Genetically Informed Studies of Victimization and Trauma - Reading (PDF)

Genetically informed studies of victimization and trauma - Reading 03 December 2023 15:20 Source Notes Genetic vulnerability to Experiencing Child Maltreatment Introduction (Pezzoli et al., 2019) Child maltreatment, encompassing physical, emotional, and sexual abuse, as well as neglect, poses a sign...

Genetically informed studies of victimization and trauma - Reading 03 December 2023 15:20 Source Notes Genetic vulnerability to Experiencing Child Maltreatment Introduction (Pezzoli et al., 2019) Child maltreatment, encompassing physical, emotional, and sexual abuse, as well as neglect, poses a significant public health concern. While environmental factors have long been recognized as contributing to child victimization, recent research suggests that genetic factors may also play a role. Genetic and Environmental Influences on Child Victimization ○ Studies have shown that both genetic and environmental factors influence the risk of experiencing child maltreatment. ○ Genetic influences account for a moderate proportion of the risk for all types of child victimization, while shared and uniqu e environmental factors also contribute. Co-occurrence of Child Victimization ○ Children who experience one form of maltreatment are more likely to experience others. ○ This co-occurrence may be explained by shared genetic and environmental factors. Genetic and Environmental Influences Across Maltreatment Types ○ The extent of genetic and environmental influences may vary across different types of child maltreatment. ○ For instance, genetic influences on child sexual abuse may be lower than for other forms of maltreatment. Unique Environmental Exposures ○ Unique environmental exposures, such as individual experiences or social circumstances, may play a more prominent role in predicting specific types of child victimization compared to genetic and shared environmental factors. Genetic Relatedness and Child Victimization ○ The extent of genetic and environmental influences may differ depending on the genetic relatedness between the victim and the perpetrator. ○ For family-specific child victimization, genetic influences may be stronger, while unique environmental factors may play a larger role in family-unspecific child victimization. Sex Differences in Child Victimization ○ Sex differences are observed in the prevalence of different types of child maltreatment. ○ These differences may be partly explained by genetic factors. Materials and Methods Participants ○ 13,024 individuals (8,415 women and 4,609 men) ○ Ages 18-49 years ○ Recruited through the Central Population Registry of Finland ○ Participated in the Genetics of Sexuality and Aggression project ○ Zygosity was determined using standard questionnaire items ○ 91% of the subsample was correctly classified based on questionnaire items Measures ○ Childhood Trauma Questionnaire Short Form (CTQ-SF) ○ Measures five types of maltreatment ○ Reliable and valid in clinical and community-based samples Analyses ○ Phenotypic and quantitative genetic analyses ○ Examined mean scores on all items ○ Estimated zero-order correlation coefficients ○ Created five-factor scores ○ Categorized items as family-specific or family-unspecific ○ Created two mean scores ○ Standardized them as z scores ○ Examined cross-twin correlations ○ Tested univariate, bivariate, and multivariate twin models ○ Examined sex limitation models Results Phenotypic Results ○ Participants reported higher levels of emotional neglect and emotional abuse compared to the other types of child victimizati on. ○ Men reported lower levels of emotional abuse and sexual abuse compared to women, but higher levels of physical abuse. ○ Participants reported higher levels of family-specific victimization compared to family-unspecific victimization. ○ Correlations between items addressing the same type of child victimization were moderate, while correlations between items addressing different types of child victimization were small. ○ Correlations between items addressing child sexual abuse were the strongest and the least correlated with the remaining items. ○ Cross-twin within-trait correlations were larger in monozygotic (MZ) twins than in dizygotic (DZ) twins, indicating additive genetic influences. Genetic Results Univariate Models ▪ Additive genetic influences were moderate for emotional abuse, sexual abuse, and emotional neglect, but modest for physical abuse and neglect. ▪ Shared environmental influences were modest for physical neglect, small for physical abuse and emotional neglect, and nonsignificant for emotional and sexual abuse. ▪ Unique environmental influences were moderate for all types of child victimization. ▪ Shared and unique environmental influences differed significantly between family-specific and family-unspecific items. ▪ Unique environmental influences were significantly larger in men compared to women for emotional abuse, sexual abuse, and emotional neglect. Genetic Correlations ▪ Genetic and shared environmental correlations were positive and moderate to large, whereas unique environmental correlations were positive but small. ▪ Bivariate correlations were substantially consistent across sexes. Multivariate Common Pathway Model ▪ The model fitted the data excellently. ▪ Additive genetic influences were smaller for all types of abuse compared to the univariate models, except for sexual abuse. ▪ Unique environmental influences