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Behavioral Science, Mental Health, Research

Pump up the bass, not the volume, to feel more powerful

Pump up the bass, not the volume, to feel more powerful

runner_iPodAs any seasoned athlete or fitness fanatic knows, a meticulously curated playlist is key when staying focused before a big game or getting through a tough workout. But what is it about music that transforms our psychological state and make us feel more powerful?

To answer this question, researchers at the Kellogg School of Management at Northwestern University identified so-called “highest power” songs (such as Queen’s “We Will Rock You“) and “lowest power” tunes (such as Fatboy Slim’s “Because We Can“) and then performed a series of experiments designed to ascertain how the music affected individuals’ sense of power, perceived sense of control, competitiveness and abstract thinking. According to a release, their findings showed “that the high-power music not only evoked a sense of power unconsciously, but also systematically generated the three downstream consequences of power.”

Since participants didn’t report increased feelings of empowerment after reading the lyrics of the songs, researchers turned their attention to how manipulation of bass levels impacted listeners. More from the release:

In the bass experiments, the researchers asked participants to listen to novel instrumental music pieces in which bass levels were digitally varied. In one experiment, they surveyed participants about their self-reported feelings of power, and in another, they asked them to perform a word-completion task designed to test implicit, or unconscious, feelings of power. They found that those who listened to the heavy-bass music reported more feelings of power and generated more power-related words in the implicit task than those listening to the low-bass music.

The effects of the bass levels support one possible explanation for why music makes people feel more powerful: the “contagion hypothesis.” The idea is that when people hear specific music components that express a sense of power, they mimic these feelings internally. “Importantly, because we used novel, never-before-heard music pieces in these experiments, it suggests that the effect may sometimes arise purely out of contagion,” [Dennis Hsu, PhD,] says. “Of course, this does not preclude the possibility that music could induce a sense of power through other processes, such as conditioning.”

The “conditioning hypothesis” suggests that certain pieces of music might trigger powerful experiences because these experiences are often paired with that particular music. For example, music used frequently at sports events may elicit powerful feelings because of the association with power, rewards, and winning (e.g., “We Are the Champions” is often played to celebrate victory).

Previously: Why listening to music boosts fitness performance, Can music benefit cancer patients? and Prescription playlists for treating pain and depression?
Photo by Bert Heird

Aging, Genetics, Imaging, Immunology, Mental Health, Neuroscience, Research, Women's Health

Stanford’s brightest lights reveal new insights into early underpinnings of Alzheimer’s

Stanford's brightest lights reveal new insights into early underpinnings of Alzheimer's

manAlzheimer’s disease, whose course ends inexorably in the destruction of memory and reason, is in many respects America’s most debilitating disease.  As I wrote in my article, “Rethinking Alzheimer’s,” just published in our flagship magazine Stanford Medicine:

Barring substantial progress in curing or preventing it, Alzheimer’s will affect 16 million U.S. residents by 2050, according to the Alzheimer’s Association. The group also reports that the disease is now the nation’s most expensive, costing over $200 billion a year. Recent analyses suggest it may be as great a killer as cancer or heart disease.

Alarming as this may be, it isn’t the only news about Alzheimer’s. Some of the news is good.

Serendipity and solid science are prying open the door to a new outlook on what is arguably the primary scourge of old age in the developed world. Researchers have been taking a new tack – actually, more like six or seven new tacks – resulting in surprising discoveries and potentially leading to novel diagnostic and therapeutic approaches.

As my article noted, several Stanford investigators have taken significant steps toward unraveling the tangle of molecular and biochemical threads that underpin Alzheimer’s disease. The challenge: weaving those diverse strands into the coherent fabric we call understanding.

In a sidebar, “Sex and the Single Gene,” I described some new work showing differential effects of a well-known Alzheimer’s-predisposing gene on men versus women – and findings about the possibly divergent impacts of different estrogen-replacement  formulations on the likelihood of contracting dementia.

Coming at it from so many angles, and at such high power, is bound to score a direct hit on this menace eventually. Until then, the word is to stay active, sleep enough and see a lot of your friends.

