by EMILY MAKOWSKI

Neuroscientist Robert Provine, known for his groundbreaking research on common but mysterious human behavior such as laughter and yawning, died October 17 of complications from non-Hodgkin’s lymphoma, according to The Washington Post. He was 76.

Provine studied human social behaviors through innovative methods. In one 1993 study, his team observed people laughing outside of the lab setting, such as in shopping malls or while walking down the street. He found that, contrary to scientific belief of the time, most instances of laughter were based not in response to overt humor, but instead in an effort to strengthen social bonds, acknowledge a superior’s authority, or, when used negatively, to exclude someone from a group.

“Laughter is part of this universal human vocabulary. Everyone speaks this language. Just as birds of a given species all sing their species’ typical song, laughter is part of our own human song,” Provine once told NPR, according to the Post.

Born on May 11, 1943 in Tulsa, Oklahoma, Provine showed an aptitude for science at a young age when he built telescopes in high school. He received his bachelor’s degree in psychology from Oklahoma State University in 1965 and PhD in psychology from Washington University in St. Louis in 1971. He was a member of the American Association for the Advancement of Science, the Association for Psychological Science, and the Psychonomic Society, and wrote two popular science books: Laughter: A Scientific Investigation in 2000 and Curious Behavior: Yawning, Laughing, Hiccupping, and Beyond in 2012.

“Provine’s research on topics such as yawning, laughter, tickling, and emotional tears provided fascinating insights into the fundamental building blocks of human social behavior,” according to a memorial on the University of Maryland, Baltimore County’s (UMBC) website. Provine taught at UMBC for four decades before becoming a professor emeritus in 2013.

“His approach was just amazing. It was different than what pretty much anyone was doing,” Robert Spencer, one of Provine’s former PhD students and currently the chief of neuropsychology at the VA Ann Arbor Healthcare System, tells The Scientist. “He was opening up a whole new set of methods, things that he would refer to as ‘sidewalk neuroscience,’ which was essentially ethology as applied to humans. And he answered questions you just can’t answer in synthetic lab situations,” he says.

Spencer remembers Provine as having a quirky personality, a distinctive Oklahoma accent, and a lab that “looked like a museum,” adding that it was “just full of equipment that he had built himself” in order to conduct experiments. In addition, he had many interests outside of the lab, such as saxophone playing, race car driving, and martial arts.

He is survived by his wife of 23 years, his son and daughter from his first marriage, and three grandchildren.

https://www.the-scientist.com/news-opinion/robert-provine–researcher-of-universal-human-behavior–dies-66622?utm_campaign=TS_DAILY%20NEWSLETTER_2019&utm_source=hs_email&utm_medium=email&utm_content=78428564&_hsenc=p2ANqtz-9rEINL9K9sYAcnp9kSxgo46D44ioSo_zR3e3MkXqwoeczqjTYDR5a4v3X7Cc4X3sqANvMx6eWvkiUiGKo7lYg5Cj8Sjw&_hsmi=78428564

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Researchers at the University of Bordeaux say the combination of ingredients in a traditional chocolate cookie trigger the same addictive response in your brain as cocaine or marijuana.

“Overall, this research has revealed that sugar and sweet reward can not only substitute to addictive drugs, like cocaine, but can even be more rewarding and attractive,” the study’s abstract posits.

Like your cookies with a dash of salt? Your brain does too. Salt consumption activates the brain’s reward centers, compounding the already addictive effects of these chocolaty treats.

So the next time your cookie cravings compel you to act against your better judgement, don’t beat yourself up about it. It’s basically a natural human response, the study shows.

Chocolate chip cookies account for about a fifth of the global cookie market, which is expected to become a $38 billion industry by 2022.

Study: Chocolate chip cookies as addictive as cocaine

Young carriers of the APOE4 allele have brains that are more connected (left, red lines illustrate connections between brain areas) and active (right, yellow indicates activity) than the brains of those without the allele.
KRISHNA SINGH, ELIFE, 8:E36011, 2019.

A growing body of evidence supports the theory that neural hyperactivity and hyperconnectivity precede the pathological changes that lead to neurodegeneration.

DIANA KWON

There are approximately 5.6 million people over the age of 65 living with Alzheimer’s disease in the United States. With the population aging, that number is projected to grow to 7.1 million by 2025. Researchers know that age, a family history of the disease, and carrying a genetic variant known as APOE4 are all associated with a higher chance of developing the condition. But the biological mechanisms leading to Alzheimer’s are still largely a mystery.