were significantly increased for all types of child victimization, except for sexual abuse. ▪ Shared environmental influences were substantial only for physical neglect and small or negligible for the remaining types of child victimization. Sex Limitation Models The difference in fit was close to significance only for emotional abuse and sexual abuse. PSYC0036 Genes and Behaviour Page 1 ○ The difference in fit was close to significance only for emotional abuse and sexual abuse. ○ For emotional abuse, sex-limited genetic effects exerted a significantly larger impact on women than men. ○ For sexual abuse, no significant difference emerged in the magnitude of the genetic influences common to both sexes, but the sexlimited genetic path was nonsignificant for men. Discussion Etiological Pathways Underlying Single and Multiple Types of Child Victimization ○ Genetic factors, in addition to environmental factors, might influence the risk of child victimization. ○ The risk of multiple victimizations might be influenced by genetic and shared environmental more than nonshared environmental factors. ○ The risk of experiencing one form of victimization rather than another might be largely influenced by unique environmental fa ctors. ○ Distinct genetic and unique environmental risk factors for sexual abuse were identified. ○ Shared and unique environmental factors might influence the risk of victimization by related and unrelated individuals, respe ctively. ○ Successful prevention of child abuse and neglect necessarily entails identifying and supporting families where parental risk factors for child maltreatment are present. ○ Unique situational factors that might increase the risk of sexual abuse should be identified. ○ Future research should clarify whether and which heritable traits might increase the risk of being taken advantage of sexuall y motivated perpetrators. ○ Further research should investigate possible clusters of extrafamilial risk factors, to better understand which situations in crease the risk of victimization outside the household. Sex Differences in the Etiology of Child Victimization ○ Sex differences emerged both in the mean levels of the reported adversities as well as in the etiological influences on them. ○ Women reported higher mean levels of emotional and sexual abuse, while men reported higher mean levels of physical abuse. ○ The phenotypic patterns of co-occurrence were similar and influenced by similar factors. ○ Smaller unique environmental influences were estimated in women, compared to men, for emotional abuse, sexual abuse, and emotional neglect. ○ Preliminary evidence suggests that different sets of genes might influence the risk of emotional and sexual abuse in girls an d boys. Limitations ○ The study employed only one psychometric scale. ○ The study employed a retrospective self-report measure. ○ The items did not measure the exact age at which child victimization had occurred. ○ How well the findings generalize to nontwins and families without twins is unclear. ○ Some cultural aspects pertinent to child victimization might not generalize to other populations. Conclusion ○ Genetic factors might influence the risk of child victimization. ○ Heritable characteristics in the child, as well as features of the rearing environment, were found to especially influence th e cooccurrence of multiple types of child victimization. ○ Both individual and familial risk factors should be addressed to develop adequate preventive strategies. ○ Unique environmental factors still influenced the risk of specific types of child victimization. ○ Substantial sex differences in the etiology of child victimization were estimated. Gene–environment correlations and causal effects of childhood maltreatment on physical and mental health: a genetically informed approach (Warrier et al., 2021) Introduction Childhood maltreatment is a global problem, affecting up to 36% of the population worldwide. Up to 80% of perpetrators are the parents or other family members of the child. Parental experience of childhood maltreatment is a risk factor for maltreating their own children. Studies have shown that childhood maltreatment has a twin and familial heritability of 6–62%. A 2020 study has shown a SNP heritability of 6% for childhood maltreatment. Gene–Environment Correlations The heritable component of childhood maltreatment is not immutable and is thought to manifest through gene–environment correlations. There are three main types of gene–environment correlations: passive, active, and reactive or evocative. Passive gene–environment correlation occurs when parental genes influence family environments and are inherited by their children. Active gene–environment correlation occurs when children's genes shape their behaviours including risk-taking behaviour. Reactive or evocative gene–environment correlation occurs when children's genes shape their behaviour and physical features, eliciting different responses from their parents or others. Observational Studies Observational studies link childhood maltreatment with severe and long-lasting mental (e.g., psychosis, depression, ADHD) and physical health problems (e.g., diabetes, cardiovascular disease). There is considerable heterogeneity in these observations, partly because studies differ in how childhood maltreatment is operationalised, whether they examine the effects of specific subtypes, and whether prospective or retrospective reports of childhood maltreatment are