Author Archives: Dr. Malcolm Kendrick

About Dr. Malcolm Kendrick

Malcolm Kendrick is a Scottish doctor and author of The Great Cholesterol Con (2008). He has been a general practitioner for over 25 years and has worked with the European Society of Cardiology.

Care homes and COVID19

1st May 2022

[Lessons must be learned]

I love the phrase ‘lessons need to be learned’. It always makes me laugh when I hear it. Usually intoned with a voice of great seriousness by the leaders of an organisation found to have made disastrous errors. It is right up there with ‘safety is our number one priority.’ About the only group I have yet to hear say this are arms manufacturers. Although I wouldn’t put it past them. Maybe … ‘You could take someone’s eye out with that.

As I have occasionally remarked about airlines … when they tell us that safety is their number one priority. Well, in that case don’t take off. Everything is perfectly safe when your plane is on the ground. It’s that hurling yourself into the air, dashing about in the skies, then landing, where all the accidents take place.

Getting back to lessons learned. The only lesson I have ever learned, about lessons being learned, is that lessons are never learned. The same disasters occur again, and again, for all the same reasons. The reasons being institutional inertia and the overwhelming desire of those at the top to protect themselves from any criticism.

What I have also learned is that the primary function of any enquiry is to make sure that no-one who actually made those terrible decisions can be blamed for anything. A few scapegoats further down the pecking order will be dragged out and punished. Then all goes quiet again.

Mistakes were made.’ This is another one I enjoy. Mistakes were made – but who made them? The use of the passive voice is all you ever need to pay attention to Here. You never hear. ‘I made this mistake. Or, that person made this mistake.’ Even more rarely will you hear ‘I, alone, made this mistake.

Yes, once the dreaded passive voice comes into play, you know that no-one is going to be singled out, no lessons are going to be learned by anyone. Instead, some vague unidentifiable entity will have to learn from the mistakes that some other vague and unidentifiable entity may, or may not, have made.

Mistakes were certainly made in the COVID19 pandemic, and I have found myself bombarded by the ‘lessons have been learned’ claptrap.

The man in charge of healthcare in the UK, when COVID19 crashed upon the world, was Matt Hancock. This was also the time when patients were being flung out of hospitals into care homes, thousands of whom then went on to die.

He chose to hide behind an excuse. ‘No-one told me, so it wasn’t my fault.’ Is that what the Captain of the Titanic thought to himself as his ship slipped beneath the waves?

Here is one article about what went on during that terrible time. I cannot reference it for everyone, because it came to me through, which is for doctors in the UK only. Here it is anyway, although, unless you are a doctor you will have no access. ‘Poor planning behind the illegal pandemic care home discharges’1. By the way, you are not missing anything. It mirrors many other articles that said exactly the same thing:

Bed shortages led to the illegal discharge policies that led to the deaths of hundreds of patients in care homes, the British Medical Association has alleged.

A court yesterday delivered a ground-breaking ruling that the government acted unlawfully in the advice it issued to the NHS on hospital discharge during the early stages of the pandemic.

The advice stated that there was not a risk from patients who had no symptoms of COVID infection. It led to the virus running amok in the care sector and a judicial review by two bereaved relatives gained the support of the courts yesterday.

I would disagree with the statement that hundreds of deaths occurred. It was in the region of twenty to thirty thousand, maybe more. What was Matt Hancock’s response?

Yesterday he (Matt Hancock) claimed the court ruling had not found him culpable, blaming Public Health England for failing to advise that the asymptomatic patients could transmit the virus.

So, what lesson do we think Matt Hancock has learned? ‘A big boy (public health England) made me do it’, seems an adequate summary. Yes, we know there was a lot going on at the time. A great deal of pressure, and panic, and suchlike.

Using pressure in a rapid changing situation as an excuse, as this Government has repeatedly done … This makes me think of a General explaining that all the mistakes he made during a battle were due to people rushing about firing guns and yelling. No-one can possibly concentrate, and get things right, with all that bloody racket going on.

The reason why you had a position of such power and responsibility, Mr Hancock, is that you needed to be the big grown-up boy. You were required to think quickly, and clearly. If people didn’t tell you things, such as the fact that an airborne virus can spread though asymptomatic people – as they all do, then, quite frankly, you bloody well needed to ask.

Of course, it seems he was told, he just doesn’t want to admit that he was … and someone has told him he can probably get away with that pathetic excuse, of an excuse:

Here is what, I think, he should have said. ‘Whilst the situation was difficult, I should have ensured that I looked at this issue in more detail. I needed to find out more about the impact of discharging elderly people back into care homes. The risk of transmission with asymptomatic patients. The difficulty in isolating elderly and often demented patients in that environment. I did not do any of these things adequately. I was the man in charge, I am deeply sorry … please hand me a gun.’

It is not as if this impending disaster was beyond the understanding of us mere mortals. On the 17th April 2020 I wrote a blog about it:

‘The government’s disregard of care home residents – old, sick people, acutely vulnerable to COVID19 – has been scandalous. As a GP, I regularly visit care homes. At one I visit, they recently had eight residents who died in a week, probably from coronavirus. But there’s no testing, so who could possibly know …

When COVID struck, many things were not known, and could not have been accurately predicted. The transmission rate, the case fatality rate, the best way to treat those infected

However, it was very clear, very early on, that COVID was killing the elderly in far greater numbers than anyone else. In Italy, the early figures released revealed that the average age of death was seventy-nine. The figures were slightly higher in Germany, and around eighty years old in pretty much every other country.

Equally, it was known that amongst the elderly who were dying, almost all of them had other serious medical conditions. Heart disease, high blood pressure, diabetes, chronic pulmonary disease and suchlike. This is often known in my line of work as “multimorbidity.”

In a world of uncertainty, one thing stood out. Which is that the unwell elderly were the ones who were most likely to die. Equally, they were the ones most likely to end up in hospital, potentially overwhelming the health services. As happened in Italy and Spain.

Ergo, you would think that someone, somewhere in the UK government, would have asked the obvious question. Where do we have the greatest concentrations of elderly, frail, people with multimorbidity? Could it possibly be that they are being looked after in care homes around the country?

Nursing homes, residential homes, care homes. They are all pretty much the same thing nowadays. Nursing homes tend to look after those with greater health needs, and they must have registered nurses looking after patients, but the distinctions have become blurred.

Many care homes are also specialised in looking after the elderly with dementia. In the UK, they are called EMI units [elderly mentally infirm]. These represent a particular problem in that residents tend to wander about from room to room.

So, in care homes we potentially had the perfect storm for the pandemic. They are full of elderly and infirm and highly vulnerable people. Environments where it is often impossible to isolate residents, and staff who have never been adequately trained in isolation measures. Equally, whilst relatives cannot visit hospitals, care homes have been continuing to allow them in.

It is not as if the warning signs were not there, flashing red.

What was the government’s strategy for dealing with nursing homes?  It has been, up until the last couple of days, to make things even worse. The instructions from the Dept of Health have been to send patients diagnosed with COVID out of hospital, and back into care homes, with further instructions to “barrier nurse” them, a term for a set of stringent infection control techniques.  Care homes were informed that they could not refuse to take the residents back …’ 2

It was after this that Dr Kathy Gardner (PhD, not medical doctor) contacted me, as her father had died of COVID19 in a care home. I wrote various lengthy replies to her lawyers about the situation, and my experience thereof. They may, or may not, have used my missives in the court case. The case that she battled so long and hard to get heard. She is quoted in the article:

At the time the Health Secretary Matt Hancock had claimed he was throwing a “protective ring” around care homes.

Yesterday he claimed the court ruling had not found him culpable, blaming Public Health England for failing to advise that the asymptomatic patients could transmit the virus.

One of the claimants, Dr Cathy Gardner, said the “protective ring” had proved to be a “despicable lie.”

Dr Gardner said: “I believed all along that my father and other residents of care homes were neglected and let down by the government. The high court has now vindicated that belief, and our campaign to expose the truth.’

Within the NHS I was also fighting my own lonely battles. Here is an e-mail (identifiers redacted) that I send to my manager in April 2020

‘I had a short chat with A yesterday about nursing homes X and Y.

Although things seem to be getting sorted out at Intermediate Care facility B there do not seem to have been any changes at nursing homes X and Y Both homes have several patients with Covid (proven positive swabs). It seems that the Hub is still sending Covid negative patients into both homes – putting these patients at immense risk. We have had staff to patient transmission at Intermediate Care facility B.

Equally patients are being discharged home without having swabs. So, they are arriving home and potentially infecting any partner living there – usually elderly and vulnerable. Equally, if community staff are going in to visit, they can also get infected – then pass the infection on to other clients in the community. The only patients being swabbed on discharge from nursing home X are those going to other care homes – at that care homes request.

Two out of three swabbed patients in nursing home X have come back positive. Which means we are clearly sending Covid positive patients back home – without a swab. I spoke to H, who said that this was still policy? I am not quite sure who’s policy?

I believe we must stop the hub sending Covid negative patients into our nursing homes. – until they are clear of infection. I also believe we cannot discharge anyone from our nursing homes without a clear swab.

I think if anyone were to be made aware that their relatives were being transferring into a Covid positive care home, where they will be at high risk of getting Covid, they would rightly be up in arms. They would rightly be up in arms because it is unsafe, it is putting staff and patients at risk. We already know that nursing homes are becoming the focus of Covid deaths, we should not be making this situation worse in nursing home X and Y.’

I am no genius. I was not the only one who could see that this was a stupid and deadly policy. I wrote about it, and complained about it, at the time. We have now had a court case saying what was done was illegal. But [squeaky voice] ‘no-one knew…’ The care home managers were all up in arms at the time. They bloody knew. But no-one chose to listen to their inconvenient truth.

So now what happens. It it almost impossible to see that anything of any value will occur as a result of this judicial health review. What lessons we be learned? None by the Department of Health and Social Care. Their comment:

‘A spokesperson for the Department of Health and Social Care, said: “We specifically sought to safeguard care home residents based on the best information at the time.’ Yup, safety was their number one priority.

Well, God only knows what would have been the result if they hadn’t decided to ‘specifically safeguard care home residents, based on the best information at the time.’ It is difficult to think of anything they could have done to make things worse.

The best information?’ Who gave them this information? The same vague unidentifiable entity who made the mistakes and will now be learning the lessons I suppose. Maybe it was the exact same god-like entity that was spoken of, in hushed tones, during the pandemic …The Science. Yes, The Mighty Science that works in mysterious ways, its wonders to perform.



Evidence Based Medicine – it was a good idea

25th April 2022

[Until it died]

Once upon a time I was a member of the General Practitioners Committee. A sub-committee of the British Medical Association that represents GPs. This was during a time when the Quality and Outcomes Framework (QOF) system was being rolled out. There is hardly anyone working in the NHS, including almost all hospital doctors, who has any idea what QOF is. But GPs [Family physicians] sure as hell do.

I donned my armour and battled against it, in a purely Don Quixote style. I was aware that I was tilting at windmills, but I felt the need to do something, however unlikely I was to succeed. This stance did offer the advantage that I could then say two things that really irritate other people. First ‘It wasn’t my fault.’ Even worse ‘I told you so.’

Ah yes, what on earth is he talking about this time? What is this QOF thingy, you ask? And what has it to do with evidence-based medicine? Well, you could say that QOF represents the inevitable end-point of evidence-based medicine. The crowning glory of a system designed to remove uncertainty from clinical practice. Replace it with carefully crafted treatment algorithms, based on the best possible evidence.

To explain in a little more detail. QOF itself is a system whereby GPs can earn points for reaching various targets. They are then paid money for each point gained. How much money? You can skip the next bit, but it makes me laugh. It is but the tip of a mighty iceberg of complexity. A system that makes filling in a tax return look like light-hearted fun.

‘To work out your actual QOF value for your practice, you need to divide your population by 8,479 to derive a factor and multiply this to the QOF point value to derive the actual QOF value for your practice.

For example, if your practice has 4000 patients.

4000/8479 = 0.4717537

0.4717537 x £187.74 = £88.57 per QOF point.’

At present it is possible to achieve a maximum of 567 points (last time I looked). This equates to an income of roughly fifty thousand pounds, for a practice of four thousand patients. If, that is, you achieve all the points on offer. Which is tricky.

What sort of activity earns points? Well, take diabetes as an example. You start by establishing, and maintaining, a register of all patients, aged seventeen or over, with diabetes. The register must also specify the type of diabetes – where a diagnosis has been confirmed.

You may think this all sounds perfectly reasonable, but then ask yourself why does it need to be done? In the UK, all GPs use computer systems. If someone has diabetes, this will be known. It will be on screen. It’s not as if the GP is going to be taken by surprise to learn that the patient has diabetes when they carry out an audit.

In short, an up-to-date list makes no difference to their management. Nor are you going to suddenly stumble across more patients with diabetes simply by the magical act of creating a list.

No, the reason why a list must be created is that you can gain points for such things as lowering the blood pressure to a ‘target’ level in the approved percentage of patients. Or driving the cholesterol level down below the ‘target level’, or getting the blood sugar (HbA1c) level below the ‘target’ level in the approved percentage of patients.

In short, for QOF to work, the GP needs to create database after database of different diseases. Then carry out audit … after audit. What a great use of clinical time it all is. Appointment after appointment filled with patients called in to have their annual blood pressure check, which just sneaks in just below target level – every single time.

For the pharmaceutical companies this is manna from heaven. Every patient with diabetes logged and audited. Every one driven to reach a ‘target’. A target that will inevitably require medication. Medication that the pharmaceutical company just, ahem, happens to have developed. Medication where they just, ahem, happen to have done all the clinical trials.

In addition to QOF, you also need to link everything into NICE guidelines. NICE stands for ‘The National Institute for Health and Care Excellence’. They produce magnificent ‘evidence based’ medical guidelines on such matters as the management of low back pain, or treatment of high blood pressure. Amongst a multitude of other things.

Some of these guideline documents are, literally, hundreds of pages long. But if you do not follow them then you are in trouble. You could find yourself struck off the medical register.

If you add NICE to QOF, what do you get?

What you get are extraordinarily rigid pathways, and algorithms, for treating patients. Soviet style central planning at its finest. Everything commanded from on high, everything measured, everything inspected. All five-year plans in place …comrade.

At this point you may well ask, why the need for highly trained clinicians? Disease X requires treatment Y, at dose Z, to achieve the desired outcome. Anyone sitting in front of a computer can do this. It requires no knowledge of why you are doing any of it.

Equally, it requires zero understanding of the complex relationship between various physiological systems, or the specific medical needs of a patient either. What if the patient has three different diseases, where you must balance one system against another? What if no-one has ever studied the use, benefit, or harms, of four different drugs given at the same time? How do you balance one set of guidelines against another?

Leaving such issues to one side, depending on your philosophy of life, you may believe this is all a fantastic idea. Repeatable and reliable treatment protocols replacing potentially flawed clinical judgement. Factory worker vs. skilled artisan. Ford vs Rolls Royce.  In general, we know who usually wins this one. Command and control vs. individual decision making. No contest.

However, if the medical authorities decide, as they have done, to go down the bureaucratic ‘command and control’ model – based on the best evidence available – then there is a critical thing. It is the absolute requirement to be certain that the evidence you use is of the highest quality. Untouched by bias … if not, your house of algorithms simply collapses.

So, how reliable is the evidence base? Here is what Richard Horton (editor of The Lancet) stated a few years ago in an article ‘Has science “taken a turn towards darkness”?

“The case against science,” wrote Richard Horton, editor of the medical journal the Lancet, “is straightforward: much of the scientific literature, perhaps half, may simply be untrue.”1

A while back I wrote a book called Doctoring Data, in which I tried to help people understand the many, many, ways in which the data from major clinical trials are manipulated and biased. How they are carefully designed to obtain only the desired results. I also attempted to clarify the endless data manipulations used to report the results themselves.

If I had to sum up the overall message of the book, it is that we are all, essentially, bunny rabbits caught in the headlights of an onrushing car. The onrushing car, in this case, being pharmaceutical company profits.

More recently the BMJ published an article entitled ‘The illusion of evidence-based medicine.’ 2

It begins, thus:

‘The advent of evidence-based medicine was a paradigm shift intended to provide a solid scientific foundation for medicine. The validity of this new paradigm, however, depends on reliable data from clinical trials, most of which are conducted by the pharmaceutical industry and reported in the names of senior academics. The release into the public domain of previously confidential pharmaceutical industry documents has given the medical community valuable insight into the degree to which industry sponsored clinical trials are misrepresented. Until this problem is corrected, evidence-based medicine will remain an illusion.’

It goes on to say:

‘Regulators receive funding from industry and use industry funded and performed trials to approve drugs, without in most cases seeing the raw data. What confidence do we have in a system in which drug companies are permitted to “mark their own homework” rather than having their products tested by independent experts as part of a public regulatory system? Unconcerned governments and captured regulators are unlikely to initiate necessary change to remove research from industry altogether and clean up publishing models that depend on reprint revenue, advertising, and sponsorship revenue.’

I have been saying this, or something pretty much like this, for years. As have many other voices … howling in the wilderness. Has anything changed? Well, yes, it has changed. It has all got considerably worse.

For example, much of the recent research done during the COVID19 pandemic was almost laughably biased and dreadful. Anything that could make a pharmaceutical company money was promoted ruthlessly – did someone say remdesivir. Anything where no little money could be made was slammed though the floor. Did someone say hydroxychloroquine?

As for the vaccine trials themselves. Let us draw a discrete veil over those …vague approximations to science.

What we currently have is a crisis in evidence-based medicine. The evidence that we use is, at best flawed and incomplete. At worst, just plain wrong. Yet, this is this evidence used to create the NICE guidelines and drive the QOF targets.

Any wonder so many GPs are completely fed up. It is not the only reason, but it is a major reason. ‘You trained me for ten years, now I cannot even make a bloody clinical decision. What is the point?’ A GP colleague calls it ‘monkey medicine.’ In that a well-trained monkey could do it.

When QOF was first being heavily promoted as the glorious future of primary care, I made a prediction. I predicted that life expectancy of the elderly (where most of the QOF points aggregate) would gently start to fall. This would happen because everyone was going to be monitored and measured. Then treated with drug after flawed ‘evidence-based ‘drug.

Two problems. First, this would inevitably drive polypharmacy [many different drugs prescribed simultaneously], and the evidence for this is overwhelming, and clear. Here is a short section from a paper examining the increasing use of multiple medications. ‘Medication usage change in older people (65+) in England over 20 years: findings from CFAS I and CFAS II.’

‘The number of people taking five or more items quadrupled from 12 to 49%, while the proportion of people who did not take any medication has decreased from around 1 in 5 to 1 in 13.’3

Polypharmacy is, in of itself, potentially dangerous, in that all the different drugs can start interacting with each other in unexpected and, often, damaging ways. Many studies have demonstrated this unequivocally. 4

These inherent problems with polypharmacy are, of course, made far worse by being driven by biased evidence. It does not take a genius to add two and two in order to predict that, in this situation, life expectancy may well go down, rather than up.

Biased evidence base + polypharmacy = increased morbidity and mortality

In support of this, here is an analysis from Imperial College London entitled ‘Life expectancy declining in many English communities even before pandemic.’

‘A substantial number of English communities experienced a decline in life expectancy from 2010-2019, Imperial College London researchers have found … For such declines to be seen in ‘normal times’ before the pandemic is alarming.’’ 5

Cause and effect? This cannot be said for certain – rather too many variables flying about. I know what I think.

However, one thing you can certainly argue is the following. If the evidence we now use to audit and treat everyone, using QOF, was of unbiased high quality, then you should expect to see some improvement in life expectancy.

But that is not what happened. What happened, was a fall. Not a huge, oh my God fall, but a fall, nonetheless. Has anyone pointed to QOF, and NICE, and the endless proliferation of guidelines as potential factors? You already know the answer to that one. Not a chance.

Whilst other countries do not have QOF, or NICE, the relentless march of evidence-based guidelines, and the subsequent clinical algorithms that they are based on, has become a world-wide phenomenon. The US, too, is seeing a fall in life expectancy.

At one time, long ago, I was a great believer in evidence-based medicine. It seemed like a good idea at the time. I now recognise that I was hopelessly naïve. First, as a student of history, I should have known that centralised command and control systems always end in disaster.

This happens, no matter how well intentioned it may have been to start with, and QOF was well intentioned. A crushing and inflexible bureaucracy will inexorably grow, and suffocate, and drain enthusiasm and energy from the workplace. The guidelines themselves would also, inevitably, end up as a Procrustean bed, upon which no patient can ever fit. So, you have to chop bits off, or stretch, as required.

Procrustes “the stretcher [who hammers out the metal]”, was a rogue smith and bandit from Attica who attacked people by stretching them or cutting off their legs, so as to force them to fit the size of an iron bed. [The process was always fatal].

In this case, the Procrustean bed has been further distorted by the fact that the evidence base itself rests of quicksand. It is a horribly biased mess. So, yes, evidence-based medicine was a good idea (sort of). It died long ago. R.I.P.

As an end-note, the impact of QOF was reviewed a few years ago. In 2017, to be precise. Nothing since that I am aware of. As the study concluded:

‘The lack of effect of the QOF on mortality is surprising, given that the indicators are based on high-quality evidence of effectiveness of interventions. Why this is the case is not clear… ‘6

Not clear… There are none so blind as those who have not eyes to see.







Pfizer and me – Best Buddies

21st March 2022

Someone once said to me that I really must despise the pharmaceutical industry. There are certainly times when this is true, and my anger with them is sharp … and hot.

But yet, and yet, I know many people who work in the industry, and they all seem nice, concerned about the world, caring. Trying to do good. The industry itself has also produced some great innovations and medications. Without which the world would be a much scarier and more unpleasant place.

In truth, I find the industry is a bit like capitalism. Both fantastic and dreadful. Which is a bit like humanity itself. Both fantastic and dreadful. Capable of the most amazing things, yet the darker side can be very dark indeed. Dr Jekyll and Mr Hyde.

To be frank, my personal problems with the pharmaceutical industry have mainly centred around cholesterol lowering. Various companies have made billions, nay tens of billions, nay hundreds of billions, pushing LDL-Cholesterol reduction with all their might.

However, I have oft sat with my head in my hands in despair at such nonsense. Pfizer with Lipitor (atorvastatin) pushed the hardest and made the most … and horribly distorted the entire world of cardiovascular disease research in so doing.

However, thirty years ago, and purely by chance, the planets Pfizer and Kendrick were in a strange alignment. Briefly, I found myself on the same side as Pfizer when it came to cardiovascular disease.

How could this possibly be so? Well, gentle reader, let me take you back to a time when Pfizer had a very different drug to promote, called Doxazocin. It was a type of blood pressure lowering agent known as an Alpha-1 blocker. It was not selling terribly well, so they were looking for other angles in an attempt to boost sales.

I should mention that this was before Pfizer had a statin. A time that you could refer to as the ‘BS’ era. (Or maybe we are now in the true BS era – discuss). Then, in the year 2000, Pfizer took over Warner Lambert, which just happened to have a statin called atorvastatin (Lipitor). Yes, Pfizer didn’t actually develop atorvastatin. They just bought out the company that did. Nifty move.

Anyway, in 1992, Pfizer was not much interested in lowering LDL-Cholesterol, as they didn’t have a statin. Which meant they had other fish to fry with their cardiovascular drugs. They were more focussed on blood pressure lowering. But their Alpha-1 blocker for this, doxazocin (Cardura) was a bit rubbish.

So, what to do? What to do indeed. What they did was to use the tried and trusted mechanisms of looking at different effects that this drug might have.

To explain, almost all drugs when they are launched are marketed for one indication, and that indication only – the thing that will make the most money. Achieving marketing approval, for any indication e.g., blood pressure lowering, costs vast sums of money. Which means that companies must keep their focus tight, to drive the drug through the clinical trials process.

However, almost all drugs will do many other things, and you cannot run separate clinical trials on them all. To long, too complex, too costly.

There may be some ‘magic bullet’ drug that hits one target, and one alone, and spares everything else. Sniper fire. However, with most of them, you select automatic, raise the gun over your head from behind a sheltering wall, close your eyes, and spray bullets vaguely towards the target. Hoping you manage to hit the thing you’re aiming at.

Just to give a few well-known examples from history. Aspirin was initially found to reduce pain, inflammation and temperature. It was later discovered it helps to prevent platelets (small blood cells) sticking together. So, it was also an anti-coagulant – it reduced the risk of blood clots forming – and thus reduced the risk of dying of a heart attack. Now, it is being used to prevent cancer.

Sildenafil (Viagra) was initially developed as a drug for angina. The rest, as they say is history. It ended up being marketed for erectile dysfunction because it had an unknown, at the time, ‘off-target effect’ that had nothing, directly to do with angina at all. Or, at least, no-one could see the connection at the time.

Thalidomide was originally developed as a sedative. It was then sold for treating colds, flu, nausea and morning sickness. As everyone now knows, it caused horrible deformities in the unborn child.

Coincidentally, it was discovered the very same mechanism that led to the terrible deformities, also meant it was pretty good at treating a whole series of different diseases, such as multiple myeloma and leprosy. It is now prescribed as Thalomid – it has many different names. But certainly not thalidomide.

Last time I bothered counting, statins had thirty-four off-target effects. These are sometimes called ‘pleiotropic’ effects. I suppose this makes them sound more scientific. I am only surprised that statins have not yet been repurposed as anti COVID19 drugs. Probably because they are all off-patent, thus cannot make vast sums of money.

In an attempt to pull all these strands together, if your drug is not selling that well, have a closer look at all the other things it may do. The off-target effects, the ‘pleiotropics’. It has already reached market, at great cost, and whilst you are not allowed advertise it for ‘off-label’ benefits i.e., benefits not studied in the clinical trials, you can hold educational meetings and produce educational booklets to promote these additional things.

You can, effectively, launch it again as ‘Cardura two point one’. Ladies and Gentlemen …. drum roll. ‘A new era in cardiovascular disease prevention has begun.’ Dun, dun, duuuuuuuuun!’

At which point you can purchase a few off the shelf cardiology opinion leaders to push Cardura two point one with great enthusiasm. Throw a few million – carefully labelled – free pens, sticky pads, and BP cuffs around as an appreciative gift to doctors. Take them to a free lunch, sorry, educational meeting. Bore them for ten minutes, then reward them with a prawn sandwich. Feed the sea-lions.

And lo it came to pass that Pfizer scrutinised Cardura in greater detail, and found that it, like aspirin, helped to stop platelets sticking together. Platelets are small cells that float around in the bloodstream and play the key role in blood clotting. They have been described as the conductors of the clotting orchestra.

If you stop platelets sticking together, you can reduce the risk of cardiovascular disease, as was discovered with aspirin. Aha! So, not only does Cardura lower blood pressure, but it also has ‘anti-coagulant’ properties. Even better, it reduced fibrinogen, and PAI-1 and increased TPa activity. These are all ‘good’ in reducing the formation and increasing the breakdown of blood clots. As Pfizer stated:

‘These recent studies suggest that doxazosin may have a range of significant antithrombotic effects in many patients…’

Unfortunately, in 1992 doctors had already been under heavy and continuous bombardment with the message that lowering cholesterol and blood pressure were, by far, the most important things you could possibly do to prevent cardiovascular disease.

Blood clotting? Well, aspirin was used, a bit. But this was mainly to help with the final event. The big blood clot that blocked a major artery. No-one was suggesting that blood clotting had anything to do with atherosclerosis itself.

After all, how can blood clotting possibly cause atherosclerotic plaques to develop? As everyone had already been told, and told, and told … and told, and then told some more, atherosclerotic plaques (the entities that gradually grow and narrow down arteries) were full of cholesterol. Not the remnants of blood clots.

Love and marriage may go together like a horse and carriage, but platelet aggregation and atherosclerotic plaques …. You certainly cannot get a rhyme out of that – go on, I challenge you. Ergo, it must be wrong.

It was certainly a big mountain to climb. ‘You know that stuff about cholesterol…. Sorry. Turns out we should have been looking at Platelets and blood clotting instead.’ Here from a booklet on Cardura in 1992:

Platelets and atherosclerosis progression

Several features of mature plaques, such as their multi-layered pattern, suggest that 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, with can stimulate plaque development.

Given the insidious nature of atherosclerosis, it is vital to consider the role of platelets and thrombosis in this process, and the serious events that may be triggered once plaques are already present.

Goodness me. Who said all this? Why, of course it was Pfizer … Pfizer, Pfizer, Pfizer.

However, they didn’t get very far with this story. Merck were hammering away with simvastatin (Zocor) and Bristol Myers Squibb were also promoting pravastatin (Pravachol) with relentless fervour. The world of cardiovascular disease prevention was moving even more firmly in the direction of cholesterol lowering and statins.

As King Cnut (Canute to you and me) once demonstrated, once the tide starts to come in, not even a king can stop it. And the statin wave was very powerful. On the basis that, if you can’t beat them, join them, Pfizer decided to ride that wave. So, they went out and bought a large part of it, then bought the surf-boards and the tinnies.

To their (money making) credit, they then rode the cholesterol wave exceptionally well. To be frank you would buy a used car from Pfizer. I don’t know how they got so brilliant at spraying bull-shit with yellow paint, to make it look like one-hundred per-cent gold bullion, but there is no doubt they are the masters of pharmaceutical marketing.

At which point the Kendrick and Pfizer, planets were no longer in alignment. We span off on different orbits. I was still slowly plodding along the ‘platelets and atherosclerosis progression’ path, trying to make sense of it all.

Pfizer, to flip my analogies, firmly jumped on the ‘all singing, all dancing’ cholesterol lowering bandwagon.’ Complete with dancing girls in fancy costumes, a brass band, champagne, hundreds of balloons – and all the key opinion leaders in cardiology singing ‘We’re in the money.’

We’re in the money

We’re in the money

We’ve got a lot of what it takes to get along

We’re in the money

The sky is sunny

Old man depression, you are through you done us wrong, oh

We never see a headline

‘Bout a breadline today

And when we see the landlord

We can look that guy right in the eye

Oh, We’re in the money

Come, on my honey

Let’s lend it, spend it, send it rolling around…

And lo it came to pass that Pfizer and I were no longer friends. But there was a time when I like to think we could have danced all night, and still have begged for more. I could have spread my wings, and done a thousand things, I’ve never done before. Yes, my bandwagon would have been much better. Better music too. John Martyn, Fleetwood Mac, Randy Newman, The Pretenders, Jools Holland ….

Yes, it’s a little bit funny that Pfizer knew, thirty years ago, that blood clotting and atherosclerosis were intimately connected. They had seen the research. They knew:

‘Important evidence is now emerging that the selective alpha-1 inhibitor, doxazosin, in addition to its beneficial effects on elevated blood pressure and the serum lipid profile, may help to intervene in the evolution of thrombosis, a key component of atherosclerosis.’

In my recent book The Clot Thickens, I said I would put up the Pfizer booklet for all to see. It proved a bit more of a technical challenge than I thought, but here it is. And when people tell me that atherosclerotic cardiovascular disease (ASCVD) is all due to raised cholesterol I can say, not even Pfizer believes that. Not really. Not deep in their hearts …. They have a ghost in the machine that still stalks the corridors of Pfizer HQ. And if it doesn’t, it should.

They knew, oh yes once upon a time, they knew. It’s just not very profitable for them to admit it. To quote John Martyn:

Half the lies I tell you are not true.’


To date, most of our attempts to prevent atherosclerosis have centered on the control of hypertension and hyperlipidaemia, as well as lifestyle factors . However, recent insights into the pathology of coronary heart disease have sharpened our focus on the natural history of atheroma and its relentless progression to acute cardiac events.

Platelets and atherosclerosis progression

Several features of mature plaques, such as their multi-layered pattern, suggest that 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, and the serious events that may be triggered once plaques are already present.


If fibrinolysis is incomplete, thrombus may become incorporated into the plaque, and may cause severe stenosis. Alternatively, any residual thrombus can act as a powerful stimulant to further platelet aggregation. The growing mass of fibrin, platelets and enmeshed red cells may become solid enough to cause complete vessel obstruction.

It is significant to note that complete obstruction and myocardial infarction often develops from mild lesion initially causing less than 50% stenosis. Rupture of these plaques and the cascade of events that leads to thrombosis can occur rapidly and it now recognized as a common and major precipitant of unstable angina, myocardial infarction and sudden cardiac death. Studies suggest that thrombotic events may account for up to 90% of acute myocardial infarction.

Triggering factors in thrombosis

Hypertensive patients are known to have greater platelet adhesiveness and aggregability, which could increase clot formation at the site of plaque injury. In addition, thrombolysis is often defective in hypertension and hyperlipidaemia, which may result in an impaired ability to dissolved clots in the presence of atherosclerosis.

Clot propagation

Any residual thrombus can act as a powerful stimulant to further platelet aggregation. The growing mass of fibbing, platelets and enmeshed red-cells may become solid enough to cause complete vessel obstruction.

It is significant to not that complete obstruction and myocardial infarction often develops form mild lesions initially causing less than 50% stenosis. Rupture of these plaques and the cascade of events that leads to thrombosis can occur rapidly and it now recognized as a common and major precipitant of unstable angina, myocardial infarction and sudden cardiac deaths. Studies suggest that thrombotic events may account for up to 90% of acute myocardial infarctions.

The atherosclerotic process begins with infiltration of low-density lipoproteins or LDL into the arterial intima to create lipid-rich foam cells which form the basis of the ‘fatty streak.’ This early lesion contains large amounts of cholesterol, but its development to atherosclerosis is not inevitable. Progression appears to depend critically upon endothelial injury, caused by oxidation of LDL by the shearing forces of hypertension and by smoking.


With each decade, new insight is gained into how drug therapy can reduce the risk of coronary heart disease and stroke, the primary goal in the management of the hypertensive patient.
Important evidence is now emerging that the selective alpha-1 inhibitor, doxazosin, in addition to its beneficial effects on elevated blood pressure and the serum lipid profile, may help to intervene in the evolution of thrombosis, a key component of atherosclerosis.

The Document is called Pathological Triggers ‘New Insights into Cardiovascular Risk.’

Produced by Medi Cine Inc
488 Madison Avenue
New York
NY 10022

For Pfizer Inc
New York
NY 10017 Copyright 1992 Pfizer Inc. All rights reserved.

An online meeting on Heart Disease

We Love Our Heart.’ 9th April 2022

Please sign up here

Ivor Cummins [not Cummings please Mr spell check] has organised an on-line meeting on the 9th of April. Ivor is a brilliant man. He must be, he asked me to give one of the talks. He has brought together a great list of presenters who have been innovative thinkers in the world of cardiovascular disease for many years.

We are all, in different ways, trying to break out of the suffocating embrace of the ‘diet-heart cholesterol hypothesis’ and move things along. Our focus and thoughts are not exactly the same – thank goodness. Ivor is highly focussed on the metabolic causes of heart disease. Essentially insulin resistance, type II diabetes and suchlike.

Others have been researching the microbiome and related issues. However, the approaches are all complementary. Those who have read my stuff will know that there is not one cause of heart disease, there are many. Equally, you are not going to protect yourself against heart disease doing one thing. You need to do many.

The purpose of this conference is to look at many different areas, and many different approaches, to discuss how each of them can provide benefit. The synergies that you can find. There is also an opportunity to discuss your specific questions with the presenters. I hope this conference will be the first of many.

Please sign up. Thank you.

Why do we have Experts?

9th March 2022

The COVID19 pandemic has thrown an issue into sharp focus that I have been observing for many years now. What is an expert? The simple answer is someone who has expertise. Deep knowledge of a subject that has been gained by spending many years researching, reading, speaking to colleagues, and suchlike.

