scholarly journals Epigenome-wide association meta-analysis of DNA methylation with coffee and tea consumption

2020 ◽  
Author(s):  
Irma Karabegović ◽  
Eliana Portilla-Fernandez ◽  
Yang Li ◽  
Jiantao Ma ◽  
Silvana C.E. Maas ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Observational Studies ◽  
Disease Risk ◽  
Association Studies ◽  
Meta Analysis ◽  
Disease Onset ◽  
Coffee Consumption ◽  
Tea Consumption ◽  
Hepatic Lipid Metabolism

AbstractCoffee and tea are extensively consumed beverages worldwide. Observational studies have shown contradictory findings for the association between consumption of these beverages and different health outcomes. Epigenetics is suggested as a mechanism mediating the effects of dietary and lifestyle factors on disease onset. We conducted epigenome-wide association studies (EWAS) on coffee and tea consumptions in 15,789 participants of European and African-American ancestries from 15 cohorts. EWAS meta-analysis revealed 11 CpG sites significantly associated with coffee consumption (P-value <1.1×10-7), nine of them annotated to the genes AHRR, F2RL3, FLJ43663, HDAC4, GFI1 and PHGDH, and two CpGs suggestively associated with tea consumption (P-value<5.0×10-6). Among these, cg14476101 was significantly associated with expression of its annotated gene PHGDH and risk of fatty liver disease. Knockdown of PHGDH expression in liver cells showed a correlation with expression levels of lipid-associated genes, suggesting a role of PHGDH in hepatic-lipid metabolism. Collectively, this study indicates that coffee consumption is associated with differential DNA methylation levels at multiple CpGs, and that coffee-associated epigenetic variations may explain the mechanism of action of coffee consumption in conferring disease risk.

scholarly journals Epigenome-wide association meta-analysis of DNA methylation with coffee and tea consumption

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Irma Karabegović ◽  
Eliana Portilla-Fernandez ◽  
Yang Li ◽  
Jiantao Ma ◽  
Silvana C. E. Maas ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Association Studies ◽  
Meta Analysis ◽  
Disease Onset ◽  
Coffee Consumption ◽  
Tea Consumption ◽  
Hepatic Lipid Metabolism ◽  
Significance Threshold ◽  
Suggestive Association

AbstractCoffee and tea are extensively consumed beverages worldwide which have received considerable attention regarding health. Intake of these beverages is consistently linked to, among others, reduced risk of diabetes and liver diseases; however, the mechanisms of action remain elusive. Epigenetics is suggested as a mechanism mediating the effects of dietary and lifestyle factors on disease onset. Here we report the results from epigenome-wide association studies (EWAS) on coffee and tea consumption in 15,789 participants of European and African-American ancestries from 15 cohorts. EWAS meta-analysis of coffee consumption reveals 11 CpGs surpassing the epigenome-wide significance threshold (P-value <1.1×10−7), which annotated to the AHRR, F2RL3, FLJ43663, HDAC4, GFI1 and PHGDH genes. Among them, cg14476101 is significantly associated with expression of the PHGDH and risk of fatty liver disease. Knockdown of PHGDH expression in liver cells shows a correlation with expression levels of genes associated with circulating lipids, suggesting a role of PHGDH in hepatic-lipid metabolism. EWAS meta-analysis on tea consumption reveals no significant association, only two CpGs annotated to CACNA1A and PRDM16 genes show suggestive association (P-value <5.0×10−6). These findings indicate that coffee-associated changes in DNA methylation levels may explain the mechanism of action of coffee consumption in conferring risk of diseases.

Environment

2013 ◽  
pp. 290-295
Author(s):  
Christopher R. Holroyd ◽  
Nicholas C. Harvey ◽  
Mark H. Edwards ◽  
Cyrus Cooper
Keyword(s):  
Rheumatoid Arthritis ◽  
Life Course ◽  
Disease Risk ◽  
Association Studies ◽  
Population Level ◽  
Environment Interaction ◽  
Disease Pattern ◽  
The Individual ◽  
The Life Course

Musculoskeletal disease covers a broad spectrum of conditions whose aetiology comprises variable genetic and environmental contributions. More recently it has become clear that, particularly early in life, the interaction of gene and environment is critical to the development of later disease. Additionally, only a small proportion of the variation in adult traits such as bone mineral density has been explained by specific genes in genome-wide association studies, suggesting that gene-environment interaction may explain a much larger part of the inheritance of disease risk than previously thought. It is therefore critically important to evaluate the environmental factors which may predispose to diseases such as osteorthritis, osteoporosis, and rheumatoid arthritis both at the individual and at the population level. In this chapter we describe the environmental contributors, across the whole life course, to osteoarthritis, osteoporosis and rheumatoid arthritis, as exemplar conditions. We consider factors such as age, gender, nutrition (including the role of vitamin D), geography, occupation, and the clues that secular changes of disease pattern may yield. We describe the accumulating evidence that conditions such as osteoporosis may be partly determined by the early interplay of environment and genotype, through aetiological mechanisms such as DNA methylation and other epigenetic phenomena. Such studies, and those examining the role of environmental influences across other stages of the life course, suggest that these issues should be addressed at all ages, starting from before conception, in order to optimally reduce the burden of musculoskeletal disorders in future generations.

