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Why Justin Trudeau Is Able to Stand Up to Donald Trump

Why Justin Trudeau Is Able to Stand Up to Donald Trump

Right now is a nice time to be Canadian. Brought up in Canada, as I was, and married to a woman so Canadian that she is both Winnipeg Icelandic and Winnipeg Jewish (you would have to be a Canadian to grasp the full glory of that combination), I have the immediate urge to praise Canada, set in motion by Justin Trudeau’s recent rebuke of Donald Trump at the G-7 summit. There, Trudeau made it plain that he and his country were not about to be bullied by the American President, not on a question of unilateral tariffs, not about anything. Trump responded with gangster-style threats and sneers, followed by more threats and sneers from his associates. Trudeau, a young man generally thought to lack the great prime-ministerial gravitas of his late father, Pierre, emerged as a statesman and a leader. On Monday, the Canadian Parliament voted its unanimous support for his statements.

Instantly and hilariously, this was recognized as Justin’s “Love Actually” moment—named for the scene in that holiday-film classic in which the British Prime Minister, played with an oddly Trudeau-like reticence and charm by Hugh Grant (O.K., how else does Grant play anything?), quietly and against the advice of his advisers, repudiates an Ugly American President, and becomes beloved by the British people. The “Love Actually” American prez, to be sure, merely combined the worst features of George W. Bush’s insularity and Bill Clinton’s lechery—the clowning cruelty of Trump being beyond the imagination of even British romantic comedies of that era.

The question worth asking is what it is in the Canadian national character, if I may call it that, that makes Canadians so ready to take on bullies? Canada has been doing this as long as there has been a Canada. The Mounties wear red coats, we were taught in school, to defy villains by their very presence. More seriously, Lester Pearson prompted Charles de Gaulle to cut short a visit to the country, in 1967, after he had insulted Canadian sovereignty. When Pierre Trudeau learned that Richard Nixon, in 1971, had called him an “asshole,” he delivered an unforgettable Canadian retort: “I’ve been called worse things by better people.” Canada also negotiated its way through a constitutional crisis of Quebec nationalism to emerge with the country reasonably, if imperfectly, elucidated by bilingualism from coast to coast, and Quebec reasonably secure within the confederation.

Famously obliging in attitude—how do you get twenty-five Canadians out of a swimming pool? You say, “Please get out of the swimming pool”—Canadians are also notoriously stubborn of spirit. What gives them backbone alongside their gift for compromise, allowing them to bend equably and then snap back sharply? One might be inclined to say that it’s their national sports. Canada has two: curling, a sport in which absolutely nothing happens, slowly; and hockey, a sport in which everything happens, too quickly to follow. But there is a genuine answer to the question: it’s love, actually.

Canadian democracy is supported by some of the strongest social capital in the world, exceeded only, by most academic measures, by that of Scandinavia and New Zealand. Trust in social institutions, in the honesty of government and the solidarity of citizens, remains strong in Canada, even when its results, as with the election of Doug Ford—the smarter brother of the late Rob Ford, the onetime mayor of Toronto—to the premiership of Ontario, is not what progressive-minded people might like. Though United States now ranks below Canada, it still scored high in recent registries. But it once led the world in social capital. Can it do so again?

What do we mean by social capital? The term seems to have originated, or at least become most closely associated, with the Harvard political scientist Robert Putnam. His book “Making Democracy Work: Civic Traditions in Modern Italy,” published in 1993, is a study of what happened after the powerful central government in Rome “democratized,“ in 1970, transferring some power to regional governments. Putnam discovered that the existence of “intermediate institutions” was crucial: in northern Italy, where citizens participate actively in sports clubs, literary guilds, service groups, and choral societies, regional governments are “efficient in their internal operation, creative in their policy initiatives and effective in implementing those initiatives.” In southern Italy, by contrast, where patterns of civic engagement are far weaker, regional governments tend to be corrupt and inefficient.

Putnam explained this relationship between strong networks of citizen participation and positive institutional performance with “social capital.” Translated from the sociologese, this makes perfect sense. If you have experience working outside your immediate clan or cohort, you’re likelier to be able to practice democratic politics. It’s the same idea that the philosopher Jürgen Habermas captured in the phrase “the public sphere,” when he showed how essential civic life was to the Enlightenment: a government is only as strong as its cafés. The most poetic term to describe the idea that I know of comes from Frederick Law Olmsted, the designer of Central Park. Olmsted is a doubly interesting liberal hero, because, although he is best known now as a kind of urban pastoralist, he was also one of the first great American journalists. In one of the first famous reports that the Times published, Olmsted compared the Southern states with those of the North and found that, for all the South’s cultural self-proclamation, it was a paralyzed, frozen society, while the Northwas full of activity. “Our young men are members and managers of reading rooms, public libraries, gymnasiums, game clubs, boat clubs, ball clubs, and all sorts of clubs, Bible classes, debating societies, military companies; they are planting road-side trees, or damming streams for skating ponds, or rigging diving-boards, or getting up fireworks displays, or private theatricals; they are always doing something,” he wrote. Olmsted called this orgy of sociability “commonplace civilization.”

By this measure, it was the strength of Canada’s commonplace civilization, the knowledge that a huge and hugely variegated country would find bullying unacceptable, that gave Trudeau the nerve to speak in ways that previously had been the province of escapist romantic comedy. He was, of course, speaking up practically for Canadian aluminium- and steelworkers. But the thing that sparked his countrymen’s admiration seems to be not simply his defense of their interests but his defense of the idea that there is more to politics than the rituals of domination and submission, which are the sum total of Donald Trump’s understanding of society. Trudeau is hardly a perfect politician, and in the months leading up to the G-7 he had plenty of political pratfalls and problems of his own, but the unanimity of support that his defiance achieved was a marker of renewed trust.

Beneath the days’ conflicts between Trudeau and Trump lay a deeper conflict between a society that, for all its difficulties, has a strong public sphere and a powerful sense of solidarity—and the American one, that is debased every day by its own leader. The bankruptcy of America’s social capital becomes more evident when we see it flourish elsewhere. It’s no accident that Trudeau, in addition to receiving the support of his own Parliament, has received that of what used to be called the free world. The American President, meanwhile, has found himself more at home with the brutal leaders of gangster governments. Not an accident at all. But certainly a tragedy.

Potassium and Vitamin K in Avocado

How to read the label

  1. Start with the serving size and servings per package.
    A serving of avocado is based on 1/3 of a medium avocado (50 grams) so there are three servings per avocado.
  2. Check calories (and calories from fat).
    Based on a 2,000 calorie diet the FDA’s general guide to calories in a serving of food is:

    • 40 Calories is low
    • 100 Calories is moderate
    • 400 Calories or more is high

    One-third of a medium avocado (50g) has 80 calories and contributes nearly 20 vitamins, minerals and beneficial plant compounds making it a good nutrient choice.

