For some women, genes may influence pressure to be thin

EAST LANSING, Mich. — Genetics may make some women more vulnerable to the pressure of being thin, a study led by Michigan State University researchers has found. From size-zero models to airbrushed film stars, thinness is portrayed as equaling beauty across Western culture, and it's an ideal often cited as a cause of eating disorder symptoms in young women. The researchers focused on the potential psychological impact of women buying into this perceived ideal of thinness, which they call thin-ideal internalization. Changes in self-perception and behavior, caused by this idealization, can lead to body dissatisfaction, a preoccupation with weight and other symptoms of eating disorders. "We're all bombarded daily with messages extoling the virtues of being thin, yet intriguingly only some women develop what we term thin-ideal internalization," said Jessica Suisman, lead author on the study and a researcher in MSU's Department of Psychology. "This suggests that genetic factors may make some women more susceptible to this pressure than others." To explore the role of genetic factors in whether women "buy in" to the pressure to be thin, the idealization of thinness was studied in sets of twins. More than 300 female twins from the MSU Twin Registry, ages 12-22, took part in the study. Suisman and colleagues measured how much participants wanted to look like people from movies, TV and magazines. Once the levels of thin idealization were assessed, identical twins who share 100 percent of their genes were compared with fraternal twins who share 50 percent. The results show that identical twins have closer levels of thin idealization than fraternal twins, which suggests a significant role for genetics. Further analysis shows that the heritability of thin idealization is 43 percent, meaning that almost half of the reason women differ in their idealization of thinness can be explained by differences in their genetic makeup. In addition to the role of genes, findings showed that influences of the environment are also important. The results showed that differences between twins' environments have a greater role in the development of thin ideal internalization than wider cultural attitudes, which women throughout Western societies are exposed to. "We were surprised to find that shared environmental factors, such as exposure to the same media, did not have as big an impact as expected," Suisman said. "Instead, non-shared factors that make co-twins different from each other had the greatest impact." Although the study did not look at specific environmental triggers, non-shared environmental influences typically include experiences that twins do not share with one another. This could include involvement by one twin in a weight-focused sport like dance, one twin being exposed to more media that promotes thinness than the other, or one of the twins having a friendship group that places importance on weight. "The take-home message," Suisman said, "is that the broad cultural risk factors that we thought were most influential in the development of thin-ideal internalization are not as important as genetic risk and environmental risk factors that are specific and unique to each twin." Kelly Klump, MSU professor of psychology and co-author on the study, said it is well established that a broad range of factors can contribute to the development of eating disorders LPC Continuing Education "This study reveals the need to take a similar approach to the ways in which women buy in to pressure to be thin, by considering how both genetic and environmental factors contribute to the development of thin-ideal internalization," Klump said. ### The study, funded by the National Institute of Mental Health, appears in the International Journal of Eating Disorders. Co-authors include Shannon O'Connor, Alexandra Burt and Cheryl Sisk from MSU; Steffanie Sperry and Kevin Thompson from the University of South Florida; Pamela Keel from Florida State University; Michael Neale from Virginia Commonwealth University; and Steven Boker from the University of Virginia.

