DR CHRIS VAN TULLEKEN: How we learned to treat Covid-19 then beat it

How we learned to treat Covid-19, then beat it! DR CHRIS VAN TULLEKEN describes the front line of a battle that humanity can’t afford to lose

The next pandemic is already in the post. This month, the authorities in Guinea in West Africa declared a new Ebola outbreak; Saudi Arabia’s health ministry has reported four new cases of MERS, a coronavirus we catch from camels, writes Dr Chris van Tulleken

As an infectious diseases doctor at the Hospital for Tropical Diseases, which is part of University College London Hospital (UCLH), I see patients with infections — and I also study viruses in the lab at University College London next door.

Yet despite my clinical and research experience, over the past year I’ve been utterly wrong about so much of this pandemic — and especially about the infection it would cause.

When I first realised in early 2020 that we were facing a global pandemic of Covid-19, I imagined that this new foe would be a virus that largely affected the lungs — a more serious version of the four coronaviruses that already circulate and cause colds.

This was the received wisdom following a very similar but far more deadly coronavirus that emerged in 2003: SARS.

That belief changed entirely last March when my twin brother, Xand, caught Covid.

His symptoms were miserable but expected: cough, fever, exhaustion and loss of smell and taste. 

He seemed to manage them well in isolation, and within a fortnight appeared to be on the road to full recovery.

But then one morning, early in his recovery, while I was working a shift on a Covid ward at UCLH, Xand came into A&E as an urgent case. 

He’d developed a dangerous heart rhythm disorder, atrial fibrillation, likely as a result of the virus inflaming his heart.

Xand had a heart rate of 170 beats per minute (it should have been around 60) and his blood pressure was low. Colleagues from the A&E and anaesthetics teams sedated Xand and cardioverted him — giving him a large electric shock to temporarily stop his heart, allowing it to restart in a normal rhythm.

It was a terrifying and, for me, tearful moment. This is a fairly routine procedure but the worst consequences are severe.

Covid is starting to make many of us wonder if contracting a virus as an adult may explain the symptoms many previous patients have been struggling with. The latest science of long Covid is just one of the topics covered in a new BBC Horizon special, to be broadcast this Thursday, that marks nearly a year since Britain first entered lockdown

Nor was this to be the last time: Xand came into the emergency room twice more as the year went on. It was clear that Covid had damaged his heart.

As this was unfolding in my own family, it was becoming clear from patients and colleagues from other specialties that Covid affects every organ system — even in those who don’t have a serious infection.

We now know from hard-won experience that it can have widespread and devastating effects, causing strokes and brain inflammation, clots and heart attacks.

And contrary to media reports, we were seeing these problems in many young and previously healthy people. A few died, but many have been left devastated by an apparently mild illness.

Xand is still taking medication to keep his heart in rhythm.

Meanwhile, other effects on the heart are still unfolding. Only last week, a study by UCL found high levels of potentially chronic heart problems among people who have survived hospitalisation with Covid — revealed in blood tests for troponin, a protein released from injured heart muscle.

The lessons learned: Doctors Chris (left) and Xand van Tulleken in a Horizon report. We now know from hard-won experience that it can have widespread and devastating effects, causing strokes and brain inflammation, clots and heart attacks

Perhaps the most worrying side-effect for younger people is long Covid — a cluster of different symptoms along with severe ongoing fatigue.

For a long time, the medical profession has been unable (and, occasionally, unwilling) to help people with fatigue syndromes such as ME (myalgic encephalomyelitis) and fibromyalgia. They often have normal test results and they can get written off.

Covid is starting to make many of us wonder if contracting a virus as an adult may explain the symptoms many previous patients have been struggling with.

Covid-19 facts

  • 10-30% of people who get Covid are responsible for 90% of further infections
  • There are 200 new Covid vaccines currently in development — 60 are in clinical trials 

The latest science of long Covid is just one of the topics covered in a new BBC Horizon special, to be broadcast this Thursday, that marks nearly a year since Britain first entered lockdown.

