The Wry Observer’s Covid-19 update (43)

It’s unusual to get started so early (0945hrs) but I began Mark Honigsbaum’s book “The Pandemic Century: A History of Global Contagion from the Spanish Flu to Covid-19” (Penguin books, 2020) over my morning cup of tea in bed. I haven’t got very far but felt I had to put a quote down from page 16 (there are pages all told):

Anomalies are a common occurrence in science. No two experiments are ever exactly alike, but by refining methods and sharing tools and technologies scientists are broadly able to reproduce each other’s observations and findings, thereby arriving at a consensus that this or that interpretation of the world is correct. That is how knowledge emerges and a particular paradigm comes to be adopted. However, there is no such thing as absolute certainty in science. Paradigms are constantly being refined by new observations and, if enough anomalies are found, faith in the paradigm may be undermined and a new one may come to supplant it. Indeed, the best scientists welcome anomalies as this is the way scientific knowledge advances.

Sound familiar?

Wearing another hat I have written a lot about statins, and how the paradigm of cholesterol-heart disease has been undermined by re-analysis of original data. It is interesting though that in that case the Inquisition (aka the hypothesis supporters, helped by statin manufacturers) have suppressed the Galileans who believe the earth is round (the Galileans being the cholesterol sceptics, marshalled by a network, THINCS). Honigsbaum uses the above paragraph to introduce the problem faced by those investigating the Spanish Flu when it became clear that it could be transmitted even when the best bacteriological filters were in place, proving that it was caused by something smaller – which of course we now know is a virus. But I use this preamble to introduce a piece of news reported today.

If you have been reading my blog regularly you will have read my views on the BAME community and why they appear to be especially susceptible to Covid-19. Blood group A? It may be more than that, if it is that at all. is a paper from Zeberg and Päälo, with this abstract:

A recent genetic association study (Ellinghaus et al. 2020) identified a gene cluster on chromosome 3 as a risk locus for respiratory failure in SARS-CoV-2. Recent data comprising 3,199 hospitalized COVID-19 patients and controls reproduce this and find that it is the major genetic risk factor for severe SARS-CoV-2 infection and hospitalization (COVID-19 Host Genetics Initiative). Here, we show that the risk is conferred by a genomic segment of ~50 kb that is inherited from Neandertals and occurs at a frequency of ~30% in south Asia and ~8% in Europe.

What, though is confusing (much as it is an explanation for the high prevalence in people of Bangladeshi origin) is that this gene cluster is almost absent in people of African descent, as the authors conclude:

Among the individuals in the 1000 Genome Project, the Neanderthal-derived risk haplotypes is almost completely absent in Africa, consistent with that gene flow from Neandertals into African populations was limited and probably indirect (Chen et al. 2020). The Neandertal haplotype occurs in South Asia at a frequency of 30%, in Europa at 8%, among admixed Americans at 4% and at lower frequencies in East Asia. The highest frequency occurs in Bangladesh, where more than half the population (63%) carries at least one copy of the Neandertal risk variant and 13% is homozygous for the variant. The Neandertal variant may thus be a substantial contributor to COVID-19 risk in certain populations.

So how do you explain the higher prevalence in them? The word multifactorial comes to mind… but I am also curious why there is such a high prevalence of this Neanderthal gene in Bangladesh.

Of course disparities have happened before. Honigsbaum notes that during the Spanish Flu epidemic the death rate in Maoris was seven times that of the white New Zealand population; in Guam one white sailor died but 5% of the local population did; white South Africans had a case fatality rate of 2.6% but for “Blacks, Indians, and Coloureds” it was almost 6%. Poverty? Genes? Previous exposure?

Meanwhile the New York Times reports a change in scientific thinking about transmission risk:

Elected officials in the United States are beginning to acknowledge that the rush to reopen was a mistake, as many of the hardest-hit areas in recent weeks have been places that lifted lockdown restrictions fastest. And one factor seems to be playing an outsize role in the uptick: indoor transmission from businesses like bars and restaurants.

…Scientists from 32 countries are now warning that airborne transmission of the virus indoors should be taken more seriously and are calling on the World Health Organization to revise its recommendations, which they say underestimate the dangers of transmission by tiny, viral particles that linger in the air indoors.

See an article by Morawska and Milton: (

The full article (pre-print, but accepted for publication) underlines the futility of a 1 or 2 metre distancing rule, as indoors spread can take place over tens of metres, not helped of course by air conditioning. As well as the two authors, 239 other scientists have approved the article. That’s an awful lot of scientists to put on a paper! Might they all yet be wrong? Meanwhile a mask seems very sensible, unless you have already had gene sequencing done on your own DNA which proves you don’t have that Neanderthal gene on Chromosome 3.

