australasian science - may 2016
TRANSCRIPT
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8/17/2019 Australasian Science - May 2016
1/52Interview with Brian Schmidt • Human Gene Editing Fails • Why Are Bigger Offspring Better?
Gene for Speed • The Psychology of Trump • The Truth about Sugar • Functional Neurology • Viruses Warm to Climate
Volume 37 | Number 4
MAY 2016 | $9.95
How to Test yewitness Reliability
How Obesity Suppresses Satiety Signals
iet used by bodybuilders alters
g lu co se me tabo lism to a llev ia te
chizophren ia
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MAY 2016 | | 3
CONTENTS
18
4
7
3
FEATURES
14 A Diet that Calms the Schizophrenic MindThe ketogenic diet favoured by bodybuilders also normalises
schizophrenia-like behaviours.
18 How Reliable Is an Eyewitness?Eyewitness identification of criminals is notoriously unreliable, but a
new study based on police records has identified factors that can
determine which witnesses are accurate and which are guessing.
21 The Stomach as a Target for ObesityObesity permanently changes the way our body processes
gastrointestinal signals about satiety. While appetite suppressants
have had limited success, the identification of an appetite-regulatingnerve channel offers a new approach to keeping weight off.
24 A Gene for SpeedA gene that may have enabled ancient humans to spread to colder
climates may also be the difference between power athletes and the
rest of us, and play a role in muscle diseases.
27 About SchmidtNobel Prize winner Brian Schmidt discusses global warming, exploding
stars, politics and Star Wars with JAY FURBY.
31 Why Are Bigger Offspring Better?Bigger offspring have greater energy needs, so why do they survive
and reproduce more successfully than their smaller siblings?
34 Generation MultiAs technology continues to become more richly embedded in our daily
lives, so too comes the increased demand and temptation to
multitask. But can we improve our ability to do two things at once?
36 Plant Viruses Threaten Crops as Climate Warms
Climate change will exacerbate the spread of a virus that reduces theyield of infected wheat by 70%.
conSCIENCE
38 Mega-Banks Unleash an Infrastructure TsunamiThe rise of investment bank lending for infrastructure projects in
developing countries is driving a “feeding frenzy” of developments
with lower environmental controls.
39 Stem Cell Industry Must Tread a Fine LineThe emerging stem cell industry needs to be able to fast-tracktherapies into clinical trials without clearing the way for clinics to offer
unproven therapies to vulnerable patients.
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4 | MAY 2016
CONTENTS
7
5
NEWS6 Browse
A round-up of science news from our shores.
COLUMNS5 Up Front
Can a sugar tax save us if obesity has already permanently suppressedthe satiety signals that tell us to stop eating?
40 Expert OpinionA second case of gene editing of human embryos has unsuccessfullyattempted to introduce resistance to HIV infection.
41 NeuropsyDonald Trump’s appeal to voters may be explained by a preference for authoritarian anti-establishment leaders.
42 The FitIs there something uniquely unhealthy about sugar above and beyondthe excess calories?
43 The Fossil FileAustralian museums don’t display any dinosaurs mounted from realbones into a life-like position.
44 Directions
Australia’s total net CO2 emissions are much lower than are implied bypublished numbers.
45 Out of this WorldAstronomers have found that Saturn’s moons may be younger thanthe dinosaurs, and may have seen a “baby Earth” forming.
46 The Bitter PillChiropractors claim that “functional neurology” can treat conditionsranging from epilepsy and Alzheimer’s disease to autism and stroke, butthe technology they use isn’t up to the task.
47 The Naked SkepticEven people who are rational about most matters can hold opinionsthat aren’t supported by science or even common sense.
48 EcoLogicInconsistent classification of species introduces systematic bias toecological studies.
49 Lowe TechInstallations of solar and wind energy will need to maintain their pace toensure that electric vehicles aren’t powered by fossil fuels.
50 QuandaryCases of sexual attraction are bound to grow as “genetic orphans”seek out their missing parents.
51 Australasian SkyYour map of the night sky this month.
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Obesity Is Winning the Hunger GamesCan a sugar tax save us if obesity has already permanently
suppressed the satiety signals that tell us to stop eating?
When I was at school I was incredulous at a health promotion campaign that urged people to find 30 minutes per day to exercise. I was a skinny, hyperactive kid who barely
had time to eat. I knew that adults had to work longer than schoolkids, but how could
they not find the time – or desire – to chase a ball for half an hour each day?
Fast forward to the present and we see many people using wearable devices to count
how many steps they take each day, as well as monitor other health parameters such as
heart rate and quality of sleep. We’re better educated about the food we should eat, and
have a wider range of healthier options available. And there’s no end of fitness equipment
and diet programs to order from the many “lifestyle” channels available 24/7.
Yet obesity rates have continued to rise, with the Victorian Health Department esti-
mating that about 80% of Australians will be overweight or obese within 9 years. This
is alarming not only because being overweight or obese is associated with cardiovascular
disease and diabetes, but also because obesity alters our metabolism permanently.
In this edition of Australasian Science , Dr Amanda Page of The University of Adelaide’s
Centre for Nutrition and Gastrointestinal Disease explains that the responses of vagal
afferent nerves in the gastrointestinal tract are significantly dampened in obese individ-
uals (see p.21), particularly where a high-fat diet has induced obesity. In these cases the
vagal nerves become less sensitive to stretching of the stomach, so the brain doesn’t
receive the signal that it’s time to put down the cutlery and step away from the table.
Page warns that dieting won’t correct this loss of our gastronomic self-control: the damp-
ened response to satiety continues even after an individual has lost weight and is no
longer obese. This would explain why dieters lose weight only to put it back on again.More encouragingly, Page’s group has identified a target for a pharmacological agent.
While these nerve channels are activated in pain-sensing nerves and are responsible for
the heat we experience when we eat hot chillies, they also play a role in satiety signalling.
Satiety is just one aspect of the battle of the bulge. As former hunter-gatherers we
have a primal urge to consume energy-rich sources of energy, so we shouldn’t be surprised
that Tim Tams are so addictive. Indeed, Australian scientists have now discovered that
drugs used to treat nicotine addiction can also stop sugar cravings (see Browse , p.7).
Sugar has become the current dietary villain, and the UK is introducing a sugar tax
to reduce consumption. Should Australia introduce one too? While Australian researchers
have found that a 20% rise in the cost of sugary drinks would save 1600 lives and prevent
thousands of heart attacks and strokes each year (http://tinyurl.com/hy4xr48), Prof TimOlds has reviewed the literature and found that sugar consumption has been falling for
15 years and the evidence against it is unconvincing (see The Fit , p.42).
We need to take matters into our own hands. If we can’t overcome the addictive
nature of sugar or restore our lost perception of when our bellies are full, we could do worse
than return to the advice given to Norm, the cartoon couch potato from my childhood:
find 30 minutes to exercise, or follow the Fitbit fad and take 10,000 steps each day.
Guy Nolch is Editor/Publisher of Australasian Science .
MAY 2016 | | 5
www.austscience.comEDITOR/PUBLISHER: Guy Nolch
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UP FRONT
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Cover StoryThe ketogenic diet is high in fiet and low in carbs, and must besupervised by a doctor. It is favoured by bodybuilders but newresearch has found that it also normalises schizophrenia-likebehaviours. Image credit: enterlinedesign/adobe
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Astronomers have captured the earliest minutes of two exploding stars, and for the first time seen a shockwave generated by a star’scollapsing core. “It’s like the shockwave from a nuclear bomb,only much bigger and no one gets hurt,” said Dr Brad Tucker of The Australian National University.
Stars explode when their fuel runs down and the core collapses.The resulting supernova explosion is brighter than the rest of itsgalaxy, and shines for some weeks.
Supernovae are so bright that they can be seen in distantgalaxies, but very little is known about the early stages of theseexplosions.
As the core of a supernova collapses to form a neutron star,energy bounces back from the core in the form of a shockwave thattravels at 30–40,000 km/s and causes the nuclear fusion that
creates heavy elements such as gold, silver and uranium.
T he n ew s tu dy , p ub li sh ed i n t he Astrophysical Journal (http://tinyurl.com/zfplud3), reports the explosions of two redsupergiants. The astronomers only saw a shockwave in the smallerstar, which has a radius 270 times that of the Sun. The shock- wave was observed as a peak in the light emitted from the explo-sion in the first few days.
