Why does putting our feelings into words — talking with a therapist or friend, writing in a journal — help us to feel better? A new brain imaging study by UCLA psychologists reveals why verbalizing our feelings makes our sadness, anger and pain less intense.

Another study, with the same participants and three of the same members of the research team, combines modern neuroscience with ancient Buddhist teachings to provide the first neural evidence for why “mindfulness” — the ability to live in the present moment, without distraction — seems to produce a variety of health benefits.

When people see a photograph of an angry or fearful face, they have increased activity in a region of the brain called the amygdala, which serves as an alarm to activate a cascade of biological systems to protect the body in times of danger. Scientists see a robust amygdala response even when they show such emotional photographs subliminally, so fast a person can’t even see them.

But does seeing an angry face and simply calling it an angry face change our brain response” The answer is yes, according to Matthew D. Lieberman, UCLA associate professor of psychology and a founder of social cognitive neuroscience.

“When you attach the word ‘angry,’ you see a decreased response in the amygdala,” said Lieberman, lead author of the study.

The study showed that while the amygdala was less active when an individual labeled the feeling, another region of the brain was more active: the right ventrolateral prefrontal cortex. This region is located behind the forehead and eyes and has been associated with thinking in words about emotional experiences. It has also been implicated in inhibiting behavior and processing emotions, but exactly what it contributes has not been known.

“What we’re suggesting is when you start thinking in words about your emotions —labeling emotions — that might be part of what the right ventrolateral region is responsible for,” Lieberman said.

If a friend or loved one is sad or angry, getting the person to talk or write may have benefits beyond whatever actual insights are gained. These effects are likely to be modest, however, Lieberman said.

“We typically think of language processing in the left side of the brain; however, this effect was occurring only in this one region, on the right side of the brain,” he said. “It’s rare to see only one region of the brain responsive to a high-level process like labeling emotions.”

Many people are not likely to realize why putting their feelings into words is helpful.

“If you ask people who are really sad why they are writing in a journal, they are not likely to say it’s because they think this is a way to make themselves feel better,” Lieberman said. “People don’t do this to intentionally overcome their negative feelings; it just seems to have that effect. Popular psychology says when you’re feeling down, just pick yourself up, but the world doesn’t work that way. If you know you’re trying to pick yourself up, it usually doesn’t work — self-deception is difficult. Because labeling your feelings doesn’t require you to want to feel better, it doesn’t have this problem.”

Thirty people, 18 women and 12 men between ages of 18 and 36, participated in Lieberman’s study at UCLA’s Ahmanson-Lovelace Brain Mapping Center. They viewed images of individuals making different emotional expressions. Below the picture of the face they either saw two words, such as “angry” and “fearful,” and chose which emotion described the face, or they saw two names, such as “Harry” and “Sally,” and chose the gender-appropriate name that matched the face.

Lieberman and his co-authors — UCLA assistant professor of psychology Naomi Eisenberger, former UCLA psychology undergraduate Molly Crockett, former UCLA psychology research assistant Sabrina Tom, UCLA psychology graduate student Jennifer Pfeifer and Baldwin Way, a postdoctoral fellow in Lieberman’s laboratory — used functional magnetic resonance imaging to study subjects’ brain activity.

“When you attach the word ‘angry,’ you see a decreased response in the amygdala,” Lieberman said. “When you attach the name ‘Harry,’ you don’t see the reduction in the amygdala response.

“When you put feelings into words, you’re activating this prefrontal region and seeing a reduced response in the amygdala,” he said. “In the same way you hit the brake when you’re driving when you see a yellow light, when you put feelings into words, you seem to be hitting the brakes on your emotional responses.”

As a result, an individual may feel less angry or less sad.

This is ancient wisdom,” Lieberman said. “Putting our feelings into words helps us heal better. If a friend is sad and we can get them to talk about it, that probably will make them feel better.”