Over the last decade, scientists have amassed evidence for a hypothesis that, prior to developing full-blown Alzheimer’s disease, patients experience a period of hyperactivity and hyperconnectivity in the brain. Several functional magnetic resonance imaging studies have reported that people with mild cognitive impairment (MCI), a condition that often precedes Alzheimer’s, appear to have higher brain activity levels than their age-matched counterparts. Researchers have also found signs of such changes in healthy people carrying the APOE4 allele, as well as in presymptomatic stages of Alzheimer’s in rodent models of the disease.

Krishna Singh, a physicist and imaging neuroscientist at the Cardiff University Brain Research Imaging Center (CUBRIC) in the UK, and his colleagues wanted to investigate this theory further. Previous studies of brain activity in young APOE4 carriers were mostly conducted using small sample sizes, according to Singh. But by the mid-2010s, his team had access to neuroimaging data from close to 200 participants studied at CUBRIC as part of an effort to build a massive dataset of healthy brains. So the researchers decided to use the data to search for signs of unusual brain activity and connectivity in people with the APOE4 allele.

Using magnetoencephalography (MEG), a neuroimaging technique that records the magnetic fields generated by electrical activity in the brain, Singh and his colleagues had measured resting-state brain activity in a group of 183 healthy adults, which included 51 individuals who carried at least one copy of APOE4. The average age of the participants was 24 years old, although ages ranged from 18 to 65 years old.

Analysis of the imaging data revealed that, compared with controls, young APOE4 carriers displayed greater activity in several regions in the right side of the brain, including parts of what’s known as the default mode network, which is active when a person is not focused on a specific task. A similar set of brain regions also showed an overall increase in connectivity.

The researchers next compared the results to brain activity and connectivity data from a previous neuro­imaging study they had conducted, which found that elderly people with early-stage Alzheimer’s disease had decreased neuronal activity and connectivity compared with that of age-matched controls. The network of brain areas that displayed increased connectivity in young APOE4 carriers, the team found, partially overlapped with the brain regions that exhibited a decrease in connectivity in people with early-stage Alzheimer’s. These findings are intriguing, Singh says, because they suggest that brain areas that end up getting impaired in Alzheimer’s may be highly active and connected early in life—long before symptoms of the disease appear.

“This study adds further evidence that hyperactivity and hyperconnectivity may play an influential role in Alzheimer’s disease,” says Tal Nuriel, a professor of pathology and cell biology at the Columbia University Medical Center who wasn’t involved in the work. Because this was an observational study, the findings can only establish a correlation between brain activity and Alzheimer’s, Nuriel adds, so it’s still unclear whether the hyperactivity and hyperconnectivity observed during the early stages of the disease are a cause or a consequence of pathological changes that lead to neurodegeneration.

Scientists used to think that increased activity was simply a compensatory effect—the brain trying to make up for a loss of neurons and synapses, says Willem de Haan, a neurologist at the Amsterdam University Medical Center who was not involved in the latest study. “But I think there’s overwhelming evidence that this may actually be pathological hyperactivity.”

Much of that evidence comes from animal experiments conducted over the last decade or so. In rodents, researchers have found that hyperactivity can increase the production and spread of amyloid-ß, the peptide that accumulates into plaques found in the brains of people with Alzheimer’s—and that amyloid-ß can in turn induce neuronal hyperactivity. These findings have led some scientists to speculate that there might be a self-amplifying loop, where a progressive hyperactivity and build-up of amyloid-ß drives pathological changes associated with the neurodegenerative disease.

Research in humans also supports the idea that hyperactivity could play a causal role in Alzheimer’s disease. In 2012, researchers at Johns Hopkins University treated individuals with MCI with the anti-epileptic drug levetiracetam and found that the therapy suppressed activity in the hippocampus and led to improved memory performance. The team is currently testing levetiracetam for MCI in clinical trials. “I think this is one of the most interesting results,” says de Haan. “It seems to show that by correcting hyperactivity we can actually find some improvements in patients that might point to a completely new type of therapy for [Alzheimer’s disease].”

For the current study, Singh’s team also trained a machine-learning algorithm to distinguish APOE4 carriers from non-carriers based on their MEG data and tested whether it would be able to predict cases of Alzheimer’s. They found that while the program was able to perform above chance, the effect was not significant. “In a way, that was kind of encouraging,” Singh says. “Because I don’t think anybody would predict that we could find a signature [for Alzheimer’s] in 20- and 30-year-olds.”

