Discrete versus dimensional models of emotion?

Eliza Bliss-Moreau

Over the last number of months as an Associate Editor at Emotion, as well as a reader of the literature, I have seen an increasing number of scholars refer to “discrete emotion models” and pit them against “dimensional emotion models” in order to set up a primary hypothesis and its alternative.  This is a false dichotomy.  My challenge as an editor is that I have not been able to find a singular “quick read” piece of writing in the literature articulating why a discrete versus dimensional contrast doesn’t make sense (although there are longer papers on this that do make this point such as thisthis, this, and this – if you know of others that are near and dear to you, send them my way).  I did a quick – entirely nonscientific – review of papers with the keyword “emotion” and “discrete or dimension or dimensional” published in 2017 and 2018 and there is some evidence that this is a problem in the published literature as well.  My first take was “I should write a manuscript about this”, and I may, ultimately. My goal here, however, is not to call people out for this analytical problem per se but to provide an explanation as to why pitting discrete emotion models against dimensional emotion models is logically problematic, so that folks can fix it if it is in their writing (or thinking) or not make it in the first place. I don’t see any way around that goal if I were to undertake writing a manuscript which would require appropriate scholarly referencing.  So, writing a blog post seemed like a good option.

The problem
There are lots of theories and models of emotion that focus on discrete emotions – how they come to be, their outputs, their functions, and so on.   They vary widely in their hypotheses about all of those features of emotion. But there is no dimensional theory of emotion.  Dimensions  – typically valence and arousal –  are characteristic of affect [i], not emotion.  According to a number of the major theories in our field, affect is thought either to be the causal foundation of emotion or one of the most important components of emotion.  Saying that affect is a causal foundation or critical component of emotion is very different, however, from saying that affect is emotion – and so, theories of emotions which recognize differences between affect and emotion are not reductionist about emotions.  According to these theories, whatever else emotion is, it is something “more” than just affect. It is therefore a mistake to talk about theories of emotions as if they are dimensional.  As a result, there is no way to pit “discrete emotion models” against “dimensional emotion models” because a) there is no dimensional emotion model, only dimensional affect models and b) emotion theories that hypothesize that multiple dimensions of affect underlie emotions in some way or another frequently hold that these emotions can be separated into distinct types and kinds, and therefore are, metaphysically speaking, discrete entities.

The background
It goes without saying that there are many different theoretical and methodological approaches to the study of emotion. Over the last decade or so, two types of theories have dominated discussion and study (despite both being around for much longer) – what we call the Classic View of Emotion (CVE) [ii] and Theories of Constructed Emotion (TCEs).  I use this terminology with very specific intentions, not just as shorthand labeling to differentiate my writing from that of other scholars.

The CVE says that emotions are precipitated by events and then produce a stereotypical set of outputs in the face, voice, autonomic/peripheral nervous system, behavior, and, or brain.  There is a predictable mapping between the types of events that cause emotions and specific emotions. Further, each emotion is thought to have some sort of specific pattern of physiological and behavioral outputs. Because of this, to understand the emotion state of another individual, an observer (who could be the self) can “read” the outputs and, because the relationship between the outputs at the emotion causing them is mapped, infer the identity of the emotion causes the relevant outputs.

The interesting unit of analysis from the CVE can be at any step of the process – the event that causes the emotions, the process by which the effects of the event are translated into the emotion, the phenomenological experience of the emotion, the process by which the emotion generates to the outputs, the type of outputs generated by the emotions.  CVEs stipulate that some special set of, or number of, emotions cannot be reduced to more fundamental or basic parts. This belief is reflected in the moniker of one type of CVE – “basic” emotion theory.

“Basic” emotion theories typically stipulate that a small set of emotions (e.g., 5 or 6) are unique kinds.  This means that they are held by the theory to be fundamental or basic [iii], irreducible, and have a modular neurobiological architecture [iv].  These theories sometimes stipulate that more “complex” emotions (e.g., guilt) may be built via combinations of basic emotions, but even those more emotions must follow the event–>emotion–>output schema according to this theory (a view articulated here, for example). Basic emotion theories argue that relationships between events, emotions, and outputs is biologically hardwired and evolutionarily conserved; these assumptions have guided investigation into the neurobiological basis of emotion (e.g., in nonhuman animals, and in humans) and evolutionary emergence of emotion (for example).

