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Objective: To test for interactions between APOE ε4 genotype and lifestyle factors on worse cognitive abilities in UK Biobank., Methods: Using UK Biobank cohort data, we tested for interactions between APOE ε4 allele presence, lifestyle factors of alcohol intake, smoking, total physical activity and obesity, and sex, on cognitive tests of reasoning, information processing speed, and executive function (n range = 70,988-324,725 depending on the test). We statistically adjusted for potential confounders of age, sex, deprivation, cardiometabolic conditions, and educational attainment., Results: There were significant associations between APOE ε4 and worse cognitive abilities, independent of potential confounders, and between lifestyle risk factors and worse cognitive abilities; however, there were no interactions at multiple correction-adjusted p < 0.05, against our hypotheses., Conclusions: Our results do not provide support for the idea that ε4 genotype increases vulnerability to the negative effects of lifestyle risk factors on cognitive ability, but rather support a primarily outright association between APOE ε4 genotype and worse cognitive ability., (© 2019 American Academy of Neurology.)

Background: The prevalence of sleep disturbance is high and increasing. The study investigated whether active, former and passive smoking were associated with sleep disturbance., Methods: This cross-sectional study used data from the UK Biobank: a cohort study of 502 655 participants, of whom 498 208 provided self-reported data on smoking and sleep characteristics. Multivariable multinomial and logistic regression models were used to examine the associations between smoking and sleep disturbance., Results: Long-sleep duration (>9 h) was more common among current smokers [odds ratio (OR): 1.47; 95% confidence interval (CI): 1.17-1.85; probability value (P) = 0.001] than never smokers, especially heavy (>20/day) smokers (OR: 2.85; 95% CI: 1.66-4.89; P < 0.001). Former heavy (>20/day) smokers were also more likely to report short (<6 h) sleep duration (OR: 1.41; 95% CI: 1.25-1.60; P < 0.001), long-sleep duration (OR: 1.99; 95% CI: 1.47-2.71; P < 0.001) and sleeplessness (OR: 1.47; 95% CI: 1.38-1.57; P < 0.001) than never smokers. Among never smokers, those who lived with more than one smoker had higher odds of long-sleep duration than those not cohabitating with a smoker (OR: 2.71; 95% CI: 1.26-5.82; P = 0.011)., Conclusions: Active and passive exposure to high levels of tobacco smoke are associated with sleep disturbance. Existing global tobacco control interventions need to be enforced.

Risk-taking behaviour is a key component of several psychiatric disorders and could influence lifestyle choices such as smoking, alcohol use, and diet. As a phenotype, risk-taking behaviour therefore fits within a Research Domain Criteria (RDoC) approach, whereby identifying genetic determinants of this trait has the potential to improve our understanding across different psychiatric disorders. Here we report a genome-wide association study in 116,255 UK Biobank participants who responded yes/no to the question "Would you consider yourself a risk taker?" Risk takers (compared with controls) were more likely to be men, smokers, and have a history of psychiatric disorder. Genetic loci associated with risk-taking behaviour were identified on chromosomes 3 (rs13084531) and 6 (rs9379971). The effects of both lead SNPs were comparable between men and women. The chromosome 3 locus highlights CADM2, previously implicated in cognitive and executive functions, but the chromosome 6 locus is challenging to interpret due to the complexity of the HLA region. Risk-taking behaviour shared significant genetic risk with schizophrenia, bipolar disorder, attention-deficit hyperactivity disorder, and post-traumatic stress disorder, as well as with smoking and total obesity. Despite being based on only a single question, this study furthers our understanding of the biology of risk-taking behaviour, a trait that has a major impact on a range of common physical and mental health disorders.

