What theory of emotion states that arousal and emotion occur at the same time and in order to experience the emotion you need a cognitive label for the arousal?

By Charlotte Nickerson, published Nov 01, 2021

Key Takeaways

• William James (1884) and Carl Lange (1885) devised two physiological theories of emotion independently. These theories had different emphases, and some scholars argue that the James-Lange theory of emotion is a distortion of both scientists’ work.
• James-Lange theory of emotion (1880s) proposed that bodily changes come first and form the basis of an emotional experience. Thus, emotions are caused by bodily sensations (you become happier when you smile, you are afraid because you run).
• The James-Lange theory of emotion has spurned over a century of research into the physiology of emotion, and notable critics of the James-Lange theory (such as the Cannon-Bard theory of emotion) have also garnered tremendous traction from researchers.
• This theory has been criticized as it cannot explain emotion without any arousal, nor the role of learning and cognition. It is also difficult to perceive different physiological states accurately (e.g. blood pressure).

Overview and History

William James (1948) and Carl Lange (1885) devised two distinct theories surrounding physiology and emotions independently. While James emphasized the various somatic and visceral responses to stimuli that can prompt conscious emotional experiences, Lange had a specific emphasis. To Lange, emotion was a cardiovascular event (Lang, 1994).

Nonetheless, both scientists agreed that emotion did not begin with the conscious experience of an emotion, but bodily responses to external events.

William James’ (1884) theory of emotion proposed that there are a set of basic emotions (such as anger), and that each of these emotions has its own associated physical state (emotional measurement).

William James’ original theory was constructionist, which means that James believed that there was no “essence” of any given equation; however, there were certain physiological states that organisms shared in response to stimuli (Meiselman, 2016).

Rather than attempting to categorize the plethora of individual emotions, James believed that the object of psychology was “a science of relations of mind and brain,” and that it “must show how the elementary ingredients of the former correspond to the elementary functions of the latter” (1920).

The James-Lange theory of emotion owes its existence to philosophical psychology. From the last decades of the 19th century sprung a field whose quiddity was studying people’s conscious experiences. Philosophical psychologists tended to see emotions as either primary and unanalyzable (one psychologist who believed this was Wilhelm Wundt (1896) or raw data to be examined (Lang, 1994).

William James took the latter approach and proposed that emotions were not the fundamental givens of human consciousness but phenomena prompted by the perception of somatic and visceral changes elicited by external stimuli (Lang, 1994).

Scholars long studied the physiology of emotion prior to James (1884) and Lange (1885). Prior to the publication of James’ article in Mind, physiologists had established an empirical, lab-based science of emotions, beginning with a series of European physiologists in the 1860s (Dror, 2013).

The major figure in the study of the physiology of emotions contemporary to James was the Italian physiologist Angelo Mosso, who established the beginnings of how modern physiologists study emotion (Mosso, 1879).

Mosso framed his study of emotion in terms of the Darwinian theory of evolution, and created, measured, and replicated emotions in provided graphic and numeric representations of emotional states.

James knew Mosso’s findings well, and indeed acknowledged how Mosso expanded the study of emotions to the so-called viscera — the brain and its internal processes.

Mosso’s experiments and instruments would in turn heavily influence numerous other psychologists who studied emotions in the late 19th and early 20th centuries, such as the German physiologist, Lehman, in Die Hauptgesetze des menschlichen Gefühlslebens (1892).

How Does the James-Lange Theory Work?

The James-Lange theory of emotion postulates that emotions occur as a result of physical responses to events (physiological responses to stimuli directly cause subjective feelings).

Our natural way of thinking about these standard emotions is that the mental perception of some fact excites the mental affection called the emotion, and that this latter state of mind gives rise to the bodily expression.

My thesis on the contrary is that the bodily changes follow directly the Perception of the exciting fact, and that our feeling of the same changes as they occur IS the emotion. Common sense says, we lose our fortune, are sorry, and weep; we meet a bear, are frightened and run; we are insulted by a rival, are angry and strike.

The hypothesis here to be defended says that this order of sequence is incorrect, that the one mental state is not immediately induced by the other, that the bodily manifestation must first be interposed between, and that the more rational statement is that we feel sorry because we cry, angry because we strike, afraid because we tremble, and not that we cry, strike, or tremble because we are sorry, angry, or fearful as the case may be.