Potential new class of drugs blocks nerve cell death

Potential new class of drugs protects nerve cells in models of Parkinson's disease and amyotrophic lateral sclerosis Diseases that progressively destroy nerve cells in the brain or spinal cord, such as Parkinson's disease (PD) and amyotrophic lateral sclerosis (ALS), are devastating conditions with no cures. Now, a team that includes a University of Iowa researcher has identified a new class of small molecules, called the P7C3 series, which block cell death in animal models of these forms of neurodegenerative disease. The P7C3 series could be a starting point for developing drugs that might help treat patients with these diseases. These findings are reported in two new studies published the week of Oct. 1 in PNAS Early Edition. "We believe that our strategy for identifying and testing these molecules in animal models of disease gives us a rational way to develop a new class of neuroprotective drugs, for which there is a great, unmet need," says Andrew Pieper, M.D., Ph.D., associate professor of psychiatry at the UI Carver College of Medicine, and senior author of the two studies. About six years ago, Pieper, then at the University of Texas Southwestern Medical Center, and his colleagues screened thousands of compounds in living mice in search of small, drug-like molecules that could boost production of neurons in a region of the brain called the hippocampus. They found one compound that appeared to be particularly successful and called it P7C3. "We were interested in the hippocampus because new neurons are born there every day. But, this neurogenesis is dampened by certain diseases and also by normal aging," Pieper explains. "We were looking for small drug-like molecules that might enhance production of new neurons and help maintain proper functioning in the hippocampus." However, when the researchers looked more closely at P7C3, they found that it worked by protecting the newborn neurons from cell death. That finding prompted them to ask whether P7C3 might also protect existing, mature neurons in other regions of the nervous system from dying as well, as occurs in neurodegenerative disease. Using mouse and worm models of PD and a mouse model of ALS, the research team has now shown that P7C3 and a related, more active compound, P7C3A20, do in fact potently protect the neurons that normally are destroyed by these diseases. Their studies also showed that protection of the neurons correlates with improvement of some disease symptoms, including maintaining normal movement in PD worms, and coordination and strength in ALS mice. Of mice and worms In the ALS mouse model, a highly active variant of the original P7C3 molecule, known as P7C3A20, which the investigators synthesized, largely prevented death of the nerve cells within the spinal cord that are normally destroyed by this disease. The P7C3 molecule also worked, but was not as effective at protecting neurons in this model. As cell survival increased in the ALS model, coordination and strength of the mice improved as well. Mice that were given P7C3A20 were able to stay on a rotating rod much longer than untreated animals or animals that received the less active compounds. Animals receiving P7C3A20 also performed better in analysis of their walking gait, which typically worsens in these animals as the disease progresses. In PD, dopamine-producing neurons necessary for normal movement are gradually destroyed. In patients, loss of these brain cells leads to tremors, stiffness, and difficulty walking. The study again showed that P7C3 protects these neurons from cell death and the more active analogue, P7C3A20, provided even greater protection. The two compounds also potently blocked cell death of dopaminergic neurons in a C. elegans worm model of PD. Moreover, reduced cell death in this model was associated with improved movement in the worms. Healthy C. elegans worms have a very characteristic swimming motion. This movement is disrupted in the PD worm. Hector De Jesus-Cortes, a graduate student of neuroscience at UT Southwestern Medical Center and lead author of the Parkinson's study, videotaped and analyzed the PD worms' mobility with and without treatment. Normal swimming was almost completely preserved with P7C3A20, and was also fairly well preserved with P7C3. Tweaking the molecule The research team compared the activity of several new P7C3-related compounds that they synthesized, in both the hippocampal neurogenesis screen and the mouse model of PD. "Every variation of our P7C3 molecule that works in the neurogenesis assay also works in the PD model," Pieper says. "As we continue to refine the molecule, our hope is that the results from the neurogenesis assay will accurately predict the neuroprotective potency of the compound, and thus aid in more rapidly optimizing a new neuroprotective agent." Nursing CEUs The team plans to continue tweaking the structure of the P7C3 molecule to improve its neuroprotective ability while eliminating potential side effects. "Our hope is that this work will form the basis for designing a neuroprotective drug that could eventually help patients," Pieper says. ### Pieper and De Jesus-Cortes conducted the study with colleagues at UT Southwestern Medical Center, including Steven McKnight, Ph.D., chairman of biochemistry, and Joseph Ready, Ph.D., professor of biochemistry. The work was funded in part by grants from the National Institute for Mental Health.

Ready for Your Close-Up?

