Differential susceptibility effects of oxytocin gene (OXT) polymorphisms and perceived parenting on social anxiety among adolescents

2017 ◽  
Vol 30 (2) ◽  
pp. 449-459 ◽  
Author(s):  
Susanne Olofsdotter ◽  
Cecilia Åslund ◽  
Tomas Furmark ◽  
Erika Comasco ◽  
Kent W. Nilsson

AbstractSocial anxiety is one of the most commonly reported mental health problems among adolescents, and it has been suggested that parenting style influences an adolescent's level of anxiety. A context-dependent effect of oxytocin on human social behavior has been proposed; however, research on the oxytocin gene (OXT) has mostly been reported without considering contextual factors. This study investigated the interactions between parenting style and polymorphic variations in the OXT gene in association with social anxiety symptoms in a community sample of adolescents (n = 1,359). Two single nucleotide polymorphisms linked to OXT, rs4813625 and rs2770378, were genotyped. Social anxiety and perceived parenting style were assessed by behavioral questionnaires. In interaction models adjusted for sex, significant interaction effects with parenting style were observed for both variants in relation to social anxiety. The nature of the interactions was in line with the differential susceptibility framework for rs4813625, whereas for rs2770378 the results indicated a diathesis–stress type of interaction. The findings may be interpreted from the perspective of the social salience hypothesis of oxytocin, with rs4813625 affecting social anxiety levels along a perceived unsafe–safe social context dimension.

2017 ◽  
Vol 41 (S1) ◽  
pp. S72-S72
Author(s):  
S. Olofsdotter ◽  
C. Åslund ◽  
T. Furmark ◽  
E. Comasco ◽  
K. Nilsson

IntroductionAdolescence is a period of increasing demands in independent social functioning where parenting style may have an impact on social anxiety. A context-dependent effect of oxytocin on human social behavior has been suggested, however research on the gene coding for oxytocin (OXT) has mostly been reported without considering contextual factors.AimThis study investigated interactions between parenting style and polymorphic variations in the OXT gene in association with social anxiety symptoms in a community sample of adolescents.MethodsThe study group consisted of 1359 adolescents. Two single nucleotide polymorphisms located near OXT, rs4813625 and rs2770378, were genotyped. Social anxiety and perceived parenting style were assessed by behavioral questionnaires.ResultsSignificant joint effects in line with the differential susceptibility framework were observed for rs4813625 with parenting style. The levels of social anxiety among C allele carriers were conditional on the level of supportive parenting style whereas homozygote G carriers’ levels of social anxiety were unaffected by supportive parenting style. The nature of the interactions between rs2770378 and parenting style was in line with the diatheses-stress model. However, associations of rs2770378 and parenting style with social anxiety became nonsignificant in nonlinear models.ConclusionsThe study provides preliminary evidence for a modifying effect of supportive parenting style on the relationship between rs4813625 and social anxiety symptoms in adolescents, independent of sex. The findings may be interpreted from the perspective of the social salience hypotheses of oxytocin, with rs4813625 affecting social anxiety levels along a perceived unsafe–safe social context dimension.Disclosure of interestThe authors have not supplied their declaration of competing interest.


2007 ◽  
Vol 28 (3) ◽  
pp. 161-164 ◽  
Author(s):  
Rosalind Arden ◽  
Nicole Harlaar ◽  
Robert Plomin

Abstract. An association between intelligence at age 7 and a set of five single-nucleotide polymorphisms (SNPs) has been identified and replicated. We used this composite SNP set to investigate whether the associations differ between boys and girls for general cognitive ability at ages 2, 3, 4, 7, 9, and 10 years. In a longitudinal community sample of British twins aged 2-10 (n > 4,000 individuals), we found that the SNP set is more strongly associated with intelligence in males than in females at ages 7, 9, and 10 and the difference is significant at 10. If this finding replicates in other studies, these results will constitute the first evidence of the same autosomal genes acting differently on intelligence in the two sexes.


