Associations of Binge Drinking With the Risks of Ischemic Heart Disease and Stroke: A Study of Pooled Norwegian Health Surveys.

Norwegian health survey data (1987-2003) were analyzed to determine if binge drinking increases the risk of incident major events from ischemic heart disease (IHD) and stroke. Among current drinkers reporting average alcohol intakes of 2.00-59.99 g/day (n = 44,476), frequent binge drinking (≥5 units at least once per month) was not associated with a greater risk of IHD (adjusted hazard ratio (HR) = 0.91, 95% confidence interval (CI): 0.76, 1.09) or stroke (adjusted HR = 0.98, 95% CI: 0.81, 1.19), in comparison with participants who reported that they never or only infrequently (less than once per month) had episodes of binge drinking. Participants with an average alcohol intake of 2.00-59.99 g/day had a lower risk of IHD in comparison with participants with very low intakes (<2.00 g/day), both among frequent binge drinkers (adjusted HR = 0.67, 95% CI: 0.56, 0.80) and among never/infrequent binge drinkers (adjusted HR = 0.75, 95% CI: 0.67, 0.84). The findings suggest that frequent binge drinking, independent of average alcohol intake, does not increase the risk of incident IHD or stroke events. However, the findings should be interpreted in light of the limitations of the study design.

Association of coincident self-reported mental health problems and alcohol intake with all-cause and cardiovascular disease mortality: A Norwegian pooled population analysis.

BACKGROUND: The disease burden attributable to mental health problems and to excess or harmful alcohol use is considerable. Despite a strong relationship between these 2 important factors in population health, there are few studies quantifying the mortality risk associated with their co-occurrence in the general population. The aim of this study was therefore to investigate cardiovascular disease (CVD) and all-cause mortality according to self-reported mental health problems and alcohol intake in the general population. METHODS AND FINDINGS: We followed 243,372 participants in Norwegian health surveys (1994-2002) through 2014 for all-cause and CVD mortality by data linkage to national registries. The mean (SD) age at the time of participation in the survey was 43.9 (10.6) years, and 47.8% were men. During a mean (SD) follow-up period of 16.7 (3.2) years, 6,587 participants died from CVD, and 21,376 died from all causes. Cox models estimated hazard ratios (HRs) with 95% CIs according to a mental health index (low, 1.00-1.50; high, 2.01-4.00; low score is favourable) based on the General Health Questionnaire and the Hopkins Symptom Checklist, and according to self-reported alcohol intake (low, <2; light, 2-11.99; moderate, 12-23.99; high, ≥24 grams/day). HRs were adjusted for age, sex, educational level, marital status, and CVD risk factors. Compared to a reference group with low mental health index score and low alcohol intake, HRs (95% CIs) for all-cause mortality were 0.93 (0.89, 0.97; p = 0.001), 1.00 (0.92, 1.09; p = 0.926), and 1.14 (0.96, 1.35; p = 0.119) for low index score combined with light, moderate, and high alcohol intake, respectively. HRs (95% CIs) were 1.22 (1.14, 1.31; p < 0.001), 1.24 (1.15, 1.33; p < 0.001), 1.43 (1.23, 1.66; p < 0.001), and 2.29 (1.87, 2.80; p < 0.001) for high index score combined with low, light, moderate, and high alcohol intake, respectively. For CVD mortality, HRs (95% CIs) were 0.93 (0.86, 1.00; p = 0.058), 0.90 (0.76, 1.07; p = 0.225), and 0.95 (0.67, 1.33; p = 0.760) for a low index score combined with light, moderate, and high alcohol intake, respectively, and 1.11 (0.98, 1.25; p = 0.102), 0.97 (0.83, 1.13; p = 0.689), 1.01 (0.71, 1.44; p = 0.956), and 1.78 (1.14, 2.78; p = 0.011) for high index score combined with low, light, moderate, and high alcohol intake, respectively. HRs for the combination of a high index score and high alcohol intake (HRs: 2.29 for all-cause and 1.78 for CVD mortality) were 64% (95% CI 53%, 74%; p < 0.001) and 69% (95% CI 42%, 97%; p < 0.001) higher than expected for all-cause mortality and CVD mortality, respectively, under the assumption of a multiplicative interaction structure. A limitation of our study is that the findings were based on average reported intake of alcohol without accounting for the drinking pattern. CONCLUSIONS: In the general population, the mortality rates associated with more mental health problems and a high alcohol intake were increased when the risk factors occurred together.

