Subjects: Psychology >> Developmental Psychology submitted time 2023-06-23
Abstract： There has been a dramatic rise in gene–environment interaction (G × E) studies of depression over the last two decades. These studies are pivotal to understanding the etiology of depression and individual differences in environmental sensitivity. However, these studies rarely take into consideration how the genotype by environment interactions change over development and how the interactions work on the developmental trajectories of depression. The brain-derived neurotrophic factor (BDNF) gene is a good candidate for the investigation of the dynamic genetic effects on depression because it is involved in several age-related changes in behavior and brain maturation. On the one hand, the effect of the BDNF gene may depend on the basal BDNF level. The BDNF level peaks during adolescence, so the effect of the BDNF gene on depression may change during development. Moreover, peer experiences change may alter epigenetic modifications of the BDNF gene, which may change the pattern of gene–environment interactions. On the other hand, according to the developmental cascades model, the differences in genetic effects on depression may increase over time in that initial depressive symptoms may evoke poor peer experiences. Taken together, this study aimed to investigate the age differences in the G × E interaction on depression and the G × E effect on the developmental trajectories of depression.
One thousand and eighty-six adolescents (aged 11–12 years with a mean of 12.32, 50% girls) were followed up for three years. Saliva samples, self-reported depressive symptoms, and peer nomination were all collected. All of the measures showed good reliability. Concurrent hierarchical regression analyses and latent growth curve models (LGCMs) were conducted. We also completed re-parameterized regression and parallel LGCMs to understand the gene by environment interaction pattern and the dynamic association between peer relationships and depression.
The results showed that the BDNF Val66Met polymorphism significantly moderated the influence of peer rejection—but not peer acceptance—on youth depressive symptoms at three time points; however, the susceptible genotype changed over time. In particular, the effect of peer rejection on depression was stronger in MetMet compared to ValMet carriers at 12 years of age; the effect of peer rejection on depression was stronger in MetMet and ValVal compared to ValMet carriers at 13 years of age; the effect of peer rejection on depression was stronger in ValVal carriers compared to ValMet carriers at 14 years of age. LGCMs suggested that adolescents’ depression increased in a linear trajectory from 12 to 14 years of age. In addition, there were significant genotype differences in the change of depression over time, but this effect was not moderated by peer relationships.
These findings may move research in the field away from the simplistic notion of risk alleles, recognizing that an allele may be a risk factor during one period and a protective factor during another. Further, this study has progressed the conceptualization of how genes and the environment interact to influence the developmental trajectories of depression during early adolescence.
Subjects: Psychology >> Social Psychology submitted time 2023-03-27 Cooperative journals: 《心理学报》
Abstract： Dopaminergic genes have been frequently found to be associated with aggressive behavior, but the results are inconsistent. One reason for the inconsistencies is there might be the U-shaped relationship between dopaminergic genetic variants and aggressive behavior. More specifically, evidence has suggested an inverted U-shaped relationship between dopamine activity and prefrontal cortex (PFC) function (a critical region related to aggression), with both dopaminergic hypofunction and hyperfunction, were related to poor PFC function. It is possible that the relationship between dopaminergic genes and aggression approximates a U-shaped function. However, such U-shaped relationship is rarely investigated in previous studies. Moreover, several concerns have been raised about the ignoring the polygenic traits of aggressive behavior when conducting gene by environment interaction (G×E) research using single loci. Therefore, the present study aimed to examine the interaction between dopaminergic genetic variants and maternal negative parenting on adolescent aggressive behavior by adopting the approach of multilocus genetic profile score (MGPS).Participants were 1044 adolescents (mean age 13.32 ± 0.49 years old at Time 1, 50.2% females) recruited from the community. The adolescents completed two assessments with an interval of one year. Saliva samples, mother-reported parenting data and data on peer-nominated aggressive behavior were collected. All measures showed good reliability. The MGPS was created by COMT rs4680 polymorphisms, DRD2 rs1799978 polymorphisms and DAT1 rs27072 polymorphisms. Genotyping in three dopaminergic genes were performed for each participant in real time with MassARRAY RT software version 3.0.0.4 and analyzed using the MassARRAY Typer software version 3.4 (Sequenom). To examine whether negative parenting moderates the effects of MGPS on adolescent aggressive behavior, hierarchical regression analyses were conducted. The results found that after controlling for gender, maternal negative parenting was a significant risk factor for adolescent aggressive behavior, with higher negative parenting related to more aggressive behavior. The main effect of the quadratic term of MGPS on adolescents’ aggressive behavior was significant at Time 2, indicating a U-shaped relationship between MGPS and adolescent aggressive behavior. Moreover, the quadratic term of MGPS significantly interacted with maternal negative parenting in predicting aggressive behavior at Time 1 and Time 2, respectively. Specifically, there was a U-shaped relationship between MGPS and adolescent aggressive behavior, indicating that adolescents with higher and lower MGPS exhibited higher levels of aggressive behavior when experiencing higher levels of maternal negative parenting. No significant effect of MGPS on adolescent aggressive behavior when experiencing lower levels of maternal negative parenting existed. This study provides evidence for the molecular mechanisms of multilocus genetic profile scores and gene-environment interactions in adolescent aggressive behavior.
