BDNF Val66Met polymorphism, life stress and depression: A meta-analysis of gene-environment interaction

2018 ◽  
Vol 227 ◽  
pp. 226-235 ◽  
Author(s):  
Mingzhe Zhao ◽  
Lu Chen ◽  
Jiarun Yang ◽  
Dong Han ◽  
Deyu Fang ◽  
...  
Keyword(s):  
Life Stress ◽  
Meta Analysis ◽  
Environment Interaction ◽  
Val66met Polymorphism ◽  
Gene Environment Interaction ◽  
Gene Environment ◽  
Bdnf Val66met Polymorphism

Childhood Abuse and the BDNF-Val66Met Polymorphism: Evidence for Gene-Environment Interaction in the Development of Adult Psychosis-Like Experiences

2011 ◽  
Vol 26 (S2) ◽  
pp. 1381-1381
Author(s):  
S. Alemany ◽  
B. Arias ◽  
M. Aguilera ◽  
H. Villa ◽  
J. Moya ◽  
...  
Keyword(s):  
Childhood Abuse ◽  
Childhood Adversity ◽  
Independent Effect ◽  
Psychotic Symptoms ◽  
Environment Interaction ◽  
Val66met Polymorphism ◽  
Gene Environment Interaction ◽  
Gene Environment ◽  
Established Relationship ◽  
Bdnf Val66met Polymorphism

IntroductionThe well-established relationship between childhood adversity and psychosis is likely to involve other factors such as genetic variants, which could help to understand why not everyone exposed to adverse events develops psychotic symptoms later in life (Van Winkel, et al. 2008; Simmons et al. 2009).AimsThe present study investigated the influence of childhood abuse and neglect on positive and negative psychosis-like experiences in adulthood and the potential moderating effect of the BDNF-Val66Met polymorphism.MethodPsychosis-like experiences and childhood adversity were assessed in 533 individuals from the general population.ResultsChildhood abuse showed a strong independent effect on the positive dimension of psychosis-like experiences (B = .16; SE = .05; p = .002). Furthermore, this association was moderated by the BDNF-Val66Met polymorphism (B = .17; SE = .09; p = .004).ConclusionsIndividuals exposed to childhood abuse are more likely to report positive psychosis-like experiences. Met carriers reported more positive psychosis-like experiences when exposed to childhood abuse than did individuals carrying the Val/Val genotype.Therefore, the observed gene-environment interaction effect may be partially responsible for individual variation in response to childhood abuse.

scholarly journals Childhood abuse, the BDNF-Val66Met polymorphism and adult psychotic-like experiences

2011 ◽  
Vol 199 (1) ◽  
pp. 38-42 ◽  
Author(s):  
Silvia Alemany ◽  
Bárbara Arias ◽  
Mari Aguilera ◽  
Helena Villa ◽  
Jorge Moya ◽  
...  
Keyword(s):  
Childhood Abuse ◽  
Childhood Adversity ◽  
Independent Effect ◽  
Psychotic Symptoms ◽  
Environment Interaction ◽  
Val66met Polymorphism ◽  
Gene Environment Interaction ◽  
Gene Environment ◽  
Established Relationship ◽  
Bdnf Val66met Polymorphism

BackgroundThe well-established relationship between childhood adversity and psychosis is likely to involve other factors such as genetic variants that can help us to understand why not everyone exposed to adverse events develops psychotic symptoms later in life.AimsWe investigated the influence of childhood abuse and neglect on positive and negative psychotic-like experiences in adulthood and the potential moderating effect of the BDNF-Val66Met polymorphism.MethodPsychotic-like experiences and childhood adversity were assessed in 533 individuals from the general population.ResultsChildhood abuse showed a strong independent effect on the positive dimension of psychotic-like experiences (β = 0.16, s.e. = 0.05, P = 0.002). Furthermore, this association was moderated by the BDNF-Val66Met polymorphism (β = 0.27, s.e. = 0.10, P = 0.004).ConclusionsIndividuals exposed to childhood abuse are more likely to report positive psychotic-like experiences. Met carriers reported more positive psychotic-like experiences when exposed to childhood abuse than did individuals carrying the Val/Val genotype. Therefore, the observed gene–environment interaction effect may be partially responsible for individual variation in response to childhood abuse.

scholarly journals Effect of polygenic risk scores on depression in childhood trauma

