Does labeling your feelings help regulate them?

Kristen Lindquist

One of the mainstays of psychotherapy is the idea that talking about your emotions—or even writing about them—can help you to regulate them. Mindfulness-based approaches from Buddhism offer similar outcomes—the idea is that if you are “mindful,” or aware, of your feelings, then they won’t seem as strong. Until recently, it was not well understood how, or even why, labeling your feelings worked to reduce them. In some ways, it seems too simple to be true. Yet growing evidence from neuroscience suggests that labeling your feelings is in fact a good idea; telling your kids (or your spouse) to “use their words” when they’re upset just might work.emotions_-_3

In a recent paper from my lab, my collaborators and I explored the neural mechanisms at play when people are prompted to label their emotions versus when they are not prompted to label their emotions. This paper was particularly powerful because it used meta-analysis to summarize the findings across 386 neuroimaging studies of emotion (for more on the neuroimaging of emotion, see our recent post). This means that we were able to say which brain regions were consistently more active across 386 studies when individuals were prompted to label their emotions versus were not prompted to label their emotions. In many cases, participants had no clue that labeling would have an effect on their emotions. In fact, most studies were not explicitly designed to even test this hypothesis, they just conveniently asked participants to label their feelings as part of their study design (to check that participants were in fact experiencing the desired emotions, to ensure that participants were paying attention, etc.). Thus, our paper offers a unique lens for examining whether drawing people’s attention to emotion labels alters their brain activity while they are experiencing emotions.

Our findings confirmed the idea that labeling helps regulate your emotions. We found that when labels were present—at any point—in an experiment (prior to experiencing emotions or during experiences of emotions), this was associated with more consistent increases in prefrontal and temporal regions of the brain during emotional feelings. Critically, these brain regions are responsible for retrieving concepts and elaborating on their meaning. Take a second and think about the concept of “anger”–what does it mean? What does it feel like? What happens when you’re angry? You’re activating these regions now. This means that merely seeing a word such as “anger,” “fear,” or “disgust” prior to viewing a negative image may cause your brain to start retrieving knowledge about specific emotions and to start categorizing what you’re feeling, putting your feelings of negativity into more specific words. Consistent with the idea that labeling your feelings reduces them, these regions are also known to be consistently involved in deliberate emotion regulation when people try to rethink, or “re-appraise” the meaning of their initial emotional responses to a situation (e.g., “maybe I don’t feel sad the new job didn’t work out, I feel relieved…”)

In contrast, when emotion words were not present in experiments and participants were just experiencing emotions unfettered, we found greater activity in the amygdala. The amygdala is well-known to show increased activation during emotions and may be particularly involved in intense or impactful experiences. We also know that the amygdala has increased activation to ambiguous stimuli and situations. Together, these findings suggest that when you’re not prompted to access emotion words prior to viewing a negative image, your feelings may be more intense and harder for you to understand. Consistent with this interpretation, other classic findings on emotion labeling demonstrate an interplay between prefrontal regions involved in representing words and the amygdala–greater increases in word-related regions result in greater decreases in the amygdala during emotional experiences.

Taken together, our findings begin to shine light on the neural basis of why putting feelings into words may work. Teaching people to become more mindful of their feelings, or to become better at labeling their feelings in nuanced ways (a facet of “emotionally intelligence”) may be a fruitful route for getting emotions under control. In fact, kids who “use their words” following emotional intelligence training do better at school and have more positive relationships with other kids and teachers. The next time you’re feeling bad, try labeling it. You might just feel better.


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Where in the brain are emotions?

Kristen Lindquist

This post is the latest in our Introduction to the Neuroscience of Emotion series. It discusses research using healthy human subjects and functional magnetic resonance imaging (or fMRI for short) to understand the brain basis of emotions. In coming months, we’ll have posts about studying individuals and animals with brain lesions as well as other neuroscience tools.

According to Aristotle, emotions come from your heart. In his view, the brain is just a pile of meat that is used to cool the blood. We’ve learned a thing or two about the structure and function of anatomy since the time of Aristotle; almost everyone today agrees that emotions—and mental life, more generally—originate in the brain. But, the question that remains for modern neuroscientists is how this happens. Philosopher David Chalmers calls this “the hard problem” for a reason – understanding how the brain creates conscious experiences such as emotions is extremely challenging. Despite how hard this problem is, we’ve learned a lot over the past several decades about how the brain creates the mind, and in particular, how the brain creates our emotions.

