• 27 December 2009 by Douglas Fox

CONTAINS zero calories! Countless soft drinks are emblazoned with that slogan as a come-on for those of us locked in a never-ending battle to rein in a spreading waistline. Calorie-free sweeteners certainly have a lot to offer. Food and drink manufacturers have become so good at blending sugar substitutes into their products that it can be almost impossible to tell them apart from the real thing - sucrose - in taste tests.

But while artificial sweeteners may be able to confuse our taste buds, the suspicion is growing that our brain is not so easily fooled. Could it be that our cravings for sugary foods run deeper than a liking for sweetness? If so, a whole bunch of weight-loss strategies may need rethinking.

Non-sugar sweeteners have come a long way. One of the first, and perhaps the worst, was lead. Romans boiled grapes in lead pots, leaching the sweet-tasting metal into their food. The practice outlived the Roman empire by many centuries, and is thought to have led to the deaths of a number of notables, including Pope Clement II, who perished in 1047. Indigenous peoples in South America use a herb called stevia, which contains chemicals that taste sweet but aren't metabolised in the human gut. These early experimenters weren't worried about shedding the kilos - just searching for a way to sweeten food in a world where refined sugar was scarce.

Saccharin, the first of the industrially manufactured artificial sweeteners, was discovered late in the 19th century and soon became popular. Taxes and restrictive patents kept the cost high, and a black market sprang up throughout Europe: a report in 1911 claimed there were 129 saccharin smugglers in the Swiss city of Zurich alone. It does, however, have a potent aftertaste. Not for nothing has it earned itself a place in the English lexicon as the epitome of sickly sweetness. Since then, a parade of sweeteners has come on stream, including cyclamate, aspartame, the sucrose-like (and very sweet) sucralose, and several others, including one called Rebiana, derived from a South American herb.

Even as manufacturers get better at blending these agents to avoid peculiar tastes, their ability to help us cut down on calories and keep our weight in check is coming into question. A handful of studies, starting in the 1980s, suggested that regular use of artificial sweeteners might even make people eat more, rather than less, by sti mulating their appetites without satisfying them. Though the methodology of some of these studies was questionable, the doubts continued.

More recently, the hunt has been joined by Guido Frank, a psychiatrist at the University of Colorado in Denver who has a particular interest in eating disorders. To compare how the brain responds to sucralose and sucrose, he fed the sweetener and the sugar to 12 women, adjusting the concentrations so that the sweetness of the two matched. "They consciously could not distinguish them," Frank says. Yet when he looked at their brain responses with functional magnetic resonance imaging (fMRI), he saw clear differences.

Pleasure response

Sucrose produced stronger activation in the "reward" areas of the brain that light up in response to pleasurable activities such as eating and drinking. Sucralose didn't activate these areas as strongly, but it synchronised the activity in a whole constellation of taste-associated brain areas - and it did this more strongly than sucrose did (NeuroImage, vol 39, p 1559). Frank suggests that sucralose activates brain areas that register pleasant taste, but not strongly enough to cause satiation. "That might drive you to eat something sweet or something calorific later on," he says.

Similar results emerged from brain-scanning experiments by Paul Smeets, a neuroscientist at Utrecht University Medical Center in the Netherlands, in which he fed volunteers two versions of an orangeade drink. One was sweetened with sugar and one with a blend of the non-calorific sweeteners aspartame, saccharin, cyclamate and acesulfame potassium. Both drinks evoked similar patterns of brain activation, except that the calorie-free blend failed to light up a cherry-sized lump of tissue within a reward area called the caudate nucleus. Smeets presented his results at a meeting of the Organization for Human Brain Mapping in June 2009 in San Francisco.

A study that goes beyond brain mapping, published in July by Edward Chambers of the University of Birmingham, UK, adds weight to the idea that there's more to the appeal of sugary foods than sweetness. Chambers made eight cyclists perform 60-minute workouts on a stationary bike while measuring their work rate. During workouts on separate days he told them to rinse their mouth with a solution of either glucose or saccharin, without swallowing either one. The glucose mouth rinse improved the cyclists' performance by a small but consistent amount compared to saccharin. It was as if the taste suggesting that more calories are on the way was enough to inspire the tired athletes' brains to drive their legs harder.