Presented by me, Xand and Dr Guddi Singh, a paediatrician at Guy’s and St Thomas’ NHS Foundation Trust, it features interviews from scientists and clinicians at the forefront of the fight.

We have learned so much in the past year, and now have the knowledge to end the pandemic and stop the appalling sickness and death caused both by the coronavirus and by lockdowns.

And the data we have seen seem to make some choices increasingly clear if we want to relegate this virus from a lethal pandemic to an occasional pestilence.

Here are some of the lifesaving lessons that we’ve learned. 

Genetics are key to beating pandemic 

What we know about the new coronavirus, how it behaves and how to tackle it, is the culmination of the revolution in genetics that started with the project to sequence the human genome.

In the 20 years since that was completed, we haven’t quite seen the promised benefit to us all. Until now.

The story of this pandemic — past, present and future — can be written with an alphabet of just four letters: those of the genetic code that’s common to all life.

These letters — A, T, C and G — are the building blocks of the DNA blueprint in all our cells, including many viruses. The ways in which these letters are combined in long sequences determine what makes all living things unique.

It is thanks to the advances in genetics, unimaginable even a few years ago, that we now know enough about how this virus spreads and mutates so we can actively end this pandemic and return to normal life.

What we know about the new coronavirus, how it behaves and how to tackle it, is the culmination of the revolution in genetics that started with the project to sequence the human genome

The sequence of the Covid-19 genome was published in January 2020 — astoundingly fast. This meant that by early February, Professor Teresa Lambe and the team in Oxford (working with AstraZeneca), along with other scientists around the world, were already designing the vaccines many of us have now had.

As Teresa explained when we interviewed her, the vaccines licensed in the UK are gene-based, which means they don’t need a sample of the virus to start testing and manufacturing: they just need the genetic code, which can be sent in an email. (This massively speeds up the development process as there’s no need to culture live virus.)

Genetics have also allowed us to diagnose the virus. The gold standard PCR test is a genetic test that looks for parts of the virus genome. It is highly accurate and has allowed us to understand so much of the virus biology.

Genetic technology has also enabled the Covid-19 Genomics UK Consortium (COG-UK) to track the emergence of new variants by sequencing diagnostic samples from all over the UK.

As Professor Sharon Peacock, who heads up COG-UK, told me, it is thanks to this work that we are now increasingly sure that our homegrown ‘Kent’ variant, which swept across England last November, is not just more transmissible but may also be more deadly, hospitalising a greater proportion of the patients who get it.

For a while, it had seemed like this virus changed relatively slowly — a couple of mutations a month. But not now.

We know that allowing a surge to spread through the population once the vulnerable are vaccinated will give an advantage to those variants capable of spreading in vaccinated people. People are seen in Regents Park, London

I also spoke with an old friend and colleague, Ravi Gupta, a professor of clinical microbiology at the Cambridge Institute of Therapeutic Immunology and Infectious Disease and member of NERVTAG (the body that advises the Government on new respiratory viruses).

He described his shock when he first saw the gene sequence for the Kent variant: it had not one or two but 23 different DNA mutations. He’d seen this exact pattern in a patient with a perilously weak immune system (as a result of chemotherapy for cancer) with Covid at Addenbrooke’s Hospital in Cambridge who’d been suffering with the virus for 100 days.

The patient was given ‘convalescent plasma’ from those who had recovered from Covid. The plasma contained antibodies that should, theoretically, kill the infection. Instead, the virus evolved to get around this by accumulating mutations in its DNA. By the time the patient had died, the virus had evolved 37 separate mutations.

This may be where some of the new variants are coming from — chronic cases in patients with immune dysfunction where the virus has a unique opportunity to try out different evasion strategies.

The genetic sequences that we use to diagnose patients are now also being used to build the next round of vaccines. We are going to see variants emerge around the globe, but instead of starting from scratch, the sequence can be plugged in and an updated vaccine produced in months, not years. I can’t imagine where we would have been now with this pandemic had it not been for genetics — but without doubt, we would be desperately worse off.

