The Elephant in the Room E-Book

Liz Kalaugher

• Herausgeber: Icon Books
• Kategorie: Wissenschaft und neue Technologien
• Sprache: Englisch

Seitenzahl: 672

Veröffentlichungsjahr: 2025

Beschreibung

Humans, animals and disease. They're all inter-related, so why do we keep ignoring the elephant in the room? It's well known that Covid-19 may have come from a bat, but diseases are often transmitted in the other direction too. Humans have passed diseases to animals countless times through history, and it's the cross-currents of this relationship between humans, animals and disease that are explored by Liz Kalaugher in The Elephant in the Room. Taking the reader on a globe-trotting journey through time, Kalaugher presents a series of fascinating case histories of human-related wildlife diseases. Among the stories featured here are the early humans who may have carried pathogens responsible for the extinction of Neanderthals, the native birds of Hawaii that have been devasted by human-introduced disease, and the Tasmanian tiger that has been lost to the sands of time. Examining these tales and drawing on first-hand accounts from experts around the world, The Elephant in the Room is both a tragic history and an inspirational call to arms. It doesn't have to be this way. By learning from the past, it's possible to create a better, healthier environment for ourselves, our wildlife and our planet.

Leseprobe

 

 

Published in the UK and USA in 2025 by

Icon Books Ltd, Omnibus Business Centre,

39–41 North Road, London N7 9DP

email: [email protected]

www.iconbooks.com

ISBN: 9781837731381

eBOOK: 9781837731404

Text copyright © 2025 Liz Kalaugher

The author has asserted her moral rights.

No part of this book may be reproduced in any form, or by any means, without prior permission in writing from the publisher.

Typeset by SJmagic DESIGN SERVICES, India

Printed and bound in the UK

To Sue, Patrick, Mags, Catherine, Justin, Dan, Tom, Josh and Krystal

Contents

Preface

1Wild Horse Chase: Grevy’s Zebra, Extinctions and Wildlife Diseases

2A Mammoth Problem: Early Travel, Disappearing Neanderthals and Vanishing Megafauna

3The Canary in the Hawaiian Chain: Honeycreepers, Colonial Ships, Accidental Imports, Avian Pox and Avian Malaria

4Measly Migration: Close Contact, War, and Rinderpest’s Deadly Jump from Cattle to African Wildlife

5Tasmanian Troubles: Sheep Farming, Extinct Tigers and ‘Distemper’

6Black Feet and Black Death: Long-distance Trade, Plague, Prairie Dog Days and Ferret Futures

7Seals Go to the Dogs: Unusual Contact and Morbilliviruses out at Sea

8A Devil of a Problem: Farming and Tasmanians Devilled by Cancer

9Fungus and Frogs: Lab Animals, Pets, Food, and Trading Amphibian Disease Internationally

10City Catches: Foxes, Mange and High-Density Living

11Warming and Westerning: Climate Change, American Crows and West Nile Virus

12Monkey Mix-up: Muriquis, Vanishing Forests and Yellow Fever

13Bats for Bushmeat: Plantations, Eco-tourism, Apes and Ebola

14Big Farma: Industrial Farming and Bird Flu

15Changing Our Stripes: Protecting Ourselves and Other Wildlife

Endnotes

Acknowledgements

Preface

One evening in early 2020, as I walked back to my cabin at a hotel near the base of Mount Kenya, creatures screeched from high in the trees. It was too dark to see but they sounded vicious and large. Once my feet had rejoined the ground, a voice in my head said, ‘Blimey, archaeopteryx. I thought flying dinosaurs had gone extinct.’ The next day, I learned the screechers were tree hyraxes – nocturnal mammals related to elephants but a little larger than guinea pigs. Over the next few evenings they bawled and rasped outside the cabin’s ground-floor bathroom like murderers with chainsaws, and howled from the chimney-top so that the sound reverberated from the stone walls as I tried to sleep.

These small animals’ bark was far more scary than their bite. Far away in China, however, a toothless but much more deadly danger had quietly emerged from the wild. As I travelled across Kenya in search of the Grevy’s zebra, a rare and threatened species that copes well with harsh, dry conditions, the SARS-CoV-2 virus, which causes Covid-19, spread around the globe. And pretty much everyone’s focus turned to zoonotic diseases – illnesses that jump from wildlife to humans.

In recent years, more and more of these diseases have emerged from the wild and made people ill – HIV, SARS-CoV-1 and SARS-CoV-2, MERS, swine flu, Zika, Ebola, mpox and more. But we’ve paid much less attention to the ways that humans have made other animals sick. We’ve done this for millennia, pretty much since we first left Africa and encountered Neanderthals.

As soon as the first anatomically modern humans left Africa, we took bugs with us in our bodies, spreading disease when we ourselves were sick. Later we grew more sophisticated in the ways we impart diseases. Some 12,000 years ago, when we started farming other animals, we began living closely alongside poultry and livestock and putting these animals in cramped conditions. That enabled bugs to spread more easily from non-human animal to non-human animal, from other animals to us, and from us to other animals. Our farming made the animals we’d domesticated sick; not just livestock like cows, sheep, goats, pigs, camels and llamas, but also working and companion animals like dogs and cats. Many of those animals have close relatives still living in the wild – goats, antelope, wild boar, wolves, big cats – that had similar biologies to their domesticated and newly disease-rich cousins. Domestic dogs, we think, have spread canine distemper virus to lions and African wild dogs. Nearly 90 per cent of mammals threatened by parasites, including viruses and bacteria, are from the orders Artiodactyla, especially the swine family and the bovid family of cloven-hoofed ruminants such as cattle, bison, buffalo and antelope, and Carnivora, particularly the dog and cat families.1 That doesn’t seem like a coincidence.

When we developed arable farming, our crop stores attracted rodents that shared pathogens – disease-causing agents – with us too. Since rodents have a live-fast-die-young approach to immune systems and don’t invest much effort in fighting germs, they were largely the major gift-givers. In turn, we shared those gifts worldwide, with other animals and other humans.

Then, of course, there’s trade. Humans started moving non-human animals around the world as we explored. We took domestic animals with us, whether by design, in the case of livestock, or accident, in the case of rats, and we began to trade wild animals – live or as carcasses – from the places we’d inhabited or invaded. We introduced invasive species to islands and continents where they didn’t exist before, taking their bugs and diseases with them. This killed off, as just one example, many species of the finch-like birds known as Hawaiian honeycreepers, leaving the lower slopes of Hawaii’s mountains desolate. More recently, trade has spread chytrid fungus around the world, devastating frog populations. The wildlife trade for pets, food, trophies, souvenirs and medicine continues today, some of it legal, much of it not.

