Posts tagged brain
Posts tagged brain
One of the smallest parts of the brain is getting a second look after new research suggests it plays a crucial role in decision making.
A University of British Columbia study published today in Nature Neuroscience says the lateral habenula, a region of the brain linked to depression and avoidance behaviours, has been largely misunderstood and may be integral in cost-benefit decisions.
“These findings clarify the brain processes involved in the important decisions that we make on a daily basis, from choosing between job offers to deciding which house or car to buy,” says Prof. Stan Floresco of UBC’s Dept. of Psychology and Brain Research Centre (BRC). “It also suggests that the scientific community has misunderstood the true functioning of this mysterious, but important, region of the brain.”
In the study, scientists trained lab rats to choose between a consistent small reward (one food pellet) or a potentially larger reward (four food pellets) that appeared sporadically. Like humans, the rats tended to choose larger rewards when costs—in this case, the amount of time they had to wait before receiving food–were low and preferred smaller rewards when such risks were higher.
Previous studies suggest that turning off the lateral habenula would cause rats to choose the larger, riskier reward more often, but that was not the case. Instead, the rats selected either option at random, no longer showing the ability to choose the best option for them.
The findings have important implications for depression treatment. “Deep brain stimulation – which is thought to inactivate the lateral habenula — has been reported to improve depressive symptoms in humans,” Floresco says. “But our findings suggest these improvements may not be because patients feel happier. They may simply no longer care as much about what is making them feel depressed.”
Floresco, who conducted the study with PhD candidate Colin Stopper, says more investigation is needed to understand the complete brain functions involved in cost-benefit decision processes and related behaviour. A greater understanding of decision-making processes is also crucial, they say, because many psychiatric disorders, such as schizophrenia, stimulant abuse and depression, are associated with impairments in these processes.
The lateral habenula is considered one of the oldest regions of the brain, evolution-wise, the researchers say.
Professor Stephen Hawking has predicted that it could be possible to preserve a mind as powerful as his on a computer - but not with technology existing today.
The cosmologist, 71, said the brain operates in a similar way to a computer programme, meaning it could in theory be kept running without a body to power it.
Prof Hawking was speaking after the premiere of a new biopic about his life, which he narrates himself, at the Cambridge Film Festival.
Asked about whether a person’s consciousness can live on after they die, he said: “I think the brain is like a programme in the mind, which is like a computer, so it’s theoretically possible to copy the brain onto a computer and so provide a form of life after death.
"However, this is way beyond our present capabilities. I think the conventional afterlife is a fairy tale for people afraid of the dark."
The film tells the story of Prof Hawking’s life, from his childhood in Oxford to his current home in Cambridge where he lives with the help of a group of carers.
It addresses how he moved from being diagnosed with motor neurone disease at the age of 21, and being told he had three years left to live, to becoming the world’s most famous living scientist.
Addressing his condition, which has afflicted him for half a century, he says in the film: “Keeping an active mind has been vial to my survival,as has been maintaining a sense of humour.”
Speaking before the premiere on Thursday, Kip Thorne, the American physicist and a close friend of Prof Hawking, said: “I think his handicap allowed him to do science he may not otherwise have done.
"He is the most stubborn man I know and that stubbornness and that drive is in part motivated by his disability."
People with severe encephalitis — inflammation of the brain — are much more likely to die if they develop severe swelling in the brain, intractable seizures or low blood platelet counts, regardless of the cause of their illness, according to new Johns Hopkins research.
The Johns Hopkins investigators say the findings suggest that if physicians are on the lookout for these potentially reversible conditions and treat them aggressively at the first sign of trouble, patients are more likely to survive.
“The factors most associated with death in these patients are things that we know how to treat,” says Arun Venkatesan, M.D., Ph.D., an assistant professor of neurology at the Johns Hopkins University School of Medicine and leader of the study published in the Aug. 27 issue of the journal Neurology.
Experts consider encephalitis something of a mystery, and its origins and progress unpredictable. While encephalitis may be caused by a virus, bacteria or autoimmune disease, a precise cause remains unknown in 50 percent of cases. Symptoms range from fever, headache and confusion in some, to seizures, severe weakness or language disability in others. The most complex cases can land patients in intensive care units, on ventilators, for months. Drugs like the antiviral acyclovir are available for herpes encephalitis, which occurs in up to 15 percent of cases, but for most cases, doctors have only steroids and immunosuppressant drugs, which carry serious side effects.