Without the bodily states following on the perception the latter would be purely cognitive in form, pale, colorless, destitute of emotional warmth. We might then see the bear and judge it best to run, receive the insult and deem it right to strike, but we would not actually feel afraid or angry.

James and Lange’s (1948; 1885) theories of emotion counter the classical idea of emotional processing, where someone imagines or experiences an emotion-eliciting event or stimulus, experiences an emotion, and then experiences a bodily reaction to that emotion (Meiselman, 2016).

Rather, the James-Lange theory of emotion argues that emotions occur due to physiological reactions to events. To illustrate this theory, consider a person who encounters an angry, barking dog.

According to the classical theory of emotional processing, the person would hear and see the dog bark, experience an emotion (such as fear), and then experience an emotional response (such as trembling) as a result. The person trembles because they are afraid.

In contrast, according to the James-Lange theory of emotion, the person would hear the dog and tremble. Consciously, they would process this trembling and come to the conclusion because they are afraid.

The person, in this case, is afraid because they are trembling. In James’ words, “My theory...is that the bodily changes follow directly the perception of the exciting fact, and that our feeling of the same changes as they occur is the emotion” (James, 1948).

James believed that there were a set of standard emotions (for example, surprise, fear and anger) but does not specify what may happen for emotions that do not have a distinct set of bodily reactions, such as shame (Meiselman, 2016).

Scholars have labeled the James-Lange theory of emotion as peripheralist (Meiselman, 2016), and have used the label of peripheralism to contrast the James-Lange theory of emotion with the rival Cannon-Bard theory of emotion.

In short, peripheralism is the view that emphasizes events at the periphery of an organism’s own body – such as, say, its skeletal muscles and sex organs, over events originating in the central nervous system.

Impact of the James-Lange Theory

James-Lange theory of emotion came to influence a century of empirical emotional research and rebuttals of the James-Lange theory of emotion, notably Cannon-Bard’s 1927 critique, have spurned long-standing debates in neuroscience and psychology (Lang, 1994).

Cannon-Bard theory of Emotion

Cannon-Bard theory of emotion (1927) states that changes of emotional state and changes in the autonomic nervous system occur simultaneously but independently, both caused by the arrival of the same sensory input at the thalamus.

Cannon-Bard’s “centralist” theory of emotion emphasizes how emotions affect, firstly, the brain and nervous system. The Cannon-Bard theory of emotion assumes that stimuli elicit physiological and “affective,” conscious emotional responses simultaneously.

Cannon-Bard (1925) proposed their theory of emotion as a direct response to the previously predominant James-Lange theory of emotion. In the article, The James-Lange Theory of Emotions: A Critical Examination and An Alternative Theory (1927), Cannon offers five main criticisms of James-Lange:

1. total separation of the viscera from the central nervous system does not alter emotional behavior;
2. the same visceral changes occur in very different emotional states and in non-emotional states;
3. the viscera are relatively insensitive structures;
4. visceral changes are too slow to be a source of emotional feeling; and finally,
5. artificial induction of the visceral changes typical of strong emotions does not produce them.

The James-Lange/Cannon-Bard debate is a classical one in understanding emotional processing, and numerous scholars have compared the merits of each theory in relation to others. Namely, academics have provoked a large amount of empirical research regarding the temporal sequence of emotion (emotional measurement).

For example, Allport and Tomkins (1962) bolstered the James-Lange theory of emotion by creating the facial feedback hypothesis. Rooted in the conjectures of Charles Darwin and William James, the facial feedback hypothesis puts forth that one’s facial expressions directly affect their emotional experience.

For example, by forcing someone’s face to contract into a smile, someone may be more likely to experience joy. A lack of facial expression, meanwhile, would result in a suppression of emotion. Nonetheless, both theories were influenced by and went on to influence others.

Example 1

To illustrate this theory in the context of the dog example, a person may see a barking dog, and tremble and consciously register “I am afraid,” at the same time. The person is not afraid because they are trembling, but because their thalamus has been triggered by the stimulus of an angry dog.

This means that, in a scenario where somehow someone’s physiological responses to emotion were disabled, the person would still feel the emotion of fear.

Conversely, in a situation away from the stimulus where all of physiological responses were triggered — for example, if the parts of the brain associated with trembling were activated by the stimulation of an electrode in the absence of a frightening stimulus – the person or organism would not consciously feel fear, according to the Cannon-Bard theory of emotion.

