scholarly journals Smoking, alcohol and coffee consumption and pregnancy loss: a Mendelian randomization investigation

Author(s):  
Shuai Yuan ◽  
Jin Liu ◽  
Susanna C. Larsson
Author(s):  
Alisa D. Kjaergaard ◽  
Yanxin Wu ◽  
Wai-Kit Ming ◽  
Zillian Wang ◽  
Mathias N. Kjaergaard ◽  
...  

Nutrients ◽  
2021 ◽  
Vol 13 (7) ◽  
pp. 2218
Author(s):  
Shuai Yuan ◽  
Paul Carter ◽  
Amy M. Mason ◽  
Stephen Burgess ◽  
Susanna C. Larsson

Coffee consumption has been linked to a lower risk of cardiovascular disease in observational studies, but whether the associations are causal is not known. We conducted a Mendelian randomization investigation to assess the potential causal role of coffee consumption in cardiovascular disease. Twelve independent genetic variants were used to proxy coffee consumption. Summary-level data for the relations between the 12 genetic variants and cardiovascular diseases were taken from the UK Biobank with up to 35,979 cases and the FinnGen consortium with up to 17,325 cases. Genetic predisposition to higher coffee consumption was not associated with any of the 15 studied cardiovascular outcomes in univariable MR analysis. The odds ratio per 50% increase in genetically predicted coffee consumption ranged from 0.97 (95% confidence interval (CI), 0.63, 1.50) for intracerebral hemorrhage to 1.26 (95% CI, 1.00, 1.58) for deep vein thrombosis in the UK Biobank and from 0.86 (95% CI, 0.50, 1.49) for subarachnoid hemorrhage to 1.34 (95% CI, 0.81, 2.22) for intracerebral hemorrhage in FinnGen. The null findings remained in multivariable Mendelian randomization analyses adjusted for genetically predicted body mass index and smoking initiation, except for a suggestive positive association for intracerebral hemorrhage (odds ratio 1.91; 95% CI, 1.03, 3.54) in FinnGen. This Mendelian randomization study showed limited evidence that coffee consumption affects the risk of developing cardiovascular disease, suggesting that previous observational studies may have been confounded.


2022 ◽  
Vol 12 (1) ◽  
Author(s):  
Shuai Yuan ◽  
Alicja Wolk ◽  
Susanna C. Larsson

AbstractWe conducted a Mendelian randomization study to determine the associations of body mass index (BMI), type 2 diabetes (T2D), systolic blood pressure (SBP), coffee and alcohol consumption and smoking initiation with senile cataract. Independent single nucleotide polymorphisms associated with the metabolic and lifestyle factors at the p < 5 × 10–8 were selected as instrument variables. Summary-level data for senile cataract were obtained from the FinnGen consortium (20,157 cases and 154,905 non-cases) and UK Biobank study (6332 cases and 354,862 non-cases). Higher genetically predicted BMI and SBP and genetic predisposition to T2D and smoking initiation were associated with an increased risk of senile cataract. The combined odds ratios were 1.19 (95% confidence interval (CI) 1.09–1.29; p < 0.001) per one standard deviation increase in BMI (~ 4.8 kg/m2), 1.13 (95% CI 1.04–1.23; p = 0.004) per 10 mmHg increase in SBP, 1.06 (95% CI 1.03–1.09; p < 0.001) per one unit increase in log-transformed odds ratio of T2D, and 1.19 (95% CI 1.10–1.29; p < 0.001) per one standard deviation increase in prevalence of smoking initiation. Genetically predicted coffee consumption showed a suggestive association with senile cataract (odds ratio per 50% increase, 1.18, 95% CI 1.00–1.40; p = 0.050). This study suggests causal roles of obesity, T2D, SBP and smoking in senile cataract.


2020 ◽  
Vol 75 (5) ◽  
pp. 753-761 ◽  
Author(s):  
Oliver J. Kennedy ◽  
Nicola Pirastu ◽  
Robin Poole ◽  
Jonathan A. Fallowfield ◽  
Peter C. Hayes ◽  
...  

2017 ◽  
Vol 46 (6) ◽  
pp. 1958-1967 ◽  
Author(s):  
Johan H Bjørngaard ◽  
Ask Tybjærg Nordestgaard ◽  
Amy E Taylor ◽  
Jorien L Treur ◽  
Maiken E Gabrielsen ◽  
...  

