Black & Decker has launched a new health division with a lineup of personal emergency response (PERS) wearables aimed at seniors. Called goVia, it includes devices that can be worn on the wrist or around the neck that can detect falls or allow seniors to call for aid via a monthly subscription powered by Medical Guardian.
The first device, called the goVia Mini ($125 on Amazon), has a battery life of five days and can be carried in bags or worn on belts or around the neck with an included lanyard. It comes with cellular coverage from Verizon’s 4G LTE network along with location tracking via GPS, WiFi and triangulation. If the wearer encounters an emergency, they can press the call button and speak with an operator directly through the device. A responder can then come directly to their location.
The goVia Move ($75) works in a similar way, but offers portable wearable help buttons that can be worn on the wrist. In case of emergency, you can press on either the button on the Move device itself or the portable button, though the latter has to be within 300 feet of the main unit. That will again connect you to an operator directly through the device, who can then send help to your location determined by a GPS.
The $45 goVia Home Classic device connects to a landline rather than a cellular service and includes a neck pendant or wristband (with a 600 foot range) that can be used to call for help at the press of a button. Black & Decker Health also offers the $50 goVia Home Wireless version that uses AT&T’s cellular services rather than a landline. Both offer a fall detection option (for an additional monthly cost) that can automatically detect motion changes caused by a fall and impact and automatically connect to emergency operators without the need for a landline.
While the devices themselves are relatively inexpensive, they all require monthly monitoring subscriptions provided by Medical Guardian that aren’t cheap. The goVia Mini’s service plan costs $39.95 per month, the goMove service is $44.95 a month, Home Classic is $29.95 monthly and Home Wireless is $34.95 per month, or $44.95 per month with fall detection.
Growing numbers of women are reporting as homeless in England as figures show rough sleeping in London has risen by 35% in five years.
More than 11,000 people were counted sleeping rough in the capital from April 2020 to March 2021, a 3% increase on the previous year, despite the push to get “everyone in” last spring. The homelessness charity Crisis described the figures as “dreadful” and said it showed progress resulting from the push to house people in hotels at the start of the pandemic was “in imminent danger of being lost”.Advertisement
After plateauing between 2014 and 2017, rough sleeping has been rising sharply since. The number of people counted sleeping in parks, doorways and other places not designated was almost double the number in 2011. The figures are commissioned by the Greater London Authority and are considered the UK’s most comprehensive data about rough sleeping.
Charities said the figures showed the battle against rough sleeping was at “a precipice”, with last month’s lifting of the eviction ban, the winding down of furlough and a chronic shortage of affordable housing all increasing the threat.
They also warned of a hidden crisis of women sleeping rough, with job losses in the hospitality sector and increasing domestic violence during the pandemic fuelling the surge. The homelessness charity Glass Door said that between 2020 and 2021, 26% of those it supported were women, up from 19% in 2018-19. New Horizon Youth Centre in London found that between April and June this year35% of its guests were female, comparedwith 10% in 2019.Advertisement
St Basils, a charity in the West Midlands, found 35% of those using services under the Everyone In scheme were young women.
Official rough sleeping statistics for England released in February show just 14% of rough sleepers were women and the new figures for London show 16% were women.
Outreach workers fear women are not being included in official rough sleeping statistics because they often go inside when the counts are happening, seeking shelter on buses or staying in A&E departments for safety.
The latest rough sleeping figures for London suggest the widely praised initiative to get people off the street was overwhelmed by new rough sleepers. Councils said more than 5,000 people were accommodated at the peak of the Everyone In initiative but the number of people bedding down in London for the first time had increased on the previous year.
“The Everyone In programme has been a huge success,” said Rick Henderson, the chief executive at the national homelessness membership charity Homeless Link. “But, by design, it was an emergency measure. Today’s news that over 7,500 people experienced sleeping rough in the capital for the first time in the past year shows that, for the government to meet its target of ending rough sleeping by 2024, it must start to address the root causes of homelessness too.”Advertisement
Jon Sparkes, the chief executive of Crisis, said: “It’s dreadful to see an increase in the numbers of people sleeping on our streets … in the past decade rough sleeping numbers have increased by a shocking 94%. There is nothing inevitable about this.”
Gemma Thapermall, a senior caseworker at Glass Door, said job loss was a key cause of homelessness for women but “when I start supporting these women I always notice there is something more going on”.
She said: “They may have come to the services with problems such as losing a job but other issues in their lives will soon become apparent, such as domestic abuse.”
Marike van Harskamp, from New Horizon, said men and women “negotiate street homelessness quite differently”, with women often not staying visible at night, meaning they do not appear in the data.
One woman helped by Glass Door, who asked to remain anonymous, moved to the UK two years ago from Romania and had been the victim of modern slavery when she first arrived. As her English improved she realised she was being exploited and got a job elsewhere as a waitress. However, she lost this job amid the pandemic and could not find anywhere to rent. She left one property due to threats of violence and ended up sleeping rough.Advertisement
She eventually received support from the charity and was able to get universal credit but said she found the experience “psychologically and physically very hard”.