Basic emotion theory is arguably the dominant theory that embodies a CVE, but it is not the only theory, hence my use of “CVE” and not “Basic Emotion Theory” (or something similar) to name this perspective.  For example, most appraisal theories embrace a CVE insofar as they evaluate the specific pattern of cognition (called appraisals) that people make following events that lead to emotion – that is the process by which the event translates to emotions.

CVEs do say there are discrete emotions, whether they stipulate that a small set of emotions is biologically basic and hardwired or focus on the process by which an event precipitates an emotion or even the numbers of discrete emotions that exist.  The unit of analysis is typically specific, discrete emotions and these emotions are thought to be the source of the lion’s share of variance in outputs.  These are the theories, I believe, that scholars think they are referring to when they discuss “discrete emotion models” because of their emphasis on specific emotions (like happiness, sadness, fear, disgust, elation, and so on). Further, CVEs do not typically discuss or evaluate the importance of valence and arousal – the dimensions of affect.

Valence and arousal are the dimensions of affect, which, according to TCEs forms the basis of discrete emotions.  TCEs stipulate that emotions are not hardwired modules. Instead, TCEs say that each emotion is a causal by-product of a complex interaction of more basic parts, and that these parts can vary dramatically depending on age, behavioral context, cultural context, conceptual knowledge, and any number of other important physiological and cognitive factors [v].  Nevertheless, TCEs still recognize that emotions are discrete things. TCEs differ to some degree in the ingredients that they think are critical for the emergence of discrete emotions – hence Theories of Constructed Emotion and not Theory of Constructed Emotion.  But all TCEs hold that affect is a critical ingredient.

Affect is a state that is characterized by some degree of valence (hedonics, pleasantness to unpleasantness) and arousal (physiological activation) and can, but need not be, felt consciously.  People can report on their affect (“I feel good” or “I feel bad”) or, people can report on their emotions and affective information can be extracted from those reports (e.g., one characteristic of happiness is a good or pleasant feeling). That is, affect can be organized according to dimensions (valence and arousal). That is the case because discrete emotions are organized in a systematic way with regards to valence and arousal.  Happiness?  Positive valence, just slightly activated/aroused.  Depression?  Negative valence, very deactivated.  Fear, anger, disgust?  Very negative, very activated/aroused, and so on.

TCEs say that affect is an essential component of emotion, but they do not say that affect is emotion – and so they do not reduce emotion to affect. According to TCEs, a discrete emotion has affective components, but the affective states that are components of emotions are not alone sufficient to determine the identity of the emotion of which they are part. For example, there are a slew of negative, high arousal emotions which share a negative, high arousal affective state but are not the same emotion – think anxiety, disgust, anger, and fear.  The same affective state can thus be part of a number of discrete emotions depending on the context, what the person knows about emotion, past experiences, the language the person speaks, social norms, and so on.  As a result, it does not follow to say that emotions, according to TCEs, are (or can be described by) dimensions. Scholars guided by TCEs, just like those guided by CVEs, study discrete emotions – but they may be equally likely to study the various other ingredients that go into cooking up emotions, including affect.

Why does the distinction between discrete emotions and the dimensions of affect matter?
It is important to be clear about whether we are testing hypotheses about emotions (which nearly everyone agrees are discrete entities) or testing hypotheses about affect (which everyone agrees can be analyzed as falling into at least two continuous but bounded dimensions), or testing hypotheses about some combination of the two–for example, when we ask whether (discrete) emotions or (degrees of the dimensions of) affect capture more of the variance in a given situation. Keeping this distinction in mind can help us develop strong, testable hypotheses about the nature of emotion.

For example, the goal of my lab is to understand some of the biological mechanisms that generate the emotions – and we do that work largely in nonhuman animals.  While there is huge debate about the nature of nonhuman animal emotions, I have argued that affect is species nomothetic – at least in mammals who share a similar central-to-peripheral nervous system structure.  If this is the case, and if a given behavioral or physiological phenomenon is driven by affect and not discrete emotions, then we can hypothesize that it has a homolog in nonhuman animals.