Trade isn’t last on the list of the ways we’ve spread diseases to wildlife. We’ve also logged forests and destroyed habitat, forcing wild animals to live more closely alongside each other and us. What’s more, damaged, less biodiverse ecosystems are less resilient and more likely to harbour pathogens. We’ve warmed the climate too. And we’ve begun farming wildlife, and farming livestock on an industrial-scale, cramming non-human animals into massive sheds. High-density poultry farms kick-started a more dangerous strain of bird flu that spilled back into the wild, and today threatens humans with a new pandemic. Even the wildlife conservation programmes that have tried to help have in some cases inadvertently introduced disease, for example by passing pathogens from one species to another during captive breeding programmes, then letting the germs loose in a new area when they let that species free. As we’ll see later, that’s how the chytrid fungus, deadly to many amphibians, reached the island of Mallorca.

Our harms broadly fall into four categories – moving pathogens to new places, encroaching on the lives of other animals, harming or destroying ecosystems, and influencing climate change. The elephant in the room is us. And it’s an elephant with many faces – the story for each species and pathogen unfolds in its own unique way.

PATHOGENS RISING

The result of all these changes? We’ve increased the threat of new diseases emerging in other animals. Like those in humans, wildlife diseases have emerged more frequently in recent decades. Wildlife biologists only recently became aware of just how big a role disease played in extinctions both ancient and modern. Disease has been the neglected problem child of the conservation world. Instead, attention has focused on its four ugly sisters: the ‘evil quartet’2 of habitat destruction, introduced species, overkill – humans slaying too many individuals – and secondary extinctions – species wipe-outs that result from other extinctions, for example the two species of louse that lived only on the passenger pigeon shot to oblivion in North America in the nineteenth century.3

American scientist and environmental historian Jared Diamond coined the term evil quartet in the early 1980s, before global warming showed its true face; many would now add climate change to the ugly sisterhood.4 The same goes for diseases. ‘Normally infectious disease is left off that list,’ says infectious disease expert Hamish McCallum of Griffith University, Australia. ‘My view is that’s probably a mistake.’ Even back in 1933 environmentalist Aldo Leopold stated that ‘the role of disease in wildlife conservation has probably been radically underestimated’.5,6 Illness is often the final straw that breaks the camel’s, or Tasmanian tiger’s, back. Today, as we’ll see, the African wild dog, Tasmanian devil and North America’s black-footed ferret are all at risk of extinction from disease.

FINDING THE ELEPHANT

To begin, The Elephant in the Room will introduce human and wildlife diseases, as well as the Grevy’s zebra – a species threatened by many of those evil step-sisters, particularly habitat loss, overkill and, increasingly, climate change. As an animal that lives alone or in small groups and has a loose social structure, the Grevy’s is, thankfully, relatively unaffected by infections. But, with conditions becoming more extreme, early signs indicate that even the Grevy’s is suffering more strongly from disease. Yet this equid’s story shows us what can happen when people change their behaviour in order to protect wildlife; the Grevy’s zebra is now a rare success story in the field of conservation. Its stripes form a lens for us to examine our actions and choose a path forward.

Next, we will head back to the dawn of modern man and explore how early humans’ germs may have killed off Europe’s Neanderthals. From then on we will journey forwards in time, through the potential role of disease in the extinction of North American woolly mammoths and giant sloths, the triple import whammy that harmed Hawaii’s native birds, the accidental introduction of cattle plague to Africa, and the demise of the Tasmanian tiger. Each chapter in this book will focus on a single wildlife case study that illustrates the animal’s unique value, the manmade factors contributing to its disease woes, and, where possible, how we can stem the emergence and spread of such diseases. I’ve largely avoided detailed descriptions of sick animals. As an animal-lover, I didn’t want to write them and they don’t make for a fun read.

As this book moves through time and the diseases come thick and fast, the manmade factors change in parallel with our lifestyles. We begin to farm. We stop walking between continents in favour of travel by ship and then planes. We chop down rainforests for ranches and plantations. We burn fossil fuels. We build industrial-scale farms. Case by case, the full picture of our planetary damage reveals itself.

As we reach the 1980s and 1990s, when wildlife diseases emerge faster, we turn to the case of the black-footed ferret, which introduces the risks associated with conservation techniques; the African wild dogs and seals that share related viruses thanks to close contact between humans and other animals; foxes that highlight the trials and tribulations of city living; frogs killed by the increasing globalisation of trade; and American crows that reveal how climate change allows diseases to take new ground.

Here in the present day, The Elephant in the Room looks at the results for monkeys, apes, bats and wild birds as people have fragmented habitats, cleared more land for agriculture and commercial plantations, come into ever closer contact with wildlife, and set up industrial-scale sheds housing chickens and pigs: outbreaks of yellow fever, Ebola, flu and more. As I wrote the chapter about bird flu, the first transmission of a bird flu virus from a cow to a farmer took place in the US; many fear the H5N1 virus is adapting to spread more easily between mammals. That prospect is terrifying.

UNIVERSAL HEALTH

The same human activities that have spread diseases to wildlife have come back to bite us too – they’ve also heightened the risk of diseases spreading from wildlife and livestock to humans, whether virally, as with the 1918 influenza or Covid-19 pandemic, or by other means, like with the chronic illness Lyme disease, which spread to us from wild mammals via ticks (partly due to habitat disruption). The pet trade introduced mpox – the pox formerly known as monkeypox that’s generally found in rodents and non-human primates in western and central Africa – to the US in 2003. That made 81 people ill. By May 2022 the disease, which had caused sporadic human cases in Africa for decades, had become better at transmitting from human to human and broke out in humans in several countries, including the UK, the US and Australia. In 2024, as this book neared completion, the World Health Organization declared a new strain of mpox a public health emergency of international concern, its strongest form of global alert, after an outbreak in the Democratic Republic of Congo and other nations nearby.7

We’ve made ourselves as well as other animals more likely to get sick. In 2008 prestigious science journal Nature published a paper that showed that 60 per cent of infectious diseases in humans originate in non-human animals, with more than 70 per cent of these zoonotic diseases coming from wildlife, and increasing over time.8

