scholarly journals CACNA1C Polymorphism (rs2283291) Is Associated with Schizophrenia in Chinese Males: A Case-Control Study

2019 ◽  
Vol 2019 ◽  
pp. 1-7 ◽  
Author(s):  
Xiaojing Zhu ◽  
Rixin Li ◽  
Guojun Kang ◽  
Qi Kang ◽  
Wenwang Rao ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Gene Interaction ◽  
Environment Interaction ◽  
Gender Stratification ◽  
Gene Environment ◽  
Increased Risk ◽  
Genetic Level ◽  
Famine Exposure ◽  
Male Patients ◽  
Prenatal Famine

Recent research has shown that prenatal famine exposure may be one of the risk factors for schizophrenia and that people born in famine years may be at an increased risk of schizophrenia due to alteration of the DNA methylation of genes. In this study, the association of rs2283291/rs4648635 and the incidence of schizophrenia and prenatal famine exposure at the genetic level were investigated to provide clues to the pathogenesis of schizophrenia. A total of 960 participants were recruited, comprising 473 prenatal famine-exposed individuals (225 patients and 248 controls) and 487 prenatal non-famine-exposed individuals (220 patients and 267 controls). The association of prenatal famine, schizophrenia, and their interaction with DNA methylation levels was analyzed using SPSS and GMDR software. Gender stratification analysis revealed a significant association between the rs2283291 genotype and schizophrenia in male patients (P=0.017), and difference still existed after correction by the Bonferroni method. It was also found that an increasing risk of schizophrenia was associated with rs2283291 in males (OR: 1.62, 95% CI: 1.13-2.33, P=0.0086, AIC=669.7) in an overdominant model. The results of gene-environment interaction and gene-gene interaction revealed no association with the risk of schizophrenia. This study reported for the first time that rs2283291 was associated with schizophrenia in Chinese males.

scholarly journals Gene–gene and gene-environment interactions on cord blood total IgE in Chinese Han children

2021 ◽  
Vol 17 (1) ◽  
Author(s):  
Li Hua ◽  
Quanhua Liu ◽  
Jing Li ◽  
Xianbo Zuo ◽  
Qian Chen ◽  
...  
Keyword(s):  
Environmental Factors ◽  
Cord Blood ◽  
Synergistic Effects ◽  
Gene Interaction ◽  
Independent Effect ◽  
Environment Interaction ◽  
Nucleotide Polymorphisms ◽  
Chinese Han ◽  
Gene Environment Interaction ◽  
Gene Environment

Abstract Background IL13, IL4, IL4RA, FCER1B and ADRB2 are susceptible genes of asthma and atopy. Our previous study has found gene–gene interactions on asthma between these genes in Chinese Han children. Whether the interactions begin in fetal stage, and whether these genes interact with prenatal environment to enhance cord blood IgE (CBIgE) levels and then cause subsequent allergic diseases have yet to be determined. This study aimed to determine whether there are gene–gene and gene-environment interactions on CBIgE elevation among the aforementioned five genes and prenatal environmental factors in Chinese Han population. Methods 989 cord blood samples from a Chinese birth cohort were genotyped for nine single-nucleotide polymorphisms (SNPs) in the five genes, and measured for CBIgE levels. Prenatal environmental factors were collected using a questionnaire. Gene–gene and gene-environment interactions were analyzed with generalized multifactor dimensionality methods. Results A four-way gene–gene interaction model (IL13 rs20541, IL13 rs1800925, IL4 rs2243250 and ADRB2 rs1042713) was regarded as the optimal one for CBIgE elevation (testing balanced accuracy = 0.5805, P = 9.03 × 10–4). Among the four SNPs, only IL13 rs20541 was identified to have an independent effect on elevated CBIgE (odds ratio (OR) = 1.36, P = 3.57 × 10–3), while the other three had small but synergistic effects. Carriers of IL13 rs20541 TT, IL13 rs1800925 CT/TT, IL4 rs2243250 TT and ADRB2 rs1042713 AA were estimated to be at more than fourfold higher risk for CBIgE elevation (OR = 4.14, P = 2.69 × 10–2). Gene-environment interaction on elevated CBIgE was found between IL4 rs2243250 and maternal atopy (OR = 1.41, P = 2.65 × 10–2). Conclusions Gene–gene interaction between IL13 rs20541, IL13 rs1800925, IL4 rs2243250 and ADRB2 rs1042713, and gene-environment interaction between IL4 rs2243250 and maternal atopy begin in prenatal stage to augment IgE production in Chinese Han children.

Gene–environment interplay in the etiology of psychosis

2018 ◽  
Vol 48 (12) ◽  
pp. 1925-1936 ◽  
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.

scholarly journals Cohort Differences in the Associations of Selected Candidate Genes With Risk of All-Cause Mortality at Advanced Ages

2020 ◽  
Vol 189 (7) ◽  
pp. 708-716
Author(s):  
Qihua Tan ◽  
Rune Jacobsen ◽  
Marianne Nygaard ◽  
Mette Soerensen ◽  
Jonas Mengel-From ◽  
...  
Keyword(s):  
Candidate Genes ◽  
Survival Data ◽  
Cohort Effect ◽  
Human Longevity ◽  
Environment Interaction ◽  
Relative Risks ◽  
Cohort Differences ◽  
Risk Of Mortality ◽  
Gene Environment ◽  
Increased Risk