Dare I return to my hobby horse?

You won’t stop the spread. Testing is unreliable. The Office for National Statistics now says that of those testing positive for SARS-CoV-2 78% are asymptomatic.  There may be ways of predicting susceptibility but they are not in common use. There is no vaccine yet. So why not concentrate on treating the cytokine storm syndrome induced by SARS-CoV-2?  We know what to use and when to use it.

Oh, and another thing. Just like in wartime there is profiteering, with contracts awarded to companies that have never traded, but appear to have connections. See Procurement is a good word to use, given its legal usage.

The Wry Observer’s Covid-19 update (42)

While I have a few reservations about the Wuhan Handbook (you can download a copy through it should be required reading for all involved in Covid-19 care, not least because the experience of clinicians in Wuhan is several weeks in advance of clinicians elsewhere in the world. I am prompted to offer this advice following the “Insight” report in yesterday’s “Sunday Times” which attempts to examine the exact origin of SARS-CoV-2. It’s most interesting but remains completely irrelevant to the management of Covid-19. We should be in collaboration with anyone and everyone to develop treatments that stop people dying, not playing a blame game on incomplete information.

Meanwhile the role of aerosol transmission is being evaluated, but the bottom line is that it is likely to produce infection at large distances if (a) there is a lot of it and (b) it’s in a relatively confined space. See As transmission can take place from asymptomatic people I believe it is impossible to eliminate spread of SARS-CoV-2, only to reduce it. But judging by the scenes in Soho, let alone Rye High Street, the likelihood of people continuing to socially distance or wear masks is close to zero.

It still appears that a lot of folk are attempting to call the crisis in every detail before all the facts are clear. And the spurious precision of death figures continues. More information is emerging about the higher risks of being in a care home, or suffering from a disability (or both) which perhaps is good news for those who are neither, however selfish that may seem – but facts are facts.

The Wry Observer’s Covid-19 update (41)

4th July 2020


I am not a lockdown sceptic, but a lockdown agnostic.  However, Toby Young’s Lockdown Sceptics website yesterday carried a remarkable piece by a doctor from Leicester.  It is a sign of the increasing authoritarianism of the NHS that they have remained anonymous in case of reprisal; shades of the new law passed in Hong Kong – criticise the organisation and end up in prison, or Coventry, with a stain on your record.  Such attempts at the suppression of dissent are not new.  I was threatened with disciplinary action for speaking out against the party line in 2010; a friend, decades ago, who helped organise a junior doctors’ protest, told me that he had a one-line reference at the end of his posting: “This man is politically unreliable”.  Many congratulations to Dr Leicester, or rather Dr Q.  I would give them a job any time; the piece shows sensible and serious reasoning, which is just what one needs in a doctor.  OK, I suffer from confirmation bias but hey.

The article has a splendid cartoon (it’s at but Toby has kindly allowed me to reproduce the text of Dr Q’s letter here.

I’m a doctor at University Hospitals Leicester NHS Trust. We have about 2000 inpatient beds across three main sites and serve roughly 1 million people in Leicester city, Leicestershire county and Rutland. Leicester is a multi-cultural city and 36% of our 16,000 health care workers are from BAME backgrounds.

Many of my colleagues are angry and confused about what is happening nationally and particularly in Leicester and Leicestershire. We are reminded daily that we are not allowed to speak to journalists or on social media, which is why I am stringently anonymous and more vague than I’d like to be here. I love being a doctor, and I risk suspension for speaking out.

I’m going to use Public Health England’s own numbers for this analysis (found here) and I’m going to explain why I think the conclusions they (and the politicians) have drawn are wrong.

The Leicester and Leicestershire experience of COVID-19 echoes the majority of cities in England, with the exception of Birmingham and London, whose peaks were harder and faster. In early March, we could see the COVID-19 crisis coming. We weren’t ready, it’s fair to say. We rapidly wrote guidelines, trained staff and fought over who needed the little PPE that was available. Every day brought new guidance from Public Health England. Each day, the guidance was different to the day before and it was incredibly stressful.

We already run at maximum capacity the vast majority of the time and with the standard shortages of doctors at middle grade “registrar” level, we were terrified about how we would manage. Suddenly, on March 16th, shielding was announced along with stringent social distancing for pregnant women. We had to protect our staff. We lost 15% of our department, who could no longer provide face-to-face care.