Vaccines get us on road to freedom 

Eventually, once as many people as possible are vaccinated, herd immunity will reduce transmission of the virus. But this will take many months — and we are a very long way off having natural immunity from the massive waves of virus that have spread.

In the meantime, reducing transmission is vital for the success of our vaccine rollout. Allowing the virus to continue to spread before widespread vaccination will not only lead to deaths and long Covid but also risks the emergence of vaccine-resistant strains.

It is a law of biology as immutable as the law of gravity that viruses mutate when they spread. Every infected person and transmission gives a chance to the virus. We know that allowing a surge to spread through the population once the vulnerable are vaccinated will give an advantage to those variants capable of spreading in vaccinated people.

We are going to see variants emerge around the globe, but instead of starting from scratch, the sequence can be plugged in and an updated vaccine produced in months, not years

Currently, our vaccines work superbly well. Surrendering an advantage to the virus by allowing it to start spreading rapidly would be a terrible waste. It will also kill many young, fit people and leave many others devastated with the consequences of infection.

Dying of Covid-19 now is like being a soldier shot dead on Armistice Day when the ink is drying on the treaty but the ceasefire is yet to begin. This is now a vaccine-preventable disease. If everyone complies with lockdown right now, that vaccine potential won’t be wasted. 

Why more patients are now surviving 

The hospital death rate from Covid has dropped spectacularly. Partly this is due to the case mix of patients (tragically, many people most likely to die have already died), but in large part it’s also due to advances in clinical care.

The high-tech solutions, especially the drugs, make the headlines — but they’re not the only thing making the difference, as I saw when I went to interview Mark Vargas, a senior charge nurse on the intensive care unit (ICU) nursing team at University College London Hospital.

I watched his team perform an emergency ‘prone’ on one of the sickest patients. This is where the patient is flipped onto their front to allow improved blood and air flow in their lungs.

Done badly, it is extraordinarily dangerous, as the ventilator tube can be pulled out. As it is such a risky procedure, in the past it was done only a few times per year, but the patient I saw flipped over while filming Horizon was the third patient expertly and safely proned that day.

Proning is just one of a huge suite of changes made in ICU so that, despite the fact that they are now looking after five patients with just two nurses (the ratio would normally be 1:1), survival rates have still improved.

We need to spot the super-shedders 

To reduce transmission and the worst effects of long Covid, it’s vital we find the people who spread the most virus and isolate them.

Scientific studies have revealed that the vast majority of people who contract Covid-19 never pass it on — and that between 10 to 30 per cent of infected people are responsible for 90 per cent of all transmissions.

This may be partly down to some people’s biology. In the Horizon programme, Mark Woolhouse, a professor of infectious disease epidemiology at Edinburgh University, refers to these people as super-shedders, because they release unusually large numbers of virus particles. 

This was starkly demonstrated in the summer of 2020, when an airliner landed in Ireland from the Middle East carrying 49 passengers.

It was later discovered that 13 were infected with Covid-19. Most of them did not go on to infect anyone else; however, five of the passengers went on to infect 43 other people.

We also know that there are super-spreader events which are crucial. If a super-shedder patient is sitting quietly at home alone, then they won’t infect anyone. But if they go to a party, say, they could infect a huge number of others present.

Super-spreader events tend to be poorly ventilated, indoor environments with lots of crowding: weddings, churches, choirs, gyms, funerals, restaurants. Loud talking or singing massively increases the risk. Clubs and pubs are prime examples.

Any case of Covid is most likely to have been infected at a superspreader event or by a super-shedder. This means that simply isolating the contacts of an infected person, as we currently do, is important — but what we would ideally do is look backwards at all the people our case may have caught it from.

This will identify the superspreader event or person and allow tracing of their contacts — which will produce many more cases who need to be isolated. This is called backward tracing and it is not trivial. It takes resources and money and needs transmission rates to be low enough to do it.

As I write, there are more than 10,000 new cases each day. It is simply not possible to trace and isolate everyone linked to every one of them.

