Wellcome Trust Science Writing Prize 2013
In association with the Guardian and the Observer
Science Writing
Prize 2013:
The shortlist
The 19 best entries in this
year’s competition
1 | Science Writing Prize 2013: The shortlist
Wellcome Trust Science Writing Prize 2013
Congratulations to our shortlisted writers –
exciting new voices in science communication.
Winners
Stroke survivors – by Patrick Russell (B)
The revenge of the Americas – by Katherine Wright (A)
Highly commended
Echoes in the sand – by Josh Davis (B)
Fighting fit – by Laura Dawes (A)
We may experience some turbulence – by James Bezer (B)
Tactical manoeuvres on the viral battlefield – by Ben Bleasdale (A)
Here comes the wild world – by Joseph Bull (A)
Not monsters – by Sarah Byrne (A)
The rhythm of life – by Abigail Hayward (B)
Taming the twinkle – by Michael Hughes (A)
What’s so funny? – by Yingying Jiang (B)
A critique of sadness – by Pamilla Kaur (B)
Blurring the line between life and death – by Fergus McAuliffe (A)
Let there be light – by Kate McAllister (A)
Termites and intelligent living buildings – by David Parr (B)
The skeleton key – by Emma Pewsey (A)
The new ‘balanced’ diet – by Maliah Roshan (A)
Treating cancer with some help from the brain – by John Wilde (B)
Windows into the mind – by Rebecca Winstanley (B)
(A = entered in category for professional scientists; B = entered in general category)
2 | Science Writing Prize 2013: The shortlist
Wellcome Trust Science Writing Prize 2013
Foreword
Did I enjoy it? Did I learn something? Was it easy
to read?
These, broadly speaking, are the judging criteria
for the Wellcome Trust Science Writing Prize.
Our aim is to encourage new voices in the
communication of science, to find writers who
can explain science in the most engaging way, and
to increase the number of people reading,
thinking and talking about science.
“Science really excites and inspires people,” said
Hilary Leevers, Head of Education and Learning
at the Trust and one of this year’s judges. “It was
great to see so many entries that tackled
challenging science in an informative,
entertaining and above all well-written manner.”
We received almost 600 entries this year. A team
of volunteers from the Trust and the Guardian
whittled those down to their top 19 – ten in
category A (professional scientists) and nine in
category B (everybody else). Then our esteemed
judges got to work.
As well as Hilary, the shortlist was assessed by
radio and television presenter Maggie Philbin,
psychologist Professor Dorothy Bishop, author
and Observer features writer Carole Cadwalladr,
physicist and broadcaster Dr Helen Czerski, and
Dr James Randerson, environment and science
news editor at the Guardian.
3 | Science Writing Prize 2013: The shortlist
“The calibre of this year’s entries was very high
and included some fascinating tales told with
great skill, intelligence and passion,” James said. “I
hope the winners and all those shortlisted go on
to use their talents to keep writing and to enrich
the national conversation about science.”
The winners – Katherine Wright in the
professional scientist category and Patrick Russell
in the general category – each received £1000 and
saw their work edited and published in the
Observer and the Guardian respectively. The entire
shortlist has now been edited and you can read all
19 pieces on the following pages.
Shortlisted writers from previous years have gone
on to write about science in a variety of
publications, including several book deals, some
even becoming fully fledged science journalists.
The Science Writing Prize can lead to fantastic
opportunities for those who want to keep writing
about science, and we hope to see the work of this
year’s shortlist in print and online in the years to
come, too. Many congratulations to all!
To find out more about the Science Writing Prize,
please visit our website: www.wellcome.ac.uk/swp
Wellcome Trust Science Writing Prize 2013
Stroke survivors: retraining the brain
Patrick Russell
Stephen Manning was head chef at a French
restaurant in Notting Hill for 25 years. Today, he
struggles to make a cup of tea. His wife Joanne
intervenes when he pours water into a cup
without a tea bag or forgets to add milk to his
cereal. But when she is not around, life can be very
difficult. It is not that Stephen doesn’t understand
what he is trying to do. He knows what a cup of
tea looks like. The problem is that he often
struggles to remember the steps to make the
perfect brew.
Last year, Stephen was one of the 150 000 people
in the UK who suffered a stroke, caused by a lack
of blood getting to parts of the brain. The classic
symptoms associated with having a stroke are
physical. Patients can end up with paralysed limbs
and problems with speech. But for Stephen,
something much more subtle underlies his
problems – and he is not alone.
Of stroke patients, 68 per cent go on to develop
apraxia and action disorganisation syndrome
(AADS). Sufferers have difficulty in sequencing
previously automatic actions, from washing
themselves to making the bed. Although the
patient’s movement is affected, AADS is primarily
a disorder of the mind. Naturally people want to
cure what they can see. AADS is hard to identify
and although it is common, it has been overlooked
in favour of physical stroke rehabilitation.
Improved brain-scanning techniques mean it is
easier to identify AADS. And now, psychologists
and engineers have joined forces in a project that
aims to help improve the lives of the thousands of
people who suffer from this condition.
4 | Science Writing Prize 2013: The shortlist
“Patients may have done basic tea-making tasks in
hospital, but there is nothing to aid cognitive
rehabilitation after that,” says Amy Arnold, a PhD
researcher at Birmingham University who is
working on the project, called Cogwatch. It aims
to restore patients’ independence by developing
personalised rehabilitation systems that can be
installed into their homes.
These systems will silently monitor patients as
they go about their daily lives and provide advice
to guide them when they make errors. It is hoped
that patients will learn to sequence tasks correctly
as a consequence.
But designing this rehabilitation system has
proved a challenge. Ultimately, patients will wear
a watch that will monitor their movements.
Electronic devices will be installed into everyday
objects in their homes, such as a toothbrush or a
vest. These will transmit information wirelessly to
a central system. This will guide patients if they
make errors, through sounds, vibrations or a
visual screen.
Manish Parekh, a PhD student who is part of the
project, explains: “We are incorporating sensors
that monitor grip strength or motion into
everyday objects. This is the same technology
used in mobile phones that detect which way up
they are being held.”
Another challenge is combining technology with
the research carried out by the project’s
psychologists. “We are trying to learn how healthy
people normally behave and the kind of errors
that occur in stroke patients,” explains Amy.
Wellcome Trust Science Writing Prize 2013
To monitor how tasks are normally undertaken,
the team has studied healthy participants. Sensors
that can monitor complex movements were used
to examine how they completed several tasks.
This information can then be used as a
comparison to AADS behaviour.
Not everyone will welcome the new technology
with open arms. Many stroke patients are above
the age of 65 and may struggle to integrate
technology into their everyday lives. “It has to be
friendly enough to make patients want to use it,”
explains Amy. “They don’t want lots of gadgetry
and to press lots of buttons, or for it to take over
their lives.”
This is the reason Cogwatch is working closely
with the Stroke Association. “It is great that they
are addressing this problem but a system like this
will only succeed if it is usable by patients,”
explains Dr Clare Walton, the Stroke Association’s
Research Communication Officer. “One of the
concerns with this project is that the tech group
will go nuts, developing all this amazing
technology, but that it will be unusable – like
developing a vibrating watch for a patient with
sensation problems.”
With the focus still on physical rehabilitation, this
project, though still in its infancy, is quietly
tackling AADS head-on for the first time. The
disorder affects a massive percentage of stroke
survivors, and for people like Stephen Manning,
that fight could not have come soon enough.
5 | Science Writing Prize 2013: The shortlist
Wellcome Trust Science Writing Prize 2013
The revenge of the Americas
Katherine Wright
In the 1490s, a gruesome new disease exploded
across Europe. It moved with terrifying speed.
Within five years of the first reported cases,
among the mercenary army hired by Charles VIII
of France to conquer Naples, it was all over the
continent and reaching into north Africa. The
first symptom was a lesion, or chancre, in the
genital region. After that, the disease slowly
progressed to the increasingly excruciating later
stages. The infected watched their bodies
disintegrate, with rashes and disfigurements,
while they gradually descended into madness.
Eventually, deformed and demented, they died.
their genitals by 1494. What if Columbus had
brought the disease back to Europe with him as an
unwelcome stowaway aboard the Pinta or the
Niña?
Some called it the French disease. To the French, it
was the Neapolitan disease. The Russians blamed
the Polish. In 1530, an Italian physician penned an
epic poem about a young shepherd named
Syphilis, who so angered Apollo that the god
struck him down with a disfiguring malady to
destroy his good looks. It was this fictional
shepherd (rather than national rivalries) who
donated the name that eventually stuck: the
disease, which first ravaged the 16th-century
world and continues to affect untold millions
today, is now known as syphilis.
However, scientists, anthropologists and
historians still disagree about the origin of
syphilis. Did Columbus and his sailors really
transport the bacterium back from the New
World? Or was it just coincidental timing that the
first cases were recorded soon after the
adventurers’ triumphant return to the Old World?
Perhaps syphilis was already present in the
population, but doctors had only just begun to
distinguish between syphilis and other disfiguring
illnesses such as leprosy; or perhaps the disease
suddenly increased in virulence at the end of the
15th century. The ‘Columbian’ hypothesis insists
that Columbus is responsible, and the ‘preColumbian’ hypothesis that he had nothing to do
with it.
As its many names attest, contemporaries of the
first spread of syphilis did not know where this
disease had come from. Was it indeed the fault of
the French? Was it God’s punishment on earthly
sinners?
Another school of thought, less xenophobic and
less religious, soon gained traction. Columbus’s
historic voyage to the New World was in 1492. The
Italian soldiers were noticing angry chancres on
6 | Science Writing Prize 2013: The shortlist
Since the 1500s, we have discovered a lot more
about syphilis. We know it is caused by a spiralshaped bacterium called Treponema pallidum, and
we know that we can destroy this bacterium and
cure the disease using antibiotics. (Thankfully we
no longer ‘treat’ syphilis with poisonous,
potentially deadly mercury, which was used well
into the 19th century.)