Mechanical Thromboprophylaxis in Critically Ill Patients: A Systematic Review and Meta-Analysis

2006 ◽  
Vol 15 (4) ◽  
pp. 402-412 ◽  
Author(s):  
Anthony Limpus ◽  
Wendy Chaboyer ◽  
Ellen McDonald ◽  
Lukman Thalib
Keyword(s):  
Intensive Care ◽  
Randomized Controlled Trials ◽  
Observational Studies ◽  
Meta Analysis ◽  
Controlled Trials ◽  
Trauma Patients ◽  
Intensive Care Patients ◽  
Randomized Controlled ◽  
Confounding Variables

• Objective To systematically review the randomized trials, observational studies, and survey evidence on compression and pneumatic devices for thromboprophylaxis in intensive care patients. • Methods Published studies on the use of compression and pneumatic devices in intensive care patients were assessed. A meta-analysis was conducted by using the randomized controlled trials. • Results A total of 21 relevant studies (5 randomized controlled trials, 13 observational studies, and 3 surveys) were found. A total of 811 patients were randomized in the 5 randomized controlled trials; 3421 patients participated in the observational studies. Trauma patients only were enrolled in 4 randomized controlled trials and 4 observational studies. Meta-analysis of 2 randomized controlled trials with similar populations and outcomes revealed that use of compression and pneumatic devices did not reduce the incidence of venous thromboembolism. The pooled risk ratio was 2.37, indicative of favoring the control over the intervention in reducing the deep venous thrombosis; however, the 95% CI of 0.57 to 9.90 indicated no significant differences between the intervention and the control. A range of methodological issues, including bias and confounding variables, make meaningful interpretation of the observational studies difficult. • Conclusions The limited evidence suggests that use of compressive and pneumatic devices yields results not significantly different from results obtained with no treatment or use of low-molecular-weight heparin. Until large randomized controlled trials are conducted, the role of mechanical approaches to thromboprophylaxis for intensive care patients remains uncertain.

scholarly journals A systematic review and meta-analysis of genetic association studies for the role of inflammation and the immune system in diabetic nephropathy

2017 ◽  
Vol 10 (3) ◽  
pp. 293-300 ◽  
Author(s):  
Maria Tziastoudi ◽  
Ioannis Stefanidis ◽  
Georgios M. Hadjigeorgiou ◽  
Konstantinos Stravodimos ◽  
Elias Zintzaras
Keyword(s):  
Systematic Review ◽  
Diabetic Nephropathy ◽  
Immune System ◽  
Genetic Association ◽  
Association Studies ◽  
Meta Analysis ◽  
Genetic Association Studies

scholarly journals Associations between socioeconomic status and chronic kidney disease: a meta-analysis

2018 ◽  
Vol 72 (4) ◽  
pp. 270-279 ◽  
Author(s):  
Xiaoxi Zeng ◽  
Jing Liu ◽  
Sibei Tao ◽  
Hyokyoung G Hong ◽  
Yi Li ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Socioeconomic Status ◽  
Kidney Disease ◽  
Observational Studies ◽  
Disease Risk ◽  
Meta Analysis ◽  
Inverse Association ◽  
Lower Income ◽  
Lower Education ◽  
Stage Renal Disease

BackgroundSocioeconomic status (SES) has long been conjectured to be associated with the incidence and progression of chronic kidney disease (CKD), but few studies have examined this quantitatively. This meta-analysis aims to fill this gap.MethodsA systematic literature review was performed using Medline and EMBASE to identify observational studies on associations between SES and incidence and progression of CKD, published between 1974 and March 2017. Individual results were meta-analysed using a random effects model, in line with Meta-analysis of Observational Studies in Epidemiology guidelines.ResultsIn total, 43 articles met our inclusion criteria. CKD prevalence was associated with several indicators of SES, particularly lower income (OR 1.34, 95% CI (1.18 to 1.53), P<0.001; I2=73.0%, P=0.05); lower education (OR 1.21, 95% CI (1.11 to 1.32), P<0.001; I2=45.20%, P=0.034); and lower combined SES (OR 2.18, 95% CI (1.64 to 2.89), P<0.001; I2=0.0%, P=0.326). Lower levels of income, occupation and combined SES were also significantly associated with progression to end-stage renal disease (risk ratio (RR) 1.24, 95% CI (1.12 to 1.37), P<0.001; I2=66.6%, P=0.006; RR 1.05, 95% CI (1.01 to 1.09), P=0.012; I2=0.0%, P=0.796; and RR 1.39, 95% CI (1.09 to 1.79), P=0.009; I2=74.2%, P=0.009). Subgroup analyses generally confirmed these results, except in a few cases, such as an inverse association related to particular socioeconomic backgrounds and where results were adjusted by more disease-related risk factors.ConclusionLower income was most closely associated with prevalence and progression of CKD, and lower education was significantly associated with its prevalence. Evidence for other indicators was inconclusive.