However, that is clearly not enough. I have spent years researching cardiovascular disease. I have written papers about it, written books, given lectures… but I have never been referred to, by any in mainstream medical research at least, as an ‘expert’. I am very much something else. A maverick, a denier, zealot a … [insert insult of choice here].

I used to joke that there must be a secret expert exam that you have to pass in order to be called an expert. Or perhaps it’s a bit like the Freemasons. Someone has a quiet word in your ear to sound you out. Then asks if you would like to join the international brotherhood of ‘experts.’ Dedicated to something, or other.

Very soon, after the COVID19 pandemic struck, Imperial College Business School had this to say on experts:

‘In 2016, when Michael Gove made his famous statement that “people in this country have had enough of experts”, it seemed experts and expert knowledge were on their way out. The opinion of populist politicians and online influencers were deemed much more relevant to decision making than the findings of scientists or the theories of economists. From the antivax movement to newly resurgent creationists, the spirit of the times was very much against the expert. Science and its evidence-based rationality were in retreat and the trend seemed unstoppable. 

Fast-forward four years and the world is suddenly a very different place. Experts like Imperial College London’s Neil Ferguson, and Peter Piot from the London School of Hygiene & Tropical Medicine are now central advisors to government and the profiles of experts are the material of front-page stories. With the arrival of a global pandemic, experts are back – and with a vengeance!

So, what has changed? And what can we learn from the recent success of the experts who are shaping government policy on coronavirus? First, the experts who are currently leading the government’s policy response to the pandemic are not just experts, they are leaders. They know that simply understanding a topic deeply and having something to say on an issue is not enough.’ Etc. etc, glory glory Imperial College 1.

I found the final sentence interesting. ‘They know that simply understanding a topic deeply and having something to say on an issue is not enough.’

In short, to be an expert you must also be a leader? I think this is probably true …. You certainly have to be at the top of some organisation or other.

Anthony Fauci for example. He was held by the mainstream media to be the number one expert about COVID19. His position unassailable – or at least it was. He was, and remains, the head of the National Institute of Allergy and Infectious Diseases. He remains the Chief Medical Advisor to the President.

Did he know more than anyone else about Sars-Cov2? Was this even a requirement? Tricky, as this was a completely new virus. Was he the perfect man for the job? He most certainly ticked all the expert boxes – so he should have been the ideal man? Hire that man right now…

Of course, there are those who have been far more sceptical about the value added by experts – to anything. David Sackett, who was a driving force behind the Evidence Based Medicine (EBM) movement – and who was also a very good man – wrote an article in 2000 entitled ‘The sins of expertness and a proposal for redemption.’

Here are a couple of sections. I suggest you read the entire article; it is not very long:

‘Is redemption possible for the sins of expertness? The only one I know that works requires the systematic retirement of experts. To be sure, many of them are sucked into chairs, deanships, vice presidencies, and other black holes in which they are unlikely to influence the progress of science or anything else for that matter.’

‘But there are still far more experts around than is healthy for the advancement of science. Because their voluntary retirement does not seem to be any more frequent in 2000 than it was in 1980, I repeat my proposal that the retirement of experts be made compulsory at the point of their academic promotion and tenure.’ 2

In this paper he refers to an earlier piece, written in 1983, where he first called for the retirement of all experts. Having voluntarily ‘retired’ himself as an expert in the field of ‘compliance with therapeutic regimes’. As he added:

I received lots of fan mail about this paper from young investigators, but almost none from experts.’

Some twenty years later he ‘retired’ himself again. This time as an expert in the field of evidence-based medicine, some would say the expert. He believed he had attained too much power and status and was therefore distorting everything around him.

As with all other acknowledged experts, he found that junior researchers deferred to him, and simply would not question him. He came to the conclusion that the very presence of an expert impaired scientific progress. [Of course, of all the experts in the world, he was the one that should not have retired].

In his opinion, experts crystallised into barriers to the progress of new ideas, and most other forms of innovative thinking. Their primary role became an immovable pillar, supporting the existing status quo. Of course, this expert problem has been recognised by many others … For example, Max Plank, in his famous quote:

‘A new scientific truth does not triumph by convincing its opponents and making them see the light, but rather because its opponents eventually die, and a new generation grows up that is familiar with it.’


Science advances one funeral at a time.’

So, who you going to call? If, that is, you are a government, and there is a pandemic? You do what everybody does. You call on the established experts. Leaders who sit at the top of the pyramid.

Those professors garlanded with honours. Opinion leaders. Even the mighty key opinion leaders (KOLs). No need to look elsewhere. All the expertise can easily be found, right? And the experts all know each other, so they can also recommend their expert friends – the ones they know and get on with.

A few years ago, there used to be an expression in business, which went something like this: ‘you never get fired for hiring IBM?’ Why not? Because IBM was huge, and they had the reputation of being the major players in IT solutions.

No-one would ever ask you to explain why you hired them. You just did. IBM was also bloated, cumbersome and vastly expensive – containing about as much innovation as a squashed cabbage. Which eventually caught up with them… eventually. Now, you tend to hire another massive company … GE, or suchlike. IBM still exists, but it came very close to the edge.

Of course, everyone needs expertise. If you want to build a bridge, then hire an architect and engineers who are capable of designing and constructing one that does not fall down. This requires skills and knowledge that take years to attain. True, validated, expertise.

Equally, if you want someone to replace your hip, find an anaesthetist and an orthopaedic surgeon, and their team of experts. Don’t pop down the local Botox clinic and hope for the best.

However, if you find yourself in a situation never seen before, where no-one really knows what to do … Then you will find experts are always going to propose doing only what they have always done. What they already know. As used to be said of generals, that they always started off any new war, using the exact same tactics that were being used at the end of the last war. Which never worked. Things had moved on … they hadn’t.

I do find it ironic that when the pandemic started, the key advisor to Boris Johnson was Dominic Cummings? The great ‘disruptor,’ the man who wanted to break apart the ‘cosy establishment’ and replace it with new thinking, and innovation. Here from the article: ‘Dominic Cummings: A model of disruptive leadership?’ [Sub-header. “The best way to spot those at the vanguard of disruption is by their unpopularity”].

The underlying problem is widespread institutional inertia that serves to contain rather than facilitate change. Leaders soon realise that being truly disruptive carries risks that either they, their board-level superiors, or those they lead find hard to tolerate. Few therefore follow through on good intentions, the common default being safety first…

Rightly or wrongly, Cummings believes the UK is being held back by a cosy establishment that stands in the way of reform. He openly disdains convention, as when deliberately bypassing traditional campaigning methods to sell Vote Leave’s ‘Take Back Control’ message, even if this means sailing close to the ethical wind.

You can tell that Cummings hits raw nerves because criticism of his modus operandi is laced with attacks on everything from his personal manner to his dress sense. But you wouldn’t bet on him lasting much longer in the Whitehall machine. The quicksand of inertia has a habit of swallowing disrupters in organisations a lot less complex and cunning than that of government … [Good call]

Change rhetoric might tell us that we need more people prepared to break the mould but our recent political experience indicates that having the will to disrupt rarely guarantees success against stubborn guardians of the ‘same old, same old’. 3

Well, as everyone in the UK knows, Dominic Cummings is now history. Disruptor no more. However, in February/March 2020 he was still very much in place – and he had Boris Johnson’s ear, as his most trusted advisor. You might have thought, therefore, that the scientific advisory group for emergencies (SAGE) would have contained a disruptor or two.

But no, we got the exact same old, same old. The well-established experts. The Chief Medical Officer, the Deputy Chief Medical Officer, the Chief Scientific Officer, the chief of this, the professor of that.

The great problem is that this ‘same old same old’ was going to have an in-built, and almost pathological resistance to risk – of any sort. In this case, by risk, I mean doing anything that is slightly different. Anything that may open you up to criticism. This is the main reason why the SAGE doomsday predictions have never matched reality.

Just as you never got fired for hiring IBM. If you are an epidemiologist, you never get fired for modelling a worst-case scenario. If you say there will be six thousand Omicron deaths a day – in the UK alone – yet the highest number reached was three hundred. Then are safe. This is the approved, standard direction of error.

On the other hand, if you said there would be three hundred deaths a day and it ended up at six thousand… all hell breaks loose. To quote Professor Graham Medley, who chaired the SAGE modelling group.

‘Professor Medley said one of the ‘worst things’ would be for the modellers to under-predict the approaching wave.

He told MPs: ‘The worst thing for me as chair of the committee is for the Government to say “why didn’t you tell us it would be that bad?”, so inevitably we are going to have a worst case that is worse than reality.4

inevitably we are going to have a worst case, that is worse than reality’… Roll that idea around for a moment or two. I did, and this was my interpretation. ‘Inevitably, our models will always be worse than the worst thing than can ever happen.’ Ergo, our models are designed to be utterly useless and inaccurate. A great way to plan your response?

Any decent disruptor would have questioned the assumptions underlying this ‘worst thing’. A disrupter would flip the question on its head. The worst thing, surely, would be to drive the Government into a massive over-reaction that could lead to such things as … thousands of deaths from undiagnosed cancers.

Or patients dying of heart attacks, terrified to attend hospital. Or care homes being flooded with COVID19 positive patients, because the hospital had to be cleared out. Or a tidal wave of mental health problems in children and adolescents. Or an increase in domestic abuse. Or … keep going, there are many damaging things that were caused by lockdown.

They would also have questioned the massive financial cost of extended lock-downs. The new hospitals that could not be built in the future. The much-needed healthcare staff not being hired – because we have run out of money. The inability to pay inflation matching pay rises, leading to staff resignations and loss of morale. The drugs that can’t be paid for, and on and on.

They would have remined those on the advisory board that this was not a zero-sum game. Every COVID19 death prevented, no matter how much it costs, is not necessarily a positive. There will be major, damaging, downsides to your actions, and these have to be taken into account.

However, if you stuff your advisory body with established experts you will get what you got. A group of people whose primary motivation is to ensure that they cannot be blamed for making a mistake. They will ‘hire IBM’. They will battle to maintain the status-quo. ‘Think of how terrible things would have been if we had not driven lock-downs on the entire country for weeks and months.’

Disruptor: ‘Look at how badly wrong your predictions have been, and the enormous and widespread damage you have caused. The cost of which may never even be known.’

Yes, as you can probably gather, I am not a great fan of experts. Of course, I do love expertise… and I love doing things as well as possible. At least those things that have been proven to work. I love innovation, and new thinking. Different ways of looking at the world.

What I hate, what we should all hate, is that any attempt to shift the status quo seems doomed to fail:

‘Change rhetoric might tell us that we need more people prepared to break the mould, but our recent political experience indicates that having the will to disrupt rarely guarantees success against stubborn guardians of the ‘same old, same old’.

When COVID19 arrived, we needed disruptors, new ways of thinking, and acting. We needed clear sighted innovators. What we got, predictably, inevitably, depressingly, were ‘experts’ to lay their cold, dead, hands on the situation. Experts desperate never to be ‘wrong.’ Having first decided what wrong meant. In this case it meant never, ever, underestimating the number of COVID19 deaths.

At this point I feel the need to quote David Sackett once more: I repeat my proposal that the retirement of experts be made compulsory at the point of their academic promotion and tenure.

Hear, hear. ‘Do I have a second for this proposal?’





Vaccination – silencing doctors in the UK

27th February 2022

My last blog discussed the possibility that mRNA COVID19 vaccines significantly increase the risk of myocarditis. Following this, a fellow doctor reached out to tell me about what has happened to them. They too, had questioned some aspects of the safety and efficacy of the vaccines.

As a result, they have been sent two threatening letters, which are both of the ‘iron fist in a velvet glove’ variety. I asked their permission to reproduce them here. One is from the General Medical Council (GMC). The other from their responsible officer – I shall explain what this title means a bit further on.

Below is the letter from the GMC:

Dear Dr….

The GMC have received several complaints regarding your recent social media posts.

All doctors have a right to express their personal opinion regarding the Covid-19 vaccine, and while the GMC in no way supports this opinion, we don’t consider your comments are sufficiently strong to open a fitness to practice investigation at this stage.

However, we are referring this matter to your Responsible Office for your reflection through the appraisal process.

We ask that you consider what implications this complaint might have for your practise when you are discussing this with your appraiser. We would also like to remind you of GMC guidance, in particular ‘Doctors’ use of social media, and of the requirement of doctors to act with honesty and integrity to justify the public’s trust in them

What we will do now

We will share the complaint with your responsible officer for them to consider in the wider context of your practice and revalidation.

‘The wider context of your practice and revalidation.’ Which means what, exactly? I sometimes wonder if there a special training scheme where you learn to write creepy and threatening phrases that can later be denied as being creepy and threatening? ‘I was only trying to be nice. They just took it the wrong way.

‘Your children look charming. However, you may want to consider their continued existence on the planet in the wider context of your practice.’

The GMC, as mentioned before, have the powers to investigate complaints made against doctors in the UK, and impose various punishments (they call them sanctions, which sounds far prettier). Ranging from nothing very much to permanent erasure from the medical performers list.

The latter means that you cannot work as a doctor ever again. Anywhere in the world. The GMC will communicate your erasure to other national statutory bodies, upon request. They do it gladly… and speedily.

On the face of it, in this case, the GMC have decided to do nothing. ‘We don’t consider your comments are sufficiently strong to open a fitness to practice investigation at this stage.’

Jolly good.Nothing to see here, move along. Although they add the rider … ‘at this stage.’ Well, what other stages are left, after deciding to take no action? The … I have changed my mind and I am going to have you guillotined, stage?

However, in reality they have not done nothing – have they dear reader? The GMC have decided to refer the complaint to this doctor’s responsible officer. A responsible officer is a doctor who is ‘responsible’ for ensuring that other doctors working in their area have met the necessary requirement for revalidation.

Revalidation is a five-year cycle whereby a doctor has to meet various requirements. A few hundred hours of medical education, keeping up do date with mandatory training. Carrying out an audit, and a patient satisfaction questionnaire, getting sufficient colleague feedback, and suchlike.

There is also a need to have a yearly appraisal. Which is a meeting with an allocated appraiser, to discuss how things have gone. A look through any complaints about you, work you have done, audits that have been completed, actions to take in the next year to improve your practice – a personal development plan. Release of thumbscrews – or a tightening.

If all this is done successfully, over a five-year period, the responsible officer ‘signs you off’ and you are now able to continue work. If not, you are removed from the performers list, and you cannot work as a doctor until you are successfully re-validated. No-one has ever explained to me how you actually do get revalidated. In fact, there is no system in place for this to happen.

If you manage to fulfil the re-validation cycle, and attend appraisals, in theory there can be no grounds for removal. You cannot actually ‘fail’ an appraisal. You simply have to turn up, and ‘reflect’ on your practice. I have never heard of a responsible officer stepping in to remove a doctor from the performers list any time they so wish.

Bearing all that in mind, here is the follow up letter from the responsible officer.

Dear Dr….

I have today received a communication from the GMC regarding an ‘incident that occurred on social media.’ The GMC have advised that they have reviewed the complaint and that it does not meet the threshold for investigation.

However, I understand that you have been asked to consider what implications this complaint may have for your practise and there is a requirement for you to reflect on this matter at your next appraisal meeting.

As your Responsible Officer I have a statutory duty to ensure that any concern or complaint about your practise is responded to and dealt with appropriately.

I would be grateful if you could let me have your views on this issue, by completing the attached form and returning it as a matter of urgency.

Can you also complete the attached Monitoring of Clinical Practise for your file, please.

Your co-operation with this process is vital in order for us to come to an acceptable resolution as soon as possible, minimising impact to your practice and cost in time and money.

If you have any questions regarding this process, please to contact me to discuss further.

Kind regards

Dr X

Responsible Officer for X region.

I love the ‘Kind regards’ sign off. For this is a letter dripping with unspoken menace. Just to highlight one phrase ‘An incident that occurred on social media…’ An ‘incident’. You mean, someone wrote something that someone didn’t like, they then complained about it. This was not an incident, in the sense that anyone would normally choose to use this word.

[I also note that the GMC spells practice, practice. The responsible officer spells it practise – maybe they need to reflect on their spelling between them].

If you look up the word ‘incident’ on the Cambridge Dictionary it gives an example of its use:

‘A youth was seriously injured in a shooting incident on Saturday night.’1

It does not say. ‘Someone wrote a blog post that upset someone, somewhere, for a bit. But it’s alright now, they are looking at pictures of kittens to recover.’

Words. Words, words, words. They can be used in so many different ways. Their true meaning hidden behind layers of sophistry. But we all know what the word ‘incident’ means in this case. Someone was badly damaged by your actions on that day – do not attempt to deny it, comrade.

Then we move onto the real threat. The responsible officer wants to ensure an acceptable resolution, thus … ‘minimising impact to your practise and cost in time and money.’

What the responsible officer here is saying is that I have the powers to stop you practising medicine in the UK. If I find that your answer to this complaint – which was not strong enough to open a fitness to practice investigation by the GMC – does not satisfy me. Indeed (subtext), I do not actually care what answer you give, I may remove you anyway. This will certainly maximise the impact on this doctor’s ‘practise and cost in time and money’.

If you think this is not what is being threatened. Then ask yourself what else it could mean? There is nothing that needs to be ‘resolved’. A complaint has been made, but the GMC didn’t think it was serious enough to take forward. No patient was harmed, no laws broken … no wrecks and nobody drowned, in fact nothing to laugh at, at all. (small prize for who knows where that came from).

At this point you may have begun to allow the thought to enter your mind that the GMC have quite deliberately handed this complaint down to the responsible officer to carry out the required sentence and execution. Whatever the accused doctor says, the responsible officer can simply respond. ‘Sorry, not satisfied with your answer. I am now going to stop you working – for as long as I wish.’ No hearing, no possibility of review, no accountability. Bosh.

In truth I have always known that responsible officers possess this amazing and unrestrained power. I tried, and failed, to stop this happening years ago – when I was on various British Medical Association (BMA) committees. I found it incredible that the legislation in this area was going to hand over, to one individual, the ability to destroy someone’s career, with no regard to anyone else, or anything else.

Yes, we live in a democracy that has created a form of local tyranny.

Tyranny (noun) def: government by a ruler or small group of people who have unlimited power of the people in their country or state and use it unfairly, and cruelly.

You could say that this situation suits the GMC very well … Very well indeed. Because, you see, the GMC has tried to remove other doctors from the medical register for criticising vaccination. [The medical register is not quite the same thing as the performer’s list, but you need to be on both of them to work as a doctor in the UK].

These punishments were quashed in the High Court. Here from a legal firm that works in this area:

‘On Friday, the High Court handed down a judgment quashing the GMC interim order of conditions previously imposed on a GP, Dr Samuel White, as a result of his actions arising from the pandemic.  Dr White came to the GMC’s attention as a result of “spreading misinformation and inaccurate details about the Coronavirus and how it is diagnosed and treated”.  His comments have included assertions that the COVID-19 vaccine “inserts a code”, masks do “absolutely nothing” and hydroxychloroquine, budesonide inhalers and ivermectin are “safe and proven treatments”.  

The interesting point arising from Dr White’s High Court appeal is the technical point on which he won. The High Court found that the Medical Practitioners Tribunal Service (MPTS – the adjudication wing of the GMC) panel made an error of law in not properly considering the test required by section 12(3) of the Human Rights Act 1998 when deciding whether to impose an interim order.2

As this company also says:

As time goes on, we’re seeing more fitness to practise cases arising from COVID-19-related activities.  We’ve previously posted about the Irish GP interim suspended after describing COVID-19 as a hoax and the first UK nurse struck off by the Nursing and Midwifery Council (NMC) as a result of COVID-19 denial activities.

‘COVID denial activities’ – what a deliciously Soviet phrase.

I have to say that I very much enjoyed the lawyers’ assertion that the GMC interim order was quashed on a ‘technical point’. Namely that the GMC had failed to consider the small matter of the Human Rights Act 1998. Riding roughshod over someone’s human rights is now a technical point of law. How quaint.

However, undeterred, the GMC have not been deterred from their vital work in punishing COVID-19 vaccine deniers – to ensure that they can never work again. They have just found another, simpler, far cheaper, and far quicker route to obliterate a doctor’s career. Call the responsible officer. No-one expects the responsible officer.

Who needs time consuming and costly hearings, where you might have to bear in mind the Human Rights act 1998 – and other such woolly liberal nonsense? When you can alert the local ‘tyrant’ to a doctor’s non-comradely Soviet ‘denial’ activities. Sorry, COVID19 ‘denial’ activities.

They will know precisely what to do, and they have the powers to do it. Why on earth did the GMC not think of this of this before? I could have told them about the ridiculous, frightening, and untrammelled powers of a responsible officer, but they never asked me.

Of course, you could argue the following. If the local responsible officer does obliterate someone’s medical career and does this without paying any heed to such things as well, the law, for example, then their actions will be over-turned in court. Well, I certainly hope so, in fact I would expect so. This may act as a deterrent … maybe.

However, during the months, or years, that it takes to get such a case to court, the doctor will be out of work and unable to earn. They will almost certainly end up bankrupt, and their reputation (have been struck off the performers’ list) will lie shattered in the gutter.

As for the responsible officer. Their punishment ‘please don’t do it again,’ would just about cover it. This is very much asymmetric warfare. I can punish you, terribly, but you can do absolutely nothing to me in return.

In the financial world they call this moral hazard. A banker can bankrupt you, and your family, and half the country, making stupid and risky decisions – that will earn them huge short-term bonuses. If, as a result, their bank goes bust, the Government simply bails them out and they keep their job, and their bonus. All gain, no pain.

As a sign off, the responsible officer (washing his hands of any personal responsibility of course) wrote this ‘I have a statutory duty to ensure that any concern or complaint about your practise is responded to and dealt with appropriately.’ Kind regards … Pontius.

However, one thing that has not happened, so far, is to actually take the time and effort to forward a copy of the complaints to the doctor concerned. Still, they must be guilty of something or other. So, it is clearly critical that they respond to these unknown complaints, of some sort or another, in some-way or other. ‘Here is a bottle of whisky, and a revolver…. You know what you must do.’

What a world this has become. I had hoped I would not live to see such a time in this country, but I have.



A few thoughts on COVID19 vaccination

23rd February 2022

The first thing I want to say here is that there should be nothing in science that is beyond analysis and potential criticism. Because, once this happens, we can find ourselves in a very dangerous situation indeed. A place of unquestioned acceptance of the accepted narrative, with criticism enforced by the authorities.

Unfortunately, I believe this is the place we have reached with COVID19 vaccination. Here is just one example from the UK.

‘GPs have been warned that criticising the Covid vaccine or other pandemic measures via social media could leave them ‘vulnerable’ to GMC* investigation.’1

*GMC = General Medical Council. This is the body that can strike doctors from the medical register so they cannot work as a doctor.

‘Vulnerable to GMC investigation’. What a deliciously creepy phrase that is, dripping with unspoken menace, whilst pretending to be helpful. It sounds like something the Mafia would come up with.

‘I would keep quiet about this, if I were you.’ Baseball bat tapping gently on the floor. ‘No, this is not a threat, think of it as advice from a friend. We don’t like to see anybody making themselves, or their family, vulnerable, and getting seriously injured now, would we?’

It seems that, unless you prostrate yourself before the mighty vaccine, and intone ‘Our vaccine, which art in heaven, hallowed be thy name…’ and suchlike, you will be attacked from all sides … simultaneously. Indeed, to suggest that vaccines are not perfect in every way is the twenty first century’s equivalent of blasphemy.

he said Jehovah. Stone him.’

This does make any discussion on vaccines somewhat tricky. To criticize any individual vaccine, indeed any aspect of any individual vaccine, is also to be instantly defined as an anti-vaxxer. Then you will be furiously fact-checked by someone with a fine arts degree, or suchlike, who will decree that you are ‘wrong’.

At which point you will be unceremoniously booted off various internet platforms – amongst other sanctions open to the ‘vulnerable’. This includes, for example, finding yourself struck off the medical register, and unable to earn any money:

            ‘Hell, we ain’t like that around here. We don’t just string people up, son. First, we have a trial to find ‘em guilty, only then do we string ‘em up. Yeeee Ha!’

Spit … ding!

Yes, it seems you must support the position that all vaccines are equally wonderful, no exceptions. Try this with any other pharmaceutical product. ‘He doesn’t think statins are that great, so he obviously believes that antibiotics are useless.’ Would this sound utterly ridiculous?

But with vaccines… All are the same, all are great, not a problem in sight? I said, NOT! a problem in sight. However, I genuinely believe there are some questions which still have not been answered and simply because of the different types of vaccines that are available, no, not all vaccines are the same.

Just for starters, vaccines come in many different forms. Live, dead, those only containing specific bits of the virus, and suchlike. Now we have the brand new, never used on humans before, messenger RNA (mRNA) vaccines. So no, all vaccines are not alike. Not even remotely.

In addition to the major difference between vaccines, the diseases we vaccinate against vary hugely. Some are viruses, others bacteria, others somewhere in between, TB for example.

Some, like influenza, mutate madly in all directions. Others, such as measles, do not. Some viruses are DNA viruses – which tend to remain unchanged over the years. Others, e.g. influenza, are single strand RNA viruses, and they mutate each year.

Adding to this variety, some of those viruses which mutate very little, also have no other host species to hide in. Smallpox, for example. Which means that the virus was unable to run away and hide in, say, a chicken, or a bat. Others are fully capable of flitting from animal species to animal species. Bird flu and Ebola spring to mind.

Some vaccines just haven’t worked at all. For over thirty years, people have tried to develop an HIV vaccine, and have thus far failed. Early trials on animal coronavirus vaccines also showed some concerning results. Here from the paper ‘Early death after feline infectious peritonitis virus challenge due to recombinant vaccinia virus immunization.’

The gene encoding the fusogenic spike protein of the coronavirus causing feline infectious peritonitis was recombined into the genome of vaccinia virus. The recombinant induced spike-protein-specific, in vitro neutralizing antibodies in mice. When kittens were immunized with the recombinant, low titers of neutralizing antibodies were obtained. After challenge with feline infectious peritonitis virus, these animals succumbed earlier than did the control group immunized with wild-type vaccinia virus (early death syndrome).’2  

Yet, despite all this massive variety flying in all directions, with some spike protein vaccines found to increase the risk of death (in a few animal studies), attach the word vaccine to any substance, and it suddenly has miraculous properties that transcend all critical thought. Vaccines move in mysterious ways, their wonders to perform.

Yes, of course, some have worked extremely well. The polio vaccine, for example, although I have seen some valid criticisms. Smallpox… I am less certain about. Even though it is held up as the greatest vaccine success story of all. Maybe it was. Smallpox has certainly gone, for which we should be truly thankful. It was a truly terrible disease.

My doubts about the unmatched efficacy of smallpox vaccine simply arise from the fact that diseases come, and diseases go. The plague, for example. This was the scourge of mankind at one time. It tore round and round the world and leaving millions of dead in its wake, over a period of hundreds of years.

We do not vaccinate against the plague, yet it is virtually unknown today. Cholera killed millions and millions, thousands each year in the UK alone. Now … gone. In the UK at least. This had nothing to do with vaccination either. Measles. There seems little doubt that the measles vaccine is effective. But vaccination cannot explain the fact that measles deaths fell off a cliff and were bumping along the bottom for years and long before we started vaccination programmes.

In the US vaccination did not begin until 1963. So, what happened here? The virus did not mutate, so far as we know. It did not mutate because apparently it cannot. Or, if it did, it would no longer be able to be infective. At least not to humans:

‘While the influenza virus mutates constantly and requires a yearly shot that offers a certain percentage of protection, old reliable measles needs only a two-dose vaccine during childhood for lifelong immunity. A new study publishing May 21 in Cell Reports has an explanation: The surface proteins that the measles virus uses to enter cells are ineffective if they suffer any mutation, meaning that any changes to the virus come at a major cost.’3

So, measles didn’t change, but it did become far less damaging. From around ten deaths per one hundred thousand in the first two decades of the twentieth century, down to much less than one.

Why? What I believe happened with measles is primarily that the ‘terrain’ changed. Nutrition greatly improved. Vitamins, perhaps most importantly vitamin D, were discovered and added to the food supply. Rickets and other manifestation of vitamin D deficiency were rife in the late nineteenth and early twentieth centuries. Virtually gone by 1940.

Of course treatments improved as well, although antibiotics (to treat secondary bacteria pneumonia following measles), did not come into play until the late 1940s, at the earliest.

What we see with measles is simply the fact that infectious diseases have far less impact when they hit a healthy, well nourished person (healthy terrain), than when they hit an impoverished and undernourished child caught in the war in the Yemen, for example.

So, yes, vaccines have played a role in improving human health and wellbeing, but we shouldn’t inflate their impact to the point where they have become the unmatched saviours of humankind. They have certainly not been the only thing that reduced the impact of infectious diseases. They were probably not even the most important thing. ‘Yes … how dare you say this… string up the unbeliever, I know, I know.

Moving on, and and I think this is even more pertinant to the disucssion that follows. If we cannot accept the possiblility that, at least some vaccines, may have significant adverse effects, if we will not permit anyone to look into this, in any meaningful way. Then we can never improve them. Criticism is good, not bad.

Speaking personally, I do not criticize things that I do not care about. Primarily, because I don’t care if they improve, or not. I only criticize things when I want them to be as good as they possibly can be. It is a character trait of mine to hunt for flaws, and potential problems. Both real and imagined.

Some criticism is, of course, close to bonkers. Suggesting that COVID19 vaccines contain transhuman nanotechnology and microchips of some kind that will become activated by 5G phones … to what end? ‘World domination Mr Bond. Mwahahahahaha etc.’ Quantum dots? Yes, these do exist. But they would be pretty useless at collecting informaiton, and suchlike. Give it fifty years and … maybe.

The problem here is that wild conspiracy theories are simply gathered together with reasonable science-based criticism, to be dismissed as a package of equally mad, unscientific woo-woo tin-foil hat wearing, conspiracy theorist, gibberish.

Which means that, when people (such as me) suggested that COVID19 mRNA vaccination could, potentially, lead to an increased risk of blood clots – this was treated with utter scathing dismissal. I did not understand ‘the science’ apparently. Fact check number one. ‘Oh, look… clots.’

When people questioned the ‘fact’ that the safety phases of the normal clincial trial pathway had been seriously truncated, and that some parts were just non-existent, they were told that they knew nothing of ‘the science’ either.

I looked on the BBC website to find out the ‘official’ party line on vaccine safety information, sanctioned and approved by HM Govt, and SAGE I presume. It was an article entitled ‘How do I know if the vaccine is safe?’ The information rapidly contradicts reality. They say:

  • There are different approved types and brands available and all have undergone rigorous testing and safety checks
  • Safety trials begin in the lab, with tests and research on cells and animals, before moving on to human studies
  • The principle is to start small and only move to the next stage of testing if there are no outstanding safety concerns

The article then looks at fast track approval for vaccines against new variants

  • The UK’s drug regulator says new vaccines can be fast tracked for approval if needed.
  • No corners will be cut, with safety paramount.
  • But lengthy clinical trials with thousands of volunteers will not be needed4

What is wrong here? Well, ‘if the principle is to start small and only move to the next stage of testing if there are no outstanding safety concerns,’ then this principle was not followed. After pre-clinical and animal testing, we move onto trials in humans. Phase I, then II and then III.

Phase I may include as few as twenty people to check that humans don’t simply drop dead on contact with the new agent (it has happened).

Phase II may include a couple of hundred individuals, and usually lasts a few months… a bit more safety, and an attempt to establish the potential size of any health benefit.

Phase III may have up to thirty or forty thousand participants. This phase often lasts for several years.

Well, with the Pfizer Biontech vaccine, the concept of waiting to move to the next stage of testing did not truly occur. Because phase II and III were combined… and the phase III trials have now been, effectively abandoned. They were not supposed to finish until May 2022 at the earliest, and now apparently, they are not going to finish at all. At least not as a double-blind placebo controlled trial.

Yet, we are still informed by the BBC, in all seriousness, that no corners were cut, or will be cut. The fact is that corners were absolutely one hundred per cent cut. Slashed to the bone would perhaps be more accurate. To pretend otherwise is simply to deny reality.

It normally takes around ten years for any drug, or vaccine, to move through the clinical trials process, with each step done in series. COVID19 vaccines took around six months from start to finish, with critical steps done in parallel, and the animal testing was rushed – to say the least. To claim that no corners were cut is nonsense. Nonsense that we are virtually forced to believe?

It is possible/quite likely/probable that vaccine development can be shortened, but please do not tell us that all the normal processes were followed.  No-one is that easily fooled.

‘Freedom is the freedom to say that two plus two make four[NK1] . If that is granted, all else follows.’ That freedom disappeared pretty early on in the COVID19 pandemic. I enjoyed the slant that ‘Important quotes explained’ had on the quote from Orwell’s 1984.

By weakening the independence and strength of individuals’ minds and forcing them to live in a constant state of propaganda-induced fear, the Party is able to force its subjects to accept anything it decrees, even if it is entirely illogical.

Of course, it could be that despite the speed with which these vaccines were pushed through nothing important was missed. It is almost certainly true that the standard ten years from start to finish in vaccine and drug development can be compressed, if everyone really wished. Bureaucracy expands to fill the space available.

But in general we are talking about a ten-year process, cut down to six months, or thereabouts. An additional concern is that this happened using mRNA vaccines, which represent a completely new form of technology. One that has never been used on humans before at all, ever.

We are not talking about the sixth drug in a long line of very similar drugs e.g. the statins.

  1. Lovastatin
  2. Fluvastatin
  3. Simvastatin
  4. Pravastatin
  5. Atorvastatin
  6. Cerivastatin
  7. Rosuvastatin etc.

Statins all do pretty much the exact same thing thing, in exactly the same way. Yet, each one fo them still had to go through the entire laborious clincial trial process. Years and years.

‘Can we not just skip this phase….please?’




Hold on one moment, just step back, what was that at number six on this list, I hear you say… cerivastatin. You mean you’ve never heard of it. Well, it got through all the pre-clinical trials, then the animal trials. It then sailed through the human Phase II and III trials without a murmur. It was then was launched to wild acclaim. In truth that may be over-egging its real impact, which was a bit more ‘who cares, do we really need another one?

Here from a 1998 paper: ‘Clinical efficacy and safety of cerivastatin: summary of pivotal phase IIb/III studies.’

‘In conclusion, these studies indicate that cerivastatin is a safe and effective long-term treatment for patients with primary hypercholesterolemia and also suggest that higher doses should be investigated.’ 5

Here from 2001, and an article entitled: ‘Withdrawal of cerivastatin from the world market.’

‘Rhabdomyolysis was 10 times more common with cerivastatin than the other five approved statins. We address three important questions raised by this withdrawal. Should we continue to approve drugs on surrogate efficacy? Are all statins interchangeable? Do the benefits outweigh the risks of statins? We conclude that decisions regarding the use of drugs should be based on direct evidence from long-term clinical outcome trials.’ 6  

Yes, as it turns out, cerivastatin caused far more cases of severe muscle breakdown, and death, in a significant number of people. Which meant that it was hoiked from the market.

The moral of this particular story is that, even if you DO do all the clinical studies, fully and completely, one step at a time, over many years, in a widely used class of drug, your particular drug may still be found in the long term, not to be safe. Not even if it is the sixth of its class to launch.

The cerivastatin withdrawal is not an isolated event. You can, if you wish, read this paper ‘Post-marketing withdrawal of 462 medicinal products because of adverse drug reactions: a systematic review of the world literature.’7. So, what happens if you try to compress the entire ten year clinical trial process into around six months, on a completely new type of agent?

