scholarly journals Are Genes Destiny? Exploring the Role of Intrauterine Environment in Moderating Genetic Influences on Body Weight

2017 ◽  
Author(s):  
Jinho Kim
Keyword(s):  
Birth Weight ◽  
Environmental Factors ◽  
In Utero ◽  
Genetic Effects ◽  
Interactive Effects ◽  
Environment Interaction ◽  
Intrauterine Environment ◽  
Fetal Origins ◽  
Gene Environment Interaction ◽  
Gene Environment

By incorporating molecular genetic variants and the fetal origins of obesity hypothesis into a gene-environment interaction framework, this study investigates the potential interactive effects of variation in the obesity-associated gene (FTO) and intrauterine environment on body mass index (BMI) in adulthood. This study draws on data from the Wisconsin Longitudinal Study, and uses sibling comparisons that allow for quasi-experimental variations in both genetic and environmental factors. Findings demonstrated that even after controlling for unobserved family background, the FTO variants and birth weight are generally associated with adult BMI. Moreover, this study found that the effects of having a risk allele of the FTO gene are largely concentrated on those who were heavier at birth, providing evidence for a gene-environment interaction on BMI and the development of obesity. Results of this study suggest that genes are not destiny and environmental factors may offset the effects of obesity-promoting genes. In particular, efforts to counteract genetic effects on obesity may begin as early as in utero. Interventions to prevent higher birth weight may help reduce the risk of obesity later in life, by directly addressing the programming effects of the in utero environment and also indirectly moderating the obesity-promoting genetic effects.

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.

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.

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.

scholarly journals Catechol-O-Methyltransferase Gene Val158Met Polymorphism Moderates the Effect of Social Exclusion and Inclusion on Aggression in Men: Findings From a Mixed Experimental Design

2021 ◽  
Vol 11 ◽  
Author(s):  
Meiping Wang ◽  
Pian Chen ◽  
Hang Li ◽  
Andrew Haddon Kemp ◽  
Wenxin Zhang
Keyword(s):  
Undergraduate Students ◽  
Interactive Effects ◽  
Environment Interaction ◽  
Mixed Design ◽  
Gene Environment Interaction ◽  
Val158met Polymorphism ◽  
Gene Environment ◽  
Methyltransferase Gene ◽  
Aggressive Motivation ◽  
Group Variable

Accumulating research has identified the interactive effects of catechol-O-methyltransferase (COMT) gene Val158Met polymorphism and environmental factors on aggression. However, available evidence was mainly based upon correlational design, which yields mixed findings concerning who (Val vs. Met carriers) are more affected by environmental conditions and has been challenged for the low power of analyses on gene–environment interaction. Drawing on a mixed design, we scrutinized how COMT Val158Met polymorphism (between-group variable) impacts on aggression, assessed by hostility, aggressive motivation, and aggressive behavior, under different social conditions (exclusion vs. inclusion, within-group variable) in a sample of 70 Chinese male undergraduate students. We found that both Val/Val homozygote and Met alleles carriers showed differences in the feelings of hostility and aggressive motivation under conditions of exclusion versus inclusion, but these differences were more pronounced for Met allele carriers. These findings implied that COMT Val158Met polymorphism did not respond to environmental stimuli in an all-or-none way and shed light on the importance of examining the gene–environment interaction using a mixed design.

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 Classification and Clustering Methods for Multiple Environmental Factors in Gene–Environment Interaction

Epidemiology ◽  
2016 ◽  
Vol 27 (6) ◽  
pp. 870-878 ◽  
Author(s):  
Yi-An Ko ◽  
Bhramar Mukherjee ◽  
Jennifer A. Smith ◽  
Sharon L. R. Kardia ◽  
Matthew Allison ◽  
...  
Keyword(s):  
Environmental Factors ◽  
Environment Interaction ◽  
Clustering Methods ◽  
Gene Environment Interaction ◽  
Gene Environment ◽  
Classification And Clustering

Assessing gene–environment interactions on anxiety symptom subtypes across childhood and adolescence

2007 ◽  
Vol 19 (4) ◽  
pp. 1129-1146 ◽  
Author(s):  
Jennifer Y. F. Lau ◽  
Alice M. Gregory ◽  
Michelle A. Goldwin ◽  
Daniel S. Pine ◽  
Thalia C. Eley
Keyword(s):  
Life Events ◽  
Environmental Effects ◽  
Separation Anxiety ◽  
Negative Life Events ◽  
Child And Adolescent ◽  
Genetic Effects ◽  
Anxiety Symptoms ◽  
Environment Interaction ◽  
Gene Environment Interaction ◽  
Gene Environment

AbstractConsistent evidence shows both genetic and stress-related risks on child and adolescent anxiety, yet few studies have considered the degree to which genetic effects are moderated by stress (gene–environment interaction). We used longitudinal data from both a child and adolescent sample of twins to examine three novel issues on the presence of gene–environment interaction on anxiety symptoms. First, we assessed moderation of genetic risks on anxiety symptoms by negative life events in each age group. Second, by distinguishing between “stable” and “age-specific” genetic factors, we explored the continuity of gene–environment interaction across time and/or its emergence at specific ages. Third, we compared the presence of gene–environment interaction across different symptom types (general, panic, social, and separation). Genetic effects on separation anxiety symptoms in childhood (mean age = 8 years, 6 months) and panic anxiety symptoms in adolescence (mean age = 15 years) increased across independent negative life events. Shared environmental effects on separation anxiety symptoms and nonshared environmental effects on general anxiety symptoms in adolescence were also moderated by negative life events. We interpret these preliminary findings tentatively in the context of gene–environment interaction on anxiety in general, and on early separation and later panic anxiety in particular.

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