“Encephalitis is really a syndrome with many potential causes, rather than a single disease, making it difficult to study,” says Venkatesan, director of the Johns Hopkins Encephalitis Center.
In an effort to better predict outcomes for his patients, Venkatesan and his colleagues reviewed records of all 487 patients with acute encephalitis admitted to The Johns Hopkins Hospital and Johns Hopkins Bayview Medical Center between January 1997 and July 2011. They focused further attention on patients who spent at least 48 hours in the ICU during their hospital stays and who were over the age of 16. Of those 103 patients, 19 died. Patients who had severe swelling in the brain were 18 times more likely to die, while those with continuous seizures were eight times more likely to die. Those with low counts in blood platelets, the cells responsible for clotting, were more than six times more likely to die than those without this condition.
The findings can help physicians know which conditions should be closely monitored and when the most aggressive treatments — some of which can come with serious side effects — should be tried, the researchers say. For example, it may be wise to more frequently image the brains of these patients to check for increased brain swelling and the pressure buildup that accompanies it.
Venkatesan says patients with cerebral edema may do better if intracranial pressure is monitored continuously and treated aggressively. He cautioned that although his research suggests such a course, further studies are needed to determine if it leads to better outcomes for patients.
Similarly, he says research has yet to determine whether aggressively treating seizures and low platelet counts also decrease mortality.
Venkatesan and his colleagues are also developing better guidelines for diagnosing encephalitis more quickly so as to minimize brain damage. Depending on where in the brain the inflammation is, he says, the illness can mimic other diseases, making diagnosis more difficult.
Another of the study’s co-authors, Romergryko G. Geocadin, M.D., an associate professor of neurology who co-directs the encephalitis center and specializes in neurocritical care, says encephalitis patients in the ICU are “the sickest of the sick,” and he fears that sometimes doctors give up on the possibility of them getting better.
“This research should give families — and physicians — hope that, despite how bad it is, it may be reversible,” he says.
Virginia Commonwealth University researchers studying a special class of potassium channels known as GIRKs, which serve important functions in heart and brain tissue, have revealed how they become activated to control cellular excitability.
The findings advance the understanding of the interaction between a family of signaling proteins called G proteins, and a special type of cell membrane ion pore called G protein-sensitive, inwardly rectifying potassium (GIRK) channels. The findings may one day help researchers develop targeted drugs to treat conditions of the heart such as atrial fibrillation.
In the study, published this week in the Online First section of Science Signaling, a publication of the American Association for the Advancement of Science (AAAS), researchers used a computational approach to predict the interactions between G proteins and a GIRK channel.
Rahul Mahajan, a M.D./Ph.D. candidate in the VCU School of Medicine’s Department of Physiology and Biophysics, undertook this problem for his dissertation work, under the mentorship of Diomedes E. Logothetis, Ph.D., chair of the Department of Physiology and Biophysics and the John D. Bower Endowed Chair in Physiology in the VCU School of Medicine. They developed a model and tested its predictions in cells, demonstrating how G proteins cause activation of GIRKs.
“Malfunctions of GIRK channels have been implicated in chronic atrial fibrillation, as well as in drug abuse and addiction,” said Logothetis, who is an internationally recognized leader in the study of ion channels and cell signaling mechanisms.
“Understanding the structural mechanism of Gβγ activation of GIRK channels could lead to rational based drug design efforts to combat chronic atrial fibrillation.”
In chronic atrial fibrillation, the GIRK channel is believed to be inappropriately open. According to Logothetis, if researchers are able to target only the specific site that keeps the channel inappropriately open, then any unrelated channels could be left unaltered, thus avoiding unwanted side effects.
Crystal structures of GIRK channels, which preceded the current study, have revealed two constrictions of the ion permeation pathway that researchers call “gates”: one at the inner leaflet of the membrane bilayer and the other close by in the cytosol, which is the liquid found inside cells.