“After living on the streets, I never in my life want to go back to that. I don’t want to sleep on the streets again even for a night,” she said.
Van Harskamp said New Horizon thought it was seeing more women due to increased levels of domestic violence during the pandemic. “Where young women are normally resourceful in finding informal arrangements with friends they found it harder during Covid, so instead presented at services,” she said.
“A third factor is that young women in normal times may be able to get early support, or it would be identified in college or via youth services, but these services closed due to coronavirus.”
What else did this research find? It found that over the course of the study the middle-aged people who did the least exercise and had the poorest sleep quality were 57% more likely to die than those who exercised most and slept best.
Tell me more. And also that physically active, young, thin, rich non-smokers with no mental health issues who eat lots of vegetables and drink little alcohol tend to sleep quite well at night.
Did they really need an 11-year study to find this out? However, people who exercised a lot and also slept poorly managed to counteract the negative effects of the latter with the benefits of the former.
I don’t understand. Poor sleep quality is, it turns out, really bad for you: those with the worst sleep scores were 67% more likely to die from a heart attack or stroke, and 45% more likely to die from cancer.
That’s exactly the sort of news that keeps me up at night. But the study found that a high level of physical activity “appeared to eliminate most of the deleterious associations of poor sleep and mortality”.
Surely the cure for not enough sleep is more sleep? Or loads of strenuous exercise.
But I’m tired! They all say that – get on that rowing machine.
How is this counteracting effect explained? The study was observational, didn’t get into causality, and its authors accept there are no widely established explanations for the association between low sleep quality and ill-health. But there may be some biological mechanism at work.
Such as? “Poor sleep has been linked with metabolic effects such as disturbed glucose control,” said Prof Mark Hamer, one of the study’s authors. “We know that physical activity has favourable effects on many metabolic pathways.”
How much exercise do I have to do to for this to work? More than the World Health Organization-recommended threshold of 600 metabolic-equivalent minutes a week.
Can I do that in bed? It’s the equivalent of 150 minutes of brisk walking or 75 minutes of running, so no.
Do say: “I couldn’t sleep, so I did press-ups all night instead.”
Don’t say: “Which is why I won’t be coming in to work today.”
The “scintillating starburst” stimulus. This stimulus is made up of several concentric pairs of scaled star polygons. Most observers perceive fleeting rays, beams, or lines emanating from the center that appear to be brighter than the background. Credit: Michael Karlovich, Recursia LLC
A new class of illusion, developed by a visual artist and a psychology researcher, underscores the highly constructive nature of visual perception.
The illusion, which the creators label “Scintillating Starburst,” evokes illusory rays that seem to shimmer or scintillate—like a starburst. Composed of several concentric star polygons, the images prompt viewers to see bright fleeting rays emanating from the center that are not actually there.
“The research illustrates how the brain ‘connects the dots’ to create a subjective reality in what we see, highlighting the constructive nature of perception,” explains Pascal Wallisch, a clinical associate professor in New York University’s Department of Psychology and Center for Data Science and senior author of the paper, which appears in the journal i-Perception.
“Studying illusions can be helpful in understanding visual processing because they allow us to distinguish the mere sensation of physical object properties from the perceptual experience,” adds first author Michael Karlovich, founder and CEO of Recursia Studios, a multidisciplinary art and fashion production company.
The authors acknowledge that the visual effects of this illusion are superficially similar to a number of previously described effects of other, grid-based illusions. However, their Scintillating Starburst, unlike known visual illusions, evokes a number of newly discovered effects, among them that fleeting illusory lines diagonally connect the intersection points of the star polygons.Play00:0000:08MuteSettingsPIPEnter fullscreenPlayThis stimulus is made up of several concentric pairs of scaled star polygons. Most observers perceive fleeting rays, beams, or lines emanating from the center that appear to be brighter than the background. Credit: Michael Karlovich, Recursia LLC
To better understand how we process this class of illusion, the researchers ran a series of experiments with more than 100 participants, who viewed 162 different versions of the Scintillating Starburst, which varied in shape, complexity, and brightness.
The research participants were then asked a series of questions about what they saw—for instance, “I do not see any bright lines, rays, or beams,” “I maybe see bright lines, rays, or beams, but they are barely noticeable,” and “I see bright lines, rays, or beams, but they are subtle and weak.”
The authors found that the confluence of several factors, including contrast, line width, and number of vertices, matters.
“In particular, a large number of prominent intersection points leads to stronger and more vivid rays, as there are more cues to indicate the implied lines,” observes Wallisch.
Thus, this research illustrates how the brain “connects the dots” to create one’s subjective reality, even on the perceptual level, highlighting the constructive nature of perception.
