Gene–Environment Correlations Affecting Children's Early Rule-Breaking and Aggressive Play Behaviors

Play among peers is an important developmental context for child socialization. We have earlier shown that children at genetic risk for aggression were more likely to be treated aggressively by unfamiliar peers during peer play, reflecting genotype-evoked behaviors manifested during play. In this study, 118 5-year-old twin pairs were paired randomly with an unfamiliar, same-age, same-sex child, thus controlling for parent- and child-chosen environments (passive and active rGE). Twins played separately from each other with unmatched children. Play behaviors were coded for aggressive and assertive behaviors. Children were also independently rated by parents for rule-breaking problem behaviors at age 5, and 97 children were rated again on these behaviors 2–10 years later. Analyses showed that children at genetic risk for early rule-breaking were more likely to have partners who behaved more aggressively, suggesting that this was evoked behavior during play. Some evidence of an ‘early bloomer’ phenomenon emerged via early difficult temperament and parent-rated delinquency significantly predicting later delinquency. Children's play, which is one of the most important influences on early development, requires further study from an rGE perspective.

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Gene–environment interplay in the etiology of psychosis

Psychological Medicine ◽

10.1017/s003329171700383x ◽

2018 ◽

Vol 48 (12) ◽

pp. 1925-1936 ◽

Cited By ~ 26

Author(s):

Alyson Zwicker ◽

Eileen M. Denovan-Wright ◽

Rudolf Uher

Keyword(s):

Environmental Factors ◽

Genetic Risk ◽

Environmental Exposures ◽

Response To Treatment ◽

Human Potential ◽

Specific Gene ◽

Environment Interaction ◽

Gene Environment ◽

Increased Risk ◽

The Impact

AbstractSchizophrenia and other types of psychosis incur suffering, high health care costs and loss of human potential, due to the combination of early onset and poor response to treatment. Our ability to prevent or cure psychosis depends on knowledge of causal mechanisms. Molecular genetic studies show that thousands of common and rare variants contribute to the genetic risk for psychosis. Epidemiological studies have identified many environmental factors associated with increased risk of psychosis. However, no single genetic or environmental factor is sufficient to cause psychosis on its own. The risk of developing psychosis increases with the accumulation of many genetic risk variants and exposures to multiple adverse environmental factors. Additionally, the impact of environmental exposures likely depends on genetic factors, through gene–environment interactions. Only a few specific gene–environment combinations that lead to increased risk of psychosis have been identified to date. An example of replicable gene–environment interaction is a common polymorphism in theAKT1gene that makes its carriers sensitive to developing psychosis with regular cannabis use. A synthesis of results from twin studies, molecular genetics, and epidemiological research outlines the many genetic and environmental factors contributing to psychosis. The interplay between these factors needs to be considered to draw a complete picture of etiology. To reach a more complete explanation of psychosis that can inform preventive strategies, future research should focus on longitudinal assessments of multiple environmental exposures within large, genotyped cohorts beginning early in life.

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Discoveries in gene-environment interactions that influence CVD, lipid traits, obesity, diabetes, and hypertension appear to be able to influence gene therapy.

10.31219/osf.io/cr5af ◽

2021 ◽

Author(s):

Moataz Dowaidar

Keyword(s):

Gene Therapy ◽

Genetic Risk ◽

Environmental Influences ◽

Biological Processes ◽

Significant Progress ◽

Therapy Outcomes ◽

Genetic Therapy ◽

Clinical Genetic ◽

Gene Environment ◽

Made In

In a relatively short amount of time, significant progress has been made in discovering gene-environment interactions that influence CVD, lipid traits, obesity, diabetes, and hypertension. These correlations appear to change genetic vulnerability, which may help researchers better understand the genetic processes that influence CVD development in the future. In order to advance the field, further research is required to confirm initial comparisons, identify the biological processes by which environmental influences modify genetic risk, and investigate strategies that use this knowledge to influence clinical genetic therapy outcomes.

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Evocative gene‐environment correlation between genetic risk for schizophrenia and bullying victimization

World Psychiatry ◽

10.1002/wps.20685 ◽

2019 ◽

Vol 18 (3) ◽

pp. 366-367

Author(s):

Giulio Pergola ◽

Marco Papalino ◽

Barbara Gelao ◽

Leonardo Sportelli ◽

Wilma Vollerbergh ◽

...