“The structure of the Gβγ -GIRK1 complex reveals that Gβγ inserts a part of it in a cleft formed by two cytosolic loops of two adjacent channel subunits,” Logothetis said. “This is also the place where alcohols bind to activate the channel. One can think of this cleft as a clam that has its shells either open or shut closed. Stabilization of this cleft in the ‘open’ position stabilizes the cytosolic gate in the open state.”
GIRKs are activated when they interact with G proteins coupled to receptors bound to stimulatory hormones or neurotransmitters. In heart tissue, acetylcholine released by the vagus nerve activates these channels, which hyperpolarize the membrane potential and slow heart rate. In brain tissue, GIRKs inhibit excitation by acting at postsynaptic cells.
G proteins are composed of three subunits, a, b, and g. Since 1987, researchers have known that the Gbgsubunits directly activate the atrial GIRK channel, but an atomic resolution picture of how the two proteins interact remained elusive until now.
Moving forward, the team would like to use computational and experimental approaches to build and test the structures of the rest of the components of the G protein complex – for example, the Ga subunits and the G protein-coupled receptor – around the Gβγ-channel complex, which is the structure the team has already achieved.
Within 24 hours of quitting the drug, your withdrawal symptoms begin. Initially, they’re subtle: The first thing you notice is that you feel mentally foggy, and lack alertness. Your muscles are fatigued, even when you haven’t done anything strenuous, and you suspect that you’re more irritable than usual.
Over time, an unmistakable throbbing headache sets in, making it difficult to concentrate on anything. Eventually, as your body protests having the drug taken away, you might even feel dull muscle pains, nausea and other flu-like symptoms.
This isn’t heroin, tobacco or even alcohol withdrawl. We’re talking about quitting caffeine, a substance consumed so widely (the FDA reports thatmore than 80 percent of American adults drink it daily) and in such mundane settings (say, at an office meeting or in your car) that we often forget it’s a drug—and by far the world’s most popular psychoactive one.
Like many drugs, caffeine is chemically addictive, a fact that scientists established back in 1994. This past May, with the publication of the 5th edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM), caffeine withdrawal was finally included as a mental disorder for the first time—even though its merits for inclusion are symptoms that regular coffee-drinkers have long known well from the times they’ve gone off it for a day or more.
Why, exactly, is caffeine addictive? The reason stems from the way the drug affects the human brain, producing the alert feeling that caffeine drinkers crave.
Soon after you drink (or eat) something containing caffeine, it’s absorbed through the small intestine and dissolved into the bloodstream. Because the chemical is both water- and fat-soluble (meaning that it can dissolve in water-based solutions—think blood—as well as fat-based substances, such as our cell membranes), it’s able to penetrate the blood-brain barrier and enter the brain.
Structurally, caffeine closely resembles a molecule that’s naturally present in our brain, called adenosine (which is a byproduct of many cellular processes, including cellular respiration)—so much so, in fact, that caffeine can fit neatly into our brain cells’ receptors for adenosine, effectively blocking them off. Normally, the adenosine produced over time locks into these receptors and produces a feeling of tiredness.
When caffeine molecules are blocking those receptors, they prevent this from occurring, thereby generating a sense of alertness and energy for a few hours. Additionally, some of the brain’s own natural stimulants (such as dopamine) work more effectively when the adenosine receptors are blocked, and all the surplus adenosine floating around in the brain cues the adrenal glands to secrete adrenaline, another stimulant.
For this reason, caffeine isn’t technically a stimulant on its own, says Stephen R. Braun, the author or Buzzed: the Science and Lore of Caffeine and Alcohol, but a stimulant enabler: a substance that lets our natural stimulants run wild. Ingesting caffeine, he writes, is akin to “putting a block of wood under one of the brain’s primary brake pedals.” This block stays in place for anywhere from four to six hours, depending on the person’s age, size and other factors, until the caffeine is eventually metabolized by the body.
In people who take advantage of this process on a daily basis (i.e. coffee/tea, soda or energy drink addicts), the brain’s chemistry and physical characteristics actually change over time as a result. The most notable change is that brain cells grow more adenosine receptors, which is the brain’s attempt to maintain equilibrium in the face of a constant onslaught of caffeine, with its adenosine receptors so regularly plugged (studies indicate that the brain also responds by decreasing the number of receptors for norepinephrine, a stimulant). This explains why regular coffee drinkers build up a tolerance over time—because you have more adenosine receptors, it takes more caffeine to block a significant proportion of them and achieve the desired effect.