More information: Michael W. Karlovich et al, Scintillating Starbursts: Concentric Star Polygons Induce Illusory Ray Patterns, i-Perception (2021). DOI: 10.1177/20416695211018720Provided by New York University
A new discovery in rats shows that the brain responds differently in immersive virtual reality environments versus the real world. The finding could help scientists understand how the brain brings together sensory information from different sources to create a cohesive picture of the world around us. It could also pave the way for “virtual reality therapy” for learning and memory-related disorders ranging including ADHD, Autism, Alzheimer’s disease, epilepsy and depression.https://fc287dedc268dbf8569bb365b57f518a.safeframe.googlesyndication.com/safeframe/1-0-38/html/container.html#xpc=sf-gdn-exp-1&p=https%3A//medicalxpress.com
Mayank Mehta, Ph.D., is the head of W. M. Keck Center for Neurophysics and a professor in the departments of physics, neurology, and electrical and computer engineering at UCLA. His laboratory studies a brain region called the hippocampus, which is a primary driver of learning and memory, including spatial navigation. To understand its role in learning and memory, the hippocampus has been extensively studied in rats as they perform spatial navigation tasks.
When rats walk around, neurons in this part of the brain synchronize their electrical activity at a rate of 8 pulses per second, or 8 Hz. This is a type of brain wave known as the “theta rhythm,” and it was discovered more than six decades ago.
Disruptions to the theta rhythm also impair the rat’s learning and memory, including the ability to learn and remember a route through a maze. Conversely, a stronger theta rhythm seems to improve the brain’s ability to learn and retain sensory information.
Therefore, researchers have speculated that boosting theta waves could improve or restore learning and memory functions. But until now, nobody has been able to strengthen these brain waves.
“If that rhythm is so important, can we use a novel approach to make it stronger?” asks Dr. Mehta. “Can we retune it?”
Damage to neurons in the hippocampus can interfere with people’s perception of space—”why Alzheimer’s disease patients tend to get lost,” says Dr. Mehta. He says he suspected that the theta rhythm might play a role in this perception. To test that hypothesis, Dr. Mehta and his colleagues invented an immersive virtual reality environment for the rats that was far more immersive than commercially available VR for humans.
The VR allows the rats to see their own limbs and shadows, and eliminates certain unsettling sensations such as the delays between head movement and scene changes that can make people dizzy.
To measure the rats’ brain rhythms, the researchers placed tiny electrodes, thinner than a human hair, into the brain among the neurons.
“It turns out that amazing things happen when the rat is in virtual reality,” says Dr. Mehta. “He goes to the virtual fountain and drinks water, takes a nap there, looks around and explores the space as if it is real.”
Remarkably, Dr. Mehta says, the theta rhythm becomes considerably stronger when the rats run in the virtual space in comparison to their natural environment
“We were blown away when we saw this huge effect of VR experience on theta rhythm enhancement,” he says.
This discovery suggests that the unique rhythm is an indicator of how the brain discerns whether an experience is real or simulated. For instance, as you walk toward a doorway, the input from your eyes will show the doorway getting larger. “How do I know I took a step and it’s not the wall coming at me?” Dr. Mehta says.
Answer: The brain uses other information, such as the shift of balance from one foot to the other, the acceleration of your head through space, the relative changes in the positions of other stationary objects around you, and even the feeling of air moving against your face to decide that you are moving, not the wall.
On the other hand, a person “moving” through a virtual reality world would experience a very different set of stimuli.
“Our brain is constantly doing this, it’s checking all kinds of things,” Dr. Mehta says. The different theta rhythms, he says, may represent different ways that brain regions communicate with each other in the process of gathering all this information.
When they looked closer, Dr. Mehta’s team also discovered something else surprising. Neurons consist of a compact cell body and long tendrils, called dendrites, that snake out and form connections with other neurons. When the researchers measured activity in the cell body of a rat brain experiencing virtual reality, they found a different electrical rhythm compared with the rhythm in the dendrites. “That was really mind blowing,” Dr. Mehta said. “Two different parts of the neuron are going in their own rhythm.”
The researchers dubbed this never-before-seen rhythm “eta.” It turned out this rhythm was not limited to the virtual reality environment: with extremely precise electrode placement, the researchers were then able to detect the new rhythm in rats walking around a real environment. Being in VR, however, strengthened the eta rhythm—something no other study in the past sixty years has been able to do so strongly, either using pharmacological tools or otherwise, according to Dr. Mehta.
Previous studies have shown that the precise frequency of the rhythm makes a big difference to neuroplasticity, he says, just as the precise pitch of a musical instrument is critical for creating the right melody. This opens up an unprecedented opportunity to design VR therapy that can retune and boost brain rhythms and as a way to treat learning and memory disorders.
“This is a new technology that has tremendous potential,” he says. “We have entered a new territory.”
Chronic pain is like a horror movie monster that sneaks up on you. It’s unpredictable, lingers silently, and when it strikes it’s often too late to tame. More diabolically, our best weapon against it—pain medication—can increase pain intensity over time. And as the opioid epidemic sadly shows, even pain medication is a double-edged sword.
It’s time for something new. This week, a group from the New York University School of Medicine said “no thank you” to medication altogether. Instead, they engineered a “neural bridge” that connects two brain regions: one critical for detecting pain, the other that dampens pain when activated.