While a shockwave could not be detected in the second star, alarge supergiant with a radius 460 times larger than the Sun, Tuckersaid that it must have existed. “The star was so large that the shock- wave did not travel all the way to the surface,” he explained.
The observation will help astronomers fine-tune their under-standing of how the size and composition of a star affects theearly moments of its death. “Supernovae made the heavy elements we need to survive, such as iron, zinc and iodine, so we are really
learning about how we are created,” Tucker said.
6 | MAY 2016
Increasing exposure to outdoor light can
stave off an “epidemic” of short-sightedness
among children, according to research
published in Investigative Ophthalmology &
Visual Science (http://tinyurl.com/hqynqu2).
A/Prof Scott Read of Queensland
University of Technology’s School of
Optometry and Vision Science said thatchildren need to spend more than an hour
and preferably at least 2 hours per day
outside to help prevent the development and
progression of myopia. Read explained that it
wasn’t “near work” on screens that caused
myopia, but a lack of adequate outdoor
light. While screens are leading children to
spend more time indoors than in previous
years, the research shows they are not the
direct cause of the increased incidence of
myopia.The QUT study measured children’s eye
growth, with study participants wearing
wristwatch light sensors to record light
exposure and physical activity for a fortnight
during warmer and then colder months to give
an overall measurement of their typical light
exposure.
“Children exposed to the least outdoor
light had faster eye growth and hence faster
myopia progression,” Read said.
In February the Brien Holden Vision
Institute predicted that half the world’spopulation will be short-sighted by 2050,
with 10% of the world’s population at risk of
blindness.
An Hour a Day Keeps Myopia at Bay
BROWSE
For the first time, a supernova shockwave has been observed in the visible spectrum as it reaches the surface of a star called KSN2011d. It took 14 days for the explosive death of this star to reach maximum brightness, but the initial shock breakout lasted only20 minutes. Credit: NASA Ames/W. Stenzel
Astronomers Glimpse Supernova Shockwave
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A Pill to Treat Sugar AddictionDrugs used to treat nicotine addiction could be used to treat sugaraddiction in animals, according to research from QueenslandUniversity of Technology.
“The latest World Health Organisation figurestell us 1.9billion people worldwide are overweight, with 600 million consideredobese,” said Prof Selena Bartlett of QUT’s Institute of HealthandBiomedical Innovation, who is corresponding author of the study published in PLOS ONE (http://tinyurl.com/jmolxof).
“Excess sugar consumption has been proven to contributedirectly to weight gain,” Bartlett said. “It has also been shown torepeatedly elevate dopamine levels, which control the brain’s rewardand pleasure centres in a way that is similar to many drugs of abuse,including tobacco, cocaine and morphine.
“After long-term consumption, this leads to the opposite: areduction in dopamine levels. This leads to higher consumption
of sugar to get the same level of reward.“We have also found that as well as an increased risk of weightgain,animals thatmaintain highsugarconsumption andbingeeating into adulthood may also face neurological and psychiatric conse-quencesaffecting mood andmotivation.Ourstudyfound thatFoodandDrugAdministration-approveddrugslike varenicline (a prescrip-tion medication trading as Champix, which treats nicotine addic-tion) can work the same way when it comes to sugar cravings.”
PhD researcher Masroor Shariff said the study also put artificialsweeteners under the spotlight. “Interestingly, ourstudy also foundthat artificial sweeteners such as saccharin could produce effectssimilarto those weobtained withtablesugar,highlightingtheimpor-tance of re-evaluating ourrelationship with sweetenedfood per se.”
Bartlett said that varenicline acted as a neuronal nicotinic
receptor modulator (nAChR), and similar results were observed with similar drugs such as mecamylamine and cytisine. “Like otherdrugs of abuse, withdrawal from chronic sucrose exposure canresult in an imbalance in dopamine levels and be as difficult asgoing ‘cold turkey’ from them,” she said.
“Further studies are required, but our results do suggest thatcurrent FDA-approved nAChR drugs may represent a novel new treatment strategy to tackle the obesity epidemic.”
MAY 2016 | | 7
S u b s c r i b e o
n l i n e
F u l l o n l i n e a c
c e s s p l u s a d
d i t i o n a l
c o n t e n t w h e n y
o u s u b s c r i b
e a t
w w w. a u s t s c i e n c e
. c o m
What if snakes or whales could regrow legs, or chickens developteeth, or humans re-evolve tails like our primate ancestors?Reversible evolution is possible under certain conditions – even aftermany millions of years – according to a study published in Evolu-tion (http://tinyurl.com/zkdj5hy).
An international team of scientists found that some of thelargest kangaroos ever to evolve resurrected crests on their teeth that were present in their distant ancestors more than 20 million yearsearlier. They speculate that changes in climate, habitat and diet provided the selection pressures that resurrected these dentalfeatures. As forests retreated towards the coastline over millions of years, kangaroos were forced to eat more grass, and their teethneeded to cut rather than grind their food.
Biologists have often discounted the potential for evolution to
shift into reverse, dismissing such occurrences as cases of conver-gent evolution. However, co-author A/Prof Gavin Prideaux of
Flinders University argues that “reanimating genetically moth-balled features may be ‘allowed’ by evolution when it aligns with pressures that determine an animal’s ecology”.
PhD candidate Aidan Couzens found that “small changes to a‘rule’ that determines how teeth form in the embryo have allowedsome kangaroos to partly turn back the clock on evolution. Using these rules, we can start to predict the pathways evolution can take.
“We found that, contrary to Dollo’s law in biology, featureslost in evolution can re-evolve when evolution ‘tinkers’ with the way features are assembled in the embryo,” Couzens says.
Prideaux says that kangaroos and wallabies have been studiedas barometers of historical climatic change in Australia. “They have been around for at least 30 million years,” he says. “We arediscovering more about how early forms were adapted to the abun-
dant soft-leaved forest plants, and how later macropods adaptedto more arid conditions.”
Evolution Goes Back to the Drawing Board
Compiled by Guy Nolch
ksena32/adobe
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MAY 2016 | | 9
The first large-scale study of ancient DNA from early American people has confirmed the devastating impact of European coloni-sation on the Indigenous American populations of the time.
Published in Science Advances (http://tinyurl.com/za9vzu9),the study reveals a striking absence of pre-Columbian genetic line-ages in modern Indigenous Americans, and thus points to theextinction of these lineages with the arrival of the Spaniards.
The research team reconstructed maternal genetic lineages of Indigenous American populations by sequencing mitochondrialgenomes extracted from bone and teeth samples taken from92 pre-Columbian human mummies and skeletons aged between500 and 8600 years old.
“Surprisingly, none of the genetic lineages we found in almost100 ancient humans were present, or showed evidence of descen-dants, in today’s Indigenous populations,” says joint lead author DrBastien Llamas of the Australian Centre for Ancient DNA at TheUniversity of Adelaide. “This separation appears to have beenestablished as early as 9000 years ago and was completely unex- pected, so we examined many demographic scenarios to try and
explain the pattern.“The only scenario that fit our observations was that shortly
after the initial colonisation, populations were established thatsubsequently stayed geographically isolated from one another, and
that a major portion of these populations later became extinctfollowing European contact. This closely matches the historicalreports of a major demographic collapse immediately after theSpaniards arrived in the late 1400s.”
The ancient genetic signals also provide a more precise timing of the first people entering the Americas via the Bering Land Bridgethat connected Asia and the north-western tip of North Americaduring the last Ice Age.
“Our genetic reconstruction confirms that the first Americansentered around 16,000 years ago via the Pacific coast, skirting around the massive ice sheets that blocked an inland corridor route which only opened much later,” says co-author Prof Alan Cooper.“They spread southward remarkably swiftly, reaching southernChile by 14,600 years ago.”
“Genetic diversity in these early people from Asia was limitedby the small founding populations which were isolated on theBeringian land bridge for around 2400 to 9000 years,” explains joint lead author Dr Lars Fehren-Schmitz of the University of California at Santa Cruz. “It was at the peak of the last Ice Age, when
cold deserts and ice sheets blocked human movement, and limitedresources would have constrained population size. This long isola-tion of a small group of people brewed the unique genetic diver-sity observed in the early Americans.”
