Cognitive abilities are heritable and influenced by socioeconomic status (SES). It is critical to understand the association between SES and cognition beyond genetic propensity to inform potential benefits of SES-based interventions and to determine if such associations vary across (i) cognitive domains, (ii) facets of SES, and/or (iii) genetic propensity for different aspects of cognition. We examined the contributions of neighborhood socioeconomic advantage, family income, and polygenic scores (PGS) for domains of cognition (i.e., general cognitive ability, executive function, learning and memory, fluid reasoning) in a sample of children (ages 9–10; n = 5549) most genetically similar to reference populations from Europe. With some variability across cognitive outcomes, family income and PGS were independently significantly associated with cognitive performance. Within-sibling analyses revealed that cognitive PGS associations were predominantly driven by between-family effects suggestive of non-direct genetic mechanisms. These findings provide evidence that SES and genetic propensity to cognition have unique associations with cognitive performance in middle childhood. These results underscore the importance of environmental factors and genetic influences in the development of cognitive abilities and caution against overinterpreting associations with PGS of cognitive and educational outcomes as predominantly direct genetic effects.

Alcohol use is influenced by genetic and environmental factors. We examined the interactive effects between genome-wide polygenic risk scores for alcohol use (alc-PRS) and social support in relation to alcohol use among European American (EA) and African American (AA) adults across sex and developmental stages (emerging adulthood, young adulthood, and middle adulthood). Data were drawn from 4,011 EA and 1,274 AA adults from the Collaborative Study on the Genetics of Alcoholism who were between ages 18–65 and had ever used alcohol. Participants completed the Semi-Structured Assessment for the Genetics of Alcoholism and provided saliva or blood samples for genotyping. Results indicated that social support from friends, but not family, moderated the association between alc-PRS and alcohol use among EAs and AAs (only in middle adulthood for AAs); alc-PRS was associated with higher levels of alcohol use when friend support was low, but not when friend support was high. Associations were similar across sex but differed across developmental stages. Findings support the important role of social support from friends in buffering genetic risk for alcohol use among EA and AA adults and highlight the need to consider developmental changes in the role of social support in relation to alcohol use.

Emotional dysregulation (ED) is a dimensional, transdiagnostic domain that is associated with multiple categorical psychiatric diagnoses from childhood to adulthood, representing a risk for increased problems in affect, behavior, and cognition [1]. Traditionally, the nature of ED trait has been studied with top down approaches: quantitative evaluation of ED is possible through “Dysregulation Profile” scoring, which is measured through composite scales of the “Achenbach System of Empirically Based Assessment” (ASEBA) [2] questionnaires. Dysregulation profile is characterized by severe anxiety and affective symptoms, impulsive and/or aggressive behaviours and metacognitive difficulties. More recently, different researchers also applied bottom up approaches to evaluate the presence of ED in both general population and clinically referred samples [3]. Also in these cases, the results showed that ED is a trait, stable through time and across different cultures and societies, associated with higher presence of psychiatric diagnosis. It is important to note that these non-traditional statistical approaches highlighted that, in adulthood, ED is characterized by elevated scores in both externalizing and internalizing areas. In this contribution, the research aimed at disentangling the etiology of ED, which is crucial to treat and prevent worst evolution associated with this trait, will be revised. Many efforts have been done to understand the complex interaction between genetic and environmental risk factors which predispose patients to develop and maintain ED. [1] Aitken, et al. (2019). JAD, 253, 87-95. [2] Achenbach & Rescorla (2001). Manual for the ASEBA school-age forms and profiles. [3] Bianchi, et al (2017). ECAP, 26(5), 549-557.

Gene-environment correlations and interactions for the relationship between emotional problems (EP) and family environment in adolescents in low- to middle-income countries (LMIC) have been rarely investigated. In total, 3207 adolescent twins aged 12–18 (Mean = 14.6 ± 1.73) years attending public schools in Lagos State in Nigeria completed measures of EP and Family Chaos (FC). Model-fitting analyses suggested that genetic and non-shared environmental influences on EP were 21% and 71%, respectively, and the corresponding estimates were 23% and 71% for FC. Shared environmental influences were not significant (8% and 6% respectively). Phenotypic correlation between EP and FC was .30 (95% CI = .27–.34), which was significantly influenced by genetic (A – 49%, 95% CI: 0.01–0.97) and non-shared environmental factors (E – 32%, 95% CI: 0.10–0.54). Shared environmental influences were not significant (C – 19%, 95% CI: −0.13 to 0.50). Moderation effects were significant whereby as FC increased, A on EP decreased (βA = −0.07, 95% CI: −0.12 to −0.02) while E increased (βE = 0.06, 95% CI: 0.03–0.09). Our findings indicate that genetic and non-shared environmental risk factors may mediate the relationship between EP and FC, and that as FC increases, protective genetic influences on EP may be attenuated, whereas environmental influences may become stronger in adolescents in LMIC.

