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Objective: Apolipoprotein E genotype (APOE) polymorphism affects lipid levels and coronary heart disease (CHD) risk. However, these associations may be modified by lifestyle factors. Therefore, we studied whether smoking, physical inactivity or overweight interact with APOE on cholesterol levels and CHD risk., Methods: Combining two Swedish case-control studies yielded 1735 CHD cases and 4654 population controls (3747 men, 2642 women). Self-reported questionnaire lifestyle data included smoking (ever [current or former regular] or never) and physical inactivity (mainly sitting leisure time). We obtained LDL cholesterol levels and APOE genotypes. CHD risk was modelled using logistic regression to obtain odds ratios (ORs) and 95% confidence intervals (CIs), adjusted for relevant covariates., Results: Smoking interacted with APOE on CHD risk; adjusted ORs for ever versus never smoking were 1.45 (95% CI 1.00-2.10) in ɛ2 carriers, 2.25 (95% CI 1.90-2.68) in ɛ3 homozygotes and 2.37 (95% CI 1.85-3.04) in ɛ4 carriers. Female ɛ4 carriers had OR 3.62 (95% CI 2.32-5.63). The adjusted ORs for physical inactivity were 1.09 (95% CI 0.73-1.61), 1.34 (95% CI 1.12-1.61), and 1.79 (95% CI 1.38-2.30) in ɛ2, ɛ3ɛ3 and ɛ4 groups, respectively. No interaction was seen between overweight and APOE for CHD risk, or between any lifestyle factor and APOE for LDL cholesterol levels., Conclusion: The APOE ɛ2 allele counteracted CHD risk from smoking in both genders, while the ɛ4 allele was seen to potentiate this risk mainly in women. Similar ɛ2 protection and ɛ4 potentiation was suggested for CHD risk from physical inactivity., (Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.)

Background: Smokers have been shown to have lower mortality after acute coronary syndrome than non-smokers. This has been attributed to the younger age, lower co-morbidity, more aggressive treatment and lower risk profile of the smoker. Some studies, however, have used multivariate analyses to show a residual survival benefit for smokers; that is, the "smoker's paradox". The aim of this study was, therefore, to perform a systematic review of the literature and evidence surrounding the existence of the "smoker's paradox"., Methods: Relevant studies published by September 2010 were identified through literature searches using EMBASE (from 1980), MEDLINE (from 1963) and the Cochrane Central Register of Controlled Trials, with a combination of text words and subject headings used. English-language original articles were included if they presented data on hospitalised patients with defined acute coronary syndrome, reported at least in-hospital mortality, had a clear definition of smoking status (including ex-smokers), presented crude and adjusted mortality data with effect estimates, and had a study sample of > 100 smokers and > 100 non-smokers. Two investigators independently reviewed all titles and abstracts in order to identify potentially relevant articles, with any discrepancies resolved by repeated review and discussion., Results: A total of 978 citations were identified, with 18 citations from 17 studies included thereafter. Six studies (one observational study, three registries and two randomised controlled trials on thrombolytic treatment) observed a "smoker's paradox". Between the 1980s and 1990s these studies enrolled patients with acute myocardial infarction (AMI) according to criteria similar to the World Health Organisation criteria from 1979. Among the remaining 11 studies not supporting the existence of the paradox, five studies represented patients undergoing contemporary management., Conclusion: The "smoker's paradox" was observed in some studies of AMI patients in the pre-thrombolytic and thrombolytic era, whereas no studies of a contemporary population with acute coronary syndrome have found evidence for such a paradox.

Background: Cardiovascular (CVD) mortality decreased abruptly in Norway during WW II but increased faster than in other European countries from the 1950's. Mean life expectancy for middle-aged men declined during 1960's., Objectives: To give a short overview of CVD epidemiology, especially changes in coronary heart disease (CHD) mortality, total serum cholesterol and diet during the latter half of the 20th century., Methods: Review of mortality statistics, reports from the previous National Health Screening Service and papers concerning risk factor and dietary changes. Data on CHD morbidity are not available., Discussion and Conclusions: CHD mortality reached its peak during 1966-1970. It declined during the next 30 years bringing Norwegian mortality rates to levels comparable to some Mediterranean countries. The main causes for the decline during the first twenty years of this time period are reduced total cholesterol levels from the 1970's to the 1990's, as well as a declined prevalence of smoking in the male population. Improved medical and interventional treatment are likely to explain the changes occurring during the last decade of the 20th century.

Background: Favourable trends in cardiovascular disease have been observed in Sweden. The aim of this study was to study secular trends in a variety of cardiovascular risk factors., Methods: Total-, low-density (LDL) and high-density lipoprotein (HDL) serum cholesterol; serum triglycerides; systolic and diastolic blood pressure; self-reported smoking and alcohol consumption were studied in repeated cross-sectional surveys. Data from four population-based samples in Goteborg, Sweden were used-WHO MONICA project 1985, 1990 and 1995, and INTERGENE 2002. A total of 2931 females and 2691 males aged 25-64 consisting of 1021-1624 randomly selected subjects at each survey period participated., Results: Serum cholesterol levels showed downward trends but the decline in both total- and LDL-cholesterol seems to be levelling off from 1995 and onwards. No significant changes were observed in serum triglyceride, HDL-serum cholesterol or blood pressure levels. The majority of the participants had higher total- and LDL-serum cholesterol levels than currently recommended. Antihypertensive medical treatment increased in women and the oldest men. The prevalence of smoking decreased from 39 to 25% in women and 35 to 20% in men respectively from 1985-2002. In contrast, the prevalence of subjects consuming strong beer and wine, respectively, at least once a week almost doubled from 1990-2002., Conclusions: Cardiovascular risk factor patterns change continuously and need to be monitored. The favourable trends in LDL-serum cholesterol and smoking in the Goteborg surveys were paralleled by less favourable trends in being overweight and alcohol consumption.

