Anger more harmful to health of older adults than sadness

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NEUROSCIENCE NEWS

MAY 9, 2019

Summary: Experiencing daily anger increases inflammation and raises the risk of developing chronic illnesses, such as heart disease and cancer, in those aged 80 and over.

Source: APA

Anger may be more harmful to an older person’s physical health than sadness, potentially increasing inflammation, which is associated with such chronic illnesses as heart disease, arthritis and cancer, according to new research published by the American Psychological Association.

“As most people age, they simply cannot do the activities they once did, or they may experience the loss of a spouse or a decline in their physical mobility and they can become angry,” said Meaghan A. Barlow, MA, of Concordia University, lead author of the study, which was published in Psychology and Aging. “Our study showed that anger can lead to the development of chronic illnesses, whereas sadness did not.”

Barlow and her co-authors examined whether anger and sadness contributed to inflammation, an immune response by the body to perceived threats, such as infection or tissue damage. While inflammation, in general, helps protect the body and assists in healing, long-lasting inflammation can lead to chronic illnesses in old age, according to the authors.

The researchers collected and analyzed data from 226 older adults ages 59 to 93 from Montreal. They grouped participants as being in early old age, 59 to 79 years old, or advanced old age, 80 years old and older.

Over one week, participants completed short questionnaires about how angry or sad they felt. The authors also measured inflammation from blood samples and asked participants if they had any age-related chronic illnesses.

“We found that experiencing anger daily was related to higher levels of inflammation and chronic illness for people 80 years old and older, but not for younger seniors,” said study co-author Carsten Wrosch, PhD, also of Concordia University. “Sadness, on the other hand, was not related to inflammation or chronic illness.”

Sadness may help older seniors adjust to challenges such as age-related physical and cognitive declines because it can help them disengage from goals that are no longer attainable, said Barlow.

This study showed that not all negative emotions are inherently bad and can be beneficial under certain circumstances, she explained.

“Anger is an energizing emotion that can help motivate people to pursue life goals,” said Barlow. “Younger seniors may be able to use that anger as fuel to overcome life’s challenges and emerging age-related losses and that can keep them healthier. Anger becomes problematic for adults once they reach 80 years old, however, because that is when many experience irreversible losses and some of life’s pleasures fall out of reach.”

 

This study showed that not all negative emotions are inherently bad and can be beneficial under certain circumstances, she explained. The image is in the public domain.

The authors suggested that education and therapy may help older adults reduce anger by regulating their emotions or by offering better-coping strategies to manage the inevitable changes that accompany aging.

“If we better understand which negative emotions are harmful, not harmful or even beneficial to older people, we can teach them how to cope with loss in a healthy way,” said Barlow. “This may help them let go of their anger.”

ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE

Source:
APA
Media Contacts: 
Michael Shulman – APA
Image Source:
The image is in the public domain.

Original Research: Open access
“Is anger, but not sadness, associated with chronic inflammation and illness in older adulthood?”. Barlow, Meaghan A.; Wrosch, Carsten; Gouin, Jean-Philippe; Kunzmann, Ute.
Psychology and Aging. doi:10.1037/pag0000348

Abstract

Is anger, but not sadness, associated with chronic inflammation and illness in older adulthood?

The discrete emotion theory of affective aging postulates that anger, but not sadness, becomes increasingly maladaptive during older adulthood in predicting health-relevant physiological processes and chronic disease (Kunzmann & Wrosch, 2018). However, it is largely unknown whether different negative emotions have distinct functional consequences in the development of older adults’ physical disease. To start examining this possibility, we investigated whether older adults’ daily experiences of anger and sadness were differentially associated with two biomarkers of chronic low-grade inflammation (interleukin-6 [IL-6] and C-reactive protein [CRP]) and the number of chronic illnesses (e.g., heart disease, cancer, etc.). In addition, we examined whether such divergent associations would become paramount in advanced, as compared with early, old age. A community-dwelling study of 226 older adults (age 59 to 93; M = 74.99, SD = 7.70) assessed participants’ anger and sadness over 1 week, inflammatory processes, number of chronic illnesses, and relevant covariates. Regression analysis showed that anger predicted higher levels of IL-6 and chronic illness in advanced, but not in early, old age. The age effect of anger on chronic illness was mediated by increased IL-6 levels. Sadness exerted a reversed, but nonsignificant, association with IL-6 and chronic illness, independent of age. No emotion or age effects were obtained for CRP. The study’s findings inform theories of health, emotion, and life span development by pointing to the age-related importance of discrete negative emotions in predicting a major physiological pathway to physical health across older adulthood.