Wildlife diseases and human pandemics are two sides of the same coin. Yet we’re mainly looking only at ‘our’ side, a selfish approach that is unlikely to serve us well. We’re animals too and our health depends on the health of our ecosystems and of other animal species, whether livestock or wild. The burgeoning academic discipline of One Health acknowledges that human, non-human animal and ecosystem health are closely linked. Indigenous cultures have aligned with this concept for tens of thousands of years.9 In the West, although ancient Greek philosopher Hippocrates was an early proponent,10 One Health only became a mainstream topic from around 2004, when scientists at a meeting in New York organised by the Wildlife Conservation Society set up twelve Manhattan Principles on ‘One World, One Health’.11 Even in this field we’re still neglecting wildlife; currently most people working in One Health focus on disease surveillance in livestock and humans, and rarely consider how the environment feeds in to emerging health threats.12

‘The stress that humanity is placing on nature is leading many [non-human] animals to become more susceptible to infection, and to be more likely to shed virus when they are infected, even if they don’t get sick themselves,’ says practising medical doctor and epidemiologist Neil Vora of Conservation International. ‘These are all factors that come back to hurt our own health because the pathogens that cause most new infectious diseases originate in animals and then jump into people. We’re all connected.’

When I set out to write the final chapter of this book, I planned to look at ways of guarding wildlife health then move on to protecting humans from pandemics. But arranging the material this way was like trying to untangle a thicket of brambles – everything was too closely entwined to tease apart without pain. Instead, I decided to ignore the artificial borders we currently imagine between the health of humans, other animals and the environment, and proceed as if humans are part of nature, which we are, no matter how divorced we feel from the wild as we tramp along the hard surfaces of city pavements. Our bodies and immune systems know it even if our minds don’t. They’ve proved it by catching diseases from other animals. Harming wildlife and the environment is a form of self-harm, though you might not guess it based on how we’re treating the natural world, ourselves included.

TAMING THE ELEPHANT

The remedies for this harm range wide. We could regulate trade and farming, protect forests and other habitats, turn away from fossil fuels. This would likely cost less than another pandemic. As yet, our efforts to stop new infectious diseases emerging for both wildlife and people have been minimal. The chances of another global pandemic are high and wildlife diseases and extinctions continue apace. Unless more people understand why and call for government and international action, we’ll see more and more wildlife loss and more and more pandemics.

Many of these changes would have a hefty side-benefit – they would also save wildlife from population declines and extinctions not linked to disease. In turn, keeping ecosystems healthy in this way would protect all living beings, by making diseases even less likely to break out. It’s a win-win situation. Let’s choose panacea not pandemic. Until we mend our ways and our ecosystems, us, the Grevy’s, the tree hyrax and all other species face an uncertain future. Let’s focus on, then usher out, this elephant in the room.

Liz Kalaugher Bristol, UK, 2024

1

Wild Horse Chase: Grevy’s Zebra, Extinctions and Wildlife Diseases

‘Our wildlife is our river of life; if we finish the wildlife it would be like the river we fetch water from drying up.’

Lmantros Lenangetai, Grevy’s Zebra Trust Ambassador

LATE JANUARY 2020, SAMBURU COUNTY, NORTHERN KENYA

It’s dusk. I’m ‘powdering my nose’ in the room behind my tent at the Grevy’s Zebra Trust HQ. I’ve climbed the six wooden steps from the stone floor of the room with the sink, then turned right. Just above my head, chicken wire frames the sky in the handspan gap between the rendered mud wall and the plant-stem roof. In the distance, a bird serenades the evening and a goat bleats. The light is fading fast, it’s not far to the equator. Better get on. As I sit, something zooms past my right ear. It comes from near the window, turns 90 degrees to head down the stairs and swoops out into the sky through the open roof of the cubicle for bucket showers. My heart beats almost as fast as the flutter of its sharp-cornered wings – it’s a bat.

I like bats. I own a bat detector. But generally, I go out to look for them in a field or park or garden. I wasn’t expecting a bat to join me in the bathroom. It must have come through the window, I think. There must be a gap in the wire.

It’s only when it comes up in conversation at dinner that I realise the bat didn’t fly through the window. It sped out of the long-drop toilet just before I blocked the exit. Over the next few nights, I become savvier. If I hear the bats flapping as they circle the exit from their cavernous roost, I move politely to one side until they’ve left. I don’t want to excrete on anybody. With the aid of my head torch, I strike a balance between being in the way and getting a good view; it’s dark down there, though I’m grateful I can’t see the bottom. One evening, I glimpse two bats flying several circuits of the long-drop before they venture out. Gradually I grow more confident. I move less far away, give the bats less space. Another evening, when I hear the flutter of a bat inside the long-drop, I shuffle forward with my head turned to look behind. The bat flaps out and up. I’m a shock to it. We’re face to face, the bat so close it’s a blur, a fuzzy shape growing larger fast. I gasp and freeze. The bat veers away over my shoulder. All it leaves is a memory of a small pink face with a prominent snout, edged by brown fur. I don’t know if that’s what I saw or what I imagine I saw. The image doesn’t arrive until the bat has gone, like a flash of nostalgia. That was close, I think. Good work, bat.

We were in each other’s faces, we breathed the same air. Should I be worried? Later, I learn that bats host a multitude of viruses; I’m fully aware of that now it’s affected my life and those around me. Bats can live symptom-free with infections that would – and do – kill us.1 These animals may be protected against becoming ill by their evolution of flight, whose stringent requirements mean that, almost as a side-effect, they developed an immune system that counteracts viruses while limiting inflammatory responses that can damage the bat itself.2 Bats make us sick with all sorts of diseases – they’ve passed us Ebola, Marburg virus, SARS-CoV-1, MERS, Nipah, Hendra and now, chances are, SARS-CoV-2, which causes Covid-19. Though humans have also made bats sick, notably by transporting across the Atlantic the fungus that causes white-nose syndrome in North American bats.

When bats make humans ill, it’s possible that the fever our bodies create to kill these viruses only makes the invaders feel more at home, by bringing our body temperature closer to that of a bat. I don’t, as far as I’m aware, catch anything from my close encounter. No fever, no cough, no loss of taste or smell. The bat’s faeces are safely inside the long-drop and the Covid-19 pandemic is a distant shadow, a flutter on the edge of my consciousness. We aren’t yet face to face.