Previously: The reefer connection: Brain’s “internal marijuana” signaling implicated in very earliest stages of Alzheimer’s pathology, The rechargeable brain: Blood plasma from young mice improves old mice’s memory and learning, Protein known for initiating immune response may set up our brains for neurodegenerative disease, Estradiol – but not Premain – prevents neurodegeneration in woman at heightened dementia risk and Having a copy of ApoE4 gene variant doubles Alzheimer’s risk for women, but not for men
Illustration by Gérard DuBois

Autism, Pediatrics, Research, Stanford News

Stanford research clarifies biology of oxytocin in autism

Stanford research clarifies biology of oxytocin in autism

For years, scientists have been trying to sort out the role oxytocin plays in autism. The developmental disorder affects one in 68 U.S. children, causing social and communication deficits, repetitive behaviors and sensory problems. Oxytocin, which functions in the blood as a hormone and in the brain as a neurotransmitter, has long been known to have roles in enhancing social ability. Based on research in animal models, some people have speculated that oxytocin deficiency might contribute to autism. But prior human studies of the purported connection have produced a confusing picture.

The previous hypotheses saying that low oxytocin was linked to autism were maybe a little bit simplistic. It’s much more complex…

Now, a new Stanford paper publishing online this week in Proceedings of the National Academy of Sciences adds interesting details to our understanding. The study is the largest ever to examine blood oxytocin levels in children with autism and two comparison groups without autism: kids who have autistic siblings and children who do not have siblings with autism.

The researchers found the same range of blood oxytocin levels across all three groups, with similar numbers of children with low, medium and high oxytocin levels in each category. Although, as expected, the kids with autism had social deficits, blood oxytocin level was clearly linked to social ability within each group. Children with autism who had low blood oxytocin had poorer social ability than autistic children with high blood oxytocin, for example, and typically developing kids with low blood oxytocin also had poor social ability compared to other typically developing children.

From our press release on the research:

“It didn’t matter if you were a typically developing child, a sibling or an individual with autism: Your social ability was related to a certain extent to your oxytocin levels, which is very different from what people have speculated,” said Antonio Hardan, MD, professor of psychiatry and behavioral sciences and the study’s senior author. Hardan is a child and adolescent psychiatrist who treats children with autism at [Lucile Packard Children's Hospital Stanford].

“The previous hypotheses saying that low oxytocin was linked to autism were maybe a little bit simplistic,” he said. “It’s much more complex: Oxytocin is a vulnerability factor that has to be accounted for, but it’s not the only thing leading to the development of autism.”

The findings suggest that, although oxytocin deficiency may not explain all cases of autism, some kids with autism may still benefit from oxytocin-like medications. The researchers caution that their study needs to be repeated with measures of oxytocin in cerebrospinal fluid, since this liquid that bathes the brain may give better information about the nuances of oxytocin biology.

A Duke University scientist commented for a story on NPR’s health blog, Shots, about what the findings imply for the potential value of oxytocin therapy:

“It could be that if a kid has low oxytocin levels then they might benefit,” says Simon Gregory, a genomics researcher at Duke University who was not involved in the study. He is part of another group investigating the use of oxytocin to treat people with autism.

Gregory says it’s not surprising that children with autism have widely varying levels of oxytocin. “Autism isn’t a disease, it’s a spectrum” that can’t be linked to any one cause, he told Shots.

Stanford’s research team is also doing more work to clarify further details of the biology of oxytocin in autism.

Previously: Volunteers sought for autism drug study, Using Google Glass to help individuals with autism better understand social cues and “No, I’m not ready yet”: A sister’s translation for her brother with autis

In the News, Public Health, Research, Science, Stanford News, Technology

NPR highlights Google’s Baseline Study and what it might teach us about human health

NPR highlights Google's Baseline Study and what it might teach us about human health

Late last month, my colleague reported on Stanford partnering with Google [x] and Duke on a research study to better understand the human body. On the most recent edition of NPR’s Science Friday, project collaborator Sanjiv Sam Gambhir, MD, PhD, professor of radiology at Stanford, discussed the project and joined Jason Moore, MD, professor of genetics at Dartmouth College, in a segment called “Will big data answer big questions on health?”

According to Gambhir, what makes the new project unique is the focus on understanding the baseline of healthy human beings. Will it ultimately yield meaningful data about what makes us healthy? Listen here for the researchers’ thoughts.