Another issue in the nonhuman animal literature that appears regularly is that scientists will make strong claims about animals’ abilities to perceive emotion stimuli when they are actually testing an affect hypothesis.  For example, in a recent study, when goats were shown pictures of human faces generating behaviors typically associated with anger and those typically associated with happiness, goats spent more time investigating the “happy faces”.   The take home message, amplified by the media, was that a) goats understand human emotions or “goats can read human emotions” and b) “goats prefer happy people”.  That may very well be true, but given the experiment as conducted, there’s actually no way to determine whether goats prefer happy people or simply pleasant, neutral arousal people compared to negative, high arousal people.   It’s entirely possible that when a happy face was compared to a serene face, goats might opt for serenity.  If this was the case, one starts to build an argument that their choice has nothing to do with valence at all (let alone emotion), but rather arousal – lower arousal faces might be favored.

The hope
What CVE and TCE theorists, as well as scientists studying discrete emotions and the dimensions of affect, all have in common is the goal of understanding the mechanisms that generate and subserve emotions. My hope is that remaining clear about the difference between a hypothesis that is about discrete emotions versus a hypothesis that is about the dimensions of affect will speed those discoveries.




[i] Thus, there is a dimensional theory of affect.  Valence and arousal aren’t the only dimensions that have been proposed to organize affect, but they are the dimensions that consistently appear in analyses of self-reports of emotion experience and judgements of emotion stimuli.  Jim Russell’s 1980 paper is a classic on this .  Here’s a resource of a broader discussion of affect.  And here’s a recent paper which proposed additional dimensions of affect.

[ii] As far as I know this labeling originated with Lisa Barrett and a version of it (the Classical View) is used throughout her book, How Emotions Are Made.

[iii] For examples of modern articulations of basic emotion theory see: here, here, here, here, and here.

[iv] There are lots of ways that a phenomenon can be modular, for example if the same stimulus or event produces a single emotion, then that Stimulus-Response link is modular.  When framed as a neuroscience argument, modularity has typically been interpreted as their being discrete neural and biological circuity for each emotions – such that emotions have, as Lisa Barrett calls them in here book, “fingerprints” in the brain (as well as voice, face, etc.).

[v] For a historical review of Theories of Constructed Emotion.  For an edited volume on Theories of Constructed Emotion (note that many of the chapters appear to be accessible on the authors’ websites).

Humans aren’t the only lonely species. Monkeys may be lonely too.

Eliza Bliss-Moreau

More than two decades of research demonstrates that people who have more social connections do better—in terms of their general health, ability to recover from illness, and longevity (for a classic, oft cited study, see here; for a review, here; for popular press coverage and a lovely long read on human loneliness, here). Perhaps unsurprisingly, it’s not just the number of people you’re connected to that matters for your well-being. Whether people’s social relationships meet their social needs also has critical importance for health outcomes  regardless of how many social connections they have (for reviews of this literature see here, here, and here). That is, it’s possible to be well-connected socially and still feel totally alone in the world. It is also possible to have very few social relationships but not feel lonely at all.

Exciting new evidence illustrates that we humans might not be the only ones to experience loneliness—rhesus macaque monkeys may as well. As part of an interdisciplinary team, Dr. John Capitanio examined the social behavior of adult male macaques at the California National Primate Research Center and identified three different patterns. Some monkeys engaged in a lot of social interactions with other males, adult females, and younger monkeys. Other monkeys did not engage in a lot of social interactions at all. What’s critical some of these “lowly social” monkeys seemed fairly content with their lot in life—they went about their daily business without trying to build new relationships.

Housing&Enrichment©K.West-CNPRC,039The other lowly social monkeys did seem to care about their lot in life, however. They often physically approached adult females and younger animals, presumably in an effort to initiate an interaction. Similarly, the monkeys would walk by those animals to see what they were doing, even when trying not to engage with them. The fact that these behaviors were observed with adult females and younger monkeys suggests that these “lonely” adult male monkeys may have been looking for easy social relationships (because of how macaque societies are structured, relationships between adult males can be challenging). This heightened social interest persisted when evaluated 1.5 years later. In other words, there were monkeys who appeared to chronically desire social relationships but did not manage to make them happen—a potential monkey homologue of human loneliness. What’s more, as Capitanio points out, these lonely monkeys may be better models for human loneliness than previous animal models because the phenomenon emerged spontaneously in the context of large naturalistic social groups, rather than as a result of experimentally separating animals.