For now, Singh says, his team’s findings simply shed light on what might be going on in the brains of people with the APOE4 allele. There are still a number of unanswered questions—such as when the transition from hyper- to hypoconnectivity and activity happens, what changes occur in the largely understudied middle-aged cohort, and whether there are differences between APOE4 carriers who go on to develop Alzheimer’s and those who don’t. Ultimately, to understand how disruptions in neuronal activity lead to behavioral and cognitive deficits, scientists need to decipher what’s going on inside a healthy brain, Singh says. “[We] require a model of how the brain works—and those are still in their infancy.”

https://www.the-scientist.com/notebook/genetic-risk-for-alzheimers-disease-linked-to-highly-active-brains-66483?utm_campaign=TS_DAILY%20NEWSLETTER_2019&utm_source=hs_email&utm_medium=email&utm_content=78081371&_hsenc=p2ANqtz-98aZf5axxCqtPYITNqfIVWKM6xuk3ni-QSpgTS4gFXzeQcntecrOf6DFFXjrf5qcktWTUz2M3xnAEJlvXTaS7WDQEKNg&_hsmi=78081371

A technology that originated at the University of Minnesota is well on its way to commercialization thanks to an investment award from Alzheimer’s Drug Discovery Foundation (ADDF).

The investment of up to $500,000 was awarded through the ADDF’s Diagnostics Accelerator initiative. Toronto, Ontario-based RetiSpec licensed through the University of Minnesota’s Technology Commercialization program. The technology harnesses hyperspectral imaging and machine learning.

“We are focused on bringing to market a noninvasive, easy-to-use, screening technology that can change when and how we detect Alzheimer’s disease at its earliest stages including before a patient presents with symptoms,” said Eliav Shaked, CEO of RetiSpec. “Early detection provides an important window of opportunity for timely therapeutic interventions that can slow or even prevent the progression of Alzheimer’s disease. ADDF’s investment represents another point of external validation of the promise of our technology.”

In preclinical studies and a pilot human study, the retinal imaging technology was effective in detecting small changes in biomarkers associated with elevated cerebral amyloid beta levels early in the disease process including before the onset of clinical symptoms.

RetiSpec is currently collaborating with Toronto Memory Program, Canada’s largest Alzheimer’s clinical trial site, to validate the accuracy and usability of the technology in patients.

“We believe that RetiSpec’s retinal scanner stands out and shows promise as a unique diagnostic tool among a range of technologies in development,” said Howard Fillit , MD, founding executive director and chief science officer of ADDF The technology has the potential to facilitate early diagnosis, improve the lives of patients and their loved ones and save the healthcare system money and resources. The technology will also be useful in making clinical trials for Alzheimer’s disease more efficient.”

https://www.mddionline.com/feast-your-eyes-new-technology-early-alzheimers-screening

· Children who were bullied by siblings and peers are more likely to develop clinical depression, self-harm and think about suicide in their early twenties

· Children bullied at home and school had no safe place to escape bullying

· Education of parents and mental health professionals is needed to reduce sibling bullying, as in turn it could reduce peer bullying and lead to a decrease in issues later on in life

Depression, self-harm and suicidal ideation are more prominent in adults in their early twenties if they were bullied at home and at school, a study by researchers at the University of Warwick have found. Researchers stress that intervention is needed to educate people in bullying to reduce it.

Previous studies have identified that sibling bullying has an effect on mental health in adolescence, however researchers Professor Dieter Wolke and Dr. Slava Dantchev have now found children who were bullied by siblings and friends are more likely to harm themselves.

In the paper ‘The Independent and Cumulative Effects of Sibling and Peer Bullying in Childhood on Depression, Anxiety, Suicidal Ideation, and Self-Harm in Adulthood’ published in the journal Frontiers in Psychiatry, researchers show there is a long shadow thrown by sibling bullying on self-harm, suicide attempts and depression at 24 years of age.

Using the Children of the 90s study, they were able to show that children who were bullied by siblings had more mental health issues in adulthood. If they were also bullied by peers this risk increased further.

The participants were asked to self-report bullying when they were 12 years old, whilst depression, anxiety, suicidal ideation and self-harm were assessed at 24 years old.

Of 3,881 youths studied it was found that 31.2% experienced bullying by a sibling. Of those who both became victims and bullied siblings 15.1% were diagnosed with clinical depression, 35.7% experienced suicidal ideation and 16.1% self-harmed with a further 4.9% with the intent of suicide.