There's more to the appeal of sugary foods than sweetness. The brain has a way of detecting calories

The really surprising result came later, however, when Chambers had the cyclists rinse their mouths with either saccharin alone or saccharin plus a calorific - but non-sweet - sugar called maltodextrin. The cyclists did slightly better when they rinsed their mouths with maltodextrin - even though both solutions carried identical saccharin tastes (The Journal of Physiology, vol 587, p 1779).

All these results suggest the brain has some way of detecting calories while food is still in the mouth. "It's an unconscious response," says Chambers - and it's independent of sweetness perception. When Chambers performed fMRI scans on his athletes, he got a glimpse of that unconscious response. The combination of saccharin and maltodextrin activated two reward-associated brain areas - the striatum and anterior cingulate - which saccharin alone failed to touch.

While this discovery might seem like bad news for zero-calorie drinks, it could be the beginning of real progress in finding ways to help people reduce their calorie intake. One approach focuses on information that has come in over the past decade describing the role of the receptor proteins on our taste buds. It is these receptors that detect the flavour molecules in our foods. While we seem to have about 30 different receptors for bitter tastes, there seems to be just one receptor for sweetness, formed by a pair of proteins called T1R2 and T1R3. It sits on taste buds near the tip of the tongue and, not surprisingly, binds to both sugars and artificial sweeteners.

These receptors have become the focus of efforts to create better sugar stand-ins - and could solve the problem of aftertaste that has long plagued artificial sweeteners (see "Lingering on") - but they tell us little about the brain's apparent ability to discriminate between sugar and artificial sweeteners. Instead, it may be texture that is the key factor says Jayaram Chandrashekar, a neuroscientist at Howard Hughes Medical Institute in Janelia Farm, Virginia, who helped identify many taste receptors.

Because saccharin is several hundred times sweeter than sugar, Chambers used far less of it - with the result that the glucose and maltodextrin drinks were more viscous than the saccharin-only drink. The brain may take these subtle texture cues into account, Chandrashekar says.

"When you eat something sweet you may activate two pathways, one for sweetness and one for texture," Chandrashekar says. "Together they give you a better feeling than just the sweet pathway alone." A non-calorific bulking agent to thicken up the zero-calorie drink might solve the problem. Such bulkers are already used in a variety of products, from smoothies to enchiladas.

An alternative approach is under investigation at Senomyx in San Diego, California. The company has developed a tasteless molecule called S6973 that does not activate the sweet receptor directly, but changes it in a way that makes it bind more tightly to sucrose. "This will cause the sugar molecule to stay on the receptor maybe two times as long," says Grant DuBois, a flavour chemist at The Coca-Cola Company in Atlanta, Georgia, which has financed research at Senomyx. "You can take a beverage that may normally contain 10 per cent sugar and make it with 5 per cent sugar, and it tastes the same."

S6973 might still disappoint those of us who like to compensate for a million-calorie festive meal by drinking zero-calorie sodas - after all, drinks with sweetener enhancers will still contain as much as half the sugar of regular drinks. But that could actually be a plus if, unlike their zero-calorie cousins, these drinks manage to convince the brain that it is getting the calories it craves.

Never mind the taste test; they might even pass the brain-scan test.

Lingering on

Aftertaste has been the Godzilla of problems for zero-calorie sweeteners. "They all have this problem of slow sweetness onset and sweetness linger," says Grant DuBois, a chemist who develops sweeteners at The Coca-Cola Company in Atlanta, Georgia. In a study published earlier this year, he and Andrew James, a neuroscientist at Emory University, also in Atlanta, reported the first known neural signature for aftertaste (NeuroReport, vol 20, p 245).

