scholarly journals Exploring the genetic correlations of antisocial behaviour and life history traits

BJPsych Open ◽  
2018 ◽  
Vol 4 (6) ◽  
pp. 467-470 ◽  
Author(s):  
Jorim J. Tielbeek ◽  
J.C. Barnes ◽  
Arne Popma ◽  
Tinca J.C. Polderman ◽  
James J. Lee ◽  
...  
Keyword(s):  
Life History ◽  
Genome Wide Association Study ◽  
Genetic Correlations ◽  
Antisocial Behaviour ◽  
Study Data ◽  
Age At First Birth ◽  
Number Of Children ◽  
Genome Wide ◽  
History Approach ◽  
Children Ever Born

SummaryPrior evolutionary theory provided reason to suspect that measures of development and reproduction would be correlated with antisocial behaviours in human and non-human species. Behavioural genetics has revealed that most quantitative traits are heritable, suggesting that these phenotypic correlations may share genetic aetiologies. We use genome-wide association study data to estimate the genetic correlations between various measures of reproductive development (N = 52 776–318 863) and antisocial behaviour (N = 31 968). Our genetic correlation analyses demonstrate that alleles associated with higher reproductive output (number of children ever born, rg = 0.50, P = 0.0065) were positively correlated with alleles associated with antisocial behaviour, whereas alleles associated with more delayed reproductive onset (age at first birth, rg = −0.64, P = 0.0008) were negatively associated with alleles linked to antisocial behaviour. Ultimately, these findings coalesce with evolutionary theories suggesting that increased antisocial behaviours may partly represent a faster life history approach, which may be significantly calibrated by genes.Declaration of interestNone.

scholarly journals Exploring the genetic correlations of antisocial behavior and life history traits

2018 ◽  
Author(s):  
Jorim J. Tielbeek ◽  
J.C. Barnes ◽  
Arne Popma ◽  
Tinca J.C. Polderman ◽  
James J. Lee ◽  
...  
Keyword(s):  
Life History ◽  
Antisocial Behavior ◽  
Reproductive Output ◽  
Behavioral Genetics ◽  
Genetic Correlations ◽  
Antisocial Behaviors ◽  
Number Of Children ◽  
Reproductive Onset ◽  
History Approach ◽  
Children Ever Born

AbstractPrior evolutionary theory provided reason to suspect that measures of development and reproduction would be correlated with antisocial behaviors in human and non-human species. Behavioral genetics has revealed that most quantitative traits are heritable, suggesting that these phenotypic correlations may share genetic etiologies. We use GWAS data to estimate the genetic correlations between various measures of reproductive development (N= 52,776 – 318,863) and antisocial behavior (N= 31,968). Our genetic correlation analyses demonstrate that alleles associated with higher reproductive output (number of children ever born, rg=0.50, p=.0065) were positively correlated with alleles associated with antisocial behavior, whereas alleles associated with more delayed reproductive onset (age of first birth, rg=-.64, p=.0008) were negatively associated with alleles linked to antisocial behavior. Ultimately, these findings coalesce with evolutionary theories suggesting that increased antisocial behaviors may partly represent a faster life history approach, which may be significantly calibrated by genes.

scholarly journals Sex-dimorphic genetic effects and novel loci for fasting glucose and insulin variability

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Vasiliki Lagou ◽  
◽  
Reedik Mägi ◽  
Jouke- Jan Hottenga ◽  
Harald Grallert ◽  
...  
Keyword(s):  
Genome Wide Association Study ◽  
Fasting Glucose ◽  
Genetic Correlations ◽  
Epidemiological Studies ◽  
Genetic Effects ◽  
Fasting Insulin ◽  
Sex Dimorphism ◽  
Waist To Hip Ratio ◽  
Genome Wide ◽  
Meta Analyses

