By Sarah Stevenson, MA- The Tini Yogini
Theories of Emotion
In this article, I will peel away the layers of emotional experiences, uncovering the underpinnings and characteristics involved in the animation and energizing of our being. Emotions like fear, anxiety, depression, and excitement elicit and suppress different physiological and cognitive attributes and directly affect how we experience and react to the world around us (Barrett et al., 2016). I will introduce you to the theorists that have contributed to how we view emotion in the present day.
William James and Carl Lange 3-Part Sequence of Experiencing Emotional Events
Psychologist William James and physiologist Carl Lange theorized that emotions exist because of our body’s physiological reaction to stimuli and events (James, 1884). According to this theory, there is a sequence of three parts to each emotional experience. It looks something like this:
- Step 1-Seeing an external stimulus (an aggressive dog).
- Step 2- The physiological response to the aggressive dog, which is likely increased heart rate, dilation of pupils, perspiration, and blood pressure rising.
- Step 3-The mind’s interpretation of physiological response that leads to feeling the emotion of fear (James, 1894).
An increase in heart rate and blood pressure rising may cause a fearful person to run, yell at the dog or become frozen and immobile with severe panic. In the picture above, the kitten sees the scary dog (step one). The kitten’s eyes dilate and are intently focused on the threat, her hair stands up, and she arches her back (step two). This kitten is frightened (step three).
How Do We Know This?
In 1890, Williams James wrote The Principles of Psychology, a 1200-page book on physiology, philosophy, and psychology that contains the basis for many of our current theories on emotion today (James & Drummond, 1890). James was an anatomy and physiology professor at Harvard University and the first to teach a psychology course in the United States and the first to look at emotions from a behavioral standpoint (Goodman, 2017). Research that relates to this theory today looks at emotions that are interconnected to the automatic nervous system. A classic study that supported the James-Lange theory looked at how facial expressions associated with anger, disgust, fear, happiness, sadness, and surprise stimulated the automatic nervous system, which causes the body to change skin temperature and heart rate (Levenson et al., 1990). Brain scan studies that link emotions to activity in specific parts of the brain are based on this theory (Lindquist et al., 2012). There has been criticism about the James-Lange theory of emotions because the studies were not done in a controlled environment and the simplicity of physical reactions being attached to a single emotion (Cannon, 1927). For example, heart rate and blood pressure can increase when one is excited, angry, afraid, or drinking too much coffee, so the physiological response does not necessarily point to a specific emotion (Wu et al., 2019).
Cannon-Bard Theory of Emotion
Walter Cannon and Philip Bard criticized the William-Lang theory and theorized that a reaction to a stimulus and the emotion associated with the stimuli happen simultaneously (American Psychological Association, n.d.). Imagine getting out of work late at night and walking to your car parked in a dark alley. You hear a gunshot off in the distance, immediately feel the sting of adrenaline in your veins and run to your car, lock your doors, and speed off to escape possible danger. This is the Cannon-Bard explanation of the experience of fear. In this theory, the thalamus, which relays sensory and motor information to other parts of the brain, sends a message to the amygdala where emotion is processed and the automatic nervous system, causing the physiological response to happen the same time the emotion happens (Fama & Sullivan, 2009). Cannon notes that physiological changes happen slower than immediate emotional changes (Cannon, 1927).
How Do We Know This?
Cannons theory brought attention to the fight-or-flight ‘emergency theory’. A frightening stimulus is present that activates the sympathetic nervous system triggering a stress response of confronting the threat or fleeing from it (Schauer & Elbert, 2010). When a person is in fight-or-flight mode, there is elevated arousal in the amygdala, blood rushes to the vital organs and away from the brain’s rational part. The person goes into survival mode, having increased strength, elevated heart rate, rapid breathing, and a fast pulse (Jansen et al., 1995). The Cannon-Bard theory of emotions has been criticized for emphasizing the thalamus during an emotional experience while not considering other parts of the brain.
Schacter-Singer Two-Factor Theory of Emotion
The Stanley Schacter and Jerome Singer two-factor cognitive theory became popular in the 1960s when the ‘cognitive revolution’ rose (Miller, 2003). The Schacter-Singer perspective draws from both James-Lange and Cannon-Bard theories of emotion, emphasizing that physical arousal plays the first part of the emotional dance, but also believes cognitive labeling is part of defining each emotion. It looks a little something like this:
- Physical arousal-I see a Japanese beetle flying towards me, so my heart begins to race, and I start shaking.
- Cognitive labeling- My racing heart and shaking body cause me to label my response to the beetle as fear.
- Emotion is felt- I feel scared (fear).
How Do We Know This?
Schacter and Singer conducted a research study of 184 male subjects given an injection of epinephrine, a hormone associated with a rapid heart rate, shaking, and quick breathing patterns (Schacter & Singer, 1962). The participants were told that the injection was given to test their eyesight. Half the group was told there were side effects to the drug, while the other half were told nothing at all. All the subjects were put in a room with a confederate who acted happy or angry. The individuals who were not told of the side-effects of the injection reported feeling more effect by the confederate’s mood (happier or angrier than informed subjects). If the participants were in a room with the confederate pretending to be happy, the subjects reported that the drug’s side-effects were happiness. If the confederate was angry, they reported side effects as anger. Schacter and Singer concluded that if people were not explained the side-effects, they were more susceptible to the confederate’s emotion and would label their feelings according to how they felt in the moment.