used. Causal Mechanisms It is unclear whether observational associations are due to causal effects of childhood maltreatment, or to genetic or environmental confounding (e.g., deprivation). Mendelian randomisation assumes that a genetic variant associated with an exposure can be used as an unconfounded proxy for that exposure to investigate its effect on potential outcomes. Research in Context Childhood maltreatment is known to be partly heritable but how different mechanisms of gene–environment correlation contribute to childhood maltreatment, and whether childhood maltreatment is causally related to mental and physical health outcomes is unknown. Previous studies have investigated the SNP heritability of childhood maltreatment and identified two genetic loci. No previous studies have investigated mechanisms of gene–environment correlations or causal effects of childhood maltreatment using Mendelian randomisation. Added Value of This Study This genome-wide meta-analysis (N=185414) of childhood maltreatment is the largest to date to our knowledge. We identified 14 independent genetic variants (13 novel) associated with childhood maltreatment. We found some direct evidence for active and reactive gene–environment correlation, but could not show an absence of passive gene– environment correlation. We identified potentially causal effects of childhood maltreatment on depression. We also identified bidirectional potentially causal effects between childhood maltreatment and both ADHD and schizophrenia. Methods The study included data from 185,414 participants from five cohorts: the UK Biobank, Adolescent Brain Cognitive Development Study, Avon Longitudinal Study of Parents and Children, Generation R, and the Psychiatric Genomics Consortium (PGC_26K). The participants were primarily of European genetic ancestry and provided information on childhood maltreatment. Methods ○ The study consisted of five main methods: GWAS meta-analysis and functional annotation, SNP heritability and genetic correlations, polygenic score (PGS) analyses, contribution of different mechanisms to childhood maltreatment, and Mendelian randomisation. Results The study identified 14 independent loci associated with childhood maltreatment. The loci were significantly associated with mental health problems, risky behaviour, smoking and cannabis use, cardiovascular health, sleep difficulties, and reduced intelligence and educational attainment. The loci were enriched for foetal and adult brain-specific histone marks and DNAse hypersensitivity sites, and for genes with high expression in the excitatory neuron subpopulation (Ex4) in the adult post-mortem brain. Between-sibling PGS analyses suggested that 58% of the variance in childhood maltreatment was due to active and reactive geneenvironment correlation. Over-transmission of PGS of GWAS child maltreatment to autistic children from their parents (mean difference 0.056 [SE 0.02]; p=0.010) supported the hypothesis that an increased risk of childhood maltreatment in autistic individuals was partly explained by increased active PSYC0036 Genes and Behaviour Page 2 supported the hypothesis that an increased risk of childhood maltreatment in autistic individuals was partly explained by increased active and reactive gene-environment correlation. Mendelian randomisation analyses found a significant causal effect of childhood maltreatment on major depressive disorder (inverse variance-weighted Mendelian randomisation analyses) and ADHD and schizophrenia (bidirectional causal effect). The study did not find a significant causal effect of childhood maltreatment on autism, bipolar disorder, coronary artery disease, type 2 diabetes, C-reactive protein concentration, or vice versa. Discussion Childhood maltreatment has modest SNP heritability (6% of total phenotypic variance) Genetic correlations among different subtypes, operationalisations, and reports of childhood maltreatment are high (range 0.24 to 1.00) Genome-wide association studies identified 14 independent loci associated with childhood maltreatment, including genes involved in neurodevelopment, chromatin accessibility, and gene expression Within-family analyses suggest that 58% of the variance in childhood maltreatment is due to active and reactive gene–environment correlation (AGEE) Over-transmission of PGS of GWAS child maltreatment to autistic children from their parents suggests that AGEE also contributes to the increased risk of childhood maltreatment in autistic individuals Mendelian randomisation analyses found a significant causal effect of childhood maltreatment on major depressive disorder (MDD) and bidirectional causal effects on ADHD and schizophrenia There was no evidence for causal effects of childhood maltreatment on autism, bipolar disorder, coronary artery disease, type 2 diabetes, or C-reactive protein concentration Limitations of the study include the small proportion of variance explained by genetic factors, non-uniform maltreatment measurement across cohorts, and lack of distinction between objective and subjective maltreatment The study suggests that the mechanisms underlying childhood maltreatment are complex and include multiple forms of gene– environment correlation (AGEE) The correlation mechanisms identified probably contribute to intergenerational transmission of childhood maltreatment The findings highlight the importance of family-based support strategies to minimise the risk of child maltreatment and limit