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Brand Logo Can Make You ‘Think Different’

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Whether you are a Mac person or a PC person, even the briefest exposure to the Apple logo may make you behave more creatively, according to recent research from Duke University’s Fuqua School of Business and the University of Waterloo, Canada.

In work to be published in the April issue of the Journal of Consumer Research, Professors Gavan Fitzsimons and Tanya Chartrand of Duke, and Gráinne Fitzsimons of Waterloo, found that even the briefest exposure to well-known brands can cause people to behave in ways that mirror those brands’ traits.

“Each of us is exposed to thousands of brand images every day, most of which are not related to paid advertising,” said Gavan Fitzsimons. “We assume that incidental brand exposures do not affect us, but our work demonstrates that even fleeting glimpses of logos can affect us quite dramatically.”

To assess the effects of brands on behavior, the researchers selected two competing brands, both well respected by consumers, with distinct and well-defined brand personalities. “Apple has worked for many years to develop a brand character associated with nonconformity, innovation and creativity,” said Chartrand, “and IBM is viewed by consumers as traditional, smart and responsible.”

The team conducted an experiment in which 341 university students completed what they believed was a visual acuity task, during which either the Apple or IBM logo was flashed so quickly that they were unaware they had been exposed to the brand logo.  The participants then completed a task designed to evaluate how creative they were, listing all of the uses for a brick that they could imagine beyond building a wall.

People who were exposed to the Apple logo generated significantly more unusual uses for the brick compared with those who were primed with the IBM logo, the researchers said. In addition, the unusual uses the Apple-primed participants generated were rated as more creative by independent judges.

“This is the first clear evidence that subliminal brand exposures can cause people to act in very specific ways,” said Gráinne Fitzsimons. “We’ve performed tests where we’ve offered people $100 to tell us what logo was being flashed on screen, and none of them could do it. But even this imperceptible exposure is enough to spark changes in behavior.”

Other than their defined brand personalities, the researchers argue there is not anything unusual about Apple and IBM that causes this effect. The team conducted a follow-up experiment using the Disney and E! Channel brands, and found that participants primed with the Disney Channel logo subsequently behaved much more honestly than those who saw the E! Channel logos.

“These experiments demonstrate that most any brand that has strong associations with particular traits could have the capacity to influence how we act,” Chartrand said.

The researchers note practical implications of their work for both consumers and marketers.

“Instead of spending the majority of their money on traditional print and television advertising, companies with established brand associations such as Apple may want to give serious consideration to shifting more marketing resources to product placement opportunities and other forms of outreach that emphasize brief brand exposures,” Gavan Fitzsimons said.

And consumers should be aware that they are susceptible to influences they may not detect and use this knowledge to their advantage. “If you know you need to perform well on some task, say something athletic, you may want to surround yourself with images and brand logos that represent success in athletics,” Gráinne Fitzsimons said.

Fitzsimons, Gráinne M., Tanya L. Chartrand and Gavan J. Fitzsimons (in press) “Automatic Effects of Brand Exposure on Motivated Behavior: How Apple Makes You “Think Different”,” Journal of Consumer Research.

Written by huehueteotl

March 31, 2008 at 12:44 pm

Posted in Psychology

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Parents In Denial About Their Children’s Weight Problems

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In a study of 104 children under treatment for type 2 diabetes at the Vanderbilt Eskind Pediatric Diabetes Clinic, the children and their parents were surveyed about their perceptions of the child’s weight, dietary and exercise practices, as well as barriers to improving diet and exercise habits.

Quite often, both the children and their parents underestimated the child’s weight status.

“You could argue the first step for overcoming obesity is recognition,” said Russell Rothman, M.D., assistant professor of Internal Medicine and Pediatrics at the Vanderbilt Center for Health Services Research, and senior author on the study in February’s Diabetes Care.

“This is a group that is already getting treatment for type 2 diabetes, including education about exercise and nutrition. If anything, you might expect them to be more aware about weight issues. This should send up a red flag about how challenging it is to treat obesity in this population, if many of the parents and patients in this group don’t even recognize the problem.”

