave, which is an accurate indicator of arterial flexibility – and thus arterial health. If your arteries are stiff this is a worrying sign, and reflects poor arterial health. The more flexible your arteries are, the better.

At last, hoorah, instead of wrapping a simple cuff round people’s arms, we can use a complicated cuff to look at two more, really important things. The central blood pressure, and arterial flexibility. This gives us far more information.

Perhaps most importantly, we can monitor the effects that different blood pressure lowering medications have, beyond their impact on the BP measured at the arm. We can see if central pressure is increased, or decreased, or if arterial compliance (flexibility) is improved.

I think that this is a major breakthrough in medical practice. So much so, that I have acquired a machine for myself, and will be using it on a regular basis. I fear it will take the wider medical profession about twenty years or so for this to become an accepted way of measuring blood pressure. This is about the normal lead time for new ideas to become standard practice.

Sweden 1967

Sweden in 1967

It may, of course, take longer. Or never happen at all. At the risk of going off on a major tangent, I remember looking at pictures of roads Sweden in 1967. This was when they switched from driving on the left, to driving on the right. 3rd Sept 1967

As you can see from the picture, a bit of a mess. But imagine if any country tried to do it now, with the extra number of cars and lorries, and roads, and signs. This would probably be just too difficult.

How about changing the way we look at measuring blood pressure. We have always measured blood pressure using a simple cuff on the arm. All the clinical studies on BP lowering were done using this technique. All the data, all the guidelines….everything, is now based on doing BP measurement in this way.

Just imagine what happens if someone now says. Hold on, this is not good enough. The measurement is inaccurate and potentially confusing, and it doesn’t’ really tell us what we need to know. Let us start again. Let us drive on the right, not the left.

In the meantime, whilst the medical world grapples (or chooses not to grapple) with a trillion dollar problem, you can do yourself a favour and get your blood pressure measured centrally.

More on this later.

1: http://www.medscape.org/viewarticle/518570

2: Port S, et al: ‘There is a non-linear relationship between mortality and blood pressure.’ European Heart Journal (2000) 21, pp. 1635 – 1638

Beradinelli-Seip Syndrome – stick that in your pipe and smoke it

We are told, ad-nauseam, that obesity is the main cause of type II diabetes. This, allegedly, follows a very simple causal chain.

Obesity > insulin resistance > raised blood sugar levels

For those not familiar with the term Insulin resistance, this is the condition whereby various organs in the body become gradually more insensitive to insulin, which forces insulin levels higher to keep the blood sugar levels down.

Eventually the resistance to insulin becomes so great that the blood sugar levels rise anyway – despite the high insulin levels.  Alternatively, or in parallel, the pancreas gives up fighting against the resistance and insulin production becomes ‘burnt-out’. Whichever process is dominant, they both result in sugar levels become very high, and you will be diagnosed with type II diabetes.

At this point I have to state that I have always found it weird that a raised blood sugar level can be defined as a disease, when it is clearly nothing of the sort. In my world a ‘disease’ is the underlying malfunction which causes various signs and symptoms to occur (of which a raised blood sugar level would be one).

Everyone agrees that insulin resistance is the basic underlying cause of a raised blood sugar level a.k.a. type II diabetes. Despite this we define the blood sugar level itself as the disease.

‘A high blood sugar level is type II diabetes….end of.’

‘So, if we lower the sugar level, we have cured the disease?’

‘Yes. Now do shut up.’

Clearly bonkers, but let us not expect too much in the way of logic in medicine. Anyway, that is a slight distraction from the main theme here, which is the: obesity > insulin resistance > raised blood sugar levels discussion.

Now, for reasons that I am not going to fully bore you with here (but maybe at a later date), I have always had problems with this causal chain.  Primarily, that it has never made much sense to me.  Insulin resistance occurs almost exclusively in two tissues; the liver and skeletal muscle, and NOT in adipose tissue. So why would having too much adipose tissue make you insulin resistant? Answers on a post-card please*.

In order to pursue this thought further I started to look at evidence from Sumo Wrestlers. These are the most obese people on the planet. At least they are if you use BMI to define obesity. Yet, none of them have type II diabetes (at least not, whilst in training). For example:

Abnormally large waist circumferences, which were determined by the criteria established by the Japanese Society of Internal Medicine, were present in all Sumo wrestlers (100%), and fifteen Sumo wrestlers (83%) had high abdominal visceral fat areas (>100cm2). Only 2 subjects were categorized with high serum triglyceride levels, and 5 subjects were classified with low HDL-C levels by established criteria. None of the Sumo wrestlers had fasting hyperglycemia (high blood sugar levels) (0%)1

Interesting, is it not, that the most obese people on the planet do not have type II diabetes (although some of them have a degree of insulin resistance – for reasons that I may explain at a later date). Yes, I know exactly what you are now thinking. They do not have diabetes because they exercise a lot. It’s true, they do.  But does that not make it more likely that a lack of exercise is the true of cause of insulin resistance, rather than obesity….yes, of course it could certainly mean that.

