scholarly journals Psychotic Experiences Are Associated With Paternal Age But Not With Delayed Fatherhood in a Large, Multinational, Community Sample

2020 ◽  
Vol 46 (5) ◽  
pp. 1327-1334
Author(s):  
Franck Schürhoff ◽  
Baptiste Pignon ◽  
Mohamed Lajnef ◽  
Romain Denis ◽  
Bart Rutten ◽  
...  
Keyword(s):  
Community Sample ◽  
Self Report ◽  
Paternal Age ◽  
Environment Interaction ◽  
The European Union ◽  
Gene Environment Interaction ◽  
Gene Environment ◽  
Increased Risk ◽  
Psychosis Risk ◽  
Subclinical Psychosis

Abstract Advanced paternal age has been consistently associated with an increased risk of schizophrenia. It is less known if such an association also exists with subclinical/attenuated forms of psychosis. Additionally, it has been suggested that it is not paternal age per se, but rather delayed fatherhood, as a marker of a genetic liability of psychosis, that is the cause of the association. The aim of the current study was to examine whether paternal age and/or delayed fatherhood (paternity age) predict self-reported positive, negative, and/or depressive dimensions of psychosis in a large sample from the general population. The sample (N = 1465) was composed of control subjects from the 6 countries participating in the European Union Gene-Environment Interaction study. The CAPE, a self-report questionnaire, was used to measure dimensions of subclinical psychosis. Paternal age at the time of respondents’ birth and age of paternity were assessed by self-report. We assessed the influence of the variables of interest (paternal age or paternity age) on CAPE scores after adjusting for potential confounders (age, gender, and ethnicity). Paternal age was positively associated with the positive dimension of the CAPE. By contrast, paternity age was not associated with any of the psychosis dimensions assessed by the CAPE. Thus, our results do not support the idea that delayed fatherhood explains the association between age of paternity and psychosis risk. Furthermore, our results provide arguments for the hypothesis of an etiologic continuum of psychosis.

scholarly journals Interaction between ELMO1 gene polymorphisms and environment factors on susceptibility to diabetic nephropathy in Chinese Han population

2019 ◽  
Vol 11 (1) ◽  
Author(s):  
Yi Hou ◽  
Yong Gao ◽  
Yan Zhang ◽  
Si-Tong Lin ◽  
Yue Yu ◽  
...  
Keyword(s):  
Diabetic Nephropathy ◽  
Alcohol Drinking ◽  
Control Group ◽  
Environment Interaction ◽  
Nucleotide Polymorphisms ◽  
Chinese Han ◽  
Gene Environment Interaction ◽  
Gene Environment ◽  
Increased Risk ◽  
Significant Gene

Abstract Background The association of diabetic nephropathy (DN) risk with single nucleotide polymorphisms (SNPs) within Engulfment and Cell Motility 1 (ELMO1) gene and gene–environment synergistic effect have not been extensively examined in, therefore, the purpose of this study is to explore the association between multiple SNPs in ELMO1 gene, and the relationship between gene–environment synergy effect and the risk of DN. Methods Genotyping for 4 SNPs was performed with polymerase chain reaction (PCR) and following restriction fragment length polymorphism (RFLP) methods. Hardy–Weinberg balance of the control group was tested by SNPstats (online software: http://bioinfo.iconologia.net/snpstats). The best combination of four SNPs of ELMO1 gene and environmental factors was screened by GMDR model. Logistic regression was used to calculating the OR values between different genotypes of ELMO1 gene and DN. Results The rs741301-G allele and the rs10255208-GG genotype were associated with an increased risk of DN risk, adjusted ORs (95% CI) were 1.75 (1.19–2.28) and 1.41 (1.06–1.92), respectively, both p-values were < 0.001. We also found that the others SNPs-rs1345365 and rs7782979 were not significantly associated with susceptibility to DN. GMDR model found a significant gene–alcohol drinking interaction combination (p = 0.0107), but no significant gene–hypertension interaction combinations. Alcohol drinkers with rs741301-AG/GG genotype also have the highest DN risk, compared to never drinkers with rs741301-AA genotype, OR (95% CI) 3.52 (1.93–4.98). Conclusions The rs741301-G allele and the rs10255208-GG genotype, gene–environment interaction between rs741301 and alcohol drinking were all associated with increased DN risk.