The parents and children were surveyed by telephone and were asked, among other things, “do you think your child’s/your weight is very overweight, slightly overweight, about right, slightly thin or very thin.”

While 87 percent of the children surveyed were obese by the most recent Centers for Disease Control and Prevention (CDC) standards, only 41 percent of parents, and 35 percent of the children reported themselves “very overweight.” Among parents who reported their child’s weight as “about right,” 40 percent had children who actually were at or over the 95th percentile for weight and were considered obese by government standards.

Girls were more likely than boys to underestimate their weight, and parents underestimated their children’s weight more often than the children did themselves. Additionally, those who underreported weight were more likely to report a poor diet and exercise than those who correctly reported their weight status. Those with misperceptions about weight also reported more barriers to better exercise and diet behaviors.

There have been other studies showing parents and children in the general population often don’t accurately perceive weight. However, Rothman said this is the first study to examine weight perception among children with type 2 diabetes — a population that should already have been informed of their weight status and its contribution to diabetes from their health care providers.

“As health care providers we need to take a step back and realize these families need better guidance about understanding their weight status before we can convince them to make lifestyle changes to improve their health,” said Rothman, who also serves as director of the Vanderbilt Program on Effective Health Communication. “We need to do a better job as providers to work on shared communication, using more clear language, goal setting with families about key behavior changes, identifying barriers and setting realistic goals.”

Diabetes Care. 2008 Feb;31(2):227-9. Epub 2007 Nov 13.
Accuracy of perceptions of overweight and relation to self-care behaviors among adolescents with type 2 diabetes and their parents.
Health Policy and Administration, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599-7411, USA.
OBJECTIVE: To examine how adolescents with type 2 diabetes and their parents/primary caregivers perceive the adolescents’ weight and the relationship of those perceptions to diet and exercise behaviors and perceived barriers to healthy behaviors. RESEARCH DESIGN AND METHODS: Interviews were conducted with adolescents and their parents about perceptions of the adolescents’ weight, diet, and exercise behaviors, as well as barriers to engaging in healthy diet and exercise behaviors. Interviews were linked with clinic records to provide BMI. RESULTS: A total of 104 parent-adolescent dyads participated. Parents and adolescents typically perceived the adolescents’ weight as less severe than it actually was. For parents and adolescents, underestimating the adolescents ‘ weight was associated with poorer diet behaviors and more perceived barriers to following healthy diet or exercise behaviors. CONCLUSIONS: Addressing misperceptions of weight by adolescents and their parents may be an important first step to improving weight in these patients.
for bodyweight perception in adults see:


Written by huehueteotl

March 5, 2008 at 12:14 pm

Cocaine’s Effects On Brain Metabolism May Contribute To Abuse

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Many studies on cocaine addiction – and attempts to block its addictiveness – have focused on dopamine transporters, proteins that reabsorb the brain’s “reward” chemical once its signal is sent. Since cocaine blocks dopamine transporters from doing their recycling job, it leaves the feel-good chemical around to keep sending the pleasure signal. Now a new study conducted at the U.S. Department of Energy’s Brookhaven National Laboratory suggests that cocaine’s effects go beyond the dopamine system. In the study, cocaine had significant effects on brain metabolism, even in mice that lack the gene for dopamine transporters.

Magnetic resonance imaging (MRI) and positron emission tomography (PET) scans showing the effect of cocaine on brain metabolism in mice with normal levels of dopamine transporter proteins (DAT +/+) and mice lacking dopamine transporters (DAT -/-). Cocaine was compared with saline treatment (vehicle). Cocaine use blunted whole brain metabolism in both groups of mice (indicated by a reduced amount of yellow visible on the cocaine images), and had a particularly significant effect on the thalamus (TH) in DAT -/- mice. These results indicate that cocaine affects the brain in ways not modulated by its blockade of dopamine transporter proteins. (Credit: Image courtesy of DOE/Brookhaven National Laboratory)

“In dopamine-transporter-deficient mice, these effects on metabolism are clearly independent of cocaine’s effects on dopamine,” said Brookhaven neuroscientist Panayotis (Peter) Thanos, who led the research. “These metabolic factors may be a strong regulator of cocaine use and abuse, and may also suggest new avenues for addiction treatments.”