In truth, finding very obese people without diabetes does not rule out obesity as the cause of diabetes. But it does rule out obesity as being both ‘necessary’ and ‘sufficient’.  At this point I need to explain the concept of necessary and/or sufficient.

It was Koch who first tried to determine a process of logic to describe whether or not something may be a true cause of a disease, or just a chance association. He introduced us to Koch’s postulates, and also the concept of necessary and/or sufficient.

For example, it is known that the bacteria vibrio cholarea causes cholera. In order to get all the signs and symptoms of cholera it is ‘necessary’ to be infected with this organism. However, infection with vibrio cholarea does not cause cholera in everyone. If you are a fit and healthy adult you can shrug off the infection with only mild symptoms. Koch proved this by drinking a glass of water known to be infected with vibrio cholarea and developing only mild symptoms of the disease

Thus it can be stated therefore that infection with vibrio cholarea is ‘necessary’ to cause cholera. However it is not, on its own, ‘sufficient.’ Other factors are needed.  On the other hand, if you could find people with cholera who had not been infected with vibrio cholarea, then you would have to declare that vibrio cholarea was neither necessary, nor sufficient, to cause cholera. So it could NOT be the cause of cholera.

This is obvious, and inarguable.

So, moving back to type II diabetes.  Can you find people with type II diabetes who are of normal weight? Or, to stretch this concept to the limit, can you find people with type II diabetes who have no adipose tissue at all? Surely not, you say. Surely impossible.

At this point I shall introduce you to ‘Berardinelli-Seip Congenital Lipodystrophy’. This condition affects about one in ten million people. So it is hardly common, but that is not the point. The point is that the primary abnormality in Berardinelli-Seip Congenital Lipodystrophy is a lack of functional adipocytes – which means that those who suffer from this condition do not have fat cells, and cannot store fat. Ergo, that they are extremely lean. The leanest of the lean, the least obese of the least obese.

From time to time I describe this condition to doctors. At which point I somewhat cheekily ask them to guess what percentage of people with Berardinelli-Seip Congenital Lipodystrophy have type II diabetes.  I say cheekily, because they inevitably get the answer wrong. They always, without exception, answer pretty much as follows:

‘Obviously, none of them.’

The correct answer is, of course, ‘Every… single…one…of…them.’ [Gasp, sounds of people collapsing to the floor in shock etc.]

Now, if you can understand why this is true, you are at least one step on the road to understanding type II diabetes. Or to be more accurate, what is the true underlying cause of insulin resistance and high blood sugar levels. You will also understand that obesity has only a small and indirect part to play in this process; that BMI has no relevance to the issue, and that the simple causal chain: Obesity > insulin resistance > raised blood sugar level……is wrong.

Of course obesity is closely associated with diabetes – to state otherwise would be nuts. However it is not the cause of type II diabetes. It is caused by it. By which I mean that obesity is (in major part) caused by that the underlying process that also leads to insulin resistance and high sugar levels. There is a causal chain here, but it is not Obesity>insulin resistance>raised blood sugar levels.

More on this later, once your brain has become unscrambled.

*Yes, for those who know about this area, you can talk about visceral fat, but this is another more interesting and completely different discussion. I am also only discussion type II diabetes, not type I (which is a completely different condition altogether).

1: http://connection.ebscohost.com/c/articles/84569721/metabolic-profiles-fat-distribution-japanese-college-sumo-wrestlers

 

811 deaths and counting

There is a doctor in the USA called Duane Graveline who I know well. He trained as an astronaut, when such things were seen as exciting. He was very much mainstream in his prescribing and thinking about medicine, until he was started on statins. He took them happily, until he suffered an episode of transient global amnesia. A complete loss of memory, re-booting his brain to the age of about eight.

On the first occasion he had no idea what had happened. He thought he could have had a stroke, but after investigations nothing was found. He asked if the statin could have caused this, and was told no – not a chance. So he started on statins again, and suffered another episode, the same as the last.