In Leicester Hospitals, we rapidly increased our numbers of inpatients and patients on ITU with COVID-19 in the last two weeks of March. It was a distressing time for staff, particularly due to the lack of equipment and the daily changing guidance. We were petrified for our families and ourselves and many were also juggling negotiating key worker school places (not automatic), trying to buy food around odd shift patterns and worried about how much worse it was going to get.

By April, we got access to PPE via the Army and the guidelines started changing weekly instead of daily. Everybody calmed down. We were going to manage. We encouraged social distancing among staff, but not rigidly. We wore masks, plastic aprons and gloves for patient care outside of theatres and ITU and still didn’t seem to catch COVID-19. Nothing seemed as bad as had been described elsewhere. Oddly, colleagues in other large English cities were also reporting fewer cases than they had expected. Our younger children were in schools or nursery and despite no social distancing at all and full mixing with all those risky key workers, nobody’s children were ill. We heard about and worried about deaths of health care workers across the UK, but locally, relatively few colleagues were ill and the vast majority recovered without needing hospital admission. The early deaths data appeared from the ONS showing that security guards and chefs had the highest risk of death, not health workers.

By May, positive cases averaged around 10 a day and deaths were continuing to fall. In late May, we started swabbing every single admission to the hospitals, and this is where things get interesting. I work in a department that isn’t respiratory medicine. This means that the patients who are in our area are there for other health issues that are not caused by COVID-19 (think surgery or mental health). Of those we swabbed, just 1% tested positive and all of them were asymptomatic. That rate has been steady since May 23rd. I believe that our patients are representative of the rate in the UK population and, for what it’s worth, it’s the same story in Manchester, Leeds and Guildford, where I’ve been comparing notes with colleagues. Unpublished data shared on an open forum from Leeds, Manchester, Sussex also confirms this – 1%, all asymptomatic when testing positive. These patients have, almost without exception, not developed any symptoms, although some have had household members with a cough.

By June we were down to between three and eight positive cases a day in UHL (also known as Pillar 1 testing, shown as dark green on the graph). This has remained unchanged throughout the whole of June.

Dr Q 1

The point of “Lockdown” has always been to ‘flatten the curve’ in order to ‘Protect the NHS’. Given we were coping on March 31st, when we had nearly ten times the number of positive cases in hospitals, with relatively little access to testing, we are certainly coping now. The issue and alleged cause of the “Local Lockdown” is our Pillar 2 numbers, which are the lighter green ones on the graph. These are the community tests outsourced to private companies. There is no guarantee that these tests are all taken from different people (unlike the Pillar 1 data, which is cross checked against a unique patient identifier). In fact, the Government accepts that the number of Pillar 2 cases is not the same as the number of people with COVID-19 because Pillar 2 data includes people who’ve been tested more than once – often because they have to re-test before they’re allowed back to work.

We have also brought in two mobile testing stations into these areas, just so we can find all of these people with the virus, which, as I say, are almost certainly no more than 1% of the population. So lets get this really clear: we have locked down based on unreliable test results which may contain multiple positives for one person, all accompanied by a falling rate of hospital admissions and deaths.

Some might say that these community rates are really serious and that all these people could be admitted to hospital in two weeks. However, these rates have been high since mid-May, and our Pillar 1 hospital numbers remain unchanged – so there’s little evidence they’re being admitted to hospital. The other key thing to note is that our Pillar 2 positive numbers have already fallen as shown by the blue line on the Public Health England graph below. Note that there’s no data about what community rates looked like when we had our actual peak of COVID-19 – they weren’t doing Pillar 2 testing then.

Dr Q 2

The final reason we don’t need to worry about the risk of overwhelming the hospital is the age of the people affected. The median age of those with a positive community test is 39. The risk of a 39 year-old dying from COVID-19 is less than that of them drowning (based on the ONS data). Thirty-nine year-olds are out at work, particularly 39 year-olds who live in North Evington, the worst affected area in Leicester city. Over 95% cases are in under-65 year-olds, again at substantially decreased risk. North Evington has a higher than average population who were not born in the UK, and have fewer qualifications and work in manual jobs. They live in smaller houses with less outside space. This means that they have not had a middle class luxury lockdown with working from home and sitting in their garden.  They are out working in the garment factories, which never closed and are poorly ventilated, in our hospitals and in food production. They are crucial to our country, and it is inevitable that some will now be carrying the virus. They are now crucial to our COVID-19 response too. They are the people, along with all the other exposed key workers, that could bring Leicester to our crucial 20% infection rate to give us the herd immunity that we need to get our vulnerable people back out of their homes.

