What is Social Inhibition?

Introduction

Social inhibition is a conscious or subconscious avoidance of a situation or social interaction.

With a high level of social inhibition, situations are avoided because of the possibility of others disapproving of their feelings or expressions. Social inhibition is related to behaviour, appearance, social interactions, or a subject matter for discussion. Related processes that deal with social inhibition are social evaluation concerns, anxiety in social interaction, social avoidance, and withdrawal.

Also related are components such as cognitive brain patterns, anxious apprehension during social interactions, and internalising problems. It also describes those who suppress anger, restrict social behaviour, withdraw in the face of novelty, and have a long latency to interact with strangers. Individuals can also have a low level of social inhibition, but certain situations may generally cause people to be more or less inhibited. Social inhibition can sometimes be reduced by the short-term use of drugs including alcohol or benzodiazepines.

Major signs of social inhibition in children are cessation of play, long latencies to approaching the unfamiliar person, signs of fear and negative affect, and security seeking. Also in high level cases of social inhibition, other social disorders can emerge through development, such as social anxiety disorder and social phobia.

Background

Social inhibition can range from normal reactions to social situations to a pathological level, associated with psychological disorders like social anxiety or social phobia. Life events are important and are related to our well-being and inhibition levels. In a lab study conducted by Buck and colleagues, social inhibition in everyday life was reviewed. Researchers observed how individuals interacted and communicated about different stimuli. In this study, there were female participants called “senders” who viewed twelve emotionally loaded stimuli. There were also participants in the study called “received” who had to guess which stimuli was viewed by the senders. The senders were either alone, with a friend, or with a stranger while viewing the slides. The results of the study revealed that being with a stranger had inhibitory effects on communication, whereas being with a friend had facilitative effects with some stimuli and inhibitory effects with others. The results show how anyone can be inhibited in daily life, with strangers or even friends. Inhibition can also be determined by one’s sensitivity levels to different social cues throughout the day. Gable and colleagues conducted a study in which they examined different events participants would record at the end of their day. Participants were also measured on the behavioural activation system and the behavioural inhibition system. The results revealed that individuals with more sensitivity on the behavioural inhibition system reported having more negative effects from daily events.

Expression can also be inhibited or suppressed because of anxiety to social situations or simple display rules. Yarczower and Daruns’ study about social inhibition of expression defined inhibition of expression as a suppression of one’s facial behaviour in the presences of someone or a perceived anxious situation. They addressed the display rules we all learn as children; we are told what expressions are suitable for what situations. Then as age increases we are socialised into not expressing strong facial emotions. However, leaving the face with a reduced expression hinders communication. In turn this makes the face a less reliable social cue during social interactions. Friedmen and Miller-Herringer bring these nonverbal expressions to the next level by studying individuals that have a greater level of emotional suppression. They state that without proper emotional expression social interactions can be much more difficult because others may not understand another individual’s emotional state.

This being said, there are also four commonly seen irrational cognitive patterns involved in social inhibition. The first pattern centres on self-esteem and perfectionism. In these cases, an individual would inhibit themselves through self-criticism; they want to do everything the “right” way. The second pattern deals with unrealistic approval needs; here individuals want to gain the approval of others and will fear rejection if they express too much. In the third pattern, unrealistic labelling of aggressive and assertive behaviour depicts how many individuals that inhibit themselves may feel as though aggression or assertiveness is bad. They believe if they express these behaviours they will receive a negative label. The last pattern discusses criticism of others, this pattern is a spin-off from the first. They will be highly critical of others much like they are to themselves. Shyness is another factor that is a part of social inhibition. Shyness is associated with low emotional regulations and high negative emotions. In many cases shy individuals have a greater change of social inhibition.

Although social inhibition is a common part of life, individuals can also have high levels of inhibition. Social Inhibition on higher levels can sometimes be a precursor to disorders such as Social Anxiety Disorder. Essex and colleagues found that some early risk factors may play a role in having chronically high inhibition. In this study, mothers, teachers, and the child reported on the child’s behavioural inhibition. The factors that were found to be contributors to social inhibition were female gender, exposure to maternal stress during infancy and the preschool period, and early manifestation of behavioural inhibition. In severe cases, clinical treatment, such as therapy, may be necessary to help with social inhibition or the manifesting social disorder.

Over the Lifespan

Social inhibition can develop over a lifespan. Children can be withdrawn, adolescents can have anxiety to social situations, and adults may have a hard time adjusting to social situations which they have to initiate on their own. To be inhibited can change and be different for many. In many cases, inhibition can lead to other social disorders and phobias.

Infants and Children

In infants and children, social inhibition is characterised by a temperament style that will have children responding negatively and withdrawing from unfamiliar people, situations and objects. In addition to cessation of play, inhibited children may display long latencies to approaching an unfamiliar person, signs of fear and negative affect, and security seeking. Avoiding behaviour can be seen at a very young age. In one study, Fox and colleagues found that even at four months of age some infants had negative responses to unfamiliar visual and audio stimuli. The study was longitudinal; therefore, follow ups revealed that half the infants who had high negative responses continued to show behavioural inhibition through the age of two. Fox’s longitudinal study reported that the expression of behavioural inhibition showed a small degree of continuity. Over time, the toddlers who were quiet and restrained continued the trend into childhood by being cautious, quiet, and socially withdrawn. The uninhibited control group of the same ages continued to interact easily with unfamiliar people and situations. There has also been a link between inhibition at childhood age with social disorders in adolescents and adulthood. Schwartz and Kagan found that in a longitudinal study from ages two to thirteen, sixty-one percent of teens who had inhibitor traits as toddlers reported social anxiety symptoms as adolescents, compared to twenty-seven percent of adolescents who were uninhibited in earlier life. However, not every child that has some withdrawn or inhibited behaviour will be inhibited as an adolescent or manifest a social disorder.

The caregiver alone is not solely responsible for inhibition in children; however, in some cases it can be a factor. Caregivers can affect the inhibition levels of their child by exposing the child to maternal stress during infancy and the preschool period. In addition, in some situations the child may simply have early manifestation of behavioural inhibition. There seems to be no parenting style that researchers agree on to be the best to combat social inhibition. Park and Crinic say that a sensitive, accepting, overprotective parenting is best to reduce the negative behaviours because it will allow the child to be themselves without judgement. However, Kagan hypothesized that firm parenting styles are better suited for socially inhibited children. Researchers supporting sensitive parenting believe that too firm of a parenting style will send a message to children that says they need to change.

Adolescence

Social inhibition has been widely studied in children; however, research on how it develops through adolescence and adulthood is not as prevalent, although anxiety-related social problems are most commonly seen in adolescents. Many of the behavioural traits are the same in adolescence as they are in childhood: withdrawing from unfamiliar people, situations and objects. However, it has been tested that adolescents are more aware of their social situations and are more likely to be inhibited in public settings. Researchers found younger individuals to be more likely to differentiate between public and private settings when inquiring about potentially embarrassing issues. It is also thought that inhibition is in many ways addressed in childhood and adolescence simply because schools facilitate interactions with others. As an adult, the same facilitating circumstance may not occur unless the individual prompts them on their own. Gest states that adults do not have as many casual peer interactions and friendship opportunities that guide and support relationships unless they facilitate them on their own. Adolescent research has also shown that social inhibition is associated with a more negative emotional state in young men than women.

This is in contrast to a study that measured inhibition levels through self reports from the adolescent and their parents. West and Newman found that young American Indian women and their parents reported higher levels of inhibition than young American Indian men; in addition, the parental reports also predicted social anxiety in young American Indian women over young American Indian men. In this same study, relationship development with peers was investigated over time. West and Newman stated that low levels of behavioural inhibition had an association with early social and school situations and that were related to greater levels of socially mediated anxiety, especially negative evaluation of fear by peers. This study then speculates about the possibility that adolescents and children who have a generally positive social experience will be more aware of the status of these positive relationships, therefore more anxious about failure in their social domain. Other studies also discussed how in many cases, early behavioural inhibition is a risk factor for the development of chronic high school-age inhibition and possible social anxiety disorder. Although social inhibition can be a predictor of other social disorders there is not an extremely large portion of adolescents who have developed an anxiety disorder and also had a history of inhibition in childhood.

Besic and Kerr believes that appearance can be a factor for social inhibition. In their study they hypothesized that a way to handle difficult situations with behavioural inhibition was to present an off-putting appearance. They examined “radical” crowds, such as those labelled as goths and punks and if their appearances fulfilled a functions for their inhibition. They state that a radical style could be used to draw away the social boundaries and relieve them of pressures or expectations to interact in unfamiliar situations with unfamiliar peers. Another possibility is that an individual may be self-handicapping to ensure that they will not have to interact with unfamiliar peers. The results revealed that radicals were significantly more inhibited than other groups. However, there are other inhibited individuals in other social classifications. The highest inhibited radical was no more inhibited than the highest inhibited individual in other groups.

Adulthood

Adult cases of social inhibition are hard to come by simply because many see it as something that happens through development. Although research is lacking, developmental considerations suggest there may be a stronger association between behavioral inhibition and peer relations in adulthood. One researcher says this lack of information may be because adults are not put in as many socially interactive situations that would guide them through the situation. It would seem that adults have an increased responsibility to initiate or structure their own social peer relationships; this is where social inhibition could have a more problematic role in adulthood than in childhood. One study that did contribute to adult research used questionnaires to study both clinical and nonclinical adults. Like in adolescence, behavioral inhibition was also found to be associated with anxiety disorders in adulthood. In addition the study found that childhood inhibition was specifically a factor in a lifetime diagnosis of social phobia. Gest also measured adult peer relations, and to what degree they had a positive and active social life. For example, researchers wanted to know if they participated in any recreational activities with others, how often they met with others, and if they had any close confiding relationships. The participants were rated on a 5-point scale on each peer relationship they disclosed. The results revealed that social inhibition had nothing to do with popularity, however it was correlated with peer relations in both genders and emotional stress in only men.

A similar study found that some shy men had a low occupational status at age forty because they entered their career later in life. However, another researcher has commented on this giving this example, perhaps remaining at home longer allows young adults to accumulate educational and financial resources, before moving out and becoming more independent. Additionally it was found that young adults who were inhibited as children were less likely to move away from their families. There is also some discussion of the inhibition through generations and children mirroring their parents. Results indicated that children whose birth mothers met criteria for the diagnosis of social phobia showed elevated levels of observed behavioural inhibition. Social inhibition can decrease with age due to cognitive deficits that can occur in old age. Age-related deficits have an effect on older adults’ ability to differentiate between public and private settings when discussing potentially embarrassing issues, leading them to discuss personal issues in inappropriately public situations. This suggests that deficits in inhibitory ability that lead to inappropriateness are out of the individual’s control.

In Different Contexts

In Schools

Schools can be a place for children to facilitate different social interactions; however, it can also uncover social and school adjustment problems. Coplan claims that Western children with inhibition problems may be at a higher risk of developmental problems in school. Although social inhibition may be a predictor of social and school adjustment problems in children, Chen argues that the effect of social inhibition on school adjustment differs between Western cultures and Chinese culture. Chen found that in Chinese children, behavioural inhibition was associated with greater peer liking, social interaction, positive school attitudes, and school competence and fewer later learning problems, which is also different from western cultures. In other studies, researchers such as Oysterman found there to be difficulties in adjustment in children that were experiencing inhibition. In Western cultures, these difficulties are seen more because of the emphasis on social assertiveness and self-expression as traits that are valued in development. In other cultures children are sometimes expected to be inhibited. This does not contrast with other cultures in which children are socialised and assert themselves. Despite these differences there are also similarities between gender. Boys were more antagonistic in peer interaction and seemed to have more learning problems in school. Girls were more cooperative in peer interaction and had a more positive outlook on school. They formed more affiliations with peers, and performed more completely in school.