But what is clear is that if our vaccines and our current tracing methods are going to work, we must ensure that transmission rates in the community are at rock bottom before we start to open up the places where it spreads best.

Rapidly opening up venues where large numbers of people are indoors with poor ventilation for prolonged periods may lead to the emergence of vaccine-resistant strains and another cycle of deaths from Covid, followed by lockdown.

I would rather catch Covid-19 now than a year ago. But knowing about long Covid, I would much rather not get it at all. And that is the point of continuing to drive down the daily infection numbers whilst we roll out mass vaccination and effective tracking and tracing. 

Danger of trusting in herd immunity 

When we do the maths, it looks like we will need to vaccinate many more people against Covid-19 than was previously hoped to achieve herd immunity, which will prevent the virus from spreading.

Indeed, we might have to vaccinate as many as 97 per cent of the population. This is because the new variants we’ve seen so far are significantly more contagious than the strain from China.

Certainly, we can’t rely on natural herd immunity emerging by sufficient people getting infected and surviving to develop their own immune resistance, as some mooted early on. That idea was always extraordinarily naïve and dangerous.

When we do the maths, it looks like we will need to vaccinate many more people against Covid-19 than was previously hoped to achieve herd immunity, which will prevent the virus from spreading

This has been underlined by the fact that high levels of natural transmission have allowed new strains to emerge — and it looks like these can go through the population and re-infect people. 

Nor do I think that anyone with expert knowledge believes we can eradicate Covid-19 in the way that we wiped out smallpox — the only virus we have managed to eradicate. But we can reduce its impact with vaccines.

I’m a great fan of vaccination, but I’m not a fan of mandatory vaccination because it generates suspicion. We need to persuade people about how great and safe these vaccines are, not threaten them with ‘no jab, no job’.

Carrots and information work better than sticks. 

Covid-19 has now killed some 2.5 million people worldwide and infected 110 million, many of whom will suffer long-term consequences, and cost the world an estimated £16 trillion.

But compared to what might have happened, we’ve got off relatively lightly. It’s estimated there are more than a million viruses in animals able to infect us, and any one may become a pandemic far worse than this. Imagine a virus that kills 5 to 10 per cent of those it infects, and that this was the death rate in children.

The next pandemic is already in the post. This month, the authorities in Guinea in West Africa declared a new Ebola outbreak; Saudi Arabia’s health ministry has reported four new cases of MERS, a coronavirus we catch from camels.

We know that the more humans invade wild ecosystems, the more we expose ourselves to deadly viruses that can jump from animal species into us. And these jumps are happening more often, driven by global consumption, health inequalities, climate change, agricultural practices and environmental destruction.

We need to improve our global surveillance systems for spotting and stopping novel viral outbreaks. If we don’t, it is a racing certainty that we will see the next pandemic within our lifetimes.

Coronavirus — A Horizon special: What We Know Now, Thursday at 9pm on BBC2.

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Why Dr. Fauci Thinks You Should Wear Two Masks

If you’ve been paying close attention to pandemic expert Dr. Anthony Fauci and you’ve been masking up, you might have noticed officials belonging to the freshly minted Biden administration going above and beyond by wearing not just one masks, but two — one on top of the other — since the Inauguration. And if you’re wondering whether official directives might have changed with regard to mask wearing, they haven’t; well, not exactly.

In an interview with NBC’s Savannah Guthrie, Dr. Fauci says that double masking “likely works” because masks are physical barriers that keep potentially infectious droplets, and the virus those could carry, from getting into our systems and getting us sick. “If you have a physical covering with one layer, you put another layer on, it just makes common sense that it likely will be more effective, and that’s the reason why you see people double masking, or doing a version of the N-95,” Dr. Fauci explained.

Dr. Fauci’s input on wearing two masks is worth considering, particularly with the news that more contagious variants of the COVID-19 virus have been spotted in the United Kingdom, South Africa, Brazil, and closer to home in California (via USA Today). He also told Guthrie on The Today Show that vaccine manufacturers are already working on creating booster shots that will help keep the inoculations effective against COVID-19.

