Rewilded elephants on Khamab Kalahari Reserve – Elephant Reintegration Trust of South Africa / SWNS
Credit – Glen Carrie / Unsplash
Andy Rouse captured antics of Kenyan family of elephants – SWNS
Rewilded elephants on Khamab Kalahari Reserve – Elephant Reintegration Trust of South Africa / SWNS
Credit – Glen Carrie / Unsplash
Andy Rouse captured antics of Kenyan family of elephants – SWNS
Institute for Basic Science
Credit: Erika FletcherIntelligence is an energetically expensive luxury – as the rise of artificial intelligence has reminded us. The human brain is no exception.
Comprising roughly 2% of the body weight, it uses one fifth the body’s energy in the resting state – compared with less than half of this in non-human primates. A five-year-old child devotes 66% of the energy they need to stay alive to their brain.
How did our ancestors foot the energy bill to run their uniquely large brains? Eating more meat is often considered to be the answer. But there’s a catch. The brain relies on a form of fuel that is not present in meat: glucose.
Our new study, published today in Science, shows that carbohydrates contributed more than half our total energy requirements over four million years of evolution. It holds important clues for why we crave sweet foods today – and how we can eat more healthily.
Many anthropologists have credited meat eating as the stimulus to produce a large brain. After all, it required tools to butcher the carcass and access the fat-rich marrow inside bones.
Protein and fat in fruit and leaves are dilute, requiring hours of chewing, while animal foods are dense sources that can be devoured quickly. Bone marrow is a rich source of essential fats.
In truth, humans do not require more protein as a proportion of energy than other primates.
Our increasingly large brains and high reproductive rate demanded carbohydrate calories (found in plants but not meat), while our taller and heavier bodies needed fat calories to move those big muscles.
Although the body can synthesise glucose from precursors such as amino acids, the process is finite and energetically inefficient. Furthermore, there are limits on using just protein as fuel. For example, it can lead to a type of poisoning known as “rabbit starvation”.
A minimum amount of dietary carbohydrate was necessary. Our new study shows that, for much of evolution, the sugars in fruit and honey were the source.
We modelled the diets of hominins – the group consisting of humans and our immediate ancestors – over four million years of evolution.
First, we calculated overall demand for glucose by the organs and tissues which use it as their primary source of energy. Apart from the brain, red blood cells and the kidneys require glucose.
We then accounted for reproductive needs. The fetus and placenta use glucose not just as an energy source but as a structural component of growing tissues. Synthesis of DNA, RNA and nerve cell membranes requires glucose. During lactation, women use about 80g of glucose each day to produce the sugars in human milk.
Then we modelled the availability of macronutrients – carbohydrates, fats and proteins – from foods, starting with the diminutive ancient ape known as Lucy (Australopithecus afarensis).
This early ancestor of ours walked on two legs, and was likely to be a ripe fruit specialist like chimpanzees today. Over two thirds of her energy came from naturally-occurring sugars.
Indeed, some scientists think frugivory – a feeding strategy primarily characterised by eating fruit – kick-started the evolution of large brains because, living in tropical forests, our ancestors required good cognition to remember when and where the best fruits were ripening. They needed strategic thinking to beat the birds and other competitors.
We finished up with the known diet composition of contemporary human foragers in warm climates. In six incremental steps, we incorporated increasing proportions of animal-based food, starting with 5% of calories and finishing with 35–50%.
Around one million years ago, mastery of fire allowed cooked starch, which unlike raw starch can be easily digested to provide glucose, to replace some of the sugars. Relatively recently, about 100,000 years ago, grinding stones and hearths indicate that the starch inside cereal grains became more accessible.
Did early hominins consume sufficient carbohydrate to cover the obligatory demands of the brain and other tissues? Yes, if you were a male, but only just if you were a pregnant female.
As we ventured out of tropical environments into cold and arid territory, the intake of carbohydrates would have become limiting. Plants would be plentiful, along with protein and marrow fat, but fruit and honey would be seasonal.
We speculate that limited amounts of dietary carbohydrate selected for genes that result in higher blood glucose levels. This would improve the growth and future survival of the fetus.
Today, the same genes likely predispose us to type two diabetes and cardiovascular disease. Low carbohydrate diets may therefore be helpful in specific clinical contexts.