The most criminal thing about the whole of this investigation is that they have only managed to track-and-trace 11 cases. That is, they’ve only managed to trace the contacts of 11 out of approximately 900 new cases in the past two weeks. You won’t be shocked to hear that they found no links between those 11 cases – statistically they wouldn’t.

The only other thing I want to address is the myth of Covid and children. We had one child with COVID-19 in our hospitals back in May and none since. Public Health England say in their report “that the number of children with positive tests remains relatively static”. We absolutely do not need to worry about our children or teachers under the age of 65. The research worldwide is clear. However, they have shut our schools again. Education is the best long-term route out of poverty, the best thing we can do for vulnerable children and we are punishing them for a disease that isn’t even making our population ill.

Local Lockdown in Leicester is purely a tool of control. It’s a threat to make us behave. We weren’t actually misbehaving for the record – our protests have had lower numbers and less violence than the national average, we haven’t been going to any beaches – there aren’t any – and the vast majority of the population have taken the random rules of lockdown very seriously. Be warned. Given our cases have already started falling, they will be able to call this a success in two weeks. By then it might be your turn.

Dr Q

If ever there was an indictment of bad science this is it.  Will I be surprised if there’s a jump in hospital admissions in one to two weeks?  Yes. Very surprised.

Meanwhile in “The Spectator” of 27th June Lionel Shriver takes a kick at the political correctness surrounding the BAME susceptibility argument.  “Political pandering won’t prevent Covid deaths” is far better written than my various expostulations from the beginning of June but re-states several of my arguments.  Great minds. But she doesn’t actually address what might prevent deaths – appropriate treatment.  And the following article by Hugh Osmond “Battle lines” is splendid, although I still have some sympathy for PHE given the infallibility of retrospectoscopes.  Read both if you can.

And just look at a summary of an article about the Kawasaki type syndrome in children at  It details a small series of neurological complications.  And how did they treat these?  And what have I been saying for weeks?

The Wry Observer’s Covid-19 update (40)

Richard Horton is editor of “The Lancet” one of the UK’s principal “general” medical journals, the other being the British Medical Journal. His journal might be deemed more scientific, although there has under his editorship been somewhat of an anti-establishment approach and some of his own writing is polemic rather than scientific.

“The Covid-19 Catastrophe: What’s gone wrong and how to stop it happening again” is a highly readable account of the pandemic up until the end of May 2020. He makes several arguments; that the UK response was based on SARS-CoV-2 being rather like just another flu virus, when all the evidence emerging from China pointed to it being something quite different, and much more dangerous. He likens some of the responses of government and the SAGE committee to being, at least initially, things that they wanted to believe or they expected – suggesting the effect of what statisticians know as confirmation bias. He believes initial recommendations were wrong because they were based on wrong assumptions – and with that I agree.

If a doctor writes a book about a disease one somehow expects to read a formula: description, distribution, epidemiology, clinical features, investigations, treatment. The utterly extraordinary thing about this book that there is no mention of treatment, with the exception of references to ventilators and intensive care, until page 111 of 127 (excluding the short series of references). Nothing. Nada. Zilch.

Confirmation bias indeed. The entire book is predicated on the premise that SARS-CoV-2 progressing to Covid-19 will kill many people. There is almost an assumption that death is if not inevitable it is almost so. In passing, some of the serious non-respiratory elements of Covid-19 are referred to but there is no analysis of what these are due to. It’s a book about an epidemic in which the clinical features of the disease are irrelevant, because it’s a book about the management of an epidemic infection. On page 111 there is a mention also of the Kawasaki-like illness seen in children, but no mention of what it might be, or how Kawasaki disease is treated (I might add very successfully). There is an earlier one-line reference to the cytokine storm element but absolutely nothing about its components, what tests might predict its development or how it might be managed. Or how important it might be.  So in blaming ethnic minority preponderance of fatal outcomes on social issues (when there is likely to be a big genetic element), and sniping at health officials by accusing them of toeing the party line for their own protection (for which he has no evidence, save the sidelining of a couple of spokespeople who indicated a teeny bit of dissent – after the book went to press) he has totally failed to address the one enormous issue.

If you can stop people dying by treating the serious acute illness that is Covid-19, then nothing else matters.

No mention, then, of the NHS Research Authority and the trials it has been running (whether these are with the right things is immaterial to my argument). No mention of why the disease spread so rapidly (because of the multiple entry points from Italy and Spain). There is simply a hanging presumption that once you get Covid-19 there is a very high chance you will die. Inshallah.

