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.

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.

1: https://advances.augusta.edu/1014#:~:text=Interestingly%2C%20in%20Japan%20the%20reference,methylmalonate%20levels%20are%20not%20checked.

2: https://onlinelibrary.wiley.com/doi/full/10.1111/bjh.12959

3: https://www.nhs.uk/news/food-and-diet/the-new-guidelines-on-vitamin-d-what-you-need-to-know/

4: https://www.webmd.com/cancer/news/20111004/low-vitamin-d-levels-linked-to-advanced-cancers#1

5: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6540771/

6: https://pubmed.ncbi.nlm.nih.gov/23924693/

7: https://vitamindforall.org/letter.html

8: https://www.mayoclinic.org/healthy-lifestyle/nutrition-and-healthy-eating/expert-answers/vitamin-d-toxicity/faq-20058108#:~:text=Advertisement&text=The%20main%20consequence%20of%20vitamin,the%20formation%20of%20calcium%20stones.

9: https://eu.usatoday.com/story/news/nation/2013/12/19/dietary-supplements-executives-criminal-records-spiked/4114451/

10: https://ethics.harvard.edu/blog/new-prescription-drugs-major-health-risk-few-offsetting-advantages

11: https://academic.oup.com/emph/article/2019/1/221/5556105

12: https://onlinelibrary.wiley.com/doi/full/10.1111/j.1538-7836.2006.01903.x

13: http://www.jlr.org/content/32/2/317.full.pdf

14: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3869438/

15: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5707683/

16: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5622757/

17: https://diabetes.diabetesjournals.org/content/55/2/480

18: https://www.ncbi.nlm.nih.gov/pubmed/24554606

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: https://www.nice.org.uk/guidance/gid-ta10703/documents/1

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.

THERE IS NO EVIDENCE THAT INCLISIRAN WORKS

Let me rephrase the second sentence

THIS MEANS, THE CURRENT COST-EFFECTIVNESS ESTIMATES ARE NONSENSE

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

Introduction:

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


Postscript:

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:

NATIONAL INSTITUTE FOR HEALTH AND CARE EXCELLENCE

Single Technology Appraisal

Inclisiran for treating primary hypercholesterolaemia or mixed dyslipidaemia

[ID1647]

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.

1: https://publications.parliament.uk/pa/cm200708/cmselect/cmhealth/27/2707.htm

2: https://www.nice.org.uk/guidance/gid-ta10703/documents/final-appraisal-determination-document

3: https://jcbmr.com/index.php/jcbmr/article/view/35/75

4: https://pubmed.ncbi.nlm.nih.gov/28514624/

5: https://www.ctsu.ox.ac.uk/research/ctt

6: https://www.ctsu.ox.ac.uk/research/ctt

7: https://www.zoeharcombe.com/2014/08/ctsu-funding-from-drug-companies/

8: https://www.ctsu.ox.ac.uk/research/orion-4 9: https://www.nice.org.uk/guidance/gid-ta10703/documents/final-matrix

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.https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7373848/

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.

1:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6046589/

2: https://www.sciencedirect.com/science/article/pii/S1074761319300937

3: https://www.sciencedirect.com/science/article/pii/S1074761319300937

4: https://www.frontiersin.org/articles/10.3389/fmed.2018.00200/full

5: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4399148/

6: https://www.nature.com/articles/s41584-020-0474-5

7: https://ccforum.biomedcentral.com/articles/10.1186/s13054-020-03077-0

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?’

(1) https://www.who.int/publications/i/item/10665-331501

(2) https://www.bmj.com/content/369/bmj.m2420/rr-5

(3) https://www.whatdotheyknow.com/request/679566/response/1625332/attach/ht…

(4) https://www.eurosurveillance.org/content/10.2807/1560-7917.ES.2020.25.32…

(5) https://www.fda.gov/media/134922/download 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.

1: https://www.bmj.com/content/370/bmj.m3379/rr-2

2: https://systematicreviewsjournal.biomedcentral.com/articles/10.1186/s13643-021-01689-3

3: https://coronavirus.data.gov.uk/?_ga=2.38943459.111756282.1590603430-1775824629.1590603430

4: https://www.bmj.com/content/373/bmj.n1411/rr

5: https://www.euromomo.eu/graphs-and-maps/

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.

1: https://journals.plos.org/plosmedicine/article?id=10.1371/journal.pmed.0020124

2: https://www.nytimes.com/1997/08/10/magazine/the-fall-and-rise-of-kilmer-mccully.html

3: https://www.sciencedirect.com/science/article/pii/S0033062021000670

4: https://www.timesofisrael.com/1-in-4-hospitalized-covid-patients-who-lack-vitamin-d-die-israeli-study

5: https://www.researchgate.net/publication/14383321_Antiviral_and_Immunomodulatory_Activities_of_Ascorbic_Acid 6: https://off-guardian.org/2021/06/25/canadian-surgeon-fired-for-voicing-safety-concerns-over-covid-jabs-for-children/

Matt Hancock ‘I tried’

16th June 2021

This article first appeared in RT.com https://www.rt.com/op-ed/526539-catastrophic-care-homes-matt-hancock/

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.’ https://www.nuffieldtrust.org.uk/news-item/COVID-19-and-the-deaths-of-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.

Sepsis

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.

COVID19

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.

Then…

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.

Vaccines

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.’ https://www.ucsusa.org/resources/merck-manipulated-science-about-drug-vioxx

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.

1: https://www.intechopen.com/books/pregnancy-thrombophilia-the-unsuspected-risk/thrombophilia-in-systemic-lupus-erythematosus-a-review-of-multiple-mechanisms-and-resultant-clinical

2: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4399148/

3: https://pubmed.ncbi.nlm.nih.gov/15141377/

4: https://covid.joinzoe.com/post/covid-symptoms-diarrhoea

5: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2614534/ 

6: https://academic.oup.com/cardiovascres/article/116/6/1097/5813131

7: https://www.karger.com/Article/FullText/512007

8: https://www.news-medical.net/news/20210310/SARS-CoV-2-spike-S1-subunit-induces-hypercoagulability.aspx

9: https://www.ema.europa.eu/en/news/astrazenecas-covid-19-vaccine-ema-finds-possible-link-very-rare-cases-unusual-blood-clots-low-blood


 

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 (https://rationalwiki.org/wiki/Malcolm_Kendrick) 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.

1: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1118019/

2: https://www.britannica.com/science/Baconian-method

COVID19: Taking Stock

24th April 2021

What has happened with COVID19 has happened. All around the world Governments and their advisors have blundered about, all claiming they did absolutely the right thing. Maybe a bit slow in locking down here and there.

However, essentially, it is very clear that the COVID narrative has been written. It has been written by those in charge, who have far too much to lose if it is found to be nonsense. So, it is not going to change.

What was the narrative? I have never seen it formally written down, but I think it is pretty much as follows:

  • COVID19 is a new, mutated coronavirus, that is far deadlier than influenza. With an infection fatality rate of around 1%*.
  • In the UK, around 500,000 people were going to die from it. Around 2.5 million in the USA, unless action was taken.
  • It was going to overwhelm health services unless drastic action was taken. Therefore, even more people would die if we just let it run its course.
  • The agreed action was lockdown, which has now been demonstrated to be highly effective at lowering the rate of infection in all countries.
  • Masks are highly effective at reducing spread.
  • More generally, PPE is highly effective at reducing spread.
  • It can be spread by asymptomatic people to almost the same extent as those with symptoms.
  • It is spread by droplets, not aerosols, which is why masks are so important.
  • Herd immunity is not possible through allowing people to become infected naturally.
  • There would be far greater damage to the economy if we allowed it to spread unchecked, than would ever be caused by lockdown.
  • Virtually everyone recorded as dying of COVID19 has died of COVID19 – not with COVID19 – or from something else altogether.
  • Vaccination provides stronger immunity than catching the disease, overcoming it, and building up natural immunity.
  • Remdesivir is effective at controlling symptoms and saving lives.
  • Hydroxychloroquine, Zinc, Vitamin D, Ivermectin, Vitamin C are all completely useless and damaging and should not be given to anyone. Doctors prescribing them should be (and have been) struck off.
  • Steroids can dampen down the immune response and reduce mortality.

*No agreement on where it actually originated. However, China and the WHO have told us it couldn’t possibly, in any way, have been due to ‘gain of function’ research in a lab in Wuhan – so that’s been cleared up then. I am fully satisfied, and you should be too.

I have not referenced any of this, because you will all have seen these messages repeated… repeatedly. In one form or another.

How much of this is likely correct? Some of it? None of it?

I think there are two things on that list that I fully agree with. COVID19 is a new, mutated, coronavirus that is more deadly than (most forms) of influenza – in the elderly at least.

I don’t think anyone is yet arguing that COVID19 has been, or will be, deadly than Spanish flu. Whether or not the Russian flu of the 1890s was worse? Maybe.

The other major influenza epidemics of 1957 and 1967/8 were pretty bad, just as bad, possibly worse?

There were, again probably, fewer overall deaths, but the world’s population was only a half of what it is now. The figures on deaths are almost impossible to make sense of anyway.

The other thing I agree with is that steroids are effective in reducing mortality. If given at the right time. As for the rest of it? I think it is pretty much wall to wall nonsense from start to finish.

I believe that the images from China, with people apparently dropping dead in the streets, spooked almost everyone. Then, when Italy was first hit, there were the images of overwhelmed hospitals filling our television screens. At which point the glass was smashed and we hit the ‘we’re all going to die’ red button. Fear was unleashed.

It certainly all happened very suddenly. On March the 26th Anthony Fauci stated the following in the New England Journal of Medicine:

” If one assumes that the number of asymptomatic or minimally symptomatic cases is several times as high as the number of reported cases, the case fatality rate may be considerably less than 1%. This suggests that the overall clinical consequences of Covid-19 may ultimately be more akin to those of a severe seasonal influenza (which has a case fatality rate of approximately 0.1%) or a pandemic influenza (similar to those in 1957 and 1968) rather than a disease similar to SARS or MERS, which have had case fatality rates of 9 to 10% and 36%, respectively.” 1

In the UK, on the 19th of March 2020, we had the following statement from the Advisory Committee of Dangerous Pathogens (ACDP):

COVID-19 is no longer considered to be a high consequence infectious disease (HCID) in the UK”.

“The 4 nations public health HCID group made an interim recommendation in January 2020 to classify COVID-19 as an HCID. This was based on consideration of the UK HCID criteria about the virus and the disease with information available during the early stages of the outbreak. Now that more is known about COVID-19, the public health bodies in the UK have reviewed the most up to date information about COVID-19 against the UK HCID criteria. They have determined that several features have now changed; in particular, more information is available about mortality rates (low overall), and there is now greater clinical awareness and a specific and sensitive laboratory test, the availability of which continues to increase.

“The Advisory Committee on Dangerous Pathogens (ACDP) is also of the opinion that COVID-19 should no longer be classified as an HCID.

“The need to have a national, coordinated response remains, but this is being met by the government’s COVID-19 response.2

However, the doomsters had already managed to grab the narrative, and all attempts at scientific discussion were blown away. Fauci rapidly and completely changed his mind. COVID19 was, in fact, absolutely deadly and we must do absolutely everything possible to control it. At which point no-one else dared say anything else. Within a week the UK began, what is now called, Lockdown. An enormous, world altering decision had been made.

I find it slightly weird that, on March the 16th, Sir Patrick Vallance was recommending lockdown. Three days before this, the Advisory Committee of Dangerous Pathogens decreed that COVID-19 should no longer be classified as a high consequence infectious disease. Make your minds up guys.

Anyway, at some point in late March 2020, across the world the narrative had spread across the world like an iron curtain. There was to be no dissent from the party line. In the UK the BBC turned into the communications department for the Government, with health correspondents telling the public what they now needed to do. No longer reporting…instructing.

There was not, and has not been, the slightest attempt by the mainstream media to ask any serious questions about lockdown, or any other aspect of the actions taken. The opposition parties have all been falling over themselves to push more, ever tighter lockdowns, more punishment of offenders.

A ten-year jail sentence for making a mistake filling in a COVID questionnaire form. Yes, that is in place, although I very doubt anyone is ever going to be prosecuted for it. UK parliamentary democracy has been replaced by a dictatorship. No parliamentary scrutiny – at all.

In another sinister development, various agencies and fact checkers sprang into action. If you dared to question the narrative, you were subjected to the modern-day equivalent of the Spanish Inquisition. Accounts suspended, posts removed, access denied. Attacks raining down. At least you didn’t get burned at the stake – only your reputation went up in flames.

In stark contrast, a company called Surgisphere managed to publish an article in the Lancet, no less, claiming that hydroxychloroquine was useless. Which suited the narrative. It turned out they had simply made up their figures. In addition, they were closely financially connected with the pharmaceutical company that makes Remdesivir 3.

Where were the fact checkers on this …yes, completely silent, as they have been about anything in support of the narrative. On the other hand, dare to question the validity of, say, mask wearing, and they are down on you like a ton of bricks.

