Subjects: Other Disciplines >> Synthetic discipline submitted time 2023-10-09 Cooperative journals: 《心理科学进展》
Abstract： Stress contagion refers to the phenomenon where people unconsciously absorb stress reactions from another individual in the stressed state, through observation or direct contact, and match their own physiological and psychological state to that individual. In experimental settings, individuals who experience stress are commonly referred to as demonstrators, while those who observe the demonstrator undergoing stress are referred to as observers. Sensory channels are important factors that influence the process of stress contagion, as different sensory channels transmit social information in varying ways. The experimental paradigm for stress contagion can be categorized into two types: vicarious stress and stress crossover. In the vicarious stress paradigm, the observer receives stress information transmitted by the demonstrator through one or multiple sensory channels, such as images, sounds, or pheromones that are emitted by the stressed demonstrator. In the stress crossover paradigm, the observer comes into direct contact with the demonstrator and receives stress information through multiple sensory channels after the demonstrator undergoes stress. Studies have found that different sensory information elicits similar behavioral responses during stress contagion, which are accompanied by decreased autonomic activity, increased anxiety-like behavior, and elevated cortisol levels. However, the underlying neural circuit and key regions differ depending on the type of sensory information. In stress contagion induced by visual information, the anterior cingulate cortex and insular cortex play crucial roles as key brain regions. On the other hand, in stress contagion induced by auditory information, the basolateral amygdala and periaqueductal gray are the key brain regions involved. The olfactory system's primary receptors that receive stress pheromones are the grueneberg ganglion cell, while the basolateral amygdala and medial prefrontal cortex are the key areas responsible for stress transmission. Additionally, significant activation of the amygdala was observed in different types of stress contagion paradigms, suggesting that the amygdala may be a hotspot brain region for stress contagion. To date, no studies have investigated stress contagion induced by touch alone, and future research should explore the neural mechanisms underlying touch-induced stress contagion by developing new experimental paradigms. Additionally, future studies should aim to identify the specific brain regions that should be investigated based on the sensory channels that influence the neural mechanisms of stress contagion.
Subjects: Psychology >> Physiological Psychology submitted time 2023-06-19
Abstract： Stress contagion refers to the phenomenon where people unconsciously absorb stress reactions from another individual in the stressed state, through observation or direct contact, and match their own physiological and psychological state to that individual. The experimental paradigm for stress contagion can be categorized into two types: vicarious stress and stress crossover. In vicarious stress paradigms, the observer receives stress information transmitted through one or more sensory channels from a demonstrator. In stress crossover paradigms, the observer comes into direct contact with the demonstrator after they have experienced stress, receiving stress information through multiple sensory channels. The behavioral responses elicited by different sensory information exhibit similarities, such as decreased autonomic activity, increased anxiety-like behavior and elevated cortisol levels. The neural circuit and key brain regions involved are not entirely consistent across all sensory channels. However, stress contagion effects tend to be stronger when multiple sensory channels are involved compared to single sensory channels (visual, auditory, or olfactory). The amygdala has been identified as a central brain region for stress contagion, consistently demonstrating significant activation across various stress contagion paradigms. In future studies, it is crucial for researchers to carefully consider the experimental paradigms employed in studying stress contagion and identify specific brain regions of interest based on the underlying neural mechanisms associated with stress contagion effects induced by different sensory channels.
Subjects: Psychology >> Social Psychology submitted time 2023-03-28 Cooperative journals: 《心理科学进展》
Abstract： One of the core symptoms of autism spectrum disorder（ASD）is persistent social dysfunction. The severity of symptoms varies from patient to patient, and there are many different clinical manifestations, such as depression, anxiety, sleep disorders and ADHD. About 30 percent of people with ASD require psychotherapy and psychiatric care, including medication for behavioral problems. In recent years, many studies have indicated that tactile input can affect social function through regulating the oxytocin system. The affective touch conducted by C-fiber promotes the synthesis and release of oxytocin and enhances social motivation and social preference. And the social salience hypothesis of oxytocin hypothesizes that oxytocin regulates the attention orientation of individuals to social information cues in external situations. For example, oxytocin may enhance aggression and competitiveness of individuals in competitive situations while enhance cooperation in social situations. According to the social salience hypothesis of oxytocin, oxytocin increases the salience of social information through enhancing activation of corresponding brain regions. Under this theoretical framework, when social interaction happens, tactile input can enhance the synthesis and release of oxytocin, and oxytocin can also increase the salience of tactile information, which further promotes the occurrence of social interaction. Previous studies have shown that people with ASD have deficits in the oxytocin system. The main manifestations are lower peripheral oxytocin concentration than normal developing individuals and the change of Single Nucleotide Polymorphism（SNP）of oxytocin receptor. People with ASD also show abnormal tactile sensitivity, including hypersensitivity and hyposensitivity. At the peripheral level, they manifest abnormal tactile threshold. At the central level, they manifest abnormal activation in the brain’s affective touch processing regions (such as insula). Compared with typical development, people with ASD show lower activation in social brain network, which maybe is the one reason of abnormal tactile sensitivity. Moderate tactile input can promote the synthesis and release of oxytocin. Thus, we can combine the exogenous oxytocin treatment with auxiliary tactile training together in the future intervening measures. And the interventions for social dysfunction need to start as early as possible. Many people with ASD exhibit abnormal sensory sensitivity in early life, which can affect the quality of parent-child interactions. If infant cannot obtain adequate sensory input from early parent-child interaction, it will cause a growth environment similar to sensory deprivation for infant patients with ASD, which will seriously affect future social functioning in adulthood. Based on the social salience hypothesis of oxytocin, this article summarizes the possible regulations between touch and oxytocin on social function. We point out that the deficits in the oxytocin system can decrease the salience of touch information in people with ASD, reducing the attention resources in social interaction and affecting the emotional feelings for touch. Abnormal tactile sensitivity results in social avoidance, which decreases the synthesis and release of oxytocin in social contact, decreasing the social motivation and social preference, ultimately resulting in social dysfunction. Exploring the interaction between touch, oxytocin system and social function can help us understand the pathogenesis of social dysfunction, and providing new ideas for the prevention and intervention in the future.
