Effect of Smoking on Blood Pressure and Resting Heart Rate: A Mendelian Randomization Meta-Analysis in the CARTA Consortium
01 Dec 2015-Circulation-cardiovascular Genetics (Lippincott Williams & Wilkins)-Vol. 8, Iss: 6, pp 832-841
TL;DR: In this paper, a Mendelian randomization meta-analysis supported a causal association of smoking heaviness with higher level of resting heart rate, but not with blood pressure, while there was no strong association with diastolic blood pressure or hypertension.
Abstract: Background-Smoking is an important cardiovascular disease risk factor, but the mechanisms linking smoking to blood pressure are poorly understood. Methods and Results-Data on 141 317 participants (62 666 never, 40 669 former, 37 982 current smokers) from 23 population-based studies were included in observational and Mendelian randomization meta-analyses of the associations of smoking status and smoking heaviness with systolic and diastolic blood pressure, hypertension, and resting heart rate. For the Mendelian randomization analyses, a genetic variant rs16969968/rs1051730 was used as a proxy for smoking heaviness in current smokers. In observational analyses, current as compared with never smoking was associated with lower systolic blood pressure and diastolic blood pressure and lower hypertension risk, but with higher resting heart rate. In observational analyses among current smokers, 1 cigarette/day higher level of smoking heaviness was associated with higher (0.21 bpm; 95% confidence interval 0.19; 0.24) resting heart rate and slightly higher diastolic blood pressure (0.05 mm Hg; 95% confidence interval 0.02; 0.08) and systolic blood pressure (0.08 mm Hg; 95% confidence interval 0.03; 0.13). However, in Mendelian randomization analyses among current smokers, although each smoking increasing allele of rs16969968/rs1051730 was associated with higher resting heart rate (0.36 bpm/allele; 95% confidence interval 0.18; 0.54), there was no strong association with diastolic blood pressure, systolic blood pressure, or hypertension. This would suggest a 7 bpm higher heart rate in those who smoke 20 cigarettes/day. Conclusions-This Mendelian randomization meta-analysis supports a causal association of smoking heaviness with higher level of resting heart rate, but not with blood pressure. These findings suggest that part of the cardiovascular risk of smoking may operate through increasing resting heart rate.
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TL;DR: Strong evidence supports the benefits of regular physical activity and exercise for the prevention and management of hypertension, and the Dietary Approaches to Stop Hypertension diet is the most effective dietary approach to prevent hypertension and to reduce blood pressure in individuals with pre-hypertension or hypertension.
Abstract: Hypertension affects approximately one third of the world's adult population and is a major cause of premature death despite considerable advances in pharmacological treatments. Growing evidence supports the use of lifestyle interventions for the prevention and adjuvant treatment of hypertension. In this Review, we provide a summary of the epidemiological research supporting the preventive and antihypertensive effects of major lifestyle interventions (regular physical exercise, body weight management and healthy dietary patterns), as well as other less traditional recommendations such as stress management and the promotion of adequate sleep patterns coupled with circadian entrainment. We also discuss the physiological mechanisms underlying the beneficial effects of these lifestyle interventions on hypertension, which include not only the prevention of traditional risk factors (such as obesity and insulin resistance) and improvements in vascular health through an improved redox and inflammatory status, but also reduced sympathetic overactivation and non-traditional mechanisms such as increased secretion of myokines.
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TL;DR: The findings revealed that the adjusted blood pressure were lower in current smokers versus nonsmokers and former smokers, and no significant dose-dependent effect of current smoking on blood pressure indices except PP was observed.
Abstract: Cigarette smoking is a known risk factor for cardiovascular disease (CVD), but the association between smoking and blood pressure is unclear. Thus, the current study examined the association between cigarette smoking and blood pressure in men. Systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial pressure (MAP) and pulse pressure (PP) were examined using digital blood pressure measuring device, and smoking status was determined with China National Health Survey. The ANCOVA showed that the adjusted DBP and MAP were lower in current smokers versus nonsmokers and the adjusted SBP was lower in current smokers versus former smokers (P < 0.05). Additionally, the adjusted PP tend to be decreased steadily as the pack·years increased in current smokers. In a fully adjusted logistic regression model, former smokers had increased ORs (95% CI) of 1.48 (1.01, 2.18) of hypertension and current smokers had not increased ORs (95% CI) of 0.83 (0.61, 1.12), compared with never smokers. The findings revealed that the adjusted blood pressure were lower in current smokers versus nonsmokers and former smokers. No significant dose-dependent effect of current smoking on blood pressure indices except PP was observed. Smoking cessation was significantly associated with an increased risk of hypertension. However, current smoking was not a risk factor of hypertension.