Much of the evidence to distinguish between
these two hypotheses comes from the skeletal
record. Late-stage syphilis causes significant and
identifiable changes in the structure of bone,
including abnormal growths. To prove that
syphilis was already lurking in Europe before
Wellcome Trust Science Writing Prize 2013
Columbus returned, anthropologists would need
to identify European skeletons with the
characteristic syphilitic lesions, and date those
skeletons accurately to a time before 1493.
This has proved a tricky exercise in practice.
Identifying past syphilis sufferers in the New
World is straightforward: ancient graveyards are
overflowing with clearly syphilitic corpses, dating
back centuries before Columbus was even born.
However, in the Old World, a mere scattering of
pre-Columbian syphilis candidates have been
unearthed.
Are these 50-odd skeletons the sought-after
evidence of pre-Columbian syphilitics? With such
a small sample size, it is difficult to definitely
diagnose these skeletons with syphilis. There are
only so many ways bone can be damaged, and
several diseases produce a bone pattern similar to
syphilis. Furthermore, the dating methods used
can be inexact, thrown off by hundreds of years
because of a fish-rich diet, for example.
A study published in 2011 has systematically
compared these European skeletons, using
rigorous criteria for bone diagnosis and dating.
None of the candidate skeletons passed both tests.
In all cases, ambiguity in the bone record or the
dating made it impossible to say for certain that
the skeleton was both syphilitic and preColumbian. In other words, there is very little
evidence to support the pre-Columbian
hypothesis. It seems increasingly likely that
Columbus and his crew were responsible for
transporting syphilis from the New World to the
Old.
7 | Science Writing Prize 2013: The shortlist
Of course, Treponema pallidum was not the only
microbial passenger to hitch a ride across the
Atlantic with Columbus. But most of the traffic
was going the other way: smallpox, measles and
bubonic plague were only some of the Old World
diseases which infiltrated the New World, swiftly
decimating thousands of Native Americans.
Syphilis was not the French disease, or the Polish
disease. It was the disease – and the revenge – of
the Americas.
Wellcome Trust Science Writing Prize 2013
Echoes in the sand
Josh Davis
Spring sunlight shimmers off the wet sand
revealed by the ebbing tide, rain patters on my
coat as I scan Formby beach one damp Sunday
afternoon. I’m with Alison Burns, an
archaeologist from Manchester University, and a
dozen brave locals. Eventually Burns finds what
we’ve been looking for in a patch of brown
sediment jutting out from under the sand. We
gather round. It is the footprint of a large red deer.
As we glance around, we notice many more – a
herd. Had we just missed them? Further along the
beach, Burns finds something else: a trail of
human footprints leading into the dunes. But
however carefully we follow them, we’ll never find
the people that made them. Not left by damp
day-trippers like us, these prints are tangible
evidence of someone passing by 6000 years ago.
was recording them. He has since documented
more than 200 human trails and countless animal
tracks, building a unique picture of the
environment in which these people lived. The list
of animal tracks includes species such as red and
roe deer, dogs or wolves, boar, oyster catchers and
cranes, as well as the extinct aurochs.
During the Mesolithic, this stretch of coast had a
large reed marsh protected from the sea by a sand
bar. As people and animals walked through the
soft mud, their prints were baked hard by the sun
and covered in a fine layer of silt from the river
flowing into the marsh. Over time the river
migrated south, the sand bar disappeared.
Millennia later, the sea now washes away the silt,
slowly giving up this secret snapshot of ancient
life. After a window of time, the tide returns to
reclaim them. By determining the age of the
sediment, scientists have been able to date the
footprints to the late Mesolithic to early Neolithic
(4000BC).
This information can give us an incredible insight
into what Neolithic people were getting up to in
this marsh. Adult male human tracks are often
found in association with those of red deer: it
appears that the men were following, possibly
even managing, the herds. There are other tracks
which lead directly out to sea where the men may
have been fishing. While the men were out
hunting, the women and children appear to have
been gathering food such as shrimp and shellfish
from the marsh itself. There are even prints from
children running and playing in the mud.
Gordon Roberts, a local resident, has been
researching these “ephemeral imprints” since 1989
when he first found tracks himself. He realised
that there were many reports of prints but no one
8 | Science Writing Prize 2013: The shortlist
But it’s the prints of our ancestors who walked
this coastline 6000 years ago which are truly
special. Rather than simply inferring a lifestyle
from artefacts, we can glimpse the life of these
people as it happened. From the footprints,
Roberts tells me, we can deduce the approximate
height and sex of an individual, and by the pace
and stride we can calculate their speed of
movement.
Burns is just as interested in what the tracks don’t
show. They span the Mesolithic-Neolithic
boundary, when farming and animal husbandry
were starting to spread within the British Isles.
But these prints show a distinct lack of change.
Men still wander out to sea to fish while women
Wellcome Trust Science Writing Prize 2013
continue to patrol the shore looking for shellfish.
The footprints seem to show a community in
stasis, unchanging while the world around adopts
new techniques. Burns believes this is because
there was simply no need to start farming or
raising livestock here. The marshlands were as
productive as ever, the game clearly still plentiful,
and quality of life apparently high.
So high in fact, that these communities were able
to support the disabled. There are imprints made
by people with deformities: missing toes,
deformed feet and evidence of club foot. We might
have thought these people would struggle to
survive within a hunter-gatherer society but, on
the contrary, the prints tell us they thrived too.
These footprints offer us more than just hard facts
and data. Standing on the beach on this Sunday
afternoon, looking at the track made by a woman
6000 years ago, I immediately feel an intimate
connection. I can’t help but wonder where she had
been, what she had been doing. Was she returning
from a successful afternoon collecting razor
clams? Did she have children waiting for her in the
forest? We’ll never know. Time and tide wait for
no one. Leaning into the rain, heading home, we
leave the returning tide to take away forever these
amazing echoes of the past.
9 | Science Writing Prize 2013: The shortlist
Wellcome Trust Science Writing Prize 2013
Fighting fit: how dieticians tested if Britain
would be starved into defeat
Laura Dawes
In December 1939, Britain had been at war with
Germany for three months. U-boat attacks
threatened incoming food shipments. And, armed
with bicycles and walking boots, a group of
medical researchers headed to the Lake District to
conduct a secret study: if Britain was totally cut
off from food imports, would starvation hand
victory to Germany?
The researchers investigating whether Britain
could win the food fight were Cambridge
University physiologists Elsie Widdowson and
Robert McCance. When war broke out, Elsie and
Mac felt they could use their expertise in food and
nutrition to answer whether, if German U-boats
crippled food imports, would Britain be dieted
into defeat?
This was an important medical question. Could
the public stay fighting fit if food was rationed to
what Britain alone could produce? If the ration
was too low in protein, people would get ‘famine
oedema’ (swelling from fluid build-up). Before the
war, Britain imported half its meat, more than
half its cheese and a third of its eggs. Much of the
protein in the British diet would therefore be lost
if a shipping blockade succeeded. Anaemia
(insufficient iron) and scurvy (lack of vitamin C)
could also become a problem.
They decided to experiment on themselves. Four
students and Mac’s mother-in-law also
volunteered. They would pretend that a German
shipping blockade had curtailed imports and they
had to eat only British food. Everyone would get
equal shares of the available produce. To work out
what this might be, Elsie and Mac sought advice
from Frank Engledow, a professor of agriculture
who later helped set wartime food policy. British
food production in 1938 became the basis for the
experimental diet: one egg a week (a third of the
pre-war consumption); a quarter of a pint of milk
a day (half the pre-war consumption); a pound of
meat and 4 oz of fish per week, assuming trawlers
would be commandeered for patrols. No butter
and just 4 oz of margarine. But they could eat as
much potato, vegetables, and wholemeal bread as
they wanted. The eight guinea pigs would follow
this diet for three months.
The rationed diet had to provide enough fuel for
the long hours in factories and farms needed for
the war effort. If people were too weakened by
lack of food, infectious diseases would pick them
off, just as surely as bullets. Disease played a key
part in deciding who won wars. Famously,
Napoleon lost his Russian campaign in 1812 after
his army was decimated by typhus and dysentery.
In total war, it wasn’t just the army who had to
stay well to win. The home front also had to
remain healthy. Having a sufficient diet was a
medical issue that went to the heart of the war
effort.
10 | Science Writing Prize 2013: The shortlist
Happily, the gloomy spectres of famine oedema,
scurvy and anaemia did not arise. The guinea pigs
felt fit and well on the ration and could do their
usual work. But there were two main difficulties.
One was that meals took a long time to eat.
Wholemeal bread without butter took ages to
chew. The sheer quantity of potato needed to
make up calories also took time to eat. All the
fibre in the diet caused 250 per cent bigger poos.
They measured it.
Wellcome Trust Science Writing Prize 2013
The other problem with eating all that starch was
the amount of flatus – gas – that it produced. The
consequences could be, in Elsie and Mac’s
description, “remarkable”.
sugar, meat and fish than Elsie and Mac’s diet.
Convoys from America were able to run the
U-boat blockade and flesh out British food
supplies.
To simulate the hardest physical work that might
be expected of people during the war, some of the
team headed to the Lake District for an intensive
fortnight of walking, cycling and mountaineering.
It was tough going with snow and ice on the paths.
But other than a sore knee for Elsie, the team did
well enough that a professional mountaineer
rated their performance “distinctly good”. And
this was on the diet that might be the lot for all
Britain if shipping imports failed.
Rationing during the Second World War caused
problems – it was hard to cook inventively with
limited ingredients, and queuing for supplies
burdened housewives. But Elsie and Mac’s study
showed that scurvy and starvation would not add
to that burden.
In 1940, the British government rationed bacon,
butter and sugar, just as the team finished their
trial. Their report and its conclusion – that Britain
could stay fighting fit even if all food imports were
lost – was circulated to government departments.
But the study was kept secret until after the war.
As more foods were rationed, the experiment
provided assurance that home front health was
secure. Had the conclusion been different, Britain
might have had to decide whether to distribute
the limited food equitably – and suffer the
consequences of widely degraded health – or give
more food to workers most important to the war
effort. Elsie and Mac’s experiment showed this
horrible reckoning was not necessary: Britain
could afford to be fair and still be fighting fit. As it
turned out, the experiment had been too severe.