For a brain implant, this one’s particularly special. It’s basically a tag-team of spy and sleeper agent. The “spy” listens to electrical chatter in a brain region that processes pain—along with dozens of other tasks—and decodes it in real time. Once it detects an electrical signal that suggests “pain found,” it sends the information to the “sleeper agent,” a computer chip implanted in the front part of the brain. The chip then automatically triggers a light beam to stimulate the region, activating neurons that can override pain signals.
Yeah, it’s pretty wild.
The beauty of this particular brain-machine interface (BMI) is it only activates when there is pain, instead of zapping the brain all the time. That is, it’s specific and efficient.
For now, the device has only been tested in rats. But it’s a “blueprint” for tuning the brain to ease pain in the future, the authors wrote.
“Our findings show that this implant offers an effective strategy for pain therapy, even in cases where symptoms are traditionally difficult to pinpoint or manage,” said Drs. Jing Wang and Valentino D.B. Mazzia, who led the study.
Closing the Loop
From the Utah Array and BrainGate, the OGs of brain implants, to Neuralink’s sleek neural interface with stitched-in electrode threads, brain implants have reached mainstream status.
But most deal with only one part of the equation: sensing and decoding. It’s already a herculean task, and allows brains to literally link to a computer. Monkeys playing Pong with their minds. Paralyzed people typing or browsing the web with brain waves.
The harder part is linking the brain to itself—or other parts of the nervous system. Rather than using decoded signals to control a cursor, here the signals control another brain region, or a body part.
Prosthetic hands, for example, can be equipped with electrical stimulators that transmit feelings of pressure, temperature, or other sensations by zapping remaining nerves. These signals are then transmitted to the brain, where it decodes them and sends orders back through a separate collection of nerve highways to control how the hand moves. Another example are brain stimulators that detect abnormal electrical patterns associated with a seizure and automatically zap brain regions to disrupt those signals.
These systems go from sensing or action alone, to intricately linking both—hence their name, “closed-loop systems.” They function similarly to our own brains: regions that receive input process the data and transmit it to other relevant regions. These signals then trigger an outcome—awareness, movement, or maybe, a change in sensation.
A Neural Bridge
Inspired by previous studies, the authors engineered a closed-loop system for pain.
Whether it worked was a coin toss. Using closed-loop brain implants is “highly speculative” for sensory disorders, the team said. Unlike motor movements—for example, controlling a cursor—pain is very difficult to pin down in the brain.
The authors said they first had to decide on “an input arm for signal detection and an output arm for treatment.”
For the input (pain-decoding) arm, they honed in on the anterior cingulate cortex (ACC), a U-shaped strip of the brain that’s been shown to process pain in animals and humans. Here, they implanted a microarray of electrodes to listen in on brain signals.
The output treatment arm was an optical fiber inserted into the prelimbic prefrontal cortex (PFC). Previous studies showed that activation of PFC neurons can dampen pain signals from the ACC in both rodents and primates. If the ACC is a crying toddler who stubbed his toe, the PFC is the parent going “it’ll be alright.” The optical fiber uses optogenetics—a method that leverages light to control genetically-engineered neurons—to activate the PFC. Together, the system forms a real-time feedback loop that, in theory, suppresses pain as soon as it sparks in the brain.
Pain Relief
The team first tested the system for sudden, acute pain in rats—the type you feel when burning your hand on a hot stove, or stepping on a Lego block. The decoder, an algorithm called a “state-space model,” could reliably parse pain signals with up to 80% accuracy and a few seconds delay. It could also reliably pick up signals for mechanical pain—a light pin prick to the rat’s footpad like the tip of a needle that catches your fingertip when sewing.
Once the team turned the stimulator on, the animals withdrew their paws 40% more slowly, suggesting pain relief.
In another test for both mechanical and chronic pain from inflammation—think arthritis, chronic back pain, or fibromyalgia—the team put the rats into a double chamber. On one side, the implant turned on when it detected pain signals. On the other, it turned on randomly. The rats spent far more time in the former chamber, suggesting the implant dampened their pain as it occurred.
Similarly, the implant also worked for neuropathic pain—a condition where the problem is pain itself. Here, the nerves and sensors that transmit pain become ultrasensitive, so even a light touch can feel painful. Here, the rats also responded to the brain implant, spending more time in the chamber where pain relief is turned on.
A New Era of Pain Management
The study breaks ground. It’s one of the first to use a smart, closed-loop brain implant to detect and relieve bursts of pain in real time. It’s also the first to target chronic pain, which often sparks without a known trigger.
But it’s just the start. Although most brain implants begin with research in rats, it’s a long road bridging rodent to primate to human. One particular challenge is where to capture pain signals. The ACC, where the team implanted electrodes to detect pain signals in this study, is a Grand Central Station of sorts. It has vast connections to other brain regions, giving it a diverse set of roles in addition to pain processing—empathy, decision-making, social behaviors.
“Currently, because we do not have specific anatomic targets for pain treatment, most brain regions…will inevitably have non-specific effects,” the authors said.
