Is smoking heaviness causally associated with alcohol use? A Mendelian randomization study in four European cohorts

Research output: Contribution to journal › Journal article › Research › peer-review

Standard

Is smoking heaviness causally associated with alcohol use? A Mendelian randomization study in four European cohorts. / Taylor, Michelle; Rode, Line; Bjørngaard, Johan; Taylor, Amy E.; Bojesen, Stig E.; Åsvold, Bjørn O.; Gabrielsen, Maiken E.; Lewis, Glyn; Nordestgaard, Børge G.; Romundstad, Pal R.; Hickman, Matthew; Munafò, Marcus R.

In: International Journal of Epidemiology, Vol. 47, No. 4, 2018, p. 1098-1105.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Taylor, M, Rode, L, Bjørngaard, J, Taylor, AE, Bojesen, SE, Åsvold, BO, Gabrielsen, ME, Lewis, G, Nordestgaard, BG, Romundstad, PR, Hickman, M & Munafò, MR 2018, 'Is smoking heaviness causally associated with alcohol use? A Mendelian randomization study in four European cohorts', International Journal of Epidemiology, vol. 47, no. 4, pp. 1098-1105. https://doi.org/10.1093/ije/dyy027

APA

Taylor, M., Rode, L., Bjørngaard, J., Taylor, A. E., Bojesen, S. E., Åsvold, B. O., Gabrielsen, M. E., Lewis, G., Nordestgaard, B. G., Romundstad, P. R., Hickman, M., & Munafò, M. R. (2018). Is smoking heaviness causally associated with alcohol use? A Mendelian randomization study in four European cohorts. International Journal of Epidemiology, 47(4), 1098-1105. https://doi.org/10.1093/ije/dyy027

Vancouver

Taylor M, Rode L, Bjørngaard J, Taylor AE, Bojesen SE, Åsvold BO et al. Is smoking heaviness causally associated with alcohol use? A Mendelian randomization study in four European cohorts. International Journal of Epidemiology. 2018;47(4):1098-1105. https://doi.org/10.1093/ije/dyy027

Author

Taylor, Michelle ; Rode, Line ; Bjørngaard, Johan ; Taylor, Amy E. ; Bojesen, Stig E. ; Åsvold, Bjørn O. ; Gabrielsen, Maiken E. ; Lewis, Glyn ; Nordestgaard, Børge G. ; Romundstad, Pal R. ; Hickman, Matthew ; Munafò, Marcus R. / Is smoking heaviness causally associated with alcohol use? A Mendelian randomization study in four European cohorts. In: International Journal of Epidemiology. 2018 ; Vol. 47, No. 4. pp. 1098-1105.

Bibtex

@article{bd9cf5505ece4fa28b1f290e95639bba,
title = "Is smoking heaviness causally associated with alcohol use?: A Mendelian randomization study in four European cohorts",
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-Tr{\o}ndelag 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 inALSPAC; 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.",
keywords = "ALSPAC, CGPS, HUNT, Licit drugs, Mendelian randomization, UK Biobank",
author = "Michelle Taylor and Line Rode and Johan Bj{\o}rngaard and Taylor, {Amy E.} and Bojesen, {Stig E.} and {\AA}svold, {Bj{\o}rn O.} and Gabrielsen, {Maiken E.} and Glyn Lewis and Nordestgaard, {B{\o}rge G.} and Romundstad, {Pal R.} and Matthew Hickman and Munaf{\`o}, {Marcus R.}",
year = "2018",
doi = "10.1093/ije/dyy027",
language = "English",
volume = "47",
pages = "1098--1105",
journal = "International Journal of Epidemiology",
issn = "0300-5771",
publisher = "Oxford University Press",
number = "4",

}

RIS

TY - JOUR

T1 - Is smoking heaviness causally associated with alcohol use?

T2 - A Mendelian randomization study in four European cohorts

AU - Taylor, Michelle

AU - Rode, Line

AU - Bjørngaard, Johan

AU - Taylor, Amy E.

AU - Bojesen, Stig E.

AU - Åsvold, Bjørn O.

AU - Gabrielsen, Maiken E.

AU - Lewis, Glyn

AU - Nordestgaard, Børge G.

AU - Romundstad, Pal R.

AU - Hickman, Matthew

AU - Munafò, Marcus R.

PY - 2018

Y1 - 2018

N2 - 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-Trøndelag 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 inALSPAC; 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.

AB - 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-Trøndelag 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 inALSPAC; 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.

KW - ALSPAC

KW - CGPS

KW - HUNT

KW - Licit drugs

KW - Mendelian randomization

KW - UK Biobank

U2 - 10.1093/ije/dyy027

DO - 10.1093/ije/dyy027

M3 - Journal article

C2 - 29509885

AN - SCOPUS:85055163211

VL - 47

SP - 1098

EP - 1105

JO - International Journal of Epidemiology

JF - International Journal of Epidemiology

SN - 0300-5771

IS - 4

ER -

ID: 215132085