  3. Look at the nutrients to help limit or increase your nutrient consumption.
    According to the FDA, eating too much-saturated fat, trans fat, or sodium may increase your risk of heart disease, some cancers, or high blood pressure. Health experts recommend limiting your intake of saturated fat, trans fat, added sugars, and sodium as part of a nutritionally balanced diet.

    Avocados, due to their mono and polyunsaturated fat content, are a great substitution for foods rich in saturated fat or added sugars.

  4. Check the % DV column to see how much of the FDA recommended Daily Value for key nutrients (based on a 2,000 calorie daily diet) the avocado provides.

For more information on FDA Guidelines for Nutrition Labeling and help on how to read the nutrition label –visit the U.S. Food and Drug Administration site here.

One cup (4.6 servings, 230g) of pureed avocado has…

  • 368 Calories
  • 4.6g of Protein
  • 19.62g of Carbohydrate
  • 1166mg of Potassium
  • 23.0mg of Vitamin C
  • 175mg Beta-sitosterol
  • 0mg Cholesterol

The information above is based on the USDA National Nutrient Database for Standard Reference.
Search the database for “avocado”.

Fresh avocados – More than Great Taste!

2015 Dietary Guidelines for Americans emphasize making small dietary shifts to achieve an overall healthy eating pattern, such as replacing foods higher in saturated fats with foods containing good fats, like avocados. The Guidelines and the American Heart Association recommend eating a variety of nutritious foods from all food groups. Eating a variety of fruits and vegetables may help one control their weight, cholesterol and blood pressure. As one step towards managing weight, the USDA recommends choosing foods that are “nutrient-rich,” like fruits and vegetables, that are low in “extras” that just add calories.

Avocados Now Defined as “Healthy”

The U.S. Food and Drug Administration (FDA) has new guidance for the use of the nutrient content claim “healthy” on food labeling, and fresh avocados meet the criteria. The new proposed guidance from FDA, in light of new scientific evidence and recommendations from the Dietary Guidelines, gives consideration to the types of fats in a food. The Dietary Guidelines for Americans state that the type of fat, rather than the total amount, is most important for good health. Avocados contain 8g of fat per 50g serving, over 75% of which are naturally good fats (monounsaturated and polyunsaturated fats).

Nutrition Facts

Serving Size1/3 medium (50g)

Amount Per Serving
Calories 80
% Daily Value*
Total Fat 8g 10%
Saturated Fat 1g 5%
Trans Fat
Polyunsaturated Fat 1g
Monounsaturated Fat 5g
Cholesterol 0mg 0%
Sodium 0mg 0%
Carbohydrates 4g 1%
Dietary fiber 3g 11%
Sugar 0g
Added sugars 0g
Protein 1g
Vitamin D 0mcg 0%
Calcium 10mg 0%
Iron 0.3mg 2%
Potassium 250mg 6%
Vitamin A 0mcg 0%
Vitamin C 4mg 4%
Vitamin E 1mg 6%
Vitamin K 11mcg 10%
Thiamin 0.04mg 4%
Riboflavin 0.1mg 8%
Niacin 1mg 6%
Vitamin B6 0.1mg 6%
Folate

(0mcg folic acid)

45mcg DFE

10%
Pantothenic Acid 0.7mg 15%
Phosphorus 30mg 2%
Magnesium 15mg 4%
Zinc 0.3mg 2%
Copper 0.1mg 10%
Manganese 0.1mg 4%

The % Daily Value (DV) tells you how much a nutrient in a serving of food contributes to a daily diet. 2,000 calories a day is used for general nutrition advice.

*The % Daily Value tells you how much a nutrient in a serving of food contributes to a daily diet. 2,000 calories a day is used for general nutrition advice.


The avocado nutrition facts label is designed to be compliant with the FDA
Guidelines for Nutrition Labeling
.

Leg Exercise is Critical to Brain and Nervous System Health

Leg Exercise is Critical to Brain and Nervous system health

Summary: Weight bearing leg exercises send signals to the brain which are vital for the production of healthy neural cells, researchers report.

Source: Frontiers.

Groundbreaking research shows that neurological health depends as much on signals sent by the body’s large, leg muscles to the brain as it does on directives from the brain to the muscles. Published today in Frontiers in Neuroscience, the study fundamentally alters brain and nervous system medicine — giving doctors new clues as to why patients with motor neuron disease, multiple sclerosis, spinal muscular atrophy and other neurological diseases often rapidly decline when their movement becomes limited.

“Our study supports the notion that people who are unable to do load-bearing exercises — such as patients who are bed-ridden, or even astronauts on extended travel — not only lose muscle mass, but their body chemistry is altered at the cellular level and even their nervous system is adversely impacted,” says Dr. Raffaella Adami from the Università degli Studi di Milano, Italy.

The study involved restricting mice from using their hind legs, but not their front legs, over a period of 28 days. The mice continued to eat and groom normally and did not exhibit stress. At the end of the trial, the researchers examined an area of the brain called the sub-ventricular zone, which in many mammals has the role of maintaining nerve cell health. It is also the area where neural stem cells produce new neurons.

Limiting physical activity decreased the number of neural stem cells by 70 percent compared to a control group of mice, which were allowed to roam. Furthermore, both neurons and oligodendrocytes — specialized cells that support and insulate nerve cells — didn’t fully mature when exercise was severely reduced.

The research shows that using the legs, particularly in weight-bearing exercise, sends signals to the brain that are vital for the production of healthy neural cells, essential for the brain and nervous system. Cutting back on exercise makes it difficult for the body to produce new nerve cells — some of the very building blocks that allow us to handle stress and adapt to challenge in our lives.

“It is no accident that we are meant to be active: to walk, run, crouch to sit, and use our leg muscles to lift things,” says Adami. “Neurological health is not a one-way street with the brain telling the muscles ‘lift,’ ‘walk,’ and so on.”

The researchers gained more insight by analyzing individual cells. They found that restricting exercise lowers the amount of oxygen in the body, which creates an anaerobic environment and alters metabolism. Reducing exercise also seems to impact two genes, one of which, CDK5Rap1, is very important for the health of mitochondria — the cellular powerhouse that releases energy the body can then use. This represents another feedback loop.