I read a largely positive review of the book on the website of “The Guardian”, jointly with another book by Debora MacKenzie titled “COVID-19: The Pandemic that Never Should Have Happened, and How to Stop the Next One”. That looks rather interesting, so it’s on order now. Well with this lockdown what else do you spend your money on? I have Mark Honigsbaum’s pandemic history on the bedside table as well. His Spanish Flu book was very good. Oh, and there’s a management manual out of Wuhan which I was pointed at by Duncan Campbell…

There is one big thing where I agree with Richard Horton. The experts have not listened to all the evidence they have had access to. They clearly have not listened to him. They certainly do not appear to have listened to me!

If you are going to appoint experts to plan your response you must ensure they are the right experts. You can have the best Nobel prize-winning epidemiologists and public health doctors in the world but if you haven’t got the experts who know how to treat the disease you are trying to get a football team to play ice hockey in a baseball stadium. Or some similar example.

Richard Horton’s book contains arguments that have already been overtaken by events, which is a good reason not to write a book analysing a war until the war is over (or to have an inquiry). All sorts of unexpected turns may appear in the road that lies in front of us. My confirmation bias (oh yes, I admit it!) is different. The differing realities of the SARS-CoV-2 pandemic as seen by epidemiological theorists and front-line clinicians may eventually coincide, or coalesce, but they have not done so yet.

The Wry Observer’s Covid-19 update (39)

Oh dear. Dryden wrote

For those whom God to ruin has designed,
He fits for fate, and first destroys their mind.

Two outbreaks of madness reported today. The first is the purchase by the United States government of the world’s stocks of remdesivir, the antiviral agent trumpeted (pun not intended) as the answer to Covid-19. For a state to invest so heavily in a single drug, whose efficacy has been published from a trial of 73 people run by the drug company, is insane. Remdesivir doesn’t even work very well. Ah well, saves us in the UK from bothering with it, then.

The second is the reimposed lockdown in the city of Leicester. It reminds me of the story of the cooling pool at Windscale in 1957, when a reactor pile overheated. It went critical, expanded, stopped being critical, cooled down, became critical again and continued to cycle until it was diluted enough not to contain a critical mass. At least that’s what my med school physics teacher told me ten years on. We are heading for a similar scenario; lockdown, release, spike in cases, another lockdown ad infinitum. I saw this coming. If Covid-19 does not kill people, is this really necessary? But then, I suppose, it still does kill people, because the policymakers are waiting for the trials, which are probably not necessary because we already know what to do. At least, some of us do.

The UK death rate is now below the average, as I expected, but the gloom merchants still preach tidings of great fear. I await with interest the full figures from Leicester (question: is the spike in infections matched by a similar spike on hospital admissions and deaths – if not, then why worry?) And bits of the meeja are weeks behind the curve; a couple of days ago there was a piece on the BBC news about a Covid-19 sufferer who had had two strokes. Really worrying. Why does it happen etc. If the journos read my blogs they would understand exactly why it happens – and understand how one stops it from happening.

Richard Horton’s little book has come. The SAGE reports are, apparently, online now. More reading to be done.

The Wry Observer’s Covid-19 update (38)

Difficult to believe that time has gone so fast, and it’s a week since the last episode of the Update, but I plead alternative commitments (writing a piece for our local newspaper, watching a web lecture, doing the allotment, going out for lunch and BREAKING THE LOCKDOWN AT LAST! It was outside, and we were properly distanced, and a swarm of bees did appear to distract us, but it was a great day. Mind you it would appear that half of England headed for Camber Sands or the Dorset beaches, and also that the concept of social distancing has been forgotten already. But at last the awful daily briefings have stopped. We stopped watching a while back as they became repetitive and uninformative; the questions from the press were irrelevantly focussed; and I got fed up with seeing the faces I had written to (who have never replied) ignoring so far as I could see any of my suggestions.

Well, you will say, they must have been deluged with stuff. Maybe so, but increasingly it seems my stuff was pretty well on the ball. The webcast I watched was presented by two rheumatologists, Professor Ernest Choy from Cardiff and Professor Dennis McGonagle from Leeds. It told me four things; first, that you have to hit Covid-19 with the immunosuppressives at just the right time (after the viral peak and at the beginning of the cytokine storm); second, that low oxygen saturation allied to abnormal blood tests predicts the latter (and yes, my protocol had an omission – the C-reactive protein also goes sky high so it should be included with the D-Dimer and ferritin); third that my protocol for treating the storm was on the nail and fourthly – beautifully illustrated with immunological slides – that rheumatologists are the best people to be treating cytokine storms because they actually understand the immunological principles and have experience of the treatments to use.

