Australasian Science - May 2016

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


2/52

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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

COLUMNISTS: David Reneke, Ian Lowe,Peter Bowditch, Michael Cook,John Long, Tim Olds, Tim Hannan

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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 shockwave 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 shockwave 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 excavations 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.


15/52

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

MAY 2016 | | 15

Terence Mendoza/adobe


16/52

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


17/52

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.

MAY 2016 | | 17


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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.

a u r e m a r / a d o b

e


19/52

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.

MAY 2016 | | 19


20/52

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

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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


22/52


23/52

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.


25/52

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.


26/52

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?


27/52

“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

Documents

Australasian Science - May 2016