Those who experienced sibling bullying and peer bullying had double the odds of developing clinical depression and consider suicide.

Dr Slava Dantchev of the University of Warwick and the University of Vienna said: “This is the first study to show that being bullied by siblings has adverse effects on mental health into adulthood, when the siblings are not living together anymore. Those bullied at home are also more likely to be bullied by peers and have no save space at school or at home. This further increased their torment and affected their mental health”

Professor Dieter Wolke of the Department of Psychology at the University of Warwick comments: “As sibling bullying often starts when children are young it will be important to educate and help parents to deal and reduce bullying between siblings in early childhood. This is an area which has been completely overlooked in mental health provision and parent support”

https://warwick.ac.uk/newsandevents/pressreleases/children_bullied_by

By Dennis Thompson

Middle-aged folks who worry about healthy aging would do well to keep an eye on their walking speed.

Turns out that the walking speed of 45-year-olds is a pretty solid marker of how their brains and bodies are aging, a new study suggests.

Slow walkers appear to be aging more rapidly, said senior researcher Terrie Moffitt, a professor of psychology and neuroscience at Duke University. They’ve lost more brain volume in middle-age than folks with a quicker walking pace, and also perform worse on physical and mental tests, she said.

“For those people who were slow walkers for their age group, they already had many of the signs of failing health that are regularly tested in a geriatric clinic,” Moffitt said.

In the study, middle-aged people who walked slower than 3.6-feet per second ranked in the lowest fifth when it comes to walking speed, and those are the individuals already showing signs of rapid aging, said Dr. Stephanie Studenski, a geriatrician with the University of Pittsburgh School of Medicine.

“It takes many body systems to have you walk well,” Studenski said. “It takes a good heart, good lungs, good nervous system, good strength, good musculoskeletal system and a variety of other things. Gait speed summarizes the health of all of your body’s systems.”

Gait speed tests are a standard part of geriatric care, and are regularly given to people 65 and older, Moffitt said.

“The slower a person walks, that is a good predictor of impending mortality,” Moffitt said. “The slower they walk, the more likely they will pass away.”

Moffitt and her colleagues suspected that gait tests might be valuable given at an earlier age, figuring that walking speed could serve as an early indicator of how well middle-aged people are aging.

To test this notion, the researchers turned to a long-term study of nearly 1,000 people born in a single year in Dunedin, New Zealand. These people have been tested regularly since their birth in 1972-1973 regarding a wide variety of medical concerns.

This group of study participants recently turned 45, and as they did, the research team tested their walking speed by asking each to repeatedly amble down a 25-foot-long electronic pad, Moffitt said.

Each person walked down the pad at their normal rate, and then again as fast as they could. They also were asked to walk as fast as possible while reciting the alphabet backward, Moffitt said.

All of the participants then were subjected to a battery of aging tests normally used in geriatric clinics.

In addition, they underwent an MRI brain scan to test the volume of their brains, since a shrinking brain has been linked to dementia and Alzheimer’s disease.

The participants also were given a variety of mental and physical tests. The physical tests involved things like balancing on one foot, standing up out of a chair as fast as they could, or gripping a monitor as tightly as they could to test hand strength.

“All these things are very subtle,” Moffitt said. “They’re not anything that would knock you over with a feather. You have to test them in order to find them.”

The findings showed that people who were in the lowest fifth for walking speed had signs of premature and rapid aging.

Studenski said, “It’s the bottom 20% that’s by far in bigger trouble than the others.”

The slower walkers also looked older to a panel of eight screeners asked to guess each participant’s age from a facial photograph.

The findings were published online Oct. 11 in JAMA Network Open.

A gait test could be an easy and low-cost way for primary care doctors to test how well middle-aged patients are aging, said Studenski, who wrote an editorial accompanying the new study.

Doctors could place sensors at the beginning and end of a hallway, and test patients’ walking speed as they head down to the examination room, she added.

However, doctors would need to be taught how to interpret gait speed for middle-aged patients, the same way that geriatricians already are trained to interpret walking speed in seniors.

Middle-aged people with a slower gait could try to slow their aging by eating healthy, exercising, quitting smoking, and maintaining better control over risk factors like high blood pressure and elevated cholesterol, Studenski and Moffitt suggested.

An even better use of walking speed could be as an early test of drugs and therapies meant to counter dementia and other diseases of aging, Moffitt said.

