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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 randomisation analyses in the UK Biobank (N=114,029), the Norwegian HUNT study (N=56,664) and the Copenhagen General Population Study (CPGS) (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 CPGS. 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:0.12,0.21), 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.
Conclusion
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.
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 randomisation analyses in the UK Biobank (N=114,029), the Norwegian HUNT study (N=56,664) and the Copenhagen General Population Study (CPGS) (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 CPGS. 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:0.12,0.21), 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.
Conclusion
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.
Original language | English |
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Article number | dyx147 |
Pages (from-to) | 1958-1967 |
Number of pages | 10 |
Journal | International Journal of Epidemiology |
Volume | 46 |
Issue number | 6 |
Early online date | 14 Aug 2017 |
DOIs | |
Publication status | Published - Dec 2017 |
Structured keywords
- Brain and Behaviour
- Tobacco and Alcohol
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Dive into the research topics of 'Heavier smoking increases coffee consumption: findings from a Mendelian randomisation analysis'. Together they form a unique fingerprint.Projects
- 2 Finished
Profiles
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Dr Amy E Taylor
- Bristol Medical School (PHS) - Research Fellow
- Bristol Population Health Science Institute
- MRC Integrative Epidemiology Unit
Person: Academic , Member