scholarly journals Gene/environment interaction and autoimmune disease

2019 ◽  
Author(s):  
Tamia A Harris ◽  
Shai Bel
Keyword(s):  
Environmental Factors ◽  
Autoimmune Diseases ◽  
Disease Onset ◽  
Environment Interaction ◽  
Gene Environment Interaction ◽  
Environmental Interactions ◽  
Gene Environment ◽  
Two Factors ◽  
Exact Etiology ◽  
Genetic And Environmental Factors

Autoimmune diseases are complex illnesses in which the body’s immune system attacks its own healthy tissues. These diseases, which can be fatal, gravely impact the quality of life of those afflicted by them with no cure currently available. The exact etiology of autoimmune diseases is not completely clear. Biomedical research has revealed that both genetic and environmental factors contribute to the development and progression of these diseases. Nevertheless, genetic and environmental factors alone cannot explain a large proportion of cases, leading to the possibility that the two factors interact in driving disease onset. Understanding how genetic and environmental factor influence host physiology in a manner that leads to the development of autoimmune diseases can reveal the mechanisms by which these diseases manifest, and bring us closer to finding a cure for them. In this chapter, we will review the current research of genetic/environmental interactions that contribute to development of autoimmune diseases, with an emphasis on interactions between the host and the multitudes of microbes that inhabit it, the microbiota.

scholarly journals Gene/environment interaction and autoimmune disease

2019 ◽  
Author(s):  
Tamia A Harris ◽  
Shai Bel
Keyword(s):  
Environmental Factors ◽  
Autoimmune Diseases ◽  
Disease Onset ◽  
Environment Interaction ◽  
Gene Environment Interaction ◽  
Environmental Interactions ◽  
Gene Environment ◽  
Two Factors ◽  
Exact Etiology ◽  
Genetic And Environmental Factors

Autoimmune diseases are complex illnesses in which the body’s immune system attacks its own healthy tissues. These diseases, which can be fatal, gravely impact the quality of life of those afflicted by them with no cure currently available. The exact etiology of autoimmune diseases is not completely clear. Biomedical research has revealed that both genetic and environmental factors contribute to the development and progression of these diseases. Nevertheless, genetic and environmental factors alone cannot explain a large proportion of cases, leading to the possibility that the two factors interact in driving disease onset. Understanding how genetic and environmental factor influence host physiology in a manner that leads to the development of autoimmune diseases can reveal the mechanisms by which these diseases manifest, and bring us closer to finding a cure for them. In this chapter, we will review the current research of genetic/environmental interactions that contribute to development of autoimmune diseases, with an emphasis on interactions between the host and the multitudes of microbes that inhabit it, the microbiota.

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.

Gene–environment interaction

2020 ◽  
pp. 343-358
Author(s):  
Craig Morgan ◽  
Marta Di Forti ◽  
Helen L. Fisher
Keyword(s):  
Mental Disorders ◽  
Environmental Factors ◽  
Statistical Modelling ◽  
Environment Interaction ◽  
Gene Environment Interaction ◽  
Working Definition ◽  
Gene Environment ◽  
Genetic And Environmental Factors ◽  
Definition Of ◽  
Study Designs

For all major mental disorders there are many factors that, in combination and through multiple pathways, increase or decrease the risk of onset. These include, to varying degrees, genetic and environmental factors. This chapter provides an introduction, from an epidemiological perspective, to the study of gene–environment interaction. It begins by providing a working definition of gene–environment interaction, rooted in a sufficient causes framework, and then considers, in turn, the prominent puzzles and challenges, including the statistical modelling of interaction, the main study designs (including strengths and weaknesses), measurement of environmental exposures, and required sample sizes. The chapter concludes with a consideration of the implications of recent advances in genetics for studies of gene–environment interaction.

scholarly journals Gene-Environment Interaction: A Genetic-Epidemiological Approach

2010 ◽  
Vol 29 (3) ◽  
pp. 131-134 ◽  
Author(s):  
Tatjana Pekmezović
Keyword(s):  
Environmental Factors ◽  
Genetic Epidemiology ◽  
Disease Risk ◽  
Environmental Exposures ◽  
Molecular Medicine ◽  
Environment Interaction ◽  
Gene Environment Interaction ◽  
Gene Environment ◽  
Genetic And Environmental Factors ◽  
Epidemiological Approach