Already in our faces, even though we’re ignoring it, is the flipside of this – how much humans have inflicted harm on wildlife by spreading diseases throughout history. Over time, our numbers have soared, from 1 billion in 1800 to 8.2 billion in 2024.3 The human population curve mimics the rise in cases at the start of an epidemic, though on a longer timescale. For the luckiest of us, lifestyles grew lavish – houses, central heating, aircon, cars, washing machines, plastic toys, televisions, laptops, mobile phones, and food, pets and lab animals flown in from other countries. So we ‘needed’ more resources to sustain these lifestyles, more land to grow timber and crops, to mine metals and minerals, and to set up factories for goods and livestock.

Often the devastating consequences, for us and other animals, of our cosseted Western lives happen far away, out of sight and out of mind, easy to ignore until they come back to hit us in the lungs. This hunger for land, for homes for our growing numbers and to meet our growing needs, has seen us encroach on wildlife territories. More people have moved deeper into areas that were recently wild, into forests and savannah. That’s disrupted ecosystems, sent species into population decline and brought us into closer contact with wildlife. As we should have learned over the centuries of our encounters with livestock, contact with other species means opportunities for pathogens to jump the species divide.

Before the road network expanded, chances were that when a deadly virus that could transmit from human to human spilled over from a rainforest, only a few people from that first victim’s village and perhaps a few neighbouring villages would die before the outbreak sputtered out. Nowadays, almost everywhere has access to a road and more people travel to, trade with, and live in towns and cities. A virus can range further, faster, the flames of its devastation spreading like wildfire across the globe rather than flickering in isolated patches that burn themselves out. International air travel means pathogens that do make it into a human can be in another continent the very next day, almost before their victim has time to cough. Or they can hide out in a wild or farmed animal – or a wild farmed animal in China – that we ship or fly around the world dead or alive. Chances are West Nile virus reached the US, where it kills birds and people, by plane or ship from Israel in 1999. Today it’s spread across the continent. Our industrial farms bring non-human animals into closer contact, chicken crammed in next to chicken near sheds packed full with pigs, while wild birds peck the dirt outside or feed in the ponds where the chicken waste falls. It’s enough to give a person chills. In fact, it does – it lets flu strains mix and match from pig to bird to human. That’s dangerous.

SHARE ALIKE

We’ve found many ways to worsen other animals’ health. Sometimes we’re almost literally hands-on and give animals that are biologically similar to us diseases directly, for example by visiting chimps and gorillas in nature reserves and passing on colds and other human respiratory viruses that may kill other apes. Some call diseases that jump from human to non-human animal zooanthroponoses, while some choose the term reverse zoonoses. Diseases that jump species in the other direction, from non-human to human, as SARS and likely Covid-19 did, are known as zoonoses or, if you have time on your hands, anthropozoonoses. Here, we’ll take the easy route and call everything a zoonosis. Often we won’t need to use the word, as the way we cause wildlife diseases isn’t always direct. Sometimes our livestock and companion animals make wildlife sick, and sometimes our harm is less direct even than that.

As biologists look back at past extinctions, they find the hand of disease caused by man in many more cases than they realised, or rather, the suspected fingerprints of the hand of disease caused by man – it’s hard to diagnose diseases when physical evidence has long decayed. It wasn’t until the seventeenth century that we first saw bacteria in early optical microscopes, and not until the nineteenth century that we linked these bacteria to disease. Virus discovery was even slower – filtering sap from a diseased plant proved the existence of viruses in the late 1800s and it wasn’t until the 1930s and the invention of the electron microscope that we could look at them in detail. Even then, it was a specialist job and not available to those on the ground seeing wildlife, livestock and their relations die.

Whether the cause was known at the time or not, the march of creatures disappearing to disease goes on, from Christmas Island’s native rats to the Hawaiian birds lost in the nineteenth and twentieth centuries, the demise of the Tasmanian tiger in the 1930s, and more recently, some 90 species of amphibians and counting, including Costa Rica’s golden toad. All gone. Vanished into the mists of the past with a helping shove from man.

The other stresses we’re imposing make matters worse. Between 1970 and 2016, global populations of vertebrates – backboned species like mammals, reptiles, birds, fish, amphibians – crashed by roughly two-thirds, according to a report by the WWF.4 Nearly a million of Earth’s species are at risk of extinction, say UN figures, and the current rate of extinctions is tens to hundreds of times higher than the average for the past 10 million years.5 In 2010 the UN Convention on Biological Diversity set 20 biodiversity targets for 2020. We haven’t fully achieved a single one.6 Habitat loss is a major factor but there are many others alongside emerging diseases – competition for resources, invasive species transplanted by man, climate change, pollution, hunting, poaching and human–wildlife conflict.

The problem is, diseases and drops in headcount are like the currents in a whirlpool sucking wildlife towards oblivion. Their forces combine and accelerate. Once numbers of an animal decline because of habitat loss or climate change or for whatever manmade reason, that species is much more likely to be wiped out by disease. A small population that lacks genetic diversity, is stressed, has lost much of its habitat so is crowded together, perhaps alongside new competition from invasive species, and in a climate that it’s not well adapted to, is not best placed to withstand an onslaught of infection. Animals become more susceptible to the pathogens that bring diseases, which could cause so many individuals to die that there wouldn’t be enough left to build numbers back. Disease can pile pressure onto animals already under threat from habitat loss or exploitation or poaching or pollution.

These losses create an even stronger push towards the centre of the whirlpool – both population declines and extinctions disrupt ecosystems, which in turn makes diseases more likely to break out. Generally, the larger, longer-lived animals go extinct first. And they tend to have better immune systems and be more disease-resistant. Take these animals out and you have an ecosystem where disease can take hold and spread more easily. This ‘dilution effect’ theory, that ecosystems with more biodiversity are more resilient against disease, has been controversial over the years but the evidence has finally tipped towards it.

Each species lost leaves a gap in the structure of an ecosystem that risks it crumbling into disarray. If nature goes, we’ll suffer too – we’re part of it. No bees to pollinate our crops, no detritivores to clean up rotting vegetation. No protection for our health. As we destroy nature further, both wildlife and humans will suffer more diseases; the rates for both have already increased. In the 1980s and 1990s, seals died in their thousands in the North Sea thanks to an outbreak of phocine distemper virus that attacked their lungs and brains. Canine distemper virus harmed African wild dogs and lions and nearly wiped out the black-footed ferret in the US. My home city of Bristol’s foxes fell to mange. Tasmanian devils caught an infectious cancer. Frogs disappeared around the globe. North American birds perished in the wild and in zoos.