These results shed light on several important health issues, ranging from concerns about cardio-vascular impacts as a result of sedentary lifestyles to insight into devastating diseases, such as spinal muscular atrophy (SMA), multiple sclerosis, and motor neuron disease, among others.

leg exercise

“I have been interested in neurological diseases since 2004,” says co-author Dr. Daniele Bottai, also from the Università degli Studi di Milano. “The question I asked myself was: is the outcome of these diseases due exclusively to the lesions that form on the spinal cord in the case of spinal cord injury and genetic mutation in the case of SMA, or is the lower capacity for movement the critical factor that exacerbates the disease?”

This research demonstrates the critical role of movement and has a range of potential implications. For example, missions to send astronauts into space for months or even years should keep in mind that gravity and load-bearing exercise play an important role in maintaining human health, say the researchers.

“One could say our health is grounded on Earth in ways we are just beginning to understand,” concludes Bottai.

ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE

Funding: Funding provided by Asamsi ONLUS, Italy and Vertical Foundation.

Source: Emma Duncan – Frontiers 
Publisher: Organized by NeuroscienceNews.com.
Image Source: NeuroscienceNews.com image is in the public domain.
Original Research: Open access research for “Reduction of Movement in Neurological Diseases: Effects on Neural Stem Cells Characteristics” by Raffaella Adami, Jessica Pagano, Michela Colombo, Natalia Platonova, Deborah Recchia, Raffaella Chiaramonte, Roberto Bottinelli, Monica Canepari and Daniele Bottai in Frontiers in Neuroscience. Published May 23 2018
doi:10.3389/fnins.2018.00336

Frontiers “Leg Exercise is Critical to Brain and Nervous System Health.” NeuroscienceNews. NeuroscienceNews, 23 May 2018.
<http://neurosciencenews.com/leg-exercise-brain-health-9118/&gt;.

Abstract

Reduction of Movement in Neurological Diseases: Effects on Neural Stem Cells Characteristics

Both astronauts and patients affected by chronic movement-limiting pathologies face impairment in muscle and/or brain performance. Increased patient survival expectations and the expected longer stays in space by astronauts may result in prolonged motor deprivation and consequent pathological effects. Severe movement limitation can influence not only the motor and metabolic systems but also the nervous system, altering neurogenesis and the interaction between motoneurons and muscle cells. Little information is yet available about the effect of prolonged muscle disuse on neural stem cells characteristics. Our in vitro study aims to fill this gap by focusing on the biological and molecular properties of neural stem cells (NSCs). Our analysis shows that NSCs derived from the SVZ of HU mice had shown a reduced proliferation capability and an altered cell cycle. Furthermore, NSCs obtained from HU animals present an incomplete differentiation/maturation. The overall results support the existence of a link between reduction of exercise and muscle disuse and metabolism in the brain and thus represent valuable new information that could clarify how circumstances such as the absence of load and the lack of movement that occurs in people with some neurological diseases, may affect the properties of NSCs and contribute to the negative manifestations of these conditions.

Is It Rational to Trust Your Gut Feelings?

Is It Rational to Trust Your Gut Feelings?

Source: The Conversation.

Imagine the director of a big company announcing an important decision and justifying it with it being based on a gut feeling. This would be met with disbelief – surely important decisions have to be thought over carefully, deliberately and rationally?

Indeed, relying on your intuition generally has a bad reputation, especially in the Western part of the world where analytic thinking has been steadily promoted over the past decades. Gradually, many have come to think that humans have progressed from relying on primitive, magical and religious thinking to analytic and scientific thinking. As a result, they view emotions and intuition as fallible, even whimsical, tools.

However, this attitude is based on a myth of cognitive progress. Emotions are actually not dumb responses that always need to be ignored or even corrected by rational faculties. They are appraisals of what you have just experienced or thought of – in this sense, they are also a form of information processing.

Intuition or gut feelings are also the result of a lot of processing that happens in the brain. Research suggests that the brain is a large predictive machine, constantly comparing incoming sensory information and current experiences against stored knowledge and memories of previous experiences, and predicting what will come next. This is described in what scientists call the “predictive processing framework”.

This ensures that the brain is always as prepared to deal with the current situation as optimally as possible. When a mismatch occurs (something that wasn’t predicted), your brain updates its cognitive models.

This matching between prior models (based on past experience) and current experience happens automatically and subconsciously. Intuitions occur when your brain has made a significant match or mismatch (between the cognitive model and current experience), but this has not yet reached your conscious awareness.

For example, you may be driving on a country road in the dark listening to some music, when suddenly you have an intuition to drive more to one side of the lane. As you continue driving, you notice that you have only just missed a massive pothole that could have significantly damaged your car. You are glad you relied on your gut feeling even if you don’t know where it came from. In reality, the car in the far distance in front of you made a similar small swerve (since they are locals and know the road), and you picked up on this without consciously registering it.

When you have a lot of experience in a certain area, the brain has more information to match the current experience against. This makes your intuitions more reliable. This means that, as with creativity, your intuition can actually improve with experience.

Biased understanding

In the psychological literature, intuition is often explained as one of two general modes of thinking, along with analytic reasoning. Intuitive thinking is described as automatic, fast, and subconscious. Analytic thinking, on the other hand, is slow, logical, conscious and deliberate.

Many take the division between analytic and intuitive thinking to mean that the two types of processing (or “thinking styles”) are opposites, working in a see-saw manner. However, a recent meta-analysis – an investigation where the impact of a group of studies is measured – has shown that analytic and intuitive thinking are typically not correlated and could happen at the same time.

So while it is true that one style of thinking likely feels dominant over the other in any situation – in particular analytic thinking – the subconscious nature of intuitive thinking makes it hard to determine exactly when it occurs, since so much happens under the bonnet of our awareness.

Indeed, the two thinking styles are in fact complementary and can work in concert – we regularly employ them together. Even groundbreaking scientific research may start with intuitive knowledge that enables scientists to formulate innovative ideas and hypotheses, which later can be validated through rigorous testing and analysis.

What’s more, while intuition is seen as sloppy and inaccurate, analytic thinking can be detrimental as well. Studies have shown that overthinking can seriously hinder our decision-making process.

brain scans

In other cases, analytic thinking may simply consist of post-hoc justifications or rationalisations of decisions based on intuitive thinking. This occurs for example when we have to explain our decisions in moral dilemmas. This effect has let some people refer to analytic thinking as the “press secretary” or “inner lawyer” of intuition. Oftentimes we don’t know why we make decisions, but we still want to have reasons for our decisions.