Previously: Stanford partnering with Google and Duke to better understand the human body

Genetics, Research, Stanford News

Surprise discovery links cancer protein with developmental disorder

Surprise discovery links cancer protein with developmental disorder

Attardi

Scores of scientific discoveries — including dynamite, penicillin, and heaps of others — were accidents. Fiddling around in the lab and wa-zam, there’s a cure for syphilis.

The same sort of thing happened recently in the Stanford lab of Laura Attardi, PhD, professor of radiation oncology and genetics. Her team studies the protein p53, a key tumor suppressor. Normally, when switched on, p53 tells other proteins to kill ailing cells — a critical role to keep cancer in check.

To investigate its behavior in an organism, the researchers created a mouse with a mutated form of p53. This mutated protein had no off switch, but it also couldn’t communicate with its “minion” proteins that kill cells, so when a mouse had two copies of the mutated protein, it survived. A mouse with two normal copies of p53 also survived.

But surprisingly, when researchers created a mouse with one copy of the mutated p53, and one normal copy, it died before birth. What was going on?

To figure it out, Jeanine Van Nostrand, PhD, a former Stanford graduate student, now a researcher at The Salk Institute for Biological Studies, tried to figure out exactly why the mice were dying. They also had a unique set of problems — inner and outer ear deformities, heart abnormalities and a rare gap in the eye among others. After consulting with developmental experts, the researchers linked the mice deaths to CHARGE syndrome, a rare developmental disorder that causes eye, ear, nasal and genital problems, among other symptoms. “It was a very big surprise and very intriguing,” Van Nostrand comments in a release. “P53 had never before been shown to have a role in CHARGE.”

The researchers learned the mice with one normal p53, and one mutant p53, had hybrid p53 proteins, Frankenstein-like molecules that lacked an off switch, but retained the ability to trigger cell death.

These proteins led to the CHARGE symptoms. And thanks to the study, which appeared online yesterday in Nature, researchers can use the new clues about CHARGE to begin developing potential therapies, said Donna Martin, MD, PhD, associate professor of pediatrics and genetics at the University of Michigan Medical School, a CHARGE expert and co-author of the paper.

Becky Bach is a former park ranger who now spends her time writing, exploring, or practicing yoga. She’s currently a science writing intern in the medical school’s Office of Communication & Public Affairs.

Photo of Attardi by Steve Fisch

Behavioral Science, Chronic Disease, Neuroscience, Pain, Research, Stanford News

Obscure brain chemical indicted in chronic-pain-induced “Why bother?” syndrome

Obscure brain chemical indicted in chronic-pain-induced "Why bother?" syndrome

why botherChronic pain, meaning pain that persists for months and months or even longer (sometimes continuing well past the time when the pain-causing injury has healed), is among the most abundant of all medical afflictions in the developed world. Estimates of the number of people with this condition in the United States alone range from 70 million to 116 million adults – in other words, as much as half the country’s adult population!

No picnic in and of itself, chronic pain piles insult on injury. It differs from a short-term episode of pain not only in its duration, but also in triggering in sufferers a kind of psychic exhaustion best described by the rhetorical question, “Why bother?”

In a new study in Science, a team led by Stanford neuroscientist Rob Malenka, MD, PhD, has identified a particular nerve-cell circuit in the brain that may explain this loss of motivation that chronic pain all too often induces. Using lab mice as test subjects, they showed that mice enduring unremitting pain lost their willingness to perform work in pursuit of normally desirable goals, just as people in chronic pain frequently do.

It wasn’t that these animals weren’t perfectly capable of carrying out the tasks they’d been trained to do, the researchers showed. Nor was it that they lost their taste for the food pellets which with they were rewarded for successful performance – if you just gave them the food, they ate every bit as much as normal mice did. But they just weren’t willing to work very hard to get it. Their murine morale was shot.

Chalk it up to the action of a mysterious substance used in the brain for god-knows-what. In our release describing the study, I explained:

Galanin is a short signaling-protein snippet secreted by certain cells in various places in the brain. While its presence in the brain has been known for a good 60 years or so, galanin’s role is not well-defined and probably differs widely in different brain structures. There have been hints, though, that galanin activity might play a role in pain. For example, it’s been previously shown in animal models that galanin levels in the brain increase with the persistence of pain.

In a surprising and promising development, the team also found that when they blocked galanin’s action in a particular brain circuit, the mice, while still in as much pain as before, were once again willing to work hard for their supper.