Other researchers like Geng have looked to understand social inhibition, effortful control, and attention in school. In Geng’s study, gender came in to play with high socially inhibited girls being extremely aware of their surroundings, possibly paying too much attention to potentially anxious situations. It is well known in a large number of research studies social inhibition had been linked to other anxiety disorders. However Degnan and colleagues believe that being able to regulate your effortful control may serve to reduce the anxiety the comes from inhibition. Nesdale and Dalton investigated inhibition of social group norms in school children between the ages of seven and nine. In schools there becomes an increase in social in-groups and out-groups as children increase in age. This study created different in-groups or exclusive groups and out-groups or inclusive groups. The results showed that students in the inclusive group liked all students more, while students in the exclusive group like their group over other groups. This study could help in the future to facilitate school peer groups more efficiently.

In the Workplace

Social inhibition can manifest in all social situations and relationships. One place that we can see the effects of social inhibition is in the workplace. Research has shown that social inhibition can actually affect the way that one completes a given amount of work. In one experiment, participants completed a task in a laboratory setting, varying whether or not another individual was present in the room with the participants while they attempted to complete the task. The results showed that when another individual was present in the room the person focused on completing the experimental task decreased their body movements, hand movements, and vocalisation, even though the other person did not speak to or even look at the participant. This suggests that just the mere presence of another person in a social situation can inhibit an individual. However, although the individual in charge of completing the experimental task was socially inhibited by the presence of another person in the laboratory, there were no significant links between their social inhibition when completing the task and improved performance on said task. These findings suggest that an individual may socially inhibit themselves in the work place if another person is also in the room, however, such inhibition does not suggest that the inhibited individual is actually performing the duties assigned to them with more accuracy or focus.

In Psychological Disorders

Depression

Links between social inhibition and depression can be found in individuals who experienced social inhibited behaviours during childhood. Researchers from the UK conducted a study in an attempt to explain possible links between social inhibition in infancy and later signs of depression. The researchers based their study on previous information from literature acknowledging that there are social and non-social forms of inhibition, and that social inhibition is significantly related to early social fears. The researchers hypothesized that social inhibition in childhood would be linked to higher levels of depression in later years. Participants completed a number of questionnaires about their experiences of social inhibition in childhood and their current levels of depression. Results showed a significant relationship between depression and recalled social fears, or, social inhibitions during childhood. Furthermore, the researchers related their findings to another study conducted by Muris et al., in 2001 which found that there is an association between social inhibition and depression in adolescents. The study compared adolescents who were not inhibited to those who are, and found that:

“adolescents experiencing high levels of behavioral inhibition were more depressed than their counterparts who experienced intermediate or low levels of behavioral inhibition”.

Another study set out to examine the link between social inhibition and depression, with the basis for their study being that social inhibition (which they explain as a part of type D personality, or distressed personality) is related to emotional distress. The researchers explain that a major factor related to social inhibition is the inhibited individual not expressing their emotions and feelings, a factor that the researchers cite in relation to the link between social inhibition and depression. Overall, the results of the study show that social inhibition (as a factor of type D personality) predicts depression, regardless of the baseline depression level of the individual. Significantly, this study was conducted with young, healthy adults, as opposed to working with those in self-help groups or with individuals who have a pre-existing medical or psychological condition.

Fear

Social inhibition can be affected by fear responses that one has in the early “toddler years” of their life. In 2011, researchers Elizabeth J. Kiel and Kristin A. Buss examined “how attention toward an angry-looking gorilla mask in a room with alternative opportunities for play in 24-month-old toddlers predicted social inhibition when children entered kindergarten”. In the study, the researchers specifically looked at the toddlers’ attention to threat and their fear of novelty in other situations. The researchers paid special attention to these two factors due to previous research suggesting that “sustained attention to putatively threatening novelty relates to anxious behavior in the first 2 years of life”. Also, it has been found in earlier research conducted by Buss and colleagues that no matter the differences, individual responses to novelty during early childhood can be related to later social inhibition. These results already link fear responses, particularly in children, to social inhibition, mainly such inhibition that manifests later on in the individual’s life. Overall, the researchers based their experiment on the notion that the more time a toddler spends being attentive towards a novel potential threat the greater the chance that they will experience issues with the regulation of distress, which can predict anxious behaviour such as social inhibition.

Through a study intended to further connect and understand links between fear and late social inhibitions, the researchers conducted a study where they worked with 24-month-old toddlers. They placed the toddlers in a room called the “risk room” which is set up with a number of play areas for the toddlers to interact with, with one of those areas being a potentially threatening stimulus, in this case, an angry looking gorilla mask. The children are left alone, with only their primary caregiver sitting in the corner of the room, to explore the play areas for three minutes, and then the experimenter returns and instructs the toddler to interact with each of the play areas. The purpose of this was to allow for other experimenters to code the reactions of the toddler to the stimuli around him or her, paying special attention to their attention to threat, their proximity to the threat, and their fear of novelty.

The results of this study indicate that attention to threat (attention given, by the toddler to the feared stimuli) predicts social inhibition in kindergarten. Further, if the child approaches the feared stimuli, the relation to later social inhibition is not significant. When a child’s behaviour is to keep more than two feet away from the threatening stimulus, their behaviour can be seen as linked to later social inhibition. Another important factor that the researchers found when looking at the prediction of social inhibition is the child paying a significant amount of attention to a feared or threatening stimuli in the presence of other, enjoyable activities. Mainly, if the child’s duration of attention to the threatening stimuli is significant even when there are other enjoyable activities available for them to interact with, the link to later social inhibition is stronger due to the fact that “toddler-aged children have increased motoric skill and independence in exploring their environments; so they are capable of using more sophisticated distraction techniques, such as involvement with other activities”.

In another study looking at social inhibition and fear, the researchers made the distinction between different forms of inhibition. Mainly looking at behavioural inhibition the researchers separated the category into two subcategories, social behavioural inhibition and non-social behavioural inhibition. The researchers cite an experiment conducted by Majdandzic and Van den Boom where they used a laboratory setting to attempt to elicit fear in the children. They did this by using both social and non-social stimuli. What Majdandizic and Van der Boom found was a variability in the way that fear was elicited in the children when using either the social or non-social stimuli. Essentially, this study realised that there is a correlation between social stimuli producing fear expressions in children, whereas non-social stimuli is not correlated to fear. This can be evidence of social inhibition due to the social stimuli that result in fear expressions in children.

The researchers of the current study took the results from the Majdandizic and Van der Boom study and expanded on their work by looking at variability in fear expressions in both socially inhibited children and non-socially inhibited children. What they found was that mainly socially inhibited children have effects such as shyness and inhibition with peers, adults, and in performance situations, as well as social phobia and separation anxiety. The stronger link with fear reactions comes mainly from those children who were non-socially behaviourally inhibited. While these results go against previous findings, what the researchers were eager to stipulate was that “the normative development of fear in children have indicated that many specific fears (e.g. fear of animals) decline with age, whereas social fears increase as children get older”.

Social Phobia

Social inhibition is linked to social phobia, in so much as social inhibition during childhood can be seen as a contributing factor to developing social phobia later on in life. While social inhibition is also linked to social anxiety, it is important to point out the difference between social anxiety and social phobia. Social anxiety is marked by a tendency to have high anxiety before a social interaction, but not experience the avoidance of the social activity that is associated with social phobia. Social phobia and social inhibition are linked in a few different ways, one being physiologically. When one is experiencing extreme levels of inhibition they can suffer from symptoms such as accelerated heart rate, increased morning salivary cortisol levels, and muscle tension in their vocal cords. These symptoms are also reported by those with social phobia, which indicates that both social inhibition and social phobia interact with the sympathetic nervous system when the individual encounters a stressful situation.

Further, it is suggested throughout literature that social inhibition during childhood is linked to later social phobia. Beyond that research has indicated that continuity in inhibition plays an important role in the later development of social phobia. Continuity of social inhibition means someone experiencing social inhibition for a number of year continuously. The research explains work done with young teenagers, which found that the teenagers who had been classified as inhibited 12 years earlier were significantly more likely to develop social phobia than young teenagers who were not classified as inhibited. This research pertains to the link between social inhibition and generalised social phobia, rather than specific phobias. When looking at continuity in social inhibition some research offers reasoning as to why the social inhibition may continue long enough to be a predictor of social phobia. Researchers have suggested that if the early childhood relationships are not satisfactory they can influence the child to respond to situations in certain inhibitory ways. When this happens it is often then associated with poor self-evaluation for the child, which can lead to increased social inhibition and social phobia. Also, if a child is neglected or rejected by their peers, rather than by their caregiver, they often develop a sense of social failure, which often extends into social inhibition, and later social phobia. The link between social inhibition and social phobia is somewhat exclusive, when testing for a possible link between non-social inhibition and social phobia no predictive elements were found. It is particularly social inhibition that is linked to social phobia.

The research also suggests that social inhibitions can be divided between different kinds of social fears, or different patterns of inhibition can be seen in individuals. The researchers suggest that certain patterns, or certain social fears, can be better predictors of social phobia than others. Mainly, the researchers suggest that there can be different patterns of social inhibition in relation to an unfamiliar object or encounter. These specific patterns should be looked at in conjunction with motivation and the psychophysiological reaction to the object or encounter to determine the specific patterns that are the better predictors of social phobia.

Another study aimed to examine the link between social inhibition and social phobia also found that social phobia is linked to the social phobic being able to recall their own encounters with social inhibition during childhood. The social phobic participants were able to recall social and school fears from their childhood, but they also were able to recall sensory-processing sensitivity which indicates that the social phobic participants in the study were able to recall having increased sensitivity to the situations and behaviours around them.

Another study explains that social phobia itself has a few different ways it can manifest. The study aims at understanding the link between social inhibition and social phobia, as well as depression in social phobia. What the study found was an important link connecting the severity of social inhibition during childhood to the severity of social phobia and factors of social phobia in later years. Severe social inhibition during childhood can be related to lifetime social phobia. Further, the researchers point out that inhibition during childhood is significantly linked to avoidant personality disorder in social phobia as well as childhood inhibition linked with major depressive disorder in social phobia that spans across the individual’s lifetime. A major suggestion related to the results of the study suggested that while inhibition can be a general predictor of risk factors related to social phobia, it may not be a specific predictor of social phobia alone

Social Anxiety Disorder

Social anxiety disorder is characterised by a fear of scrutiny or disapproval from others. Individuals believe this negative reaction will bring about rejections. Individuals with social anxiety disorder have stronger anxious feeling over a long period of time and are more anxious more often. In many cases, researchers have found that social inhibition can be a factor in developing other disorders such as social anxiety disorder. Being inhibited does not mean that an individual will develop another disorder; however, Clauss and colleagues conducted a study to measure the association between behavioural inhibition and social anxiety disorder. The results of the study discovered that 15% of all children have behavioural inhibition and about half of those children will eventually develop social anxiety disorder. This is why behavioural inhibition is seen as a larger risk factor.

That being said, Lim and colleagues researched the differences between early and late onset of social anxiety disorder and its relation to social inhibition. Through the duration of their study, they found those diagnosed as early onset had complaints other than ones about social anxiety symptoms. Early onset individuals would frequently have more severe symptoms and higher levels of behavioural inhibition. Additional behavioural inhibition was more severe especially in social and school situations with only the early onset cases. Lorian and Grisham researched the relationship between behavioural inhibition, risk-avoidance, and social anxiety symptoms. They found that all three factors correlated with each other and risk avoidance is potentially a mechanism linked to an anxiety pathology.

Reduction

Alcohol Consumption

Social inhibition can be lowered by a few different factors, one of them being alcohol. Alcohol consumption can be seen to lower inhibitions in both men and women. Social inhibitions generally act to control or affect the way that one conducts themselves in a social setting. By lowering inhibitions alcohol can work to increase social behaviours either negatively or positively. Importantly, one must remember that the higher the dosage of alcohol, the greater the damage it will cause to inhibitory control.

By lowering inhibitions, alcohol can cause social behaviours such as aggression, self disclosure, and violent acts. Researchers have suggested that situational cues used to inhibit social behaviours are not perceived the same way after someone consumes enough alcohol to qualify them as drunk:

“interacting parties who are impaired by alcohol are less likely to see justifications for the other’s behavior, are thus more likely to interpret the behavior as arbitrary and provocative, and then, having less access to inhibiting cues and behavioral standards, are more likely to react extremely.”