scholarly journals Epigenome-wide meta-analysis of blood DNA methylation and its association with subcortical volumes: findings from the ENIGMA Epigenetics Working Group

2019 ◽  
Author(s):  
Tianye Jia ◽  
Congying Chu ◽  
Yun Liu ◽  
Jenny van Dongen ◽  
Evangelos Papastergios ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Nucleus Accumbens ◽  
Large Scale ◽  
Biomarker Discovery ◽  
Association Studies ◽  
Meta Analysis ◽  
Hippocampal Volume ◽  
Small Sample ◽  
Small Sample Sizes ◽  
Meta Analyses

AbstractDNA methylation, which is modulated by both genetic factors and environmental exposures, may offer a unique opportunity to discover novel biomarkers of disease-related brain phenotypes, even when measured in other tissues than brain, such as blood. A few studies of small sample sizes have revealed associations between blood DNA methylation and neuropsychopathology, however, large-scale epigenome-wide association studies (EWAS) are needed to investigate the utility of DNA methylation profiling as a peripheral marker for the brain. Here, in an analysis of eleven international cohorts, totalling 3337 individuals, we report epigenome-wide meta-analyses of blood DNA methylation with volumes of the hippocampus, thalamus and nucleus accumbens (NAcc)—three subcortical regions selected for their associations with disease and heritability and volumetric variability. Analyses of individual CpGs revealed genome-wide significant associations with hippocampal volume at two loci. No significant associations were found for analyses of thalamus and nucleus accumbens volumes. Cluster-based analyses revealed additional differentially methylated regions (DMRs) associated with hippocampal volume. DNA methylation at these loci affected expression of proximal genes involved in learning and memory, stem cell maintenance and differentiation, fatty acid metabolism and type-2 diabetes. These DNA methylation marks, their interaction with genetic variants and their impact on gene expression offer new insights into the relationship between epigenetic variation and brain structure and may provide the basis for biomarker discovery in neurodegeneration and neuropsychiatric conditions.

scholarly journals Association between DNA methylation and ADHD symptoms from birth to school age: a prospective meta-analysis

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Alexander Neumann ◽  
Esther Walton ◽  
Silvia Alemany ◽  
Charlotte Cecil ◽  
Juan Ramon González ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Neurotransmitter Release ◽  
Association Studies ◽  
Meta Analysis ◽  
School Age ◽  
Adhd Symptoms ◽  
Future Studies ◽  
Hyperactivity Disorder ◽  
Causal Pathways ◽  
Nominal Significance

AbstractAttention-deficit and hyperactivity disorder (ADHD) is a common childhood disorder with a substantial genetic component. However, the extent to which epigenetic mechanisms play a role in the etiology of the disorder is unknown. We performed epigenome-wide association studies (EWAS) within the Pregnancy And Childhood Epigenetics (PACE) Consortium to identify DNA methylation sites associated with ADHD symptoms at two methylation assessment periods: birth and school age. We examined associations of both DNA methylation in cord blood with repeatedly assessed ADHD symptoms (age 4–15 years) in 2477 children from 5 cohorts and of DNA methylation at school age with concurrent ADHD symptoms (age 7–11 years) in 2374 children from 9 cohorts, with 3 cohorts participating at both timepoints. CpGs identified with nominal significance (p < 0.05) in either of the EWAS were correlated between timepoints (ρ = 0.30), suggesting overlap in associations; however, top signals were very different. At birth, we identified nine CpGs that predicted later ADHD symptoms (p < 1 × 10–7), including ERC2 and CREB5. Peripheral blood DNA methylation at one of these CpGs (cg01271805 in the promoter region of ERC2, which regulates neurotransmitter release) was previously associated with brain methylation. Another (cg25520701) lies within the gene body of CREB5, which previously was associated with neurite outgrowth and an ADHD diagnosis. In contrast, at school age, no CpGs were associated with ADHD with p < 1 × 10−7. In conclusion, we found evidence in this study that DNA methylation at birth is associated with ADHD. Future studies are needed to confirm the utility of methylation variation as biomarker and its involvement in causal pathways.

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