The right ventrolateral prefrontal cortex undergoes much of its development during a child’s preteen and teenage years. It is possible that interaction with friends and family during these years could shape the strength of this brain region’s response, but this is not yet established, Lieberman said.

One benefit of therapy may be to strengthen this brain region. Does therapy lead to physiological changes in the right ventrolateral prefrontal cortex” Lieberman, UCLA psychology professor Michelle Craske and their colleagues are studying this question.

Combining Buddhist Teachings and Modern Neuroscience

After the participants left the brain scanner, 27 of them filled out questionnaires about “mindfulness.” Mindfulness meditation, which is very popular in Southeast Asia and elsewhere, originates from early Buddhist teachings dating back some 2,500 years, said David Creswell, a research scientist with the Cousins Center for Psychoneuroimmunology at the Semel Institute for Neuroscience and Human Behavior at UCLA.

Mindfulness is a technique in which one pays attention to his or her present emotions, thoughts and body sensations, such as breathing, without passing judgment or reacting. An individual simply releases his thoughts and “lets it go.”

“One way to practice mindfulness meditation and pay attention to present-moment experiences is to label your emotions by saying, for example, ‘I’m feeling angry right now’ or ‘I’m feeling a lot of stress right now’ or ‘this is joy’ or whatever the emotion is,” said Creswell, lead author of the study, which will be featured in an upcoming issue of Psychosomatic Medicine, a leading international medical journal for health psychology research.

“Thinking, ‘this is anger’ is what we do in this study, where people look at an angry face and say, ‘this is anger,’” Lieberman noted.

Creswell said Lieberman has now shown in a series of studies that simply labeling emotions turns down the amygdala alarm center response in the brain that triggers negative feelings.

Creswell, who conducted the mindfulness research as an advanced graduate student of psychology at UCLA, said mindfulness meditation is a “potent and powerful therapy that has been helping people for thousands of years.”

Previous studies have shown that mindfulness meditation is effective in reducing a variety of chronic pain conditions, skin disease, stress-related health conditions and a variety of other ailments, he said. Creswell and his UCLA colleagues — Lieberman, Eisenberger and Way — found that during the labeling of emotions, the right ventrolateral prefrontal cortex was activated, which seems to turn down activity in the amygdala. They then compared participants’ responses on the mindfulness questionnaire with the results of the labeling study.

“We found the more mindful you are, the more activation you have in the right ventrolateral prefrontal cortex and the less activation you have in the amygdala,” Creswell said. “We also saw activation in widespread centers of the prefrontal cortex for people who are high in mindfulness. This suggests people who are more mindful bring all sorts of prefrontal resources to turn down the amygdala. These findings may help explain the beneficial health effects of mindfulness meditation, and suggest, for the first time, an underlying reason why mindfulness meditation programs improve mood and health.

“The right ventrolateral prefrontal cortex can turn down the emotional response you get when you feel angry,” he said. “This moves us forward in beginning to understand the benefits of mindfulness meditation. For the first time, we’re now applying scientific principles to try to understand how mindfulness works.

“This is such an exciting study because it brings together the Buddha’s teachings — more than 2,500 years ago, he talked about the benefits of labeling your experience — with modern neuroscience,” Creswell said. “Now, for the first time since those teachings, we have shown there is actually a neurological reason for doing mindfulness meditation. Our findings are consistent with what mindfulness meditation teachers have taught for thousands of years.”

Source: UCLA

Compared to people with normal vision, those who were blind at birth tend to have excellent memories. A new study shows that blind individuals are particular whizzes when it comes to remembering things in the right order.

The findings are a good example of the familiar adage that “practice makes perfect” and reveal that mental capabilities may be refined or adjusted in order to compensate for the lack of a sensory input, according to researchers Noa Raz and Ehud Zohary of Hebrew University.

“Our opinion is that the superior serial memory of the blind is most likely a result of practice,” Zohary said. “In the absence of vision, the world is experienced as a sequence of events. Since the blind constantly use serial-memory strategies in everyday circumstances, they tend to develop superior skills.”

