New research at the University of Colorado Cancer Center shows how to stop both.

Specifically, cells signal themselves to survive, grow, reproduce, and migrate. Two years ago, researchers at the CU Cancer Center showed that turning off a family of signals made brain cancer cells less robust – it sensitized these previously resistant cells to chemotherapy.

But the second major problem – migration – potentially remained.

“I thought, aha, I have this great way to treat this cancer, but needed to check that we weren’t going to cause other problems. We wondered if turning off TAM family signaling would make brain cancer cells crawl away to a new spot where they might make new problems,” says Amy Keating, MD, investigator at the CU Cancer Center and senior author of the study, recently published in the journal Nature: Oncogene.

So Keating and colleagues went inside this TAM signaling family to explore how its members affect not only proliferation but migration. When they inhibited signaling through the other family member Axl, little changed (actually this was good: at least turning off this signaling pathway didn’t promote cancer cell migration).

But when Keating and colleagues turned off signaling through the Mer pathway, it was neither too hot nor too cold – it was just right, and these affected cancer cells were not only more sensitive to chemotherapy, but also unable to escape to safer areas of the brain.

Currently glioblastoma multiforme affects 45,000 people in the United States every year, the majority of whom will not survive 14 months after diagnosis.

“This represents a new targeted therapy, offering a potential new direction that nobody’s tried before,” says Keating, assistant professor of pediatrics at the University of Colorado School of Medicine.

After these extremely promising results with cell lines, Keating and colleagues are currently testing the technology in mice, after which all involved hope to move soon to human clinical trials.

Linguists and psychologists have debated how much the parts of the brain that mediate direct sensory experience are involved in understanding metaphors. George Lakoff and Mark Johnson, in their landmark work ‘Metaphors we live by’, pointed out that our daily language is full of metaphors, some of which are so familiar (like “rough day”) that they may not seem especially novel or striking. They argued that metaphor comprehension is grounded in our sensory and motor experiences.

New brain imaging research reveals that a region of the brain important for sensing texture through touch, the parietal operculum, is also activated when someone listens to a sentence with a textural metaphor. The same region is not activated when a similar sentence expressing the meaning of the metaphor is heard.

The results were published online this week in the journal Brain & Language.

“We see that metaphors are engaging the areas of the cerebral cortex involved in sensory responses even though the metaphors are quite familiar,” says senior author Krish Sathian, MD, PhD, professor of neurology, rehabilitation medicine and psychology at Emory University. “This result illustrates how we draw upon sensory experiences to achieve understanding of metaphorical language.”

Sathian is also medical director of the Center for Systems Imaging at Emory University School of Medicine and director of the Rehabilitation R&D Center of Excellence at the Atlanta Veterans Affairs Medical Center.

Seven college students who volunteered for the study were asked to listen to sentences containing textural metaphors as well as sentences that were matched for meaning and structure, and to press a button as soon as they understood each sentence. Blood flow in their brains was monitored by functional magnetic resonance imaging. On average, response to a sentence containing a metaphor took slightly longer (0.84 vs 0.63 seconds).

In a previous study, the researchers had already mapped out, for each of these individuals, which parts of the students’ brains were involved in processing actual textures by touch and sight. This allowed them to establish with confidence the link within the brain between metaphors involving texture and the sensory experience of texture itself.

“Interestingly, visual cortical regions were not activated by textural metaphors, which fits with other evidence for the primacy of touch in texture perception,” says research associate Simon Lacey, PhD, the first author of the paper.

The researchers did not find metaphor-specific differences in cortical regions well known to be involved in generating and processing language, such as Broca’s or Wernicke’s areas. However, this result doesn’t rule out a role for these regions in processing metaphors, Sathian says.

Also, other neurologists have seen that injury to various areas of the brain can interfere with patients’ understanding of metaphors.

“I don’t think that there’s only one area responsible for metaphor processing,” Sathian says. “Actually, several recent lines of research indicate that engagement with abstract concepts is distributed around the brain.”

“I think our research highlights the role of neural networks, rather than a single area of the brain, in these processes. What could be happening is that the brain is conducting an internal simulation as a way to understand the metaphor, and that’s why the regions associated with touch get involved. This also demonstrates how complex processes involving symbols, such as appreciating a painting or understanding a metaphor, do not depend just on evolutionarily new parts of the brain, but also on adaptations of older parts of the brain.”