But our findings provide an evolutionary explanation why healthy humans require about half their energy as carbohydrates. They also give us insight into why humans crave sweetness – a pleasurable signal on the tongue that encouraged foods that fuelled the mind and body millions of years ago.
Intrinsically, sugars are highly reactive molecules that are bundled in nature with antioxidants and other natural compounds that reduce harm within the cell.
Ideally, we consume them in that form – as fruit – rather than refined sugars.![]()
Jennie Brand-Miller, Emeritus Professor of Human Nutrition, University of Sydney; David Raubenheimer, Leonard P. Ullman Chair in Nutritional Ecology, Nutrition Theme Leader Charles Perkins Centre, University of Sydney, and Les Copeland, Professor of Agriculture, University of Sydney
This article is republished from The Conversation under a Creative Commons license. Read the original article.
What causes a dog to slink away from a cranky person, when they will quietly approach and lean against someone who is weeping? We’ve all seen it – they can respond to our feelings. And science agrees dogs have emotions too.
These social skills could underpin dogs’ success in living with us. But do you think your dog could tell an angry person’s face from a sad or fearful one?
New research published in the journal iScience explored that question, and revealed interesting findings from magnetic resonance imaging (MRI) scans of dogs’ brains.
Dogs are sensitive to human faces. They look longer in response to our emotional expressions and sounds compared with neutral ones.
Scientists weren’t sure whether dogs were just differentiating “good mood” (happy) from “bad mood” (angry, fearful or sad), or treating these expressions as genuine indicators of different emotions.
The new study, by Raúl Hernández-Pérez, a neuroscientist at the University of Vienna, and colleagues, explored this gap using MRI to scan pet dogs’ brains while they were viewing photos of human faces.
Building on their earlier work, the researchers found evidence that dogs do process images of our distinct emotional expressions differently.
The researchers used machine learning and showed that when looking at a dog’s whole brain, a different brain region was activated to distinguish between fear and sadness (the right rostral suprasylvian gyrus, to be precise), than between fear and anger (this was in the right mid ectosylvian gyrus and left splenial gyrus).
The analysis didn’t detect a difference in the brain areas activated when dogs were shown images of human anger and sadness. Fear stood out from the other negative emotions.
This raises the question: why?
It might be that fear and anger are simply more attention-grabbing than sadness.
Other research has found dogs react to fear and anger faster, and with a bigger physical response, such as a raised heart rate. This is likely because they’re the expressions most likely to call for a quick response from dogs to stay safe.
Sadness is less likely to pose a direct threat to dogs living with people, so they experience less urgency to respond to it. We know some dogs don’t respond with the heroic Lassie behaviour we might like when we are in distress.
Although the numbers in this new research were small (eight and twelve dogs across the two parts of the study), this is the first MRI-based proof-of-concept evidence that dog brains can distinguish between two human facial expressions of distinct negative emotions. It indicates dogs’ neural representation of our emotion goes beyond a simple valence (good/bad) split.
This shows us that perceiving emotion in others (even across species) isn’t handled by one single “emotion centre” in the brain – in dogs, in humans, or in other animal species. It’s spread across a network of regions working together as part of living socially.
The authors of this study point out that using still images of humans is a very people-centred way to explore how dogs interpret our emotional states.
We know dogs live in rich sensory worlds where the scent and sound of our speech also convey emotions, shaping how dogs respond to us.
In fact, even wolves who have grown up around people show the same kind of response to the odour of human fear as dogs. This highlights the important role of learning, as distinct from evolutionary differences in canid bodies or how they respond to people. Dogs (and wolves) are learning about us in every interaction we have with them.
Dogs are adept at watching, smelling, and listening to our emotions, learning how these signals predict our behaviours toward them, and using this information to live with people harmoniously.
Returning the favour, learning more about how dogs express their emotions seems like the least we can do.![]()
Mia Cobb, Research Fellow, Animal Welfare Science Centre, The University of Melbourne
This article is republished from The Conversation under a Creative Commons license. Read the original article.
Colobus congoensis – credit, released by Daniel Rosengren, Frankfurt Zoological Society
Can spiders swim?