Subjects: Psychology >> Developmental Psychology submitted time 2022-11-08
Abstract：
Dopaminergic genes have been frequently found to be associated with aggressive behavior, but the results are inconsistent. One reason for the inconsistencies is there might be the U-shaped relationship between dopaminergic genetic variants and aggressive behavior. More specifically, evidence has suggested an inverted U-shaped relationship between dopamine activity and prefrontal cortex (PFC) function (a critical region related to aggression), with both dopaminergic hypofunction and hyperfunction, were related to poor PFC function. It is possible that the relationship between dopaminergic gene and aggression approximates a U-shaped function. However, such U-shaped relationship is rarely investigated in previous studies. Moreover, several concerns have been raised about the ignoring the polygenic traits of aggressive behavior when conducting gene by environment interaction (G×E) research using single loci. Therefore, the present study aimed to examine the interaction between dopaminergic genetic variants and maternal negative parenting on adolescent aggressive behavior by adopting the approach of multilocus genetic profile score (MGPS).
Participants were 1044 adolescents (mean age 13.32 ± 0.49 years old at Time 1, 50.2% females) recruited from the community. The adolescents completed two assessments with an interval of one year. Saliva samples, mother-reported parenting data and data on peer-nominated aggressive behavior were collected. All measures showed good reliability. The MGPS was created by COMT rs4680 polymorphisms, DRD2 rs1799978 polymorphisms and DAT1 rs27072 polymorphisms. Genotyping in three dopaminergic genes were performed for each participant in real time with MassARRAY RT software version 3.0.0.4 and analyzed using the MassARRAY Typer software version 3.4 (Sequenom). To examine whether negative parenting moderates the effects of MGPS on adolescent aggressive behavior, hierarchical regression analyses were conducted.
The results found that after controlling for gender, maternal negative parenting was a significant risk factor for adolescent aggressive behavior, with higher negative parenting related to more aggressive behavior. The main effect of the quadratic term of MGPS on adolescents’ aggressive behavior was significant at Time 2, indicating a U-shaped relationship between MGPS and adolescent aggressive behavior. Moreover, the quadratic term of MGPS significantly interacted with maternal negative parenting in predicting aggressive behavior at Time 1 and Time 2, respectively. Specifically, there was a U-shaped relationship between MGPS and adolescent aggressive behavior, indicating that adolescents with higher and lower MGPS exhibited higher levels of aggressive behavior when experiencing higher levels of maternal negative parenting. No significant effect of MGPS on adolescent aggressive behavior when experiencing lower levels of maternal negative parenting existed.
This study provides evidence for the molecular mechanisms of multilocus genetic profile scores and gene-environment interactions in adolescent aggressive behavior.