Scientists May Have Just Found a Way to Prevent the Brain From Aging

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themindunleashed.com

Elias Marat

Apr 5, 2019

A team of Stanford neuroscientists may have stumbled onto a way to prevent the brain from aging–and if the results of tests on old mice are any indicator, the research is promising.

Hailed as a “stunning piece of research” by New Atlas, the study–published in peer-reviewed international journal Nature–managed to pinpoint a specific gene called CD22 that is responsible for cognitive loss resulting from aging. The gene, common to both mice and humans, apparently degrades certain cells’ ability to conduct normal brain activity.

That same gene was found to be three times more prevalent among older mice than younger ones in follow-on experiments.

With this data in mind, the researchers devised antibodies to block CD22–specifically, molecules that bind to proteins and can be generated in a lab.

The Stanford team then injected the antibodies into the hippocampus on one side of the brains of the test mice. After a month of injecting the CD22-blocking antibody into both sides of their brains, the mice that received the injection began outperforming their counterparts in various intelligence tests.

The researchers believe that this is because as we age, the microglia–the class of brain cells responsible for routine cleanup and immune responses–decline and lose their ability to engage in the sort of “maintenance” work that brains require.

In a statement, study author and professor of neurology and neurological sciences Tony Wyss-Coray said:

“The mice became smarter … Blocking CD22 on their microglia restored their cognitive function to the level of younger mice. CD22 is a new target we think can be exploited for treatment of neurodegenerative diseases.”

This research could open the path to reverse a range of cognitive effects of aging–including such diseases as Parkinson’s and Alzheimer’s.

Wyss-Coray noted:

“Many of the genes whose high-risk variants have recently been linked to Alzheimer’s disease are known to be active in the brain only in microglia … Microglial genes’ activation patterns are abnormal in Alzheimer’s patients, and in other neurodegenerative disorders including Parkinson’s disease and amyotrophic lateral sclerosis.”

Yet the new research could be promising, especially when–or if–it eventually reaches human trials. The Stanford team remains optimistic, with Wyss-Coray noting:

“We think we may have discovered a way to get these cells back on track and make them work the way they used to when we were young.”

CRISPR twins who had their genes edited also had their brains altered to make them smarter, scientists believe

Source: CRISPR twins who had their genes edited also had their brains altered to make them smarter, scientists believe / Boing Boing

boingboing.net

Feb 22, 2019

Scientists believe that the “CRISPR twins,” who had their genes edited last year before birth, will now have an easier time learning and memorizing. Apparently, the gene alteration, which was meant to make the girls immune to HIV, also altered their brains.

According to Technology Review:

Now, new research shows that the same alteration introduced into the girls’ DNA, to a gene called CCR5, not only makes mice smarter but also improves human brain recovery after stroke, and could be linked to greater success in school.

“The answer is likely yes, it did affect their brains,” says Alcino J. Silva, a neurobiologist at the University of California, Los Angeles, whose lab has been uncovering a major new role for the CCR5 gene in memory and the brain’s ability to form new connections.

“The simplest interpretation is that those mutations will probably have an impact on cognitive function in the twins,” says Silva. He says the exact effect on the girls’ cognition is impossible to predict, and “that is why it should not be done.”

There is no evidence that He Jiankui, the lead scientist from the Southern University of Science and Technology in Shenzhen, China, set out to alter their intelligence. He is now under investigation for the controversial experiment that “has been widely condemned as irresponsible.”

 

Hearing Hate Speech Primes the Brain For Hateful Actions

Researchers report on how the brain is spurred into action by hearing certain words. They propose a new simulation theory that perceiving words can drive brain systems into states almost identical to what would be evoked by directly experiencing what the word describes.

“Dan Slobin suggested that habitual ways of speaking lead to habitual ways of thinking about the world. The language that you hear gives you a vocabulary for discussing the world, and that vocabulary, by producing simulations, gives you habits of mind.”

Source: Hearing Hate Speech Primes the Brain For Hateful Actions – Neuroscience News

Neuroscience News

January 12, 2019

Summary: Researchers report on how the brain is spurred into action by hearing certain words. They propose a new simulation theory that perceiving words can drive brain systems into states almost identical to what would be evoked by directly experiencing what the word describes.