Extremely low birth weight babies grown up: Gene–environment interaction predicts internalizing problems in the third and fourth decades of life

2016 ◽  
Vol 29 (3) ◽  
pp. 837-843 ◽  
Author(s):  
Ayelet Lahat ◽  
Ryan J. van Lieshout ◽  
Karen J. Mathewson ◽  
James Mackillop ◽  
Saroj Saigal ◽  
...  
Keyword(s):  
Birth Weight ◽  
Low Birth Weight ◽  
Internalizing Problems ◽  
Self Report ◽  
Extremely Low Birth Weight ◽  
Environment Interaction ◽  
Region Gene ◽  
The Third ◽  
Gene Environment ◽  
Increased Risk

AbstractExtremely low birth weight (ELBW; <1000 g) infants have been exposed to stressful intrauterine and early postnatal environments. Even greater early adversity has been experienced by ELBW survivors who were also born small for gestational age (SGA; <10th percentile for GA) compared to those born appropriate for GA (AGA). ELBW survivors, particularly those born SGA, face increased risk for internalizing problems compared to normal BW (NBW; ≥2500 g) controls. Internalizing problems are related to allelic variations in the promoter region of the serotonin transporter linked polymorphic region gene (5-HTTLPR). We followed the oldest longitudinal cohort of ELBW survivors to adulthood. Participants provided buccal cells and reported on internalizing problems, using the Young Adult Self-Report when they were in their mid-20s (ELBW/SGA, N = 28; ELBW/AGA, N = 60; NBW, N = 81) and mid-30s (ELBW/SGA, N = 27; ELBW/AGA, N = 58; NBW, N = 76). The findings indicate that ELBW/SGAs carrying the 5-HTTLPR short allele reported increased internalizing problems, particularly depression, during the third and fourth decades of life. This is the first known report on gene–environment interactions predicting psychopathology among ELBW survivors. Our findings elucidate putative neurobiological pathways that underlie risk for psychopathology.

The effect of DTNBP1 and comt risk variants and comorbid drug-abuse in patients with schizophrenia: A Gene-Environment Interaction?

2011 ◽  
Vol 26 (S2) ◽  
pp. 1345-1345
Author(s):  
J. Benkovits ◽  
P. Polgár ◽  
Á. Fábián ◽  
P. Czobor ◽  
I. Bitter ◽  
...  
Keyword(s):  
Substance Abuse ◽  
Self Report ◽  
Environment Interaction ◽  
Psychoactive Substance ◽  
Symptom Scale ◽  
Comt Val158met ◽  
Gene Environment Interaction ◽  
Negative Factor ◽  
Risk Variants ◽  
Gene Environment

IntroductionEarlier studies have shown that candidate gene risk polymorphisms and psychoactive substance abuse influence the frequency and severity of psychosis.ObjectivesIn this study we examined whether the most studied schizophrenia risk polymorphisms and psychoactive substance abuse interact in their influence on symptom severity and neurocognition.MethodsWe analyzed the clinical data of 280 schizophrenia patients, including genotyping data of the candidate genes NRG1, DTNBP1, RGS4, G72/G30 and PIP5K2A. Patients were assessed clinically by the Positive and Negative Symptom Scale (PANSS) and information about substance abuse was based on self-report and reviewing patient charts. We tested for possible interactional effects using the General Linear Model (GLM) analysis.Results15,8% of patients reported episodic or regular substance abuse, the vast majority (92%) used cannabis or the combination of cannabis and another drug. Substance abuse was associated with higher scores of the PANSS hostility/excitement factor, independent of sex, age, or genetic results (F = 4,02;p = 0,04). We found significant interactional effects of the DTNBP1 gene risk polymorphisms and substance abuse on different PANSS factors: rs2619528 and positive substance abuse interaction were associated with higher scores on the PANSS negative factor (F = 4,6;p = 0,03), and the PANSS depression factor (F = 4,75;p = 0,03). Moreover the rs3213207 - substance abuse interaction was associated with higher scores on the PANSS cognitive factor (F = 7,55;p = 0,006). Carriers of the Val allele of the COMT Val158Met polymorphism demonstrated significantly higher scores on the PANSS depression factor (F = 5,53;p = 0,02).ConclusionsOur results underscore the importance of gene-environment interactions in the phenotypic heterogeneity of schizophrenia.