Sathian’s future plans include asking whether similar relationships exist for other senses, such as vision. The researchers also plan to probe whether magnetic stimulation of the brain in regions associated with sensory experience can interfere with understanding metaphors.

In a paper published January 31 in the journal Molecular Psychiatry, researchers at Sanford-Burnham Medical Research Institute (Sanford-Burnham) reveal how antipsychotic drugs interfere with normal metabolism by activating a protein called SMAD3, an important part of the transforming growth factor beta (TGFbeta) pathway.

The TGFbeta pathway is a cellular mechanism that regulates many biological processes, including cell growth, inflammation, and insulin signaling. In this study, all antipsychotics that cause metabolic side effects activated SMAD3, while antipsychotics free from these side effects did not. What’s more, SMAD3 activation by antipsychotics was completely independent from their neurological effects, raising the possibility that antipsychotics could be designed that retain beneficial therapeutic effects in the brain, but lack the negative metabolic side effects.

“We now believe that many antipsychotics cause obesity and diabetes because they trigger the TGFbeta pathway. Of all the drugs we tested, the only two that didn’t activate the pathway were the ones that are known not to cause metabolic side effects,” said Fred Levine, M.D., Ph.D., director of the Sanford Children’s Health Research Center at Sanford-Burnham and senior author of the study.

In a previous study aimed at developing new insights into diabetes, Dr. Levine and his team used Sanford-Burnham’s high-throughput screening capabilities to search a collection of known drugs for those that alter the body’s ability to generate insulin, the pancreatic hormone that helps regulate glucose. That’s when they first noticed that many antipsychotics alter the activity of the insulin gene.

In this current study, the researchers set out to connect the dots between antipsychotics and insulin. In doing so, experiments in laboratory cell-lines showed that antipsychotics known to cause metabolic side effects also activated the TGFbeta pathway—a mechanism that controls many cellular functions, including the production of insulin—while the drugs without these side effects did not.

Wondering whether their initial laboratory observations were relevant to the human experience, the researchers reanalyzed previously published gene expression patterns in brain tissue from schizophrenic patients treated with antipsychotics. What they found supported their earlier findings—TGFbeta signaling was activated only in those patients receiving antipsychotic treatment. Looking further, they found that the extent to which each antipsychotic drug activated the TGFbeta pathway in human brains correlated very closely with the extent to which those same drugs activated SMAD3 and affected the insulin promoter in their cell culture experiments.

The TGFbeta pathway also plays an important role in metabolic disease in people who don’t take antipsychotic medications. “It’s known that people who have elevated TGFbeta levels are more prone to diabetes. So having a dysregulated TGFbeta pathway—whether caused by antipsychotics or through some other mechanism—is clearly a very bad thing,” said Dr. Levine. “The fact that antipsychotics activate this pathway should be a big concern to pharmaceutical companies. We hope this new information will lead to the development of improved drugs.”

“When people say, ‘I’m committed to my relationship,’ they can mean two things,” said study co-author Benjamin Karney, a professor of psychology and co-director of the Relationship Institute at UCLA. “One thing they can mean is, ‘I really like this relationship and want it to continue.’ However, commitment is more than just that.”

A deeper level of commitment, the psychologists report, is a much better predictor of lower divorce rates and fewer problems in marriage.

“It’s easy to be committed to your relationship when it’s going well,” said senior study author Thomas Bradbury, a psychology professor who co-directs the Relationship Institute. “As a relationship changes, however, shouldn’t you say at some point something like, ‘I’m committed to this relationship, but it’s not going very well — I need to have some resolve, make some sacrifices and take the steps I need to take to keep this relationship moving forward. It’s not just that I like the relationship, which is true, but that I’m going to step up and take active steps to maintain this relationship, even if it means I’m not going to get my way in certain areas’?

“This,” Bradbury said, “is the other kind of commitment: the difference between ‘I like this relationship and I’m committed to it’ and ‘I’m committed to doing what it takes to make this relationship work.’ When you and your partner are struggling a bit, are you going to do what’s difficult when you don’t want to? At 2 a.m., are you going to feed the baby?”