This also explains why suddenly giving up caffeine entirely can trigger a range of withdrawal effects. The underlying chemistry is complex and not fully understood, but the principle is that your brain is used to operating in one set of conditions (with an artificially-inflated number of adenosine receptors, and a decreased number of norepinephrine receptors) that depend upon regular ingestion of caffeine. Suddenly, without the drug, the altered brain chemistry causes all sorts of problems, including the dreaded caffeine withdrawal headache.
The good news is that, compared to many drug addictions, the effects are relatively short-term. To kick the thing, you only need to get through about 7-12 days of symptoms without drinking any caffeine. During that period, your brain will naturally decrease the number of adenosine receptors on each cell, responding to the sudden lack of caffeine ingestion. If you can make it that long without a cup of joe or a spot of tea, the levels of adenosine receptors in your brain reset to their baseline levels, and your addiction will be broken.
Autism affects different parts of the brain in females with autism than males with autism, a new study reveals. The research is published today in the journal Brain as an open-access article.
Scientists at the Autism Research Centre at the University of Cambridge used magnetic resonance imaging to examine whether autism affects the brain of males and females in a similar or different way. They found that the anatomy of the brain of someone with autism substantially depends on whether an individual is male or female, with brain areas that were atypical in adult females with autism being similar to areas that differ between typically developing males and females. This was not seen in men with autism.
“One of our new findings is that females with autism show neuroanatomical ‘masculinization’,” said Professor Simon Baron-Cohen, senior author of the paper. “This may implicate physiological mechanisms that drive sexual dimorphism, such as prenatal sex hormones and sex-linked genetic mechanisms.”
Autism affects 1% of the general population and is more prevalent in males. Most studies have therefore focused on male-dominant samples. As a result, our understanding of the neurobiology of autism is male-biased.
“This is one of the largest brain imaging studies of sex/gender differences yet conducted in autism. Females with autism have long been under-recognized and probably misunderstood,” said Dr Meng-Chuan Lai, who led the research project. “The findings suggest that we should not blindly assume that everything found in males with autism applies to females. This is an important example of the diversity within the ‘spectrum’.”
Dr Michael Lombardo, who co-led the study, added that although autism manifests itself in many different ways, grouping by gender may help provide a better understanding of this condition.
He said: “Autism as a whole is complex and vastly diverse, or heterogeneous, and this new study indicates that there are ways to subgroup the autism spectrum, such as whether an individual is male or female. Reducing heterogeneity via subgrouping will allow research to make significant progress towards understanding the mechanisms that cause autism.”
In a retrospective study, Saint Louis University researchers have found that patients with melanoma brain metastases can be treated with large doses of interleukin-2 (HD IL-2), a therapy that triggers the body’s own immune system to destroy the cancer cells.
The study that was recently published in Chemotherapy Research and Practice, reviews cases of eight patients who underwent this therapy at Saint Louis University.
John Richart, M.D., associate professor of internal medicine at SLU and principal investigator of the study, first treated a patient with the disease using the HD IL-2 treatment in 1999.
"Traditionally, melanoma patients with brain metastases have not been considered for HD IL-2 because treatment was thought to be futile," Richart said. "Our study shows that having this condition does not exclude a patient from getting this treatment and can in fact improve the length of their life."
Melanoma is the most dangerous form of skin cancer that begins in the melanin-producing cells called melanocytes. In some melanoma patients, the cancer spreads to the brain, causing multiple tumors that are difficult to treat. According to the CDC, melanoma is the third most common cancer causing brain metastases in the U.S. Richart said the median overall survival of patients with melanoma brain metastases is approximately four months whereas in the study, the median overall survival for patients was 8.7 months.
During the treatment, patients are given an IV medication - a chemical the body naturally makes that stimulates the immune system to recognize and destroy melanoma cells - for a period of six days while they are admitted to the hospital and are closely monitored by doctors and nurses. A patient requires four such six-day admission cycles in order to complete the course of the treatment.
