Extremely shy and genetically close
Investigating neurobiological endophenotypes of Social Anxiety Disorder
- Janna Marie Bas-Hoogendam
- 14 January 2020
Social anxiety disorder (SAD) is a serious psychiatric condition, which typically evolves during late childhood and early adolescence. Patients are ‘extremely shy’: they are afraid of a negative evaluation by others and avoid social situations as much as possible, leading to significant adverse effects on important areas of functioning. As SAD is characterized by a chronic course, insight in the factors that make children and adolescents vulnerable to develop SAD is pivotal to get a grip on the disorder and to prevent its lifelong negative consequences.
Previous work on SAD has identified several biological, psychological, and social factors that play a role in the development and the maintenance of SAD. In her work, Janna Marie has built upon the results of family- and twin studies, which demonstrated that the genetic makeup of individuals is one of the contributing factors to the development of SAD: being ‘genetically close’ to a patient with SAD leads to an elevated risk to develop the disorder. Previous studies reported heritability estimates of SAD around 50 %, but little is known about the genetic variations underlying the susceptibility to SAD.
The unique Leiden Family Lab study on Social Anxiety Disorder (LFLSAD) was designed to examine the genetic vulnerability to develop SAD. More than 100 family-members from eight families genetically enriched for SAD were investigated. Using magnetic resonance imaging (MRI), Janna Marie Bas-Hoogendam explored within the LFLSAD sample which brain characteristics were associated with social anxiety, and had a genetic background. She summarized her results in her PhD thesis ‘Extremely Shy & Genetically Close’ (9 research articles, 8 already published in peer-reviewed journals), and described several promising candidate endophenotypes of SAD: measurable characteristics on the pathway from genotype to phenotype, which shed light on the genetic vulnerability to develop SAD. These endophenotypes involved alterations in the structure (anatomy) and function of the brain (for example enhanced activity in response to faces with a neutral expression and increased responses to unintentional social norm violations). Thereby, this work provides new insights in the neurobiological vulnerability to develop SAD.