Associations of tobacco smoking with body mass distribution; a population-based study of 65,875 men and women in midlife.

BACKGROUND: Studies indicate an effect of smoking toward abdominal obesity, but few assess hip and waist circumferences (HC and WC) independently. The present study aimed to assess the associations of smoking status and volume smoked with HC and WC and their ratio in a population with low prevalence of obesity together with high prevalence of smoking. METHODS: We used cross-sectional survey data from 11 of a total 19 Norwegian counties examined in 1997-99 including 65,875 men and women aged 39-44 years. Analysis of associations were adjusted for confounding by socioeconomic position, health indicators, and additionally for BMI. RESULTS: Compared with never-smokers, when adjusting for confounders and in addition for BMI, mean HC remained lower while mean WC and waist-hip-ratio (WHR) were higher in current smokers. The finding of a lower HC and higher WHR level among smokers was consistent by sex and in strata by levels of education and physical activity, while the finding of higher WC by smoking was less consistent. Among current smokers, BMI-adjusted mean HC decreased whereas WC and WHR increased by volume smoked. Compared with current smokers, former smokers had higher BMI-adjusted HC, lower WHR and among women WC was lower. CONCLUSIONS: The main finding in this study was the consistent negative associations of smoking with HC. In line with the hypothesis that lower percentage gluteofemoral fat is linked with higher cardiovascular risk, our results suggest that smoking impacts cardiovascular risk through mechanisms that reduce the capacity of fat storage in the lower body region.

Sociodemographic disparities in hypertension prevalence: Results from the first Portuguese National Health Examination Survey.

INTRODUCTION: Cardiovascular disease is an important cause of death and disability worldwide, and hypertension is responsible for at least 45% of all deaths due to heart disease and 51% of deaths due to stroke. This study aimed to estimate and describe the distribution of prevalence, awareness, treatment and control of hypertension in the Portuguese population in 2015. METHODS: A national survey using a representative sample of 4911 individuals residing in Portugal and aged between 25 and 74 years was implemented. Trained nurses performed a health interview and a physical examination, including blood pressure measurement (right arm, three measurements at 1-min intervals). The prevalence of hypertension was stratified by gender, age group, marital status, education, occupation and type of residential area. Associations between hypertension prevalence and sociodemographic factors were assessed using bivariate and multivariate Poisson regression. RESULTS: The overall hypertension prevalence was 36.0%. The highest rates were observed in males (39.6%), in individuals aged between 65 and 74 years (71.3%), and in those with low levels of education (62.6%) and with no formal occupation (64.5%). Among hypertensive individuals, 69.8% were aware of their condition and 69.4% were under treatment, of whom 71.3% were controlled. Rates of awareness and medical treatment were significantly higher among women and older individuals. CONCLUSIONS: A large majority of the adult Portuguese population are likely to reach blood pressure levels defined as hypertension in adulthood. Significant differences in hypertension prevalence were found according to gender, age and socioeconomic status, which highlights the importance of population strategies in public health policies.

Impact of snus use in teenage boys on tobacco use in young adulthood; a cohort from the HUNT Study Norway.