AbstractDifferences between sexes contribute to variation in the levels of fasting glucose and insulin. Epidemiological studies established a higher prevalence of impaired fasting glucose in men and impaired glucose tolerance in women, however, the genetic component underlying this phenomenon is not established. We assess sex-dimorphic (73,089/50,404 women and 67,506/47,806 men) and sex-combined (151,188/105,056 individuals) fasting glucose/fasting insulin genetic effects via genome-wide association study meta-analyses in individuals of European descent without diabetes. Here we report sex dimorphism in allelic effects on fasting insulin at IRS1 and ZNF12 loci, the latter showing higher RNA expression in whole blood in women compared to men. We also observe sex-homogeneous effects on fasting glucose at seven novel loci. Fasting insulin in women shows stronger genetic correlations than in men with waist-to-hip ratio and anorexia nervosa. Furthermore, waist-to-hip ratio is causally related to insulin resistance in women, but not in men. These results position dissection of metabolic and glycemic health sex dimorphism as a steppingstone for understanding differences in genetic effects between women and men in related phenotypes.

A Proteome-Wide Association Study Identified Candidate Human Brain Proteins Associated with Coffee Consumption

2021 ◽  
Author(s):  
Chun'e Li ◽  
Xiao Liang ◽  
Yumeng Jia ◽  
Yan Wen ◽  
Huijie Zhang ◽  
...  
Keyword(s):  
Human Brain ◽  
Association Study ◽  
Plasma Proteins ◽  
Genome Wide Association Study ◽  
Genetic Correlations ◽  
Coffee Consumption ◽  
Genetic Associations ◽  
Brain Proteins ◽  
Genome Wide ◽  
Brain Proteome

Abstract Background Increasing evidence suggests the association between caffeine and the brain and nervous system. However, there is limited research on the genetic associations between coffee consumption subtypes and brain proteome, plasma proteomes, and peripheral metabolites. Methods First, proteome-wide association study (PWAS) of coffee consumption subtypes was performed by integrating two independent genome-wide association study (GWAS) datasets (91,462–502,650 subjects) with two reference human brain proteomes (ROS/MAP and Banner), by using the FUSION pipeline. Second, transcriptome-wide association study (TWAS) analysis of coffee consumption subtypes was conducted by integrating the two gene expression weight references (RNAseq and splicing) of brain RNA-seq and the two GWAS datasets (91,462–502,650 subjects) of coffee consumption subtypes. Finally, we used the LD Score Regression (LDSC) analysis to evaluate the genetic correlations of coffee consumption subtypes with plasma proteomes and peripheral metabolites. Results For the traits related to coffee consumption, we identified 3 common PWAS proteins, such as MADD (P PWAS−Banner−dis=0.0114, P PWAS−ROS/MAP−rep =0.0489). In addition, 11 common TWAS genes were found in two cohorts, such as ARPC2 (P TWAS−splicing−dis =2063×10− 12, P TWAS−splicing−dis =1.25×10− 10, P TWAS−splicing−dis =1.24e-08, P TWAS−splicing−rep =3.25×10− 9 and P TWAS−splicing−rep =3.42×10− 13). Importantly, we have identified 8 common genes between PWAS and TWAS, such as ALDH2 (P PWAS−banner−rep =1.22×10− 22, PTWAS− splicing−dis = 4.54×10− 92). For the LDSC analysis of human plasma proteome, we identified 11 plasma proteins, such as CHL1 (P dis = 0.0151, P rep =0.0438). For the LDSC analysis of blood metabolites, 5 metabolites have been found, such as myo-inositol (P dis = 0.0073, P dis = 0.0152, P dis =0.0414, P rep =0.0216). Conclusions We identified several brain proteins and genes associated with coffee consumption subtypes. In addition, we also detected several candidate plasma proteins and metabolites related to these subtypes.

scholarly journals A loop-counting method for covariate-corrected low-rank biclustering of gene-expression and genome-wide association study data

2018 ◽  
Vol 14 (5) ◽  
pp. e1006105 ◽  
Author(s):  
Aaditya V. Rangan ◽  
Caroline C. McGrouther ◽  
John Kelsoe ◽  
Nicholas Schork ◽  
Eli Stahl ◽  
...  
Keyword(s):  
Gene Expression ◽  
Association Study ◽  
Genome Wide Association Study ◽  
Study Data ◽  
Genome Wide Association ◽  
Low Rank ◽  
Counting Method ◽  
Genome Wide

scholarly journals Genome-wide association study identifies 48 common genetic variants associated with handedness