Levels of censorship like this have never been seen before in the West. Ever. Even the President of the US was being censored – by unelected and faceless individuals. Whatever you may have thought of The Donald, the office of President should command respect and it should have been several steps too far to shut him down.

In amongst all this censorship, where is the truth? Where are the facts? I am finding it very difficult to know. I consider myself pretty good at finding out what is going on, digging down to the truth. Analysing papers, sifting the evidence and suchlike. Helping others make sense of data. It’s kind of my thing.

Unfortunately, when I look to the voices on ‘the other side’ for balance they seem to have gone just as mad in the opposite directions. ‘Vaccination will kill hundreds of millions, women will be made sterile, it will drive the virus to mutate into a deadly, deadly, deadly, killer.’ Look, I am perfectly willing to accept that these vaccines were rushed through and may cause some significant health problems – some deaths. Which have already happened. But nothing destroys credibility faster than screaming blue bloody murder.

In my last blog I commented on a strategy known as OODA. Observe, orientate, decide, act. I have done a lot of observing. As for orientating. My current orientation is that everything we see around us has led from one error. As often happens.

The decision to lockdown was so massive, that it became impossible to question. If it was the wrong decision, all of those involved in making it would inevitably be held responsible for economic chaos, hundreds of thousands of unnecessary deaths, massive job losses and unprecedented social upheaval.

‘What was your legacy Boris’.

‘Well, harrumph, I made millions of people unemployed. In addition, by terrifying the public, I caused tens of thousands to stop attending hospital, who died unnecessarily. I blew four hundred billion, or thereabouts. I crushed personal freedoms. I prevented cancer diagnoses and treatments, and increased waiting lists by years – so people continued to suffer for years to come.’

‘Yes, but apart from that. How was lockdown?’

‘Well, to be quite frank, it achieved bugger all. Anyway, do you like my hairstyle. It does make people think I’m a bloody good chap.’

Can’t quite see anyone admitting to having made the greatest mistake in the history of the world. So now, everything is directed to the cause of ensuring that lockdown was seen to be the best thing to do, the only possible action that could have been taken. We had to the stop the infection spreading or everything would have been worse.

Anything, or any country, that does not follow that narrative has been attacked or explained away. For example, Sweden didn’t lockdown as much as the UK, or most other countries in Europe, and their actions have been ruthlessly attacked from all sides. They could not possibly be seen to have done better – than anyone. They have actually done far worse…look how badly it is going in Sweden… say what?

Standing in direct contradiction, but never commented on, it is simultaneously stated that they actually did lockdown. In fact, because the Swedes are so naturally law abiding, they locked themselves down. Suddenly everyone was a world leading expert on Swedish psychology.

Japan didn’t lock down. Ah, but they all wear masks, and don’t interact in the same way. Belarus didn’t lock down. Ah, but we don’t believe their figures. But we do believe the Chinese figures?

A randomised controlled study from Denmark showing that masks don’t really work was dismissed as useless and stripped apart by the Fact Checkers…. Studies from the US demonstrated that states that locked down tightly did no better than those that didn’t…. Oh, it was population density, atmospheric pressure, ethnic make-up, temperature. Throw whatever made-up evidence free explanation you like into the air.

This is the scientific equivalent of a fighter plane releasing chaff into the air to confuse and misdirect an incoming missile. You no longer have one target, you have thousands.

It is something I have been battled against in my cardiovascular research. Attack the ‘cholesterol hypothesis’ and it disintegrates into hundreds of different pieces in front your eyes. HDL, LDL, particle number, small dense LDL, light fluffy LDL, dyslipidaemia…. On and on it goes. A lifetime can be fully wasted examining each piece of chaff in minute detail. My advice, don’t bother, just learn to recognise chaff when you see it.

Which all gets us where?

Where, is that nothing is going to alter the direction of the narrative right now. It has the support of everyone in positions of power, almost everywhere around the world. Science is being bent to fit the narrative, and you can see it happening, if you know what to look for. Recently Boris Johnson stated that vaccination hasn’t really made any difference to falling rates in the UK, lockdown did the heavy lifting.

Why is he saying this? Because the pro-lockdowners are building the narrative fortress higher and higher to protect it from the inevitable future attacks. The likes of Imperial College London, and Neil Ferguson, who have massive responsibility for lockdown, can see there are now more and more scientists who are readying the evidence against lockdown. And it is starting to look strong.

A battle will be fought, and the pro-lockdowners are trying to get politicians to nail their colours fully to the lockdown side. They know that politicians around the world will happily throw all the pro-lockdown scientists to the wolves the moment it begins to look politically expedient. ‘They made us do it. We just followed their advice. Boo Hoo, it wasn’t my fault. Don’t be nasty to me.

Yes, we have realpolitik in place. Maybe we should call it realscientik. Neil Ferguson, and his ilk, pressed the emergency red button. It is a button they have been itching to press for years, decades. It is the ‘Here is the infection that is going to kill us all’ button. That infection may turn up at some point. COVID19 isn’t it. The button should never have been pressed.

The truth about the actions taken, and the true effectiveness of lockdown, and the damage of lockdown. This will not emerge for many years. By which time, the likes of Boris and Angela and Emmanuel, and Scott and Jacinda will be long gone, and won’t care. In my opinion there should be a reckoning. However, there won’t be.

1: https://www.nejm.org/doi/full/10.1056/nejme2002387

2: https://www.gov.uk/guidance/high-consequence-infectious-diseases-hcid?fbclid=IwAR0VTwze8V8AORcSTAiBHZjw502Qav36yg-5WtGPazMuyL4YeEpGrGXzmdY#status-of-covid-19

3: https://www.theguardian.com/world/2020/jun/10/surgisphere-sapan-desai-lancet-study-hydroxychloroquine-mass-audit-scientific-papers

A book on COVID by Sebastian Rushworth

8th April 2021

Early on in the COVID19 saga I came in contact with Sebastian Rushworth. He was, and is, working as an emergency care doctor in Sweden. It seemed we shared very similar ideas about what was going on. It was fascinating as he was working in Sweden, which has been attacked from all sides, for following WHO advice on the best actions to take in a pandemic.

Sweden did not fully lockdown, most schools remained open, as did bars and restaurants etc. As a result of this everyone died… Start again. As a result of this Sweden suffered around the average number of deaths (per head of population) in Europe.

European countries, above a certain size, that have done worse than Sweden, so far, include:

  1. Czechia
  2. Hungary
  3. Bosnia and Herzegovina
  4. Bulgaria
  5. Belgium
  6. North Macedonia
  7. Slovenia
  8. Slovakia
  9. Italy
  10. UK
  11. Portugal
  12. Spain
  13. Peru
  14. Croatia
  15. Poland
  16. France
  17. Lithuania

(NB: I left out micro-countries’ such as Gibraltar, San Marino, Andorra etc.)

You would think, from the howls of anguish that Sweden was now a smoking ruin, with hospitals full of the dead and dying. Which serves them bloody well right. They should have done what every other country did.

Anyway, it was interesting to link up with Sebastian to get a first-hand account of what was going on. You hear so much rubbish from the mainstream media, that it is difficult to know what is really going on. We live in a scary, censored world. Patrolled by self-appointed fact-checking dementors.

Sebastian has his own website at https://sebastianrushworth.com/ which I recommend as a good place for sensible thinking.

Now he has written a book. I should know, because he asked me to write the foreword for it, which I gladly did. It isn’t long, it is very readable, and you will learn a lot if you read it. It covers:

  • How Dangerous is COVID
  • Are the tests effective?
  • Does lockdown work?
  • Why did Sweden have more deaths than Norway?
  • Do face masks stop the virus?
  • Are the vaccines safe and effective?

I recommend it to everyone, and you can find a link to it on his website.

COVID19, hidden figures and OODA

20th March 2021

What figures about COVID19 do you believe?

Indeed, what figures can you believe?

Do you simply take them all at face value, and work from there? That would certainly be nice, but it’s not really possible, and you would come to some pretty weird conclusions.

For example, I was running through the Worldometer site the other day. Yes, what an exciting life I now lead.  Sitting right on top to each-other, on ‘deaths per million’ of the population were: Singapore, New Zealand and China. They are way down towards the very bottom of the list.

Deaths per million

  • Singapore (188) = 5 deaths per million (total deaths 30)
  • New Zealand (189) = 5 deaths per million (total deaths 26)
  • China (190) = 3 deaths per million (total deaths 4,636)

Just to give you a quick comparison with countries rather closer to the top of that list, where the deaths per million are around four hundred times higher, on average:

Deaths per million

Czechia (3)                                        = 2,206 deaths per million

UK (6)                                                = 1,843 deaths per million

USA (12)                                            = 1,649 deaths per million

Returning to Singapore, New Zealand and China. What do they have in common? From a COVID19 perspective they all locked down pretty hard. At least they say they did. They are all pretty wealthy countries. Apart from that… not much.

On the surface, there is nothing much to get excited, or confused about, yet. However, when you start looking a little more closely, you begin to notice stranger things. For example, if we look at total ‘cases.’

Total COVID19 cases

  • Singapore = 60,121
  • New Zealand = 2,432
  • China = 90,062

So, China with a population of 1.4Bn (One billion, four hundred million) had ninety thousand cases. Singapore with population of just over five and a half million, had sixty thousand cases. Just in case you cannot do the mental arithmetic. Singapore’s population is two hundred and forty-six times smaller than China’s.

Which means that Singapore had two thirds the number of cases in China – resulting in almost the same rate of deaths per million but in a population two hundred and fifty times smaller.

Where does this then take us? It takes us to a place where the case fatality rates are widely different. Not just between China and Singapore, but in all three countries. In fact, these figures are not even in the same ballpark. Not even in the same city. By case fatality rate (CFR) I mean the percentage of people with a clear-cut infection, who then died [terms and conditions apply].

Here are the resultant case fatality rates from the three countries, in order.

Case fatality rates

China                                                 = 5%

New Zealand                                    = 1%

Singapore                                          = 0.05%

Which means that, using the figures provided, the case fatality rate from COVID19 is one hundred times higher in China than in Singapore. Or, to put it another way, you are one hundred times more likely to die if you get COVID19 in China than in Singapore.

On the other hand, you are only twenty times more likely to die in New Zealand than in Singapore. So, should we all rush to Singapore and find out what on earth they can be doing to cure so many people. Or….

Yes, you’re right. These figures simply do not add up. Not even remotely. Medical interventions, sadly, have made very little difference to mortality rates from COVID19. A few percentage points here or there. So that cannot even remotely explain such massive differences.

What is the other explanation? It is, and can only be, that we cannot possibly be comparing like with like. Which, in turn, means that the figures in one, or all of these countries, are so incomplete, biased or wrong, as to be utterly useless.

Are they missing cases, or not counting cases, or defining cases and deaths from COVID19 in completely different ways? Whichever of these is true it doesn’t really matter. The only thing that really matters is that at least two of these three countries are reporting figures that are of absolutely no use to man nor beast. Perhaps all three.

Equally, if you’re planning what do to next in this pandemic, you must have figures that you can trust, otherwise you are simply floundering about in a sea of confusion. What’s the other choice. Delete the statistics from the countries where you simply do not believe them. And where would you start with that?

There is a military strategy called OODA: Observe, Orientate, Decide Act. It was used in the Gulf War, and by Dominic Cummins to achieve victory in the Brexit referendum – so it is claimed. It sounds simple, but it actually becomes complex, quite quickly.

With COVID19 you can observe all you like, and I have done a lot of observing. However, if the data you are looking at are clearly nonsense, it becomes impossible to orientate. Then, in turn, it becomes impossible to decide how to act.

It is why, up to this point, I have mainly contented myself with pointing out that the data that we have been presented with thus far is almost perfectly meaningless. Let’s consider another example. Which is that the gold standard for diagnosis of COVID19 is to use a system known as PCR (polymerase chain reaction). We do not use symptoms, or clinical signs, as has been the case for all other diseases known to humanity over the ages.  A major problem in itself.

Another major problem is we know that if you run PCR test processing for forty-five amplification cycles, the results become entirely meaningless. No-one will officially provide the data on how many cycles are being done. But it does seem that, in the UK at least, many labs were using forty-five cycles.

Now, the numbers of cases are falling, they have reduced PCR processing to thirty cycles. But, who knows?  Perhaps it is because they have reduced PCR to thirty cycles, that the cases have gone down. Or maybe it is the fact that we are using millions of lateral flow tests which has led to the number of positive tests falling. Because you get far fewer positive results with lateral flow kits than PCR.

In addition to that area of confusion and conflict, recorded deaths from COVID19 in the UK are based on having a positive test within twenty-eight days of dying. Yet we know that COVID19 tests can remain positive for months after someone has recovered. So, you can have had a positive test in November, go into hospital in January – for whatever reason – where you will have another test, that has remained positive. You then die of something completely unrelated. You become a COVID19 death statistic. What nonsense.