Gene-Environment Interaction: A Genetic-Epidemiological ApproachClassical epidemiology addresses the distribution and determinants of diseases in populations, and the factors associated with disease causation, with the aim of preventing disease. Both genetic and environmental factors may contribute to susceptibility, and it is still unclear how these factors interact in their influence on risk. Genetic epidemiology is the field which incorporates concepts and methods from different disciplines including epidemiology, genetics, biostatistics, clinical and molecular medicine, and their interaction is crucial to understanding the role of genetic and environmental factors in disease processes. The study of gene-environment interaction is central in the field of genetic epidemiology. Gene-environment interaction is defined as »a different effect of an environmental exposure on disease risk in persons with different genotypes,« or, alternatively, »a different effect of a genotype on disease risk in persons with different environmental exposures.« Five biologically plausible models are described for the relations between genotypes and environmental exposures, in terms of their effects on disease risk. Therefore, the study of gene-environment interaction is important for improving accuracy and precision in the assessment of both genetic and environmental factors, especially in disorders of less defined etiology. Genetic epidemiology is also applied at the various levels of disease prevention.

A six-year longitudinal population-based cohort for the extended psychosis phenotype: An epidemiological study of the gene-environment interactions (TürkSch)

2016 ◽  
Vol 33 (S1) ◽  
pp. s237-s237
Author(s):  
K. Alptekin ◽  
T. Binbay ◽  
U. Kırlı ◽  
H. Elbi ◽  
B. Kayahan ◽  
...  
Keyword(s):  
Mental Health ◽  
Environmental Factors ◽  
Stage I ◽  
Environment Interaction ◽  
Psychotic Experiences ◽  
Cross Sectional ◽  
Gene Environment Interaction ◽  
Gene Environment ◽  
Genetic And Environmental Factors ◽  
Prospective Longitudinal

IntroductionBoth genetic and environmental factors play a role in the extended psychosis phenotype which covers psychotic experiences, symptoms and disorders.ObjectivesThe respective contributions of genetic and environmental factors over time remain largely unknown.AimsTo describe the objectives and design of a multistage study.MethodsThe TürkSch (Izmir mental health survey for gene-environment interaction in psychoses) is a prospective-longitudinal study consisted of several data collection stages to screen extended psychosis phenotype in a general population sample, and to assess individual, familial, genetic and neighbourhood level variables.ResultsThe study aimed to assess the prevalence of psychotic experiences and symptoms in Izmir-Turkey (stage I, cross-sectional; n: 4011), the socioeconomic deprivation and the social capital of neighbourhoods in a separate sample (stage II, cross-sectional; n: 5124) in 2008. A nested case-control study (stage III) recruited individuals with psychotic outcomes and healthy controls from stage I, and included blood sampling for gene-environment interaction and clinical reappraisal as well. After 6 years, follow-up study (stage IV) was set to assess the mental health outcomes with a focus on extended psychosis phenotype, environmental exposures of the eligiable sample (n: 2192) from the stage I, and to collect blood samples for further genetic analysis. On both stages, Composite International Diagnostic Interview was used by clinically trained interviewers, and was able to provide broad assessment of psychotic experiences, experience-related disabilities, help-seeking and health care utilization.ConclusionsThe TürkSch has a unique study design and yields data of high quality in the Turkish population, with a specific focus on psychosis.Disclosure of interestThe authors have not supplied their declaration of competing interest.

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.

Twin Study on Myopia

1987 ◽  
Vol 36 (4) ◽  
pp. 535-540 ◽  
Author(s):  
L.L.-K. Lin ◽  
C.-J. Chen
Keyword(s):  
Intraclass Correlation ◽  
Correlation Coefficients ◽  
Environment Interaction ◽  
Ophthalmological Examination ◽  
Genetic Determination ◽  
Intraclass Correlation Coefficients ◽  
Gene Environment Interaction ◽  
Gene Environment ◽  
Genetic And Environmental Factors ◽  
Mz Twins

AbstractIn order to reassess the relative importance of genetic and environmental factors in the development of myopia in Chinese schoolchildren, 90 pairs of MZ and 36 pairs of like-sex DZ twins were enrolled for detailed ophthalmological examination about their ocular refractions. Corneal curvatures and axial lengths were also measured. With equivalent settings of the range for concordance, corneal curvatures showed higher concordance rate (84%) than ocular refractions (65%) and axial lenghts (59%) in MZ twins. F-test on the intrapair variances between MZ and DZ twins revealed a significant hereditary role in determining the ocular refraction and its optical components. The degree of genetic determination was expressed by heritability indices, which were derived from intraclass correlation coefficients. The diversity of sample ages and refractions, while making the obtained data difficult to further explore the gene-environment interaction, led to the observation of more intrapair differences with age and myopic progression in MZ twins.