DNA Confirms European Wipe-out of Early Americans
Human remains discovered in the burial site at the Huaca Pucllana great adobe pyramid in Lima, Peru.
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10 | MAY 2016
Mecysmaucheniidae spiders, which live only in New Zealand and southern South
America, are drab and tiny spiders that huntfor prey on the ground. However, a study publis hed in Current Biology (http://tinyurl.com/hyg9ulv) has found that thesespiders have a remarkable ability to striketheir prey with lightning speed.
Lead author Hannah Wood of theSmithsonian Institution’s NationalMuseum of Natural History says that the
Mecysmaucheniid family of spiders sit withtheir jaw-like chelicerae open and ready to
snap when insect prey come close enough tostrike. “The high-speed predatory attacksof these spiders were previously unknown,”she says. “Many of the species I have been working with are also unknown to the scien-tific community.”
While this kind of predatory behaviourhad been seen before in some ants, Woodsays it was unknown in arachnids. Further-
more, Wood’s team estimated that thishigh-speed, power-amplified strike hasevolved at least four different times withinMecysmaucheniids.
High-speed videos of 14 species revealed
a great range of cheliceral closing speeds.The fastest species snaps its chelicerae morethan two orders of magnitude faster thanthe slowest species.
In fact, the power output from four of the spider species exceeded the known poweroutput of their muscles. Therefore, Woodexplains, the spiders’ movements can’t bedirectly powered by their tiny muscles, partic-ularly given the short times and smalldistances covered during a strike. This meansother structural mechanisms must allow the
spiders to store the energy required to produce such powerful movements.
The researchers have already describedsome anatomical differences in the power-amplified trap-jaw spiders, but Wood saysthey aren’t quite sure how it works and arenow conducting further investigations tofind out.
In addition to providing new insightsinto spiders and their evolution, the new findings may also have broader implications.“Studying these spiders could allow humans
to design robots that move in novel waysthat are based on how these spiders move,” Wood says.
Looking at the face of a trap-jaw spider.The long chelicerae are in front and thefangs are at the tip. Credit: Hannah Wood
Trap-jaw Spiders Strike like Lightning
A series of massive supernova near our solar system showered theEarth with radioactive debris, according to evidence derived fromradioactive iron-60 found in sediment and crust samples takenfrom the Pacific, Atlantic and Indian oceans.
The iron-60 was concentrated in a period 1.7–3.2 million yearsago, which is relatively recent in astronomical terms, said researchleader Dr Anton Wallner of The Australian National University.“We were very surprised that there was debris clearly spread across1.5 million years,” Wallner said. “It suggests there were a series of supernovae, one after another. It’s an interesting coincidence thatthey correspond with when the Earth cooled and moved from thePliocene into the Pleistocene period.”
The international research team also found evidence of iron-60from an older supernova around 8 million years ago, coinciding
with global faunal changes in the late Miocene. The research hasbeen published in Nature (http://tinyurl.com/hwukuxs).
Supernovae eject heavy elements and radioactive isotopes into thecosmos. One of these isotopes is iron-60, which decays with a half-
life of2.6millionyears.Therefore anyiron-60datingfrom the Earth’sformation more than 4.6 billion years ago has long since disappeared.
Wallner was intrigued by the first hints of iron-60 in samplesfrom the Pacific Ocean floor a decade ago, so he assembled aninternational team to search for interstellar dust from 120 ocean-floor samples spanning the past 11 million years.
The first step was to extract all the iron from the ocean cores andthen separate the tiny traces of interstellar iron-60 from the otherterrestrial isotopes using the Heavy-Ion Accelerator at the ANU.The team found that it occurred all over the globe.
The age of the cores was determined from the decay of beryl-lium-10 and aluminium-26 radioactive isotopes. The dating showedthat the fallout had only occurred in two time periods, 1.7–3.2million years ago and 8 million years ago.
A possible source of the supernovae is an ageing star clusterthat has since moved away from Earth. The cluster has no largestars left, suggesting they have already exploded as supernovae andthrown out waves of debris.
Supernovae Showered Earth with Radioactive Debris
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MAY 2016 | | 11
An Australian research team has designed a nanophotonic chip that
can achieve unparalleled levels of control over the angular
momentum of light. The work, published in Science (http://
tinyurl.com/hqzoqb3), opens new opportunities to use angular
momentum for the generation, transmission, processing and
recording of information, and could also be used to help scientistsbetter understand the evolution and nature of black holes.
While travelling approximately in a straight line, a beam of light
also spins and twists around its optical axis. The angular momentum
of light measures the amount of this dynamic rotation, and could be
harnessed to improve the capacity of optical fibres by creating
parallel light channels – an approach known as “multiplexing”.
However, the creation of angular momentum multiplexing on a
chip has remained a major challenge as there is no material in
nature capable of sensing twisted light.
“By designing a series of elaborate nano-apertures and
nanogrooves on the photonic chip, our team has enabled the on-chip
manipulation of twisted light for the first time,” said Prof Min Gu of
RMIT University. “The design removes the need for any other bulkyinterference-based optics to detect the angular momentum signals.
“Our discovery could open up truly compact on-chip angular
momentum applications such as ultra-high definition displays, ultra-
high capacity optical communications and ultra-secure optical
encryption. It could also be extended to characterise the angular
momentum properties of gravitational waves to help us gain more
information on how black holes interact with each other in the
universe.”
The team devised nanogrooves to couple angular momentum-carrying beams into different plasmonic angular momentum fields,
with the nano-apertures subsequently sorting and transmitting the
different plasmonic angular momentum signals. “Our specially
designed nanophotonic chip can precisely guide angular momentum
data signals so they are transmitted from different mode-sorting
nano-ring slits without losing any information,” said Haoran Ren, a
PhD candidate at Swinburne University of Technology.
Gu added that the research offers a precise method of studying
black holes as it enabled full control over twisted light, including
both spin angular momentum and orbital angular (Oangular)
momentum. “Due to the fact that rotating black holes can impart
Oangular momentum associated with gravitational waves, anunambiguous measuring of the Oangular momentum through the sky
could lead to a more profound understanding of the evolution and
nature of black holes in the universe,” he said.
Burial Ground DiscoveryDeepens Laos Jar MysteryArchaeologists from The Australian National University have
unearthed a 2500-year-old burial ground at one of Asia’s mostmysterious sites – the Plain of Jars in Laos.The project in central Laos is the first major
archaeological dig since the 1930s at any of the90 sites that make up the Plain of Jars. The sitesfeature ancient carved stone jars up to 3 metrestall, but their purpose remains a mystery.
“This will be the first major effort since the1930s to attempt to understand the purpose of the jars and who created them,” said projectleader Dr Dougald O’Reilly. “One theory is thatthey were used to decompose the bodies. Later,after the flesh was removed, the remains may have been buried around the jars.
“What is now clear is that these are mortu-aries and were used for the disposal of the dead.The jars can number between one and 400 ateach site, ranging in size from 1 metre to 2 metrestall.”
O’Reilly said the dig had revealed threedistinct types of burial. “There are pits full of bones with a large limestone block placed overthem, and other burials where bones have been placed in ceramic vessels,” he said. “Our exca- vations have also revealed, for the first time at one
of these sites, a primary burial where a body was placed in a grave.”
O’Reilly explained that it was difficult to determine the statusof the buried individuals due to a lack of material objects buried with them. Genetic analysis might shed some light on whom these people were related to.
The Laos government is pushing for the Plain of Jars to be listed
as a UNESCO World Heritage site.
Nanochip Captures the Power of Twisted Light
Excavations at the Plain of Jars (inset) unearthedfor the first time at one of these sites a primaryburial, where a body was placed in a grave.
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12 | MAY 2016
Where Have the LargestWhale Sharks Gone?Marine biologists have raised concerns about the whereabouts
of the world’s biggest whale sharks after finding that the largest
sharks observed in recent years were smaller than those recorded
more than a decade ago.Dr Ana Sequeira of The University of Western Australia’s
Oceans Institute, who led the study, said it was important toknow the size of whale sharks because it provided informationabout their population status. However, it’s difficult to obtain
accurate size estimates as this needs to be done while they arefreely swimming.
