The role that stress and emotion play in the regulation of blood pressure is similarly intriguing. People who are prone to “white coat syndrome” tend to record lower readings at home but even in a home environment the mere fact of wrapping a cuff around your upper arm and feeling it tighten can cause anxiety. Moreover, it is well known that people who report higher levels of stress at home or work, or who have suffered a recent “life” blow such as the death of a spouse or a pet, are more likely to suffer a stroke or heart attack (in one study of work-related stressors, for instance, approaching deadlines were associated with a sixfold increase in myocardial infarction).

Frequent anger and hostility have also been shown to predict coronary events. Thus, in one community study patients with normal blood pressure but high anger temperament scores (as characterised by frequent or long-lasting anger reactions with little or no provocation) were shown to have an odds ratio of 2:3 for fatal or non-fatal cardiac events. While expert opinion differs over the extent to which BP may be a factor, people exposed to stressful situations tend to experience greater BP volatility. “I know that when I have to chair an important meeting or give a series of lectures my systolic reading can be as high as 180; that’s almost certainly due to stress,” explains Peter Rothwell, professor of clinical neurology at the John Radcliffe hospital, Oxford. But while the relationship between emotions and blood pressure is embedded in everyday language – we talk of people being “sanguine” or “hot-blooded” – the average GP has little time for such insights.

Pressure drop

Following my visit to West Middlesex, I was determined to address my hypertension but first I had to know whether my BP was really as high as the hospital reading suggested. To rule out white coat syndrome, I was advised to take one reading at home every morning shortly after waking and another in the evening before bedtime. Once I had a week’s worth of readings, I should add the morning and evening readings together and divide by 14 to get the seven-day average. To ensure the readings were as accurate as possible I took two readings five minutes apart (this was to rule out the “first-reading effect” where the initial measurement tends to run slightly higher, partly due to the cuff inflating for the first time and mild anticipatory tension).

The good news is that my seven-day average was 142/95, putting me at the lower end of the range for stage 1 hypertension. However, there was considerable variation throughout the day. One evening, I was alarmed to see that my BP had spiked to 155/99 and, one morning when I took my BP after drinking a cup of coffee, it was as high as the hospital reading – 165/100 (a single dose of caffeine tends to raise systolic BP by about 3–8 mmHg and diastolic by about 3–6 mmHg). Clearly, I could do more – cutting out coffee for a start - but what else?

I booked a consultation with my GP. After being diagnosed with hypertension in my late 40s, I’d been prescribed the ACE-inhibitor Rampiril and the channel calcium blocker Amlodipine, both at 5mg. A few years later, I upped the dose of Rampiril to 10mg but had left the the Amlodipine dosage unchanged for fear of side effects such as swollen ankles and dizziness. However, after confirming my BP was elevated and quizzing me about my salt intake, my GP suggested I increase the Amlodipine to 10mg and monitor my BP for another week. For the first three days, there was no noticeable improvement, with the same variations I’d observed before – spikes as high as 155/98 some mornings, followed by lows of 128/83 in the evening. By day seven, however, my average systolic reading was 139 and the diastolic reading averaged 93. The new regimen had reduced by BP by 3mgHG and 2mmHG respectively. The effect was small but indicated I was moving in the right direction. The question was, could I get my BP lower still? And was there a better way of monitoring it?

Simulating intimacy

Social media thrives on our anxieties. Hence, if you Google hypertension your feeds will soon be filled with unsolicited ads for supplements that claim to be able to reduce BP naturally. Whereas healthcare professionals are required to be dispassionate when issuing medical advice and make clear if they have a conflict of interest, no such restrictions apply to this influencers online. Typically, the posts begin with an anecdote about some crisis – the declining efficacy of your standard hypertensive medication, for example – before moving to revelation – “this is what your doctor won’t tell you” – followed by cure and transformation – “after taking X my blood pressure is normal again”.

Most insidious of all is the way these posts simulate intimacy in order to sell you a cure. “Each personal revelation, each seemingly candid moment… strengthens the follower’s sense they’re developing a real friendship,” writes Deborah Cohen, whose book Bad Influence, analyses the strategies and claims of health influencers. “This one-sided simulation of intimacy can create a powerful marketing dynamic.”

The ads in my feed typically begin with the phrase, “I’m a cardiologist and high blood pressure is the single most common thing I treat” or some variation thereof. They then go on to describe the cardiologist’s struggle to regulate their BP and how the standard medical regimens have resulted in unwanted side effects. Then, a patient walks into their consulting room and describes how they have achieved miraculous results with beetroot extract or aged garlic or some other naturally occurring compound. “I’ll be honest, I was very skeptical,” reads an ad for Beetwise, a concentrated beetroot extract marketed by Zenther. “Patients bring me supplements every week and 99% of them are nonsense”. No surprise to learn that Beetwise proves superior to other beetroot products on the market. “I’m sharing this because I hope it helps someone else. After 26 years as a cardiologist, I thought I knew every option for blood pressure. Turns out, my patient knew something I didn’t.”

Like most products marketed by the wellness industry, the claims have some basis in fact. Beetroot is a rich source of nitrates. When consumed, oral bacteria convert these nitrates into nitric oxide, a gas that relaxes and widens blood vessels, easing blood flow. Several clinical trials have shown that a single dose of beetroot juice (roughly 250-500ml, or an equivalent nitrate dose) can lower systolic blood pressure by around 4-10 mmHg within a few hours, with the effects often peaking around 3-6 hours after ingestion. Other studies in runners, cyclists and other elite athletes show that dietary nitrate supplementation can also lead to improved endurance and performance. However, because variations in oral bacteria affect how efficiently nitrate gets converted into nitrite, some people are “non-responders” and in those individuals the effects can be modest and short-lived. Beetroot supplements are also not suitable for people at risk of kidney stones and gout. Nevertheless, to judge by the reviews, many people swear by them, claiming that within weeks of taking the supplement their blood pressure was normal and they also felt more energised and enjoyed better sleep quality.

Zenther claims Beetwise contains 400mg per serving and is more effective than other beetroot products on the market because it uses a “cold-extraction” process (apparently, when beetroot is dried or extracted at high temperatures, the nitrate content degrades significantly). I had no way of verifying this but thought, “hey, what have I got to lose”, and ordered a 30-day starter pack. Shipped from Texas, it arrived five days later.

“Beetwise Root Formula, ancient vitality restored”, read the legend on the front of the bottle. Inside were 60 capsules with an instruction to take two a day. On its website Zenther says that each serving delivers “400mg of verified nitrates”. However, confusingly, the label on the bottle stated that each serving was 1300mg. That was more than twice the dose mentioned in the scientific literature and nearly five times the dose were I to take two pills. Was it really necessary to consume so much or was this a ploy to ensure I ran through my supply quicker? I also noticed that Beetwise was marketed as a “dietary supplement” and came with a prominent disclaimer, saying it had not been approved by the Food and Drug Administration and was “not intended to diagnose, treat, cure or prevent disease”.

On the first day and for several days after, there was no substantive change in my BP. By the second week, however, my readings began to track downward, particularly in the evenings before bedtime. My lowest reading was 123/76 but there was also considerable volatility: on some days, my systolic reading was in the 130s or 140s and on other days the gap between my systolic and diastolic readers was as high as 60mmHG. That gap is a measure of pulse pressure – the force needed to push blood during to and from the heart. Ideally, the gap between the systolic and diastolic readings should be no more 40mmHg. A gap of 60mmHG was further evidence of the reduced elasticity in my blood vessels – a condition known as “isolated systolic hypertension”.

Sensors and sensitivity

To get a better gauge of the swings in my BP, I also decided to invest in a wearable device. Typically worn around the wrist, these bands are fitted with photosensitive sensors that claim to be able to track your BP round-the-clock using a system known as photoplethysmography. In the first stage, the light source illuminates the vessels in your wrist; in the second, a photodetector measures variations in light intensity caused by changes in blood volume with each heartbeat. Once the waveform has been captured by the device it is analysed to estimate BP. The idea is that some features of the waveform correlate with physical features, such as arterial stiffness and systemic vascular resistance and, in turn, these can be read as surrogates for BP. The waveforms can also be analysed by algorithms trained on large data sets in order to learn statistical relationships between BP and waveform shape.

It didn’t take me long to identify the two market leaders – Hilo (formerly Aktiia) and HTLH. The advantage of Hilo is that it also comes with an upper-arm calf. This is used to calibrate the wrist band on first use by taking four reference readings. These readings are then used to train Hilo’s proprietary algorithm. Once it has sufficient data points, the band measures blood pressure and heart rate automatically around 25 times a day, including overnight when you are asleep. At the same time, an accelerometer helps Hilo pick moments when you’ve been still long enough to get a clean reading and if conditions aren’t ideal (movement, poor signal), Hilo won’t display a reading. To ensure the band is as accurate as possible, recalibration with the cuff is recommended every 30 days. This clinical validation meets the international standard for blood pressure devices and allows Hilo to be marketed as a medical device. However, Hilo retails at just under £200, plus another £120 for an annual subscription to its app, making it too expensive for most users, including me.

A cheaper option is the HLTH band. Costing £79, the HTLH band 1.0 also uses PPG-style sensors to estimate BP and other metrics, such as heart rate and sleep stages. The difference is it comes with a free-to-use app. However, there is no arm cuff calibration option, meaning the band cannot be marketed as a medical advice. Nonetheless, HTLH’s website claimed that the optical sensors and algorithms in the band had been “clinically validated”.

Fed up with my clunky inflatable cuff, I went ahead and ordered the HTLH band. Short of wearing a halter, I figured it was the best way of getting a snapshot of what my BP was doing while I slept. The band was remarkably easy to charge and I was soon wearing it 24/7. As well as recording my BP, heart rate and blood oxygen, the app gave me the option to take an instant reading at any point during the day. To get a sense of the band’s accuracy, I periodically tested it against my Omron arm cuff. To my disappointment, there was a significant discrepancy. For instance, when I began this article, the HTLH band estimated my BP at a 116/75. However, when I checked it against the Omron, my reading was 135/85. That was hypertensive territory. I have since repeated the exercise several times and on average the discrepancy between the HTLH and Omron is 20 mmHG for the systolic number and 10mm HG for the diastolic. Hardly reassuring.

HTLH does not appear to have published, independent peer-reviewed validation studies in major journals and a recent study of wearables found that many users stop using trackers after only a few months, citing demotivation and a perceived lack of usefulness. This was my experience. Unsure whether I should persevere with the device, I approached a spokesperson for the company, only to be told: “The HLTH Band is a wellness tracking device, not a medical device…[the] readings are designed to help you spot patterns over time rather than to provide clinical-grade numbers.”

Eric Topol, a cardiologist who blogs regularly on medical matters and who has tested the Hilo band, argues that it is too early to say whether such wearables will prove accurate in large scale trials. In particular, he worries they may not catch extreme in BP, whether too high or too low. However, based on his clinical experience, Topol says it is hard to get patients with hypertension to take multiple readings per day and impossible at the night, and that smartphone summaries may be a useful tool for tracking swings in BP and optimising treatment. I am not a cardiologist but in my experience that is sage advice. The problem with blood pressure is that the more you check it the more anxious you become about the numbers. Is my systolic reading too high this morning? What is my pulse pressure doing? How can I get both numbers to rise and fall in synch?

It’s important to keep an eye on the peaks and troughs of course but it’s the averages that matter most and the HTLH band helps me to track my BP trend at a glance. To that extent, it is a useful adjunct to a medically approved device. But it’s no substitute, and if I really want to be sure the pills are working I get out the cuff.

I find it also helps to keep things in historical perspective. CT scans of ancient Egyptian mummies estimated to be more than 40 years old at the time of death show that half had atherosclerosis – cholesterol build up in their arteries. Similarly, studies of the DNA of Ötzi, the 5,300-year-old Iceman who was found murdered high in the Italian Alps with an arrow in his back, revealed several single nucleotide polymorphisms (variations in a single DNA building block) that are linked with atherosclerosis in modern humans. This suggests that had Ötzi, who is estimated to have been 45 at the time of death, not been shot in the back he may have died of a heart attack in later life. In other words, heart disease is the price we moderns pay for living longer.

It is also important to realise that it is perfectly normal for BP to increase with age. Indeed, prior to the SPRINT trial, doctors used a simple rule of thumb – your age plus 100 – to estimate what was an acceptable systolic number. On that measure, my reading of 165/100 at West Middlesex was within range.

My aberrant ECG trace was another matter, however. Given my father’s experience, I’m grateful it triggered further investigation. Without the heart scans, I wouldn’t have known that my heart was showing signs of stress and that, if I wished to avoid the same fate as my father, I needed to control my BP better. If that meant adhering to a medical regimen recommended by my GP and checking my BP more regularly, then so be it. For the time being, I’m also persevering with the beetroot pills. However, I’ve decided to block the ads on my social media feeds and am no longer using the HTLH band to monitor my BP round-the-clock. That is simply a recipe for more anxiety.

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In her new book, Bad Influence, the science journalist Deborah Cohen, describes how a new breed of medical influencers are increasingly employing story-telling techniques and personal anecdotes to sell us wellness products of dubious efficacy. One example she gives is the Oura ring. Retailing for around $500 in the US, the ring claims to be able to track sleep patterns with 95 percent accuracy but is now the subject of a class action lawsuit for allegedly misleading consumers.

What makes these posts so insidious is that they look to be promoting “serious medical products, seemingly backed by reams of scientific evidence and apparently credible healthcare professionals”, writes Cohen. However, conflicts of interest are rarely disclosed and on closer examination the claims often turn out to be exaggerated or lacking scientific rigour.

I’m a medical historian, not a cardiologist, but having struggled with hypertension for several years I figure my experience might provide a useful counterweight to health influencers and wellness boosters.

I was first diagnosed with hypertension in 2008 during a routine visit to my GP. It was a stressful time at work and I was having trouble sleeping so she asked if she could measure my BP. My reading was 150/95 millimetres of mercury (mmHG) putting me firmly in the category of stage 1 hypertension – defined in the UK as BP in excess of 140/90 mmHG but less than 160/100 mmHG.

The discovery sent my heart racing. Four years earlier, at the age of 77, my father had suffered a massive aortic dissection – a rupture to the artery carrying blood from his heart – dying soon afterwards. Like me, my father had been fit and healthy at the time of his crisis and had none of the usual risk factors (he had an athletes’ build, played tennis three times a week and didn’t smoke or drink). According to my GP, if I wanted to avoid a similar fate, I had two choices – to drastically reduce my consumption of salt or commit to taking BP medications for the rest of my life (sodium directly raises BP by causing your body to retain water, which puts extra pressure on the walls of blood vessels; excessive salt consumption also causes the vessels to harden and lose their elasticity).

The advice didn’t sit easily. I have a slim build, exercise regularly, drink moderately and eat plenty of fruit and green vegetables. Indeed, until my mid-40s my BP had always been around 120/80 mmHG, which used to be considered perfect. Now, all of a sudden at the age of 47, I was being told I was at risk of a heart attack.

In the weeks and months that followed, I cut out processed foods and bread (one slice of bread contains an average of 0.5 grams of salt, a sixth of your daily salt allowance) and upped my consumption of fruit and vegetables. I also tried to ensure I got at least seven hours sleep at night and that, rather than opening my laptop the moment I got up, began the day with a dog walk (studies suggest that through their “bonding effect” dogs encourage the release of the love hormone, oxytocin, and that by promoting contact with strangers they counteract feelings of loneliness and reduce spikes in blood pressure).

But no matter how hard I tried to lead a healthy, stress-free life, my BP rarely fell to 120/80 mmHG and on most days it was stubbornly high. When, in 2012, I wrote about the experience in The Observer, I was inundated with inquiries from friends and former colleagues (mostly men) who had had a similar diagnosis. Like me, they were reluctant to submit to a permanent two or three-pill regimen. Long story short, I opted to take the pills and by the time I turned 50 had settled on a low-dose ACE-inhibitor combined with a calcium channel blocker.

For the first ten years of so this combination worked, reducing my blood pressure to around 130/80 mmHG (the first number records the pressure in your arteries when your heart contracts and is known the systolic reading; the second, the diastolic reading, shows the pressure on your heart when it rests between beats). Then, in my 60s, my BP began creeping up again and during particularly stressful periods, such as the pandemic of Covid-19 when I was writing and teaching full time, my systolic reading could be as high as 148 mmHG. However, it wasn’t until I turned 65 last year and attended hospital for a routine foot operation that I learned that my BP was higher than I had realised and had already caused significant injury to my heart. Those changes, about which more later, put me at risk of the same crisis that had killed my father. When I tell you that both my father’s father and his grand-father (my great grandfather) also died of heart-related conditions, you can imagine my alarm.

I immediately bought an Omron home blood pressure monitor and began obsessively checking my BP. The numbers were not encouraging and the more I checked the more anxious I became. Clearly, I had to find a solution. Should I up my dosage or ask the GP to recommend a different pill? Or should I look to alternative therapies and the wellness industry?