BACKGROUND: As smoking rates decreased, the use of Swedish snus (smokeless tobacco) concordantly increased in Norway. The role of snus as possible contributor to the reduction of smoking has been widely discussed. Our aim was to quantitate transitions in snus use, smoking and dual use of snus and cigarettes in a young male population. METHODS: This prospective cohort study includes 1346 boys participating in the Nord-Trøndelag Health Study in Young-HUNT1 1995-97, age 13-19 and in HUNT3 2006-08, age 23-30. Participants reported on tobacco use at both points of time. Models with binominal regression were applied to examine relative risks (RRs), of adolescent ever snus users, dual users or smokers (reference: never tobacco use), to be current snus only users, smokers (including dual users), or tobacco free in adulthood. RESULTS: Current tobacco use in this male cohort increased from 27% in adolescence to 49% in adulthood, increasing more for snus only use and dual use than for smoking only. The adjusted RR (95% CI) of becoming a smoker as young adult, was 2.2 (CI 1.7-2.7) for adolescent snus users, 3.6 (CI 3.0-4.3) for adolescent dual users, and 2.7 (CI 2.2-3.3) for adolescent smokers. RR to become snus only users as adults was 3.1 (2.5-3.9) for adolescent dual users, 2.8 (2.2-3.4) for adolescent snus users and 1.5 (1.0-2.2) for adolescent smokers. The adjusted RR for the transition from adolescent tobacco use to no tobacco use in adulthood was similar for snus users and smokers with RR 0.5 (CI 0.4-0.7), but considerably lower for dual users with RR 0.2 (CI 0.2-0.3). CONCLUSIONS: The use of snus, with or without concurrent smoking, carried a high risk of adult smoking as well as adult snus only use. Dual use seemed to promote the opportunity to become snus only users in adulthood, but made it also more difficult to quit. The benefit of snus use for harm reduction is not evident in our cohort, as the combination of smoking and dual use resulted in high smoking rates among the young adults.

The educational gradient in premature cardiovascular mortality: Examining mediation by risk factors in cohorts born in the 1930s, 1940s and 1950s.

AIMS: Educational inequality in cardiovascular disease and in modifiable risk factors changes over time and between birth cohorts. We aimed to assess how cardiovascular disease risk factors mediate educational differences in premature cardiovascular disease mortality and how this varies over birth cohorts and sex. METHODS: We followed 360,008 40-45-year-olds born in the 1930s, 1940s or 1950s from Norwegian health examination surveys (1974-1997) for premature cardiovascular disease mortality. Cox proportional hazard and Aalen's additive survival analyses provided hazard ratios and rate differences of excess deaths in participants with basic versus tertiary education. RESULTS: Relative educational differences in premature cardiovascular disease mortality were stable, whereas absolute differences narrowed from the 1930s to the 1950s cohorts; rate differences per 100 000 person years declined from 170 (95% confidence interval 117, 224) to 49 (36, 61) in men and from 60 (34, 85) to 23 (16, 29) in women. Cardiovascular disease risk factors attenuated rate differences by 69% in both cohorts in men, and in women by 102% in 1930s and 61% in 1950s cohorts. Smoking had the single strongest influence on the educational differences for men in all three cohorts, and for women in the two most recent cohorts. CONCLUSION: Smoking appeared to be the driving force behind educational differences in premature cardiovascular disease mortality in the 1930s to 1950s birth cohorts for men and in the two recent birth cohorts for women. This suggests that strategies for smoking prevention and cessation might have the strongest impact for reducing educational inequality in premature cardiovascular disease mortality.

Educational inequalities in midlife risk factors for non-communicable diseases in two Norwegian counties 1974-2002.

Background: The absolute educational differences in the mortality of Norwegian women and men increased during 1960-2000 and thereafter levelled off in men, but continued to widen in women. Which of the risk factors for non-communicable diseases (NCDs) might explain these trends? Aim: The aim of this study was to investigate trends in gender-specific, absolute educational differences in established risk factors during 1974-2002. Methods: We used cross-sectional data from 40-45-year-old women and men who participated in one of three health surveys in two counties, from the years 1974-1978, 1985-1988 and 2001-2002. To account for increasing educational attainment through the period we used a regression-based index of inequality (Slope Index of Inequality) to assess the educational gradients over time. Results: From 1974 to 2002, the mean levels of serum total cholesterol and blood pressure decreased and body mass index (BMI) increased in all subgroups by education in both sexes. In men, the educational gradient tended to diminish toward the null for serum total cholesterol and narrowed for systolic blood pressure, but increased for BMI. In women, the educational gradient increased to the double for smoking and increased for triglycerides. Conclusions: In two Norwegian counties, the NCD risk factors showed dynamic patterns during 1974-2002. For blood pressure and serum total cholesterol, the levels showed consistent beneficial changes in all educational subgroups, with a narrowing tendency for educational gradients in men. In women, the educational gradient for smoking increased markedly. Knowledge on midlife trends in the educational gradients of risk factors may help to explain recent and future NCD mortality.