Even if you truly have COVID19, then die, how do we know if the main cause of death was COVID19, or something else? I have seen terminally ill patients close to death from cancer, or suchlike, who have had a positive swab. They then died, and they became another ‘COVID19 death.’ Really? Is that what killed them?

We do know that at least ninety-five per-cent of people who are recorded as dying of COVID19 had other serious medical conditions. Claiming that COVID19 was the primary/recordable cause of death in all of these cases is just ridiculous. Beyond ridiculous.

Frankly, anyone who asks me to trust in any data about COVID19 is going to have a pretty tough sell. Right now, I feel that there is almost no statistic which has not been wildly bent out of shape to suit the narrative.

At this point, I shall change direction slightly, and point you at the most incomprehensible statistic of all.

It comes from the UK. In this data set, the UK has been split into four countries. England, Northern Ireland, Scotland and Wales. Here, we are looking at the figures on overall mortality – that is deaths from all causes – during the period January 1st, 2017 up until the present day. These data cover the age group of forty-five to sixty-four (I set the graphs to specifically show this age group).

What you would expect to see, I think, is that all four countries that make up the UK should show almost exactly the same pattern of deaths. All four countries are virtually identical in their demographics, life expectancy, and suchlike. All four countries ‘locked down’ in almost exactly the same way, at almost exactly the same times.

Below, are the figures (z-scores/deviation from the mean) on overall mortality. https://www.euromomo.eu/graphs-and-maps#z-scores-by-country

We can see an enormous spike in England in the forty-five to sixty-four age group in Spring 2020, and Autumn/Winter 2021. We observe nothing, or virtually nothing, in the other three countries.

Just in case you are wondering. I do believe in these overall mortality data. If someone is dead, they are dead. It is difficult to misdiagnose or diagnose in any other way. So, these figures represent the real deal.

Observe, orientate, decide, act.

I observe that overall mortality rates went up sharply in England in the spring of 2020 and again in the autumn/winter of 2020/21 in the age group 45-64. I observe that the rates barely moved in Northern Ireland, Scotland or Wales.

Orientate

Something of great significance happened in England, that did not happen in the other three countries. I cannot orientate, because I have absolutely no idea what these figures are telling me.

Orientate

These data, unremarked open by anyone else – as far as I am aware – are trying to tell us something. Something that may well be of absolutely critical importance. These are the figures that we should be using to base our decisions and actions upon. If we could only understand what they were telling us.

There is one other country which has a pattern similar to England’s, and that is Spain.

Nowhere else looks remotely similar. For example, here is Sweden.

Orientate

What have England and Spain got in common? Or, at least, somewhat in common?

Decide

Do not decide anything until you are orientated. In turn, do not act until your decision is made on a good understanding of the environment you are operating in.

Do not decide what to do until you can explain why, for example, China has a case fatality rate that is one hundred times higher than in Singapore.

Equally, you cannot possibly claim to be orientated until you can explain why England, alone of all the countries in the UK, suffered such massive spikes in overall mortality in the forty-five to sixty-four year age groups.

In super-short summary, until you can rely on the figures that are provided from around the world, you cannot claim to be orientated.

Our glorious political leaders have decided that they are, indeed, oriented. Because of this false orientation, they have made decisions and acted. Based upon foundations of, precisely, nothing.

So, what are the odds that they acted in the right way?

What is an Anti-Vaxxer?

13th March 2021

I am particularly interested in the whole concept of being ‘anti-‘ or a ‘denier’, or a sceptic. I think in great part this is due to constant attacks I have had to put up with because of my views of cholesterol and statins. I am often called a statin ‘denier’. I have also been referred to as a professional contrarian, a sceptic, a zealot and suchlike. The best general insult was from Steven Nissen, perhaps the world’s most influential cardiologist:

‘A leading cardiologist has unleashed a blistering attack on “statin denial,” which he calls “an internet-driven cult with deadly consequences 1.”’

What a result! I am now, officially, a cult member. That is, in addition to all my other, myriad flaws. Or maybe it is my cult he was referring to, and other people have joined it. Who knows? The truth is that if I did actually manage to join a cult, or start a cult, I wasn’t aware of it. But then, that’s how they do it, they sneakily pull you in these invisible people with no obvious organisation.

‘It is the very fact that they don’t even exist that makes them so dangerous, my friend. Yes, they truly are that sneaky.’

A closely related insult is that I am part of a ‘sect’. People who read my blog are sometimes insultingly referred to as my ‘acolytes’, or ‘followers’, and so on and so forth. In truth, one thing I don’t think I have ever been called is ‘anti-statinator’, but it could have slipped by without me noticing.

I am often, though, called a cholesterol sceptic. Which is fair enough. I did join a loose alliance of doctors and researchers called The International Network of Cholesterol Sceptics (THINCS), so I can hardly object to being called one.

However, I am not actually a cholesterol sceptic, nor a denier. I am not denying cholesterol exists. I just happen to believe it is not harmful – probably beneficial. To be accurate, it is the other side who attack cholesterol and who should be called cholesterol sceptics. I am really an anti-anti-cholesterol sceptic. This must make me twice as bad. I am not just anti. I am anti-anti.

Do I object to all these attacks? Well, you know, to be perfectly honest, if you can’t take the heat you should stay out of the kitchen. In addition, I don’t think I would be doing things right if people were not hurling insults at me on a regular basis.

It also encourages me to carry on. Because, as Gandhi once said:

“First they ignore you, then they laugh at you, then they fight you, then you win.’

You may prefer Schopenhauer’s take:

‘First, it is ridiculed. Second, it is violently opposed. Third, it is accepted as being self-evident.’

Once you have reached the violent, ridiculing, insulting, stage you know you are pretty much directly over the target:

‘Bombs away! We will crack that bloody dam one way or another chaps – just don’t refer to my bloody dog by name, or we will never fly another mission.

Anyway, because of my personal history I have taken a particular interest in the matter of personal insults used as a debating technique. Rather than relying on the use of terribly boring tactics like facts, and data. Why debate when you can achieve the same result with a pinpoint laser guided insult?

It is something that has been around for a long time. Schopenhauer in his essay ‘The art of being right’ discussed thirty-eight ways to win an argument. It includes a few techniques that I see used regularly. ‘Appeal to authority rather than reason’ and ‘bewilder your opponent by mere bombast’. At number thirty-eight ‘Become personal, insulting, rude…argumentum ad personam.’

The sad fact is that number thirty-eight works brilliantly. Always has, and it seems that it always will. Find something, anything, a person has said at some point in the past. Use that to relentlessly attack them. Once you have destroyed their character and motivations that is, pretty much, that. It is not really an argument, of course, it is simply a way of stating, about someone else, that ‘you are a disgusting person, and no-one should listen to anything you say, ever again.’

This has echoes with the argument that Wagner was a Nazi (before there were Nazis), so no-one should ever listen to his music. I rather like his stuff, actually. Maybe a bit right wing in parts, a bit loud and brash, but there you go. Clearly not as acceptably left-wing as Debussy. Light and fluffy, wanders about, never really gets anywhere.

Nowadays, things have become far worse. You can spend your entire life building up a spotless reputation. Never do a single thing wrong, ever. But, if you dare to make one mistake, that can be the end of you, forever. This, the obliteration by personal insult, seems to have become more and more popular since the internet took over the world.

I recently read the book ‘So you’ve been publicly shamed’ by John Ronson. It describes people who, in some instances, said one thing, and one thing only, and their entire lives were shredded on-line – then off-line too. In several cases they hadn’t really said anything ‘wrong’. Although they had been rather clumsy in their use of words.

However, someone else had decided to interpret what they said in a certain way and then decided to become insulted. There was no judge, no jury, at work here. They were guilty – and gone. Dragged off by the baying mob for a metaphorical lynching.

The medical and scientific world are, sadly, no different, and never have been. If you hold views that the mainstream finds… finds… I am not sure what the exact word here is. Wrong, misguided, unacceptable, dangerous? Perhaps a combination of all four, and more, you are attacked with exactly the same level of implacable hatred.

A hero of mine is Dr Bernard Lown. Many decades ago, he and his mentor decided to stand against a piece of universally accepted medical dogma. Which was strict bedrest following a heart attack. These two dangerous fools, instead of forcing patients to lie virtually motionless in bed for six weeks, allowed them to sit up in a chair at the end of the bed. Shock, horror.

‘Although I knew that the project would be a chore, I didn’t expect it to be an act of martyrdom. Little did I realize that violating firmly held traditions can raise a tsunami of opposition. The idea of moving critically ill patients into a chair was regarded as off‑the‑wall. Initially the house staff refused to cooperate and strenuously resisted getting patients out of bed. They accused me of planning to commit crimes not unlike those of the heinous Nazi experimentations in concentration camps. Arriving on the medical ward one morning I was greeted by interns and residents lined up with hands stretched out in a Nazi salute and a “Heil Hitler!” shouted in unison.’ 2

It is now well recognised that strict bed rest is deadly, was deadly. An action that killed tens of million world-wide. However, those daring to question it were treated with Nazi salutes. A particularly galling insult for a Jew, I would imagine. And somewhat ironic, as strict bed rest probably wiped out more people than the Nazi’s ever managed.

Moving track to another hero of mine. I used to communicate with Thomas Gold now, sadly, dead. Although he did make it to eighty-four. He was a professor of astronomy at Cornell University. He also had many other broad scientific interests, which included Geology.

In the 1950s he was a great supporter of Alfred Wegener’s theory of tectonic plate movement – to explain the structure of the Earth’s surface. Gold, and anyone else who dared to support this ridiculous and idiotic idea, were flung out of any meetings of the American Geological Society. They were attacked and insulted and disbarred by the great and the good. He was denied tenure at Harvard but was hired by Carl Sagan instead. A good result, I would say. By the way, all geologists now fully support the tectonic plate movement hypothesis, and would viciously attack anyone who question it!

Gold was attacked again, decades later, for putting forward his ideas on the ‘abiogenic theory’ of petroleum generation. Basically, he believed that there is a lot of life deep down in the Earth’s crust, and it creates petroleum as a waste product, which seeps to the Earth’s surface, which then gets trapped in certain places.

‘Gold has been derided by geologists, such as Harmon Craig and John Hunt, who are strongly opposed to Gold’s abiogenic petroleum theory. Others had even started campaigns to prevent Gold from publishing his findings.3

Twice attacked and derided by the establishment. Attempts to prevent his work even being published. I am deeply envious. If you do enjoy a hypothesis that is widely considered ridiculous, then have a read around ‘The Deep Hot Biosphere’. If you are the sort who welcome ideas that seem whacky, you’ll love it. If you prefer to accept scientific consensus without challenge, I’d give it a miss.

So, where was I. Yes, the tried and tested use of derision and personal insults to destroy someone’s credibility. ‘Climate change denier…’ is another example. In this case you will not merely be a denier. ‘You’ are almost certainly being paid by the oil industry … in some way. Find any connection, no matter how tenuous, and pump it for all it is worth. Sorry, I have a pension fund that includes BP and Shell. I think …’burn the unbeliever.’

Now we have the deadliest insult of all. ‘Anti-vaxxer.’ Two relatively short words, but if you dare to touch them, they explode into maelstrom of poison that spreads far and wide, destroying anyone and everyone in range. Today, to mix my metaphors, there is probably no deeper abyss to be dropped into, than the abyss of being labelled an ‘anti-vaxxer.’

Of course, the term has no definition. It doesn’t even have any discernible boundaries. You can be wandering about quite innocently and suddenly find you have become an ‘anti-vaxxer.’ I mentioned that the phase III clinical trials on AstraZeneca’s COVID19 vaccine will not be completed until 2023.

This, it seems, to some people on a medical website called doctors.net makes me an anti-vaxxer. Highly suspicious at the very least ‘And vhy, Dr Kendrick do you find it necessary to point out such matters. Have no doubt my friend that ve shall be vatching you very closely in future.’ I think I am channelling Raiders of the Lost Ark here.

We have now reached the position where, to state an incontrovertible fact about a clinical trial, makes you an anti-vaxxer. Which means that there truly are no longer any places to go. If, that is, you want to discuss vaccines in any way.

The only approved position to take, particularly if you are a doctor, is the following… ‘All vaccines are entirely safe. They have no adverse effects, and they are one hundred per cent effective in all cases. Anyone who questions vaccines in any way does not understand anything about science and they are putting millions of lives at risk. In fact, they should probably be treated as criminals.’

Here is the view of one doctor, from the BMJ

‘….criminalising people who intentionally hurt others through false information should also be considered. The freedom to debate, and to allow the public to raise legitimate vaccine concerns to fill the knowledge void, should not extend to causing malicious harm 4.’

And who, exactly, is to decide what constitutes malicious harm? I feel that this would be a rather large step – backwards – for mankind. This moves well beyond obliterating someone’s reputation. We should be flinging anti-vaxxers in jail.

That will certainly help to silence the bastards. A little ‘anti-vaxx’ symbol to be delicately pinned onto clothing whilst outdoors, perhaps. Otherwise, they could be walking amongst you, killing your children and elderly relatives, and you wouldn’t even know. Maybe we should build special camps to house them in at the same time.