Rationing was always more generous with butter,
11 | Science Writing Prize 2013: The shortlist
Wellcome Trust Science Writing Prize 2013
We may experience some turbulence
James Bezer
I always make tea in a glass. It makes it so much
more exciting. Pouring milk into tea is one of
those dull things we do every day without
thinking, but looking at the liquid through
transparent walls exposes intricate patterns,
currents and swirling vortices created by the
simple action of your hand. This complex motion
is incredibly striking, and strangely beautiful. But
what makes it all the more amazing is that, in
peering into your tea, you’re gazing into one of the
greatest mysteries in physics.
Since the 19th century, we have had a pretty good
theoretical description of how liquids and gases
move around. By simply applying Newton’s laws
describing the motion of solid objects to a
continuum of particles you reach a few short lines
of maths that describe the behaviour of fluids.
These are the Navier-Stokes equations.
In principle, these equations should apply in any
situation. If you’re interested in a slow-moving or
viscous fluid, they can easily be used to make
accurate predictions about how it will behave.
Under these conditions, flows are smooth and
steady; a stream of dye injected into a current like
this would remain together in a line throughout
its length, without spreading about and breaking
apart. Nice and easy.
However, as with many things in science, it’s not
quite as simple as that. Outside a narrow range of
conditions, the system becomes rather
uncooperative. Seemingly random disturbances
are created in the flow, forming swirling vortices
(called eddies), and making different parts of the
fluid mix together. These disturbances, known as
12 | Science Writing Prize 2013: The shortlist
turbulence, are why, if you injected a narrow
stream of red dye into a river, it would quickly
spread and turn the fish a lovely shade of pink.
Turbulence affects almost all fluids in nature, to at
least some extent. It forms the motion of the
atmosphere. It’s why your heartbeat makes a
noise. And it stirs up your tea.
It’s also extremely complicated. The eddies that
make up turbulent flows happen at all scales
within the fluid: big vortices are made up of small
vortices, which are made up of even smaller
vortices and so on. But, unlike in some areas of
science, we can’t just ignore what’s going on at
scales much too small to see because we’re more
interested in the big picture. All those little
perturbations, growing out of immeasurably
small variations in the initial conditions, add up
and contribute to significant changes in the
large-scale structure of the flow.
This unimaginable complexity in almost every
real-world situation means that the Navier-Stokes
equations could only be solved by supercomputers
many orders of magnitude more powerful than
anything we have today. In fact, mathematicians
still don’t have a clue whether there are some
circumstances in which they simply don’t have a
solution. In 2000, this was named one of the most
important unsolved problems in mathematics,
and if you happen to stumble upon a case where
they don’t work, or prove that they always do, you
would be lavishly rewarded with the milliondollar Millennium prize.
So if the Navier-Stokes equations are too hard to
solve in almost any real situation, what can we use
Wellcome Trust Science Writing Prize 2013
to model turbulence? Simplified forms are widely
used in engineering and applied sciences, as they
make the maths slightly less impossible in real
situations. Another approach is to work
backwards from experimental data about a flow to
a mathematical framework that sticks all the
numbers together. Both of these approaches are
very useful, helping to design everything from jet
engines to hair dryers, but in some circumstances,
the predictions they make are not just wrong, but
physically impossible.
This inability to make perfectly accurate
predictions about the real world remains hugely
frustrating, and means engineers still rely on
experimental data to see how the object in their
computers would behave in the real world. You
can rest assured that wind tunnels are still of vital
importance in aeroplane design.
This is what marks fluid dynamics out from many
other areas of physics. Solid objects, for instance,
can be precisely modelled using simple maths and
fundamental laws. If you threw a ball in the air, a
school student could predict, using its initial
speed and angle to the ground, exactly where and
when it would land. Yet turbulence remains a
mystery; not only is the maths fiendishly difficult,
but we still don’t really know what causes this
weird phenomenon to occur in the first place. It is
still the case, therefore, that we know more about
relativity, quantum mechanics and the first
nanosecond after the Big Bang than the
movement of the liquids and gases that constantly
surround us.
Still using teacups? You’re really missing out.
13 | Science Writing Prize 2013: The shortlist
Wellcome Trust Science Writing Prize 2013
Tactical manoeuvres on the viral battlefield
Ben Bleasdale
“Let’s make them work for us,” Professor Laura
Kasman tells me.
She’s talking about viruses, the tiny replicating
machines that infect everything on the planet –
from minuscule bacteria to mighty elephants.
Scientists have studied these remarkable
replicators for more than a century, learning how
to avoid them and the diseases they cause. Yet
they remain one of the biggest threats to our
survival as a species. Research into
understanding and combating this threat is a
global effort. This is war on a grand scale, and
every advantage must be exploited.
The fact is that we’re all jam-packed with viruses;
when someone tells you that they’re full of cold,
they’re actually just slightly more full than usual.
The average, healthy human being carries
around trillions of viruses with them every day.
Mostly, we’re blissfully unaware of this
ecosystem of competing, infectious predators
within our bodies. Only when one gets out of
control do we notice.
The traditional, laborious approach for
researching such pathogens has been to purify
each virus and study it in isolation. Laura was
trained in the same way. “That makes sense for
finding out basic information about a virus,” she
tells me, “but it was apparent to me that it had
very little to do with real-life infections”. She
thinks we’re missing part of the story.
14 | Science Writing Prize 2013: The shortlist
In the crowded battlefield, it’s not just how
viruses interact with their hosts – us – that
matters, it’s also how they interact with each
other. Yet this aspect of infection isn’t getting the
attention it deserves: “The search terms ‘virus–
host interaction’ found thousands of published
articles [on PubMed], whilst ‘virus–virus
interaction’ found zero,” Laura tells me. Not
content to let this stand, she is pioneering a
movement to harness this hidden aspect of
infection, for our own benefit.
Working at the Medical University of South
Carolina in the USA, Laura has been
spearheading a team that seeks to draw together
the early findings within this underappreciated
field. They hope this will empower researchers
across the globe, spurring on new ideas and
experiments that could ultimately lead to better
antiviral treatments. Based on the same concept
as Wikipedia, they’ve established the Virus–Virus
Interactions Database, an open and free online
hub for scientists to consult and contribute to.
The encyclopedia, with its increasing number of
entries, is already revealing exciting new links
between research that was previously scattered
far and wide. It shows, for example, how one
virus can dramatically change the way another
virus replicates, creating huge differences in the
spread of disease across the world.
Understanding the powerful effects of
competition and interaction between viruses
may hold the secret to new treatments,
potentially changing the lives of millions.
Wellcome Trust Science Writing Prize 2013
And Laura’s bold move is already being
vindicated. After the Database was established, a
ground-breaking study from Australia has shown
that, surprisingly, getting sick might actually
stop you getting sicker. The research revealed
that patients who’d recently been infected with a
common cold virus were protected from more
severe viruses, like influenza, even after the cold
had disappeared.
This temporary protective effect seems to stem
from the ‘smash-and-grab’ approach used by cold
viruses, which leaves the body’s immune system
on high alert, giving it a head start against
incoming flu viruses. This was also an excellent
example of one virus influencing another, proof
for Laura that her work could make a difference
for patients. “That was a really great feeling that
we were able to predict it, and then it was there,”
she says. Such results are spurring a new wave of
research, aimed at protecting patients using
nature’s existing tools – viruses themselves.
This movement is starting small but, having
planted the seed, Laura is optimistic that it can
help other scientists uncover further exciting
discoveries. “I hope that it will inspire virologists
to move away from artificial one-virus systems
and look for these interactions,” she says. This
change won’t happen overnight, but Laura’s
pioneering work has got researchers thinking
and talking – the first step on a long road that
could benefit everyone.
15 | Science Writing Prize 2013: The shortlist
At the moment, only the tip of the iceberg has
been glimpsed. The idea of getting a cold to ward
off influenza is far from ideal, but we already
know that our bodies are full of countless other
viruses that give us no noticeable symptoms at
all. It might be that, by helping the right side in
this hidden battlefield of infection, we can
harness these viruses to fight back against other
dangerous diseases. As Laura succinctly puts it,
“If we are going to be infected with all of these
symptom-less viruses anyway, let’s make them
work for us.”
And why not, they’ve been fighting this war much
longer than we have.
Wellcome Trust Science Writing Prize 2013
Here comes the wild world
Joseph Bull
The far northwest of Uzbekistan is a place of dust
and wind and fermented camel’s milk, where
there is never anything between you and the
horizon. The locals joke (sometimes through
gritted teeth) that it is not the middle of nowhere,
it is the end of nowhere. This remote, semi-arid
scrubland is an ancient arena in which tigers and
eagles used to chase an ice-age relic: the saiga
antelope. Now that the hungry herbivorous
antelope are all but gone, poached to the brink of
extinction, you might think there would be a lot
more vegetation around. But the opposite is true:
the wilderness is turning into a desert.
“Beyond the Wild Wood, comes the wide world,”
Ratty warns in The Wind in the Willows. How
many children have read that and immediately
wanted to explore the wild woods and the world
beyond? But the Earth is not as wild as it once was
and scientists are beginning to ask whether we
have tamed the wilderness too much. Do we need
wildernesses? And if so, can we rebuild them?
Desertification is affecting many of the drylands
in the world, which cover 41 per cent of global land
surface and are where some 38 per cent of all
people live. In Uzbekistan, the saiga antelope don’t
only eat the shrubs, they also break up the soil
with their hooves and fertilise it with their dung.
This maintains soil structure and allows the
vegetation to reseed itself, preventing the entire
landscape from becoming a wasteland. So one way
to help solve the desertification problem in this
part of the world might be ‘re-wilding’: bring back
the saiga and they’ll do the rest.
16 | Science Writing Prize 2013: The shortlist
Re-wilding is not limited to remote corners of
Central Asia. There are far too many deer in the
UK, for instance, because we have removed their
natural predators. In such high numbers, deer
undermine and overwhelm native woodlands that
we need for flood control, carbon sequestration
and more. We could carry on spending a large
amount of money culling the deer every year, or
we could consider re-wilding parts of the British
countryside. Scientists have simulated what
would happen if originally native predators, like
wolves or lynx, were reintroduced into large
fenced wilderness reserves. Get the area and the
fence right, and they predict that the deer could
return to manageable levels within a few decades.