This idea of increased extreme social behaviours is believed to come as a result of lowered inhibitions after consuming alcohol. Alcohol can lower inhibitions for a number of reasons, it can reduce one’s self-awareness, impair perceptual and cognitive functioning, allows for instigator pressures to have more influence over an individual, and can reduce one’s ability to read inhibitory social cues and standards of conduct.

When attempting to examine the effects that alcohol consumption has on social inhibition researchers found that after being provoked sober individuals used inhibiting cues, such as the innocence of the instigator and the severity of the retaliation to control their response to the aggressive provocation. However, the researchers found that an intoxicated individual did not have these same inhibitions and, as a result, exhibited more extreme behaviours of retaliated aggression to the provocation without processing information they would normally consider about the situation. On average, drunken individuals exhibited more aggression, self-disclosure, risk taking behaviours, and laughter than sober individuals. Extreme behaviours are not as common in sober individuals because they are able to read inhibitory cues and social conduct norms that drunken individuals are not as inclined to consider. These negative social behaviours, then, are a result of lowered social inhibitions.

Alcohol consumption also has the ability to lower inhibitions in a positive way. Research has been conducted looking at the way an intoxicated person is more inclined to be helpful. Researchers were of the same opinion that alcohol lowers inhibitions and allows for more extreme behaviours, however, they tested to see if this would be true for more socially acceptable situations, such as helping another person. The researchers acknowledged that, generally, an impulse to help another is initiated but then inhibitions will cause the potential helper to consider all factors going into their decision to help or not to help such as, lost time, boredom, fatigue, monetary costs, and possibility of personal harm. The researchers suggest that while one may be inhibited and therefore less likely to offer help when completely sober, after consuming alcohol enough damage will be done to their inhibitory functioning to actually increase helping. While this suggestion differs from socially negative behaviours that are seen after social inhibitions have been lowered, it is consistent with the idea that alcohol consumption can lower inhibitions and, as a result, produce more socially extreme behaviours when compared to a sober counterpart.

Alcohol consumption can lower social inhibitions in both men and women, producing social behaviours not typical in the individuals’ day-to-day sober lives. For example, in social settings women will tend to be uncomfortable with sexual acts and provocations as well as feeling uncomfortable in social settings that are generally male dominated such as strip clubs or bars. However, consumption of alcohol has been seen to lower these inhibitions, making women feel freer and more ready to participate socially in events and behaviours that they would normally feel inhibited from participating in if they were sober. As an example, women participating in bachelorette parties generally consume copious amounts of alcohol for the event. As a result, the females feel less inhibited and are more likely to then engage in behaviour that they would normally view as deviant or inappropriate. In an examination of bachelorette parties it was found that when those attending the party consumed only a couple of drinks behaviour minimally reflected any alcohol consumption, assuming that the party guests were still socially inhibited and less inclined to perform deviant behaviours. Similarly, “levels of intoxication were correlated with the atmosphere of the party, such that parties with little or no alcohol were perceived as less ‘wild’ than parties a lot of alcohol consumption.” Conceivably, the bachelorette parties show tendencies of “wild” behaviour after excessive alcohol consumption, which consequently lowers the inhibitions of the consumers.

When surveyed a number of women who had attended a bachelorette party, or had one in their honour, in the past year reported that their behaviour when under the influence of alcohol was different from their behaviour when sober. One party guest reported:

“People drink … to lose inhibitions and stuff that is done… I would never do sober. It lowers inhibitions – that is the main point of it.”

These reports suggest that “alcohol was used to lower inhibitions about being too sexual, about the risk of being perceived as promiscuous, or about being sexual in public. Women commented that they felt freer to talk about sex while under the influence of alcohol, to flirt with male strangers, or to dance with a male stripper.” The research collected surrounding women and their alcohol consumption in these settings provide examples of the reduction of social inhibitions in relation to excess alcohol consumption

Power

Social inhibitions can also be reduced by means unrelated to an actual substance. Another way that social inhibition can be decreased is by the attainment of power. Research has examined the way that having either elevated or reduced power affects social interactions and well-being in social situations. Such research has shown a relationship between elevated power and decreased social inhibitions. This relationship of those with elevated power and those with reduced power can be seen in all forms of social interactions, and is marked by elevated power individuals often having access to resources that the reduced power individuals do not have. Decreased social inhibition is seen in those with elevated power for two main reasons, one being that they have more access to resources, providing them with comforts and stability. The second reason is that their status as a high power individual often provides the powerful individual a sense of being above social consequences, allowing them to act in ways that a reduced power individual may not.

The elevated power individuals will experience reduced social inhibition in various ways, one being that they are more likely to approach, rather than avoid, another person. Also, with the reduced inhibition associated with high power individuals, they are more likely to initiate physical contact with another person, enter into their personal space, and they are more likely to indicate interest in intimacy. High power people tend to be socially disinhibited when it comes to sexual behaviour and sexual concepts. Consistent with this expectation, a study working with male and female participants found that when the male and female felt equally powerful they tended to interact socially with one another in a disinhibited manner.

Further, the research suggests that as a result of their reduced social inhibition, powerful individuals will be guided to behave in a way that fits with their personality traits in a social situation in which they feel powerful. Similarly, in a laboratory study it was found that when one person in a group feels powerful their reduced social inhibition can result in decreased manners. The study found that, when offered food, the powerful individual is more likely to take more than the other individuals in the room. This can be seen as the powerful individual exhibiting reduced social inhibitions, as they reduce their attention to common social niceties such as manners and sharing.

Increase

Power

Certain factors can increase social inhibition in individuals. Increased inhibitions can occur in different situations and for different reasons. One major factor that contributes to the increase of social inhibition is power. Reduced power is linked to an array of negative affect, one of which being increased social inhibitions. Power, in this instance, can be defined as a fundamental factor in social relationships that is central to interactions, influencing behaviour and emotional display. Further, power is such an essential factor in social relationships because power determines who is the giver and who is the receiver in the exchange of rewards and resources. Power is present in all social relationships, not just typical hierarchical establishments such as in employment or school settings. Power, then, is related to increased social inhibitions when an individual feels that they are in a powerless or diminished power position. Those who are deemed to be high in power are generally richer in resources and freedom, as well as decreased levels of social inhibition, whereas those who are deemed to be low in power are generally low in resources, constrained, and prone to experiencing increased social inhibition.

Research shows that individuals who are considered to be low in power experience more social threats and punishments, and generally have less access to social resources. As a result of this these individuals are prone to developing more sensitivity to criticism from others, and are more susceptible to accepting when someone constrains them. These factors contribute to increasing social inhibition in those individuals. Similarly, studies have shown that the absence of power can heighten the processes associated with social inhibition. Experiments on the interaction between power and inhibition have shown that when participants are in a situation where they perceive more punishments and threats their cognition and behaviour will show more signs of social inhibition related affect. Environments which distinguish the differences between the powerful and the powerless can lead to the social inhibition of the power reduced individuals as a response to their social interactions with the heightened power individuals.

Some of the social inhibited behaviours that a low-power individual will experience in these social situations will be embarrassment and fear and they may even go on to feel guilt, sadness, and shame. Further, low power individuals can be seen socially inhibiting themselves in ways that can, in the end, favour the high-power individuals. These can include inhibiting themselves from providing input on ideas, hesitating in normal speech, and even increasing their facial muscle actions in order to keep themselves from displaying emotions. When the low-power individuals are in a social situation with a high-power individual they will also commonly exhibit social inhibition by inhibiting their postural constriction and reducing their gestures. Researchers have generalised these suggestions of interaction between a high-power individual and low-power individuals to say that these expressions of social inhibition are expected to carry over into all areas of social interaction for the low-power individual. That is to say that low-power individuals will not only exhibit social inhibition when in the presence of a high-power individual. They will continue to be socially inhibited in all social aspects of their lives as a result of their low-power status. Further, low-power individuals tend to devote increased attention to the actions and behaviours of others.

Biological Factors

Another possible explanation for increased social inhibition has to do with biological factors. A study of brain activity in those who rate high on the scale for social inhibition showed a number of brain areas that are related to the heightened inhibitions. In their study the researchers aimed to find the link between socially inhibited individuals and an over activation of the cortical social brain network. The researchers did this by examining the brain activity of individuals who rate high in social inhibition as they respond to video clips of facial and bodily expressions that were potentially threatening. What the researchers found was that those who rate high in social inhibition show an overactive orbitofrontal cortex, left temporo-parietal junction, and right extrastriate body area. When the threat -related activity was being presented to the participants, these areas of the brain showed increased activity in comparison to those who do not rate high for social inhibition. What the researchers speculate is that, in this instance, hyperactivity in these brain structures does not mean better functioning. Further, “the orbitofrontal cortex is connected with areas that underlie emotional function and empathy”. This relates to one’s ability to stimulate how another person feels in their own facial displays. The over activity and decreased function of these brain structures can affect individuals by increasing social inhibition and behaviours related to social inhibition.

Personality Traits

Further, there is speculation that social inhibition can also be increased by the type of personality an individual has and behaviours that those individuals inherently display. Namely, those who are dependent and reassurance seeking are more commonly likely to display increased social inhibition.

Clinical Levels

Although social inhibition can occur as part of ordinary social situations, a chronically high level of social inhibition may lead some individuals to develop other social or anxiety disorders that would also need to be handled clinically. Through childhood, adolescence, and adulthood, clinical levels of social inhibition can be measured. Social inhibition can be a precursors for other social disorders that can develop in adolescence or adulthood

Measures

There are many implications for the diagnoses of social inhibition, however there are many cost-efficient ways to measure and treat this social disorder. One measure that has reliably assessed the traits of social inhibition is the seven-item inhibition scale of the Type D Scale-14. Another measure is the Behavioural Inhibition Observation System (BIOS). In clinical trials this measure is to be used for children completed by parents, teachers, and clinicians. Other scales are the:

  • Behavioural Inhibition Questionnaire (BIQ);
  • Behavioural Inhibition Instrument (BII);
  • Behavioural Inhibition Scale (BIS);
  • Preschool Behavioural Inhibition Scale (P-BIS); and
  • Behavioural Inhibition Scale for children ages 3-6.

There are also many versions of these scales that are specifically for parents, teachers, or even the child or possibly an inhibited individual to take. There are also times when these measures are grouped together; in many cases the Behavioural Inhibition System scale and Behavioural Activation System scale are used together. These two measure are the most widely used and together they consist of behavioural inhibition and behavioural activation scales that deal with reward response and fun seeking. The Behavioural Paradigm System is an observation system that allows measurements of behavioural inhibition in systematic natural environments. With this system researchers will observe cessation of play and vocalisation, long latencies to approaching the unfamiliar person, signs of fear and negative affect, and security seeking in environments such as classrooms, playgrounds, and in home settings. This paradigm was followed by many adaptations, one specifically was the adaptation of the Observational Paradigm. In an additional study by Ballespi and colleagues the paradigm was changed to be more suitable for a school environment. The adapted paradigm met three important criteria, the tests were suitable for a school environment, there had to be materials for the test that could be transported easily, and the observation of behavioural inhibition signs had to have the potential to be seen in a short period of time.

Ballespi and colleagues discussed one of the most recent measurement systems in the Behavioural Inhibition Observation System. This new system will allow clinicians to provide a quick measure for behavioural inhibition. This system is used during the first meeting with the child. In this first meeting, the child will be exposed to a strange, unfamiliar situation. The scale will then be completed after the therapist has time to observe the child in an interview setting. Researchers want to find a way to have an actual measure for inhibition, however this is difficult. There is a difference in observations, a parent or teachers is going to observe the child over long periods of time in several natural situations. The parents do not actually observe the child but instead rate the behaviour inhibition on the ideas they have formed about the child. The clinician will not have all this information and will base his or her first measure on observation alone; they measure state while parents and teachers measure traits. This is where the differences come up in measure however after several visits the measures of the clinicians, teachers, and parents become more similar.

Treatments

Treatments used for social inhibition are primarily assertive trainings introduced by therapies. These treatments are about teaching the inhibited individual to express and assert their feeling instead of inhibiting them. Assertiveness training is an important operation for behavioural therapist because it can help with behavioural issues, as well as interpersonal inadequacies, and anxiety in adults. In some cases this training can go by a different name because assertiveness is sometimes categorised by aggression therefore it can also be called appropriate expression training.

