M B Johnsen1,2,3, B S Winsvold2,4, S Børte1,2, G Å Vie5, L M Pedersen2, K Storheim2, F Skorpen6, K Hagen7,8, J H Bjørngaard5,9, B O Åsvold3,10, J A Zwart1,2,4. 1. Faculty of Medicine, Institute of Clinical Medicine, University of Oslo, Oslo, Norway. 2. Research and Communication Unit for Musculoskeletal Health, Oslo University Hospital, Oslo, Norway. 3. K.G. Jebsen Center for Genetic Epidemiology, Department of Public Health and Nursing, NTNU, Norwegian University of Science and Technology, Trondheim, Norway. 4. Department of Neurology, Oslo University Hospital, Oslo, Norway. 5. Department of Public Health and Nursing, NTNU, Norwegian University of Science and Technology, Trondheim, Norway. 6. Department of Clinical and Molecular Medicine, Faculty of Medicine and Health Sciences, NTNU, Norwegian University of Science and Technology, Trondheim, Norway. 7. Department of Neuromedicine and Movement Science, NTNU, Norwegian University of Science and Technology, Trondheim, Norway. 8. Norwegian Advisory Unit on Headaches, St Olavs Hospital, Trondheim University Hospital, Trondheim, Norway. 9. Forensic Department and Research Centre Brøset, St Olavs Hospital, Trondheim University Hospital, Trondheim, Norway. 10. Department of Endocrinology, St Olavs Hospital, Trondheim University Hospital, Trondheim, Norway.
Abstract
BACKGROUND AND PURPOSE: Headache has been associated with various lifestyle and psychosocial factors, one of which is smoking. The aim of the present study was to investigate whether the association between smoking intensity and headache is likely to be causal. METHOD: A total of 58 316 participants from the Nord-Trøndelag Health (HUNT) study with information on headache status were genotyped for the rs1051730 C>T single-nucleotide polymorphism (SNP). The SNP was used as an instrument for smoking intensity in a Mendelian randomization analysis. The association between rs1051730 T alleles and headache was estimated by odds ratios with 95% confidence intervals. Additionally, the association between the SNP and migraine or non-migrainous headache versus no headache was investigated. All analyses were adjusted for age and sex. RESULTS: There was no strong evidence that the rs1051730 T allele was associated with headache in ever smokers (odds ratio 0.99, 95% confidence interval 0.95-1.02). Similarly, there was no association between the rs1051730 T allele and migraine or non-migrainous headache versus no headache. CONCLUSION: The findings from this study do not support that there is a strong causal relationship between smoking intensity and any type of headache. Larger Mendelian randomization studies are required to examine whether higher smoking quantity can lead to a moderate increase in the risk of headache subtypes.
BACKGROUND AND PURPOSE:Headache has been associated with various lifestyle and psychosocial factors, one of which is smoking. The aim of the present study was to investigate whether the association between smoking intensity and headache is likely to be causal. METHOD: A total of 58 316 participants from the Nord-Trøndelag Health (HUNT) study with information on headache status were genotyped for the rs1051730 C>T single-nucleotide polymorphism (SNP). The SNP was used as an instrument for smoking intensity in a Mendelian randomization analysis. The association between rs1051730 T alleles and headache was estimated by odds ratios with 95% confidence intervals. Additionally, the association between the SNP and migraine or non-migrainous headache versus no headache was investigated. All analyses were adjusted for age and sex. RESULTS: There was no strong evidence that the rs1051730 T allele was associated with headache in ever smokers (odds ratio 0.99, 95% confidence interval 0.95-1.02). Similarly, there was no association between the rs1051730 T allele and migraine or non-migrainous headache versus no headache. CONCLUSION: The findings from this study do not support that there is a strong causal relationship between smoking intensity and any type of headache. Larger Mendelian randomization studies are required to examine whether higher smoking quantity can lead to a moderate increase in the risk of headache subtypes.