Fear: a natural emotional response of the human body to dangerous stimuli. Some people are said to be fearless, but are they really?
Fear is thought of as an evolutionary advantage because it can allow species to avoid danger or prepare the organism to face dangerous stimuli (Garcia, 2017). Fear and the concept of the fight-or-flight response of the sympathetic nervous system can help an organism survive and maintain necessary regulatory functioning. Despite fear having such a critical role and being undoubtedly present throughout our lives, the theories of why we are afraid rely mainly on perfunctory knowledge of the fear circuitry; however, many attempts have been made at developing therapies and drugs to ease the adverse effects of disrupted fear brain circuits, such as through Cognitive Behavioral Therapy (CBT).
The most well-known hypothesis of why we are afraid is the classical conditioning theory proposed by Pavlov. A neutral stimulus itself—let’s say a balloon—does not elicit a fear response. However, when paired with an unconditioned stimulus, such as a loud noise of a balloon popping, it causes a conditioned fear response. Additionally, if we were shown a yellow block every time before the burst of the balloon, despite the two not being directly related, seeing the yellow block itself would eventually frighten us, as we begin to associate it with this loud, sudden noise (UKEssays, 2018).
An interesting idea of acquiring fear and phobias is also presented through the social transmission of fear, a theory that posits that fear can be learned from others (Garcia, 2017). For example, an individual may display the conditioned fear response after watching another subject’s response to an assumed dangerous stimulus. The evolutionary advantage of social transmission of fear helps us avoid trouble and harm, especially in the early years. For instance, by observing the maternal figure, the child learns to avoid touching hot objects. Additionally, the child’s emotions can be modified based on the feelings of the mother, which involves a disrupted regulation of infant emotional circuitry, as well as increased difficulty to calm down after the termination of a distressing stimulus in infants of mothers with PTSD after birth (Bosquet Enlow et al., 2011). The results of the study also suggest possible future problems with mental health among the studied infants. Moreover, the results of a study on twins by Eley et al. have shown that genetic predisposition was not the main cause of children experiencing anxiety when exposed to parental fear. This suggests that environmental factors and social transmission are of significance in establishing the child’s fear response (Eley et al., 2015). However, despite the emerging evidence of the contribution of social transmission of fear to our perception of dangerous stimuli, it is not used widely in research, and scientists tend to refer to other approaches to study fear circuitry in the brain and explain how the fear response is maintained.
The maintenance of acquired fear response is thought to happen through operant conditioning, a theory proposed by leading behavioral psychologist B. F. Skinner. Essentially, behavior that is rewarded will be reinforced and repeated in the future, whereas behavior that is punished tends to decrease the frequency of that behavior. The main contributor to maintaining phobias is negative reinforcement. For example, taking away restrictions when a child behaves in an appropriate way (according to rules) is seen as negative reinforcement—the child is more likely to follow the rules again, as something undesirable is removed (Ackerman, 2022).
Currently, despite the proposed surrounding psychological theory, more research is being done into the neural basis of fear response and phobias, resulting in the identification of several brain regions involved in fear circuitry. The main regions identified, on the basis of studies using classical conditioning to elicit fear, are the amygdala, the hippocampus, and the medial prefrontal cortex (Tovote et al., 2015). The amygdala, as the main emotion processing center in the brain, receives input from various cortical areas as well as the thalamus. At the same time, the neuronal changes related to brain plasticity are controlled by signals from the basal amygdala to the hippocampus and the prelimbic cortex via excitatory pathways (Tovote et al., 2015). Results of fear research have shown that plasticity in the amygdala and the changes following fear response occur first before similar modifications are visible in the higher processing centers like the cortex (Tovote et al., 2015). The permanence of conditioned fear responses relies on synaptic modulation and neuronal plasticity (Tovote et al., 2015). Additional aspects to the research on fear circuits include the role of NMDA glutamate receptors, which, when blocked, result in a decreased fear response or affinity to acquire one (Tovote et al., 2015). However, this idea has yet to be fully characterized, as there is the certainty that many more receptors and circuits contribute to adjacent behavioral responses.