In one study discussing assertive training Ludwig and Lazarus found irrational cognitive patterns that inhibited individuals have to deal with and how to overcome them. The four patterns are self-criticism/Perfectionism, unrealistic approval needs, unrealistic labelling of aggression/assertive behaviour, and criticism of others. There are three different phases that work to combat the irrational cognitive patterns and inhibitory actions during social situations. These phases are meant to be actively practiced. The individual will receive homework assignments, and have to do role-playing exercises to overcome their inhibitions. The first phase discussed was about talking more. Ludwig states that there cannot just be an increase in talking but also an increase in expressing and talking about how one feels. The point of this phase is to get an individual talking no matter how ridiculous or trivial it may seem. Phase two is about dealing with the responses that come from talking more. When an inhibited individual starts talking more they may become embarrassed. However, with positive reactions from others they will learn that being embarrassed about some of the comments made is not devastating, and in turn the individual may talk and act more freely. In addition to the positive feedback the individual will review particularly embarrassing moment to assess why they were embarrassed to help combat those thoughts. If the inhibited person can understand the irrational thoughts they will eventually feel less embarrassed and act more freely. Role playing is also a way to help the individual understand different social behaviours. Mirroring is a way some therapist will show the client their own behaviour. The last phase deals with additional strategies that can help through social situation such as expressing disagreement, dealing with interruptions, initiating more conversations topics, and more self-disclosure. Ludwig and colleagues also make sure to explain that no one should compulsively apply these behavioural techniques in all situations. An individual should not go over board using them; additionally there are times when initiating some conversation topics and talking more are inappropriate.

Group therapies are also used in the treatment using assertiveness. Hedquist and Weinhold investigated two group counselling strategies with socially anxious and unassertive college students. The first strategy is a behavioural rehearsal group, which aims to assist members to learn more efficient responses in social situations. This was to be accomplished by rehearsing several difficult social situations. The second strategy was a social learning group that was about honesty about everything; any withholding behaviours were seen as being dishonest. Another rule was every individual had to take responsibility for everything that said. The results of this study showed that both strategies helped significantly in treating the anxiety and unassertiveness.

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What is Sertraline?

Introduction

Sertraline, sold under the brand name Zoloft among others, is an antidepressant of the selective serotonin reuptake inhibitor (SSRI) class.

The efficacy of sertraline for depression is similar to that of other antidepressants, and the differences are mostly confined to side effects. Sertraline is better tolerated than the older tricyclic antidepressants, and it may work better than fluoxetine for some subtypes of depression. Sertraline is effective for panic disorder, social anxiety disorder, generalised anxiety disorder (GAD), and obsessive-compulsive disorder (OCD). However, for OCD, cognitive behavioural therapy (CBT), particularly in combination with sertraline, is a better treatment. Although approved for post-traumatic stress disorder, sertraline leads to only modest improvement in this condition. Sertraline also alleviates the symptoms of premenstrual dysphoric disorder and can be used in sub-therapeutic doses or intermittently for its treatment.

Sertraline shares the common side effects and contraindications of other SSRIs, with high rates of nausea, diarrhoea, insomnia, and sexual side effects, but it appears not to lead to much weight gain, and its effects on cognitive performance are mild. Similar to other antidepressants, the use of sertraline for depression may be associated with a higher rate of suicidal thoughts and behaviour in people under the age of 25. It should not be used together with MAO inhibitor medication: this combination causes serotonin syndrome. Sertraline taken during pregnancy is associated with a significant increase in congenital heart defects in newborns.

Sertraline was invented and developed by scientists at Pfizer and approved for medical use in the United States in 1991. It is on the World Health Organisation’s List of Essential Medicines. It is available as a generic medication. In 2016, sertraline was the most commonly prescribed psychiatric medication in the US and in 2019, it was the twelfth most commonly prescribed medication in the US, with over 37 million prescriptions.

Brief History

The history of sertraline dates back to the early 1970s, when Pfizer chemist Reinhard Sarges invented a novel series of psychoactive compounds, including lometraline, based on the structures of the neuroleptics thiothixene and pinoxepin. Further work on these compounds led to tametraline, a norepinephrine and weaker dopamine reuptake inhibitor. Development of tametraline was soon stopped because of undesired stimulant effects observed in animals. A few years later, in 1977, pharmacologist Kenneth Koe, after comparing the structural features of a variety of reuptake inhibitors, became interested in the tametraline series. He asked another Pfizer chemist, Willard Welch, to synthesize some previously unexplored tametraline derivatives. Welch generated a number of potent norepinephrine and triple reuptake inhibitors, but to the surprise of the scientists, one representative of the generally inactive cis-analogues was a serotonin reuptake inhibitor. Welch then prepared stereoisomers of this compound, which were tested in vivo by animal behavioural scientist Albert Weissman. The most potent and selective (+)-isomer was taken into further development and eventually named sertraline. Weissman and Koe recalled that the group did not set up to produce an antidepressant of the SSRI type – in that sense their inquiry was not “very goal driven”, and the discovery of the sertraline molecule was serendipitous. According to Welch, they worked outside the mainstream at Pfizer, and even “did not have a formal project team”. The group had to overcome initial bureaucratic reluctance to pursue sertraline development, as Pfizer was considering licensing an antidepressant candidate from another company.

Sertraline was approved by the US Food and Drug Administration (FDA) in 1991 based on the recommendation of the Psychopharmacological Drugs Advisory Committee; it had already become available in the United Kingdom the previous year. The FDA committee achieved a consensus that sertraline was safe and effective for the treatment of major depression. During the discussion, Paul Leber, the director of the FDA Division of Neuropharmacological Drug Products, noted that granting approval was a “tough decision”, since the treatment effect on outpatients with depression had been “modest to minimal”. Other experts emphasized that the drug’s effect on inpatients had not differed from placebo and criticised poor design of the clinical trials by Pfizer. For example, 40% of participants dropped out of the trials, significantly decreasing their validity.

Until 2002, sertraline was only approved for use in adults ages 18 and over; that year, it was approved by the FDA for use in treating children aged 6 or older with severe OCD. In 2003, the UK Medicines and Healthcare products Regulatory Agency issued a guidance that, apart from fluoxetine (Prozac), SSRIs are not suitable for the treatment of depression in patients under 18. However, sertraline can still be used in the UK for the treatment of OCD in children and adolescents. In 2005, the FDA added a boxed warning concerning paediatric suicidal behaviour to all antidepressants, including sertraline. In 2007, labelling was again changed to add a warning regarding suicidal behaviour in young adults ages 18 to 24.

Medical Uses

Sertraline has been approved for major depressive disorder (MDD), obsessive-compulsive disorder (OCD), posttraumatic stress disorder (PTSD), premenstrual dysphoric disorder (PMDD), panic disorder, and social anxiety disorder (SAD). Sertraline is not approved for use in children except for those with OCD.

Depression

Multiple controlled clinical trials established efficacy of sertraline for the treatment of depression. Sertraline is also an effective antidepressant in the routine clinical practice. Continued treatment with sertraline prevents both a relapse of the current depressive episode and future episodes (recurrence of depression).

In several double-blind studies, sertraline was consistently more effective than placebo for dysthymia, a more chronic variety of depression, and comparable to imipramine in that respect. Sertraline also improves the depression of dysthymic patients to a greater degree than psychotherapy.

Limited paediatric data also demonstrates reduction in depressive symptoms in the paediatric population though remains a second line therapy after fluoxetine.

Comparison with Other Antidepressants

In general, sertraline efficacy is similar to that of other antidepressants. For example, a meta-analysis of 12 new-generation antidepressants showed that sertraline and escitalopram are the best in terms of efficacy and acceptability in the acute-phase treatment of adults with depression. Comparative clinical trials demonstrated that sertraline is similar in efficacy against depression to moclobemide, nefazodone, escitalopram, bupropion, citalopram, fluvoxamine, paroxetine, venlafaxine, and mirtazapine. Sertraline may be more efficacious for the treatment of depression in the acute phase (first 4 weeks) than fluoxetine.

There are differences between sertraline and some other antidepressants in their efficacy in the treatment of different subtypes of depression and in their adverse effects. For severe depression, sertraline is as good as clomipramine but is better tolerated. Sertraline appears to work better in melancholic depression than fluoxetine, paroxetine, and mianserin and is similar to the tricyclic antidepressants such as amitriptyline and clomipramine. In the treatment of depression accompanied by OCD, sertraline performs significantly better than desipramine on the measures of both OCD and depression. Sertraline is equivalent to imipramine for the treatment of depression with co-morbid panic disorder, but it is better tolerated. Compared with amitriptyline, sertraline offered a greater overall improvement in quality of life of depressed patients.

Depression in Elderly

Sertraline used for the treatment of depression in elderly (older than 60) patients is superior to placebo and comparable to another SSRI fluoxetine, and tricyclic antidepressants (TCAs) amitriptyline, nortriptyline and imipramine. Sertraline has much lower rates of adverse effects than these TCAs, with the exception of nausea, which occurs more frequently with sertraline. In addition, sertraline appears to be more effective than fluoxetine or nortriptyline in the older-than-70 subgroup. Accordingly, a meta-analysis of antidepressants in older adults found that sertraline, paroxetine and duloxetine were better than placebo. On the other hand, in a 2003 trial the effect size was modest, and there was no improvement in quality of life as compared to placebo. With depression in dementia, there is no benefit of sertraline treatment compared to either placebo or mirtazapine.

Obsessive-Compulsive Disorder

Sertraline is effective for the treatment of OCD in adults and children. It was better tolerated and, based on intention-to-treat analysis, performed better than the gold standard of OCD treatment clomipramine. Continuing sertraline treatment helps prevent relapses of OCD with long-term data supporting its use for up to 24 months. It is generally accepted that the sertraline dosages necessary for the effective treatment of OCD are higher than the usual dosage for depression. The onset of action is also slower for OCD than for depression. The treatment recommendation is to start treatment with a half of maximal recommended dose for at least two months. After that, the dose can be raised to the maximal recommended in the cases of unsatisfactory response.

CBT alone was superior to sertraline in both adults and children; however, the best results were achieved using a combination of these treatments.

Panic Disorder

Sertraline is superior to placebo for the treatment of panic disorder. The response rate was independent of the dose. In addition to decreasing the frequency of panic attacks by about 80% (vs. 45% for placebo) and decreasing general anxiety, sertraline resulted in improvement of quality of life on most parameters. The patients rated as “improved” on sertraline reported better quality of life than the ones who “improved” on placebo. The authors of the study argued that the improvement achieved with sertraline is different and of a better quality than the improvement achieved with placebo. Sertraline is equally effective for men and women, and for patients with or without agoraphobia. Previous unsuccessful treatment with benzodiazepines does not diminish its efficacy. However, the response rate was lower for the patients with more severe panic. Starting treatment simultaneously with sertraline and clonazepam, with subsequent gradual discontinuation of clonazepam, may accelerate the response.

Double-blind comparative studies found sertraline to have the same effect on panic disorder as paroxetine or imipramine. While imprecise, comparison of the results of trials of sertraline with separate trials of other anti-panic agents (clomipramine, imipramine, clonazepam, alprazolam, and fluvoxamine) indicates approximate equivalence of these medications.

Other Anxiety Disorders

Sertraline has been successfully used for the treatment of social anxiety disorder. All three major domains of the disorder (fear, avoidance, and physiological symptoms) respond to sertraline. Maintenance treatment, after the response is achieved, prevents the return of the symptoms. The improvement is greater among the patients with later, adult onset of the disorder. In a comparison trial, sertraline was superior to exposure therapy, but patients treated with the psychological intervention continued to improve during a year-long follow-up, while those treated with sertraline deteriorated after treatment termination. The combination of sertraline and CBT appears to be more effective in children and young people than either treatment alone.

Sertraline has not been approved for the treatment of generalised anxiety disorder; however, several guidelines recommend it as a first-line medication referring to good quality controlled clinical trials.