… Well then, it may be time to cross your fingers and hope for the best. But please do not insult my intelligence, or the intelligence of anyone else, by trying to tell me that vaccines have undergone: Rigorous testing and safety checks. Compared to what, exactly? Certainly not any other drug or vaccine launched in the last fifty years. ‘We rushed them through, and launched two years before the phase III clinical trials were due to finish.’ would be considerably more accurate.

Two plus two does not equal five, it never has, and it never will. However much you try to browbeat me, and everyone else, into accepting that it does. Indeed, as I write this, the simple fact is that not a single phase III clinical trial has yet ever been completed, on any mRNA COVID19 vaccine, and possibly not ever will be, in truth.

To repeat, this does not mean that mRNA vaccines may not be entirely safe. However, it has become impossible to to claim that we have not seen significant adverse effects from the mRNA vaccines. Effects that were not picked up in any phase of the clincial trials. Here, from the Journal of the American Medical Association in February. One of the most highly cited medical journals in the world:

‘Based on passive surveillance reporting in the US, the risk of myocarditis after receiving mRNA-based COVID-19 vaccines was increased across multiple age and sex strata and was highest after the second vaccination dose in adolescent males and young men.8

I highlighted the first bit here. Namely, the words ‘based on passive surveillance reporting in the US.’ Whilst this adverse effect was not seen, or reported in the clinical trials it was picked up by the passive surveillance reporting system a.k.a. spontaneous reporting systems.

Drug adverse event reporting systems

Frankly, it is surprising that anything at all is ever seen using passive surviellance. In the UK we have the passive/spontaneous reporting system, known as the ‘Yellow Card system.’ In this US (specifically for vaccines) there is ‘VAERS’ (Vaccine Adverse Event Reporting System).

When I use the term ‘spontaneous reporting’, I mean a system whereby someone may (or more likely may not) report an adverse effect to a healthcare professional. They may (or more likely may not) fill in a form, whereupon it goes through to VAERS, who then look at it and can decide whether or not the adverse effect may (or more likely may not) be due to the vaccine. Same basic principle in the UK.

How good are these types of spontaneous reporting system in picking up adverse effects?

Well, as far as I am aware, only one serious attempt has been made to look at how many drug and vaccine-related events were actually reported in the US. Here, from a study by The Agency for Healthcare Research and Quality:

‘Adverse events from drugs and vaccines are common, but under-reported. Although 25% of ambulatory patients experience an adverse drug event, less than 0.3% of all adverse drug events and 1-13% of serious events are reported to the Food and Drug Administration (FDA). Likewise, fewer than 1% of vaccine adverse events are reported.’ 9

Fewer than one per cent of vaccine adverse events are reported. Their words, not mine. Even though, in the US, unlike the UK, there is a legal responsibility to report adverse events – I believe.

When the authors of this report tried to follow up with the CDC and perform further assessment of the system, with testing and evaluation, the doors quietly, but firmly, shut:

‘Unfortunately, there was never an opportunity to perform system performance assessments because the necessary CDC contacts were no longer available and the CDC consultants responsible for receiving data were no longer responsive to our multiple requests to proceed with testing and evaluation.’

This study was done over ten years ago, but nothing about the VAERS system has changed since, as far as I know, or can find out.

In the UK the Yellow Card system may be better, or it may not be. No-one has carried out the sort of detailed analysis that was attempted in the US. However it has been accepted that:

…all spontaneous reporting schemes have a problem with numbers: the MHRA (Medicines and Healthcare products Regulatory Agency) itself says that only 10% of serious reactions and 2 – 4% of all reactions are reported using the Yellow Card Scheme. This means that most iatrogenic* morbidity goes unreported.’ 10

*Iatrogenic means – damage/disease caused by the treatment itself.

Frankly, I see no reason why the Yellow Card system would be any better than VAERS. The barriers to reporting are exactly the same. As the US report states:

‘Barriers to reporting include a lack of clinician awareness, uncertainty about when and what to report, as well as the burdens of reporting: reporting is not part of clinicians’ usual workflow, takes time, and is duplicative.’9

In other words, reporting an adverse event takes an enormous amount of time and effort. You don’t get paid for doing it, you certainly don’t get thanked for it, and you have no idea if anyone paid any attention to it. All made worse if you are not sure if the adverse event was due to the vaccine, or not.

I have filled in yellow cards three times, and several hours of work followed each one. As directed, I searched though patient notes for all previous drugs prescribed, the patient’s medical conditions, a review of the consultations and on, and on. Back and forth from the pharmaceutical company the questions went. Until the will to live was very nearly lost.

If you wanted to devise a system to ensure that adverse effects were under-reported, you could not devise anything better. Yes, doctor, please do report adverse effects to us. The result will be endless hours of work, with no attempt to report back that what you did had the slightest effect, on anything. Thank you for your continued and future co-operation. And yet this, ladies and gentlemen, is the system we have in place to monitor and review all drug and vaccine-related adverse effects.

Which becomes even more worrying because, as mentioned before a couple of times so far, nothing else of much use is going to come out of the clinical trials. With the Pfizer BioNTech trial, crossover occurred in Oct 2020. By crossover I mean the point at which they started giving the vaccine to those in the placebo group as well. End of randomisation, end of useful data. End of … well of anything of any use.

mRNA vaccines and myocarditis

Anyway, getting back to the JAMA study. Even with all the formidable barriers in place to reporting adverse events, JAMA reported an increase in the rate of myocarditis of around thirty-two-fold, as reported via the VAERS system.

I should make it clear that this was the increase seen in the most highly affected population. Males aged eighteen to twenty-four. [Myocarditis = inflammation and damage to heart muscle]. The risk was lower in females, and also in other age groups, although still high. But, to keep things simple, I am going to focus on this, the highest risk group, as far as possible.

The first thing to say is that a thirty-two-fold increase probably does sound enormous. Another way to report this would be, a three thousand one hundred per cent increase, which may sound even more dramatic?

However, myocarditis is not exactly common. In this age group, over a seven-day period, you would expect to see around one and three-quarter cases per million of the population. Multiplying this by thirty-two still only gets you to fifty-six cases per million.

Which is not exactly the end of the world. In addition, most cases may fully recover. Although, having just said this, I have no long-term data to support that statement. The closest condition we have to go on as a comparator, is post-viral infectious myocarditis. And this has a mortality rate of 20% after one year and 50% after five years.11

Which means that myocarditis is certainly not a benign condition of little concern.

Anyway, at this point, you could argue that if around only one in twenty thousand men, in the highest risk population, suffer from myocarditis post-vaccination, then this does not represent a major problem.

It could indeed be worse to allow them to catch COVID19, where the risk of myocarditis is even higher than with vaccination. In reality, we may be protecting them from myocarditis through vaccination. This certainly seems to be the current party line. I might even agree with it…. maybe. So, as is my wont, I looked deeper.

I looked for the highest rate of (reported) post-viral infection myocarditis, in younger people. I believe it can be found here. ‘Risk of Myocarditis from COVID-19 Infection in People Under Age 20: A Population-Based Analysis’ 12

Here, the reported rate was around four-hundred-and-fifty cases per million. On the face of it, this is much higher than the fifty-six cases per million post-vaccination. Approximately ten times as high. But … there are, as always, several very important buts here. There were two key factors that alter the equation.

First, in the JAMA post-vaccine study, the time period for reporting myocarditis was limited to seven days after vaccination. Any case appearing after that was not considered to be anything to do with the vaccine and was thus ‘censored’. In the study above, the time period was far longer. Anything up to ninety days post-infection was counted. A period thirteen times as long.

In addition, although it is difficult to work out exactly what was done from the details provided, the four-hundred-and fifty study only looked at young people who attended outpatients at hospital. These would have been the most severely affected by COVID19, or who had other underlying medical conditions. So, they represent a small proportion, of a small proportion …. of everyone who was actually infected. The vast majority of whom would only have suffered very mild symptoms, or none at all.

In short, we are not remotely comparing like with like here. I find that we very rarely are. We are not only going to vaccinate a small proportion, of a small proportion, of the population who are at high risk of myocarditis. We are going to vaccinate virtually everybody. So, the two populations are completely different.

Leaving that to one side, where else can we look for a comparison between the risk of post-vaccine myocarditis vs post-infection myocarditis. The CDC published this statement.

‘During March 2020–January 2021, patients with COVID-19 had nearly 16 times the risk for myocarditis compared with patients who did not have COVID-19, and risk varied by sex and age.’ 13 

Their figure appears to have been entirely derived from a paper published in the British Medical Journal: ‘Risk of clinical sequelae after the acute phase of SARS-CoV-2 infection: retrospective cohort study’ 14. Different age groups were studied here which, again, makes any direct comparison tricky.

This study found a sixteen-fold increased risk, rather than a four hundred and fifty-times risk. A sixteen times risk is around half of the post-vaccination myocarditis risk reported in JAMA, in the eighteen-to twenty-four-year-old group.

Again, though, there were major differences. In the BMJ paper the observation period for inclusion of myocarditis considered to be ‘caused by’ COVID19, was one hundred- and forty-days post infection, not seven days. Twenty times as long for cases to build up.

Equally, after looking at nine million patients records over a year, slightly over two hundred thousand were diagnosed as having had COVID19. Of these, only fourteen thousand had post-infection problems, known as clinical sequelae. In this sub-group, which represents, one point two per-cent of one per-cent of the total, population there were so few cases of myocarditis that they didn’t even appear in the chart published in the main paper. You had to go to supplemental tables and figures 15

To be frank, there are far too many unknowns and uncontrolled variables kicking around here to make any accurate comparisons. However, I do not think it would be unreasonable to suggest that the risk of myocarditis post-vaccination, from these studies, is roughly the same as if you are infected with COVID19.

Once again though, we need to take a further step back. All of our figures here only make sense if all – or the majority of cases of myocarditis – are actually being picked up. What if they are not?

Worst case scenario

SAGE – the UK Governments scientific advisory group for emergencies – have been accused of scaremongering, and only presenting worst case scenarios for COVID19 hospital admissions and deaths. They are not the only ones. This is a worldwide phenomenon.

However, as Sir Patrick Vallance – one of the key members of (SAGE) – has stated, in response to such criticism.

‘It’s not my job to be an optimist’: Sir Patrick Vallance takes swipe at critics accusing scientists of scaremongering over Covid saying ministers need to ‘hear the information whether uncomfortable or encouraging.’ 16

SAGE believe it is their role to highlight the worst possible scenarios, the highest possible death tolls, and such like. So, let us now do the same, and focus on the worst-case scenario regarding mRNA vaccines and myocarditis. Whether ‘uncomfortable or encouraging’.

The worst-case scenario starts like this. If the VAERS system only picks up one per cent of vaccine related adverse effects, this means that we can start by multiplying the JAMA figures by one hundred.

Thus, instead of fifty-six cases per million, the reality is that we could be looking at five thousand six hundred cases per million, post-vaccination. Or very nearly one in two hundred.

If, in this model, we then include the possibility that post-vaccination myocarditis is as damaging as post-viral infection myocarditis, it means that one in four hundred eighteen to twenty-four-year-olds could be dead five years after vaccination.

Do I think that this is likely? I have to say that no, I don’t, really. Although this is where the figures, such as they can be relied upon, inevitably take you. Just to run you through the process a bit more slowly.

  • Relying on the VAERS system, JAMA reported a thirty-three-fold increase in myocarditis post COVID19 vaccination. An increase from 1.76, to 56.31 cases per million (in the seven-day period post vaccination)
  • It has been established that VAERS may pick up only one per cent of all vaccine related adverse effects
  • Therefore, the actual number could be as high as five-thousand six-hundred cases per million ~ 1 in 200.
  • Myocarditis (post viral infection) has a mortality rate of 50% over 5 years. So, we need to consider the possibility that post-vaccination myocarditis will carry the same mortality.
  • Therefore, the rate of death after five years could be one in four hundred (males aged 18-24)

There are approximately sixteen million men aged between eighteen and twenty-four in the US.

Total number of deaths within five years (men aged eighteen to twenty-four in the US)

16,000,000 ÷ 400                 = 40,000

(Divide by five for the UK) = 8,000.

Now, if I were in charge of anything, which I am not, which is probably a good thing, I would hope to have been made aware of these worst-case scenario figures. I would then immediately have begun to do everything I possibly could to verify them.

For starters I would want to know two critical things:

1: Is the VAERS system truly only picking up one per cent of vaccine related adverse effects?

2: Does vaccine related myocarditis lead to the same mortality and morbidity as caused by a viral infection?

If the answer to both of these questions were, yes, then I would have to decide what to do. And that could not possibly, be nothing. At least I would hope not. Yet, nothing appears to be exactly what is currently happening.

As you can tell, I still cling to the concept of ‘first do no harm.’ Today, with COVID19, it seems this this idea has become hopelessly naïve. The current attitude seems to be. ‘We are at war; you must expect casualties’ ‘Also, careless talk costs lives.So, my friend, I advise you to keep your ‘vulnerable’ mouth shut, if you know what is good for you.’

Well then, I just hope for everyone’s sake, that these figures are completely wrong. They are, after all, only a model. A worst-case scenario created using the most accurate information available at this time. However, as per the SAGE underlying philosophy, I believe it is important to present the information whether uncomfortable or encouraging.

The thing that most concerns me the most is that we have a worrying signal emerging about the mRNA vaccines. A signal surrounded by a lot of noise, admittedly. Yet, the ‘official’ response continues to be to sweep the entire thing under the carpet. ‘Nothing to see here, move along.’


As with regard to the GMC, and the threat of sanctions, as you can see, I am only following their guidance

‘Healthcare professionals must also be open and honest with their colleagues, employers and relevant organisations, and take part in reviews and investigations when requested. They must also be open and honest with their regulators, raising concerns where appropriate. They must support and encourage each other to be open and honest, and not stop someone from raising concerns.’ 17

What do you do if it is the GMC itself that may be stopping someone from raising concerns. Should I report the GMC to the GMC? I imagine they will find themselves innocent of any wrongdoing. Quis custodiet Ipsos custodes?


















My interview with Joe Mercola

12th February 2022

Catch it while you can.

Dr Joe Mercola – a man who I admire – interviewed me about The Clot Thickens recently. This is my latest book, in case you are unaware of this majestic tome… if so, where have you been? It was all over the mainstream press, all major news channels… then I woke up.

This interview is now going to be available from Sunday 13th February, for forty-eight hours only* [unless you go behind the pay wall]. I am not entirely sure what hour it will posted, as the US is several hours behind the UK.

As some of you may know, various authorities tried very hard to shut down Mercola’s website, as he had many articles critical of the mainstream response to COVID. He ended up having to take down all his articles after forty-eight hours, then put them behind a pay wall. Some weird compromise or other, that I don’t fully understand. Anyway, you can hear my great words of wisdom if you wish, from Sunday the 13th for forty-eight hours only*. You have been warned.

*at least officially. You may want to try the link now to see if it works.

“The_Clot_ThickensThe Clot Thickens is available worldwide in Paperback and eBook through Amazon:
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Some observations on the infection fatality rate of COVID19

10th February 2022

Some observations on the infection fatality rate of COVID19
[Mainly that it does not really exist]

When COVID struck the world two years ago, or thereabouts, the first thing that happened was rather unfortunate. Namely, the instant and widespread distortion, nay destruction, of data. This happened so fast that it became almost impossible to know what on earth was going on. Who to believe … what to believe?

I have never been so naïve as to think that we are not constantly subjected to certain ‘truths’, which may or may not be true. After all, I have been battling against the dreaded ‘cholesterol hypothesis’ for decades. In doing so I have become something of an expert in recognising seriously distorted data when I see it.

I have learned to search for things not said, which are usually far more important than the things that are. I have also learned to treat the words used with great distrust. Words such as ‘fact’ for example. Facts have a disturbing tendency to crumble under pressure … note to the dreaded dementors, sorry fact checkers.

However, I felt I had become pretty expert in navigating the games played. I had learned to sail the stormy waters of scientific truths, or facts, reasonably well. Then came COVID, and the world of fact distortion achieved warp drive. Alleged facts flashed past so fast, and in such great numbers, that it all became a blur.

In this blog I will attempt to remove some of the blur surrounding the issue which became key to ‘The Great COVID Wars’. This is the Infection fatality rate (IFR) of COVID19.

You may not feel this was central to everything that occurred, or remains so, but I hope to convince you that it is the single most important ‘fact’ of them all. The keystone. Also, the one most jealously guarded by the fact checkers. ‘Put your weapon down, place both hands in the air, and step away from your IFR.

To begin. There was a time when epidemiologists, with regard to infectious diseases, used two different terms. Infection fatality rate (IFR) and case fatality rate (CFR). Although it has to be said that the distinction between the two was never exactly black and white.

After all, how do you decide when someone who is ‘infected ‘with a disease, reaches the point when they become a ‘case?’ Historically this happened when someone became so unwell that they were admitted to hospital. Whereupon the disease itself would be diagnosed with a test of some sort – sometimes. Sometimes clinical signs and symptoms were all that were used.

Which means that ‘cases’ have always been somewhat easier to count and compare. However, no-one has ever really known how many people were infected in the first place. By which I mean those people who were not seen anywhere, by anyone, and so never managed to the reach the status of a ‘case.’

In general, those with a mild infection just lay in bed, for a while feeling a bit sorry for themselves. Indeed, the advice for those with ‘flu’ always used to be to stay at home, drink plenty, and take some medication to control the temp and the aches and pains. This represents the traditional three Ps management technique. ‘Take two paracetamol and piss off.’ [Paracetamol is called acetomenophin in the US – take two As and piss off … nah, doesn’t really work]

Ergo, those with few symptoms, or no symptoms, were never seen or counted. So, the Infection Fatality Rate (IFR), which represent the total number of people who become infected, who then die, has always been subject to a great deal of guesswork.

A whole series of the underlying problems with defining IFR [and also CFR] were highlighted in the paper ‘case fatality risk of influenza A (HIN1pdm09): a systemic review.’ The authors looked at the Swine Flu epidemic of 2009, and also reviewed data on infection and case fatality rates from the past.

I shall paraphrasetheir main findings. ‘We haven’t a clue what the infection fatality rate was for this, or any other flu. In truth, neither does anyone else, because the data are complete rubbish.’

Their actual conclusion, couched in more scientific language:

‘A consensus is needed on how to define and measure the seriousness of infection before the next pandemic.’1

Did this consensus ever happen? You must be joking.

As you may have noticed, we have begun the move into very blurry waters indeed. You may ask how it is possible to compare the Infection Fatality Rate of COVID19 with previous influenza epidemics, when we have no idea what the IFR rate of previous influenza epidemics may have been.

Despite such great uncertainty, this IFR rapidly become a red line issue for the COVID wars.

On one side were the CDC, Fauci, Neil Ferguson and Imperial College London – and suchlike. The ‘establishment’ – the ‘experts’. They confidently stated, from the very beginning, that the Infection Fatality Rate of COVID19 was around one per cent. Meaning that for every one hundred people infected, one person would die (on average).

Quite how they knew this is beyond any real understanding? They say modelling. I say guesswork. Which, in truth, is pretty much the same thing. A brand new, never seen before disease, and they just knew what the IFR was.

This was also at a time before any accurate testing existed, and we had no idea how many people had actually been infected? Indeed, at this point, they were primarily relying on information from China … Oh well, at least we know that Chinese data are always fully reliable … thank God. Just don’t mention that pesky laboratory in Wuhan, or gain of function research. Or pretty much anything else that emanates from China, in truth.

On the other side were…. Well, there wasn’t really another side so to speak of. A rag tag bunch of researchers and epidemiologists who were fascinated by the data coming in, and what it was saying. It included those such as Professor John Ioannidis and Professor Carl Heneghan at the Centre of Evidence Based Medicine in Oxford, and suchlike.

I just watched with interest, at first. My own bias has always been to be very wary of any expert consensus that springs into life. This is because it will almost always be a slave to the inherent problems with human thinking that ride roughshod over a disinterested pursuit of the truth. Particularly in a crisis.

Problems such as: groupthink, confirmation bias, fast thinking rather than slow thinking, deference to ‘experts’, the desperate need to come up with ‘the answer’ and stick to it, and suchlike. We all know what they are. They all came into play, as expected.

Anyway, a key question here was, how did their one per cent figure compare with more common or garden influenza? This is very hard to say. I have seen figures of 0.67% for the flu epidemic of 1967. I have seen far less. ‘Spanish flu’, the big daddy of them all, was estimated to have had an IFR of around two to three per cent.

But how accurate can these figures be? In the paper I quoted above, the IFR estimates for swine flu (HIN1pdm09) ranged from less than one death, per hundred thousand infections, to more than ten thousand. Yes, from one in a hundred thousand, all the way up to ten per cent. This is what scientists call…. A pretty wide range.  You could call it other things.

Cutting to the chase, the reality is that, at the start of the COVID19 epidemic we had no idea what the IFR of a severe influenza epidemic was, nor did we know the IFR of COVID19. You would think that this would make any comparison somewhat tricky.

However, the mainstream consensus rapidly coalesced around two ‘facts’.

Fact one: a severe seasonal influenza has an IFR of around point one per cent. Or, to put it another way, one death per one thousand infections.

Fact two: COVID19 has an IFR of around one per cent. Which meant that COVID19 was going to be ten times as deadly. This, then, became our starting point.

What would this mean in the real world?

The UK has a population of sixty-seven million people. Which meant that if everyone were infected, we would end up with almost exactly two thirds of a million deaths. Which is one per cent of the entire population. The population of the US is three hundred and thirty million, so there would be three point three million deaths

Hold on a minute. The models also predicted that not everyone would get COVID19. Full herd immunity would kick in once about eighty per cent of the population – or thereabouts – had been infected. This, by the way, was another thing that the experts just knew, right from the very beginning. [But what about mutations, and variants, and re-infections I hear you cry…. ‘Oh, do shut up’].

In effect, the COVID19 epidemic would come to an end when eighty per cent of people had become ill, maybe slightly less. Ergo, the overall death figure would be about five hundred thousand in the UK, and just over two million in the US. Or thereabouts.

This is a lot of deaths. Around the entire world pop: ~7.9 billion. We could see nearly seventy million deaths.

This one per cent figure, then, became the trigger for everything that followed. I think of it as the ‘justification’ figure. It was used to justify lockdowns, and everything else that went along with them. Here, after all, was a disease ten times as deadly as a bad influenza epidemic. Something must be done, or millions will die.

A further complication

Of course, things are rarely this simple. Even if the one per cent figure were true, it is essential to ask a follow up question. Who exactly is dying?

The average age of death caused by the Spanish flu was estimated at twenty-eight. Yes, twenty-eight.2 The average age of death caused by COVID19 is around eighty-one – in the UK.3

I feel that the fact [and unusually this fact is almost certainly true] that COVID19 almost exclusively kills the elderly, and almost always the elderly who have many other comorbidities, had to be taken into consideration. But it wasn’t.

Instead of a disease that can wipe out young healthy people, aged twenty-eight, we had a disease on our hands that primarily kills those close to the end of their lives. Children and young adults, even middle-aged adults, even nearly old adults, have been almost remarkably unaffected by COVID19. This was known very early on.

What are the actual figures here? Turning attention specifically to the UK, we have had, at the time of writing, around one hundred and fifty thousand COVID19 deaths. Defined as… those deaths with COVID19 mentioned on the death certificate [whatever this actually means – another whole can of worms].

On the other hand, the number of people under the age of sixty, who have died from COVID19, with no other disease mentioned on the death certificate, is five hundred and forty-two. That was, by the 1st of February 2022.4

This is slightly under one per day during the epidemic. Or, to frame it another way, the risk of dying, for a healthy (or at least believed to be healthy – who knows for sure if they are or not) person under the age of sixty has been one in 79,131. [UK pop < 60 = 42,869,306].5

This risk, however, has been over very nearly two years. So, the yearly risk of death from COVID19 per years is 1:158,263. Or ~ 0.0075% … for this population. Just to give a comparator. The risk of dying from a road traffic accident in the UK, per year, is around eight times higher 6.

1in 20,000 per year vs 1 in 160,000

Thus, for more than two thirds of the population, the risk of dying from COVID19 has been 0.0075%. Instead of one per cent… it has been seven thousandths of one per cent.

Some people will say that this doesn’t matter. All deaths are of equal importance, we cannot discriminate on grounds of age, illness etc. In which case, taking the UK population as a whole, we have had 158,000 deaths with COVID19 mentioned on the death certificate. This represents a total risk of death of 1 in 424. Or ~ 0.25%.

Again, this has been over two years, so the total risk of death, per year [which is how risk is normally presented] has been 1 in 848, or ~ 0.125% per year. Which, as you may have noted, is around seven times less than one per cent.

Strangely, with COVID19, we have not stopped counting at the end of one year, and then started again. We have just kept on adding the figures year upon year – and will continue to do so? We have also continued to add in people who have been infected more than once…Double, treble, nay quadruple counting.

If we keep doing this, the IFR of COVID19 will eventually reach one. Not one per cent, but one. As in the entire population of the world will end up dying of COVID19. Although, at 0.125% per year this, as you may have worked out yourself, will take about seven hundred years. You may want to go and lie down and think about this.

Of course, the rough figures I have calculated above do not represent the Infection Fatality Rate. Instead, they represent the population fatality rate (PFR) i.e., forgetting about IFR and CFR, how many people, in total, have actually died. The population fatality has to be significantly lower than the infection fatality rate because not everyone has been infected… or have they?

The terrain is all?

We must now venture into yet another layer of complication. Yes, this onion has many layers. Most of which, you may be glad to know, I am not going to consider, or else this blog becomes a book. But the next layer is critical.

What does being ‘infected’ actually mean, and can we even know that it has happened?

At the risk of terrible oversimplification, historically there are two camps in the infectious disease world.

  • Camp one: the microbe is all (The germ theory).
  • Camp two: the terrain is all (The terrain theory).

Camp one believes that if you become exposed to an infectious agent you will inevitably become ‘infected’. You will then inevitably suffer (at least some) symptoms from the infection. You will then become unwell – maybe very unwell – and may even die. The germ theory. The severity of the disease is almost entirely dependent on the ‘viral load’ that you encounter.

Camp two states that the ‘terrain’ of the human body is far more important. We are surrounded by, and harbour microorganisms in our bodies. When exposed to pathogens ‘germs’ we become ill if our defences are weakened by deficiencies or toxicities. The germ itself is pretty much unimportant.

This is the ‘terrain’ theory. It means that many/most people, may not become ‘infected’ at all. Or that they may not even notice it – they simply shrug the infection off.

Historically, the two camps were led by Louis ‘the germ’ Pasteur and Claude ‘the terrain’ Bernard. It is said that, on his death bed Pasteur admitted. ‘Bernard was right, the pathogen is nothing, the terrain is everything.’

Well, yes and no. It is difficult to suffer any symptoms from a disease if you are never exposed to the germ. Which means that the pathogen clearly is something, not nothing. But … but we are making a greater mistake if we think that everyone is going to respond the same way to a germ. An assumption upon which our response has been predicated.

You may not think it, but the thinking behind all the actions taken is that COVID19 will inevitably ‘infect’ anyone who comes into contact with it. It will spread from person to person in a predicable manner, it will cause illness in everyone, and suchlike. In effect therefore, we have acted as if the terrain truly is nothing. Therefore, we must do everything possible to reduce contact, in order to reduce morbidity and mortality. In essence, the microbe is all.

The next assumption, following on from this, is that those who have not demonstrated any signs of symptoms have simply not been exposed to it, or not exposed to a sufficient ‘viral load’.

Personally, I find this impossible to believe. My daughter, a junior doctor who caught COVID19 working on a COVID ward in Wales, stayed at our house, suffered anosmia, and was diagnosed with COVID19 – with a PCR test, no less. No-one else got a snuffle.

At one point during the first couple of months of the epidemic, in May 2020 to be precise, I was standing next to two unmasked nurses in a small treatment room (we were not allowed to wear masks at this time) who were both coughing repeatedly in my face. Both were diagnosed with COVID19 the very next day and went off ill.

Every working day for six months, I went into nursing homes and an intermediate care centre. During which time, thirty-six patients died of – probably – COVID19. All of whom I saw and examined at least once. However, I did not become infected, and I never have. I also showed no antibodies – in a test in Autumn 2020.

If anyone tries to tell me that I was not exposed to the virus, or a sufficient viral load to cause infection, I can only laugh. I would reckon myself to be amongst an elite ‘most exposed to SARS-Cov2 virus in the world’ workforce. For at least two months I was working with no PPE – at all. Surrounding by staff and patients – many of whom died of COVID19 [no staff members, only patients].

If I was not infected, and officially I have not been, it raises the question. What, exactly, does infected mean? I speak as someone who also had to have seven Hepatitis B injections before I was able to raise a feeble, and pretty transient, antibody response. A friend and colleague had, if memory serves, over thirty Hep B vaccinations, and never raised a single antibody.

What does this, in turn, mean? That neither of us has any immunity to Hep B? That antibody tests are hopelessly flawed. That ‘immunity’ exists in ways that we have no idea how to measure – my current view.

Looking more specifically at COVID19, what happens if someone is found to be infected, as part of routine testing, yet has no symptoms, and produces no antibodies. Can you state that they were ‘infected’?

You may want to have a look at ‘The Flawed Science of Antibody Testing for SARS-CoV-2 Immunity.’ 7

It quotes this FDA statement

‘…results from currently authorized SARS-CoV-2 antibody tests should not be used to evaluate a person’s level of immunity or protection from COVID-19 at any time, and especially after the person received a COVID-19 vaccination.’

So, antibody tests cannot tell us if someone has been infected, or effectively, vaccinated, nor if they are immune to SARS-Cov2. Just run that idea round your head for a while. Then see what answer pops out.

One small study further suggested that if you were diagnosed with [had a positive test for], COVID19, but suffered no symptoms, there was a 92% chance that you would show no measurable immune response post infection. 8

These people, with a positive test, yet no symptoms, and no antibodies, were clearly ‘infected’ – they had a positive test after all [another can of worms]. However, these people must represent the most immune population of all. COVID19 hit them but was simply shrugged off. Leaving behind no sign that it was ever there.

Before I spin off down another hundred complications and side-issues – all of which are fascinating in themselves – I will attempt to highlight one immutable fact.

We have no idea how many people have been infected with SARS-Cov2, primarily because we have no idea how many people have been ‘infected’ yet demonstrate no sign of contact with the virus (unless they were coincidentally tested at the time). People such as, to pluck an example from the air … me.

It follows, therefore, that we cannot know what IFR rate might be. All we really have to go on (for all its further myriad flaws) is the Population Fatality Rate. Namely, how many people have actually died of COVID19.

In this end, this is the key figure. The one that counts [even if I have serious doubts about how this figure is created].

Thus far, across the world, over a period of very nearly two years, we have officially had five point seven million deaths from COVID19.

The total population of the world is seven point nine billion. Therefore:

  • The total population fatality rate is 0.072%
  • The total population fatality rate per year is 0.036%

This is a long, long way from the IFR of one per cent. Indeed, per year, it is around thirteen times less.

Is this because only one thirteenth of the world’s population have been infected? This is extraordinarily unlikely. The recent REACT study in the UK, found that 65% of those infected with the Omicron variant in January 2022 had previously been diagnosed with COVID-19.9

Seven per cent more had symptoms strongly suggestive of previous infection but had not had a confirmatory test at the time. Ergo, very nearly three quarters of those getting COVID19 in January 2022 had been infected before.

The authors are now attempting to backtrack from this finding. Why? Because, if it is correct that the vast majority of people infected represent re-infections, it means that the infection rate must be extremely high, much higher than anyone admits.

It also follows that exposure and transmission is extremely high. This, in turn, means that the IFR is significantly lower than anyone admits – or indeed can admit.

It is no surprise then to find that those running the REACT study are based in Imperial College London. Which is where all the original IFR estimates came from. The lair of Neil Ferguson et all. The originator of the ‘justification’ figure. Those who are now doing all they can to suggest that the number of people who have been infected with COVID19 remains low.

Even more telling, although this is less easy to confirm, we have cases of people with three, or even four, infections. How can anyone get infected four times, when people around them have not been infected once? Are they dancing naked around a flagpole, breathing in deeply from an inverted loudhailer in a COVID19 ward?

No, they are not. The explanation is that those getting re-infected are those who are unable to simply shrug of COVID19, for whatever reasons. Their terrain was different. Which means that they will likely keep on getting infected as new variants appear. Hopefully in milder and milder versions.

On the other hand, if we look at those individuals who show no evidence of infection – those who have never suffered symptoms and developed no antibodies – it is not that they have never been exposed, or ‘infected’. It is that they have more robust defences. As Claude Bernard argued, the most important thing here is not the germ, it is the terrain. It always was, and always will be.

As you may have gathered, I am convinced that we have all been exposed to and ‘infected’ with COVID19, probably all within the first year [even if I don’t know how you determine being infected]. Which means, in turn, that the PFR and the IFR – after two years of the virus spreading around – will have will be very much the same.

Can I prove this. No. If a large number of people develop no symptoms, and there is no test used that can accurately determine infection/exposure, I cannot possibly prove this. Equally, no-one can prove anything in the opposite direction.

A bit of a standout clue, however, is that three quarters of those found to be infected had been infected before. This could only have happened if people have been repeatedly exposed to a sufficient ‘viral load’ to get COVID19. And if they have, so has everyone else.

Of course, if we cannot accurately define what we mean by ‘infected’ no prediction can have been right. In turn, this means that we bet the house on an outcome measure so deeply flawed as to be virtually meaningless.

A strong clue that has been more widely recognised to be meaningless, is that it no longer exists. How so, I hear you cry? Well, it was decreed fairly early on that any positive COVID19 test represents a ‘case’ of COVID19. Something that kind of slipped through, without anyone noticing.

It was a worldwide thing, but the text below is taken from an NHS press briefing conference, using data from The bit in bold is most important.

Number of daily cases, UK:
Number of people who have had at least one positive COVID-19 test result, either lab-reported or lateral flow device (England only), by date reported – the date the case was first included in the published totals. COVID-19 cases are identified by taking specimens from people and testing them for the presence of the SARS-CoV-2 virus. If the test is positive, this is referred to as a case.

Once this happened, any historical comparison of IFRs, or CFRs, became impossible. If everyone who is infected is also a ‘case’ then everyone is an I/C, (infected/case). There is no longer an IFR. Nor can there be a CFR. There is a combination I/CFR.

This, in turn, means that the IFR rate has been artificially boosted. Case fatality rates will always higher than IFRs [people who become very ill from a disease are always more likely to die from the disease, than those who suffer no symptoms].

Add them together and the IFR jumps up. Or at least it does if no-one notices that you are flipping between, and combining IFR and CFR, at speed, and continue talking about the IFR as if it remains the same thing. Oh, the tricks that are played to inflate the IFR and ‘prove’ that the experts were right all along.

Despite the fact that it is now devoid of any meaning, the one per cent IFR for COVID19 remains the most fiercely guarded figure of all. Dare to state the IFR is significantly lower than the one per cent ‘justification’ figure and the dreaded dementors, sorry fact-checkers, descend from on high.

They will attack you, your personal habits, your professionalism, your motivations, your clear ‘anti-vaxx’ stance, your lack of being an expert – and anything else they can think of to personally denigrate and humiliate.

They will countenance no arguments, no discussion. It will be determined that you are simply wrong, certainly stupid, and unable to understand The Science and probably in the pay of someone evil cabal, or other. It is somewhat irritating. I want to discuss science, if not ‘THE SCIENCE’. They want me crushed and silenced.