These therapies usually are difficult to assess because researchers have to wait years for people to grow old and display the hoped-for benefits, she noted.

“They need something cheap and effective they can do now to evaluate these treatments,” Moffitt said. “If they give it to people and it speeds up their walking, we’ve really got something there.”

SOURCES: Terrie Moffitt, Ph.D., professor, psychology and neuroscience, Duke University, Durham, N.C.; Stephanie Studenski, M.D., MPH, geriatrician, University of Pittsburgh School of Medicine; Oct. 11, 2019, JAMA Network Open, online

https://consumer.healthday.com/senior-citizen-information-31/misc-aging-news-10/how-fast-you-walk-might-show-how-fast-you-re-aging-751167.html

Andrew A. Nierenberg, MD

It is all too easy for politicians to, yet again, blame people with mental illness for the epidemic of mass shootings in the United States. It is also wrong.1 Study after study shows that those who live with serious mental illness are far more likely to be the victims of violence rather than the perpetrators.1 The narrative is, however, complicated because mental illness is associated with a statistically significant increase in violence, but accounts for only 4% of violent acts.2 In an FBI study of active shooters, 25% had a diagnosable psychiatric disorder and based on the literature determined that a psychiatric diagnosis was not a specific predictor of violence.3 In contrast, the group most likely to commit acts of mass violence are alienated young adult white males who have access to guns, especially high capacity automatic rifles. And if the cause is not mental illness in these young men, then what seems to be among the common variables? Alienation, isolation, rage in response to rejection or humiliation—especially by women, revenge after getting fired from a job, perceptions that one’s group is under attack (eg, that immigrants are taking over and threatening white control and white supremacy) or feeling screwed by the “system” magnified by social media, and sometimes a desire for fame or infamy.

To falsely blame those with mental illness for mass shootings is not only expedient, but leads to hollow calls for more facilities to lock up patients who have mental health challenges to protect the public; although it would be laudable to increase funding for psychiatric care and research, increases in funding rarely follow the hollow calls after a disaster. Rather than protecting the public, to blame the blameless leads instead to an increase in stigma for people who live with mental illness and their families.

To call those young men “sick” makes them “other” and confuses evil with illness. The argument goes that they must be sick to commit such heinous acts. But one does not need to have mental illness to act in ways that are vindictive, destructive, and evil. Then how can our society decrease the risk of these all too often mass shooting disasters? We cannot eliminate the conditions under which these men become enraged and violent. We can, however, restrict access to high capacity automatic rifles as was done in Australia in 1996, which led to a dramatic decline in mass shootings. As tragic and dramatic as mass shootings are, they account for a small fraction of the total deaths due to guns in the US; instead, two-thirds of all gun deaths are due to suicide and the risk of suicide by guns is higher than the risk of violence to others.4 This means that those who oppose reasonable gun control laws want people to have the right to go ahead and kill themselves.

To the politicians who oppose reasonable gun control laws, stop blaming people with mental illness and instead, consider banning automatic weapons as was done in Australia. And while you are at it, increasing funding for psychiatric care and research is still a good idea in and of itself.

References
Rozel JS, Mulvey EP. The link between mental illness and firearm violence: implications for social policy and clinical practice. Annu Rev Clin Psychol. 2017;13:445–469. doi:10.1146/annurev-clinpsy-021815-093459 [CrossRef]28375722
McGinty EE. Mental illness and gun violence: disrupting the narrative. Psychiatr Serv. 2018;69:842–843. doi:10.1176/appi.ps.201800172 [CrossRef]29921191
FBI.gov. A study of pre-attack behaviors of active shooters in the United States between 2000 and 2013. https://www.fbi.gov/file-repository/pre-attack-behaviors-of-active-shooters-in-us-2000-2013.pdf/view. Accessed September 10, 2019.
Baumann ML, Teasdale B. Severe mental illness and firearm access: is violence really the danger?Int J Law Psychiatry. 2018;56:44–49. doi:10.1016/j.ijlp.2017.11.003 [CrossRef]29701598
Authors

Andrew A. Nierenberg, MD, is the Thomas P. Hackett, MD, Endowed Chair in Psychiatry, the Director, Bipolar Clinic and Research Program, and the Director, Training and Education, MGH Research Institute, Massachusetts General Hospital; and a Professor of Psychiatry, Harvard Medical School.

Address correspondence to Andrew A. Nierenberg, MD, via email: psyann@Healio.com.