My blood pressure journey

What follows is my account of my blood pressure journey. According to the British Heart Foundation (BHF), hypertension accounts for one in four deaths in England and Wales and costs the NHS an estimated £10 billion a year (£16bn for the UK). Moreover, half of us will develop a cardiovascular condition in our lifetimes and, as populations age and survival rates improve, the BHF estimates there could be as many as 10 million people living with cardiovascular disease by 2040 – two million more than today. This is why, in an effort to reduce costs to the NHS, the National Institute for Clinical Excellence has set the threshold for hypertension deliberately low.

The American Heart Association sets it even lower at 130/80 mmHg, conferring a diagnosis of hypertension on nearly half of all US adults. But this one-size-fits-all approach may say more about the medicalisation of the condition and the cost of treating it, than it does about the fitness, or otherwise, of “hypertensives”. As the cardiologist John Hay observed in 1931:

“There is some truth in the saying that the greatest danger to a man with a high blood pressure lies in its discovery because then some fool is certain to try and reduce it.”

A remarkable organ

The heart is a remarkable organ but for centuries it’s structure and mode of operation could only be guessed at. Aristotle likened the heart to a furnace and thought the job of the arteries was to supply it with its vital life force, known as pneuma – literally “wind” or “breath of life” (by contrast, Aristotle thought of blood as a product of food and water). The second century Roman physician Galen concurred. Arguing that the arteries and veins were two separate systems, Galen posited that the heart possessed “invisible pores” that enabled blood to pass from one side to the other.

Like Galen, Leonardo da Vinci could only guess at the heart’s true function. Though he made numerous anatomical drawings of hearts, he never saw a human heart beating in situ. Nonetheless, he showed it comprised four separate chambers (two atria and two ventricles) and that the atria and ventricles contracted asynchronously. He also looked closely at the actions of the heart valves and the flow of blood and, after performing autopsy on a centenarian, produced the first known description of coronary artery disease.

But although da Vinci recognised that the heart was a muscle and used his knowledge of fluids, weights, levers and engineering to try to understand how it worked, he remained wedded to the Galenic system.

It took the English physician William Harvey to overturn the Galenic orthodoxy. In his 1628 book, On the Motion of the Heart and Blood in Animals, Harvey employed experiment and deductive logic to show that the arteries and veins are functionally, if not structurally, connected in the lung and the peripheral tissues. Drawing an analogy with the engines used to supply London’s water systems, Harvey viewed the heart as a muscular pump rather than a furnace. He arrived at this view by studying living animals and observing that it was the contraction of the heart (systole) that forced blood into the arteries. He also realised that the heart pumps so much blood per hour that it is biologically impossible for the body to constantly manufacture and consume it: blood must be recycled and recirculated. In other words, the heart and the body’s arteries and veins were a closed loop.

Today we know that the heart continuously pushes 1.5 gallons of fluid per minute (about 5.5 litres) through some 60,000 miles of blood vessels. That’s enough to go round the world twice. The effort required to maintain this continual flow is extraordinary, equivalent to squirting water five feet into the air out of a garden hose.

Monitors and gauges

The ability to measure blood pressure is quite recent. In 1733 the English clergyman Stephen Hales connected a long, vertical glass tube directly to the artery of a horse and watched as the pressure pushed a column of blood to a height of over eight feet.

This was followed, in 1891, by the invention of the sphygmomanometer (sphygmos being Greek for “pulse”). However, the key breakthrough came five years later with the cuff-based version. For the first time, doctors were able to measure BP in the clinic and compare the readings to those of other individuals with or without heart disease. In 1911, Eberhard Frank described elevated BP for which no cause could be found and labelled it “essential hypertension”. Then, in 1928, physicians at the Mayo Clinic coined the term “malignant hypertension” to describe a syndrome of high BP and inadequate kidney function, which usually resulted in death within a year due to stroke, heart failure, or kidney failure. However, it took the death of Franklin D. Roosevelt to impress the dangers of untreated hypertension on the medical profession and the wider public.

Roosevelt was first diagnosed with hypertension in 1937 when he grew pale on a return flight from Europe and an anaesthesiologist at the Mayo Clinic thought to check his blood pressure. At the time, the recommended treatment was to take frequent holidays and naps and avoid “stress and strain”, something that was impossible for a president on the brink of a world war. The result was that by 1944 Roosevelt’s readings had risen to 200/120 mmHg and he was manifesting clear signs of heart failure. By the time of the Yalta conference in February 1945, Roosevelt’s BP was 260/150 mmHg and he was audibly wheezing. Two months later, at the age of 63, he died of a cerebral haemorrhage.

Roosevelt’s death so shocked Americans that, three years later, Congress passed the National Heart Act, paving the way for the first population-wide study of cardiovascular disease. Launched in 1948 under the joint stewardship of the National Heart, Lung and Blood Institute and Boston University, the Framlingham study – named after the town in Framlingham, Michigan, where the study was conducted - initially recruited 5,209 men and women between the ages of 30 and 62. By the turn of the millennium it had enrolled 15,000 participants across three generations, making it the most influential longitudinal study in the history of modern medicine.

In 1948, little was known about the causes of heart disease and stroke but because death rates for cardiovascular disease had been increasing steadily in the United States since the beginning of the century it was labelled an “American epidemic”. Through lifestyle interviews and regular physical exams, researchers were able to show that hypertension was associated with a nearly four-fold increase in heart attacks and that the key risk factors were cholesterol and smoking. However, at the time, diastolic pressure was the main measure of hypertension and no systolic target was given. This changed in the 1970s when it was recognised that ageing causes the progressive stiffening and narrowing of major arteries, particularly the aorta, leading to higher systolic pressures. By 1977 the consensus was that patients whose BP was in excess of 160/95 were borderline hypertensive. By that measure, my BP would have been within the normal range. But since the late 1970s the threshold for hypertension has been steadily revised downward.

The most significant revision came in 2015 following the SPRINT (Systolic Blood Pressure Intervention Trial) in which 9361 people with a higher cardiac risk but without diabetes were randomly assigned to a systolic blood-pressure target of either 120 mm Hg or 140mm HG. The former experienced significantly fewer cardiovascular events and lower mortality than the 140 mm Hg target group. In response, out of caution, the American Heart Association recommended a target of 130/80 mm Hg, conferring a diagnosis of hypertension on nearly half of all US adults. By contrast, in the UK, where the threshold is 140/90, a third of British adults – 16 million people – are currently considered hypertensive.

A wake-up call

One of the problems of relying on a mechanical cuff to measure BP is that it is prone to error. And as the phenomenon known as “white coat syndrome” attests, the mere fact of having one’s blood pressure taken by a medical professional is sufficient to send some people’s readings soaring. This had been my experience when in April this year I attended West Middlesex Hospital for pre-assessment prior to my operation and recorded a reading of 165/100 mmHG. Even allowing for white coat syndrome, by current measures that was too high (studies have shown that for every 20 mmHg increase in systolic blood pressure above normal levels, the risk of death from heart disease and stroke doubles).

Further cause for concern came when I was hooked up to an electrocardiogram (ECG). A normal ECG trace appears as a series of low troughs punctuated by sharp, jagged peaks, with the peaks rising and falling with the same frequency. But on my trace, there was a small secondary blip before the wave subsided. To my eyes, it looked like a hiccup. The nurse’s expression suggested otherwise.

Worse news came when, following my visit to West Middlesex, I was sent to another clinic for transthoracic echocardiography followed by a full scan of my heart using magnetic resonance imaging. In the first, ultrasound is used to capture moving images of the heart’s valves and chambers. In the second, a powerful magnet and radio waves create an even more accurate image. Once doctors have a snapshot of the heart under normal conditions, a dye is injected into a vein in your arm to speed up the heart rate. This shows how your heart functions under pressure (like exercising) and is used to identify inflammation and structural weaknesses.

Both read outs showed evidence of aortic regurgitation and a left bundle branch block (LBBB). In a healthy heart during the systole phase both ventricles contract, causing the left ventricle to push blood into the arteries and out to the body. Simultaneously, the right ventricle pumps blood into the lungs to absorb oxygen. This is followed by the dystole phase as the ventricles refill with blood. But when, following the systole phase, the aortic valve fails to close tightly, blood flows back along the descending abdominal aorta into the left ventricle, causing aortic regurgitation. This, in turn, delays or blocks the electrical signals to the LBBB, prompting the right ventricle to beat before the left.

That explained the second small peak on my ECG but thankfully the regurgitation was “mild”. I would need regular check-ups to ensure the condition didn’t worsen but, for the present, it was a matter of monitoring my blood pressure regularly and keeping an eye on the peaks and troughs.

To be continued tomorrow….

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Now imagine that this pathogen spreads via coughs and sneezes like Covid-19 and has been engineered so that its victims initially feel euphoric, making it more likely they will spread the infection to others. Now imagine that the pathogen has also been “booby-trapped” so that it is resistant to antibiotics, confusing doctors and undermining trust in medical science.

This is the Doomsday scenario the journalist Annie Jacobsen invites us to consider in her new book, Biological Warfare, imagining the release of a weaponised plague virus from a secret Soviet research facility. Unlike nuclear war, which is theoretically survivable, the release of a germ modified to be hyper-virulent and for which there is no known cure “could be twenty-first-century humans’ last invention”, she writes.

But it doesn’t necessarily have to be a deliberate act of war. Humans could just as easily be wiped out by an accident at a laboratory where scientists have been engineering pandemic pathogens in search of medical countermeasures with which to neutralise them. By inserting genes to make the pathogens more communicable or to help them evade the immune system, the argument goes, these experiments also enable scientists to develop new vaccines and antivirals before disaster strikes.

To the Pentagon and the CIA, this is an entirely legitimate exercise that falls under the rubric “biodefence”. Unfortunately, it also describes the “gain-of-function” (GOF) experiments involving SARS-like bat viruses that were being conducted at the Wuhan Institute of Virology (WIV) in China prior to the pandemic of COVID-19.

Following the sudden emergence of SARS-CoV-2, the virus of COVID-19, in Wuhan in December 2019, GOF has become a dirty word in US government circles. Spurred by conspiracy theories about nefarious Chinese actors and speculation about a “lab leak”, in late July the Trump administration rewrote the rules governing GOF research.

Under the new policy, the US government will end its support for what it calls “dangerous” gain-of-function (DGOF) research and strengthen oversight of life sciences research that “could pose significant risks to public health, biosecurity, or national security”. GOF research would not be banned outright. However, in practice the new policy would make it far harder for scientists studying pathogens such as influenza, Ebola and SARS with known pandemic potential to manipulate their genomes. Instead, such research would be assessed by an independent third-party review body using a “risk-based framework”.

The problem is risk is in the eye of the beholder and the new directive does not say who will sit on the review body and how they will make such adjudications. This could not only be bad for biodefense, it could be bad for public health, making it more difficult for scientists to study and develop counter-measures against pathogens with a theoretical but currently unknown potential to spark major epidemics and pandemics.

As the ASM, formerly the American Society for Microbiology, put it in a statement responding to the US directive: “The new policy … broadly defines several categories of research that, if shut down, will impede our ability as a nation to address infectious disease threats and respond to future outbreaks.”

Privately, many scientists go further, worrying that the new policy will be “a “bureaucratic nightmare” and have a “chilling effect” on research that uses recombinant DNA and gene-splicing techniques to explore ways of counteracting viruses and other pathogens that arise spontaneously in nature. The fear is that instead of judgements as to what constitutes DGOF being made by experts, in future it will be made by politicians hostile to mainstream science and vaccinology.

Even scientists who have questioned the benefits of GOF research worry that the new directive may be unworkable. “The error bars for how [the policy] could be implemented range from too permissive to too restrictive,” Marc Lipsitch, an epidemiologist at Stanford University who has advocated in the past for stricter controls on GOF, told Science.

It is no coincidence that the policy announcement came days ahead of Anthony Fauci’s appearance in August at the Senate Homeland Security Committee. The panel’s chairman, Senator Rand Paul, holds Fauci, the former director of the National Institutes of Health (NIH), who was pardoned by Biden in anticipation of a Republican witch hunt, personally responsible for the supposed lab-leak at the WIV and the research that led up to it.

From 1984 until his retirement in 2022, Fauci headed the National Institute of Allergy and Infectious Diseases (NIAID), a sub-division of NIH. During that period, scientists at the NIAID succeeded in reconstructing the genome of the 1918 “Spanish influenza” virus – a feat that had previously been thought impossible (for more information, see my podcast, “Resurrecting a killer”).

That research provided scientists with invaluable insights into what made the virus, which killed an estimated 50 million people worldwide, so deadly – insights that were subsequently used to identify virulence factors in other influenza viruses, including H5N1 bird flu. At the same time, the NIH supported GOF experiments on bat-derived SARS viruses at WIV and elsewhere. Although Chinese scientists created versions of these viruses so they could infect and study their virulence in mice, Fauci has long insisted these viruses were genetically far removed from SARS-CoV-2 and could not have caused the pandemic. That view is backed by biosafety experts and scientists with relevant expertise of the virology and epidemiology of COVID-19 – in a recent survey, 77 percent said they believed the pandemic was the result of a natural zoonosis. That position is endorsed by 23 of the 27 original members of the Scientific Advisory Group for the Origins of Novel Pathogens – the group commissioned by the World Health Organisation (WHO) to analyse the peer-reviewed literature on the pandemic.

Not that any of this matters to Paul, who opened last week’s Senate hearing by accusing Fauci of being personally responsible for the pandemic lockdowns by “aiding and abetting” scientists to conduct dangerous GOF experiments in Wuhan. Rather than risk incriminating himself, Fauci elected to take the Fifth and now faces being held in contempt of Congress.

Paul’s narrative is seductive precisely because it is simplistic, reducing a complex scientific topic to a digestible soundbite. “The American people weren’t asking for a semantics debate over what is gain of function,” said the Senator at one point, seemingly unaware or the irony of his statement.

Unfortunately, Jacobsen’s book feeds off this narrative and is guilty of falling into many of the same traps. “Gain-of-function is a euphemism… another way of saying ‘biological weapons engineering’”, insists one of Jacobsen’s “expert” interviewees.

Except it isn’t – at least not when the object is a pandemic vaccine aimed at preventing needless death and suffering.

Nor, despite acknowledging that the debate over Covid’s origins is responsible for “the deepest rupture in truth since the Vietnam War’, is Jacobsen much interested in the more scientifically plausible account of Covid’s origins. Instead, we are told there is no such thing as “safe” GOF research. “Gain-of-function is evil”, a senior presidential advisor on weapons of mass destruction informs her flatly (“no nuance there,” Jacobsen writes).

Jacobsen is right to point out the dangers of GOF. According to a recent survey, there are currently 110 top security BSL-4 labs scattered across 34 countries and more than 3,000 BSL-3 labs in 149 countries. That presents a lot of opportunities for things to go wrong – and, from time to time, things do go wrong: in 1988, a Soviet biological weapons engineer was fatally wounded when he accidentally pricked himself with a syringe containing Marburg, a deadly haemorrhagic virus similar to Ebola; another example is the surprise “re-emergence” in 1977 of a strain of H1N1 influenza that had been circulating in the 1950s (the fact that the virus was almost genetically unchanged after a 20+ year hiatus points to an accidental release from a Russian or Chinese laboratory or a vaccine trial, though the exact source has never been confirmed).

There have also been laboratory accidents involving the species of SARS responsible for the 2002-2003 global outbreak - the first, and until COVID-19, biggest outbreak involving the virus. And in 2019, a researcher conducting GOF research at the University of Wisconsin was scratched by a ferret infected with a lab-enhanced strain of H5N1. That accident had followed a brief moratorium on such experiments and the issuing, in 2014, by President Obama of the Dual Use Research of Concern (DURC) policy, followed, in 2017, by a new framework for research involving “Enhanced Potential Pandemic Pathogens”, involving influenza, SARS and MERS, among other viruses. The new Trump directive rewrites those policies.

But given the explosion of GOF research since the advent of recombinant DNA techniques in the 1970s, perhaps the biggest surprise is that there haven’t been more lab accidents. It is also misleading to suggest that GOF research always aims to make pathogens more virulent or transmissible. A good example is modifying E.coli to enable the bacteria to produce insulin for diabetics, or using GOF techniques to train viruses to attack tumour cells while leaving non-cancerous tissue unaffected.

“Unlike nuclear war,” the former Senate majority leader Tom Daschle, whose office was subject to a mysterious anthrax attack in 2001, tells Jacobsen, a major biological attack will be “a long painful, slow death.” But the same is true of outbreaks by naturally occurring pathogens such as Ebola.

Take the Bundibugyo species of the virus currently sparking a major emergency in the Democratic Republic of Congo (DRC). To date, 2,000 people have suffered slow and painful deaths from the virus and, according to the WHO, the outbreak in the DRC could soon “eclipse” the 2014-16 West African outbreak which killed in excess of 11,000.

Little wonder then that many scientists argue it is nature, not man, that is the biggest bioterrorist of all.

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I write “privilege” because in 2018 Fauci was not the MAGA hate figure he is today but a respected biomedical researcher and beacon of public health. As director since 1984 of the National Institute of Allergy and Infectious Diseases (NIAID), a division of NIH, Fauci had fast-tracked antiretroviral drugs for people living with HIV, bolstered America’s bio-defence capabilities following the 2001 anthrax attacks and helped coordinate the US’s medical response to the 2014-2016 Ebola outbreak in West Africa.