submitted time 2023-03-25 Cooperative journals: 《心理科学进展》
Abstract： One of the core symptoms of autism spectrum disorder（ASD）is persistent social dysfunction. The severity of symptoms varies from patient to patient, and there are many different clinical manifestations, such as depression, anxiety, sleep disorders and ADHD. About 30 percent of people with ASD require psychotherapy and psychiatric care, including medication for behavioral problems. In recent years, many studies have indicated that tactile input can affect social function through regulating the oxytocin system. The affective touch conducted by C-fiber promotes the synthesis and release of oxytocin and enhances social motivation and social preference. And the social salience hypothesis of oxytocin hypothesizes that oxytocin regulates the attention orientation of individuals to social information cues in external situations. For example, oxytocin may enhance aggression and competitiveness of individuals in competitive situations while enhance cooperation in social situations. According to the social salience hypothesis of oxytocin, oxytocin increases the salience of social information through enhancing activation of corresponding brain regions. Under this theoretical framework, when social interaction happens, tactile input can enhance the synthesis and release of oxytocin, and oxytocin can also increase the salience of tactile information, which further promotes the occurrence of social interaction. Previous studies have shown that people with ASD have deficits in the oxytocin system. The main manifestations are lower peripheral oxytocin concentration than normal developing individuals and the change of Single Nucleotide Polymorphism（SNP）of oxytocin receptor. People with ASD also show abnormal tactile sensitivity, including hypersensitivity and hyposensitivity. At the peripheral level, they manifest abnormal tactile threshold. At the central level, they manifest abnormal activation in the brain’s affective touch processing regions (such as insula). Compared with typical development, people with ASD show lower activation in social brain network, which maybe is the one reason of abnormal tactile sensitivity. Moderate tactile input can promote the synthesis and release of oxytocin. Thus, we can combine the exogenous oxytocin treatment with auxiliary tactile training together in the future intervening measures. And the interventions for social dysfunction need to start as early as possible. Many people with ASD exhibit abnormal sensory sensitivity in early life, which can affect the quality of parent-child interactions. If infant cannot obtain adequate sensory input from early parent-child interaction, it will cause a growth environment similar to sensory deprivation for infant patients with ASD, which will seriously affect future social functioning in adulthood. Based on the social salience hypothesis of oxytocin, this article summarizes the possible regulations between touch and oxytocin on social function. We point out that the deficits in the oxytocin system can decrease the salience of touch information in people with ASD, reducing the attention resources in social interaction and affecting the emotional feelings for touch. Abnormal tactile sensitivity results in social avoidance, which decreases the synthesis and release of oxytocin in social contact, decreasing the social motivation and social preference, ultimately resulting in social dysfunction. Exploring the interaction between touch, oxytocin system and social function can help us understand the pathogenesis of social dysfunction, and providing new ideas for the prevention and intervention in the future.
Subjects: Psychology >> Physiological Psychology Subjects: Psychology >> Medical Psychology submitted time 2022-12-28
Abstract：
One of the core symptoms of autism spectrum disorder (ASD)is persistent social dysfunction. In recent years, many studies have indicated that tactile input can affect social function through regulating the oxytocin system. The affective touch conducted by C-fiber promotes the synthesis and release of oxytocin and enhances social motivation and social preference. According to the social salience hypothesis of oxytocin, oxytocin increases the salience of social information through enhancing activation of corresponding brain regions. Under this theoretical framework, when social interaction happens, tactile input can enhance the synthesis and release of oxytocin, and oxytocin can also increase the salience of tactile information, which further promotes the occurrence of social interaction. Previous studies have shown that people with ASD have deficits in the oxytocin system. The main manifestations are lower peripheral oxytocin concentration than normal developing individuals and the change of Single Nucleotide Polymorphism (SNP)of oxytocin receptor. People with ASD also show abnormal tactile sensitivity, including hypersensitivity and hyposensitivity. At the peripheral level, they manifest abnormal tactile threshold. At the central level, they manifest abnormal activation in the brain’s affective touch processing regions (such as insula). Based on the social salience hypothesis of oxytocin, this article summarizes the possible regulations between touch and oxytocin on social function. We point out that the deficits in the oxytocin system can decrease the salience of touch information in people with ASD, reducing the attention resources in social interaction and affecting the emotional feelings for touch. Abnormal tactile sensitivity results in social avoidance, which decreases the synthesis and release of oxytocin in social contact, decreasing the social motivation and social preference, ultimately resulting in social dysfunction. Exploring the interaction between touch, oxytocin system and social function can help us understand the pathogenesis of social dysfunction, and providing new ideas for the prevention and intervention in the future.
Peer Review Status:
Awaiting Review
Hits
YES
Hits
Downloads
Comment