End thoughts

We understand far less about infections than we like to think. We are simply scratching at the surface at present. It is all extremely complex. If you are up for it, you may wish to read this paper. ‘Pathogenesis of COVID-19 described through the lens of an undersulfated and degraded epithelial and endothelial glycocalyx.11

This paper represents a monstrously complex discussion of ‘the terrain.’ Namely, why do some people shrug off COVID19, whereas others may become so seriously ill that they may die?

According to this paper, it has nothing whatsoever to do with the things that we think of as part of the classic ‘immune response.’ T-cells, B-cells, cytokines, antibodies and suchlike. It is almost entirely to do with the ability of cells in our body to prevent viral entry.

Keeping things as simple as possible. If COVID19 (or other viruses) cannot get into an endothelial cell – or find it very difficult to do so – because the glycocalyx is healthy and robust, then SARS-Cov2 simply bounces off, and you will not become seriously ‘infected’. Yes, you will ‘shrug’ the virus off. It may enter your bloodstream, but that is about as far as it is going to get.

I mean, I have always been aware of the importance of cell entry in viral diseases. Both HIV and the Ebola virus enter a cell by hijacking a protein called CCR5 attached to cell membranes. There are a few people who have a thing called the CCR5delta32 mutation. If you have this mutation, it means that HIV and Ebola cannot attach themselves to the protein. Neither virus can then get into the cell and ‘infection’ cannot occur. The terrain is all.

Have any of those on SAGE, or Fauci, or Ferguson, or the CDC paid any heed to such things? I would be very surprised if any of them had even heard of the glycocalyx. A perfect example of the Dunning-Kruger* effect, I feel.

Yet, despite their stunning ignorance about such things, certain individuals and organisations grabbed the reins of influence in order to convince those in power that they had the answer.

The most important ‘answer’ being that COVID19 has an IFR of one per cent, which is at least ten times that of a serious influenza epidemic. Then, as the ‘germ’ is obviously everything, the only way to prevent hundreds of thousands, nay millions, of deaths was through lockdown, mask wearing, societal control, and suchlike.

We must stop spread, the ‘the germ is everything brigade’ cried. Although, with a 75% re-infection rate it is hard to argue that we have managed anything of the sort.

If this IFR figure was grossly inflated, which certainly seems to be the case, then all that we did was to create untold damage – for no good reason. I shall leave you with a post that I put up in a WhatsApp group recently. It followed a study from John Hopkins which estimated that COVID19 lockdowns only reduced deaths by 0.2%. [A study that will be attacked remorselessly, no doubt].12

‘Did lockdown work? No, the difference it made was marginal, at best. Were the models that we relied on accurate? No, they were bloody useless. Are the vaccines safe and effective? – Jury is out. Is there anything that was done justifiable by the evidence, in so much as it can be relied upon. I do not believe so.  What we certainly did was to explode the economy, pile vast debt on UK Plc. create a massive backlog of work for the NHS. Fail to diagnose and treat hundreds of thousands of cases of cancer, and suchlike and create a tsunami of mental health problems. We also ran roughshod over incredibly important human rights, that have taken centuries to take hold and grow. In my opinion, almost everything that was done has caused more harm than good. What is the counter-argument? If we hadn’t done all these things, it would have been far worse. The evidence to support this position is sadly lacking.’

*Dunning-Kruger effect is, in psychology, a cognitive bias whereby people with limited knowledge or competence in a given intellectual or social domain greatly overestimate their own knowledge or competence in that domain relative to objective criteria or to the performance of their peers or of people in general.













Don’t just do something, stand there!

14th January 2022

A few months ago, I resolved not to write anything more about COVID19. I was having zero apparent effect on anything, or anybody, and I was just getting increasingly despondent at the destruction of science, debate, logic, humanity, personal freedoms … life.

However, my New Years resolution was to not have any more resolutions. Which lead to an almost inescapable logic loop from which I have only just managed to extricate myself.

In truth, I believe that I still have a few things left to say about COVID19 that may be useful in stopping some of the most egregious nonsense being repeated. [Fat chance, says the little man on my shoulder].

What I am about to write, I have written about before, in various different guises. However, I think it is worth going back over some old ground again. Hopefully in a more effective manner.

In this blog what I want to do is to look at how we think about a few things, primarily in medicine, and medical science. To try and highlight how some repeated flaws in thought have influenced the reaction to COVID19.

I hope that by doing this, it may help to prevent some us travelling down the terribly well-worn ‘paths of pointlessness’ again. Or, at least, to get people to stop and question how they are thinking, before throwing themselves into the fray.

To begin.

What I saw happening with COVID19 is a pattern that repeats in medicine over and over again:

  • We have a serious illness – panic
  • Something must be done – grab the pitchforks, run about screaming
  • An influential person, or organisation, grabs the initiative – ‘‘experts’ move in.’
  • I/We know what to do, you must follow me/us – simple idea + soothing paternalism
  • Frightened people latch onto their ideas – two legs good, four legs bad
  • A path is chosen – along the side of a cliff
  • Momentum builds – the unstoppable charge of the light brigade
  • Those who object to the path taken are crushed – 1984

Fast forward a few decades… ‘Oh, it seems that the thing we always do as standard medical practice… Turns out it does more harm than good.’ See under: removal of toxic colon, the radical mastectomy, strict bed rest following a heart attack, cutting teeth, use of radium water, plombage, mercury for syphilis, pre-frontal lobotomy etc.

Of course, this pattern is not true of every medical intervention, not by any manner of means. Sometimes the influential person, or organisation, promotes the best course of action. This has been known to happen from time to time… believe it or not. In addition, medical practice does eventually auto-correct – and ends up doing the right thing. Almost always. We no longer remove toxic colons to cure female neurosis.

But what never, ever, seems to happen is OODA. Defined as ‘a practical concept designed to function as the foundation of rational thinking in confusing or chaotic situation’.

OODA stands for. ‘Observe, Orient, Decide Act.’

It was developed by the Air Force Colonel, John Boyd.

What John Boyd taught was simple. If you don’t know what is going on, do not make immediate decisions. First, work out what is happening, then orientate yourself – before you decide what to do. That way you avoid most, if not all, stupid mistakes. For many years, without knowing anything of OODA my own medical strategy has tended towards ‘don’t just do something, stand there.

Unfortunately, the medical profession has always battled ferociously against doing nothing. It has always greatly favoured the ‘You must do something, anything, I don’t care what it is so long as it sounds like a good idea. Chaaarge!’ Strategy.

This, the ‘do something strategy’, has always proven far more seductive, and almost always wins. It is easier to attract followers to do something, than to than to do nothing. Why not whack a hole in the skull and split the brain apart to cure various mental diseases? Why not… indeed. Ah yes, the good old pre-frontal lobotomy.

A.N. Other doctor: ‘If you do nothing people will surely die. You cannot just stand there doing nothing.

Me:                             ‘But what if those things we do end up causing more damage, or killing more people?’

Many years ago, my father said to me. ‘You will always be blamed for failures of omission, rath than commission.’ At the time I was young,  I knew everything, and thought he was talking rubbish. In truth I didn’t really understand his point. Now that I know that… I know nothing, I fully understand how profound his comment was. I wish I had listened to him more.

Yes, doing something will always be looked on in a positive light. Effort has been made, decisions have been taken, activity carried out. In medicine this is reflected in a comment that I have had directed at me, from time to time. ‘At least you tried, doctor.’ Well, seeing as they are now dead, my efforts achieved very little. But thanks anyway.

In addition, if you do nothing, you can be accused of laziness, of being uncaring. You just stood there and watched them suffer, even die. You cruel swine. I see this overwhelming urge to do something, anything, in the person who cannot swim, jumping into a river to try and save their dog from drowning.

What exactly did they think they were going to achieve? Oh well, at least they tried, you may say. No… they were stupid. They drowned along with their dog. But who can stand on the riverbank watching their dog die?

Well, me, actually.

This also moves into the area of survival guilt. How am I still alive when others have died? Better to die trying than to have done nothing? It all further wraps round into it the almost irresistible urge to be seen to be doing something. I think it is hard-wired into our psyche. We must fight to protect those in our tribe and be seen to be doing it. Chop, chop, busy, busy, work, work, bang, bang 1.  

I am, however, reminded of the philosophy behind recruitment to the German army in the good old days – as recounted to me. Men were divided in to four categories:

  • Intelligent and lazy
  • Intelligent and hardworking
  • Stupid and lazy
  • Stupid and hardworking

At which point

  • Intelligent and lazy men were taken for officer training
  • Intelligent and hardworking men were turned into NCOs (non-commissioned officers)
  • Stupid and lazy men became privates – squaddies, to use the UK vernacular
  • Those who were both stupid, and hardworking, were taken out and shot, before they could do too much damage

Doing things, doing things, doing things. We place great value on it. Too much.

As Kurt Vonnegut Jnr noted in Cat’s Cradle:

“We do, doodley do, doodley do, doodely do,
What we must, muddily must, muddily must, muddily must;
Muddily do, muddily do, muddily do, muddily do,
Until we bust, bodily bust, bodily bust, bodily bust.”

Of course, if there are things to be done, they should be done. But that does not mean we should rush around doing stuff, just because it seems better than doing nothing. Here is what Vinay Prasad has to say in his blog ‘Will science do better post COVID19?’

‘When faced with a pandemic, we re-treated to all the old delusions. Bioplausibilty was sacrosanct— that’s why #maskswork! We can’t run RCTs— these are parachutes. Doing something is always better than doing nothing! More is better than less! Keep boosting, young man!! Newer is better than older. Disease bad; treatments good. Bad people (John Ioannidis) are always wrong (never mind, that a year ago we all thought he was brilliant).’ 2

The additional problem with doing things is that, once you have started doing them, it becomes damned difficult to stop again. After you have decided to blow four hundred billion pounds on lockdown, or thereabouts, then you are pretty much stuck with it. Or else, you are going to look pretty stupid. ‘Sorry, ahem, I seem to have wasted a teensy bit of money. Sorry, my mistake.

If everyone is ordered to wear a mask, on pain of death, you are stuck with that too. Back pedalling from instant decisions is very, very, difficult. For the scientists and politicians involved you cannot be seen to have been wrong. Reputations must be protected.

At which point, vast amounts of time and effort are expended in trying to batter down anyone who dares to suggest that we rushed into doing things that were completely pointless, even damaging. Science then becomes twisted and bent to justify the errors made. Those in power must retain power. The narrative must be supported:

  • COVID19 is really, really deadly
  • Lockdowns really, really, work
  • Masks really, really, work

If you question these narratives, people will demand an answer to this rhetorical question. Do you want people to die! (That’s always an effective weapon). The correct answer to this question by the way, is usually no – although I am willing to make exceptions.

The other terrible flaw in thinking here, especially in medicine, was also mentioned by Vinay Prasad. It is Bioplausibility. Often closely associated with fast thinking a.k.a. jumping to conclusions, because they just seem right.

Masks, indeed, must surely work. Because? Because they prevent the virus from spreading. In fact, masks represent an almost perfect example of bioplausibility a.k.a. sheer common sense. No-one can argue against using them. If you do, your arguments must be pure sophistry, or simply nonsense. ’You do not understand science.’ That’s a good one, I get that a lot.

‘I think you will find it is not I that fails to understand science.’ I think to myself. But I don’t say it, because it makes you sound like a prat.

Let me remind you of a time when, after a heart attack you had to rest in bed doing nothing for six weeks. The heart has been damaged and must be given a chance to rest. Yes, perfect Bioplausibility, believed by virtually everyone. To question it was to be cast into the outer darkness.

It is now known that the worst thing you can possibly do is to enforce strict bed rest post heart attack. This advice, in place from 1912 to about 1960(ish), killed tens of millions. Maybe hundreds of millions.

As for masks – the sort of masks worn by almost everyone.

‘The use of cloth facemasks in community settings has become an accepted public policy response to decrease disease transmission during the COVID-19 pandemic. Yet evidence of facemask efficacy is based primarily on observational studies that are subject to confounding and on mechanistic studies that rely on surrogate endpoints (such as droplet dispersion) as proxies for disease transmission. The available clinical evidence of facemask efficacy is of low quality and the best available clinical evidence has mostly failed to show efficacy, with fourteen of sixteen identified randomized controlled trials comparing face masks to no mask controls failing to find statistically significant benefit in the intent‐​to‐​treat populations. Of sixteen quantitative meta‐​analyses, eight were equivocal or critical as to whether evidence supports a public recommendation of masks, and the remaining eight supported a public mask intervention on limited evidence primarily on the basis of the precautionary principle. Although weak evidence should not preclude precautionary actions in the face of unprecedented events such as the COVID-19 pandemic, ethical principles require that the strength of the evidence and best estimates of amount of benefit be truthfully communicated to the public.3

How can masks possibly fail to work?

Well, unfortunately, our brains work one way, and the world often works in quite another way. As does, therefore, science. For centuries people thought that heavier than air flight would only be possible if you flapped things that looked very like wings. Why, because birds and bats were the only flying things people had ever seen flying [apart from lemmings] and they mostly flapped about like mad – using wings.

Except that, if you looked closely, they didn’t – not really. If you thought flapping was the key to flight, you were not really looking. An albatross can stay aloft for hours, gliding above the waves, using the wind and updrafts, and barely moving its wings at all.

Yet, and yet, no-one was able to see this. When I say ‘see’ this I mean – look beyond the obvious, in your face, flappy stuff. Observe properly, deeply, to really understand what you are looking at – in this case aerodynamics. Eventually, of course, some people did. Et voila, the Wright Brothers.

With masks… Yes, it is both true, and self-evident, that a mask stops droplets being catapulted across a room after a cough or sneeze, or suchlike. So, they must stop spread…mustn’t they? I mean, you can even see it working in slow motion videos. A man coughs in London, virus ends up in New York – or something. Ah, the dreaded Bioplausibility… that can also be visualised. Double bubble.

But a mask can also turn droplets into an aerosol by breaking the droplet down into far smaller particles. Particles will float in the air for longer, and thus be inhaled for longer. Possibly, probably4. You didn’t think of that, did you?

A mask can also become damp and keep viral particles viable for longer. Once discarded – as many masks are – they represent receptacles for viruses and can spread disease when picked up. What happens when masks are used and used, and re-used? As they often are. Superspreading here we come. Blowing viral particles out of a wet mask.

As a wise man also said. Using cloth masks to prevent viral spread it like trying to pick up sand with a tennis racket. Virus particle size ‘x’. Holes in mask size 1000x.

A mask can also mean that people stand closer to each other than they otherwise would. A mask may, simply, never had had a chance to work at all. After all, we breathe in and breathe out the same amount of air whilst wearing a mask than not.

If there is virus in floating in the air, we are still going to breathe it in, and out. Masks do not stop us breathing, and the air has to come from somewhere. Unless masks act as a type of black hole, trapping, then transporting viral particles from here into another universe… I’m not putting much money on that hypothesis.

Some months ago, I wrote about the last people to be infected with smallpox. In one hospital, in Germany, a patient with smallpox was being treated on the ground floor. The patient in the room above, and then the room above that, become infected. Which means that viral particles must have got out the window, drifted upwards and infected those above.

Which just gives you some idea of how few viral particles were needed to spread a disease that was, up to that time, not even believed to spread through the air. No droplets required.

Early on, with COVID19 it was noted that ferrets could be infected with the virus. So, researchers put one ferret in a cage, with another ferret above with a solid barrier between them. The one below was infected with COVD19.

The only route for COVID19 to travel from one ferret to the other was through a tube that bent through ninety degrees, bent again to go upwards through the barrier, then across, and back round through ninety degrees

In essence, this tube was specifically designed to ensure that droplet spread was impossible. As droplets cannot go round corners, travel upwards, turn another ninety degrees… and suchlike.

Despite this, all of the uninfected ferrets became, very rapidly, infected. Conclusion – COVID19 can travel and infect through aerosol spread. Secondary conclusion – masks cannot stop this. At least not the sort of masks that virtually everyone wears, and then re-uses.

Of course, there are masks that you can use to prevent the spread of viral particles. But they have to be airtight, they have to have filters. They are uncomfortable to wear for any length of time, and they need to be changed regularly. They also prevent a great deal of communication, as people hard of hearing will tell you. Oh yes, there are serious downsides to mask wearing.

I only focus on masks here to make the point that masks appear totally ‘Bioplausible’. If, that is, you don’t think about all the issues too deeply. Also, getting everyone to wear masks represents doing ‘something.’ Doing something, especially something visible, is always better than doing nothing.

Yes… doing something, anything, and Bioplausibility. Two bear traps in human thought. Traps that seem impossible to eradicate.

There is another, major trap, which is the urge to draw ourselves into tribes. Then attack and attempt destroy anyone who does not agree with us. Humiliate and silence. Turn the ‘other’ into someone with evil intent. I am not getting into this in any depth here. We have all seen too much of it. The terrible seductive pleasure of righteous anger. Which so easily flips into hatred.

As also mentioned by Vinay Prasad. Bad people (John Ioannidis) are always wrong (never mind, that a year ago we all thought he was brilliant).’

As we all know, it is not just Ioannidis who is attacked. Dare to breathe one word of caution about vaccines and you become ‘dirty anti-vaxxer scum. You deserve to lose your job. Ha!’

This is no way for humans to act towards each other. Crush debate, silence those who dare to think differently. Bring in the Spanish Inquisition a.k.a. fact checkers. All bought and paid for by those who have vested interests in obliterating the opposition, of course.

Question:     When is a fact checker not a fact checker?

Answer:        When they are called a fact checker. [Especially if they work for a company that used to begin with Face and ended in Book. Or Witterpedia]

Also Meta…as in, I meta  ‘n’ idiot – who think it’s okay to silence anyone they disagree with, and claim this is science. Spare me.

Anyway, what do we do next time? How do we do better? How do we think better? Well, I suppose that first of all you have to get those in power to accept that they made mistakes…. Ho hum.

Frankly, that ain’t going to happen. Therefore, we need new people in power. People who can understand that things are complicated. That the immediate Bioplausible and simplistic ‘answer’ is as likely to be wrong, as it is right. More likely in truth.

We really need people to think better:

‘We have a crisis in medicine when it comes to understanding and appraising science. We do not teach this explicitly in medical schools, and it gets short shrift to mechanistic science. Our overemphasis on molecular mechanisms fuels the cognitive distortion that a reductionistic view is superior to empiricism*’ 2

*empiricism is the view that all concepts originate in experience, that all concepts are about or applicable to things that can be experienced, or that all rationally acceptable beliefs or propositions are justifiable or knowable only through experience.

Were there any examples of doing things better from which we could learn? In Sweden they did things differently – at least from most of the rest of Europe. Anders Tegnell, the state epidemiologist (yes they have such a post) was the man who led the Swedish response. It was to bring in very few restrictions and make almost everything voluntary. Lockdown ‘lite’ if you like.

He was ruthlessly attacked from all directions, but remained superficially calm. Although I imagine he felt most terribly bruised and battered inside. TIME magazine ran a story about the Swedish response entitled ‘The Swedish COVID-19 Response Is a Disaster. It Shouldn’t Be a Model for the Rest of the World.’5

You don’t really need to read the article. The title makes it entirely clear what tone was adopted, and also what the conclusion was going to be. Sweden = death and mayhem, run for the hills. Frankly, I am amazed that the Swedish Government held firm in supporting him.

At one point even the Swedish King, Carl XVI Gustaf ‘Gustaf –  the eminent epidemiologist’ as I believe he is also known – had a pop at poor old Anders. But the Government did support Tegnell’s light touch strategy – mostly. They held their nerve.

What was Anders thinking, the mad mass murdering fool? As he calmly stated in the British Medical Journal, after COVID19 deaths in Sweden had settled into the lower half of European figures. Not as good as some, better than most:

there is still disagreement among scientists about which measures are effective against the spread of infection. “This is what we are still struggling to understand: some measures work in some places, but it is difficult to see patterns.”

“Countries that went through lockdowns are not doing that much better,”6

Yes, he is describing his OODA journey. Anders is still observing and attempting to orientate, but he cannot see what to do. He still believes that the evidence for severe lockdowns, and mask wearing, simply does not exist. To put it another way, he cannot yet decide what should be done. So, he isn’t doing it.

Good man. We need far more like Anders Tegnell, and less of those like the members of SAGE in the UK. Screaming blue bloody murder with threats of hundreds of thousands dying if WE DO NOT ACT NOW! The sky is falling, the sky is falling. OMCIRON will kill us all… all I tell ee’. Beware the black spot Cap’n.

We also need more people to be sceptical. To look at the science and the evidence. We need, quite frankly, to learn to think… and grow up. Also, importantly, learn the incredibly difficult trick of doing nothing at all.

As they used to say in a UK advert. ‘Nothing acts faster than Anadin (a painkiller)’

Solution… take nothing

Nothing acts faster than a damn good lockdown

Solution…do nothing

Or, to quote the famous physician William Osler. ‘One of the first duties of the physician is to educate the masses not to take medicine.’ I shall now leave you with two things to consider. The first is an open letter, written by Professor Ehud Qimron, head of the Department of Microbiology and Immunology at Tel Aviv University and one of the leading Israeli immunologists:

Ministry of Health, it’s time to admit failure

In the end, the truth will always be revealed, and the truth about the coronavirus policy is beginning to be revealed. When the destructive concepts collapse one by one, there is nothing left but to tell the experts who led the management of the pandemic – we told you so.

Two years late, you finally realize that a respiratory virus cannot be defeated and that any such attempt is doomed to fail. You do not admit it, because you have admitted almost no mistake in the last two years, but in retrospect it is clear that you have failed miserably in almost all of your actions, and even the media is already having a hard time covering your shame.

You refused to admit that the infection comes in waves that fade by themselves, despite years of observations and scientific knowledge. You insisted on attributing every decline of a wave solely to your actions, and so through false propaganda “you overcame the plague.” And again, you defeated it, and again and again and again.

You refused to admit that mass testing is ineffective, despite your own contingency plans explicitly stating so (“Pandemic Influenza Health System Preparedness Plan, 2007”, p. 26).

You refused to admit that recovery is more protective than a vaccine, despite previous knowledge and observations showing that non-recovered vaccinated people are more likely to be infected than recovered people. You refused to admit that the vaccinated are contagious despite the observations. Based on this, you hoped to achieve herd immunity by vaccination — and you failed in that as well.

You insisted on ignoring the fact that the disease is dozens of times more dangerous for risk groups and older adults, than for young people who are not in risk groups, despite the knowledge that came from China as early as 2020.

You refused to adopt the “Barrington Declaration”, signed by more than 60,000 scientists and medical professionals, or other common-sense programs. You chose to ridicule, slander, distort and discredit them. Instead of the right programs and people, you have chosen professionals who lack relevant training for pandemic management (physicists as chief government advisers, veterinarians, security officers, media personnel, and so on).

You have not set up an effective system for reporting side effects from the vaccines, and reports on side effects have even been deleted from your Facebook page. Doctors avoid linking side effects to the vaccine, lest you persecute them as you did with some of their colleagues. You have ignored many reports of changes in menstrual intensity and menstrual cycle times. You hid data that allows for objective and proper research (for example, you removed the data on passengers at Ben Gurion Airport). Instead, you chose to publish non-objective articles together with senior Pfizer executives on the effectiveness and safety of vaccines.

Irreversible damage to trust

However, from the heights of your hubris, you have also ignored the fact that in the end the truth will be revealed. And it begins to be revealed. The truth is that you have brought the public’s trust in you to an unprecedented low, and you have eroded your status as a source of authority. The truth is that you have burned hundreds of billions of shekels to no avail – for publishing intimidation, for ineffective tests, for destructive lockdowns and for disrupting the routine of life in the last two years.

You have destroyed the education of our children and their future. You made children feel guilty, scared, smoke, drink, get addicted, drop out, and quarrel, as school principals around the country attest. You have harmed livelihoods, the economy, human rights, mental health and physical health.

You slandered colleagues who did not surrender to you, you turned the people against each other, divided society and polarized the discourse. You branded, without any scientific basis, people who chose not to get vaccinated as enemies of the public and as spreaders of disease. You promote, in an unprecedented way, a draconian policy of discrimination, denial of rights and selection of people, including children, for their medical choice. A selection that lacks any epidemiological justification.

When you compare the destructive policies you are pursuing with the sane policies of some other countries — you can clearly see that the destruction you have caused has only added victims beyond the vulnerable to the virus. The economy you ruined, the unemployed you caused, and the children whose education you destroyed — they are the surplus victims as a result of your own actions only.

There is currently no medical emergency, but you have been cultivating such a condition for two years now because of lust for power, budgets and control. The only emergency now is that you still set policies and hold huge budgets for propaganda and psychological engineering instead of directing them to strengthen the health care system.

This emergency must stop!

Professor Udi Qimron, Faculty of Medicine, Tel Aviv University7

I suppose I should say that the opinions of Professor Udi Qimron are not necessarily those of the senior management of this blog. I, in exactly the same way as Google and Facebook (Sorry, Alphabet and Meta. ‘As I was going to St Ives I meta man with seven wives’… how many idiots were going to St Ives), and suchlike, am merely the repository for information, and articles. A warehouse if you like. I have no editorial control over content, so you cannot sue me for anything written.

Unfortunately, I am not rich enough to employ Fact Checkers and unleash them upon anyone who disagrees with me. Yet. You have been warned.

The second thing, that I shall leave you with, is the fact that doing nothing can be very rewarding, and sometimes pretty hard work. As outlined by this article in The International Journal of Doing Very little:

‘We’re busy doin’ nothin’
Workin’ the whole day through
Tryin’ to find lots of things not to do
We’re busy goin’ nowhere
Isn’t it just a crime
We’d like to be unhappy, but
We never do have the time,’

‘I have to watch the river
To see that it doesn’t stop
And stick around the rosebuds
So they’ll know when to pop
And keep the crickets cheerful
They’re really a solemn bunch
Hustle, bustle
And only an hour for lunch.’


‘We’re busy doin’ nothin’
Workin’ the whole day through
Tryin’ to find lots of things not to do
We’re busy goin’ nowhere
Isn’t it just a crime
We’d like to be unhappy, but
We never do have the time.’

‘I have to wake the Sun up
He’s liable to sleep all day
And then inspect the rainbows
So they’ll be bright and gay
I must rehearse the songbirds
To see that they sing in key
Hustle, bustle
And never a moment free.’

‘We’re busy doin’ nothin’
Workin’ the whole day through
Tryin’ to find lots of things not to do
We’re busy going nowhere
Isn’t it just a crime
We’d like to be unhappy, but
We never do have the time.’

‘I have to meet a turtle
I’m teachin’ him how to swim
Then I have to shine the dewdrops
You know they’re looking rather dim
I told my friend, the robin
I’d buy him a brand-new vest

Hustle, bustle
We never do have
We never do have
We never do, never do
Never do, never do, never do have the time
Never do have the time.’8

And if that don’t cheer you up, nothing will. And follow my motto. ‘Don’t just do something stand there….’ Whilst observing and orientating of course. Think first, act later.







7: It’s an open letter you can go and find it yourself


Vitamins once more – mainly B vitamins and homocysteine – with a special mention for magnesium

6th December 2021

Here I am on vitamins again. I don’t wish to give the impression that all I care about is vitamins. However, I have been thinking about them recently for various reasons.

The first thing to say is that I do find it slightly strange that we have substances which are absolutely essential for life, that we must eat, because our bodies cannot make them. It seems a design flaw. I want my money back.

Added to this absolute reliance on them, we do not get any hint that we are running out. If we become dehydrated, we feel thirsty, and we drink. If our energy supplies are running down, we feel hungry and we eat.

On the other hand, if our Vitamin B12 supplies are becoming perilously low – we might end up feeling bloody awful. In the final stages we could end up paralyzed, then dead, without knowing why. Vitamin B12 is essential for the health of neurones (amongst other things). But there is nothing that triggers our desire to forage around for foodstuffs rich in vitamin B12. Supposing we knew what they were anyway.

I presume this means that whilst we were evolving from the primeval soup, there were plenty of vitamins (and minerals) about. We had no need to seek them out specifically, because they were always present in the things we ate. In ample supply? Always …? Of course, it is not just vitamins, there are minerals we need too.


Most people are probably blissfully unaware they need magnesium. If you don’t have enough, how would you know? The first recognisable symptom may be … suddenly dropping dead.

Israel gives us a stark warning of what happens when magnesium goes missing, with no-one noticing. For many years, most of the water supply in Israel has been provided by desalination. This process does not just get rid of salt (NaCl), it also removes the other salts, and minerals, at the same time.

In normal circumstances people get most of the magnesium they need from drinking water. Which means there was clearly a potential for a major deficiency problem building up in Israel. As most of their water contained nothing but pure H20.

Did anyone notice? As in, did anyone say, ‘golly I feel low in magnesium today, I must go and eat a substance high in magnesium…’ Nope. Did anyone die. Yup, they did. As outlined in the paper ‘Association between exposure to desalinated sea water and ischemic heart disease, diabetes mellitus and colorectal cancer; A population-based study in Israel.’ 1

 There were possibly as many as 4,000 deaths a year:

‘An estimated 4,000 Israelis die in an average year due to an inadequate amount of magnesium in their bodies – and the amount they get from natural potable water sources is increasingly declining due to the growing desalination of sea water. The figure is 10-fold the death toll from road accidents.’ 2

The population of Israel is just over nine million. The equivalent death rate in the UK would be 30,000 deaths a year, or 180,000 in the US. A silent killer indeed.

Anyway, yes, magnesium is critical stuff. It is extremely important for health, especially heart health. It is required for the correct functioning of the electrical system in your heart, and a low level increases the risk of atrial fibrillation. Here from the paper ‘Low serum magnesium and the development of atrial fibrillation in the community: the Framingham Heart Study.’

‘…individuals in the lowest quartile of serum magnesium were ~50% more likely to develop AF…compared with those in the upper quartiles.’ 3

Unfortunately, despite its importance, we don’t feel magnesium depleted. We do not crave magnesium rich foods – as if we would have any idea what they might be … I certainly don’t. The symptoms of severe deficiency are also non-specific. The first symptom might be that your heart decides to stop beating.

It’s not just Israel. Here from the paper: ‘Subclinical magnesium deficiency: a principal driver of cardiovascular disease and a public health crisis.’

‘Furthermore, because of chronic diseases, medications, decreases in food crop magnesium contents, and the availability of refined and processed foods, the vast majority of people in modern societies are at risk for magnesium deficiency.’ 4

Have you ever heard of any of this? Did you even know you had magnesium in your body – or that it did anything important? I suspect not. However, from the same paper:

‘…magnesium deficiency can lead to serious morbidity and mortality and has been implicated in multiple cardiovascular diseases such as hypertension, cardiomyopathy, cardiac arrhythmia, atherosclerosis, dyslipidaemia and diabetes. Unfortunately, the western diet is often low in magnesium due to the refining and processing of foods, and hypomagnesaemia is often underdiagnosed in hospitalised patients.’4

My advice, take a supplement. Especially if you live in an area with ‘soft’ water – which generally means not many minerals. Doubly especially if you have atrial fibrillation. It might just go away. How much do you need to take? Around 400mg a day is fine.

Back to vitamins – in this case, Vitamin(s) B

The reason for the detour is that I really wanted to make it clear that it is certainly not a given that we routinely get all the essential micro-nutrients we need from our diet.

Modern living, modern food production and farming, modern food processing … have all have a significant impact on what our food, and water, contains.

The lazy mainstream assumption that micronutrient deficiencies simply do not exist is, therefore, wrong. Try looking at Iodine deficiency in Switzerland sometime. In addition, I am extremely dubious that we truly know what the optimal intake of micronutrients may be. The research in this area is sketchy, to say the least.

This, eventually, takes us onto vitamins, more specifically, the B vitamins. There are many of them – eight, in fact.

  • B1 (thiamine)
  • B2 (riboflavin)
  • B3 (niacin)
  • B5 (pantothenic acid)
  • B6 (pyridoxine)
  • B7 (biotin)
  • B9 (folate ak.a. folic acid)
  • B12 (cobalamin)

The first question that springs to mind is the following. Where are numbers four, eight, ten and eleven? What happened to them? It’s a bit like clotting factors. We have VII, VIII, IX etc. But there is no factor one, or two. Who gets to name things in medicine anyway?

Moving on. My main interest in the B vitamins is that, if you are low in three of them, maybe four of them: three, six, nine and twelve, this can lead to an increased level of a protein in the blood called homocysteine. [I think B6 is more important than B3, but we shall let this go for now].

The reason why this is important is if you have a high level of homocysteine then this is strongly associated with an increased risk of cardiovascular disease. The mechanism of action appears to be that homocysteine is toxic to endothelial cells.

‘Elevated homocysteine (Hc) levels have a well-established and clear causal relationship to epithelial damage leading to coronary artery disease.’ 5

On the other hand, low levels of homocysteine are associated with a lower risk:

‘In observational studies, lower homocysteine levels are associated with lower rates of coronary heart disease and stroke. Folic acid and vitamins B6 and B12 lower homocysteine levels.’[i]

As you may have gathered from that short quote, if you have a high homocysteine level, and you take B vitamins, your homocysteine levels will fall. As confirmed in a study in the American Journal of Clinical Nutrition:

‘Elevated levels of homocysteine is an indication of inadequate folate and vitamin B-12 in the diet, writes lead author Giovanni Ravaglia, a researcher with University Hospital S. Orsola-Malpighi in Bologna, Italy. His paper appears in the March American Journal of Clinical Nutrition….High homocysteine levels can be treated very easily with vitamins, including folate, niacin, and B-12.’ 6

I think the connection between B vitamins, and homocysteine, were first noted by Kilmer McCully. He studied the area in detail at Harvard University. At least he did so for a while, before he was unceremoniously booted out for carrying out research that threatened to undermine the almighty cholesterol hypothesis. A sorry tale, as reported in the New York Times:

‘Thomas N. James, a cardiologist and president of the University of Texas Medical Branch who was also the president of the American Heart Association in 1979 and ’80, is even harsher [regarding the treatment of McCully]. ”It was worse than that you couldn’t get ideas funded that went in other directions than cholesterol,” he says. ”You were intentionally discouraged from pursuing alternative questions. I’ve never dealt with a subject in my life that elicited such an immediate hostile response.

It took two years for McCully to find a new research job. His children were reaching college age; he and his wife refinanced their house and borrowed from her parents. McCully says that his job search developed a pattern: he would hear of an opening, go for interviews and then the process would grind to a stop. Finally, he heard rumors of what he calls ”poison phone calls” from Harvard. ”It smelled to high heaven,” he says.’

McCully says that when he was interviewed on Canadian television after he left Harvard, he received a call from the public-affairs director of Mass. General. ”He told me to shut up,” McCully recalls. ”He said he didn’t want the names of Harvard and Mass. General associated with my theories.’ 7

And you wonder why researchers are wary of questioning the cholesterol hypothesis? Yes, crushing scientific debate has a long and inglorious history, starting long before COVID19 first appeared over the horizon. In the world of cholesterol, it has been going on for well over sixty years.

Homocysteine, B vitamins and dementia

Now, dear reader, having just focussed on B vitamins, homocysteine and cardiovascular disease, I am going to abruptly change tack. I shall now move away from heart disease to Alzheimer’s disease. The reason for this is straightforward.

As I began to research this area in more detail, it become increasingly clear that there was a worrying association between raised homocysteine, brain damage, and dementia. This certainly attracted my attention. Because I like my brain, and I want to keep it healthy for a long as possible.