WILD HORSES

The point of my travels, the Grevy’s zebra, is unusually resistant to disease, even for a relatively large and long-lived animal. Unlike plains zebras, Grevy’s don’t live in harems – groups of females and their young headed by a male. Instead, Grevy’s have a more flexible social structure known as fission-fusion, because the animals split apart and come together depending on their needs, an approach that helps the Grevy’s cope with dry conditions where resources are patchy. About one-tenth of adult males are territorial and guard a patch of land with grass and water that attract females.

This loose social structure also makes the Grevy’s zebra relatively hardy to disease. Under normal circumstances, the Grevy’s suffers less from parasitic worms than the more sociable plains zebra, for example. Though the Grevy’s can, if humans relocate it, pass on a virus it carries symptom-free. In 2007, a Grevy’s killed a polar bear at a zoo in San Diego, by giving it equine herpesvirus-9. And nowadays we’ve made even the relatively hardy Grevy’s zebra sick. Recently two Grevy’s at a nature reserve were so stressed by food shortage due to a drought most likely caused by climate change that they fell to intestinal parasites, an infestation they’d normally be able to live with.

The Grevy’s I see in Kenya, however, all look healthy. Like my encounter with the bats, my first sighting of these animals was also a surprise. The story of the Grevy’s zebra stands out in a conservation landscape that’s otherwise bleak. After twelve years writing about climate change, I was desperate for good news. On my very first afternoon in Kenya I found myself on an upholstered bench on the veranda of a former colonial ranch house in the central highlands, at Mpala Research Centre. On the horizon, far beyond a wooded valley, lay the foothills of Mount Kenya; the mountain itself was shrouded in cloud. Superb starlings with petrol-blue chests and oil-sheen backs flitted onto the lawn in front of me while lesser-striped swallows swooped their copper heads and sparkling navy wings into a nest in the eaves above. This isn’t real, I thought. This is paradise. From a tree, a red-chested cuckoo cried as if saying ‘it will rain’ in three mournful notes descending in pitch, and rock hyraxes grazed like oversized guinea pigs or scuttled up the veranda steps. One peered at me from the gutter above, beady-eyed. At night, I’d soon discover, they and the vervet monkeys would scamper across my bedroom roof, the scraping of their claws like stones bumping down corrugated iron.

Seven hours after leaving Nairobi, I was in a scene that could have been in Out of Africa, lazingon a veranda, deep in white privilege. It was an accident because I had booked late and the working accommodation for researchers was full. So I was a special guest. About three-quarters of an hour after taking my seat, I looked away from the lawn and the trees and the hyraxes and hornbills and superb starlings, and glanced at the hill on the other side of the valley. Two Grevy’s zebras grazed, heads down, near a termite mound in a patch of open ground edged by thickets and small thorned trees. Distracted by the birds, I hadn’t seen them arrive. They weren’t there and then they were, fawn shapes against the dry grass highlighted only by the white of their ears and bellies. In places, on a neck, on a rump, I could just about make out their thin black and white stripes. I imagined the sound of grazing, a gentle munching, the ripping of grass stems, the swish of a tail, the buzz of flies. This is why I’m here, I thought. This seems too easy. The animal I’d travelled more than 6,000 kilometres, or 4,000 miles, to see had wandered into my path within an hour of my arrival.

The zebra on the left faced away from me and was swiping the brush of dark brown hairs at the end of its tail from side to side to ward off flies. The patch of white on this animal’s hindquarters gleamed in the sunshine; the Samburu name for these animals is Loiborkurum, or white-rumped. Some have used other names. The Romans paraded ‘imperial zebras’ into colosseums before gladiators battled, prizing them for their upright bearing and regal stripes. Centuries later, in 1882, Abyssinian emperor Menelik II presented one to French president Jules Grévy. When a French naturalist realised this gift was a separate species, he gave it a new name, after its new host.

Until recent times, Grevy’s roamed only the Horn of Africa, from the coast of the Arabian Gulf down into northern Kenya. Like the water in a reservoir during a drought, Grevy’s homelands have shrunk into small, isolated patches. Today these zebras make the leader board of African mammals whose range has dwindled the most. Grevy’s no longer graze the arid lands of Eritrea, Djibouti or Somalia, and only a couple of hundred linger in the deserts of Ethiopia, mainly in the Aledeghi Nature Reserve. The rest dwell in dry and semi-arid northern and central Kenya, chiefly in the north’s Samburu County, where the Grevy’s Zebra Trust has its field HQ, and in the Laikipia region around Mpala Research Centre.7 Mpala is further south than Grevy’s traditional habitat, where the growth in the number of humans pushed them out.

In 2023 estimates put the Grevy’s population at some 3,000,8 a drop of more than four-fifths from the near 15,000 alive in the late 1970s.9 In that decade zebra hides were bang on trend for Western interiors and accessories, and trade in this ‘commodity’ flourished. Even after Kenya banned commercial hunting in 1977, the population continued to fall. By then, the nation’s human population had boomed – from nearly 8 million in 1960 to more than 56 million in 2024 – and pastoral herders had stopped moving around the landscape so much, increasingly settling near schools and health clinics. This degraded the land and reduced the availability of vegetation, forcing wildlife and livestock into smaller spaces. Like a million of Earth’s other species, the Grevy’s zebra is on a slow slide to extinction; in 1983 Andy Warhol featured a Grevy’s, brightly coloured but dejected, in a screen-print for his Endangered Species series. The International Union for the Conservation of Nature (IUCN) classifies this species as endangered – very likely to become extinct in the near future.

REVERSE REVERSE

As I watch these Grevy’s graze in the sunshine, Covid-19 is spreading west into Europe. In December 2019, cases of unexplained pneumonia spiked in Wuhan, a city of some 11 million people in Hubei province, eastern China. By the end of the year, doctors had implicated the previously unknown virus 2019-nCoV – the letters stand for novel coronavirus – as the culprit for the disease they dubbed Covid-19. By 11 January, Chinese scientists had released the genetic code of the virus; the next day, given its similarity to the SARS virus that caused a pandemic in 2002 and 2003, the World Health Organization renamed 2019-nCoV as SARS-CoV-2. And by 23 January, four days before I encountered the bat at Grevy’s HQ, Wuhan was in lockdown following 540 official cases of Covid-19 and 17 deaths. The lockdown didn’t stop the spread of the virus around the globe. All most likely because of a bat, though people, as we’ll see, must share the blame. Chances are that encroachment into wildlife territory, close contact between humans and wildlife, trade and international travel were all factors.