An extreme form of fear response are phobias, which often interfere with our daily life and have an impact on a person’s psychological state. They can be classified as either nonexperiential-specific (caused by genetic predisposition) and experiential-specific (the result of a distressing event) (Garcia, 2017). Nonexperiential-specific phobias can be emphasized by sensitization, which is based on a repeated exposure of a person to the object of their fear in order to amplify the fear response (Perusini et al., 2015). Sensitization is linked to the involvement of the amygdala, which strengthens the anxious and fearful behavior. Phobias without previous conditioning are thought to be caused by a lack of habituation, which results in reduced response to fearful stimulus with time and multiple exposure (Avery & Blackford, 2016; Garcia, 2017). Usually, with a correctly functioning habituation mechanism, the phobia would go away when we realize that the feared stimulus does not cause us any harm. However, as is the case of nonexperiential phobias, the habituation mechanism is disrupted and results in poor genetic component regulation, and therefore, the fear persists.
Experiential-specific phobias are based on decreased efficacy of the extinction mechanism, defined as the fading of conditioned fear as a result of repeated exposure to a conditioned stimulus (Garcia, 2017). Such phobias, which result from a traumatic experience, are thought to have basis in classical conditioning, described previously (Garcia, 2017). Both experiential and non-experiential phobias have been the focus of treatments such as cognitive behavioral therapy, where the patient is exposed to the feared stimulus and is able to discuss their feelings with a therapist. The prescription for drugs, such as antidepressants like SSRIs, can also be obtained to increase the serotonin levels in the synapses between neurons in the brain and therefore alleviate one’s mood and decrease one’s state of anxiety. Additionally, if the fear and panic response is especially strong, tranquilizing medicine may be used to help calm the individual, lowering the heart rate.
From a scientific point of view, it would be very hard to be truly fearless. Feeling fear has given us a big evolutionary advantage and remains heavily conserved because of this. However, following the words of motivational speakers and ‘I am fearless’ affirmations, it is possible to suppress the fear response and not let the emotion overwhelm you, as is often seen in individuals who are exposed to fearful or adrenaline-inducing stimuli—such as first responders. Even though their innate fear circuitry is hard at work, they are able to focus on something else like a momentary distraction or perhaps a bigger fear in order to deflate the fear of a given situation (Ketteler, 2018). Nevertheless, it is important to remember that experiencing fear is a natural and innate part of life, and trying to suppress our sympathetic nervous system in dangerous situations may have unintended consequences.
About the Author
Kaja Posnik is a freshman at University College London, United Kingdom concentrating in Neuroscience.
References
Ackerman, C. E. (2022, March 28). 12 examples of positive punishment & negative reinforcement. PositivePsychology.com. Retrieved April 3, 2022, from https://positivepsychology.com/positive-punishment/
Avery, S. N., & Blackford, J. U. (2016). Slow to warm up: The role of habituation in Social Fear. Social Cognitive and Affective Neuroscience, 11(11), 1832–1840. https://doi.org/10.1093/scan/nsw095
Bosquet Enlow, M., Kitts, R. L., Blood, E., Bizarro, A., Hofmeister, M., & Wright, R. J. (2011). Maternal posttraumatic stress symptoms and infant emotional reactivity and emotion regulation. Infant Behavior and Development, 34(4), 487–503. https://doi.org/10.1016/j.infbeh.2011.07.007
Eley, T. C., McAdams, T. A., Rijsdijk, F. V., Lichtenstein, P., Narusyte, J., Reiss, D., Spotts, E. L., Ganiban, J. M., & Neiderhiser, J. M. (2015). The intergenerational transmission of anxiety: A children-of-twins study. American Journal of Psychiatry, 172(7), 630–637. https://doi.org/10.1176/appi.ajp.2015.14070818
Garcia, R. (2017). Neurobiology of fear and specific phobias. Learning & Memory, 24(9), 462-471. https://doi.org/10.1101/lm.044115.116
Ketteler, J. (2018, December 11). Can we ever be truly fearless? The New York Times. Retrieved March 13, 2022, from https://www.nytimes.com/2018/12/11/well/mind/fear-psychology-trauma-stress.html
Perusini, J. N., Meyer, E. M., Long, V. A., Rau, V., Nocera, N., Avershal, J., Maksymetz, J., Spigelman, I., & Fanselow, M. S. (2015). Induction and expression of fear sensitization caused by acute traumatic stress. Neuropsychopharmacology, 41(1), 45–57. https://doi.org/10.1038/npp.2015.224
Tovote, P., Fadok, J. P., & Lüthi, A. (2015). Neuronal circuits for fear and anxiety. Nature Reviews Neuroscience, 16(6), 317-331. https://doi.org/10.1038/nrn3945
UKEssays. (2018, November). Concepts and Theories of Classical Conditioning. Retrieved April 1, 2022, from https://www.ukessays.com/essays/psychology/concepts-theories-classical-7396.php?vref=1
Fear is thought of as an evolutionary advantage because it can allow species to avoid danger or prepare the organism to face dangerous stimuli (Garcia, 2017). Fear and the concept of the fight-or-flight response of the sympathetic nervous system can help an organism survive and maintain necessary regulatory functioning. Despite fear having such a critical role and being undoubtedly present throughout our lives, the theories of why we are afraid rely mainly on perfunctory knowledge of the fear circuitry; however, many attempts have been made at developing therapies and drugs to ease the adverse effects of disrupted fear brain circuits, such as through Cognitive Behavioral Therapy (CBT).