Trusting instincts

So should we just rely on our intuition, given that it aids our decision-making? It’s complicated. Because intuition relies on evolutionarily older, automatic and fast processing, it also falls prey to misguidances, such as cognitive biases. These are systematic errors in thinking, that can automatically occur. Despite this, familiarising yourself with common cognitive biases can help you spot them in future occasions: there are good tips about how to do that here and here.

Similarly, since fast processing is ancient, it can sometimes be a little out of date. Consider for example a plate of donuts. While you may be attracted to eat them all, it is unlikely that you need this large an amount of sugars and fats. However, in the hunter-gatherers’ time, stocking up on energy would have been a wise instinct.

Thus, for every situation that involves a decision based on your assessment, consider whether your intuition has correctly assessed the situation. Is it an evolutionary old or new situation? Does it involve cognitive biases? Do you have experience or expertise in this type of situation? If it is evolutionary old, involves a cognitive bias, and you don’t have expertise in it, then rely on analytic thinking. If not, feel free to trust your intuitive thinking.

It is time to stop the witch hunt on intuition, and see it for what it is: a fast, automatic, subconscious processing style that can provide us with very useful information that deliberate analysing can’t. We need to accept that intuitive and analytic thinking should occur together, and be weighed up against each other in difficult decision-making situations.

ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE

Funding: Valerie van Mulukom has worked on analytical and intuitive thinking research for projects funded by BIAL Foundation grants (62/06 and 380/14) awarded to Dr Miguel Farias (Coventry University).

Source: Valerie van Mulukom – The Conversation 
Publisher: Organized by NeuroscienceNews.com.
Image Source: NeuroscienceNews.com image is credited to Valerie van Mulukom.

New Algorithm Determines Ideal Caffeine Dosage and Timing For Alertness

New Algorithm Determines Ideal Caffeine Dosage and Timing For Alertness

Summary: Researchers have developed a new algorithm that can determine the ideal time to consume, and correct dosage of caffeine that can maximize alertness under sleep loss conditions.

Source: AASM.

According to a recent study, a newly developed algorithm may be the key to optimizing alertness with caffeine.

Caffeine is the most widely consumed stimulant to counter the effects of sleep loss on neurobehavioral performance. However, to be safe and most effective, it must be consumed at the right time and in the right amount. This study proposed an automated optimization algorithm to identify safe and effective caffeine-dosing strategies that maximize alertness under any sleep-loss condition.

“We found that by using our algorithm, which determines when and how much caffeine a subject should consume, we can improve alertness by up to 64 percent, while consuming the same total amount of caffeine,” said principal investigator and senior author Jaques Reifman, PhD. “Alternatively, a subject can reduce caffeine consumption by up to 65 percent and still achieve equivalent improvements in alertness.”

Reifman is a senior research scientist and director of DoD Biotechnology High Performance Computing Software Applications Institute and the Telemedicine and Advanced Technology Research Center at the U.S. Army Medical Research and Materiel Command in Ft. Detrick, Maryland.

The study used a validated mathematical model, which predicts the effects of sleep loss and caffeine on psychomotor vigilance task (PVT) performance and combined it with a computationally efficient optimization algorithm to determine when and how much caffeine to consume to safely maximize alertness during sleep loss. The algorithm takes a user-provided sleep/wake schedule and maximum allowed caffeine as inputs and provides a caffeine-dosing strategy as the output.

The algorithm was assessed by computing and comparing dosing strategies for four previously published experimental studies of sleep loss. For each study, two dosing strategies were computed–one which enhanced the predicted PVT performance using the same total amount of caffeine as in the original studies, and another which achieved an equivalent level of performance as in the original studies using a lower amount of caffeine.

coffee beans in a cup

Compared to the original dosing strategies used in the studies, the U.S. Army’s algorithm identified strategies that enhanced neurobehavioral performance by up to 64 percent, or reduced caffeine consumption by up to 65 percent. According to the authors, these results suggest that the algorithm can tailor the timing and amount of caffeine to the particular sleep/wake schedule of each study condition to maximize its benefits.

“Our algorithm is the first quantitative tool that provides automated, customized guidance for safe and effective caffeine dosing to maximize alertness at the most needed times during any sleep-loss condition,” said Reifman.

ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE

Source: Corinne Lederhouse – AASM 
Publisher: Organized by NeuroscienceNews.com.
Image Source: NeuroscienceNews.com image is in the public domain.
Original Research: The study “Caffeine Dosage Strategies that Efficiently Enhance Alertness during Sleep Loss” by Vital-Lopez F, Ramakrishnan S, Doty TJ, Balkin TJ, and Reifman J will be presented at SLEEP 2018.

AASM “New Algorithm Determines Ideal Caffeine Dosage and Timing For Alertness.” NeuroscienceNews. NeuroscienceNews, 4 June 2018.
<http://neurosciencenews.com/ai-caffeine-alertness-9236/&gt;.

Abstract

Caffeine Dosage Strategies that Efficiently Enhance Alertness during Sleep Loss

Introduction: Caffeine is the most widely consumed stimulant to counter the effects of sleep loss on neurobehavioral performance. However, to be safe and most effective, it must be consumed at the right time and in the right amount. Caffeine-dosing recommendations offered by prior studies are not readily adaptable to any arbitrary sleeploss condition. Here, we propose an automated optimization algorithm to identify safe and effective caffeine-dosing strategies that maximize alertness under any sleep-loss condition.

Methods: We used our validated unified model of performance, which predicts the effects of sleep loss and caffeine on psychomotor vigilance task (PVT) performance, and combined it with a computationally efficient optimization algorithm to determine when and how much caffeine to consume to safely maximize alertness during sleep loss. The algorithm takes a user-provided sleep/wake schedule and maximum allowed caffeine as inputs, and provides a caffeine-dosing strategy as the output. We assessed the algorithm by computing and comparing dosing strategies for six previously published experimental studies of sleep loss. For each study, we computed two dosing strategies—one which enhanced the predicted PVT performance using the same total amount of caffeine as in the original studies, and another which achieved an equivalent level of performance as in the original studies using a lower amount of caffeine.

Results: Compared to the original dosing strategies used in the studies, our algorithm identified strategies that enhanced neurobehavioral performance by up to 64%, or reduced caffeine consumption by up to 65%. These results suggest that the algorithm can tailor the timing and amount of caffeine to the particular sleep/wake schedule of each study condition to maximize its benefits.

Conclusion: Our algorithm is the first quantitative tool that provides automated, customized guidance for safe and effective caffeine dosing to maximize alertness at the most needed times during any sleep-loss condition.

Support (If Any): This work was sponsored by the Military Operational Medicine Program Area Directorate of the U.S. Army Medical Research and Materiel Command, Ft. Detrick, MD, and by the U.S. Department of Defense Medical Research and Development Program (Grant No. DMRDP_13200).