intergenerational transmission Review of twin studies on the heritability of trauma and PTSD (Afifi et al., 2010) Background: The study focuses on twin studies to understand the influence of genetic and environmental factors on trauma exposure and PTSD symptoms. Previous review articles have largely focused on molecular genetics, with limited attention to twin studies and behavioral-genetics. Heritability of traumatic events: Twin studies have found that exposure to certain traumatic events, such as assaultive trauma, is moderately heritable (approximately 20% of the variance), while exposure to non-assaultive trauma is largely attributable to non-shared environmental factors (61%). Heritability of PTSD symptoms: Twin studies have found that PTSD symptoms, such as re-experiencing, avoidance, and hyperarousal, are moderately heritable (approximately 28% to 36% of the variance). Shared environmental factors were not found to contribute to PTSD symptoms. Comorbidity of PTSD with other mental disorders: Twin studies have found that the comorbidity of PTSD with other mental disorders, such as generalized anxiety disorder, panic disorder, alcohol dependence, drug dependence, nicotine dependence, and major depression, may be partly due to common additive genetic and non-shared environmental influences. Gene-environment interactions: Twin studies have found that there is evidence of gene-environment interactions for PTSD. For example, genetic factors have been found to partially mediate the relationship between assaultive trauma and antisocial personality traits. Key Findings: Exposure to assaultive trauma is moderately heritable, with genetic factors accounting for about 20% of the variance. PTSD symptoms are moderately heritable, with genetic factors accounting for about 28% of the variance. Comorbidity of PTSD with other disorders (such as major depression and generalized anxiety disorder) may be partly due to shared genetic and environmental influences. There is some evidence of gene–environment interactions for PTSD, such that the effects of trauma exposure may be amplified or attenuated by genetic factors. Limitations: The majority of twin studies on PTSD have been conducted with male combat veterans, so it is not clear whether the findings generalize to other populations. Studies have not yet been able to identify specific genes that are associated with PTSD. Implications: Twin studies suggest that PTSD is a complex disorder with a combination of genetic and environmental influences. Further research is needed to identify the specific genes and environmental factors that are involved in the development and course of PTSD. Research on gene–environment interactions could help to identify the factors that make some people more or less resilient to the effects of trauma exposure. Future Directions: Conduct twin studies with more diverse populations (e.g., females, civilians, non-veterans) to determine whether the findings generalize to other groups. Develop and validate new methods for identifying genes that are associated with PTSD. Conduct more research on gene–environment interactions for PTSD. Critical analysis: The study emphasizes the importance of twin studies in providing insights into the genetic and environmental factors that influence trauma exposure and PTSD. ○ It suggests that integrating behavioral-genetics with molecular genetics and cognitive-behavioral approaches can deepen our understanding of the complex etiology of PTSD However, the limitations of the current literature, such as small sample sizes, lack of generalizability, and the inability to identify specific genes involved in PTSD development, are acknowledged. ○ The study also highlights the need for larger sample sizes, sex differences research, and investigation of gene -environment interactions in future studies. In summary, while the provided excerpts offer some insights into the importance of twin studies and the need for integrating different research approaches, they do not provide specific details on the study's background, methods, results, or critical analysis. Review on the intergenerational transmission of Intimate Partner Violence Part 1 Background Information ○ Violence in intimate relationships is a widespread problem in the United States. ○ Approximately 16% of married American couples experienced an incident of physical assault in the previous year. ○ There is no difference in the amount of violence in a married relationship versus a dating relationship. ○ Cohabiting couples have the highest rate of violence. ○ Males and females commit violence at approximately the same rate within their relationships. ○ Males and females who are victims of violence in intimate relationships can experience a variety of psychological problems, including alcoholism, drug abuse, post-traumatic stress disorder, and depression. (Hines & Saudino, 2002) PSYC0036 Genes and Behaviour Page 3 Key Findings of the Research Review ○ Intimate partner violence passes through the generations, in that children who are exposed to violence in their families of o rigin are more likely to use violence in their families as adults. ○ Social learning theory has been the primary theory to explain the intergenerational transmission of intimate partner violence. ○ Because the transmission of violence is not 100%, a social learning theory approach may be overly simplistic. ○ One explanation for the intergenerational transmission of intimate partner violence that