DuBois and James ran fMRI brain scans on subjects as they sipped solutions of either sucrose or the artificial sweetener aspartame. When the researchers compared scans they discovered that a marble-sized nugget of tissue in an area called the insula, which is known for responding to sweet tastes, turned on for 15 seconds when people sipped sucrose, but for 30 seconds with aspartame. "Only in the insula did we see this prolonged response," says James. "We conclude that we were seeing a neural response which corresponds with aftertaste."

Such studies could provide the first objective tool for measuring aftertastes of up-and-coming sweeteners. But developing those aftertaste-free molecules will be tricky, says DuBois, who has studied artificial sweeteners on and off since the 1970s. "Over my career I have tasted in the ballpark of 1000 compounds," he says. "None of these compounds has sugar-like tastes. They all linger."

This may be down to a fundamental conflict that comes with using artificial sweeteners. They are expensive to produce, so they are only economic if they work in trace amounts. They must therefore be potent. Aspartame, for example, is 200 times sweeter than sucrose, and DuBois believes that this potency is what causes the problem. "You're just not going to find a high-potency [sweet] compound that has no aftertaste," he says.

No one knows for sure why there is this link between potency and aftertaste, but Michael Naim, a food chemist at the Hebrew University of Jerusalem, Israel, has an idea. When sweetness receptors bind to sugars, the cell sends sweetness signals to nearby nerves for a few seconds, until a protein switch inside the cell flips, turning off the signal. But zero-calorie sweeteners are soluble in both water and fat - a property which may contribute to their potency by making them bind strongly to the receptor - and so can do something that sugars can't, Naim reasons. They ooze across the cell's fatty membrane, and once inside they gum up the stop switch, so the sweetness lingers.

DuBois has designed around 100 chemicals which resemble sugars more closely - and so shouldn't cross the cell membrane - in the hope that they would be useful replacements for sucrose. Sure enough, they were sweet, but unfortunately none were sweeter than sucrose, making them non-starters as industrial sweeteners.

Douglas Fox is a writer based in San Francisco

Psychedelic Science in the 21st Century

April 15-18, 2010 in the San Francisco Bay Area

An International Conference
Offering Continuing Medical Education (CME) Credits.

Open to Physicians,
Other Therapeutic and Medical Professionals,
and the General Public

Psychedelic Science will bring together international experts to present on psychedelic research and psychedelic psychotherapy topics for the largest conference dedicated solely to psychedelics in the U.S. in 17 years. There will be three full days of programming with concurrent tracks exploring clinical applications, issues relevant to healthcare professionals, and social and cultural issues surrounding the therapeutic and recreational uses of psychedelics.

Psychedelic Science will offer pre- and post-conference workshops with Stanislav Grof, M.D., Rick Doblin, Ph.D., Michael Mithoefer, M.D., Annie Mithoefer, B.S.N., Alex and Allyson Grey, David Nichols, Ph.D., Franz Vollenweider, M.D., Ralph Metzner, Ph.D., and Ann Harrison and Carolyn "Mountain Girl" Garcia of the Women's Visionary Congress.

***Take advantage of our early registration rates before December 31, 2009.***

Photo Source: Van Wedeen  

This article was taken from the January issue of Wired UK magazine. Be the first to read Wired's articles in print before they're posted online, and get your hands on loads of additional content by subscribing online

Van Wedeen, a Harvard radiology professor, is awestruck: "We've never really seen the brain - it's been hiding in plain sight." Conventional scanning has offered us a crude glimpse, but scientists such as Wedeen aim to produce the first ever three-dimensional map of all its neurons. They call this circuit diagram the "connectome", and it could help us better understand everything from imagination and language to the miswirings that cause mental illness. But with 100 billion neurons hooked together by more connections than there are stars in the MilkyWay, the brain is a challenge that represents petabyte-level data.

So how much detail do they need? Wedeen, or the like-minded Human Connectome Project in the US, will tell you that it's enough to chart the average pathways between areas of the brain (and that even this could take a decade to complete). However, this opinion has its critics: other scientists claim that a "true" connectome has to drill deeper, tracing each neuron and its hydra-headed links. It could be a fool's errand, but for some it's already their life's work.