One of the major focuses of my laboratory is to understand how emotions emerge from the complex firing of neurons across the brain. We typically study emotions in healthy adults, meaning that we’re interested in how emotions work when people are functioning optimally. Knowing how the brain creates emotions in healthy people helps scientists to begin to target what goes wrong when someone suffers from a mental disorder such as anxiety or depression. The majority of our research uses neuroimaging—or what is called functional magnetic resonance imaging (fMRI for short). We use the same MRI machine that your doctor uses when she examines a tear in your knee, although we put people in the scanner head-first to examine their brain activity. This feat is accomplished via a fortunate property of the blood—it has different magnetic properties when it is carrying oxygen to your neurons v. when the neurons have used up all its oxygen; changes in how much oxygen are present in brain tissue can be detected by the MRI machine. Since “active” neurons need more oxygen, we can identify regions that are relatively more active during one mental event (e.g., feeling excited about an upcoming party) v. another (e.g., feeling neutral about making dinner tonight). In our studies, we ask people to experience certain emotions by showing them evocative images (e.g., a picture of a striking snake), having them recall emotional events (e.g., the death of a loved one), or even putting them in emotional situations (e.g., telling them they need to give a speech that we will evaluate) and examine which brain regions are more “active.” Decades of research have now examined this question and have revealed some interesting and surprising findings.

From Lindquist et al. (2012)

For a long time it was assumed that each emotion has its own neural real estate in the form of dedicated neural circuitry that is responsible for its creation. This can be seen in the belief that an emotion comes from certain brain area (e.g., the amygdala) or a network of areas in the evolutionarily “old” portion of the brain (e.g., a network in the brainstem and other regions below the evolutionarily “new” cortex). However, despite what many people (scientists and non-scientist alike) believe to be true, we do not find that there is one region or circuit for a given emotion (e.g., fear). One of our most comprehensive projects was a “meta-analysis” that summarized the findings of all of the existing fMRI studies to date. Our method was designed to reveal which brain regions were consistently active across different studies and types of emotion (anger, disgust, fear, happiness, sadness) and which brain regions were specifically active during certain emotions (anger v. disgust v. fear v. happiness v. sadness). We found that much of the brain is consistently active when someone is “having an emotion”—not just the brainstem and subcortical regions (see figure above: regions in pink, orange and yellow represent regions that are consistently active across all studies of anger, disgust, fear, happiness and sadness). What was interesting about these consistently active regions was that they included brain areas that we know are involved in the types of “hot” body changes that accompany emotions (e.g., increases in heart rate, respiration, etc.), but they also included regions associated with the type of “cool” so-called cognitive functions aren’t generally associated with emotions such as attention, memories, and language. Each type of brain region was involved in all the emotions studied. Moreover, not a single brain region in our analysis was specific to any given emotion. For instance, the amygdala was not the brain basis of fear as is typically assumed (for another recent discussion from renowned neuroscientist Joe LeDoux see here). Instead, the amygdala was active across every type of emotion experience we looked at in our analysis (including fear but also anger, disgust, sadness, and happiness).


My latest research demonstrates that these brain regions are not just acting alone, but in concert with one another as parts of complex networks (see figure to the left for an image of what brain networks might look like–dots represent regions in the brain and lines represent connections between different regions). Take a minute and think about your social networks—you are probably part of several different social networks consisting of people who are connected by some function: you might have your work network, your family network, your neighborhood network, your exercise network, your school network, etc. Brain networks are just like this, except they are groups of brain regions working together to serve some function.

An emerging idea in neuroscience is that these groups of brain networks—what we call functional networks—are kind of like the basic “ingredients” of the brain. Just like ingredients in your pantry, they combine together to produce more complex products. Just as oil, flour, baking soda, and water can be combined to make cookies, pancakes, breads, etc. different brain networks supporting basic functions combine to create emotions, thoughts, perceptions, and all the mental stuff we experience on a day to day basis. We are finding that the particular combination of these network-based “ingredients” differs when you’re experiencing anger v. fear (see here), and even when you’re experiencing a thought v. an emotion (see here).

What’s compelling about these findings is that it appears that your emotions, and all your mental states for that matter, are created out of the same basic “ingredients” of the mind (for a more in-depth discussion, see here). These ingredients probably serve very basic functions such as activating your body for engaging in actions, representing your body changes as feelings, representing your past experiences in order to make meaning of the present, processing visual and auditory information from the world, and directing your attention to changes outside in the world or inside your body. The idea that your mental states are the complex products of basic “ingredients” is fundamentally different from the idea that each brain region serves its own special function for its own specific mental state. This new view also begins to chart a different path forward for understanding mental illness—a person with anxiety might not have something amiss with their “fear center,” but might instead have something wrong with a system that activates the body or a system that shifts attention (or both). We’re still just scratching the surface of how your brain creates emotions and fMRI offers only a single lens, but it’s already telling us important new things about how our brain creates our mental lives.