Background: The individual physical activity level is an independent risk factor for cardiovascular disease and death, as well as a possible target for improving health outcome. However, today´s widely adopted risk score charts, typically do not include the level of physical activity. There is a need for a simple risk assessment tool, which includes a reliable assessment of the level of physical activity. The aim of this study was therefore, to analyse the association between the self-reported levels of physical activity, according to the Saltin-Grimby Physical Activity Level Scale (SGPALS) question, and cardiovascular risk factors, specifically focusing on the group of individuals with the lowest level of self-reported PA. Methods: We used cross sectional data from the Intergene study, a random sample of inhabitants from the western part of Sweden, totalling 3588 (1685 men and 1903 women, mean age 52 and 51). Metabolic measurements, including serum-cholesterol, serum-triglycerides, fasting plasma-glucose, waist circumference, blood pressure and resting heart rate, as well as smoking and self-reported stress were related to the self-reported physical activity level, according to the modernized version of the SGPALS 4-level scale. Results: There was a strong negative association between the self-reported physical activity level, and smoking, weight, waist circumference, resting heart rate, as well as to the levels of fasting plasma-glucose, serum-triglycerides, low-density lipoproteins (LDL), and self-reported stress and a positive association with the levels of high-density lipoproteins (HDL). The individuals reporting the lowest level of PA (SGPALS, level 1) had the highest odds-ratios (OR) for having pre-defined levels of abnormal risk factors, such as being overweight (men OR 2.19, 95% CI: 1.51-3.19; women OR 2.57, 95 % CI: 1.78-3.73), having an increased waist circumference (men OR 3.76, 95 % CI: 2.61-5.43; women OR 2.91, 95% CI: 1.94-4.35) and for reporting stress (men OR 3.59, 95 % CI: 2.34-5.49; women OR 1.25, 95% CI: 0.79-1.98), compared to the most active individuals, but also showed increased OR for most other risk factors analyzed above. Conclusion: The self-reported PA-level according to the modernized Saltin-Grimby Physical Activity Level Scale, SGPALS, is associated with the presence of many cardiovascular risk factors, with the most inactive individuals having the highest risk factor profile, including self-reported stress. We propose that the present SGPALS may be used as an additional, simple tool in a routine risk assessment in e.g. primary care, to identify inactive individuals, with a higher risk profile. [ABSTRACT FROM AUTHOR]

Introduction: Central ghrelin signaling is required for the rewarding effects of alcohol in mice. Because ghrelin is implied in other addictive behaviors such as eating disorders and smoking, and because there is co-morbidity between these disorders and alcohol dependence, the ghrelin signaling system could be involved in mediating reward in general. Furthermore, in humans, single nucleotide polymorphisms (SNPs) and haplotypes of the pro-ghrelin gene (GHRL) and the ghrelin receptor gene ( GHSR) have previously been associated with increased alcohol consumption and increased body weight. Known gender differences in plasma ghrelin levels prompted us to investigate genetic variation of the ghrelin signaling system in females with severe alcohol dependence ( n = 113) and in a selected control sample of female low-consumers of alcohol from a large cohort study in southwest Sweden ( n = 212). Methods: Six tag SNPs in the GHRL (rs696217, rs3491141, rs4684677, rs35680, rs42451, and rs26802) and four tag SNPs in the GHSR (rs495225, rs2232165, rs572169, and rs2948694) were genotyped in all individuals. Results: We found that one GHRL haplotype was associated with reports of paternal alcohol dependence as well as with reports of withdrawal symptoms in the female alcohol-dependent group. Associations with 2 GHSR haplotypes and smoking were also shown. One of these haplotypes was also negatively associated with BMI in controls, while another haplotype was associated with having the early-onset, more heredity-driven, type 2 form of alcohol dependence in the patient group. Conclusion: Taken together, the genes encoding the ghrelin signaling system cannot be regarded as major susceptibility genes for female alcohol dependence, but is, however, involved in paternal heritability and may affect other reward- and energy-related factors such as smoking and BMI. [ABSTRACT FROM AUTHOR]

Aims: The aim was to evaluate total and cardiovascular disease (CVD) mortality in relation to use of oral contraceptives (OC) in a cohort of women with a relatively high prevalence of smoking and high serum lipid levels. Methods: In all 29,053 women aged 20–49 years were invited to a health survey in 1985–88. Of the total 82% attended and 20,282 women free of known CVD were included in this analysis. The relative risk (RR) of mortality during 14 years of follow-up was compared between OC users and non-users by means of proportional hazards regression. Results: About 50% of 827 OC users were daily cigarette smokers, and the mean total cholesterol level in the cohort was 5.9 mmol/l. There were 518 deaths, of which 10 occurred among the women taking OC at baseline. Of three deaths from CVD among OC users, two occurred in the first year of follow-up. Among non-smokers using OC three women died during the follow-up; none of the deaths was due to CVD. Women using OC of any type had no different adjusted total mortality (RR 0.87; 95% CI 0.46–1.65) or CVD mortality (RR 1.41; 95% CI 0.44–4.56) compared with non-users. Conclusions: The results were consistent with previous evidence which does not indicate that mortality from all causes or CVD is elevated in women using OC. [ABSTRACT FROM AUTHOR]