“A common technique is to compare the sharks withan object of known size while swimming alongsidethem. However, these estimates are often inaccurate,”Sequeira said. “We found the margin for error increasedas the actual size of the target increased, which meant
that big sharks of around 10–11 metres were mistak-enly thought to be up to about 3 metres smaller.”
The new study, published in Royal Society OpenScience (http://tinyurl.com/jle7hpm), “compared visualestimates of whale shark sizes with those obtained using an underwater stereo-video system”. This found that thelargest sharks observed at Ningaloo Reef in recent years were smaller than those recorded at the same locationmore than a decade ago. “The majority of whale sharksseen at Ningaloo were juveniles with mean lengths of around 6 metres which, given the fact that the fish reachmaturity when they are about 9 metres long, prompts
the question: where are the adults?”Study co-author Dr Mark Meekan of the Australian Institute
of Marine Science said that, apart from groups of large femalesreported at two locations in the eastern Pacific Ocean, there wasa lack of adult whale shark sightings around the world. “Co-occur-rence of adult males and females ensures the survival of a species,so not knowing the whereabouts of adult whale sharks and how many still exist presents a challenge for understanding their conser- vation status,” he said.
Meekan said that more research is needed to help locate large whale sharks and to clarify the number of mature animals still inexistence. “Understanding the whereabouts of the biggest whale
sharks will also help us understand how human activity such asindustrial developments, fisheries and boat strike might impactthe animals,” he said.
Gravitational Waves Can BeFound Closer to Home While gravitational waves were detected a billion light years away earlier this year, they may soon be identified throughout “theobservable universe”.
Prof David Blair of the Australian International Gravitational
Research Centre at The University of Western Australia said that“cat-flap” pendulums less than 1 mm in size could be retrofittedto existing gravitational wave detectors, enabling physicists torecord hundreds of gravity wave events every day.
“Currently the detectors can only detect huge tsunami-like waves, but with the new technology we would be able to extendthat range about seven times,” Blair said. “One of our PhD students, Jiayi Qin, has tested the concept as part of her thesis with very good results, and we will now look to test the technology further.”
Blair is part of an international team that has spent the past7 years putting together detector equipment that uses powerfullasers to measure vibrations of mirrors suspended 4 km apart at
the ends of huge vacuum pipes.The gravitational waves announced earlier this year were produced
during the final fraction of a second of the merger of two black holesto produce a single, more massive spinning black hole. This collision
of two black holes had been predicted but never observed.
However, the detectors have industrial applications too. “Grav-itational wave technology is already being applied to mineral explo-ration, time standards, quantum computing, precision sensors,ultra-sensitive radars and pollution monitors,” Blair explained.
Jiayi Qin and Prof David Blair test the new technology.
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MAY 2016 | | 13
New Gecko SpeciesA new species of fat-tailed gecko has been discovered by scientists in outback Queensland.
Diplodactylus ameyi is a specialised termite predator
found in outback Queensland and northern NSW. It isup to 8.5 cm in length and has a distinctive, broadly rounded snout.
The gecko is tan to medium-dark brown with palespots, and is well camouflaged in the dry arid environ-ments it inhabits. Like many other terrestrial geckos, it shel-ters during the day in disused spider burrows.
Queensland Museum herpetologist Patrick Couperand his colleague, Paul Oliver from the Australian NationalUniversity, named the species in honour of fellow herpetol-ogist Dr Andrew Amey, who manages QueenslandMuseum’s reptile and amphibian collections.
The gecko is formally described in Zo ot axa(http://tinyurl.com/h5tmf5x).
Models Predict Locationof New Megafauna FossilsAn international team of scientists has used the estimated ages andspatial distribution of Australian megafauna fossils to develop mathe-matical models that predict the most likely locations of undiscovered fossildeposits. Published in PLOS ONE (http://tinyurl.com/jkxh3jf), themodels were developed for Australia but can be adapted for fossil-hunters in other continents.
“A chain of ideal conditions must occur for fossils to form, whichmeans they are extremely rare, so finding as many as possible can tell usmore of what the past was like, and why certain species went extinct,”says Prof Corey Bradshaw of The University of Adelaide.
“Typically, however, we use haphazard ways to find fossils. Mostly people just go to excavation sites and surrounding areas where fossils havebeen found before. We hope our models will make it easier for palaeon-tologists and archaeologists to identify new fossil sites that could yield vast treasures of prehistoric information.”
The team modelled the past distribution of species, the geological suit-ability of fossil preservation and the likelihood of fossil discovery in thefield. They applied this information to a range of Australian megafaunathat became extinct over the last 50,000 years, such as the giant terrorbird Genyornis, the rhino-sized “wombat” Diprotodon and the marsu- pial “lion” Thylacoleo.
To produce the species distribution models of these long-extinctanimals, the researchers used “hindcasted” global circulation models to
predict temperature and rainfall during the deep past, and matched this with the estimated ages of the fossils.
“What we did was build a probability map for each of these layers –the species distribution, the right sort of geological conditions for fossilformation (for example, sedimentary rocks, or caves and lakes), and theease of discovery (for example, open areas rather than dense forest),”Bradshaw says. “We combined each of these for an overall ‘suitability forfossil discovery’ map.”
The model identified areas south of Lake Eyre and west of LakeTorrens in South Australia, a large area around Shark Bay in WesternAustralia and other areas in the south-west of Australia as places witha high potential to yield new megafauna fossils.
One Jab for Flu VaccineResearchers are a step closer to creating a universal one-
shot influenza vaccine following the discovery that T cells
can recognise and attack emerging mutant strains of the
virus.
An international research collaboration led by A/Prof
Katherine Kedzierska from the Peter Doherty Institute for
Infection and Immunity and Dr Stephanie Gras from
Monash University used cutting-edge technology to capture
the response of individual T cells to the various strains.
The study, published in Proceedings of the National
Academy of Sciences (http://tinyurl.com/h77ejfe),
determined how the T cells reacted to new mutant strains of
influenza as well as viruses to which they had previously
been exposed.
The team used the Australian Synchrotron to scrutinise
the structure of the cells and identify how they recognise
the mutant strains. They found that their flexibility and
ability to adapt enabled the T cells to “bully” the new strains
into submission.
Kedzierska said that finding this piece of the puzzle wasa major step forward on the path to creating a one-shot T
cell-mediated influenza vaccine that provided life-long
immunity against the virus. “Previous research has shown us
that T cells provide universal protective immunity to
influenza, but we didn’t know why or how until now… This
study enabled us to dissect the immune response to
understand how this immunity occurs.”
However, further research is necessary before a
universal vaccine can be created. “Our past research has
shown that only a seventh of the world’s population have the
tissue make-up that provides universal immunity to
influenza – the difference between a runny nose and beingbed-ridden,” Kedzierska said. “Now we know what to look for,
our challenge is to find these receptors in those with a
different tissue composition and elicit a similar response.”
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S
chizophrenia has long been treated, with limited
success, with drugs that block the brain neuro-
transmitter dopamine. Pharmaceutical companies
have spent billions of dollars developing yet another
drug with a slightly different mechanism of action to
also block dopamine transmission.
Is it possible that a dietary intervention can help people
suffering from this devastating mental illness, or is this idea no
better than the fad diets promoted in the pages of celebrity
gossip magazines?
Our research found that the ketogenic diet, which is very
high in fat and extremely low in carbohydrates, effectively
normalised a wide range of schizophrenia-like behaviours in a well-established mouse model of the disorder.
What does this diet do that makes the symptoms disappear?
Is this approach safely translatable to humans?
I think it is translatable, and there is some fascinating new
science behind it as well.
Beyond Dopamine
I was in the middle of my psychiatry rotation in the last year of
medical school when my brother told me of the strange, highly
disturbing behaviour of his classmate. “He locks himself in his
room, closes the curtains and the shutters on the window. He
does not talk to his mother and has not been taking much food
for a week in the fear of being poisoned. When he does talk he
is talking nonsense about some voices he is hearing.”
The very next morning, an 18-year-old man was taken to
our psychiatry ward. He was very agitated and needed to be
physically restrained by police. He attacked his mother because
he thought she wanted to kill him.