Life course socioeconomic position, alcohol drinking patterns in midlife, and cardiovascular mortality: Analysis of Norwegian population-based health surveys.

BACKGROUND: Socioeconomically disadvantaged groups tend to experience more harm from the same level of exposure to alcohol as advantaged groups. Alcohol has multiple biological effects on the cardiovascular system, both potentially harmful and protective. We investigated whether the diverging relationships between alcohol drinking patterns and cardiovascular disease (CVD) mortality differed by life course socioeconomic position (SEP). METHODS AND FINDINGS: From 3 cohorts (the Counties Studies, the Cohort of Norway, and the Age 40 Program, 1987-2003) containing data from population-based cardiovascular health surveys in Norway, we included participants with self-reported information on alcohol consumption frequency (n = 207,394) and binge drinking episodes (≥5 units per occasion, n = 32,616). We also used data from national registries obtained by linkage. Hazard ratio (HR) with 95% confidence intervals (CIs) for CVD mortality was estimated using Cox models, including alcohol, life course SEP, age, gender, smoking, physical activity, body mass index (BMI), systolic blood pressure, heart rate, triglycerides, diabetes, history of CVD, and family history of coronary heart disease (CHD). Analyses were performed in the overall sample and stratified by high, middle, and low strata of life course SEP. A total of 8,435 CVD deaths occurred during the mean 17 years of follow-up. Compared to infrequent consumption (

Menopausal hormone therapy and colorectal cancer: a linkage between nationwide registries in Norway.

OBJECTIVES: With the present study, we aimed to investigate the association between menopausal hormone therapy (HT) and risk of colorectal cancer (CRC). SETTING: Cohort study based on the linkage of Norwegian population-based registries. PARTICIPANTS: We selected 466822 Norwegian women, aged 55-79, alive and residing in Norway as of 1 January 2004, and we followed them from 2004 to 2008. Each woman contributed person-years at risk as non-user, current user and/or past HT user. OUTCOME MEASURES: The outcome of interest was adenocarcinoma of the colorectal tract, overall, by anatomic site and stage at diagnosis. Incidence rate ratios (RRs) with 95% CIs were estimated by Poisson regression and were used to evaluate the association between HT and CRC incidence. RESULTS: During the median follow-up of 4.8 years, 138 655 (30%) women received HT and 3799 (0.8%) incident CRCs occurred. Current, but not past, use of HT was associated with a lower risk of CRC (RR 0.88; 95% CI 0.80 to 0.98). RRs for localised, regionally advanced and metastatic CRC were 1.13 (95% CI 0.91 to 1.41), 0.81 (95% CI 0.70 to 0.94) and 0.79 (95% CI 0.62 to 1.00), respectively. RRs for current use of oestrogen therapy (ET) were 0.91 (95% CI 0.80 to 1.04) while RR for current use of combined oestrogen-progestin therapy (EPT) was 0.85 (95% CI 0.70 to 1.03), as compared with no use of HT. The same figures for ET and EPT in oral formulations were 0.83 (95% CI 0.68 to 1.03) and 0.86 (95% CI 0.71 to 1.05), respectively. CONCLUSIONS: In our nationwide cohort study, HT use lowered the risk of CRC, specifically the most advanced CRC.

Menopausal hormone therapy and risk of melanoma: Do estrogens and progestins have a different role?