The scientists used positron emission tomography, or PET scanning, to measure brain metabolism in dopamine-transporter deficient mice (known as DAT knockouts) and in littermates that had normal dopamine transporter levels. In this technique, the scientists administer a radioactively labeled form of sugar (glucose) – the brain’s main “fuel” – and use the PET scanner to track its site-specific concentrations in various brain regions. They tested the mice before and after cocaine administration, and compared the results to mice treated with saline instead of the drug.

Before any treatment, mice lacking dopamine transporters had significantly higher metabolism in the thalamus and cerebellum compared with normal mice. This elevated metabolism may be linked to chronically high levels of dopamine in the DAT knockout mice. It also suggests that dopamine levels may play an important role in modulating glucose levels in these brain areas, which play important roles integrating sensory information, learning, and motor function.

Interestingly, DAT knockout mice have been suggested as an animal model for attention-deficit hyperactivity disorder (ADHD). Elevated metabolism due to persistent elevated dopamine levels may be a factor contributing to the symptoms of ADHD, Thanos said.

After the scientists administered cocaine, whole brain metabolism decreased in both groups of mice, but more significantly in normal mice than in DAT knockouts. The scientists were able to detect this reduction in metabolism in a wide range of brain regions in the normal mice, suggesting that these decreases in metabolism are somehow associated with the blockade of dopamine transporters by cocaine.

The scientists also observed a reduction in metabolism in the thalamus region in the DAT knockout mice. This effect may likely be due to the effect of cocaine on other neurotransmitter systems, for example, norepinepherine or serotonin.

In summary, cocaine exposure has an effect on regional brain activity, which is mostly driven by dopamine action and to a secondary degree norepinephrine or serotonin. These results also support the idea that the thalamus and the cerebellum play key roles in cocaine’s mechanism of effect on sensory input, learning, and motor function. This is particularly of interest in better understanding the mechanism of cocaine addiction as well as the neurobiology of ADHD.

Synapse. 2008 Feb 19;62(5):319-324 [Epub ahead of print]
The effects of cocaine on regional brain glucose metabolism is attenuated in dopamine transporter knockout mice.

Behavioral Neuropharmacology Lab, Medical Department, Brookhaven National Laboratory, Upton, New York 11973‐5000.

Cocaine’s ability to block the dopamine transporter (DAT) is crucial for its reinforcing effects. However the brain functional consequences of DAT blockade by cocaine are less clear since they are confounded by its concomitant blockade of norepinephrineand serotonin transporters. To separate the dopaminergic from the non-dopaminergic effects of cocaine on brain function we compared the regional brain metabolic responses to cocaine between dopamine transporter deficient (DAT(-/-)) mice with that of their DAT(+/+) littermates. We measured regional brain metabolism (marker of brain function) with 2-[18F]-fluoro-2-deoxy-D-glucose (FDG) and microPET (muPET) before and after acute cocaine administration (i.p. 10 mg/kg). Scans were conducted 2 weeks apart. At baseline DAT(-/-) mice had significantly greater metabolism in thalamus and cerebellum than DAT(+/+). Acute cocaine decreased whole brain metabolismand this effect was greater in DAT(+/+) (15%) than in DAT(-/-) mice (5%). DAT(+/+) mice showed regional decreases in the olfactory bulb, motor cortex, striatum, hippocampus, thalamus and cerebellum whereas DAT(-/-) mice showed decreases only in thalamus. The differential pattern of regional responses to cocaine in DAT(-/-) and DAT(+/+) suggests that most of the brain metabolic changes from acute cocaine are due to DAT blockade. Cocaine-induced decreases in metabolism in thalamus (region with dense noradrenergic innervation) in DAT(-/-) suggest that these were mediated by cocaine’s blockade of norepinephrine transporters. The greater baseline metabolism in DAT(-/-) than DAT(+/+) mice in cerebellum (brain region mostly devoid of DAT) suggests that dopamine indirectly regulates activity of these brain regions. Synapse, 62:319-324, 2008. Published 2008 Wiley-Liss, Inc.