I came across papers such as this: ‘Plasma Homocysteine as a Risk Factor for Dementia and Alzheimer’s Disease.

‘An increased plasma homocysteine level is a strong, independent risk factor for the development of dementia and Alzheimer’s disease.’ 8

There were many more such papers, but you probably get the general idea. Raised homocysteine … Bad.

At this point I already knew that the B vitamins can lower the homocysteine level – if it is high. In addition, B vitamins are well known to have vital functions in the central and peripheral nervous system.

Here, from the paper: ‘B Vitamins in the nervous system: Current knowledge of the biochemical modes of action and synergies of thiamine, pyridoxine, and cobalamin.’

Neurotropic B vitamins play crucial roles as coenzymes and beyond in the nervous system. Particularly vitamin B1 (thiamine), B6 (pyridoxine), and B12 (cobalamin) contribute essentially to the maintenance of a healthy nervous system. Their importance is highlighted by many neurological diseases related to deficiencies in one or more of these vitamins, but they can improve certain neurological conditions even without a (proven) deficiency.’ 9

So, not only do certain B vitamins lower homocysteine levels. A number of them play a critical role in the growth and support of nerve cells, and suchlike.

None of this is exactly news. It has been known for centuries that excess alcohol consumption – which blocks Vitamin B1 absorption from the gut – can cause a specific form of dementia called Korsakoff’s dementia. Because of this, people with alcohol problems are often prescribed high dose vitamin B1 (Thiamine).

Which means that it was never a stretch to suggest that giving people B vitamins might be an extremely good thing if you want to prevent, or delay, the progression of Alzheimer’s/brain shrinkage. Either through the benefits on lowering raised homocysteine, or via the critical functions of B vitamins on the structure and function of the brain.

That, anyway, was the underlying science. But does giving B vitamins actually work? Well researchers at Cambridge University certainly believed it was a splendid idea:

‘In an initial, randomized controlled study on elderly subjects with increased dementia risk, we showed that high-dose B-vitamin treatment (folic acid 0.8 mg, vitamin B6 20 mg, vitamin B12 0.5 mg) slowed shrinkage of the whole brain volume over 2 years.’ 10

In a follow-up study, this group of researchers then found that, in people with raised homocysteine levels, who already had signs of dementia, B-vitamins reduced brain destruction and slowed, even halted, the progression of Alzheimer’s. In their own words, from the paper ‘Preventing Alzheimer’s disease-related gray matter atrophy by B-vitamin treatment’:

‘….we showed that high-dose B-vitamin treatment (folic acid 0.8 mg, vitamin B6 20 mg, vitamin B12 0.5 mg) slowed shrinkage of the whole brain volume over 2 years. Here, we go further by demonstrating that B-vitamin treatment reduces, by as much as seven-fold, the cerebral atrophy in those gray matter (GM) regions specifically vulnerable to the AD (Alzheimer’s Disease) process, including the medial temporal lobe. In the placebo group, higher homocysteine levels at baseline are associated with faster GM atrophy, but this deleterious effect is largely prevented by B-vitamin treatment. We additionally show that the beneficial effect of B vitamins is confined to participants with high homocysteine.’ 11

Yes, it was all looking quite good. By the way, this study came out in 2013.

But then we need to factor in the knowledge that B vitamins are very cheap. Very cheap indeed. In addition, they cannot be patented. Which makes it extremely difficult for any pharmaceutical company to make money from them. You can, of course sell them for a small profit, but pharmaceutical companies need billions to feed the machine. They require unique, patentable, blockbuster drugs. Drugs my precious.

Had any drug shown such a significant effect on brain shrinkage, I am one hundred per cent certain that the finding would have been shouted from the rooftops. We would be looking at a massive blockbuster. Probably the biggest selling drug in the world – ever.

As it was, the research from Cambridge was passed over in virtual silence … I suspect you never heard anything about it. Then, with a certain inevitability, the findings were, effectively squashed.

How was this done?

It was done through the power of the meta-analysis. A meta-analysis is a fancy term describing an attempt to bring together all the relevant trials that have been done in a therapeutic area. In order to construct a ‘meta’ study, or meta-analysis.

They can be a very useful way to bring together all of the relevant research, where there have been a large number of different studies done. In an attempt to establish the definitive answer to a medical question. Does drug x, or intervention y, actually work. If so, what are the true benefits? Assuming that the trials have all showed subtle, or not so subtle, differences in their effects.

Meta-analyses are often treated as though they are the very pinnacle of medical research. Tablets of stone handed down by Gods. In realty, they need to be treated with a very large pinch of salt, and a healthy dose of scepticism.

This is because meta-analyses often ram together studies with very different populations, using different doses of drugs, or vitamins. Or completely different drugs or vitamins, for different lengths of time.

Just to add to the potential messiness, studies can be included that have completely unrelated outcomes. You end up comparing apples and bananas, in order to decide if pomegranates actually work. In computing it would be called garbage in, garbage out – GIGO.

Moving on, in 2014, the year after the Cambridge study, a whole number of different studies on B-vitamins were brought together in a ‘meta-analysis.’ I use the term meta-analysis very loosely here. It was called: ‘Effects of homocysteine lowering with B vitamins on cognitive aging: meta-analysis of 11 trials with cognitive data on 22,000 individuals.’ 12

Sounds good, so far. In fact, the total number of individuals they looked at was 20,431 – which is a lot nearer to twenty thousand than twenty-two thousand. But, hey ho, what’s sixteen hundred or so people between friends? Having said this deliberate figure inflation is an important indication of researchers trying to ‘big up’ their findings – in my book.

Here’s another thing. A number of the studies had absolutely nothing to do with cognitive function … at all. One of the studies included was HOPE-2. Here is the background to the study.

‘In observational studies, lower homocysteine levels are associated with lower rates of coronary heart disease and stroke. Folic acid and vitamins B6 and B12 lower homocysteine levels. We assessed whether supplementation reduced the risk of major cardiovascular events in patients with vascular disease.’ 13

Yes HOPE-2 was a study on cardiovascular disease. It has absolutely nothing to do with Alzheimer’s, or any other form of dementia. The title of HOPE-2 was ‘Homocysteine Lowering with Folic Acid and B Vitamins in Vascular Disease.’ Cognition, or brain function, was not measured. Yet, it was still included in a meta-analysis of ‘11 trials with cognitive data on 22,000 individuals.’ [20,431 individuals, actually].

Moving on, and this is perhaps more mission critical. In only just over seven thousand of the individuals studied did anyone measure cognitive function at the start of the trial and then again, at the end. Leaving aside such studies as HOPE-2 where it was not measured at all. Which, straight off, means that the vast bulk of this meta-analysis is utterly meaningless.

How can you possibly know what happened to anyone’s cognitive state, if you only measured it once? Did it improve, did it worsen – not the faintest. In two thirds of the individuals included in this meta-analysis we have no idea what happened to cognitive function – at all.

It doesn’t stop here. There were others who felt that this was not meta-analyses finest hour:

‘First and foremost, this meta-analysis excluded trials on mild cognitive impairment (MCI) and Alzheimer’s disease. As a possible consequence, most of the trials included in this meta-analysis either did not see any significant cognitive change (between the start and the end of the trial) in the placebo group or did not look at such change. 14

Yes, they specifically excluded people with existing cognitive impairment, or Alzheimer’s, which would be, by far, most important group to study. As they actually have the condition you are interested in.

Which leads on to the next obvious problem:

people included in these trials included in the meta-analysis were healthy and did not show any cognitive decline, whether they received B-vitamin treatment or not. So, B-vitamins could hardly prevent or slow down something not happening in the first place.’ 14

Just to make this point a little clearer, in the minority of studies, where they bothered to measure cognitive function at the start, and also at the end, they found that almost no individuals developed any degree of cognitive impairment – in either group. Not in the treatment group, or the placebo groups. As virtually nothing happened to anyone, nothing could have been proved one way or another.

Attempting to study the progress of dementia, in people who do not have dementia, and who may never get dementia, nor have any signs of cognitive decline … is like doing a blood pressure lowering study on people who do not have a raised blood pressure.

Then, on finding there was no difference in cardiovascular event in either arm of the trial, you proceed to claim that blood pressure lowering does not work. Because there was no difference between those given the drug, and those taking the placebo. Do you think this makes any sense? Answers on a postcard, that should be sent to the Willie Wonka chocolate factory. Care of A.N. Idiot.

Despite begin riddled with fatal flaws, this analysis was greeted as though it was the definitive study. B-vitamins have no effect on cognitive decline, end of. This is what the head of Alzheimer’s Research UK had to say:

‘Although one trial in 2010 showed that for people with high homocysteine, B vitamins had some beneficial effect on the rate of brain shrinkage, this comprehensive review of several trials shows that B vitamins have not been able to slow mental decline as we age, nor are they likely to prevent Alzheimer’s. While the outcome of this new and far-reaching analysis is not what we hoped for, it does underline the need for larger studies to improve certainty around the effects of any treatment.

New and far-reaching analysis. Comprehensive review … ho hum. If I were given the job of marking this meta-analysis, I would hand it back in a rather grumpy fashion. ‘I asked you to look at the benefit of lowering homocysteine, using B-vitamins, in people with cognitive problems, or early-stage Alzheimer’s. Yet, you have not even bothered to look at these groups. In fact, you deliberately excluded them.

In addition, you included trials where the researchers failed to measure mental decline. Added to this, in most of these trials, no-one even had a high homocysteine level to start with, so they cannot – by definition – have had low levels of B-vitamins. So, how could vitamin B supplementation possible have been of any benefit … I am most disappointed. Please try again, and this time READ the brief.’

One of the trials lasted for four months, another for six months. What measurable different in cognitive function can anyone possibly expect to see in those timescales… This was not a flawed meta-analysis. It was simply gibberish.

There was a time when I would have questioned my own sanity in reading a meta-analysis such as this. Surely, I had got it wrong. Researchers would never put together such a steaming pile. If they did, then no-one would publish it. Nowadays I find myself far more in agreement with Drummond Rennie: deputy editor of the Journal of the American Medical Association:

‘There seems to be no study too fragmented, no hypothesis too trivial, no literature citation too biased or too egotistical, no design too warped, no methodology too bungled, no presentation of results too inaccurate, too obscure, and too contradictory, no analysis too self-serving, no argument too circular, no conclusions too trifling or too unjustified, and no grammar and syntax too offensive for a paper to end up in print.’ 15

A famous quote… in certain circles.

As it turns out, this analysis was done by exactly the same people who rule the research world of cholesterol lowering, known as the Cholesterol Treatment Triallists Collaboration (CTT) in Oxford. This paper came under the banner of the ‘B-vitamin treatment triallists collaboration’. Who knew such a group existed? One wonders exactly why they exist? Does the world really require such an organisation?

They sure as hell slammed the door shut on vitamin B/homocysteine research in cognitive function. Which was, some may say, possibly whey they were set up in the first place.

In my opinion, you can either believe the B-vitamin treatment triallists collaboration from Oxford with their meta-analysis. Which some would call complete and utter rubbish. Not me, of course. Personally, I have never seen a more detailed and error free research paper. I can hardly praise it highly enough.

Or, you can believe the Cambridge researchers, who demonstrated a seven-fold reduction in cerebral atrophy with B-vitamins – in those with raised homocysteine levels. The choice is entirely up to you.

















The enduring mystery of heart disease – The Clot Thickens

4th November 2021

And so, after only thirty short years of research, my book on heart disease is finally finished, and is published today. Up to now my books, and blogs, have mainly consisted of telling people what does not cause heart disease. Or to be slightly more accurate, cardiovascular disease.

Hint, it is not cholesterol, or LDL, or LDL/cholesterol, or the good cholesterol/bad cholesterol ratio – or whichever term is in favour today.

So, what does cause cardiovascular disease? Those few, those happy few, who have read this blog over the years may already know a great deal of what is in the book. For others this will be a new and, hopefully, fascinating foray into a completely different way of thinking.

The first point I want to make, then emphasize, then re-emphasize, is that there is no ‘the’ cause of cardiovascular disease. By which I mean that there is not, and never has been, any one single factor that can be considered to be ‘the’ cause. Instead, there are many. They can work by themselves or combine with others.

So you can say that, for example, diabetes is ‘a’ cause of cardiovascular disease. But you cannot say that it is ‘the’ cause. Yes ‘a’ cause but not ‘the’ cause. This is not purely semantics. Whilst the difference may seem subtle, it is critical. A table, or the table. A man, or the man. An answer, or the answer.

If there is no ‘the’ cause, what does this mean in practice? It means that many different things, or factors, or whatever term you use to describe them, can lead to exactly the same disease. You may then ask; can they all be described as causes? Boy, oh boy, it all gets very complicated. I have found that the language used here has become perhaps the greatest barrier to understanding.

Laying that admittedly complex issue to one side for the moment, and trying to keep things concrete, rather than abstract, the inescapable fact is that many, many, different factors can increase the risk of/cause cardiovascular disease. So, how can they all be fitted together into a unified theory?  

It has been tricky, very tricky.

Mainstream medicine has effectively stuck its fingers in its ears, yelled ‘la, la, la, I’m not listening,’ and run away from this entire issue. The current position is simply to state that cardiovascular disease is multifactorial. No need to think beyond that. Just find the important risk factors, then deal with each one separately. This works up to a point. Stop smoking, keep the blood pressure down, control diabetes and the risks will fall. I can’t argue with any of these actions, but they only get you so far.

In the end, you cannot just bring a whole bunch of wildly different factors together, declare that cardiovascular disease is ‘multifactorial’, and everything is now, officially, sorted. No need to look further. Move on, nothing to see here.

Many years ago, the French mathematician and science philosopher Henri Poincaré stated the following, which I find describes the situation almost perfectly. ‘Science is built of facts, as a house is with stone. But a collection of facts is no more a science than a heap of stones is a house.’

In the same way, calling cardiovascular disease “multifactorial” is just a clever sounding way of describing a pile of stones. There is no structure, no understanding, no hypothesis.

Below, for example, is a list of factors that are closely associated with an increased risk of cardiovascular disease. It comes from the latest UK cardiovascular risk factor calculator, called Qrisk3, which you can see here

You input your personal data e.g., age, sex, diabetes, blood pressure and suchlike, it then purports to calculate your risk of a cardiovascular event in the next ten years. In truth, not that accurately.

I deconstructed the Qrisk3 factors and put them into a list:

  • Age
  • Sex
  • Smoking
  • Diabetes
  • Total cholesterol/HDL ratio
  • Raised blood pressure.
  • Variation in two blood pressure readings
  • BMI
  • Chronic kidney disease
  • Rheumatoid arthritis
  • Systemic Lupus Erythematosus (SLE)
  • History of migraines
  • Severe mental illness
  • On atypical antipsychotic medication
  • Using steroid tablets
  • Atrial fibrillation
  • Diagnosis of erectile dysfunction
  • Angina, or heart attack in first degree relative under the age of 60
  • Ethnicity
  • Postcode

Fine…ish. It is true that all these things are associated with an increased risk of cardiovascular disease, in the UK, at present. However, to create a coherent hypothesis, you have to explain how they fit together. Where’s the house?

For example, you need to link a ‘history of migraines’ together with smoking. Then explain how they both lead to exactly the same disease. Or diabetes and severe mental illness. Or ethnicity and chronic kidney disease. Someone, anyone. Good luck.

As a quick aside, you may notice that the low-density lipoprotein level plays no part in this list of ‘most important’ risk factors in Qrisk3. None. Instead, we have the total cholesterol/HDL ratio – which is a very different thing indeed. It is only very indirectly related to the low-density lipoprotein level, if at all.

Moving on, the more I studied cardiovascular disease, the more I became aware of an inescapable fact. Which was that, in order to claim that I understood it, I had to establish how such very disparate factors can all lead to exactly the same disease.

This, in turn, meant giving up on the causal model. Because all that the causal model had produced was an ever-growing pile of ‘stones.’ Beneath which, the structure of an underlying house was becoming increasingly difficult to discern.

The process model

What I had to do, as pointed out to me by the late, great, Paul Rosch, was to turn my attention to the disease process. As in, what is actually going on? What is cardiovascular disease? What are we looking at?

What became very clear to me, very early on, is that what we cannot be looking at LDL molecules leaking through artery walls – or to be more exact, the endothelial cells that line all artery walls – then gradually building up into cholesterol plaques/thickenings.

This blog is not long enough to describe in any great detail why this ‘LDL leaking through’ process makes no sense. There is a great deal of information to be covered. Most of which is described, in some detail, in the book.

However, just to give you a couple of thoughts to consider. All blood vessels are lined by cells called endothelial cells. These cells, and indeed all cells in the body, have enormously complex mechanisms in place to regulate what gets into them, and what can then escape from them.

This regulation can control the movement of the largest molecule, down to the very smallest. Including tight control of the entrance, and exit, of single atoms e.g., sodium, or potassium, or calcium (in truth, in the body, these atoms exist as ions – which is just the name for a charged atom).

In short, nothing can gain entry to a cell unless the cell grants entry. Nothing [Unless you are a virus e.g., COVID19, whereby you hijack a receptor to sneak in – the cunning little devils]. For anything to gain entry, the cell must open a channel of some sort i.e., an ion channel. Or it has to manufacture a receptor. The receptor will then lock onto the substance floating in the bloodstream and drag it through the cell membrane and into the cell.

Just to pluck an example from the air. In order to get low-density lipoprotein into a cell, the cell must first synthesize a low-density lipoprotein (LDL) receptor. It then transports the receptor to the cell membrane. Once in place, it locks on to a passing LDL molecule, and then drags the entire LDL/receptor complex back inside – before breaking it down. Without this machinery getting to work, there is no way to get LDL into a cell. None.

Just to repeat this, from a slightly different direction. Cells can control the movement of single ions/atoms through their cell membranes. An LDL molecule is massive in comparison to an ion. Think rowing boat vs. super tanker.

Yet, if we are to accept the LDL hypothesis, we are supposed to believe that cell membranes simply step aside, or part like the red sea, to wave through a super-tanker sized molecule.

It all gets more unlikely. The cell must then allow the LDL molecule to propel itself from one cell membrane to the other. A very clever trick for an inanimate molecule, with no means of propulsion. Looked at from a human scale, if I were an LDL molecule, a cell would be about half a mile across.

Even if the LDL managed this, once it reached the other side of the cell, the LDL would need to pop back out of the cell and into the artery wall behind – using an inside-out LDL receptor perhaps?

Some people have therefore suggested the LDL molecules simply sneak between endothelial cells. But this, too, is impossible. Endothelial cells are tightly bound to each other, with a whole series of protein bridges a.k.a. ‘tight junctions.’ These too, can prevent the passage of single ions. Which means that nothing can get from the blood and into the artery wall though a side entrance either:

‘Tight junctions prevent the passage of molecules and ions through the space between plasma membranes of adjacent cells, so materials must actually enter the cells, in order to pass through the tissue.’1

If this were not the case, if the ‘endothelium’ did not represent a perfect barrier, we would all die immediately. To quote from a paper in the journal ‘Tissue Barriers’ yes indeed, there is such a journal:

Physiological barriers provide the framework for a boundary between circulating blood and interstitial fluid, a pre-requisite for mammalian life.’2

So, yes, there is simply no way for LDL to sneak between cells either.

Just to give you one example of what happens if you loosen the tight junctions between cells, we can look at the Ebola virus. This virus opens up the tight junctions between endothelial cells. At which point the endothelial barrier function is critically compromised, and blood can now escape into the tissues, and organs.

This leakage is the reason why Ebola is also known as a form of haemorrhagic fever. Blood appears in the cornea, so your eyes become bloodshot. You cough up the blood that that has escaped into your lungs. Your tongue falls off. Your urine is filled with blood from your kidneys, your bowel motions turn black, and then…. Bang, dead, from massive fluid loss and vascular collapse.

Ebola demonstrates very clearly the critical importance of tight junctions between cells. Open them up… and you die. How did you think Ebola actually kills you? I imagine that you, like me, before I started looking at this area in detail, probably never really thought much about it. You just vowed never to catch it:

Ebola patients experience a breakdown in endothelial barrier integrity that leads to massive fluid losses and vascular collapse.’3 

That would be where the ‘pre-requisite for mammalian life’ comes in.

Anyway, forgetting about that for the moment. Let me take you back to think about an alternative process model. To ask, so what is the disease process that allows you link smoking to, say, systemic lupus erythematosus? Because both things are most certainly causal. ‘A’ cause, rather than ‘the’ cause, of course.

And what of the many, many, other factors, not mentioned in Qrisk3? This is a very long list indeed. For example: cocaine use, antiphospholipid syndrome, Avastin, use of steroids, periodontitis, Sjogren’s syndrome, sickle cell disease, high fibrinogen levels. I could go on… for a few pages.

The harder you look, the more stones you unearth. In the end I had this massive pile of stones which became my two-thousand-piece jigsaw puzzle – just to change metaphors abruptly. A puzzle that didn’t even have a box to go with it, so I didn’t know what the picture was supposed to look like once I fitted all the pieces together. Was it a cow, or a lake, or a mountain scene?

At this point, you may get some insight as to why I called the book ‘the enduring mystery of heart disease’. Admit defeat …me? Well, usually, I am quite good at chucking in the towel. If at first you don’t succeed, give up, why make an idiot of yourself. But for some reason I did not, could not.

This bloody thing kept nagging away. I would lie awake at night considering the morphology (structure) of plaques. I contemplated the blood clotting system in all of its massively complex detail. I read papers outlining the thirty-two different types of HDL (good cholesterol). I discussed plaques with cardiologists and pathologists. I stumbled across entirely new entire worlds of research that I didn’t know existed. There were few rabbit holes down which I did not disappear.

The answer, when it finally lodged in my brain, was surprisingly simple. Not only was it simple, but it has also been kicking around for very nearly one hundred and seventy years. In 1852 Karl von Rokitansky published his ‘encrustation hypothesis.’ Describing what he saw when he closely examined atherosclerotic plaques.

‘Rokitansky proposed that the disease is the result of an excessive intimal deposition of blood components (blood clots) including fibrin. He maintained that localized thickening, atheromatous changes and calcification of the arterial wall are due to the repeated deposition of blood elements and their subsequent metamorphosis and degeneration on the lining membrane of the vascular wall.

There you go, that’s it. Blood clots, blood clots… and more blood clots.

In fact, I am being slightly disingenuous here. I had been thinking about blood clots for many years, but in a rather uninformed and directionless way. Many moons ago, when I was a medical student at Aberdeen, I was briefly taught cardiology by Dr Elspeth Smith. In a small group tutorial, she mentioned to us fresh faced students that LDL cannot penetrate the endothelium. Bing!

This was almost an off the cuff remark. Almost… but the way she said it… I knew that there was something critical here. A secret never to be told. Or, it was like a good murder mystery, where a chance remark represents the most important clue. My antennae pricked up at that moment and have not stopped twitching since.

She also wrote this over forty years ago:

‘After many years of neglect, the role of thrombosis (blood clots) in myocardial infarction is being reassessed. It is increasingly clear that all aspects of the haemostatic [blood clotting] system are involved: not only in the acute occlusive event, but also in all stages of atherosclerotic plaque development from the initiation of atherogenesis to the expansion and growth of large plaques.’

Yes, she knew what causes cardiovascular disease. I now know, for sure, that she knew. She never knew that I knew she knew. I was daft and did not take the opportunity to discuss things with her. Too much ego, I suppose. I also went off in other daft directions for many years. Looking for ‘the’ cause: the lost chord, the Ark of the Covenant, the Holy Grail. Of course, I never found ‘the’ cause, because it does not exist. Oh, well.

It was only when I was directed to return to process, that I came to fully recognise her genius – and the genius of others. I only hope that this book will help to raise her status up to where it belongs. Along with Rokitansky, Duguid, Ross and all those who pursued the blood clotting route over the decades, nay, centuries now.

Yes, I know this probably sounds very simple, and possibly completely wrong. There is no way you are going to believe straightaway that atherosclerotic plaques are just blood clots, ‘in various stages of metamorphosis and degeneration’. How can this possibly be true?

The reason why it can be true, is because it fits all the known facts about cardiovascular disease, and atherosclerotic plaques, and heart attacks, and strokes, and suchlike. Yes, everything.

For example. It is widely known, and accepted, that the single most common ‘final’ event in cardiovascular disease is the formation of a large blood clot – almost inevitably on top of an existing plaque. This can fully block an artery, leading to downstream mayhem.

It is also widely accepted that thrombus formation, on top of an already existing plaque, can make plaques suddenly jump in size. Here, for example, is a passage from a paper in the journal Atherosclerosis. This is about as mainstream a publication as you can get in cardiovascular disease research. The paper was called: ‘The role of plaque rupture and thrombosis in coronary artery disease.

In addition, plaque rupture and subsequent healing is recognized to be a major cause of further rapid plaque progression.’ 4

I could find a million quotes confirming this mechanism, without even breaking sweat.

In short, it is not remotely controversial to say that blood clots represent the final event, the thing that kills you. Nor is it controversial to say that plaques grow through the deposition of a new clot on top of an existing plaque. I would get very little argument from any cardiologist about this sequence of events. I know, I have had many such discussions.

But what is not accepted, will simply not be accepted, is that the arrival of a blood clot on the ‘healthy’ arterial wall is what initiates atherosclerotic plaque formation. Instead, it is almost universally accepted that it is LDL that does this, and LDL alone. Therefore, current conventional wisdom is that we have a three-step process:

  • The plaque starts – due to LDL leaking through the artery wall
  • The plaque grows – due to deposition of new blood clots on top of the existing plaque (which has become a point of clotting vulnerability)
  • A ‘final’ obstructive blood clot forms on the already grown plaque, causing a heart attack, or stroke – due to a blood clot

In one way, all I have done in this book is to make it clear that, yes, we do have a three-stage process. However, low-density lipoprotein plays no part in it. It is entirely driven by blood clots, from start to finish. Which means that the first step is not:

  • The plaque starts – due to LDL leaking through the artery wall

The first step is that:

  • The plaque starts, due to endothelial damage, and resultant clot formation (creating the ‘focus’ for further plaque growth)

Then, everything else follows, as described earlier by Elspeth Smith:

It is increasingly clear that all aspects of the haemostatic [blood clotting] system are involved: not only in the acute occlusive event, but also in all stages of atherosclerotic plaque development from the initiation of atherogenesis to the expansion and growth of large plaques.

Yes indeed, the Clot Thickens.

In truth, this is not a major leap in thinking? All I actually needed to do was remove low density lipoprotein from the picture. Once I did that, the jigsaw actually fitted together. Leave it in, and you cannot create a coherent hypothesis. Everything is distorted, nothing works, the picture is a mess. Take it out and it all makes sense.

I hope this brief foray into the process of cardiovascular disease has left you suitably enthused to buy the book, read it, and find out in much greater detail what is really going on here. And also, what you can do to prevent heart disease. It has been my life’s work. I hope I am right. I hope you can learn from it and enjoy it.



3: 4:

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Let’s talk about C – just you and me

22nd October 2021

Studying cardiovascular disease for over thirty years can take you to some very interesting and seemingly strange places. Places where I never expected to find myself. Connections appear where you least thought they would be, and entirely new worlds of research open up. Very often, into places where mainstream medical thinking simply does not go.

The fascinating thing is how so many things end up looping back round, in ways that you would never have considered. One of those places is within the world of vitamins. Vital…amines, and the connections to cardiovascular disease.

Unfortunately, mainstream medicine has firmly locked vitamins into a tightly constrained box. Yes, it is accepted that vitamins are vital, because you die without them – that is where the ‘vital’, in vitamins, comes from after all.

However, it is universally believed that the exact requirements for all vitamins – known as the recommended daily allowance (RDA) – which were established decades ago. It is also universally believed that everyone gets sufficient vitamin intake from their diet, so there is absolutely no need for supplementation.

But how true are these comfortable assumptions? At one point I looked into Vitamin B12 deficiency. Even mainstream medicine agrees that this can, and does, occur and can lead to very serious medical problems. Irreversible nerve damage and paralysis, for example.

The normal range for Vitamin B12 in the UK varies from 190 to 950 picograms/ml (pg/ml).  [A picogram (pg) is one trillionth of a gram]. This at least is the normal range, in some laboratories… in some places the UK. In truth, it is almost impossible to find a consistent figure.

This ‘normal’ range also varies enormously from country to country. In Japan, for example, it is 500 – 1300 pg/ml. Thus, the lower range is nearly three times higher in Japan than the UK1. If you went to your GP in the UK with a level of four hundred and said you were Vitamin B12 deficient they would point you to the door. In Japan, they would treat you.

Another thing to note here is that the range is almost always ridiculously wide. It can vary by a factor of five! This alone suggests that people are pretty much guessing at what “is” normal. Despite this, most doctors remain perfectly content that a normal/healthy level has been well established and is based on robust science. There is no need to look again.

This is not the case, not even remotely. Here, for example, are the first three key recommendations on determining what constitutes Vitamin B12 ‘deficiency’ from the British Society for Haematology – with some of the highly technical text removed. They use the term cobalamin here, not Vitamin B12, although it is (basically) the same thing [Cobalamin (Vitamin B12) comes in several different formulations e.g., hydroxycobalamin, methylcobalamin, cyanocobalamin]

  • The clinical picture is the most important factor in assessing the significance of test results assessing cobalamin status because there is no ‘gold standard’ test to define deficiency
  • Serum cobalamin currently remains the first‐line test… Serum holotranscobalamin has the potential as a first‐line test, but an indeterminate ‘grey area’ may still exist.
  • Definitive cutoff points to define clinical and subclinical deficiency states are not possible, given the variety of methodologies used and technical issues, and local reference ranges should be established2

There you are, clear…. as mud. What the British Haematology Society informs us is that: there is no gold standard test for vitamin B12 deficiency, there are also ‘grey’ areas, and ‘definitive cut-off points to define deficiency states are not possible.’

As with almost all areas of medical research, the more you dig down, the more uncertain things become. The authors of the report are not even sure if you should be measuring cobalamin, or holotranscobalamin – whatever that may be. It sounds like something from Star Trek.

When it comes to vitamin D there is a similar lack of clarity. In the UK, recent guidelines on vitamin D suggested more people should take supplements… finally. However, the NHS advice on vitamin D then goes on to make this statement:

‘…although roughly one in five people has low vitamin D levels, this is not the same as a vitamin D deficiency. It is not accurate to say that millions of people are at risk of deficiency.’3

So, according to the NHS, a low level is not a deficiency. However, a low level cannot, by definition, be normal. For, if it were normal, you could not call it “low”! So, what is it? Here is where words really start tripping over each other. Low, deficient, normal…optimal, inadequate, sub-optimal? Trying to pin any clear definition down is, I can assure you, like trying to pick up mercury using your fingertips.

In the same article it is stated that a blood level of 20nmol/l is ‘sufficient’. Again, what does sufficient mean? Is it the same thing as normal, or is it optimal? Is this really the level we should be aiming for? The National Institutes of Health in the US provides completely different figures for vitamin D deficiency. Or, as they choose to call it – ‘inadequacy.’

‘Some people are potentially at risk of inadequacy at 30 to 50 nmol/L (12–20 ng/mL). Levels of 50 nmol/L (20 ng/mL) or more are sufficient for most people. In contrast, the Endocrine Society stated that, for clinical practice, a serum 25(OH)D concentration of more than 75 nmol/L (30 ng/mL) is necessary to maximize the effect of vitamin D on calcium, bone, and muscle metabolism.

The truth is that, wherever you look the figures are all over the place. Made more complicated by the fact that the US uses different units of measurement to everyone in the civilised world, by which I mean Europe… of course. When they say seventy-five, they really mean thirty. ‘You say nanograms per millimole, I say nanomoles per litre – let’s call the whole thing off.

So, should you be aiming for 20nmol/l? Or is it thirty or forty, or fifty? If in doubt aiming higher would be my advice, better safe than sorry. After all, it has been found that the majority of people with cancer have ‘low’, if not ‘deficient’ levels of Vitamin D.

‘More than three-fourths of people with a variety of cancers have low levels of vitamin D, and the lowest levels are associated with more advanced cancers, a new study suggests.’4

If having a low level of Vitamin D means you are more likely to get cancer, then I would certainly define this as deficient, not low, and I would certainly want to do something about it.

And it is not just cancer. There are studies linking low vitamin D to many other diseases, such as kidney disease and, more importantly for the sake of this article, diabetes, and cardiovascular disease. As highlighted in this paper: ‘Vitamin D deficiency increases risk of nephropathy and cardiovascular diseases in Type 2 diabetes mellitus patients.’

‘Vitamin D (VD) deficiency is associated with insulin function and secretion. It is linked with diabetes mellitus (DM) progression, and complications were also recorded…The evidence from this study suggest that patients with Type 2 diabetes with vitamin D deficiency are at higher risk for developing CVD and nephropathy [kidney damage].5

Additionally, a low Vitamin D level can be a factor that drives obesity and diabetes in the first place. Here, from the study: ‘Vitamin D deficiency is a risk factor for obesity and diabetes type 2 in women at late reproductive age.’

‘Our results showed that vitamin D insufficiency is highly prevalent in the population of healthy women. Low 25(OH)D [a form of vitamin D] levels correlated with high body fat, glucose levels and decreased insulin sensitivity. We conclude that vitamin D deficiency is a potential risk factor for obesity and development of insulin resistance leading to diabetes type 2. 6  

If you choose to look, the evidence for the potential harms of low… deficient… inadequate…insufficient… suboptimal Vitamin D stretch on, and on, and on. Cancer, diabetes, obesity, kidney failure, cardiovascular disease. In the era of COVID19, there are also significant benefits from vitamin D in boosting of the immune system and reducing the risk of infection.7

Cutting to the chase, most doctors are eager to dismiss the benefits of Vitamin D on, pretty much, anything. However, I think the evidence for benefits on overall, and cardiovascular health are overwhelming.

Of equal importance is the fact that vitamin D is incredibly safe to take. It is true that toxicity has been seen in a few people, very few. However, it took sixty thousand units a day for several months to reach this point.

‘Taking 60,000 international units (IU) a day of vitamin D for several months has been shown to cause toxicity.8

Frankly, taking that dose would be nuts, and would not be required by anyone, ever. Personally, I take nine thousand units a day from October to March. I am l looking to get my levels above 50nmol/l, and keeping them there, if possible.

And why on earth would you not?  Vitamin D is remarkably safe, and cheap. In the summer you don’t need to take any at all. You can get all you need by going out in the sun when it shines and, shock, horror, exposing your skin for an hour or so. Even more if you like.

Why do doctors dislike vitamins so much? It is complicated, but primarily driven by the pharmaceutical industry, who absolutely hate the idea of people buying ‘health’ products that they cannot make any money from. So, they make wild claims about vitamins damaging health, and suchlike. They are simply trying to take out the opposition, usual tactics. For example:

‘….a USA TODAY investigation finds that a wide array of dietary supplement companies caught with drug-spiked products are run by people with criminal backgrounds and regulatory run-ins. Consumers buying products from these firms are in some cases entrusting their health and safety to people with rap sheets for crimes involving barbiturates, crack cocaine, Ecstasy and other narcotics, as well as arrests for selling or possessing steroids and human growth hormone. Other supplement company executives have records of fraud, theft, assault, weapons offenses, money laundering or other offenses, the investigation shows.9

Blah de blah. I amuse myself by reading the title of the book by Peter Gøtzsche: ‘Deadly Medicines and Organised Crime. How big pharma has corrupted healthcare.’ As he says. ‘If you don’t think the system is out of control, 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…

Something reinforced by Richard Smith (previous long-time editor of the British Medical Journal) in the foreword to Gøtzsche’s book:

‘It is scary how many similarities there are between this industry (the pharmaceutical industry) and the mob. The mob makes obscene amounts of money, as does this industry. The side effects of organised crime are killings and death, and the side effects are the same in this industry. The mob bribes politicians and others, and so does the drug industry.’