I remain convinced despite their positive analysis of the RECOVERY trial – which has a complex protocol which we rheumatologists don’t normally have recourse to – may have proved the point about steroids but still had flaws and also introduced a delay in treating seriously sick people. What harm could it have done to bang in a large slug of steroid? The risk of making infection worse, or allowing infection with something else, was small and manageable set against the likely suppression of the cytokine storm that was going to do all the damage.

As the lockdown begins to lift the post-mortems on the handling of the pandemic are beginning to be aired. In a way much of these are unfair, because at the outset what has become clear, or at least clearer, was completely not clear.  International comparisons are thoroughly confusing (reason not clear). Why was there an excess death spike in England but not, apparently, in the other home nations (reason not clear)? How reliable are the Covid-19 tests (not as reliable as first thought)? Should we maintain the 2-metre distancing rule (well, it’s down to 1 metre + whatever the + means)? Why are BAME people more likely to die (lots of talk about inequality and poverty, none about genetics)? Why exactly was there such a problem in care homes (people being displaced from hospital, close contact spread, infected carers)? Why don’t children appear to spread the virus (don’t know)? Should we open schools (on balance, straightaway; they should never have been closed)? What role did the media play in inducing mass hysteria (a big one, and often based on ignorance of science and medicine)? And so on.

I do wonder whether my 37,000 words so far have materially affected the management of the great plague. Writing them, and all the associated articles and letters has certainly kept me quiet, but it has been extremely frustrating to watch as the powers that be came to their conclusions days or weeks after I had. And I had told them, too. I sent links to the blog, emails with suggestions, even a full treatment protocol. Not a word.

If you can’t stop the virus from spreading (and as lockdowns ease across the world it appears you can’t), you can’t apply reliable tests to prove that you have it – or haven’t – or that you have had it – in which case it’s unclear whether immunity is long-lasting – we will have to live with SARS-CoV-2 for a while. Meanwhile there remains one thing you can do. You can stop people dying if they get it. That is a scientific issue; the moral issue is how you might determine which sufferers you prioritise, on the basis that applying treatments to restore a miserable existence may not be the right thing to do. The one certainty of life is death.

The Wry Observer’s Covid-19 update (37)

The 2 metre social distancing rule may be bent; some doubt has been cast on the studies used to recommend it on the basis that they are not direct evidence, but projections and deductions that may not be scientifically sound.  Indeed one can imagine, as one pushes through the crowd outside the door of one of our pubs, that unless someone puffs directly in your face or cough or sneezes, no droplets containing virus can possible come near you.  It makes economic sense to reduce the distance whatever the science of course.

The heightened risk to BAME people has also been in the headlines.  A preliminary inquiry was criticised for redacting the recommendations but when these finally came out I thought they should have stayed redacted.  There was no science in them at all, merely a pile of “woke” jargon about developing culturally competent assessments, involving communities and one bit that really stuck in my throat: ““In the absence of some of the more textured data it would be difficult to drill down into a very local, community level, understanding and, therefore, would limit the ability to decide how best to target and allocate resources”.  What on earth does that mean?  Will it help explain why Bangladeshis are more susceptible than Africans?  Does it unravel the likely contributions of sex, weight, diabetes, Vitamin D levels?  Does it research the possible, likely even, effects of genetic difference?  All that requires proper scientific research, not some socially aware, politically correct guff.  Where is reference to the research suggesting having blood group A might be a factor (it’s less common in white people).  Deprivation and poverty are not exclusively BAME issues, and certainly the hospital consultants of Asian origin who have tragically died in service could not remotely be described as deprived (I just hope their families are properly compensated).

And of course the whole BAME issue has been stirred into the Black Lives Matter protests.  All lives matter (careful, Wry Observer, people are being hounded for saying that) but readers will know that I recommended withdrawing BAME staff from front-line Covid-19 care a long while back until we knew why they were at higher risk.  But apropos the wild calls to knock down every statue, rename every road and investigate every possible connection with slavery and expunge it, just remember that everybody was in the slave trade; the British, Portuguese and others bought their slaves from African or Arabs, so we had better start investigating which groups did the selling, and expunge them also.  And anyone in the sugar or tobacco industries.  And cotton while we are about it.