For example, the blind tend to navigate the world by forming “route-like” sequential representations. Blind people also rely on serial-memory strategies to identify otherwise indistinguishable objects, such as different brands of yogurt that vary only in their labeling, the researchers noted. According to their own reports, in order to correctly choose a desired item, the blind typically place objects in a fashioned order and give them ordinal tags, such as “the 3rd item on the left.” Thus, a memory for the order in which items are encountered may be especially important for blind people’s ability to create mental pictures of a scene.

In the new study, the researchers tested the performance of 19 congenitally blind individuals and individually matched sighted controls in two types of memory tasks: item memory and serial memory. In the item-memory tasks, subjects were asked to identify 20 words from a list they heard. In the serial-memory tasks, subjects had to remember not only the words, but also their ordinal position in the list.

Those who were blind recalled more words than the sighted, indicating a better memory overall, they found. Their greatest advantage, however, was the ability to remember longer word sequences according to their original order.

The blind individuals’ remarkable edge in item recall resulted not from a specific advantage in remembering the first words in the list, or the most recent words. Rather, the blind showed a better memory for all of the words, regardless of where they fell. That result suggested that the key to their success may lie in representing item lists as word chains, perhaps by generating associations between adjacent items.

The researchers said they plan to further explore the underlying mental processes responsible for the differences in memory skill by using imaging techniques that measure brain activity.

The researchers include Noa Raz, Ella Striem, Golan Pundak, Tanya Orlov, and Ehud Zohary of Hebrew University in Jerusalem, Israel. This study was funded by the McDonnell Foundation grant #220020046.

Raz et al.: “Superior Serial Memory in the Blind: A Case of Cognitive Compensatory Adjustment.” Publishing in Current Biology 17, 1–5, July 3, 2007. DOI 10.1016/j.cub.2007.05.060. www.current-biology.com

Researchers have discovered a sophisticated neural computer, buried deep in the cerebellum, that performs inertial navigation calculations to figure out a person’s movement through space.

These calculations are no mean feat, emphasized the researchers. The vestibular system in the inner ear provides the primary source of input to the brain about the body’s movement and orientation in space. However, the vestibular sensors in the inner ear yield information about head position only. Also, the vestibular system’s detection of head acceleration cannot distinguish between the effect of movement and that of gravitational force.

Angelaki and colleagues based their brain studies on the predictions of a theoretical mathematical model postulating that the brain could compute inertial motion by combining rotational signals from the semicircular canal in the inner ear with gravity signals.

They concentrated their search for the brain’s inertial navigation system on particular types of neurons, called Purkinje cells, in a region of the cerebellum known to receive signals from the vestibular system. This region is known as the posterior cerebellar vermis, a narrow, worm-like structure between the brain’s hemispheres.

In their experiments, the researchers measured the electrical activity of these Purkinje cells in monkeys as the animals’ heads were maneuvered through a precise series of rotations and accelerations. After analyzing the electrical signals measured from the Purkinje cells during these movements, the researchers concluded that the specialized Purkinje cells were, indeed, computing earth-referenced motion from head-centered vestibular information.

The researchers concluded that the output of the Purkinje cells indicates an “elegant solution” to the computational problems involved in inertial navigation.

The researchers include Tatyana A. Yakusheva, Aasef G. Shaikh, Andrea M. Green, Pablo M. Blazquez, J. David Dickman, and Dora E. Angelaki of Washington University School of Medicine in St. Louis, MO.

“Purkinje Cells in Posterior Cerebellar Vermis Encode Motion in an Inertial Reference Frame.” Yakusheva et al.: Neuron 54, 973–985, June 21, 2007. DOI 10.1016/j.neuron.2007.06.003

Subjecting mice to repeated emotional stress, the kind we experience in everyday life, may contribute to the accumulation of neurofibrillary tangles, one of the hallmarks of Alzheimer’s disease, report researchers at the Salk Institute for Biological Studies. While aging is still the greatest risk factor for Alzheimer’s disease, a number of studies have pointed to stress as a contributing factor.