Wearing two masks could be a good idea under certain circumstances

There is a practical reason why double masking could be a good idea. As The New York Times points out, there is a need to think about the kind and quality of the masks we are using to keep ourselves and our loved ones safe against this potentially deadly virus that continues to spread across the country.

Because not all masks are created equal, you might want to double up on yours, especially if you’re not entirely certain about the quality of the masks that you might be using. The latest research on masks and mask wearing urges us to remember that the quality of your mask matters, and that better filters mean better protection against the coronavirus.

So, what exactly do you need to know when choosing a mask during the pandemic? Keep reading to find out some key tips.

Certain masks work best against the coronavirus

A study done earlier by scientists at Virginia Tech and reported by the New York Times pointed out that the best mask “has two tightly woven layers of outer material with a filter material sandwiched in the middle.” The study suggests you make use of masks that are made with material that features tight weaves and also fits your face better, and that face shields should be used with a mask, since the plastic barriers don’t offer much protection — if at all.

If masks don’t appear to work, it’s because they are either too thin, or wearers don’t use them properly. Still, “Something is better than nothing,” Dr. Linsey Marr, who was part of the research team, told the New York Times. “Even the simplest cloth mask of one layer of material blocks half or more of aerosols we think are important to transmission. If you go to a tighter weave and more layers, you’ll get even better performance.”

Double masks and N-95s only work if you wear them properly

One doctor thinks venturing out into the public wearing two masks may be a bit much, because doubling up on masks doesn’t exactly mean you’re doubly safe from the new coronavirus variants. Dr. Graham Snyder of WakeMed tells ABC News, “[Wearing two masks] will decrease the transmission of the virus by a small amount. [But] it’s, it’s not going to make it to zero and it’s not going to be a big jump, but it would help a little bit more.” There’s also the added grief of finding that it might be too difficult to breathe if you have two masks on so you’re tempted to not wear any masks at all. His advice: go ahead and pull two masks on — but only if you’re able to keep them on.

And before you think about heading out and buying a stock of high-performance, medical-grade N-95s in place of wearing two masks, consider this advice from Baltimore’s former health commissioner, emergency physician Dr. Leana Wen. “You could have a very good N95 mask, but let’s say that somebody isn’t wearing it properly or is only wearing it 50 percent of the time. I would rather that someone wear a surgical mask or cloth mask 100 percent of the time, correctly and consistently,” she tells NBC.

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DR MARTIN SCURR answers your health questions

‘My nightmares are so bad that I scream out loud’: DR MARTIN SCURR answers your health questions

A few times a year, I have terrible nightmares during which I scream — but I don’t remember them in the morning. I am in my 70s, the only health problem I have is high blood pressure and I haven’t suffered trauma. Should I be concerned?

Jane Thornton, via email.

This is understandably distressing for you, but the good news is that the cause is not sinister. Your email amounts to a textbook description of sleep terrors, one of a group of disorders called parasomnias, which cause unusual or unwanted behaviour while you sleep.

Although more common in children, they can affect people of any age, occurring during the deepest stage of non-rapid eye movement sleep (one of the two main cycles of sleep). They typically involve intense fear and screaming and last a few minutes.

In the morning, those affected won’t recall anything because it all happened while they were sleeping (usually they only know about it through their partner).

A visit to your GP should confirm the diagnosis and reassure you that this is nothing to worry about [File photo]

Research suggests such episodes are triggered by physical and emotional stress, including excessive fatigue, fever and certain medication (for example, the sleeping tablets zolpidem and zopiclone).

None of these factors appears to be relevant in your case, however, and I have not been able to find any research linking night terrors to high blood pressure, nor the drug felodipine, which you take to treat this.

Knowing that these episodes are night terrors, a recognised disorder, and nothing more sinister is usually enough for most patients.

There is some evidence that clonazepam (an anti-convulsant and sedative) may be helpful in the short term — but to take such medication long term for brief episodes that occur only two or three times a year does not seem ideal.