89 citations
TL;DR: It is suggested that occupational and non-occupational noise exposure is associated with elevations in average heart rate, which may in turn predict potential cardiovascular damage.
Abstract: Electronic waste (e-waste) is a growing occupational and environmental health issue around the globe. E-waste recycling is a green industry of emerging importance, especially in low-and middle-income countries where much of this recycling work is performed, and where many people’s livelihoods depend on this work. The occupational health hazards of e-waste recycling have not been adequately explored. We performed a cross-sectional study of noise exposures, heart rate, and perceived stress among e-waste recycling workers at a large e-waste site in Accra, Ghana. We interviewed 57 workers and continuously monitored their individual noise exposures and heart rates for up to 24 h. More than 40% of workers had noise exposures that exceeded recommended occupational (85 dBA) and community (70 dBA) noise exposure limits, and self-reported hearing difficulties were common. Workers also had moderate to high levels of perceived stress as measured via Cohen’s Perceived Stress Scale, and reported a variety of symptoms that could indicate cardiovascular disease. Noise exposures were moderately and significantly correlated with heart rate (Spearman’s ρ 0.46, p < 0.001). A mixed effects linear regression model indicated that a 1 dB increase in noise exposure was associated with a 0.17 increase in heart rate (p-value = 0.01) even after controlling for work activities, age, smoking, perceived stress, and unfavorable physical working conditions. These findings suggest that occupational and non-occupational noise exposure is associated with elevations in average heart rate, which may in turn predict potential cardiovascular damage.
64 citations
TL;DR: It is confirmed that smoking increases the risk of sudden cardiac death and any further studies should investigate in more detail the effects of duration of smoking, number of cigarettes per day, pack-years, and time since quitting smoking.
Abstract: Smoking is an established risk factor for cardiovascular disease including coronary heart disease and stroke, however, data regarding smoking and sudden cardiac death have not been summarized in a meta-analysis previously We therefore conducted a systematic review and meta-analysis to clarify this association We searched the PubMed and Embase databases for studies of smoking and sudden cardiac death up to July 20th 2017 Prospective studies were included if they reported adjusted relative risk (RR) estimates and 95% confidence intervals (CIs) for smoking and sudden cardiac death Summary RRs were estimated by use of a random effects model Twelve prospective studies were included The summary RR was 306 (95% CI 246–382, I2 = 41%, pheterogeneity = 012, n = 7) for current smokers and 138 (95% CI 120–160, I2 = 0%, pheterogeneity = 055, n = 7) for former smokers compared to never smokers For four studies using non-current (never + former) smokers as the reference category the summary RR among current smokers was 208 (95% CI 170–253, I2 = 18%, pheterogeneity = 030) The results persisted in most of the subgroup analyses There was no evidence of publication bias These results confirm that smoking increases the risk of sudden cardiac death Any further studies should investigate in more detail the effects of duration of smoking, number of cigarettes per day, pack-years, and time since quitting smoking and sudden cardiac death
58 citations
TL;DR: Combining genetic and mechanistic studies of nicotine dependence and smoking heaviness may reveal novel targets for medication development and inform genetic therapeutic interventions for smoking cessation and tobacco-related diseases.
57 citations
References
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TL;DR: Mendelian randomization provides new opportunities to test causality and demonstrates how investment in the human genome project may contribute to understanding and preventing the adverse effects on human health of modifiable exposures.
Abstract: Associations between modifiable exposures and disease seen in observational epidemiology are sometimes confounded and thus misleading, despite our best efforts to improve the design and analysis of studies. Mendelian randomization-the random assortment of genes from parents to offspring that occurs during gamete formation and conception-provides one method for assessing the causal nature of some environmental exposures. The association between a disease and a polymorphism that mimics the biological link between a proposed exposure and disease is not generally susceptible to the reverse causation or confounding that may distort interpretations of conventional observational studies. Several examples where the phenotypic effects of polymorphisms are well documented provide encouraging evidence of the explanatory power of Mendelian randomization and are described. The limitations of the approach include confounding by polymorphisms in linkage disequilibrium with the polymorphism under study, that polymorphisms may have several phenotypic effects associated with disease, the lack of suitable polymorphisms for studying modifiable exposures of interest, and canalization-the buffering of the effects of genetic variation during development. Nevertheless, Mendelian randomization provides new opportunities to test causality and demonstrates how investment in the human genome project may contribute to understanding and preventing the adverse effects on human health of modifiable exposures.
3,646 citations
TL;DR: The Avon Longitudinal Study of Parents and Children (ALSPAC) is a transgenerational prospective observational study investigating influences on health and development across the life course and is currently set up as a supported access resource.