Abstract Considerable efforts have been made to identify the genetic basis of human longevity, with only limited progress. One important drawback of current genetic studies is the limited knowledge of gene-environment interaction. Using 2 cohorts of long-lived individuals born in 1905 and 1915 in Denmark, we performed survival analysis to estimate risk of mortality for major candidate genes of aging and longevity and their cohort effects. Through statistical modeling that combines individual genetic and survival information with cohort-specific survival data, we estimated the relative risks of mortality from ages 95 to 103 years associated with genetic variants in apolipoprotein E (APOE), forkhead box class O3a, clusterin, and phosphatidylinositol binding clathrin assembly protein. Our analysis estimated a decreased risk of carrying the APOE$\varepsilon $4 allele (change in risk = –0.403, 95% confidence interval (CI): −0.831, 0.021; P = 0.040) in men of the later cohort, although the allele itself was harmful to survival across sexes (relative risk = 1.161, 95% CI: 1.027, 1.345; P = 0.026). We also estimated a cohort effect of increased risk for the minor allele of rs3851179 in phosphatidylinositol binding clathrin assembly protein with borderline significance (change in risk = 0.165, 95% CI: −0.010, 0.331; P = 0.052) in women. Our estimated significant cohort effect on APOE$\varepsilon $4 is indicative of the interplay between the gene and the changing environment that modulates survival at extreme ages.

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.

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 Erratum: Corrigendum: DNA methylation signatures link prenatal famine exposure to growth and metabolism

2015 ◽  
Vol 6 (1) ◽  
Author(s):  
Elmar W. Tobi ◽  
Jelle J. Goeman ◽  
Ramin Monajemi ◽  
Hongcang Gu ◽  
Hein Putter ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Famine Exposure ◽  
Prenatal Famine

scholarly journals Interactions between genetic polymorphisms of glucose metabolizing genes and smoking and alcohol consumption in the risk of type 2 diabetes mellitus

2017 ◽  
Vol 42 (12) ◽  
pp. 1316-1321 ◽  
Author(s):  
Kaiping Gao ◽  
Yongcheng Ren ◽  
Jinjin Wang ◽  
Zichen Liu ◽  
Jianna Li ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Lifestyle Factors ◽  
Environment Interaction ◽  
Nucleotide Polymorphisms ◽  
Gene Environment ◽  
Increased Risk ◽  
The Impact

The impact of gene-environment interaction on diabetes remains largely unknown. We aimed to investigate if interaction between glucose metabolizing genes and lifestyle factors is associated with type 2 diabetes mellitus (T2DM). Interactions between genotypes of 4 glucose metabolizing genes (MTNR1B, KCNQ1, KLF14, and GCKR) and lifestyle factors were estimated in 722 T2DM patients and 759 controls, using multiple logistic regression. No significant associations with T2DM were detected for the single nucleotide polymorphisms of MTNR1B, KLF14 and GCKR. However, rs151290 (KCNQ1) polymorphisms were found to be associated with risk of T2DM. Compared with AA, the odds ratios (ORs) of AC or CC genotypes for developing T2DM were 1.545 (P = 0.0489) and 1.603 (P = 0.0383), respectively. In stratified analyses, the associations were stronger in smokers with CC than smokers with AA (OR = 3.668, P = 0.013); drinkers with AC (OR = 5.518, P = 0.036), CC (OR = 8.691, P = 0.0095), and AC+CC (OR = 6.764, P = 0.016) than drinkers with AA. Compared with nondrinkers with AA, drinkers who carry AC and CC had 12.072-fold (P = 0.0007) and 8.147-fold (P = 0.0052) higher risk of developing T2DM. In conclusions, rs151290 (KCNQ1) polymorphisms are associated with increased risk of T2DM, alone and especially in interaction with smoking and alcohol.

Prenatal famine exposure, health in later life and promoter methylation of four candidate genes

2012 ◽  
Vol 3 (6) ◽  
pp. 450-457 ◽  
Author(s):  
M. V. Veenendaal ◽  
P. M. Costello ◽  
K. A. Lillycrop ◽  
S. R. de Rooij ◽  
J. A. van der Post ◽  
...  
Keyword(s):  
Candidate Genes ◽  
Promoter Methylation ◽  
Peripheral Blood ◽  
Methylation Status ◽  
Later Life ◽  
Proximal Promoter ◽  
Promoter Regions ◽  
Increased Risk ◽  
Famine Exposure ◽  
Prenatal Famine

Poor nutrition during fetal development can permanently alter growth, cardiovascular physiology and metabolic function. Animal studies have shown that prenatal undernutrition followed by balanced postnatal nutrition alters deoxyribonucleic acid (DNA) methylation of gene promoter regions of candidate metabolic control genes in the liver. The aim of this study was to investigate whether methylation status of the proximal promoter regions of four candidate genes differed between individuals exposed to the Dutch famine in utero. In addition, we determined whether methylation status of these genes was associated with markers of metabolic and cardiovascular disease and adult lifestyle. Methylation status of the GR1-C (glucocorticoid receptor), PPARγ (peroxisome proliferator-activated receptor gamma), lipoprotein lipase and phosphatidylinositol 3 kinase p85 proximal promoters was investigated in DNA isolated from peripheral blood samples of 759 58-year-old subjects born around the time of the 1944–45 Dutch famine. We observed no differences in methylation levels of the promoters between exposed and unexposed men and women. Methylation status of PPARγ was associated with levels of high-density lipoprotein cholesterol and triglycerides as well as with exercise and smoking. Hypomethylation of the GR promoter was associated with adverse adult lifestyle factors, including higher body mass index, less exercise and more smoking. The previously reported increased risk of cardiovascular and metabolic disease after prenatal famine exposure was not associated with differences in methylation status across the promoter regions of these candidate genes measured in peripheral blood. The adult environment seems to affect GR and PPARγ promoter methylation.

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