The Role of Gene–Environment Interaction in Determining Bone Mineral Density in a Twin Population

2007 ◽  
Vol 10 (1) ◽  
pp. 191-197 ◽  
Author(s):  
Vasi Naganathan ◽  
Alexander J. MacGregor ◽  
Philip N. Sambrook
Keyword(s):  
Bone Mineral Density ◽  
Lumbar Spine ◽  
Environmental Factors ◽  
Bone Mineral ◽  
Genetic Component ◽  
Total Variance ◽  
Environment Interaction ◽  
Mineral Density ◽  
Gene Environment Interaction ◽  
Gene Environment

AbstractThe possibility that specific environmental factors such as smoking and estrogen use modify the genetic influences (gene–environment interaction) on bone mineral density (BMD) has not been explored in genetic epidemiological studies such as twin studies. The aim of this study was to look for evidence of gene–environment interaction in BMD determination by analyzing data collected on a large number of healthy female twins. BMD of the hip, distal forearm and lumbar spine were measured by dual-energy X-ray absorptiometry on 287 identical and 265 nonidentical volunteer female twin pairs. The environmental factors examined were hormone replacement therapy (HRT) and smoking. In genetic modeling analysis using path analysis, there was evidence of ‘HRT-specific’ genetic component of BMD variance at the forearm (50% of total variance) but not at the hip. At the lumbar spine the magnitude of the genetic component of variance in HRT users (> 60-month HRT use) was less than the genetic component of variance for little or no exposure to HRT (48% vs. 84%). There was no evidence of gene–environment interaction for smoking. The main evidence for gene–environment interaction was the finding that forearm BMD variance was influenced by a significant HRT-specific genetic component. There was also evidence that in HRT users, the genetic component of total variance for lumbar BMD was lower.

scholarly journals Effects of Gene-Environment Interaction on Obesity among Chinese Adults Born in the Early 1960s

Genes ◽  
2021 ◽  
Vol 12 (2) ◽  
pp. 270
Author(s):  
Weiyan Gong ◽  
Hui Li ◽  
Chao Song ◽  
Fan Yuan ◽  
Yanning Ma ◽  
...  
Keyword(s):  
Socioeconomic Status ◽  
Waist Circumference ◽  
Environmental Factors ◽  
Central Obesity ◽  
Environment Interaction ◽  
Sedentary Behaviors ◽  
Chinese Adults ◽  
Gene Environment Interaction ◽  
Gene Environment ◽  
Fto Rs9939609

The prevalence of obesity has been increasing sharply and has become a serious public health problem worldwide. Gene–environment interaction in obesity is a relatively new field, and little is known about it in Chinese adults. This study aimed to provide the effects of gene–environment interaction on obesity among Chinese adults. A stratified multistage cluster sampling method was conducted to recruit participants from 150 surveillance sites. Subjects born in 1960, 1961 and 1963 were selected. An exploratory factor analysis was used to classify the environmental factors. The interaction of single nucleotide polymorphisms (SNPs) and environmental factors on body mass index (BMI) and waist circumference were analyzed using a general linear model. A multiple logistic regression model combined with an additive model was performed to analyze the interaction between SNPs and environmental factors in obesity and central obesity. A total of 2216 subjects were included in the study (mean age, 49.7 years; male, 39.7%, female, 60.3%). Engaging in physical activity (PA) could reduce the effect of MC4R rs12970134 on BMI (β = −0.16kg/m2, p = 0.030), and also reduce the effect of TRHR rs7832552 and BCL2 rs12454712 on waist circumference (WC). Sedentary behaviors increased the effects of SNPs on BMI and WC, and simultaneously increased the effects of FTO rs9939609 and FTO rs8050136 on obesity and central obesity. A higher socioeconomic status aggravated the influence of SNPs (including FTO rs9939609, BNDF rs11030104, etc.) on BMI and WC, and aggravated the influence of SEC16B rs574367 on central obesity. The MC4R rs12970134 association with BMI and the FTO rs8050136 association with central obesity appeared to be more pronounced with higher energy intake (β = 0.140 kg/m2, p = 0.049; OR = 1.77, p = 0.004, respectively). Engaging in PA could reduce the effects of SNPs on BMI and WC; nevertheless, a higher socioeconomic status, higher dietary energy intake and sedentary behaviors accentuated the influences of SNPs on BMI, WC, obesity and central obesity. Preventative measures for obesity should consider addressing the gene–environment interaction.

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