In and of itself, the finding that nonhuman animals might have the capacity to be lonely is an interesting one. It suggests that experiencing a mismatch between one’s social realities and one’s social desires is evolutionarily old, raising questions about what function loneliness might have served for our ancestors.

But perhaps more importantly, animal models of human psychological phenomena, such as a monkey model of loneliness, are critical to understanding the biological processes that contribute to them. Nonhuman primate (e.g., monkey) models are particularly important for understanding human function and dysfunction because we share so many biological and social features. Monkey models allow for precise experimental control (e.g., the ability to manipulate social environment, diet, sleep-cycles, etc.), intensive long-term longitudinal studies (i.e., the ability to track and evaluate many individual animals over the course of their entire lives), and the development of causal biological models. Understanding biological mechanisms is critical for developing effective early interventions and treatments for deleterious psychological experiences. Studying lonely monkeys may therefore unearth the biological and social processes that can be harnessed to help lonely humans in the future.

Photo: Adult male rhesus monkey at the CNPRC eating a zucchini. Photo Credit: Kathy West, CNPRC.

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.https://flic.kr/p/off1YF

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.

 Photo credit:  https://flic.kr/p/off1YF

Introduction to the Neuroscience of Emotion Series

Eliza Bliss-Moreau

In the coming months, we will be posting a number of stories on the neurobiology of emotion. Understanding how the brain creates emotion has important consequences for everything from whom we charge with crimes (are crimes that occur due to a brain disorder that changes emotions different from those that are not?) to how we treat depression (is using chemicals that effect the brain a better option than talk therapy?) to the ethics associated with meat production (if pigs have brains capable of emotions, does that change how we treat them as we turn them into meat?).

As neuroscientists in the 21st century, we are equipped with powerful tools to ask questions about emotion. Modern neuroscience techniques are comparable to the methods detailed in science fiction decades ago—we can “see” into the brain of a normal person while they are in a MRI scanner experiencing emotions; we can turn on and off areas of animal brains with a beam of light; we can record activity of single cells in the brain of animals and nerves throughout the body.  The experiments that use these tools and the data that are produced by these tools are complex and often indirect measures of brain function and the emotion produced by brain activity.  Their portrayal in the modern media often does not do justice to their complexity.https://flic.kr/p/dLbzPm

Over a series of posts, we’ll explain how different neuroscience methods actually work, how they are used to study emotion, and what the take home messages are about how the brain creates emotions.  We hope to paint a picture of how exciting and challenging research on the brain basis of emotion is, how powerful our existing tools are, and how much we still have to learn.

Neuroscience stories about emotion make the national and international news frequently these days (like this, this, and this, for example). With the abundance of these stories, it’s easy to forget that it wasn’t that long ago that we had very limited tools to study the brain in a living, breathing person or nonhuman animal. [In later posts, we’ll talk about what we’ve learned about emotion from brains that are not in living beings.] Prior to the advent of neuroimaging technology which lets us measure activity in the brain (either electrical activity, blood flow, or the movement of chemicals), most studies of human emotion occurred when people incurred brain damage.

Perhaps the most famous case of accidental brain damage interfering with emotion, is the case of Phineas Gage. Phineas Gage was a railroad worker born in the 1820s.  In 1848, he was working to build a railroad in Vermont when a terrible accident occurred.   He was using a long metal rod and blasting powder to blast rock away at the site.  During one of the blasts, he lost control of the rod and it flew through his head.   The metal rod entered his skull under his left eye and exited out of the top of his head, damaging a large area of frontal cortex in the process (see).  Surprisingly, Gage lived.  But he was never the same again.  Prior to the accident, he was a responsible, upstanding guy.  After the accident he was said to be vulgar, unable to control his behavior, and generally intolerable.  [Although, there’s a fair amount of debate about the extent to which his behavior actually changed on account of poor records, see].  Modern studies of the brain areas damaged in Gage’s case suggest that those areas contribute to the regulation of emotions.