It is a testament to Fauci’s capabilities that, unlike today, in 2018 he commanded wide bipartisan support and the NIH had just been award $37 billion by Congress for research into a range of diseases. Most of the funding was earmarked for Alzheimer’s disease and the US’s opioid epidemic, but it also included $40 million for research on a universal flu vaccine.

This was one of the subjects I had come to talk to him about.

The timing of our meeting was no accident. May 2018 marked the 100^th anniversary of the 1918 Spanish influenza pandemic and, in anticipation, I had been commissioned to make a podcast about its history and science (full disclosure: the podcast was funded by the Wellcome Trust, whose then director, Jeremy Farrar, was a confidante of Fauci’s and would soon face allegations of having helped him suppress concerns that SARS-CoV-2, the virus of Covid-19, may have been deliberately engineered at a Chinese lab).

In preparation, I had already spoken to several leading experts on “gain-of-function” experiments involving the 1918 H1N1 virus and the H5N1 bird flu virus, then the principal focus of pandemic concerns. But walking into Fauci’s office the first thing that struck me were the wall-to-wall framed photos of him alongside prominent politicians and celebrities from the worlds of film and showbiz.

Following the publication on Tuesday of Fauci’s private notes and diaries by Rand Paul, a long-term critic who heads the Senate’s Homeland Security panel, the media zeroed in on the juiciest revelations in Paul’s document dump. These showed Fauci revelling in his connections to Barbara Streisand and other Hollywood celebrities – Streisand wrote to Fauci regularly on a range of topics including whether she and her husband James Brolin should get booster vaccines for COVID-19. The diaries also painted a picture of Fauci as someone obsessed with his public image.

“It is not hyperbole to say that today I am the most famous and talked about person in the country and one of the most recognizable in the world,” he wrote after a flattering front-page story in The Washington Post.

But the potentially most damaging disclosures were that at the same time as Fauci had been telling the public that SARS-CoV-2 had emerged from a live animal market in Wuhan, in his diary he wrote that the market was merely “the amplifier” for the outbreak. His notes also contain emails and meetings with Farrar and other scientific experts were they discuss the possibility that the virus could have been engineered at the Wuhan Institute of Virology. You can read more about that theory and why most reputable experts consider it unlikely in my post on the likely natural origins of Covid.

It should be said that there is nothing particularly new in the latest disclosures as most of the information was already in the public domain. Instead, Paul’s decision to publish Fauci’s confidential musings looks like a blatant attempt to make Fauci the fall guy for the Covid lockdowns and the economic harms that followed. Little wonder that Fauci, who was pardoned by Biden at the end of his presidential term, opted to take the Fifth when questioned by Paul on Wednesday.

Nor was it a secret that Fauci was proud of his showbiz connections. When I visited him at his office in 2018, the first thing I noticed was the prominent picture of him and Streisand on the wall, followed by photos of Fauci alongside Bono and Michael Jackson. But taking pride of place were a series of photos of Fauci with Ronald Reagan, Bushes senior and junior, Bill Clinton and Barack Obama. There was just one president missing: Donald Trump.

I asked Fauci about this and he confirmed that 13 months into Trump’s first term he had yet to meet with the 45^th president of the United States. This changed, however, when the pandemic hit and Trump, apparently impressed by Fauci’s scientific credentials and reputation for being a “smart” bureaucratic operator, appointed him to his Coronavirus Task Force. This is confirmed in Fauci’s diary. Noting that Trump seemed to be “enamoured” of him, Fauci observed: “We are developing a very unique and interesting relationship.”

However, this changed when Fauci began advocating for face masks, school closures and stay-at-home measures. And his relationship with Trump soured further when the president began amplifying coronavirus conspiracy theories and advocating for unproven cures, such as Invermectin.

As the child of Italian immigrants, Fauci was more than a match for Trump, who grew up in the lap of luxury in Queens (as a child, Fauci had helped out at his father’s drugstore in Brooklyn). Despite standing just 5 feet 7 inches, Fauci had captained his school basketball team and exuded the energy of a guy used to motoring up and down a basketball court. On meeting him, I was immediately reminded of other leading biomedical researchers of the postwar era, such as Jonas Salk and Stanley Plotkin, whose passion for public health had been fired by the New York public school system and their experience growing up during a period when polio and measles could end or severely impair a child’s life.

Our conversation on that unseasonably hot winter’s afternoon covered a range of topics, from emerging and re-emerging infectious diseases such as Ebola, Nipah and Zika, to the threat posed by unknown pathogens. But the subject that occupied Fauci’s waking and sleeping hours was influenza and the prospect of another respiratory pandemic on the scale of 1918. This was two years before anyone had heard of Covid remember but in retrospect Fauci’s words strike me as prophetic. You can listen to the interview on my podcast,“Vax and the Facts”.

“The panic associated with a disease like that that could be spread by the respiratory route would be unimaginable,” he told me. “That’s why we need to take the possibility of a pandemic very seriously”.

“One of the lessons [of 1918] is that really bad pandemics can and have occurred…. If you look at the numbers – 50 million people died – and put that in the context of the population of the United States and the population of the world today, that number would be three, four, five times [higher].”

However, the most interesting part of our interview came when I asked Fauci about his current research priorities. This was a cue for a passionate speech about the latest vaccine technologies and his dream of a universal influenza vaccine.

Fauci explained that the West African Ebola epidemic had resulted in around 12,000 deaths but in a typical year seasonal influenza accounted for the same number of fatalities in the US alone. And in a severe flu year, US deaths could be as high as 51,000. Indeed, this is what had happened in in 2014-15 when Ebola had been raging inSierra Leone and Liberia. Even in the 2016-17 season just passed, flu deaths had totalled 38,000 and Fauci told me he feared the 2017-18 season could be even worse (he was right: that year, 58,000 men, women and children in the US died of flu).

Interestingly, Fauci credited the NIAID’s involvement in vaccine research to Clinton and a chance meeting with him in 1996. Clinton had called him to the White House on a whim for an update on HIV and during their conversation had wondered why there was still no vaccine against AIDS. Fauci explained that the HIV virus was extremely complex and that research was silo-ed at different centres, adding: “It would be wonderful if we could put [the researchers] in one place and have them talk to each other every single day.”

To Fauci’s surprise, five months later, at a university commencement address, Clinton, announced he was creating the NIH Vaccine Center. That decision would prove critical when SARS-CoV-2 emerged in 2019 and there was an urgent need to fast-track vaccines for COVID-19 using the latest RNA vaccine technology.

At the time, Trump praised Fauci’s expertise and foresight, but following Tuesday’s diary dump Trump predictably told the press that Fauci had been “a much bigger player in the Biden administration” than in his and he soon “grew tired of him”.

It would be fascinating to know what Fauci has to say about that but for the moment his lips are sealed. However, for a clue we need look no further than his diaries.

“Apparently the WH [White House] is very upset that I am being profiled and it looks like I am putting down the POTUS and becoming a star that outshines him,” reads Fauci’s entry for May 23, 2020. “The press is playing into this, as is the tweet storm. Very stressful!!”

Boy, do we know it!

After England’s disappointing exit from the World Cup last week at the hands of their arch-rivals Argentina, it is hard to escape the conclusion that when the opportunity came to advance to their first final in 60 years, England blew it. Or rather, Thomas Tuchel, England’s German-born coach, blew it with his bizarre decision in the 72^nd minute to swap Antony Gordon for a defender in an attempt to protect England’s narrow 1-0 lead.

We all know what happened next. Scenting blood, Lionel Messi upped the tempo and in two moments of footballing genius assisted Argentina to two goals and a place in tonight’s final with Spain. In psychological terms, you could say Tuchel misjudged the moment whereas Messi rose to it.

Or as an ontologist friend puts it, “One was operating in ‘Kairos time’, the other wasn’t”.

From the Kairos Palestine II document calling for an end to the “genocide” in Gaza and incursions by Israeli settlers, to the Kairos collective of theologists, academics and journalists calling for serious engagement with climate change, the notion of Kairos time is everywhere.

As the authors of “The Dawn of Everything”, which challenges the notion of Western civilization as a story of lineal progress and calls for a profound shift in our thinking to meet the challenge of climate change, put it: “We appear to be heading into what the ancient Greeks called Kairos, a window of opportunity when our capacity for change is put to the test.”

Andy Burnham, who will become Prime Minister tomorrow, invoked a similar spirit of Kairos in his first speech as leader of the Labour Party on Friday. Addressing colleagues at a special session of the Trade Union Congress in central London, he promised to break with the “deindustrialisation of the 1980s” and neo-liberalism, describing his victory in the Makerfield by-election as “the most significant change moment in our politics for 40 years”.

“It will take us to a country where life is more affordable and all people and places are lifted from where they are now,” he promised, before adding:

“This is the moment to speak for all parts of the country and unite people in a common cause.”

In Greek myth, the god Kairos personifies exactly this sense of an auspicious or opportune moment. The youngest son of Zeus, he is usually depicted with a forelock at the front of his head and shorter hair at the back and sides (think a Greek Erling Haaland).

During the Olympiad, Kairos’s altar stood at the entrance to the stadium opposite Hermes, the god of speed. But whereas Hermes is shown with wings on his heels, Kairos also has wings on his shoulders and balances a set of scales in his arms.

On sighting Kairos, athletes at the Olympiad thought they could steal a march on rivals by grabbing hold of his forelock as they passed, much as a runner grabs a baton during a relay race. However, the timing had to be just so since with one kick of his winged feet Kairos would be gone and the moment would have passed.

Another analogy is with weaving and archery. Think of the moment when the weaver draws the yarn through a gap that opens in a warp in a piece of cloth. Or the legendary “trial of the bow” in The Odyssey where Homer’s hero must shoot an arrow cleanly through the aligned eyelets of 12 axe heads in order to prove he’s Penelope’s returning husband and the king of Ithaca.

It is the marshalling of Odysseus’s talent at precisely the right moment in time and place that dictates the outcome of Homer’s epic poem and, by extension, other turning points in history.

For England, that window opened at precisely 55 minutes into their semi-final with Argentina when Morgan Rogers crossed the ball from the right and Gordon stole into into the Argentine penalty area from the left to sweep the ball into the net, and it closed when Argentina equalised 30 minutes later. Although England later redeemed themselves - and to a lesser extent Tuchel - with their surprise 6-4 victory over France on Saturday, there is no telling when or where such an opportunity might present itself again.

Nor is there any way of knowing whether Burnham has what it takes to grasp the opportunity afforded him by his victory in Makerfield to deliver on his radical agenda to devolve power and wealth to the regions. However, in recognising that in order for that to happen, it has to happen now rather than later, Burnham has taken the crucial first step.

Whether there is still time to reverse climate change and provide justice to Palestinians driven from their homes in Gaza, is harder to say. Certainly, when it comes to climate change our efforts have been faltering and, so far, have fallen far short of what is required. Despite governments’ repeated pledges to cut carbon emissions, human-induced global heating is currently running at 1.37°C above pre-industrial levels. Unless something changes quickly, it is hard to see how we can avoid breaching the critical 1.5°C threshold by 2030.

At time of writing, an end to the war in Gaza appears similarly unlikely. The Palestinian Christian Ecumenical Initiative (PCEI) drafted the first Kairos document calling for Palestinians to be allowed to “live in dignity” in their homeland in 2009. Since then, animosities between the warring parties and the loss of life in Gaza has only worsened. However, argues the PCEI, as awful as the decades-long animosities have been, something shifted with the October 7th Hamas attacks and Israel’s devastating and, arguably, criminal response.

“We live now in a time of genocide, ethnic cleansing and forced displacement unfolding before the eyes of the world,” write the authors of Kairos II. “This moment - a moment of truth - demands from us a new stand unlike any before it.”

Many will disagree with the characterisation of Israel’s assault on Gaza as a “genocide”, let alone other parts of the document crudely portraying Israel as an “apartheid, colonialist-settler state.”

But if the last few years and the 23rd FIFA World Cup have taught us anything, it is that fine words and heartfelt promises will only get you so far. It’s what you do in that moment on the pitch when Kairos suddenly presents himself that matters.

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Then, as with outbreaks of measles today, the Legionnaires’ Disease outbreak coincided with celebrations marking the adoption of the Declaration of Independence. And then, as now, the United States was a deeply divided society and conspiracy theories were rampant.

For some, the fact that the outbreak occurred during the American Bicentennial and that many of the victims were veterans of World War II and Korea, was no accident. Speculating that the “Philly killer”, as the press labelled the mysterious pathogen, was the work of a malign foreign power, the Philadelphia Veterans of Foreign Wars described it as “a sneak attack against the finest kind of Americans.”

Philadelphia’s mayor, Frank Rizzo, a tough talking former policeman and close friend of Richard Nixon, blamed activists opposed to the Vietnam War, while his spokesman, Albert Gaudiosi, suggested the outbreak might be the result of a covert CIA operation using chemical and biological weapons.

Today, we know better. After an exhaustive six-month investigation, in January 1977 the CDC announced it had isolated the infective agent – a common organism that grows readily in ponds and stagnant water, including the cooling towers of hotels. Labelling the bacterium, Legionella pneumophila, the CDC speculated the organism had become aerosolised when water had been sprayed across the fill at the top of Bellevue-Stratford’s cooling tower, splintering the bacteria-rich film into tiny droplets. It was thought that some of these droplets had been drawn into the air intake vents of the hotel’s air conditioning system and circulated throughout the hotel’s suites and bars where the droplets were drawn into peoples’ lungs. Other droplets had cascaded down the side of the hotel, infecting people on the sidewalk. Unfortunately, conclusive proof evaded the CDC as by the time investigators had identified the organism the cooling towers had been cleaned and Legionella from the water tower could not be recovered.

Despite this, following the outbreak at the Bellevue-Stratford public health agencies began routinely monitoring and testing water sources like cooling towers and plumbing for Legionella pneumophila and although the organism continues to spark occasional outbreaks, like the one on the Upper East Side of New York this week (see below for more details), it no longer poses a major threat to public health and is no longer the subject of conspiracy theories.

If only the same were true of other pathogens whose source or cause has yet to be identified. From Ebola to Covid-19 to hantavirus, epidemics of emerging and poorly understood infectious diseases are regularly linked to theories about bioweapons, population control and “lab leaks”, to name a few common conspiracy tropes. That they might be the result of natural processes and the by-product of climate change and alterations to the built environment is something that many people find hard to accept.

Why is this the case? Why do epidemics provoke so much mistrust and dissent? And what lessons does the 1976 Legionnaires’ Disease outbreak hold for the management of other outbreaks, now and in the future?

These are pertinent questions on the 250^th anniversary of the Declaration of Independence. It is an anniversary that is supposed to bring Americans together but judging by Trump’s intemperate Independence Day address at Mount Rushmore, in which he warned of a growing “communist menace”, Americans remain as divided as ever.

Conspiracy theories and uncertain knowledge

Nature abhors a vacuum but conspiracy theories thrive when knowledge of epidemics is uncertain or wanting. This is particularly true at times of epidemic crisis. Psychologically, it is comforting to believe that outbreaks happen for a reason. An invisible threat of unknown provenance challenges our sense of security, spreading fear and fuelling the search for alternative explanations.

In the pre-microbial era, before the birth of bacteriology and the science of epidemiology, the belief that epidemics were expressions of Divine wrath was a source of psychological comfort. The solution was to repent one’s sins and cleave more keenly to religious strictures. But when during the 14^th century Black Death, recurrent outbreaks of bubonic plague reduced Europe’s population by between a third and a half, the punishment seemed disproportionate. With their faith challenged, people looked for scapegoats, blaming Jews for poisoning the wells form which Christians drew their drinking water. Later, observing that many epidemics originated in the East, this scapegoating was directed at the Chinese and other Asiatic peoples – hence the designation of cholera as the “yellow peril”.

By the early 19^th century, as epidemiologists began to link infectious diseases to environmental and social conditions, such as poor sanitation and overcrowding, conspiracy theorists began to direct their ire at health authorities instead.

For instance, during the 1832 Parisian cholera epidemic, the German poet Heinrich Heine reported that the Parisian sanitary commission ordered mounds of rubbish that could be a source of contamination to be hauled beyond the city limits. In response, ragmen who made their living sorting through the debris spread rumours that those who had died of cholera had been poisoned by the health authorities and took to the streets in protest. “The more extraordinary these reports were, the more eagerly they were received by the multitude”, noted Heine in an echo of today’s coronavirus conspiracy theories.

Soon, physicians and surgeons who were perceived to be profiting from treatments and cures predicated on their science also became a focus of suspicion – hence the rumours that doctors, like the Edinburgh physicians Burke and Hare, were murdering cholera patients to harvest their bodies for medical dissection, or the rumours during the 1889 “Russian” influenza epidemic that doctors were exaggerating the dangers of influenza to market quinine and other proprietary remedies.