Premenstrual Dysphoric Disorder

Sertraline is effective in alleviating the symptoms of premenstrual dysphoric disorder (PMDD), a severe form of premenstrual syndrome. Significant improvement was observed in 50-60% of cases treated with sertraline vs. 20-30% of cases on placebo. The improvement began during the first week of treatment, and in addition to mood, irritability, and anxiety, improvement was reflected in better family functioning, social activity and general quality of life. Work functioning and physical symptoms, such as swelling, bloating and breast tenderness, were less responsive to sertraline. Taking sertraline only during the luteal phase, that is, the 12-14 days before menses, was shown to work as well as continuous treatment. Continuous treatment with sub-therapeutic doses of sertraline (25 mg vs. usual 50-100 mg) is also effective.

Other Indications

Sertraline is approved for the treatment of post-traumatic stress disorder (PTSD). National Institute of Clinical Excellence recommends it for patients who prefer drug treatment to a psychological one. Other guidelines also suggest sertraline as a first-line option for pharmacological therapy. When necessary, long-term pharmacotherapy can be beneficial. There are both negative and positive clinical trial results for sertraline, which may be explained by the types of psychological traumas, symptoms, and comorbidities included in the various studies. Positive results were obtained in trials that included predominantly women (75%) with a majority (60%) having physical or sexual assault as the traumatic event. Contrary to the above suggestions, a meta-analysis of sertraline clinical trials for PTSD found it to be not significantly better than placebo. Another meta-analysis relegated sertraline to the second line, proposing trauma focused psychotherapy as a first-line intervention. The authors noted that Pfizer had declined to submit the results of a negative trial for the inclusion into the meta-analysis making the results unreliable.

Sertraline when taken daily can be useful for the treatment of premature ejaculation. A disadvantage of sertraline is that it requires continuous daily treatment to delay ejaculation significantly.

A 2019 systematic review suggested that sertraline may be a good way to control anger, irritability and hostility in depressed patients and patients with other comorbidities.

Contraindications

Sertraline is contraindicated in individuals taking monoamine oxidase inhibitors or the antipsychotic pimozide. Sertraline concentrate contains alcohol and is therefore contraindicated with disulfiram. The prescribing information recommends that treatment of the elderly and patients with liver impairment “must be approached with caution”. Due to the slower elimination of sertraline in these groups, their exposure to sertraline may be as high as three times the average exposure for the same dose.

Side Effects

Nausea, ejaculation failure, insomnia, diarrhoea, dry mouth, somnolence, dizziness, tremor, headache, excessive sweating, fatigue, and decreased libido are the common adverse effects associated with sertraline with the greatest difference from placebo. Those that most often resulted in interruption of the treatment are nausea, diarrhoea and insomnia. The incidence of diarrhoea is higher with sertraline – especially when prescribed at higher doses – in comparison with other SSRIs.

Over more than six months of sertraline therapy for depression, people showed a nonsignificant weight increase of 0.1%. Similarly, a 30-month-long treatment with sertraline for OCD resulted in a mean weight gain of 1.5% (1 kg). Although the difference did not reach statistical significance, the average weight gain was lower for fluoxetine (1%) but higher for citalopram, fluvoxamine and paroxetine (2.5%). Of the sertraline group, 4.5% gained a large amount of weight (defined as more than 7% gain). This result compares favourably with placebo, where, according to the literature, 3-6% of patients gained more than 7% of their initial weight. The large weight gain was observed only among female members of the sertraline group; the significance of this finding is unclear because of the small size of the group.

Over a two-week treatment of healthy volunteers, sertraline slightly improved verbal fluency but did not affect word learning, short-term memory, vigilance, flicker fusion time, choice reaction time, memory span, or psychomotor coordination. In spite of lower subjective rating, that is, feeling that they performed worse, no clinically relevant differences were observed in the objective cognitive performance in a group of people treated for depression with sertraline for 1.5 years as compared to healthy controls. In children and adolescents taking sertraline for six weeks for anxiety disorders, 18 out of 20 measures of memory, attention and alertness stayed unchanged. Divided attention was improved and verbal memory under interference conditions decreased marginally. Because of the large number of measures taken, it is possible that these changes were still due to chance. The unique effect of sertraline on dopaminergic neurotransmission may be related to these effects on cognition and vigilance.

Sertraline has a low level of exposure of an infant through the breast milk and is recommended as the preferred option for the antidepressant therapy of breast-feeding mothers. There is 29-42% increase in congenital heart defects among children whose mothers were prescribed sertraline during pregnancy, with sertraline use in the first trimester associated with 2.7-fold increase in septal heart defects.

Abrupt interruption of sertraline treatment may result in withdrawal or discontinuation syndrome. Dizziness, insomnia, anxiety, agitation, and irritability are its common symptoms. It typically occurs within a few days from drug discontinuation and lasts a few weeks. The withdrawal symptoms for sertraline are less severe and frequent than for paroxetine, and more frequent than for fluoxetine. In most cases symptoms are mild, short-lived, and resolve without treatment. More severe cases are often successfully treated by temporary reintroduction of the drug with a slower tapering off rate.

Sertraline and SSRI antidepressants in general may be associated with bruxism and other movement disorders. Sertraline appears to be associated with microscopic colitis, a rare condition of unknown aetiology.

Sexual

Like other SSRIs, sertraline is associated with sexual side effects, including sexual arousal disorder, erectile dysfunction and difficulty achieving orgasm. While nefazodone and bupropion do not have negative effects on sexual functioning, 67% of men on sertraline experienced ejaculation difficulties versus 18% before the treatment. Sexual arousal disorder, defined as “inadequate lubrication and swelling for women and erectile difficulties for men”, occurred in 12% of people on sertraline as compared with 1% of patients on placebo. The mood improvement resulting from the treatment with sertraline sometimes counteracted these side effects, so that sexual desire and overall satisfaction with sex stayed the same as before the sertraline treatment. However, under the action of placebo the desire and satisfaction slightly improved. Some people continue experiencing sexual side effects after they stop taking SSRIs.

Suicide

The US Food and Drug Administration (FDA) requires all antidepressants, including sertraline, to carry a boxed warning stating that antidepressants increase the risk of suicide in persons younger than 25 years. This warning is based on statistical analyses conducted by two independent groups of FDA experts that found a 100% increase of suicidal thoughts and behaviour in children and adolescents, and a 50% increase – in the 18-24 age group.

Suicidal ideation and behaviour in clinical trials are rare. For the above analysis, the FDA combined the results of 295 trials of 11 antidepressants for psychiatric indications in order to obtain statistically significant results. Considered separately, sertraline use in adults decreased the odds of suicidal behaviour with a marginal statistical significance by 37% or 50% depending on the statistical technique used. The authors of the FDA analysis note that “given the large number of comparisons made in this review, chance is a very plausible explanation for this difference”. The more complete data submitted later by the sertraline manufacturer Pfizer indicated increased suicidal behaviour. Similarly, the analysis conducted by the UK Medicines and Healthcare Products Regulatory Agency (MHRA) found a 50% increase of odds of suicide-related events, not reaching statistical significance, in the patients on sertraline as compared to the ones on placebo.

Overdose

Acute overdosage is often manifested by emesis, lethargy, ataxia, tachycardia and seizures. Plasma, serum or blood concentrations of sertraline and norsertraline, its major active metabolite, may be measured to confirm a diagnosis of poisoning in hospitalised patients or to aid in the medicolegal investigation of fatalities. As with most other SSRIs its toxicity in overdose is considered relatively low.

Interactions

As with other SSRIs, sertraline may increase the risk of bleeding with NSAIDs (non-steroidal anti-inflammatory drugs such as ibuprofen, naproxen, mefenamic acid), antiplatelet drugs, anticoagulants, omega-3 fatty acids, vitamin E, and garlic supplements due to sertraline’s inhibitory effects on platelet aggregation via blocking serotonin transporters on platelets. Sertraline, in particular, may potentially diminish the efficacy of levothyroxine.

Sertraline is a moderate inhibitor of CYP2D6 and CYP2B6 in vitro. Accordingly, in human trials it caused increased blood levels of CYP2D6 substrates such as metoprolol, dextromethorphan, desipramine, imipramine and nortriptyline, as well as the CYP3A4/CYP2D6 substrate haloperidol. This effect is dose-dependent; for example, co-administration with 50 mg of sertraline resulted in 20% greater exposure to desipramine, while 150 mg of sertraline led to a 70% increase. In a placebo-controlled study, the concomitant administration of sertraline and methadone caused a 40% increase in blood levels of the latter, which is primarily metabolized by CYP2B6.

Sertraline had a slight inhibitory effect on the metabolism of diazepam, tolbutamide and warfarin, which are CYP2C9 or CYP2C19 substrates; the clinical relevance of this effect was unclear. As expected from in vitro data, sertraline did not alter the human metabolism of the CYP3A4 substrates erythromycin, alprazolam, carbamazepine, clonazepam, and terfenadine; neither did it affect metabolism of the CYP1A2 substrate clozapine.

Sertraline had no effect on the actions of digoxin and atenolol, which are not metabolised in the liver. Case reports suggest that taking sertraline with phenytoin or zolpidem may induce sertraline metabolism and decrease its efficacy, and that taking sertraline with lamotrigine may increase the blood level of lamotrigine, possibly by inhibition of glucuronidation.

CYP2C19 inhibitor esomeprazole increased sertraline concentrations in blood plasma by approximately 40%.

Clinical reports indicate that interaction between sertraline and the MAOIs isocarboxazid and tranylcypromine may cause serotonin syndrome. In a placebo-controlled study in which sertraline was co-administered with lithium, 35% of the subjects experienced tremors, while none of those taking placebo did.

Sertraline may interact with grapefruit juice.

Pharmacology

Pharmacodynamics

Sertraline is a selective serotonin reuptake inhibitor (SSRI). By binding serotonin transporter (SERT) it inhibits neuronal reuptake of serotonin and potentiates serotonergic activity in the central nervous system. Over time, this leads to a downregulation of pre-synaptic 5-HT1A receptors, which is associated with an improvement in passive stress tolerance, and delayed downstream increase in expression of brain-derived neurotrophic factor (BDNF), which may contribute to a reduction in negative affective biases. It does not significantly affect norepinephrine transporter (NET), serotonin, dopamine, adrenergic, histamine, acetylcholine, GABA or benzodiazepine receptors.

Sertraline also shows relatively high activity as an inhibitor of the dopamine transporter (DAT) and antagonist of the sigma σ1 receptor (but not the σ2 receptor). However, sertraline affinity for its main target (SERT) is much greater than its affinity for σ1 receptor and DAT. Although there could be a role for the σ1 receptor in the pharmacology of sertraline, the significance of this receptor in its actions is unclear. Similarly, the clinical relevance of sertraline’s blockade of the dopamine transporter is uncertain.

Pharmacokinetics

Absorption

Following a single oral dose of sertraline, mean peak blood levels of sertraline occur between 4.5 and 8.4 hours. Bioavailability is likely linear and dose-proportional over a dose range of 150 to 200 mg. Concomitant intake of sertraline with food slightly increases sertraline peak levels and total exposure. There is an approximate 2-fold accumulation of sertraline with continuous administration and steady-state levels are reached within one week.

Distribution

Sertraline is highly plasma protein bound (98.5%) across a concentration range of 20 to 500 ng/mL. Despite the high plasma protein binding, sertraline and its metabolite desmethylsertraline at respective tested concentrations of 300 ng/mL and 200 ng/mL were found not to interfere with the plasma protein binding of warfarin and propranolol, two other highly plasma protein-bound drugs.

Metabolism

Sertraline is subject to extensive first-pass metabolism, as indicated by a small study of radiolabelled sertraline in which less than 5% of plasma radioactivity was unchanged sertraline in two males. The principal metabolic pathway for sertraline is N-demethylation into desmethylsertraline (N-desmethylsertraline) mainly by CYP2B6. Reduction, hydroxylation, and glucuronide conjugation of both sertraline and desmethylsertraline also occur. Desmethylsertraline, while pharmacologically active, is substantially (50-fold) weaker than sertraline as a serotonin reuptake inhibitor and its influence on the clinical effects of sertraline is thought to be negligible. Based on in vitro studies, sertraline is metabolized by multiple cytochrome 450 isoforms; however, it appears that in the human body CYP2C19 plays the most important role, followed by CYP2B6. In addition to the cytochrome P450 system, sertraline can be oxidatively deaminated in vitro by monoamine oxidases; however, this metabolic pathway has never been studied in vivo.