Background: Both active smoking and second-hand smoke (SHS) are important risk factors for many age-related diseases. Active smoking is associated with shortened telomere length. However, whether SHS accelerates telomere attrition with age is uncertain. The aim of this study was to examine the association between SHS exposure and shortening by age of leukocyte telomere length among adult non-smokers., Methods: We undertook a cross-sectional study of the association between self-reported levels of SHS exposure and telomere length shortening per annum on a subgroup of participants from the Scottish Family Health Study. Inclusion was restricted to non-smokers aged ≥ 18 years, who had provided self-reported overall usual SHS exposure (total hours per week) and blood samples for telomere analysis. Linear regression models were used to compare the ratio of telomere repeat copy number to single copy gene number (T/S)by age according to SHS exposure., Results: Of the 1303 eligible participants, 779 (59.8%) reported no SHS exposure, 495 (38.0%) low exposure (1-19 h per week) and 29 (2.2%) high exposure (≥20 h per week). In the univariate linear regression analyses, relative T/S ratio declined with increasing age in all exposure groups. Telomere length decreased more rapidly with increasing age among those with high exposure to SHS [adjusted coefficient -0.019, 95% confidence interval (CI) -0.031- -0.007) when compared with both those with no exposure to SHS (adjusted coefficient -0.006, 95% CI -0.008- -0.004) (high vs no SHS: P = 0.010) and those with low exposure to SHS (adjusted coefficient -0.005, 95% CI -0.007- -0.003) (high vs low SHS: P = 0.005)., Conclusions: Our findings suggest that high SHS exposure may accelerate normal biological ageing, and support efforts to protect the public from SHS exposure. Further studies on relevant mechanisms should be conducted., (© The Author 2017; all rights reserved. Published by Oxford University Press on behalf of the International Epidemiological Association)

Objectives: Using data from a prospective birth cohort, we aimed to test for an association between exposure to tobacco smoke in utero or during early development and the experience of hypomania assessed in young adulthood., Methods: We used data on 2957 participants from a large birth cohort (Avon longitudinal study of parents and children [ALSPAC]). The primary outcome of interest was hypomania, and the secondary outcome was "hypomania plus previous psychotic experiences (PE)". Maternally-reported smoking during pregnancy, paternal smoking and exposure to environmental tobacco smoke (ETS) in childhood were the exposures of interest. Multivariable logistic regression was used and estimates of association were adjusted for socio-economic, lifestyle and obstetric factors., Results: There was weak evidence of an association between exposure to maternal smoking in utero and lifetime hypomania. However, there was a strong association of maternal smoking during pregnancy within the sub-group of individuals with hypomania who had also experienced psychotic symptoms (OR=3.45; 95% CI: 1.49-7.98; P=0.004). There was no association between paternal smoking, or exposure to ETS during childhood, and hypomania outcomes., Conclusions: Exposure to smoking in utero may be a risk factor for more severe forms of psychopathology on the mood-psychosis spectrum, rather than DSM-defined bipolar disorder., (Copyright © 2016 Elsevier Masson SAS. All rights reserved.)

Background: Serving military personnel are more likely to smoke, and to smoke more heavily, than civilians. The aim of our study was to examine whether veterans have an increased risk of a range of smoking-related cancers compared with non-veterans, using a large, national cohort of veterans., Methods: We conducted a retrospective cohort study of 57,000 veterans resident in Scotland and 173,000 age, sex and area of residence matched civilians. We used Cox proportional hazard models to compare the risk of any cancer, lung cancer and other smoking-related cancers overall, by sex and by birth cohort, adjusting for the potential confounding effect of socioeconomic deprivation., Results: Over a mean of 29 years follow-up, 445 (0.79 %) veterans developed lung cancer compared with 1106 (0.64 %) non-veterans (adjusted hazard ratio 1.16, 95 % confidence intervals 1.04-1.30, p = 0.008). Other smoking-related cancers occurred in 737 (1.31 %) veterans compared with 1883 (1.09 %) non-veterans (adjusted hazard ratio 1.18, 95 % confidence intervals 1.08-1.29, p < 0.001). A significantly increased risk was observed among veterans born 1950-1954 for lung cancer and 1945-1954 for other smoking-related cancers. The risk of lung cancer was decreased among veterans born 1960 onwards. In comparison, there was no difference in the risk of any cancer overall (adjusted hazard ratio 0.98, 95 % confidence intervals 0.94-1.01, p = 0.171), whilst younger veterans were at reduced risk of any cancer (adjusted hazard ratio 0.88, 95 % confidence intervals 0.81-0.97, p = 0.006)., Conclusions: Military veterans living in Scotland who were born before 1955 are at increased risk of smoking-related cancer compared with non-veterans, but younger veterans are not. The differences may reflect changing patterns of smoking behaviour over time in military personnel which may, in turn, be linked to developments in military health promotion policy and a changing military operational environment, as well as to wider societal factors.