Surprising, because galanin is a mighty obscure brain chemical, and because its role in destroying motivation turns out to be so intimate and specific. Promising, because the discovery suggests that a drug that can inhibit galanin’s activity in just the implicated brain circuit, without messing up whatever this mystery molecule’s more upbeat functions in the brain might be, could someday succeed in bringing back that drive to accomplish things that people in chronic pain all too often lose.

Previously: “Love hormone” may mediate wider range of relationships than previously thought, Revealed: the brain’s molecular mechanism behind why we get the blues, Better than the real thing: How drugs hot-wire our brain’s reward circuitry and Stanford researchers address the complexity of chronic pain
Photo by Doug Waldron

Neuroscience, Parenting, Pediatrics, Research

Can’t remember being a baby? Rapid growth of new neurons in young brains may explain why

Can't remember being a baby? Rapid growth of new neurons in young brains may explain why

baby_073014A close friend once told me that one of her favorite aspects about being a parent is that she could experience what it was like to be a baby and toddler. “As adults, we have no recollection of what it was like to be that young,” she said. “Watching my son grow up offers me a window into that part of my life.”

The inability to remember memories in early childhood is known as “infantile amnesia”. Few adults can remember events in their lifetime that occurred before the age of three. A past study shows that these memories tend to fade away around the age of seven.

But why can’t we remember our days as a crawling, toddling, babbling youngster? Recent research suggests the answer many have to do with how quickly the brain develops during this stage in our lives. According to a Scientific American article published earlier this week:

In a new experiment, the scientists manipulated the rate at which hippocampal neurons grew in young and adult mice. The hippocampus is the region in the brain that records autobiographical events. The young mice with slowed neuron growth had better long-term memory. Conversely, the older mice with increased rates of neuron formation had memory loss.

Based on these results, published in May in the journal Science, [neuroscientists Paul Frankland, PhD, and Sheena Josselyn, PhD] think that rapid neuron growth during early childhood disrupts the brain circuitry that stores old memories, making them inaccessible. Young children also have an underdeveloped prefrontal cortex, another region of the brain that encodes memories, so infantile amnesia may be a combination of these two factors.

Previously: Study finds age at which early-childhood memories fade and Individuals’ extraordinary talent to never forget could offer insights into memory
Photo by D Sharon Pruitt

Genetics, Research, Stanford News

A molecular “flag” marks key genes

A molecular "flag" marks key genes

metronome - smallPoint to an important gene in a cell, any cell, from most any creature, and it’s likely to have a particular elongated molecular flag stuck onto the proteins wrapped around its DNA.

This isn’t just a pretty flag, plopped in for decoration. It’s thought to regulate how often this gene is transcribed, according to Anne Brunet, PhD, associate professor of genetics here. She’s the senior author of a study appearing in the July 31 issue of Cell.

Little is known about the importance of transcriptional consistency — how regularly a gene is transcribed, Brunet said. “I think the notion of transcriptional consistency is new, and it’s very important,” she commented in a release. “This is completely uncharted territory.”

It surely matters if a polymerase — that molecular workhorse that kicks off the protein-making process — spurts out dozens of copies, then chills for a bit, picking up only when it is good and ready.

This flag, abbreviated as H3K4me3, physically standardizes the transcription process, ensuring the polymerase pops off copies as if governed by a metronome — tic, tic, tic, tic, tic, tic…

The genes that are important enough to merit this transcriptional timekeeper — about 1,000 per cell, although it’s a different 1000 in each type of cell — can provide clues to the cell’s function, Brunet said. Her team plugged all the data into an online database, which other researchers can use to find the key genes in the cells of their choice.

The opportunities are endless and Brunet, for one, is psyched. Her lab focuses on the biology of aging, but this molecular flag holds all kinds of research promise.

And, as Brunet is keen to point out, it wouldn’t be possible without the megadata-crunching that’s possible at top research universities like Stanford. Other researchers had spotted this stretched-out H3K4me3, but no one had taken the time, or the computing power, to determine its extent and function, Brunet said.

“This is the new era of using available data to make really new hypotheses and new discoveries,” Brunet said.

Becky Bach is a former park ranger who now spends her time writing, exploring, or practicing yoga. She’s currently a science writing intern in the medical school’s Office of Communication & Public Affairs.