Just in case you think Gøtzsche and Smith are over-reacting, here is what Harvard University states:

‘Few know that systematic reviews of hospital charts found that even properly prescribed drugs (aside from misprescribing, overdosing, or self-prescribing) cause about 1.9 million hospitalizations a year. Another 840,000 hospitalized patients are given drugs that cause serious adverse reactions for a total of 2.74 million serious adverse drug reactions. About 128,000 people die from drugs prescribed to them. This makes prescription drugs a major health risk, ranking 4th with stroke as a leading cause of death. The European Commission estimates that adverse reactions from prescription drugs cause 200,000 deaths; so together, about 328,000 patients in the U.S. and Europe die from prescription drugs each year. The FDA does not acknowledge these facts and instead gathers a small fraction of the cases.10

Ouch. And there are those who think I am highly critical of the pharmaceutical industry. I’m a pussy cat in comparison. How many deaths have there been from vitamins? Last time I looked; it was one, over a ten-year period. I think a large crate of vitamin D fell off a lorry and squashed someone… (joke).

Anyway, yes, as you may have noticed, I have not yet talked about C… Vitamin C. I have just been setting the scene. Rearranging the mental furniture. So, now to vitamin C. How much do you need? What good does it do?

I find it somewhat strange that almost all animals can synthesize their own Vitamin C, but we cannot. Along with a few great apes, a couple of fruit bats and guinea pigs. Animals synthesize it from glucose, in four steps.

Humans have retained the first three steps but lack the fourth. We lost this fourth step about forty million years ago. Perhaps because we learned to re-cycle vitamin C within our red blood cells, so we need far less of it. The ‘electron transfer hypothesis.’ If making Vitamin C uses up resources that we need for other things… why bother. Just eat it, there is plenty about11.

Anyway, for whatever the exact reason, we lost the ability to make vitamin C. So, we now have to eat it. Mostly from fruit and plants. Tricky if you are Inuit. However, animal meat does contain enough vitamin C to keep the Inuit going.

There is a hypothesis that the Inuit ensure that they eat the adrenal glands of various animals they kill, because this is where there is the highest concentration of vitamin C lies. I don’t think I have seen this proven. Anyway, how could the Inuit possibly have known where vitamin C was concentrated? A clever trick indeed. Do they have secret biochemical labs hidden within glaciers?

Moving on. What happens if you do not eat enough vitamin C? Well, a whole lot of different things. But the most serious problem is that vitamin C is required to create collagen. Think of collagen as being like the steel bars in concrete, providing support and strength for tissues around the body. Without collagen, things can start to break apart quite dramatically.

Blood vessels, for example, need a lot of collagen, as they have to withstand a lot of pressure, and squeezing and bending and suchlike. So, one of the first clinical signs of scurvy (Vitamin C deficiency) is often bleeding gums. Followed by bleeding everything else. Followed by bleeding to death. Not recommended.

What is both pertinent, and fascinating at this point in the vitamin C story, is that evolution came up with a plug to reduce the risk of bleeding to death in vitamin C deficiency. Until enough vitamin C could be found and consumed again, and collagen synthesis got back to normal.

This plug is called Lipoprotein(a). Or Lp(a).

If blood vessels start to crack, this action attracts a Lp(a) to the scene. It then flings itself at the cracks, to form a plug that is highly resistant to being broken apart. More so, than any other part of a blood clot. It achieves this resistance by using a very clever trick, which is that it blocks the activation of the enzyme specifically designed to break down blood clots.

At this point I need to explain a bit more about blood clots… So, off we go once more, on a detour.

The enzyme designed to break clots apart is plasmin, which does the job of slicing apart strands of fibrin. Fibrin is the very tough strand of protein that wraps around all blood clots, then binds them together, then tightens up the entire clot up and makes it very tough and difficult to ‘lyse’ i.e. slice apart.

Fibrin is constructed when smaller pieces of protein, called fibrinogen are linked up, end to end, to form the much longer fibrin strand. This is the final step of the monstrously complex ‘clotting cascade’. [You could not allow long strands of fibrin to float about freely in the blood. They would just end getting tangled around everything else and getting stuck in various vital places.]

So, whilst fibrin has a critical function in blood clot formation, if you cannot break it down – once the bleeding has stopped, and repair has started – then you cannot break apart the blood clot either – at least not easily. And if you cannot break apart blood clots, then they are going to hang around – almost forever. Which is not a good thing, as you can probably imagine.

Which is where the enzyme known as plasmin comes in. Once bleeding has stopped, plasmin is ‘activated’ to slice – or lyse – the clot apart, and then it is gone.

How do you activate plasmin? Well, this process starts with another protein called plasminogen – which is incorporated into all blood clots as they form. Plasminogen then sits there doing nothing much. However, you can convert plasminogen into plasmin using another enzyme called tissue plasminogen activator (TPa).

TPa + plasminogen → plasmin → fibrin sliced apart ‘lysed’

Yes, step after step… after step. Tissue plasminogen activator is now made commercially and is colloquially known as a ‘clotbuster’. It is often given to people having a stroke to ‘bust’ the clot apart. [Unless you are having a stroke due to a bleed, not a clot, at which point given TPa would not be a great idea].

So, and keep holding on here, because I am going to get back to Vitamin C in a bit… so, what if you could not break up clots? At least, not so easily. Well, whilst this is a good thing if your blood vessels are cracking due to a lack of collagen, as the blood clot ‘plugs’ will need to last for a long time. At least until Vitamin C intake goes up, and collagen can be made.

However, if you do not have scurvy, having blood clots that resist lysis is a bad thing, because these clots are more likely going to hang around for ages. They will be stuck to blood vessel walls for quite a long time. Which means that they can become the focus for atherosclerotic plaques. [At least this is what happen if you believe in the thrombogenic hypothesis – which I do].

Now, getting back to Lp(a). How does it stop clots being broken down? Well, the(a) in Lp(a) stands for apolipoprotein(a). This protein is almost identical to plasminogen – the protein that is incorporated into all blood clots as they form. However, apolipoprotein(a) cannot be converted to plasmin by tissue plasminogen activator. Instead, it acts as a tissue plasminogen activator inhibitor. It jams up the active site of TPa.

So, deep breath. If you have a lot of Lp(a) around, you are in danger of creating difficult to shift blood clots. As outlined in the paper ‘Lipoprotein(a) as a modifier of fibrin clot permeability and susceptibility to lysis.’

‘We here provide the first evidence that elevated plasma Lp(a) levels correlate with decreased fibrin clot permeation and impaired susceptibility to fibrinolysis both in apparently healthy subjects and patients with advanced coronary artery disease. The relationship between Lp(a) and clots …are associated with extremely unfavourable clot properties12.

Therefore, if you have a lot of Lp(a) in you blood, you will have blood clots with ‘extremely unfavourable clot properties.’ And so, you may end up dying of cardiovascular disease. Here is an article from the New York Times:

‘To millions of Americans, Bob Harper was the picture of health, a celebrity fitness trainer who whipped people into shape each week on the hit TV show “The Biggest Loser.”

But last February, Mr. Harper, 52, suffered a massive heart attack at a New York City gym and went into cardiac arrest. He was saved by a bystander who administered CPR and a team of paramedics who rushed him to a hospital, where he spent two days in a coma.

When he awoke, Mr. Harper was baffled, as were his doctors. His annual medical checkups had indicated he was in excellent health. How could this have happened to someone seemingly so healthy?

The culprit, it turned out, was a fatty particle in the blood called lipoprotein(a). While doctors routinely test for other lipoproteins like HDL and LDL cholesterol, few test for lipoprotein(a), also known as lp(a), high levels of which triple the risk of having a heart attack or stroke at an early age.

You may think, why have I never heard of Lp(a). Fear not, you are not alone, as most doctors have never heard of it either. The surprising fact is that, although you may think you have never heard of Lp(a) you have. Because it is actually….

Drum roll, great suspense…

It is…. Low Density Lipoprotein (LDL). Yes, it is ‘bad cholesterol’ itself. The evil substance of doom itself. What a remarkable coincidence…

You think I am pulling your leg. I am, but only slightly. In fact, to be fully accurate, Lp(a) is actually low-density lipoprotein (LDL), with an extra strand of protein attached to it. And that protein is apolipoprotein(a).

Yes, apolipoprotein(a), the very protein that pretends to be plasminogen. The protein that inhibits blood clots from being broken apart. This is all a bit like a Sherlock Holmes story. Ladies and Gentlemen, I give you…

‘The tragic case of mistaken identity.’

‘I put it to you sir, that when you looked at atherosclerotic plaques and saw LDL within them, you were actually looking at Lp(a) molecules, but you did not recognise them. Because you miserably failed to look for the apolipoprotein(a).’

Or, to switch metaphors in a heavy-handed manner to Cluedo.

‘It was Lp(a) wot done it, in the left anterior descending artery, with an apolipoprotein(a) molecule.’

Or, to put it more technical speak, from the paper ‘Quantification of apo[a] and apoB in human atherosclerotic lesions.’:

These results suggest that Lp[a] accumulates preferentially to LDL in plaques, and that plaque apo[a] is directly associated with plasma apo[a] levels and is in a form that is less easily removable than most of the apo B. This preferential accumulation of apo[a] as a tightly bound fraction in lesions, could be responsible for the independent association of Lp[a] with cardiovascular disease in humans13.’  

Oh, my goodness, it is all so very complicated, is it not? Well, it is both complicated, and fascinating. You start looking at Vitamin C, and you end up comparing the molecular structure of plasminogen and apolipoprotein(a). Then you find that Lp(a) is, to all intents and purposes, LDL.

Now, let me see. Where does vitamin C properly fit into this tale?

Well, if you don’t have enough vitamin C, then you are more likely to end up with cracks in your blood vessels. These cracks will then be plugged by small blood clots, containing a lot of Lp(a). If you have a high Lp(a) level, then these small blood clots will be even bigger, and even more difficult to remove.

Which means that if you have a high Lp(a) level, it would be a splendid idea to ensure that you never become vitamin C deficient. Indeed, even if you do not have a high Lp(a) level it would be a splendid idea to ensure that you do not become vitamin C deficient. Because cracks in blood vessel walls are never a good thing. Ending up, potentially, as the focus for atherosclerotic plaques.

Linus Pauling, a famous double Nobel Prize winner, believed that ‘sub-clinical’ Vitamin C deficiency was ‘the’ cause of cardiovascular disease. He also believed that if everyone took enough vitamin C, cardiovascular disease would disappear.

Personally, I do not think it is ‘the’ cause of cardiovascular disease, but I do think that it is ‘a’ cause. That is, whether or not you have a high Lp(a) level. Of course, a high Lp(a) level is likely to make things far worse, were you to end up vitamin C deficient.

However, the vitamin C, cardiovascular disease story does not end here. Because vitamin C has many other critical functions that link back to cardiovascular disease in one way, or another. For example, it has a more general function in protecting endothelial cells from harm, and supports the integrity of the vascular system. Here, from the paper ‘Role of Vitamin C in the function of the vascular endothelium’:

‘Vitamin C, or ascorbic acid, has long been known to participate in several important functions in the vascular bed in support of endothelial cells. These functions include increasing the synthesis and deposition of type IV collagen in the basement membrane, stimulating endothelial proliferation, inhibiting apoptosis (endothelial cell death), scavenging radical species, and sparing endothelial cell-derived nitric oxide to help modulate blood flow. Although ascorbate may not be able to reverse inflammatory vascular diseases such as atherosclerosis, it may well play a role in preventing the endothelial dysfunction that is the earliest sign of many such diseases.’

Supplementation to upper normal plasma ascorbate levels is clearly indicated in most diseases and conditions in which ascorbate is depleted. However, it is seldom a priority, because patients, physicians, and health authorities are unaware of the increasing evidence for multiple potentially important functions of ascorbate. With regard to the endothelium, it is worth emphasizing observations made more than 50 years ago that early scurvy generates endothelial disruption in guinea pigs, which resembles atherosclerosis and is fully and rapidly reversible with ascorbate repletion.14

Yes, with regard to the last part about guinea pigs. Many years ago, a researcher deliberately made guinea pigs ‘scorbutic’ – the medical term for the state of vitamin C deficiency, a.k.a. scurvy. At which point they developed atherosclerotic plaques.

When the vitamin C was added back into their diet, the atherosclerotic plaque disappeared. [Unless you left it too long, in which case, the plaques remained]. Best animal experiment on atherosclerosis ever done – never repeated.

Having just said all of this. I do not believe that most of us, most of the time, are lacking vitamin C – to any degree. At least I do not think so. However, if we become infected – with almost anything – the requirement for vitamin C shoots up. Because Vitamin C gets burned up protecting the endothelium, and it also supports the immune system

‘The role of vitamin C in lymphocytes is less clear, but it has been shown to enhance differentiation and proliferation of B- and T-cells, likely due to its gene regulating effects. Vitamin C deficiency results in impaired immunity and higher susceptibility to infections. In turn, infections significantly impact on vitamin C levels due to enhanced inflammation and metabolic requirements.15

Another key thing to know about vitamin C, again closely related, is that people with type II diabetes, and people who smoke, have reduced circulating levels of Vitamin C.

‘Although T2DM [type II diabetes mellitus] is not traditionally considered a risk factor for vitamin C deficiency, our research indicates that those with prediabetes or T2DM are more likely to have inadequate or deficient plasma vitamin C concentrations. This did not appear to be due to a lower dietary vitamin C intake, so dietary advice needs to emphasise the importance of consuming high vitamin C foods.16

What links smoking, type II diabetes, and vitamin C? Here I am hypothesizing a little. What links them is that with smoking, and type II diabetes, the endothelium is under ‘attack’. High blood sugar levels damage the glycocalyx (the protective lining of endothelium), and so do the nanoparticles that enter the bloodstream if you smoke.

Here is a quote from the paper: ‘Loss of endothelial glycocalyx during acute hyperglycemia coincides with endothelial dysfunction and coagulation activation in vivo.’ (In vivo means in a real live person, not just in vitro – in a test tube). Jargon alert:

‘Hyperglycemia is associated with increased susceptibility to atherothrombotic stimuli. The glycocalyx, a layer of proteoglycans covering the endothelium, is involved in the protective capacity of the vessel wall. We therefore evaluated whether hyperglycemia affects the glycocalyx, thereby increasing vascular vulnerability…

In the present study, we showed that the glycocalyx constitutes a large intravascular compartment in healthy volunteers that can be estimated in a reproducible fashion in vivo. More importantly, we showed that hyperglycemic clamping elicits a profound reduction in glycocalyx volume that coincides with increased circulating plasma levels of glycocalyx constituents like hyaluronan, an observation that is consistent with the release of glycocalyx constituents into the circulation17.’

Looking specifically at smoking:

‘Vascular dysfunction induced by smoking is initiated by reduced nitric oxide (NO) bioavailability and further by the increased expression of adhesion molecules and subsequent endothelial dysfunction. Smoking-induced increased adherence of platelets and macrophages provokes the development of a procoagulant and inflammatory environment.18 

Essentially, smoking and high blood glucose both damage the endothelium, which results in low vitamin C levels, as the endothelial cells burn through Vitamin C to maintain themselves. Ergo, fi you have type II diabetes, or smoke, you need more Vitamin C to maintain healthy levels….

Now, before I introduce you to far too many new and difference concepts – I did mention everything starts linking back together in completely unexpected ways – it is time to draw our little tale of Vitamin C together.

The first thing to say about vitamin C is that it is vital. I have only covered a few of the essential functions that it has in the human body. Those most closely related to cardiovascular disease. Importantly, it is almost impossible to cause harm by overconsumption. It is just about as safe to take, as anything can possibly be.

The next thing to say is that most of us, most of the time, probably have sufficient vitamin C intake, and require no supplements.

However, if you have a high Lp(a) level, then any damage caused by a lack of vitamin C will be amplified, dure the fact that Lp(a) sticks very tightly to areas of endothelial damage, making the resultant blood clot very difficult to remove. So, for those with high Lp(a) levels, I would recommend one gram of vitamin C a day – forever.

If you smoke, or have diabetes, the lining of your artery walls (glycocalyx and endothelium) are under constant attack from nasty substances – smoke nanoparticles and high blood glucose. This, too, will create ‘cracks’ in blood vessels.

In both situations Vitamin C is also used up more rapidly, trying to protect against this damage. So your vitamin C level is likely to be low. Which means that you too, should take one gram of vitamin C a day – forever. [Or you could try stopping smoking]

In addition, in many infections, the endothelium is under severe attack. Either directly from the microorganisms entering and killing endothelial cells (see under COVID19), or from the exotoxins (toxic waste products) released by any bacteria in the bloodstream.

The most severe endothelial attack occurs in sepsis (infection of the blood), where the exotoxins strip away the endothelium, resulting in widespread blood clotting (disseminated intravascular coagulation DIC). Which is the thing that, primarily, kills you with sepsis.

Whilst sepsis represents an extreme situation, it is still the case that if you are suffering from an infection, of any sort (gingivitis or periodontal disease) your requirement for vitamin C will shoot up. Which means that you should take as much Vitamin C as you can tolerate. Up to ten grams a day. I cannot take this amount due to the impact it has on my gastrointestinal tract. Loose, is the word. Very loose. Looser than loose.

But if you can tolerate it, Vitamin C will help to protect your endothelium. It will also boost the functioning of your immune system.

So, there we are then, vitamin C. My second favourite vitamin, after vitamin D. In the winter I take a gram a day. Along with my nine thousand units of vitamin D. Almost all medics will instantly dismiss this as ‘woo woo’ nonsense. I would tend to argue that this is because they know absolutely nothing about vitamins, or their critical roles in human physiology, and have never bothered to find out.

Pop quiz for your doctor, next time you see them. Ask them how a lack of vitamin C causes scurvy. What is the primary disease process? Watch them scrabble to bring up a Google search. Then ask them about Lp(a). What it is, what it does… I guarantee that silence will be the stern reply.



















Inclisiran sneaks through under cover of COVID19

23rd September 2021

With all medical eyes on COVID19, a cardiovascular drug with no proven benefit – at all – has been approved by NICE (The UK National Institute for Health and Care Excellence). Once a drug is approved by NICE it can, and will, be prescribed by doctors in England and Wales and Northern Ireland. Scotland has its own system.

NICE is also hugely influential beyond this small island. A NICE approval usually means a green light for approval in many other countries as well. Countries who assume that NICE will have carried out an in-depth ‘expert’ analysis using a set-up that they don’t have yet.

Which means that drug companies are always very keen to get NICE approval. It is a de-facto quality stamp. ‘This drug is both safe and cost-effective. You may now prescribe it everywhere in the world…’

Cost-effectiveness means that a drug does not just provide some clinical benefit. It must provide benefits that give you decent bang for your bucks. The ‘bang for your bucks’ measure used is the Quality Adjusted Life Year (QALY).

A QALY = one year of perfect health.

Of course, no healthcare intervention will ever give you one extra year of perfect health. Nothing is ever as clear cut as that. However, if you are suffering from a painful arthritic hip – and your quality of life is 50% perfect, or 0.5 – and you get a hip replacement, then your quality of life may rise from 0.5 to 0.9. So, you get 0.4 of a QALY/per year improvement.

After five years you have gained 0.4 (QALYs) x 5 (years) = 2 QALYs.

If the hip replacement operation has cost £10,000. The cost per QALY = £5,000. The cost per QALY obviously goes down if you live longer. That is a very simple example, most calculations become exceedingly complex. Measuring quality of life, for example, is fraught with difficulties.

In general NICE will approve a healthcare intervention if the cost per QALY is less than £30,000. This figure can never be pinned down. I often liken it to a blob of mercury. If you try to pick it up, it just slips, and slides, and fragments.

Indeed, this £30,000 figure never had any economic basis, or any other basis. It was simply plucked from the air because … well, because it seemed reasonable.

Here, from a discussion in the UK Parliament when NICE was first starting up:

‘There is clearly confusion about the cost per QALY threshold. Witnesses questioned whether there was any evidence to support the level that appears to be used. Professor Devlin told us that, “the threshold has no explicit basis or location in evidence”. Others agreed that it was “arbitrary”. Professor Smith confirmed…

Professor Rawlins admitted that the threshold was not based on “empirical research” as no such research existed anywhere in the world. He told us instead that the threshold was: …really based on the collective judgment of the health economists we have approached across the country. There is no known piece of work which tells you what the threshold should be.

No public discussion has ever taken place of the suitability of the threshold used. The American Pharmaceutical Group pointed out that the threshold has “never been the subject of public debate or Parliamentary approval. Cancer Research UK also argued that the threshold should be discussed openly and the reasons for its level should be determined in consultation with interested organisations.’ 1

I love it when people say things like ‘the threshold has no explicit basis or location in evidence.’ The short word – no – would have done nicely. As in, there is no evidence. Instead, we get the concept of no explicit basis or location in evidence. Listen guys, just get rid of the words: explicit, basis, or, and location. Why use five words when one will do?

Anyway, it has always amused me that NICE spends vast amounts of time and effort trying to establish with great accuracy whether a healthcare intervention meets a cost per QALY threshold… that was simply made up.

You might as well have got a cane with a hook on the end to pluck one of a thousand plastic yellow ducks floating in a pond with a random number written on the bottom. ‘Oooh look, it says thirty thousand… so that is the figure we shall use.’ Yes, really.

Anyway, as custom is king, this £30K figure – which has remained unaltered for twelve years [has anyone at NICE ever heard of inflation – or maybe a made-up figure cannot be affected by inflation] is unquestioned, and unquestionable. It is carved in stone. ‘And God did sayeth unto the multitude that thirty thousand pounds per QALY shalt be my law unto the end of time. Amen.’ Anyway, following that little history lesson, let us gaze upon the cost per QALY calculations that NICE used for Inclisiran – a new LDL lowering injection to be given twice a year. And below are the calculations [or at least the calculations that I could be bothered to copy]:

As you can see Inclisiran meets the cost per QALY criteria with ease. Well, actually, in truth, you cannot see anything because all the figures have been redacted. It amuses me further that NICE have decided that a table which contains no information of any use is ‘confidential’. Well, of course, it is not very confidential, because I can see it, and so can you, if you decide go to:

So, which part of that completely pointless table is confidential? It is clearly not confidential that it is confidential. Maybe this is some strange double-bluff. Perhaps you can scrape away the black areas to reveal the numbers beneath, and win a million-pound prize?

I suspect that written beneath them will be the phrases. ‘How much?’ ‘You’re having a laugh.’ Or ‘We will not release your family unless you pay this as ransom.’ And suchlike.

Enough of this. NICE is a public funded organisation that is supposed to work on our behalf. They have decided that Inclisiran is cost-effective, yet they will not let anyone see the figures that they used? You would think they would be shouting it from the rooftops. ‘Look how fantastic it is. Look at the size of that discount. Gaze with wonder on the magnificent cost-effectiveness of Inclisiran.’ No, instead, they are very shy about it. Like little meercats sensing danger and scurrying down into the darkness.

Without any figures, the NICE appraisal is essentially hundreds of pages of utterly meaningless guff. As I used to say, once upon a time, when teaching my children to count. ‘One two, miss a few, ninety-nine, one-hundred’.

How much are we paying for Inclisiran? Nobody knows. Because NICE won’t tell us. We know it should be/could be around £4,000/year ($5,000). So, some sort of discount has been negotiated. How much … well, that’s a secret. A secret. Why? In case we all rush round to Novartis headquarters and try and buy some at a bigger discount?

Secret or not, the truth is that I do not need to know the exact cost of Inclisiran. Because I already know that whatever it costs, the cost per QALY current stands at infinity i.e., ∞. I know this because, at present, there is no evidence that it provides any benefit, on any clinical outcome. By which I mean no evidence that it prevents strokes, heart attacks or, in fact, anything.

Based on this knowledge the Cost per QALY equation goes something like this:

Cost per year of Inclisiran/benefit in QALYs = cost per QALY

With Inclisiran let us set the cost per year at £4,000, and benefit at zero:

£4,000/ 0 = ∞ (infinity)

Let us set the cost at £1 and run the equation again

£1/0 = ∞ (infinity)

You see how simple it is to work out the cost per QALY when there is no benefit. It always ends up at infinity. If it cost one Turkish lira, the cost per QALY would still be infinity. I certainly did not need several hundred pages of guff to tell me this. You ought to try reading an endless NICE report sometime. My advice is, don’t bother.

Anyway, if you do read what NICE has to say about Inclisiran you will find the following key sentences in the NICE appraisal documentation.

‘There is also no long-term evidence on whether Inclisiran reduces cardiovascular events. This means the clinical evidence and the cost-effectiveness estimates are very uncertain.’2

Let me rephrase the first sentence.


Let me rephrase the second sentence


Yes, it lowers LDL (low density lipoprotein), we do know that. We do not know if this will have an impact on cardiovascular deaths, or overall mortality. NICE assumes that if you lower LDL, you will reduce cardiovascular death – and suchlike.

However, this is not necessarily true. Repatha (evolucamab) is a drug which has exactly the same mechanism of action as Inclisiran but needs to be given every two weeks instead of twice a year. Both Inclisiran and evolucamab are PCSK9-inhibitors. [They block the breakdown of LDL-receptors in the cell, which means that more LDL receptors are available to pluck LDL molecules from the blood, thus reducing the blood levels]. Both drugs reduce the LDL level by pretty much the same amount.

In the FOURIER study on Repatha the results were the following

Cardiovascular mortality – total numbers:

Repatha          = 251

Placebo          = 240

Overall mortality

Repatha         = 444

Placebo         = 4263

Yes, Repatha lowered LDL to the same degree as Inclisiran and yet slightly more people died taking Repatha than died taking placebo. Repatha has been approved and launched, although you may wonder how or why.

In short, just because a drug lowers LDL does not mean it does any good. Just to give another example, the drug evacetrapib lowered LDL by 37% (and increased HDL by 132%). It, too, had absolutely no impact on cardiovascular mortality.

‘Although the cholesteryl ester transfer protein inhibitor evacetrapib had favorable effects on established lipid biomarkers, treatment with evacetrapib did not result in a lower rate of cardiovascular events than placebo among patients with high-risk vascular disease.’ 4 

Just in case you are wondering, Evacetrapib did not launch. Nor did another three drugs in the same class that all had ‘favourable effects on established lipid biomarkers’ but achieved nothing. One of them, torcetrapib, increased cardiovascular death by 50%.

In short, approving drugs, or launching drugs before you have any evidence that they do anything – other than having a favourable effect on an established lipid biomarker – is ridiculous. But never mind, longer term studies on Inclisiran will be completed by 2023, and 2026. When will they actually be published?

Who cares, by the time they are published, Inclisiran will have made billions, and no-one will care if the results are positive, or negative, as it will have become established as ‘standard’ treatment.

A number of us found the NICE approval of Inclisiran so ridiculous that we wrote them a letter. (See below). I do not imagine it will have the slightest impact.

To: Sharmila Nebhrajani OBE,

Chair: National Institute for Health and Care Excellence

2nd Floor, 2 Redman Place

London E20 1JQ

cc. The Right Honourable Sajid Javid, MP Secretary of State for Health and Social Care Department of Health

Richmond House 79 Whitehall London, SW1A 2NS

15th Sept 2021

Concerns about the latest NICE draft guidance on Inclisiran


We are concerned about your draft final guidance recommending the novel anti-cholesterol drug inclisiran (Leqvio and made by Novartis) for people with primary hypercholesterolaemia or mixed dyslipidaemia who have already had a cardiovascular event such as a heart attack or stroke.

We would ask for this decision to be over-turned immediately until there is enough data to support any hard outcome benefit of Inclisiran, namely the prevention of heart attacks, strokes or death.

Our main concerns are addressed in six key areas:

1. Inclisiran is an investigational drug in the UK

Inclisiran gained approval by the European Medicines Agency in Dec 2020, however, the drug remains unapproved in the UK (which is not part of the European Union) since 31 Jan 2020 and other major nations. The novel PCSK-9 inhibitor has not been approved by the US Food and Drug Administration.

We would recommend however, that a full appraisal of the Inclisiran trial data and marketing license be obtained by UK’s Medicines and Healthcare products Regulatory Agency prior to rolling out the drug to patients in the NHS.

2. Lack of transparency in NICE decision making process

The decision for NICE follows an agreement on a population-level commercial deal between NHS England and NHS Improvement and Novartis which will make inclisiran available with a discount to its list price.

The full details to the pricing agreement have been kept confidential and not available for independent scrutiny. This lack of transparency should be of concern to the British public, prescribing doctors and taxpayers who fund NICE.

3. No long-term data on effectiveness or safety

To date, the trials are short term, only 18 months. NICE’s daft guidelines acknowledge this issue. “The committee was concerned that there was a lack of long-term data on cardiovascular outcomes from the clinical trials that compared Inclisiran with placebo. However, it noted that ongoing clinical trials would provide more data on these outcomes.”

We propose that more long-term data on safety and efficacy is accumulated before recommending Inclisiran, even as an adjunct to statin therapy.

4. Decision based on a surrogate marker (LDL-C)

Inclisiran, the novel PSCK-9 inhibitor is effective at lowering Low Density Lipoprotein cholesterol (LDL-C), however, mounting evidence demonstrates that it is a weak surrogate marker of cardiovascular disease.

The push to lower cholesterol with statins to prevent heart disease has been hugely influenced over the years by meta-analyses performed by the Cholesterol Treatment Trialists Collaboration at Oxford University researchers.

The CTT suggests that there is a linear relationship between LDL-C reduction by statins and the reduction in risk of cardiovascular disease. The individual patient data, upon which they make these claims, is not accessible to third parties for independent scrutiny.

NICE justifies its decision to be guided by the CTT in its recommendations “The clinical experts stated that the CTT meta-analyses were appropriate and that a similar relationship between LDL-C lowering and a reduction in cardiovascular event risk as seen with statin use could be expected with Inclisiran.”

However, it should be noted that statins have pleotrophic effects – anti-inflammatory and anti-thrombotic – that may be responsible for the benefits seen in secondary prevention patients.

Further, there is conflicting evidence that LDL-C is a causal factor in heart disease. A 2020 recent study published by Danish researchers, for example, demonstrated that LDL-C the lowest risk of all-cause mortality was found at an LDL-C concentration of 3.6 mmol/L (140 mg/dL).

In comparison the highest association with all-cause mortality was actually at LDL-C levels of less than 1.8mmol (70mg/dL).

Notably, NICE recommendations suggest that people with LDL-C concentrations persistently 2.6 mmol/l or more, despite maximum tolerated lipid-lowering therapy, should be on Inclisiran. This has no independent scientific basis.

Although the NICE recommendation is specific to patients with either previous cardiovascular disease or FH such a well-publicised recommendation feeds into a false narrative that the lower the LDL-C the better when it comes to overall health and/or managing cardiovascular disease. It’s instructive to note that there is also no difference in levels of LDL-C in patients with FH who developpremature heart disease versus the one’s that don’t suggesting that LDL-C is not the main driving factor for the development of coronary artery disease in these patients.

Furthermore, an independent peer reviewed systematic review of drug trials carried out by three cardiologists in 2020 published in BMJ Evidence Based Medicine revealed that there was no clear relationship with reduction in LDL in both high risk and low risk patients in reducing cardiovascular events.

5. No evidence for cardiovascular benefit with Inclisiran lowering LDL-C

Low Density Lipoprotein cholesterol (LDL-C) has been the primary outcome of the clinical trials. While we agree that Inclisiran demonstrates effective reduction in LDL-C, we find that the clinical data to support the benefit of cholesterol lowering is absent.

An analysis by the European Medicines Agency (EMA) found there was a “lack of cardiovascular outcome data” in the regulatory documents sent to the drug agency.

 It also found that “the number and percentage of deaths was comparable between the placebo and the Inclisiran group, but numbers are too small for clear conclusions.”

“In addition, no definite data on cardiovascular morbidity and mortality are currently available,” the report stated.

NICE’s own guidelines state, “there is also no long-term evidence on whether inclisiran reduces cardiovascular events. This means the clinical evidence and the cost-effectiveness estimates are very uncertain”.

Given that Inclisiran has not proven to reliably reduce major cardiovascular events, cardiovascular morbidity, or mortality, we believe a decision to recommend this drug based is premature.

Two studies, ORION-4 in secondary prevention and ORION-17 in primary prevention are currently underway.

6. Loss of professional confidence

The lack of transparency in the decision-making process may undermine professional and public confidence in NICE and its decision-making processes. This could be critically damaging to professional confidence in the delivery of evidence-based healthcare in the UK

In light of our concerns, we urge you to withdraw the current guidance on Inclisiran for people with primary hypercholesterolaemia or mixed dyslipidaemia who have already had a cardiovascular event such as a heart attack or stroke until further important clinical data with clear cardiovascular benefits are made available.

Your Sincerely,

Dr Aseem Malhotra FRCP, Consultant Cardiologist, Professor of Evidence Based Medicine and Chairman of The Public Health Collaboration.

Sir Richard Thompson, Past President of The Royal College of Physicians

Dr JS Bamrah CBE, Consultant Psychiatrist and Chairman of BAPIO (British Association of Physicians of Indian Origin)

Dr Campbell Murdoch, General Practitioner and Royal College of General Practitioners – Clinical Advisor

Dr David Unwin FRCGP, General Practitioner, Vice Chair – The Public Health Collaboration.

Dr Malcolm Kendrick, General Practitioner and author.

Sherif Sultan, Professor of Vascular Surgery, President of International Society of Vascular Surgeons. Shahriar Zehtabchi, MD, Professor of Emergency Medicine, State University of New York


The Cholesterol Treatment Triallists Collaboration (CTT) in Oxford is the group that hold all evidence from cholesterol lowering trials that have been done on statins. They will not release this evidence, or allow anyone else to come into their unit see it.

The meta-analyses carried out by the Cholesterol Treatment Triallists Collaboration (CTT), using the data that only they can see, using the evidence only they hold, has established that the risk of cardiovascular event is reduced by a set amount, for every 1mmol/l that LDL is lowered. (1mmol/l = 38.67mg/dl. Mg/dl is the form of measurement used in the US)

‘The CTT Collaboration has shown that lowering LDL cholesterol using statin therapy reduces the risk of major vascular events (heart attacks, stroke or coronary revascularisation procedures) by about one fifth for each 1 mmol/L reduction in LDL cholesterol achieved.5

This was the evidence used by NICE to establish that LDL lowering can be used as a ‘surrogate end-point’ i.e., the CTT ‘know’ that if LDL is lowered this will – for certain – result in a known reduction in cardiovascular end-points.

‘The company (Novartis) used the Cholesterol Treatment Trialist Collaboration (CTT)meta-analyses, which reported change in cardiovascular event risk per1 mmol/l reduction in LDL-C by statin use. The ERG agreed that these analyses were appropriate and noted that earlier versions of this source were used in past NICE technology appraisals in this disease area.’

It should be noted that the Cholesterol Treatment Triallists Collaboration (CTT) is part of the Clinical Trials Service Unit in Oxford (CTSU) 6. This unit has received hundreds of millions of pounds in funding from pharmaceutical companies, primarily those who market cholesterol lowering drugs.7

The Clinical Trials Service Unit (CTSU) in Oxford is currently running, and co-ordinating, the various ORION studies that are being done on Inclisiran. For example, ORION-4, as can be found on the CTSU website:

‘ORION-4 is a research study which aims to find out if a new cholesterol lowering injection safely reduces the risk of heart attacks and strokes in people who have already had one of these conditions, or who have had an operation or procedure to unblock their arteries.’8   

Thus, NICE are using the meta-analysis created by the CTT to make the decision that Inclisiran will reduce cardiovascular events, purely due to the effect on LDL lowering.