A visit to your GP should confirm the diagnosis and reassure you that this is nothing to worry about.

I had stents fitted nine years ago to help with angina and have since been taking beta blockers. Lately, my COPD (chronic obstructive pulmonary disease) has been worsening after exercise. I know beta blockers can cause breathlessness, but my GP won’t remove them from my prescription. Would it be dangerous to stop taking them?

Roger Jones, St Albans, Herts.

This is a reasonable question, but I urge you not to stop taking the beta-blocker (bisoprolol, as you mention in your longer letter), which is key to keeping your heart health in check.

COPD is the umbrella term for chronic lung conditions that are characterised by breathlessness, such as severe asthma. You say this is now worse with exercise — known as exertional dyspnoea — but no one has explained why.

Your heart disease (caused by a narrowing of the coronary arteries) was eased by stents, small metal cages used to prop open the blood vessels, almost a decade ago.

The beta blocker you’ve been prescribed improves blood supply to the heart muscle by slowing your heart rate and improving the efficiency of each beat. This has worked as your chest pain, caused by angina, has gone.

COPD is the umbrella term for chronic lung conditions that are characterised by breathlessness, such as severe asthma. You say this is now worse with exercise — known as exertional dyspnoea — but no one has explained why [File photo]

Through your own research you found that beta blockers can cause breathlessness. This is correct in the case of the first-generation beta blockers (e.g. propranolol), but second-generation beta blockers, including bisoprolol, do not.

Instead, a possible cause is that your COPD has deteriorated due to factors such as pollution, which can trigger more inflammation in the airways.

Or this may be an sign of a further restriction of blood flow in the coronary arteries. This could be the case even without chest pain and notwithstanding your long-term treatment with the statin simvastatin (to lower cholesterol) and aspirin (to thin the blood).

For this reason, I think it is essential that you see a cardiologist. Further investigations might include a form of heart X-ray and, depending on the findings, your medication will be reviewed.

You should also consult your GP to organise for an expert to reassess the severity of your COPD.

Write to Dr Scurr

Write to Dr Scurr at Good Health, Daily Mail, 2 Derry Street, London W8 5TT or email [email protected] Replies should be taken in a general context and always consult your own GP with any health worries.

Vitamin D is very much the nutrient du jour; its role in immunity is being studied closely as a result of the pandemic. But another, less well-known, benefit is its role in resolving dizziness.

I receive many letters about dizziness — in particular benign paroxysmal positional vertigo (BPPV), which triggers the kind of spinning and unsteadiness you would feel after jumping off a children’s roundabout.

It can be a very unpleasant and disabling experience. And, while it often resolves itself, the condition can recur.

But now research suggests it may be prevented by taking vitamin D (400IU, international units, daily) and calcium carbonate (500mg twice daily) supplements. It seems that the treatment is especially effective in those with low vitamin D levels.

In short, a very real and exciting advance for those plagued with this condition. And yet another reason to keep your levels topped up.

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DR MICHAEL MOSLEY: Why won't the NHS tell you how to treat diabetes?

DR MICHAEL MOSLEY: Why won’t the NHS tell you the secret to treating diabetes? (Clue: It costs nothing)

Eight years ago I managed to beat type 2 diabetes by going on my 5:2 diet (cutting my calories two days a week) and losing weight — 9kg to be precise. 

Since then I’ve become something of a broken record on the importance of shedding body fat to improve your blood sugar levels.

So I was delighted last week by the news from the Norfolk Diabetes Prevention Study — the largest of its kind in the world — which showed that even modest weight loss can have a big impact.

A recent review by Danish researchers found more than 70 per cent of people with type 2 diabetes who had lost significant amounts of weight were still medication-free more than five years later [File photo]

The Norfolk study recruited more than 1,000 people with pre-diabetes (meaning they had raised blood sugar levels). They were asked to lose weight, then were monitored for more than eight years. Those who managed to lose 2kg to 3kg, and keep it off, almost halved their risk of developing full-blown type 2.