Author(s):  
L. P. Kuzmina ◽  
A. G. Khotuleva ◽  
L. M. Bezrukavnikova

Based on an examination of 102 employees of lead-acid batteries recycling plant, there have been determined associations of single nucleotide polymorphisms of calcium metabolism regulators genes VDR (rs10735810) and CALCR (rs187197) and blood lead levels, urine ALA, erythrocytic parameters, that indicates significance of these genetic markers as indicators of susceptibility to lead exposure.


2002 ◽  
Vol 383 (6) ◽  
pp. 983-987 ◽  
Author(s):  
Yuanqi Zhu ◽  
Mark A. Doll ◽  
David W. Hein

Abstract Nacetyltransferase 2 (NAT2) catalyzes Nacetylation and Oacetylation of many drugs and environmental carcinogens. Genetic polymorphisms in the NAT2 gene have been associated with differential susceptibility to cancers and drug toxicity from these compounds. Single nucleotide polymorphisms (SNPs) have been identified in the human NAT2 coding region. A new allele, NAT2*19, possessing the C190T (R64W) exchange, was recently identified. In order to understand the effect of this new SNP, recombinant NAT2*4 (reference) and NAT2*19 were expressed in yeast (Schizosaccharomyces pombe). The C190T (R64W) SNP in NAT2*19 caused substantial reduction in the NAT2 protein level and stability, but did not cause significant reduction in transformation efficiency or mRNA level. The enzymatic activities for Nacetylation of two arylamine carcinogens (2-aminofluorene, 4-aminobiphenyl), and a sulfonamide drug (sulfamethazine) were over 100-fold lower for NAT2 19 compared to reference NAT2 4. Kinetic studies showed a reduction in Vmax but no significant change in substrate Km. In addition, the SNP caused significant reduction in the Oacetylation of the Nhydroxy 2-amino-1-methyl-6-phenylimidazo [4,5-b] pyridine. These results show that NAT2*19 possessing the C190T (R64W) SNP encodes a slow acetylator phenotype for both N and Oacetylation, due to a reduction in the amount and stability of the NAT2 19 allozyme.


2020 ◽  
Vol 63 (1) ◽  
Author(s):  
Viktoria Chubar ◽  
Karla Van Leeuwen ◽  
Patricia Bijttebier ◽  
Evelien Van Assche ◽  
Guy Bosmans ◽  
...  

Abstract Background. Social anxiety symptoms (SAS) are among the most common mental health problems during adolescence, and it has been shown that parenting influences the adolescent’s level of social anxiety. In addition, it is now widely assumed that most mental health problems, including social anxiety, originate from a complex interplay between genes and environment. However, to date, gene–environment (G × E) interactions studies in the field of social anxiety remain limited. In this study, we have examined how 274 genes involved in different neurotransmission pathways interact with five aspects of perceived parenting as environmental exposure (i.e., support, proactive control, psychological control, punitive control, and harsh punitive control) to affect SAS during adolescence. Methods. We have applied an analytical technique that allows studying genetic information at the gene level, by aggregating data from multiple single-nucleotide-polymorphisms within the same gene and by taking into account the linkage disequilibrium structure of the gene. All participants were part of the STRATEGIES cohort of 948 Flemish adolescents (mean age = 13.7), a population-based study on the development of problem behaviors in adolescence. Relevant genes were preselected based on prior findings and neurotransmitter-related functional protein networks. Results. The results suggest that genes involved in glutamate (SLC1A1), glutathione neurotransmission (GSTZ1), and oxidative stress (CALCRL), in association with harsh punitive parenting, may contribute to social anxiety in adolescence. Isolated polymorphisms in these genes have been related to anxiety and related disorders in earlier work.Conclusions: Taken together, these findings provide new insights into possible biological pathways and environmental risk factors involved in the etiology of social anxiety symptoms’ development. Conclusions. Taken together, these findings provide new insights into possible biological pathways and environmental risk factors involved in the etiology of social anxiety symptoms’ development.