Caltech study shows that the distance at which facial photos are taken influences perception PASADENA, Calif.—As the saying goes, "A picture is worth a thousand words." For people in certain professions—acting, modeling, and even politics—this phrase rings particularly true. Previous studies have examined how our social judgments of pictures of people are influenced by factors such as whether the person is smiling or frowning, but until now one factor has never been investigated: the distance between the photographer and the subject. According to a new study by researchers at the California Institute of Technology (Caltech), this turns out to make a difference—close-up photo subjects, the study found, are judged to look less trustworthy, less competent, and less attractive. The new finding is described in this week's issue of the open-access journal PLoS One. Pietro Perona, the Allen E. Puckett Professor of Electrical Engineering at Caltech, came up with the initial idea for the study. Perona, an art history enthusiast, suspected that Renaissance portrait paintings often featured subtle geometric warping of faces to make the viewer feel closer or more distant to a subject. Perona wondered if the same sort of warping might affect photographic portraits—with a similar effect on their viewers—so he collaborated with Ralph Adolphs, Bren Professor of Psychology and Neuroscience and professor of biology, and CNS graduate student Ronnie Bryan (PhD '12) to gather opinions on 36 photographs representing two different images of 18 individuals. One of each pair of images was taken at close range and the second at a distance of about seven feet. "It turns out that faces photographed quite close-up are geometrically warped, compared to photos taken at a larger distance," explains Bryan. "Of course, the close picture would also normally be larger, higher resolution and have different lighting—but we controlled for all of that in our study. What you're left with is a warping effect that is so subtle that nobody in our study actually noticed it. Nonetheless, it's a perceptual clue that influenced their judgments." That subtle distance warping, however, had a big effect: close-up photos made people look less trustworthy, according to study participants. The close-up photo subjects were also judged to look less attractive and competent. "This was a surprising, and surprisingly reliable, effect," says Adolphs. "We went through a bunch of experiments, some testing people in the lab, and some even over the Internet; we asked participants to rate trustworthiness of faces, and in some experiments we asked them to invest real money in unfamiliar people whose faces they saw as a direct measure of how much they trusted them." Alcoholism and Drug Abuse Counselors Continuing Education Across all of the studies, the researchers saw the same effect, Adolphs says: in photos taken from a distance of around two feet, a person looked untrustworthy, compared to photos taken seven feet away. These two distances were chosen by the researchers because one is within, and the other outside of, personal space—which on average is about three to four feet from the body. In some of the studies, the researchers digitally warped images of faces taken at a distance to artificially manipulate how trustworthy they would appear. "Once you know the relation between the distance warp and the trustworthiness judgment, you could manipulate photos of faces and change the perceived trustworthiness,'' notes Perona. He says that the group is now planning to build on these findings, using machine-vision techniques—technologies that can automatically analyze data in images. For example, one application would be for a computer program to have the ability to evaluate any face image in a magazine or on the Internet and to estimate the distance at which the photo was taken. "The work might also allow us to estimate the perceived trustworthiness of a particular face image," says Perona. "You could imagine that many people would be interested in such applications—particularly in the political arena." The study, "Perspective Distortion from Interpersonal Distance Is an Implicit Visual Cue for Social Judgments of Faces," was funded by grants from the National Institute of Mental Health and from the Gordon and Betty Moore Foundation. Written by Katie Neith