2019 ◽  
Author(s):  
Gabriel Cuellar Partida ◽  
Joyce Y Tung ◽  
Nicholas Eriksson ◽  
Eva Albrecht ◽  
Fazil Aliev ◽  
...  
Keyword(s):  
Association Study ◽  
Genetic Variants ◽  
Complex Traits ◽  
Genome Wide Association Study ◽  
Genetic Correlations ◽  
Genome Wide Association ◽  
Left Handedness ◽  
Left Handed ◽  
Genome Wide ◽  
Common Genetic Variants

AbstractHandedness, a consistent asymmetry in skill or use of the hands, has been studied extensively because of its relationship with language and the over-representation of left-handers in some neurodevelopmental disorders. Using data from the UK Biobank, 23andMe and 32 studies from the International Handedness Consortium, we conducted the world’s largest genome-wide association study of handedness (1,534,836 right-handed, 194,198 (11.0%) left-handed and 37,637 (2.1%) ambidextrous individuals). We found 41 genetic loci associated with left-handedness and seven associated with ambidexterity at genome-wide levels of significance (P < 5×10−8). Tissue enrichment analysis implicated the central nervous system and brain tissues including the hippocampus and cerebrum in the etiology of left-handedness. Pathways including regulation of microtubules, neurogenesis, axonogenesis and hippocampus morphology were also highlighted. We found suggestive positive genetic correlations between being left-handed and some neuropsychiatric traits including schizophrenia and bipolar disorder. SNP heritability analyses indicated that additive genetic effects of genotyped variants explained 5.9% (95% CI = 5.8% – 6.0%) of the underlying liability of being left-handed, while the narrow sense heritability was estimated at 12% (95% CI = 7.2% – 17.7%). Further, we show that genetic correlation between left-handedness and ambidexterity is low (rg = 0.26; 95% CI = 0.08 – 0.43) implying that these traits are largely influenced by different genetic mechanisms. In conclusion, our findings suggest that handedness, like many other complex traits is highly polygenic, and that the genetic variants that predispose to left-handedness may underlie part of the association with some psychiatric disorders that has been observed in multiple observational studies.

scholarly journals Genome-wide analysis identifies genetic effects on reproductive success and ongoing natural selection at the FADS locus

2020 ◽  
Author(s):  
Iain Mathieson ◽  
Felix R. Day ◽  
Nicola Barban ◽  
Felix C. Tropf ◽  
David M. Brazel ◽  
...  
Keyword(s):  
Natural Selection ◽  
Reproductive Success ◽  
European Ancestry ◽  
Age At First Birth ◽  
Hormone Regulation ◽  
Number Of Children ◽  
Two Generations ◽  
Reproductive Ageing ◽  
Children Ever Born ◽  
Using Data

AbstractIdentifying genetic determinants of reproductive success may highlight mechanisms underlying fertility and also identify alleles under present-day selection. Using data in 785,604 individuals of European ancestry, we identify 43 genomic loci associated with either number of children ever born (NEB) or childlessness. These loci span diverse aspects of reproductive biology across the life course, including puberty timing, age at first birth, sex hormone regulation and age at menopause. Missense alleles in ARHGAP27 were associated with increased NEB but reduced reproductive lifespan, suggesting a trade-off between reproductive ageing and intensity. As NEB is one component of evolutionary fitness, our identified associations indicate loci under present-day natural selection. Accordingly, we find that NEB-increasing alleles have increased in frequency over the past two generations. Furthermore, integration with data from ancient selection scans identifies a unique example of an allele—FADS1/2 gene locus—that has been under selection for thousands of years and remains under selection today. Collectively, our findings demonstrate that diverse biological mechanisms contribute to reproductive success, implicating both neuro-endocrine and behavioural influences.

scholarly journals Tuberculosis infection and lung adenocarcinoma: Mendelian randomization and pathway analysis of genome-wide association study data from never-smoking Asian women