Goodbye age of enlightenment. So long scientific debate. Finally killed by COVID19. You will be missed. I hope some small groups may manage to keep the flame alive. Right now, it seems to have been stamped out.

1: http://www.cardiobrief.org/2017/07/24/nissen-calls-statin-denialism-a-deadly-internet-driven-cult/

2: https://bernardlown.wordpress.com/2011/02/03/a-chair-to-the-rescue/

3: https://en.wikipedia.org/wiki/Thomas_Gold

4: https://www.bmj.com/content/372/bmj.n272?utm_source=etoc&utm_medium=email&utm_campaign=tbmj&utm_content=weekly&utm_term=20210219

Believing in impossible things – and COVID19

6th March 2021

“Alice laughed: “There’s no use trying,” she said; “one can’t believe impossible things.”

“I daresay you haven’t had much practice,” said the Queen. “When I was younger, I always did it for half an hour a day. Why, sometimes I’ve believed as many as six impossible things before breakfast.”

1: ‘The Concept of Coronavirus Herd Immunity Is Deadly and Dangerous’ https://www.self.com/story/coronavirus-herd-immunity

Since COVID19 first hurtled over the horizon, before landing upon us all with great force, I find that I have been asked to believe in many impossible things. First, I was told that attempting to create herd immunity was not achievable. It would also be extremely dangerous and would inevitably result in many hundreds of thousands of excess deaths.

Then the vaccines arrived at fantastical speed and I was told that mass vaccination, by creating herd immunity, would be the factor that would allow us to conquer COVID19 and return to normal life. I am not entirely sure which of these things is impossible, but one of them must be.

2: ‘Vaccines, on the other hand, are believed to induce stronger and longer lasting immunity.’ https://www.huffingtonpost.co.uk/entry/does-the-vaccine-give-better-protection-than-having-fought-off-the-virus_uk_601c0663c5b62bf30754c563

I was then told the vaccine would provide greater immunity than being infected with COVID19. Which was interesting. I am not sure if this is actually impossible, but it seemed unlikely that anyone could make such statements after about three hundred people had actually been studied, and just two months had passed.

At the time I was aware of two people proven to have been re-infected with COVID19, out of about ten million cases. So, getting infected certainly seemed to provide a pretty good degree of immunity. A re-infection rate of 0.00005%

I also know that vaccinations can only ever really create an attenuated response. Whereas a full-blown infection triggers a full-blown immune response. So, I think it is pretty close to impossible that vaccination can provide greater protection than that from getting the actual disease. Which is why I think it is utterly bonkers we are actually vaccinating people who have circulating antibodies in their blood.

3: ‘Universal mask use could save 130,000 U.S. lives by the end of February, new study estimates.https://www.statnews.com/2020/10/23/universal-mask-use-could-save-130000-lives-by-the-end-of-february-new-modeling-study-says/

I am also being asked to believe that face masks are essential to stop the spread of COVID19 and prevent millions of deaths worldwide. The use of masks to prevent viral spread is something I actually researched in depth before COVID19 arrived (for various reasons), as did the WHO. They looked at non-pharmaceutical interventions for prevention of influenza, and produced a hefty report, which covered the use of masks.

Yes, I agree, influenza is not exactly the same as COVID19. But it is pretty much the same size of virus, and it is thought to spread in much the same way. Anyway, the WHO reported their views on masks in 2019, using data from randomised controlled trials (RCTs) – the gold standard.

‘Ten RCTs were included in the meta-analysis, and there was no evidence that facemasks are effective in reducing transmission of laboratory-confirmed influenza.https://apps.who.int/iris/bitstream/handle/10665/329438/9789241516839-eng.pdf?ua=1

Since then, there has only been one RCT done on COVID19 transmission, in Denmark. It did not find any significant benefit from masks in reducing spread. https://pubmed.ncbi.nlm.nih.gov/33205991/

Never has a trial been subjected to such immediate and hostile reporting. Fact-checkers (whoever exactly they might be, or what understanding they have of medical research) immediately attacked it. One such, called PolitiFact, made the following judgement, which amused me.

“Social media posts claim, “The first randomized controlled trial of more than 6,000 individuals to assess the effectiveness of surgical face masks against SARS-CoV-2 infection found masks did not statistically significantly reduce the incidence of infection.”

The study concluded that wearing masks did not offer a very high level of personal protection to mask wearers in communities where wearing masks was not common practice. The study noted, however, that the data suggested masks provided some degree of self-protection.

We rate this claim Mostly False. https://pubmed.ncbi.nlm.nih.gov/33205991/

So, according to PolitiFact, masks provided self-protection, but not personal protection. An interesting concept. Note to self, try to find out the difference between these two things.

In fact, this was just one of hundreds of critical articles, with self-anointed fact checkers clearly desperate to pull it to pieces. Yes, we have now entered a world when political fact checkers feel free to attack and contradict the findings of scientific papers, using such scientific terms as ‘Mostly false.’ Maybe they should have called it ‘very unique’ at the same time. Or, like the curate’s egg, that was good in parts.

Ignoring the modern-day Spanish Inquisition, and their ill-informed criticisms, I will simply call this study. More evidence that face masks don’t work. Perhaps someone will come along with a study proving that face masks work. So far … nada. Another impossible thing.

4: As of the 2nd March 2021 there have been 122,953 deaths from COVID19 in the UK.

Unlike many people I have actually written COVID19 on death certificates. Mostly they have been educated guesses. On at least five of them, early last year, there had been no positive swab to go on. So, I was just going on probable symptoms. As were many other doctors at the time.

Which means that you can take five off that number for starters. Although, of course, once written, that is very much, that … when it comes to death certificates. In fact, early on in the pandemic, we were probably underdiagnosing as often as over diagnosing deaths from COVID19. Although no-one will ever know. With no positive swab – and few swabs were being done – and almost no post-mortems – you were simply guessing.

As for now … NOW we have the very strange concept that any death within twenty-eight days of a positive COVID19 swab is recorded as a COVID19 death. Simultaneously, I am told that if I have a positive test at work, and then take some time off work (I can never remember the latest guidance). I am not to have another swab for ninety days.

How so? Because it now seems (I actually knew this a long time ago), that swabs can remain positive for months after the infection has been and gone [or was maybe never there to begin with]. Or to put this another way, you can have a positive swab long after you have been infected – and recovered. There are just some bits of virus up your nose that can be magnified, through the wonders of the PCR test, into a positive result.

Which means that an elderly person, infected months ago, can be admitted to hospital for any reason whatsoever. The they can have a positive swab – everyone is swabbed. Then they can die, from whatever it was they were admitted for in the first place. Then, they will be recorded as a COVID19 death.

In truth, this is just the start of impossible things when it comes to the number of COVID19 deaths. Do not get me started on PCR cycle numbers, and false positives. We would be here all day.

Equally, how many people have truly died of COVID19, instead of simply with COVID19? If I painted a blue circle on your forehead, then you died, I would not say that you died of a blue circle painted on your forehead. I would say that you died with a blue circle painted on your forehead.

5: The Swedish COVID-19 Response Is a Disaster. It Shouldn’t Be a Model for the Rest of the World

This was actually the headline title from an article in TIME magazine. The article went on to state that ‘The Swedish way has yielded little but death and misery. And this situation has not been honestly portrayed to the Swedish people or to the rest of the world.’  https://time.com/5899432/sweden-coronovirus-disaster/

Death and misery. Hmmmm, I might make this the title of my next book. Bound to be a best seller.

Yes, Sweden has been attacked from all sides with terrific venom, for holding out against imposing severe lockdown. How dare they… follow the WHO’s initial advice. That everyone else ignored.

So, have they done well with regard to COVID19 deaths? Not particularly. Have they done badly?Not particularly. On Worldometer they rank twenty fourth highest for deaths per million of the population. Which is pretty much bang on average for Western Europe.

One reason why they might not have appeared to do better is that, in the year 2019, they had their lowest rate of death for at least ten years. Three and a half thousand less in total than in 2018 https://www.statista.com/statistics/525353/sweden-number-of-deaths/ . In Norway, a country  used to beat Sweden with, due to their very low COVID19 deaths there was no difference in death rate between 2018 and 2019. To be blunt, the elderly population in Sweden had some catching up to do.

Once you factor this in, the much-lauded difference in deaths, between Norway and Sweden, kind of disappears.

‘Our study shows that all-cause mortality was largely unchanged during the epidemic as compared to the previous four years in Norway and Sweden, two countries which employed very different strategies against the epidemic. Excess mortality from COVID-19 may be less pronounced than previously perceived in Sweden, and mortality displacement might explain part of the observed findings.’ https://www.medrxiv.org/content/10.1101/2020.11.11.20229708v1.full

In absolute figures. Sweden had

  • 92,185 deaths in 2018
  • 88,766 deaths in 2019
  • 97,941 deaths in 2020

A drop, then a rebound. Perhaps another way to look at the figures is to compare 2020 with a bad Swedish year in the past. In 2012, 91,938 people died. However, the population was lower at 9.5 million vs 10.2 million. So:

  • The absolute death rate in 2012 was 0.957%.
  • The absolute death rate in 2020 was 0.969%.

The difference between 2012 and 2020 is 0.012%. That is 120 extra deaths per million of the population, which is 1,224 people in population of 10.2 million. The statistics tell us that twelve thousand people died from COVID19 in Sweden. Maybe you can make all that add up. Frankly, I find it impossible.

6: Lockdowns have worked.

Before COVID19 came along, no country had ever attempted a lockdown – ever. So, no-one had any idea if such a thing could possibly work. There was no evidence, from anywhere, to support its use.

It was the Chinese who started it, and who claimed great success for their jackboot lockdown tactics. Well, they convinced me… not. Frankly, if I had to choose a country from which to obtain high quality, unbiased information, about anything, China would not feature in my top one hundred and ninety-four countries

But there you go, lockdown worked under the control of the kind and caring CCP. Hoorah, cheering all round, and the first person to stop cheering gets shot. Well, we don’t want any damned nay-sayers, do we? After that, according to almost everything I have read, everywhere, it worked for everyone else too. Remarkable.

Yes, it is certainly true you can find countries that locked down, closed their borders, and kept the rates low. That, however, is not proof of anything at all. The scientific method requires a little more rigour than this.

In fact, the main thing that scientific rigour requires is that you specifically do not go around looking for facts that support your hypothesis. Because that, I am afraid, is the exact opposite of science. What you need to do, instead, is to go around looking for facts that disprove your hypothesis. This is what Karl Popper called falsification.

For example, my hypothesis is that “all swans are white”. I seek, and find, only white swans. So, this makes my hypothesis is correct? No. What science requires you do is to hunt tirelessly for black swans. If you never find one, fine. However, you need to be aware that the moment you do, your hypothesis has just been disproven. In real life things are very rarely as simple as this, but that is the basic principle.

However, with lockdown (and I recognise that no two countries locked down in the same way) the hypothesis is that countries which did not lockdown will have higher rate of death for COVID19 than those that did.

So, let us look, first, at the countries with the highest rate of COVID19. Excluding very small countries e.g., San Marino, or Gibraltar, we have, in descending order of deaths per million of the population https://www.worldometers.info/coronavirus/ .

  • Czechia
  • Belgium
  • Slovenia
  • UK
  • Italy
  • Montenegro
  • Portugal
  • USA
  • Hungary
  • Bosnia and Herzegovina
  • North Macedonia
  • Bulgaria
  • Spain
  • Mexico
  • Peru
  • Croatia
  • Slovakia
  • Panama
  • France

Every single country in this list carried out fairly strict lockdowns. The UK, apparently, has the strictest lockdown in the world, this winter.

Four countries that have been roundly criticized for having far less restrictive lockdowns are: Sweden, Japan, Belarus and Nicaragua (Realistically there are others, in poorer countries, where lockdowns have not happened – because they can’t afford it)

In these four ‘non-lockdowns’ countries, the death rate is, on average 391 per million.

In the top twenty ‘lockdown’ countries, the death rate is, on average 1,520 per million.

The only non-lockdown country in the top ninety for death rates is Sweden. It comes just below France, at number twenty-four.

Now, if the difference between lockdown and non-lockdown countries were ten per cent, or even fifty per cent, I would fully accept that there are many other variables that could explain such finding away. Although, of course, we should really look at a higher rate in the non-lockdown countries, not a lower rate.

Yet although this evidence is out there, I am being asked to believe that lockdowns work. At least the WHO agrees with me on this impossible thing. As Dr David Nabarro, the WHO special envoy on COVID19 said:

“We really do appeal to all world leaders, stop using lockdown as your primary method of control,” he said.

“Lockdowns have just one consequence that you must never ever belittle, and that is making poor people an awful lot poorer.” https://www.abc.net.au/news/2020-10-12/world-health-organization-coronavirus-lockdown-advice/12753688

Lockdowns, according to the WHO, in unguarded moments, have just one consequence. They make poor people an awful lot poorer.