And so it has continued to the present day with conspiracy theories claiming that Covid-19 is a “hoax’ designed to boost the uptake of vaccines. Nor is there anything new about theories linking disease outbreaks to biowarfare. In 1918, the “Spanish” influenza was blamed on biological weapons released by German U-boats and in the 1990s, the KGB seeded a widely believed conspiracy theory that HIV had been engineered at a U.S. military lab.

The appeal of these theories is that they offer a simple explanation for complex biological events. The same was true of the conspiracy theories surrounding the 1976 Legionnaire’s Disease outbreak.

The outbreak occurred just two years after Gerald Ford had assumed the presidency following Nixon’s resignation over the break-in at the Watergate building in Washington DC. Coming in the wake of the Vietnam War, Watergate undermined trust in politicians and democratic institutions. It didn’t help that in 1976, the US economy was in recession and consumers were still reeling from the 1973 oil embargo which, as with Iran war and the closure of the Strait of Hormuz today, had sent energy prices soaring.

The paranoid style

In 1964 the historian Richard Hofstadter had coined the term paranoid style to describe “the sense of heated exaggeration, suspiciousness and conspiratorial fantasy”, he detected in extreme right-wing movements, such as the 1964 campaign for the White House by Barry Goldwater, the militant anti-communist Republican senator from Arizona. By the 1970s this paranoid style was arguably no longer confined to the Right but, following the assassination of leading lights of the civil rights movement, had also begun to infect the Left, hence the popularity of conspiracy theories blaming the deaths of Jack and Bobby Kennedy and Martin Luther King on variously the CIA, the Mafia and the Ku Klux Klan.

Nor did it help that in 1975 the Rockefeller Commission had revealed that the CIA had been conducting secret mind-control experiments using LSD and other chemical and psychological means. Or that in 1972, a medical whistleblower had revealed the truth about the Tuskegee Syphilis Study, an unethical 40-year medical experiment in Alabama in which 600 impoverished African-American share-croppers had been allowed to develop untreated syphilis so that researchers could observe the natural progression of the disease.

On July 2 1976, two weeks before the outbreak at the Bellevue-Stratford, Ford had sought to unite the nation with a Bicentennial address in which he described the Declaration of Independence as “the Polaris of our political order – the fixed star of freedom”. Ironically, given subsequent events, one of the few American institutions which still commanded wide public support at the time was the CDC.

In the 1950s, the agency had eliminated malaria from north America and spearheaded vaccination drives against polio and other disease. And abroad, its Epidemic Intelligence Service (EIS) was at the frontline of the global campaign to eradicate smallpox – a campaign which would achieve its goal in 1980. Thanks to these efforts and other public health initiatives, it seemed to many experts that infectious disease would soon be a problem of the past.

The puzzle of the century

The Legionnaire’s Disease outbreak, followed by the outbreak of HIV/AIDs six years later shattered that hubristic conviction. Deploying classic epidemiological methods, David Fraser, the head of the CDC’s Special Pathogens Branch, ordered his officers to compile line lists of the victims at the Bellevue-Stratford and map the distribution of the infections in time and space. The disease, whatever it was, caused an aggressive form of pneumonia but laboratory tests for influenza and common bacterial causes of pneumonia, such as psittacosis and Q fever, proved negative. Not knowing whether the pathogen was airborne or transmitted via food and/or water, Fraser ordered EIS officers to comb the hotel’s suites and conference rooms for common environmental and chemical contaminants. They began by checking the cadmium pitchers in which bar staff had mixed the Legionnaires’ Bloody Marys (cadmium poisoning resembles influenza). Next, they swept the elevators and hospitality suites. But once again the tests were negative.

The longer the mystery remained unresolved the wilder the speculation became. Perhaps the Legionnaires had been exposed to phosgene gas, a pulmonary agent first deployed by the Germans in World War I and which causes choking and shortness of breath. Or perhaps they had been poisoned with nickel carbonyl, a highly toxic liquid that can trigger chemical pneumonia and cardiorespiratory failure.

By December, Fraser was at a loss. “The illness resembles an infectious disease, but there is no secondary spread and microbiological studies have been negative”, he admitted in his final report on the outbreak. “No toxin is known that causes just this pattern of disease and toxicological studies are also negative so far.” Despairing of finding the pathogen, Robert Sharrar, chief of communicable disease control for Philadelphia, described the outbreak as “the epidemiological puzzle of the century”.

It didn’t help that by now the search for the pathogen was in danger of being overshadowed by the fiasco over what became known as the “swine flu affair”. Four months before the outbreak at the Bellevue-Stratford, the US Army had isolated a new strain of swine influenza at Fort Dix, New Jersey. Worried that it might be a pandemic strain similar to the 1918 “Spanish” influenza, scientists at the CDC and other agencies persuaded Ford to immunise millions of Americans. But in the event the swine flu proved no more severe than a regular seasonal influenza, prompting criticism that the threat had been hyped for the benefit of pharmaceutical companies.

It took a low-ranking CDC microbiologist to solve the mystery of the Legionnaires’ outbreak. Stung by the criticism of the CDC, Joseph McDade had returned to his laboratory shortly after Christmas determined to have another go at identifying the pathogen. A specialist in rickettsial diseases, McDade had fairly limited experience in public health microbiology, much less the politics surrounding major disease outbreaks. But his lack of expertise would work in his favour, prompting him to depart from standard laboratory procedures and conventional patterns of thought.

While examining smears of liver sections from guinea pigs inoculated with lung tissue from Legionnaires’ patients, McDade had noticed occasional clusters of peculiar rod-shaped bacteria. On a hunch, he applied a stain that had been developed for rickettsial organisms in the hope of bringing the bacteria into sharper view. Then, having allowed the bacteria to grow freely in the liver tissue, McDade injected the material into chicken egg embryos. The embryos immediately started to die and when McDade stained the tissue he found the same rod-shaped bacteria growing in clusters. The final proof came when he mixed the organism with serum from Legionnaires’ patients and the bacteria “lit up”, signalling a strong antibody reaction.

Science and the “unprepared mind”

McDade’s breakthrough is a classic example of the importance of scientists thinking outside the box. The reason other CDC microbiologists had missed the Legionella organisms is that they did not react to standard bacterial stains. But McDade was a novice to public health microbiology and had not been schooled in the same thought processes and techniques as his colleagues. Instead, he used a stain that no one else had considered. In this regard, he represented an exception to Pasteur’s dictum that “fortune favours the prepared mind”.

The discovery of Legionella pneumophila enabled Fraser to account for the peculiar epidemiological pattern observed at the Bellevue-Stratford. During the latter stages of the investigation, suspicion had centred on leaky refrigeration units in the basement of the hotel. One theory was that coolant from the units could have got into the air vents or elevator shafts and become overheated, causing the release of phosgene gas. After further outbreaks of Legionnaires’ Disease in the summer of 1977, however, it was established that Legionella (there are some 23 species in all) thrive in the cooling towers of large buildings. Under normal conditions, water rarely reaches the temperatures necessary for the bacteria to multiply. However, when temperatures rise the organism grows more readily and if the towers are not serviced regularly hey can be drawn into air intake vents and shafts.

The American Legion convention had opened to sweltering conditions and the following day, July 22, there had been a sharp temperature inversion. The result was that the towers on roof of the hotel had become superheated. In other words, the epidemic was very much the product of modern technology and the built urban environment. Another lesson is that although cooling towers are now regularly inspected for Legionella, climate change increases the likelihood of superheating events.

To be sure, every now and again these controls fail and there are fresh outbreaks. On Monday, New York’s Department of Health announced it was examining 160 cooling towers on the city’s Upper East Side following the hospitalisation of 18 people with Legionnaires’ Disease. The outbreak coincided with a dangerous heat wave that saw temperatures in Central Park soar to 38 degrees C (100 Fahrenheit) over the July 4 holiday weekend. One theory is that, as in Philadelphia in 1976, the extreme weather caused a heat inversion that prevented spray and fine mist from the top of cooling towers evaporating. Instead, the mist plunged to ground level where the droplets and aerosols were inhaled by passersby.

Due to climate change and New York’s “urban heat island effect”, heat inversions are becoming more common in Manhattan where paved sidewalks and treeless streets add another two to five degrees F to ambient temperatures. This make Legionnaires’ outbreaks more likely: last summer, for instance, 100 people were sickened in an outbreak in central Harlem and nine people died. Unlike in 1976, however, there is no longer any mystery about the cause – officials say buildings that test positive for Legionella will be instructed to drain, clean and disinfect towers – and outbreaks are no longer the subject of conspiracy theories.

To be sure, every now and again these controls fail and there are fresh outbreaks – last year, for instance, an outbreak at Harlem Hospital resulted in the hospitalization of 90 people and seven deaths. But there is no longer any mystery about the cause and the outbreaks are no longer the subject of conspiracy theories.

Sadly, this is not true of other pathogens. The ongoing Ebola outbreak in the Democratic Republic of the Congo is a case in point. Although scientists have long known about the threat posed by the Bundibugyo strain of the virus, there is currently no vaccine for it and, like other types of Ebola, it is not known where the virus resides between outbreaks (the leading suspects are fruit bats). The result is that the outbreak has become a fertile ground for conspiracy theorists, hence claims that the outbreak is a hoax got up by DRC health authorities to attract much needed foreign aid .

The failure to recover SARS-CoV-2, the virus of Covid-19, from animals sold at the Huanan wet market in Wuhan – the likely ground zero of the outbreak – has fuelled similar conspiracy theories, as well as unproven claims that the pandemic is the result of experiments on related SARS viruses at the Wuhan Virology Institute.

As Don DeLillo observed in his novel Libra about the life of Lee Harvey Oswald and his participation in a fictional CIA conspiracy to assassinate Jack Kennedy, conspiracy theories “gleam like jade idols”. Employing 20/20 hindsight, they are seductive precisely they provide simple, easy-to-understand explanations for seismic cultural events. When the events coincide with significant anniversaries and periods of political turmoil – and expert knowledge is wanting - it is natural for people to look elsewhere for explanations.

The problem today is that, unlike in 1976 when Ford trusted the CDC to solve the Legionnaires’ mystery, its capacity to launch similar outbreak investigations has been severely reduced by Trump’s cuts to the agency and his amplification of conspiracy theories about Covid-19.

Sad to say, the biggest threat to our ability to control infectious disease outbreaks no longer comes from pathogens but the President himself.

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The answer, evident across a pattern of recent outbreaks from mpox to Marburg to Andes hantavirus, reveals a fundamental paradox in how the international health community manages on-going threats posed by emerging infectious diseases (EIDs).

On one hand, we have what might be termed the securitisation of EIDs – viruses that threaten the security of the global order initially galvanise health bureaucracies to action, commanding political attention and attracting research funding. On the other hand, once the acute phase of the crisis has passed, these same EIDs tend to slip down the political agenda and fall into institutional neglect.

Between this securitisation and neglect lies a vast gap where preparedness should lie but is rarely found.

Bundibugyo first emerged as a distinct viral species in 2007 when it sparked an outbreak in south-western Uganda, causing 131 cases and 42 deaths. In response, international health teams were deployed to the site of the outbreak to collect samples and study the virus. Then something curious happened: the world largely forgot about it.

For the next eighteen years, Bundibugyo languished on the margins of global health. There was no vaccine development programme. No governments prepared medical countermeasures. No coordinated surveillance system watched and waited for its re-emergence.

By contrast, after the 2014-2016 West African Ebola epidemic killed over 11,000 people, resources flowed to the region and vaccines for Zaire ebolavirus were developed at unprecedented speed. Monoclonal antibody treatments were created. Countries built the infrastructure to respond. But Bundibugyo? It seemed manageable, containable – a medical curiosity and artefact of the past.

Then in 2025, the virus re-emerged in Ituri Province in the eastern Democratic Republic of the Congo (DRC) and health responders discovered the medical arsenal was empty. “Unlike other Ebola strains, there are currently no approved Bundibugyo-specific therapeutics or vaccines,” the WHO noted in its emergency declaration on May 17.

By then, cases had been circulating for months undetected or unconfirmed in the region. A Congolese man died in Kampala, Uganda’s capital, before the outbreak was officially recognized. Across the DRC and Uganda, there were reports of over 80 suspected deaths. The real numbers were almost certainly higher but because of the absence of rapid diagnostics, the WHO acknowledged there were “significant uncertainties” about the precise number of people infected and the extent of the virus’s “geographic spread”. In a war-torn region of Africa with high population mobility that is something that should concern us all.

This pattern of delayed response and institutional unpreparedness has become familiar across multiple EID threats. The same cyclical failure – securitisation followed by neglect — has characterised responses to other recent viral outbreaks, exposing a global health system organised around panic rather than along rational scientific lines.

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It was with the aim of truly “losing ourselves” then that my wife and I decided to take a short city break in Genoa. To give us the best chance of escaping the tyranny of modern communications, we selected an Airbnb in Genoa’s centro historico – a UNESCO world heritage site and the largest intact medieval city in Europe.

Centuries before the invention of the skyscraper, Genovese merchants were erecting grand palazzos here to advertise their wealth. Over the years, these palazzos grew taller and taller, each seeking to overlook their neighbours in pursuit of the best views of the Ligurian coast.

The legacy is a maze of narrow, canyon-like alleyways – known as caruggi – that could have been purpose-built for travellers in search of a digital detox. Even on the brightest Mediterranean day, little light penetrates these caruggi and most electromagnetic waves are neutered, sending Google maps haywire. Instead, you are thrown into an analogue world with only your wits to guide you.

If Genoa’s topography is a revelation, so is its social life.

“In the close crepuscular alleyways,” wrote Henry James in 1874, “the people are forever moving to and fro or standing in their cavernous doorways, calling, chattering, laughing, lamenting, living their lives in the conversational Italian fashion… I hadn’t for a long time seen people elbowing each other so closely or swarming so thickly out of populous hives.”

One hundred and fifty-two years later, we found little had changed. Our apartment was in a caruggi just behind the Piazza Caricamento. Turn right and we were plunged into the chaos of the Portico Antico with its aquarium and Museo del Mare, featuring a reconstruction of the harbour wall erected by the Genovese to repel Ottoman raiding parties in the fifteenth century. Turn left and we were rubbing shoulders with clerks on their way to work in the Via Bianci and housewives queuing for focaccia bread and pesto, Genoa’s most famous culinary products.

Luckily, we set off for the sights before the cruise boats had disgorged their passengers into the caruggi and arrived at the Palazzo Biancho just as it was opening. There, we had 15 minutes alone with Ecce Homo, Caravaggio’s masterwork showing Pontius Pilate presenting the bound and tortured figure of Christ to the crowd prior to his crucifixion (incredibly, the painting languished undiscovered in the Bianchi’s collections until 1921 and was initially dismissed as a copy!).

By the time we re-emerged onto the Via Garibaldi it was midday and the thoroughfare was heaving. Ducking into a side alley, we ran straight into a tour party just off the boat and – languishing in a nearby doorway – two women who, judging from their gaudy makeup and figure-hugging one pieces, were already open for business.

Unfortunately, our digital detox did not last long as back at our ninth-floor apartment the reception was perfect and I soon found myself falling into an AI rabbit hole. It began with a New Yorker podcast about the strides being made by Large Language Models (LLMs), such as Claude Opus, and continued when I clicked on an article about “AI companions”. Apparently, in a world where many people find it difficult to form flesh-and-blood relationships and loneliness is on the rise, more and more people are turning to chatbots for friendship. Unlike real friends, these synthetic personas are available 24/7 and always have plenty of time to chat. And when you’re feeling down, they can give you a “digital hug”. Some people find the experience so rewarding, they have begun forming romantic relationships with their AIs and discussing the practicalities of raising children, albeit with one “co-parent” stuck in the digital world.

There is nothing new about the decline of community and the connection between urbanisation and social isolation. As the French philosopher Jean-Jacques Rosseau recognised in his 1760 novel Julie or la nouvelle Heloise, with its fast pace modern city life can be extremely alienating. Writing to Julie from Paris, the protagonist of Rousseau’s novel complains:

“I am in the whirlpool of the world, where I struggle and am carried away like a straw… I am overwhelmed by a multitude of sensations but not one of them touches me deeply.”

Daisy Miller, the heroine of Henry James’s 1878 novella of the same name, experiences a similar sense of anomie in Rome as she wanders the city alone at night.

Genoa is different, however. As we discovered when we returned to street level and lost our phone signals, the city has a way of drawing you in. In our case, the transformation occurred the moment we stepped into the Via Banchi and were entranced by a haunting melody coming from the church opposite our apartment. Looking up, we saw that a dance troupe had gathered on the balcony of the church and were performing spins and handstands on the balustrades. The next moment, they clambered up and over the iron gate in front of the church and dropped stealthily into the crowd.

Soon, one of the dancers – a young man with dreadlocks – had cleared a space in front of us and was doing handstands and tumble turns. Meanwhile, the rest of the troupe began swinging each other from side to side and lifting one another onto their shoulders and outstretched hands. But the most transfixing part of the performance were the subtle looks and glances prior to each acrobatic feat.

It was a mesmerising and deeply human spectacle and, pressed elbow to elbow, we soon found ourselves following the troupe along a narrow alleyway to another square around the corner. There, the performance continued for a further 20 minutes.