How far can we go with this new science of
re-wilding? Once we begin to understand the roles
that various species have to play in maintaining
the landscape, the potential is staggering. Take
the Oostvaardersplassen wetlands in the
Netherlands. Here, animals have been introduced
where they never existed naturally, in order to play
a part that other creatures used to fulfil. Freeroaming ponies and cattle now take the place of
absent wild horses and aurochs. Wetlands are an
important component of the human water supply
but the new, semi-wild species maintain wetlands
better than human management ever could.
It is only a short conceptual leap to the really
groundbreaking idea of ‘Pleistocene re-wilding’.
This involves reintroducing species to large
reserves in places where they haven’t lived
abundantly since the last ice age. Some scientists
are exploring the concept of bringing leopards and
Wellcome Trust Science Writing Prize 2013
hippos back to Europe and introducing lions and
elephants to the USA in place of long-extinct dire
wolves and ground sloths. Others wouldn’t stop
there, and there is a growing body of research into
the possibilities for ‘de-extinction’, whereby DNA
samples could be used to resurrect species such as
the sabre-toothed tiger and woolly mammoth.
Controversial? Yes, and not without challenges.
But the argument here is the same as for saiga
antelope and wolves: wildernesses, and the beasts
they contain, play roles that support the economy
in ways that people simply cannot feasibly replace
with technology.
We need wildernesses. That is not to say we
shouldn’t heed Ratty’s warning about the
potential dangers that lurk in the wild. But we
should also consider what Badger had to say in
that same story: “They built to last, for they
thought their city would last for ever. People
come…and they go. But we remain.” If we clear all
the wild spaces, the cities we build in their place
will be undermined and, eventually, will fall.
17 | Science Writing Prize 2013: The shortlist
Wellcome Trust Science Writing Prize 2013
Not monsters: neurodiversity, acceptance and
changing perspectives on autism
Sarah Byrne
“She looked at it, screamed aloud, hit her hands
together above her head, and cried out in despair, that
this was not her child: It howled in such an inhuman
manner that it was nothing like the child she knew.”
(‘A Changeling is Beaten with a Switch’, Jacob and
Wilhelm Grimm)
European folklore is full of stories about
changelings – children and babies supposedly
stolen by fairies or demons and replaced with an
alien version. These tales may actually have been
about children with developmental disorders such
as autism, in which a seemingly normal child can
seem to suddenly regress and lose abilities such as
speech.
April 2013 was Autism Acceptance Month, the
third since its founding in the US in 2011 as a
response to traditional ‘awareness’ campaigns.
We’ve clearly come a long way since the days of
folklore, but we are still far from fully
understanding autism. There are two big
questions: what causes it, and what can we do
about it?
It is now generally accepted that autism –
characterised by language and social difficulties
and repetitive behaviours – is heritable. Other
proposed causes, including parenting styles,
environmental pollution and childhood
vaccinations, probably contain about as much
truth as the changeling legends.
Tracking down the genetic causes of such a
complex disorder is difficult though. There isn’t a
single ‘gene for autism’. And even when we know
18 | Science Writing Prize 2013: The shortlist
that changes in certain genes are associated with
the condition, it is not straightforward to map
these changes to actual behaviours or changes in
the brain’s workings. Finding the genes – and
we’re far from finding all of them – is only the
beginning. Next we need to understand the
complex interplay between them, and between
these genes and our environment. We are a long
way from a genetic test (and further still from any
gene-related therapy) for autism.
The other way of trying to understand what’s
going on is to look at the brain itself. Brain scans
of autistic and non-autistic people show some
significant differences – and the more severe the
symptoms, the bigger the differences. Although
this is interesting, it doesn’t help us much with
potential treatments.
“The nobleman said to her: ‘Woman, if you think that
this is not your child, then do this one thing. Take it
out to the meadow where you left your previous child
and beat it hard with a switch.’”
The child in this fairytale got off lightly. Common
advice in such stories was to put the ‘changeling’
in a pot of boiling water or on a fire, or outside to
freeze or starve to death. The idea was that the
mythical kidnappers would appear just in time to
stop the sacrifice, and return the rightful child.
Autism has no magical cures, and despite their
promises, today’s alternative treatments – from
diets to electric shocks – lack evidence, and can do
more harm than good. Early diagnosis and
intervention with behavioural therapies may work
Wellcome Trust Science Writing Prize 2013
better, but although this is a widely used and
mainstream approach, the evidence is still
surprisingly tentative. There have been some
studies of hormone treatment, with the so-called
‘cuddle hormone’ oxytocin appearing to improve
empathy and sociability.
But now some are asking not just can we find a
cure, but should we?
A recent research study showed that autistic
children actually reasoned in a more logical
manner than their normally developing peers.
The children watched an adult solving a simple
puzzle, with some unnecessary steps included,
and then were asked to repeat the process
themselves. Most children copy the adult exactly,
even when they know their actions are ‘silly’. The
autistic children, however, simply cut out the
irrelevant steps and performed the task efficiently
– to which the only response can be: sensible
children!
Acceptance goes a step further than traditional
awareness campaigns. Some talk about
‘neurodiversity’: the idea that autistic traits are
just another way of being human, more
comparable to racial or gender differences than a
disorder to be pitied or fixed. According to this
perspective, championed by many autistic people
themselves, it is society that needs to change to
overcome its prejudices and accommodate these
differences. Others are more cautious, however,
voicing concerns that such normalisation may
stifle research, and disadvantage those who are
severely disabled by their condition.
19 | Science Writing Prize 2013: The shortlist
Awareness and acceptance are needed, because
too often the stereotypes haven’t moved on from
the days of folklore. The screaming, unreachable,
mindlessly violent monster of a child still persists
in the popular imagination. So does the hope of a
miracle cure that will restore the ‘real’ person
stolen by the disease.
Maybe now is the time to leave those fairytales in
the past and realise that people on the autistic
spectrum are not changelings or aliens, but
valuable and contributing members of society.
The human experience is varied and diverse. And
that is not necessarily a bad thing.
Wellcome Trust Science Writing Prize 2013
The rhythm of life: a powerful beat
Abigail Hayward
Birds sing in the trees. Whales sing in the depths.
Humans sing in concert halls.
Music is a quality that makes our species unique.
Even if you haven’t deliberately gone to a concert,
or plugged yourself into your iPod, music blares
from cars, shops, bars and houses. Music is
virtually inescapable. The world is never on mute.
Practically all humans have the ability to perceive
tones, harmony, pitch and rhythm – the
fundamental building bricks of what we define as
music. But where does this capacity come from?
Are humans evolutionarily adapted to listening to
music? What, when it comes down to it, is the
point of music?
This question has been asked many times,
famously in Arthur C Clarke’s novel Childhood’s
End, where aliens come down to Earth and are
quite perturbed at man’s obsession with making
and listening to music. They might have a point.
Even Darwin wrote that “neither the enjoyment
nor the capacity of producing musical notes are
faculties of the least use to man”. For many years,
the evolution of music was a murky subject, but
within the last 50 years there has been a surge of
interest. We are starting to identify where the
mechanisms involved in music perception have
come from, and possibly even the reasons why
music perception evolved.
A study conducted by Ava R Chase in 2001 found
that goldfish had the potential to tell the
difference between blues and baroque music. This
suggests that an apparatus which evolved tens of
thousands of years ago in these fish has, many
20 | Science Writing Prize 2013: The shortlist
years on, been adapted to make music perception
possible. For example, our middle ear bones,
which now function in hearing, acted as jaw
supports. Our lungs, which acted as a floatation
control system in fish (the swim bladder), now
enable us to vocalise and breathe.
Sometimes people forget that current function
doesn’t necessarily match ancestral function. The
evolution of music didn’t start with sound
perception. Instead, it developed as it became
necessary, as tetrapods advanced onto land.
Thanks to these mechanisms, humans have
always had the ability to perceive and distinguish
between different sounds. However, as is true
today, this occurs to different degrees – some
people are just more naturally musical than
others. If music is an adaptation, what aspects of
it allowed more musical people to outcompete
people with lesser musical abilities?
Firstly, there is Steven Pinker’s “auditory
cheesecake” hypothesis. The idea was that music
stimulated our pleasure centres, “an exquisite
confection crafted to tickle the sensitive spots of...
our mental faculties”. Although it attracted a lot of
criticism at the time of its proposal, recent
research has given this hypothesis more
credibility. It has been shown that listening to
music triggers the brain to release the chemical
dopamine, which is part of a reward-driven
learning process (in other words, learning is
‘rewarded’ with dopamine). In this way, music may
actuate and actually develop our mental
capacities.
Wellcome Trust Science Writing Prize 2013
Music could also be a factor in mate choice.
Darwin himself mused that people “endeavoured
to charm each other with musical notes and
rhythm”. Music doesn’t seem evolutionary helpful,
as it may attract predators. However, musical
aptitude requires a large mental capacity, or ease
of learning, which would have allowed ancient
man to evade predators. Learning music also
requires a large amount of patience, which is an
attractive trait in terms of establishing a longlasting relationship. Patience can also be applied
to the skills needed to raise a family.
Singing lullabies could be considered to be one of
these skills and is this is actually the only genre of
music that can be considered universal. Lullabies
can be found across all cultures, ranging from
Sweden’s Mors Lilla Olle, to Kenya’s Rock, Rock,
Rock. Mother–infant song has roots in ancient
times, and is another possible reason for the
evolution of music. Firstly, lullabies are a means of
communication between mother and child – the
language is simple, making them easy to learn and
understand. Lullabies also stimulate the area of
the brain responsible for perception, which could
be important for the development of the mind.
Given that an infant’s cries could attract
unwanted attention, being able to soothe them
would surely be adaptive to save the family from
predation.
21 | Science Writing Prize 2013: The shortlist
Music may be an adaptive trait. You may choose
the logic that everything happens for a reason.
That music must have given people an
evolutionary advantage, as it still persists today.