Wired spoke to three scientists, each using a different technique to create their own extraordinary mammalian connectome.

Above: Owl-monkey brain mapped by Van Wedeen

Wedeen used a souped-up MRI scanner to detect water diffusing along the fibres that link the different areas of an owl-monkey's brain. He then traced where the broad circuitry lies and colour-coded it based on the direction of the tissue. The green, treelike structure on the left is the cerebellum, which handles perception. A next-generation scanner will allow him to image human brains. Wedeen says he wants to reveal "the symmetry and beauty in objects - from the outside, the brain is fairly ugly, but its architecture is beautiful and rational".

• 18:20 15 December 2009 by Ewen Callaway

A paralysed man has "spoken" three different vowel sounds using a voice synthesiser controlled by an implant deep in his brain.

If more sounds can be added to the repertoire of brain signals the implant can translate, such systems could revolutionise communication for people who are completely paralysed.

"We're very optimistic that the next patient will be able to say words," says Frank Guenther, a neuroscientist at Boston University who led the study along with Philip Kennedy at Neural Signals, a firm based in Duluth, Georgia, that produces neural implants.

Conventional speech

Eric Ramsey is 26 and has locked-in syndrome, in which people are unable to move a muscle but are fully conscious.

A brain implant, which requires invasive surgery, may sound drastic. But lifting signals directly from neurons may be the only way that locked-in people like Ramsey, or those with advanced forms of ALS, a neurodegenerative disease, will ever be able to communicate quickly and naturally, says Guenther.

Devices that rely on interpreting residual muscle activity, such as eye blinks, are no good for people who are completely paralysed, while those that use brain signals captured by scalp electrodes are slow, allowing typing on a keyboard at a rate of one to two words per minute.

"Our approach has the potential for providing something along the lines of conventional speech as opposed to very slow typing," he says.

Messy signals

His team's breakthrough was to translate seemingly chaotic firing patterns of neurons into the acoustic "building blocks" that distinguish different vowel sounds. Ramsey, who suffered a brain-stem stroke at the age of 16, has an electrode implanted into a brain area that plans the movements of the vocal cords and tongue that underlie speech.

Over the past two decades, the team has developed models that predict how neurons in this region fire during speech. Using these predictions, they were able to translate the firing patterns of several dozen brain cells in Ramsey's brain into the acoustical building blocks of speech.

"It's a very subtle code; you're looking over many neurons. You don't have one neuron that represents 'aaa' and another that represents 'eee'. It's way messier than that," Guenther says.

Next, Guenther's team provided Ramsey with audio feedback of the computer's interpretation of his neurons, allowing him to tune his thoughts to hit a specific vowel. Over 25 trials across many months, Ramsey improved from hitting 45 per cent of vowels to 70 per cent.

Listen: Eric Ramsey repeating target vowel sounds here

Laptop control

Of course, the ability to produce three distinct vowels from brain signals won't allow for much communication, let alone real-time natural conversation. But Guenther says technological improvements should have a next-generation decoder producing whole words in three to five years.

This next device will read from far more neurons and so should be able to extract the brain signals underlying consonants, says Guenther. The team plan to have it controlled by a laptop, so people can practise speaking at home as much as they like. Two people interested in having this device implanted have already contacted Guenther's team, he says.

Niels Birbaumer, a neuroscientist at the University of Tübingen, Germany, who has developed a prosthetic that records brain activity beneath the skin to type out words, is sceptical that the new approach will yield fluent speech.

He also worries about its reliance on an invasive brain surgery. "In most cases an invasive procedure like this where you hurt the brain is not necessary," he says.

Guenther agrees that "if patients have enough residual movement they can control some sort of device". But he says that his implant is intended principally for people who suffer from severe forms of paralysis or significant vocal tract damage that means even these interventions won't work.

Journal reference: PLoS One, DOI: 10.1371/journal.pone.0008218

The Neurocritic has compiled a collection of interesting neurological studies where a number of patients seems to have experienced a profound change in their sexual preferences as a result of brain disturbance.