In summary, genetics, as well as foetal and early life environmental factors shape the size or capacity of our monoamine systems, of which the serotonergic one might play a leading role. Those constitutional properties then form the biological basis for personality traits, such as impulsiveness and “sensation seeking”, which interact with psychosocial settings and life events to form a pattern of reactivity to a current life event or psychosocial situation, shown as a high or low order of magnitude of gene-environment interaction. In the present paper emphasis is put on the role of genotypes of the serotonin transporter, of monoamine oxidases A and B, and of platelet monoamine oxidase B activity, which all have been shown to be of importance for behaviour and with obvious effects of interactions with environment. Under unfortunate circumstances constitutional properties might be strong enough to result in vulnerability for suicide, even with a modest influence of environment.

Elevated number of parental Communication Deviance (CD) has been connected with psychiatric and thought disorders in their offspring. However, no earlier systematic efforts have been made to review this issue. The aim of this study was to survey the existing literature systematically and perform a meta-analysis of this association. A literature search for published and unpublished observational studies on the association of parental Communication Deviance with psychopathology in the offspring was conducted. Multiple electronic databases were searched (from 1960 to 2012) and the reference lists of the resulting publications were scanned. The findings were pooled using random effect meta-analysis. A total of 19 relevant papers were found and accessed. The results showed that a high level of parental CD is associated with schizophrenia spectrum disorders in the offspring. A large overall effect size (0.79) was found in the meta-analysis. No meta-analysis could be performed on the association of parental CD with an offspring's thought disorders, but the results suggest that such an association may exist. Parental Communication Deviance is associated with schizophrenia spectrum disorders in the offspring. High parental CD could be treated as an indicator of a risk of developing a schizophrenia spectrum disorder, at least among high-risk groups.

Research suggests that genetic variants linked to hypothalamic-pituitary-adrenal (HPA)-axis functioning moderate the association between environmental stressors and depression, but examining gene–environment interactions with single polymorphisms limits power. The current study used a multilocus genetic profile score (MGPS) approach to measuring HPA-axis–related genetic variation and examined interactions with acute stress, chronic stress, and childhood adversity (assessed using contextual threat interview methods) with depressive symptoms as outcomes in an adolescent sample (ages 14–17, N = 241; White subsample n = 192). Additive MGPSs were calculated using 10 single nucleotide polymorphisms within HPA-axis genes (CRHR1, NR3C2, NR3C1, FKBP5). Higher MGPS directly correlated with adolescent depressive symptoms. Moreover, MGPS predicted stronger associations between acute and chronic stress and adolescent depressive symptoms and also moderated the effect of interpersonal, but not noninterpersonal, childhood adversity. Gene–environment interactions individually accounted for 5%–8% of depressive symptom variation. All results were retained following multiple test correction and stratification by race. Results suggest that using MGPSs provides substantial power to examine gene–environmental interactions linked to affective outcomes among adolescents.

Nature and nurture are not separate. Instead it is important to investigate the interplay between genes and environment and how they influence on another. To an important degree, genetic effects on behavior come about because they either influence the extent to which the individual is likely to be exposed to individual differences in environmental risk or they affect how susceptible the individual is to environmental adversities.

The current inability to explain or predict which genetically predisposed individuals will finally become schizophrenic has forced us to confront our ignorance of the precise mechanism and mode of the transmission of this disorder. Zubin's proposal to view the schizophrenic as a vulnerable individual who develops a temporary episode only under certain provocations can help place the controversy in proper perspective. Vulnerability (predisposition, diathesis) to schizophrenia can be defined as the individual's characteristic treshold beyond which stressful events produce decompensation manifest in the clinically diagnosable symptom picture.