‘Freedom is the freedom to say that two plus two makes four. If this is granted all else follows.’

How deadly is COVID19?

17th February 2021

I have spent large chunks of my life trying to untangle medial data and research. COVID19 has long since defeated me. I have been unable to make any sense of the information we are bombarded with daily. So, I decided to go back to basics.

At the start of the COVID19 saga, I was interested to know what the infection fatality rate (IFR) was likely to be. I felt I could then have a go at comparing it to other diseases, primarily influenza.

The infection fatality is the number of people infected with the virus who then die. This is very different to the case fatality rate (CFR), which is the number of people infected with the disease who become unwell enough (sometimes, but not always) to be admitted to hospital – the ‘cases’. Who then die.

Before COVID19 appeared, there used to be a reasonably clear distinction between the infection fatality rate (IFR), and the case fatality fate (CFR) and it is important that they should not get mixed up. Because the case fatality rate is almost always far higher than the infection fatality rate – as you would expect. People who are ill enough to go into hospital are far more likely to die than people who do not suffer any symptoms. Bear this in mind.

Another thing to bear in mind is that, at the start of any epidemic it is simpler to establish the case fatality rate, because most people who are seriously ill end up in hospital and/or will have tests to see if they have the disease in question. Those with no symptoms may never cross the path of a medical professional and are very unlikely to be tested.

What is the ratio between the two? It depends on the virus. With Ebola the infection fatality rate and case fatality rate are closely matched – more than fifty per cent of people who are infected, die. With the common ‘coronavirus’ cold, the spread is far wider, maybe a hundred to one, or a thousand to one – perhaps more.

The fact that most infections are never noted, is one of the reasons why the infection fatality rate for previous flu epidemics can vary so wildly from paper to paper. However, with influenza the CFR/IFR ratio has generally been estimated to be about ten to one. By which I mean that, for each ten infections, one will be severe, and it is amongst the severe infections that you get the deaths.

Armed with such knowledge, and assuming COVID19 had a similar case: infection ratio to influenza you could have a go at working out the infection fatality rate. Always bearing in mind that people with no symptoms, who are not tested, are very unlikely to appear in any figures.

You are always guessing – to some degree or another.  

However, you always know three things:

1: The infection fatality rate must always be lower than the case fatality rate.

2: The case fatality rate will appear to fall as less severely infected people are tested.

3: The infection fatality rate will also appear to fall as more people with no symptoms are found to have had the infection.

For example, in China, at the start of the COVID19 pandemic, the infection fatality rate was reported to be three to four per-cent. This rapidly fell. Then it went up a bit, then it fell, then it went up. Then, everyone started giving different figures. The highly influential Imperial College group, led by Professor Neil Ferguson, decided to use an infection fatality rate of 0.9% for their modelling.

Somewhat later on, John Ioannidis, an influential figure in the world of medical research, estimated the infection fatality rate to be 0.27%. This was a couple of months after the Imperial College figure was published 1.

Peter Gotzsche, who established the highly regarded Nordic Cochrane collaboration, put the figure even lower than this. He looked at a study in Denmark, where blood donors were tested for antibodies. Using these data, the researchers established an infection fatality rate of 0.16% 2. Other figures came in higher, some lower.

The most tested population in the World – per head of population – is Iceland. Last time I looked, Iceland had 6,033 ‘cases,’ and twenty-nine deaths. This represents a case fatality rate of 0.5%, which suggests an infection fatality rate of 0.05% 3.

However, these figures I am quoting from Iceland come from a time after everything changed. At some point, difficult to put an exact date on this, it was decreed that if you had a positive PCR COVID19 test, with or without symptoms, you were to be defined as a case. No matter if you had symptoms, or not. This had the result of making the infection fatality rate, and case fatality rate, the same thing. Suddenly, all cases are infections, and all infections are cases.

Which means that any comparisons of the infection fatality rate with COVID19, and other diseases became virtually meaningless. The infection fatality rate suddenly shot up to match the case fatality rate, which point I gave up trying to work out the infection fatality rate. I doubly gave up when I tried to find out the accuracy of the PCR tests. Were these tests over-diagnosing, or under-diagnosing?

So, I thought I would turn my attention to the population fatality rate instead. That is, how many people has COVID19 killed in a population, or country. This figure is the bald, unvarnished, death rate. It does not, necessarily, tell you how many people have been infected. It does not tell you the percentage of cases, that die. It simply tells you how many people have died… with COVID19 written somewhere on their death certificate. [Or even not written on their death certificate]

At present, in the UK, the total number who have died is one hundred and seventeen thousand. This represents a population death rate of 0.17%. if you knew how many people had been infected, in total, you could work out the infection fatality rate from this. But we don’t know how many people were infected, and now we never will. Because so many people are now being vaccinated. They will show antibodies, and it will not be known if that is because of an infection, or due to vaccination.

So, where to turn to next. If you look at the entire world, the current figure of COVID19 deaths, on the fourteenth of February, stood at 2,406,689 3. Which is a little over one in three thousand, or 0.033%. How many people in the world have been infected? Nobody knows that answer to this question. There are some countries that have done very little testing, others far more.

On the basis that there are so many questions, with very few clear-cut answers, I thought I would try to compare the two point four million figure with previous influenza epidemics.

A study was done in 2016, looking at the influenza epidemic of 1957 – one of the worst in recent history. They extrapolated the mortality figures from 1957 to 2005, because the World’s population doubled during that time period (I am not entirely sure why they chose 2005). Their conclusion was that a flu epidemic of similar magnitude to that of 1957 could kill two point seven million people.

‘In conclusion, our study fills a gap in the availability of global mortality estimates for historical influenza pandemics, which can help guide pandemic planning. Our model extrapolates 2.7 million influenza-related deaths (95% CI, 1.6 million–3.4 million deaths) should a virus of similar severity to the 1957 pandemic influenza A(H2N2) virus return in the 2005 population, which is intermediate between global estimates for the 2009 pandemic (0.3 million–0.4 million deaths and a devastating 1918-like pandemic (62 million deaths; range, 51 million–81 million deaths)’ 4.

Extrapolating onwards to 2020, where the population is significantly greater than in 2005, then the figure from the 1957 epidemic would now be just over three million deaths. Which means that, up to this point COVID19 has been thirty per-cent less deadly than the influenza epidemic of 1957 – per head of population.

If the Imperial College infection fatality rate of 0.9% is accurate, once around eighty per cent of the world’s population has been infected [at which point population wide immunity would be reached] we should see fifty-four million deaths. We are currently nowhere near that figure, and at the current rate of deaths, per year, it will take twenty-two and a half years to reach the fifty-four million figure.

Of course, people will argue that this outbreak is far from over, and millions more will certainly die. Yes, more people will die, but the current number of new cases and deaths is falling pretty rapidly worldwide, rather than rising. We may reach three million, we may not. It is exceedingly hard to believe we would ever have reached fifty-four million even without any vaccines.

So, how deadly is COVID19? It seems, so far, to be equivalent to a bad flu pandemic. Worse than most in recent times. However, it seems to have had an extremely variable impact.

In Singapore, there have been nearly sixty thousand ‘cases’ and twenty-nine deaths. A case fatality rate of around one in two thousand, or 0.02%. The UK has had four million cases and one hundred and seven thousand deaths. A case fatality rate of 3%. Therefore, if you get COVID19 you are one hundred and fifty times more likely to die of it in the UK, than in Singapore 3.

Yes, I went back to basics and the figures still didn’t make any sense.

 

1: https://www.who.int/bulletin/online_first/BLT.20.265892.pdf

2: https://www.bmj.com/content/371/bmj.m4509/rr

3: https://www.worldometers.info/coronavirus/

4: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4747626/

Does Lockdown work, or not?

27th January 2021

This blog was published on RT-com, after much discussion and a few changes. It can be seen here  It took a few days. The editors were concerned about the fact-checkers having a go at it and demanding retraction.

We went back and forward. I assured them that all my quoted facts were correct, so the fact-checkers could only attack the ‘opinion’ stated. Which they may well do. If so, fact checkers are no longer checking facts, they are decreeing which scientific opinions are correct, and which are wrong.

Which puts them in a very dangerous place indeed. We do not know who the fact checkers are, we do not know how much they are paid, we do not know what editorial control is exerted over them. We know nothing about them, yet their pronouncements are decreed final on all matters.

This is the recreation of Soviet show trials of another era. “We know you are guilty, you will be found guilty, all that is required of you is that you admit your guilt. We, the judges in this case, however, are subject to no control, no-one can find us in the wrong, or punish us in any way.”

Anyway, the main concerns of Russia Today were that I did not look at enough variable factors. What about population density? What about secondary lockdowns etc. I replied it was impossible to assess all variables fully. I sat and thought about the confounding variables inherent in lockdown, that you would probably need to include in any study on them:

Number of tests carried out
False positives
False negatives
How deaths are recorded/validated
Population density
Percentage of population living in cities [not the same as population density]
Population density within cities
Number of single person households
Average age of population
Age distribution
Percentage of ethnic minorities
Primary ethnicity of population
Number of people with multimorbidity’s
ICU beds per head of population
Time of first lockdown
Time of relaxation of first lockdown
How well lockdown measures were followed.
Time of second lockdown
Restrictions within lockdowns curfews etc.
Test and trace set-up
Vitamin D levels
Northern or Southern hemisphere
Strain 1 COVID
Strain 2 COVID
Strain 3 COVID
Air pollution
Main method of commuting, underground, buses etc.

That’s just for starters.

The total number of interactions between these twenty-seven factors is twenty-seven factorial 27 x 26 x 25….x 3 x 2 x 1

Which is …

10,888,869,450,418,352,160,768,000,000 possible interactions.

So, if anyone says you have not taken the interactions of all variables into account, you can say that this is – effectively – impossible. Perhaps they would like to demonstrate they have done so.

I also pointed out I was not the only person to believe that lockdowns had little, or no effect on transmission rates and death from COVID. Here is part of an article from South Africa, based on the paper ‘COVID-19 in South Africa’

The article was published on Prevention Web:

Lockdown didn’t work in South Africa: why it shouldn’t happen again

By Benjamin T H Smart, Alex Broadbent and Herkulaas MvE Combrink

At the start of October, the World Health Organisation (WHO) and the Chinese government lauded South Africa’s response to the global COVID-19 pandemic. Yet data concerning both the spread of the virus and the indirect consequences of the lockdown suggest that the severe restrictions imposed in South Africa – some of the strictest in the world – were far from effective.

We recently reviewed the evidence for the effectiveness of the lockdown at slowing the spread of the pandemic. The mitigation strategies initially implemented may well have gone some way to “flattening-the-curve” – that is, reducing the rate at which the virus spreads through the population. But we found no decline in either daily new cases or deaths between around 27 March, which was the first day of level 5; and the latter part of July, when cases began to tail off during level 3.

Lockdown level 5 in South Africa was one of the world’s strictest. Citizens weren’t allowed to leave their residence except for essential purposes such as grocery shopping and medical care. All non-essential businesses were shut down, and cigarette and alcohol sales were banned.

If this “hard lockdown” had been effective, the rate of infection would have dropped significantly 7-14 days after lockdown was implemented. Note that one must look for a delay due to the disease’s 5-6 day average incubation period, and time for test results to be released. This simply did not happen.

Of course, the number of cases did increase over time, but what counts is whether the rate of increase changed when lockdowns changed. We found no such changes. As lockdown restrictions were relaxed and South Africa entered levels 4 and 3, when much of the economy re-opened and restrictions on movement were substantially reduced, there was no increase in the rate of infection.

In fact, during level 3, the pandemic peaked. And as the country entered level 2, the pandemic started to recede. If lockdown regulations were having the intended effect, one would expect the rate of infection to spike as restrictions were relaxed. This did not happen…..

Here is the article that first appeared in RT-com:

The scientific evidence so far on COVID lockdowns suggests that they don’t work – and may actually increase the death rate

We are being told that lockdowns halt the spread of the infection, but where’s the proof? The places with the worst death rates all followed that path – and the ones who didn’t have generally fared better. 

‘Paradoxically, human beings, when compelled to act, learn to justify a chosen course with an assurance unwarranted by the evidence for the course chosen.’ Bernard Lown.

I have studied the history of medicine, and medical interventions, for many years. The most extreme disasters have always followed a fairly distinct pattern. A series of steps, if you like.

Step one = we have a serious disease that is killing lots of people.

Step two = it creates great fear, and the medical profession has nothing much in place to deal with it.

Step three = a charismatic leader emerges to decree that he (almost always a ‘he’ up to now) knows how to treat it/control it, etc. This is ‘the idea’.

Step four = The ‘idea’ is enthusiastically taken up around the world and becomes mainstream thinking.

Step five = the ‘idea’ becomes standard practice.

Step six – the ‘idea’ is taught to medics and becomes accepted truth, a fact.

Step six = anyone who goes against the ‘idea’ is ruthlessly attacked.