The association between use of menopausal hormone therapy (HT) and occurrence of skin malignant melanoma (SMM) is controversial. We investigated the issue in a nationwide cohort of 684,696 Norwegian women, aged 45-79 years, followed from 2004 to 2008. The study was based on linkage between Norwegian population registries. Multivariable Poisson regression models were used to estimate the effect of HT use, different HT types, routes of administration and doses of estrogen and progestin on the risk of SMM. During the median follow-up of 4.8 years, 178,307 (26%) women used HT, and 1,476 incident SMM cases were identified. Current use of HT was associated with increased risk of SMM (rate ratios (RR) = 1.19; 95% confidence interval (CI) 1.03-1.37). Plain estrogen therapy was associated with an increased risk of SMM (RR 1.45; 95% CI 1.21-1.73), both for oral (RR 1.45; 95% CI 1.09-1.93) and vaginal (RR 1.44; 95% CI 1.14-1.84) formulations, while combined estrogen and progestin therapy (EPT) was not (RR 0.91; 95% CI 0.70-1.19). We performed a dose-response analysis of estrogen and progestin in women using tablets, and found that use of estrogens was associated with increased risk (RR 1.24; 95% CI 1.00-1.53 per 1 mg/day) and use of progestins with decreased risk (RR 0.71; 95% CI 0.57-0.89 per 10 mg/month) of SMM. In conclusion, estrogens were associated with increased risk of SMM, while combinations of estrogens and progestins were not. Our results suggest that estrogens and progestins might affect the risk of SMM in opposite ways.

The educational gradient in cardiovascular risk factors: impact of shared family factors in 228,346 Norwegian siblings.

BACKGROUND: Various indicators of childhood socioeconomic position have been related to cardiovascular disease (CVD) risk in adulthood. We investigated the impact of shared family factors on the educational gradient in midlife CVD risk factors by assessing within sibling similarities in the gradient using a discordant sibling design. METHODS: Norwegian health survey data (1980-2003) was linked to educational and generational data. Participants with a full sibling in the health surveys (228,346 individuals in 98,046 sibships) were included. Associations between attained educational level (7-9 years, 10-11 years, 12 years, 13-16 years, or >16 years) and CVD risk factor levels in the study population was compared with the corresponding associations within siblings. RESULTS: Educational gradients in risk factors were attenuated when factors shared by siblings was taken into account: A one category lower educational level was associated with 0.7 (95% confidence interval 0.6 to 0.8) mm Hg higher systolic blood pressure (27% attenuation), 0.4 (0.4 to 0.5) mmHg higher diastolic blood pressure (30%), 1.0 (1.0 to 1.1) more beats per minute higher heart rate (21%), 0.07 (0.06 to 0.07) mmol/l higher serum total cholesterol (32%), 0.2 (0.2 to 0.2) higher smoking level (5 categories) (30%), 0.15 (0.13 to 0.17) kg/m2 higher BMI (43%), and 0.2 (0.2 to 0.2) cm lower height (52%). Attenuation increased with shorter age-difference between siblings. CONCLUSION: About one third of the educational gradients in modifiable CVD risk factors may be explained by factors that siblings share. This implies that childhood environment is important for the prevention of CVD.

Validity of self-reported myocardial infarction and stroke in regions with Sami and Norwegian populations: the SAMINOR 1 Survey and the CVDNOR project.

OBJECTIVE: Updated knowledge on the validity of self-reported myocardial infarction (SMI) and self-reported stroke (SRS) is needed in Norway. Our objective was to compare questionnaire data and hospital discharge data from regions with Sami and Norwegian populations to assess the validity of these outcomes by ethnicity, sex, age and education. DESIGN: Validation study using cross-sectional questionnaire data and hospital discharge data from all Norwegian somatic hospitals. PARTICIPANTS AND SETTING: should read '16 865 men and women aged 30 and 36­79 years participated in the first survey of the Population-based Study on Health and Living Conditions in Sami and NorwegianPopulations (the SAMINOR 1 Survey) in 2003­2004. Information on SMI and SRS was available from self-administered questionnaires for 15 005 and 15 088 of these participants, respectively. We compared this information with hospital discharge data from 1994 until SAMINOR 1 Survey attendance. PRIMARY AND SECONDARY OUTCOMES: Sensitivity, specificity, positive predictive value (PPV), negative predictive value and κ. RESULTS: The sensitivity and PPV of SMI were 90.1% and 78.9%, respectively; the PPV increased to 93.1% when all ischaemic heart disease (IHD) diagnoses were included. The SMI prevalence estimate was 2.3% and hospital-based 2.0%. The sensitivity and PPV of SRS were 81.1% and 64.3%, respectively. The SRS prevalence estimate was 1.5% and hospitalisation-based 1.2%. Moderate to no variation was observed in validity according to ethnicity, sex, age and education. CONCLUSIONS: The sensitivity and PPV of SMI were high and moderate, respectively; for SRS, both of these measures were moderate. Our results show that SMI from the SAMINOR 1 Survey may be used in aetiological/analytical studies in this population due to a high IHD-specific PPV. The SAMINOR 1 questionnaire may also be used to estimate the prevalence of acute myocardial infarction and acute stroke.