Waubra Preschool students, Victoria, Australia
What a great question!
Most spiders don’t swim by choice. But they sure can survive in water when they need to. From floating like a boat, to paddling like a rower, to carrying their own scuba bubbles, spiders have developed brilliant ways to deal with water.
Let’s dive into the science in some more detail, and look at how spiders handle getting their paws wet, with examples from our local bush.
Water has surface tension – this acts like a kind of invisible skin that can hold up small, light objects.
Many spiders are tiny and have water-repellent hairs on their legs, so they can stand or run on water without sinking.
For example, fishing spiders wait at the water’s edge and scuttle across the surface to grab insects, tadpoles or even small fish.
If prey escapes underwater, this spider can even hide beneath the water’s surface briefly, then come back up.
Spiders don’t have gills, so they can’t get oxygen from water like fish do. But they have evolved clever strategies for staying alive if they stay in the water for a long time.
For example, the Australian Sydney funnel-web spider often falls into backyard swimming pools. People might see one and think it drowned, but it can actually survive underwater for hours by holding its breath much longer than a human could.
That’s because it breathes much more slowly than we do. Like many spiders, it has both tracheae (tiny air tubes) and book lungs (they look like a book with many pages) for breathing. Some spiders can close these and become watertight, to hold their breath for a long time.
Some trapdoor spiders have been recorded only taking a breath every six minutes.
Some spiders take the air with them like a scuba diver.
On the Great Barrier Reef coast, a little intertidal spider called Desis bobmarleyi actually lives part of its life under seawater. At high tide, it hides in a silk-lined air pocket in coral or shells. It uses the long hairs on its legs and body to trap a bubble around itself so it can breathe underwater between the tides. When the tide goes out, this spider comes out to hunt on the wet reef.
And in other parts of the world, there’s the famous diving bell spider, the only spider that spends its whole life entirely underwater.
It weaves an underwater silk web that it fills with air – like an underwater house. This spider can stay underwater for more than a day at a time by letting its air-bubble vessel actively pull oxygen from the water.
Some spiders sit tight and make their homes flood-proof. Remember those trapdoor spiders we mentioned? Trapdoor spiders live snug in burrows underground with a silken lid on top (like a little trapdoor).
In areas that get sudden heavy rains, a trapdoor spider might build its burrow with a raised entrance – a bit like a chimney – so water flows around or over it rather than straight in.
Some Australian trapdoor spiders in the outback clay pans have been found to build thick muddy silk doors that fit perfectly like a bath plug into the surrounding soil. The water just goes straight over the top.
Even if water does get in, some trapdoor spiders can seal their bodies and essentially hold their breath. They don’t swim in their flooded burrows, but they can wait out a flood without drowning.
If you ever find a spider struggling in water – say in a swimming pool or even in a bucket – you can help as long as you’re careful.
First, always ask an adult before trying to assist a spider. Nobody has died in Australia in 60 years from spider venom. But some (such as the Sydney funnel-web) can still be fatal, so you must be sure not to touch or provoke it.
A good way to save a spider in a pool is to use a net or a scoop with a long handle. Gently lift the spider out and put it on the ground away from the water. The spider might look dead at first, but don’t be surprised if it “comes back to life” as it dries out – just like trapdoor spiders do.
And remember: never poke a spider with your bare hands, even if it seems lifeless. Spiders such as funnel-webs can still bite underwater or right after being rescued, and they will defend themselves if they feel threatened. So, play it safe and use tools or ask an adult or a spider expert to help.
If anyone is bitten, get an adult to seek medical attention immediately.
Next time you’re exploring nature (or even looking into the toilet), keep an eye out for our eight-legged friends and how they interact with water. You might spot a little spider boat captain or an air-bubble diver right in your backyard.![]()
Leanda Denise Mason, Vice Chancellor Research Fellow in Conservation Ecology, Edith Cowan University
This article is republished from The Conversation under a Creative Commons license. Read the original article.

The fastest serve so far at this year’s Wimbledon tennis championships was struck by the Argentinian Thiago AgustÃn Tirante on the opening day.