Written by huehueteotl

February 25, 2008 at 2:47 pm

Socialising Makes Us Smart

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Humans are social animals, in the tradition of Aristotle Thomas Aquinas calls us rational animals and social beings. How are the two sides connected?

Article lead author Oscar Ybarra* and his colleagues at the University of Michigan explored the possibility that social interaction improves mental functioning. In a series of related studies, they tested the participants’ level of cognitive functioning, comparing it to the frequency of participants’ social interactions.

They found that people who engaged in social interaction displayed higher levels of cognitive performance than the control group. Social interaction aided intellectual performance.

“Social interaction,” the authors suggest, “helps to exercise people’s minds. People reap cognitive benefits from socializing,” They speculate that social interaction “exercises” cognitive processes that are measured on intellectual tasks. “It is possible,” the authors conclude, “that as people engage socially and mentally with others, they receive relatively immediate cognitive boosts.”

Pers Soc Psychol Bull 2008; 34; 248 DOI: 10.1177/0146167207310454

Mental Exercising Through Simple Socializing: Social Interaction Promotes General Cognitive Functioning

Oscar Ybarra, Eugene Burnstein, Piotr Winkielman, Matthew C. Keller, Melvin Manis, Emily Chan and Joel Rodriguez

The online version of this article can be found at:

Social interaction is a central feature of people’s life and engages a variety of cognitive resources. Thus, social interaction should facilitate general cognitive functioning. Previous studies suggest such a link, but they used special populations (e.g., elderly with cognitive impairment), measured social interaction indirectly (e.g., via marital status), and only assessed effects of extended interaction in correlational designs. Here the relation between mental functioning and direct indicators of
social interaction was examined in a younger and healthier population. Study 1 using survey methodology found a positive relationship between social interaction, assessed via amount of actual social contact, and cognitive functioning in people from three age groups including younger adults. Study 2 using an experimental design found that a small amount of social interaction (10 min) can facilitate cognitive performance. The findings are discussed in the context of the benefits social relationships have for so many aspects of people’s lives. 

Written by huehueteotl

February 19, 2008 at 3:36 pm

Amygdala And Learning Fear

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Very young rat brains process memories of fear differently than more mature ones, new research indicates. The work significantly advances scientific understanding of when and how fear is stored and unlearned, and introduces new thinking on the implications of fear experience early in life.

“This important paper raises questions that are the ‘tip of the iceberg’ related to the very complex series of events that occur as we learn to fear something. In the real world, we become fearful, extinguish that fear, reacquire it at another time, and then conquer it yet again,” says John Krystal, MD, of Yale University and director of the clinical neuroscience division of the VA National Center for Post-Traumatic Stress Disorder. “Typically, we think about long-term, negative impact of fear learning, such as lifelong problems with anxiety. But this work highlights an avenue for adapting to early stresses that apparently can occur only early in life: to erase a learned fear from memory.” Krystal was not affiliated with the research.

Study co-authors Jee Hyun Kim and Rick Richardson, PhD, of the University of New South Wales in Sydney, homed in on the amygdala, using anesthesia to temporarily inactivate it and therefore isolate its role. The amygdala is critical for emotional learning and plays a central role in dulling the memory of a fear.

Kim and Richardson trained rats that were 16 and 23 days old–the human equivalent of children and budding adolescents–to associate a specific sound with a mild shock to the foot. After subsequent training, when the sound was not followed by a shock, the animals’ fearful reaction to hearing the sound faded. Technically, this is known as “extinction,” and depended on the function of the amygdala.