There’s much we don’t yet know about SARS-CoV-2. What we do know for sure is its genetic code and that it’s a coronavirus. At its heart it has strands of RNA, which is a nucleic acid like the DNA that forms our genes, but curls in single-stranded spirals, not the twisting coupled ladders of DNA’s famous double helix. Sheathing these strands of RNA is a coat embellished with the protein spikes that give the family its name; they fan out around the virus like a crown. SARS-CoV-2 basically consists of RNA, proteins and a double layer of lipid molecules that link the proteins in its coat. That’s it – genetic code in a bag. A very small bag, roughly one thousandth of the diameter of a human hair. Under a powerful microscope SARS-CoV-2 looks innocuous, like a child’s drawing or a fluffy burr. It’s what it does that harms.

Despite their simple structures and small size, viruses kill. In humans, SARS-CoV-2’s club-shaped protein spikes chiefly latch on to the ACE2 (Angiotensin-converting enzyme 2) protein receptors coating the cells that line our airways – nose, throat, lungs. The virus tricks its way inside a cell via these protein receptors. Once there, it subverts the cell’s DNA-reading machinery to read viral RNA instead. So the cell replicates the viral proteins that the RNA codes for instead of making more of its own proteins. ‘Don’t copy you,’ the virus whispers inside the cell. ‘Copy me.’ And, bewitched or bewildered, the cell does, over and over again. It helps its own invader multiply. These home-grown copies of the virus sneak back out through the cell wall and infect other cells, where they replicate again in an ever-expanding onslaught. Some people become infected but don’t show symptoms, others cough or lose their sense of taste or smell or burn a fever as their immune system fights back. An unlucky few per cent, a number that soon becomes hundreds of thousands of individuals when millions are infected, struggle to breathe when their lungs fill with fluid, and the unluckiest of these people die. Millions of people around the world lost their lives to SARS-CoV-2; my heart goes out to everyone who didn’t make it and to those they left behind, especially those forced to grieve alone.

SARS-CoV-2 is a killer. Yet not all coronaviruses are this lethal. There’s diversity here too; researchers estimate there are around 3,000 to 5,000 coronaviruses, all of them likely to have originated in bats. The virus doesn’t care which animal’s cells it enters, as long as its proteins hold the key to getting inside and it can take over the cell’s workings to replicate. Coronaviruses have probably existed alongside us and other animals for thousands, if not millions of years. Science identified the first only in 1931, on a farm in the US state of North Dakota, where it caused avian infectious bronchitis in chickens and killed up to 90 per cent of infected chicks.10 In the 1960s, researchers discovered that some coronaviruses give humans colds, although most colds are caused by rhinoviruses, which are three times smaller than SARS-CoV-2. In people and birds, coronaviruses mainly affect the respiratory system. Other species react differently. In mice, coronaviruses cause brain inflammation and hepatitis, while in cows and pigs they bring diarrhoea. In bats too, coronaviruses tend to thrive in the gut; bats typically shed particles of these viruses in their faeces. Given what we now know, the traditional practice in Chinese medicine of treating diseases by sprinkling powdered bat faeces into people’s eyes doesn’t seem a great idea; some practitioners have called for a ban.

In November 2002 we discovered coronaviruses could give us something more deadly than a cold when Severe Acute Respiratory Syndrome, or the SARS virus, made itself known in Guangdong province in southern China. This virus infected more than 8,000 people around the world,11 and killed around one in ten,12 a rate some ten times higher than SARS-CoV-2. The SARS virus hasn’t infected a human since 2004 but that doesn’t mean it couldn’t jump species to us again. It’s likely that SARS came from horseshoe bats in a cave in China’s Yunnan province, also in the south. When scientists tested these bats’ faeces and swabbed their insides, they found that although none were infected with SARS, they did harbour a number of different bat coronaviruses.13 Together these viruses contained all the genetic building blocks for making the SARS virus. Jumbling – or recombination – of these building blocks when a bat had two or more viruses at once could over time, the team believes, have created a SARS-like virus. Spread of this SARS-like virus to an intermediate animal such as the cat-sized masked palm civet,14 may have let the virus evolve into a form that could spread between humans. When one of these intermediate hosts ended up at a wet market, a forum for selling unrefrigerated vegetables and meat, sometimes freshly killed, it passed the virus to the first human. And SARS was ready to run rife from one person to the next.

There are probably many more spillovers of non-human animal diseases into humans each year than we ever realise. In the events that disappear without trace, the crucial difference is that the person who catches the disease doesn’t pass it on; the pathogen isn’t well enough adapted to us to use our bodies to transmit itself. The virus or bacterium cadging a ride inside us doesn’t have the right ticket to transfer vehicles, if you like, and the human it enters becomes a terminus, a dead end. Perhaps literally. But that can change, as it did with SARS, probably with the help of a civet. Ten years after SARS, in 2012, Middle East Respiratory Syndrome coronavirus, MERS-CoV for short, was detected in Jeddah, Saudi Arabia. MERS transmitted, scientists think, from an African bat to a North African camel then moved to humans in the Middle East via the camel trade.15 Also known as camel flu, MERS has killed roughly one-third of the 2,000 or so people it’s infected to date,16 mainly through contact with diseased camels or in hospitals.17

When Covid-19 came on the scene and scientists learned that the virus that causes this disease is genetically 80 per cent similar to the original SARS virus, both viruses got new names. Original SARS unofficially became SARS-CoV-1 and 2019-nCoV became SARS-CoV-2.18 The two share a common ancestor; SARS-CoV-2 is not a direct descendant of SARS-CoV-1 but a cousin, perhaps a distant one. Together with similar viruses in bats, the pair are known as severe acute respiratory syndrome-related coronaviruses, or SARSr-CoV. This is not a field of snappy titles. Since different viruses often mix and match – or recombine – their genetic material, virus family history tends to be murky and hard to trace. To find out where SARS-CoV-2 came from, researchers strip out its recombinant regions – the mixed-in parts – and look at them individually,19 as if they were tracing the history of a car that’s had new doors, a new engine and a change of upholstery piece by piece. Such analysis indicates that, like its relative, SARS-CoV-2 also has its origins among horseshoe bats; it’s more than 96 per cent similar to several different bat coronaviruses found in South-west China,20 as well as northern Laos.21 It’s the viruses further from Wuhan, in Laos, which have genes related to binding to host cells – the make-or-break part when it comes to the ability to infect humans – that are more similar to those of SARS-CoV-2.22 These viruses last had a common ancestor with – or in other words, diverged from – SARS-CoV-2 only a couple of years before it emerged in humans in Wuhan.23 ‘Given the extent of recombination going on, we’re unlikely to find an individual bat hosting the SARS-CoV-2 virus,’ says virologist David Robertson of the University of Glasgow, UK. But it does mean that horseshoe bats host other viruses that could infect humans too.