Background: There is a general perception that smoking protects against weight gain and this may influence commencement and continuation of smoking, especially among young women., Methods: A cross-sectional study was conducted using baseline data from UK Biobank. Logistic regression analyses were used to explore the association between smoking and obesity; defined as body mass index (BMI) >30 kg/m2. Smoking was examined in terms of smoking status, amount smoked, duration of smoking and time since quitting and we adjusted for the potential confounding effects of age, sex, socioeconomic deprivation, physical activity, alcohol consumption, hypertension and diabetes., Results: The study comprised 499,504 adults aged 31 to 69 years. Overall, current smokers were less likely to be obese than never smokers (adjusted OR 0.83 95% CI 0.81-0.86). However, there was no significant association in the youngest sub-group (≤40 years). Former smokers were more likely to be obese than both current smokers (adjusted OR 1.33 95% CI 1.30-1.37) and never smokers (adjusted OR 1.14 95% CI 1.12-1.15). Among smokers, the risk of obesity increased with the amount smoked and former heavy smokers were more likely to be obese than former light smokers (adjusted OR 1.60, 95% 1.56-1.64, p<0.001). Risk of obesity fell with time from quitting. After 30 years, former smokers still had higher risk of obesity than current smokers but the same risk as never smokers., Conclusion: Beliefs that smoking protects against obesity may be over-simplistic; especially among younger and heavier smokers. Quitting smoking may be associated with temporary weight gain. Therefore, smoking cessation interventions should include weight management support.

Objective: Both active smoking and exposure to secondhand smoke (SHS) are associated with cardiovascular disease, but sidestream smoke contains higher levels of small particles and toxic gases than mainstream smoke. The relationship between the concentration of cotinine and a number of cardiovascular biomarkers among nonsmokers and active smokers was examined., Methods: A cross-sectional study using the Scottish Health Surveys conducted between 1998 and 2010 was undertaken. Inclusion was restricted to participants aged ≥16 years who had provided saliva and blood samples. Uni- and multivariate regression models were used to examine the relationships between the concentration of cotinine and C-reactive protein (CRP), high-density lipoprotein (HDL) cholesterol, and fibrinogen concentrations, as well as total:HDL cholesterol ratios., Results: Of the 10,018 eligible participants, 7,345 (73.3%) were confirmed to be nonsmokers (cotinine <15.0 ng/mL) and 2,673 (26.7%) were confirmed to be current smokers (cotinine ≥15.0 ng/mL). CRP and total:HDL cholesterol increased, and HDL cholesterol decreased, with increasing cotinine concentration across nonsmokers and smokers (all p < .001). However, there were step changes at the interface, whereby nonsmokers with a high exposure to SHS had lower concentrations of cotinine than light active smokers but comparable concentrations of CRP (p = .709), HDL cholesterol (p = .931), and total:HDL cholesterol (p = .405). Fibrinogen concentrations were significantly raised in moderate and heavy active smokers only (both p < .001)., Conclusion: Exposure to SHS is associated with disproportionately higher biomarkers of cardiovascular risk compared with active smoking. Protection from exposure to SHS should be a public health priority., (Copyright © 2014 European Society for Vascular Surgery. Published by Elsevier Ltd. All rights reserved.)

Context: Smoking is an important risk factor for peripheral arterial disease (PAD)., Objective: To undertake a meta-analysis of the association between cigarette smoking and PAD., Data Sources: Medline, Embase, PubMed and Web of Science databases., Study Selection: Relevant studies published up to 30 April 2012 were identified., Data Extraction: Performed by two researchers. Overall and stratified random effects meta-analyses, cumulative meta-analyses and metaregression analyses were conducted. Heterogeneity was tested using the I(2) test, and publication and small study bias using funnel plots and Egger's test., Results: Fifty-five eligible studies were identified: 43 cross-sectional, 10 cohort and 2 case-control. Of the 68 results for current smokers, 59 (86.8%) were statistically significant and the pooled OR was 2.71 (95% CI 2.28 to 3.21). There was a high level of heterogeneity (I(2) 94.9%, p<0.001) and Egger's test was significant (p=0.023). The association with smoking was significant among both general (OR 3.08, 95% CI 2.56 to 3.69) and disease populations (OR 1.54, 95% CI 1.31 to 1.83). Of the 40 results for ex-smokers, 29 (72.5%) were statistically significant and the pooled OR was 1.67 (95% CI 1.54 to 1.81). There was moderate heterogeneity (I(2) 54.7%, p<0.001) and Egger's test was significant (p<0.001)., Conclusions: There is now substantial evidence of an association between active smoking and PAD. The magnitude of the association is greater than that reported for coronary heart disease. The risk is lower among ex-smokers but, nonetheless, significantly increased compared with never smokers. The results highlight the need for interventions both to encourage quitting among existing smokers and discourage commencement among never smokers.