Popular HIV drug may cause memory declines

Johns Hopkins study suggests the commonly prescribed anti-retroviral drug efavirenz attacks brain cells The way the body metabolizes a commonly prescribed anti-retroviral drug that is used long term by patients infected with HIV may contribute to cognitive impairment by damaging nerve cells, a new Johns Hopkins research suggests. Nearly 50 percent of people infected with HIV will eventually develop some form of brain damage that, while mild, can affect the ability to drive, work or participate in many daily activities. It has long been assumed that the disease was causing the damage, but Hopkins researchers say the drug efavirenz may play a key role. People infected with HIV typically take a cocktail of medications to suppress the virus, and many will take the drugs for decades. Efavirenz is known to be very good at controlling the virus and is one of the few that crosses the blood-brain barrier and can target potential reservoirs of virus in the brain. Doctors have long believed that it might be possible to alleviate cognitive impairment associated with HIV by getting more drugs into the brain, but researchers say more caution is needed because there may be long-term effects of these drugs on the brain. "People with HIV infections can't stop taking anti-retroviral drugs. We know what happens then and it's not good," says Norman J. Haughey, Ph.D., an associate professor of neurology at the Johns Hopkins University School of Medicine. "But we need to be very careful about the types of anti-retrovirals we prescribe, and take a closer look at their long-term effects. Drug toxicities could be a major contributing factor to cognitive impairment in patients with HIV." For the study led by Haughey and described online in the Journal of Pharmacology and Experimental Therapeutics, researchers obtained samples of blood and cerebrospinal fluid from HIV-infected subjects enrolled in the NorthEastern AIDS Dementia study who were taking efavirenz. Researchers looked for levels of the drug and its various metabolites, which are substances created when efavirenz is broken down by the liver. Performing experiments on neurons cultured in the lab, the investigators examined the effects of 8-hydroxyefavirenz and other metabolites and found major structural changes when using low levels of 8-hydroxyefavirenz, including the loss of the important spines of the cells. Haughey and his colleagues found that 8-hydroxyefavirenz is 10 times more toxic to brain cells than the drug itself and, even in low concentrations, causes damage to the dendritic spines of neurons. The dendritic spine is the information processing point of a neuron, where synapses — the structures that allow communication among brain cells — are located. In the case of efavirenz, a minor modification in the drug's structure may be able block its toxic effects but not alter its ability to suppress the virus. Namandje N. Bumpus, Ph.D., one of the study's other authors, has found a way to modify the drug to prevent it from metabolizing into 8-hydroxyefavirenz while maintaining its effectiveness as a tool to suppress the HIV virus. "Finding and stating a problem is one thing, but it's another to be able to say we have found this problem and here is an easy fix," Haughey says. Haughey says studies like his serve as a reminder that while people infected with HIV are living longer than they were 20 years ago, there are significant problems associated with the drugs used to treat the infection. "Some people do seem to have this attitude that HIV is no longer a death sentence," he says. "But even with anti-retroviral treatments, people infected with HIV have shortened lifespans and the chance of cognitive decline is high. It's nothing you should treat lightly." HIV and AIDS CE Course ### The study was supported by grants from the National Institute on Alcohol Abuse and Alcoholism (AA0017408), the National Institute of Mental Health (MH077543, MH075673 and MH71150), the National Institute on Aging (AG034849) and the National Institute of Neurological Disorders and Stroke (NS049465). Other Hopkins researchers involved in the study include Luis B. Tovar y Romo, Ph.D.; Lindsay B. Avery, Ph.D.; Ned Sacktor, M.D.; and Justin McArthur, M.B.B.S., M.P.H. For more information: http://www.hopkinsmedicine.org/neurology_neurosurgery/research/jhu_nimh/researchers

Mentally Ill Often Targets of Violence

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Suicide Now Kills More Americans Than Car Crashes: Study

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Suicide Now Kills More Americans Than Car Crashes: Prevention efforts lowered traffic fatalities, more attention needed for suicide, experts say ***************************************************** Suicide Prevention CE Course (7 hours) Description $ - For course pricing details, see our Pricing page by clicking on the "Pricing" tab This course is designed to help you: Increase awareness of suicide prevention methods Increase familiarity with broad based support systems Become familiar with strategies to reduce stigma Learn how to promote efforts to reduce efforts to lethal means of self harm. Identify at risk behavior Implement appropriate treatment and resources Develop and Promote Effective Clinical and Professional Practices CEU LPC, ceus mft, ceu’s for social workers, BBS approved, NBCC provider, nursing ceus, online ceus, ceus for MFTs, ce courses for counselors, Social Worker ceus, continuing education units for LPCs, MHC ceus, LCSW, ASW and MFT Intern ceus, Board approved ceus in many states, national board approval ceus, alcohol and drug abuse counselor ceus. See chart below for your state and license.