But what we may not be able to conclusively
explain is this: after a bird serenades his potential
partner, he can just fly away. After a whale’s last
song, he sinks back to the depths. But at the end of
a musical performance, a person can sit with tears
in their eyes, unable to explain why. Music has
done something to us emotionally as a species.
And it’s something we may never be able to truly
fathom.
Wellcome Trust Science Writing Prize 2013
Taming the twinkle
Michael Hughes
For poets and composers of nursery rhymes, the
twinkling of the stars is a delight. For
astronomers, it’s a disaster. Try to take a
photograph of a star through a telescope and
you’ll find out why. The constant motion and
distortion of the light corrupts the image, blurring
out small features. We don’t even need a telescope
to see this twinkling, just find a break in the
clouds and take a look at the night sky. The stars
seem to dance around, left to right, up and down,
sometimes fainter and sometimes brighter, never
quite seeming to rest in one place.
If you were to travel a few hundred miles straight
up, and sit just outside the Earth’s atmosphere, the
twinkling would stop. Now the stars would be
fixed points: steady, constant and unmoving.
Their light has travelled this way across the
vastness of space, undisturbed and undistorted.
It’s only in the final moments of its journey,
passing through our turbulent atmosphere, that it
is bent and twisted out of shape.
What scientists call the resolution of an image –
the minimum separation needed between two
objects before they blur together – is limited by
the atmosphere. No matter how expensive the
telescope, or how large its mirrors and lenses, the
limit doesn’t change. This is one reason why
billions of dollars were spent putting the Hubble
Space Telescope into orbit, safely above the
influence of the atmosphere.
Much to the relief of government bean-counters,
there is another way. It’s called adaptive optics.
The idea is to ‘undo’ the effect of the atmosphere
22 | Science Writing Prize 2013: The shortlist
by reversing the distortions it causes. A
‘deformable’ mirror is added to the telescope. The
surface of this kind of mirror can be reshaped
under computer control. So, if the distortions
from the atmosphere can be measured, then the
opposite distortion can be simulated by the
deformable mirror, and so much of the effect of
the atmosphere can be cancelled out.
If it sounds simple, then think again. Firstly,
because the atmosphere is constantly shifting, so
are the distortions. This means that a new shape
for the deformable mirror has to be calculated and
applied many times a second. Secondly, the
instruments used to measure the distortions,
called wavefront sensors, need a relatively bright
light source to work on. The objects that the
astronomers actually want to study usually aren’t
suitable, so they need to find a second, brighter
star in the same region of the sky. The distortions
measured using this ‘guide-star’ are then used to
correct the interesting image.
Unfortunately, this all relies on there being a
bright-enough star close by. The further away the
guide-star, the poorer the correction will be. Not
content to live with this limitation, astronomers
have resorted to making their own guide-stars by
bouncing an intense laser beam off the upper
atmosphere. This allows them to correct images
from any point in the sky.
While adaptive optics systems are allowing us to
probe ever deeper into space, they can also be used
to deal with troublesome optical distortions closer
to home. Modern microscopy techniques allow
Wellcome Trust Science Writing Prize 2013
scientists to look several millimetres into
biological tissue. But, like the atmosphere, the
tissue distorts the focus of the light, limiting the
penetration and resolution of the microscope.
Scientists around the world are now using
adaptive optics techniques to improve the quality
of their images.
Some retinal imaging cameras now include
systems to correct for distortions caused by the
eye, allowing individual photo-receptors – the
light-sensitive cells on our retinas – to be seen.
And as costs fall, we are even beginning to see
simple adaptive optics built into consumer
electronics devices such as DVD players.
While we might not notice adaptive optics in
these everyday devices, there is something on the
horizon that will be difficult to miss. The
European Southern Observatory, a 15-nation
organisation that funds observatories in Chile,
has approved construction of the European
Extremely Large Telescope. When it becomes
operational in the early 2020s, it will be the largest
optical telescope in the world, boasting a primary
mirror nearly 40 metres across.
Just as important will be its adaptive optics
system, which is likely to include two deformable
mirrors and multiple laser guide-stars. Without
these, the telescope would be an expensive folly.
With them, it will be able to track down Earth-like
planets orbiting nearby stars, and study galaxies at
the edge of the known universe. We don’t yet
know what these stars and galaxies will tell us
about our place in the universe. But one thing is
for sure: thanks to adaptive optics, nothing will be
twinkling.
23 | Science Writing Prize 2013: The shortlist
Wellcome Trust Science Writing Prize 2013
What’s so funny?
Yingying Jiang
What causes irregular breathing, is highly
contagious and can start an epidemic? No, not a
new strain of bird flu, but something much more
pleasant: laughter.
Whether it’s the chortling of a baby in a pushchair,
a group of giggling teenagers on the bus or a
hearty belly laugh in the office as someone cracks
a joke, we laugh and hear laughter every day. But
for a behaviour that is so easy and natural, it raises
some intriguing questions that scientists don’t yet
fully understand: Why do we laugh? Are laughing
individuals ‘fitter’ for survival? Why does the sight
of strangers in hysterics set us giggling too? Just
what is so funny?
Why we laugh seems obvious at first – it’s because
we find something amusing. However, the next
time you are out among groups of people, listen
carefully to when they actually laugh, and you
might notice that laughter and humour are not
inseparable. In a study of laughter, Robert
Provine, professor of psychology and neuroscience
at the University of Maryland, Baltimore County,
recorded hours of real conversations in public
places. From 1200 ‘laugh episodes’, he found that
only 10 to 20 per cent of laughs followed what
seemed like attempts at humour. The majority of
chuckles were generated by completely banal
statements like ‘I’ll see you guys later’ and ‘I think
I’m done’. Are we just being polite when we titter
at these non-witticisms?
After his initial study, Provine soon realised that
the essential ingredient of laughter is not a punch
line but another person. Laughter is a social
24 | Science Writing Prize 2013: The shortlist
activity. In the absence of anything that tries to
make us laugh, like a film comedy or a stand-up
routine, we are 30 times more likely to laugh when
we’re in company than when alone. You might
think that your laughter is solely a form of
self-expression, but in fact it serves a more
fundamental purpose. It elicits positive feelings in
other people. Brain scans have revealed that the
sound of laughter triggers a response in the part of
our brain that is activated when we smile, thus
priming our facial muscles for laughter. Just as we
yawn when others yawn, we also feel the urge to
laugh when we see other people laugh. Laughter is
highly contagious. Just search for ‘laughing
weatherwoman’ on YouTube and try to keep a
straight face.
A common misconception about laughter is that it
is unique to humans, but a look at our ape
relatives would suggest that the human laugh
might be an echo of the chimpanzee chuckle. To
investigate the origins of laughter, psychologist
Marina Davila-Ross and her team at the
University of Portsmouth conducted what might
just be the greatest experiment in the world:
tickling primates.
Juvenile orang-utans, chimps, gorillas and
bonobos, as well as humans, were tickled in the
armpits, palms and feet for their reaction. DavilaRoss found that the apes responded in the same
way as human children when being tickled:
squirming and vocalising laugh-like sounds. For
example, a chimp’s laugh is rapid and breathy,
which has been dubbed ‘play-panting’. Though the
vocalisation was different between species,
Wellcome Trust Science Writing Prize 2013
probably due to anatomical differences, this
variability matched the well-established genetic
relationship between them, suggesting that our
laughter comes from the last common ancestor of
great apes and humans.
It’s easy to understand why natural selection
might favour individuals with a strong fight-orflight response, but what might be the
evolutionary advantage of laughing? According to
Jaak Panksepp, a neuroscientist and psychologist
at Washington State University, primal laughter
could have evolved as a ‘signalling device’, giving
an honest indication of an individual’s emotional
health, just as a peacock’s tail feathers indicate
physical health. Laughter can be used to show
readiness for friendly interaction, as well as to
defuse tension.
Panksepp also believes that laughing animals may
have appeared more attractive to the opposite sex,
since laughter indicates a positive temperament,
leading to interaction and ultimately to
reproduction. On a less positive note, mocking,
jeering laughter towards outsiders can be used to
reinforce a group’s solidarity – the difference
between laughing with and laughing at someone.
Laughter is therefore a vital social lubricant,
fostering a sense of group unity while
maintaining a subtle status hierarchy, both of
which could have been especially important for
small groups of early humans.
25 | Science Writing Prize 2013: The shortlist
The human brain is still a complex puzzle. With
the development of higher cognitive functions,
the repertoire of things that trigger our laughter
has increased since our ancestors’ time. Although
humans may have the last laugh in the
evolutionary sense, we still have a long way to go
to fully understand the mystery of laughter.
Wellcome Trust Science Writing Prize 2013
A critique of sadness
Pamilla Kaur
Signs of heartbreak, loss or any other form of
emotional pain that sends your lacrimal glands
into overdrive, emotional tears are unique to
humans. You won’t come home to find your dog
having a breakdown to a Celine Dion CD, or turn
to see your cat’s eyeballs secreting tears when Rose
lets go of Jack in Titanic. Even though animals can
experience sadness, they don’t produce tears like
we can, in response to films or music for example,
and that’s pretty crucial.
Charles Darwin was one of the first scientists to
investigate crying by studying animals such as
Indian elephants, but he never once saw them
emotionally tearing or met anyone who could
testify to such an event. Like us, animals produce
tears as a reflex to foreign bodies that enter the
eye, such as dust particles, which makes sense: an
enzyme in tears is essentially the Pac-Man of the
biology world, engulfing bacteria to maintain the
health of the eye. However, why should sad
situations from films to funerals cause humans to
reach for the tissues too? What is it about sadness
that can make us produce the same teary response
as to a physical irritant?
Research in this field is sadly lacking. It could
provide us with some fundamental information
about the behaviour of humans but, considering
the complex neurological stimulation involved, it’s
no wonder scientists still find the process of crying
to be elusive.
Nevertheless, scientists are trying, and some of the
most interesting research is the result of seemingly
bizarre methods. A study by Israeli scientists from
26 | Science Writing Prize 2013: The shortlist
the Weizmann Institute of Science involved
bottling tears produced by women welling up over
a sad film, then asking male test subjects to inhale
the vapour. The men’s testosterone levels
decreased as a direct result of inhaling the tear
vapour, suggesting tears are a chemical signal of
sadness.