This adds to extensive research carried out by British scientists showing that, as well as pre-diabetes, type 2 diabetes can be put into remission by going on a rapid weight-loss diet. And, as we’ve known for 20 years, weight-loss surgery can also reverse type 2.

In fact, a recent review by Danish researchers found more than 70 per cent of people with type 2 diabetes who had lost significant amounts of weight were still medication-free more than five years later.

Despite all this, the NHS Choices website still tells you type 2 diabetes is a ‘progressive’ disease that ‘usually gets worse over time’, with most people needing ever increasing levels of medication. What a depressing — and I would argue inaccurate — message.

So why aren’t they being a bit more encouraging? The situation with type 2 diabetes reminds me of a tussle I had with the medical establishment more than 25 years ago. 

In 1993 I was looking around for a subject to make a science documentary, when I came across the work of two Australians, Dr Barry Marshall and Dr Robin Warren, who had a striking new theory about stomach ulcers.

I was delighted last week by the news from the Norfolk Diabetes Prevention Study — the largest of its kind in the world — which showed that even modest weight loss can have a big impact [File photo]

At the time, stomach or duodenal ulcers (affecting the first part of the small intestine) were incredibly common but, like type 2, were seen as something of a mystery.

Gut ulcers can be excruciatingly painful and lead to internal bleeding. Doctors knew they were caused by excess acid and they could be managed by drugs such as ranitidine, which stopped the stomach from producing acid. These drugs, known as proton pump inhibitors, were expensive but there was a lot of incentive to use them because if you didn’t, or if the drugs stopped working, there was a high chance you’d need some of your stomach and intestines removed.

Robin and Barry, however, were convinced they had a cheap and effective cure. Their research showed that most patients with ulcers were infected with a bacterium, which the two doctors called Helicobacter pylori.

The patients’ stomachs were producing more acid to get rid of the bacterium, but this failed because Helicobacter is resistant to acid attack. But it is vulnerable to the right antibiotics.

To prove the point, Barry deliberately infected himself with Helicobacter (he swallowed a flask of it) and soon developed gastritis — massive inflammation — which he cured with a short course of antibiotics. This was in 1984.

Nine years later, when I began filming with Robin and Barry, there was still widespread resistance to their claims, despite extensive proof they were right.

When I asked Barry how long he thought it would take to persuade his colleagues to take their claims seriously, he laconically replied, ‘Well it’s been ten years and ten per cent of doctors are treating ulcers this way. Perhaps in 100 years they will all be doing it.’

In fact, within ten years almost all doctors were doing it. Not least because Barry and Robin won the Nobel Prize for Medicine in 2004 for their work.

But back in 1994, when my documentary, Ulcer Wars, detailing their work, came out, the medical reaction was either indifference or hostility. A review in The British Medical Journal by a leading gastroenterologist described the film as ‘one sided and tendentious’.

However, patients with duodenal ulcers who’d watched the programme soon began demanding antibiotic treatment.

Many later wrote to me and as one man put it: ‘I saw your programme a week before I was due to have surgery, and it was only because my doctor was prepared to listen that I was cured by antibiotics rather than having a chunk of my guts removed.’

Why did it take so long for doctors to adopt this approach, despite overwhelming evidence that eradicating Helicobacter could change patients’ lives? This was a question that researchers from Harvard asked in 2019 — concluding that it was mainly because doctors get much of their information from pharmaceutical companies, and these companies had no incentive to promote a cheap alternative to their acid-reducing drugs (which, of course, you took for life).

The parallels with type 2 diabetes are clear. As the millions of those affected in the UK will know, type 2 is usually treated with medication. 

While this will reduce the long-term damage caused by high blood sugar levels, it doesn’t deal with the underlying disease — and like all medication, the drugs can have significant side-effects, particularly when you move on to injecting insulin.

So how long before there’s widespread acceptance that most cases of type 2 diabetes can be put into remission by a rapid weight-loss diet? 