2014 ◽  
Vol 205 (2) ◽  
pp. 113-119 ◽  
Author(s):  
Wouter J. Peyrot ◽  
Yuri Milaneschi ◽  
Abdel Abdellaoui ◽  
Patrick F. Sullivan ◽  
Jouke J. Hottenga ◽  
...  
Keyword(s):  
Childhood Trauma ◽  
Meta Analysis ◽  
Genetic Effect ◽  
Risk Scores ◽  
Environment Interaction ◽  
Polygenic Risk ◽  
Gene Environment Interaction ◽  
Gene Environment ◽  
Genome Wide ◽  
Direct Genetic Effect

BackgroundResearch on gene×environment interaction in major depressive disorder (MDD) has thus far primarily focused on candidate genes, although genetic effects are known to be polygenic.AimsTo test whether the effect of polygenic risk scores on MDD is moderated by childhood trauma.MethodThe study sample consisted of 1645 participants with a DSM-IV diagnosis of MDD and 340 screened controls from The Netherlands. Chronic or remitted episodes (severe MDD) were present in 956 participants. The occurrence of childhood trauma was assessed with the Childhood Trauma Interview and the polygenic risk scores were based on genome-wide meta-analysis results from the Psychiatric Genomics Consortium.ResultsThe polygenic risk scores and childhood trauma independently affected MDD risk, and evidence was found for interaction as departure from both multiplicativity and additivity, indicating that the effect of polygenic risk scores on depression is increased in the presence of childhood trauma. The interaction effects were similar in predicting all MDD risk and severe MDD risk, and explained a proportion of variation in MDD risk comparable to the polygenic risk scores themselves.ConclusionsThe interaction effect found between polygenic risk scores and childhood trauma implies that (1) studies on direct genetic effect on MDD gain power by focusing on individuals exposed to childhood trauma, and that (2) individuals with both high polygenic risk scores and exposure to childhood trauma are particularly at risk for developing MDD.

scholarly journals Characterization of 9p24 Risk Locus and Colorectal Adenoma and Cancer: Gene–Environment Interaction and Meta-Analysis

2010 ◽  
Vol 19 (12) ◽  
pp. 3131-3139 ◽  
Author(s):  
Jonathan D. Kocarnik ◽  
Carolyn M. Hutter ◽  
Martha L. Slattery ◽  
Sonja I. Berndt ◽  
Li Hsu ◽  
...  
Keyword(s):  
Colorectal Adenoma ◽  
Meta Analysis ◽  
Environment Interaction ◽  
Cancer Gene ◽  
Gene Environment Interaction ◽  
Gene Environment ◽  
Risk Locus

scholarly journals Role of the Common PRSS1-PRSS2 Haplotype in Alcoholic and Non-Alcoholic Chronic Pancreatitis: Meta- and Re-Analyses

Genes ◽  
2020 ◽  
Vol 11 (11) ◽  
pp. 1349
Author(s):  
Anthony F. Herzig ◽  
Emmanuelle Génin ◽  
David N. Cooper ◽  
Emmanuelle Masson ◽  
Claude Férec ◽  
...  
Keyword(s):  
Chronic Pancreatitis ◽  
Risk Allele ◽  
Genetic Model ◽  
Meta Analysis ◽  
Risk Haplotype ◽  
Environment Interaction ◽  
Gene Environment Interaction ◽  
Alcoholic Chronic Pancreatitis ◽  
Gene Environment ◽  
Association Data

The association between a common PRSS1-PRSS2 haplotype and alcoholic chronic pancreatitis (ACP), which was revealed by the first genome-wide association study of chronic pancreatitis (CP), has been consistently replicated. However, the association with non-ACP (NACP) has been controversial. Herein, we sought to clarify this basic issue by means of an allele-based meta-analysis of currently available studies. We then used studies informative for genotype distribution to explore the biological mechanisms underlying the association data and to test for gene-environment interaction between the risk haplotype and alcohol consumption by means of a re-analysis. A literature search was conducted to identify eligible studies. A meta-analysis was performed using the Review Manager software. The association between the risk genotypes and NACP or ACP was tested for the best-fitting genetic model. Gene-environment interaction was estimated by both case-only and multinomial approaches. Five and eight studies were employed for the meta-analysis of ACP and NACP findings, respectively. The risk allele was significantly associated with both ACP (pooled odds ratio (OR) 1.67, 95% confidence interval (CI) 1.56–1.78; p < 0.00001) and NACP (pooled OR 1.28, 95% CI 1.17–1.40; p < 0.00001). Consistent with a dosage effect of the risk allele on PRSS1/PRSS2 mRNA expression in human pancreatic tissue, both ACP and NACP association data were best explained by an additive genetic model. Finally, the risk haplotype was found to interact synergistically with alcohol consumption.