In a second round of training, the researchers reintroduced the fear and tried to re-extinguish it. This time around, they found, only the older rats were able to do so without the amygdala.

The researchers concluded that the age at which the initial extinction training occurred was critical to whether or not the rats’ fear faded the second time independently of the amygdala. The authors suggest that in the very young, it is primarily the amygdala that extinguishes fearful memories, but that mechanisms independent of the amygdala develop later.

This raises the possibility that fears unlearned at an early enough age are, in fact, erased. As brains develop, however, and related structures near the amygdala mature, these structures take on a greater role. Thus, fear in adolescence and later in life may not be erased, but instead be, for example, inhibited by a process of overlaying neutral memories on top of the initial fear reaction. The initial memory could still exist and be called on again.

“Extinction in the young brain might forever erase early traumatic learning–but accepting this hypothesis will have to wait for more research,” says Mark Bouton, PhD, of the University of Vermont, who did not participate in the esearch. “What might change as the brain develops is where and how fear learning and extinction are stored and how they can be retrieved.”

J Neurosci. 2008 Feb 6;28(6):1282-90.
The effect of temporary amygdala inactivation on extinction and reextinction of fear in the developing rat: unlearning as a potential mechanism for extinction early in development.

School of Psychology, The University of New South Wales, Sydney 2052, Australia.

It is well accepted that fear extinction does not cause erasure of the original conditioned stimulus (CS)-unconditioned stimulus association in the adult rat because the extinguished fear often returns (e.g., renewal and reinstatement). Furthermore, extinction is NMDA and GABA dependent, showing that extinction involves new inhibitory learning. We have recently observed each of these extinction-related phenomena in 24-d-old but not in 17-d-old rats. These results suggest that different neural processes mediate extinction early in development. However, the neural processes underlying extinction in the developing rat are unknown. Therefore, the present study investigated amygdala involvement in extinction and reextinction during development. In experiment 1, temporary inactivation of the amygdala (using bupivacaine, a sodium channel modulator) during extinction training impaired extinction of conditioned fear in 17- and 24-d-old rats. In experiment 2, 17- and 24-d-old rats were conditioned, extinguished, and then reconditioned to the same CS. After reconditioning, the CS was reextinguished; at this time, some rats at each age had their amygdala temporarily inactivated. Reextinction was amygdala independent in 24-d-old rats, as previously shown in adult rats. However, reextinction was still amygdala dependent in 17-d-old rats. In Experiment 3, the age at conditioning, reconditioning, reextinction, and test was held constant, but the age of initial extinction varied across groups; reextinction was found to be amygdala independent if initial extinction occurred at 24 d of age but amygdala dependent if it occurred at 17 d of age. Consistent with previous findings, these results show that there are fundamental differences in the neural mechanisms of fear extinction across development.

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February 19, 2008 at 11:32 am

Prior Experience Shapes How Consumers Compute New Information

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Over time, consumers develop a set of cues that we then use to make inferences about products, such as “all French restaurants have great service” or “more expensive candles smell better.” However, this set of predictable beliefs can make it difficult for us to learn and recognize other real, positive qualities that are indicated by the same cues, reveals a new study.

“Once people learned that a cue predicted an outcome, they became less likely to learn about this very same cue with respect to a different outcome,” write Marcus Cunha Jr. (University of Washington), Chris Janiszewski, and Juliano Laran (both University of Florida). “The implication is that the learning system is designed to discourage single cue–multiple outcome learning.”

In the pilot study of a series of five experiments, the researchers used cheese tasting to explore the development of predictive knowledge structures, a phenomenon also known as “protection of prior learning.” They first had participants taste an orange rind Raclette cheese that was mild and creamy, and a purple rind Drunken Goat cheese that was much stronger tasting and dry. They then had participants rate the cheeses on a scale of mild to strong to induce the association with an orange rind and a mild flavored cheese. A control group also tasted two different types of cheese but did not rate them.