Executive functions (EF) are a complex set of neurodevelopmental, higher-ordered processes that are especially salient during adolescence. Disruptions to these processes are predictive of psychiatric problems in later adolescence and adulthood. The objectives of the current study were to characterize the latent structure of EF using bifactor analysis and to investigate the independent and interactive effects of genes and environments on EF during adolescence. Using a representative young adolescent sample, we tested the interaction of a polymorphism in the serotonin transporter gene (5-HTTLPR) and parental supervision for EF through hierarchical linear regression. To account for the possibility of a hierarchical factor structure for EF, a bifactor analysis was conducted on the eight subtests of the Delis-Kaplan Executive Functions System (D-KEFS). The bifactor analysis revealed the presence of a general EF construct and three EF subdomains (i.e., conceptual flexibility, inhibition, and fluency). A significant 5-HTTLPR by parental supervision interaction was found for conceptual flexibility, but not for general EF, fluency or inhibition. Specifically, youth with the L/L genotype had significantly lower conceptual flexibility scores compared to youth with S/S or S/L genotypes given low levels of parental supervision. Our findings indicate that adolescents with the L/L genotype were especially vulnerable to poor parental supervision on EF. This vulnerability may be amenable to preventive interventions. (JINS, 2014, 20, 62–73)

The Sri Lankan Twin Registry (SLTR), established in 1997, is a unique resource for twin and genetic research in a low- and middle-income country (LMIC). It comprises of a volunteer cohort of 14,120 twins (7,060 pairs) and 119 sets of triplets, and a population-based cohort of 19,040 (9,520 pairs) twins and 89 sets of triplets. Several studies have been conducted using this registry, including the Colombo Twin and Singleton Study (CoTaSS 1; 4,387 twins, 2,311 singletons), which have explored the prevalence and heritability of a range of psychiatric disorders as well as gene-environmental interplay. Currently, a follow-up study (CoTaSS 2) of the same cohort is underway, looking at the prevalence and interrelationship of key cardiovascular and metabolic risk markers (e.g., metabolic syndrome). A significant feature of CoTaSS 2 is the establishment of a biobank. Current SLTR work is extending beyond mental health and the interface between mental and physical health to new horizons, extending collaborations with the wider global twin research community. Ethics and governance have been given special emphasis in the initiative. Capacity building and public engagement are two crucial components. Establishment of a state-of-the-art genetic laboratory was a major accomplishment. SLTR is a classic showcase of successful North–South partnership in building a progressive research infrastructure in a LMIC.

The Interplay of Genes and Environment across Multiple Studies (IGEMS) group is a consortium of eight longitudinal twin studies established to explore the nature of social context effects and gene-environment interplay in late-life functioning. The resulting analysis of the combined data from over 17,500 participants aged 25–102 at baseline (including nearly 2,600 monogygotic and 4,300 dizygotic twin pairs and over 1,700 family members) aims to understand why early life adversity, and social factors such as isolation and loneliness, are associated with diverse outcomes including mortality, physical functioning (health, functional ability), and psychological functioning (well-being, cognition), particularly in later life.

Adolescents' evaluations of family functioning may have a significant impact on their subjective well-being and adjustment. The aim of the study was to investigate the degree to which genetic and environmental influences affect variation in evaluations of general family functioning, family conflict, and quality of life and the overlap between them. We assessed whether genetic and environmental influences are moderated by parental divorce by analyzing self-report data from 6,773 adolescent twins and their non-twin siblings. Genetic, shared, and nonshared environmental influences accounted for variation in general family functioning and family conflict, with genetic influences being relatively more important in girls than boys in general family functioning. Genetic and nonshared environmental influences accounted for variation in quality of life, with genetic influences being relatively more important in girls. Evidence was found for interaction between genetic factors and parental divorce: genetic influence on general family functioning was larger in participants from divorced families. The overlap between general family functioning and quality of life, and family conflict and quality of life was accounted for the largest part by genetic effects, with nonshared environmental effects accounting for the remaining part. By examining the data from monozygotic twins, we found evidence for interaction between genotype and nonshared, non-measured, environmental influences on evaluations of general family functioning, family conflict, and quality of life.

Aims – Genetics can offer new resources to epidemiology. This review will consider recent findings regarding the link between stress and depression as an example to illustrate the added value of employing genetics in epidemiological studies. Methods – Systematic review of medical and psychological databases. Results – Genetic and environmental factors may correlate. This suggests the potential for genetic mediation of the exposure to the environment. Gene-environment correlations can help epidemiologists to better understand causal pathways and suggest effective therapeutic strategies. Genetic and environmental factors may also interact. This suggests the potential for genetic modification of environmental effects on disease risk. Gene-environment interactions can help epidemiologists to identify vulnerable individuals and strata-specific environmental effects. Conclusions – New models of disease based on the interplay between genes and environments are providing epidemiology with a new set of testable hypotheses that will advance our understanding of mental health and illness.

Declaration of Interest: Dr. Danese is holder of the Wellcome Trust Research Training Fellowship in Clinical Science.