Source: The Conversation.

A mark on a page, an online meme, a fleeting sound. How can these seemingly insignificant stimuli lead to acts as momentous as participation in a racist rally or the massacre of innocent worshippers? Psychologists, neuroscientists, linguists and philosophers are developing a new theory of language understanding that’s starting to provide answers.

Current research shows that humans understand language by activating sensory, motor and emotional systems in the brain. According to this new simulation theory, just reading words on a screen or listening to a podcast activates areas of the brain in ways similar to the activity generated by literally being in the situation the language describes. This process makes it all the more easy to turn words into actions.

As a cognitive psychologist, my own research has focused on developing simulation theory, testing it, and using it to create reading comprehension interventions for young children.

Simulations are step one

Traditionally, linguists have analyzed language as a set of words and rules that convey ideas. But how do ideas become actions?

Simulation theory tries to answer that question. In contrast, many traditional theories about language processing give action short shrift.

Simulation theory proposes that processing words depends on activity in people’s neural and behavioral systems of action, perception and emotion. The idea is that perceiving words drives your brain systems into states that are nearly identical to what would be evoked by directly experiencing what the words describe.

Consider the sentence “The lovers held hands while they walked along the moonlit tropical beach.” According to simulation theory, when you read these words, your brain’s motor system simulates the actions of walking; that is, the neural activity elicited by comprehending the words is similar to the neural activity generated by literal walking. Similarly, your brain’s perceptual systems simulate the sight, sounds and feel of the beach. And your emotional system simulates the feelings implied by the sentence.

So words themselves are enough to trigger simulations in motor, perceptual and emotional neural systems. Your brain creates a sense of being there: The motor system is primed for action and the emotional system motivates those actions.

Then, one can act on the simulation much as he’d act in the real situation. For example, language associating an ethnic group with “bad hombres” could invoke an emotional simulation upon seeing members of the group. If that emotional reaction is strong enough, it may in turn motivate action – maybe making a derogatory remark or physically lashing out.

Although simulation theory is still under scientific scrutiny, there have been many successful tests of its predictions. For example, using neuroimaging techniques that track blood flow in the brain, researchers found that listening to action words such as “lick,” “pick” and “kick” produces activity in areas of the brain’s motor cortex that are used to control the mouth, the hand and the leg, respectively. Hearing a sentence such as “The ranger saw an eagle in the sky” generates a mental image using the visual cortex. And using Botox to block activity in the muscles that furrow the brow affects the emotional system and slows understanding of sentences conveying angry content. These examples demonstrate the connections between processing speech and motor, sensory and emotional systems.

Recently, my colleague psychologist Michael McBeath, our graduate student Christine S. P. Yu and I discovered yet another robust connection between language and the emotional system.

Consider pairs of single-syllable English words that differ only in whether the vowel sound is “eee” or “uh,” such as “gleam-glum” and “seek-suck.” Using all such pairs in English – there are about 90 of them – we asked people to judge which word in the pair was more positive. Participants selected the word with the “eee” sound two-thirds of the time. This is a remarkable percentage because if linguistic sounds and emotions were unrelated and people were picking at the rate of chance, only half of the “eee” words would have been judged as the more positive.

We propose that this relation arose because saying “eee” activates the same muscles and neural systems as used when smiling – or saying “cheese!” In fact, mechanically inducing a smile – as by holding a pencil in your teeth without using your lips – lightens your mood. Our new research shows that saying words that use the smile muscles can have a similar effect.

We tested this idea by having people chew gum while judging the words. Chewing gum blocks the systematic activation of the smile muscles. Sure enough, while chewing gum, the judged difference between the “eee” and “uh” words was only half as strong. We also demonstrated the same effects in China using pairs of Mandarin words containing the “eee” and “uh” sounds.

Practice through simulation makes actions easier

Of course, motivating someone to commit a hate crime requires much more than uttering “glum” or “suck.”

Inflammatory words can prime a mind.

But consider that simulations become quicker with repetition. When one first hears a new word or concept, creating its simulation can be a mentally laborious process. A good communicator can help by using hand gestures to convey the motor simulation, pointing to objects or pictures to help create the perceptual simulation and using facial expressions and voice modulation to induce the emotional simulation.