The couples that were willing to make sacrifices within their relationships were more effective in solving their problems, the psychologists found. “It’s a robust finding,” Bradbury said. “The second kind of commitment predicted lower divorce rates and slower rates of deterioration in the relationship.”

Of the 172 married couples in the study, 78.5 percent were still married after 11 years, and 21.5 percent were divorced. The couples in which both people were willing to make sacrifices for the sake of the marriage were significantly more likely to have lasting and happy marriages, according to Bradbury, Karney and lead study author Dominik Schoebi, a former UCLA postdoctoral scholar who is currently at Switzerland’s University of Fribourg.

For the study, the couples — all first-time newlyweds — were given statements that gauged their level of commitment. They were asked to what extent they agreed or disagreed with statements like “I want my marriage to stay strong no matter what rough times we may encounter,” “My marriage is more important to me than almost anything else in my life,” “Giving up something for my partner is frequently not worth the trouble” and “It makes me feel good to sacrifice for my partner.” The psychologists videotaped the couples’ interactions and measured how they behaved toward each other.

The psychologists also conducted follow-ups with the couples every six months for the first four years (and again later in their marriages), The couples were asked about their relationship history, their feelings toward each other, the stress in their lives, their level of social support, and their childhood and family, among other subjects.

The research is published online in the Journal of Personality and Social Psychology, the premier journal in social psychology, and will be published in an upcoming print edition.

‘We’re not saying it’s easy’

So what does it mean to be committed to your marriage?

“It means do what it takes to make the relationship successful. That’s what this research is saying. That’s what commitment really means,” Karney said. “In a long-term relationship, both parties cannot always get their way.”

When a couple has a dispute, they have many choices of how to respond, the psychologists said.

“One choice,” Karney said, “is if you dig your heels in, then I can dig my heels in too. I can say, ‘You’re wrong. Listen to me!’ But if this relationship is really important to me, I’m willing to say, ‘I will compromise.’ What is my goal? Is it to win this battle? Is it to preserve the relationship? The behaviors I might engage in to win this conflict are different from those that are best for the relationship. The people who think more about protecting the relationship over the long term are more likely to think this is not that big a problem.”

“When the stakes are high, our relationships are vulnerable,” Bradbury said. “When we’re under a great deal of stress or when there is a high-stakes decision on which you disagree, those are defining moments in a relationship. What our data indicate is that committing to the relationship rather than committing to your own agenda and your own immediate needs is a far better strategy. We’re not saying it’s easy.”

How do you do this when it’s difficult?

“Find ways to compromise, or at least have the conversation that allows you and your partner to see things eye to eye,” Bradbury said. “Often, we don’t have the big conversations that we need in our relationship. The very act of communicating in difficult times can be as important as the outcome of the conversation. Everybody has the opportunity to engage in a conflict, or not, to say, ‘You’re wrong, I’m right.’ When people are in it for the long term, they are often willing to make sacrifices and view themselves as a team. They both are.”

The couples whose marriages lasted were better at this than the couples who divorced, Bradbury and Karney said.

“The people who ended their marriages would have said they were very committed to the marriage,” Bradbury said. “But they did not have the resolve to say, ‘Honey, we need to work on this; it’s going to be hard, but it’s important.’ The successful couples were able to shift their focus away from whether ‘I win’ or ‘you win’ to ‘Are we going to keep this relationship afloat?’ That is the ideal.”

In a marriage, disagreement is inevitable, but conflict is optional — a choice we make, Bradbury and Karney said. When the psychologists give workshops for couples, they encourage them to discuss a source of disagreement. Finding such a topic is rarely, if ever, a problem.

The psychologists recommend against “bank-account relationships,” in which you keep score of how often you get your way and how often you compromise.

The research was funded by the National Institute of Mental Health and the National Institute of Child Health and Human Development (both part of the National Institutes of Health) and the UCLA Academic Senate.

The ‘invisible forces’ in your marriage

Have you ever noticed that some couples seem to be in sync with each other while other couples are much less so, and wondered why?

In another new study that used data on the couples who were still married after 11 years, Karney, Bradbury, Schoebi and Baldwin Way, an assistant professor of psychology at Ohio State University and former UCLA psychology postdoctoral scholar, suggest that some people, on the basis of their genetic makeup, appear to be more responsive to their spouse’s emotional states.