Keyword(s):

Genetic Risk ◽

Bullying Victimization ◽

Gene Environment

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Parkinson’s disease determinants, prediction and gene–environment interactions in the UK Biobank

Journal of Neurology Neurosurgery & Psychiatry ◽

10.1136/jnnp-2020-323646 ◽

2020 ◽

Vol 91 (10) ◽

pp. 1046-1054 ◽

Cited By ~ 2

Author(s):

Benjamin Meir Jacobs ◽

Daniel Belete ◽

Jonathan Bestwick ◽

Cornelis Blauwendraat ◽

Sara Bandres-Ciga ◽

...

Keyword(s):

Risk Factors ◽

Parkinson’S Disease ◽

Parkinson's Disease ◽

Family History ◽

Genetic Risk ◽

Positive Family History ◽

Risk Scores ◽

Uk Biobank ◽

Gene Environment ◽

History Of

ObjectiveTo systematically investigate the association of environmental risk factors and prodromal features with incident Parkinson’s disease (PD) diagnosis and the interaction of genetic risk with these factors. To evaluate whether existing risk prediction algorithms are improved by the inclusion of genetic risk scores.MethodsWe identified individuals with an incident diagnosis of PD (n=1276) and controls (n=500 406) in UK Biobank. We determined the association of risk factors with incident PD using adjusted logistic regression models. We constructed polygenic risk scores (PRSs) using external weights and selected the best PRS from a subset of the cohort (30%). The PRS was used in a separate testing set (70%) to examine gene–environment interactions and compare predictive models for PD.ResultsStrong evidence of association (false discovery rate <0.05) was found between PD and a positive family history of PD, a positive family history of dementia, non-smoking, low alcohol consumption, depression, daytime somnolence, epilepsy and earlier menarche. Individuals with the highest 10% of PRSs had increased risk of PD (OR 3.37, 95% CI 2.41 to 4.70) compared with the lowest risk decile. A higher PRS was associated with earlier age at PD diagnosis and inclusion of the PRS in the PREDICT-PD algorithm led to a modest improvement in model performance. We found evidence of an interaction between the PRS and diabetes.InterpretationHere, we used UK Biobank data to reproduce several well-known associations with PD, to demonstrate the validity of a PRS and to demonstrate a novel gene–environment interaction, whereby the effect of diabetes on PD risk appears to depend on background genetic risk for PD.

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Environmental and genetic risk factors and gene-environment interactions in the pathogenesis of chronic obstructive lung disease.

Environmental Health Perspectives ◽

10.1289/ehp.00108s4733 ◽

2000 ◽

Vol 108 (suppl 4) ◽

pp. 733-742 ◽

Cited By ~ 27

Author(s):

R Walter ◽

D J Gottlieb ◽

G T O'Connor

Keyword(s):

Risk Factors ◽

Lung Disease ◽

Genetic Risk ◽

Obstructive Lung Disease ◽

Chronic Obstructive Lung Disease ◽

Genetic Risk Factors ◽

Chronic Obstructive ◽

Gene Environment

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Student Classroom Misbehavior: An Exploratory Study Based on Teachers' Perceptions

The Scientific World JOURNAL ◽

10.1100/2012/208907 ◽

2012 ◽

Vol 2012 ◽

pp. 1-8 ◽

Cited By ~ 10

Author(s):

Rachel C. F. Sun ◽

Daniel T. L. Shek

Keyword(s):

Problem Behavior ◽

Problem Behaviors ◽

Teaching And Learning ◽

Secondary School Student ◽

Teachers Perceptions ◽

Individual Interviews ◽

Junior Secondary School ◽

Junior Secondary ◽

Rule Breaking ◽

Student Problem

This study aimed to examine the conceptions of junior secondary school student misbehaviors in classroom, and to identify the most common, disruptive, and unacceptable student problem behaviors from teachers' perspective. Twelve individual interviews with teachers were conducted. A list of 17 student problem behaviors was generated. Results showed that the most common and disruptive problem behavior was talking out of turn, followed by nonattentiveness, daydreaming, and idleness. The most unacceptable problem behavior was disrespecting teachers in terms of disobedience and rudeness, followed by talking out of turn and verbal aggression. The findings revealed that teachers perceived student problem behaviors as those behaviors involving rule-breaking, violating the implicit norms or expectations, being inappropriate in the classroom settings and upsetting teaching and learning, which mainly required intervention from teachers.