scholarly journals Gene-Environment Interaction between the IL1RN Variants and Childhood Environmental Tobacco Smoke Exposure in Asthma Risk

2020 ◽  
Vol 17 (6) ◽  
pp. 2036
Author(s):  
Yongzhao Shao ◽  
Yian Zhang ◽  
Mengling Liu ◽  
Maria-Elena Fernandez-Beros ◽  
Meng Qian ◽  
...  
Keyword(s):  
Environmental Tobacco Smoke ◽  
Tobacco Smoke ◽  
Early Onset ◽  
Adult Population ◽  
Interleukin 1 ◽  
Tobacco Smoke Exposure ◽  
Environment Interaction ◽  
Gene Environment Interaction ◽  
Gene Environment ◽  
Increased Risk

(1) Background: Variants of the interleukin-1 receptor antagonist (IL1RN) gene, encoding an anti-inflammatory cytokine, are associated with asthma. Asthma is a chronic inflammatory disease of the airway influenced by interactions between genetic variants and environmental factors. We discovered a gene–environment interaction (GEI) of IL1RN polymorphisms with childhood environmental tobacco smoke (ETS) exposure on asthma susceptibility in an urban adult population. (2) Methods: DNA samples from the NYU/Bellevue Asthma Registry were genotyped for tag SNPs in IL1RN in asthma cases and unrelated healthy controls. Logistic regressions were used to study the GEI between IL1RN variants and childhood ETS exposures on asthma and early onset asthma, respectively, adjusting for population admixture and other covariates. (3) Results: Whereas the rare genotypes of IL1RN SNPs (e.g., GG in SNP rs2234678) were associated with decreased risk for asthma among those without ETS exposure (odds ratio OR = 0.215, p = 0.021), they are associated with increased risk for early onset asthma among those with childhood ETS (OR = 4.467, p = 0.021). (4) Conclusions: We identified a GEI between polymorphisms of IL1RN and childhood ETS exposure in asthma. Analysis of GEI indicated that childhood ETS exposure disrupted the protective effect of some haplotypes/genotypes of IL1RN for asthma and turned them into high-risk polymorphisms for early onset asthma.

scholarly journals Environment and Lifestyle: Their Influence on the Risk of RA

2020 ◽  
Vol 9 (10) ◽  
pp. 3109
Author(s):  
Carine Salliot ◽  
Yann Nguyen ◽  
Marie-Christine Boutron-Ruault ◽  
Raphaèle Seror
Keyword(s):  
Large Scale ◽  
Complex Disease ◽  
Dietary Factors ◽  
Environment Interaction ◽  
Food Groups ◽  
Gene Environment Interaction ◽  
Gene Environment ◽  
Increased Risk ◽  
Environmental Agents ◽  
Hormonal Exposures

Background: Rheumatoid arthritis (RA) is a complex disease in which environmental agents are thought to interact with genetic factors that lead to triggering of autoimmunity. Methods: We reviewed environmental, hormonal, and dietary factors that have been suggested to be associated with the risk of RA. Results: Smoking is the most robust factor associated with the risk of RA, with a clear gene–environment interaction. Among other inhalants, silica may increase the risk of RA in men. There is less evidence for pesticides, pollution, and other occupational inhalants. Regarding female hormonal exposures, there is some epidemiological evidence, although not consistent in the literature, to suggest a link between hormonal factors and the risk of RA. Regarding dietary factors, available evidence is conflicting. A high consumption of coffee seems to be associated with an increased risk of RA, whereas a moderate consumption of alcohol is inversely associated with the risk of RA, and there is less evidence regarding other food groups. Dietary pattern analyses (Mediterranean diet, the inflammatory potential of the diet, or diet quality) suggested a potential benefit of dietary modifications for individuals at high risk of RA. Conclusion: To date, smoking and silica exposure have been reproducibly demonstrated to trigger the emergence of RA. However, many other environmental factors have been studied, mostly with a case-control design. Results were conflicting and studies rarely considered potential gene–environment interactions. There is a need for large scale prospective studies and studies in predisposed individuals to better understand and prevent the disease and its course.