Their study appears in the online edition of the journal Emotion, published by the American Psychological Association. It will also be published in an upcoming print edition of the journal.

Building on prior research, the psychologists hypothesize that a gene — the serotonin transporter gene 5-HTTLPR — might play a role in making us more, or less, responsive to our spouse’s emotions. Some people have one variant of the gene, and some have a second variant.

The two variants of the gene strengthen or weaken the link between your emotions and your spouse’s emotions, the psychologists report. People with one variant (called the “short form”) tend to stay angry, sad or happy longer than people with the other variant.

“The extent to which we are connected, to which my emotions become your emotions, is stronger or weaker as a function of the serotonin transporter gene 5-HTTLPR,” Bradbury said.

“In the face of a negative event, your genes control how long your reaction lasts,” Karney said. “What we are showing in this paper is that if I have one form of this gene, I’m more responsive to my partner’s emotional states, and if I have the other form, I’m less responsive.”

“I think this creaks open a door,” Bradbury said, “to a field of psychology that helps people to realize that who they are and who their partner is, is actually in their biology. Who you are and how you respond to me has a lot to do with things that are totally outside your control. My partner’s biology is invisible to me; I have no clue about it. The more I can appreciate that the connection between who I am and who my partner is may be biologically mediated leads me to be much more appreciative of invisible forces that constrain our behavior.”

While the researchers suspect the role of 5-HTTLPR is important, they say there is probably a “constellation of important genes” that plays a role in how responsive we are to emotions.

“It’s much more complex than a single gene,” Bradbury said.

This research may imply that we should be forgiving of the behavior of a loved one and not demand that a spouse change her or his behavior, the psychologists said.

“If it’s so easy for you to tell your partner to change, perhaps you should just change yourself,” Bradbury said. “Go ahead and take that on, see how that goes.”

Bradbury and Karney are writing a book tentatively titled “Love Me Slender,” scheduled for publication next year, which connects one’s relationship with one’s physical health. Decisions we make about our health when we’re in a relationship are closely connected with our partner and his or her health, they argue.

Perhaps all this research is a reminder than when choosing a relationship, choose carefully and wisely — and even then, don’t expect it to be easy.

The discovery by researchers at Washington University School of Medicine in St. Louis may lead doctors and researchers to change the way Alzheimer’s disease is classified.

They report their findings Feb. 1 in the online journal PLoS One (Public Library of Science).

“We probably shouldn’t think of early-onset disease as inherited and late-onset as sporadic because sporadic cases and familial clustering occur in both age groups,” says senior investigator Alison M. Goate, DPhil. “I think it’s reasonable to assume that at least some cases among both early- and late-onset disease have the same causes. Our findings suggest the disease mechanism can be the same, regardless of the age at which Alzheimer’s strikes. People who get the disease at younger ages probably have more risk factors and fewer protective ones, while those who develop the disease later in life may have more protective factors, but it appears the mechanism may be the same for both.”

The researchers used next-generation DNA sequencing to analyze genes linked to dementia. They sequenced the APP (amyloid precursor protein) gene, and the PSEN1 and PSEN2 (presenilin) genes. Mutations in those genes have been identified as causes of early-onset Alzheimer’s disease. They also sequenced the MAPT (microtubule associated protein tau) gene and GRN (progranulin) gene, which have been associated with inherited forms of another illness involving memory loss called frontotemporal dementia.

“We found an increase in rare variants in the Alzheimer’s genes in families where four or more members were affected with late-onset disease,” says Goate, the Samuel and Mae S. Ludwig Professor of Genetics in Psychiatry, professor of neurology, of genetics and co-director of the Hope Center Program on Protein Aggregation and Neurodegeneration. “Changes in these genes were more common in Alzheimer’s cases with a family history of dementia, compared to normal individuals. This suggests that some of these gene variants are likely contributing to Alzheimer’s disease risk.”

The study also found mutations in the MAPT and GRN genes in some Alzheimer’s patients, suggesting they had been incorrectly diagnosed as having Alzheimer’s disease when they instead had frontotemporal dementia.