He was my brother’s classmate. He was diagnosed with an
acute psychotic episode, promptly received an antipsychotic
injection and admitted to the ward.
I soon moved on to another rotation and a year later acci-
dentally bumped into the psychiatrist who had admitted the
young man. I asked him about his young patient.
“He died, unfortunately... committed suicide,” the psychi-atrist answered.
“But he was looked after properly, received his antipsychotic
medication and should have not ended up like this,” I protested
in my youthful enthusiasm.
Perhaps now, one-quarter of a century later, we are in a much
better position to help people who are suffering from this devas-
tating mental illness.
For many years, schizophrenia research and drug develop-
ment was driven by the idea that there seems to be an increased
activity of dopamine in the brain. A lot of evidence pointed in
that direction. For example, drugs used in the treatment of
schizophrenia all blocked the receptor protein for dopamine,
and drugs that stimulated brain dopamine tend to induce
psychosis.
Animal models with hyperactive dopamine neurotrans-
mission churned out drugs that all resembled the original
antipsychotics used in the validation of these animal models
in the first place. A bit of a Catch 22, isn’t it?
Then, in the dawn of the “genomic age”’ at the turn of the
millennium, human genetics research started to uncover a
number of other possible disease mechanisms. Researchersstarted to discover schizophrenia susceptibility genes that play
a role in brain development and in the formation of the synapse
that connects one nerve cell to the next. They also identified that
14 | MAY 2016
A Diet that Calms theSchizophrenic MindZOLTÁN SARNYAI
The ketogenic diet favoured by bodybuilders also normalises schizophrenia-like behaviours.
Ketogenic Diet Warning!The typical ketogenic diet (also called the “long-chain
triglyceride diet”) is a high-fat, low-carbohydrate diet that has
been in use since 1921.
The diet provides 3–4 grams of fat for every 1 gram of
carbohydrate and protein. It is provided by a medical
practitioner working together with a registered dietitian, and
should NOT be done without medical supervision.
The diet itself is challenging, especially at the beginning. It
requires strict compliance, precise food measurements, a
hospital stay for observation and plenty of patience.
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environmental events associated with schizophrenia, such as
maternal virus infection and malnutrition as well as exposure
to stress and early adversity, influence the expression of these
genes, resulting in abnormal brain development and patho-
logical behaviour in experimental animals.
Schizophrenia has therefore been reconceptualised as a
disease of abnormal neural development caused by the inter-
action of many genes and adverse early events.
Insulin Resistance
About 10 years ago researchers at The University of Cambridge
discovered abnormal expression of genes responsible for the
proper breakdown and utilisation of glucose in the prefrontalcortex of patients with schizophrenia. This brain region is
involved in higher cognitive functions that are abnormal in
schizophrenia, such as attention, planning and executive control
of other brain areas. Other groups confirmed that these enzyme
proteins are abnormally low in this brain region. They also
identified changes in the structure and function of the mito-
chondria, the “power stations” that fuel all of the processes
required for proper communication between nerve cells. These
discoveries have given rise to the hypothesis that abnormal
glucose and energy metabolism may contribute to the devel-
opment of schizophrenia.
This wasn’t surprising. Maudsley, the famous 19th century
British psychiatrist, had already observed that patients suffering
from “insanity”, as well as their first-degree relatives, showed a
disproportionately higher rate of diabetes mellitus. This was
the first hint that glucose and energy metabolism might beabnormal in schizophrenia.
Before the discovery of modern antipsychotic agents, psychi-
atrists at the beginning of the 20th century employed insulin
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Terence Mendoza/adobe
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coma therapy to drive down circulating
glucose in the hope that this would improve
the symptoms of patients with a variety of
mental illnesses. They found that patients
with schizophrenia required much moreinsulin to achieve the same effect. This
supports the notion that some sort of
insulin resistance is involved in schizo-
phrenia.
One hundred years later, researchers
using modern analytical tools and diag-
nostic criteria have reported that unmed-
icated patients experiencing their first
episode of schizophrenia showed resistance
to the effects of insulin. This also suggests
that there might be a problem with glucose
metabolism in and beyond the brain.
This all makes a lot of sense. The brain
is an extremely energy-hungry organ that
uses a disproportionately high amount of
glucose compared with other parts of the
body, such as the heart and the muscles.
Glucose in the brain is converted into
chemical energy in the form of adenosine-
triphosphate (ATP) molecules in order to:
• maintain communication between nervecells;
• synthesise the main excitatory neuro-
transmitter, glutamate;
• synthesise the main inhibitory neuro-
transmitter, gamma-amino-butyric acid
(GABA); and
• synthesise molecules that deal with toxic
free radicals produced by normal
neuronal activity.
If the utilisation and processing of
glucose is abnormal, neurons cannot func-tion properly, will not communicate effi-
ciently and their connections may get
damaged due to high levels of toxic free
radicals. If these changes occur in brain
areas that underlie key cognitive functions
such as the prefrontal cortex, the symp-
toms of schizophrenia may emerge. These
include hallucinations, delusions, impaired
attentional and other cognitive functions.
Here Comes the DietIf schizophrenia is driven, at least partly,
by abnormal glucose metabolism, we
hypothesised that we might be able tonormalise the disease process if we provide
energy sources in a way that circumvents
glucose metabolism. If this energy supply is
adequate, nerve cells would be able to
communicate properly through the synapse
and remove harmful free radicals more effi-
ciently.
One such roundabout way of feeding
nerve cells with molecules that can be used
for the production of energy and the key neurotransmitters glutamate and GABA
is the use of fatty acids instead of glucose.
In the absence of glucose and other carbo-
16 | MAY 2016
The ketogenic diet is preferred bybodybuilders who need a high energyintake that doesn’t promote theconversion of fat from excesscarbohydrates. Credit: tankist276/adobe
DODairy:
✓ butter
✓ mayonnaise
✓ heavy whipping cream
✓ cheese
✓ eggs
Oils:
✓ olive oil
✓ canola oil
Meat:
✓
bacon✓ chicken
✓ ground beef
✓ tuna
✓ frankfurts
✓ sausages, salami
Fruit & Veg:
✓ green vegetables
✓ lettuce
✓ spring onions
✓ mushrooms
✓
celeriac✓ strawberries
✓ blueberries
✓ avocado
✓ macadamia nuts
✓ almonds
Artificial sweeteners
DON’TSugar and high-sugar content
products:
malt sugar
corn syrup
chocolate, lollies, etc.
ice cream, etc.
tropical fruits
grape and grape juice
fruit extracts and juices
carrot
Flour and high-starch content
products:
bread and related products pasta
potato, fries, chips
rice
A Ketogenic Diet
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hydrates, fatty acids are broken down to beta-hydroxybutyrate
(BHB) and acetone in the liver.
BHB travels easily to the brain, where it’s taken up by nerve
cells. Here BHB is further broken down to molecules that can
enter into the energy production pathways downstream of the
point where energy metabolism breaks down in schizophrenia.
This metabolic pathway is a normal physiological process
that takes places during starvation, when the body accesses its
fat deposits to produce energy. In fact, it is likely that this could
have been a dominant metabolic process during most of human
evolution, when food was always scarce and carbohydrates played a very small role as energy substrates.
My student, Ann Katrin Kraeuter, tested our hypothesis by
putting mice on a ketogenic diet for 3 weeks. She then admin-
istered a drug that has been known to induce psychosis in
humans and schizophrenia-like behaviours in mice.
Mice on the normal diet promptly exhibited a variety of
schizophrenia-like behaviours, such as hyperactivity, excessive
stereotyped behaviours, abnormal social interactions as well as
impaired working memory. The latter indicates that prefrontal
cortical functions are compromised.
Mice on the ketogenic diet, however, showed none of these
symptoms. They were lean, weighed less than mice on a normal
diet and had lower circulating blood glucose levels.
These results suggested that the ketogenic diet might be a
useful approach to manage schizophrenia, not only because it
normalised schizophrenia-like behaviours but also because of
its beneficial metabolic effects.
Antipsychotic drugs used in the treatment of schizophrenia produce weight gain, elevated blood glucose, insulin resistance
and ultimately metabolic syndrome. These can contribute to the
patient’s early death due to cardiovascular disorders.
The ketogenic diet seems to counteract these deleterious
metabolic effects.
