A Research On Social Anxiety Disorder From Environmental And Genetic Perspective

The DSM-5 defines social anxiety disorder as when a person experiences fear in a social context which appears excessive or unreasonable, and that the person must be aware of their excessive/unreasonable fear. This disorder can affect nearly all aspects of someone’s life, whether it be a speech in front of class, or even asking someone for directions; this social anxiety leads a person to feel as though they are being judged negatively and this causes more anxiety. There has been much debate on what is the best explanation for the cause of social anxiety disorder; this is the conflict between environmental influences on social anxiety disorder which can come through forms like psychological stress and pressure from peers. The conflict is also between genetic influences, potentially in the form of the genes for the disorder being present at birth, or through neurological imbalances. In this essay, I will discuss research into both environmental causes and explanations, and genetic causes and explanations.

One study by Pickering et al. (2019) looked into the environmental explanation of social anxiety disorder, particularly in adolescent girls. This study found that the main risk factors for teenage girls were negative experiences with friends such as arguments and falling out with friends and family, as well as a lack of close friendships whom the girls need as a support system. From this evidence, the researchers suggested that ‘frameworks’ must be developed in order to reduce the risk of social anxiety but in gender specific ways. It is clear that this study highlights the issues that are faced by young females, which is important as most research focuses on the male experience and little light is shed on females in scientific research. Yet, it is important to note that as the study is gynocentric it does not consider the risk factors in young males, and therefore we cannot generalise the results to the whole population since there is a lack of population validity. Despite the lack of population validity, this study does have great temporal validity as the study was conducted recently and therefore the findings are up to date and we can trust the results more. However, this study fails to consider whether these young females were biologically predisposed to social anxiety to begin with, and therefore it is very difficult to fully trust these findings since potential confounding variables were not controlled in the first place. The findings of this research do suggest that there is an environmental influence in social anxiety disorder, yet we cannot truly be certain that this is the case due to the issue of gender bias in this particular study. Barnett et al. (2020) also looked at environmental influences on social anxiety disorder, and focused on the relationship between social anxiety and perceived social support and if this relationship was different for each gender. The researchers had 813 university students (both male and female) conduct an online survey. They found that for both men and women, social anxiety had a high correlation and relationship with lower social support through less expressiveness with each other. There was a difference between men and women, which was that for men with lower perceived social support through lower preciseness had a relationship with social anxiety, meanwhile women found a link with lower verbal aggressiveness as well as higher emotions. The researchers stated that psychotherapy would be the best treatment for social anxiety in regards to perceived social support. An advantage of this study is that it considers both genders and shows that different environmental influences, regarding perceived social support, do show a strong relationship with social anxiety disorder. However, even though the relationship between these co-variables are strong, we cannot establish causation because there were no experimental conditions that can prove that lower perceived social support causes social anxiety disorder. Similar to Pickering et al. (2019), this study also ignores the potential biological influences that may have affected these results, and we cannot automatically assume that it is only environmental influences that can explain social anxiety disorder. It is clear that despite any limitations of the empirical evidence, they show a pattern that suggests that there is an environmental influence on social anxiety disorder.

There is also research that looks into the genetic explanation for social anxiety disorder. The study by Forstner et al. (2017) looked at the serotonin gene SLC6A4 and how this contributes towards social anxiety disorder in 321 German SAD patients. The researchers found that there are numerous genes that contribute to social anxiety disorder, as SNPs (single-nucleotide polymorphisms) were found near SLC6A4 which is the main area where SSRIs work to treat anxiety disorders. This study was done in a lab experimental condition, which is great to increase the reliability of the findings, and highlights that the findings can be trusted. Furthermore, the findings were statistically significant which highlights that there is an association between genetics and social anxiety disorder. However, this study focuses on the relationship between the variables, but we cannot establish causation as we do not know whether social anxiety disorder is caused by this gene, or if social anxiety disorder has caused the variances in the gene instead, which needs to be investigated further. Although, there is a large sample size in this study, which we can infer that there is high population validity since we are likely to generalise these findings to other cases of social anxiety disorder. Stein et al. (2017) conducted a study on army service members where they looked at the heritability of social anxiety by looking at a New Soldier Study (NSS) and a pre/post Deployment Survey (PPDS). The NSS consisted of genotyping the cohort and picked samples based on different phenotypes and collecting a subset (mainly focused in PTSD) for genotyping. PPDS is a survey that took baseline data from US soldiers approximately six weeks during their deployment in Afghanistan. They found that there was a SNP-based heritability for social anxiety (12%) and confirmed that social anxiety disorder has heritability, and highlights the importance of finding genetic risks for SAD. One limitation of this study is that it has a small sample size, and is therefore less likely to find genes that will have an impact on social anxiety. Moreover, this small sample size makes it difficult to generalise the results since there are so little participants and lacks population validity. Although, this study is very reliable due to the laboratory experimental conditions, since all extraneous and confounding variables have been controlled. Yet, neither one of these studies refers to any environmental influences, in particular, the harsh surroundings of being in a war-like setting are likely to trigger anxiety-like symptoms for those who do not have a genetic predisposition. Although this research does present some issues with methodology, it is clear that there is a genetic influence, even though more research does need to be done in this area.

It is important to consider the power of both explanations combined – an interactionist approach. Perhaps a person may have a genetic predisposition, but the exposure to a negative social situation may trigger the disorder. Gazelle (2013) looked into a more interactionist explanation in young girls, who were assigned to different play groups and they had to play with their familiar play group for 5 days and unfamiliar for another 5 days. Gazelle found that social anxiety is already pre-existing in a child but social anxiety is also triggered by the child’s surroundings. She also found that children who were in the anxious solitary excluded group experienced the most distress when they experienced rejection, and also saw that anxious solitary children carried their behaviour style across all different contexts, implying that anxiety is already existent in the child. This study has some benefits, it has high ecological validity as the study was done in a manner that would be realistic to the children, therefore the results would be authentic. Furthermore, this study highlights the impact of both genetic predisposition as well as the environment, which reduces the reductionism that the other studies promoted. However, it is difficult to generalise these results since the study was done on young children; adults may not experience these same effects and so it is difficult to confirm if these findings are completely valid. The main importance of this explanation is that this has implications on treatments, an interactionist treatment of both SSRIs and CBT would be more effective for patients with social anxiety.

All empirical research that has been discussed has provided an insight on how we could explain social anxiety disorder. It is clear that there is an environmental influence on SAD, predominantly from peer stress and due to lower perceived social support. Furthermore, there is some supporting evidence to show that there is a genetic influence on social anxiety due to variances in the gene important for serotonin reuptake, as well as finding a heritability for social anxiety. Yet, it appears that when we combine both explanations there is more valid and reliable findings, and this interactionist approach has demonstrated that treatment for social anxiety is more effective when both SSRIs and CBT are used.