scholarly journals Early-onset Alzheimer's disease in Scotland: environmental and familial factors

2001 ◽  
Vol 178 (S40) ◽  
pp. s53-s59 ◽  
Author(s):  
Lawrence J. Whalley
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Environmental Factors ◽  
Disease Model ◽  
Environmental Data ◽  
Paternal Age ◽  
Environment Interaction ◽  
Gene Environment Interaction ◽  
Gene Environment ◽  
Genetic And Environmental Factors

BackgroundAlzheimer's disease (AD) is a common, complex, age-related disorder in which both genetic and environmental factors are important.AimsTo integrate recent studies on genetic and environmental factors in AD into a multi-factorial disease model.MethodDisease models to explain gene-environment interaction in cardiovascular disease are related to observations on AD.ResultsInformative, community-based studies on the genetic epidemiology of AD are rare. Putative risk factors from the Scottish studies include increased paternal age in AD men and coal mining as paternal occupation in both AD and vascular dementia. Migration effects suggest that environmental factors in high-incidence AD areas are important during adult life.ConclusionsThe studies summarised do not provide sufficient data to support a single comprehensive disease model of gene-environment interaction in AD. Future studies will require very large (≥600) sample sizes, molecular genetic analysis, and environmental data that span neurodevelopment and the period between disease onset and appearance of clinical symptoms.

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.

scholarly journals War exposure, 5-HTTLPR genotype and lifetime risk of depression

2011 ◽  
Vol 199 (1) ◽  
pp. 43-48 ◽  
Author(s):  
Sylvaine Artero ◽  
Jacques Touchon ◽  
Anne-Marie Dupuy ◽  
Alain Malafosse ◽  
Karen Ritchie
Keyword(s):  
Depressive Disorders ◽  
Stressful Life Event ◽  
Community Sample ◽  
Environment Interaction ◽  
Gene Environment Interaction ◽  
Gene Environment ◽  
Gender Education ◽  
Life Threatening ◽  
Long Term Impact

BackgroundIn 1962 approximately 1.5 million French people living in Algeria were repatriated to France in very poor and often life-threatening conditions. These people constitute a cohort for the study of the long-term impact of gene–environment interaction on depression.AimsTo examine the interaction between a highly stressful life event and subsequent depression, and its modulation by a length polymorphism of the serotonin transporter gene (5–HTTLPR).MethodA community sample of people aged 65 years and over residing in the Montpellier region of the south of France was randomly recruited from electoral rolls. Genotyping was performed on 248 repatriated persons and 632 controls. Current and lifetime major and minor depressive disorders were assessed according to DSM-IV criteria.ResultsA significant relationship was observed between exposure to repatriation and subsequent depression (P<0.002), but there was no significant effect of gene alone (P = 0.62). After controlling for age, gender, education, disability, recent life events and cognitive function, the gene–environment interaction (repatriation×5-HTTLPR) was globally significant (P<0.002; OR = 3.21, 95% CI 2.48–5.12). Individuals carrying the two short (s) alleles of 5-HTTLPR were observed to be at higher risk (P<0.005; OR = 2.34, 95% CI 1.24–4.32), particularly when repatriation occurred before age 35 years (P<0.002; OR = 2.91, 95% CI 1.44–5.88), but this did not reach significance in those who were older at the time of the event (P = 0.067).ConclusionsThe association between depression and war repatriation was significantly modulated by 5-HTTLPR genotype but this appeared to occur only in people who were younger at the time of exposure.

scholarly journals Effects of Childhood Adversity and Its Interaction with the MAOA, BDNF, and COMT Polymorphisms on Subclinical Attention Deficit/Hyperactivity Symptoms in Generally Healthy Youth