The Schacter-Singer Two Factor Theory has faced criticism in that other researchers have found results that only moderately support this theory or results that completely negate this theory. Several people replicated this study and found that regardless of the confederate’s mood, the participants’ effect was negative (Maslach, 1979; Marshal & Zimbardo, 1979). While other researchers have found that some emotions occur before cognition occurs, supporting the James-Lange theory of emotion (Reisenzein, 1983).
Physiological Responses Involved in Emotions
Physiological responses to emotion occur in the autonomic nervous system (ANS) (Barrett et al., 2016). Two systems within the ANS function without consciousness and are responsible for regulating and activating the body. The sympathetic nervous system (SNS) is responsible for fight or flight, and the parasympathetic nervous system (PNS) is responsible for resting and bring the body back to homeostasis (Alshak & Das, 2021).
The first system is the sympathetic nervous system (SNS), which prepares the body to physically react to its environment (Alshak & Das, 2021). When a person is presented with threatening stimuli, the hypothalamus (responsible for reactive emotional response) activates the sympathetic nervous system. The endocrine system has glands that release hormones into our bloodstream, and each hormone has unique characteristics that send signals to the body. The sympathetic nervous system causes adrenal glands to secrete epinephrine (adrenaline), norepinephrine, and cortisol which wakes up the fight or flight response that brings increased blood flow to the body to feel less pain and quickly respond to threatening stimuli. When triggered, the SNS causes an increased heart rate, which creates an upsurge of oxygen in the blood. Digestion in the stomach and intestines decreases so oxygen and blood can go to other parts of the body. The pupils dilate to allow more light in, and fine-tune focus on objects. Blood pressure increases, and the body can begin to sweat and shake (Britannica Editors of Encyclopedia, 2019). The body goes into the survival mode, also known as fight-or-flight (Jansen et al., 1995).
The parasympathetic Nervous System (PNS) brings the body back to homeostasis. The adrenal glands secrete acetylcholine to put the brakes on the SNS. Body temperature cools down, heart rate slows down and blood pressure lowers. The person’s breathing starts to ease back to a regular cycle, pupils constrict, the bladder contracts and the stomach begins digestion again. A healthy body should automatically slip into the parasympathetic nervous system when the sympathetic nervous system runs out of energy. When people have issues with naturally switching to the PNS and are continually triggered into the SNS, it can cause hypertension, obesity, depression, kidney disease, cardiovascular disease, and type 2 diabetes (Fisher et al., 2009; Young & Landsberg, 1982).
How Do We Know This?
The fight-or-flight response to stressful stimuli links us to our ancient ancestors (Britannica Editors of Encyclopedia, 2019). When we feel a present threat, the autonomic nervous system turns on, and the sympathetic nervous system goes to work, secreting hormones, turning certain things on and other things off to protect ourselves from the perceived present danger (Jansen et al., 1995). New findings in research suggest that the fight-or-flight response may not be entirely an autonomic nervous system response (Berger et al., 2019).
Recent research suggests this fight-or-flight emotional instinct is even in our bones (Berger et al., 2019). Columbia University Irving Medical Center’s Dr. Karsenty, a physician and geneticist, studied the hormone osteocalcin found in the skeleton and bloodstream. He accidentally fell upon this hormone when looking at bone calcification (hardening of bone) and found a large amount of osteocalcin present. Humans and mice were tested in stressful situations, and blood levels were measured to determine how much osteocalcin was present. Human participants were asked to give a 10-minute speech, and the rodents were physically restrained for 45-minutes. Both human and rodent subjects showed a surge in osteocalcin in the bloodstream. The fascinating piece about this study is that when the researchers injected osteocalcin into the bloodstream, it did not turn on the SNS but ignited the PNS, decreasing heart rate, thus turning off the autonomic nervous system so another part of the body could take on the fight-or-flight response. In this study, bone, not adrenaline, was taking on the stress response. These new findings open a plethora of questions regarding stress response. There is so much we know about the human body, and even more, we must uncover.
Alshak, M. N., & Das, J. M. (2021). Neuroanatomy, sympathetic nervous system. https://search.ebscohost.com/login.aspx?direct=true&AuthType=ip,sso&db=cmedm&AN=31194352&site=eds-live
American Psychological Association. (n.d.). Canon-bard theory. APA Dictionary of Psychology. https://dictionary.apa.org/cannon-bard-theory
Barret, L. F. (2006). Are emotions natural kinds? Perspectives on Psychological Science, 1(1), 28–58. https://doi.org/10.1111/j.1745-6916.2006.00003.x
Barrett, L. F., Lewis, M. & Haviland-Jones, J. M. (2016). Handbook of emotions (4th ed.). The Guilford Press.