Peer Review Status:
Awaiting Review
Subjects: Psychology >> Developmental Psychology submitted time 2021-05-23
Abstract： Prosocial behaviour, that is, behaviour intended to benefit others, has been linked to a variety of desirable traits, including positive relationships, better academic performance and lower levels of antisocial behaviours. As such, the origins and the mechanisms underlying the remarkable individual differences in prosocial behaviour are the focus of an increasing number of studies, with numerous research consistently documenting the important role of positive parenting and empathy. Notably, differentiating between cognitive and emotional components of empathy may help further clarify the processes by which parenting eventuates in prosocial behaviour. Although all children may be impacted by parenting, some children benefit more than others from good-quality rearing. Recent research has suggested that the oxytocin receptor (OXTR) gene rs53576 polymorphism could determine the degree to which a child is influenced by environment. The biological function of rs53576 polymorphism has yet to be delineated, and the literature is mixed with regard to heterozygote (AG) grouping; thus, the implications for AG grouping are not well understood. Therefore, the dummy coding, additive coding, dominant coding and recessive coding models were all investigated in this study to test the nature of gene effect. This study aimed to extend previous studies on the association between parenting and prosocial behaviour by examining the mediating role of cognitive and emotional empathy and the moderating role of the OXTR gene. The participants were 1082 mother–offspring dyads (adolescents’ mean age: 12.32 ± 0.48 years, 50.3% females) recruited from the community. At Time 1, mothers reported their positive parenting via the Chinese version of the Child-Rearing Practices Report (CRPR) and peer-rated adolescents’ prosocial behaviours. At Time 2, adolescent-reported perspective-taking and empathic concern, peer-rated prosocial behaviours and saliva samples were collected. All measures showed good reliability. Genotyping at OXTR gene was performed with MassARRAY RT software version 3.0.0.4 and analysed using the MassARRAY Typer software version 3.4 (Sequenom). Results showed that adolescents who received higher levels of maternal positive parenting exhibited more prosocial behaviours. However, the direct effect of positive parenting on prosocial behaviour became nonsignificant after controlling for baseline prosocial behaviour. Cognitive empathy, but not emotional empathy, mediated the association between positive parenting and prosocial behaviour. Specifically, positive parenting was positively associated with cognitive empathy, which in turn was positively associated with adolescent prosocial behaviour. Further, this mediation was moderated by the OXTR gene rs53576 polymorphism. For adolescents with AA and GG genotypes, positive parenting was related to higher levels of cognitive empathy, which increased prosocial behaviour. However, this mediation effect was not observed among adolescents with AG genotype. In addition, the results revealed evidence for an overdominance model for OXTR rs53576. Moreover, the G × E term predicted cognitive empathy but not prosocial behaviour. This finding suggests that cognitive empathy may be an endophenotype closer along the causal chain to the genotype and that the strength of the G × E effects was greater for empathy than for distal behavioural outcomes. These findings add to our understanding of how empathy and genetic factors contribute to adolescents’ prosocial behaviour within the family context. In addition, these results suggest that cognitive and emotional aspects of empathy are likely to be involved—in somewhat different psychosocial mechanisms—in the development of prosocial behaviour. Notably, the overdominance effect of OXTR should be interpreted with caution until replicated. However, when a three-category polymorphic genotype is used, as is commonly applied when modelling a dominant or recessive effect, both false positive and false negative results can occur, and the nature of the interaction can be misrepresented.