Children ◽  
2020 ◽  
Vol 7 (9) ◽  
pp. 122
Author(s):  
Meng-Che Tsai ◽  
Kai-Jyun Jhang ◽  
Chih-Ting Lee ◽  
Yu-Fang Lin ◽  
Carol Strong ◽  
...  
Keyword(s):  
Community Sample ◽  
Univariate Analysis ◽  
Childhood Adversity ◽  
Monoamine Oxidase A ◽  
Environment Interaction ◽  
Adhd Symptoms ◽  
Gene Score ◽  
Gene Environment Interaction ◽  
Gene Environment ◽  
Interaction Term

We aimed to investigate the effects of childhood adversity and its interaction with the polymorphisms in the monoamine oxidase A (MAOA), brain-derived neurotrophic factor (BDNF), and catechol-O-methyltransferase (COMT) genes on attention and hyperactivity disorder (ADHD) symptoms in a community sample of generally healthy youth. Participants (N = 432) completed questionnaires assessing ADHD symptoms (i.e., inattention, hyperactivity, and impulsiveness) and adverse childhood experiences, such as adverse environments (AEs) and childhood maltreatment (CM). Salivary genomic DNA was used to test polymorphisms in MAOA, BDNF, and COMT genes. A gene score (GS) was created based on the number of risk allele in the studied genes. Multiple linear regressions were used to examine the genetic and environmental effects on ADHD symptoms. The univariate analysis indicated that CM was significantly associated with inattention (β = 0.48 [95% confidence interval 0.16–0.79]), hyperactivity (0.25 [0.06–0.45]), and impulsiveness (1.16 [0.26–2.05]), while the GS was associated with hyperactivity (0.22 [0.11–0.33]) and impulsiveness (0.56 [0.06–1.05]). Only the GS remained significantly associated with hyperactivity (0.25 [0.12–0.37]) and impulsiveness (0.79 [0.20–1.38]) when the gene-environment interaction term was added in the model. No effects were found for AE and the gene-environment interaction term. In conclusion, CM was associated with ADHD symptoms in emerging adulthood. Genetic factors may also play a significant role in the association with these outcomes.

scholarly journals Differential vulnerability to neighbourhood disorder: a gene×environment interaction study

2019 ◽  
Vol 73 (5) ◽  
pp. 388-392 ◽  
Author(s):  
Jennifer Williams Robinette ◽  
Jason D Boardman ◽  
Eileen M Crimmins
Keyword(s):  
Genetic Risk ◽  
Chronic Health Condition ◽  
Health Condition ◽  
Environment Interaction ◽  
Gene Environment Interaction ◽  
Gene Environment ◽  
Increased Risk ◽  
Polygenic Scores ◽  
Significant Gene ◽  
Neighbourhood Disorder

BackgroundType 2 diabetes (T2D) is preventable, it is increasing in prevalence and it is a major risk factor for morbidity and mortality. Importantly, residents of neighbourhoods with high levels of disorder are more likely to develop T2D than those living in less disordered neighbourhoods and neighbourhood disorder may exacerbate genetic risk for T2D.MethodWe use genetic, self-reported neighbourhood, and health data from the Health and Retirement Study. We conducted weighted logistic regression analyses in which neighbourhood disorder, polygenic scores for T2D and their interaction predicted T2D.ResultsGreater perceptions of neighbourhood disorder (OR=1.11, p<0.001) and higher polygenic scores for T2D (OR=1.42, p<0.001) were each significantly and independently associated with an increased risk of T2D. Furthermore, living in a neighbourhood perceived as having high levels of disorder exacerbated genetic risk for T2D (OR=1.10, p=0.001). This significant gene×environment interaction was observed after adjusting for years of schooling, age, gender, levels of physical activity and obesity.ConclusionFindings in the present study suggested that minimising people’s exposure to vandalism, vacant buildings, trash and circumstances viewed by residents as unsafe may reduce the burden of this prevalent chronic health condition, particularly for subgroups of the population who carry genetic liability for T2D.

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