One of the most well-known of these studies is a recent case of a man who was convicted of paedophilia late in life, but was later found to have a brain tumour, and on removal of the tumour his sudden interest in children disappeared. It reappeared again when the tumour once more began to grow.

The case has raised questions about free will and self-determination in light of the fact that such morally reprehensible acts seemed only to occur when a tumour was affecting brain function.

It's importantly to mention that brain damage rarely causes such tragic events, although sexual difficulties, in general, are not uncommon. Problems can range from difficulties with arousal and enjoyment, to behavioural disturbances and inappropriate behaviour.

In some rare cases, preferences themselves seem to be affected, although it's never clear whether it's actually that the person has different desires, or whether they always had them but now are, perhaps, less able to stop themselves acting on them.

It's easier to think that damage has changed people's desires when the behaviour markedly unusual, such as this case of a man who was, to put it bluntly, screwing the coin return tray of a public telephone after brain deterioration.

But one thing we know from the forensic literature and cases of healthy people who accidentally die during sexual practices (for example, these two), is that no matter how strange the attraction seems to you, someone is out there expressing it.

Not all of the cases of changes sexuality after brain damage are where people act outside of the norm, of course. In one, admittedly, not brilliantly detailed case, an apparently exclusively homosexual man found he developed heterosexual attraction after a stroke.

Sadly, this area is massively under-researched so we really know relatively little about how different aspects of desire, emotional attachment and sexual behaviour are handled by the brain, but these case studies give us a window into the possibilities.

Link to The Neurocritic on 'Unusual Changes in Sexuality'.

—Vaughan.

 

 

 

 

 

 

 

I've just discovered a curious medical finding that can be detected on MRI brain scans called the 'face of the giant panda sign' where, quite literally, it looks like there's a panda face in the middle of the brain, indicating a specific pattern of neural damage.

The image you can see on the left is the 'face of the giant panda sign' that appeared in a brain scan of a patient with multiple sclerosis who started showing unusual sexual behaviour and is taken from a 2002 study. Click the image if you want to see the whole scan.

The pattern is apparently caused by "high signal in the tegmentum, normal signals in the red nuclei and lateral portion of the pars reticulata of the substantia nigra, and hypointensity of the superior colliculus".

It is most associated with Wilson's disease, a genetic condition which causes a toxic build-up of copper in the body, but obviously can appear in other disorders as well.

Thanks to Twitter user @sarcastic_f for alerting me to this.

It's not just pandas that appear in brain scans of course, the Virgin Mary has also been known to make an appearance.

Link to PubMed entry for MS study.
Link to brief description from Neurology.

Out of your head: Leaving the body behind

• 13 October 2009 by Anil Ananthaswamy

THE young man woke feeling dizzy. He got up and turned around, only to see himself still lying in bed. He shouted at his sleeping body, shook it, and jumped on it. The next thing he knew he was lying down again, but now seeing himself standing by the bed and shaking his sleeping body. Stricken with fear, he jumped out of the window. His room was on the third floor. He was found later, badly injured.

What this 21-year-old had just experienced was an out-of-body experience, one of the most peculiar states of consciousness. It was probably triggered by his epilepsy (Journal of Neurology, Neurosurgery and Psychiatry, vol 57, p 838). "He didn't want to commit suicide," says Peter Brugger, the young man's neuropsychologist at University Hospital Zurich in Switzerland. "He jumped to find a match between body and self. He must have been having a seizure."

In the 15 years since that dramatic incident, Brugger and others have come a long way towards understanding out-of-body experiences. They have narrowed down the cause to malfunctions in a specific brain area and are now working out how these lead to the almost supernatural experience of leaving your own body and observing it from afar. They are also using out-of-body experiences to tackle a long-standing problem: how we create and maintain a sense of self.

Dramatised to great effect by such authors as Dostoevsky, Wilde, de Maupassant and Poe - some of whom wrote from first-hand knowledge - out-of-body experiences are usually associated with epilepsy, migraines, strokes, brain tumours, drug use and even near-death experiences. It is clear, though, that people with no obvious neurological disorders can have an out-of-body experience. By some estimates, about 5 per cent of healthy people have one at some point in their lives.