Goate and her colleagues studied the five genes in members of 440 families in which at least four individuals per family had been diagnosed with Alzheimer’s disease. They found rare variants in key Alzheimer’s-related genes in 13 percent of the samples they analyzed.

“Of those rare gene variants, we think about 5 percent likely contribute to Alzheimer’s disease,” says first author Carlos Cruchaga, PhD, assistant professor of psychiatry. “That may not seem like a lot, but so many people have the late-onset form of Alzheimer’s that even a very small percentage of patients with changes in these genes could represent very large numbers of affected individuals.”

Goate, who in 1991 was the first scientist to identify a mutation in the APP gene linked to inherited, early-onset Alzheimer’s disease, now wants to look closely at families with multiple cases of Alzheimer’s but no mutations in previously identified Alzheimer’s genes. She says it’s likely they carry mutations in genes that scientists don’t yet know about. And she believes that new sequencing techniques could speed the discovery of these genes. In fact, the researchers say a study like this would have been impossible only a few years ago.

“With next-generation sequencing technology, it’s now possible to sequence all of these genes at the same time,” Cruchaga says. “One reason we didn’t do this study until now is that 15 to 20 years ago when these genes were first identified, it would have taken years to sequence each gene individually.”

Cruchaga and Goate say the new technology and their new findings suggest that it may be worthwhile to sequence these genes in people with a strong family history of Alzheimer’s disease.

“We would like to see physicians who treat patients with late-onset disease ask detailed questions about family history,” Goate says. “I’m sure many probably do that already, but in those families with very strong histories, it’s not unreasonable to think about screening for genetic mutations.”

She says such screenings also may weed out people thought to have Alzheimer’s disease who actually have changes in genes related to frontotemperal dementia.

Both Goate and Cruchaga agree that one result of their discovery that the same genes can be connected with both early- and late-onset forms of Alzheimer’s disease may be changes in the way the disease is classified.

“It’s always been somewhat arbitrary, figuring out where early-onset ends and late-onset begins,” Goate says. “So I no longer look at early- and late-onset disease as being different illnesses. I think of them as stages along a continuum.”

Andrew Carton, assistant professor of management and organization at Penn State Smeal College of Business, and Ashleigh Shelby Rosette of Duke University, suggest in the current issue of the Academy of Management Journal that what steers people’s perceptions of African Americans are stereotypes about blacks’ leadership failings, biases that may not even be conscious.

The researchers found evidence of this phenomenon in a source seemingly remote from the corporate world — newspaper stories about college football quarterbacks.

Buried in those press reports is a consistent pattern of associating losses with failed leadership when quarterbacks are black but not when they are white, and associating victories with quarterbacks’ native athletic ability when they are black but not when they are white.

“Evaluators adjust the way they use stereotypes according to performance outcomes,” the researchers report. “Specifically, negative leader-based stereotypes will be applied after [a black quarterback's] performance failure and non-leader compensatory stereotypes (i.e., black leaders succeed because of marginal qualities that ‘compensate’ for negative qualities) will be applied after performance success.”

This stereotyping, Carton and Rosette observe, “may provide an important missing link in our understanding of bias against black leaders and may serve as an important contributor to barriers that impede the advancement of black leaders in organizations.”

The study owed its genesis in part to Carton’s own experience as a member of his college’s varsity football team.

“I became aware of certain racial biases, and when I later enrolled as a graduate student at Duke, I mentioned my experience to Professor Rosette, whose research included bias in the workplace. Quarterbacks are a good focus for any research on leadership, because they have an executive role on the field that is unique in sports.

The researchers analyzed newspaper reports over the course of a season for 119 teams in the Football Championship Subdivision, the highest level of competition in college football. They randomly sampled one story a week from the leading newspaper of each school’s locale, and coders unaware of the nature of the study were assigned to extract words or phrases that evaluated the quarterback and his performance — for example, where reporters cited a quarterback for “intelligence” or for being “fleet-footed.” Evaluative text was identified for 113 quarterbacks, 82 white and 31 black.

Analysis focused particularly on text that conveyed competence or incompetence and athleticism or its lack, the former two intimately related to leadership. Of special interest was how writers accounted for teams’ success in view of this presumption of black incompetence and whether they accounted for success or failure differently depending on quarterbacks’ race.