Background: Previous studies have reported a reduction in acute coronary events following smoke-free legislation. Evidence is lacking on whether stroke is also reduced. The aim was to determine whether the incidence of stroke, overall and by sub-type, fell following introduction of smoke-free legislation across Scotland on 26 March 2006., Methods and Findings: A negative binomial regression model was used to determine whether the introduction of smoke-free legislation resulted in a step and/or slope change in stroke incidence. The model was adjusted for age-group, sex, socioeconomic deprivation quintile, urban/rural residence and month. Interaction tests were also performed. Routine hospital administrative data and death certificates were used to identify all hospital admissions and pre-hospital deaths due to stroke (ICD10 codes I61, I63 and I64) in Scotland between 2000 and 2010 inclusive. Prior to the legislation, rates of all stroke, intracerebral haemorrhage and unspecified stroke were decreasing, whilst cerebral infarction was increasing at 0.97% per annum. Following the legislation, there was a dramatic fall in cerebral infarctions that persisted for around 20 months. No visible effect was observed for other types of stroke. The model confirmed an 8.90% (95% CI 4.85, 12.77, p<0.001) stepwise reduction in cerebral infarction at the time the legislation was implemented, after adjustment for potential confounders., Conclusions: Following introduction of national, comprehensive smoke-free legislation there was a selective reduction in cerebral infarction that was not apparent in other types of stroke.

Background: Weight control is cited by some people, especially adolescent girls, as a reason for commencing smoking or not quitting. The aim of this study was to explore the relationship between smoking behaviour and being overweight or obese, overall and by age and sex sub-groups., Methods: We used data from the six Scottish Health Surveys conducted to date (1995-2010) to undertake a population-based, cross-sectional study on 40,036 participants representative of the adult (≥16 years) Scottish population. Height and weight were measured by a trained interviewer, not self-reported., Results: 24,459 (63.3%) participants were overweight (BMI ≥25 kg/m²) and 9,818 (25.4%) were obese (BMI ≥30 kg/m²). Overall, current smokers were less likely to be overweight than never smokers. However, those who had smoked for more than 20 years (adjusted OR 1.54, 95% CI 1.41-1.69, p < 0.001) and ex-smokers (adjusted OR 1.18, 95% CI 1.11-1.25, p < 0.001) were more likely to be overweight. There were significant interactions with age. Participants 16-24 years of age, were no more likely to be overweight if they were current (adjusted OR 1.01, 95% CI 0.84-1.20, p = 0.944) or ex (adjusted OR 0.88, 95% CI 0.67-1.14, p = 0.319) smokers. The same patterns pertained to obesity., Conclusions: Whilst active smoking may be associated with reduced risk of being overweight among some older adults, there was no evidence to support the belief among young people that smoking protects them from weight gain. Making this point in educational campaigns targeted at young people may help to discourage them from starting to smoke.