For a prototype approach, activity recorded from the ACC could be used for pain detection, the authors explained, adding that the interface may reveal better targets for recording chronic pain signals in animal models—and potentially in humans.
What’s especially neat is that the stimulated brain region normally doesn’t generate any sense of euphoria, the downfall of opioids. This means it’s likely to decrease the chance of addiction. And because the system only stimulates the brain when it detects pain signals, it lowers the chance the brain adapts to the stimulation. That is, instead of turning the brain into an alcoholic requiring increasingly more booze, it’s more like being the occasional social drinker.
While brain implants may seem like overkill to treat pain, for chronic sufferers, they could represent a new choice—similar to the choice given to people with epilepsy, who were some of the first to implant closed-looped BCIs to curb their seizures, giving them hope when drugs didn’t work.
We can decode pain from signals in the brain as they occur, the authors said. Our results show it’s possible to counteract those signals, with a new “blueprint for therapy.”
SHELLY FANShelly Xuelai Fan is a neuroscientist-turned-science writer. She completed her PhD in neuroscience at the University of British Columbia, where she developed novel treatments for neurodegeneration. While studying biological brains, she became fascinated with AI and all things biotech. Following graduation, she moved to UCSF to study blood-based factors that rejuvenate aged brains.
Neuroscientists have developed a method for predicting when your mind might go blank or completely forget whatever it was we were talking about.
Slow waves, a pattern of neural activity commonly associated with the transition to sleep, could be a good prediction of that unedifying moment in a meeting when you’ve forgotten the name of the person you’re talking to and indeed the subject about which you are supposed to be talking, while instead idly daydreaming of tonight’s dinner.
Such lapses occur more often when people are tired, and researchers argue they could be linked to a neural phenomenon called “local sleep”, where certain brain regions show signs of being in slow-wave sleep while the rest of the brain is alert. Although the link has been made in sleep-deprived rodents and humans, it had not been demonstrated in well-rested humans.
That is until Thomas Andrillon, a research fellow at the Institut du Cerveau, or Paris Brain Institute, and his colleagues recorded whole brain electrical activity with electroencephalography in 26 well-rested adult humans.
Subjects were asked to perform tasks focusing on images of faces or numbers for an average of 1.7 hours. They were also told to press a button in response to certain facial expressions or digits to maintain their focus.
But – and here’s the tricky part – the participants were interrupted at random every 30 to 70 seconds. Then researchers asked whether their mental state was “task-focused, mind-wandering or mind-blanking” and about their levels of sleepiness. At the same time eye pupil size was measured.
According to a paper published in Nature Communications today, researchers showed that slow waves in frontal brain areas preceded daydreaming and impulsive behaviour. However, when the same wave patterns occur further back in the brain they seemed to indicate mind blanking and slow responsiveness.
“The location of slow waves could distinguish between sluggish and impulsive behaviours, and between mind wandering and mind blanking. Our results suggest attentional lapses share a common physiological origin: the emergence of local sleep-like activity within the awake brain,” the paper said.
The importance of the study is underscored by the observation that both in-lab and real-life studies show humans spend up to half of their waking lives not paying attention to their environment or any task at hand, remarkable for a species with such a strong evolutionary track record. At least now the researchers can suggest a physiological link to predict a wandering or blank mind.
“We propose that these slow waves reflect local intrusions of sleep within waking and constitute a mechanistic and proximate cause to explain attentional lapses. Identifying a proximate mechanism of attentional lapses could inspire novel applications leveraging brain-machine interfaces in educational or professional settings,” the paper said.
It does not elaborate further on the precise “novel applications”, but we’re imagining a bucket of cold water propelled from behind the monitor, or a cartoon-like slap about the chops should the machine side of the interface suspect the human of not being “all there” following a large lunch.
During their everyday life, humans can regulate their negative emotions in different ways, most of which do not require any conscious cognitive engagement. For instance, they might take a bath, step outside for fresh air or listen to music.
Researchers at Radboud University Nijmegen in The Netherlands, the Norwegian University of Science and Technology (NTNU), and University Hospital Aachen, Germany have recently carried out a study aimed at investigating the effects of a short-term musical training on implicit emotion regulation. Their paper, published in BMC Neuroscience, specifically examined whether musical training helped people to reduce the negative emotions elicited by unpleasant or disgusting odors.
“At the time of conception, my colleagues and I worked in the same department in Aachen,” Nils Kohn, one of the researchers who carried out the study, told MedicalXpress. “The project was born out of our curiosity for emotions and the power of mood induction that is harbored by music. Mark Berthold-Losleben, being more of a trained musician than myself, was the perfect person to discuss this with.”
Kohn, Berthold-Losleben and their colleagues decided to investigate whether, in a controlled environment, music could change people’s emotional responses to unpleasant smells. They focused on olfaction because previous studies found that odors can consistently lead to emotional responses.
Their paper draws on previous knowledge about the stability of olfaction and its neuroanatomical connections, which was gathered by their research group in the past. In addition, it builds on Kohn’s theoretical interpretation of how implicit emotion regulation works.