The most well-known hypothesis of why we are afraid is the classical conditioning theory proposed by Pavlov. A neutral stimulus itself—let’s say a balloon—does not elicit a fear response. However, when paired with an unconditioned stimulus, such as a loud noise of a balloon popping, it causes a conditioned fear response. Additionally, if we were shown a yellow block every time before the burst of the balloon, despite the two not being directly related, seeing the yellow block itself would eventually frighten us, as we begin to associate it with this loud, sudden noise (UKEssays, 2018).
An interesting idea of acquiring fear and phobias is also presented through the social transmission of fear, a theory that posits that fear can be learned from others (Garcia, 2017). For example, an individual may display the conditioned fear response after watching another subject’s response to an assumed dangerous stimulus. The evolutionary advantage of social transmission of fear helps us avoid trouble and harm, especially in the early years. For instance, by observing the maternal figure, the child learns to avoid touching hot objects. Additionally, the child’s emotions can be modified based on the feelings of the mother, which involves a disrupted regulation of infant emotional circuitry, as well as increased difficulty to calm down after the termination of a distressing stimulus in infants of mothers with PTSD after birth (Bosquet Enlow et al., 2011). The results of the study also suggest possible future problems with mental health among the studied infants. Moreover, the results of a study on twins by Eley et al. have shown that genetic predisposition was not the main cause of children experiencing anxiety when exposed to parental fear. This suggests that environmental factors and social transmission are of significance in establishing the child’s fear response (Eley et al., 2015). However, despite the emerging evidence of the contribution of social transmission of fear to our perception of dangerous stimuli, it is not used widely in research, and scientists tend to refer to other approaches to study fear circuitry in the brain and explain how the fear response is maintained.
The maintenance of acquired fear response is thought to happen through operant conditioning, a theory proposed by leading behavioral psychologist B. F. Skinner. Essentially, behavior that is rewarded will be reinforced and repeated in the future, whereas behavior that is punished tends to decrease the frequency of that behavior. The main contributor to maintaining phobias is negative reinforcement. For example, taking away restrictions when a child behaves in an appropriate way (according to rules) is seen as negative reinforcement—the child is more likely to follow the rules again, as something undesirable is removed (Ackerman, 2022).
Currently, despite the proposed surrounding psychological theory, more research is being done into the neural basis of fear response and phobias, resulting in the identification of several brain regions involved in fear circuitry. The main regions identified, on the basis of studies using classical conditioning to elicit fear, are the amygdala, the hippocampus, and the medial prefrontal cortex (Tovote et al., 2015). The amygdala, as the main emotion processing center in the brain, receives input from various cortical areas as well as the thalamus. At the same time, the neuronal changes related to brain plasticity are controlled by signals from the basal amygdala to the hippocampus and the prelimbic cortex via excitatory pathways (Tovote et al., 2015). Results of fear research have shown that plasticity in the amygdala and the changes following fear response occur first before similar modifications are visible in the higher processing centers like the cortex (Tovote et al., 2015). The permanence of conditioned fear responses relies on synaptic modulation and neuronal plasticity (Tovote et al., 2015). Additional aspects to the research on fear circuits include the role of NMDA glutamate receptors, which, when blocked, result in a decreased fear response or affinity to acquire one (Tovote et al., 2015). However, this idea has yet to be fully characterized, as there is the certainty that many more receptors and circuits contribute to adjacent behavioral responses.