These bats don’t usually migrate,24 and are unlikely to have dispersed fast enough to transport the virus hundreds of kilometres on this timescale. So it looks like humans helped, moving the virus to Hubei province inside an as-yet unknown intermediate species via the trade in wild and farmed animals.25

Once there, SARS-CoV-2 jumped to a human at a wet market in Wuhan.26,27 ‘There’s certainly no evidence for any lab involvement, while there’s lots of evidence for a spillover event very much like SARS,’ says Robertson. ‘The evidence that SARS-CoV-2 got into humans through an intermediate animal host at the Huanan market in Wuhan is now very compelling.’ It’s notable that some of those who called most strongly for further inquiries into whether the virus leaked from the Wuhan Institute of Virology were politicians, who may have been lobbied by those with vested interests in our continued exploitation of the environment. If the virus escaped from a lab, the lobbyists can argue, then the myriad ways we’re harming nature simply aren’t relevant, and politicians are in no way to blame for failing to regulate this. Yet the lab leak theory itself creates an anti-science agenda that leaves us more vulnerable to future pandemics.28

Some have touted pangolins, also known as scaly anteaters, as the intermediary where the virus developed the ability to transmit itself from human to human. But Robertson doesn’t believe this happened. Only a few of the pangolin viruses studied have the same human-ready receptor-binding sequence as SARS-CoV-2. And no one has found evidence of a pangolin carrying SARS-CoV-2 at the Huanan market.29 The pangolin may be a wild-goose chase, along with the snakes, civets, ferrets and members of the cat family who were on the early suspect lists as intermediaries. On my travels, someone joked that the link to pangolins was a rumour spread by conservationists – these animals are severely endangered, chiefly because of the demand for their body parts from traditional Chinese medicine. Though, since these animals can carry SARSr-CoV-like viruses, they’re still a possible culprit and remain a potential source of future spillovers.30

Whether or not pangolins contributed, SARS-CoV-2 isn’t a lone phenomenon, a single chance happening with incredibly low odds. This is no black swan. At least 60 per cent of the 335 infectious human diseases that emerged between 1940 and 2004 came from other animals, according to ecologist Kate Jones of University College London and colleagues.31 Since 2015 the World Health Organization has kept a list, updated each year, of up to ten of the most serious emerging infectious diseases, those ‘likely to cause severe outbreaks in the near future’ and for which there are no good treatments, cures or vaccines. Every single disease on that first list was zoonotic, found in a non-human animal with the potential to jump to humans: SARS and MERS, which came from bats; Crimean Congo haemorrhagic fever, carried from livestock via ticks; Ebola and Marburg virus diseases from bats; Lassa Fever spread by rodents in West Africa; Nipah virus and henipaviral disease, which jumped to us from fruit bats in Asia via pigs; and Rift Valley Fever, transmitted by mosquitoes from livestock in North and East Africa, including Kenya.32

Given that it’s never spread in the country where I live, it’s not rational, but it’s Ebola that scares me the most – up to 90 per cent of its hosts die. Named after a river in the Democratic Republic of Congo, this snake-shaped filovirus has killed thousands since its discovery in 1976, in outbreaks in Sudan and across West and Central Africa, most notably in West Africa in 2014–16. Even when we’ve stamped out one human outbreak of the virus, it lingers in chimp, gorilla and bat ‘reservoirs’, ready to emerge from the forest and flare up into the next human epidemic. It’s only a matter of time. The harm caused by our lifestyles is catching up with us.

SAVING OUR STRIPES

So how do we save wildlife and ourselves? Here the Grevy’s provides signs of hope. In the early twenty-first century, the Grevy’s fortunes turned around when Samburu livestock herders monitored the zebras’ behaviour with the aid of GPS receivers. Once they realised chasing Grevy’s away from water sources and the best grass harmed them, particularly the youngsters, they changed their ways. Grevy’s numbers stabilised in 2015, with infants and juveniles making up nearly 28 per cent of the group, a promising sign for population growth. Behaviour change by a few humans made a big difference to wildlife survival. This zebra has, for now, ceased to slip towards the void, though outside forces still loom.

A couple of nights after the bat and I come face to face at the Grevy’s Trust field HQ, the Trust staff and their visitors eat around a campfire in the dry riverbed. Only the glow of the flames lights the night; there are no streetlamps and the buildings – the kitchen and the gathering area – lie behind the trees. I look up at the stars, bright spots in a sea of navy. Most of the constellations are new to me, though Orion, who hangs outside my home on winter nights, is here too. There are so many stars, this universe has depth. Something falls into my eye. It stings and I blink as tears form. My first thought is that it’s a bat taking its revenge by weeing on me. More likely, it’s ash from the fire.

The fates of humans and wildlife are closely linked and a stinging eye is the least of our worries. Now that we’ve seen and felt the human, social and economic damage of a pandemic close to home, will we be wise enough to jolt into action to prevent the next? To stop destroying habitat, exploiting wildlife, wiping out species, cramming farm animals into industrial-scale sheds and shipping them around the globe? Or will we put our heads back in the sand and distract ourselves by rebuilding the economy? Or become waylaid by techno-fixes – cataloguing viruses from the wild, developing universal vaccines – that deal with symptoms of the problem, not the cause? Although they could be useful, focusing on techno-fixes is like plugging a hole in a leaking boat from the outside while a man on the inside hacks at the hull with an axe, splintering it to pieces. It can’t work long-term. And we need to fix this now, for good, for all animals including ourselves.

CROSS COUNTRY

As I travel across Kenya, to the national parks in the south and the Indian Ocean, then back to Nairobi by train with a seat-side view of elephants and antelope, I track progress of the coronavirus from afar. It lurches across Asia and Europe. At a hostel in Kilifi, near the coast, in early March, I chat to a couple of German tourists. Germany has far more cases of Covid-19 than the UK but fewer deaths. We work out the percentages in our heads and look at each other confused. Why is the UK death rate so much worse? At the poolside a Kenyan man sneezes loudly and effusively. ‘Corona,’ he says and laughs. Then he looks at me and says, ‘Sorry, I shouldn’t joke.’ Kenya is not yet reporting any cases and the comments beneath the story on a national news website say that black people can’t catch the virus. I wish this was true. Kenya doesn’t have many hospitals.