Background: Both active smoking and environmental tobacco smoke exposure are associated with pregnancy complications. In March 2006, Scotland implemented legislation prohibiting smoking in all wholly or partially enclosed public spaces. The aim of this study was to determine the impact of this legislation on preterm delivery and small for gestational age., Methods and Findings: We conducted logistic regression analyses using national administrative pregnancy data covering the whole of Scotland. Of the two breakpoints tested, 1 January 2006 produced a better fit than the date when the legislation came into force (26 March 2006), suggesting an anticipatory effect. Among the 716,941 eligible women who conceived between August 1995 and February 2009 and subsequently delivered a live-born, singleton infant between 24 and 44 wk gestation, the prevalence of current smoking fell from 25.4% before legislation to 18.8% after legislation (p<0.001). Three months prior to the legislation, there were significant decreases in small for gestational age (-4.52%, 95% CI -8.28, -0.60, p = 0.024), overall preterm delivery (-11.72%, 95% CI -15.87, -7.35, p<0.001), and spontaneous preterm labour (-11.35%, 95% CI -17.20, -5.09, p = 0.001). In sub-group analyses, significant reductions were observed among both current and never smokers., Conclusions: Reductions were observed in the risk of preterm delivery and small for gestational age 3 mo prior to the introduction of legislation, although the former reversed partially following the legislation. There is growing evidence of the potential for tobacco control legislation to have a positive impact on health.

Objectives: In Scotland, legislation was implemented in March 2006 prohibiting smoking in all wholly or partially enclosed public spaces. We investigated the impact on attempts to quit smoking and smoking prevalence., Methods: We performed time series models using Box-Jenkins autoregressive integrated moving averages (ARIMA) on monthly data on the gross ingredient cost of all nicotine replacement therapy (NRT) prescribed in Scotland in 2003-2009, and quarterly data on self-reported smoking prevalence between January 1999 and September 2010 from the Scottish Household Survey., Results: NRT prescription costs were significantly higher than expected over the three months prior to implementation of the legislation. Prescription costs peaked at £1.3 million in March 2006; £292,005.9 (95% CI £260,402.3, £323,609, p<0.001) higher than the monthly norm. Following implementation of the legislation, costs fell exponentially by around 26% per month (95% CI 17%, 35%, p<0.001). Twelve months following implementation, the costs were not significantly different to monthly norms. Smoking prevalence fell by 8.0% overall, from 31.3% in January 1999 to 23.7% in July-September 2010. In the quarter prior to implementation of the legislation, smoking prevalence fell by 1.7% (95% CI 2.4%, 1.0%, p<0.001) more than expected from the underlying trend., Conclusions: Quit attempts increased in the three months leading up to Scotland's smoke-free legislation, resulting in a fall in smoking prevalence. However, neither has been sustained suggesting the need for additional tobacco control measures and ongoing support.

Objective: To assess the evidence for a reduced risk of acute coronary events following comprehensive smoke-free legislation., Methods: Two independent systematic reviews were undertaken using PubMed, Embase and Science Direct with no date restrictions imposed. Meta-analysis was undertaken using a random effects model to obtain a pooled estimate of the relative risk. Linear regression was used to examine possible bias and meta-regression was used to investigate possible causes of heterogeneity., Main Outcome Measure: Acute coronary events., Results: The 17 eligible studies (10 from North America, 6 from Europe and 1 from Australasia) provided 35 estimates of effect size. Apart from five subgroup analyses, all of the published results suggested a reduction in the incidence of acute coronary events following the introduction of smoke-free legislation. Meta-analysis produced a pooled estimate of the relative risk of 0.90 (95% CI 0.86 to 0.94). There was significant heterogeneity (overall I(2)=95.1%, p<0.001) but there was no evidence of small study bias (p=0.714). On univariate random effects meta-regression analysis, studies with longer data collection following legislation produced greater estimates of risk reduction and remained significant after adjustment for other study characteristics (adjusted coefficient -0.005, 95% CI -0.007 to -0.002, multiplicity adjusted p=0.006)., Conclusions: There is now a large body of evidence supporting a reduction in acute coronary events following the implementation of comprehensive smoke-free legislation, with the effect increasing over time from implementation. Countries that have not yet adopted smoke-free legislation should be encouraged to do so.