Ketamine and Psychedelic Drugs Change Structure of Neurons

Ketamine and Psychedelic Drugs Change Structure of Neurons

Summary: A new study reveals psychedelics increase dendrites, dendritic spines and synapses, while ketamine may promote neuroplasticity. The findings could help develop new treatments for anxiety, depression and other related disorders.

Source: UC Davis.

A team of scientists at the University of California, Davis is exploring how hallucinogenic drugs impact the structure and function of neurons — research that could lead to new treatments for depression, anxiety, and related disorders. In a paper published on June 12 in the journal Cell Reports, they demonstrate that a wide range of psychedelic drugs, including well-known compounds such as LSD and MDMA, increase the number of neuronal branches (dendrites), the density of small protrusions on these branches (dendritic spines), and the number of connections between neurons (synapses). These structural changes suggest that psychedelics are capable of repairing the circuits that are malfunctioning in mood and anxiety disorders.

“People have long assumed that psychedelics are capable of altering neuronal structure, but this is the first study that clearly and unambiguously supports that hypothesis. What is really exciting is that psychedelics seem to mirror the effects produced by ketamine,” said David Olson, assistant professor in the Departments of Chemistry and of Biochemistry and Molecular Medicine, who leads the research team.

Ketamine, an anesthetic, has been receiving a lot of attention lately because it produces rapid antidepressant effects in treatment-resistant populations, leading the U.S. Food and Drug Administration to fast-track clinical trials of two antidepressant drugs based on ketamine. The antidepressant properties of ketamine may stem from its tendency to promote neural plasticity — the ability of neurons to rewire their connections.

“The rapid effects of ketamine on mood and plasticity are truly astounding. The big question we were trying to answer was whether or not other compounds are capable of doing what ketamine does,” Olson said.

Psychedelics show similar effects to ketamine

Olson’s group has demonstrated that psychedelics mimic the effects of ketamine on neurons grown in a dish, and that these results extend to structural and electrical properties of neurons in animals. Rats treated with a single dose of DMT — a psychedelic compound found in the Amazonian herbal tea known as ayahuasca — showed an increase in the number of dendritic spines, similar to that seen with ketamine treatment. DMT itself is very short-lived in the rat: Most of the drug is eliminated within an hour. But the “rewiring” effects on the brain could be seen 24 hours later, demonstrating that these effects last for some time.

image shows neurons under psychedelics and ketamine

Behavioral studies also hint at the similarities between psychedelics and ketamine. In another recent paper published in ACS Chemical Neuroscience, Olson’s group showed that DMT treatment enabled rats to overcome a “fear response” to the memory of a mild electric shock. This test is considered to be a model of post-traumatic stress disorder (PTSD), and interestingly, ketamine produces the same effect. Recent clinical trials have shown that like ketamine, DMT-containing ayahuasca might have fast-acting effects in people with recurrent depression, Olson said.

These discoveries potentially open doors for the development of novel drugs to treat mood and anxiety disorders, Olson said. His team has proposed the term “psychoplastogen” to describe this new class of “plasticity-promoting” compounds.

“Ketamine is no longer our only option. Our work demonstrates that there are a number of distinct chemical scaffolds capable of promoting plasticity like ketamine, providing additional opportunities for medicinal chemists to develop safer and more effective alternatives,” Olson said.

ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE

Additional coauthors on the Cell Reports study are Calvin Ly, Alexandra Greb, Sina Soltanzadeh Zarandi, Lindsay Cameron, Jonathon Wong, Eden Barragan, Paige Wilson, Michael Paddy, Kassandra Ori-McKinney, Kyle Burbach, Megan Dennis, Alexander Sood, Whitney Duim, Kimberley McAllister, and John Gray.

Olson and Cameron were coauthors on the ACS Chemical Neuroscience paper along with Charlie Benson and Lee Dunlap.

Funding: The work was partly supported by grants from the National Institutes of Health.

Source: Andy Fell – UC Davis 
Publisher: Organized by NeuroscienceNews.com.
Image Source: NeuroscienceNews.com image is credited to Calvin and Joanne Ly.
Original Research: Open access research for “Psychedelics Promote Structural and Functional Neural Plasticity” by Calvin Ly, Alexandra C. Greb, Lindsay P. Cameron, Jonathan M. Wong, Eden V. Barragan, Paige C. Wilson, Kyle F. Burbach, Sina Soltanzadeh Zarandi, Alexander Sood, Michael R. Paddy, Whitney C. Duim, Megan Y. Dennis, A. Kimberley McAllister, Kassandra M. Ori-McKenney, John A. Gray, and David E. Olson in Current Biology. Published April 6 2018
doi:10.1016/j.celrep.2018.05.022

CITE THIS NEUROSCIENCENEWS.COM ARTICLE
UC Davis “Ketamine and Psychedelic Drugs Change Structure of Neurons.” NeuroscienceNews. NeuroscienceNews, 12 June 2018.
<http://neurosciencenews.com/ketamine-psychedelics-neuron-structure-9314/&gt;.

Abstract

Psychedelics Promote Structural and Functional Neural Plasticity

Highlights
•Serotonergic psychedelics increase neuritogenesis, spinogenesis, and synaptogenesis
•Psychedelics promote plasticity via an evolutionarily conserved mechanism
•TrkB, mTOR, and 5-HT2A signaling underlie psychedelic-induced plasticity
•Noribogaine, but not ibogaine, is capable of promoting structural neural plasticity

Summary
Atrophy of neurons in the prefrontal cortex (PFC) plays a key role in the pathophysiology of depression and related disorders. The ability to promote both structural and functional plasticity in the PFC has been hypothesized to underlie the fast-acting antidepressant properties of the dissociative anesthetic ketamine. Here, we report that, like ketamine, serotonergic psychedelics are capable of robustly increasing neuritogenesis and/or spinogenesis both in vitro and in vivo. These changes in neuronal structure are accompanied by increased synapse number and function, as measured by fluorescence microscopy and electrophysiology. The structural changes induced by psychedelics appear to result from stimulation of the TrkB, mTOR, and 5-HT2A signaling pathways and could possibly explain the clinical effectiveness of these compounds. Our results underscore the therapeutic potential of psychedelics and, importantly, identify several lead scaffolds for medicinal chemistry efforts focused on developing plasticity-promoting compounds as safe, effective, and fast-acting treatments for depression and related disorders.

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The Art of Switching Antiepileptic Medications: Keep Trying or Just Let It Be

The Art of Switching Antiepileptic Medications: Keep Trying or Just Let It Be

Commentary

Seizure Recurrence and Remission After Switching Antiepileptic Drugs.