He then started investigating and found that thousands of others had suffered from episodes of transient global amnesia whilst on statins. A very, very, rare thing to happen to anyone, but increasingly common nowadays. I wonder why? Dr. Graveline then started to develop a neuromuscular disease, similar to amyotrophic lateral sclerosis (ALS) which he attributes to the statin. Statins can certainly cause neuropathy – but I shall say no more on this issue at present.

Dr. Graveline is not so keen on statins now, nor does he believe that cholesterol causes heart disease – having looked at the evidence again with a fresh eye. For those who do not know, he has a website www.spacedoc.com. Here are listed all of the many adverse effects of statins, and the suffering of many thousands of people.

He believes that the authorities are, basically, turning a blind eye to the many and varied problems with statins. So he has laboriously gone through the Food and Drug Administration (FDA) database of Adverse Drug Events (Medwatch), to find out just exactly how many deaths statins have caused.

This is extremely difficult to analyse as the coding system in Medwatch is complex, poorly linked and many things – frankly – do not seem to make sense. Whilst going through this stuff is an absolute nightmare, it can be done – although you have to make some assumptions along the way.

What Dr. Graveline did was to look for case of rhabdomyolysis (catastrophic breakdown of muscle tissue) linked to statins. Rhabdomyolysis is a pretty specific, and well-accepted, adverse effect of al statins. However, it is considered as so vanishingly rare as to be not worth bothering about by most doctors.

Rhabdomyolysis carries a very high mortality rate, because the waste products of dissolving muscles travel to the kidneys, where they block up the nephrons, causing acute kidney failure. In around ten per-cent of cases rhabdomyolysis is fatal. So you can assume, with reasonable accuracy, that for every ten reported cases of rhabomyolysis, you will get one death. You will also get a number of people with destroyed kidneys who end up on dialysis – hey ho.

At this point I should also point out that adverse drug events are widely known to be a massively under-reported. It is difficult to be certain on the exact figures. However, having read many papers on this subject the general feeling is that about 1 – 5% of all events are actually reported by anyone – ever. Which means that any figures in Medwatch can be pretty reliably multiplied by twenty to one hundred? Which is a topic for another day.

Anyway, with this pre-amble out of the way, I have copied Dr. Graveline’s blog on statins (with his full permission). What he has found is that, over a six year period there were 8,111 cases of rhabodmyolysis reported to Medwatch associated with statins. This represents, at least, 811 deaths in this period. [If you were to multiply this figure by twenty, this is 16,200. Multiply by one hundred and you have 81,110.]

A few years ago one of the statins called Baycol was rapidly removed by the FDA after sixty people died from rhabdomyolysis whilst taking statins. Well, all statins can cause rhabdomyolysis. Hundreds have died, probably more, since Baycol was yanked from the market. Yet there is absolute radio silence on this issue.

Below is Dr. Graveline’s blog…

Relative risk of Statin Associated Rhabdomyolysis

A recent study comparing the relative risks of muscle problems with the use of the various statin drugs has recently been reported. Generally the risk of muscle adverse effects varies with the strength of the statin used except for the statin fluvastatin (Lescol). Lescol, usually considered to be the weakest of the commonly used statins now shares with rosuvastatin (Crestor), the strongest of the statins, in being consistently linked to higher adverse muscle events relative to the other commonly used statins. Atorvastatin (Lipitor) and simvastatin (Zocor) showed intermediate risks and pravastatin (Pravachol) and lovastatin (Mevacor) had the lowest risk rates. Designating rosuvastatin’s and fluvastatin’s relative risk as 100%, comparative rates for atorvastatin, simvastatin, pravastatin, and lovastatin were, respectively, 55%, 26%, 17%, and 7.5%.

     There were a total of 186,796 case reports listed within the Adverse Event database (Medwatch) during the study period 1 Jul 2005 to 31 Mar 2011. Choosing rhabdomyolysis as one of the more discrete and credible of the muscle diagnoses, a total of 8,111 cases of rhabdomyolysis were reported during this study period, averaging 1,350 cases yearly. Sidney Wolfe MD has previously estimated the statin associated rhabdomyolysis death rate to be 10 percent (giving a total of 811 deaths during this 6 year 4 month time period). Of the total number of rhabdomyolysis cases, fluvastatin was involved in 164, rosuvastatin in 1146, simvastatin in 3395, atorvastatin in 1641, pravastatin in 267 and lovastatin in 161.