Photo credit: licensed for use


Understanding the Early-Life Origins of Extreme Anxiety—Role of the Amgydala

Alex Shackman

The internalizing disorders—anxiety and depression—are a major human blight. According to the World Health Organization and National Institute of Mental Health, depression is responsible for more years lost to illness and disability than any other medical condition, including such familiar scourges as diabetes and chronic respiratory disorders. Anxiety disorders are the most common family of psychiatric disorder in the United States and rank sixth as a worldwide cause of disability. These disorders, which commonly co-occur, also impose a substantial and largely hidden burden on the global economy: hundreds of billions of dollars in healthcare costs and lost productivity each year. Unfortunately, existing therapeutic approaches are inconsistently effective or, in the case of many pharmaceutical approaches, are associated with significant side effects. Not surprisingly, the internalizing disorders have become an important priority for clinicians, economists, research funding agencies, and policy makers.

The internalizing disorders generally have their roots in the first three decades of life and there is clear evidence that children with a fearful, shy, or anxious temperament are more likely to suffer from anxiety disorders, major depression, or both as they grow older. As a postdoctoral fellow in Ned Kalin’s lab at the University of Wisconsin and, more recently, as the director of my own lab at the University of Maryland, I’ve used a range of tools and techniques to understand the brain systems that contribute to extreme anxiety early in life. Building on a tradition that dates back to pioneering studies at Wisconsin by Harry Harlow, Karl Pribram, and others, much of the work that I conducted as a postdoc used nonhuman primates to model and understand key features of childhood anxiety. Young rhesus monkeys are useful for deciphering the brain circuits that underlie childhood anxiety. Owing to the relatively recent evolutionary divergence of humans and Old World monkeys (~25 million years ago), the brains of monkeys and humans are biologically similar. Similar brains endow monkeys and children with a common repertoire of social and emotional behaviors, which makes it possible to measure anxiety in monkeys using procedures similar to those used with kids. Another virtue of working with monkeys is the opportunity to collect high-resolution measures of brain activity (using positron emission tomography or PET) while the animals freely respond—hiding in the corner, barking, and so on—to naturalistic threats, such as an unfamiliar human ‘intruder’s’ profile. This would be difficult or impossible to do in children and, somewhat surprisingly, has rarely been attempted in adults (most human imaging studies use fMRI, which requires that the subject remain dead still throughout the scan).

Large-scale brain imaging studies, each including hundreds of young monkeys—in humans terms, roughly equivalent to children and teens—show that anxious individuals respond to signs of potential threat with heightened activity in a number of brain regions. For present purposes, I’ll focus on the contribution of the amygdala, a small, almond-shaped region buried beneath the temporal lobe of the brain (the red regions in the accompanying animation).

Collectively, these studies teach us that amygdala activity systematically differs across individuals. Some individuals show chronically elevated activity; others consistently show much lower levels. Notably, elevated activity is associated with exaggerated reactions to potential danger: Monkeys with higher levels of metabolic activity in the amygdala tend to show higher levels of the stress hormone cortisol and to freeze longer (in an attempt to evade detection) in encounters with the human intruder. Like many other qualities that distinguish one individual from another, work by our group demonstrates that amygdala activity is:

1. Consistent over time and context: We can think of amygdala activity as a trait, like personality or IQ.

2. Heritable: Amygdala activity partially reflects the influence of genes. Parents marked by higher levels of amygdala activity are more likely to have offspring with this trait.

Of course, like any brain imaging study, it’s important to remember that these results do not let us to claim that the amygdala causes anxiety. From this perspective, it is reassuring that mechanistic work in monkeys and rodents demonstrates that it does: selective lesions and other biological manipulations of the amygdala sharply reduce (but do not entirely abolish) anxiety (see for example this very recent rodent study). This is consistent with observations of a handful of human patients with near-complete amygdala damage. For example, one relatively well-known patient (identified as ’SM,’ to protect her identity), has normal intellect, but reports a profound lack of fear and anxiety in response to scary movies, haunted houses, tarantulas, and snakes.

According to Justin Feinstein, Ralph Adolphs, and other researchers who have studied SM over the past two decades,

She has been held up at knife point and at gun point, she was once physically accosted by a woman twice her size, she was nearly killed in an act of domestic violence, and on more than one occasion she has been explicitly threatened with death…What stands out most is that, in many of these situations, SM’s life was in danger, yet her behavior lacked any sense of desperation or urgency. Police reports…corroborate SM’s recollection of these events and paint a picture of an individual who lives in a poverty-stricken area replete with crime, drugs, and danger…Moreover, it is evident that SM has great difficulty detecting looming threats in her environment and learning to avoid dangerous situations.