Elimination

The elimination half-life of sertraline is on average 26 hours, with a range of 13 to 45 hours. The half-life of sertraline is longer in women (32 hours) than in men (22 hours), which leads to 1.5-fold higher exposure to sertraline in women compared to men. The elimination half-life of desmethylsertraline is 62 to 104 hours.

In a small study of two males, sertraline was excreted to similar degrees in urine and faeces (40 to 45% each within 9 days). Unchanged sertraline was not detectable in urine, whereas 12 to 14% unchanged sertraline was present in faeces.

Pharmacogenomics

CYP2C19 and CYP2B6 are thought to be the key cytochrome P450 enzymes involved in the metabolism of sertraline. Relative to CYP2C19 normal (extensive) metabolisers, poor metabolisers have 2.7-fold higher levels of sertraline and intermediate metabolisers have 1.4-fold higher levels. In contrast, CYP2B6 poor metabolisers have 1.6-fold higher levels of sertraline and intermediate metabolisers have 1.2-fold higher levels.

Society and Culture

Generic Availability

The US patent for Zoloft expired in 2006, and sertraline is available in generic form and is marketed under many brand names worldwide.

In May 2020, the FDA placed Zoloft on the list of drugs currently facing a shortage.

Other Uses

Lass-Flörl et al., 2003 finds sertraline significantly inhibits phospholipase B in the fungal genus Candida, reducing virulence. It is also a very effective leishmanicide. Specifically, Palit & Ali 2008 find that sertraline kills almost all promastigotes of Leishmania donovani.

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What is Exposure Therapy?

Introduction

Exposure therapy is a technique in behaviour therapy to treat anxiety disorders. Exposure therapy involves exposing the target patient to the anxiety source or its context without the intention to cause any danger. Doing so is thought to help them overcome their anxiety or distress. Procedurally, it is similar to the fear extinction paradigm developed studying laboratory rodents. Numerous studies have demonstrated its effectiveness in the treatment of disorders such as generalised anxiety disorder (GAD), social anxiety disorder, obsessive-compulsive disorder (OCD), post traumatic stress disorder (PTSD), and specific phobias.

Brief History

The use of exposure as a mode of therapy began in the 1950s, at a time when psychodynamic views dominated Western clinical practice and behavioural therapy was first emerging. South African psychologists and psychiatrists first used exposure as a way to reduce pathological fears, such as phobias and anxiety-related problems, and they brought their methods to England in the Maudsley Hospital training programme.

Joseph Wolpe (1915-1997) was one of the first psychiatrists to spark interest in treating psychiatric problems as behavioural issues. He sought consultation with other behavioural psychologists, among them James G. Taylor (1897-1973), who worked in the psychology department of the University of Cape Town in South Africa. Although most of his work went unpublished, Taylor was the first psychologist known to use exposure therapy treatment for anxiety, including methods of situational exposure with response prevention – a common exposure therapy technique still being used. Since the 1950s several sorts of exposure therapy have been developed, including systematic desensitisation, flooding, implosive therapy, prolonged exposure therapy, in vivo exposure therapy, and imaginal exposure therapy.

Medical Uses

Generalised Anxiety Disorder

There is empirical evidence that exposure therapy can be an effective treatment for people with generalised anxiety disorder, citing specifically in vivo exposure therapy, which has greater effectiveness than imaginal exposure in regards to generalized anxiety disorder. The aim of in vivo exposure treatment is to promote emotional regulation using systematic and controlled therapeutic exposure to traumatic stimuli.

Phobia

Exposure therapy is the most successful known treatment for phobias. Several published meta-analyses included studies of one-to-three hour single-session treatments of phobias, using imaginal exposure. At a post-treatment follow-up four years later 90% of people retained a considerable reduction in fear, avoidance, and overall level of impairment, while 65% no longer experienced any symptoms of a specific phobia.

Agoraphobia and social anxiety disorder are examples of phobias that have been successfully treated by exposure therapy.

Post Traumatic Stress Disorder

Virtual reality exposure (VRE) therapy is a modern but effective treatment of post-traumatic stress disorder (PTSD). This method was tested on several active duty Army soldiers, using an immersive computer simulation of military settings over six sessions. Self-reported PTSD symptoms of these soldiers were greatly diminished following the treatment. Exposure therapy has shown promise in the treatment of co-morbid PTSD and substance abuse.

Obsessive Compulsive Disorder

Exposure and response prevention (also known as exposure and ritual prevention; ERP or EX/RP) is a variant of exposure therapy that is recommended by the American Academy of Child and Adolescent Psychiatry (AACAP), the American Psychiatric Association (APA), and the Mayo Clinic as first-line treatment of obsessive compulsive disorder (OCD) citing that it has the richest empirical support for both youth and adolescent outcomes.

ERP is predicated on the idea that a therapeutic effect is achieved as subjects confront their fears, but refrain from engaging in the escape response or ritual that delays or eliminates distress. In the case of individuals with OCD or an anxiety disorder, there is a thought or situation that causes distress. Individuals usually combat this distress through specific behaviours that include avoidance or rituals. However, ERP involves purposefully evoking fear, anxiety, and or distress in the individual by exposing him/her to the feared stimulus. The response prevention then involves having the individual refrain from the ritualistic or otherwise compulsive behaviour that functions to decrease distress. The patient is then taught to tolerate distress until it fades away on its own, thereby learning that rituals are not always necessary to decrease distress or anxiety. Over repeated practice of ERP, patients with OCD expect to find that they can have obsessive thoughts and images but not have the need to engage in compulsive rituals to decrease distress.

The AACAP’s practise parameters for OCD recommends cognitive behavioural therapy, and more specifically ERP, as first line treatment for youth with mild to moderate severity OCD and combination psychotherapy and pharmacotherapy for severe OCD. The Cochrane Review’s examinations of different randomised control trials echoes repeated findings of the superiority of ERP over waitlist control or pill-placebos, the superiority of combination ERP and pharmacotherapy, but similar effect sizes of efficacy between ERP or pharmacotherapy alone.

Techniques

Exposure therapy is based on the principle of respondent conditioning often termed Pavlovian extinction. The exposure therapist identifies the cognitions, emotions and physiological arousal that accompany a fear-inducing stimulus and then tries to break the pattern of escape that maintains the fear. This is done by exposing the patient to progressively stronger fear-inducing stimuli. Fear is minimised at each of a series of steadily escalating steps or challenges (a hierarchy), which can be explicit (“static”) or implicit (“dynamic” – refer to Method of Factors) until the fear is finally gone. The patient is able to terminate the procedure at any time.

There are three types of exposure procedures. The first is in vivo or “real life.” This type exposes the patient to actual fear-inducing situations. For example, if someone fears public speaking, the person may be asked to give a speech to a small group of people. The second type of exposure is imaginal, where patients are asked to imagine a situation that they are afraid of. This procedure is helpful for people who need to confront feared thoughts and memories. The third type of exposure is interoceptive, which may be used for more specific disorders such as panic or post-traumatic stress disorder. Patients confront feared bodily symptoms such as increased heart rate and shortness of breath. All types of exposure may be used together or separately.

While evidence clearly supports the effectiveness of exposure therapy, some clinicians are uncomfortable using imaginal exposure therapy, especially in cases of PTSD. They may not understand it, are not confident in their own ability to use it, or more commonly, they see significant contraindications for their client.

Flooding therapy also exposes the patient to feared stimuli, but it is quite distinct in that flooding starts at the most feared item in a fear hierarchy, while exposure starts at the least fear-inducing.

Exposure and Response Prevention

In the exposure and response prevention (ERP or EX/RP) variation of exposure therapy, the resolution to refrain from the escape response is to be maintained at all times and not just during specific practice sessions. Thus, not only does the subject experience habituation to the feared stimulus, but they also practice a fear-incompatible behavioural response to the stimulus. The distinctive feature is that individuals confront their fears and discontinue their escape response. The American Psychiatric Association recommends ERP for the treatment of OCD, citing that ERP has the richest empirical support.

While this type of therapy typically causes some short-term anxiety, this facilitates long-term reduction in obsessive and compulsive symptoms. Generally, ERP incorporates a relapse prevention plan toward the end of the course of therapy.

Mindfulness

A 2015 review pointed out parallels between exposure therapy and mindfulness, stating that mindful meditation “resembles an exposure situation because [mindfulness] practitioners ‘turn towards their emotional experience’, bring acceptance to bodily and affective responses, and refrain from engaging in internal reactivity towards it.” Imaging studies have shown that the ventromedial prefrontal cortex, hippocampus, and the amygdala are all affected by exposure therapy; imaging studies have shown similar activity in these regions with mindfulness training.

Research

Exposure therapy can be investigated in the laboratory using Pavlovian extinction paradigms. Using rodents such as rats or mice to study extinction allows for the investigation of underlying neurobiological mechanisms involved, as well as testing of pharmacological adjuncts to improve extinction learning.

What is Anxiety?

Introduction

Anxiety is an emotion characterised by an unpleasant state of inner turmoil, often accompanied by nervous behaviour such as pacing back and forth, somatic complaints, and rumination. It includes subjectively unpleasant feelings of dread over anticipated events.

Anxiety is a feeling of uneasiness and worry, usually generalised and unfocused as an overreaction to a situation that is only subjectively seen as menacing. It is often accompanied by muscular tension, restlessness, fatigue and problems in concentration. Anxiety is closely related to fear, which is a response to a real or perceived immediate threat; anxiety involves the expectation of future threat. People facing anxiety may withdraw from situations which have provoked anxiety in the past.

Anxiety disorders differ from developmentally normative fear or anxiety by being excessive or persisting beyond developmentally appropriate periods. They differ from transient fear or anxiety, often stress-induced, by being persistent (e.g. typically lasting 6 months or more), although the criterion for duration is intended as a general guide with allowance for some degree of flexibility and is sometimes of shorter duration in children.

Anxiety vs Fear

Anxiety is distinguished from fear, which is an appropriate cognitive and emotional response to a perceived threat. Anxiety is related to the specific behaviours of fight-or-flight responses, defensive behaviour or escape. It occurs in situations only perceived as uncontrollable or unavoidable, but not realistically so. David Barlow defines anxiety as “a future-oriented mood state in which one is not ready or prepared to attempt to cope with upcoming negative events,” and that it is a distinction between future and present dangers which divides anxiety and fear. Another description of anxiety is agony, dread, terror, or even apprehension. In positive psychology, anxiety is described as the mental state that results from a difficult challenge for which the subject has insufficient coping skills.

Fear and anxiety can be differentiated in four domains:

  1. Duration of emotional experience;
  2. Temporal focus;
  3. Specificity of the threat; and
  4. Motivated direction.

Fear is short-lived, present-focused, geared towards a specific threat, and facilitating escape from threat; anxiety, on the other hand, is long-acting, future-focused, broadly focused towards a diffuse threat, and promoting excessive caution while approaching a potential threat and interferes with constructive coping.

Joseph E. LeDoux and Lisa Feldman Barrett have both sought to separate automatic threat responses from additional associated cognitive activity within anxiety.

Symptoms

Anxiety can be experienced with long, drawn-out daily symptoms that reduce quality of life, known as chronic (or generalised) anxiety, or it can be experienced in short spurts with sporadic, stressful panic attacks, known as acute anxiety. Symptoms of anxiety can range in number, intensity, and frequency, depending on the person. While almost everyone has experienced anxiety at some point in their lives, most do not develop long-term problems with anxiety.

Anxiety may cause psychiatric and physiological symptoms.

The risk of anxiety leading to depression could possibly even lead to an individual harming themselves, which is why there are many 24-hour suicide prevention hotlines.

The behavioural effects of anxiety may include withdrawal from situations which have provoked anxiety or negative feelings in the past. Other effects may include changes in sleeping patterns, changes in habits, increase or decrease in food intake, and increased motor tension (such as foot tapping).