Top left: In unstressed animals the hippocampus, which is involved in the formation of memories and learning, is free of phosphorylated tau. Top right: Subjecting mice to low-level chronic emotional stress–the kind we experience in everyday life–leads to widespread tau phosphorylation, a key step in the formation of neurofibrillary tangles (black streaks), one of the hallmarks of Alzheimer’s disease. Bottom: While acute stress effects are reversible, repeated stress leads to cumulative increases in phosphorylated tau, a portion of which is sequestered in an insoluble, and potentially pathogenic, form. Image courtesy of Dr. Paul E. Sawchenko and Dr. Robert A. Rissman, Salk Institute for Biological Studies

“A long-term study of about 800 members of religious orders had found that the people who were most prone to stress were twice as likely to develop Alzheimer’s disease, but the nature of the link between the two has been elusive,” says Paul E. Sawchenko, Ph.D., a professor in the Neuronal Structure and Function Laboratory, who led a phalanx of Salk researchers contributing to the current study.

The group’s findings, detailed in this week’s Journal of Neuroscience, suggest that the brain-damaging effects of negative emotions are relayed through the two known corticotropin-releasing factor receptors, CRFR1 and CRFR2, which are part of a central switchboard that mediates the body’s responses to stress and stress-related disorders.

Alzheimer’s disease is defined by the accumulation of amyloid plaques and neurofibrillary tangles. While plaques accumulate outside of brain cells, tangles litter the inside of neurons. They consist of a modified form of the tau protein, which—in its unmodified form—helps to stabilize the intracellular network of microtubules. In Alzheimer’s disease, as well as various other neurodegenerative conditions, phosphate groups are attached to tau. As a result, tau looses its grip on the microtubules, and starts to collapse into insoluble protein fibers, which ultimately cause cell death.

Previous studies had shown that extreme physiological stress, such as plunging mice into ice water or starving them for three days, can induce tau phosphorylation. “But what we wanted to know was whether exposure to milder stress, of the kind we experience in our daily lives, can induce tau phosphorylation,” explains senior research associate and first author Robert A. Rissman, Ph.D.

Restraining mice for half an hour, a situation that replicates the body’s reaction to low-level anxiety, fear or social stress, resulted only in a transient phosphorylation of tau. However, when Rissman simulated chronic stress by repeating the procedure every day for two weeks, the modification lasted long enough to let tau molecules tumble off the cytoskeleton and pile up in insoluble heaps of protein.

The first thing you consider when you think about stress-induced changes in the brain is glucocorticoids because they are such pervasive mediators of stress responses, says Rissman. But even without available glucocorticoids, tau was still modified under stressful conditions and he had to look elsewhere. “The next obvious candidate was the CRF system, which has been broadly implicated in many kinds of stress adaptation,” he says.

So, Rissman and Sawchenko teamed up with their Salk colleagues Kuo-Fen Lee, Ph.D., and Wylie W. Vale, Ph.D., both professors in the Clayton Foundation Laboratories for Peptide Biology. Vale, Lee and their colleagues have been instrumental in piecing together a global view of how the corticotropin-releasing family of molecules regulate our bodies’ responses to physiological and emotional stress.

Lee made available his mice that had been genetically engineered to lack either CRFR1 or CRFR2. “And sure enough, the CRF receptors turn out to be integrally and differentially involved,” says Sawchenko. In the absence of CRFR1, stress-induced tau phosphorylation was abrogated, while in mice missing CRFR2 the effect was amplified. Pharmacological studies with small molecule inhibitors replicated the effect.

Currently, several companies are actively pursuing small molecule drugs that bind CRF receptors and a few of them are already in stage 2 clinical trials for depression and other mood disorders. “We may have discovered another application. Such drugs could have a prophylactic effect or delay the progression of Alzheimer’s disease,” Sawchenko says.

Source: Salk Institute