Wang SP, Mintzer S, Skidmore CT, Zhan T, Stuckert E, Nei M, Sperling MR. [Published online ahead of print August 29, 2012, Epilepsia. doi: 10.1111/j.1528-1167.2012.03652.x.]

PURPOSE: Studies of seizure outcome in patients undergoing serial antiepileptic drug trials have all been uncontrolled, with no account made for the spontaneous changes in disease state that could confound the elucidation of drug effects.

In addition, no study has ever looked at outcome following antiepileptic drug switch in seizure-free patients, despite the fact that this is done routinely in clinical practice.

We aimed to address both of these issues using a matched case-cohort design. METHODS: We followed patients taking phenytoin or carbamazepine in monotherapy for focal epilepsy who were being crossed over to a newer agent as part of studies on the metabolic effects of anticonvulsant therapy.

Many had been seizure-free but were being switched nonetheless due to side effects or concerns about long-term adverse consequences. Each patient was matched with two controls of the same seizure status who were taking anticonvulsant monotherapy and whose drug was not switched. Seizure freedom over the ensuing 6 months was the primary end point.

KEY FINDINGS:

There were 43 cases and 86 matched controls. Twenty-three patients (cases) had been seizure-free on their old drug; 5 (21.7%) had seizure recurrence after drug switch compared to 2 (4.3%) of 46 matched controls. Twenty patients (cases) were having seizures on their old drug; 6 (30%) entered remission after drug switch, compared to 8 of 40 matched controls (20%).

The two groups differed at baseline in number of anticonvulsants previously failed, which was the most important factor for prognosis. After statistical adjustment to account for this, seizure-free patients had 6.53 times higher odds of seizure recurrence if switched to a new drug (95% confidence interval [CI] 1.02–61.19; p = 0.06).

Non-seizure-free patients had 1.66 times higher odds of remission if they remained on the same drug compared to switching, although this was not significant (95% CI 0.36–8.42; p = 0.532). Neither dose changes, nor drug mechanism, nor duration of seizure freedom had any bearing upon the results.

SIGNIFICANCE:

Although the large majority of seizure-free patients remain so when switched to another agent, about one sixth have a recurrence attributable to the change. Conversely, our study design provides the first evidence to suggest that most improvements in drug-resistant patients are likely due to spontaneous remissions, not new drug introductions.

These findings have conflicting implications for two competing models of comparative antiepileptic drug efficacy, which will require further study to elaborate.

 

The study by Wang et al. raises two very interesting questions:

First, what is the risk of switching patients with well-controlled seizures to another medication because of adverse events? Second, is it worthwhile to change medications in patients with uncontrolled seizures, or are we just fooling ourselves with the natural course of the disease?

The study reports that switching phenytoin and carbamaze-pine to newer agents resulted in recurrent seizures in approximately 20% of patients as compared with 4% with unchanged therapy. This amounts to a six times higher likelihood of recurrent seizures, although this only marginally reaches significance considering all confounding factors in a multiple regression analysis.

The dilemma—the rationale for switching AEDs was to reduce metabolic side effects of older AEDs. Although this is a serious problem, is it worthwhile for the patient to take the risk of recurrent seizures with all of its psychosocial implications (e.g., loss of driving privileges and employment)? An unexpected seizure is the foremost concern of epilepsy patients ().

Seizure recurrence can be costly and detrimental (). A similar scenario occurs when the patient’s seizures are well controlled, but the patient experiences noticeable side effects such as cognitive slowing or psychiatric problems.

Patients may be more interested in switching antiepileptic medications if the adverse events are immediately bothersome, but it is certainly more difficult to convince a patient, who has been seizure free and very tolerant of phenytoin or carbamazepine for years, to switch to another agent for cardiovascular consequences that seem far in the future.

Are the newer AEDs as effective as the older AEDs in treating focal seizures? A possible supposition from Wang et al. could be that older AEDs are simply more effective, and therefore the recurrence rate is higher when switched over to newer AEDs. This is an unanswered, controversial, and complicated question. Unfortunately, only comparative studies could answer such questions. Our medical system is not set up to fund comparative studies.

The only comparative AED study in the United States was performed long before the advent of newer AEDs and showed that carbamazepine and phenytoin were superior to phenobarbital and primidone (). This is not much help in our current AED environment, but it certainly confirms that phenytoin and carbamazepine are effective. The SANAD study performed in the U.K. is an unblinded study that reported that lamotrigine may, at least, not be inferior to carbamazepine for focal epilepsy ().

However, the study generated a lot of controversy, and reports of shortfalls are multiple (). Another significant problem is that comparative studies are already outdated before they are published (). For example, SANAD did not include levetiracetam, which is now preferentially used in many countries.

If we just assume that most AEDs are equally effective, maybe our attention should go to the side-effect profile. However, comparing adverse events of AEDs is even more difficult. What is the weight of cardiovascular risk, sedation, cognition, irritability, psychiatric side effects, headaches, and multiple other adverse reactions? Which ones are more acceptable than others? It seems unreasonable to make generalized statements that specific medications should always or never be used. Therefore, as treating physicians, we attempt to tailor medications to each specific patient.

In the above study, the new AED was titrated up to the full dose before reducing the previous one. What is the right way to switch from one medication to another? With two AEDs, the patient may be experiencing more significant side effects during the titration period but is probably less at risk for seizures. Is tapering one while titrating the other equally safe? Should we more closely assess metabolic interactions between the two AEDs?

The second claim the authors make seems challenging, at first. They suggest that “most improvements in drug-resistant patients are likely due to spontaneous remissions, not new drug introductions.” Their control group with unchanged medications experienced as many seizures as patients whose medications were switched. This basically translates into No matter what we do with AEDs, it does not have any effect.

Certainly many patients feel that way. Should we as epileptologists, nevertheless, keep recommending AED changes to our patients? The above study has a strength in using controls compared with many other observational studies, although the controls are not entirely equal to the study patients. We generally seem to ignore the natural history of epilepsy. Spontaneous remissions do certainly occur and may be more frequent than we assume (). Whether this occurs more frequently in patients with more benign syndromes, and may exclude certain syndromes such as temporal lobe epilepsy, remains unclear ().

Wang et al. also only address monotherapy. The claim that whatever we do in intractable patients is ineffective seems invalidated by the fact that patients in well-controlled add-on studies of focal epilepsy hardly ever become seizure free in the placebo group, but a small percentage usually achieves seizure freedom with the active ingredient.