“Black quarterbacks were perceived to be significantly more incompetent than whites when their respective teams lost, but this difference was not found when their respective teams won,” the researchers said.

For example, black quarterbacks of defeated teams were more likely than defeated white quarterbacks to be tasked by reporters for making bad decisions under pressure.

To help rule out explanations other than bias for the difference in reporters’ perceptions of incompetence, the researchers looked for intellectual or scholastic factors. Neither the academic ratings of the colleges quarterbacks attended nor their grade point averages from high school were significantly associated with these perceptions.

Carton and Rosette say that one way to combat corporate CEO biases is for companies to institute “perception-based reform.” This might involve fostering one-on-one or small-group interactions that can serve to enhance people’s awareness of each other as individuals and not stereotypes.

The researchers also suggest that black leaders themselves can make their colleagues and subordinates more aware of their qualifications and experience, and of biases caused by stereotyping.

Neuromaging suggests they do. When applying a placebo, scientists see activity in the dorsolateral prefrontal cortex. That’s the part of the brain that controls high-level cognitive functions like working memory and attention—which is what you use to do that distracting puzzle.

Now a new study challenges the theory that the placebo effect is a high-level cognitive function. The authors—Jason T. Buhle, Bradford L. Stevens, and Jonathan J. Friedman of Columbia University and Tor D. Wager of the University of Colorado Boulder—reduced pain in two ways – either by giving them a placebo, or a difficult memory task. lacebo.

But when they put the two together, “the level of pain reduction that people experienced added up. There was no interference between them,” says Buhle. “That suggests they rely on separate mechanisms.” The findings, published in Psychological Science, a journal of the Association for Psychological Science, could help clinicians maximize pain relief without drugs.

In the study, 33 participants came in for three separate sessions. In the first, experimenters applied heat to the skin with a little metal plate and calibrated each individual’s pain perceptions. In the second session, some of the people applied an ordinary skin cream they were told was a powerful but safe analgesic. The others put on what they were told was a regular hand cream.

In the placebo-only trials, participants stared at a cross on the screen and rated the pain of numerous applications of heat—the same level, though they were told it varied. For other trials they performed a tough memory task—distraction and placebo simultaneously. For the third session, those who’d had the plain cream got the “analgesic” and vice versa. The procedure was the same.

The results: With either the memory task or the placebo alone, participants felt less pain than during the trials when they just stared at the cross. Together, the two effects added up; they didn’t interact or interfere with each other. The data suggest that the placebo effect does not require executive attention or working memory.

So what about that neuroimaging? “Neuroimaging is great,” says Buhle, “but because each brain region does many things, when you see activation in a particular area, you don’t know what cognitive process is driving it.” This study tested the theory about how placebos work with direct behavioral observation.

The findings are promising for pain relief. Clinicians use both placebos and distraction—for instance, virtual reality in burn units. But they weren’t sure if one might diminish the other’s efficacy. “This study shows you can use them together,” says Buhle, “and get the maximum bang for your buck without medications.”

A group of psychological scientists explore the relationship between silence and memories in a new paper published in Perspectives on Psychological Science, a journal of the Association for Psychological Science.

“There’s this idea, with silence, that if we don’t talk about something, it starts fading,” says Charles B. Stone of Université Catholique de Louvain in Belgium, an author of the paper. But that belief isn’t necessarily backed up by empirical psychological research—a lot of it comes from a Freudian belief that everyone has deep-seated issues we’re repressing and ought to talk about. The real relationship between silence and memory is much more complicated, Stone says.

“We are trying to understand how people remember the past in a very basic way,” Stone says. He cowrote the paper with Alin Coman of the University of Pittsburgh, Adam D. Brown of New York University, Jonathan Koppel of the University of Aarhus, and William Hirst of the New School for Social Research.

“Silence is everywhere,” Stone says. He and his coauthors divide silence about memories into several categories. You might not mention something you’re thinking about on purpose—or because it just doesn’t come up in conversation. And some memories aren’t talked about because they simply don’t come to mind. Sometimes people actively try not to remember something.