This and other evidence—spanning a range of species, populations, and measurement tools—indicates that anxious individuals’ exaggerated distress in the face of potential danger reflects hyper-reactivity in a brain circuit that includes the amygdala. Systematic differences in amygdala activity and connectivity first emerge early in life and can foretell the future development of anxious and depressive symptoms in humans. These and other observations suggest that enduring differences in amygdala function contribute to key features of childhood temperament, like shyness, and confer increased risk for the development of internalizing disorders, particularly among individuals exposed to stress or trauma. More importantly, this work lays a solid, brain-based foundation for developing better strategies for treating or even preventing these debilitating illnesses.

To learn more about the emotional disorders, please visit the Anxiety & Depression Association of America (ADAA) website, which features a number of useful videos, fact sheets, and other resources for patients, clinicians, and researchers.

Photo credit: The amygdala animation was generated by Life Science Databases, obtained from Wikimedia Commons, and is freely used under a Creative Commons license.


The emotional potency of peers during adolescence

Leah Somerville

If you had to choose one event that epitomizes your experience as a teenager, what would it be? For me, I immediately think of that moment at the school dance while I was dancing with my middle school crush to November Rain by Guns n Roses. Our slow dancing skills were passable during the first part of the song, but then the tempo picked up … and let’s just say, we were not very smooth at adapting our dancing styles. Although I hope (for your sake) that the same thing didn’t happen to you, I’d bet that whatever memory you do conjure when you think back to your own adolescence is socially and emotionally charged.

It turns out that my adolescent experiences were completely typical of most adolescents—social experiences take on heightened emotional and motivational importance during adolescence as compared to other stages of life. In a study we conducted, we wanted to see how sensitive adolescents were to even the simplest, most innocuous social provocation: being looked at by a peer. During our study, we measured brain activity with functional magnetic resonance imaging in tandem with physiological arousal (measured with the skin conductance response—how much sweat is secreted on the skin during emotional events). We observed that even the simple act of being looked at by a peer was enough to induce heightened emotion reports, physiological responses, and brain activity in adolescents (when compared to adults and younger children). For instance, we saw biased activity in regions of the brain important for representing the emotional value of stimuli and in brain regions involved in thinking about ourselves (to read more, see here). All of these findings add up to the general conclusion that adolescents are highly attuned and reactive to their social environments – even very subtle ones – and that this fact influences a variety of their daily choices and feelings.


The author of this post at age 13 showing off her spiral perm.

What’s interesting about these findings is that they seem not to be unique to human adolescents. The term ‘adolescence’ is a sociocultural construct that refers only to humans, defined by simultaneous physical and psychological change that ends when an individual takes on adult roles in society (adolescence is most often defined as the approximate ages ~13-17 years). However, some aspects of biological changes during this age range, including hormone changes that define puberty, occur in other mammals as well. Some surprising results have arisen from the study of pubertal-linked changes in social behavior in non-human mammals. Pubertal rats enjoy ‘social play’ (kind of like wrestling) more frequently than adult rodents, and also seek out more novel and potentially thrilling experiences. Perhaps most intriguingly, rodents undergoing puberty also approach potential rewards (in this case, consuming alcoholic beverages) more when in social groups. Whereas adult mice spent the same amount of time consuming alcoholic substances when alone and with peer animals, juvenile animals in the pubertal stage spent more time consuming alcohol when in a cage with familiar peer animals. And it wasn’t just a motivation to consume the tasty cocktail before others got to it – they each had their own sipper.

What lessons can we learn from our furry friends about adolescence and the social potency that characterizes this age range? It is often assumed that peers take on heightened importance in adolescence due to overt concern about social status. However, it seems unlikely that such complicated, strategic motivations would drive rodents to behave differently around peers. This raises a second possibility, that there are “undercover” or non-deliberate ways that adolescents are influenced by social contexts. We believe that adolescents’ brains are biased to assign importance to social information, which imbues social settings with an extra boost in power to shape their feelings, motivations, and decisions. Although more research needs to be done to address questions like “why” and “how”, I guess that’s why I’m still mildly embarrassed by my tragic bout of dancing (and simultaneously thankful I grew up before the days of smartphone cameras).