has not been tested is a behavioral genetic explanation. ○ Because families share both genes and environments, the transmission of intimate partner violence could be due to genetic as well as environmental causes. ○ Social learning theory takes into account only environmental causes, but without a genetically sensitive design, we cannot be sure if the causes are due only to environments and not genes. ○ In a related area, it has consistently been found that aggression in adults is genetically influenced; therefore, aggression in intimate relationships may also be genetically influenced. ○ Behavioral genetic studies are needed to better understand the intergenerational transmission of intimate partner violence. Conclusion ○ Intimate partner violence is a complex problem that is influenced by a variety of factors, including social learning, psychol ogical factors, and genetic factors. ○ More research is needed to understand the specific factors that contribute to intimate partner violence and to develop effect ive interventions. Part 2 Background Information Adoption Studies: ▪ Parent-offspring design: Compares behavioral similarity between adopted children and their biological parents and adoptive parents. ▪ Adoptive/nonadoptive sibling design: Compares the similarity of adoptive and nonadoptive sibling pairs. Intimate Partner Violence Research from a Behavioral Genetic Point of View: ▪ Familial resemblance in intimate partner violence can be explained by social learning theory, which suggests that children learn violence from their parents. ▪ A strictly social learning theory account would imply shared environmental influences. ▪ Behavioral genetic research methods can provide a more nuanced understanding of the contributions of genes and environments to intimate partner violence. Key Findings ○ Behavioral Genetic Results in Areas Related to Intimate Partner Violence: ○ MZ twins are more similar than DZ twins in their perpetration and victimization of intimate partner violence. ○ Adoptees are more similar to their biological relatives than their adoptive relatives in their perpetration and victimization of intimate partner violence. ○ Nonshared environmental influences consistently account for 40% to 50% of the variance in antisocial behaviors and criminalit y. ○ Genetic factors play a larger role than environmental factors in antisocial behaviors and criminality. ○ The combination of genetic and environmental risk factors leads to the greatest incidence of adulthood criminality. ○ The contribution of genes and environment to intimate partner violence may vary depending on the age group studied. ○ The research on extremely violent criminal behavior has led to equivocal results. ○ The research on aggressive behavior, as measured by self-report, may be more relevant to the issue of intimate partner violence. ○ There are many similarities between aggression in intimate relationships and aggression in the community. Conclusions and Recommendations ○ Appling Behavioral Genetic Methods to the Study of Intimate Partner Violence: ○ Providing an explicit test of the social learning theory as it relates to the intergenerational transmission of violence in i ntimate relationships. ○ Examining if shared genes or shared environments are responsible for the familial resemblance in intimate partner violence. ○ Exploring possible genetic mediators for intimate partner violence, such as personality, intelligence, attachment, or substan ce use. ○ Identifying specific shared and nonshared environmental influences that contribute to intimate partner violence. Implications for Practice, Policy, and Research: Practice: ▪ Therapists should understand that genes do not equal destiny and that environment can also influence intimate partner violence. ▪ Therapy should focus on environmental factors within, not between, families. Policy: ▪ Policymakers should understand that genes do not equal destiny and that people with a genetic predisposition to violence can be helped. ▪ Educational programs should be developed to inform policymakers about the implications of behavioral genetic studies. Research: ▪ Conducting genetically sensitive studies to determine the role of genes and environment in intimate partner violence. ▪ Assessing possible genetic mediators of intimate partner violence. ▪ Studying environmental influences that affect intimate partner violence to develop prevention and intervention strategies. Longitudinal twin study on negative life events (Johnson et al., 2013) Introduction Objectives: To examine the genetic and environmental influences on the stability and change in stressful life events (SLEs) from childhood to adolescence in a sample of twins. Negative dependent life events were more stable across time than negative independent life events. Genetic influences on negative dependent life events increased during adolescence. Shared environmental influences on negative dependent life events decreased during adolescence. Nonshared environmental influences on negative dependent life events were consistent across time. The pattern of genetic and environmental influences on negative independent life events was less consistent than for dependent life events. Study Overview This study examined the genetic and environmental influences on exposure to stressful life events (SLEs) during adolescence. The researchers used data from a sample of 457 same-sex twin pairs who were assessed annually from ages 9 to 16. The