Be historical, not hysterical.  The last time this happened in a big way in England was about 500 years ago, when churches were stripped of their statues of saints, wall paintings and other symbols of Catholicism.  It was indeed the Great Iconoclasm.  Must we repeat it?  Why not leave things as they are and be reminded of the sins of the past – not that they were sins back then, always.

Off-topic.  Sorry.


The Wry Observer’s Covid-19 update (36)

Today the papers are full of the “amazing” advance in Covid-19 treatment using a cheap drug.  Not as amazing as I would like, and I wonder how long it will be before the researchers lose their timidity about steroids and actually try a blockbuster dose.  Dexamethasone in small doses does work, but curiously is better in the late, serious patients than in ones treated earlier (I have yet to see the whole data set, so don’t know what early and late may mean, nor what doses were used, or what with).  Hit early and hit hard, I say, and get on with it.  I recall an article many decades ago pointing out that the success of high-dose steroids in a condition called dermatomyositis was so striking that a clinical trial would have been both unnecessary and unethical.  Same here.

Another report flagged to me (I don’t read “The Guardian”) is an apparent government review into Vitamin D and its possible benefits particularly in ethnic minorities.  Yet another piece of the jigsaw that I and some others have already put in.

I am still waiting for a response to my letter and protocol sent to Matt Hancock at the Department of Health.  I sent a copy to my own MP and had a note back, thanking me and saying it would be passed on – to the Department of Health…

There’s an excellent article on the problems of testing from Johns Hopkins at


The Wry Observer’s Covid-19 update (35)

I do hate to say “I told you so” when lives are at stake, but I did say way back that firing steroids at patients should be part of the medical management of Covid-19.  The RECOVERY trial has now reported – no, you’ll never guess – that dexamethasone reduces deaths in ventilator patients by one-third.  See

I suppose that a hypothesis required proving.  How long will it be before high-dose steroid is administered as soon as it becomes plain that the clinical situation is serious, but before it gets to a ventilator situation?  Er, like I suggested

You learned it here first.

Meanwhile deaths continue to fall, and the argument between the “The lockdown should have happened earlier” and the “The lockdown should not have happened at all” continues to simmer, or occasionally rage.  Masks were not thought necessary for the public; now some evidence suggests they might reduce transmission by 40% so perhaps they are necessary.  I think they are, especially having observed the complete abandonment of social distancing among visitors to Rye.  But, as Matthew Parris wrote in his “Spectator” piece, what do I know?

I have written a piece for our local online newspaper “Rye News” which seems to be welcome.  The first part is at

Meanwhile Richard Horton, editor of “The Lancet”, has launched a coruscating attack on the way the coronavirus has been handled, saying “The UK response to coronavirus is the greatest science policy failure for a generation”.  His small book setting this out is on its way, and I will comment on it in due course, but given “The Lancet” had to retract a paper on the benefit of hydroxychloroquine in Covid-19, not to mention its publication of Andrew Wakefield’s fraudulent trial suggesting a link between measles vaccine and autism which resulted in loss of herd immunity to the measles virus, I have to wonder if the pot is calling the kettle black.

The Wry Observer’s Covid-19 update (34)

On 24th April I asked whether the apparent predisposition of ethnic minority groups to Covid-19 was genetic, and subsequently I have emphasised the likelihood, partly because of my concern that the arguments over causation appeared to have moved from the clinical and scientific to the socio-economic.  I have also suggested that trying to run an inquiry now would be like writing a book about a holiday halfway through it, and either inventing or guessing what will happen during the half you haven’t had yet.  As the data change, so will the conclusions.  Yes, we should have an inquiry.  No, we should not have it now; there are still too many unknowns.

Well.  Today “The Times” reports a large study that seems to indicate that being of blood group A is a risk factor.  See  Ok, it hasn’t been peer reviewed yet, but still.  And does this fit with the known additional risks in different BAME groups?  Yes it does.  So before we get hung up on deprivation, racial prejudice etc let’s be sure that it isn’t in the genes, just like sickle-cell anaemia or thalassaemia.

Two good articles in “The Spectator” of 30th May.  The first by pathologist John Lee, whose elegant piece “Count for nothing” underlines my earlier concerns that lack of confirmation of SARS-CoV-2 being present bedevils counting, and advice to pathologists not to do autopsies has hampered research into the pathological processes in the lungs (and elsewhere in the body, for that matter). See It is absurd on the one hand to allow Covid-19 to be implicated by presumption alone while on the other quoting death figures to several decimal places.  While some Covid-19 deaths may be missed, other deaths are quite possibly nothing to do with the virus.  Curiously we appear to have fallen into the same counting trap that was earlier decried in Belgium, which like us has a very high death rate per 100,000 population. It reminds me of an old joke.