To test whether an association between an orange rind and mild flavor would make it more difficult for consumers to gauge other existing qualities, such as texture, tasters were then asked to rate the creaminess of a mild, creamy Port Salut with an orange rind and a dry Manchego with no rind. Surprisingly, participants were less likely than the control group to expect the second orange rind cheese to be creamy, even though the first one had also been creamy. As the researchers explain, “Learning that the orange rind predicted a difference in the strength of flavor . . . attenuated the learning that the orange rind predicted creaminess.”

This research has important implications for marketers, policy makers and consumers. For instance, the researchers point to Merck’s introduction of the cholesterol-lowering drug Simvastatin under the brand name Zocor. Recently, researchers found that Simvastatin may be also effective at preventing the onset of Alzheimer’s disease.

“This opportunity creates a branding dilemma for Merck,” the researchers write. “Our findings suggest that consumers may be slower to learn the Alzheimer’s relief association to [Zocor] than to a new brand name.”

Similarly, from a public policy standpoint, the results suggest that people may be resistant to adopt new health and safety standards when information conflicts with prior learning. Beyond creating awareness, successful campaigns might present new information in a way that does not utilize attributes already associated with another outcome.

Journal of Consumer Research, Page 000–000, DOI: 10.1086/523293 Electronically published October 10, 2007

Marcus Cunha Jr. Chris Janiszewski Juliano Laran, John Deighton served as editor and Susan Broniarczyk served as associate editor for this article.
As a product category evolves, consumers have the opportunity to learn a series of feature-benefit associations. Initially, consumers learn that some features predict a critical benefit, whereas other features do not. Subsequently, consumers have the opportunity to assess if previously predictive features, or novel features, predict new product benefits. Surprisingly, later learning is characterized by attenuated learning about previously predictive features relative to novel features. This tendency to ignore previously predictive features is consistent with a desire to protect prior learning.

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February 18, 2008 at 11:28 am

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Neural Basis Of ‘Number Sense’ In Young Infants

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Behavioral experiments indicate that infants aged 4½ months or older possess an early “number sense” that allows them to detect changes in the number of objects.
Distinct cerebral pathways for object identity and number have been identified in the brain of human infants. (Credit: Izard V, Dehaene-Lambertz G, Dehaene S)

However, the neural basis of this ability was previously unknown.

In new research, Véronique Izard, Ghislaine Dehaene-Lambertz, and Stanislas Dehaene provide brain imaging evidence showing that very young infants are sensitive to both the number and identity of objects, and these pieces of information are processed by distinct neural pathways.

The authors recorded the electrical activity evoked by the brain on the surface of the scalp as 3-months-old infants were watching images of objects. The number or identity of objects occasionally changed.

The authors found that the infant brain responds to both changes, but in different brain regions, which map onto the same regions that activate in adults. These results show that very young infants are sensitive to small changes in number, and the brain organization that underlies the perception of object number and identity are established early during development.

PLoS Biology Vol. 6, No. 2, e11 doi:10.1371/journal.pbio.0060011

Distinct Cerebral Pathways for Object Identity and Number in Human Infants

Izard V, Dehaene-Lambertz G, Dehaene S 

All humans, regardless of their culture and education, possess an intuitive understanding of number. Behavioural evidence suggests that numerical competence may be present early on in infancy. Here, we present brain-imaging evidence for distinct cerebral coding of number and object identity in 3-mo-old infants. We compared the visual event-related potentials evoked by unforeseen changes either in the identity of objects forming a set, or in the cardinal of this set. In adults and 4-y-old children, number sense relies on a dorsal system of bilateral intraparietal areas, different from the ventral occipitotemporal system sensitive to object identity. Scalp voltage topographies and cortical source modelling revealed a similar distinction in 3-mo-olds, with changes in object identity activating ventral temporal areas, whereas changes in number involved an additional right parietoprefrontal network. These results underscore the developmental continuity of number sense by pointing to early functional biases in brain organization that may channel subsequent learning to restricted brain areas.

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February 11, 2008 at 9:39 am