2015 ◽  
Vol 130 (2) ◽  
pp. 116-122 ◽  
Author(s):  
Ji Li ◽  
Hong Zhao ◽  
Ju-Min Song ◽  
Jing Zhang ◽  
Yin-Lan Tang ◽  
...  

2021 ◽  
Author(s):  
Jiuling Li ◽  
Tasnim Choudhury ◽  
Miaoran Zhang ◽  
Lanlan Chen ◽  
Jianping Wen ◽  
...  

AbstractBackground and aimsCoffee is one of the most widely consumed beverages in the world and has received considerable concerns regarding its impact on human health. Mendelian randomization (MR) could be valuable to explore the potential health effects of coffee via instrumental variables. In this study, we aim to identify novel genetic loci associated with habitual coffee consumption using genome-wide meta-analysis (GWMA) and to evaluate the broad impact of coffee consumption on human health and disease risk via a large-scale, phenotype-wide, two sample Mendelian randomization (TSMR) analysis.MethodsWe conducted a genome-wide association study (GWAS) among 283,926 coffee consumers of European ancestry in the UK Biobank (UKBB) to identify single nucleotide polymorphisms (SNPs) associated with the amount of coffee consumption (cups/day, GWAS 1), caffeine intake (GWAS 2) as well as the intake of non-caffeine substance in coffee (GWAS 3). The GWAS 1 results were further combined with the published results from the Coffee and Caffeine Genetics Consortium (CCGC) for a GWMA. TSMR were performed to evaluate the causal-relationship between coffee/caffeine/non-caffeine substance consumption and 1,101 diseases and health traits.ResultsThe GWMA identified 50 lead SNPs among 19 genomic regions for habitual coffee consumption. Nine out of the 19 loci were novel, including ADAMTSL4-AS1, CACNA2D2, LINC02123-ADCY2, UBD-SNORD32B, SEMA4D-GADD45G, LOC101929457-LINGO1, RAI1, HCN2,and BRWD1. The GWAS 2 and 3 identified 2 (SORCS2 and SLC39A8) and 5 (LINC02060-LINC00461, AGR3-AHR, PRR4-TAS2R14, CYP1A1-CYP1A2, and FTO) genomic regions, respectively. TSMR analysis indicated that coffee consumption increased the risk of high blood lipids, obesity, and diabetes. Meanwhile, intake of caffeine and non-caffeine coffee components decreased and increased some of the blood lipids levels, respectively.ConclusionsOur study provided evidence that habitual coffee consumption could increase the risk of metabolic perturbations. The bioactive components in coffee, other than caffeine, may be more harmful to human health. Our findings have significant implications for global public health given the increasing burden of metabolic diseases.


2020 ◽  
Author(s):  
Merete Ellingjord-Dale ◽  
Nikos Papadimitriou ◽  
Michalis Katsoulis ◽  
Chew Yee ◽  
Niki Dimou ◽  
...  

AbstractBackgroundObservational studies have reported either null or weak protective associations for coffee consumption and risk of breast cancer.MethodsWe conducted a two-sample Mendelian randomization randomization (MR) analysis to evaluate the relationship between coffee consumption and breast cancer risk using 33 single-nucleotide polymorphisms (SNPs) associated with coffee consumption from a genome-wide association (GWA) study on 212,119 female UK Biobank participants of White British ancestry. Risk estimates for breast cancer were retrieved from publicly available GWA summary statistics from the Breast Cancer Association Consortium (BCAC) on 122,977 cases (of which 69,501 were estrogen receptor (ER)-positive, 21,468 ER-negative) and 105,974 controls of European ancestry. Random-effects inverse variance weighted (IVW) MR analyses were performed along with several sensitivity analyses to assess the impact of potential MR assumption violations.ResultsOne cup per day increase in genetically predicted coffee consumption in women was not associated with risk of total (IVW random-effects; odds ratio (OR): 0.91, 95% confidence intervals (CI): 0.80-1.02, P: 0.12, P for instrument heterogeneity: 7.17e-13), ER-positive (OR=0.90, 95% CI: 0.79-1.02, P: 0.09) and ER-negative breast cancer (OR: 0.88, 95% CI: 0.75-1.03, P: 0.12). Null associations were also found in the sensitivity analyses using MR-Egger (total breast cancer; OR: 1.00, 95% CI: 0.80-1.25), weighted median (OR: 0.97, 95% CI: 0.89-1.05) and weighted mode (OR: 1.00, CI: 0.93-1.07).ConclusionsThe results of this large MR study do not support an association of genetically predicted coffee consumption on breast cancer risk, but we cannot rule out existence of a weak inverse association.


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