To be eligible for HD IL-2 treatment, melanoma patients with brain metastases have to be in healthy shape with good brain function - that is they cannot have brain lesions that are growing rapidly or show any symptoms of brain lesions. In the past, melanoma patients with brain metastases have been considered ineligible for this treatment because doctors thought that the treatment would cause life-threatening cerebral edema, a complication that causes excess accumulation of fluids in the brain, and neurotoxicity, or irreversible damage to the brain or the nervous system.
"In this review, we found that there were no episodes of treatment-related mortality. Our findings demonstrate that HD IL-2 can be considered as an option for patients with melanoma brain metastases," said Melinda Chu, M.D., a first year dermatology resident at SLU and first author of the study.
SLU is the only medical center in the region that provides this treatment.
"We need a highly skilled nursing staff for the HD-IL-2 program to be successful," Richart said. "Our nursing team at SLU is with each patient every step of the way, 24 hours a day. They help patients get through and continue the treatment."
"I told my daughter her living room TV was out of sync. Then I noticed the kitchen telly was also dubbed badly. Suddenly I noticed that her voice was out of sync too. It wasn’t the TV, it was me."
Ever watched an old movie, only for the sound to go out of sync with the action? Now imagine every voice you hear sounds similarly off-kilter – even your own. That’s the world PH lives in. Soon after surgery for a heart problem, he began to notice that something wasn’t quite right.
"I was staying with my daughter and they like to have the television on in their house. I turned to my daughter and said ‘you ought to get a decent telly, one where the sound and programme are synchronised’. I gave a little chuckle. But they said ‘there’s nothing wrong with the TV’."
Puzzled, he went to the kitchen to make a cup of tea. “They’ve got another telly up on the wall and it was the same. I went into the lounge and I said to her ‘hey you’ve got two TVs that need sorting!’.”
That was when he started to notice that his daughter’s speech was out of time with her lip movements too. “It wasn’t the TV, it was me. It was happening in real life.”
PH is the first confirmed case of someone who hears people speak before registering the movement of their lips. His situation is giving unique insights into how our brains unify what we hear and see.
It’s unclear why PH’s problem started when it did – but it may have had something to do with having acute pericarditis, inflammation of the sac around the heart, or the surgery he had to treat it.
Brain scans after the timing problems appeared showed two lesions in areas thought to play a role in hearing, timing and movement. “Where these came from is anyone’s guess,” says PH. “They may have been there all my life or as a result of being in intensive care.”
Several weeks later, PH realised that it wasn’t just other people who were out of sync: when he spoke, he registered his words before he felt his jaw make the movement. “It felt like a significant delay, it sort of snuck up on me. It was very disconcerting. At the time I didn’t know whether the delay was going to get bigger, but it seems to have stuck at about a quarter of a second.”
Light and sound travel at different speeds, so when someone speaks, visual and auditory inputs arrive at our eyes and ears at different times. The signals are then processed at different rates in the brain. Despite this, we normally perceive the events as happening simultaneously – but how the brain achieves this is unclear.
To investigate PH’s situation, Elliot Freeman at City University London and colleagues performed a temporal order judgement test. PH was shown clips of people talking and was asked whether the voice came before or after the lip movements. Sure enough, he said it came before, and to perceive them as synchronous the team had to play the voice about 200 milliseconds later than the lip movements.
The team then carried out a second, more objective test based on the McGurk illusion. This involves listening to one syllable while watching someone mouth another; the combination makes you perceive a third syllable.
Since PH hears people speaking before he sees their lips move, the team expected the illusion to work when they delayed the voice. So they were surprised to get the opposite result: presenting the voice 200 ms earlier than the lip movements triggered the illusion, suggesting that his brain was processing the sight before the sound in this particular task.
And it wasn’t only PH who gave these results. When 37 others were tested on both tasks, many showed a similar pattern, though none of the mismatches were noticeable in everyday life.
Freeman says this implies that the same event in the outside world is perceived by different parts of your brain as happening at different times. This suggests that, rather than one unified “now”, there are many clocks in the brain – two of which showed up in the tasks – and that all the clocks measure their individual “nows” relative to their average.
In PH’s case, one or more of these clocks has been significantly slowed – shifting his average – possibly as a result of the lesions. Freeman thinks PH’s timing discrepancies may be too large and have happened too suddenly for him to ignore or adapt to, resulting in him being aware of the asynchrony in everyday life. He may perceive just one of his clocks because it is the only one he has conscious access to, says Freeman.