The emotional effects of anxiety may include “feelings of apprehension or dread, trouble concentrating, feeling tense or jumpy, anticipating the worst, irritability, restlessness, watching (and waiting) for signs (and occurrences) of danger, and, feeling like your mind’s gone blank” as well as “nightmares/bad dreams, obsessions about sensations, déjà vu, a trapped-in-your-mind feeling, and feeling like everything is scary.” It may include a vague experience and feeling of helplessness.

The cognitive effects of anxiety may include thoughts about suspected dangers, such as fear of dying. “You may … fear that the chest pains are a deadly heart attack or that the shooting pains in your head are the result of a tumour or an aneurysm. You feel an intense fear when you think of dying, or you may think of it more often than normal, or can’t get it out of your mind.”

The physiological symptoms of anxiety may include:

  • Neurological, as headache, paraesthesia’s, fasciculations, vertigo, or presyncope.
  • Digestive, as abdominal pain, nausea, diarrhoea, indigestion, dry mouth, or bolus.
  • Respiratory, as shortness of breath or sighing breathing.
  • Cardiac, as palpitations, tachycardia, or chest pain.
  • Muscular, as fatigue, tremors, or tetany.
  • Cutaneous, as perspiration, or itchy skin.
  • Uro-genital, as frequent urination, urinary urgency, dyspareunia, or impotence, chronic pelvic pain syndrome. Stress hormones released in an anxious state have an impact on bowel function and can manifest physical symptoms that may contribute to or exacerbate IBS.

Types of Anxiety

There are various types of anxiety. Existential anxiety can occur when a person faces angst, an existential crisis, or nihilistic feelings. People can also face mathematical anxiety, somatic anxiety, stage fright, or test anxiety. Social anxiety refers to a fear of rejection and negative evaluation by other people.

Existential

The philosopher Søren Kierkegaard, in The Concept of Anxiety (1844), described anxiety or dread associated with the “dizziness of freedom” and suggested the possibility for positive resolution of anxiety through the self-conscious exercise of responsibility and choosing. In Art and Artist (1932), the psychologist Otto Rank wrote that the psychological trauma of birth was the pre-eminent human symbol of existential anxiety and encompasses the creative person’s simultaneous fear of – and desire for – separation, individuation, and differentiation.

The theologian Paul Tillich characterised existential anxiety as “the state in which a being is aware of its possible nonbeing” and he listed three categories for the nonbeing and resulting anxiety: ontic (fate and death), moral (guilt and condemnation), and spiritual (emptiness and meaninglessness). According to Tillich, the last of these three types of existential anxiety, i.e. spiritual anxiety, is predominant in modern times while the others were predominant in earlier periods. Tillich argues that this anxiety can be accepted as part of the human condition or it can be resisted but with negative consequences. In its pathological form, spiritual anxiety may tend to “drive the person toward the creation of certitude in systems of meaning which are supported by tradition and authority” even though such “undoubted certitude is not built on the rock of reality”.

According to Viktor Frankl, the author of Man’s Search for Meaning, when a person is faced with extreme mortal dangers, the most basic of all human wishes is to find a meaning of life to combat the “trauma of nonbeing” as death is near.

Depending on the source of the threat, psychoanalytic theory distinguishes the following types of anxiety:

  • Realistic.
  • Neurotic.
  • Moral.

Test and Performance

According to Yerkes-Dodson law, an optimal level of arousal is necessary to best complete a task such as an exam, performance, or competitive event. However, when the anxiety or level of arousal exceeds that optimum, the result is a decline in performance.

Test anxiety is the uneasiness, apprehension, or nervousness felt by students who have a fear of failing an exam. Students who have test anxiety may experience any of the following: the association of grades with personal worth; fear of embarrassment by a teacher; fear of alienation from parents or friends; time pressures; or feeling a loss of control. Sweating, dizziness, headaches, racing heartbeats, nausea, fidgeting, uncontrollable crying or laughing and drumming on a desk are all common. Because test anxiety hinges on fear of negative evaluation, debate exists as to whether test anxiety is itself a unique anxiety disorder or whether it is a specific type of social phobia. The DSM-IV classifies test anxiety as a type of social phobia.

While the term “test anxiety” refers specifically to students, many workers share the same experience with regard to their career or profession. The fear of failing at a task and being negatively evaluated for failure can have a similarly negative effect on the adult. Management of test anxiety focuses on achieving relaxation and developing mechanisms to manage anxiety.

Stranger, Social, and Intergroup Anxiety

Humans generally require social acceptance and thus sometimes dread the disapproval of others. Apprehension of being judged by others may cause anxiety in social environments.

Anxiety during social interactions, particularly between strangers, is common among young people. It may persist into adulthood and become social anxiety or social phobia. “Stranger anxiety” in small children is not considered a phobia. In adults, an excessive fear of other people is not a developmentally common stage; it is called social anxiety. According to Cutting, social phobics do not fear the crowd but the fact that they may be judged negatively.

Social anxiety varies in degree and severity. For some people, it is characterised by experiencing discomfort or awkwardness during physical social contact (e.g. embracing, shaking hands, etc.), while in other cases it can lead to a fear of interacting with unfamiliar people altogether. Those suffering from this condition may restrict their lifestyles to accommodate the anxiety, minimising social interaction whenever possible. Social anxiety also forms a core aspect of certain personality disorders, including avoidant personality disorder.

To the extent that a person is fearful of social encounters with unfamiliar others, some people may experience anxiety particularly during interactions with outgroup members, or people who share different group memberships (i.e. by race, ethnicity, class, gender, etc.). Depending on the nature of the antecedent relations, cognitions, and situational factors, intergroup contact may be stressful and lead to feelings of anxiety. This apprehension or fear of contact with outgroup members is often called interracial or intergroup anxiety.

As is the case with the more generalised forms of social anxiety, intergroup anxiety has behavioural, cognitive, and affective effects. For instance, increases in schematic processing and simplified information processing can occur when anxiety is high. Indeed, such is consistent with related work on attentional bias in implicit memory. Additionally recent research has found that implicit racial evaluations (i.e. automatic prejudiced attitudes) can be amplified during intergroup interaction. Negative experiences have been illustrated in producing not only negative expectations, but also avoidant, or antagonistic, behaviour such as hostility. Furthermore, when compared to anxiety levels and cognitive effort (e.g. impression management and self-presentation) in intragroup contexts, levels and depletion of resources may be exacerbated in the intergroup situation.

Trait

Anxiety can be either a short-term ‘state’ or a long-term personality “trait”. Trait anxiety reflects a stable tendency across the lifespan of responding with acute, state anxiety in the anticipation of threatening situations (whether they are actually deemed threatening or not). A meta-analysis showed that a high level of neuroticism is a risk factor for development of anxiety symptoms and disorders. Such anxiety may be conscious or unconscious.

Personality can also be a trait leading to anxiety and depression. Through experience, many find it difficult to collect themselves due to their own personal nature.

Choice or Decision

Anxiety induced by the need to choose between similar options is increasingly being recognised as a problem for individuals and for organisations. In 2004, Capgemini wrote: “Today we’re all faced with greater choice, more competition and less time to consider our options or seek out the right advice.”

In a decision context, unpredictability or uncertainty may trigger emotional responses in anxious individuals that systematically alter decision-making. There are primarily two forms of this anxiety type. The first form refers to a choice in which there are multiple potential outcomes with known or calculable probabilities. The second form refers to the uncertainty and ambiguity related to a decision context in which there are multiple possible outcomes with unknown probabilities.

Panic Disorder

Panic disorder may share symptoms of stress and anxiety, but it is actually very different. Panic disorder is an anxiety disorder that occurs without any triggers. According to the US Department of Health and Human Services, this disorder can be distinguished by unexpected and repeated episodes of intense fear. Someone who suffers from panic disorder will eventually develop constant fear of another attack and as this progresses it will begin to affect daily functioning and an individual’s general quality of life. It is reported by the Cleveland Clinic that panic disorder affects 2% to 3% of adult Americans and can begin around the time of the teenage and early adult years. Some symptoms include: difficulty breathing, chest pain, dizziness, trembling or shaking, feeling faint, nausea, fear that you are losing control or are about to die. Even though they suffer from these symptoms during an attack, the main symptom is the persistent fear of having future panic attacks.

Anxiety Disorders

Anxiety disorders are a group of mental disorders characterised by exaggerated feelings of anxiety and fear responses. Anxiety is a worry about future events and fear is a reaction to current events. These feelings may cause physical symptoms, such as a fast heart rate and shakiness. There are a number of anxiety disorders: including generalised anxiety disorder, specific phobia, social anxiety disorder, separation anxiety disorder, agoraphobia, panic disorder, and selective mutism. The disorder differs by what results in the symptoms. People often have more than one anxiety disorder.

Anxiety disorders are caused by a complex combination of genetic and environmental factors. To be diagnosed, symptoms typically need to be present for at least six months, be more than would be expected for the situation, and decrease a person’s ability to function in their daily lives. Other problems that may result in similar symptoms include hyperthyroidism, heart disease, caffeine, alcohol, or cannabis use, and withdrawal from certain drugs, among others.

Without treatment, anxiety disorders tend to remain. Treatment may include lifestyle changes, counselling, and medications. Counselling is typically with a type of cognitive behavioural therapy. Medications, such as antidepressants or beta blockers, may improve symptoms.

About 12% of people are affected by an anxiety disorder in a given year and between 5%-30% are affected at some point in their life. They occur about twice as often in women than they do in men, and generally begin before the age of 25. The most common are specific phobia which affects nearly 12% and social anxiety disorder which affects 10% at some point in their life. They affect those between the ages of 15 and 35 the most and become less common after the age of 55. Rates appear to be higher in the United States and Europe.

Short- and Long-Term Anxiety

Anxiety can be either a short-term “state” or a long-term “trait”. Whereas trait anxiety represents worrying about future events, anxiety disorders are a group of mental disorders characterized by feelings of anxiety and fear.

Co-Morbidity

Anxiety disorders often occur with other mental health disorders, particularly major depressive disorder, bipolar disorder, eating disorders, or certain personality disorders. It also commonly occurs with personality traits such as neuroticism. This observed co-occurrence is partly due to genetic and environmental influences shared between these traits and anxiety.

Anxiety is often experienced by those with obsessive compulsive disorder and is an acute presence in panic disorder.

Risk Factors

Anxiety disorders are partly genetic, with twin studies suggesting 30-40% genetic influence on individual differences in anxiety. Environmental factors are also important. Twin studies show that individual-specific environments have a large influence on anxiety, whereas shared environmental influences (environments that affect twins in the same way) operate during childhood but decline through adolescence. Specific measured ‘environments’ that have been associated with anxiety include child abuse, family history of mental health disorders, and poverty. Anxiety is also associated with drug use, including alcohol, caffeine, and benzodiazepines (which are often prescribed to treat anxiety).

Neuroanatomy

Neural circuitry involving the amygdala (which regulates emotions like anxiety and fear, stimulating the HPA Axis and sympathetic nervous system) and hippocampus (which is implicated in emotional memory along with the amygdala) is thought to underlie anxiety. People who have anxiety tend to show high activity in response to emotional stimuli in the amygdala. Some writers believe that excessive anxiety can lead to an overpotentiation of the limbic system (which includes the amygdala and nucleus accumbens), giving increased future anxiety, but this does not appear to have been proven.

Research upon adolescents who as infants had been highly apprehensive, vigilant, and fearful finds that their nucleus accumbens is more sensitive than that in other people when deciding to make an action that determined whether they received a reward. This suggests a link between circuits responsible for fear and also reward in anxious people. As researchers note, “a sense of ‘responsibility’, or self-agency, in a context of uncertainty (probabilistic outcomes) drives the neural system underlying appetitive motivation (i.e. nucleus accumbens) more strongly in temperamentally inhibited than noninhibited adolescents”.

The Gut-Brain Axis

The microbes of the gut can connect with the brain to affect anxiety. There are various pathways along which this communication can take place. One is through the major neurotransmitters. The gut microbes such as Bifidobacterium and Bacillus produce the neurotransmitters GABA and dopamine, respectively. The neurotransmitters signal to the nervous system of the gastrointestinal tract, and those signals will be carried to the brain through the vagus nerve or the spinal system. This is demonstrated by the fact that altering the microbiome has shown anxiety- and depression-reducing effects in mice, but not in subjects without vagus nerves.