Background: Previous studies have shown that after the adoption of comprehensive smoke-free legislation, there is a reduction in respiratory symptoms among workers in bars. However, it is not known whether respiratory disease is also reduced among people who do not have occupational exposure to environmental tobacco smoke. The aim of our study was to determine whether the ban on smoking in public places in Scotland, which was initiated in March 2006, influenced the rate of hospital admissions for childhood asthma., Methods: Routine hospital administrative data were used to identify all hospital admissions for asthma in Scotland from January 2000 through October 2009 among children younger than 15 years of age. A negative binomial regression model was fitted, with adjustment for age group, sex, quintile of socioeconomic status, urban or rural residence, month, and year. Tests for interactions were also performed., Results: Before the legislation was implemented, admissions for asthma were increasing at a mean rate of 5.2% per year (95% confidence interval [CI], 3.9 to 6.6). After implementation of the legislation, there was a mean reduction in the rate of admissions of 18.2% per year relative to the rate on March 26, 2006 (95% CI, 14.7 to 21.8; P<0.001). The reduction was apparent among both preschool and school-age children. There were no significant interactions between hospital admissions for asthma and age group, sex, urban or rural residence, region, or quintile of socioeconomic status., Conclusions: In Scotland, passage of smoke-free legislation in 2006 was associated with a subsequent reduction in the rate of respiratory disease in populations other than those with occupational exposure to environmental tobacco smoke. (Funded by NHS Health Scotland.)

Background: Previous studies have suggested a reduction in the total number of hospital admissions for acute coronary syndrome after the enactment of legislation banning smoking in public places. However, it is unknown whether the reduction in admissions involved nonsmokers, smokers, or both., Methods: Since the end of March 2006, smoking has been prohibited by law in all enclosed public places throughout Scotland. We collected information prospectively on smoking status and exposure to secondhand smoke based on questionnaires and biochemical findings from all patients admitted with acute coronary syndrome to nine Scottish hospitals during the 10-month period preceding the passage of the legislation and during the same period the next year. These hospitals accounted for 64% of admissions for acute coronary syndrome in Scotland, which has a population of 5.1 million., Results: Overall, the number of admissions for acute coronary syndrome decreased from 3235 to 2684--a 17% reduction (95% confidence interval, 16 to 18)--as compared with a 4% reduction in England (which has no such legislation) during the same period and a mean annual decrease of 3% (maximum decrease, 9%) in Scotland during the decade preceding the study. The reduction in the number of admissions was not due to an increase in the number of deaths of patients with acute coronary syndrome who were not admitted to the hospital; this latter number decreased by 6%. There was a 14% reduction in the number of admissions for acute coronary syndrome among smokers, a 19% reduction among former smokers, and a 21% reduction among persons who had never smoked. Persons who had never smoked reported a decrease in the weekly duration of exposure to secondhand smoke (P<0.001 by the chi-square test for trend) that was confirmed by a decrease in their geometric mean concentration of serum cotinine from 0.68 to 0.56 ng per milliliter (P<0.001 by the t-test)., Conclusions: The number of admissions for acute coronary syndrome decreased after the implementation of smoke-free legislation. A total of 67% of the decrease involved nonsmokers. However, fewer admissions among smokers also contributed to the overall reduction., (2008 Massachusetts Medical Society)

C-reactive protein (CRP) levels predict coronary heart disease (CHD) risk. Levels are raised among smokers, but the effect of smoking cessation is unclear. Exposure to secondhand smoke (SHS) may be a confounder. Lifetime smoking exposure may have a dose effect on CRP among smokers, but it is unclear if this persists after cessation. We analyzed cross-sectional data on 4,072 adults recruited to a Scotland-wide population health survey who did not have CHD and were not on nicotine replacement therapy. CRP fell with time from cessation but was still raised up to 5 years after adjustment for case-mix (p<.001). SHS exposure was greater among ex-smokers than never-smokers (median cotinine 0.5 ng/ml vs. 0.4 ng/ml, p<.001) but did not explain the difference. Among smokers, there was a dose relationship between pack years and CRP on both univariate, F(4,1279) = 31.841, p<.001, and multivariate, F(4,1085) = 3.499, p = .008, analysis. Among ex-smokers there was also a dose relationship between pack-years and CRP, F(4,751) = 14.108, p<.001, which was independent of time from cessation and case-mix, F(4,466) = 3.744, p = .005. That CRP does not fall to normal levels immediately and that lifetime smoking exposure continues to impact on CRP levels post cessation suggest that CRP is not raised as a direct effect of cigarette smoke but rather via a secondary mechanism, such as tissue damage causing an inflammatory stimulus. Our results reinforce the need to encourage smoking cessation as early as possible.