No one solicited contributions or asked us for money. At one point, my wife, who had been drawn to the front of the crowd, was even rewarded with a hug. It was an incredibly intimate moment, a reminder that there are some things the digital realm cannot and will never be able to replicate.

But perhaps the most extraordinary part of the performance was the bond it created within the audience. We were strangers, yet plunging back into Genoa’s centro historico we felt connected in a way we hadn’t before. The performance had fostered a physical and emotional intimacy, reminding us that we were embodied social beings. Truly, it was an experience for the ages.

These were not the only diseases that Europeans brought with them to the Americas – in 1518, Christopher Columbus inadvertently introduced measles and smallpox to the Yucatan, decimating the local Aztec population. Thanks to the Spanish conquistadors, other Old World diseases soon followed.

However, with the exception of syphilis, which some scientists believe was brought to Europe by Spanish explorers returning from the Caribbean, the Andean hantavirus is, to my knowledge, the first significant pathogen to have crossed the Atlantic in the opposite direction (I’m exempting the 2007 swine flu and the bird flu virus which, like other influenza viruses, continually circulate between the Southern and Northern hemispheres).

At time of writing, the outbreak on the Hondius, a luxury Dutch cruise ship, has sickened eight of the 150 passengers who boarded the vessel on March 20 at Tierra del Fuego, in Argentina, and killed three. The boat is now en route to Tenerife, in the Canary Islands, where it is expected to dock on Sunday, at which point anyone confirmed to be infected will be transported directly to the airport for repatriation to their home countries. However, that is unlikely to be the end of the story as it is thought that several other passengers who disembarked this modern-day “plague ship” earlier in its voyage from South America may have been infected with the virus without realising it. Given that hantavirus can incubate for up to ten weeks before the appearance of symptoms that means it may be June before we can all breath easily again.

It is important to say from the outset that though the outbreak on the Hondius resembles the outbreak of Covid-19 on the Diamond Princess cruise ship in February 2020, hantavirus is nothing like as catchy as the coronavirus, SARS-CoV-2, and is unlikely to trigger a global pandemic, much less a regional epidemic comparable to the outbreak of Ebola that devastated West Africa in 2013-2016.

But, as Dr David Berger, an expert on aerosol infections, points out, while the risk of a hantavirus pandemic is low, it is not zero. Nor should we rely on the World Health Organization’s assurances that hand hygiene measures should be sufficient to contain the onboard outbreak. Cruise ships are floating petri dishes and, as with SARS-CoV-2, there is a theoretical risk of aerosol spread in the confined spaces below deck. Berger also notes that the official in charge of the WHO’s response to the Hondius outbreak is Dr Maria van Kerkhove – the same WHO official responsible for the notorious “Covid is not airborne” tweet from March 22, 2020.

I am a supporter of the WHO and believe that, despite Trump’s disengagement from the organisation, it remains essential for our ability to monitor and respond to international disease outbreaks in a timely fashion. However, I also wonder how wise it is to allow suspected cases to be repatriated to their home countries without knowing the full risk of aerosol spread (a KLM flight attendant, who briefly shared cabin space with the 69-year-old Dutch woman, was initially hospitalised with suspected hantavirus in Amsterdam only to be cleared this morning; however, by all accounts, the KLM flight from Johannesburg was packed and several other crew members and passengers might have been infected).

Given this uncertainty, the obvious solution in the interim would be some form of port quarantine. Cape Verde, where the Hondius sought permission to dock on May 4, does not possess this capacity – hence the authorities’ insistence that it anchor off the port of Praia before sailing for Tenerife.

However, Spain, and other European countries such as Italy and France, have a long history of maritime quarantines. Indeed, in the eighteenth century, lazarettos were a standard feature of European entrepots from Venice to Marseille and in 1817 the Bourbons opened a huge quarantine station on an island opposite the Menorcan capital Mahón,

For the next 100 years, some 40,000 souls passed through the Llatzeret de Maó’s imposing Lions Gate. Passengers and crew “suspected” of infection, or who had briefly “touched” an infected plague port, were typically detained for between twenty to thirty days. However, those with confirmed plague, cholera or yellow fever were not so lucky. These unfortunates were carried or carted (depending on their condition) directly onto ramps leading from the dock to a separate area of the compound where they spent forty days contemplating the sky and scudding clouds – hence the term quarantena, Italian for forty days.

Three years ago, I had the opportunity to visit the Llatzeret de Maó with a group of medical historians and explore its grounds. The compound occupies an astonishing 470,000 square metres and boasts 7.5 metre-high double-walls along its perimeter. In addition to a “fumigation” dock where boats suspected of harbouring infectious diseases were submerged in sea-water for 24 hours before being re-floated, the lazaretto has 141 rooms, seven warehouses and an astonishing 49 kitchens, some of which, as we discovered during our sojourn, are still capable of turning out a delicious paella. In bygone days, those who could afford it paid to stay in the “French Quarters”, whose rooms came with maid service, laundry facilities and the Bourbon-equivalent of a mini-bar.

You can read about my visit to the Llatzeret de Maó – and our subsequent discussions on quarantines and the parallels with the Covid lockdowns – here.  

The lazaretto was decommissioned in 1917 and it would be impractical to reopen it today. But I cannot help feeling that a stripped-down version equipped with state-of-the-art healthcare facilities and diagnostics for typing hantaviruses and other poorly understood pathogens would be a better solution to the ongoing risks presented by the Hondius and other plague ships on the high seas.

Board a cruise boat, take your chances.

But what if the opposite is true? What if instead of damaging our immune systems, vaccines increase our chances of living long and healthy lives free from debilitating diseases and conditions associated with senescence? That is the surprising conclusion of several studies looking at the indirect benefits of vaccination.

Perhaps the best example is the Bacillus Calmette–Guérin (BCG) vaccine. First introduced in the UK in 1952, BCG is an effective prophylactic against tuberculosis, reducing the risk of the bacterial disease by half. Less well known is that BCG also provides protection against neonatal sepsis and a range of respiratory tract infections and can be used to treat bladder cancer and genital warts.

Or take the shingles vaccine. A retrospective study of more than 300,000 elderly people in Wales found that as well as reducing the chances of developing shingles, the Zostavax vaccine was associated with a 20 percent reduction in dementia (the study was based on a natural experiment in which researchers compared the health records of 80-year-olds who qualified for the roll-out of the vaccine in Wales on September 1, 2013, and those who were born earlier and therefore missed out on immunisation).

As dementia affects more than 55 million people worldwide, with an estimated 10 million new cases per annum, that means that in theory two million cases of dementia could be avoided each year by getting the shingles jab. It’s also far more cost effective than treating the painful rash and fluid-filled blisters that result from the reactivation of the varicella-zoster virus (for older patients, treatment in England averages £445 per case as opposed to £230 per vaccine dose).

As a late Boomer, I avoided most of the diseases that afflicted my parents’ generation. In 1957, three years before I was born, the NHS introduced the pertussis vaccine, which prevents whooping cough, into the child immunisation schedule, alongside the diphtheria vaccine. This was followed in 1961 by the tetanus vaccine and in 1962 by the live oral polio vaccine (no jab was required as it came in the form of a sugar cube). I can’t remember exactly when I received the BCG vaccine – most likely at primary school - but I still bear the raised circular scar on my left shoulder resulting from the blister that developed a few weeks later.

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As the meningitis outbreak at the University of Kent sparks alarm across southern England, you could be forgiven for thinking we are witnessing a replay of Covid-19. And just when Baroness Heather Hallet, the chair of the UK Covid Inquiry, is about to deliver her long-awaited report on the impact of the pandemic on healthcare systems i the four nations.

Of course, meningitis is a very different pathogen from SARS-CoV-2, the virus of Covid-19 – for starters, the Kent outbreak is due to a bacterium, not a virus, and is typically spread by close contact with respiratory droplets rather than via highly infectious aerosols. And the good news is we have a vaccine against the “B” strain at the centre of the Kent outbreak, something that wasn’t the case during Covid when vaccines had to be manufactured from scratch. Nonetheless the echoes are striking, reminding us that while history doesn’t repeat it often rhymes.

So far, the outbreak that begun in Kent last weekend has killed two students and left 15 gravely ill. Whether viral or bacterial, meningitis presents a particular risk in communal settings such as universities and schools – one of the victims was an 18-year-old Kent schoolgirl, the other a 21-year-old female student. But it can affect people at any age, including adults in the prime of life.

For me, the latest outbreak immediately brought to mind the sudden death of a journalist friend from meningitis a little over thirteen years ago. It was shortly before Christmas 2012 when John, a reporter for Lloyds’ List, first felt the premonitory signs of fatigue and fever at his home in Bath. Thinking he had a mild case of flu, John ignored the symptoms and set off for London accompanied his wife and sons. The plan was to catch the Eurostar to Paris, where they were scheduled to meet up with John’s sister-in-law and her husband before heading to their home in Fontainbleu for the festive season. But John never made it to Fontainbleu. Instead, by the time the Eurostar emerged from the Channel tunnel, he was running a high fever and his wife was sufficiently worried to ask a guard if he could stop the train and let them off.

“Impossible”, came the reply.

The result was that by the time the Eursotar pulled into the Gare du Nord, John was complaining of a stiff neck and muscle and back pains – hallmarks of a severe meningitis infection. And by the time he reached his sister-in-law’s apartment near Bastille, he was having trouble standing up.

They immediately dialled the emergency services but when the medics arrived at the fifth floor apartment John was ice cold. Then, on turning him over, the medics spotted a dark purple rash on his back – another sign of meningitis.

Suspecting John had a systemic infection, the medics called the fire brigade. The next thing his wife knew, pompiers had brought a crane up to the balcony of the apartment and were stretchering John out the louvre windows.

Whisked to the Val-de-Grace hospital in the 14^th arrondisement, John was admitted to intensive care as doctors tried to figure out what was wrong with him. Fit, middle-aged men with no underlying medical conditions do not usually collapse going about their daily business, unless they have suffered a heart attack or a brain aneurism. But John’s symptoms did not match those of a heart attack or other common catastrophic conditions and, although it was the flu season, there were no unusually virulent strains circulating that winter.

Fearing that John was at risk of toxic shock, he was placed him on a heart monitor while doctors ran a series of tests to rule out common viral infections. Then, thinking that his immune system may have been compromised, they screened him for HIV and leukaemia but these tests were also negative. It was only when they took a lumbar puncture and saw a mass of tiny, kidney-shaped diplococci in John’s spinal fluid that they realised it was Neisseria meningitidis.

The bacterium lives in the membranes of the nose and throat and usually presents little risk to healthy adults. However, every now and then, for reasons that are unclear, it gets into the bloodstream, causing septicaemia and catastrophic systemic changes. And if it crosses the meninges, the thin membrane that protects the brain, it can trigger paralysis and lasting brain damage.

Fearing the bacteria had already crossed the blood-brain barrier, John was placed in a coma, while doctors fed him intravenous antibiotics. But by now John had sepsis and his kidneys were beginning to fail. The final stage came 48 hours later when John’s immune system went into overdrive, flooding his lungs with fluids that cut the flow of oxygen to his heart. The doctors upped the antibiotics and put him on a respirator to help his breathing but it was to no avail and on Christmas Day John died. He was 53.

Meningitis mystery

To this day, John’s family has no idea how he caught meningitis. At Lloyd’s List, John’s speciality was Italian shipping, a beat that required him to keep tabs on the comings and goings of tankers and cruise liners at various ports in the Meditteranean and the Aegean. Perhaps he’d the caught the bug while interviewing the crew of a ship that had recently returned from Sudan or Senegal – one of the most virulent strains of meningitis is the W135 serogroup, a type associated with periodic epidemics in countries in sub-Saharan Africa and pilgrims returning from the Haj in Mecca. Or perhaps he’d caught a different strain during his regular travels in Europe.

The chances of contracting meningitis are about 1 in 100,000. Close to half of cases are in adults aged 25 and over. The best way to avoid infection is to be vaccinated. The MenACWY vaccine is usually offered to school-age children to protect against four common meningococcal groups and can be given up to age 25. However, the vaccine against the B strain – known as Bexsero - is expensive and is typically only given to infants, though it can also be obtained privately.

Bexsero is now being offered to some students at Kent as part of what the health secretary Wes Streeting is describing as a “targeted” programme (four of the 15 confirmed cases are meningitis B). However, at time of press it was too early to say whether the outbreak, which appears to have begun at a nightclub in Canterbury on March 5, will be contained or if cases will spread to other parts of the UK. With many parents now evacuating their children from Kent, that possibility cannot be ruled out. And who can blame parents for panicking?

In educational settings, once a second linked case has occurred, the chances of a third case occurring are as high as 30 to 50 per cent. Risk factors including kissing and – if some reports are to be believed - sharing vapes. But as John’s case and the death of the schoolgirl and student in Kent illustrate, the truth is no one is immune from meningitis and when outbreaks occur, cases can progress rapidly with devastating consequences.

That is why whenever a pathogen – whether it be meningitis, Ebola, bird flu or SARS – makes the news, I cannot help but think of John and reflect, “there but for the grace of God go I”.

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Following an outbreak of influenza in 1789 in Hartford, Connecticut, the American lexicographer Noah Webster scoured the historical literature for accounts of epidemics and found that they tended to coincide with earthquakes, volcanic eruptions and other natural phenomena such as the appearance of comets in the night sky.

Speculating that these phenomena ignited subterranean fires and that these fires caused subtle electrical changes to the Earth’s atmosphere, Webster concluded that “the cause must be the action of fire, the most energetic principle in nature” and its effect on “the general properties of the air.”[1]

Fast forward one hundred years and the advent of bacteriology and modern epidemiological methods had done little to dispel these superstitions, hence the way that in 1889-90 medical authorities blamed the pandemic of “Russian influenza” on the flooding of the Yellow River in China the previous winter and the “burning heat” of the following summer. According to no less an authority than E. Symes Thompson, Gresham Professor of Medicine and expert on respiratory disease at London’s Brompton Hospital, the sun’s rays had acted on the corpses of Chinese flood victims buried in the mud, sending “countless of millions of organic spores” into the higher atmosphere”. Once there, all it took was the trade winds to spread influenza to every corner of the globe.

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Today, armed with modern virological and genetic techniques, we know better. Sure, earthquakes and floods may spark epidemics but only indirectly through, by example, the destruction of sanitary systems that keep pathogens like cholera from contaminating water supplies, or by displacing rats that carry diseases like plague and hantavirus from their burrows.

Indeed, from serological sampling in areas where bats and other virus-carrying wildlife live cheek-by-jowl with humans and comparative phylogenetic analysis, we know that 70 percent of new human infections originate in animals. However, in the absence of hard virological evidence, in practice it has proved very difficult to identify the progenitor animal viruses of pandemics. Thus, we still do not know precisely where the 1918-19 influenza pandemic originated or whether it was first transmitted to humans by a pig, chicken or wild waterfowl. Nor do we know how or where HIV, which is closely related to simian viruses that circulate in the Congo and other parts of Africa, made the jump to humans.

This question is nowhere more important than in the case of Covid-19. Six years on from the biggest pandemic of modern times, we still do not know whether SARS-CoV-2 came directly from a bat or an intermediate animal host, such as a pangolin or racoon dog, or whether it was the result of laboratory experimentation.

Little wonder then that the same superstitions and racist Asiatic tropes that attached to previous historical pandemics have attached to Covid-19, not least the idea that it must all be the fault of the Chinese because of supposedly reckless experiments conducted at a laboratory in Wuhan.

Like other pandemics, the origins of Covid-19 are unlikely to ever be settled. That would entail retrieving an identical virus from a bat or some other intermediary host and showing that this virus was the first to exhibit the key mutations that enabled SARS-CoV-2 to spread efficiently between humans.

But now, a new study in Cell has called into question one of the central planks of the “lab leak” hypothesis: namely, that when SARS-CoV-2 emerged in Wuhan in December 2019 it was already suspiciously well-adapted to people.

By analysing viral genomes from previous outbreaks of influenza, Ebola, Marburg and SARS 1 and 2, researchers at the University of California San Diego were able to demonstrate that none showed evidence of special evolutionary adaptation before spilling over into humans. Instead, across these diverse viruses, investigators found that selection pressures prior to zoonotic emergence were indistinguishable from those acting during routine circulation in animal reservoirs, and that measurable changes in selection typically appeared only after sustained transmission had begun in people.

“Rather than requiring rare, finely tuned adaptations in animals, many viruses may already possess the basic capacity to infect and transmit between humans,” explains Joel Wertheim, senior author and professor of medicine in the Division of Infectious Diseases and Global Public Health at UC San Diego School of Medicine. “What matters most is human exposure to a diverse array of animal viruses.”

In other words, pandemic viruses do not require prior adaptation in order to jump species. They just need the right opportunity.

Investigators found just one exception to this rule: the 1977 Russian influenza. Unlike the other viruses they studied, the 1977 H1N1 strain showed both unusually limited genetic divergence from similar 1950s viruses and a clear shift in selection consistent with viruses that had been propagated in cell culture or in laboratory animals. The finding is consistent with the long-held suspicion that the 1977 Russian flu escaped from a lab as a result of an accident – perhaps a vaccine trial that had gone wrong in the Soviet Union or China.