“In the first draft of our paper, we also wanted to explore implicit emotion regulation among professional musicians and/or composers,” Berthold-Losleben said. “Therefore, we initiated a cooperation with the school for music and dance in Cologne to recruit participants. Unfortunately, most musicians didn’t meet our schedule or the study’s inclusion criteria. Another problem was that professional musicians, or at least those we tried to recruit, did not like the positive auditory stimuli as much as non-professionals did. We assumed that this was because of their professional and therefore more complex approach to music. Maybe our stimuli were too well-known and boring to them.
To investigate the effects of musical training on implicit emotion regulation, Kohn, Berthold-Losleben and their colleagues designed a simple experiment in which they paired negative olfaction (eliciting a negative emotion) with positive music to create four different combinations of stimuli. They then recruited 31 healthy participants to take part in their experiment.
Essentially, participants were either exposed to an odor similar to rotten eggs or to no odors at all. Simultaneously, they either listened to an excerpt of classical music or to a neutral range of tones.
“We then added three weeks of passive listening to classical music as our musical intervention for participants and re-did the test,” Kohn explained. “In the task, subjects had to always rate how disgusting the smell was, how they liked the music and how they felt in general. This was done while the subjects lay in the fMRI scanner.”
Overall, the findings gathered by the researchers suggest that listening to music two times per day for three weeks can reduce negative emotions elicited by a bad odor, particularly if one hears music again. In other words, music could improve wellbeing and help people to regulate negative emotions elicited by an external stimulus.
If they were also applicable to individuals with psychiatric disorders, the findings gathered by this team of researchers could have important implications. For instance, they could highlight the value of musical interventions for increasing stress resilience and helping people with affective disorders to better regulate their emotions.
“Patients suffering from affective disorders like depression often find themselves in an endless circle of sameness,” Berthold-Losleben said. “Once confronted with triggers that lead to negative affect, they react with negative emotions/feelings, negative body experiences and negative thinking. All of that itself can trigger a new negative affect. These patients tend to end up in a negative circle or spiral which it is difficult or impossible to get out of.”
The overreaching goal of the work by Kohn, Berthold-Losleben and their colleagues is to devise simple musical interventions for people with depression or other affective disorders, which are easy to implement and could improve their ability to regulate negative emotions. Firstly, however, they had to gain a better understanding of emotion regulation and of the stimuli that can elicit or reduce negative emotions.
“We are now trying to initiate a collaboration between Radboud University Nijmegen and the Norwegian University of Science and Technology in Trondheim to continue this line of research, as I’m still very interested in what challenges our abilities to regulate ourselves in our daily life and what can support us,” Kohn said. “Music would truly be such an easy, powerful and supportive tool for emotion regulation.”
More information: Short-term musical training affects implicit emotion regulation only in behavior but not in brain activity. BMC Neuroscience(2021). DOI: 10.1186/s12868-021-00636-1.Journal information:BMC Neuroscience
A brain imaging study published in Frontiers in Behavioral Neuroscience found evidence that the low mood that accompanies a romantic breakup can affect executive functioning. The researchers found that greater depressive symptomology among heartbroken subjects was associated with reduced activation of a network of brain areas involved in working memory.
The study’s authors Anne M. Verhallen and her colleagues were motivated by numerous studies suggesting that stress and depression are associated with neural and behavioral changes in executive functioning — and particularly, changes in working memory. The researchers proposed that one way to investigate these effects might be by studying people experiencing a recent breakup.
As expected, depressive symptomology was greater among the heartbreak group than the relationship group. Interestingly, while the two groups performed similarly during the high workload trials, the heartbreak group showed greater accuracy and a faster reaction time during the low workload trials when compared to the relationship group. The study authors say that this superior performance among the heartbreak group might be evidence of improved sensory information processing, which has previously been reported among people dealing with acute stress.
Next, the researchers looked for group differences in brain activation during the tasks. Compared to the relationship group, the heartbreak group showed reduced activation in the precuneus, an area of the brain implicated in memory retrieval. They also found that when the heartbreak group took part in the high workload trials, changes in precuneus activation were accompanied by changes in brain regions that make up the working memory network — the anterior cingulate gyrus, the supplementary motor cortex, and the lateral occipital cortex.
Moreover, among the heartbreak group, as depressive symptomology increased, activation decreased among a cluster of brain regions that included the anterior cingulate gyrus, precuneus, and the supplementary motor cortex — again, key areas involved in working memory processing.
“Given that our heartbreak sample includes otherwise healthy individuals reporting elevated depression scores after a stressful event, this specific working memory-related network may be of importance with regard to the transition from healthy behavior, and corresponding brain activity, to depressive behavior during a disturbing period in life,” Verhallen and her colleagues discuss.
While the sample did not include many subjects with clinical-level depressive symptoms (only a quarter of subjects), the findings offer evidence that even those who present with mild depressive symptomology can show changes in brain activation during a working memory task.