Subsequently, other scientists have theorised
about the evolutionary significance of this. Lower
levels of testosterone reduce the amount of anger
and arousal a male feels. Perhaps, as humans
evolved to live in social groups, the chemical signal
released by crying allowed other humans,
especially men, to protect those who were more
vulnerable.
As well as a chemical signal, tears are physical
signs of sadness. Studies at the University of
Maryland showed that viewing images of crying
faces with the tears Photoshopped out didn’t
generate the same level of empathy in their test
subjects as images with the tears in. This shows it
is the actual tears that are perceived as a signal of
sadness, not just the crumpled, dissolving facial
expressions that act as a fleshy canvas for your
salty tears.
Probably the most familiar role of tears is to
provide a sense of relief. There is a lot of scientific
debate on whether crying provides a feeling of
calmness. On the one hand, nervous activity has
been shown to increase with tears. However,
anyone who’s ever sobbed their heart out after a
bad day will know the comforting feeling of
contentment after having a good cry. So some
Wellcome Trust Science Writing Prize 2013
scientists (maybe those who have had a bad day
recently) do believe tears can be interpreted as an
evolutionary coping mechanism to expel pent-up
emotions through stress hormones and toxins, as
well as to express our feelings to others. It’s not
hard to see how this could have been particularly
useful before the evolution of human language:
watching someone cry is powerful in itself.
What is clear, though, is that research in this field
is helping scientists understand more about how
we behave. So the next time Jack and Rose reduce
you to a snivelling, slobbering mess, remember
that it’s because complex and fundamental
biological processes are at play, that potentially
evolved to protect you from danger.
27 | Science Writing Prize 2013: The shortlist
Wellcome Trust Science Writing Prize 2013
Blurring the line between life and death
Fergus McAuliffe
How clear is the line between life and death? At
first glance, the distinction seems quite clear. We
all have a beating heart – it is what keeps us alive.
If your heart stopped beating, you’d be in cardiac
arrest. This would, left untreated, lead to your
death.
When spring begins and the temperature rises,
something remarkable happens. The frogs begin
to thaw out. Their hearts start to beat again, and
their lungs start to breathe. In a matter of hours
the wood frog is hopping around like nothing
happened.
But what if an animal didn’t need a beating heart
to be alive?
So, if a wood frog can do this, why can’t we? When
the cells in our bodies begin to freeze they
dehydrate. Water is sucked out of the cells and
freezes in the area around them. With less water
inside them to provide shape and structure, the
cells collapse, split and die. Even if these cells thaw
out they can no longer function. It is this
mechanism that kills human fingers and toes in
severe cases of frostbite.
To explore this question we must go on a journey
all the way to the cold, dark forests of northern
Canada. This isn’t a story of fantasy or of fairytale,
but it does involve a frog. Each winter the wood
frog (Rana sylvaica) blurs the line between life and
death as it hibernates.
Unlike humans, frogs are cold-blooded. Their
body temperature closely follows the temperature
of their environment. The wood frog is the only
species of North American frog that lives north of
the Arctic Circle. It has evolved in such a way that
it can survive this freezing environment.
As the temperature drops below zero degrees
Centigrade at the onset of winter, the wood frog
starts to freeze. First its skin cells freeze, then its
legs. Next is the chest, head and – finally – the
heart. The wood frog has no heartbeat or pulse
and exists in cardiac arrest. It stays in this deathlike state for weeks at a time. With up to 70 per
cent of their bodies frozen solid, these amphibians
are so inanimate that they don’t even respond to
the kiss of a princess.
28 | Science Writing Prize 2013: The shortlist
Rather than migrating to avoid the cold weather,
like so many other animals do, the wood frog has
evolved a safety mechanism to elude the lethal
effects of freezing. This mechanism has become
the focus of research by Professor Ken Storey and
Janet Storey of Carleton University, Ottawa,
Canada. Through years of observation and
experimentation, the Storeys have elucidated
many of the biological pathways that the wood
frogs use to enable them to freeze and thaw.
When frogs begin to freeze, their organs start to
dehydrate. Water lost in this way freezes in the
frog’s internal spaces such as the abdominal cavity.
By ensuring that water freezes in these spaces and
not around the cells (as in humans), the frogs limit
the damage to their organs caused by ice crystals.
Wellcome Trust Science Writing Prize 2013
But why don’t the dehydrated cells in the frog die?
As water leaves the cells it is replaced with a simple
sugar, glucose, that the wood frog makes in its
liver. This glucose combines with the remaining
water inside the cells to form a natural sugary
antifreeze, or cryo-protectant, which keeps the
cell’s vital machinery from freezing. While up to
70 per cent of the water in the wood frog is frozen
solid in cavities, the crucial parts in the inside of
the cells are protected and retain their function.
While preparing to hibernate, the wood frog starts
making extra glucose in its liver. Its forward
planning is so good that glucose levels can be up to
40 times higher at the moment of freezing onset
than during the summer. While these high levels
of glucose would be toxic to human cells, this is
not the case with the wood frog. In the spring,
when the frog thaws out, water re-enters the cells,
which then resume their normal function. The
glucose is removed and excreted from the body in
sugary urine.
This freeze–thaw adaptation allows the wood frog
to survive, not by avoiding the cold but by
embracing it. This small creature – no longer than
two inches in length and found only in North
America – challenges our understanding of what it
means to be alive: the beating heart. This is how
the wood frog is blurring the line between life and
death. Not by freezing to death, but freezing to
live.
29 | Science Writing Prize 2013: The shortlist
Wellcome Trust Science Writing Prize 2013
Let there be light
Kate McAllister
The most scientific thing most people would
associate with flickering office lights would
perhaps be the direct correlation between
flickering and expletives uttered. As it turns out,
however, the strip lights barely illuminating my
workspace might also be having some sinister
effects on my physiology.
A growing area of science known as chronobiology
is beginning to understand how light is involved
in almost everything, from how we feel to how we
age. We are evolved to sleep when it is dark and to
be alert in the day. Scientists have known for
decades that our daily cycle, or circadian rhythm,
is carefully controlled by internal timers. The
master clock, the suprachiasmatic nuclei or SCN,
is found deep in the ancient parts of our brains.
The ticking over of this internal clock is entwined
with external cues, which scientists refer to as
zeitgebers, or time givers. For almost all animals,
the main zeitgeber is light – bright sunshine is our
cue to leap out of bed and get to it. If we don’t get
enough light our physiology is knocked out of
whack, impacting on everything from urine
production to body temperature.
Families of people with dementias and other
degenerative diseases won’t be surprised to hear
that disrupted sleep is one the primary reasons
that patients have to be taken in to residential
care. Daytime napping and disrupted sleep
through the night are distressing and disorienting
for families and patients alike. Circadian rhythm
disruption has also been associated with
‘sundowning’, the tendency for people with
dementia to experience confusion, mood swings
and agitation through the evening.
30 | Science Writing Prize 2013: The shortlist
Our circadian rhythms change as we age, with
sleep abnormalities common in the elderly
population. In older life we are less likely to spend
time outside in natural sunlight (for a number of
reasons such as less social opportunities and
increasing frailty). For some, this is aggravated by
age-related deterioration in the eye. Cataracts and
glaucoma, which are common in the elderly and
even more so in dementia patients, further
obscure light getting to photosensitive cells.
Visiting an elderly relative with Alzheimer’s
disease in a residential care home I was always
struck at the dimly lit corridors, the dark rooms,
the tiny windows. I had suspected that the lack of
natural light didn’t do much for his spirits, but it
didn’t occur to me that the constant time indoors
with just the faint glow of the television may
actually have been doing harm.
Speaking at the 2012 Cambridge Science Festival,
Professor Russell Foster from the University of
Oxford explained that nursing homes typically
have a light level of around 20 lux during the day
(a bright sunny day would be around 100 000 lux).
Add ocular problems, such as cataracts, and you
can see why people in residential homes struggle
to maintain healthy sleep–wake rhythms.
Considering that disrupted sleep can lead to
cognitive problems, reduce wellbeing and increase
irritability, the consequences of low light become
clear.
In recent years, bright light therapy – sitting with
a box emanating very bright light – has been
trialled with Alzheimer’s disease patients. Light
therapy has been shown to positively influence
Wellcome Trust Science Writing Prize 2013
fragmented sleep–wake cycles in some
participants. And there is theoretical science to
support it. The light box increases the intensity of
stimulation to the SCN, via the retinohypothalamic tract, a corridor of brain cells
linking the eye to the hypothalamus. Strikingly,
bright light therapy has also been shown to reduce
agitated behaviours in dementia. Such steps,
although not disease-modifying, are crucial to
lessening the burden of the disease on both
patient and carer.
Encouragingly, it appears that the importance of
chronobiology is being taken more seriously in a
wide range of areas, including architecture. Better
lighting in hospitals has been shown to impact on
recovery rates of patients and further research
studies are investigating how substantial this
effect is. Electronics giant Philips have recently
created an in-hospital lighting system to improve
the levels of daytime light, incorporating a
two-hour light boost in the mornings that they
claim supports healthy sleep. How this will impact
patients in the long term remains to be seen.
Chronobiology is a growing field in science, but
like much of biomedicine, there is much yet to be
understood. One thing is for certain, though: the
average light level in an office is around 400 lux,
and that’s not high enough to entrain my SCN.
This strip light will have to go…
31 | Science Writing Prize 2013: The shortlist
Wellcome Trust Science Writing Prize 2013
Termites and intelligent living buildings
David Parr
Life can be hard to define. A traditional biological
definition is structures of organised cells that eat
in order to grow, adapt, react, maintain and
regulate their internal state, with the capacity to
reproduce. Sometimes, though, organisms need to
maintain and regulate the climate outside of their
own bodies. Termites in Nigeria, for example,
have trouble surviving when exposed to the
normal conditions of their native land. For a
species famed for its animal architecture, it is
often overlooked that the grand form actually
follows vital function. Termites even build tunnels
to move through when foraging outside the nest
in order to maintain their own requirements for
temperature and humidity.
that the structure promotes gas exchange through
enhanced diffusion in the finest tunnels, not just
as a bulk flow of buoyant air, in the same way that
gas movement occurs in the alveolar ducts. He
told Pearce: “It was only when I began to see
things as a process... and not an object that I began
to understand how it worked. It is all physiology.”