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Gene–environment correlation in the development of adolescent substance abuse: Selection effects of child personality and mediation via contextual risk factors

Development and Psychopathology ◽

10.1017/s0954579412000946 ◽

2013 ◽

Vol 25 (1) ◽

pp. 119-132 ◽

Cited By ~ 24

Author(s):

Brian M. Hicks ◽

Wendy Johnson ◽

C. Emily Durbin ◽

Daniel M. Blonigen ◽

William G. Iacono ◽

...

Keyword(s):

Substance Abuse ◽

High Risk ◽

Genetic Risk ◽

Social Engagement ◽

Developmental Trajectory ◽

Selection Effects ◽

Adolescent Substance Abuse ◽

Adolescent Substance ◽

Contextual Risk ◽

Gene Environment

AbstractWe used a longitudinal twin design to examine selection effects of personality traits at age 11 on high-risk environmental contexts at age 14 and the extent to which these contexts mediated risk for substance abuse at age 17. Socialization at age 11 (willingness to follow rules and endorse conventional values) predicted exposure to contextual risk at age 14. Contextual risk partially mediated the effect of socialization on substance abuse, though socialization also had a direct effect. In contrast, boldness at age 11 (social engagement and assurance, thrill seeking, and stress resilience) also predicted substance abuse directly but was unrelated to contextual risk. There was substantial overlap in the genetic and shared environmental influences on socialization and contextual risk, and genetic risk in socialization contributed to substance abuse indirectly via increased exposure to contextual risk. This suggests that active gene–environment correlations related to individual differences in socialization contributed to an early, high-risk developmental trajectory for adolescent substance abuse. In contrast, boldness appeared to index an independent and direct genetic risk factor for adolescent substance abuse.

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Gene-Gene and Gene-Environment Interactions Determine Risk of Thrombosis in Families With Inherited Antithrombin Deficiency

Blood ◽

10.1182/blood.v94.8.2590.420k40_2590_2594 ◽

1999 ◽

Vol 94 (8) ◽

pp. 2590-2594 ◽

Cited By ~ 91

Author(s):

H.H. van Boven ◽

J.P. Vandenbroucke ◽

E. Briët ◽

F.R. Rosendaal

Keyword(s):

Risk Factors ◽

Risk Factor ◽

Venous Thromboembolism ◽

Genetic Risk ◽

Factor V Leiden ◽

Genetic Defects ◽

Factor V ◽

Antithrombin Deficiency ◽

Gene Environment ◽

Genetic And Environmental Factors

To analyze inherited antithrombin deficiency as a risk factor for venous thromboembolism in various conditions with regard to the presence or absence of additional genetic or acquired risk factors, we compared 48 antithrombin-deficient individuals with 44 nondeficient individuals of 14 selected families with inherited antithrombin deficiency. The incidence of venous thromboembolism for antithrombin deficient individuals was 20 times higher than among nondeficient individuals (1.1% v 0.05% per year). At the age of 50 years, greater than 50% of antithrombin-deficient individuals had experienced thrombosis compared with 5% of nondeficient individuals. Additional genetic risk factors, Factor V Leiden and PT20210A, were found in more than half of these selected families. The effect of exposure to 2 genetic defects was a 5-fold increased incidence (4.6% per year; 95% confidence interval [CI], 1.9% to 11.1%). Acquired risk factors were often present, determining the onset of thrombosis. The incidence among those with exposure to antithrombin deficiency and an acquired risk factor was increased 20-fold (20.3% per year; 95% CI, 12.0% to 34.3%). In conclusion, in these thrombophilia families, the genetic and environmental factors interact to bring about venous thrombosis. Inherited antithrombin deficiency proves to be a prominent risk factor for venous thromboembolism. The increased risks among those with exposure to acquired risk factors should be considered and adequate prophylactic anticoagulant therapy in high-risk situations seems indicated in selected families with inherited antithrombin deficiency.

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