Example 2

To clarify the James-Lange theory of emotion, consider someone who experiences road rage while driving a car. Say that this person has just been cut off by a nearby car. This event is an external stimulus.

In response to being cut off, the person’s heart may race, their face may flush, their jaw may clench, and their hands may shake. The James-Lange theory of emotion would argue that these physiological reactions are characteristic of anger.

Thus, the person experiencing these symptoms may feel angry as a direct response to these reactions, and behave accordingly.

The James-Lange theory of emotion would also argue that, if someone had these physiological reactions without a stimulus — say, if a machine somehow could raise their heart rate and clench their jaw — then the person would still register the emotion of anger.

James-Lange and Schacter and Singer’s Two-Factor Theory of Emotion

The James-Lange vs. Cannon-Bard debate has influenced major findings in emotion research. Some sources argue that the both theories of emotion garnered a great amount of influence in early emotional physiology because of its testability (Meiselman, 2016).

Two of the most notable findings, Schachter and Singer’s two-factor theory of emotion (1962) and Damsio’s theory of emotion draw heavily on Jamesian concepts.

The two-factor theory of emotion focuses on the interaction between emotional arousal and how organisms label that arousal. In particular, the theory argues that emotion arises from both the physiological arousal resulting from a stimulus and the reasoning that surrounds that emotion.

To use the previous example, a person may see an angry, barking dog and begin to tremble. That person then needs to consciously appraise their physiological response to the angry dog in order to determine that they are afraid.

The point of differentiation between the James-Lange and two-factor theories of emotion is subtle and lies in this cognitive appraisal. While the James-Lange theory proposes that emotion happens because of physiological arousal, the two-factor theory of emotion contends that there is a conscious appraisal of that physiological response that leads to the emotion.

For example, while, according to the James-Lange theory of emotion, an afraid person may say, “I am afraid because I am trembling,” that same person would say, “I am afraid because I have consciously assessed that I am trembling and this is a response to fear.”

In other words, both the physiological response to and assessment of that response contribute to the experience of emotion, according to Schacter and Singer’s theory, and that both physiological arousal and cognition need to work together in order for someone to perceive an emotion.

James-Lange and Damasio’s neo-Jamesian Theory of Emotion

Damasio (1994) devised the second major theory of emotion influenced by James-Lange. Damasio proposed “somatic markers,” which are physiological reactions tied to past emotional events.

New events trigger these somatic markers and influence how people make decisions. For example, someone who has had past positive experiences with dogs (for example, a dog cuddling and protecting a person) would have a series of markers that would influence that person to, say, pet the next dog that they see.

The most notable testing of the concept of somatic markers has been the Iowa gambling task. The Iowa gambling task is a way of studying decision making using cards. In these experiments, notably Bechara, Damasio, Damasio and Anderson (1994), participants can choose one of four card decks, and win or lose money.

Two sets of decks were “high risk,” (with the possibility of losing or gaining large amounts of money) while the others were lower risk.

Bechara et. al.’s original study on patients with damage to the prefrontal cortex postulated that those with brain damage were less sensitive to the consequences of their decision making due to the “somatic marker” of brain damage.

Facial Feedback Hypothesis

The facial feedback hypothesis stems from the underlying principles of the James-Lange theory of emotion in the belief that physiological responses to stimuli generate emotion.

In the words of facial feedback researcher Tomkins (1962), emotions are “sets of muscle and glandular responses located in the face.”

Scientists have extended this facial feedback hypothesis to posture (Stepper and Strack, 1993) and more recently have conducted studies using Botox to fix facial expressions.

In one such study, Hennenlotter (2007) asked participants to perform a facial expression imitation task before and after being injected with Botox, which paralyzes and restricts the movement of facial muscles.

The researchers found that those who had been injected with Botox experienced less activation of brain regions associated with emotional processing when asked to imitate angry facial expressions.

Unable to imitate negative facial expressions, Hennenlotter et. al. postulated that Botox injections would lead to fewer negative emotions, and that the drug could be used to treat symptoms of depressions. Further studies have supported the facial feedback hypothesis.

For example, there has been evidence that smiling while reading cartoons correlates with greater levels of amusement (Hennenlotter, 2007), and that those with facial paralysis are more likely to experience depression (Hennenlotter, 2007).

This hypothesis was tested by Hennenlotter, who used Botox to treat ten patients with depression by means of suppressing muscles associated with frowning. Negative effects decreased in all patients, with nine no longer experiencing depressive symptoms.