     Returning to the death rate estimate of 811, this strikes me as extraordinarily high and I cannot believe I am just now discovering this. Back in the Baycol crisis of 2004, sixty deaths caused FDA to rise up and Bayer to take its problematic product off the shelves. Six years later, 811 deaths do not even deserve a mention. What has happened? Where is the media uproar that we had back in 2004? I knew the Medwatch figures for Lipitor because I had obtained a copy of the Medwatch data and counted the rhabdomyolysis cases myself. I counted 2731 cases of rhabdomyolysis from the period 1997 to 2011 from Lipitor alone which fits quite well with this recently published work. So I had a heads up. I predicted the total rhabdomyolysis cases would be 6,000 for all the statins never suspecting I would underestimate by several thousand.

     Medwatch exists for FDA to monitor these outrageous post marketing events and report back to the medical community. Where is the FDA report? This is incredible!

The most unutterable balls

A couple of night’s ago, I was watching a programme called ‘Long Live Britain’ on the BBC, co-presented by Phil Hammond. He is a UK doctor whom I greatly admire, and who mostly talks common sense. So I hesitate to criticise him. But on this programme I heard him say these very words to a volunteer on the programme (sic) ‘A lifetime of eating fatty food has made your liver fatty……’  In truth, he may have used slightly different words, but I cannot bear to watch again.

He then went on to present a lengthy clip of a very unwell lady with (I presume, though not stated), non-alcoholic steatohepatitis NASH. This is the name for a damaged, fatty, liver. A condition that can worsen and worsen and may, eventually, lead to liver failure.

Sorry Phil, but when I heard you say that eating fat caused a fatty liver, I had to switch the television off and take a few deep breaths, lest my blood pressure became too high.

What is it about diet that no-one has even the faintest damned idea what they are talking about, especially when I comes to fat consumption. I think we have demonised fat for so long that you can say anything about fat and, so long as it is sufficiently damning; no-one dares question anything you say. Science goes straight out the window.

A.N. Idiot:                           ‘Did you know that eating fat can make your liver explode.’

A.N. Other Idiot:                ‘OMG, I never knew that.’

A.N. Idiot:                           ‘It’s true. It must be, I saw it on the telly.’

Well, here are a few facts that really are facts. When you eat fat it is absorbed in the small bowel, turned into triglycerides, and packaged into a lipoprotein called a chylomicron. Chylomicrons are then fed directly into the bloodstream via the thoracic duct – bypassing the liver completely.  As they pass fat cells, the cells strip almost all of the fat out of them, so the chylomicrons shrink down and down in size, becoming chylomicron remnants. Once almost all fat is gone, these remnants are absorbed into the liver.

As should be clear from this, at no point in this process does the vast, vast, majority of fat we eat get anywhere near the liver. It is carried from the bowel directly into adipose tissue.  So, Phil, how does eating fat make your liver fatty…exactly? When the liver has no part of play in the absorption, transport and storage of any fat we eat? Oh, sorry, you’re right, it can’t.

Carbohydrates, on the other hand, now here you are talking. All the carbohydrates we eat are converted into glucose and/or fructose in the gut [apart from fibre, and starch, which we cannot digest]. Glucose and fructose then pass directly into the liver where, if your body’s sugar stores are full, they are converted into…you guessed it…fat. [Your body can only store about fifteen hundred calories of energy as glucose/sugar before the stores are full – which is not a lot].

Imagine, if you will, a body with full sugar stores* – this would be most people, most of the time. You eat carbohydrate a.k.a. proto-sugar. With sugar stores full, there is nowhere for this excess sugar to go, so the liver converts it all into fat a.k.a. triglycerides. The liver tries to stick this excess triglyceride into a lipoprotein called a VLDL (Very Low Density Lipoprotein). However, this process is complex, so the liver starts to fill up with fat.

At the same time insulin does battle with the liver, in order to drive lipogenesis (the making of fat from sugar) in the liver. Which means that you are more likely to end up with diabetes. This is not rocket science. This is basic human metabolism/physiology. And you know what, the way to reverse this process is…TO EAT FAT.

The simple fact is that there is no way on God’s earth that eating fat can give you a fatty liver. However, the process by which eating excess carbohydrate could give you a fatty liver, and then diabetes, is simple and straightforward. Yet we have a BBC programme, with a real doctor on it, stating the exact opposite.

I suppose I don’t really blame Phil Hammond too much. We have all been fed with such unutterable balls about the dangers of eating fat for so long now that the science behind nutrition long since became an inconvenience. ‘Do not bother me with facts, for my mind is made up.’

Or ‘don’t bother me with the fats; I am going to kill myself eating carbohydrates.’ Long Live Britain indeed.

*sugar/glucose is stored in the body as glycogen, a polymer of glucose (lots and lots of glucose molecules stuck together). The body does this to reduce the amount of water required to encircle individual glucose molecules.