There is always, of course, the possibility that the ‘idea’ is the best thing to do. This happens from time to time. However, there seems to be little or no correlation between the enthusiasm, and speed, with which ideas are taken up, and the likelihood they are correct.

The problem, as I came to recognise, lies between step two and step four. By which I mean that a charismatic figure convinces everyone that they have the answer, before there is any evidence to support it. The person may not be charismatic, simply someone who has the ability to grab attention and push the ‘idea’ forward. Such as the Chinese Premier.

Another thing that leads to disaster, which is perhaps of even greater importance, is that the ‘idea’ must sound like the most obvious common sense. It should trigger a response along the lines of ‘Yes, of course, that sounds perfectly reasonable’. Once that’s been achieved, the ‘idea’ drops neatly into people’s minds, settles down, and grows roots, creating not a ripple of cognitive dissonance.

At which point it cements itself in, and becomes difficult, even painful, to remove.

To quote the film Inception: ‘What is the most resilient parasite? Bacteria? A virus? An intestinal worm? An idea. Resilient… highly contagious. Once an idea has taken hold of the brain it’s almost impossible to eradicate. An idea that is fully formed – fully understood – that sticks; right in there somewhere.’

We love ideas, they make us who we are. We defend them, sometimes with our very lives.

“Why do people insist on defending their ideas and opinions with such ferocity, as if defending honour itself? What could be easier to change than an idea?” J.G. Farrell.

So, yes, I have no illusions about the strength of ideas. They are so powerful, and so dangerous that you must be very careful where you aim them. Because ideas also have a God-like power, which is that they are immortal.

The damage inflicted by medical ideas

You can kill a person who holds an idea. You can kill thousands of people who hold the same idea – but you cannot kill that idea. Unless you kill every single person who believes in it, then wipe it from the historical record, so that no-one can ever think it again. See 1984.

I will give you a couple of examples of horribly damaging medical ideas. The first is the radical mastectomy. An idea first driven by William Halsted, a US surgeon from the end of the nineteenth century. He believed, as did almost everyone else at the time, that breast cancer spread locally – as did all cancers. Therefore, anything located anywhere near the cancer had to be cut away in case it had already been polluted.

With a radical mastectomy the entire breast, the other breast, muscles on the chest wall, lymph nodes, more muscles were cut out. Almost anything that could be removed without actually killing the women in the process.

The mutilated women were immensely grateful, and the surgeons proud of their expertise. They were doing a good thing, because the idea was considered to be inarguably correct. Questioning it was to be met with the response like, ‘Do you want these women to die – you heartless swine?

Except that it wasn’t correct. Breast cancer does not spread locally. At least, when it does, it does so very slowly. The spread that causes problems, and kills women, is not local. Cancer cells get into the lymphatic system, and the bloodstream, and spread widely around the body, very early on. Often, long before the primary cancer can be detected.

Those who questioned the radical mastectomy, were attacked. Geoffrey Keynes, brother of John Maynard, tried less radical surgery in the 1920s. It did not go down well:

‘Halsted’s followers in America ridiculed this approach, and came up with the name “lumpectomy” to call the local surgery. In their minds, the surgeon was simply removing “just” a lump, and this did not make much sense. They were aligning themselves with the paradigm of Radical Mastectomy. In fact, some of the surgeons even went further to come up with “superradical” and “ultraradical” procedures that were morbidly disfiguring procedures where the breast, underlying muscles, axillary nodes, the chest wall, and occasionally the ribs, part of the sternum, the clavicle and the lymph nodes inside the chest were removed. The idea of “more was better” became prevalent.’

More is better… this is another of the deadly repeating themes of ‘the idea.’ The idea can never be wrong, it is just that people are not doing with sufficient vigour. If women are still dying from metastatic breast cancer, even after radical mastectomies (and they were), the answer could not possibly be that the procedure doesn’t work. The answer is that we are not being radical enough: ‘Hack away more, and then more.’

 ‘I was greeted with hands stretched out in a Nazi salute’

Another big medical idea is that of bed rest following a heart attack. It was thought, at one time, that all heart attacks were fatal. James Herrick, another US doctor, described the first non-fatal heart attack in 1912, then suggested that following such an attack, strict bed rest was important. This would take pressure off the heart and allow it a chance to heal. Again, this sounds perfectly reasonable. As described by Dr Bernard Lown, a professor of cardiology and the developer of the  defibrillator:

“To a medical novice like me, the justification for enforced bed rest was persuasive. It was based on a sacrosanct therapeutic principle, the need to rest a diseased body part, be it a fractured limb or a tuberculosis-affected lung. Unlike a broken bone, which could be immobilized in a cast, or a lung lobe, which could be collapsed by inflating the chest cavity with air, the heart could not be cradled into quietude. The only approximation for a diseased heart was to diminish its workload. It was long known that during recumbency the heart rate slows and blood pressure drops, both indices of less oxygen usage and therefore of decreased cardiac work. Heart rest was therefore equated with bed rest.”

And so it became standard practice. It was simply what you did:

“Patients were confined to strict bed rest for four to six weeks. Sitting in a chair was prohibited. They were not allowed to turn from side to side without assistance. During the first week, they were fed. Moving their bowels and urinating required a bedpan. For the constipated, which included nearly every patient, precariously balancing on a bedpan was agonizing as well as embarrassing.

“Because world events might provoke unease, some physicians prohibited their patients from listening to the radio or reading a newspaper. Visits by family members were limited. Since recumbency provoked much restiveness and anxiety, patients required heavy sedation, which contributed to a pervasive sense of hopelessness and depression. Around one in three patients died.”

Bed rest started as a relatively mild thing. However, as it is with almost all things, it became increasingly ‘radical’. Lown, along with his mentor Dr Samuel Levine, tried to change this. He became involved in trying to get patients up out of bed to sit in a chair:

“Little did I realize that violating firmly held traditions can raise a tsunami of opposition. The idea of moving critically ill patients into a chair was regarded as off‑the‑wall. Initially the house staff refused to cooperate and strenuously resisted getting patients out of bed. They accused me of planning to commit crimes not unlike those of the heinous Nazi experimentations in concentration camps. Arriving on the medical ward one morning I was greeted by interns and residents lined up with hands stretched out in a Nazi salute and a “Heil Hitler!” shouted in unison.”

Step six = anyone who goes against the ‘idea’ is ruthlessly attacked

No evidence, no problem

Then, among all the other problems with ‘the idea’, between steps two and three, is one that I have not yet mentioned. It is that no study is ever done to find out if the idea works, or not. It is just conceived to be so obviously beneficial, such common sense, that there would be no point in wasting time and resources trying to prove it works.

No-one ever did a study to find out if the radical mastectomy improved survival. No-one ever did a study to prove that bed rest saved lives. They were both introduced on the back of absolutely nothing. In time, eventually, the folly of both was finally recognised. It took seventy years for radical mastectomy, fifty for bed rest.

Which takes us to lockdowns. The most expensive, invasive, and potentially destructive medical intervention ever attempted by humanity.  Was there any evidence from anywhere, in history, that lockdowns would work? No, there was none. But we have the six steps on full display here.

Step one = we have a serious disease that is killing lots of people – check.

Step two = it creates great fear, and the medical profession has nothing in place to deal with it – check.

Step three = a charismatic leader emerges to decree that he (almost always a ‘he’ up to now) knows how to treat it/control it etc. This is the ‘idea’ – check.

Step four = The ‘idea’ is enthusiastically taken up around the world and becomes ‘mainstream thinking’ – check.

Step five = the ‘idea’ becomes standard practice – check.

Step six – the ‘idea’ is taught to medics and becomes accepted truth, a fact – check.

Step six = anyone who goes against the ‘idea’ is ruthlessly attacked – check.

Does it work – have lockdowns worked? You can pick and choose countries to support the case that it does and dismiss any evidence you don’t much like. Unfortunately, once you introduce a medical intervention that affects everyone, everywhere, you have lost the possibility of carrying out a controlled experiment of any sort.

Despite the lack of any randomised evidence, most people are absolutely convinced that lockdowns work to control the spread of COVID-19. They point to various countries, e.g. New Zealand, Norway, Australia and Taiwan, to prove their case. They always have a ready explanation as to why countries that underwent lockdown still have high death rates and vice-versa.

The ‘idea’ has become the truth. Its proponents now demand that those who doubt the efficacy of lockdowns prove that they don’t work. However, I don’t believe it’s up to those who don’t believe that lockdowns work, to prove that case.

The starting point, for any scientific hypothesis, is for the proponents to disprove the null hypothesis. Demanding that those who believe something may not work, to prove that it doesn’t, is to turn the scientific method upside down. You can never prove a negative.

The null hypothesis, by the way, is that there is no difference between two things. Randomised Controlled Trials (RCTs) in medicine are designed to prove, statistically, that there is an actual difference between doing A or B. This is how science is done, how research is done.

We must look carefully at the death rates

Unfortunately, it is not possible to do a controlled trial with COVID-19. The possibility of doing any randomised study was lost very early on. Which means that we are forced to rely, instead, on observational studies. We can look at country X, that did Y, and see how it compares with country Z that did not do Y.

Or we can look at two countries that did Y, to see how they compare. Or two countries that did not do Y. With COVID, of course, no two countries did exactly the same thing. Not even the four ‘countries’ within the UK. So any observations become more difficult to rely on due to this ‘confounding variable’.

In some UK countries, six people could meet up, in others it was eight, or two households, or only one household etc. In some, restaurants were open, in others they were shut – at varying times. From a scientific perspective, it’s a mess.

Anyway, to simplify things, let’s look at the 10 countries around the world with the highest death rate from COVID. That is, deaths per million population (I have left out countries with population of less than one million, such as Monaco, or Liechtenstein, or Andorra because a few deaths here or there can distort the death rate considerably)

What did they do differently, what did they do the same? Looking only at first lockdown dates:

Belgium first locked down on March 18th, 2020.

Slovenia first locked down on March 20th, 2020.

Czechia first locked down on March 16th, 2020.

The UK first locked down March 23rd, 2020.

Bosnia-Herzegovina first locked down March 16th, 2020.

Italy first locked down March 9th, 2020.

North Macedonia first locked down March 18th, 2020.

The USA is highly federal and different states took different approaches – seven states did not issue lockdown orders: Arkansas, Iowa, Nebraska, North and South Dakota, Utah, and Wyoming. In those seven states the death rate from COVID averaged at 1,280 per million vs. 1,254 as the US average.

In comparison, New Jersey first locked down March 21st, 2020, and its current death rate is 2,310 per million. New York locked down on March 12th – its current death rate is 2,130 per million. These states have the highest COVID related deaths in the US.

Bulgaria first locked down on March 13th, 2020.

Hungary first locked down on March 28th, 2020.

All countries locked down, Italy first, Hungary last.  As you can see, the date of first lockdown is unrelated to the death rate. The other stand out facts are that these are all ‘European’ countries. All with majority Caucasian populations. They are all in the Northern hemisphere.

If I were thinking of running a clinical trial where the hypothesis was that a lockdown was the best way to prevent deaths from COVID, then I would start by looking at observational data such as this.

I would find that the ten countries in the world with the highest death rates all locked down at similar times, with similar restrictions.

I would look at the US where the death rate in states that locked down, and those that did not, were almost the same rate (or vastly higher in the cases of New Jersey and New York), and I would conclude that the observational studies had – thus far – failed to disprove the null hypothesis. In fact, the evidence up to this point could suggest that lockdowns may actually increase the death rate.

In short, I would look for another idea.

What is left to say?

30th December 2020

I have not written much about COVID19 recently. What can be said? In my opinion the world has simply gone bonkers. The best description can be found in Dante’s Inferno, written many hundreds of years ago.

In it, Dante describes the outcasts, who took no side in the rebellion of angels. They live in the vestibule. Not in heaven, not in hell, forever unclassified. They reside on the shores of the Acheron. Naked and futile, they race around through a hellish mist in eternal pursuit of an elusive, wavering banner, symbolic of their pursuit of ever-shifting self-interest.

I find this description of the desperate pursuit of an elusive wavering banner rings rather true. This, it seems, is pretty much the place we have arrived at. Which banner have you decided to follow?

The ‘COVID19 s the most terrible infection ever, and we must do everything in our power to stop it, whatever the cost’ banner.

Or the ‘What on earth are we doing? This is no worse than a bad flu, and we are destroying the world economy, stripping away basic human rights and killing more people than we are saving’ banner.

There may be others.

Between these two, main, completely incompatible positions, lies the truth. It is in pretty poor shape. It has been crushed, and bent out of shape, smashed, and left as a broken heap in the corner. I search where I can, to find the fragments, in an attempt to bring together a picture that makes some kind of sense.

But what to believe? Who to believe?

I feel somewhat like Rene Descartes. In order to find the ineluctable truth he scraped everything away until he was left with ‘Cogito, ergo sum’. ‘I think, therefore I am.’

I have stripped away at the accuracy of PCR COVID19 testing. I found myself left with nothing I could make any sense of. I hacked down to establish the way that COVID19 deaths are recorded. All I found were assumptions and difficulties.