By contrast, investigators could find no evidence that SARS-CoV-2 was shaped by selection in a laboratory or prolonged evolution in an intermediate host prior to its emergence in 2019. Instead, it steadily acquired mutations as it spread between bats, just like other SARS-like bat coronaviruses. And it was only after the virus emerged in humans that it underwent a marked genetic shift, resulting in radically new variants with mutations that made them well-adapted to humans.

(For a detailed account of this process, see my earlier Substack post putting the case for a natural origin for Covid-19).

As every schoolboy knows, absence of evidence is not evidence of absence. But in this case, argues Wertheim, the study’s findings are “exactly what we would expect from a natural zoonotic event – and it represents another nail in the coffin for theories invoking laboratory manipulation”.

No doubt proponents of the lab-leak theory will disagree with that verdict. But then they’ve long been reluctant to look at Covid within the context of other spillover events and pathogens that sparked pandemics long before scientists had the means to enhance their transmissibilty in a lab.

As a group of experts assigned by the World Health Organization to examine Covid’s origins pointed out in a study last month, most of the peer-reviewed scientific evidence supports the theory that SARS-CoV-2 originated in a natural bat reservoir from where it passed to animals that were being sold at a market in Wuhan.

Unless and until evidence emerges to suggest otherwise, that remains the most parsimonious explanation.

[1] Noah Webster, A brief history of epidemic and pestilential diseases, two volumes. Hartford: Hudson & Goodwin, 1799.

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Not long after, similar images of mass graves appeared in Manaus, Brazil, and Pretoria, South Africa. But it wasn’t until April 2020, when drone footage emerged of mortuary workers on Hart Island in Long Island Sound filling trenches with wooden coffins, that it became clear that nowhere in the world was safe from Covid-19 and that, epidemiologically speaking, we were one people.

How is it then that as bombs rain down on Tehran once more and as cemeteries fill with new casualties, the world is more than divided than ever? Was it inevitable that the military stand-off between Iran and Israel, which pre-dated the pandemic, would spark a war in the Middle East? Or is the current conflagration further evidence of how the coronavirus pandemic has destabilised our world, plunging us into permacrisis?

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Certainly, the last few years have been among the most turbulent in history. No sooner did Britain and other European countries begin lifting lockdown restrictions than Russia invaded Ukraine. Eight months later, in October 2022, the then Prime Minister Liz Truss and her chancellor Kwasi Kwarteng, triggered a sudden rise in UK government borrowing costs with their disastrous mini autumn budget. The subsequent bond market meltdown was a reminder that, like other countries which had borrowed heavily to fund furlough schemes during Covid-19, the pandemic had left Britain with record levels of sovereign debt making it vulnerable to bond vigilantes.

Next came the global energy crisis, followed by the cost-of-living crisis, and the October 7 attacks on Israel. None of these can be traced directly to the pandemic but collectively they added to the sense that, post-Covid, the world had become a less stable and more unpredictable place.

Perhaps, had the Democrats managed to hold onto the White House in 2024, new life could have been breathed into the dying liberal order. But if it wasn’t clear before the US presidential election, it is clear now that the unprecedented health response to Covid paved the wave for Trump II by weaponizing conspiracy theories and undermining trust in science and other sources of authority. To the extent that the pandemic left countries with ailing workforces and weaker, heavily indebted economies, it also reduced politicians’ room for maneouvre, hollowing out the centre ground and fuelling the rise of populist movements each with their own grievances.

These grievances predated the pandemic of course. But Covid saw them configured in new and disturbing ways – hence the way that the US president’s chief medical advisor, Anthony Fauci, became a lightning rod for bizarre Nazi/ Holocaust tropes from both the antisemitic Right and the anti-Zionist Left. The result is that six years on from the biggest pandemic of modern times the old certainties and the old ways of doing things have been swept away, leaving a vacuum for the worst kind of science denialists and disrupters.

But today we have an opportunity to pause and take stock. For Sunday March 8 marks the UK’s second national Day of Reflection of Covid-19. For some, this will be a chance to remember absent loved ones and the 230,000 dead. For others, to applaud the doctors and nurses who kept the National Health Service from collapsing under the weight of unprecedented numbers of sick. For still others it will be an opportunity to reflect on the “lessons learned” from the pandemic, of what we got right and what we got wrong.

This week Baroness Heather Hallett, the chair of the UK’s independent public inquiry into Covid-19, took evidence from the final witnesses. In a series of ten interlocking investigations over three years she has laid bare the UK’s lack of preparedness, interrogated the scientific assumptions underlying decision-making before and during the lockdowns, and examined the shuttering of care homes and Covid’s on-going impact on the economy and society. But of all the lessons of the pandemic, perhaps none is more urgent than the need to repair our broken social care system.

As Louise Casey, the head of the UK’s independent commission into adult social care, spelled out in her report last week, the current system is held together with “sticking plasters and glue”. This is because unlike other parts of the welfare state, social care in Britain never had a “Beveridge moment”and has been starved of meaningful investment for decades.

The pandemic is estimated to have cost the UK government £375 billion – a staggering sum. But if Covid showed us anything, it is that in the event of another pandemic a pound spent now could save thousands if not millions later. How much better to avoid another lockdown and more disruption to childrens’ education by ensuring that the elderly and vulnerable are properly protected and cared for.

Those who complain that we didn’t need an inquiry costing £200 million to reach this conclusion and that the money would have been better spent interrogating the murky origins of the pandemic are wrong. It is precisely because of the neglect of social care and other health services that Britain ended up with one of the highest fatality rates among developed nations. And it is because of the ongoing neglect of social care at a time when growing numbers of people are succumbing to chronic illnesses and conditions like dementia and Alzheimer’s that a second pandemic would prove just as devastating.

The alternative - more graves and more avoidable deaths – does not bear thinking about.

As Glen Grundell, whose mother died of Covid in hospital during the first wave of the pandemic, told Lady Hallett last week: “My mum left in an ambulance and I never saw her again. I have no acceptance, no closure… there’s an aftermath [and] many of us are trapped in the rubble.”

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You can imagine the thoughts that flashed through my mind as we flew parallel to the Andalusian coast. Had Putin launched a sneak attack on “the Rock” in the latest attempt to test Britain’s air defences? Or had a member of the ground staff failed to set their alarm and overslept?

In the event, the answer lay in the novel I’d brought on holiday. In What We Can Know, Ian McEwan transports us to 2119 when most of Europe is underwater and people have migrated to the last remaining areas of high ground, together with the records and artefacts from the before times. Without going into too much detail, the plot revolves around a climate-denying poet and the attempt 105 years later by a literary scholar to track down his last great work, a collection of sonnets known as a Corona. Part literary detective story, part ode to our vanishing post-pandemic present, the novel is animated by McEwan’s reflections on the “great derangement” – a term, he informs us, that came into use in the mid-2030s to denote “the vengeful fury of weather systems” and our failure to address climate change.

That fury had just unleashed a series of storms on Andalusia – an “atmospheric river” as one meteorologist put it – that saw Cadiz and the surrounding countryside receive a year’s worth rain in the space of a month. Damns overflowed, rivers broke their banks and 20 percent of the region’s vegetable crop was destroyed.

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The storms also brought gusts of up to 80mph and, although on the morning we set off from Heathrow, the winds had eased, the rain had not, and the ground staff at Gibraltar were only just coming to terms with the damage. At first, the captain announced there had been a power outage at the airport; then, that Gibraltar’s radar was down. He’d tried calling the air tower repeatedly. I imagined men in high-vis jackets perched on top of the Rock straining to upright the radar mast.

After an hour hovering over the Mediterranean, during which no word or sign came from below, the captain had had enough and bent the wing toward Malaga. Bussed back to Gibraltar, we were only three hours late, but now the heavens had opened again and we had a new problem: where to take shelter?

Luckily, my wife and I had booked an Airbnb in a white village on a limestone outcrop high above Conil and the floodplain of the Barbate River. Over the centuries, Vejer de la Frontera has been a refuge for Romans, Visigoths, Vandals, Arabs, Jews and Christians. In the 1930s, it even provided sanctuary for rebels fleeing General Franco’s fascist forces. However, it was the Moors, who occupied Vejer from 711 to the Christian reconquest in 1248, who left the most indelible impression. Their influence can still be seen in Vejer’s principal church with its minaret disguised as a bell tower and its castle with its crenelated battlements dating to the eleventh century.

The houses are built directly into the castle’s wall and walking the town’s cobbled alleyways with their narrow passages and blind turns one has the sense of having wandered into a maze. The streets have evocative names that speak to Vejer’s rich history of confinement – a particular favourite of mine is Paseo de las Cobijadas, “Walkway of the Sheltered Ones”, a reference to the nuns in dark cloaks who used to stroll here in search of cooling breezes. We had no such problems and took shelter in the Jewish quarter near the Puerta Cerada, a door on the southwestern side of the castle, that in medieval times had kept out marauding pirates. Every now again the clouds parted, bathing our terrace in sunlight, but most days were spent hunkered down as rain lashed the windows and we chased drips around our bedroom.

We were not the only ones. For the past six weeks, most of Europe has been similarly confined. The rain and floods have been Biblical, exceeding the forty days and forty nights described in the Book of Genesis. When will the deluge end, many have been asking? But what if it has only just begun? And if so, what are we going to do about it?

To judge by Trump’s latest announcement, F-all. On Thursday, the day after scientists warned that the Earth’s climate was closer than had been thought to a “point of no return”, the Deranged One repealed a scientific finding that required the US’s Environmental Protection Agency to combat global warming, paving the way for even more greenhouse emissions. From now on US car manufacturers will no longer be required to transition to electric vehicles and companies will be free to ignore carbon caps.

And what of us? Boarding a plane at Heathrow in the dead winter and flying 1,500 miles south in the hope of escaping the incessant rain is the definition of wishful thinking. But if so, we are not the only ones. Despite the delays and cancellations, record numbers of Brits are holidaying abroad this year, with adults aged 25 to 34 leading the charge. No doubt this reflects pent-up demand from the “lost years” of the pandemic. But if so, it is further evidence of our collective derangement because if Covid-19 taught us anything it is that pandemics are also a product of climate change and a world out of balance.

And with the arrival of AI and its seemingly insatiable demand for energy, that imbalance is only going to worsen. Perhaps, rather than venturing outside, we should all be hunkering down and preparing for “the great sheltering”.

Maybe we won’t get on that return flight to London. After all, where better to see out the end of days than a hilltop village with views ( on a good day) of Africa?

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The answer in one word: deference.

I first became suspicious of Mandelson in October 1996 when I learnt he’d bought a four-storey house in Northumberland Place in Bayswater, west London. In 1961 when my parents moved to Northumberland Place, their house came with a sitting tenant and cost them just £6,000. But following financial deregulation in the 1980s and the “Big Bang”, house prices in Bayswater and nearby streets in Notting Hill had soared and properties in Northumberland Place were changing hands for in excess of £450,000.

How was it then, I wondered, that Mandelson, then a backbench MP earning just over £40,000 a year, could afford to live there? At the time, average mortgage rates were 7.58% and the most a bank or building society would lend was three times a person’s salary. In Mandelson’s case, I calculated, the maximum loan he could afford was £120,000.[1] The question was, how had he bridged the difference?

In fact, as I later discovered when I checked the sales details in the land registry, Mandelson had paid £475,000 for his house at No. 9 Northumberland Place. So, assuming he’d covered the rest with a personal mortgage, that left him with a shortfall of £355,000.

At the time, I was working as a feature writer on the Evening Standard, so, smelling a story, I began digging. I wasn’t alone. Unbeknownst to Mandelson, five doors down from him in Northumberland Place lived another journalist, Phillip Knightley. A member of the Sunday Times investigation team that broke the thalidomide scandal and a former reporter of the year, Knightley had been helpful to me when I was looking to break into journalism, so it was natural I should ask his advice.

“Follow the money,” he suggested. So I did.

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So why is it that within moments of sitting down to watch Hamnet – Chloé Zhao’s adaptation of Maggie O’Farrell’s book based on the death in 1596 of Shakespeare’s 11-year-old son - my eyes were welling and that by the end of the movie my cheeks were streaked with tears?

The answer, according to some critics, is that I had fallen victim to “grief porn”, a formulaic and emotionally manipulative device that produces a false sense of catharsis in the viewer. According to this interpretation, the emotions I felt at the closing scene as Jessie Buckley, playing Shakespeare’s wife Anne Hathaway, reaches out from the pit of the Globe Theatre to the ghost of Hamlet’s father – who in O’Farrell’s telling represents her dead son Hamnet – was nothing more than a theatrical sleight of hand. A staged emotion, in other words, not unlike the scene at the end of E.T when the home-bound extraterrestrial promises Elliott he will always live in his heart, or words to that effect.

It’s a verdict seemingly shared by several critics and members of my social circle. Some are put off by Zhao’s “shameless deployment” of Max Richter’s “On the Nature of Daylight” to prime our lachrymal glands. Others find it difficult to connect with Buckley’s portrayal of “Agnes” – as Hathaway is known in both the film and the book – as a free-thinking woodland spirit. The opening shot shows Buckley curled up in a tree root in the forest of Arden, before panning out to show an ominous hollow in the tree’s trunk.

The hollow represents the Abyss which Agnes and we must all confront. But the image appears too frequently and obviously for some tastes. The result is that rather suspending disbelief, some viewers are immediately put on their guard. Consequently, they are unable to feel what Buckley’s Agnes feels when the inevitable happens.

But what if despite its clumsy recurring motifs, Hamnet qualifies as great art and is a deserved contender for best picture at the Oscars? (It has already won a Golden Globe in that category and best performance by a female actor for Buckley). Ultimately, that is a question that can only be answered by each viewer. Whether you are mourning a dead pet or an absent family member, everyone brings their own experience of grief to the movie theatre. Sitting alone in a darkened auditorium, or with your partner beside you (as I was), from the point of art it matters little that there is someone to witness your emotions and that you are seen to be an empathetic and “feeling” individual. What matters is the “truth” of the emotions on screen and your willingness to connect with them.

Ultimately, such judgements are subjective. As Zoe Williams argues in The Guardian, the claim that they rest on the veracity of the performances is also somewhat tautological.

You only get to decide whether it’s art if you’re already feeling it so deeply that it must be… If the death left you cold and you found the ensuing emotionality manipulative and domineering, this logic is quite annoying.

Such considerations notwithstanding, leaving my local movie theatre I had little doubt I had witnessed a cinematic masterpiece. This was largely due to Buckley’s magnetic performance. As Agnes (pronounced An-yes in Shakespeare’s time and throughout the film) the camera is rarely off her. Her wails of grief as she grasps Hamnet’s buboe-ridden body to her breast are both agonising and unforgiving. Although she has seen a vision of two children at her death bed, Agnes had assumed that Hamnet’s twin sister, Judith, would be the one to be taken by the plague, rather than Hamnet or her eldest child, Susanna. She cannot accept that Judith and Hamnet have swapped places or that Will, played by Paul Mescal, was in London pursuing his metier when he could have been at his son’s deathbed. It is a fury that threatens to undermine their marriage and the chemistry that brought them together in the first place.

But Zhao’s screen adaptation is more than a story of unrequited grief and a romance soured by loss. What qualifies it as great art is how Zhao and O’Farrell, who collaborated closely on the screenplay, succeed in connecting Agnes’s experience to those of other women who have experienced similar losses. For Agnes is not the only mother who has lost a child to the Black Death.

The key scene comes when Shakespeare’s mother Mary, played by Emily Watson, assists Agnes in nursing Judith back to health only to see Hamnet die of the same disease. In a speech taken almost word from word from O’Farrell’s book, whose original subtitle was “A Novel of Plague”, Mary, who has also seen several of her children pre-decease her, reminds Agnes:

What is given may be taken away, at any time. The trick is never to let down your guard. Never think you are safe. Never take for granted that your children’s hearts beat, that they sup milk, that they draw breath… Never for a moment forget they may be gone, snatched from you in the blink of an eye.

It is not until the final scene, however, that Agnes realises that her grief is shared just as much by her husband who has been feverishly crafting his own tribute to their dead son in London. In Shakespeare’s time, we are informed, the names Hamnet and Hamlet were interchangeable. But Agnes has wrongly assumed that Will has been working on a comedy and at first is unable to recognise her son’s name on the playbill. Entering the Globe Theatre, she has no inkling that Hamlet is a tragedy in which the ghost of Hamlet’s father stands for her son and the fury of the prince of Denmark is a proxy for Will’s own grief.

For those who have not read Farrell’s book and have yet to see the film, I hesitate to describe the ending, suffice to say that watching the play of emotions on Buckley’s face as Agnes realises she has cruelly misjudged her husband is spellbinding. Equally moving is the reaction of the crowd as, mimicking Agnes, they reach out to Hamlet’s stricken form on stage.

“To be or not to be”. Hamlet is Hamnet, and Hamnet is Hamlet, both alive and dead. By inverting the tragedy and taking the role of the ghost, Will has resurrected his son’s spirit and ensured his name will live on.