Knock, knock!

Who’s there?


Barack who?

What short memories people have!

The second article is by Matthew Parris: “Why has coronavirus fled London?”  ( but you may need a subscription to read it online).  He suggests his partner thinks he is treading on dangerous ground, as he’s not an epidemiologist, saying ‘Nobody’s interested in your theories.’  Sadly that may be true as far as the high-ups are concerned, but the piece exhibits classical hypothesis development.  It notes facts, finds questions to ask about them, draws out contradictions and comes up with an explanation.  Never mind if it’s not the right one; the thought process is immaculate.

I have argued in my book “Mad Medicine” that the duty of scientists is to question facts, find out what cannot fit with a hypothesis and with a plan try and find one reason why it won’t work.  Parris demonstrates a great scientific brain, judged on my criteria, and I think he should be put immediately onto the SAGE committee, as he clearly is a sage.

He ends ‘…who cares what I think?’  Well, Matthew, if it’s any consolation, I do!  But then nobody seems to care much for what I think, either.

A BMJ piece today points yet another finger at the risks of relying on published research as being The Real, Absolute, Science Honesty, or TRASH for short.  The respected journals The Lancet and the New England Journal of Medicine have each retracted a Covid-19 article because the data could not be accessed, and thus could not be verified. Surprise!

Here also is my Rapid Response to today’s BMJ Editorial entitled: Ethnicity and Covid-19:

The rapid pace of scientific research into SARS-CoV-2 shows how reports can be overtaken by events.  The editorial by Patel et al suggests that PHE’s report of disparities between ethnic groups, with a higher incidence of Covid-19 in Black, Asian and Minority Ethnic groups (BAME) has missed a trick by failing to identify why.  I would suggest that when the report was written a “Don’t know” conclusion was better than a false one.  But today a report emerges that the disparity may be due to blood group (1).  This report, albeit awaiting full peer review, points to blood group A as a risk factor.  This may not be sufficient to explain all of the ethnic differences, but it appears to be significant, and confirms earlier small-scale results from China.  BAME people have a higher incidence of Group A than Caucasians.  It also provides a hypothesis as to why:

” Our data thus aligns with the suggestions that blood group O is associated with lower risk compared with non-O blood groups whereas blood group A is associated with higher risk of acquiring Covid-19 compared with non-A blood groups. Unlike for Chromosome 3, we found no difference between patients receiving oxygen supplementation only and those with mechanical ventilation any kind. However, it should be noted that the lead SNP at the ABO locus in our study (rs657152) has been associated with elevated interleukin-6 (IL6) levels in childhood obesity in previous GWAS, providing a hypothetical link to the established association of elevated IL-6 with severity and mortality of Covid-19.  Furthermore, genetic variation at the ABO locus has previously been associated with a number of procoagulant markers such as von Willebrand factor and Factor VIII, and the potential relationship between our genetic findings and the significant coagulopathy that is observed in severe Covid-19 warrants further attention”

This research shows the risk of jumping to conclusions of the basis of unproven hypotheses that fit a non-evidenced sociological construct.  The management of Covid-19 has nothing whatever to do with “systemic racism” in any case.  Racism must be dealt with, but it is dangerous and distracting to conflate unrelated events.

I first suggested that BAME workers in the NHS be protected by withdrawal from front-line care in my blog on April 26th.  I hold to that, whatever the reason for disparity; I am relieved though to note that, despite my Asian ethnic origin (in part) I am blood group O.


1..Ellinghaus D et al.  The ABO blood group locus and a chromosome 3 gene cluster associate with SARS-CoV-2 respiratory failure in an Italian-Spanish genome-wide association analysis.  medRxiv preprint:

I can barely turn the page without finding something else to comment on.  Another article bewails the PHE review and asks why no recommendations have been included.  Obviously the review authors have not listened to my pleas for BAME staff to be protected…  and guess what?!  Later on is a review of hospital Covid-19 admissions in the States.  (BMJ 2020369 doi: ).  Its conclusions are

“Age and comorbidities were found to be strong predictors of hospital admission and to a lesser extent of critical illness and mortality in people with Covid-19; however, impairment of oxygen on admission and markers of inflammation were most strongly associated with critical illness and mortality. Outcomes seem to be improving over time, potentially suggesting improvements in care.”

Impairment of oxygen on admission.  Markers of inflammation.  Fancy that!  Now, what have I been saying for weeks… keep up!