His serve of almost 148mph (238km/h) was still some way under the Wimbledon record of 153mph, set by Frenchman Giovanni Mpetshi Perricard in 2025. And despite Tirante giving his opponent less than a fifth of a second to play each serve, he lost the match in straight sets.
Which means his rocket serves were successfully returned on lots of points. Our emerging understanding of how the human brain works can help explain how this feat is achieved.
Whether you’re a player or a spectator, the ability to see a tennis ball travelling that quickly across the court is a marvel of human physiology. At nearly 150mph, the ball is travelling faster than anyone can watch it move.
By the time your brain has processed the sight of the ball leaving the racket, it is already well on its way to the other end of the court. Yet professional tennis players return these high-powered serves with astonishing accuracy.
The reason is that they do not rely on reaction alone. Returning a tennis serve depends on one of the brain’s most remarkable abilities: predicting the future.
Tennis players – and spectators – face the same basic problem: the visual information arrives in their brain slightly late.
Before a player becomes aware of a tennis ball hurtling across the court, light reflected from its surface has to be detected by their eyes’ retinas, converted into electrical signals, then transmitted along the optic nerves to the brain. There, the visual cortex begins analysing its colour, shape, speed and direction.
Even under ideal conditions, this takes around a tenth of a second. During that time, a ball travelling at nearly 148mph will have covered several metres.
For a spectator, this delay is rarely noticeable. The brain’s predictions are so accurate that the ball appears to move smoothly across the court, despite what you are seeing being a fraction of a second out of date.
But the player standing at the other end of the court needs to do a lot more than just watch the ball. They must move their body to that specific point on the court, position their racket and time their swing with great precision if they want to be in with a chance of winning the point.
In fact, much of this process begins before the ball has even left the opponent’s racket. It is an extraordinarily complex system.
As the server prepares to strike the tennis ball, the receiver is already gathering information. The height and position of the ball toss, the rotation of the server’s trunk, the movement of their shoulder and forearm, the angle of the racket face and the speed of the swing all provide clues about what is about to happen.
Elite players have, of course, spent many thousands of hours learning to recognise these subtle biomechanical cues. Their brains combine the latest cues with all that previous experience to estimate the likely speed, direction and spin of the serve – before the ball has even crossed the net.
Central to this is the cerebellum, a densely folded structure tucked beneath the back of the brain. Although best known for coordinating movement and balance, advances in brain imaging and computational neuroscience have revealed it is also one of the brain’s great prediction engines.
Rather than simply responding to sensory information as it arrives, the cerebellum continuously generates internal models of how the body and external world behave. As fresh visual information reaches the brain, these models are updated almost instantaneously, allowing movements to be adjusted before conscious awareness has caught up.
But the cerebellum does not work alone. A specialised region of the visual cortex, known as area MT or V5, is exquisitely sensitive to movement, and calculates the speed and direction of the ball as it crosses the player’s visual field.
This information travels along the dorsal visual stream – often called the brain’s “where pathway” – to the posterior parietal cortex, where the ball’s position is integrated with information about the player’s own body.
The brain’s two visual streams
From there, premotor regions begin preparing possible movements. The supplementary motor area helps organise their sequence, and the primary motor cortex sends commands to the muscles of the trunk, shoulder, arm and wrist.
At the same time, the frontal eye fields and the superior colliculus (a small structure in the midbrain that rapidly redirects the eyes towards objects of interest) generate rapid eye movements towards where the ball is expected to be next – rather than where it was a fraction of a second ago.
This is why the fastest returns in tennis are not simply feats of lightning-fast reflexes. They are the product of a brain that is constantly making, testing and refining predictions. The players who appear to have more time have become exceptionally good at anticipating what will happen next.
Neuroscientists are still trying to understand why some tennis players acquire these remarkable predictive skills faster than others. Is it simply a matter of hours spent on court, or are some brains naturally better equipped to build the internal models that underpin elite performance?
For now, the answer appears to be a combination of both.
Understanding how the brain predicts movement has implications far beyond tennis. Similar neural mechanisms help us catch a falling glass before it hits the floor, judge when it is safe to cross a busy road, or drive through traffic.
These predictive systems are becoming an important focus of neuroscience research. Insights into how the cerebellum and wider motor networks anticipate movement are helping researchers improve rehabilitation after neurological injury, understand disorders of movement and coordination, and design robots capable of interacting more naturally with an unpredictable world.