Subjects: Psychology >> Developmental Psychology submitted time 2020-08-07
Abstract： Depression is one of the most prevalent mental health problems during adolescence. Research has indicated that distal stress and proximal stress as well as their interaction are important predictors of adolescent depressive symptoms. There are two different hypotheses — cumulative stress hypothesis and match-mismatch hypothesis — to understand the interaction between distal stress and proximal stress. It has been suggested that an individual’s genetic susceptibility may determine which of these two hypotheses is relevant, but very little empirical research has considered the impact of genetic predisposition on these issues. Furthermore, recent researchers have paid attention to the cumulative genetic score (CGS) of multiple loci rather than to single polymorphism. The present study was designed to extend prior research by exploring whether the interaction effects of distal maternal negative parenting and proximal peer victimization were consistent with the cumulative stress hypothesis or the match-mismatch hypothesis, for adolescents who carried higher or lower CGS of FKBP5 gene. In this study, 970 adolescents (48.8% male) were followed from Grade 6 to Grade 9. At T1 (Mage = 12.31 years, SD = 0.47), adolescent depressive symptoms were assessed using Children’s Depression Inventory (CDI). Mothers reported their negative parenting via the Chinese version of Child-Rearing Practices Report (CRPR). At T2 (Mage = 15.32 years, SD = 0.47), saliva samples of adolescents were collected and genotyped for three FKBP5 gene polymorphisms. Peer victimization and depressive symptoms were tested using Multidimensional Peer Victimization Scale (MPVS) and CDI, respectively. A series of hierarchical regressions and internal replication analyses were conducted to test the three-way interaction among maternal negative parenting, peer victimization and CGS of FKBP5 on depressive symptoms, separately for male and female adolescents. The results showed that, after T1 depressive symptoms were controlled for, maternal negative parenting, peer victimization and CGS had a significant three-way interaction on male adolescent depressive symptoms at T2. Specifically, among male adolescents who had higher CGS, maternal negative parenting negatively predicted depressive symptoms in the context of higher peer victimization, which fitted better with the match-mismatch hypothesis. The interaction between negative parenting and peer victimization was not significant among males with lower CGS, but showed a cumulative stress trend.The three-way interaction was not observed among females. By examining the interaction effect of maternal negative parenting, peer victimization and CGS on depressive symptoms, the present study highlights the important role of individuals’ genetic susceptibility in understanding the distal and proximal stress interactions during adolescence. This underscores the complex environmental and multiple loci underpinnings of depressive symptoms and lends some support for both the cumulative stress and match-mismatch hypotheses on the etiology of depressive symptoms.
Subjects: Psychology >> Developmental Psychology submitted time 2019-07-22
Abstract： For decades, there is increasing evidence for the importance of single-gene by environment interactions (G × E) in understanding the etiology of depression. However, several concerns have been raised about the ignoring the polygenic traits of depression when conducting G × E research using single loci. Within this context, the multilocus genetic profile score (MGPS) have recently emerged as an approach of capturing polygenic nature across multiple genes. In line with the monoamine deficiency hypothesis, recent research has begun to show that the combined effects of multiple dopaminergic genetic variants are stronger than the influence of any single gene examined in isolation. Additionally, genes related to the functioning of the dopaminergic system, which coordinates individual’s response to stress. However, existing G × E research has largely focused on adverse family environments (i.e., maltreatment, maternal unresponsiveness) and to a lesser extent on positive environment, such as positive parenting. Therefore, the present study aimed to examine the interaction between dopaminergic genetic variants and maternal parenting on adolescent depressive symptoms, by adopting the approach of multilocus genetic profile score. Participants were 1052 mother–offspring (adolescents mean age 12.31 ± 0.37 years old at the first time point, 50.2% females) dyads recruited from the community. Youth completed assessments twice with an interval of one year. Saliva samples, self-reported depressive symptoms and mother-reported parenting were collected. All measures showed good reliability. Genotyping in three dopaminergic genes were performed for each participant in real time with MassARRAY RT software version 3.0.0.4 and analyzed using the MassARRAY Typer software version 3.4 (Sequenom). To examine whether multilocus genetic profile score moderates the effects of parenting on adolescent depressive symptoms and whether this potential moderating effect act in a diathesis–stress or differential susceptibility manner, hierarchical regression analyses were conducted. We also tested above questions by recoding into categorical variables and re-conducted analyses. The results found that multilocus genetic profile score was a significant risk factor of depression, with higher dopamine genetic risk scores (indicating lower dopaminergic neurotransmission) predicting higher levels of depression. After controlling for gender and prior depressive symptoms, the G × E effect with positive and negative parenting were also significant, suggesting that G × E interaction significantly predicted change in depression level between Time 1 and Time 2. Specifically, adolescents with higher MGPS exhibited higher risk for depression when encountered with lower levels of positive parenting and higher levels of negative parenting, compared to their counterparts with lower MGPS. The results support the diathesis-stress model and highlight the complex ways that genes and environment interact to influence development. These finding underscores complex polygenic underpinnings of depression and lends support for the mulitlocus genetic profile scores–environment interactions implicated in the etiology of depressive symptoms.
Hits
YES
Hits
Downloads
Comment