Are These Findings Translatable to People?
We know that the ketogenic diet can be safely given to humans.
In fact, it has been used for the management of drug-resistant
epilepsy in children for a long time. The ketogenic diet has alsobeen used as a weight loss diet, and seems to be preferred by
bodybuilders who need a high energy intake that doesn’t
promote the conversion of fat from excess carbohydrates.
Long-term feeding trials of the ketogenic diet in mice showed
no deleterious consequences when used for up to a year, which
is about half of the life span of a mouse. This is encouraging, but
we need to demonstrate the efficacy of the ketogenic diet in
other animal models of schizophrenia before we can move to
clinical trials.
One might argue that the ketogenic diet is not easy to follow and can be especially challenging for patients who are suffering
from schizophrenia. This prompts us to seek alternative ways to
deliver the diet, perhaps in the form of a supplement that mimics
its effects. This requires a better understanding of what is
happening in the body and brain of someone on a ketogenic diet.
Using dietary means to manage schizophrenia is not unheard
of. Recent pioneering work at The University of Melbourne has
shown that omega-3 fatty acids in fish oils decrease the devel-
opment of psychosis in individuals who have a high genetic
risk of developing schizophrenia.
Perhaps we areenteringinto theeraof nutritionalpsychiatry.
Zoltán Sarnyai is Associate Professor and Head of the Laboratory of Psychiatric
Neuroscience at the Australian Institute of Tropical Health and Medicine, James CookUniversity.
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E yewitness misidentification is the single greatest
cause of wrongful convictions in theUnited States,
havingplayed a role inmore than70% oforiginal
convictions lateroverturnedbynew DNA evidence
(www.innocenceproject.org).
This is consistent with a great deal of psychological research
using simulated crimes and lineups. This research shows that
our memories can be surprisingly fallible – we forget impor-
tant details of events, even whole events themselves, and we
remember things that have never happened. What’s worse, wecan make these mistakes even when we seem very confident
that our memories are correct.
Findings like these have cast doubt on the reliability of
eyewitnesses. Even when witnesses appear to remember some-
thing, or someone, strongly and with high confidence, they can
still be wrong.
Our research challenges this widespread view. Rather than
relying on laboratory studies, we were interested in the reliability
of eyewitnesses in actual police lineups and tested two impor-
tant conclusions drawn from laboratory research: that confi-
dence is not a good guide to accuracy, and that sequential lineups
are better than simultaneous lineups.
In a simultaneous lineup, the eyewitness is given all the
photos, usually laid out in a grid, and asked to identify the
person they remember committing the crime. In a sequential
lineup, each photo is presented one-by-one and the eyewitness
is asked to identify whether or not each photo is the culprit.
There is laboratory evidence that accuracy can be greater in
a sequential lineup than in a simultaneous lineup. This is
surprising, because more information is available to the witness
in a simultaneous lineup. While this could aid their decision-making, it may instead make the decision more confusing.
The data for our study was collected by a member of our
team, William Wells, in collaboration with the Robbery Divi-
sion of the Houston Police Department, where 45 police offi-
cers had presented photo lineups to more than 700 eye witnesses
over a 12-month period. Each lineup included a photo of a
suspect that had been identified by the police as possibly respon-
sible for the crime, as well as photos of five innocent “fillers”.
Half the lineups were presented simultaneously and the other
half were presented sequentially.
The lineups were conducted fairly – the administering officer
was unaware which photo was of the suspect. Eyewitnesses who
identified a photo as the culprit were asked to rate their confi-
dence on a three-point scale: low, medium or high confidence.
Our first question was whether confidence was a reliable
indicator of accuracy. Unlike laboratory studies, we didn’t
know if the suspect in the photo lineup was innocent or guilty
so we weren’t able to measure accuracy directly. We therefore
approached this problem in two different ways.First, because the suspect could be the culprit but none of the
innocent fillers could be, high accuracy would be reflected in a
high level of suspect identification coupled with a low level of
18 | MAY 2016
How Reliable Isan Eyewitness?JOHN DUNN
Eyewitness identification of criminals is notoriouslyunreliable, but a new study based on police recordshas identified factors that can determine which
witnesses are accurate and which are guessing.
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filler identification. This is exactly what we found.
At the lowest level of confidence, most identifications were of
fillers – as we would expect if witnesses were simply guessing.
However, identifications at the medium level of confidence were
evenly divided between suspect and fillers. At the highest level of
confidence more than 80% of identifications were of suspects.
This shows that while eyewitnesses do make mistakes, and
falsely identify innocent people, they usually have little confi-
dence in such decisions. On the other hand, when their confi-
dence is high they make many fewer mistakes.
We also found that the number of identifications of suspects
with corroborating evidence increased systematically from low
to high confidence, reaching more than 90% in the latter cate-
gory. This result further supports the idea that when eyewitnesses
have high confidence they have a high probability of identi-
fying the culprit.Although our findings provide strong indirect evidence that
eyewitness accuracy is related to confidence, we were unable
to measure accuracy directly because we didn’t know the propor-
tion of lineups in which the suspect was guilty of the crime.
However, the mathematics of choosing from a lineup can
provide useful insights.
If the suspect is not the culprit and the witness identifies a
photo, there is a one-in-six chance that the identified individual will be the suspect. On the other hand, if the suspect is the
culprit and the witness identifies a photo, the probability that
they choose the suspect is a measure of their accuracy. If accu-
racy is zero (the witness is guessing) then this probability will
be one-in-six. On the other hand, if accuracy is 100% then they
will always identify the suspect.
However, to measure this probability we have to know the
number of lineups conducted at the Robbery Division of the
Houston Police Department in which the police suspect was
indeed the culprit. To solve this problem we turned to a math-
ematical model of memory used by other members of our team
(John Wixted, Laura Mickes, John Dunn and Steven Clark) to
understand the relationship between confidence and accuracy.
According to the model, the different levels of low, medium
and high confidence simply reflect whether memory strength
exceeds a low, medium or high criterion. This is analogous to
the bar of a high jump: strong, medium and weak jumpers can
all get over a low bar, but only strong and medium jumpers can
get over a medium bar, and only strong jumpers can get over the
high bar. Similarly, weak memories that are likely to be inaccurate
may be still be strong enough to exceed a low criterion, butonly strong memories that are likely to be accurate can exceed
the high criterion.
As well as helping us to understand our results, a remark-
able feature of the model is that we could use it to estimate the
proportion of lineups in which the suspect was also the culprit.
However, before we applied it to our data, we first tested the
model against a large-scale simulation conducted by a different
group of researchers in Australia.
Because it was a simulation, the researchers arranged the
test so that the suspect was the culprit in half of the lineups. We
used the results from this study to construct eyewitness iden-tification rates for lineups in which the culprit was present or
absent. When we applied the model to these different combi-
nations it determined the proportion of culprit-present lineups
with a very high level of accuracy.
Armed with this knowledge, we then applied the model to
our real-world data and estimated the proportion of culprit-
present lineups. Unlike almost all laboratory-based studies,
where usually 50% of lineups are culprit-present, our results
suggested that only 35% of lineups at the Robbery Division of
the Houston Police Department contained the culprit. In many ways this is not surprising, as it is likely that the police would
want to know if a person responsible for one crime was also
responsible for similar crimes.
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More importantly, we replicated our earlier analyses
suggesting that accuracy increased with confidence. In partic-
ular, we found that identification of the culprit when present
in the lineup was close to 100% at the highest level of witness
confidence. In other words, when viewing lineups at the Robbery Division of the Houston Police Department, if an eyewitness
identified the suspect with high confidence, that person was
almost always the culprit.
This result does not completely depend on our 35% base
rate estimate. We also estimated accuracy based on different
estimates of the proportion of culprit-present lineups(25–75%).
Identification accuracy was unaffected and remained close to
100% when witnesses were highly confident.
Finally,we usedthe mathematical model to comparememory
strength between simultaneous and sequential lineups. Unlike
many laboratory studies, we found that memory strength was
always greaterfor simultaneouslineupsthan for sequential lineups.The results of our study are important for two reasons. First,
we were able to investigate eyewitness reliability for crimes
conducted in the real-world rather for simulated crimes in labo-
ratory settings. Second, in contrast to the conclusions reached
from many laboratory-based simulations, we found that eyewit-
ness identifications are highly accurate when they have high
confidence in their identification.Furthermore, and again in contrast to the conclusions reached
from many laboratory-based simulations, we found that a simul-
taneous lineup led to higher levels of memory strength than a
sequential lineup.