PH says that in general he has learned to live with the sensory mismatch but admits he has trouble in noisy places or at large meetings. Since he hears himself speak before he feels his mouth move, does he ever feel like he’s not in control of his own voice? “No, I’m definitely sure it’s me that’s speaking,” he says, “it’s just a strange sensation.”
Help may be at hand: Freeman is looking for a way to slow down PH’s hearing so it matches what he is seeing. PH says he would be happy to trial a treatment, but he’s actually not that anxious to fix the problem. “It’s not life-threatening,” he says. “You learn to live with these things as you get older. I don’t expect my body to work perfectly.”
A new study from Rush University Medical Center in Chicago claims reading and writing may preserve memory into old age. By keeping your brain active, says study author Robert S. Wilson, PhD, you’re able to slow the rate at which your memory decreases in later years.
This is not the first time researchers have arrived at such a conclusion, of course. Previous studies have also found keeping the brain active by reading, writing, completing crossword puzzles and more can essentially exercise the brain and keep it limber far into old age. One study also concluded that keeping television consumption to a minimal amount may also boost brain power over the years. Wilson’s study was recently published in the journal Neurology.
“Our study suggests that exercising your brain by taking part in activities such as these across a person’s lifetime, from childhood through old age, is important for brain health in old age,” said Wilson in a statement.
For his study, Wilson gathered nearly 300 people around the age of 80. He then gave them tests which were designed to measure both their memory and cognition each year until they passed away at an average age of 89. The same participants also answered questions about their past, such as whether they read books, did any writing, or engaged in any other mentally stimulating activities. The volunteers answered these questions for every part of their life, from childhood to adolescence, middle age and beyond.
When the participants passed away, their brains were then examined at an autopsy as Wilson’s team looked for physical evidence of dementia, such as lesions in the brain, tangles or plaques. After examining the brains of these volunteers and compiling the data from the questionnaires, Wilson’s team found those who had kept their minds active throughout their lives had a slower rate of memory decline than those who did not often participate in mentally challenging activities. Based on the amount of plaques and tangles in the brains, keeping your brain active is responsible for a 15 percent differential in memory decline.
The study also found the rate of memory decline was reduced by 32 percent in people who kept their brains active late in life. Those who were not mentally active had it much worse; their memories declined 48 percent faster than their actively reading and writing peers.
“Based on this, we shouldn’t underestimate the effects of everyday activities, such as reading and writing, on our children, ourselves and our parents or grandparents,” said Wilson.
And this news is hardly surprising. Doctors, teachers and parents have been admonishing children to turn off the television and pick up a book for years. There is no shortage of studies to back up their claims. A 2009 study, for example, found people who keep their brains active saw a 30 to 50 percent decrease in risk of developing memory loss. This study, conducted by doctors at the Mayo Clinic in Rochester, Minnesota observed people between the ages of 70 and 89 with and without diagnosed memory loss.
Those who were likely to read magazines or engage in other social activities were 40 percent less likely to develop memory loss than homebodies who did not read. Furthermore, those who spent less than seven hours a day watching television were 50 percent less likely to develop memory loss than those who planted themselves in front of the tube for long stretches of time.
Snakes and fish do it. Cats and dogs do it. Even human babies do it inside the womb. And maybe after seeing the picture above, you’re doing it now: yawning.
Yawning appears to be ubiquitous within the animal kingdom. But despite being such a widespread feature, scientists still can’t explain why yawning happens, or why for social mammals, like humans and their closest relatives, it’s contagious.
As yawning experts themselves will admit, the behavior isn’t exactly the hottest research topic in the field. Nevertheless, they are getting closer to the answer to these questions. An oft-used explanation for why we yawn goes like this: when we open wide, we suck in oxygen-rich air. The oxygen enters our bloodstream and helps to wake us up when we’re falling asleep at our desks.
Sounds believable, right? Unfortunately, this explanation is actually a myth, says Steven Platek, a psychology professor at Georgia Gwinnett College. So far, there’s no evidence that yawning affects levels of oxygen in the bloodstream, blood pressure or heart rate.