Pearce himself cites this as a turning point in his
outlook: “We should try to see things in nature
not as objects and copy their form, but as
processes and systems”.
Mick Pearce watched this story of design and
survival unfold through a David Attenborough
documentary. The iconic chimneys and galleries
of termite nests led him to design the Eastgate
Centre, a large retail/office structure built in
Harare, Zimbabwe, in 1996. By learning from
nature, a technique now called biomimicry, his
design team built one of the most sophisticated
green buildings of the time. The design links
thermal mass and ventilation, and responds to the
local climate. It maintains and regulates its
internal state and reacts to stimulus, core
principles of life.
Turner and Soar’s resulting paper, ‘Beyond
Biomimicry’, proposes that the mound is not a
static, isolated structure, but the lungs themselves
of a macro-organism; the termites are analogous
to cells in a larger, cohesive whole, surrounded by
the nest as a second skin. Current building design,
they argue, sees the building fabric as a barrier
separating internal spaces from the outside world.
However, as the internal space needs air, light and
heat to function, these things are then ‘bolted on’
in air conditioning and electric lights. Living
systems, however, resolve this paradox by seeing
membranes as “adaptive interfaces, where fluxes
of matter and energy across the wall are not
blocked, but managed by the [structure] itself”, a
statement they see as true for termite mounds as
well as for human skin.
Three years ago, Scott Turner and Rupert Soar
made contact with Pearce. They were also
learning from termites and were intrigued by
Eastgate. As the conversation developed, Turner
shared his view of termite nests: that the central
structure may operate not just as a chimney, but
in a way much closer to human lungs. He believes
Soar works in 3D printing and material science,
and his current project is seeking to develop
‘intelligent’ buildings. The ability for a building to
grow and adapt is yet to be realised; yet again
termites have got there first. They are constantly
‘tuning’ their structure – by acting as the senses of
the wider macro-organism, they continually
32 | Science Writing Prize 2013: The shortlist
Wellcome Trust Science Writing Prize 2013
assess the conditions of the nest, adding and
removing material in an attempt to balance the
internal requirements against a range of everchanging external conditions. This is the growth
and adaptation portion of defining a living
building. It could be argued that our buildings
already achieve this. We add extensions if we want
more space, we open windows for more air, but in
reality we are very bad at this, and especially at
doing this for the lowest energy costs. The
Eastgate Centre was extensively tuned over a
period of years by the design team in order to
achieve the best balance between energy usage
and the required internal conditions.
Soar’s new challenge is to create a building that
grows and adapts itself, without relying on human
decision-making and action, and he is looking to
the final part of the definition of life to solve this:
genetics and reproduction. Together with Julian
Vincent, Soar is developing a framework based on
DNA that can ‘evolve’ a building from information
on the intended usage and location. The building
form and materials would be derived from
computer algorithms, and manufactured using
new 3D printing tools. Further, the building would
be adaptive, forever refining itself through
multiple iterations by tuning its structure to a
minute scale in response to its self-monitoring
processes. If successful, this project could be the
next step to a living building, an achievement
already 20 years in the making, but one which
termites have been doing for centuries.
33 | Science Writing Prize 2013: The shortlist
Wellcome Trust Science Writing Prize 2013
The skeleton key
Emma Pewsey
I love you to your bones.
That might be a bit forward, but I make no
apologies. Bones are brilliant. Unlike buildings,
which are over-engineered to cope with extreme
events, bones react to the forces that you impose
on them to give you exactly the strength you need.
Every time you go for a walk, you make your bones
stronger. As your foot hits the ground, the stress
sent through the bones supporting you stimulates
cells called osteoblasts. These then lay down the
foundations for new bits of the hard, supportive
outer shell of calcium-containing minerals that
coat your bones.
Swap your walk for a week in bed and your bones
will become measurably weaker. With bone, it’s
use it or lose it.
But why do bones weaken? Well, your skeleton
doesn’t only support your body physically. Bones
are also the body’s 24-hour one-stop calcium shop.
Calcium is crucial not just for keeping bones
strong, but also for generating the electrical
signals that keep the heart beating and your
muscles moving. So drinking that glass of milk
won’t just keep your bones strong, it will keep your
heart beating too!
To release the calcium, another group of cells
called osteoclasts swing into action. These break
down the hard surface of the bone, expelling the
minerals into the bloodstream. This also has
benefits for the strength of your skeleton. Tiny
cracks, shorter than the width of a hair, form in
your bones as part of everyday activities. A sudden
34 | Science Writing Prize 2013: The shortlist
shock can turn these cracks into fractures. The
work of the osteoclasts therefore cleans up these
fragile regions so the osteoblasts can replace them
with fresh, strong bone.
So the magic of bones comes from this careful
balance of destruction and renewal processes,
which ensures your skeleton is the most perfectly
adapted structure on Earth. Unfortunately, trips
into space present new problems.
Astronauts lose 1 to 2 per cent of their bone
density every month they’re in space. This bone
loss can be partially reversed when they’re back on
Earth, but even a year after they’ve returned, their
bones still won’t be back to full strength.
You might think that losing bone density in space
would be an expected consequence of being in
microgravity. With fewer forces acting on the
skeleton there will be less stimulation of the
bone-forming osteoblasts. However, in space bone
formation continues more or less normally.
Instead, bone destruction speeds up.
Weaker bones aren’t the only consequence. The
calcium released from bones has to go somewhere
– astronaut pee. Processing this extra calcium
puts astronauts at an increased risk of kidney
stones – a particularly painful prospect halfway to
Mars. It damages equipment too. The drink of
‘choice’ in space is processed urine. However, the
Urine Processing Assembly on the International
Space Station needed emergency repairs in 2009
after the high calcium concentrations flowing
through it formed a scale which blocked it.
Wellcome Trust Science Writing Prize 2013
So what can be done to keep astronaut bones
strong, and space toilets flowing freely? This is
where life on Earth and life in space help each
other out. Osteoporosis has a similar boneweakening effect as space travel, though six times
less severe. Research into preventing osteoporosis
can therefore help astronaut bones, and vice versa.
There are currently two big weapons used in the
war against weak bones. The first is exercise.
Weight-bearing exercise stimulates osteoblasts to
form new bone, and has been shown to be an
effective treatment for osteoporosis. Space
agencies are well aware of this, and have developed
a range of complicated-looking exercise
contraptions for astronauts to strap themselves in
to. However, despite years of research these aren’t
quite perfect, and astronauts still return to Earth
with weaker bones.
The second weapon is another straightforward
piece of health advice. Health’s current bad boy is
sodium chloride – common table salt. Eating too
much salt may cause a grim-sounding condition
called acidosis, where the fluids in your body
become more acidic. To neutralise this acidity,
more calcium is released from your bones,
weakening them.
35 | Science Writing Prize 2013: The shortlist
It turns out that the highly processed nature of
space food means the average astronaut consumes
twice their recommended daily allowance of salt.
So is cutting down on salt the key to lessening the
misery of brittle bones in space (and of cleaning
blocked-up space toilets)?
It’s a possible solution that’s being investigated,
but since your sense of taste is dampened in space,
reducing salt risks making astronauts unhappy as
without it, food becomes even blander.
On Earth we have more choice over what we eat.
So support your bones by reducing your salt
intake. After all, they support you in more ways
than you might think.
Wellcome Trust Science Writing Prize 2013
The new ‘balanced’ diet
Maliah Roshan
Imagine being able to guzzle just exactly what you
want, and as much as you fancy, with no negative
consequences. No more limiting yourself to a
small pack of crinkle-cut cheddar crisps that
vanishes in a few seconds: now you could scoff a
family-sized pack, no worries. All you’d have to do
to achieve this calorific nirvana is override those
problematic calories with some more beneficial
ones. It sounds like wishful thinking, yet a recent
spate of nutritional research publications is
showing how it might be done.
Groups of researchers from the US to China have
fed rats, mice and hamsters the sort of high-fat,
high-sugar diet guaranteed to lead to obesity,
clogged arteries and diabetes. However, they
found that the animals could largely be saved
from such a fate if they were supplied with some
other specially selected nutrient that appeared to
counter the damage. Extracts of chokeberries,
peanuts, turmeric and chickpeas are just some of
these, and the list of nutrients capable of
offsetting unhealthy foods or even lifestyle is
constantly expanding.
Coffee, for example. American researchers
conducted one of the largest surveys on the effects
of coffee consumption on mortality, by following
over 400 000 US citizens aged over 50 across 13
years. The coffee drinkers in the study were
generally an unhealthy bunch of couch potatoes
compared to non-coffee drinkers. They were more
likely to smoke, take no vigorous physical exercise,
consume a lot of alcohol and eat more red meat,
while eating very few fresh fruits or vegetables.
They also had lower levels of education, which is
known to lead to poorer health.
36 | Science Writing Prize 2013: The shortlist
The coffee drinkers had higher rates of mortality,
but once these relevant lifestyle details were taken
into account the scientists found something
surprising: coffee was actually protecting people
against a broad range of illnesses ranging from
stroke and lung diseases to infections and
diabetes. And the more coffee they consumed the
more protection they got: 10–15 per cent lower
mortality in coffee drinkers who downed six cups
a day.
This counters our usual assumptions about
caffeine – all that caffeine surely can’t be good for
us? In fact, the caffeine in coffee does cause a spike
in blood sugar levels and therefore also insulin –
definitely unhealthy over the long term. And yet
coffee drinkers are less likely to develop diabetes
than non-drinkers.
How? It would appear there is a sort of offsetting
effect at work here. The clues behind this lie in the
components found in coffee, and in the selected
nutrients used in the animal studies mentioned
earlier.