Genomics ◽  
2020 ◽  
Vol 112 (2) ◽  
pp. 1223-1232
Author(s):  
Jason Y.Y. Wong ◽  
Han Zhang ◽  
Chao A. Hsiung ◽  
Kouya Shiraishi ◽  
Kai Yu ◽  
...  
Keyword(s):  
Lung Adenocarcinoma ◽  
Association Study ◽  
Pathway Analysis ◽  
Genome Wide Association Study ◽  
Mendelian Randomization ◽  
Study Data ◽  
Tuberculosis Infection ◽  
Genome Wide Association ◽  
Asian Women ◽  
Genome Wide

scholarly journals Genome-Wide Association Study Data Reveal Genetic Susceptibility to Chronic Inflammatory Intestinal Diseases and Pancreatic Ductal Adenocarcinoma Risk

2020 ◽  
Vol 80 (18) ◽  
pp. 4004-4013
Author(s):  
Fangcheng Yuan ◽  
Rayjean J. Hung ◽  
Naomi Walsh ◽  
Han Zhang ◽  
Elizabeth A. Platz ◽  
...  
Keyword(s):  
Association Study ◽  
Pancreatic Ductal Adenocarcinoma ◽  
Genetic Susceptibility ◽  
Genome Wide Association Study ◽  
Study Data ◽  
Genome Wide Association ◽  
Ductal Adenocarcinoma ◽  
Intestinal Diseases ◽  
Genome Wide

scholarly journals Insights into Pancreatic Cancer Etiology from Pathway Analysis of Genome-Wide Association Study Data

PLoS ONE ◽  
2012 ◽  
Vol 7 (10) ◽  
pp. e46887 ◽  
Author(s):  
Peng Wei ◽  
Hongwei Tang ◽  
Donghui Li
Keyword(s):  
Pancreatic Cancer ◽  
Association Study ◽  
Pathway Analysis ◽  
Genome Wide Association Study ◽  
Study Data ◽  
Genome Wide Association ◽  
Cancer Etiology ◽  
Genome Wide

scholarly journals Assessing causality in associations between cannabis use and schizophrenia risk: a two-sample Mendelian randomization study

2016 ◽  
Vol 47 (5) ◽  
pp. 971-980 ◽  
Author(s):  
S. H. Gage ◽  
H. J. Jones ◽  
S. Burgess ◽  
J. Bowden ◽  
G. Davey Smith ◽  
...  
Keyword(s):  
Fixed Effects ◽  
Genome Wide Association Study ◽  
Mendelian Randomization ◽  
Causal Effect ◽  
Positive Control ◽  
Negative Control ◽  
Study Data ◽  
Nucleotide Polymorphisms ◽  
Genome Wide ◽  
Genome Wide Data

BackgroundObservational associations between cannabis and schizophrenia are well documented, but ascertaining causation is more challenging. We used Mendelian randomization (MR), utilizing publicly available data as a method for ascertaining causation from observational data.MethodWe performed bi-directional two-sample MR using summary-level genome-wide data from the International Cannabis Consortium (ICC) and the Psychiatric Genomics Consortium (PGC2). Single nucleotide polymorphisms (SNPs) associated with cannabis initiation (p < 10−5) and schizophrenia (p < 5 × 10−8) were combined using an inverse-variance-weighted fixed-effects approach. We also used height and education genome-wide association study data, representing negative and positive control analyses.ResultsThere was some evidence consistent with a causal effect of cannabis initiation on risk of schizophrenia [odds ratio (OR) 1.04 per doubling odds of cannabis initiation, 95% confidence interval (CI) 1.01–1.07, p = 0.019]. There was strong evidence consistent with a causal effect of schizophrenia risk on likelihood of cannabis initiation (OR 1.10 per doubling of the odds of schizophrenia, 95% CI 1.05–1.14, p = 2.64 × 10−5). Findings were as predicted for the negative control (height: OR 1.00, 95% CI 0.99–1.01, p = 0.90) but weaker than predicted for the positive control (years in education: OR 0.99, 95% CI 0.97–1.00, p = 0.066) analyses.ConclusionsOur results provide some that cannabis initiation increases the risk of schizophrenia, although the size of the causal estimate is small. We find stronger evidence that schizophrenia risk predicts cannabis initiation, possibly as genetic instruments for schizophrenia are stronger than for cannabis initiation.

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