The real function of yawning, according to one hypothesis, could lie in the human body’s most complex system: the brain.
Yawning—a stretching of the jaw, gaping of the mouth and long deep inhalation, followed by a shallow exhalation—may serve as a thermoregulatory mechanism, says Andrew Gallup, a psychology professor at SUNY College at Oneonta. In other words, it’s kind of like a radiator. In a 2007 study, Gallup found that holding hot or cold packs to the forehead influenced how often people yawned when they saw videos of others doing it. When participants held a warm pack to their forehead, they yawned 41 percent of the time. When they held a cold pack, the incidence of yawning dropped to 9 percent.
The human brain takes up 40 percent of the body’s metabolic energy, which means it tends to heat up more than other organ systems. When we yawn, that big gulp of air travels through to our upper nasal and oral cavities. The mucus membranes there are covered with tons of blood vessels that project almost directly up to the forebrain. When we stretch our jaws, we increase the rate of blood flow to the skull, Gallup says. And as we inhale at the same time, the air changes the temperature of that blood flow, bringing cooler blood to the brains.
In studies of mice, an increase in brain temperature was found to precede yawning. Once the tiny rodents opened wide and inhaled, the temperature decreased. “That’s pretty much the nail in the coffin as far as the function of yawning being a brain cooling mechanism, as opposed to a mechanism for increasing oxygen in the blood,” says Platek.
Yawning as a thermoregulatory system mechanism could explain why we seem to yawn most often when it’s almost bedtime or right as we wake up. “Before we fall asleep, our brain and body temperatures are at their highest point during the course of our circadian rhythm,” Gallup says. As we fall asleep, these temperatures steadily decline, aided in part by yawning. But, he added, “Once we wake up, our brain and body temperatures are rising more rapidly than at any other point during the day.” Cue more yawns as we stumble toward the coffee machine. On average, we yawn about eight times a day, Gallup says.
Scientists haven’t yet pinpointed the reason we often feel refreshed after a hearty morning yawn. Platek suspects it’s because our brains function more efficiently once they’re cooled down, making us more alert as result.
A biological need to keep our brains cool may have trickled into early humans and other primates’ social networks. “If I see a yawn, that might automatically cue an instinctual behavior that if so-and-so’s brain is heating up, that means I’m in close enough vicinity, I may need to regulate my neural processes,” Platek says. This subconscious copycat behavior could improve individuals’ alertness, improving their chances of survival as a group.
Mimicry is likely at the heart of why yawning is contagious. This is because yawning may be a product of a quality inherent in social animals: empathy. In humans, it’s the ability to understand and feel another individual’s emotions. The way we do that is by stirring a given emotion in ourselves, says Matthew Campbell, a researcher at the Yerkes National Primate Research Center at Emory University. When we see someone smile or frown, we imitate them to feel happiness or sadness. We catch yawns for the same reasons—we see a yawn, so we yawn. “It isn’t a deliberate attempt to empathize with you,” Campbell says. “It’s just a byproduct of how our bodies and brains work.”
Platek says that yawning is contagious in about 60 to 70 percent of people—that is, if people see photos or footage of or read about yawning, the majority will spontaneously do the same. He has found that this phenomenon occurs most often in individuals who score high on measures of empathic understanding. Using functional magnetic resonance imaging (fMRI) scans, he found that areas of the brain activated during contagious yawning, the posterior cingulate and precuneus, are involved in processing the our own and others’ emotions. “My capacity to put myself in your shoes and understand your situation is a predictor for my susceptibility to contagiously yawn,” he says.
Contagious yawning has been observed in humans’ closest relatives, chimpanzees and bonobos, animals that are also characterized by their social natures. This begs a corollary question: is their capacity to contagiously yawn further evidence of the ability of chimps and bonobos to feel empathy?
Along with being contagious, yawning is highly suggestible, meaning that for English speakers, the word “yawn” is a representation of the action, a symbol that we’ve learned to create meaning. When we hear, read or think about the word or the action itself, that symbol becomes “activated” in the brain. “If you get enough stimulation to trip the switch, so to speak, you yawn,” Campbell says. “It doesn’t happen every time, but it builds up and at some point, you get enough activation in the brain and you yawn.”