Genetic risk and gene?environment interaction in coronary artery spasm in Japanese men and women

ABSTRACTWhile psychotic experiences are core symptoms of mental health disorders like schizophrenia, they are also reported by 5-10% of the population. Both smoking behaviour and genetic risk for psychiatric disorders have been associated with psychotic experiences, but the interplay between these factors remains poorly understood. We tested whether smoking status, maternal smoking around birth, and number of packs smoked/year were associated with lifetime occurrence of three psychotic experiences phenotypes: delusions (n=2067), hallucinations (n=6689), and any psychotic experience (delusions or hallucinations; n=7803) in 144818 UK Biobank participants. We next calculated polygenic risk scores for schizophrenia (PRSSCZ), major depression (PRSDEP) and attention deficit hyperactivity disorder (PRSADHD) in the UK Biobank participants to assess whether association between smoking and psychotic experiences was attenuated after adjustment of diagnosis of psychiatric disorders and the PRSs. Finally, we investigated whether smoking exacerbates the effects of genetic predisposition on the psychotic phenotypes in gene-environment interaction models. Smoking status, maternal smoking, and number of packs smoked/year were significantly associated with psychotic experiences (p<1.77×10−5). Except for packs smoked/year, effects were attenuated but remained significant after adjustment for diagnosis of psychiatric disorders and PRSs (p<1.99×10−3). Gene-environment interaction models showed the effects of PRSDEP and PRSADHD(but not PRSSCZ) on delusions (but not hallucinations) were significantly greater in current smokers compared to never smokers (p<0.0028). There were no significant gene-environment interactions for maternal smoking nor for number of packs smoked/year. Our results suggest that both genetic risk of psychiatric disorders and smoking status may have independent and synergistic effects on specific types of psychotic experiences.

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Gene–environment interaction in coronary artery disease: apolipoprotein E and smoking and the interleukin-6 gene and inflammation as examples

Coronary Heart Disease Epidemiology ◽

10.1093/acprof:oso/9780198525738.003.0032 ◽

2005 ◽

pp. 528-544

Author(s):

S. E. Humphries

Keyword(s):

Coronary Artery Disease ◽

Coronary Artery ◽

Apolipoprotein E ◽

Interleukin 6 ◽

Environment Interaction ◽

Gene Environment Interaction ◽

Gene Environment ◽

Artery Disease

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Inclusion of a gene‐environment interaction between alcohol consumption and the aldehyde dehydrogenase 2 genotype in a risk prediction model for upper aerodigestive tract cancer in Japanese men

Cancer Science ◽

10.1111/cas.14573 ◽

2020 ◽

Vol 111 (10) ◽

pp. 3835-3844

Author(s):

Motoki Iwasaki ◽

Sanjeev Budhathoki ◽

Taiki Yamaji ◽

Sachiko Tanaka‐Mizuno ◽

Aya Kuchiba ◽

...

Keyword(s):

Alcohol Consumption ◽

Environment Interaction ◽

Upper Aerodigestive Tract ◽

Aldehyde Dehydrogenase 2 ◽

Japanese Men ◽

Tract Cancer ◽

Gene Environment Interaction ◽

Gene Environment ◽

Upper Aerodigestive Tract Cancer ◽

Aerodigestive Tract Cancer

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Genetic and environmental pathways to suicidal behavior: Reflections of a genetic epidemiologist

European Psychiatry ◽

10.1016/j.eurpsy.2010.01.005 ◽

2010 ◽

Vol 25 (5) ◽

pp. 300-303 ◽

Cited By ~ 22

Author(s):

K.S. Kendler

Keyword(s):

Psychiatric Disorders ◽

Suicidal Behavior ◽

Indirect Effects ◽

Genetic Risk ◽

Developmental Pathways ◽

Early Adversity ◽

Environment Interaction ◽

Direct Effects ◽

Gene Environment Interaction ◽

Gene Environment

AbstractThis paper presents a tentative typology of genetic and environmental pathways to suicidal behavior. Ten pathways are proposed and briefly illustrated: (i) direct effects from psychiatric disorders; (ii) direct effects from personality; (iii) direct effects of early adversity; (iv) direct effects of current adversity; (v) indirect effects of genes on selection into adversity (gene–environment correlation); (vi) interactions between genetic risk and current adversity: gene–environment interaction; (vii) interactions between early and current adversity: environment–environment interaction; (viii) interactions between culture and genes; (ix) dynamic developmental pathways involving causal loops from genes to environment and back again; and (x) gene × environment × development interaction.

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Comparison of weighting approaches for genetic risk scores in gene-environment interaction studies

BMC Genetics ◽

10.1186/s12863-017-0586-3 ◽

2017 ◽

Vol 18 (1) ◽

Cited By ~ 14

Author(s):

Anke Hüls ◽

Ursula Krämer ◽

Christopher Carlsten ◽

Tamara Schikowski ◽

Katja Ickstadt ◽

...

Keyword(s):

Genetic Risk ◽

Risk Scores ◽

Environment Interaction ◽

Genetic Risk Scores ◽

Gene Environment Interaction ◽

Interaction Studies ◽

Gene Environment

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Gene–environment interaction between peer victimization and child aggression

Development and Psychopathology ◽

10.1017/s0954579408000229 ◽

2008 ◽

Vol 20 (2) ◽

pp. 455-471 ◽

Cited By ~ 40

Author(s):

Mara Brendgen ◽

Michel Boivin ◽

Frank Vitaro ◽

Alain Girard ◽

Ginette Dionne ◽

...

Keyword(s):

Aggressive Behavior ◽

Peer Victimization ◽

Genetic Risk ◽

Environment Interaction ◽

Child Aggression ◽

Gene Environment Interaction ◽

Genetic Modeling ◽

Gene Environment ◽

Teacher Reports ◽

Peer Nominations

AbstractAlthough peer victimization places children at serious risk for aggressive behavior, not all victimized children are aggressive. The diathesis–stress hypothesis of disease proposes that an environmental stressor such as peer victimization should to lead to maladjustment mostly in those individuals with preexisting genetic vulnerabilities. Accordingly, this study examined whether the link between peer victimization and child aggression is moderated by children's genetic risk for such behavior. Using a sample of 506 6-year-old twins, peer victimization was assessed through peer nominations and aggressive behavior was assessed through peer and teacher reports. Children's genetic risk for aggression was estimated as a function of their co-twin's aggression and the pair's zygosity. Genetic modeling showed that peer victimization is an environmentally driven variable that is unrelated to children's genetic disposition. Results also provided support for the notion of a gene–environment interaction between peer victimization and child's genetic risk for aggressive behavior, albeit only in girls. For boys, peer victimization was related to aggression regardless of the child's genetic risk for such behavior. Different socialization experiences in girls' compared to boys' peer groups may explain the different pattern of results for girls and boys.

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