researchers used three quantitative genetic models to examine the stability and change in SLEs across time: the Cholesky model, the common factor model, and the simplex model. Key Findings There was evidence of phenotypic stability in both dependent and independent SLEs. For dependent SLEs, genetic influences increased from childhood to adolescence, while shared environmental influences decreased. For independent SLEs, the pattern of genetic and environmental influences was more complex. Genetic influences were present, but were smaller in magnitude than for dependent SLEs. Shared environmental influences were also present, but were inconsistent across time. The results suggest that a combination of genetic and environmental factors contributes to the development of SLEs during adolescence. Methods: Participants: A sample of 457 same-sex twin pairs (245 monozygotic, 212 dizygotic) was recruited from the Longitudinal Twin Study. Participants completed the Life Events Scale for Adolescence (LESA) annually from ages 9 to 16. Measures: PSYC0036 Genes and Behaviour Page 4 Measures: Life events: The LESA measures the frequency of occurrence of 54 life events in three domains: family, school, and peer. Genetic models: Cholesky model: A model that decomposes the covariance of SLEs across ages into genetic (a²), shared environmental (c²), and nonshared environmental (e²) influences. Common factor model: A model that assumes that there is one consistent underlying factor explaining influences on SLEs at each age. Simplex model: A model that explains phenotypic stability by assuming that past influences on SLEs are transmitted over time (continuation effects), via autoregressive effects among the latent variables. Results: Correlations: ○ Dependent events: Positive correlations between SLEs across time suggest some stability in life events during adolescence. MZ correlations were larger than DZ correlations, suggesting genetic influences on the stability of SLEs. ○ Independent events: There was also evidence of phenotypic stability over time. MZ correlations were generally higher than DZ correlations in girls, but not in boys. Variance components: ○ Dependent events: ▪ Genetic influences increased from childhood to adolescence. ▪ The majority of genetic influences were common to all ages. ▪ Shared environmental influences decreased from childhood to adolescence and were mostly due to common influences. ▪ Nonshared environmental influences were generally age specific and consistent across ages. ○ Independent events: ▪ Genetic influences were relatively small and did not differ across gender. ▪ Shared environmental influences were generally age specific and consistent across gender in girls, but were less stable in boys. ▪ Nonshared environmental influences were generally age specific and consistent across gender in both boys and girls. Gender differences: ○ Dependent events: There were no gender differences in the genetic or environmental influences on the stability of dependent events. ○ Independent events: There were gender differences in the genetic influences on independent events. ▪ Girls had higher genetic correlations than boys at all ages, and the difference between MZ and DZ correlations was greater in girls than boys. Conclusions: Dependent events: ○ The findings suggest that both genetic and environmental factors contribute to the stability of dependent SLEs during adolescence. ○ Genetic influences increase from childhood to adolescence, while shared environmental influences decrease. ○ Nonshared environmental influences are generally age specific and consistent across ages. Independent events: ○ The findings suggest that genetic influences are relatively small for independent SLEs, and that shared environmental influen ces are more important. ○ Shared environmental influences are generally age specific and consistent across gender in girls, but are less stable in boys. ○ Nonshared environmental influences are generally age specific and consistent across gender in both boys and girls. Exposure to negative life events was stable over time. This means that people who experienced a lot of negative life events in childhood were also more likely to experience them in adolescence. The magnitude of etiological influences on the stability of life events changed considerably throughout this developmental period. This means that the factors that contributed to exposure to negative life events changed as people got older. Strengths and limitations: Strengths: ○ The study used a large sample of twins, which allowed for a more precise examination of the genetic and environmental influences on stressful life events. ○ The study used a longitudinal design, which allowed for the examination of how genetic and environmental influences change over time. ○ The study used a well-validated measure of stressful life events. Limitations: ○ The study only examined stressful life events that are negative. It is possible that the pattern of genetic and environmental influences on positive life events is different. ○ The study was conducted in a sample of twins from Colorado, which may limit the generalizability of the findings to other populations. ○ The study did not examine the specific mechanisms through which genetic and environmental factors influence stressful life events. ○ Retrospective report of life events ○ Correlational nature of the data ○ Limited generalizability to non-twin samples PSYC0036 Genes and Behaviour Page 5