Did someone die with COVID19, of COVID19 – or did it have absolutely nothing whatsoever to do with COVID19? Who knows? I certainly don’t, and I wrote some of the death certificates myself.

Have we overestimated deaths, or underestimated deaths? I do not know … and so it goes on.

So, what do I know? I know that COVID19 exists – or I am as certain of this as I can be. Was it a natural mutation from a bat, or was it created in a laboratory? Well, I suppose it doesn’t really matter. It’s here, and there is no chance that any Government, anywhere, would ever admit responsibility for creating the damned thing. So, we will never know. If you asked me to bet, I would say it was created in a lab, then escaped by accident.

Is it deadlier than influenza? Well, it is certainly deadlier than some strains of influenza. Indeed, most strains. However, Spanish flu was estimated to have killed fifty million, when the world’s population was about a fifth of what it is now. So, COVID19 is definitely less deadly than that one. About as deadly as the influenzas of 1957 and 1967. Probably.

Will it mutate into something worse? Who knows.

Will the current vaccines work on mutated strains? Who knows.

Can it be transmitted by asymptomatic carriers? Who knows.

How effective are the current vaccines going to be? Who knows.

What are we left with?

At the beginning, I kept relatively quiet on how deadly COVID19 would prove to be. Because I didn’t know. The figures raged up and down. The infection fatality rate become a battle scene, with warriors lined up on either side to defend their positions.

I even got attacked by factcheckers, the self-appointed know-it-alls who are, it seems, capable of judging on all matters of scientific dispute. Truly, the Gods have descended to live amongst us. Those who can determine what is true, and what is not. No need for any further clinical trials, or any more scientific studies of any sort, ever. We just need to ask the Fact Checkers for the answer, to any given question.

Anyway, it appeared that tens of thousands died in some countries, almost none in others. What I was waiting to see, was the impact on the one outcome that you cannot alter, or fudge. The outcome that is overall mortality i.e. the chances of dying, of anything.

I did this because, when it comes to recording deaths from a specific illness, things can go in and out of fashion. A couple of years ago I looked at deaths from sepsis. At one time this was a condition of far lower priority. Doctors didn’t routinely search for it, or routinely record it, on death certificates.

Sepsis is an infection that gets into the blood, toxins are released, and people die. Everyone knew it happened. Or at least I hope they did.

Then, all of a sudden, there was a gigantic push to look for it more diligently, diagnose it more, treat it better. I think this was generally a good thing. Sepsis is eminently treatable, if you think to look for it, and lives can be saved. We now have initiatives like ‘Sepsis six’ and warnings that pop up on computers. ‘Have you considered sepsis,’ and suchlike. I love it … not. Because I do not love being told how to think, and do my job, by a computer algorithm programmed with ‘zero risk’ as their touchstone. But, hey ho.

In 2013, in the UK, a report was published by the health ombudsman ‘Time to Act – severe sepsis, rapid diagnosis and treatment saves lives.’ As the report stated.

‘Sepsis is a more common reason for hospital admission than heart attack – and has a higher mortality.’ The UK Sepsis Trust 1

That last statement is somewhat disingenuous, as many people with sepsis are very elderly, often with multiple morbidities, and suchlike. They were probably going to die, shortly, from something else.

Anyway. With all this activity, with all this increased sepsis recognition and treatment, you would expect the rate of deaths from sepsis to fall. It did not. The rate has gone up, by around 30% since 2013. Does this mean there is far more sepsis going about? Or, that it is just more often written on death certificates? I suggest the latter. I use this example, simply to make it clear that even the cause of death written on a death certificate is far from rock solid evidence.

With COVID19, this is a massive problem. In the UK, and several other countries if you have had a COVID19 positive test (which may, or may not, be accurate) and you die within twenty-eight days of that positive test, you will be recorded as a COVID19 death. I do not know much for sure about COVID19, but I do know that is just complete nonsense.

There are so many cases where – even if the COVID19 test was accurate – COVID19 would have had nothing whatsoever to do with the death. Another thing known, or at least we probably know, is that the vast majority of people who die had many other things wrong with them.

In the US, the Centre of Disease Control (CDC) found that ninety-four per cent of people who died of COVID19 ‘related deaths’ had other significant diseases (co-morbidities) 2.  This ninety-four per-cent figures would only be the co-morbidities that were known about – who knows what lurked beneath? Especially as people stopped doing post-mortems (i.e., autopsies in the US).

So yes, they had COVID19 (or at least they had a positive test – which may not be the same thing), but they were often very old, and already severely ill. Using an extreme example, someone with terminal cancer who is a week from death, catches COVID19 in hospital, and dies. What killed them? The statistics say COVID19. I say, bollocks.

When I started in medicine, ‘bronchopneumonia’ (a bad chest infection) used to be known as the ‘old man’s friend.’ For those who were very old, and frail, often demented, lying in care homes, often incontinent, a chest infection represented a reasonably painless way to die.

Very often we would not actively treat it, instead we allowed for a peaceful death. Indeed, this still happens. Less so now, as someone, somewhere, often a relative from a country far, far, away – who has not visited for years – is far more likely to sue you.

Did they really die of bronchopneumonia? You could argue yes, you could argue no. Yes, it was the thing that finally pushed them over the edge. No, they were already slowly dying as their body gave out. In the end, what does anyone actually die of? My Scottish grannie, who lived to one hundred and two, used to say ‘they die frae want of breath.’ Entirely accurate, but, alas, also completely useless.

So, what you need to do, is look beyond what is written on death certificates. You need to look at what is happening to the overall mortality. Whilst you can argue endlessly, pointlessly, about specific causes of death. What you cannot argue about is whether or not someone is alive, or dead. Even I usually get this one right. No pulse, no breathing, no reaction of the pupils to light, no response to pain… and suchlike. Yup, dead. Now… what they die of? Um… let me think.

Thus, I have tended to look to EuroMOMO. The European Mortality Monitoring project. As they say, of themselves:

‘The overall objective of the original European Mortality Monitoring Project was to design a routine public health mortality monitoring system aimed at detecting and measuring, on a real-time basis, excess number of deaths related to influenza and other possible public health threats across participating European Countries.

Mortality is a basic indicator of health. Therefore, understanding its epidemiology is fundamental for effective public health planning and action.

Mortality monitoring becomes pivotal during influenza or other pandemics for several reasons. In a severe pandemic, mortality monitoring can be a robust way to monitor the pandemics progression and its public health impact when other systems are failing, due to an overburdened health care sector. Decision makers will require data on the pandemics impact and on deaths by age and geographical area in various stages of the pandemic. Mortality monitoring can provide such estimates, which will be important to guide and prioritize health service response and decision-making, i.e. use of antivirals and vaccines.’ 3  

Here are the data that you can therefore, pretty much, fully rely on. It is where I go to see what is really happening across Europe. Not all of Europe, as some countries do not participate. However, there are more than enough, to get a good picture. It encompasses key countries such as Spain, Italy, the UK (split into four separate countries), Sweden and suchlike.

Here is the graph of overall mortality for all ages, in all countries. The graph starts at the beginning of 2017 and carries on to almost the end of 2020.

As you can see, in each winter there is an increase in deaths. In 2020, nothing much happened at the start of the year, then we had – what must have been – the COVID19 spike. The tall pointy bit around week 15.

It started in late March and was pretty much finished by mid-May. Now, we are in winter, and the usual winter spike appears. It seems to be around the same size as winter 2017/18. It also seems to have passed the peak and is now falling. But it could jump up again. [The figures in the most recent weeks can always be a bit inaccurate, as it can take some time for all the data to arrive]

Two things stand out. First, there was an obvious ‘COVID19 spike’. Second, what we are seeing at present does not differ greatly from previous years. The normal winter spike in deaths.

If we split this down into individual countries, this reasonably clear pattern falls apart.

Here are the figures from England

Unlike the first graph, the scale on the left is not absolute numbers. It is a thing called the Z-score. Which means standard deviation from the mean. Sorry, maths. If the Z-score goes above five, this means something significant is happening. The red, upper, dotted line is Z > 5. As you can see, despite the howls of anguish from England about COVID19 overwhelming the country, we are really not seeing much at all.

What of Sweden, that pariah country? They did not fully lock-down, the irresponsible fools (all they did was follow WHO guidance – by the way), and we are now told they are suffering terribly, they should have enforced far more rigid lockdown, their ‘experiment’ failed etc. etc. COVID19 shall have its vengeance. Or to quote Arnie – I’ll be back.

As you can see, nothing much happening in Sweden either.

Then, if you look further, there are anomalies all over the place. Northern Ireland, which is part of the UK, and did exactly the same things as the rest of the UK with regard to lockdown, masks etc. At least it did in the earlier part of the year. However, it shows a completely different pattern to England. Or, to be fully accurate, it shows no pattern at all. No waves, and nobody drowning.

What of Slovenia?

As you can see absolutely nothing happened earlier in the year in Slovenia. Now, it has the biggest spike of all – apart from, maybe, Switzerland. Earlier in the year it was held up as a great example of how brilliantly effective masks were. Now… you don’t hear so much about masks. Maybe masks only work in months beginning with M. [Maybe, whisper it, they don’t work at all].

So, what have I learned from euroMOMO? First that it appears to have made absolutely no difference if a country locked down hard, and early, or did not. Everyone points at Norway and Finland as examples of great and early government action, and how wonderful everything would have been if we had done the same.

Well, look up at Northern Ireland. Then look at Finland

Spot the difference. There is none.

Of course, much of the most heated debate surrounded what happened during the so-called first wave. Who dealt with it well, or badly. Now, everyone in Europe is doing much the same things. Lockdown, restrictions on travel, restrictions on meeting other people, everyone wearing masks, etc. etc. Yet some countries are having a new wave, and others are not.

There is a special prize for anyone who can match up the severity of restrictions in various countries, to the Z-score. I say this, because no correlation exists.

So, again, what have I learned about COVID19? I learned that all Governments are floundering about, all claiming to have exerted some sort of control over this disease and ignoring all evidence to the contrary. In truth, they have achieved nothing. As restrictions and lockdowns have become more severe, in many cases the number of infections has simply risen and risen, completely unaffected by anything that has been done.

The official solution is, of course, more restrictions. ‘We just haven’t restricted people enough!’ Sigh. When something doesn’t work, the answer is not to keep doing it with even greater fervour. The real answer is to stop doing it and try something else instead.

I have also learned that, in most countries, COVID19 appears to be seasonal. It went away – everywhere – in the summer. It came back in the autumn/winter, as various viruses do.

On its return is has been, generally, far less deadly. Much you would expect. The most vulnerable died on first exposure, and far fewer people had any resistance to it, at all. Now, a number of people do have some immunity, and may of the vulnerable are already dead.

Which means that, in this so-called second wave COVID19 is of no greater an issue than a moderately bad flu season.

If I were to recommend actions. I would recommend that we stop testing – unless someone is admitted to hospital and is seriously ill. Mass testing is simply causing mass panic and achieves absolutely nothing. At great cost. We should also just get on with our lives as before. We should just vaccinate those at greatest risk of dying, the elderly and vulnerable, and put this rather embarrassing episode of mad banner waving behind us.

Hopefully, in time, we will learn something. Which is that we should not, ever, run about panicking, following the madly waved banners… ever again. However, I suspect that we will. This pandemic is going to be a model for all mass panicking stupidity in the future. Because to do otherwise, would be to admit that we made a pig’s ear of it this time. Far too many powerful reputations at stake to allow that.

1: https://www.ombudsman.org.uk/sites/default/files/Time_to_act_report.pdf

2: https://www.cdc.gov/nchs/nvss/vsrr/covid_weekly/index.htm?fbclid=IwAR3-wrg3tTKK5-9tOHPGAHWFVO3DfslkJ0KsDEPQpWmPbKtp6EsoVV2Qs1Q&_ga=2.83596054.1497558416.1598967201-386365132.1598967194#Comorbidities

3: https://www.euromomo.eu/about-us/history/

The case for Keto – a review

9th December 2020

Gary Taubes has a new book out called ‘The Case for Keto,’ which he sent to me in the form of a real book with real pages, that he wanted me to read. Which I have.

I then suggested I should do a review and stick it up on my blog. I shall say, right up front, that I strongly recommend this book.

This may not be a surprise to those who know my thoughts on diet, heart disease and suchlike. In my case Gary is preaching to the converted. This is a book which covers the fact that fats, saturated fats, indeed any fats (other than trans-fats, and the industrially produced fats from grains) are perfectly healthy. Humans have eaten them for millennia.

You don’t see cave paintings of early humans out scything autumn wheat fields. No, you see pictures of men, because men always get the easy jobs, chasing woolly mammoths with spears. They are not just taking the mammoths out on early morning exercise, and throwing the spears to play catch. They are throwing those spears at the mammoths, and chasing them into spike filled pits, then eating them – saturated fats and all.

Anyway, as Gary makes very clear, despite the endless claims that animal fats are bad for us, when you get down to it, the evidence simply does not exist. The idea that fats make us fat and diabetic and kill us with heart disease is simply a ‘meme.’