Feeling Guilty Versus Feeling Angry – Who Can Tell the Difference?

When you rear-end the car in front of you at a stoplight, you may feel a mix of different emotions such as anger, anxiety, and guilt. The person whose car you rear-ended may feel angered and frustrated by your carelessness, but it’s unlikely that he’ll feel much guilt. The ability to identify and distinguish between negative emotions helps us address the problem that led to those emotions in the first place. But while some people can tell the difference between feeling angry and guilty, others may not be able to separate the two. Distinguishing between anger and frustration is even harder. In a study forthcoming in Psychological Science, a journal of the Association for Psychological Science, psychological scientist Emre Demiralp of the University of Michigan and his colleagues hypothesized that clinically depressed people would be less able to discriminate between different types of negative emotions compared to healthy individuals. Clinically depressed people often experience feelings of sadness, anger, fear, or frustration that interfere with everyday life. “It is difficult to improve your life without knowing whether you are sad or angry about some aspect of it,” says Demiralp. “For example, imagine not having a gauge independently indicating the gasoline level of your car. It would be challenging to know when to stop for gas. We wanted to investigate whether people with clinical depression had emotional gauges that were informative and whether they experienced emotions with the same level of specificity and differentiation as healthy people.” The researchers recruited 106 people between the ages of 18 and 40 to participate in their study. Half of the participants were diagnosed with clinical depression and half were not. Over the course of seven to eight days, they carried a Palm Pilot, which prompted them to record emotions at 56 random times during the day. To report their emotions, they marked the degree to which they felt seven negative emotions (sad, anxious, angry, frustrated, ashamed, disgusted, and guilty) and four positive emotions (happy, excited, alert, and active) on a scale from one to four. Demiralp and his colleagues looked at participants’ tendency to give multiple emotions (e.g., disgusted and frustrated) similar rankings at a given point in time. According to their methodology, the more two emotions were reported together the less the person differentiated between these emotions. The researchers found that clinically depressed people had less differentiated negative emotions than those who were healthy, supporting their hypothesis. Notably, they did not find the same difference between groups for positive emotions—people with and without diagnosed clinical depression were equally able to differentiate between positive emotions. It is possible that people who are clinically depressed differentiate more between positive emotions as a coping mechanism. Demiralp and his colleagues argue that the procedure used in the study to record emotions may be particularly useful in studying the emotional experience of clinically depressed people, paving the way for more treatment and therapy options in the future. “Our results suggest that being specific about your negative emotions might be good for you”, says Demiralp. “It might be best to avoid thinking that you are feeling generally bad or unpleasant. Be specific. Is it anger, shame, guilt or some other emotion? This can help you circumvent it and improve your life. It is one of our overarching goals to investigate approaches for facilitating this kind of emotional intelligence at a large scale in the population.” *** This research was supported by NIMH grants MH60655 to John Jonides, MH59259 to Ian H. Gotlib, and F32 MH091831 to Renee J. Thompson, SNF Fellowship PA001/117473 to Susanne Jaeggi, and fellowships SFRH/BPD/35953/2007 from Fundação para a Ciência e a Tecnologia and Wi3496/41 from the Deutsche Forschungsgemeinschaft awarded to Jutta Mata. Jutta Mata is now at the University of Basel, Switzerland LPCC Continuing Education ### For more information about this study, please contact: Emre Demiralp at emredemi@umich.edu. The APS journal Psychological Science is the highest ranked empirical journal in psychology. For a copy of the article "Feeling Blue or Turquoise? Emotional Differentiation in Major Depressive Disorder" and access to other Psychological Science research findings, please contact Anna Mikulak at 202-293-9300 or amikulak@psychologicalscience.org.