The CTT hold all the data that make up the meta-analysis used by NICE – and will not allow any independent researchers to see it.

The CTT are part of the CTSU which has run, and continues to run, many pharmaceutical company sponsored studies on LDL/cholesterol lowering drugs. For which they have received hundreds of millions in funding. The CTSU is the group primarily responsible for running the clinical trials on Inclisiran.

Yet, and yet. If you look at the final stakeholder list of consultees and commentators for the Single Technology Appraisal:


Single Technology Appraisal

Inclisiran for treating primary hypercholesterolaemia or mixed dyslipidaemia


Final stakeholder list of consultees and commentators

…if you look closely, the CTT and CTSU do not get a mention 9. It is as if they simply do not exist. And there are literally hundreds of stakeholders. Running from the British Cardiology Society, to the Cochrane Cystic Fibrosis and Genetic Disorders Group, and NHS Bradford City CCG.  

Yet, the CTT/CTSU hold on the data for the meta-analysis upon which the entire approval process rests. They are the people running the clinical trials on Inclisiran. And no-one at NICE thought it might be a good idea to speak to them? Are they not, stakeholder number one? Why so coy?

One could even argue that NICE have breached their own guidelines by failing to speak to the most important stakeholder of all.








8: 9:

COVID19 and CVD – Bridging the gap

16th September 2021

Bridging the gap between cardiovascular disease and COVID19

[Where two diseases meet]

Having announced that I will not discuss COVID19 anymore, I am about to do so – at least in part. Yes, you may now be thinking… how can we believe anything this man says?

However, I do have an excuse for this. Because, as part of my transition back to more familiar waters, I am going to look at the links that COVID19 has to cardiovascular disease… my life-long obsession.

The reason is that I have found it amazing how two apparently unrelated diseases can be linked so closely, and greatly increase your knowledge of both.

I will start with a quote that I would like to you read slowly, and carefully, taking a little time to think about – if you can get through the jargon.

‘Host defense against infection is based on two crucial mechanisms: the inflammatory response and the activation of coagulation. Platelets are involved in both hemostasis (blood clotting) and immune response. These mechanisms work together in a complex and synchronous manner making the contribution of platelets of major importance in sepsis. This is a summary of the pathophysiology of sepsis-induced thrombocytopenia*, microvascular consequences, platelet-endothelial cells and platelet–pathogens interactions.’ 1

*thrombocytopenia = drastic fall in platelet levels (small cells that conduct the entire blood clotting orchestra).

Yes, as you may have noticed, this passage says nothing about COVID19. On the face of it, it has nothing to do with cardiovascular disease either. It also contains a lot of jargon which most people without a medical background will struggle to understand. To me, however, it is fascinating, as it opens an entirely new way of thinking about critical disease processes.

What these researchers are saying, in the typically impenetrable prose of medical writing, is that the immune system, and the blood clotting (coagulation) system, have been designed to work together to fight off infective agents. Indeed, from an evolutionary perspective, they started off as the same thing. As discussed in an article in the Journal ‘Immunity’. ‘The Coagulation and Immune Systems Are Directly Linked through the Activation of Interleukin-1α by Thrombin.’

‘Ancient organisms have a combined coagulation and immune system, and although links between inflammation and hemostasis (blood clotting) exist in mammals, they are indirect and slower to act. Here we investigated direct links between mammalian immune and coagulation system….The identification of a direct link between the coagulation system and the activation of the IL-1α* inflammatory cascade raises important questions.’ 2

*Interleukin 1 alpha (IL-1α) also known as hematopoietin 1 is a cytokine** of the interleukin 1 family that in humans is encoded by the IL1A gene. In general, Interleukin 1 is responsible for the production of inflammation, as well as the promotion of fever and sepsis. [Which is why you get hot and shivery when you get infected]

**a cytokine is a small protein that normally passes messages from cells to other cells and the immune system. Cytokines are key players in the immune response to infections, and there are many of them.

Anyway, put at its simplest. If you become infected (with almost any micro-organism,) you are far more likely to produce blood clots. Why? Well, it is probably because serious and life-threatening infections will often enter the body through a wound, or damage of some sort. Therefore, it makes sense that the body tries to seal off such wounds, or entry points, with a blood clot. This will not only stop the bleeding, but it will also trap the invading bacteria and viruses to prevent them spreading.

At which point the immune system gets to work on the trapped micro-organisms. Indeed, what better way to neutralize a virus, or bacteria, than by wrapping it up inside platelet fibrin complexes – two of the main constituents of blood clots?

At this point you may well ask, so what has this to do with cardiovascular disease, atherosclerosis and atherosclerotic plaques? Well, as the same paper goes on to say:

‘Many diseases are driven by the interplay between coagulation and inflammation. Inflammation drives atherosclerosis and IL-1α can play a dominant role independent of inflammasomes suggesting another mechanism activates IL-1α. Plaques contain thrombin-antithrombin complexes and show fibrin localized throughout, implying thrombin activation occurs throughout atherogenesis. Thus, p18 IL-1α might drive atherogenesis.’ 3

In super-short version:

Infection → inflammation + coagulation → (if regularly repeated) atherosclerotic plaques = cardiovascular disease

I find it a remarkable coincidence that I was studying the impact of infectious agents on cardiovascular disease when the COVID19 tsunami broke upon the world. Then I started delving into what the Sars-Cov2 virus does to a wide range of physiological systems. It opened doors into new passageways of thinking, and research, that I never even knew existed.

Primarily, that there is a tight connection between the blood clotting system and the immune system. Who knew? Well, some people obviously did, because they were researching it and writing about it. However, until COVID19 came along I didn’t have the faintest idea. I hadn’t even thought to connect the two processes.

Yes, I already knew that infectious diseases, such as Influenza, could greatly increase the risk of a fatal blood clot in the days and weeks following infection. I knew that sepsis (bacterial infection of the blood) causes damage to endothelial cells that line all blood vessels, triggering small blood clots all around the body. A condition known as Disseminated Intravascular Coagulation (DIC), which is the primary cause of death in sepsis.

I also knew that ‘inflammation’ of the blood vessels, a condition often known as vasculitis, could greatly increase the risk of cardiovascular disease. Vasculitis essentially means damage of the endothelium (the layer of glycocalyx, and endothelial cells, that line all blood vessel walls).

The impact of vasculitis on cardiovascular disease is highlighted by the fact that the form of vasculitis associated with Systemic Lupus Erythematosus (SLE) a.k.a. ‘lupus’ can increase the risk of death from cardiovascular disease by – up to – 4,900% in young women. 4

Indeed, all the vasculitides – plural of vasculitis – can greatly increase the risk of CVD, and thrombosis (blood clotting):

‘The relationship between inflammation and thrombosis is not a recent concept, but it has been largely investigated only in recent years. Nowadays inflammation-induced thrombosis is considered to be a feature of systemic autoimmune diseases such as Systemic Lupus Erythematosus (SLE), Rheumatoid Arthritis (RA), or Sjögren Syndrome (SS). Moreover, both venous and arterial thrombosis represents a well-known manifestation of Behçet syndrome (BS).5

Then, of course, along comes COVID19, which brought a number of these strands into tight focus. It became clear that COVID19 also links infection + coagulation + vasculitis.

How so? Well, it was rapidly established that COVID19 enters cells by linking onto a receptor known as the ACE2 receptor (Angiotensin Converting Enzyme 2 receptor), before being dragged into the cell.

ACE2 receptors form an important part of the enormously complex Renin Aldosterone Angiotensin System (RAAS). Sorry, this is yet another strand, but please bear with me for a while, because it is important.

What is the Renin aldosterone angiotensin system? Well, keeping it super-simple, the RAAS controls blood pressure. If your blood pressure drops the RAAS kicks into action. [It also kicks into action if sodium levels fall, but that is an entirely different world of discussion]. The RAAS forces the heart to pump harder, it constricts blood vessels, it drives the kidneys to keep a hold of sodium and water etc. etc.

Although there are all sorts of hormones involved in the RAAS, with feedback and amplification loops here and there, they basically all end up triggering the conversion of a hormone called angiotensin I to angiotensin II. Angiotensin II is the active hormone that locks onto receptors in various organs, causing them to do their blood pressure raising thing.

[If you block the conversion of angiotensin I to angiotensin II, you will lower the blood pressure. This is what the class of drugs known as ACE-inhibitors do. They inhibit the enzyme that turns angiotensin I into angiotensin II. Which means that they are called angiotensin converting enzyme inhibitors. This reduces the amount of angiotensin II in the blood, and stops the heart rate increase, the blood vessel contraction, and suchlike. These drugs are widely prescribed]

As you might imagine therefore, ACE2 receptors are present in high numbers on the surface of membranes of cells that play a role in the RAAS. Basically, any cells involved in blood pressure control.

A large number are found in the cells in the lungs, because the lungs are where Angiotensin I (the inactive pro-hormone) is converted to Angiotensin II – the active form. Why does this conversion occur in the lungs, not the kidneys or liver? No idea. Something to do with evolution probably.

ACE2 receptors are also found in the cells that line all blood vessels – the endothelial cells. Why? Because angiotensin II links to these receptors to create messages commanding blood vessels to constrict – thus raising the blood pressure.

[In fact, sorry to add yet another complication, ACE2 receptors represent part of the ‘control feedback system’ for RAAS. When activated, ACE2 receptors block the effects of angiotensin II. They are ‘anti-angiotensin II’ receptors, if you like. They work to keep the effects of angiotensin II from running out of control. However, they are still an integral part of the RAAS system, and a critical part of the negative feedback loop to control blood pressure. Thus, wherever you have an ACE-receptor, you will also have an ACE2 receptor. Yin and Yang].

Why is all of this important, you may ask. Because it explains which cells are going to be most damaged by COVID19, and why. Essentially, the cells that are most damaged will be the cells that play a role in the RAAS. They are damaged because they have ACE2 receptors on their membranes.

Without this receptor, it is impossible for a cell to be infected by Sars-Cov2, and no damage can occur.

Years ago, I was looking at the Ebola virus. I found out that this virus gains entry through a protein stuck to the cell membrane known as the CCR5 protein. As with COVID19 and the ACE2 receptor, Ebola must find something on the cell membrane to link onto, before it can gain entry to the cell. A lock and key if you like. If the lock doesn’t fit the key – there can be no entry for the virus.

It was found that some people have a variant of this protein known as the ‘CCR5 Delta 32 mutation’. Because this protein has a different structure to the normal CCR5 protein, the Ebola virus cannot link to it. Therefore, it cannot enter any cells. Which means that people with the CCR5 Delta mutation cannot become infected with Ebola. Or at least, it cannot enter any cells in the body, so it cannot multiply, so it cannot cause any damage.  

It is of interest that HIV also enters cells using the CCR5 protein, and people with the CCR5 delta 32 mutation cannot be infected with HIV either.

Anyway, trying desperately to bring things back together… deep breath. Once inhaled, COVID19 gets into lung cells using the ACE2 receptor – creating lung damage. It gets into kidney cells – creating further damage. It gets into heart cells (myocytes, pericytes) – causing even more damage. It gets into endothelial cells – creating vasculitis. It also stimulates the coagulation system into action – as almost all infectious agents do.

If you survive the initial lung damage – which most people probably will do – then the thing you need to start worrying about is the vasculitis/blood clotting that will be triggered throughout the rest of the body. This will all be worsened by the fact that infected endothelial cells will be sending out cytokines (distress messages) to the immune system. Stating, simply. ‘I am infected, come and kill me and the virions within.’

This, then, is the basis of the ‘cytokine storm’ which you may have read about with COVID19. Ironically, the body’s own defence system, the immune system, can become the very thing that kills you with COVID19. It revs up, starts attacking the infected cells, and creates major problems such as myocarditis (inflammation/damage to heart muscle). Kidney damage/failure, and a more widespread severe vasculitis develops as the endothelial cells are machine gunned by their own side.

All of this creates widespread blood clotting, which was recognised quite early on. Here from the paper ‘Emerging evidence of a COVID-19 thrombotic syndrome has treatment implications.’

‘Reports of widespread thromboses and disseminated intravascular coagulation (DIC) in patients with coronavirus disease 19 (COVID-19) have been rapidly increasing in number. Key features of this disorder include a lack of bleeding risk, only mildly low platelet counts, elevated plasma fibrinogen levels, and detection of both severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and complement components in regions of thrombotic microangiopathy (TMA). This disorder is not typical DIC. Rather, it might be more similar to complement-mediated TMA syndromes, which are well known to rheumatologists who care for patients with severe systemic lupus erythematosus or catastrophic antiphospholipid syndrome.’ 6

Again, much jargon. However, the final sentence which provided me with the intellectual equivalent of sipping a twelve-year-old malt whisky… Roll it around the palate with deep pleasure. Please read again, and think about it:

‘Rather, it might be more similar to complement-mediated TMA syndromes, which are well known to rheumatologists who care for patients with severe systemic lupus erythematosus or catastrophic antiphospholipid syndrome.’

On the face of it, a rather boring sentence. What it is telling us, however, is that with COVID19 we are looking at almost the same pathological process as seen in Systemic Lupus Erythematosus (SLE), with an added dash of antiphospholipid syndrome.

Lupus, as mentioned before, causes vasculitis, because the immune system attacks endothelial cells. It is made worse when the person also has antiphospholipid syndrome (sometimes called Hughes’s syndrome).

Phospholipids essentially, are cell membranes. Two layers of phospholipids stuck back-to-back like Velcro. Within this bi-layer of phospholipids are various channels and gates and receptors and (as you may have noticed), lots of cholesterol – which stabilises the cell membrane. No cholesterol, no cell membrane, it simply falls apart.

Getting back to anti-phospholipid syndrome, it means exactly what you would think it means. The immune system starts to attack the phospholipid bi-layer that makes up the endothelial cell membrane, it becomes an ‘anti-phospholipid system’. This creates damage, the damage exposes the underlying clotting factors, and you end up with blood clots forming on blood vessel walls. Thrombotic microangiopathy (TMA).

Thus SLE/antiphospholipid syndrome, and COVID19, although they are completely different diseases, can create almost the same damage. The immune system and clotting system combining – along with severe endothelial disruption. This is also, almost certainly, why some children develop a severe vasculitis following shortly after the acute phase of COVID19 infection.

Here, from the article ‘COVID-19-associated vasculitis and vasculopathy.’

‘COVID-19 is a SARS–CoV-2 syndrome that can involve all organs, including the circulatory system. Endothelial cell inflammation occurs within arteries, arterioles, capillaries, venules and veins and contributes to pathological events; including tissue hypoperfusion, injury, thrombosis and vascular dysfunction in the acute, subacute and possibly chronic stages of disease. Beyond re-writing the textbooks that hence will include SARS–CoV-2 as a causal pathogen for multi-bed vasculitis, the data will show that it is a new category of systemic vasculitis forever captured in the annals of medicine.

Look, I understand this is all complex, and I have taken you through it all at a bit of a rush, but I was hoping to give you a sense of my scientific excitement. When COVID19 hit, I was looking at vasculitis and how it caused cardiovascular disease. Here, are the very words I was writing.

‘Vasculitis means damage and inflammation to the blood vessels. Vascular = blood vessels; ‘itis’ = inflammation. As in tonsillitis = inflammation of the tonsils, or appendicitis = inflammation of the appendix.

There are many, many different sorts of vasculitis, and they all have impossible to remember names. However, I do love them, as they are so evocative of a bygone era in medicine. Here are several of them, not including systemic lupus erythematosus or rheumatoid arthritis:

  • Polyarteritis nodosa
  • Waldenström’s macroglobulinaemia
  • Sjogren’s disease
  • Giant cell arteritis
  • Behcet’s disease
  • Buerger’s disease
  • Churg-Strauss syndrome
  • Cryoglobulinemia
  • Granulomatosis with polyangiitis
  • Henoch-Schonlein purpura
  • Kawasaki disease
  • Takayasu’s arteritis

This is Harry Potter stuff. Wave your wand about and exclaim…’Vasculitis obliterans!’ Actually, that is another form of vasculitis. The reason why they don’t all appear on Qrisk3 is because many of them are considerably rarer than hen’s teeth. In addition, they not widely recognised to increase CVD risk – although they all do. If you choose to look.

Apart from increasing the risk of CVD, another characteristic they have in common is that they are also, what are termed as auto-immune conditions. ‘Autoimmune’ describes the situation whereby the body decides to attack itself….’

Immune system + vasculitis + coagulation.

How strange that a virus would come along and create an almost perfect model to highlight this world, I thought.

As a sign-off, I did wonder what it was with COVID19 that so directly stimulated the blood clotting system. As it turns out, it appears to be the spike protein itself. Here, from the paper ‘The unique characteristics of COVID-19 coagulopathy.’

‘Thrombosis is a major pathological driver in COVID-19. Evolving evidence suggests that in addition to the activated leukocytes and derangement of antithrombotic property of endothelial cells, hyperactive platelets participate in thrombogenesis. The direct and indirect effects of SARS-CoV-2 spike protein on platelets stimulate the release of platelet factor 4. The spike protein also upregulates inflammation and coagulation through the binding to ACE2 on macrophages/monocytes, lung epithelial cells, and possibly vascular endothelial cells, reactions that lead to micro and macro circulatory clotting known as CAC (COVID19 associated coagulopathy).’ 7

Yes, the spike protein. This, it appears, is the key antigen, the key driver of the immune/thrombotic system in COVID19. This is the factor that can lead to blood bloods, strokes heart attacks…sudden death.

‘The number of out-of-hospital sudden death episodes has increased since COVID-19 outbreaks. One of the possible reasons is the high incidence of major thrombotic events in patients with COVID-19.’

It would therefore seem that caution would be required, if you were to find a way to stimulate the creation of trillions of spike proteins within the human body. Caution.

Anyway, now you know – I hope – why I became so interested in COVID19. Because it links together a whole series of processes that, I believe, are key to understanding cardiovascular disease. Endothelial damage, blood clot formation, the central role of the blood clotting system.

Of course, COVID19 represents an acute vasculitis which comes and goes at some speed and is unlikely to lead to the longer-term damage required to create the repeated clot deposition necessary to drive atherosclerotic plaque formation. However, it can still cause acute clot formation, which can lead to strokes and heart attacks and kidney damage, and suchlike.

It is why, after I got vaccinated, I took aspirin for a month.

Next, fully back to cardiovascular disease – and associated stuff. I will even start to promote my new book – due to launch in October. ‘The enduring mystery of heart disease – The Clot Thickens.’ Yes, it was my son who came up with the title. Not that I will ever let anyone know it was him.








I have not been silenced

3rd September 2021

Thank you to the many people who have e-mailed me recently and asked if I have been silenced. I have not. I have had letters from Public Health England and the General Medical Council, informing me that I was under investigation for daring to question anything about COVID19, particularly vaccines.

The good news is the investigations ended up nowhere, and were closed down. I have also had irate phone calls from doctors, telling me that I must not question vaccination and suchlike. This has been somewhat wearing and has caused me to remain silent for a while and think about things.

However, I do know how to play the medical regulations game. Don’t make a statement you cannot reference from a peer-reviewed journal. Don’t give direct advice to people over the internet. Provide facts, and do not make statements such as ‘vaccines are killing thousands of people.’ Or suchlike.

Not that I ever would. My self-appointed role within the COVID19 mayhem, was to search for the truth – as far as it could be found – and to attempt to provide useful information for those who wish to read my blog.

The main reason for prolonged silence, and introspection, is that I am not sure I can find the truth. I do not know if it can be found anymore. Today I am unsure what represents a fact, and what has simply been made up. A sad and scary state of affairs.

This is not just true of the mainstream and the mainstream media, which has simply decided to parrot all Government and WHO statements without any critical engagement…or thought. For example, the BBC intones that ‘In the last day, fifty people died within twenty-eight days of a positive COVID19 test…’ Or a hundred, or six. What the hell is this supposed to mean? It means nothing, it is the very definition of scientific meaninglessness.

Especially when it seems that very nearly a half of those admitted to hospital with COVID19 were not admitted to hospital with COVID19. They were admitted with something else entirely, then had a positive test whilst in hospital. In short, they were not admitted to hospital with COVID19, and almost certainly did not die of COVID19. They died with a positive COVID19 test. With, not of.

But the misinformation is equally a problem for those on the other side. Claims are made for the benefits of Ivermectin and hydroxychloroquine that simply do not stand up to scrutiny. Yes, I believe both drugs may provide some benefit, but not the claimed 90% reduction in deaths that I have seen trumpeted.

So, I have given up on COVID19. It is a complete mess, and I feel that, without being certain of the ground under my feet, I have nothing to contribute. I too am in danger of starting to make statements that are not true.

However, before leaving the area entirely, I would like to make clear some of the things I currently believe to be true, and what I do not believe to be true. If this is of any assistance to anyone. Very little is referenced, because I can very easily find a contradictory reference to any reference I provide. For each fact, there is an equal and opposite fact.

1: SARS-CoV2 exists

Many people have stated, probably correctly, that the SARS-CoV2 virus has never been fully isolated. Whatever exactly that means. Have Koch’s postulates been met? [see a bit later on] I think for viruses, Koch’s postulates are very rarely, if ever, met. Does it matter, not really.

Despite this gap I believe that SARS-CoV2 truly is a ‘new’ virus that did not exist before. So, it must have mutated somewhere, or been mutated somewhere, from another coronavirus… probably. Although it seems that SARS-CoV2 does not mutate. Instead, it creates variants which, somehow or other, is a completely different process to a mutation! I have found that language in this area means little, and words are simply twisted to suit a particular narrative.

I feel it is most likely this mutation occurred within a laboratory in Wuhan during gain of function research. But I don’t suppose we will ever know. It seems unlikely to be something that the Chinese authorities are ever going to admit… ever. As a general rule, the more fervently, and angrily, the Chinese state denies something – the more likely it is to be true.

This is a special case of a general rule that I modestly call the ‘Kendrick reverse meaning law.’ Which developed from P.G. Wodehouse’s observation that ‘When an Englishman says ‘trust me’ it is time to start counting the spoons.

This reverse meaning was seen clearly when Matt Hancock (UK Health Secretary at the time) stated that ‘Right from the start we’ve tried to throw a ring of steel around our care homes.’ Which actually meant that ‘Right from the start we threw care homes under a bus.’ Unless, what he actually meant was that the ring of steel was put up to stop care home residents escaping. ‘Halt, who goes there….’ Sound of heavy machine gun fire, whistles screeching, attack dogs baying at the leash. ‘Go for the Zimmer frames, that should bring them down.’

2: SARS-CoV2 is generally more deadly than influenza

Of course, SARS-CoV2 is most certainly not deadlier than the influenza epidemic of 1918-19. Which is estimated to have wiped out 2% of the entire world’s population. It is probably not more deadly than the 1957 epidemic, or the 1967 influenza epidemic. But it seems more deadly than anything in the last forty years, or so. So, a bit more deadly than most influenzas that sweep through humanity every year, or so. Give or take.

Currently, SARS-CoV2 is reckoned to have killed four and half million people across the Globe. Which is 0.07% of the world’s population. However, there is an immediate problem here. With influenza, we count for one year, then start again the next year. With COVID19 we have just kept on counting, adding this year figures to last years, and so on!

Eventually, therefore, assuming COVID19 comes and goes like the flu, and we just keep on counting without end, it will end up killing a hundred million. Making it the deadliest virus ever. Far worse than any influenza? At the current rate this will take another thirty years, or so. Within one thousand six hundred and sixty-six years it will have killed everyone. Of course, there will have been a few billion replacement humans created during that time.

What is far more important is to know the infection fatality rate (IFR)? That is, what percentage of those infected with SARS-CoV2 will die? This, I am afraid, we are never going to know, as the definition of what the word ‘infected’ means has flipped this way and that and can never be pinned down.

Does it mean a positive test? Does it mean a positive test plus symptoms? [Which used to be called a ‘case’] Does it mean something else. What does infected actually mean…

Here, I defer to the Master – Lewis Carroll:

‘When I use a word,” Humpty Dumpty said in rather a scornful tone, “it means just what I choose it to mean — neither more nor less.”

The question is,” said Alice, “whether you can make words mean so many different things.”

The question is,” said Humpty Dumpty, “which is to be master – – that’s all.”

Accepting that no-one will define what COVID19 infection actually means, I believe the infection fatality rate is, (using previous used definitions) settling at around 0.15%. At least it was last time I looked. This was never enough to justify the panicked actions that have taken place around the globe. Never.

3: The figures make no sense – and never will

One of the central problems here, form which all other problems flow, is that the PCR (polymerase chain reaction) test is the test against which the PCR test itself is tested. We have nothing better. So, we are completely reliant on it being accurate. However, we cannot know how accurate it truly is, because there is no test against which to compare it.

I mentioned Koch’s postulates earlier. These are the tests which can prove if a ‘micro-organism’ is actually causing the disease. The ultimate gold standard:

  • The microorganism must be found in abundance in all organisms suffering from the disease, but should not be found in healthy organisms.
  • The microorganism must be isolated from a diseased organism and grown in pure culture.
  • The cultured microorganism should cause disease when introduced into a healthy organism.
  • The microorganism must be re-isolated from the inoculated, diseased experimental host and identified as being identical to the original specific causative agent.

And good luck with all of that. The truth is that these postulates can work for bacteria, but not really for viruses. Because it is very difficult to meet them. I am not sure if they have ever been truly met for any virus.

On the matter of finding out if the virus is truly present, in anyone diagnosed with COVID19, here is a letter that was published in the BMJ in October last year

‘We are told that the virus is everywhere – in the air, in our breath, on fomites, trapped in masks – yet public health authorities seem not to be in possession of any cultivable clinical samples of the offending pathogen.

In March 2020, the World Health Organisation instructed authorities not to look for a virus but to rely instead on a genome test, the RT-PCR, which is not specific for SARS-CoV-2 (1) (2).

A Freedom of Information request to Public Health England about cultivable clinical samples or direct evidence of viral isolation has no information and refers to the proxy RT-PCR test, quoting Eurosurveillance (3).

Eurosurveillance states: “Virus detection by reverse transcription-PCR (RT-PCR) from respiratory samples is widely used to diagnose and monitor SARS-CoV-2 infection and, increasingly, to infer infectivity of an individual. However, RT-PCR does not distinguish between infectious and non-infectious virus. Propagating virus from clinical samples confirms the presence of infectious virus but is not widely available (and) requires biosafety level 3 facilities” (4).

The CDC admits that, “no quantified virus isolates of the 2019-nCoV are currently available”, and used a genetically modified human lung alveolar adenocarcinoma cell culture to, “mimic clinical specimen”(5).

It appears, therefore, that we have public health bodies without clinical samples, a test which is non-specific and does not distinguish between infectivity and non-infectivity, a requirement for biosafety level 3 facilities to even look for a virus, yet we are led to believe that it is up all our noses.

So, where is the virus?’





(5) 1

After reading this, do I still think SARS-CoV2 exists? Yes, I do. I firmly believe that I watched people dying of it, from it. They died in a way I have never seen people do so before, and I have seen a lot of people die. They seemed quite well, then suddenly their oxygen sats dropped like a stone – they still seemed okay otherwise – then they died. The end.

Very strange, and rather disturbing. I started slipping an oxygen saturation monitor onto my finger from time to time. Just in case. 99% is my average reading, if you are interested. It never dropped.

However, getting back to the testing. If you truly want to confirm the presence of a virus in a sample, you need to send it to biosafety level 3 facilities to isolate it, grow it (not really the correct word for a virus), and suchlike. This is never done in the clinical setting.

You could argue that if you wait for antibodies to develop, you can ‘prove’ that someone was infected, or not, and thus work out how accurate the PCR test has been retrospectively. Perhaps…

I speak as someone who needed seven Hepatitis B vaccinations before I produced any detectable antibodies. Did I have immunity after the first six, or not? Am I someone who simply does not make many antibodies, but still have immunity through other mechanisms?  Do others simply not produce antibodies, or their level drops so fast, that they effectively disappear?

Yes, serological testing (looking for antibodies), has its own very significant problems.

‘Serological tests for SARS-CoV-2 have accuracy issues that warrant attention. They measure specific antibody responses which may take some weeks to develop after disease onset reducing the sensitivity of the assay. If blood samples were collected during the early stage of the infection, they may produce false negative results. They do not directly detect the presence of the virus. Further, antibodies may be present when SARS-CoV-2 is no longer present giving false positive case diagnosis.’ 2

In reality, we are relying on a PCR test to diagnose SARS-CoV2 infection, the accuracy of which is entirely dependent on believing that the test is accurate. Yes, that is the route to madness.

At present, in the UK, we are doing about one million tests a day 3.

We are getting about thirty thousand ‘positive’ results. Or, about 3% positive. How many of these are truly positive? Well, you can take a wild guess on that one. At one point, the CDC stated that 30% of the PCR tests were false positives. A ‘false positive’ means that test says you have the disease, when you do not. [A false negative informs you that you do not have the disease, when you do] 4.

The thirty per cent cannot be the case currently, because that would mean if you did one million tests, you would get more than three hundred thousand false positives. Instead we are getting thirty thousand, which means that it is impossible for the false positive rate to be higher than three per cent.

So, what is the true rate? Well, if is three percent, then virtually every single positive test is a false positive test. [Three per cent of one million is thirty thousand] Which would mean that no-one in the UK currently has COVID19, and everything we are doing is completely pointless. It also means that people admitted to hospital with COVID19 do not have the disease, they are suffering from, and dying from, something else with a false positive COVID19 false test stamped on their forehead.

Is it possible that no-one actually is infected with SARS-CoV2? Well, it is certainly not impossible. Here is a graph of overall mortality (risk of dying of anything) from England. These figures, unlike most others, are pretty much fully reliable. Someone is either dead, or they are not. It is a difficult thing to get wrong, or manipulate. There can be some delay in registering a death, but this is not normally a major issue.

The graph starts in last quarter 2017. As you can see, a spike in overall mortality in Spring 2020, A spike in Winter 2020/21. Currently, no excess mortality at all. So, if COVID19 is infecting hundreds of thousands of people each week, it is not showing up as any excess deaths… at all 5.

Does this mean that COVID19 has gone, and we are rushing around panicking about false positive tests? Or is it still here? Still here I think… but who knows… who knows.

This is the main reason I have given up. I just don’t know what to believe – apart from overall mortality figures. The figures are spun and massage, twisted and mangled.

Another reason why I have given up trying to make any sense of COVID19 is the enormous differences in overall mortality seen in countries that are virtually identical in life expectancy, healthcare systems, actions taken against COVID19 etc. etc.

Afters studying the figures from England, I looked at the figures from Northern Ireland.

Both countries [yes, Northern Ireland is not actually a separate country, it is part of the UK] did almost exactly the same things when it came to COVID19. They both have the National Health Service, they are as close to each other as can be – in terms of COVID19, and most other things. Here is the graph of overall morality for Northern Ireland.

Which means that something very dramatic happened in England, with regard to COVID19? Yet nothing happened in Northern Ireland. This, to me, is fascinating, although I cannot explain it. However, I know that if you were able explain why these two graphs are so weirdly different, you will be unearthing some critical truths with regard to COVID19.

Of course, no-one is remotely interested in such anomalies. Instead, they point to a country like Norway and say – ‘Look how well they did with their rapid lockdown, and preventing people crossing the border’. No-one points to Northern Ireland and says, ‘look how well they did with all their….’ All their what? All their doing exactly the same as England.

Yes, Northern Ireland does not fit with the approved narrative, so it is ignored. Anything that does not fit with the mask wearing, social isolating, vaccination will save the world narrative is simply ignored.

Or it is shouted down or censored by the self-appointed Fact-checkers. Those mighty intellects who can determine what is true, and what is not. It was thoughtful of them to descend from Mount Olympus to mingle amongst feeble minded humanity and tell us what we should, and should not, be thinking. We must all be eternally grateful that the ‘Truth Gods’ now live amongst us, to firmly inform us all what, and how, we should be thinking. And shut us down if we veer from the official narrative.

Anyway, faced with a situation where there are almost no facts that can be relied upon, from anywhere, I have officially removed myself from all discussions on the matter of COVID19.

Instead, I shall return to other areas where, whilst the truth is constantly battered and bruised, and lying in a bruised heap the corner, it is still breathing … just about alive. Sometimes it is capable of weakly raising its head and whispering quietly into my ear. I shall let you know what it says.






Covid19 – the final nail in coffin of medical research

28th June 2021

“The lamps are going out all over Europe, we shall not see them lit again in our life-time.” Edward Grey

Several years ago, I wrote a book called Doctoring Data. It was my attempt to help people navigate their way through medical headlines and medical data.

One of the main reasons I was stimulated to write it, is because I had become deeply concerned that science, especially medical science, had been almost fully taken over by commercial interests. With the end result that much of the data we were getting bombarded with was enormously biased, and thus corrupted. I wanted to show how some of this bias gets built in.

I was not alone in my concerns. As far back as 2005, John Ioannidis wrote the very highly cited paper ‘Why most Published Research Findings are False’. It has been downloaded and read by many, many, thousands of researchers over the years, so they can’t say they don’t know:

‘Moreover for many current scientific fields, claimed research findings may often be simply accurate measures of the prevailing bias.’1

Marcia Angell, who edited the New England Journal of Medicine for twenty years, wrote the following. It is a quote I have used many times, in many different talks:

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

Peter Gotzsche, who set up the Nordic Cochrane Collaboration, and who was booted out of said Cochrane collaboration for questioning the HPV vaccine (used to prevent cervical cancer) wrote the book. ‘Deadly Medicine and Organised Crime. [How big pharma has corrupted healthcare]’.

The book cover states… ‘The main reason we take so many drugs is that drug companies don’t sell drugs, they sell lies about drugs… virtually everything we know about drugs is what the companies have chosen to tell us and our doctors… if you don’t believe the system is out of control, please e-mail me and explain why drugs are the third leading cause of death.’

Richard Smith edited the British Medical Journal (BMJ) for many years. He now writes a blog, amongst other things. A few years ago, he commented:

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

In 2002 I spent eight marvellous weeks in a 15th palazzo in Venice writing a book on medical journals, the major outlets for medical research, and the dismal conclusion that things were badly wrong with journals and the research they published. My confidence that ‘things can only get better’ has largely drained away.’

Essentially, medical research has inexorably turned into an industry. A very lucrative industry. Many medical journals now charge authors thousands of dollars to publish their research. This ensures that it is very difficult for any researcher, not supported by a university, or a pharmaceutical company, to afford to publish anything, unless they are independently wealthy.

The journals then have the cheek to claim copyright, and charge money to anyone who actually wants to read, or download the full paper. Fifty dollars for a few on-line pages! They then bill for reprints, they charge for advertising. Those who had the temerity to write the article get nothing – and nor do the peer reviewers.

It is all very profitable. Last time I looked the Return on Investment (profit) was thirty-five per-cent for the big publishing houses. It was Robert Maxwell who first saw this opportunity for money making.

Driven by financial imperative, the research itself has also, inevitably, become biased. He who pays the paper calls the tune. Pharmaceutical companies, food manufacturers and suchlike. They can certainly afford the publication fees.

