scholarly journals The interaction between serotonin transporter allelic variation and maternal care modulates sociability on Instagram

Author(s):  
Andrea Bonassi ◽  
Ilaria Cataldo ◽  
Giulio Gabrieli ◽  
Moses Tandiono ◽  
Jia Nee Foo ◽  
...  

Human social interactions ensure recognition and approval from others, both in offline and online environments. This study applies a model from behavioural genetics on Instagram sociability to explore the impact of individual development on the behaviour on social networks.We hypothesize that sociable attitudes on Instagram resulted from an interaction between serotonin transporter gene alleles and the individual’s social relationship with caregivers. We assess environmental and genetic components of 57 Instagram users. The self-report questionnaire Parental Bonding Instrument is adopted to determine the quality of parental bonding. The number of posts, followed users (“followings”), and followers are collected from Instagram as measures of online social activity. Additionally, the ratio between the number of followers and followings (“Social Desirability Index”) was calculated to estimate the asymmetry of each user’s social network. Finally, buccal mucosa cell samples were acquired, and the polymorphism rs25531 (T/T homozygotes vs C-carriers) within the serotonin transporter gene was examined.In the preliminary analysis, we identified a gender effect on the number of followings. In line with our predictions, we specifically found a gene- environment interaction on the standardized Instagram “Social Desirability Index”: users with the genotype more sensitive to environmental influences (T/T homozygotes) showed a higher Instagram “Social Desirability Index” than non-sensitive ones (C-carriers) when they experienced positive maternal care.This result may contribute to the understanding of online social behaviour from a gene*environment perspective.

2009 ◽  
Vol 24 (S1) ◽  
pp. 1-1 ◽  
Author(s):  
M. Melchior ◽  
T.E. Moffitt ◽  
R. Poulton ◽  
K. Sugden ◽  
A. Caspi

Background:High work demands (i.e. a heavy workload, tight time pressures, conflicting work tasks) put individuals at high risk of depression. Our aim was to test whether the relationship between high work demands and depression is moderated by genetic vulnerability to depression and by work control.Methods:Participants are members of the Dunedin Study, a 1972-73 longitudinal birth cohort assessed most recently in 2004-2005, at age 32 (96% response rate). This analysis included all participants who were employed at age 32. Depression was measured using the Diagnostic Interview Schedule. Work demands and work control were assessed in an interview. Genetic vulnerability to stress was ascertained by the serotonin transporter gene (5-HTT).Results:Among individuals exposed to high work demands, symptoms of depression were significantly higher among those who carried two short alleles of the 5-HTT gene (‘s/s’ group) than among ‘l’ carriers (interaction between 5-HTT gene and work demands: β=4.22, se=1.86, p=0.02). However, this gene-environment interaction was only present among those individuals who had low control over their work (interaction between 5-HTT gene and high work demands: β: 7.21, se: 2.73, p=0.009), not among those who had high work control (interaction between 5-HTT gene and high work demands: β: 1.32, se: 2.53, p=0.60).Conclusion:Pending replication, the serotonin transporter gene appears to moderate the effects of high work demands on symptoms of depression. This gene-environment interaction is attenuated by high work control.


2006 ◽  
Vol 188 (3) ◽  
pp. 210-215 ◽  
Author(s):  
Kay Wilhelm ◽  
Philip B. Mitchell ◽  
Heather Niven ◽  
Adam Finch ◽  
Lucinda Wedgwood ◽  
...  

BackgroundA relationship between the serotonin transporter gene, adverse events and onset of major depression has been reported.AimsTo replicate a gene × environment interaction in a cohort with longitudinal data for life events, experience of depression, parental bonding and neuroticism.MethodAtthe 25-year follow-up, genomic DNA was obtained from 127 cohort members (mean age 48 years) to determine the genotype of the serotonin transporter gene-linked promoter region (5-HTTLPR). Associations were investigated between the 5-HTTLPR genotype, positive and adverse life events and the gene × environment interaction, and also between the 5-HTTLPR genotype and risk factors for depression.ResultsNo relationship was found between 5-HTTLPR genotype and either risk factors for depression or positive life events. Adverse life events had a significantly greater impact on the onset of depression for individuals with the s/s genotype.ConclusionsThe 5-HTTLPR genotype is a significant predictor of onset of major depression following multiple adverse events. This is one of the more robust findings concerning specific biological risk factors for depression.


2009 ◽  
Vol 194 (5) ◽  
pp. 404-410 ◽  
Author(s):  
Kay Wilhelm ◽  
Bettina Meiser ◽  
Philip B. Mitchell ◽  
Adam W. Finch ◽  
Jennifer E. Siegel ◽  
...  

BackgroundRecent studies show that adverse life events have a significantly greater impact on depression onset for those with the s/s allele of the genotype for the 5-HT gene-linked promoter region. Research in genes related to risk of depression leads to the question of how this information is received by individuals.AimsTo investigate factors related to the response to receiving one's own serotonin transporter genotype results.MethodPredictors of the impact of receiving individual genotype data were assessed in 128 participants in a study of gene–environment interaction in depression onset.ResultsTwo-thirds decided to learn their individual genotype results (receivers) and prior to disclosure this decision was associated with a perception of greater benefit from receipt of the information (P=0.001). Receivers completing the 2-week (n=76) and 3-month follow-up (n=78) generally reported feeling pleased with the information and having had a more positive experience than distress. However, distress was related to genotype, with those with the s/s allele being most affected.ConclusionsThere was high interest in, and satisfaction with, learning about one's serotonin transporter genotype. Participants appeared to understand that the gene conferred susceptibility to depression rather than a direct causal effect.


Author(s):  
Leandra Kuhn ◽  
Hannes Noack ◽  
Nadine Skoluda ◽  
Lisa Wagels ◽  
Ann-Kristin Röhr ◽  
...  

AbstractThe experience of stress is related to individual wellbeing and vulnerability to psychopathology. Therefore, understanding the determinants of individual differences in stress reactivity is of great concern from a clinical perspective. The functional promotor polymorphism of the serotonin transporter gene (5-HTTLPR/rs25531) is such a factor, which has been linked to the acute stress response as well as the adverse effect of life stressors. In the present study, we compared the impact of two different stress induction protocols (Maastricht Acute Stress Test and ScanSTRESS) and the respective control conditions on affective ratings, salivary cortisol levels and cognitive performance. To this end, 156 healthy young males were tested and genotyped for the 5-HTTLPR/rs25531 polymorphism. While combined physiological and psychological stress in the MAST led to a greater cortisol increase compared to control conditions as well as the psychosocial ScanSTRESS, subjective stress ratings were highest in the ScanSTRESS condition. Stress induction in general affected working memory capacity but not response inhibition. Subjective stress was also influenced by 5-HTTLPR/rs25531 genotype with the high expression group showing lower stress ratings than lower expression groups. In line with previous research, we identified the low expression variant of the serotonin transporter gene as a risk factor for increased stress reactivity. While some dimensions of the human stress response may be stressor specific, cognitive outcomes such as working memory performance are influenced by stress in general. Different pathways of stress processing and possible underlying mechanisms are discussed.


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