However, it could be that epilepsy requiring polytherapy is overall a different clinical syndrome and may not be comparable to the patients studied by Wang et al. The study certainly confirms that once seizures are intractable, however this is defined, then nothing in terms of medication changes is as successful as epilepsy surgery.

The authors elegantly propose two theoretical models about AED efficacy. In the first model, no matter what AED we use, treatment will only be successful in some patients, and patients will be intractable no matter which AED they receive. So, “keep on trying” will be to no avail. Studies that report on early intractability support that model (). The second model suggests an incomplete overlap in efficacy, so some AEDs may be more effective than others in certain patients or epilepsy syndromes. If the latter is true, we certainly have not done very well in identifying those patients or epilepsy syndromes.

The study has some shortcomings in terms of selection bias, sample size, and confidence intervals. However, it certainly points out some fundamental concepts about AEDs. We, as a community, are called to find more conclusive answers. It also demonstrates that no study can be large enough or inclusive enough to provide us with definitive answers. The conclusion can only be that prescribing AEDs remains an art, weighing all risks and benefits in every particular patient and circumstance. We just need to get better at it.

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New Mechanism by Which Alzheimer’s Spreads Through the Brain

New Mechanism by Which Alzheimer’s Spreads Through the Brain

Summary: According to researchers, exosomes can transport toxic aggregates of amyloid beta to new neurons in the brain.

Source: Linkoping University.

The waste-management system of the cell appears to play an important role in the spread of Alzheimer’s disease in the brain. A new study has focused on small membrane-covered droplets known as “exosomes”. It was long believed that the main task of exosomes was to help the cell to get rid of waste products. In simple terms, they were thought of as the cell’s rubbish bags. However, our understanding of exosomes has increased, and we now know that cells throughout the body use exosomes to transmit information. It’s now known that the exosomes can contain both proteins and genetic material, which other cells can absorb.

The Linköping researchers have shown in the new study that exosomes can also transport toxic aggregates of the protein amyloid beta, and in this way spread the disease to new neurons. Aggregated amyloid beta is one of the main findings in the brains of patients with Alzheimer’s disease, the other being aggregates of the protein tau. As time passes, they form ever-increasing deposits in the brain, which coincides with the death of nerve cells. The cognitive functions of a person with Alzheimer’s disease gradually deteriorate as new parts of the brain are affected.

“The spread of the disease follows the way in which parts of the brain are anatomically connected. It seems reasonable to assume that the disease is spread through the connections in the brain, and there has long been speculation about how this spread takes place at the cellular level,” says Martin Hallbeck, associate professor in the Department of Clinical and Experimental Medicine at Linköping University and senior consultant of clinical pathology at Linköping University Hospital.

In a collaboration with researchers at Uppsala University, he and his co-workers have investigated exosomes in brain tissue from deceased persons. The research team at Linköping University found more amyloid beta in exosomes from brains affected by Alzheimer’s disease than in healthy controls. Furthermore, the researchers purified exosomes from the brains from people with Alzheimer’s disease, and investigated whether they could be absorbed by cells cultured in the laboratory.

the researcher looking through a microscope

“Interestingly, exosomes from patients were absorbed by cultured neurons, and subsequently passed on to new cells. The cells that absorbed exosomes that contained amyloid beta became diseased,” says Martin Hallbeck.

The researchers treated the cultured neurons with various substances that prevent exosomes from being formed, released, or absorbed by other cells. They were able to reduce the spread of the aggregated amyloid beta between cells by disrupting the mechanism in these ways. The methods used in these laboratory experiments are not yet suitable for treating patients, but the discovery is important in principle. “Our study demonstrates that it is possible to influence this pathway, and possibly develop drugs that could prevent the spreading. The findings also open up the possibility of diagnosing Alzheimer’s disease in new ways, by measuring the exosomes,” says Martin Hallbeck.

ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE

Funding: The research has received financial support from donors that include the Swedish Research Council, the Swedish Alzheimer’s Foundation, and the Swedish Brain Foundation.

Source: Karin Söderlund Leifler – Linkoping University 
Publisher: Organized by NeuroscienceNews.com.
Image Source: NeuroscienceNews.com image is credited to Thor Balkhed/Linköping University.
Original Research: Open access research for “Alzheimer’s disease pathology propagation by exosomes containing toxic amyloid-beta oligomers” by Maitrayee Sardar Sinha, Anna Ansell-Schultz, Livia Civitelli, Camilla Hildesjö, Max Larsson, Lars Lannfelt, Martin Ingelsson, and Martin Hallbeck in Acta Neuropathologica. Published June 13 2018
doi:10.1007/s00401-018-1868-1

CITE THIS NEUROSCIENCENEWS.COM ARTICLE
Linkoping University “New Mechanism by Which Alzheimer’s Spreads Through the Brain.” NeuroscienceNews. NeuroscienceNews, 13 June 2018.
<http://neurosciencenews.com/alzheimers-spread-mechanism-9332/&gt;.

Abstract

Alzheimer’s disease pathology propagation by exosomes containing toxic amyloid-beta oligomers

The gradual deterioration of cognitive functions in Alzheimer’s disease is paralleled by a hierarchical progression of amyloid-beta and tau brain pathology. Recent findings indicate that toxic oligomers of amyloid-beta may cause propagation of pathology in a prion-like manner, although the underlying mechanisms are incompletely understood. Here we show that small extracellular vesicles, exosomes, from Alzheimer patients’ brains contain increased levels of amyloid-beta oligomers and can act as vehicles for the neuron-to-neuron transfer of such toxic species in recipient neurons in culture. Moreover, blocking the formation, secretion or uptake of exosomes was found to reduce both the spread of oligomers and the related toxicity. Taken together, our results imply that exosomes are centrally involved in Alzheimer’s disease and that they could serve as targets for development of new diagnostic and therapeutic principles.

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Higher Empathy People Process Music Differently in the Brain

Higher Empathy People Process Music Differently in the Brain

Higher Empathy People Process Music Differently in the Brain

Summary: Researchers report people with higher empathy process music with greater involvement in the brain’s reward system and areas of the brain associated with social information processing.

Source: Southern Methodist University.

People with higher empathy differ from others in the way their brains process music, according to a study by researchers at Southern Methodist University, Dallas and UCLA.

The researchers found that compared to low empathy people, those with higher empathy process familiar music with greater involvement of the reward system of the brain, as well as in areas responsible for processing social information.

“High-empathy and low-empathy people share a lot in common when listening to music, including roughly equivalent involvement in the regions of the brain related to auditory, emotion, and sensory-motor processing,” said lead author Zachary Wallmark, an assistant professor in the SMU Meadows School of the Arts.