An idea so widely held that everyone just believes it must be true. So much so that there is no need to even think about it. Fat gets into your body, floats about and gets stuck to your artery walls. Fat, cholesterol, same thing innit? ‘My mind is made up, don’t confuse me with facts.’

I think I should mention that Gary first gained considerable fame in this area with his book ‘Good Calories, Bad Calories.’ In the UK and Australia, it was called. ‘The Diet Delusion.’ This is where he first looked at the idea that fats were bad for us and found it to be based almost entirely on hot air.

So, if it is not fat in the diet that is capable of causing weight gain, diabetes, heart disease, and other such nasty things, what is it? As Gary points out clearly, and inarguably, the answer is sugar. By sugar, he means carbohydrates (all sugars are just simple carbohydrates).

Slightly more complex carbohydrates are bread, and pasta, and rice and potatoes. These are just made up of lots of glucose molecules stuck together. Many people are unaware that our body takes in pasta, bread, rice etc. and simply breaks them down into sugar. So, pasta = sugar. Bread = sugar. Potatoes = sugar. Just as much as sugar = sugar. They all have the same effect.

Gary goes through the history of the brave individuals who have been those pointing out the damage that can be caused by excess carbohydrate intake for decades. Those who have been squashed flat by the mainstream. An English professor of nutrition, John Yudkin, tried to make this all clear in his book on sugar(s): ‘Pure, white and Deadly’ first published in the early 1970s. He was attacked and shouted down by Ancel Keys – the main promoter of the diet/heart hypothesis.

Gary maintains a calm and reasonable tone when discussing some of these events. Which is admirable. If I were him, I would be breaking the furniture, and chewing the curtains. He also calmly points out where the evidence is strong, and where it is weak, or where it does not exist at all. He does not overclaim, nor suggest that cutting down on carbs is a panacea that will benefit everyone. It is the calm reasonable tone that is actually most impressive. He knows his stuff, and he lays it out carefully and clearly.

What of the title of the book itself? ‘The case for Keto.’ For those who know this area ‘Keto’ is the metabolic state achieved when the body stops using sugar for energy and starts to break down the stored fats instead. These stored ‘fatty acids’ are converted to molecules known as ketone bodies in the liver. The body is perfectly happy to use them for energy. This is ‘ketosis’. Explaining the title of the book.

Many people think ketones are the preferred energy source for most organs in the body. Virtually the only exception being some processes in the brain, that require glucose, and only glucose, to function.

The downstream benefit to entering ketosis is that, when you burn up fats and ketones, you are also using up your “energy stores” aka fat. So, once you stop burning glucose, and start using ketones, you can finally lose weight. Also, your blood glucose levels fall, your insulin levels fall, and the body has a chance to reset itself.

Gary has spoken to many, many doctors and researchers who are now absolutely convinced that the best way to prevent, even reverse, the wave of obesity and diabetes sweeping the modern world is to change from eating carbohydrates and eat more fats. I agree with him. If you read this book, I believe you will agree with him too. He makes a compelling case. It is the Case for Keto.

A YouTube interview you may want to listen to

28th November 2020

This YouTube interview is me, speaking to Ivor Cummins, and discussing many things COVID. Lockdown, the weird statistics, the absolute lack of any real science, the crushing of dissent, and suchlike.

I have known Ivor for years, as he has been a long-term critic of the dietary guidelines, and a fervent supporter of the low carbohydrate high fat (LCHF) diet as a way of treating type II diabetes.

I find it interesting that many of the people I know who are critical of the mainstream thinking on diet and heart disease also find themselves critical of the mainstream response to COVID. I like to think this means we are all highly intelligent, with a clear understanding of the scientific method. Maybe we are all just stroppy buggers, who like a bit of controversy. I think that is for others to decide.

Anyway, the interview is on YouTube, and can be found here

Stamping on the ‘anti-vaxxers’ – a very stupid idea

17th November 2020

The COVID19 pandemic has thrown into sharp relief the concerns that a number of people have about vaccination. However, such is the eagerness to develop a vaccine, and get everyone to take it, that authorities are now looking to ban anyone who raises doubts. For example, the Labour Party in the UK is now calling for emergency ‘anti-vaccine’ laws:

‘Emergency laws to “stamp out dangerous” anti-vaccine content online should be introduced, Labour has said. The party is calling for financial and criminal penalties for social media firms that do not remove false scare stories about vaccines.

It follows news of progress on the first effective coronavirus vaccine. The government said it took the issue “extremely seriously” with “a major commitment” from Facebook, Twitter and Google to tackle anti-vaccine content.’ 1

There are so many things that could be said about this, that it is difficult to know where to start. Or to finish. I think in this blog I am just going to stick to focussing on a single issue. Which is that, if the intention of such laws is to ensure more people are keen to be vaccinated then I have news for the Labour party.

It will almost certainly backfire.

This is because state censorship does not change minds, never has. Whilst debate, at least superficially, has been silenced, the concerns do not disappear. Instead, the doubts are often redoubled. Once you start banning and censoring and fining and arresting, people start to wonder if you are just afraid to make your case. As Wendell Phillips said, and many people think:

‘He who stifles free discussion, secretly doubts whether what he professes to believe is really true.’

Once censorship starts, people are also reminded of the worst, most dreadful periods in history the world has even seen. It has always been one of the primary tools of totalitarian regimes:- Nazi Germany, Russia under Stalin, North Korea, China and Iran today.

One of the greatest books of the twentieth century is George Orwell’s 1984. It is a book mainly concerned with how facts, and truth, are tightly controlled by the party.

‘And if all others accepted the lie which the Party imposed — if all records told the same tale — then the lie passed into history and became truth.’

Of course, Orwell was not the first to notice the critical importance of freedom of speech

‘Liberty is meaningless where the right to utter one’s thoughts and opinions has ceased to exist. That, of all rights, is the dread of tyrants. It is the right which they first of all strike down. They know its power. Thrones, dominions, principalities, and powers, founded in injustice and wrong, are sure to tremble, if men are allowed to reason of righteousness, temperance, and of a judgment to come in their presence.’ Frederick Douglass

‘Freedom of speech is a principal pillar of a free government; when this support is taken away, the constitution of a free society is dissolved, and tyranny is erected on its ruins. Republics and limited monarchies derive their strength and vigor from a popular examination into the action of the magistrates.’ Benjamin Franklin.

Deep down we all know this. We know that this essential freedom – to say what you really believe to be true – is the essential pillar of any free society. It carries a cost, of course it carries a cost. People say stupid things, people say wrong and misguided things. They can be damaging things, but the alternative will always be much worse in the end.

I say this because people also say things that, whilst angrily dismissed at the time as dangerous foolishness, are later found to have been correct all along. I have spent many years looking at the history of medical science (if that is not, at times, an oxymoron). I have seen many activities considered to be of inarguable benefit, turn out to be indefensible malpractice.

Bernard Lown is, I think, my number one medical hero. His motto ‘Do as much as possible for the patient, and as little as possible to the patient.’

As he also said:

‘From my earliest days in medicine, I have struggled against the prevailing model of health care. My opposition in part was provoked by the growing prevalence of overtreatment. Resorting to excessive interventions seemed to be the illegitimate child of technology in the age of market medicine.’ 2

He tells a tale from the 1950s where the orthodoxy of the time was to ensure strict bed rest following a heart attack. In the face of considerable hostility, he and his mentor, Dr Samuel Levine allowed patients to sit up in a comfortable chair at the end of the bed. Shock horror. In his own words:

‘The idea of moving critically ill patients into a chair was regarded as off‑the‑wall. Initially the house staff refused to cooperate and strenuously resisted getting patients out of bed. They accused me of planning to commit crimes not unlike those of the heinous Nazi experimentations in concentration camps. Arriving on the medical ward one morning I was greeted by interns and residents lined up with hands stretched out in a Nazi salute and a “Heil Hitler!” shouted in unison.’  3

Heil Hitler indeed. An almost perfect irony, I suppose.

It turns out that strict bed rest was absolutely and completely and totally the worst possible single thing you could do. I estimated, some years ago, that this action resulted in the premature death of around one hundred million people, worldwide. It could well have been more.

I imagine the ‘Heil Hitler’ shouting interns and residents would have happily endorsed censorship of any criticism of strict bed rest … for the good of society, no doubt.

Of course, had this happened, we would probably still be enforcing strict bed rest to this very day. Once a treatment becomes ‘standard practice’, there is no longer anything else against which to compare it, so you have no idea if it is beneficial, or harmful. That is what happens when you ban freedom of thought, and speech.

Leaving aside the principle that freedom of speech is our single most important freedom and must be handled with exquisite care. If we crush dissent, we also crush progress. Stupid ideas will, in the end, be shown to be stupid. Nonsense will be exposed as nonsense. However, if no criticism allowed, stupid ideas that are widely believed to be true, cannot be challenged and we will be stuck – forever.

I think most people recognise this truth. I also think most people, when they see things being banned and censored … wonder why. You immediately raise doubts. Why are they doing this, are they attempting to hide something? You will not convince anyone, ever, by censoring them, or shutting them up. You will, instead, make them more certain that you are hiding something, and that they are right.

Censorship always hardens attitudes; it does not change minds. Anti-vaxxers (whatever that stupid deliberately demeaning term means) will become more anti-vaxx. Discussion will be driven underground. Heroes and martyrs will be created. You will have done the exact oppositive of what you hoped to achieve.

You don’t win arguments by clubbing people into submission. All you do is silence them and redouble their determination.

1: https://www.bbc.co.uk/news/uk-politics-54947661

2: https://myheartsisters.org/2019/11/17/bed-rest-overtreatment-dr-bernard-lown/ 3: https://bernardlown.wordpress.com/2011/02/03/a-chair-to-the-rescue/

3: https://bernardlown.wordpress.com/2011/02/03/a-chair-to-the-rescue/

Ninety per cent

10th November 2020

‘Ladies and gentlemen, roll-up, roll-up, roll-up. My new product, just brought to the market this very day, prevents ninety per-cent, yes ninety per-cent of all known things happening to you. Yes, a remarkable ninety per cent. Not sixty per cent, not seventy per cent, no…not even eighty per cent. But ninety of your finest American per cent – of things’.

‘What is a thing, madam? What a very good question, and by the way your child is a most beautiful young girl, is she not. And your hair, someone did a most fantastic job on that. You must have paid a fortune for such magnificent styling… you sir.’

‘You are asking how much it costs. Cost sir, now cost doesn’t come into it. I can promise that I will never make a penny from selling this product, this year…. Not a penny, as I promise on my mother’s grave sir, my mother’s grave.’

‘Lady at the back there what was that …you say that my mother is still alive, you met her for coffee last week. Gracious, she does get about doesn’t she.’

‘Back to you sir. Cost, this product .. it does have to be kept at a very low temperature, so valuable is it sir. The cost of the refrigeration unit. Now, that is pricey sir very pricey.  Pricey indeed.

‘How pricey sir. I can tell you are a very clever man, there is no way I could fool you, is there. But pricey sir…made by top scientists, and they do not come cheap, no they do not. I wish with all my heart it were otherwise, but you cannot buy the product without the refrigeration. It would not make sense otherwise, would it sir. But you know, my good fellow, how can anyone quibble about the costs of keeping this remarkable product cold, when it will prevent ninety per cent….of things.’

‘But do not simply take my word for it. No. Here is a young lady who was injected with this product just the other day. Yes, just the other day. And do you know what… Well, don’t listen to me. Here she is…. big round of applause for this very brave young lady. Now Miss Fauci, for that is your name is it not… yes it is. You were injected with this very product seven days ago and what has happened to you?’

Miss Fauci: ‘Nothing.’

‘Yes, absolutely nothing happened to young Miss Fauci. Nothing at all. When you think of all the things that could have happened, and yet none of them did, did they. Well, this is remarkable, truly remarkable. No fevers, no loss of smell, no cough….?’

Miss Fauci: ‘Yes, nothing at all.’

‘Ladies and gentlemen, can you believe it. Nothing happened to this young lady at all after seven whole days.’

‘What was that madam, nothing happened to you either. Goodness me, you have been lucky haven’t you. You must be one of the lucky ten per cent. Here, have a free PCR swab to celebrate. Yes, keep it madam, its yours. Your day just got even better. Yes, have two, one could be positive, the other negative, we never really know do we. Ha, ha… my little joke.’

‘You sir, you still want to know what a thing is. Goodness me, you’re not one of those anti-product protestors are you. Our products undergo the most rigorous testing for safety, the most rigorous. How many, why, at least thirty people sir. We are not one of those fly-by-night organisations.’

‘You still want more information on things? Have I not just told you everything you could possibly need to know sir? Our product can prevent ninety per cent of things. If that is not enough to convince you sir, then I have not idea what else I can say.

‘Roll up, roll up. Only twenty billion for you, Mr Johnson – you know a bargain when you see one, don’t you. You’re certainly no mug, are you.’