toggle visibility Search & Display Options

Select All    Deselect All
 |   | 
Details
   print
  Records Links
Author (up) Bjorngaard, J.H.; Nordestgaard, A.T.; Taylor, A.E.; Treur, J.L.; Gabrielsen, M.E.; Munafo, M.R.; Nordestgaard, B.G.; Asvold, B.O.; Romundstad, P.; Davey Smith, G. url  doi
  Title Heavier smoking increases coffee consumption: findings from a Mendelian randomization analysis Type Journal Article
  Year 2017 Publication International Journal of Epidemiology Abbreviated Journal Int J Epidemiol  
  Volume Issue Pages  
  Keywords Coffee, tea, smoking, Mendelian randomization  
  Abstract Background: There is evidence for a positive relationship between cigarette and coffee consumption in smokers. Cigarette smoke increases metabolism of caffeine, so this may represent a causal effect of smoking on caffeine intake. Methods: We performed Mendelian randomization analyses in the UK Biobank ( N = 114 029), the Norwegian HUNT study ( N = 56 664) and the Copenhagen General Population Study (CGPS) ( N = 78 650). We used the rs16969968 genetic variant as a proxy for smoking heaviness in all studies and rs4410790 and rs2472297 as proxies for coffee consumption in UK Biobank and CGPS. Analyses were conducted using linear regression and meta-analysed across studies. Results: Each additional cigarette per day consumed by current smokers was associated with higher coffee consumption (0.10 cups per day, 95% CI: 0.03, 0.17). There was weak evidence for an increase in tea consumption per additional cigarette smoked per day (0.04 cups per day, 95% CI: -0.002, 0.07). There was strong evidence that each additional copy of the minor allele of rs16969968 (which increases daily cigarette consumption) in current smokers was associated with higher coffee consumption (0.16 cups per day, 95% CI: 0.11, 0.20), but only weak evidence for an association with tea consumption (0.04 cups per day, 95% CI: -0.01, 0.09). There was no clear evidence that rs16969968 was associated with coffee or tea consumption in never or former smokers or that the coffee-related variants were associated with cigarette consumption. Conclusions: Higher cigarette consumption causally increases coffee intake. This is consistent with faster metabolism of caffeine by smokers, but could also reflect a behavioural effect of smoking on coffee drinking.  
  Address School of Social and Community Medicine, University of Bristol, Bristol, UK  
  Corporate Author Thesis  
  Publisher Place of Publication Editor  
  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 0300-5771 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:29025033 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 1881  
Permanent link to this record
 

 
Author (up) Skaaby, T.; Taylor, A.E.; Jacobsen, R.K.; Paternoster, L.; Thuesen, B.H.; Ahluwalia, T.S.; Larsen, S.C.; Zhou, A.; Wong, A.; Gabrielsen, M.E.; Bjorngaard, J.H.; Flexeder, C.; Mannisto, S.; Hardy, R.; Kuh, D.; Barry, S.J.; Tang Mollehave, L.; Cerqueira, C.; Friedrich, N.; Bonten, T.N.; Noordam, R.; Mook-Kanamori, D.O.; Taube, C.; Jessen, L.E.; McConnachie, A.; Sattar, N.; Upton, M.N.; McSharry, C.; Bonnelykke, K.; Bisgaard, H.; Schulz, H.; Strauch, K.; Meitinger, T.; Peters, A.; Grallert, H.; Nohr, E.A.; Kivimaki, M.; Kumari, M.; Volker, U.; Nauck, M.; Volzke, H.; Power, C.; Hypponen, E.; Hansen, T.; Jorgensen, T.; Pedersen, O.; Salomaa, V.; Grarup, N.; Langhammer, A.; Romundstad, P.R.; Skorpen, F.; Kaprio, J.; R Munafo, M.; Linneberg, A. url  doi
  Title Investigating the causal effect of smoking on hay fever and asthma: a Mendelian randomization meta-analysis in the CARTA consortium Type Journal Article
  Year 2017 Publication Scientific Reports Abbreviated Journal Sci Rep  
  Volume 7 Issue 1 Pages 2224  
  Keywords  
  Abstract Observational studies on smoking and risk of hay fever and asthma have shown inconsistent results. However, observational studies may be biased by confounding and reverse causation. Mendelian randomization uses genetic variants as markers of exposures to examine causal effects. We examined the causal effect of smoking on hay fever and asthma by using the smoking-associated single nucleotide polymorphism (SNP) rs16969968/rs1051730. We included 231,020 participants from 22 population-based studies. Observational analyses showed that current vs never smokers had lower risk of hay fever (odds ratio (OR) = 0.68, 95% confidence interval (CI): 0.61, 0.76; P < 0.001) and allergic sensitization (OR = 0.74, 95% CI: 0.64, 0.86; P < 0.001), but similar asthma risk (OR = 1.00, 95% CI: 0.91, 1.09; P = 0.967). Mendelian randomization analyses in current smokers showed a slightly lower risk of hay fever (OR = 0.958, 95% CI: 0.920, 0.998; P = 0.041), a lower risk of allergic sensitization (OR = 0.92, 95% CI: 0.84, 1.02; P = 0.117), but higher risk of asthma (OR = 1.06, 95% CI: 1.01, 1.11; P = 0.020) per smoking-increasing allele. Our results suggest that smoking may be causally related to a higher risk of asthma and a slightly lower risk of hay fever. However, the adverse events associated with smoking limit its clinical significance.  
  Address Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark  
  Corporate Author Thesis  
  Publisher Place of Publication Editor  
  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 2045-2322 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:28533558; PMCID:PMC5440386 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 1980  
Permanent link to this record
 