Meanwhile, insights from neuroscience might also help hone a future Wimbledon tennis champion.![]()
Michelle Spear, Professor of Anatomy, University of Bristol
This article is republished from The Conversation under a Creative Commons license. Read the original article.
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Some of the strongest parental instincts happen without conscious thought. The urge to check on a sleeping baby. To stay close. To pick them up when they cry.
Becoming a mother also brings about an extraordinary shift in priorities. As the late British psychotherapist and author Naomi Stadlen wrote, “motherhood can be relentless. The dependency, the need, the constant pull of being someone’s entire world…”
For all mammals, raising young demands enormous time, energy and resources, requiring mothers to place their offspring’s needs ahead of almost everything else.
So just how precisely does the brain make that shift? Our newly published research sought to answer that question.
Using studies in mice, we identified part of the brain circuitry that drives a mother’s urge to interact with her newborn. We found an essential pathway linking a hormone-sensing region of the brain to its reward network.
Activated by the pregnancy hormone placental lactogen and the milk-production hormone prolactin, this pathway helps make caring for a newborn rewarding rather than simply necessary. Remarkably, we were even able to switch that drive on and off experimentally.
We focused on a brain region called the medial preoptic area, known for decades to be a key controller of parenting behaviours. Many of its neurons carry receptors for placental lactogen and prolactin.
In earlier studies, we showed that mice without these receptors in this region were unable to care for their offspring after birth. What remained unclear was exactly how these neurons helped drive parenting behaviour.
Using specialised neuroscience techniques to observe these neurons in living mice, we found they became highly active when females came into close contact with pups. The response was much stronger in mothers than in females that had never given birth, with the biggest surge occurring at the very first meeting.
We then traced where these neurons send their signals. A subset of these neurons connect directly to the brain’s reward system, triggering the release of dopamine – the neurochemical that helps make experiences feel rewarding. Recent advances in neuroscience allowed us to watch dopamine being released in real time as mice interacted with their pups.
When we artificially activated this pathway, female mice that had never given birth behaved much more like new mothers. Faced with a barrier separating them from newborn pups, they climbed over it more quickly and repeatedly returned to the pups.
Interestingly, when we blocked the pathway, the opposite happened. Mice no longer showed the normal dopamine surge when meeting the pups and were slower to engage with them. Removing prolactin receptors from the pathway also reduced mother–pup interactions, while leaving other aspects of maternal care largely unchanged.
These new insights help explain why caring for a newborn becomes such a powerful priority after birth. Prolactin acts through this pathway to tune the brain’s reward system, making time with offspring rewarding rather than simply another task.
Although our work was conducted in mice, the same reward pathways are found in human mothers, with prolactin serving as the key milk-production hormone in all mammals.
The human brain undergoes huge and long-lasting changes during pregnancy, yet very little neuroscience research has focused on females – and even less has looked at how pregnancy causes changes in the brain.
The Ministry of Health estimates that 12–18% of New Zealand women experience depression, anxiety or other mental health conditions during pregnancy or after birth.
The World Health Organisation reports that globally, about 10% of pregnant women and 13% of women who have just given birth experience a mental disorder, primarily depression. In developing countries, this rate is even higher.
Yet there are few treatments that target the biological changes driving these disorders.
Our research aims to understand how the brain adapts during pregnancy and early motherhood to support healthy mood, with the goal of developing better ways to prevent and treat poor peripartum mental health.
We also hope this work will help reduce the stigma faced by parents who struggle to bond with their baby. Rather than personal failing, difficulties with bonding may reflect brain pathways that have not adapted as expected.
Given the profound changes the brain undergoes during pregnancy, it is perhaps unsurprising that this process does not always unfold smoothly. Parents and families deserve better understanding, support and treatment during this critical period.![]()
Rosie Brown, Associate Professor in Physiology, University of Otago; Jenny Clarkson, Research Fellow and Lecturer, Department of Physiology, University of Otago, and Michael Perkinson, Postdoctoral Research Fellow, Department of Physiology, University of Otago
This article is republished from The Conversation under a Creative Commons license. Read the original article.