People without any obvious neurological disorder can have an out-of-body experience

So what exactly is an out-of-body experience? A definition has recently emerged that involves a set of increasingly bizarre perceptions. The least severe of these is a doppelgänger experience: you sense the presence of or see a person you know to be yourself, though you remain rooted in your own body. This often progresses to stage 2, where your sense of self moves back and forth between your real body and your doppelgänger. This was what Brugger's young patient experienced. Finally, your self leaves your body altogether and observes it from outside, often an elevated position such as the ceiling. "This split is the most striking feature of an out-of-body experience," says Olaf Blanke, a neurologist at the Swiss Federal Institute of Technology in Lausanne.

Surprisingly pleasant

Some out-of-body experiences involve just one of these stages; some all three, in progression. Bizarrely, many people who have one report it as a pleasant experience. So what could be going on in the brain to create such a seemingly impossible sensation?

The first substantial clues came in 2002, when Blanke's team stumbled across a way to induce a full-blown out-of-body experience. They were performing exploratory brain surgery on a 43-year-old woman with severe epilepsy to determine which part of her brain to remove in order to cure her. When they stimulated a region near the back of the brain called the temporoparietal junction (TPJ), the woman reported that she was floating above her own body and looking down on herself.

This makes some kind of neurological sense. The TPJ processes visual and touch signals, balance and spatial information from the inner ear, and the proprioceptive sensations from joints, tendons and muscles that tell us where our body parts are in relation to one another. Its job is to meld these together to create a feeling of embodiment: a sense of where your body is, and where it ends and the rest of the world begins. Blanke and colleagues hypothesised that out-of-body experiences arise when, for whatever reason, the TPJ fails to do this properly (Nature, vol 419, p 269).

More evidence later emerged that a malfunctioning TPJ was at the heart of the out-of-body experience. In 2007, for example, Dirk De Ridder of University Hospital Antwerp in Belgium was trying to help a 63-year-old man with intractable tinnitus. In a last-ditch attempt to silence the ringing in his ears, Ridder's team implanted electrodes near the patient's TPJ. It did not cure his tinnitus, but it did lead to him experiencing something close to an out-of-body experience: he would feel his self shift about 50 centimetres behind and to the left of his body. The feeling would last more than 15 seconds, long enough to carry out PET scans of his brain. Sure enough, the team found that the TPJ was activated during the experiences.

Insights from neurological disorders or brain surgery can only take you so far, however, not least because cases are rare. Larger-scale studies are required, and to achieve this Blanke and others have used a technique called "own-body transformation tasks" to force the brain to do things that it seemingly does during an out-of-body experience. In these experiments, subjects are shown a sequence of brief glimpses of cartoon figures wearing a glove on one hand. Some of the figures face the subject, others have their back turned (see diagram). The task is to imagine yourself in the position of the cartoon figure in order to work out which hand the glove is on. To do this, you may have to mentally rotate you own body as one image succeeds another. As volunteers performed these tasks, the researchers mapped their brain activity with an EEG and found that the TPJ was activated when the volunteers imagined themselves in a position different from their actual orientation - an out-of-body position.

The team also zapped the TPJ with transcranial magnetic stimulation, a non-invasive technique that can temporarily disable parts of the brain. With a disrupted TPJ, volunteers took significantly longer to do the own-body transformation task (The Journal of Neuroscience, vol 25, p 550).

Other brain regions have been implicated too, including ones close to the TPJ. The emerging consensus is that when these regions are working well, we feel at one with our body. But disrupt them, and our sense of embodiment can float away.

This does not, however, explain the most striking feature of out-of-body experiences. "It's a great puzzle why people, from their out-of-body locations, visualise not only their bodies but things around them, such as other people," says Brugger. "Where does this information come from?"