 
Author (up) Taylor, A.E.; Carslake, D.; de Mola, C.L.; Rydell, M.; Nilsen, T.I.L.; Bjorngaard, J.H.; Horta, B.L.; Pearson, R.; Rai, D.; Galanti, M.R.; Barros, F.C.; Romundstad, P.R.; Davey Smith, G.; Munafo, M.R. url  doi
  Title Maternal Smoking in Pregnancy and Offspring Depression: a cross cohort and negative control study Type Journal Article
  Year 2017 Publication Scientific Reports Abbreviated Journal Sci Rep  
  Volume 7 Issue 1 Pages 12579  
  Keywords  
  Abstract Previous reports suggest that offspring of mothers who smoke during pregnancy have greater risk of developing depression. However, it is unclear whether this is due to intrauterine effects. Using data from the Avon Longitudinal Study of Parents and Children (ALSPAC) from the UK (N = 2,869), the Nord-Trondelag health study (HUNT) from Norway (N = 15,493), the Pelotas 1982 Birth Cohort Study from Brazil (N = 2,626), and the Swedish Sibling Health Cohort (N = 258 sibling pairs), we compared associations of maternal smoking during pregnancy and mother's partner's smoking during pregnancy with offspring depression and performed a discordant sibling analysis. In meta-analysis, maternal smoking during pregnancy was associated with higher odds of offspring depression (OR 1.20, 95% CI:1.08,1.34), but mother's partner's smoking during pregnancy was not (OR 1.05, 95% CI:0.94,1.17). However, there was only weak statistical evidence that the odds ratios for maternal and mother's partner's smoking differed from each other (p = 0.08). There was no clear evidence for an association between maternal smoking during pregnancy and offspring depression in the sibling analysis. Findings do not provide strong support for a causal role of maternal smoking during pregnancy in offspring depression, rather observed associations may reflect residual confounding relating to characteristics of parents who smoke.  
  Address UK Centre for Tobacco and Alcohol Studies, School of Experimental Psychology, University of Bristol, Bristol, United Kingdom  
  Corporate Author Thesis  
  Publisher Place of Publication Editor  
  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 2045-2322 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:28974730; PMCID:PMC5626710 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 2010  
Permanent link to this record
 

 
Author (up) Taylor, M.; Rode, L.; Bjorngaard, J.; Taylor, A.E.; Bojesen, S.E.; Asvold, B.O.; Gabrielsen, M.E.; Lewis, G.; Nordestgaard, B.G.; Romundstad, P.R.; Hickman, M.; Munafo, M.R. url  doi
  Title Is smoking heaviness causally associated with alcohol use? A Mendelian randomization study in four European cohorts Type Journal Article
  Year 2018 Publication International Journal of Epidemiology Abbreviated Journal Int J Epidemiol  
  Volume 47 Issue 4 Pages 1098-1105  
  Keywords  
  Abstract Background: Observational studies have shown that tobacco and alcohol use co-occur, but it is not clear whether this relationship is causal. Methods: Using data from the Avon Longitudinal Study of Parents and Children (ALSPAC) and UK Biobank, we used observational methods to test the hypothesis that smoking heaviness increases alcohol consumption. Mendelian randomization (MR) analyses were then used to test the causal relationship between smoking heaviness and alcohol consumption using 55 967 smokers from four European studies [ALSPAC, The Nord-Trondelag Health Study (HUNT), the Copenhagen General Population Study (CGPS) and UK Biobank]. MR analyses used rs1051730/rs16969968 as a genetic proxy for smoking heaviness. Results: Observational results provided evidence of an association between cigarettes per day and weekly alcohol consumption (increase in units of alcohol per additional cigarette smoked per day = 0.10, 95% confidence interval (CI) 0.05 to 0.15, P </= 0.001 in ALSPAC; and 0.48, 95% CI 0.45 to 0.52, P </= 0.001 in UK Biobank). However, there was little evidence for an association between rs1051730/rs16969968 and units of alcohol consumed per week across ALSPAC, HUNT, CGPS and UK Biobank (standard deviation increase in units of alcohol per additional copy of the risk allele = -0.004, 95% CI -0.023 to 0.016, P=0.708, I2 = 51.9%). We had 99% and 88% power to detect a change of 0.03 and 0.02 standard deviation units of alcohol per additional copy of the risk allele, respectively. Conclusions: Previously reported associations between smoking and alcohol are unlikely to be causal, and may be the result of confounding and/or reverse causation. This has implications for public health research and intervention research.  
  Address UK Centre for Tobacco and Alcohol Studies, School of Experimental Psychology, University of Bristol, Bristol, UK  
  Corporate Author Thesis  
  Publisher Place of Publication Editor  
  Language English Summary Language Original Title  
  Series Editor Series Title Abbreviated Series Title  
  Series Volume Series Issue Edition  
  ISSN 0300-5771 ISBN Medium  
  Area Expedition Conference  
  Notes PMID:29509885; PMCID:PMC6124618 Approved no  
  Call Number HUNT @ maria.stuifbergen @ Serial 2181  
Permanent link to this record
Select All    Deselect All
 |   | 
Details
   print

Save Citations:
Export Records: