scholarly journals DNA methylation variant, B-vitamins intake and longitudinal change in body mass index

2018 ◽  
Vol 43 (3) ◽  
pp. 468-474
Author(s):  
Xiang Li ◽  
Tiange Wang ◽  
Min Zhao ◽  
Tao Huang ◽  
Dianjianyi Sun ◽  
...  
2018 ◽  
Author(s):  
Amy E. Taylor ◽  
Rebecca C. Richmond ◽  
Teemu Palviainen ◽  
Anu Loukola ◽  
Jaakko Kaprio ◽  
...  

AbstractBackgroundGiven clear evidence that smoking lowers weight, it is possible that individuals with higher body mass index (BMI) smoke in order to lose or maintain their weight.Methods and FindingsWe undertook Mendelian randomization analyses using 97 genetic variants associated with BMI. We performed two sample Mendelian randomization analyses of the effects of BMI on smoking behaviour in UK Biobank (N=335,921) and the Tobacco and Genetics consortium genomewide association study (GWAS) (N≤74,035) respectively, and two sample Mendelian randomization analyses of the effects of BMI on cotinine levels (N≤4,548) and nicotine metabolite ratio (N≤1,518) in published GWAS, and smoking-related DNA methylation in the Avon Longitudinal Study of Parents and Children (N≤846).In inverse variance weighted Mendelian randomization analysis, there was evidence that higher BMI was causally associated with smoking initiation (OR for ever vs never smoking per one SD increase in BMI: 1.19, 95% CI: 1.11 to 1.27) and smoking heaviness (1.45 additional cigarettes smoked per day per SD increase in BMI, 95% CI: 1.03 to 1.86), but little evidence for a causal effect with smoking cessation. Results were broadly similar using pleiotropy robust methods (MR-Egger, median and weighted mode regression). These results were supported by evidence for a causal effect of BMI on DNA methylation at the aryl-hydrocarbon receptor repressor (AHRR) locus. There was no strong evidence that BMI was causally associated with cotinine, but suggestive evidence for a causal negative association with the nicotine metabolite ratio.ConclusionsThere is a causal bidirectional association between BMI and smoking, but the relationship is likely to be complex due to opposing effects on behaviour and metabolism. It may be useful to consider BMI and smoking together when designing prevention strategies to minimise the effects of these risk factors on health outcomes.


2021 ◽  
Vol 2021 ◽  
pp. 1-7
Author(s):  
Andrea Maugeri ◽  
Martina Barchitta ◽  
Roberta Magnano San Lio ◽  
Giuliana Favara ◽  
Claudia La Mastra ◽  
...  

Uncovering the relationship between body mass index (BMI) and DNA methylation could be useful to understand molecular mechanisms underpinning the effects of obesity. Here, we presented a cross-sectional study, aiming to evaluate the association of BMI and obesity with long interspersed nuclear elements (LINE-1) methylation, among 488 women from Catania, Italy. LINE-1 methylation was assessed in leukocyte DNA by pyrosequencing. We found a negative association between BMI and LINE-1 methylation level in both the unadjusted and adjusted linear regression models. Accordingly, obese women exhibited lower LINE-1 methylation level than their normal weight counterpart. This association was confirmed after adjusting for the effect of age, educational level, employment status, marital status, parity, menopause, and smoking status. Our findings were in line with previous evidence and encouraged further research to investigate the potential role of DNA methylation markers in the management of obesity.


Epigenetics ◽  
2018 ◽  
Vol 13 (10-11) ◽  
pp. 1072-1087 ◽  
Author(s):  
Jian V. Huang ◽  
Andres Cardenas ◽  
Elena Colicino ◽  
C. Mary Schooling ◽  
Sheryl L. Rifas-Shiman ◽  
...  

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Fan He ◽  
Arthur Berg ◽  
Yuka Imamura Kawasawa ◽  
Edward O. Bixler ◽  
Julio Fernandez-Mendoza ◽  
...  

2017 ◽  
Vol 168 (1) ◽  
pp. 241-248 ◽  
Author(s):  
Arielle S. Gillman ◽  
Casey K. Gardiner ◽  
Claire E. Koljack ◽  
Angela D. Bryan

Author(s):  
Gemma C Sharp ◽  
Rossella Alfano ◽  
Akram Ghantous ◽  
Jose Urquiza ◽  
Sheryl L Rifas-Shiman ◽  
...  

AbstractBackgroundAccumulating evidence links paternal adiposity in the peri-conceptional period to offspring health outcomes. DNA methylation has been proposed as a mediating mechanism, but very few studies have explored this possibility in humans.Methods and findingsIn the Pregnancy And Childhood Epigenetics (PACE) consortium, we conducted a meta-analysis of co-ordinated epigenome-wide association studies (EWAS) of paternal prenatal Body Mass Index (BMI) (with and without adjustment for maternal BMI) in relation to DNA methylation in offspring blood at birth (13 datasets; total n= 4,894) and in childhood (six datasets; total n = 1,982). We found little evidence of association at either time point: for all CpGs, the False Discovery Rate-adjusted P-values were >0.05. In sex-stratified analyses, we found just four CpGs where there was robust evidence of association in female offspring. To compare our findings to those of other studies, we conducted a systematic review, which identified seven studies, including five candidate gene studies showing associations between paternal BMI/obesity and offspring or sperm DNA methylation at imprinted regions. However, in our own study, we found very little evidence of enrichment for imprinted genes.ConclusionOur findings do not support the hypothesis that paternal BMI around the time of pregnancy is associated with offspring blood DNA methylation, even at imprinted regions.Author SummaryPrevious small, mostly candidate gene studies have shown associations between paternal pre-pregnancy BMI and offspring blood DNA methylation. However, in our large meta-analysis of co-ordinated EWAS results from a total of 19 datasets across two timepoints, we found little evidence to support these findings, even at imprinted regions. This does not rule out the possibility of a paternal epigenetic effect in different tissues, at regions not covered by the 450k array, via different mechanisms, or in populations with greater extremes of paternal BMI. More research is warranted to help understand the size and nature of contributions of paternal adiposity to offspring epigenetics and health outcomes.


Author(s):  
Emily S. Wan ◽  
Weiliang Qiu ◽  
Helene Bacherman ◽  
Vincent J. Carey ◽  
Andrea Baccarelli ◽  
...  

Placenta ◽  
2020 ◽  
Vol 93 ◽  
pp. 74-82
Author(s):  
Keshari M. Thakali ◽  
Ying Zhong ◽  
Mario Cleves ◽  
Aline Andres ◽  
Kartik Shankar

Respiration ◽  
2020 ◽  
pp. 1-11
Author(s):  
Eun Kyung Kim ◽  
Dave Singh ◽  
Joo Hun Park ◽  
Yong Bum Park ◽  
Seung-Il Kim ◽  
...  

<b><i>Background:</i></b> Low body mass index (BMI) is an important prognostic factor in chronic obstructive pulmonary disease (COPD). However, the prognostic value of longitudinal BMI change in COPD has not been well studied. <b><i>Objective:</i></b> We aimed to evaluate the association between longitudinal change of BMI and prognosis of COPD in Korean COPD cohort. <b><i>Methods:</i></b> This study was conducted in a prospective Korean Obstructive Lung Disease (KOLD) cohort where COPD patients were recruited on an outpatient basis at 17 hospitals in South Korea. Annual BMI was measured over a period of 3 years or more. All patients were categorized into underweight (UW), normal weight (NW), and overweight (OW) groups by BMI. Clinical characteristics and outcomes including exacerbation and mortality were compared based on initial BMI grade and longitudinal change of BMI. <b><i>Results:</i></b> This analysis included 537 COPD patients (mean age = 67.4 ± 7.9 years, male = 97.0%, mean BMI = 23.0 ± 3.1) of KOLD cohort. The proportions of UW, NW, and OW groups were 6.9% (<i>n</i> = 37), 68.9% (<i>n</i> = 370), and 24.2% (<i>n</i> = 130) respectively. The UW group showed lower forced expiratory volume in 1 s (FEV<sub>1</sub>) (<i>p</i> &#x3c; 0.001), shorter 6-minute walk distance (<i>p</i> &#x3c; 0.001), higher modified Medical Research Council score (<i>p</i> = 0.002), higher St. George Respiratory Questionnaire score (<i>p</i> &#x3c; 0.001), higher emphysema index (<i>p</i> &#x3c; 0.001) and air-trapping index (<i>p</i> &#x3c; 0.001), and more frequent (<i>p</i> &#x3c; 0.001) and severe exacerbations (<i>p</i> = 0.003). Multivariable analyses demonstrated that decrease of BMI (hazard ratio [HR] = 0.786, <i>p</i> = 0.038) and the descent of BMI group (HR = 3.167, <i>p</i> = 0.016) at 3-year follow-up along with age, initial BMI, post-bronchodilator FEV<sub>1</sub>, and severe exacerbations were significantly associated with mortality. <b><i>Conclusions:</i></b> This study demonstrated that BMI decrease during follow-up was independently associated with exacerbation and higher mortality of COPD, suggesting BMI reduction in COPD should be carefully managed.


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