There is no evidence that Hamnet died of plague or that Mary Shakespeare’s daughters were also taken by the pestilence. And of course, several other Shakespeare plays, including two comedies, came between the death of Hamnet and the creation of Hamlet.

Hamlet is usually interpreted as a revenge play. The genius of Zhao’s film is that in seeing Hamlet through Agnes’s disbelieving eyes it also becomes a play about grief – one that resonates both with Agnes and other members of the Globe audience. Recreating that feeling in a movie theatre takes a special kind of alchemy.

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The fighting had been particularly fierce that year in Southern Sudan, sparking a famine that drove millions of refugees to seek refuge in northern Uganda. There, the refugees were greeted by officials from the World Food Programme (WFP), or what was left of it following the deep cuts to USAID initiated by Elon Musk and Donald Trump in the first weeks of his presidency.

The cuts had decimated WFP’s stocks of maize and pearl millet but fortunately there just enough sorghum to go round. However, there had been no time to construct storage sheds to keep the sorghum dry. Instead, officials had stacked the sacks of sorghum in the open, where they were exposed to the elements.

By the time the refugees reached Uganda some of the sorghum had turned mouldy but it was better than the roots and leaves they had devoured on the trek from Sudan. Afterwards, having filled their bellies, they fell into exhausted stupors, dreaming of absent loved ones and their abandoned villages and farms.

The following morning, their hunger was as keen as ever so they filled their stomachs with more sorghum. By the week’s end, the sacks of sorghum were empty but now the refugees had a new problem – the children were sobbing. Whether it was the unfamiliar feeling of fullness or the realisation that they would never return to their homes, no one could say, but the sobbing went on late into the night and the next morning several children suffered epileptic fits.

Then, one by one, the children started nodding their heads and weeping uncontrollably. As their tears mixed with the remains of the mouldy sorghum, the sky turned dark and their tears were lifted high into the atmosphere by a dry wind from the east. Then, at the Gulf of Guinea, the tear-laden particles began to drift across the Atlantic and north toward Europe.

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On Good Friday, a baker in the Marais noticed a fine dust on the pavement in front of his shop and a smell like burnt almonds. Had he left some frangipane out overnight by mistake? Then he remembered he had shut his ovens for the holidays. The odour reminded him of his father, a hero of the resistance, who everyone agreed had made the best madeleines in Paris. In an instant his eyes welled with hot, salty tears and he began nodding and weeping.

On Easter Sunday, in what would be his final public outing, Pope Francis appeared on the balcony of the Vatican to reassure the crowds gathered in St Peter’s Square. “Sisters and brothers, especially those of you experiencing pain and sorrow, your silent cry has been heard and your tears have been counted - not one of them has been lost!”

Francis’s words resonated with people of all faiths, not just Catholics. Some speculated that the tears were a reaction to the “genocide” in Gaza and the incessant shelling of Kyiv; others, a response to the famine in Sudan and the Horn of Africa.

People cried for small things and big things. They cried for their deceased goldfish and the boats laden with desperate refugees in the Mediterranean; at soppy pop songs and people queuing outside soup kitchens. But most of all they cried for their lost innocence and their helplessness in the face of so much misery.

At first, commentators on X blamed the epidemic of weeping on “the woke mind virus”. The government, fearing social meltdown, urged people to show more “grit”. “Whatever happened to the stiff-upper lip?”, asked a member of the Reform Party. But as trains ground to a halt and offices shuttered, it became clear that this was no ordinary crying jag.

The epidemic was worst of all in Japan, where people trained to believe that tears were a sign of weakness, began covering their eyes in shame. But the bandages soon grew wet and heavy. Unable to stem the torrents, people began nodding even harder in the hope of shaking the tears from their heads, for where else could they be coming from? But the well ran deep and all it took was the sight of a fellow blubberer to re-open the floodgates.

Come December the medical press was full of accounts of “inconsolables”. Some experts were convinced that, despite the glorious weather, the crying fits were a form of Seasonal Affective Disorder. Others, that the tears were a type of emotional contagion. Sales of magic mushrooms and MDMA spiked on the Dark Web. The hashtag “mindfulness” trended on Tiktok.

“It was sad,” everybody agreed, “to see so many sad people”. At which point, the World Health Organization decided to name the disease. SAD was already taken so the WHO added another S for “severe”.

The SSAD epidemic continued into 2026. Then, on a wan day in early March something remarkable happened: people stopped cradling their heads in their hands and looked up. Not in the way they had in the “before times” when another person’s tears were a source of unease but with eyes cleansed by salt and electrolytes. That’s when people realised that no one had a monopoly on tears and that each tear was part of a rivulet that fed into a great river that cut across national, religious and ethnic divides.

Lyrics that the day before had provoked waves of involuntary gushing suddenly took on new meaning. Perhaps the song that best caught the public mood was Billy Bragg’s tribute to the Four Tops singer Levi Stubbs with its refrain, “When the world falls apart, some things stay the same”.

Yes, the world was falling apart; yes, images of fires, famines and cluster bombs continued to fill people’s screens. Yes, people contined to die for oil and other valuable commodities. But for better or worse it was their world and in the new republic of tears forged by the mouldy sorghum everyone was in it together.

A note on the sources that inspired this story:

Nodding syndrome (NS) is a neurologic disorder of children with typical onset between the ages of 5-15. First identified in Tanzania in the 1960s, NS is characterized by head dropping movements, cognitive impairment and seizures. One of the best-documented outbreaks occurred in Kitgum, in northern Uganda, in 1998 during an internal armed conflict that displaced thousands of children into refugee camps.

In 2001–2002, during an outbreak in Southern Sudan, experts from the WHO noted a strong association with the ingestion of red sorghum delivered by the World Food Programme. It is hypothesized that the practice of storing sorghum in outdoor stacks encourages the build-up of moisture, promoting the growth of mycotoxins (toxic fungi). Other suspected causal agents include prior infection with measles, a parasite transmitted by blackflies that breed beside rivers and post-traumatic stress disorder.

The quote from Pope Francis is from his final public appearance on Easter Sunday 2025 in St Peter’s Square.

In Japan, crying tends to be regarded as a sign of weakness. In recent years, “crying cafes” have sprung up in Tokyo and other Japanese cities to address the stigma and persuade people that crying regularly is a healthy way of relieving stress.

Further reading:

Michael S. Pollanen, et.al., Nodding syndrome in Uganda is a tauopathy. Acta Neuropathology, 136, 5 (2018 ):691-697.

WHO East Mediterranean Region, Determining current levels of mycotoxin contamination in Sudanese sorghum.

Florence Miettaux, The fight to cure South Sudan’s mysterious neurological disorder. The Guardian, 25 March, 2024.

Mark Honigsbaum, Read it and Weep: why regular crying is cathartic. The Observer, 24 May 2025.

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Department stores and other buildings where people congregated in large numbers were particularly hard hit with patients complaining they felt as if they had been “thrashed with sticks”. Others reported “searing pains” in their eyeballs.

Like the so-called super flu threatening to overwhelm the NHS this Christmas, the outbreaks were likely due to an H3 influenza virus. The difference was the virus had a much higher attack rate and made a profound impression on the medical profession and Victorian society and culture.

I am referring to the “Russian influenza” which swept the globe in 1889-1890, sickening people on every continent, and which was followed by further severe outbreaks in 1891,1892 and 1893. Up to 60 percent of urban populations were affected. By contrast, the current H3N2 virus – known as “subclade K” – has an attack rate of just 5 to 10 percent.

The Russian influenza was so named because the first well-documented outbreak occurred in St Petersburg in November 1889. In fact, as I described in a previous post, the pandemic originated in Western Siberia, from where is spread south and east to China and west to Bukhara, a Muslim trading post on the Silk Road in what was then Tsarist-controlled Uzbekistan.

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Today, we are used to flu and other viruses sparking annual winter crises. It happened last year when a “quademic” of flu, Covid-19, RSV and norovirus also threatened to overwhelm the NHS in the run-up to Christmas. And it also happened in 2022-23. The difference this winter is that the surge in infections has come two weeks earlier than usual and coincides with the threat of strikes by junior doctors. The result is that around 2,660 patients a day are now being treated in hospitals, the highest level ever recorded for this time of year. A&E attendances for flu and other respiratory illnesses area also running at record levels. If infections continue to grow at the current rate and junior doctors carry through with industrial action tomorrow (Wednesday, 17 December) the crisis will almost certainly worsen.

By contrast, in 1889, no one had experienced an influenza pandemic for 41 years. At first, doctors were baffled by the symptoms, confusing the disease with malaria and dengue. Adding to their confusion was the fact that the flu attacked the respiratory, gastric and nervous systems simultaneously. The headaches and shooting pains in the abdomen and eyeballs were only the tip of the iceberg. Patients also complained of profound fatigue, accompanied by bouts of insomnia and, in some cases, psychosis.

“I am so weak that if I read or write for half an hour I become so tired and faint that I have to lie down,” the English social reformer and women’s rights campaigner Josephine Butler informed a friend in 1892. The British Prime Minister Lord Roseberry suffered such a severe nervous attack that he spent six weeks confined to his bed at his home in Epsom.

At a wedding attended by 100 guests, it was reported, all but three had fallen ill. London police constables – perhaps because they were out in public and more exposed to the virus - appeared to be particularly badly affected, leading to the flu’s characterisation as a “fiend”.

According to official records, the Russian flu pandemic accounted for 125,000 excess deaths in England and Wales in 1890-93, a total which approaches the mortality of the better-known 1918-20 Spanish influenza pandemic. But, in truth, the Russian flu never went away. “It seems only too clear that we must reckon an outbreak of influenza among our regular yearly visitations”, remarked The Times in February 1895. Indeed, in her correspondence Butler was still complaining of the depredations of Russian flu in 1899.

As I and a colleague wrote in The Lancet, the result was that by the turn of the century, the Russian flu was being blamed in England for everything from the suicide rate to the general sense of malaise that marked the fin de siècle and the image of a nation of convalescents, too debilitated to work or return to daily routines, and plagued with mysterious symptoms and chronic illnesses, had become central to the period’s medical and cultural iconography.

While the present level of hospitalisations is alarming, so far there is no evidence that the current H3 is a “super flu”. Rather, it is a mutation of the same H3N2 virus that sparked a pandemic in 1968. Dubbed “Hong Kong flu”, that pandemic was responsible for between 1 million to 4 million deaths globally. Sera collected in 1956-57 from people aged 68 years or over showed strong cross-reactivity with antibodies from the Hong Kong flu. This suggests that people who survived the Russian flu and lived to an old age had protective antibodies against the H3N2 virus.

However, we cannot be sure the Russian flu was an H3 because in 1890 there were no diagnostic tests for influenza and no viral genetic material has been recovered from victims of the pandemic that would allow us to type the virus (by contrast, we know the Spanish flu was an H1N1 virus because its genome has been reconstructed from archival autopsy material).

Another intriguing theory is that the Russian flu may have been due to a coronavirus or a mixed pandemic of flu and corona.

One of the hallmarks of SARS-CoV-2, the virus of Covid-19, is that it is a highly efficient aerosol that spreads in unventilated spaces, such as choirs, cruise ships and night clubs. These super-spreader events resemble the outbreaks seen at department stores and other crowded settings in the winter of 1889-90. The fact that these outbreaks affected so many people at the same time baffled contemporary observers and led to competing theories about the disease’s mode of spread, with some scientists arguing it was due to mysterious atmospheric “influences” and others that it was a contagious disease spread by direct contact between affected individuals.

These debates mirrored the disputes 130 years later about whether Covid-19 was an aerosol or droplet infection and the degree of asymptomatic spread. The diverse clinical symptoms of Russian flu and its effects on the respiratory, gastric and nervous systems also suggest that, like Covid-19, it was a multi-organ disease. Finally, Russian flu transmitted easily from humans to cats – a feature that has been observed with Covid-19 but not with influenza.

Given that Covid is still causing widespread illness – with the Stratus and Nimbus strains currently dominant – that would provide yet another parallel with the 1890s. If so, the current hospitalisations may only be the beginning of a winter of misery.

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Organised by the Committee for Academic Freedom, the event was billed as “a rigorous [and] engaging exchange” on the pros and cons of lockdowns and an antidote to the UK Covid inquiry, which, having spent two years collecting evidence and interrogating 167 witnesses at a cost of nearly £200m, is now the most expensive in British history.

Even though the panel featured such prominent lockdown sceptics as Sunetra Gupta – Professor of Theoretical Epidemiology at Oxford University and a leading advocate of the “herd immunity” approach - I was confident that we would be able to agree on some basic facts and explore the evidence dispassionately, something that had proved nigh impossible during the pandemic.

Going into the debate my view was that lockdown had been a blunt instrument that had inflicted considerable damage on the economy and people’s mental health. But by the third week of March 2020 there had been no other way of slowing transmission of the coronavirus and relieving the strain on the NHS.

As Lady Hallett put it the following day: “The failure to appreciate the scale of the threat, or the urgency of response it demanded, meant that – by the time the possibility of a mandatory lockdown was first considered – it was already too late and a lockdown had become unavoidable.”

I made a similar point during the panel discussion, citing the findings of Imperial modellers that had Britain locked down on 16 March rather than 23 March, as many as 23,000 lives might have been saved. The message “stay home, protect the NHS, save lives” had come a week too late.

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But as rapidly became clear, this was not a conclusion that Gupta, who as a signatory of the Great Barrington Declaration had advocated shielding the elderly and most vulnerable while allowing the virus to spread to the rest of the population, was prepared to accept. Nor was it one that met with the approval of the Oxford audience.

During the Q&A that followed our discussion, speaker after speaker expressed fury with the damage that lockdowns and school closures had inflicted on young people’s mental health to cheers from the audience. Nor were Oxonians in a mood to hear that in March 2020, when Imperial’s Neil Ferguson came out with his infamous model predicting that as many as half a million Brits might die if we did not lockdown immediately, there had been no alternative.

In the spirit of fostering an open debate, CAF had extended an invitation to Ferguson but he declined to join the panel (his last public appearance was on 25 April 2020 when he was interviewed by UnHerd’s Freddy Sayer). I subsequently learned that such was the bad blood between Gupta and other prominent proponents of lockdown, such as Christina Pagel and Devi Sridhar, that they had been unwilling to share the same stage. Thus, it fell to yours truly to provide “balance” to the other speakers who, besides Gupta, included Toby Green, professor of African history at King’s College, London, and a prominent Left-wing critic of the lockdowns, and Hugh Montgomery, Chair of Intensive Care Medicine at University College London, who could speak directly to the experience of physicians on the Covid frontline.

It was an odd position to find myself in – I am a historian, not an epidemiologist – and at times it felt as if I was there to provide a target for point-scoring. Indeed, midway through our discussion Green quoted a passage from the first edition of my book, which was published six months before the emergence of Covid-19, in which I had pointed out that the World Health Organization had a poor record when it came to predicting pandemics and that in 2009 it had fostered widespread panic about a novel swine flu, only for the virus to turn out to be no more severe than a regular seasonal influenza.

It is always disconcerting to find oneself quoted out-of-context. The swine flu, as we now know, was a very different virus to SARS-CoV-2, the coronavirus that causes Covid-19. For one thing, in 2020 no one had immunity to the coronavirus, whereas the 2009 swine flu was a mutation of a pre-existing H1N1 influenza virus. Moreover, SARS-CoV-2 had a much lower infection fatality rate than Covid – around 0.03 as opposed to 0.66 - and although the unexpected emergence of the swine flu in Mexico in the spring of 2009 had led to the outlay of billions of dollars on emergency vaccines, there was never a possibility that the National Health Service would be overwhelmed.

This was not the case in 2020. On the contrary, as early as late February and certainly by the second week in March, it was clear that a “wait-and-see” approach of allowing the virus to spread while mitigating its worst impacts risked disaster and that, in the absence of a vaccine, restrictive measures aimed at suppressing transmission would be necessary.

Note that I write “risked” disaster. In the spring of 2020, there was no way of knowing that the NHS would be overwhelmed and whether the Imperial model was accurate. Nor can we know for certain if the then Prime Minister Boris Johnson’s failure to heed the call for a brief “circuit breaker” in September 2020, only to order a second lockdown six weeks later, contributed to the 70,000 deaths during the second wave in the winter of 2020-2021.

In her report on Friday, Hallett described Johnson’s dithering as “inexcusable” and argued that had Johnson brought in a circuit breaker then the second lockdown “might conceivably have been avoided altogether” (italics inserted).

But as Carl Heneghan, the director of Oxford’s Centre for Evidence-Based Medicine and a close associate of Gupta, pointed out on BBC Radio 4’s Today programme the day after the publication of Hallett’s report, words like “might” and “may” indicate that Hallet’s conclusion rested on Ferguson’s disputed model and were hypotheses, not evidence. “What we really needed to understand the causal chains of transmission … was to have a proper epidemiological investigation,” he complained.

I have some sympathy with Heneghan’s criticisms. His complaint was echoed this week by Unherd and other long-standing critics of the inquiry process such as the former Spectator editor Fraser Nelson. Writing in the Guardian, even Devi Sridhar, who broadly supported Hallett’s conclusions, wondered “what it adds to our understanding of what happened politically, and what lessons it offers for the future”.