Abstract: The Avon Longitudinal Study of Parents and Children (ALSPAC) is a transgenerational prospective observational study investigating influences on health and development across the life course. It considers multiple genetic, epigenetic, biological, psychological, social and other environmental exposures in relation to a similarly diverse range of health, social and developmental outcomes. Recruitment sought to enroll pregnant women in the Bristol area of the UK during 1990-92; this was extended to include additional children eligible using the original enrollment definition up to the age of 18 years. The children from 14541 pregnancies were recruited in 1990-92, increasing to 15247 pregnancies by the age of 18 years. This cohort profile describes the index children of these pregnancies. Follow-up includes 59 questionnaires (4 weeks-18 years of age) and 9 clinical assessment visits (7-17 years of age). The resource comprises a wide range of phenotypic and environmental measures in addition to biological samples, genetic (DNA on 11343 children, genome-wide data on 8365 children, complete genome sequencing on 2000 children) and epigenetic (methylation sampling on 1000 children) information and linkage to health and administrative records. Data access is described in this article and is currently set up as a supported access resource. To date, over 700 peer-reviewed articles have been published using ALSPAC data.
2,440 citations
TL;DR: The Avon Longitudinal Study of Children and Parents (ALSPAC) was established to understand how genetic and environmental characteristics influence health and development in parents and children.
Abstract: Summary The Avon Longitudinal Study of Children and Parents (ALSPAC) was established to understand how genetic and environmental characteristics influence health and development in parents and children. All pregnant women resident in a defined area in the South West of England, with an expected date of delivery between 1st April 1991 and 31st December 1992, were eligible and 13 761 women (contributing 13 867 pregnancies) were recruited. These women have been followed over the last 19–22 years and have completed up to 20 questionnaires, have had detailed data abstracted from their medical records and have information on any cancer diagnoses and deaths through record linkage. A follow-up assessment was completed 17–18 years postnatal at which anthropometry, blood pressure, fat, lean and bone mass and carotid intima media thickness were assessed, and a fasting blood sample taken. The second follow-up clinic, which additionally measures cognitive function, physical capability, physical activity (with accelerometer) and wrist bone architecture, is underway and two further assessments with similar measurements will take place over the next 5 years. There is a detailed biobank that includes DNA, with genome-wide data available on >10 000, stored serum and plasma taken repeatedly since pregnancy and other samples; a wide range of data on completed biospecimen assays are available. Details of how to access these data are provided in this cohort profile.
1,902 citations
TL;DR: A common variant in the nicotinic acetylcholine receptor gene cluster on chromosome 15q24 with an effect on smoking quantity, ND and the risk of two smoking-related diseases in populations of European descent is identified.
Abstract: Smoking is a leading cause of preventable death, causing about 5 million premature deaths worldwide each year. Evidence for genetic influence on smoking behaviour and nicotine dependence (ND) has prompted a search for susceptibility genes. Furthermore, assessing the impact of sequence variants on smoking-related diseases is important to public health. Smoking is the major risk factor for lung cancer (LC) and is one of the main risk factors for peripheral arterial disease (PAD). Here we identify a common variant in the nicotinic acetylcholine receptor gene cluster on chromosome 15q24 with an effect on smoking quantity, ND and the risk of two smoking-related diseases in populations of European descent. The variant has an effect on the number of cigarettes smoked per day in our sample of smokers. The same variant was associated with ND in a previous genome-wide association study that used low-quantity smokers as controls, and with a similar approach we observe a highly significant association with ND. A comparison of cases of LC and PAD with population controls each showed that the variant confers risk of LC and PAD. The findings provide a case study of a gene-environment interaction, highlighting the role of nicotine addiction in the pathology of other serious diseases.
1,459 citations
TL;DR: The findings strongly suggest that regular use of three or more drinks of alcohol per day is a risk factor for hypertension.
Abstract: We studied blood pressure in relation to known drinking habits of 83,947 men and women of three races (83.5 per cent white). Using health-check-up questionnaire responses, we classified persons as nondrinkers or according to usual daily number of drinks: two or fewer per day, three to five per day, or six or more per day. As compared to nondrinkers blood pressures of men taking two or fewer drinks per day were similar. Women who took two or fewer drinks per day had slightly lower pressures. Men and women who took three or more drinks per day had higher systolic pressures (P less than 10(-24) in white men, and less than 10(-12) in white women), higher diastolic pressures (P less than 10(-24) in white men, and less than 10(-6) in white women), and substantially higher prevalence of pressures greater than or equal to 160/95 mm Hg. The associations of blood pressure and drinking were independent of age, sex, race, smoking, coffee use, former "heavy" drinking, educational attainment and adiposity. The findings strongly suggest that regular use of three or more drinks of alcohol per day is a risk factor for hypertension.
848 citations