Gage’s case was just one of many that point to a link between particular areas of the brain and the generation and regulation of emotions.  The next post in this series will address what we’ve learned about emotion from other instances in which humans acquire brain damage.  Sometimes damage is created intentionally—typically to treat intractable diseases (like seizure disorders).  Sometimes damage occurs during strokes.  Finally, there are some diseases out there that target specific brain areas and render them nonfunctional.

In addition to exploring what the emotional lives of people with brain damage have taught us about the neuroscience of emotion, we’ll also be answering questions like: How does neuroimaging really work?  What have animal studies of the brain and emotion taught us? What are the biggest and most dramatic misconceptions about the neuroscience of emotion? How do different brain areas work together to create emotions?

If there are other specific topics you would like to see covered, please email one of the founders or leave a comment for us below.

Fido feels?

Eliza Bliss-Moreau

The emotional lives of dogs has become a hot topic as of late and made some big splashes in the media. In a recently published study, Christine Harris and Caroline Prouvost claim that dogs, like humans, experience jealousy.

The researchers tested pet dogs and their owners while their owners interacted with three different objects:  a toy dog that moved and made noise, a jack-o-lantern figure, and a children’s book that made noise.  Owners were instructed to interact with the objects and ignore their dogs.  When owners were interacting with the toy dog (compared to the other objects), their pets were more likely to touch them or the objects, move between the owner and object, and look more at the owner and object.  Dogs also “snapped” more at the animated toy dog than the other objects.  The authors state that these behaviors are “indicative of” jealously.

The report makes three fairly substantial, critical assumptions—two about the nature of emotion and one about how dogs behave with toys.

3210109272_df9c66d773_oThe first assumption is that behaviors map on to emotions in a specific way.  The idea here is that we can know the internal state of an individual based on his or her behavior.  In other words, if behavior X occurs, then emotion Y is present.  This is an intuitive idea that resonates with people.  But, the scientific evidence suggests this is not true. The problem is that there is a substantial amount of evidence that suggests this is not the case, even in humans who can tell us how they feel while they are behaving.  Overt behaviors don’t relate in specific ways to specific emotions.  Physiological patterns (e.g., what your heart is doing during an emotion) don’t relate in specific ways to specific emotions.  And so on.  Sometimes people (and rodents and dogs and monkeys) fight when they’re fearful and sometimes they run away.  Sometimes people smile when they’re happy, sometimes they make no facial behaviors at all, and sometimes people smile when they’re angry.   So particular behaviors aren’t “indicative of” particular emotions.

The second, related, assumption is that behaviors in animals are indicative of emotional states that are human-like.  This logical leap has been made for decades (particularly in studies of fear).  A freezing rat is said to be a fearful rat.  In actually, we have no way of knowing (yet) whether a freezing rat is experiencing human like fear at all.  Freezing is a fairly simple neurobiological reflex.  It’s hard to equate it with human experiences of emotion. Like for example, the experience you might have when you hear that a plane has crashed and your lover was on it, or the feeling you might have when you’re walking down a dark alley and hear heavy footsteps behind you.  Making the assumption that rat freezing is the same as one of those human experiences is a fairly large (and as I and others argue, problematic) logical leap.

The third assumption is that dogs’ behaviors differed with the toy dog because of emotion and not some other psychological state.  But there are a number of other possibilities.  For example, it’s possible that dogs were simply more interested in the toy dog because it was more complex or interesting or because it looked like a dog.  It’s possible that the dogs wished to play with it themselves, or were confused because it emulated a dog without being one.  Since the dogs were never tested with the objects and without the owner, or when the owner was not paying attention to the toy, none of these hypotheses can be excluded.

So, can Fido feel jealous? Possibly.  Humans have selectively breed dogs over thousands of years, creating modern day dog that is particularly responsive to human emotions, gestures, and eye-gaze.  Some of these capacities are unmatched even in our closest genetic relatives—the nonhuman primates.  Dogs also have fairly complex brains that may be capable of the computations needed for a complex socially oriented emotion like jealously.

But, based on this single study alone, the jealously jury is definitely still out.