Another key pathway is the HPA axis, as mentioned above. The microbes can control the levels of cytokines in the body, and altering cytokine levels creates direct effects on areas of the brain such as the hypothalmus, the area that triggers HPA axis activity. The HPA axis regulates production of cortisol, a hormone that takes part in the body’s stress response. When HPA activity spikes, cortisol levels increase, processing and reducing anxiety in stressful situations. These pathways, as well as the specific effects of individual taxa of microbes, are not yet completely clear, but the communication between the gut microbiome and the brain is undeniable, as is the ability of these pathways to alter anxiety levels.

With this communication comes the potential to treat anxiety. Prebiotics and probiotics have been shown to reduced anxiety. For example, experiments in which mice were given fructo- and galacto-oligosaccharide prebiotics and Lactobacillus probiotics have both demonstrated a capability to reduce anxiety. In humans, results are not as concrete, but promising.

Genetics

Genetics and family history (e.g. parental anxiety) may put an individual at increased risk of an anxiety disorder, but generally external stimuli will trigger its onset or exacerbation. Estimates of genetic influence on anxiety, based on studies of twins, range from 25%-40% depending on the specific type and age-group under study. For example, genetic differences account for about 43% of variance in panic disorder and 28% in generalised anxiety disorder. Longitudinal twin studies have shown the moderate stability of anxiety from childhood through to adulthood is mainly influenced by stability in genetic influence. When investigating how anxiety is passed on from parents to children, it is important to account for sharing of genes as well as environments, for example using the intergenerational children-of-twins design.

Many studies in the past used a candidate gene approach to test whether single genes were associated with anxiety. These investigations were based on hypotheses about how certain known genes influence neurotransmitters (such as serotonin and norepinephrine) and hormones (such as cortisol) that are implicated in anxiety. None of these findings are well replicated, with the possible exception of TMEM132D, COMT and MAO-A. The epigenetic signature of BDNF, a gene that codes for a protein called brain derived neurotrophic factor that is found in the brain, has also been associated with anxiety and specific patterns of neural activity. and a receptor gene for BDNF called NTRK2 was associated with anxiety in a large genome-wide investigation. The reason that most candidate gene findings have not replicated is that anxiety is a complex trait that is influenced by many genomic variants, each of which has a small effect on its own. Increasingly, studies of anxiety are using a hypothesis-free approach to look for parts of the genome that are implicated in anxiety using big enough samples to find associations with variants that have small effects. The largest explorations of the common genetic architecture of anxiety have been facilitated by the UK Biobank, the ANGST consortium and the CRC Fear, Anxiety and Anxiety Disorders.

Medical Conditions

Many medical conditions can cause anxiety. This includes conditions that affect the ability to breathe, like COPD and asthma, and the difficulty in breathing that often occurs near death. Conditions that cause abdominal pain or chest pain can cause anxiety and may in some cases be a somatisation of anxiety; the same is true for some sexual dysfunctions. Conditions that affect the face or the skin can cause social anxiety especially among adolescents, and developmental disabilities often lead to social anxiety for children as well. Life-threatening conditions like cancer also cause anxiety.

Furthermore, certain organic diseases may present with anxiety or symptoms that mimic anxiety. These disorders include certain endocrine diseases (hypo- and hyperthyroidism, hyperprolactinemia), metabolic disorders (diabetes), deficiency states (low levels of vitamin D, B2, B12, folic acid), gastrointestinal diseases (celiac disease, non-celiac gluten sensitivity, inflammatory bowel disease), heart diseases, blood diseases (anaemia), cerebral vascular accidents (transient ischemic attack, stroke), and brain degenerative diseases (Parkinson’s disease, dementia, multiple sclerosis, Huntington’s disease), among others.

Substance-Induced

Several drugs can cause or worsen anxiety, whether in intoxication, withdrawal or as side effect. These include alcohol, tobacco, cannabis, sedatives (including prescription benzodiazepines), opioids (including prescription pain killers and illicit drugs like heroin), stimulants (such as caffeine, cocaine and amphetamines), hallucinogens, and inhalants. While many often report self-medicating anxiety with these substances, improvements in anxiety from drugs are usually short-lived (with worsening of anxiety in the long term, sometimes with acute anxiety as soon as the drug effects wear off) and tend to be exaggerated. Acute exposure to toxic levels of benzene may cause euphoria, anxiety, and irritability lasting up to 2 weeks after the exposure.

Psychological

Poor coping skills (e.g. rigidity/inflexible problem solving, denial, avoidance, impulsivity, extreme self-expectation, negative thoughts, affective instability, and inability to focus on problems) are associated with anxiety. Anxiety is also linked and perpetuated by the person’s own pessimistic outcome expectancy and how they cope with feedback negativity. Temperament (e.g. neuroticism) and attitudes (e.g. pessimism) have been found to be risk factors for anxiety.

Cognitive distortions such as overgeneralising, catastrophising, mind reading, emotional reasoning, binocular trick, and mental filter can result in anxiety. For example, an overgeneralised belief that something bad “always” happens may lead someone to have excessive fears of even minimally risky situations and to avoid benign social situations due to anticipatory anxiety of embarrassment. In addition, those who have high anxiety can also create future stressful life events. Together, these findings suggest that anxious thoughts can lead to anticipatory anxiety as well as stressful events, which in turn cause more anxiety. Such unhealthy thoughts can be targets for successful treatment with cognitive therapy.

Psychodynamic theory posits that anxiety is often the result of opposing unconscious wishes or fears that manifest via maladaptive defence mechanisms (such as suppression, repression, anticipation, regression, somatisation, passive aggression, dissociation) that develop to adapt to problems with early objects (e.g. caregivers) and empathic failures in childhood. For example, persistent parental discouragement of anger may result in repression/suppression of angry feelings which manifests as gastrointestinal distress (somatisation) when provoked by another while the anger remains unconscious and outside the individual’s awareness. Such conflicts can be targets for successful treatment with psychodynamic therapy. While psychodynamic therapy tends to explore the underlying roots of anxiety, cognitive behavioural therapy has also been shown to be a successful treatment for anxiety by altering irrational thoughts and unwanted behaviours.

Evolutionary Psychology

An evolutionary psychology explanation is that increased anxiety serves the purpose of increased vigilance regarding potential threats in the environment as well as increased tendency to take proactive actions regarding such possible threats. This may cause false positive reactions but an individual suffering from anxiety may also avoid real threats. This may explain why anxious people are less likely to die due to accidents. There is ample empirical evidence that anxiety can have adaptive value. Within a school, timid fish are more likely than bold fish to survive a predator.

When people are confronted with unpleasant and potentially harmful stimuli such as foul odours or tastes, PET-scans show increased blood flow in the amygdala. In these studies, the participants also reported moderate anxiety. This might indicate that anxiety is a protective mechanism designed to prevent the organism from engaging in potentially harmful behaviours.

Social

Social risk factors for anxiety include a history of trauma (e.g. physical, sexual or emotional abuse or assault), bullying, early life experiences and parenting factors (e.g. rejection, lack of warmth, high hostility, harsh discipline, high parental negative affect, anxious childrearing, modelling of dysfunctional and drug-abusing behaviour, discouragement of emotions, poor socialisation, poor attachment, and child abuse and neglect), cultural factors (e.g. stoic families/cultures, persecuted minorities including the disabled), and socioeconomics (e.g. uneducated, unemployed, impoverished although developed countries have higher rates of anxiety disorders than developing countries). A 2019 comprehensive systematic review of over 50 studies showed that food insecurity in the United States is strongly associated with depression, anxiety, and sleep disorders. Food-insecure individuals had an almost three (3) fold risk increase of testing positive for anxiety when compared to food-secure individuals.

Gender Socialisation

Contextual factors that are thought to contribute to anxiety include gender socialisation and learning experiences. In particular, learning mastery (the degree to which people perceive their lives to be under their own control) and instrumentality, which includes such traits as self-confidence, self-efficacy, independence, and competitiveness fully mediate the relation between gender and anxiety. That is, though gender differences in anxiety exist, with higher levels of anxiety in women compared to men, gender socialisation and learning mastery explain these gender differences.

Treatment

The first step in the management of a person with anxiety symptoms involves evaluating the possible presence of an underlying medical cause, whose recognition is essential in order to decide the correct treatment. Anxiety symptoms may mask an organic disease, or appear associated with or as a result of a medical disorder.

Cognitive behavioural therapy (CBT) is effective for anxiety disorders and is a first line treatment. CBT appears to be equally effective when carried out via the internet. While evidence for mental health apps is promising, it is preliminary.

Psychopharmacological treatment can be used in parallel to CBT or can be used alone. As a general rule, most anxiety disorders respond well to first-line agents. First-line drugs are the selective serotonin reuptake inhibitors and serotonin-norepinephrine reuptake inhibitors. Benzodiazepines are not recommended for routine use. Other treatment options include pregabalin, tricyclic antidepressants, buspirone, moclobemide, and seratriline, among others.

Prevention

The above risk factors give natural avenues for prevention. A 2017 review found that psychological or educational interventions have a small yet statistically significant benefit for the prevention of anxiety in varied population types.

Pathophysiology

Anxiety disorder appears to be a genetically inherited neurochemical dysfunction that may involve autonomic imbalance; decreased GABA-ergic tone; allelic polymorphism of the catechol-O-methyltransferase (COMT) gene; increased adenosine receptor function; increased cortisol.

In the central nervous system (CNS), the major mediators of the symptoms of anxiety disorders appear to be norepinephrine, serotonin, dopamine, and gamma-aminobutyric acid (GABA). Other neurotransmitters and peptides, such as corticotropin-releasing factor, may be involved. Peripherally, the autonomic nervous system, especially the sympathetic nervous system, mediates many of the symptoms. Increased flow in the right parahippocampal region and reduced serotonin type 1A receptor binding in the anterior and posterior cingulate and raphe of patients are the diagnostic factors for prevalence of anxiety disorder.

The amygdala is central to the processing of fear and anxiety, and its function may be disrupted in anxiety disorders. Anxiety processing in the basolateral amygdala has been implicated with dendritic arborisation of the amygdaloid neurons. SK2 potassium channels mediate inhibitory influence on action potentials and reduce arborisation.

Emotional Information Processing & Assessment of Cognitive Functions in Social Anxiety Disorder

Research Paper Title

Emotional Information Processing and Assessment of Cognitive Functions in Social Anxiety Disorder: An Event-Related Potential Study.

Background

The aim of the study was to determine deficits in cognitive areas, including social cognition such as emotion recognition capacity, theory of mind, and electrophysiological alterations in patients with social anxiety disorder (SAD) and to identify their effects on clinical severity of SAD.

Methods

Enrolled in the study were 26 patients diagnosed with SAD and 26 healthy volunteers. They were administered the Liebowitz Social Anxiety Scale (LSAS), Reading Mind in the Eyes Test (RMET), and Cambridge Neuropsychological Test Automated Battery. EEG monitoring was performed for electrophsiologic investigation.

Results

In the patient group, total reading the mind scores were lower (P = .027) while P300 latencies and emotion recognition latency during the Emotion Recognition Task (ERT) were longer (P = .038 and P = .012, respectively). The false alarm scores in the Rapid Visual Information Processing Task (RVP) were higher in the patient group (P = .038).

In a model created using multivariate linear regression analysis, an effect of ERT and RVP scores on LSAS scores was found.

Conclusions

The researches suggest the results of the study confirm that particularly impairment of cognitive functions such as sustained attention and emotion recognition may seriously affect the clinical presentation negatively. P300 latency in the parietal region may has the potential to be a biological marker that can be used in monitoring treatment.

Reference

Tetik, D., Gica, S., Bestepe, E.E., Buyukavsar, A. & Gulec, H. (2020) Emotional Information Processing and Assessment of Cognitive Functions in Social Anxiety Disorder: An Event-Related Potential Study. Emotional Information Processing and Assessment of Cognitive Functions in Social Anxiety Disorder: An Event-Related Potential Study. Clinical EEG and Neuroscience. doi: 10.1177/1550059420981506. Online ahead of print.