Coffee is rich in chlorogenic acids, which are
potent antioxidants (molecules that mop up
unstable oxygen and other such molecules). These
have been shown to lower blood pressure in both
healthy and mildly hypertensive people. Roasted
coffee extracts activate antioxidant elements in a
number of genes, protecting cells from the sort of
oxidative stress associated with inflammatory
processes such as those found in diabetes. In fact,
one of the key players in that process, NF-κB, is
blocked by caffeic acid, formed when chlorogenic
acids are broken down in the intestine.
Wellcome Trust Science Writing Prize 2013
Chokeberries are also very high in antioxidant
molecules, such as anthocyanins and flavonoids,
and, like coffee, these appear to counter an
unhealthy diet. When rats were fed a diabetespromoting high-fructose diet, as well as gaining
weight they showed the metabolic markers
typically seen in the run-up to developing diabetes
and heart disease. However, those rats who were
given an additional chokeberry extract gained less
weight and showed fewer of the pre-diabetes
signals. Analysis of the rats’ gene expression
showed that the chokeberry extract was blocking
the expression of genes involved in inflammation
and insulin signalling.
Another study using peanuts echoed some of the
results seen with the chokeberries. Hamsters on a
high-fat, atherosclerosis-inducing diet fed a
peanut extract were saved from the worst effects
of the diet. This can be explained by peanuts’ long
list of heart-friendly ingredients, from mono- and
polyunsaturated fats to high levels of ß-sitosterol,
known to reduce serum cholesterol levels, and
resveratrol, a broadly acting antioxidant that
results in improved insulin sensitivity and lessens
the risk of heart disease.
What coffee, peanuts and chokeberry extract have
in common is they all contain a cocktail of
ingredients including antioxidants that put a
brake at various stages in the processes leading to
obesity, insulin resistance and cardiovascular
disease.
37 | Science Writing Prize 2013: The shortlist
This suggests that if you love your food too much
and want to be able to have your cake and eat it,
you need to look further than having your five a
day. By selecting the right nutrients in the right
amounts you may be able to tip the balance of
healthy versus damaging foods in your favour. A
‘balanced’ diet may soon mean something quite
different.
Wellcome Trust Science Writing Prize 2013
Treating cancer with some help
from the brain
John Wilde
Just a sniff is all it takes. It’s that distinctive aroma
of tequila which, thanks to a foolish night in my
youth, leaves me feeling ill at even the slightest
whiff. My brain has gone through a process called
associative learning in which the smell and taste
of tequila has become linked with the presence of
alcohol, triggering a physiological response which
leaves me feeling rather off-colour. This isn’t a
problem for me – thankfully I don’t need tequila.
But what about cancer patients and
chemotherapy?
Anticipatory nausea and vomiting (ANV) is a
well-documented phenomenon in oncology and
can be incredibly debilitating. Around 25–30 per
cent of patients experience severe nausea and
vomiting when they enter the chemotherapy clinic
following just one treatment session. It can be so
severe that some patients will opt to end their
therapy before they have had sufficient doses to
have any beneficial effect, while those who do
continue with their treatment must endure
several horrible hours each time they return for a
round.
But how and why does this happen?
The side-effects of chemotherapy occur due to the
defence mechanisms of the body: chemotherapy is
a cocktail of poisons which the body tries to avoid
by inducing nausea and vomiting. These
unpleasant side-effects still arise despite drugs
used to combat them. In associative theory this is
an ‘unconditioned response’ as it is a direct cause
of the chemotherapy treatment, the
‘unconditioned stimulus’. In ANV the entire
38 | Science Writing Prize 2013: The shortlist
clinical context (the smell of the clinic, the
location, the décor and even the nurses
themselves) becomes associated with the
unpleasant effects of chemotherapy. The result of
this is that exposure to the clinical context alone
is enough to generate the feeling of illness.
One potential intervention is ‘stimulus
scapegoating’. This uses associative theory to
prevent the association from forming. A key
element in associative learning is that an event
(e.g. chemotherapy-induced illness) becomes
linked with the stimulus most easily identified
from a group of stimuli. Scapegoating uses this
principle by introducing a new, attentiongrabbing stimulus to overshadow the clinical
context. This is usually done using a strong
flavour that is new to the individual.
This idea has proven effective in animal studies
conducted by Michelle Symonds and Geoffrey
Hall at the University of York. Rats were given
either a sour flavour or water while being trained
to associate nausea and a distinct context. The
rats given the sour flavour were happier to drink a
sucrose flavour, compared to control rats given
water, when they were returned to the training
context. This indicates that the rats associated
nausea with the sour flavour as opposed to the
context.
This effect has also been demonstrated in
humans. Ursula Stockhurst and her team at the
University of Düsseldorf found that when cancer
patients were given a novel fruit juice as an
overshadowing stimulus, there were no cases of
Wellcome Trust Science Writing Prize 2013
ANV, whereas the control group given water
produced two.
Scapegoating and its potential uses are still being
investigated, with studies by Friedemann Geiger
and Levke Wolfgram in Kiel, Germany, due to
begin in 2013. Their study will use 52 newly
diagnosed paediatric cancer patients to examine
the effectiveness of the scapegoating procedure
using flavoured or tasteless sweets.
The results could further prove how simply
adding a distinctive flavour could vastly improve a
patient’s quality of life by making their time
before sessions more palatable. Moreover, there is
some evidence that the benefits of scapegoating
may extend even further. Stockhurst and
colleagues’ study also found a beneficial effect in
reducing nausea and vomiting after chemotherapy
treatment, as well as before it. Stockhurst thinks
this may be because the patient records nausea
and vomiting in the same context as that of the
treatment, causing an interaction between the
conditioned side-effects and those actually caused
by the drugs. By removing the conditioned nausea
using the scapegoating intervention, the patient
has a reduction in overall feelings of nausea and
illness. If this proves replicable and usable in the
clinic then it could lead to a reduction in the
number and dosage of anti-nausea drugs, which
have their own side-effects, that patients need to
take.
39 | Science Writing Prize 2013: The shortlist
Cancer is on the rise in the developed world; 1 in 3
people will be affected by it at some point in their
lives. Thankfully our growing understanding of
psychology should allow us to make its treatment
less unpleasant. Maybe one day all chemotherapy
treatments will come with drink, although be sure
it’s not something you’re partial to.
Wellcome Trust Science Writing Prize 2013
Windows into the mind
Rebecca Winstanley
Throughout history, people have imagined that
the eyes are the windows into the soul. Most of
these people could not have envisaged the modern
methods putting this philosophy to the test. Over
the past few decades, advances in eye-tracking
technology have transformed psychology: tiny
changes in the speed and direction of eye
movements can reveal profound insights into the
inner workings of the brain.
For example, observing eye movements can reveal
the extent to which we are aware of other people’s
perspectives. To investigate this, a team of
researchers at the University of Queensland used
the famous Sally–Anne paradigm: participants see
Sally placing a ball in a box and leaving the room.
Following this, Anne (the villain of the story)
hides the ball in a different box. While we know
the ball is no longer there, most of us recognise
that Sally, when she comes back into the room,
will look for it in the original box.
Even when the participants were distracted by
another task and not consciously paying attention
to the actors, their eye movements still identified
with the belief state of the Sally character –
participants looked sympathetically towards the
first box. The researchers dubbed this ‘implicit
mentalising’.
The same test has helped shape our
understanding of when young children learn to
deduce the views of those around them. Children
under the age of three typically fail in tasks that
test for a ‘theory of mind’ – that is, the ability to
recognise that the views of others are different to
your own. However, recent studies have
40 | Science Writing Prize 2013: The shortlist
demonstrated that when children between 6 and
18 months view a Sally–Anne video, they
preferentially look towards Sally’s box even when
the ball is no longer there. The finding that a
theory of mind may exist in an implicit form
earlier than believed not only brings exciting new
challenges to the field of developmental
psychology, but suggests eye movements could
potentially be used as an early-age diagnostic tool
for autism spectrum disorders, where theory of
mind abilities are impaired.
When we see other people moving, our brains
unconsciously generate ‘motor plans’ to perform
the same action, but we generally inhibit these
plans and prevent any actual movement. A study
published earlier this year revealed that watching
videos of dancers improved the control of eye
movements in individuals with Parkinson’s
disease. The study’s authors suggest that by
watching the dancers, participants formed and
inhibited dance-related motor plans. Inhibiting
this movement then strengthened their ability to
control more automatic movements in subsequent
tasks. If true, this may be used to develop
therapies to help people with Parkinson’s disease
maintain more control over the movement of their
bodies.
Studying eye movements has also shed light on
how memory is organised in the brain. It is well
documented that generating sequences of rapid
eye movements before trying to remember
something considerably enhances recall for things
like lists of words, childhood memories, details of
stories and visual landmarks.
Wellcome Trust Science Writing Prize 2013
The left and right hemispheres of the brain are
connected by a bundle of nerve fibres called the
corpus callosum – this is crucial for
communication between the two sides of the
brain. Cognitive psychologists have confirmed
that activities which stimulate the corpus
callosum can, in turn, bolster memory. Because
the right hemisphere controls movement in the
left eye and the left hemisphere the right eye,
sequences of rapid eye movements actively
stimulate the corpus callosum, which may help
the successful encoding and retrieval of
information.
Whether it’s in the processing of everyday
information or in simple ways to improve day-today functioning, when it comes to the inner
workings of the brain, our eyes are surprisingly
telling.
41 | Science Writing Prize 2013: The shortlist
Wellcome Trust
We are a global charitable foundation dedicated to
achieving extraordinary improvements in human and
animal health.
We support the brightest minds in biomedical research
and the medical humanities. Our breadth of support
includes public engagement, education and the application
of research to improve health.
We are independent of both political and commercial
interests.
Wellcome Trust
Gibbs Building
215 Euston Road
London NW1 2BE, UK
T +44 (0)20 7611 8888
F +44 (0)20 7611 8545
E contact@wellcome.ac.uk
wellcome.ac.uk
The Wellcome Trust is a charity registered in England and Wales,
no. 210183. Its sole trustee is The Wellcome Trust Limited, a company
registered in England and Wales, no. 2711000 (whose registered office
is at 215 Euston Road, London NW1 2BE, UK). MC-5686.18/12-2013/JS
42 | Science Writing Prize 2013: The shortlist