It makes sense that the echo chamber of social media provides the practice needed to both speed and shape the simulation. The mental simulation of “caravan” can change from an emotionally neutral string of camels to an emotionally charged horde of drug dealers and rapists. And, through the repeated simulation that comes from repeatedly reading similar posts, the message becomes all the more believable, as each repetition produces another instance of almost being there to see it with your own eyes.

Psycholinguist Dan Slobin suggested that habitual ways of speaking lead to habitual ways of thinking about the world. The language that you hear gives you a vocabulary for discussing the world, and that vocabulary, by producing simulations, gives you habits of mind. Just as reading a scary book can make you afraid to go in the ocean because you simulate (exceedingly rare) shark attacks, encountering language about other groups of people (and their exceedingly rare criminal behavior) can lead to a skewed view of reality.

Practice need not always lead down an emotional rabbit hole, though, because alternative simulations and understandings can be created. A caravan can be simulated as families in distress who have the grit, energy and skills to start a new life and enrich new communities.

Because simulation creates a sense of being in a situation, it motivates the same actions as the situation itself. Simulating fear and anger literally makes you fearful and angry and promotes aggression. Simulating compassion and empathy literally makes you act kindly. We all have the obligation to think critically and to speak words that become humane actions.

The neuroscience of creativity (and yes, right brain/left brain is mostly bullshit)

Source: The neuroscience of creativity (and yes, right brain/left brain is mostly bullshit) / Boing Boing

boingboing.net

David Pescovitz

Jan 10, 2019

Anna Abraham literally wrote the book on creativity and the brain. The Leeds Beckett University psychology professor is the author of a new textbook titled The Neuroscience of Creativity. From an interview with Abraham by psychologist Scott Barry Kaufman in Scientific American:

SBK: Why does the myth of the “creative right brain” still persist? Is there any truth at all to this myth?AA: Like most persistent myths, even if some seed of truth was associated with the initial development of the idea, the claim so stated amounts to a lazy generalization and is incorrect. The brain’s right hemisphere is not a separate organ whose workings can be regarded in isolation from that of the left hemisphere in most human beings. It is also incorrect to conclude that the left brain is uncreative. In fact even the earliest scholars who explored the brain lateralization in relation to creativity emphasized the importance of both hemispheres. Indeed this is what was held to be unique about creativity compared to other highly lateralized psychological functions. In an era which saw the uncovering of the dominant involvement of one hemisphere over the other for many functions, and the left hemisphere received preeminent status for its crucial role in complex functions like language, a push against the tide by emphasizing the need to also recognize the importance of the right hemisphere for complex functions like creativity somehow got translated over time into the only ‘creative right brain’ meme. It is the sort of thing that routinely happens when crafting accessible sound bites to convey scientific findings.

SBK: Is brain plasticity truly possible? If so, to what extent? How can creative thinking both induce and be caused by brain plasticity?

AA: Brain plasticity is a fact. Our brains change throughout our lifespan and this is readily evidenced by the everyday observation that we never stop learning. The extent of brain plasticity is harder to define and hasn’t been systematically examined. Creative thinking involves the discovery of novel connections and is therefore tied intimately to learning. Arthur Koestler pointed this out rather beautifully several decades ago: “Creative activity is a type of learning process where the teacher and pupil are located in the same individual.”

The Neuroscience of Creativity (Amazon)

Decreased Deep Sleep Linked to Early Alzheimer’s Disease

A new study links poor sleep quality in older adults with elevated levels of tau, a protein associated with Alzheimer’s disease. Researchers report poor sleep quality later in life may be associated with declining brain health and may be an early indicator of Alzheimer’s disease.

Source: Decreased Deep Sleep Linked to Early Alzheimer’s Disease – Neuroscience News

Neuroscience News

January 9, 2019

Summary: A new study links poor sleep quality in older adults with elevated levels of tau, a protein associated with Alzheimer’s disease. Researchers report poor sleep quality later in life may be associated with declining brain health and may be an early indicator of Alzheimer’s disease.

Source: WUSTL.

Poor sleep is a hallmark of Alzheimer’s disease. People with the disease tend to wake up tired, and their nights become even less refreshing as memory loss and other symptoms worsen. But how and why restless nights are linked to Alzheimer’s disease is not fully understood.