How do our results square with the
Innocence Project, which found that
a high number of false convictions
were based on unreliable eyewitness
identifications? The answer to this
question lies in where and when confi-
dence is measured.
Our results support the view that
confidence expressed at the time of
identification from a fair lineup is a
reliable index of accuracy. However,
confidence can increase over time as
more information is learned by the
witness, reducing its usefulness as an
index of accuracy.
This effect has been known for a
long time. In a well-known psycho-logical study conducted in the 1950s,
people were asked to judge whether
two straight lines were continuous or slightly disjointed. Most
people were not initially confident in their original decision, but
when surrounded by other people who all appeared very confi-
dent in one decision or the other (because they were coached
by the experimenter to say this), most people increased their
stated confidence in that decision even when the evidence of
their own eyes stayed exactly the same.
The story for lineups is much the same – only initial confi-
dence counts.
John Dunn is Professor of Psychology at The University of Adelaide, and Chair of theAustralian Psychology Accreditation Council.
20 | MAY 2016
Make sense of scienceSubscribe at www.austscience.com for access to past andpresent editions, plus additional content.
R i c h
L e g g i S t o c k p h o t o
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A ustralia is now ranked as one of the fattest
nations in theworld, with 14 million Australians
currently overweight or obese. By 2025 it is
predicted that about 80% of Australians will
be overweight or obese (tinyurl.com/z8apzug).
Dueto the increasing prevalence of diseases associated with
obesity, it is now the biggest threat to public health in Australia.It has overtaken smoking as the leading cause of illness and
premature death. To put this into perspect ive, the World
Health Organisation estimates that overweight and obesity are
responsible for about 45% of diabetes, 23% of heart disease
and 7–41% of certain types of cancer globally.
One of the major problems is that obesity is very resistant to
behavioural interventionssuch as diet and exercise. Of theindi-
viduals who manage to lose weight, only about 5% maintain
that weight loss –and this only with a high degree of self-moni-
toring.People who become obese no longer regulate their appetite
or metabolism in the same way as an individual who has never
been obese. While drug therapies have targeted the central
nervous system to control appetite, theyhave had limited effect
or unacceptable side-effects.
Currentlythemost effectivetreatment forobesity is bariatric
surgery. However, surgery is not a practical solution for the
increasing number of obese people due tothe highcosts and asso-
ciated mortality rates. Bariatric surgery is reserved for severely
obese individuals with a body mass index (BMI) greater than40,or individuals with a BMI greater than 35 but with obesity-
related comorbidities where drug therapies or lifestyle changes,
such as diet and exercise, have been unsuccessful.
If we can develop safe and relatively inexpensive medica-
tions that mimic the effect of bariatric surgery then perhaps
we can prevent the onset of severe obesity and the co-morbidi-
ties associated with it. With this in mind there is renewed
interest in therole of thegastrointestinal tract in appetite regu-
lation, energy intake and blood glucose control.
The stomach and small intestine play complementary butdistinct roles in appetite regulation. In the stomach wall there
arevagalafferent nervesthat detect stretching as foodenters and
gradually fills the stomach. The activated nerves signal to the
MAY 2016 | | 21
The Stomach as aTarget for ObesityAMANDA PAGE
Obesity permanently changes the way our body processes gastrointestinal signals aboutsatiety. While appetite suppressants have had limited success, the identification of anappetite-regulating nerve channel offers a new approach to keeping weight off.
MartesiaBezuidenhout/adobe
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reduction in the response to stretch. This
suggests that the dampened satiety signalling
in cases of obesity induced by a high-fat diet is
due to disrupted TRPV1-mediated responses
within nerves innervating the stomach.If we can restore or improve the func-
tion of TRPV1 channels in these nerves
then perhaps we can enhance the feelings
of fullness and terminate food intake sooner.
This is particularly relevant because an indi-
vidual’s metabolic response after weight loss
does not return to its pre-obesity state.
If mice are placed back on a normal diet for
an equivalent amount of time that they were
on the high-fat diet then the response to stretch
is not returned to normal; the dampened
response of nerves innervating the stomach to
stretch remains. Therefore it’s possible that the
disruption in function of TRPV1 channels is
maintained even after weight loss.
This may be one of the reasons it is so diffi-
cult to maintain weight loss. If we can restore
or improve the function of TRPV1 channels
it will have implications not only on weight loss
but also weight maintenance.
In addition to the dampened responseto mechanical stretch there are also
changes in the effect of gastric hormones
on nerves innervating the stomach. As
mentioned before, the gastric hormone ghrelin
reduces the response of gastric nerves to stretch. This
reduction is enhanced in high-fat diet-induced obesity,
further reducing the satiety signal from the stomach.
Perhaps more significant is the change in effect of the satiety
hormone leptin, which is secreted by fat cells. Leptin circulates
to the brain, where it controls the long-term regulation of food
intake.
Leptin is also found in the stomach, where it modulates the
activity of nerves in response to mechanical stimulation. Inter-
estingly, the effect of leptin on gastric nerves switches from
appetite suppression in lean conditions to appetite stimulation
in high-fat diet-induced obesity.
The mechanism behind this switch in effect is unknown
and currently under investigation. An understanding of this
switch could have huge implications for the pharmacological
treatment of obesity.
In summary, vagal nerves relay information about food intakefrom the gastrointestinal tract to the central nervous system,
where it is processed and initiates feedback on the control of food
intake. It is a highly plastic system that adapts to changes in
energy levels and appropriately signals the requirements for
food intake.
However, this system is susceptible to disruption by condi-
tions such as high-fat diet-induced obesity. Understanding the
mechanisms behind these disruptions in function will reveal
ways to overcome the changes observed in high-fat diet-induced
obesity and establish new peripheral targets for the pharma-cotherapy of obesity.
Amanda Page is a Senior Research Fellow at The University of Adelaide’s Centre forNutrition and Gastrointestinal Disease.
MAY 2016 | | 23
Nerves that respond to stretching of the stomach, and thereforetrigger feelings of satiety, are significantly dampened in cases of obesity induced by a high-fat diet. Credit: freshidea/adobe
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T
he health of our skeletal muscle is crucial for
everyday activities. It provides structural support
and stability to bones and joints and is also a key
powerhouse for energy production and use.
Our research team at the Murdoch Childrens Research Insti-tute focuses on how our genes effect the ability of our skeletal
muscle to perform across the spectrum of health, including
both inherited and acquired muscle diseases. By examining
both athletes and people affected by muscle diseases we are able
to look at the contrasting role our genes play under these
extremely different settings.
In 1999 we discovered a variant of the ACTN3 gene, which
encodes the protein α-actinin-3. This structural protein is found
in the fast-twitch skeletal muscle fibres that produce the rapid,
powerful movements that set elite sprinters and weightliftersapart from the rest of us.
The ACTN3gene variant R577X is common, and results in
complete deficiency of α-actinin-3 in almost 20% of the general
population (or 1.5 billion people worldwide). In contrast, we
found that α-actinin-3 deficiency is extremely rare in sprint
athletes, suggesting that this protein plays a crucial role in the
function of fast-twitch muscle fibres.
The association between ACTN3and athletic performancehas since been replicated in athletes from around the world.
The effect in sprint athletes is particularly strong: of the 74
Olympic-level sprint athletes that have so far been tested for
ACTN3, not a single one is deficient for α-actinin-3.
Hence α-actinin-3 is commonly referred to as the “gene for
speed” and is now one of the best characterised and most
frequently studied genes related to sport and exercise perform-
ance.
In our laboratory we have generated an ACTN3 gene
knockout mouse to determine how α-actinin-3 influencesmuscle performance and metabolism. We are also interested
in its role in health and disease, including its interaction with
the inherited muscle disorder Duchenne muscular dystrophy.
24 | MAY 2016
A Gene for SpeedPETER HOUWELING & KATHRYN NORTHA gene that may have enabled ancient humans to spread to colder climates may also be thedifference between power athletes and the rest of us, and play a role in muscle diseases.