The researchers conclude that studying people who are going through a relationship breakup can offer insight into the relations between stressful events, depression, and executive functioning. Importantly, such research might shed light on possible risk factors for the development of clinical depression following stress.
Is your sleep not what it used to be? Does your mind race when your head hits the pillow? Do you wake up at 4am and struggle to fall back asleep? Are you feeling drowsy and sleep-deprived no matter how many hours you spend in bed?
For many people, sleeping poorly was the norm before the pandemic. Then the stress, anxiety and disruptions made our nightly slumber worse, giving rise to terms such as “coronasomnia” to describe the surge in sleep disturbances last year. But recently, sleep experts noticed something that astonished them: more than a year into the pandemic, our collective sleep only continued to deteriorate.
In a survey of thousands of adults last summer, the American Academy of Sleep Medicine found that 20 per cent of people said they had trouble sleeping because of the pandemic. But when the academy repeated its survey 10 months later, in March, those numbers rose drastically. Roughly 60 per cent of people said they struggled with pandemic-related insomnia, and nearly half reported that the quality of their sleep had diminished — even though infection rates have fallen and the country is opening back up.
“A lot of people thought that our sleep should be getting better because we can see the light at the end of the tunnel — but it’s worse now than it was last year,” says Dr Fariha Abbasi-Feinberg, a sleep medicine specialist and spokesperson for the American Academy of Sleep Medicine. “People are still really struggling.”
Chronically bad sleep is more than just a nuisance. It weakens the immune system, reduces memory and attention span, and increases the likelihood of chronic conditions such as depression, type 2 diabetes and heart disease. The shorter your sleep, studies suggest, the shorter your life span. And for people over 50, sleeping less than six hours a night may even heighten the risk of dementia.
“Over the past year, we’ve had the perfect storm of every possible bad thing that you can do for your sleep,” says Dr Sabra Abbott, an assistant professor of neurology in sleep medicine at Northwestern University Feinberg School of Medicine in Chicago.
Those who benefited the most were people who naturally tend to go to bed late but no longer had to set an early alarm to commute to work or get their children ready for school
Studies show that in the pandemic, people tended to keep irregular sleep schedules, going to bed far later and sleeping in longer than usual, which can disrupt our circadian rhythms. We slashed our physical activity levels and spent more time indoors; gained weight and drank more alcohol; and erased the lines that separate work and school from our homes and our bedrooms — all of which are damaging to sleep.
Most striking of all, our stress and anxiety levels skyrocketed, which are two of the root causes of insomnia. In a report published in May, the American Psychiatric Association found that a majority of Americans were still anxious about their health, their finances and the possibility of a loved one getting Covid-19. More than half of parents said they were worried about the mental state of their children, and 41 per cent of adults said they had more anxiety today than they did during the first few months of the pandemic.
Not everyone, of course, is suffering from disrupted sleep. A team of international researchers who studied 3 million people in New York, London, Los Angeles, Seoul and Stockholm found that on average, people gained an extra 25 minutes of sleep each night during the pandemic compared with a year earlier. Those who benefited the most were people who naturally tend to go to bed late but no longer had to set an early alarm to commute to work or get their children ready for school, says Matthew Walker, a professor of neuroscience and psychology at the University of California, Berkeley, and author of the bestselling book Why We Sleep.about:blankjavascript:void(0)javascript:void(0)✕
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“If there is a success story, it is revenge of the night owls when it comes to Covid and sleep,” Walker says. “The night owls are finally starting to sleep a little more in synchrony with their biology.”
But for millions of others who suffer from insomnia, the extra time in bed can paradoxically make matters worse. When people struggle to fall or stay asleep, their brains associate their beds with stressful experiences. “Your brain learns that your bed is the place where you don’t fall asleep,” Abbott says. “The more time you spend in bed, the more you reinforce that idea.”https://b8de3cbe1522c28da8cb50d06388ca53.safeframe.googlesyndication.com/safeframe/1-0-38/html/container.html
One of the standard treatments for insomnia is a strategy called sleep restriction, which makes people better and more efficient sleepers by teaching them to spend less time in bed, not more.
So what more can we do to get our disrupted sleep back on track? Read on.
How to beat insomnia
It’s normal to have trouble sleeping during big changes in your life. But when the sleep disruptions last longer than three months, it can qualify as chronic insomnia, which can have long-term health consequences. One of the most effective treatments is cognitive behavioral therapy, or CBT. This approach helps you address the underlying thoughts, feelings and behaviors that are ruining your sleep. Here are some CBT-inspired ways to combat insomnia.
If you get into bed and can’t fall asleep after 25 minutes, or you wake up at night and can’t get back to sleep after 25 minutes, then don’t stay in bed. Get up and do a quiet activity that calms your mind and makes you drowsy. “Just get up, don’t fret,” Walker says. “If you stay in bed awake for long periods of time, your brain thinks, ‘Every time I get into bed, this is the place where I should be awake.’ And you need to break that association.”