One line of evidence comes from the condition known as sleep paralysis, in which healthy people find their body immobilised as in sleep despite being conscious (see "The twilight zone"). In a survey of nearly 12,000 people who had experienced sleep paralysis, Allan Cheyne of the University of Waterloo in Ontario, Canada, found that many reported sensations similar to out-of-body experiences. These included floating out of their body and turning back to look at it.

Cheyne suggests that this might be the result of conflicts of information in the brain. During sleep paralysis, it is possible to enter a REM-like state in which you dream of moving or flying. Under these circumstances you are conscious of a sensation of movement, yet your brain is aware that your body cannot move. In an attempt to resolve this sensory conflict, the brain cuts the sense of self loose (Cortex, vol 45, p 201). "It resolves by splitting the self from its body," says Cheyne. "The self seems to go with the movement and the body gets left behind." Perhaps similar sensory conflicts cause classic out-of-body experiences.

The brain resolves sensory conflict by splitting the self from the body. The body gets left behind

Brugger, meanwhile, has a suggestion for how someone might see things even though their eyes are shut, based on one of his patients who reported an out-of-body experience. According to this patient's father, who was sitting by the bedside, he had his eyes closed. Yet he later reported seeing, from a perspective above his bed, his father going to the bathroom, returning with a wet towel and towelling his forehead.

The patient presumably heard his father walk to the bathroom and run some water, and must have felt the wet towel on his head. Brugger speculates that his brain converted those stimuli into a visual image, not unlike what happens in synaesthesia. This still does not, however, explain the external vantage point. "It's not clear how the brain constructs that," says cognitive philosopher Thomas Metzinger of the Johannes Gutenberg University in Mainz, Germany.

Metzinger does have a suggestion. Imagine an episode from a recent holiday. Do you visualise it from a first-person perspective, or from a third-person perspective with yourself in the scene? Surprisingly, most of us do the latter. "In encoding visual memories, the brain already uses an external perspective," says Metzinger. "We don't know much about why and how, but if something is extracted from such a database [during an out-of-body experience], there may be material for seeing oneself from the outside."

Whatever the mechanism, the study of out-of-body experiences promises to help answer a profound question in neuroscience and philosophy: how does self-consciousness emerge? It's abundantly clear to us that we have a sense of self that resides, most of the time, in our bodies. Yet it is also clear from out-of-body experiences that the sense of self can seemingly detach from your physical body. So how are the self and the body related?

To address that question, Metzinger has teamed up with Blanke and his colleagues in an experiment that induces an out-of-body experience in healthy volunteers. They film each volunteer from behind and project the image into a head-mounted display worn by the volunteer so that they see an image of themselves standing about 2 metres in front. The experimenters then stroke the volunteer's back - which the volunteers see being done to their virtual self. This creates sensory conflict, and many reported feeling their sense of self migrating out of their physical bodies and towards the virtual one (Science, vol 317, p 1096).

To Metzinger, these experiments demonstrate that self-consciousness begins with the feeling of owning a body, but there is more to self-consciousness than the mere feelings of embodiment. "Selfhood has many components," says Metzinger. "We are trying to fill them in, building block by building block. This is just the beginning."

Anil Ananthaswamy is a contributing editor for New Scientist

"THE EIGHT CIRCUIT BRAIN: Navigational Strategies for the Energetic Body". LIMITED FIRST EDITION. (2009; 312 pages. Illustrated. Paperback. Cover art by James Koehnline. $19.95 retail). This book advances the material in Alli's groundbreaking first book, "ANGEL TECH" (Original Falcon), a compendium of techniques and practical applications of Dr. Timothy Leary’s 8-Circuit Brain model for Intelligence Increase. After twenty-plus years of research and experimentation, Antero's earlier findings have been significantly updated and enriched in this new body of work. Includes a comprehensive 8-week course of study and practice, the author's "Neurological Autobiography of Outside Shocks and Hedonic Upgrades," a forum featuring Alli's responses to questions from former students, accounts of his in-depth encounters with Christopher S. Hyatt and Robert Anton Wilson, and much, much more. Published by Vertical Pool.