In addition to all the financial and peer-review pressure, if you dare swim against the approved mainstream views you will, very often, be ruthlessly attacked. As many people know, I am a critic of the cholesterol hypothesis, along with my band of brothers…we few, we happy few. In the 1970s, Kilmer McCully, who plays double bass in our band, was looking into a cause of cardiovascular disease that went against the mainstream view. This is what happened to him:

‘Thomas N. James, a cardiologist and president of the University of Texas Medical Branch who was also the president of the American Heart Association in 1979 and ’80, is even harsher [regarding the treatment of McCully]. ”It was worse than that – you couldn’t get ideas funded that went in other directions than cholesterol,” he says. ”You were intentionally discouraged from pursuing alternative questions. I’ve never dealt with a subject in my life that elicited such an immediate hostile response.

It took two years for McCully to find a new research job. His children were reaching college age; he and his wife refinanced their house and borrowed from her parents. McCully says that his job search developed a pattern: he would hear of an opening, go for interviews and then the process would grind to a stop. Finally, he heard rumors of what he calls ”poison phone calls” from Harvard. ”It smelled to high heaven,” he says.’

McCully says that when he was interviewed on Canadian television after he left Harvard, he received a call from the public-affairs director of Mass. General. ”He told me to shut up,” McCully recalls. ”He said he didn’t want the names of Harvard and Mass. General associated with my theories.’ 2

More recently, I was sent a link to an article outlining the attacks made on another researcher who published a paper which found that being overweight meant having a (slightly) lower risk of death than being of ‘normal weight. This, would never do:

‘A naïve researcher published a scientific article in a respectable journal. She thought her article was straightforward and defensible. It used only publicly available data, and her findings were consistent with much of the literature on the topic. Her coauthors included two distinguished statisticians.

To her surprise her publication was met with unusual attacks from some unexpected sources within the research community. These attacks were by and large not pursued through normal channels of scientific discussion. Her research became the target of an aggressive campaign that included insults, errors, misinformation, social media posts, behind-the-scenes gossip and maneuvers, and complaints to her employer.

The goal appeared to be to undermine and discredit her work. The controversy was something deliberately manufactured, and the attacks primarily consisted of repeated assertions of preconceived opinions. She learned first-hand the antagonism that could be provoked by inconvenient scientific findings. Guidelines and recommendations should be based on objective and unbiased data. Development of public health policy and clinical recommendations is complex and needs to be evidence-based rather than belief-based. This can be challenging when a hot-button topic is involved.’ 3

Those who lead the attacks on her were my very favourite researchers, Walter Willet and Frank Hu. Two eminent researchers from Harvard who I nickname Tweedledum and Tweedledummer. Harvard itself has become an institution, which, along with Oxford University, comes up a lot in tales of bullying and intimidation. Willet and Hu are internationally known for promoting vegetarian and vegan diets. Willet is a key figure in the EAT-Lancet initiative.

Where is science in all this? I feel the need to state, at this point, that I don’t mind attacks on ideas. I like robust debate. Science can only progress through a process of new hypotheses being proposed, being attacked, being refined and strengthened – or obliterated. But what we see now is not science. It is the obliteration of science itself:

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

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

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

I was already pretty depressed with the direction that medical science was taking. Then COVID19 came along, the distortion and hype became so outrageous that I almost gave up trying to establish what was true, and was just made up nonsense.

For example, I stated, right at the start of the COVID19 pandemic, that vitamin D could be important in protecting against the virus. For having the audacity to say this, I was attacked by the fact checkers. Indeed, anyone promoting vitamin D to reduce the risk of COVID19 infection, was ruthlessly hounded.

 Guess what. Here from 17th June:

‘Hospitalized COVID-19 patients are far more likely to die or to end up in severe or critical condition if they are vitamin D-deficient, Israeli researchers have found.

In a study conducted in a Galilee hospital, 26 percent of vitamin D-deficient coronavirus patients died, while among other patients the figure was at 3%.

“This is a very, very significant discrepancy, which represents a big clue that starting the disease with very low vitamin D leads to increased mortality and more severity,” Dr. Amir Bashkin, endocrinologist and part of the research team, told The Times of Israel.’ 4

I also recommended vitamin C for those already in hospital. Again, I was attacked, as has everyone who has dared to mention COVID19 and vitamin C in the same sentence. Yet, we know that vitamin C is essential for the health and wellbeing of blood vessels, and the endothelial cells that line them. In severe infection the body burns through vitamin C, and people can become ‘scrobutic’ (the name given to severe lack of vitamin C).

Vitamin C is also known to have powerful anti-viral activity. It has been known for years. Here, from an article in 1996:

‘Over the years, it has become well recognized that ascorbate can bolster the natural defense mechanisms of the host and provide protection not only against infectious disease, but also against cancer and other chronic degenerative diseases. The functions involved in ascorbate’s enhancement of host resistance to disease include its biosynthetic (hy-droxylating), antioxidant, and immunostimulatory activities. In addition, ascorbate exerts a direct antiviral action that may confer specific protection against viral disease. The vitamin has been found to inactivate a wide spectrum of viruses as well as suppress viral replication abd expression in infected cell.’ 5

I like quoting research on vitamins from way before COVID19 appeared, where people were simply looking at Vitamin C without the entire medico-industrial complex looking over their shoulder, ready to stamp out anything they don’t like. Despite a mass of evidence that Vitamin C has benefits against viral infection, it is a complete no-go area and no-one even dares to research it now. Facebook removes any content relating to Vitamin C and COVID19.

As of today, any criticism of the mainstream narrative is simply being removed. Those who dare to raise their heads above the parapet, have them chopped off:

‘Dr Francis Christian, practising surgeon and clinical professor of general surgery at the University of Saskatchewan, has been immediately suspended from all teaching and will be permanently removed from his role as of September.

Dr Christian has been a surgeon for more than 20 years and began working in Saskatoon in 2007. He was appointed Director of the Surgical Humanities Program and Director of Quality and Patient Safety in 2018 and co-founded the Surgical Humanities Program. Dr. Christian is also the Editor of the Journal of The Surgical Humanities.

On June 17th Dr Christian released a statement to over 200 of his colleagues, expressing concern over the lack of informed consent involved in Canada’s “Covid19 vaccination” program, especially regarding children.

To be clear, Dr Christian’s position is hardly an extreme one.

He believes the virus is real, he believes in vaccination as a general principle, he believes the elderly and vulnerable may benefit from the Covid “vaccine”… he simply doesn’t agree it should be used on children, and feels parents are not being given enough information for properly informed consent.6

When I wrote Doctoring Data, a few years ago, I included the following thoughts about the increasing censorship and punishment that was already very clearly out in the open:

…where does it end? Well, we know where it ends.

First, they came for the communists, and I didn’t speak out because I wasn’t a communist

Then they came for the socialists, and I didn’t speak out because I wasn’t a socialist

Then they came from the trade unionists, and I didn’t speak out because I wasn’t a trade unionist

Then they came for me, and there was no-one left to speak for me

Do you think this is a massive over-reaction? Do I really believe that we are heading for some form of totalitarian stated, where dissent against the medical ‘experts’ will be punishable by imprisonment? Well, yes, I do. We are already in a situation where doctors who fail to follow the dreaded ‘guidelines’ can be sued, or dragged in front the General Medical Council, and struck of. Thus losing their job and income…

Where next?

The lamps are not just going out all over Europe. They are going out, all over the world.





5: 6:

Matt Hancock ‘I tried’

16th June 2021

This article first appeared in

As a GP working mainly with elderly patients in Care Homes and Intermediate Care I witnessed, at first hand, the absolute disaster that was the Government policy at the start of the COVID19 outbreak. Elderly patients who were COVID19 positive, or not tested, perhaps even negative, were simply shovelled out of hospitals and into care homes. ‘The hospitals must be cleared out… nothing else matters.

At the time there was no personal protection equipment (PPE) available… at all. In fact, in many care homes staff were actually ordered by the management not to wear PPE. This was also the case in hospitals. Not that it would have made a great deal of difference in most care homes where patients with dementia often wander happily from room-to-room without masks, and oblivious to any potential danger. I had to usher one or two out of the nurse’s office from time to time.

In my work with Intermediate Care patients, looking after those who were too well to be in an acute hospital bed, but not yet well enough to be at home, we were placed under massive pressure to just send everyone home. That is if they were COVID19 positive, or not, or untested, where they could spread it to their – often elderly – relatives. Alternatively, they could infect their carers who would then travel to the homes of other elderly people they were looking after, without PPE.

In fact, if you wanted to design a system of ensuring that every single, vulnerable person in the country gained full exposure to COVID19, you could not have a done a better job. I wrote several increasingly frustrated e-mails to various managers, but they simply stated they were just following policy so ‘you can’t blame me’. Policy set at the very top.

Here is an example of the type of e-mail I was sending in April 2020. You may sense the frustration (I have changed the names of the unit and wards for confidentiality reasons).

I think this is very simple, Unit A is currently ‘hot’. We have five patients and four staff ‘COVID positive’ swabbed. Eight patients have now died of COVID.

If we admit COVID negative patients into Unit A this is putting them at great risk of being infected. So, we should stop admissions. The only ones that should come in are those found positive, recovered, and 14 days post positive swab – at least.

Equally if we discharge patients, we are, almost certainly, spreading COVID around the entire care community. Until fourteen days have passed.

There is also a plan to send COVID positive patients to ward B, and keep Unit A as green (no COVID). The only way Unit A can be green is if we stop admitting patients. Because, once new patients reach Unit A they are likely to get infected, then another 14 – 21 days must pass. So, we will go round and round, forever.

Also, another plan is to send high risk staff to Unit A, and have low risk staff in ward B, so the staff will be swapped around. Again, Unit A is currently red hot. We will be endangering high risk staff if we send them to Unit A. Some of them will get infected. Then, they will incubate for 7 – 14 days. They will infect patients, and other staff, then they will go off sick. Then, some of them may well die.

The current plan seems to be to admit elderly vulnerable patients into a high risk COVID ‘hot’ environment and hope they don’t get COVID. We have already seen staff to patient transmission in Unit A. So, some of these patients will get infected, with a very high risk of dying….

In a way, it is hard to blame management who were trying to follow ever-changing edicts from above. Edicts often directly contradicting what they had been told the day before. It was chaos. Now, we have Matt Hancock, the UK Health Secretary stating, amazingly without being struck down by a lightning bolt, that he threw a ring of steel around care homes and elderly hospital units at the time. A… ring… of… steel. This was presumably to stop anyone escaping somewhere safer. Of course, he now says that the most important word in his statement is ‘tried’ as in ‘We tried to throw a ring of steel…’

This will now be his perfect defence. I didn’t say we succeeded, I only said that we tried. How completely pathetic. First, he did the exact opposite of trying. He put in place policies that were directly responsible for the massive number of deaths in care homes. He commanded that hospital were emptied out of elderly patients. What’s his next excuse. ‘Lots of the other countries did the same thing.’ Which is true. But you can hardly claim you are a leader, if all you managed to do was follow others down a disastrous policy failure.

How many deaths did this cause? Well, during the first wave of COVID19 it has been estimated that forty per cent of deaths occurred in care homes. Here from the Nuffield trust:

‘…the burden of the virus fell much more severely on care homes (relative to the population generally) in the first wave. Of the 48,213 COVID deaths registered between mid-March and mid-June, 40% were care home residents.’

There are around half a million residents in care homes, which is nought point seven per-cent (0.7%) of the entire population. Yet they had forty per cent (40%) of the deaths.

Yes, the elderly, especially those in care homes were most likely to die from COVID19. But this was known very early on. In Italy, where COVID19 first hit Europe, the average age of death was eighty two, and almost all of those who died had other, significant diseases.

If there was one population that needed to be protected it was elderly, vulnerable care home residents. Matt Hancock presided over policy decisions that threw care home residents under a bus. Now he is trying to claim he did all he could to protect them. Anyone who works in the health service, or in the care sector, knows exactly what he did.

COVID19 – the spike protein and blood clotting

3rd June 2021

When COVID19 came along I was in the midst of writing my latest book on heart disease. What causes it – and what does not.

One section I was working on covers the wide range of conditions known as the vasculitis(es). I could immediately see a whole series of connections between COVID19, spike proteins, the immune system and blood clots. Some of which are deeply concerning, for reasons that should become apparent.

Before getting started, you can see an immediate problem here is there does not seem to be a plural form of vasculitis. A bit like octopus. You can have one octopus, but what happens then… two octupuses… or is it two octopi? Wars have been fought over less.

Anyway, a vasculitis is a condition whereby a factor, of some sort, causes damage to the vascular system. The vascular system being, essentially, the blood vessels and the heart. The suffix itis simplymeans inflammation. As in appendicitis, or tonsillitis. Or, in this case vasculitis.

There are many different vasculitis(es) or vasculiti? They range from Kawasaki’s disease to antiphospholipid syndrome, rheumatoid arthritis, scleroderma, Sjogren’s disease and suchlike. They are many, and varied, and quite fascinating. At least they are, to me.

In all of them you have two things in common… that are most relevant to this discussion. First, with any form of vasculitis, the body decides to attack the lining of the blood vessels – causing inflammation and damage. Second, the rate of death from cardiovascular disease goes up dramatically. In some cases, a fifty-fold increase. This was seen in young women with Systemic Lupus Erythematosus (SLE) with additional antiphospholipid syndrome1.

Why does the body decide to attack itself? This is a good question that I cannot really answer. If I could, I would be claiming my Nobel prize, right now. However, I can say that, for various reasons, the immune system makes the decision that it doesn’t like something about the lining of the blood vessels and believes it to have become ‘alien’ in some way. It then proceeds to attack. Which does not answer the question as to exactly why the attack happens? But it does tell you a bit about what happens.

Another major problem with vasculitis is that blood clots spring to life throughout the vascular system. This is because the blood is always ready to clot, at any time, and if you take away some of vital the anti-clotting mechanisms, the balance will be tilted firmly towards coagulation.

One of the most powerful anti-clotting mechanisms/systems is the protective layer that lines your entire vascular system, known as the glycocalyx. This is made up of glycoproteins (glucose and proteins stuck together). Under an electron microscope the glycocalyx looks like a tiny forest, or a badly mown lawn.

Many fish are covered with glycocalyx, which makes them very slippery, and difficult to get hold of. The glycocalyx also stops bacteria and viruses from gaining entry, in both fish and humans.

In your blood vessels, the glycocalyx protrudes out from endothelial cells, the cells that line all your blood vessels, and into the bloodstream. The layer of glycocalyx contains many, many, anticoagulant factors. Below is a short list of all the things the glycocalyx does:

The glycocalyx:

  • Forms the interface between the vessel wall and moving blood.
  • Acts as the exclusion zone between blood cells and the endothelium.
  • Acts as a barrier against leakage of fluid, proteins and lipids across the vascular wall.
  • Interacts dynamically with blood constituents.
  • Acts as the “molecular sieve” for plasma proteins.
  • Modulates adhesion of inflammatory cells and platelets to the endothelial surface.
  • Functions as a sensor and mechano-transducer of the fluid shear forces to which the endothelium is exposed; thus, the glycocalyx mediates shear-stress-dependent nitric oxide production.
  • Retains protective enzymes (e.g., superoxide dismutase).
  • Retains anticoagulation factors, e.g.: Tissue factor inhibitor, Protein C, Nitric Oxide (NO), Antithrombin.

Complicated stuff – that hardly anyone has ever heard of.

Anyway, if you damage the glycocalyx, or damage the underlying endothelial cells that synthesizes the glycocalyx layer, you will tip the balance very strongly towards the creation of blood clots. These can then then stick to the artery, or vein, wall. Sometimes they will fully block a blood vessel, leading to such things as a stroke or heart attack.

The interaction between vasculitis and thrombosis has been a relatively unexplored area of medicine. But it remains critically important in many diseases:

‘The relationship between inflammation and thrombosis is not a recent concept, but it has been largely investigated only in recent years. Nowadays inflammation-induced thrombosis is considered to be a feature of systemic autoimmune diseases such as Systemic Lupus Erythematosus (SLE), Rheumatoid Arthritis (RA), or Sjogren’s Syndrome (SS)2.

In super-short version. If you damage the lining of blood vessel walls, blood clots are far more likely to form. Very often, the damage is caused by the immune system going on the attack, damaging blood vessel walls, and removing several of the anti-clotting mechanisms.


Moving sideways for a moment. There are other things that can damage the blood vessel wall, leading to widespread blood clot formation. One of them is the condition known as sepsis. Which used to be called blood poisoning.

In sepsis, bacteria gain entry to the bloodstream through such things as a cut, an insect bite, a severe urine infection, and suchlike. When bacteria get into the blood, and start multiplying, they release exotoxins. Which are, effectively, the waste products of the bacteria.

These exotoxins then attack blood vessel walls, damaging the glycocalyx and endothelial cells. This drives the formation of blood clots throughout the body. The medical term for this is disseminated intravascular coagulation (DIC) = widespread blood clots in the vascular system.

The attacks not only cause clots, they can also cause the smaller blood vessels to weaken and burst. Which is why one sign of an infection with the meningococcal bacteria (the one that causes meningitis), is a rash. The rash is made up of dark, almost black, bruises. Once these start to appear, things are very bad. Potentially fatal, it means blood vessels are under severe attack and are breaking apart. Creating both bleeding and clots.

In truth, the ‘rash’ in meningitis is not really a rash at all. It is a sign of underlying, severe, vasculitis. The individual small bruises can also be called petechiae. Just to be scientific.

Another sign of widespread blood vessel damage, with the formation of multiple blood clots, is that the level of platelets in the bloodstream falls dramatically. For those who have never heard of such things, platelets are small cells that float about in the bloodstream. Their primary role is to co-ordinate the blood clotting system. If a red blood cell was the size of the Earth, a platelet would be about this size of the Moon.

If there is damage to blood vessels, platelets fling themselves at the area, and stick together to form a solid plug. They also release chemicals and enzymes that cause fibrin to be formed. Fibrin is the long sticky strand of protein that binds clots tightly together. Platelets also drag in red blood cells, and suchlike to make bigger and tougher clots. They have been called the conductors of the clotting orchestra.

In the process of doing all of these things, the number of platelets starts to fall. This is not surprising, as they are being used up to make blood clots/thrombi. Which means that one sign of widespread clot formation is a fall in the level of platelets (thrombocytopenia). This reliable sign of widespread coagulation, or disseminated intravascular coagulation (DIC).

Time for a quick re-cap.

What do we know?

What we now know, on the journey towards COVID19, are three important things.

  • If you damage the endothelial cells/glycocalyx, blood clots will form and stick to the side of blood vessels.
  • Damage is often caused by immune system attack.
  • Falling platelet levels are a sign of widespread blood clotting.


What do we know about COVID19? First, it can only enter cells that have a receptor known as the angiotensin II receptor (ACE2 receptor). Cells with these receptors are mainly found in the lining of the lungs, and endothelial cells that line all blood vessels. Also, the epithelial /endothelial cells than line the intestines. If a cell does not have an ACE2 receptor, COVID19 simply cannot gain entry.

This was known years ago, when SARS-CoV was identified, the precursor of SARS-Cov2. Here from a paper in 2004:

‘The most remarkable finding was the surface expression of ACE2 protein on lung alveolar epithelial cells and enterocytes of the small intestine. Furthermore, ACE2 was present in arterial and venous endothelial cells and arterial smooth muscle cells in all organs studied. In conclusion, ACE2 is abundantly present in humans in the epithelia of the lung and small intestine, which might provide possible routes of entry for the SARS-CoV. This epithelial expression, together with the presence of ACE2 in vascular endothelium, also provides a first step in understanding the pathogenesis of the main SARS disease manifestations3.’

So, SARS-CoV gets into the body through the lungs and bowels. These are the places where the virus can gain access because it is where ACE2 receptors can mainly be found. Of course, SARS-Cov2 gets into the body in exactly the same way.

What happens once SARS-Cov2 gets into cells? Well, it does what all viruses do. It takes over various cellular mechanisms and forces the cell to produce more SARS-CoV2 viruses. This then kills, or severely damages those cells. This mainly occurs when ‘virions’ start to escape from within the cell. This damages the cell membrane, and in some cases can cause the cell to burst apart.

Essentially, SARS-Cov2 starts by damaging endothelial cells in the lungs, because it usually arrives here first. Fluid is released, and there is the breakdown of small blood vessels in the lungs, and the small airways. In this situation, the lungs begin to fail, and oxygen levels in the blood can fall dramatically.

Infection can also cause diarrhoea, as the epithelial cells in the intestines are damaged. To quote from ‘the COVID19 symptoms’ study:

‘We think COVID-19 causes diarrhoea because the virus can invade cells in the gut and disrupt its normal function 4.’

As far as I know, no-one has died of COVID19 diarrhoea. However, COVID19 can create such severe lung damage that people have died from respiratory failure or lung damage… call this form of disruption what you will. However, many/most people survive this phase.

It is what happens next that that kills the majority of people who become severely infected.

What happens next is that SARS-Cov2 gets into the bloodstream. It then invades endothelial cells, also pericytes and myocytes in the heart.  Both of which have a high level of ACE2 receptors. Both of which are kind of vital for heart function 5,6.


What we now have is a major widespread vasculitis on our hands, with severe endothelial cell damage and disruption and damage to the glycocalyx. Blood clots, blood clots, blood clots, everywhere.

‘Coronavirus disease 2019 (COVID-19) causes a spectrum of disease; some patients develop a severe proinflammatory state which can be associated with a unique coagulopathy and procoagulant endothelial phenotype. Initially, COVID-19 infection produces a prominent elevation of fibrinogen and D-dimer/fibrin(ogen) degradation products. This is associated with systemic hypercoagulability and frequent venous thromboembolic events. The degree of D-dimer elevation positively correlates with mortality in COVID-19 patients. COVID-19 also leads to arterial thrombotic events (including strokes and ischemic limbs) as well as microvascular thrombotic disorders (as frequently documented at autopsy in the pulmonary vascular beds). COVID-19 patients often have mild thrombocytopenia* and appear to have increased platelet consumption, together with a corresponding increase in platelet production.7

*a low level of platelets

The spike protein

Then, of course, we have the spike protein to consider. If this is the thing that the immune system recognises and attacks – which it almost certainly is – then cells which are growing SARS-Cov2 inside them, which then express the spike protein on their surface as the virions escape, will be identified as ‘the enemy’.

At which point, the immune system will start to attack the endothelium (and glycocalyx) in an attempt to wipe out the virus. This will tend to happen two or three weeks after the initial infection (sometimes sooner). This is after the immune system has had a real chance to identify the spike protein, then properly wind itself up to produce antibodies against it. This is the time of maximum attack on the endothelium.

This moment is often referred to as a cytokine storm. A point where every system in the immune system gets revved up and charges into action. At one point I wasn’t sure if I really believed in the cytokine storm. But I do now think it is a real thing. It is almost certainly why steroids (which very powerfully reduce the immune response) have been found to reduce mortality in severely ill patients.

All of which means it may well be the body’s own infectious disease defence system that creates much of the damage to the cardiovascular system. Not necessarily the virus itself.

Alternatively, it may be that the spike protein itself creates most of the blood clots. Here from the paper ‘SARS-CoV-2 spike S1 subunit induces hypercoagulability.’

‘When whole blood was exposed to spike protein even at low concentrations, the erythrocytes (red blood cells) showed agglutination, hyperactivated platelets were seen, with membrane spreading and the formation of platelet-derived microparticles8.’

Translation. Introduce SARS-CoV2 spike proteins into bloodstream, and it makes it clot – fast. Which is a worry.


It is a worry because the entire purpose of vaccination against SARS-Cov2 is to force cells to manufacture the spike protein(s) and then send them out into the bloodstream.

So, quick recap again, what do we know?

We know that a very high percentage of the people who die following a COVID19 infection, die as result of blood clots. We also know that they can also suffer severe myocarditis (inflammation of the heart muscle), and suchlike.

We know that the spike protein can stimulate blood clots all by itself.

We know that the immune system attack on ‘alien’ proteins, such as the spike protein, can cause vasculitis.

We know that vaccines are designed to drive the rapid production of spike proteins that will enter the blood stream specifically to encounter immune cells, in order to create a powerful response that will lead to ‘immunity’ against future SARS-CoV2 infection.

We know that a number of people have died from blood clots following vaccination. To quote from the European Medicines Agency website report on the AZ COVID19 vaccine:

‘The PRAC (pharmacovigilance risk assessment committee) noted that the blood clots occurred in veins in the brain (cerebral venous sinus thrombosis, CVST) and the abdomen (splanchnic vein thrombosis) and in arteries, together with low levels of blood platelets and sometimes bleeding 9.’

This was all pretty much predictable, if you understood what was going with SARS-CoV – nearly seventeen years ago.

My concern at this point is that, yes, we have identified very rare manifestations of blood clotting: cerebral venous sinus thrombosis (CVST) and splanchnic (relating to the internal organs or viscera) vein thrombosis (SVT). These are so rare that it is unlikely that anything else – other than a novel vaccine – could have caused them. I have never seen a case and I had never even heard of them before COVID19 came along. And I have spent years studying the blood coagulation system, and vasculitis, and suchlike.

So, if someone is vaccinated, then has a cerebral venous sinus thrombosis, or a splanchnic vein thrombosis, this is almost certainly going to be noted and recorded – and associated with the vaccination. Fine.

However, if there is an increase in vanishingly rare blood clots, could there also be an increase in other, far more common blood clots at the same time. If this was the case, then it would be far more difficult to spot this happening.

Millions and millions of people suffer strokes and heart attacks every year. Millions more suffer deep vein thrombosis and pulmonary emboli. In fact, around the world, tens of millions die each and every year as a result of a blood clots forming somewhere in the body.

That is a hell of a lot of background blood clotting noise. Which means that it could be extremely difficult to disentangle cause and effect, especially if you are not looking. If an elderly person is vaccinated, then dies of a stroke a couple of weeks later. What caused the blood clot that led to the stroke? It is unlikely that any doctor would record this as a post-vaccine adverse event.

To give you one example of the difficulty of disentangling cause and effect, when you are looking at very common events, a few years ago Merck launched a drug called Vioxx (an anti-inflammatory like ibuprofen, or naproxen but not exactly the same class of drug).  It didn’t go well. Here from the article ‘Merck Manipulated the Science about the Drug Vioxx.’

‘To increase the likelihood of FDA (Food and Drug Administration) approval for its anti-inflammatory and arthritis drug Vioxx, the pharmaceutical giant Merck used flawed methodologies biased toward predetermined results to exaggerate the drug’s positive effects. Internal documents made public in litigation revealed that a Merck marketing team had developed a strategy called ADVANTAGE (Assessment of Differences between Vioxx And Naproxen To Ascertain Gastrointestinal tolerability and Effectiveness) to skew the results of clinical trials in the drug’s favor.

As part of the strategy, scientists manipulated the trial design by comparing the drug to naproxen, a pain reliever sold under brand names such as Aleve, rather than to a placebo.’

The scientists highlighted the results that naproxen decreased the risk of heart attack by 80 percent, and downplayed results showing that Vioxx increased the risk of heart attack by 400 percent. This misleading presentation of the evidence made it look like naproxen was protecting patients from heart attacks, and that Vioxx only looked risky by comparison. In fact, Vioxx has since been found to significantly increase cardiovascular risk, leading Merck to withdraw the product from the market in 2004.

Tragically, Merck’s manipulation of its data—and the FDA’s resulting approval of Vioxx in 1999—led to thousands of avoidable premature deaths and 100,000 heart attacks.’

Yes, not exactly their finest hour. However, the point that I want to highlight from this sorry tale is that it is estimated that Vioxx caused 100,000 additional heart attacks, in the US alone, and nobody noticed. This figure was only worked out when researchers analysed the figures on increased risk, that had been seen in the clinical trials – at least the figures that were finally seen when Merck were forced to release the data.

You may think. How could one hundred thousand heart attacks simply be missed? Well, there are very nearly one million physicians in the US. If the heart attacks caused by Vioxx were evenly distributed, only one in five physicians would have seen anyone suffer because of taking Vioxx. In those physicians that did see one, or two, would they have made the connection? No, they would not. Not in a million years. There would not even be a record of any possible connection made.

Elderly person has a stroke, or heart attack. Elderly person took Vioxx. And…?

All of which means I am not gigantically concerned about CVST and SVT. Blood clots in these veins are rare, and remain rare, even after vaccination – and will never be missed, particularly when they happen in younger people. Because when younger people die, great efforts are made to establish the cause of death.

However, I can see no reason why these specific blood vessels would be targeted by blood clots. Perhaps there is some reason why clots only occur in the central venous sinus vein, or splanchnic vein following vaccination. If so, I have been unable to find out. I am more than willing to be educated on this.

Time to move on to the other worrying observation, that can be found within the report by the pharmacovigilance risk assessment committee (PRAC) – as mentioned above:

‘The PRAC noted that the blood clots occurred in veins in the brain (cerebral venous sinus thrombosis, CVST) and the abdomen (splanchnic vein thrombosis) and in arteries, together with low levels of blood platelets and sometimes bleeding.

One blood clot, in one relatively small vein, is not going to cause a low platelet level. Nor will it cause bleeding – a sign of very low platelet levels. Which means that those unfortunate people who developed CVST and SVT almost certainly had widespread problems with other clots as well. Then, for reasons unknown, they triggered these forms of, vanishingly rare blood clot. The ones that killed them. The ones that were recognised – because they are so rare.

I shall finish here. You can join the dots yourself. Or not.











COVID19 – the end of scientific discussion?

24th May 2021

I haven’t written a blog for a while. Instead, I have been sorting out two complaints about my blog made to the General Medical Council. Also, a complaint from NHS England, and two irate phone calls from other doctors, informing me I shouldn’t make any negative comments about vaccines.

For those in other countries, who don’t know about such things, doctors in the UK are ruled by many different organisations, all of whom feel able to make judgement and hand down various sanctions. The deadliest of them, the ‘Spanish Inquisition’ if you like, is the General Medical Council (GMC) who can strike you off the medical register and stop you working as a doctor. They have great power, with no oversight.

Prior to this, I had been phoned by, and attacked by, two journalists and a couple of fact-checking organisations that have sprung up which can decide your guilt or innocence with regard to any information about COVID19. Of course, no-one can check the fact-checkers. They are the self-appointed guardians of ‘truth.’ quis custodiet ipsos custodes – indeed. (Who guards the guardians?)

In truth they have not scared me off, just greatly annoyed me. The problem is that if they really decide to hunt you down, then you are wiped from the system. Dr Mercola, for example, is having to remove information from his site in great haste. Once wiped from the internet, it becomes very difficult for anyone to read anything you write or listen to anything you say. A major problem if this is how one makes a living.

I was removed from Wikipedia a couple of years ago, but I do have a couple of insulting pages on Rational W ( to take their place. Edited and controlled by – who knows?

I think it is the extreme wing of the Vegan party who decided to write my history, and thoughts, on rational Wikipedia. I say this because a large number of other people I know who are critical of the diet-heart hypothesis, those who dared to suggest that eating animal products is perfectly healthy, were also obliterated from Wikipedia at pretty much the same time.

I did rather like the idea of Wikipedia when it started, but it has been taken over by people, some may say zealots, with their own agendas. This is particularly true of a few scientific areas I am particularly interested in. Diet, heart disease and COVID19.

Frustratingly, there is nothing you can do if Wikipedia decides to wipe you out. There is no appeal. Those who have gained the power to edit Wikipedia are answerable to no-one. They rule their little empires with absolute power. They are, of course, exactly the sort of people who should have absolutely nothing whatsoever to do with science. Their minds were made up years ago. They have agendas, they are the anti-science, anti-scientist brigade.

The main purpose of science is to question and attack. To subject ideas to the greatest scrutiny.  Those who decide to shut down and stifle debate … whatever they may believe themselves to be doing, they are in fact traitors to the cause of science. Stranglers of the enlightenment, assassins of progress.

They are not alone, and things have got far worse, in the last year or so. Science has taken a terrible battering with COVID19, I have always known that dissent against a widely held scientific hypothesis is difficult.

Just trying to get published is a nightmare. The peer-review system is one of the many weapons used against innovative thinking. ‘Let’s see what the current experts think of this new idea which threatens to overturn everything they have researched and taught over the last thirty years, and have built their reputations on… I wonder if they will like it, and approve it?’

Experts certainly create a formidable barrier to change. As described by David Sackett (a founding father of evidence-based medicine) in his article ‘The sins of expertness and a proposal for redemption.

‘….It then dawned on me that experts like me commit two sins that retard the advance of science and harm the young. Firstly, adding our prestige to our opinions gives the latter far greater persuasive power than they deserve on scientific grounds alone. Whether through deference, fear, or respect, others tend not to challenge them, and progress towards the truth is impaired in the presence of an expert.

The second sin of expertness is committed on grant applications and manuscripts that challenge the current expert consensus. Reviewers face the unavoidable temptation to accept or reject new evidence and ideas, not on the basis of their scientific merit, but on the extent to which they agree or disagree with the public positions taken by experts on these matters.’ 1

And his proposal:

‘But there are still far more experts around than is healthy for the advancement of science. Because their voluntary retirement does not seem to be any more frequent in 2000 than it was in 1980, I repeat my proposal that the retirement of experts be made compulsory at the point of their academic promotion and tenure.’

Expertise is great. ‘Experts’… well, that is a completely different matter. We certainly have a few formidable ones kicking about with COVID19. In the UK we have the great and good of the SAGE committee made up of – who knows? – chosen for whatever reasons. They wield enormous power, and never disagree on anything. In the US we have Fauci and the CDC. Ditto.

In the background we have the WHO … who can tell you what way the wind is blowing if nothing else. They remind me of Groucho Marx’s famous comment. ‘These are my principles. And you if you don’t like them…. I have others.’ However, we at the WHO would like to make it clear that nothing about COVID19 has anything to do with China, in any way. Can we have more money please?

Anyway, where are we with COVID19, and science?

In my opinion COVID19 succeeded in breaking my last vestiges of faith in medical scientific research. I cannot believe anything I read. I accept no mainstream facts or figures.

We are told such utter nonsense. For example, the ‘fact. that vaccination protects against COVID19 more effectively than having had the disease itself… This is just utter nonsense.

We were told that COVID19 was spread by touching contaminated surfaces… Really? We were told it spread though droplets, not aerosols. Which is the most complete garbage. We were told that everyone has to wear a mask. We were told it could easily be passed on by asymptomatic people. Based on nothing at all. I could go on.

Yet, no-one seems remotely bothered by any of this utter nonsense. The public seem to lap it up, and attack anyone who questions the current narrative. I feel that I am clinging onto a dying religion. The religion of Francis Bacon and the enlightenment.

Baconian method, methodical observation of facts as a means of studying and interpreting natural phenomena. This essentially empirical method was formulated early in the 17th century by Francis Bacon, an English philosopher, as a scientific substitute for the prevailing systems of thought, which, to his mind, relied all too often on fanciful guessing and the mere citing of authorities to establish truths of science.

After first dismissing all prejudices and preconceptions, Bacon’s method, as explained in Novum Organum (1620; “New Instrument”), consisted of three main steps: first, a description of facts; second, a tabulation, or classification, of those facts into three categories—instances of the presence of the characteristic under investigation, instances of its absence, or instances of its presence in varying degrees; third, the rejection of whatever appears, in the light of these tables, not to be connected with the phenomenon under investigation and the determination of what is connected with it.2

This way of thinking it seems, lasted from 1620 to 2020. Four hundred years of immense scientific progress. The age of enlightenment. We are moving back to the prevailing systems of thought… on fanciful guessing and the mere citing of authorities to establish truths of science.

The Dark Ages are returning.