Charlotte Nickerson is a member of the Class of 2024 at Harvard University. Coming from a research background in biology and archeology, Charlotte currently studies how digital and physical space shapes human beliefs, norms, and behaviors and how this can be used to create businesses with greater social impact.

How to reference this article:

Nickerson, C. (2021, Nov 01). The James-Lange Theory of Emotion. Simply Psychology. www.simplypsychology.org/what-is-the-james-lange-theory-of-emotion.html

References

Bechara, A., Damasio, A. R., Damasio, H., & Anderson, S. W. (1994). Insensitivity to future consequences following damage to human prefrontal cortex. Cognition, 50(1-3), 7-15.

Bernard, C. (1866). Leçons sur les propriétés des tissus vivants: Germer Baillière.

Cannon, W. B. (1915). Bodily Changes in Pain, Hunger, Fear and Rage. Ed. Appleton & Company.

Cannon, W. B. (1927). The James-Lange theory of emotions: A critical examination and an alternative theory. The American Journal of Psychology, 39(1/4), 106-124.

Cannon, W. B., & Britton, S. W. (1925). Studies on the conditions of activity in endocrine glands: XV. Pseudaffective medulliadrenal secretion. American Journal of Physiology-Legacy Content, 72(2), 283-294.

Darwin, C., & Wundt, W. Emotion Psychologische Erklärungsmodelle.

de Cyon, E. (1873). Principes d'électrothérapie: Baillière.

Dror, O. E. (2013). The Cannon–Bard Thalamic Theory of Emotions: A Brief Genealogy and Reappraisal. Emotion Review, 6(1), 13-20. doi:10.1177/1754073913494898

Ellsworth, P. C. (1994). William James and emotion: is a century of fame worth a century of misunderstanding? Psychological Review, 101(2), 222.

Fehr, F. S., & Stern, J. A. (1970). Peripheral physiological variables and emotion: the James-Lange theory revisited. Psychological Bulletin, 74(6), 411.

Friedman, B. H. (2010). Feelings and the body: The Jamesian perspective on autonomic specificity of emotion. Biological Psychology, 84(3), 383-393.

Hennenlotter, A., Dresel, C., Ceballos-Baumann, A., Wohlschläger, A., Castrop, F., & Haslinger, B. (2007). Denervation of frown muscles with botulinum toxin disrupts facial feedback to central circuitry of emotion. Aktuelle Neurologie, 34(S 2), P408.

James, W. (1920). Collected essays and reviews: Longmans, Green and Company.

James, W. (1890). The principles of psychology (Vol. 1). New York, NY: Henry Holt. Find this resource.

James, W. (1894). The physical basis of emotion. Psychological Review, 1, 516-529.

James, W. (1884). What is an emotion? Mind, 19, 188-205. Republished in K. Dunlap (Ed.), The emotions. Baltimore: Williams & Wilkins.

James, W. (1922). The emotions. Chap. XXV in Principles of Psychology, 1890. Republished in K. Dunlay (Ed.), The Emotions. Baltimore: Williams & Wilkins.

Lange, C. (1922). The emotions. In K. Dunlap (Ed.), The emotions (I. A. Haupt, Trans.; pp. 33-90). Baltimore: Williams & Wilkins. (Original work published 1885)

Lang, P. J. (1994). The varieties of emotional experience: a meditation on James-Lange theory. Psychological Review, 101(2), 211.

Lange, C. G. (1885). The mechanism of the emotions. The Classical Psychologists, 672-684.

Meiselman, H. L. (2016). Emotion measurement. Woodhead publishing.

Schachter, S., & Singer, J. (1962). Cognitive, social, and physiological determinants of emotional state. Psychological Review, 69(5), 379.

Stepper, S., & Strack, F. (1993). Proprioceptive determinants of emotional and nonemotional feelings. Journal of Personality and Social Psychology, 64(2), 211.

Tomkins, S. (1963). Affect imagery consciousness: Volume II: The negative affects: Springer publishing company.

Wundt, W. (1896). Grundriss der psychologic (C. H. Judd, Trans., 1897). Leipzig, Germany: Engelmann.

Home | About Us | Privacy Policy | Advertise | Contact Us

Simply Psychology's content is for informational and educational purposes only. Our website is not intended to be a substitute for professional medical advice, diagnosis, or treatment.

© Simply Scholar Ltd - All rights reserved

report this ad