2020 ◽  
Vol 24 (1) ◽  
pp. 17
Author(s):  
Chin Wen Cong ◽  
Chuah Peng Aik ◽  
Mohtaram Rabbani ◽  
Arianna Oh Zhing Ni

Author(s):  
Salma Rehman ◽  
Madiha Asghar

Current study was planned to find out the difference between the perceived parenting styles of drug addict and non-addict medical students. Total sample of the study was two hundred (N=200) medical students that comprised of one hundred addict (n=100) and one hundred (n=100) non-addict medical students with age range of 18 to 29 years. Data was collected from different medical colleges in Khyber Pakhtunkhwa through convenient and snow ball techniques. Data was collected through adolescent’s alcohol and drug usage scale (Moberg, 1991)and parenting styles questionnaire (Buri, 1991) . The results of the study indicated that authoritative parenting style was significantly reported by non-addict medical students, whereas addict medical students reported higher scores on authoritarian parenting style. It can be therefore concluded from the findings of the study that parenting styles play a significant role in the mental wellbeing and promotion of healthy habits among youth. The study supports the idea that controlling parenting style may contribute to promote mental health problems among youth such as drug addiction.


Author(s):  
L. P. Kuzmina ◽  
A. G. Khotuleva ◽  
N. N. Anokhin

Associations of single nucleotide polymorphisms of the cytokine genes TGFb1 (rs1800471), IL1b (rs16944), IL4 (rs2243250), IL6 (rs1800795) with the development and severity of asbestosis have been identified.


2014 ◽  
Vol 24 (58) ◽  
pp. 223-232 ◽  
Author(s):  
Alessandra Turini Bolsoni-Silva ◽  
Sonia Regina Loureiro

Social anxiety is one of the most frequent mental health problems and there is no consensus regarding the relation between social skills and anxiety. This study aimed to compare the behavioral indicators of social skills presented by university students with social anxiety in relation to a non-clinical group, and to verify the predictive value of the social skills for social anxiety. Participants were 288 university students, 144 with Anxiety Disorder and 144 non-clinical. Social skills were assessed using the QHC-University (Social Skills, Behaviors and Context Assessment Questionnaire for University Students) and the IHS-Del-Prette instruments. Mental health indicators were assessed through screening and diagnostic instruments. Through univariate and multivariate analysis an association was found between social skills and anxiety, highlighting public speaking, potential, difficulties, and the total social skills score as predictors of social anxiety, which contributes to demonstrating the role the resources and difficulties play in this.


2020 ◽  
Vol 218 (2) ◽  
Author(s):  
Katharina Richard ◽  
Kurt H. Piepenbrink ◽  
Kari Ann Shirey ◽  
Archana Gopalakrishnan ◽  
Shreeram Nallar ◽  
...  

Two cosegregating single-nucleotide polymorphisms (SNPs) in human TLR4, an A896G transition at SNP rs4986790 (D299G) and a C1196T transition at SNP rs4986791 (T399I), have been associated with LPS hyporesponsiveness and differential susceptibility to many infectious or inflammatory diseases. However, many studies failed to confirm these associations, and transfection experiments resulted in conflicting conclusions about the impact of these SNPs on TLR4 signaling. Using advanced protein modeling from crystallographic data of human and murine TLR4, we identified homologous substitutions of these SNPs in murine Tlr4, engineered a knock-in strain expressing the D298G and N397I TLR4 SNPs homozygously, and characterized in vivo and in vitro responses to TLR4 ligands and infections in which TLR4 is implicated. Our data provide new insights into cellular and molecular mechanisms by which these SNPs decrease the TLR4 signaling efficiency and offer an experimental approach to confirm or refute human data possibly confounded by variables unrelated to the direct effects of the SNPs on TLR4 functionality.


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