Early Explorations of the Final Frontier: The Human Brain

Eliza Bliss-Moreau

Yesterday, that National Institutes of Health (NIH) announced the awarding of $46 million as part of the new BRAIN Initiative (Brain Research through Advancing Innovative Neurotechnologies).  The BRAIN Initiative is a multi-agency funding program aimed at developing the technologies necessary to map the functions of the brain. We’ve learned a lot about the brain over the last century, but there’s so much more to learn that many neuroscientists consider the brain “the final frontier”.  Dr. Francis Collins, Director of the NIH, has likened the BRAIN Initiative to President Kennedy’s race to the moon. In a world of discovery where we use methods like optogenetics, positron emission topography, magnetic resonance imaging, DREADDs (designer receptors exclusively activated by designer drugs), electrocorticography (which we’ll discuss in future posts) to understand how areas and circuits of the brain work and how they contribute to emotion, it’s easy to forget how far the neuroscience of emotion has come in the last half-century or so.  And, of course, it’s also easy to forget how far we have to go.

The goal of today’s post is to take a *very* brief walk back down memory lane to remember whence we’ve come (circa early 20th century) and the lessons from the pioneers of the neuroscience of emotion that we should carry with us as we continue to explore the brain.

Before we could look into the human brain using neuroimaging, our knowledge of how the human brain functioned was largely made possible by people with diseases or injury. In some cases, people got tumors that required surgery.  When the tumor was removed, a given brain area was disturbed.  Changes in the person’s behavior following surgery were therefore logically linked to the damage. Sometimes people had strokes or aneurysms that damaged the brain.  Sometimes people had injuries that damaged the brain (e.g., Phineas Gage).  In yet other cases, surgery was performed on the brain to alleviate epilepsy or psychological illness. One important point to keep in mind is that regardless of the cause of damage, studies of these sorts were not studies of the healthy, normal human brain; they were studies of the diseased or injured brain.  It wasn’t until different sorts of neuroimaging or recording techniques arrived on the scene as methodological tools that we were able to evaluate the healthy human brain.

Damage that occurred because of a tumor, a stroke, or injury most often crossed multiple anatomical areas somewhat randomly.  This made it challenging to conclude which psychological functions were generated by which brain areas. But damage that occurred to alleviate illness was typically targeted, or what neuroscientists call “focal”. Studying people with this sort of damage allowed the pioneers of emotion neuroscience some of the first glimpses into the role of particular brain areas in the generation of emotions. By combining observations from the clinic with animal studies in which comparable brain damage was made or in which regions of the brain were electrically stimulated (which will be discussed in a future post), the neuroscience of emotion was propelled forward.

These early emotion neuroscientists—men like Cannon, Papez, and MacLean—used what their fairly rudimentary tools (by modern standards) to reveal some truths about emotion that still ring true today:

Emotions don’t live in particular areas of the brain but rather came to be via distributed circuitry throughout the whole brain. The expression, experience, and perception of emotion are made possible by slightly different circuitry.  Emotion comes to be in part via the activity in the peripheral nervous system—that is, we “feel” emotions in our bodies.  Certain brain areas are “hubs” of activities—central areas much like bus terminals in a big city where lots of signals arrive and are subsequently transmitted to other areas for further processing.

For examples classic early papers see here, here, here, and here.

Over the years, these important messages that stand the test of time (and modern methods) were often lost in attempts to localize particular emotions to particular neural regions.  [The most pervasive of the localization hypotheses is that the amygdala is the locus of fear.  The hypothesis is so pervasive and the evidence to support it so lacking, that we’ll take on that idea in another full post.] Localization attempts focused on mapping discrete emotions to discrete neural structures, often relying on poor operationalization of emotion related variables.

An early scientist might label a phenomena “rage” without ever defining what rage actually was (By answering questions like: are we talking about the perception of rage? The expression of rage? The experience of rage? How do we tell the difference between rage and anger? If this phenomena is being observed in animals how do we know that it maps on to the human experience of rage?) or indicating a specific way to measure it. Another important, often overlooked point is that changes to emotion observed in these human patients were typically described in diffuse, nonspecific terms—for example a patient’s psychiatry symptoms might have “improved” following surgery.  Improvement in anxiety or depression symptomology, for example, were taken as evidence that particular brain areas removed during psychosurgery were involved in emotion.  Advancement of emotion neuroscience requires carefully defining emotion terms and characterizing emotion phenomena in ways that can be systematically measured.

Despite these caveats, the lessons from early studies of the emotional brain are powerful and not to be ignored as we enter an era of the BRAIN Initiative—careful experimentation and measurement can yield impressive gains in knowledge, even with fairly rudimentary tools.

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