One well-studied example used by Stone and his colleagues to demonstrate how subtle the effects of silence can be, establishes that silences about the past occurring within a conversation do not uniformly promote forgetting.  Some silences are more likely to lead to forgetting than others.  People have more trouble remembering silenced memories related to what they or others talk about than silenced memories unrelated to the topic at hand.

If President Bush wanted the public to forget that weapons of mass destruction figured in the build-up to the Iraq War, he should not avoid talking about the war and its build-up.  Rather he should talk about the build-up and avoid any discussion of WMDs.  And at a more personal level, when people talk to each other about the events of their lives, talking about happy memories may leave the unhappy memories unmentioned, but in the future, people may have more trouble remembering the unmentioned happy memories than the unmentioned sad memories.

Or to supply another example of the subtle relation between memory and silence:  If your mother is asking you about your boyfriend and you tell her about yesterday’s date, while thinking—but not talking—about the exciting ending of the date, that romantic finish may linger longer in your memory than if you just answered her questions without thinking about the later part of the evening.

“Silence has important implications for how we remember the past beyond just forgetting,” Stone says. “In terms of memory, not all silence is equal.”

“They don’t want to rock the boat or upset the sense of social harmony,” says Julie Exline, a Case Western Reserve psychologist and lead author of the study.

Turning down cake or cookies when others are indulging is tough for everyone, but it poses a special problem for people-pleasers, Exline says. If people-pleasers feel a sense of social pressure to eat, they will often eat more in an attempt to match what others around them are eating.

But even if people-pleasers overeat in order to keep others comfortable, they may pay an emotional price.

“Those who overeat in order to please others tend to regret their choices later. It doesn’t feel good to give in to social pressures,” Exline says.

The research findings were reported in the Journal of Social and Clinical Psychology article, “People-Pleasing through Eating: Sociotropy Presents Greater Eating in Response to Perceived Social Pressure.”

This study looked at the eating habits, but, Exline says, the same behaviors that affect food consumption can surface in other areas of the individual’s life. For example, people-pleasers may feel anxious or guilty if they outperform others in areas such as academics, athletics or relationship success. People-pleasers have a strong desire to avoid posing a threat to others, so they often put a lot of energy into trying to keep others comfortable.

Exline led a two-part study of 101 college students (41 men and 60 women) who completed a questionnaire that assessed characteristics for people-pleasing, also known as “sociotropy.” Students high in people-pleasing were those who tended to put others’ needs before their own, worried about hurting others, and were sensitive to criticism, among other behaviors.

After answering these questions along with some other background measures, students were seated with a female actor who was posing as a second participant in the study. The experimenter handed a bowl of M&M candies to the actor, who took a small handful of candies (about 5) before offering the bowl to the participant. After taking the candies, participants reported how many they took and why. Researchers also assessed the number of candies taken.

High sociotropy (people-pleasing) scores were associated with taking more candy, both in this laboratory experiment and in a second study involving recall of real-life eating situations.

“People-pleasers feel more intense pressure to eat when they believe that their eating will help another person feel more comfortable,” Exline says. “Almost everyone has been in a situation in which they’ve felt this pressure, but people-pleasers seem especially sensitive to it.”

“Neurologists see patients with neurologic disorders that may make them more susceptible to abuse or neglect,” said lead author Elliott A. Schulman, MD, of Lankenau Medical Center in Wynnewood, Penn., and a Fellow of the American Academy of Neurology. “They also see patients with neurologic issues that may be either directly or indirectly related to mistreatment.”

More than 90 percent of all injuries from intimate partner violence occur to the head, face or neck region, and can lead to traumatic brain injury, according to the position statement. People with neurologic disorders such as Parkinson’s disease, Alzheimer’s disease or stroke may be at higher risk for abuse and neglect.

“By routinely asking about violence and abuse, the neurologist increases the opportunity for both identifying ongoing abuse and intervening when appropriate,” Schulman said. “In addition to further physical and emotional harm, consequences of not asking about abuse might include failure of treatments and, when children are exposed to abuse, perpetuation of the cycle of abuse from generation to generation.”

The position statement outlines 10 principles of intervention by the neurologist when meeting with patients, beginning with integrating questions about abuse into the medical history and routinely screening all patients for past and ongoing violence.

The Academy is also offering free training to members interested in seeking to help address domestic violence issues in their communities.