But there is at least one significant difference.

Highly empathic people process familiar music with greater involvement of the brain’s social circuitry, such as the areas activated when feeling empathy for others. They also seem to experience a greater degree of pleasure in listening, as indicated by increased activation of the reward system.

“This may indicate that music is being perceived weakly as a kind of social entity, as an imagined or virtual human presence,” Wallmark said.

Researchers in 2014 reported that about 20 percent of the population is highly empathic. These are people who are especially sensitive and respond strongly to social and emotional stimuli.

The SMU-UCLA study is the first to find evidence supporting a neural account of the music-empathy connection. Also, it is among the first to use functional magnetic resonance imaging (fMRI) to explore how empathy affects the way we perceive music.

The new study indicates that among higher-empathy people, at least, music is not solely a form of artistic expression.

“If music was not related to how we process the social world, then we likely would have seen no significant difference in the brain activation between high-empathy and low-empathy people,” said Wallmark, who is director of the MuSci Lab at SMU, an interdisciplinary research collective that studies — among other things — how music affects the brain.

“This tells us that over and above appreciating music as high art, music is about humans interacting with other humans and trying to understand and communicate with each other,” he said.

This may seem obvious.

“But in our culture we have a whole elaborate system of music education and music thinking that treats music as a sort of disembodied object of aesthetic contemplation,” Wallmark said. “In contrast, the results of our study help explain how music connects us to others. This could have implications for how we understand the function of music in our world, and possibly in our evolutionary past.”

The researchers reported their findings in the peer-reviewed journal Frontiers in Behavioral Neuroscience, in the article “Neurophysiological effects of trait empathy in music listening.”

The co-authors are Choi Deblieck, with the University of Leuven, Belgium, and Marco Iacoboni, UCLA. The research was carried out at the Ahmanson-Lovelace Brain Mapping Center at UCLA.

“The study shows on one hand the power of empathy in modulating music perception, a phenomenon that reminds us of the original roots of the concept of empathy — ‘feeling into’ a piece of art,” said senior author Marco Iacoboni, a neuroscientist at the UCLA Semel Institute for Neuroscience and Human Behavior.

“On the other hand,” Iacoboni said, “the study shows the power of music in triggering the same complex social processes at work in the brain that are at play during human social interactions.”

Comparison of brain scans showed distinctive differences based on empathy

Participants were 20 UCLA undergraduate students. They were each scanned in an MRI machine while listening to excerpts of music that were either familiar or unfamiliar to them, and that they either liked or disliked. The familiar music was selected by participants prior to the scan.

Afterward each person completed a standard questionnaire to assess individual differences in empathy — for example, frequently feeling sympathy for others in distress, or imagining oneself in another’s shoes.

The researchers then did controlled comparisons to see which areas of the brain during music listening are correlated with empathy.

brain scans taken while people listened to music

Analysis of the brain scans showed that high empathizers experienced more activity in the dorsal striatum, part of the brain’s reward system, when listening to familiar music, whether they liked the music or not.

The reward system is related to pleasure and other positive emotions. Malfunction of the area can lead to addictive behaviors.

Empathic people process music with involvement of social cognitive circuitry

In addition, the brain scans of higher empathy people in the study also recorded greater activation in medial and lateral areas of the prefrontal cortex that are responsible for processing the social world, and in the temporoparietal junction, which is critical to analyzing and understanding others’ behaviors and intentions.

Typically, those areas of the brain are activated when people are interacting with, or thinking about, other people. Observing their correlation with empathy during music listening might indicate that music to these listeners functions as a proxy for a human encounter.

Beyond analysis of the brain scans, the researchers also looked at purely behavioral data — answers to a survey asking the listeners to rate the music afterward.

Those data also indicated that higher empathy people were more passionate in their musical likes and dislikes, such as showing a stronger preference for unfamiliar music.

Precise neurophysiological relationship between empathy and music is largely unexplored

A large body of research has focused on the cognitive neuroscience of empathy — how we understand and experience the thoughts and emotions of other people. Studies point to a number of areas of the prefrontal, insular, and cingulate cortices as being relevant to what brain scientists refer to as social cognition.

Activation of the social circuitry in the brain varies from individual to individual. People with more empathic personalities show increased activity in those areas when performing socially relevant tasks, including watching a needle penetrating skin, listening to non-verbal vocal sounds, observing emotional facial expressions, or seeing a loved one in pain.

In the field of music psychology, a number of recent studies have suggested that empathy is related to intensity of emotional responses to music, listening style, and musical preferences — for example, empathic people are more likely to enjoy sad music.

“This study contributes to a growing body of evidence,” Wallmark said, “that music processing may piggyback upon cognitive mechanisms that originally evolved to facilitate social interaction.”

ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE

Funding: The research was supported by UCLA Office of the Vice Chancellor for Research.

Source: Nancy George – Southern Methodist University 
Publisher: Organized by NeuroscienceNews.com.
Image Source: NeuroscienceNews.com image is credited to SMU, UCLA.
Video Source: Video credited to SMUVideo.
Original Research: Open access research for “Neurophysiological Effects of Trait Empathy in Music Listening” by Zachary Wallmark, Choi Deblieck, and Marco Iacoboni in Frontiers in Behavioral Neuroscience. Published April 6 2018
doi:10.3389/fnbeh.2018.00066

Southern Methodist University “Higher Empathy People Process Music Differently in the Brain.” NeuroscienceNews. NeuroscienceNews, 12 June 2018.
<http://neurosciencenews.com/empathy-music-processing-9313/&gt;.

Abstract

Neurophysiological Effects of Trait Empathy in Music Listening

The social cognitive basis of music processing has long been noted, and recent research has shown that trait empathy is linked to musical preferences and listening style. Does empathy modulate neural responses to musical sounds? We designed two functional magnetic resonance imaging (fMRI) experiments to address this question. In Experiment 1, subjects listened to brief isolated musical timbres while being scanned. In Experiment 2, subjects listened to excerpts of music in four conditions (familiar liked (FL)/disliked and unfamiliar liked (UL)/disliked).

For both types of musical stimuli, emotional and cognitive forms of trait empathy modulated activity in sensorimotor and cognitive areas: in the first experiment, empathy was primarily correlated with activity in supplementary motor area (SMA), inferior frontal gyrus (IFG) and insula; in Experiment 2, empathy was mainly correlated with activity in prefrontal, temporo-parietal and reward areas. Taken together, these findings reveal the interactions between bottom-up and top-down mechanisms of empathy in response to musical sounds, in line with recent findings from other cognitive domains.

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