Wikimedia Commons
Olympic gold medallist Usain Bolt is regardedas the fastest man alive. He is the first man to
hold both the 100 and 200 metre worldrecords, as well as the 4 x 100 metre relay.
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Fast or Slow? Long or Strong?Our skeletal muscle consists of two α-actinin proteins, α-actinin-
2 and α-actinin-3. While it was originally thought that these
proteins provide structural support to our muscles during
contraction, we now know that they interact with many different proteins that have structural, metabolic and signalling roles.
Functional differences in these pathways have been identified
in α-actinin-3-deficient muscle, and these differences combine
to alter muscle function.
α-Actinin-3 is predominately expressed in the fast-twitch
fibres of our skeletal muscle. These fibres are responsible for
rapid and forceful contractions but they fatigue quickly and
are prone to injury. This is the opposite of our slow-twitch
muscle fibres, which generate less force but are resistant to
fatigue.
The R577X variant plays an important role in our muscles’
ability to generate strength. Through changes in muscle struc-
ture, metabolism and cellular signals, people who are α-actinin-
3-deficient have a shift in their fast-twitch muscle fibres towards
the properties of a slower muscle fibre. Therefore α-actinin-3-
deficient muscles generate less power during contractions but
recover more quickly from fatigue.
Deficiency of α-actinin-3 does not cause muscle disease, but
is a natural variant that influences muscle function and perform-
ance.
Athletes Are a Breed ApartIn 2003 we examined 439 elite Australian athletes and 436
unrelated controls to demonstrate that the loss of α-actinin-3
is detrimental to sprint performance in elite athletes. In this
study the number of α-actinin-3-deficient sprint/power indi-
viduals was significantly lower in both male and female sprinters,
with no Olympic sprint athlete being α-actinin-3-deficient.
This landmark study has now been repeated in at least 15
independent studies of athletes from around the world. To
date, no elite sprint athlete has been found who is α-actinin-3-
deficient. On the other-hand, α-actinin-3 deficiency was foundto be higher in female Australian endurance athletes.
In addition, the R577X variant also influences normal muscle
function in non-athletes. Both men and women deficient in
α-actinin-3 show reduced muscle strength and take longer to
complete timed sprints. These findings are consistent with the
athlete data, and suggest that α-actinin-3 deficiency has a detri-
mental effect on sprint/power performance and potentially
benefits endurance sports.
In order to study the loss α-actinin-3 in more detail we devel-
oped an ACTN3
knockout mouse that doesn’t expresses α-actinin-3 in its skeletal muscle. While the knockout mice look
the same as their wild-type littermates, we observed clear differ-
ences in muscle function and metabolism.
ACT 3 knockout mice generate less force but run further
on a motorised treadmill, mirroring the performance of α-
actinin-3-deficient human muscles. Knockout mice also show
a shift in the metabolic characteristic of their muscles.
Given the specific expression of α-actinin-3 in fast fibres,
the functional effects on sprint and endurance performance
and the interaction between the α-actinins and many meta-
bolic proteins, we investigated whether the loss of α-actinin-3
produced changes in skeletal muscle metabolism. We exam-
ined the two principal metabolic pathways in skeletal muscle:anaerobic metabolism (predominantly fast-twitch muscles)
and the slower, more efficient aerobic metabolism predomi-
nantly found in slow-twitch muscles.
The data indicated a shift in the muscle metabolism of
ACTN3 knockout fast fibres away from their traditional reliance
on anaerobic metabolism to the aerobic metabolism of slow-
twitch muscles.
We have also begun to identify the molecular switches that
cause these changes in muscle strength and metabolism. In
2013 we demonstrated that calcineurin activity – a key signalling protein that influences the fast-to-slow skeletal muscle fibre
type change – is higher in the absence of α-actinin-3. We believe
this drives many of the features associated with the loss of α-
MAY 2016 | | 25
Staining reveals the different muscle fibres in the quadricepsmuscle of a mouse: blue (type I), red (type II) and black (typeIIx/a) fibers. The muscle fibre boarders are green. α-Actinin-
3 is specifically expressed in the type II (red) muscle fibres.
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actinin-3, including reduced muscle strength and increased
endurance performance.
It’s important to note that no single gene can be used to
determine our athletic ability. Like many physical features,
athletic performance is a complex characteristic that involves
both our genes and the environment. There are likely to be
many genes that contribute to athletic performance, but α-
actinin-3 was the first for which a clear association has been
demonstrated in many athlete and non-athlete groups.
An Adaptation to Cold?By studying α-actinin-3-deficient humans and the ACTN3
knockout mouse, significant progress has been made in under-
standing how ACTN3 expression alters muscle function. This
has led to an appreciation of the diverse roles that α-actinin-3
plays in our skeletal muscle. But how did this variation become
so common in modern humans?
The ACTN3 gene is estimated to be over one million years
old. However, the genetic signatures surrounding the ACTN3
R577X variant suggests recent positive selection for the loss of
α-actinin-3 as modern humans migrated out of Africa into
colder climates around 15–30,000 years ago. This means thatthe number of people who possess the R577X allele is at its
highest in places with reduced mean annual temperature and
food availability. This suggests that the R577X allele may have
conferred resistance to cold exposure or famine.
R577X is one of only two known examples in the human
genome where a gene variant results in a clear selection advan-
tage. (The other is a variant in the CASP12 gene, which influ-
ences our ability to resist serious infection).
As such, there is great interest in understanding how α-
actinin-3 deficiency provides an advantage and why the absenceof this protein alters human muscle function today. We have
already shown that the loss of α-actinin-3 appears to be detri-
mental to sprint/power performance but may benefit muscle
endurance. The current theory for this increase in α-actinin-3
deficiency is that a shift towards slower muscle fibres that use
energy more efficiently provides a survival advantage during
exposure to cold and famine.
Muscle Diseases
It is now well established that ACTN3 influences performance
in elite athletes, but the ultimate goal of our laboratory is to
find cures for children suffering from severe muscle diseases.
Recently we have started to explore how ACTN3 influences
the severity and progression of diseases associated with muscle weakness.
To understand the effect of α-actinin-3 in muscle develop-
ment and disease we examined our ACTN3 knockout mouse
in response to muscle disease. Using a method that is similar to
prolonged bed rest in humans, which results in muscle wasting
over time, we examined how wild-type and ACTN3knockout
mice responded to immobilisation. Interestingly, we were able
to show that α-actinin-3 deficiency protects against muscle
breakdown in response to immobilisation. ACTN3 knockout
mice resisted muscle wasting compared with wild-type controls.
Currently we are building on the knowledge we have gainedby studying elite athletes and the ACTN3 knockout mouse to
determine the role of α-actinin-3 in inherited muscle disorders
such as Duchenne muscular dystrophy, as well as muscle-wasting
conditions seen during ageing some types of cancer. We propose
that the changes in muscle strength and metabolism induced
by ACTN3 will influence the way individuals respond to and
develop different disease conditions.
Australia has a fantastic track record in the science of sport
performance, and it would be great if we can build on that
knowledge to help find new treatments for inherited musclediseases and wasting conditions.
Peter Houweling is Senior Research Officer at the Murdoch Childrens Research Institute,where Kathryn North is Group Leader and Director.
26 | MAY 2016
A world map that shows theproportion of 577X (red) and577R (blue) alleles in the localpopulations. The 577X allele hasincreased as modern humansmigrated out of Africa (redarrows) into the colder Eurasianclimate. The mechanism for thischange is yet to be determinedbut may be due to resistance tocold, famine or increasedendurance performance.
Resistance to cold
Resistance to famine
Endurance capacity?
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“The first thing I did when I won the Nobel Prize
was to sit my wife down. I told her I was sorry. I
knew everything was about to change.”
It’s not every day you meet a Nobel Prize winner, and while
Brian P. Schmidt appears, at first glance, no different than the
average guy you’d bump into at a bus stop, the reality couldn’t
be further from the truth.
Schmidt is 48. Born in Montana, he married an Australian
and emigrated here in 1994. Described by some as a militant
agnostic, his tagline of “I don’t know and neither do you” often
raises a smile. He believes in global warming, and has even
placed a $10,000 bet on temperatures rising with the chairman
o