Photo by Niki Odolphie

Autism, Neuroscience, Pediatrics, Research, Stanford News

Finding of reduced brain flexibility adds to Stanford research on how the autistic brain is organized

Finding of reduced brain flexibility adds to Stanford research on how the autistic brain is organized

A Stanford brain-imaging study has just shown that the brains of children with autism are less able to switch from rest to taking on a new task than the brains of typically developing children.

According to the study, which appears this week in the scientific journal Cerebral Cortex, instead of changing to accommodate a job, connectivity in key brain networks of autistic children looks similar to connectivity in the resting brain. The degree of inflexibility was linked to the intensity of children’s autism symptoms: those with less flexibility had more severe restrictive and repetitive behaviors, one of the hallmarks of the developmental disorder.

From our press release on the research:

“We wanted to test the idea that a flexible brain is necessary for flexible behaviors,” said Lucina Uddin, PhD, a lead author of the study. “What we found was that across a set of brain connections known to be important for switching between different tasks, children with autism showed reduced ‘brain flexibility’ compared with typically developing peers.” Uddin, who is now an assistant professor of psychology at the University of Miami, was a postdoctoral scholar at Stanford when the research was conducted.

“The fact that we can tie this neurophysiological brain-state inflexibility to behavioral inflexibility is an important finding because it gives us clues about what kinds of processes go awry in autism,” said Vinod Menon, PhD, the Rachel L. and Walter F. Nichols, MD, professor of psychiatry and behavioral sciences at Stanford and the senior author of the study.

The study is the first to examine unusual patterns of connectivity in the brains of children with autism while they are performing tasks; Menon’s team has previously published research on connectivity between different regions of the autistic brain at rest. Some regions of the autistic brain are over-connected to each other, that work has shown, and the degree of over-connection is linked to children’s social deficits, perhaps in part because it interferes with their ability to derive pleasure from human voices. Menon’s lab has also explored how differences in the organization of the autistic brain may contribute to better math performance in some people with autism.

“We’re making progress in identifying a brain basis of autism, and we’re starting to get traction in pinpointing systems and signaling mechanisms that are not functioning properly,” Menon told me. “This is giving us a better handle both in thinking about treatment and in looking at change or plasticity in the brain.”

Previously: Greater hyperconnectivity in the autistic brain contributes to greater social deficits, Unusual brain organization found in autistic kids who best peers at math and Stanford study reveals why human voices are less rewarding for kids with autism

Research, Science, Stanford News

They said “Yes”: The attitude that defines Stanford Bio-X

They said "Yes": The attitude that defines Stanford Bio-X

bio-X peopleI write a lot about interdisciplinary research (it’s my job), but it was just recently that I heard the best description of what it is that makes interdisciplinary collaborations possible. It came from Carla Shatz, PhD, who directs Stanford Bio-X — an interdisciplinary institute founded in 1998 that brings together faculty from the schools of medicine, humanities & sciences and engineering. She told me:

You have to be able to walk into someone’s lab and say, “You know, I have this problem in my lab. Would you like to have a cup of coffee and talk about it?” And then that person needs to say, “Yes.”

We were talking about a recent report by the National Research Council of the National Academies. They had put together a workshop and then published a report giving advice and best practices for supporting interdisciplinary research. The report used Bio-X as a success story for the type of innovation that can come out of programs that cross disciplines.

Nowhere in the report is there a subhead reading, “Faculty have to say yes,” but a lot of the other advice is straight out of the Bio-X playbook. The institute needs to be located at the cross section of several schools or departments (check). The institute needs a building that brings people together (check). The institute needs to support students (check). The institute needs to be a financial value add rather than taxing participating departments (check).

This isn’t specifically called out in the report, but Shatz added that a good interdisciplinary institute also needs good food. She pointed out that people come from all over campus to eat at Nexus, located in the middle of the Clark Center that houses Bio-X and serves as a focus for its activities. It turns out scientists are just like the rest of us: offer good food and they will come. And then they will chat, and the next thing you know they’ll be collaborating.

I wrote a Q&A with Shatz based on our conversation. From now on, when I hear the phrase “She said yes” I’ll think of her, and her great description of the attitude that underlies collaboration.

Previously: Bio-X Kids Science Day inspires young scientists, Dinners spark neuroscience conversation, collaboration, Stanford’s Clark Center, home to Bio-X, turns 10 and Pioneers in science
Photo from Bio-X

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