On my last full day in Kenya, Friday 13 March, I visit the elephant orphanage in Nairobi. It’s shutting, they announce while I’m there, as Kenya had its first confirmed case the day before, in a woman who flew in from the US via London, and the government has banned public gatherings. On the way back to the hostel I ask the taxi driver to stop at a shopping mall in the suburbs so I can buy eye drops. One of my eyes is itchy and red. Instead of seeking out powdered bat faeces I opt for a Western-style pharmacy. Inside, a white woman has put three giant bottles of hand sanitizer – they must contain a litre each – in her shopping trolley. The transparent gel gleams under the fluorescent lights. Trade, as we’ll see, was part of the problem that brought us to this point. Now it’s providing this woman a solution, of sorts.

On the flight home, the sky is clear as we pass above Mount Kenya; her jagged peaks stand proud of the low cloud at her base. After flying by Lake Turkana, home to some of the very first hominins, we cross miles and miles of rippled umber sand and the Nile leads us north to the sudden stop of the Egyptian coastline. Greek islands adorn the blue sea like jewels before they are cut. Who knows what pathogens I’m bringing with me, inside my body or on my clothes? And what their risk is to other people, and to wildlife that is already struggling in the face of numerous troubles? By the time we reach mainland Europe clouds have gathered. The view is gone.

2

A Mammoth Problem: Early Travel, Disappearing Neanderthals and Vanishing Megafauna

‘Trust not the horse, O Trojans.

Be it what it may, I fear the Grecians even when they offer gifts.’

Virgil, Aeneid (c. 29–19 BCE), II, 4 Translated by J. W. Mackail

MARCH 2020, BRISTOL BUS STATION

Arriving home is a big relief. I’d worried, at one point, that transport would stop and I’d have to wheel my suitcase down the side of a spookily traffic-free motorway. I’d worried too that I might bring Covid back with me, hidden inside. The taxi driver when I arrive at Bristol coach station from Heathrow is wearing a thick coat. For a moment, I’m confused. Then I realise it’s winter and the air is cold. It takes my body a second to catch up, and then I’m cold too. It’s a shock. I shrink from the raw air, huddling into the jumper I’ve just put on as the chill grasps at my bones. And what of the very first people to leave the African continent, our early forebears? How did they fare? No fleeces for them, just furs. And no Covid either, though likely plenty of other bugs.

Setting off at least 120,000 years ago, these early travellers would have experienced very different journeys to mine. The biggest challenge I faced was finding a boy already sitting in my seat. He’d misread the row numbers so I sat in his seat instead and waved at the air stewards every time I saw a vegetarian meal heading his way. Back then, the journey probably lasted generations, not one day, and meals weren’t provided. The first anatomically modern humans – humans for short, from now on – travelled north-east to leave Africa on foot, walked on into the Levant then east to Asia and, later, west into Europe. The lands they reached were already inhabited, not by other humans but by Neanderthals.

This group of hominins had evolved some 300,000 years earlier from a branch of the human family tree that left Africa a million years before. They were smaller than today’s humans; at a little over 1.68 metres (5 feet 6 inches), I’m taller than the average Neanderthal man. Neanderthals were also stocky, which helped protect against the cold, as did their large noses that warmed and humidified freezing air before it entered their lungs.

Some Neanderthals made it to southern England, where I live today. As a human from outside Africa, chances are that my DNA is between 1 and 4 per cent Neanderthal.1 I have blue eyes, one of my sisters has red hair and some days I only want to grunt at things, especially in the mornings. So I reckon I’m at the higher end of this range. But that’s just a hunch, so, like a true scientist, I order a DNA test. Having questioned previous customers about their traits, the company will be able to reveal what my genetic heritage might mean for my ability to match musical pitch, how often mosquitoes bite me and my favourite flavour of ice cream. On the webpage where I checked which tests include Neanderthality (a word that should definitely exist), an image displays a group of Neanderthals warming their hands around a fire. Furs drape their torsos and the men wear some kind of trousers, but the women and children have bare legs and everyone has bare, surprisingly hair-free arms. Woolly mammoths plod across a snow-clad ridge in the background and I can’t help thinking the Neanderthals would have benefited from inventing sleeves. Nevertheless, they were the first hominins to survive a glacial ecosystem.

WHY DID WE WIN?

The Neanderthal man sculpted by the Natural History Museum in London has dark eyes that twinkle beneath his strong eyebrow ridge, a wide nose above a gentle smile and a Charles Darwin-style full beard.2 Yet the Neanderthal of legend is hairy, grunty, violent, stupid and short. The species was simply inferior to humans, according to some of the first explanations for why Neanderthals died out and humans didn’t – the last Neanderthal we know of lived 38,000 years ago, some 7,000 years after humans reached Europe.

There’s evidence for short – Neanderthal skeletons show they were around 1.5–1.6 metres tall (4 feet 11 inches to 5 feet 3 inches). Hairy, grunty, violent and stupid are more debatable, I learn. Since they possessed the FOXP2 gene that brought humans language, Neanderthals may have been able to speak, while ancient pollen reveals that they may have placed flowers on the graves of their dead, from species with medicinal powers, though others believe that bees may have transported at least some of the pollen.3 In any case, there’s good evidence that Neanderthals cared for individuals who could no longer look after themselves,4 and may have decorated shells and painted the walls of their caves.5

Over the years, we’ve discovered that humans weren’t any cleverer or faster than Neanderthals; we didn’t have better tools, our hunting skills weren’t sharper and Neanderthals may have communicated just as we did. When today’s archaeologists find stone tools on a dig site, they can only tell whether they belonged to Neanderthals or humans if they discover the toolmakers’ bones alongside their creations. The cultures of Neanderthals and early humans were equally advanced. If anything, humans were less strong and less well adapted to living in the cold. Put a Neanderthal and a human in one of those hypothetical ‘which would win a fight?’ pub arguments and the answer wouldn’t be clear. Yet Neanderthals were the ones who vanished, not us.

In 2019, Gili Greenbaum, an expert in computational genomics at the Hebrew University of Jerusalem in Israel, came up with a new theory to explain the Neanderthals’ disappearance.6 ‘Thinking has changed quite dramatically in the last couple of decades,’ he tells me carefully. ‘Neanderthals had the brain capacity to do what modern humans did.’ It’s clear Greenbaum is passionate about his subject and he wants to get this right. And he doesn’t think humans persisted because we were ‘better’ than Neanderthals.