scholarly journals Life stress, the dopamine receptor gene, and emerging adult drug use trajectories: A longitudinal, multilevel, mediated moderation analysis

2012 ◽  
Vol 24 (3) ◽  
pp. 941-951 ◽  
Author(s):  
Gene H. Brody ◽  
Yi-Fu Chen ◽  
Tianyi Yu ◽  
Steven R. H. Beach ◽  
Steven M. Kogan ◽  
...  
Keyword(s):  
Drug Use ◽  
Emerging Adults ◽  
Dopamine Receptor ◽  
Life Stress ◽  
Receptor Gene ◽  
Saliva Sample ◽  
Environment Interaction ◽  
Gene Environment Interaction ◽  
Gene Environment ◽  
Status Interaction

AbstractThis study was designed to examine the prospective relations of life stress and genetic status with increases in drug use. African Americans (N = 399) in rural Georgia (Wave 1 mean age = 17 years) provided three waves of data across 27.5 months and a saliva sample from which the dopamine receptor D4 (DRD4) gene was genotyped. Multilevel growth curve modeling analysis indicated that emerging adults manifested the highest escalations in drug use when they reported high life stress and carried an allele of DRD4 with 7 or more repeats (7 + R allele). In addition, emerging adults who reported high life stress and carried the 7 + R allele evinced the largest increases in two proximal risk factors for drug use: affiliations with drug-using companions and drug use vulnerability cognitions. Furthermore, when the Gene × Environment interaction effects on the increases in affiliations with drug-using companions and vulnerability cognitions were entered into the model forecasting drug use, the Life Stress × DRD4 Status interaction on drug use became nonsignificant in the presence of the risk mechanisms. This finding provides an example of “second generation” Gene × Environment interaction research in which the interaction's effects on proximal risk mechanisms account for its effects on outcomes.

scholarly journals Meta-analysis of gene-environment interaction: joint estimation of SNP and SNP × environment regression coefficients

2010 ◽  
Vol 35 (1) ◽  
pp. 11-18 ◽  
Author(s):  
Alisa K. Manning ◽  
Michael LaValley ◽  
Ching-Ti Liu ◽  
Kenneth Rice ◽  
Ping An ◽  
...  
Keyword(s):  
Meta Analysis ◽  
Joint Estimation ◽  
Regression Coefficients ◽  
Environment Interaction ◽  
Gene Environment Interaction ◽  
Gene Environment

Oral Clefts, Maternal Smoking, and TGFA: A Meta-Analysis of Gene-Environment Interaction

2005 ◽  
Vol 42 (1) ◽  
pp. 58-63 ◽  
Author(s):  
Joanna S. Zeiger ◽  
Terri H. Beaty ◽  
Kung-Yee Liang
Keyword(s):  
Logistic Regression ◽  
Maternal Smoking ◽  
Meta Analysis ◽  
Case Control ◽  
Environment Interaction ◽  
Oral Clefts ◽  
Gene Environment Interaction ◽  
Gene Environment ◽  
Increased Risk ◽  
Polytomous Logistic Regression

Objective A meta-analysis was performed to examine the association among maternal cigarette smoking, infant genotype at the Taq1 site in the transforming growth factor α (TGFA) locus, and risk of nonsyndromic oral clefts, both cleft palate (CP) and cleft lip with or without cleft palate (CL/P). Design Five published case-control studies were included in the meta-analyis. Pooled Mantel-Haenszel odds ratios (OR) and 95% confidence intervals (CIs) were computed. Gene-environment interaction was also assessed by using the pooled data in a case-only analysis and polytomous logistic regression. Results Among nonsmoking mothers, there was no evidence of any increased risk for CP if the infant carried the TGFA Taq1 C2 allele. If the mother reported smoking, however, there was an overall increased risk for CP if the infant carried the C2 allele (ORsmokers = 1.95; 95% CI = 1.22 to 3.10). TGFA genotype did not increase risk to CL/P, regardless of maternal smoking status. Polytomous logistic regression revealed a significant overall smoking effect for CL/P (OR = 1.64, 95% CI = 1.33 to 2.02) and CP (OR = 1.42, 95% CI = 1.06 to 1.90). Conclusions While maternal smoking was a consistent risk factor for both CL/P and CP across all studies, the suggestive evidence for gene-environment interaction between the infant's genotype at the Taq1 marker in TGFA and maternal smoking was limited to CP. Furthermore, evidence for such gene-environment interaction was strongest in a case-control study drawn from a birth defect registry where infants with non-cleft defects served as controls.

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