– credit Tony Kershaw via SWNS
Tipah and her litter of cubs – credit Tony Kershaw via SWNS


For many people, the thought of a tasty burger or a cold pint of beer conjures up a vivid mental image and drives behaviour.
This link between thinking and doing serves a clear function – it motivates us to get the necessities for life.
But for some, this process can malfunction. Preoccupation with these rewarding stimuli can lead to disorders of substance overuse, including overeating to the point of obesity and alcohol abuse.
Studies going back to the 1970s have linked vivid mental imagery with drug abuse.
Understanding this link between craving and consuming is central to understanding addiction. This has eluded neuroscience for decades, but the introduction of a new class of drugs for weight loss may have given us just the lever we need to understand it.
These new drugs – including Ozempic and Wegovy – mimic the GLP-1 hormone to stimulate insulin release, slow digestion, and increase feelings of fullness. They are known as GLP-1 agonists and were originally used to treat type 2 diabetes because they help control blood sugar.
As a side effect, people using these drugs also lost a lot of weight, in some cases almost as much as might be expected from bariatric surgery.
But there is another less well publicised effect. Human studies show that GLP-1 agonists reduce alcohol consumption. Preclinical animal studies suggest these drugs also reduce the use of cocaine, amphetamines, opiates and nicotine.
These drugs are changing how we think about the brain’s reward system. They may also open new treatment options for obesity, alcohol dependence and the consumption of other addictive substances.
We have a reasonable understanding of the brain’s “reward circuitry” associated with regions that produce the neurotransmitter dopamine.
These brain parts – the ventral tegmental area (VTA) and nucleus accumbens (NAc) – have been the subject of research on reward for decades. They are the obvious candidate regions to look for a mechanism for GLP-1 action in the brain. But they lack significant density of receptors for GLP-1 and are unlikely to be the direct mechanism.
We must, therefore, consider other brain regions to understand the anti-consumption effect of GLP-1 drugs.
One jump “upstream” from the dopamine-producing brain parts is a region called the lateral septum. This brain structure has been historically implicated in emotional regulation.
Back in 1953, pioneering US behavioural researchers Joseph Brady and Walle Nauta coined the term “septal rage” when animals with damage in the lateral septum showed increased aggression, while direct stimulation of this brain region reduced aggression.
Much more recent work has placed the lateral septum at the centre of a neural connectivity network. This has reframed how we think about its function.
While a link between the lateral septum and another region called the hypothalamus is probably responsible for septal rage, the lateral septum links with many other regions with various functions.
The lateral septum inherits much of its primary input from a brain region called the hippocampus.
This region is well known as the place that lets us form long-term “episodic memories”. A famous case of hippocampal damage, Henry Molaison (patient HM), was unable to form new memories after his surgery for epilepsy. He effectively lived without a past, in permanent present tense.
The hippocampus also contains the remarkable “place cells” – neurons that fire corresponding to a person’s thoughts about their position in space and, as recent research has shown, time.
This “where and when am I” information gets forwarded to the lateral septum. Key research has recently shown the lateral septum also contains place cells, but these cells strongly respond to rewards. They effectively add “what is good in this place” to the “where and when am I” information from the hippocampus.
Critically, the lateral septum shares this information with the dopamine-producing regions we would normally associate with reward.
Neuroscientists now think of the lateral septum as the brain region that lets us “think about” rewards – our conscious perception of them – and communicates with the machinery in the brain’s reward system that produces dopamine to make us feel good about them.
There is one last reason to suspect the lateral septum as the mechanism behind the anti-consumption effect of GLP-1 agonists. It is absolutely loaded with GLP-1 receptors.
Emerging research points to this as the mechanism. GLP-1 activation directly in the lateral septum has recently been shown to reduce food consumption in mice. Earlier this year, another study showed the same for alcohol consumption.
My own lab has shown this year that GLP-1 drugs reduce a type of activity in the lateral septum that may prevent it communicating so effectively with other brain regions.
These findings are reshaping our understanding of how the brain processes rewards and have put the spotlight firmly on the lateral septum as the home of cravings.![]()
Robert Munn, Senior Lecturer, University of Otago
This article is republished from The Conversation under a Creative Commons license. Read the original article.