Do any activity that relaxes you. Get up and stretch. Sit on your couch and meditate or read a magazine. Read a book in dim light. Do deep-breathing exercises. Listen to a soothing podcast. You could sit in a chair and draw or knit. Then, when you start to feel drowsy again, get back into bed and try to go to sleep. Just don’t get into bed unless you are tired. “You would never sit at the dinner table waiting to get hungry,” Walker says. “So why would you lie in bed waiting to get sleepy?”
Throw away your worries
Sit down with a blank piece of paper one to two hours before bed each night. Then write down all of your thoughts, especially anything that is bothering you. It could be what you’re going to do at work tomorrow, the phone calls you have to make or the bills you have to pay. “If most of what you’ve written down is stuff that you’re worried about, then crumple up the paper and throw it in the trash — that’s called discharging your thoughts,” says Dr Ilene M. Rosen, a sleep medicine doctor and associate professor of medicine at the Perelman School of Medicine at the University of Pennsylvania. The act of dumping your thoughts on a piece of paper and throwing it away is a symbolic gesture that empowers you and calms your mind, Rosen says. “You had those thoughts and now they’re gone.”
Screens in the bedroom
One reason sleep has suffered this past year is that people are sacrificing their slumber to catch up on all the fun things that they missed out on during the day, such as scrolling through Instagram and watching YouTube videos. This phenomenon, known as revenge bedtime procrastination, is made worse by our attachment to our phones and screens, which often follow us into our beds. (How many times have you been glued to your phone long past your bedtime?)
We all know that we shouldn’t look at bright screens late at night because the blue light they emit tells your brain that it’s time to be awake. But many of us do it anyway. So follow this guideline: if you are going to use your phone or device after your bedtime, then use it only while standing. When you feel like sitting or lying down, you have to put the device away. “You’ll find after about 10 minutes of standing up at your normal bedtime that you’re going to say, ‘I need to lie down’ — and that’s your body telling you that you need to put the phone away and get to sleep,” Walker says.
Good sleep starts long before bedtime. Many of the things you do during the day will impact the quality of your slumber. So try these sleep-promoting habits.
Wake up at the same time
Our bodies follow a daily circadian rhythm, and waking up at different times throws it out of whack. It is best to keep your wake-up time consistent. Don’t sleep in, even on weekends. “When the alarm goes off, get out of bed and start your day regardless of how much you’ve slept,” Rosen says. “You may not feel great for a few days, but you’re reinforcing that when you’re in bed, you sleep.” The same goes for your bedtime: keep it consistent. The less you deviate from your normal bed and wake-up times, the better you’ll sleep.
Get sunlight every morning
If you don’t commute to work, it can be easy to spend your entire mornings inside. But exposure to sunlight serves an important purpose: it shuts down the release of melatonin, a hormone that promotes sleep. “Most brain fog in the morning is caused by continued melatonin production,” says Michael Breus, a clinical psychologist and author of The Power of When. “When sunlight hits your eye, it sends a signal to your brain to tell the melatonin faucet to turn off.” Aim to get at least 15 minutes of sunlight first thing every morning.
Make your bed a haven
Working from home — sometimes from our beds — has erased a lot of the boundaries between work and sleep. But turning your mattress into an office can condition your brain to view your bed as a place that makes you stressed and alert, which can lead to insomnia. That’s why sleep experts say you have to reserve your bed for two activities only. “The bed is for sleeping or sex,” Rosen says. “If you’re not doing either of those things, then get out of bed. If you have the luxury of going to a different room, then that’s even better. You have to break the association of being awake in bed.”
‘The closer you drink to your bedtime, the worse your sleep is going to be’(Getty/iStock)
Exercise for better sleep
The pandemic led people to cut back on physical activity. But exercise is the easiest way to improve sleep, Breus says. “Sleep is recovery,” he added. “If you don’t have anything to recover from, your sleep isn’t going to be that great.” At least 29 studies have found that daily exercise, regardless of the type or intensity, helps people fall asleep faster and stay asleep longer, especially among people who are middle-aged or older. According to the Sleep Foundation, people with chronic insomnia can fall asleep about 13 minutes faster and gain up to 20 extra minutes of sleep per night by starting an exercise routine. One caveat: end your exercise at least four hours before bedtime; otherwise, it could interfere with your sleep by raising your core body temperature, Breus says.
Cut off caffeine at 2pm
Caffeine has a half-life of six to eight hours and a quarter-life of about 12 hours. That means that if you drink coffee at 4pm, “you’ll still have a quarter of the caffeine floating around in your brain at 4am,” Breus says. Avoiding caffeine in the evening is a no-brainer. But, ideally, you should steer clear of caffeine after 2pm so your body has enough time to metabolise and clear most of it from your system.
Follow the two-drink rule
If you drink alcohol, limit yourself to two drinks in the evening and stop at least three hours before bed. Alternate each drink with a glass of water. Because alcohol is a sedative, some people drink a nightcap to help them fall asleep faster. But alcohol suppresses rapid eye movement (REM) sleep and causes sleep disruptions, which will worsen the overall quality of your sleep. “The closer you drink to your bedtime, the worse your sleep is going to be,” Breus says.
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