It is beginning to happen, but I wouldn’t guarantee that NHS Choices will be telling you the good news any time soon.

Like us, worms need to sleep. And the way their bodies prepare for sleep is also surprisingly similar to humans — one of the key triggers for a bit of shut eye is the release of melatonin, also known as the ‘hormone of darkness’.

Melatonin is produced in your brain and levels rise when it gets dark (synthetic melatonin is a popular sleep aid and is used to treat jet lag — I find it very effective).Now researchers at the University of Connecticut have discovered how melatonin actually works — in worms at least.

It slows the release of neurotransmitters, substances that allow messages to travel between nerve cells. So melatonin effectively tells your brain cells to stop chatting to each other — the chemical equivalent of a giant ‘shhh’!

Covid-19 vaccines are like buses; you wait for one, then two come along, almost together, with other contenders coming close behind.

This week we learnt that the vaccine made by Moderna may be even more effective than Pfizer’s. That both are more than 90 per cent effective is fantastic news and a real poke in the eye for the sceptics who claimed we might never get a vaccine against Covid-19, let alone several.

These findings also suggest that our immune system is doing what evolution designed it to do: mount a strong response to the virus.

There was a fear that Covid-19 might mutate into a more resistant form — or that our immune response might weaken. 

Yet recent research suggests that while antibody levels tend to fall over time, your immune system retains a ‘memory’ of the virus. So if you encounter it again, your body is ready to begin churning out antibodies and T-killer cells.

Which makes me wonder why Boris, who’s had Covid, is self-isolating. He’s unlikely to be ‘bursting with antibodies’ as he claims, but he’s also very unlikely to get it again, or to be infectious, so I can’t see how he’s a threat to others. 

Our immune system has been severely tested by Covid, but as the new vaccines show, it just needs a bit of help to get back on top.

Covid-19 vaccines are like buses; you wait for one, then two come along, almost together, with other contenders coming close behind [File photo]

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Dr. Adalja advises Pence to self-quarantine despite negative coronavirus test after aides test positive

Dr. Amesh Adalja: Pence is at ‘very high risk of getting coronavirus’

Five staffers test positive for coronavirus; infectious disease expert joins ‘America’s News HQ’ with insight.

Infectious disease expert Dr. Amesh Adalja told “America’s News Headquarters” on Sunday that he would advise Vice President Mike Pence to cancel any travel and self-quarantine after four staffers and an outside adviser tested positive for the coronavirus.

Pence, who with second lady Karen Pence tested negative Sunday, is still at “significant” risk of exposure. Nine days from Election Day, he plans to maintain his planning campaign travel to Kinston, N.C., Sunday, his office said.

“The vice president is at very high risk for developing coronavirus,” Adalja said. “Him getting daily tests is only going to take the risk down a little bit. There probably is a need for him to self-quarantine for 14 days based on the amount of people around him that are positive.”

5 CLOSE TO PENCE TEST POSITIVE FOR CORONAVIRUS, VP TO MAINTAIN CAMPAIGN SCHEDULE, OFFICE SAYS

Adalja said he’d like to know the nature of the interactions Pence has had with his aides prior to confirmed infection, and if masking was involved.

Pence waves to supporters Saturday Oct. 24, 2020 in Tallahassee, Fla. (AP Photo/Steve Cannon)

Adalja said he “can’t say that it’s safe” to continue to campaign.

“He likely was significantly exposed,” he said. “And we know that a test is just one moment in time and that you can’t test yourself out of self-quarantine.”

Adalja suggested Pence follows Centers for Disease Control and Prevention guidance surrounding coronavirus exposure by quarantining regardless of test results, holding the vice president to the standard “every American is held to.”

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The New York Times is reporting White House Chief of Staff Mark Meadows has tried to keep news of the recent outbreak quiet, which Adalja said is a public safety hazard.

“You want to be as transparent as possible,” he said. “And we want people to know who might’ve interacted with the vice president that they could’ve been significantly exposed. … That's how we move forward in this pandemic is being very open about who's at risk.”

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