Now, researchers at Washington University School of Medicine in St. Louis may have uncovered part of the explanation. They found that older people who have less slow-wave sleep – the deep sleep you need to consolidate memories and wake up feeling refreshed – have higher levels of the brain protein tau. Elevated tau is a sign of Alzheimer’s disease and has been linked to brain damage and cognitive decline.

The findings, published Jan. 9 in Science Translational Medicine, suggest that poor-quality sleep in later life could be a red flag for deteriorating brain health.

“What’s interesting is that we saw this inverse relationship between decreased slow-wave sleep and more tau protein in people who were either cognitively normal or very mildly impaired, meaning that reduced slow-wave activity may be a marker for the transition between normal and impaired,” said first author Brendan Lucey, MD, an assistant professor of neurology and director of the Washington University Sleep Medicine Center. “Measuring how people sleep may be a noninvasive way to screen for Alzheimer’s disease before or just as people begin to develop problems with memory and thinking.”

The brain changes that lead to Alzheimer’s, a disease that affects an estimated 5.7 million Americans, start slowly and silently. Up to two decades before the characteristic symptoms of memory loss and confusion appear, amyloid beta protein begins to collect into plaques in the brain. Tangles of tau appear later, followed by atrophy of key brain areas. Only then do people start showing unmistakable signs of cognitive decline.

The challenge is finding people on track to develop Alzheimer’s before such brain changes undermine their ability to think clearly. For that, sleep may be a handy marker.

To better understand the link between sleep and Alzheimer’s disease, Lucey, along with David Holtzman, MD, the Andrew B. and Gretchen P. Jones Professor and head of the Department of Neurology, and colleagues studied 119 people 60 years of age or older who were recruited through the Charles F. and Joanne Knight Alzheimer’s Disease Research Center. Most – 80 percent – were cognitively normal, and the remainder were very mildly impaired.

The researchers monitored the participants’ sleep at home over the course of a normal week. Participants were given a portable EEG monitor that strapped to their foreheads to measure their brain waves as they slept, as well as a wristwatch-like sensor that tracks body movement. They also kept sleep logs, where they made note of both nighttime sleep sessions and daytime napping. Each participant produced at least two nights of data; some had as many as six.

The researchers also measured levels of amyloid beta and tau in the brain and in the cerebrospinal fluid that bathes the brain and spinal cord. Thirty-eight people underwent PET brain scans for the two proteins, and 104 people underwent spinal taps to provide cerebrospinal fluid for analysis. Twenty-seven did both.

After controlling for factors such as sex, age and movements while sleeping, the researchers found that decreased slow-wave sleep coincided with higher levels of tau in the brain and a higher tau-to-amyloid ratio in the cerebrospinal fluid.

“The key is that it wasn’t the total amount of sleep that was linked to tau, it was the slow-wave sleep, which reflects quality of sleep,” Lucey said. “The people with increased tau pathology were actually sleeping more at night and napping more in the day, but they weren’t getting as good quality sleep.”

Reduced amounts of slow brain waves – the kind that occur in deep, refreshing sleep – are associated with high levels of the toxic brain protein tau. This computer-generated image maps the areas where the link is strongest, in shades of red and orange. A new study from Washington University School of Medicine in St. Louis has found that decreased deep sleep is associated with early signs of Alzheimer’s disease. NeuroscienceNews.com image is credited to Brendan Lucey.

If future research bears out their findings, sleep monitoring may be an easy and affordable way to screen earlier for Alzheimer’s disease, the researchers said. Daytime napping alone was significantly associated with high levels of tau, meaning that asking a simple question – How much do you nap during the day? – might help doctors identify people who could benefit from further testing.

“I don’t expect sleep monitoring to replace brain scans or cerebrospinal fluid analysis for identifying early signs of Alzheimer’s disease, but it could supplement them,” Lucey said. “It’s something that could be easily followed over time, and if someone’s sleep habits start changing, that could be a sign for doctors to take a closer look at what might be going on in their brains.”

Anil Seth: Your brain hallucinates your conscious reality (17 min)

TED

Published on 18 Jul 2017

Right now, billions of neurons in your brain are working together to generate a conscious experience — and not just any conscious experience, your experience of the world around you and of yourself within it. How does this happen? According to neuroscientist Anil Seth, we’re all hallucinating all the time; when we agree about our hallucinations, we call it “reality.” Join Seth for a delightfully disorienting talk that may leave you questioning the very nature of your existence.