An extreme form of fear response are phobias, which often interfere with our daily life and have an impact on a person’s psychological state. They can be classified as either nonexperiential-specific (caused by genetic predisposition) and experiential-specific (the result of a distressing event) (Garcia, 2017). Nonexperiential-specific phobias can be emphasized by sensitization, which is based on a repeated exposure of a person to the object of their fear in order to amplify the fear response (Perusini et al., 2015). Sensitization is linked to the involvement of the amygdala, which strengthens the anxious and fearful behavior. Phobias without previous conditioning are thought to be caused by a lack of habituation, which results in reduced response to fearful stimulus with time and multiple exposure (Avery & Blackford, 2016; Garcia, 2017). Usually, with a correctly functioning habituation mechanism, the phobia would go away when we realize that the feared stimulus does not cause us any harm. However, as is the case of nonexperiential phobias, the habituation mechanism is disrupted and results in poor genetic component regulation, and therefore, the fear persists.
Experiential-specific phobias are based on decreased efficacy of the extinction mechanism, defined as the fading of conditioned fear as a result of repeated exposure to a conditioned stimulus (Garcia, 2017). Such phobias, which result from a traumatic experience, are thought to have basis in classical conditioning, described previously (Garcia, 2017). Both experiential and non-experiential phobias have been the focus of treatments such as cognitive behavioral therapy, where the patient is exposed to the feared stimulus and is able to discuss their feelings with a therapist. The prescription for drugs, such as antidepressants like SSRIs, can also be obtained to increase the serotonin levels in the synapses between neurons in the brain and therefore alleviate one’s mood and decrease one’s state of anxiety. Additionally, if the fear and panic response is especially strong, tranquilizing medicine may be used to help calm the individual, lowering the heart rate.
From a scientific point of view, it would be very hard to be truly fearless. Feeling fear has given us a big evolutionary advantage and remains heavily conserved because of this. However, following the words of motivational speakers and ‘I am fearless’ affirmations, it is possible to suppress the fear response and not let the emotion overwhelm you, as is often seen in individuals who are exposed to fearful or adrenaline-inducing stimuli—such as first responders. Even though their innate fear circuitry is hard at work, they are able to focus on something else like a momentary distraction or perhaps a bigger fear in order to deflate the fear of a given situation (Ketteler, 2018). Nevertheless, it is important to remember that experiencing fear is a natural and innate part of life, and trying to suppress our sympathetic nervous system in dangerous situations may have unintended consequences.
About the Author
Kaja Posnik is a freshman at University College London, United Kingdom concentrating in Neuroscience.
References
Ackerman, C. E. (2022, March 28). 12 examples of positive punishment & negative reinforcement. PositivePsychology.com. Retrieved April 3, 2022, from https://positivepsychology.com/positive-punishment/
Avery, S. N., & Blackford, J. U. (2016). Slow to warm up: The role of habituation in Social Fear. Social Cognitive and Affective Neuroscience, 11(11), 1832–1840. https://doi.org/10.1093/scan/nsw095
Bosquet Enlow, M., Kitts, R. L., Blood, E., Bizarro, A., Hofmeister, M., & Wright, R. J. (2011). Maternal posttraumatic stress symptoms and infant emotional reactivity and emotion regulation. Infant Behavior and Development, 34(4), 487–503. https://doi.org/10.1016/j.infbeh.2011.07.007
Eley, T. C., McAdams, T. A., Rijsdijk, F. V., Lichtenstein, P., Narusyte, J., Reiss, D., Spotts, E. L., Ganiban, J. M., & Neiderhiser, J. M. (2015). The intergenerational transmission of anxiety: A children-of-twins study. American Journal of Psychiatry, 172(7), 630–637. https://doi.org/10.1176/appi.ajp.2015.14070818
Garcia, R. (2017). Neurobiology of fear and specific phobias. Learning & Memory, 24(9), 462-471. https://doi.org/10.1101/lm.044115.116
Ketteler, J. (2018, December 11). Can we ever be truly fearless? The New York Times. Retrieved March 13, 2022, from https://www.nytimes.com/2018/12/11/well/mind/fear-psychology-trauma-stress.html
Perusini, J. N., Meyer, E. M., Long, V. A., Rau, V., Nocera, N., Avershal, J., Maksymetz, J., Spigelman, I., & Fanselow, M. S. (2015). Induction and expression of fear sensitization caused by acute traumatic stress. Neuropsychopharmacology, 41(1), 45–57. https://doi.org/10.1038/npp.2015.224
Tovote, P., Fadok, J. P., & Lüthi, A. (2015). Neuronal circuits for fear and anxiety. Nature Reviews Neuroscience, 16(6), 317-331. https://doi.org/10.1038/nrn3945
UKEssays. (2018, November). Concepts and Theories of Classical Conditioning. Retrieved April 1, 2022, from https://www.ukessays.com/essays/psychology/concepts-theories-classical-7396.php?vref=1