However, Hallett’s brief was to “assess decision-making about non-pharmaceutical measures and the factors that contributed to their implementation”. It was never part of her terms of reference to examine the epidemiological modelling and the reliability of the projections made at the time. That would have been a very different inquiry, one that would have been better conducted by an organisation like the Royal Society.

It is also worth pointing out that during the inquiry Hallett took witness statements from both Heneghan and Gupta, where they set out their concerns about the assumptions underlying Ferguson’s model and why by March 2020 they thought sufficient immunity had accumulated in the population to obviate the need for a lockdown. Heneghan was also given ample opportunity to explain why, in September 2020, when he and Gupta met with Johnson and other experts to discuss a circuit breaker, he believed Covid was already “endemic” to the UK. However, during cross-examination last October by the inquiry’s deputy counsel Andrew O’Connor, Heneghan struggled to explain what he meant by endemic and why there had been a surge in deaths during the second wave – something that suggested we were still very much in the epidemic phase of the pandemic.

You can see Connor’s cross-examination of Heneghan here (the key exchanges are at 6.06.25). I leave it you to judge whether he was a convincing witness.

Underpinning these disputes was the claim made by Gupta in March 2020 that up to half the British population may have already been infected with Covid. If true, this would have meant that we were already on course to achieve herd immunity and that infections would soon peak, obviating the need for the spring lockdown (by contrast, the Imperial model assumed that by March less than three percent of the UK population had been infected and recovered, leaving 97 percent of the population susceptible to infection and hospitalisation).

In his book Spiked, Jeremy Farrar, the former director of the Wellcome Trust and a prominent member of SAGE, points out that even by September antibody data suggested that just six percent of the population had been infected. Describing the Great Barrington Declaration as “ideology masquerading as science”, Farrar writes that the only way Declaration proponents could explain the discrepancy between their theory and the antibody data was to posit that people were protected by “immunological dark matter”. But no evidence was presented to support this claim at the time and, to my knowledge, no evidence has emerged for it since.

I went into the panel discussion willing to be corrected. But when I cited the antibody data, Gupta insisted the government statistics were misleading because people who had been infected and who had cleared Covid infections prior to the commencement of testing in February 2020 would not necessarily have detectable antibodies six months later. This may well have been the case – absence of evidence is not evidence of absence - but it is no basis on which to make decisions affecting peoples’ chances of living or dying in a rapidly developing pandemic crisis. And that, as Hallett put it, was the “unenviable” position politicians found themselves in March 2020 when they were faced with the “agonising” decision whether or not to lock down.

But as I have argued elsewhere, in January 2020 we didn’t need epidemiologists to tell us that Covid-19 was a “once in a century pathogen” and that we were on a collision course with an asteroid. The images from China of deserted city centres and hospitals being constructed overnight should have told us that something unprecedented was coming our way. And when in February we saw those pictures from Lombardy of intensive care wards filling with elderly patients and military trucks loaded with corpses there could be little doubt.

But as Hallett pointed out, February had been a “lost month” for decision-makers. That the UK avoided similarly apocalyptic scenes to Italy was only thanks to the last-minute repurposing of NHS wards and the heroism of doctors and nurses working round the clock to relieve the pressure on intensive care units (ICUs).

As Kevin Fong, the national clinical advisor for NHS England’s Emergency Preparedness Resilience and Response, told Hallett when he testified at the inquiry last year, “the scale of death was truly astounding” and by June 2020, when the first wave ended, the system was “broken”.

At the panel discussion, Hugh Montgomery, who served on ICU wards throughout the pandemic and whose patients included the children’s author Michael Rosen, made a similar point. It wasn’t just elderly patients like Rosen who threatened to overwhelm ICUs but people in their 40s with comorbidities. Covid was a “systemic multi-organ infection” that proved “far worse” than anyone had anticipated, he said.

Writing in today’s Observer, the NHS palliative care specialist Rachel Clarke concurred.

“People died who could have been saved. These deaths are facts that cannot be denied.”

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James A. Garfield, the 20^th president of the United States, is a largely forgotten figure today, one of those shadowy members of the Gilded Age that the novelist Thomas Wolfe memorably described as one of the generation of “lost Americans”:

Garfield, Arthur, Harrison, Hayes… their gravely vacant and bewhiskered faces mixed, melted, swam together… Which had the whiskers, which the burnsides: which was which?

There are certainly plenty of whiskers and mutton chops on display in Death by Lightning, the new Netflix miniseries based on the 1881 assassination of Garfield. And while several scenes are invented, it is worth watching for its attention to historical and medical detail – not least its depiction of post-bellum Washington D.C. as a fever-ridden swamp and Garfield’s lingering death at the hands of his surgeon, Dr William Bliss.

I first came across the story of Garfield’s assassination when I was looking for a follow-up to The Fever Trail, my book on malaria. During my research, I learnt that Washington DC had once been highly malarious due to the mosquitoes that bred in marshes beside the Potomac River. Indeed, in 1882, an English obstetrician with the magnificent name Albert Freeman Africanus King had delivered a paper to the Philosophical Society listing 19 reasons why mosquitoes were the vectors of malaria and challenging the city’s fathers to erect a massive wire screen around the capital as high as the Washington Monument.

Alas, King was ahead of his time – it would be another five years before, in 1887, the British Army surgeon Ronald Ross confirmed that malaria was transmitted by female Anopheles mosquitoes – and King’s suggestion was dismissed (ironically, King is best remembered today for attending Lincoln on the night he was assassinated at the Ford’s Theatre).

However, I was fascinated to learn that as Garfield lay mortally wounded in the White House during the summer of 1881, the first lady, four White House servants and Guiteau himself had contracted malaria. Hoping to save Garfield from a similar fate, Bliss fed him large doses of quinine, which, while causing intestinal cramping, may have saved Garfield from a similar fate.

Unfortunately, Bliss didn’t have much time for germ theory and the insights of the German physician Ignaz Semmelweis into sepsis and refused to disinfect his instruments before attempting to extract the bullet from Garfield’s abdomen. Seventy-nine days later, after much prodding and probing, Garfield died of a massive haemorrhage caused by the bursting of the aneurysmal sac that had formed around the wound. At autopsy, it was discovered that Guiteau’s bullet had missed Garfield’s vital organs and lodged behind his pancreas. Had Bliss simply sewn up the wound, Garfield would almost certainly have survived.

The details of Garfield’s confinement and the trial afterwards of Charles Guiteau struck me as having all the elements of a major Hollywood screenplay and in 2003 I drafted a book proposal with the title “The President and the Madman”.

“It is a story of courage, love and medical incompetence set against the backdrop of party-political infighting in a parochial disease-infested city very different from the Washington of today,” I wrote my agent. “And it is the story of one of the most celebrated American “insanity trials” of the nineteenth century.”

Alas, my proposal failed to find a publisher. Imagine my surprise then when I saw the trailer for Death by Lightning with the tag line: “A president. A madman. A bullet.”

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American Killer

Credit for bringing the story to the small screen belongs to Mark Makowsky, who based the series on Candice Millard 2011 book Destiny of the Republic, and who, together with director, Matt Ross, does an excellent job of describing Giteau’s troubled upbringing and the delusions of grandeur that led to his fateful encounter with Garfield.

More’s the pity then that Makowsky skirts over Giteau’s subsequent trial. Instead, he fast forwards to the gallows where in the final scene Guiteau, played by Matthew Macfadyen, is shown reading a mawkish poem before being dispatched by the hangman. That caveat aside, Makowsky’s portrayal of Guiteau is sensitive and nuanced and in Macfadyen, who is no stranger to playing creeps (think of his role as Tom Wambsgans in Succession), Makowsky has found the perfect foil.

“The most reductive view of Guiteau is ‘chaotic evil’ but that’s the least interesting rendering of this person,” Makowsky recently told the Los Angeles Times. Instead, Makowsky sees Guiteau as a latter-day Rupert Pupkin, the obsessive fanboy portrayed by Robert De Niro in Martin Scorsese’s film The King of Comedy.

“[Guiteau] felt like a direct historical antecedent to the Rupert Pupkins and the Travis Bickles of the world. He fell through the cracks and we lost potentially one of our greatest presidents because of it.”

The question that interests Makowsky is “what are the societal factors that alienate a man like Guiteau from his fellow human beings?”

At a time of resurgent political violence marked by the 2024 assassination attempt on Trump and the assassination in September of Charlie Kirk, that is question pertinent to our own troubled times. At one point in the series, Garfield, played by Michael Shannon, likens the risk of assassination to a lightning strike – hence the show’s title. However, in Makowsky’s telling Garfield’s shooting is an accident waiting to happen and Guiteau is an instantly recognisable type of American assassin.

But we’re getting ahead of ourselves. As one of Makowsky’s characters asks on discovering a jar containing Guiteau’s embalmed brain in the stores of a medical museum, “Who the fuck was Guiteau?” One might equally add, who the f*** was Garfield?

A hero of the Gilded Age

Strong, athletic and ruthless in debate, Garfield cut a romantic figure in post-bellum Washington. Born like Abraham Lincoln in a log cabin, Garfield had escaped rural poverty in Cleveland, Ohio, rising via a church ministry to a college presidency and a generalship in the Union Army. Decorated for heroism during the Civil War, he championed the rights of former slaves and after resigning his commission to run for Congress as an Abolitionist enjoyed a meteoric rise through the ranks of the Republican party.

It was at the 1880 Republican National Convention that he became he surprise Republican pick for the presidency, defeating Ulysses Grant, who was seeking an unprecedented third term. Grant had been the preferred candidate of the “Stalwarts”, old guard Republicans who advocated for the civil rights of African-Americans but opposed civil service reform. By contrast, Garfield allied with James Blaine, the Senator from Maine and representative of the so-called “Half Breeds” who opposed New York’s hold on political patronage. Garfield, who was fluent in Latin and Greek, had come to the convention to speak on Blaine’s behalf but his oratory so impressed delegates that when the voting led to a stalemate, he emerged as the compromise candidate, clinching the nomination on the 36^th ballot. Shannon is particularly good in the role, playing Garfield with a quiet confidence and moral clarity reminiscent of Barack Obama in his heyday.

By contrast, with his sallow complexion, whiskers and a slight build, Guiteau was Garfield’s opposite. Born in Illinois to a hard-working Huguenot family, Guiteau proved a disappointment to his father and after dropping out of university, joined a millenarian religious cult, the Oneida Community, in New York. However, its philosophy of communal living and free love was not to his liking – in one of the show’s more amusing scenes, Guiteau refuses to indulge in the alfresco bonking encouraged by the community earning himself the derogatory nickname “Git-out” from his fellow Oneidans.

Giteau next tried to set up a newspaper and, when that failed, studied for the bar. But his legal career was also a bust and in New York he garnered a reputation as a shyster and wife beater. By the late 1870s, when Guiteau turned to preaching to earn a living, his life was on a downward spiral. Publishing a companion to the Bible entitled, The Truth, he began crisscrossing America, delivering surreal sermons and leaving a trail of unpaid bills in his wake. Soon, he found himself in Washington where, swept up in Garfield fervour, he began writing speeches and lobbying the president for a consular position. In this respect, he was no different from the hundreds of other undeserving office seekers who descended on Washington in search of lucrative appointments. But, as Makowsky makes clear, Garfield was a staunch opponent of the “spoils system” and was determined to break the hold of the New York Republican party and the Stalwarts on government offices.

Long story short, Garfield rejected Guiteau’s entreaties and on 2 July 1881 Guiteau took his revenge by firing two bullets into him from behind as Garfield was about to board a train at the Baltimore and Potomac depot. Following his arrest, police retrieved a letter intended for the newspapers in which Guiteau admitted shooting the president and described his death as “a political necessity because he proved a traitor to the men who made him” (this was a reference to the Stalwarts, the faction to which Guiteau had allied himself after being rebuffed by Garfield). The first bullet grazed Garfield’s right arm and flew harmlessly away. The second hit him in the abdomen, lodging near his pancreas. Blaine, who Garfield had appointed Secretary of State, was the first to his side, followed by his Secretary of War, Robert Todd Lincoln, the son of Abraham Lincoln. “How many hours of sorrow I have passed in this town,” Lincoln would later reflect.

On learning that her husband had died of sepsis, Garfield’s wife Lucretia was similarly disbelieving, exclaiming: “Oh why am I made to suffer this cruel wrong?” It was a sentiment shared by Garfield’s supporters. More than 70,000 mourners filed past his casket for the two days he lay in state on Capitol Hill and a further 150,000 visited Garfield’s bier when he was brought back to his farmstead in Cleveland for burial.

Garfield’s stoicism coupled with the First Lady’s pain at his death had stirred the nation. But if the manner of Garfield’s departure was remarkable, the trial of his assassin was even more extraordinary.\

Trial of the century

Charles Guiteau entered the District courthouse on 14 November 1881 and did not leave it until 26 January the following year. Reported daily in the newspapers, the three-month trial mesmerized the nation. According to the medical historian Charles Rosenberg, the prosecution called more than 90 direct and rebuttal witnesses, the defence another 50. It was one of the nineteenth century’s most celebrated insanity trials.

Sitting beside his attorneys as co-counsel, Guiteau turned the courtroom into a circus with his repeated outbursts. But the most dramatic exchanges were between the “alienists” – as the psychiatrists who studied the insane were then known.Although the role of genetics in behaviour was widely accepted, these psychiatrists fiercely debated whether heredity had predisposed Guiteau to assassinate Garfield or whether his upbringing and environmental and social conditions were also partly to blame. Was Guiteau a madman and thus not responsible for his actions? Or was he, as the district attorney maintained, a “cool, calculating blackguard”?

The psychiatrists’ attempts to answer that question would raise issues at the heart of the insanity defence to this day. For instance, following John Hinckley’s assassination attempt on Reagan in 1981, psychiatrists argued that Hinckley was suffering from a “narcissistic personality disorder” and was so deluded by his obsession with the actress Jodie Foster that he could not be held criminally responsible for his actions. Hinckley was acquitted by a jury and sent to St Elizabeth’s Hospital, a psychiatric institution in Washington, where he received treatment until his release in 2022.

“A fit subject for a lunatic asylum”

Today, most experts agree that Giteau’s conviction for murder was a travesty and that, like Hinckley, he should have been found innocent by reason of insanity. As early as 1875, Guiteau’s father, despairing at his son’s erratic behaviour, wrote that he was a “fit subject for a lunatic asylum”. And so convinced was Guiteau’s brother-in-law, George Scoville, that a jury would see that Guiteau was insane, that when no other attorney would defend him, he took the case.

Unfortunately for Guiteau, at the time of his trial the test for insanity was the McNaghten rule. Named after Daniel McNaghten, the British man tried in 1843 for the murder of Robert Peel’s private secretary, the rule held that a defendant was considered responsible if he was aware of the nature of his act and knew it to be forbidden by law. Guiteau had already admitted as much in his letter. Moreover, American juries had tired of defendants employing what they regarded as the “insanity dodge”. The only acceptable defence was the one formulated by John Gray, the superintendent of New York’s Utica Asylum: if a man had lived a good life and suddenly went out and killed his neighbour, then insanity was possible, Gray argued, but if the person had lived a bad life, then insanity was not possible.

It did not help Guiteau’s defence that when Gray was recruited as a witness for the prosecution and asked Guiteau how he’d come by the insanity defence, he admitted that from the time he conceived the act he knew that if he could convince the jury that the assassination was an act inspired by God, he could not be held responsible before the law. “The responsibility lies on the Deity and not on me,” he informed Gray. “And that, in law, is insanity.”

Despite this, Guiteau bridled at Scoville’s attempts to portray him as a self-deluding fool. “I don’t want to have the case tried this way,” he informed his brother-in-law at one point in the trial. “When you say I am a fool, I am down on you.”

The upshot was that his defence failed and on 30 June 1882 he was hung for Garfield’s murder. Yet, within a dozen years of his execution few psychiatrists doubted Guiteau had been insane and that his trial had been a miscarriage. Although they classified Guiteau as a “degenerate of the regicidal class” – a hereditary concept of criminality that has no place in theories of mental illness today – their diagnosis would prove a milestone in psychiatry, one that would revolutionise the law’s attitude to mental illness.

It would have been interesting to see how Macfadyen would have handled the trial scenes. His performance up to Guiteau’s arrival at the gallows leaves little doubt that Guiteau was clinically insane, albeit with that peculiar perspicacity that is the hallmark of madmen.

Indeed, like Booth and Oswald, he appears to have been a type peculiar to America. For as Stephen Sondheim argues in Assassins, his brilliant musical about presidential assassins and would-be assassins, one of America’s most cherished national myths is that in the United States everyone has the right to succeed. And if you are unable to realise your dream, then someone or something must be to blame.

With his overbearing sense of entitlement and toxic feelings of impotence, Guiteau fits this mould perfectly. It wasn’t God that made him pull the trigger but an America that teaches it’s citizens that celebrity is their God-given right.

As Sondheim puts it in Assassins: “If you can shoot a president, you can get the prize.”

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