Berger, J. M., Singh, P., Khrimian, L., Morgan, D. A., Chowdhury, S., Arteaga-Solis, E., Horvath, T. L., Domingos, A. I., Marsland, A. L., Yadav, V. K., Rahmouni, K., Gao, X. B., & Karsenty, G. (2019). Mediation of the Acute Stress Response by the Skeleton. Cell metabolism, 30(5), 890–902.e8. https://doi.org/10.1016/j.cmet.2019.08.012
Britannica, T. Editors of Encyclopedia (2019, September 13). Sympathetic nervous system. Encyclopedia Britannica. https://www.britannica.com/science/sympathetic-nervous-system
Cannon, W. (1927). The James-Lange Theory of Emotions: A Critical Examination and an Alternative Theory. The American Journal of Psychology, 39(1/4), 106-124. https://www.jstor.org/stable/1415404?origin=crossref
Fama, R., & Sullivan, E. V. (2015). Thalamic structures and associated cognitive functions: Relations with age and aging. Neuroscience and Biobehavioral Reviews, 54, 29–37. https://doi.org/10.1016/j.neubiorev.2015.03.008
Fisher, J. P., Young, C. N., & Fadel, P. J. (2009). Central sympathetic overactivity: maladies and mechanisms. Autonomic neuroscience: basic & clinical, 148(1-2), 5–15. https://doi.org/10.1016/j.autneu.2009.02.003
Goodman, R. (2017). William james. The Stanford Encyclopedia of Philosophy. https://plato.stanford.edu/entries/james/#PrinPsyc
James, W. (1884). What is an emotion? Mind, 9(34), 188-205. https://doi.org/10.1093/mind/os-IX.34.188
James, W. (1894). Discussion: The physical basis of emotion. Psychological Review, 1(5), 516–529. https://doi.org/10.1037/h0065078
James, W. & Drummond, R. (1890). The principles of psychology. New York: Henry Holt and Company. https://archive.org/details/theprinciplesofp00jameuoft
Jansen, A. S. P., Nguyen, X. V., Karpitskiy, V., Mettenleiter, T. C., & Loewy, A. D. (1995). Central Command Neurons of the Sympathetic Nervous System: Basis of the Fight-or-Flight Response. Science, 270(5236), 644–646. https://search.ebscohost.com/login.aspx?direct=true&AuthType=ip,sso&db=edsgao&AN=edsgcl.17755802&site=eds-live
Levenson, R. W., Ekman, P., & Friesen, W. V. (1990). Voluntary facial action generates emotion-specific autonomic nervous system activity. Psychophysiology, 27(4), 363–384. https://search.ebscohost.com/login.aspx?direct=true&AuthType=ip,sso&db=s3h&AN=11030941&site=eds-live&custid=s1229530
Lindquist, K., Wager, T., Kober, H., Bliss-Moreau, E., & Barrett, L. (2012). The brain basis of emotion: A meta-analytic review. Behavioral and Brain Sciences, 35(3), 121-143. https://www.cambridge.org/core/journals/behavioral-and-brain-sciences/article/brain-basis-of-emotion-a-metaanalytic-review/80F95F093305C76BA2C66BBA48D4BC8A
Marshall, G. D., & Zimbardo, P. G. (1979). Affective consequences of inadequately explained physiological arousal. Journal of Personality and Social Psychology, 37(6), 970–988. https://doi.org/10.1037/0022-35220.127.116.110
Maslach, C. (1979). Negative emotional biasing of unexplained arousal. Journal of Personality and Social Psychology, 37(6), 953–969. https://doi.org/10.1037/0022-3518.104.22.1683
Miller G. A. (2003). The cognitive revolution: a historical perspective. Trends in cognitive sciences, 7(3), 141–144. https://doi.org/10.1016/s1364-6613(03)00029-9
Reisenzein, R. (1983). The Schachter theory of emotion: Two decades later. Psychological Bulletin, 94(2), 239–264. https://doi.org/10.1037/0033-2909.94.2.239
Schachter, S., & Singer, J. (1962). Cognitive, social, and physiological determinants of emotional state. Psychological Review, 69(5), 379–399. https://doi.org/10.1037/h0046234
Schauer, M., & Elbert, T. (2010). Dissociation following traumatic stress. Journal of Psychology, 218(2), 109-127. https://doi.org/10.1027/0044-3409/a000018
Sullivan, L. E. (2009). Cannon-bard theory. SAGE glossary of the social and behavioral sciences 1, 60. https://www.doi.org/10.4135/9781412972024.n289
Young, J. B., & Landsberg, L. (1982). Diet-induced changes in sympathetic nervous system activity: possible implications for obesity and hypertension. Journal of chronic diseases, 35(12), 879–886. https://doi.org/10.1016/0021-9681(82)90118-7
Wu, Y., Gu, R., Yang, Q., & Luo, Y. J. (2019). How do amusement, anger, and fear influence heart rate and heart rate variability? Frontiers in neuroscience, 13, 1131. https://doi.org/10.3389/fnins.2019.01131
Zaragoza Bernal, J. M. (2021). A change of pace: The history of (emotional) experiences. History of Psychology, 24(2), 130–135. https://doi.org/10.1037/hop0000173