Postmenopausal Hormone Therapy and Breast Cancer Prognostic Characteristics: A Linkage between Nationwide Registries.

BACKGROUND: The effects of use of different types of hormone therapy on breast cancer risk according to prognostic factors are largely unknown. METHODS: We linked data from the Norwegian Prescription Database and the Cancer Registry of Norway during 2004 to 2009 on all women ages 45 to 79 years (N = 686,614). We estimated rate ratios and 95% confidence intervals for breast cancer in relation to hormone therapy using Poisson regression. RESULTS: During an average 4.8 years of follow-up, 7,910 invasive breast cancers were diagnosed. Compared with nonusers of hormone therapy, users of estradiol and tibolone were more likely to be diagnosed with grade I, lymph node-negative, and estrogen receptor-positive (ER+)/progesterone receptor-positive (PR+) tumors. However, compared with nonusers, users of the most common estrogen and progestin combinations [estradiol-norethisterone acetate (NETA) preparations (Kliogest, Activelle or Trisekvens)] were at a 4- to 5-fold elevated risk of grade I tumors, 3-fold elevated risk of lymph node-negative tumors, and 3- to 4-fold elevated risk of ER+/PR+ tumors. Importantly, estradiol-NETA users were also at a 2- to 3-fold increased risk of medium differentiated (grade II) tumors and tumors with lymph node involvement. CONCLUSIONS: Use of oral estradiol, tibolone, and estradiol-NETA predominantly increases the risk of breast cancer with favorable prognosis characteristics. However, use of estradiol-NETA preparations also increases the risk of breast cancers with less favorable characteristics. IMPACT: The hormone therapy preparations most commonly used in the Nordic countries are associated with both breast cancers with good and less favorable prognosis characteristics. Cancer Epidemiol Biomarkers Prev; 25(11); 1464-73. ©2016 AACR.

Physical activity, resting heart rate, and atrial fibrillation: the Tromsø Study.

AIMS: The objective was to examine the association of physical activity and resting heart rate (RHR) with hospital-diagnosed atrial fibrillation (AF) in a Norwegian cohort. METHODS AND RESULTS: This prospective study included 20 484 adults (50.3% men) who participated in the third Tromsø Study survey in 1986-87. At baseline, physical activity was assessed by a validated questionnaire, and RHR was objectively measured. Participants were followed from baseline through 2010 with respect to incident cases of hospital-diagnosed AF documented on an electrocardiogram. During a mean follow-up period of 20 years (409 045 person-years), 750 participants (70.5% men) were diagnosed with AF. Compared with the low physical activity group, moderately active individuals had a 19% lower risk of any AF [adjusted hazard ratio (HR) 0.81, 95% confidence interval (CI) 0.68-0.97], whereas highly active had similar risk of AF. Vigorously active individuals showed a non-significantly higher risk of AF (adjusted HR 1.37, 95% CI 0.77-2.43). Risk of AF increased with decreasing RHR (adjusted HR 0.92, 95% CI 0.86-0.98 for each 10 b.p.m. increase in RHR), and RHR < 50 b.p.m. was a risk factor for AF (P < 0.05). CONCLUSION: In this prospective cohort study, leisure time physical activity was associated with AF in a J-shaped pattern. Moderate physical activity was associated with a reduced risk of AF, whereas higher activity levels attenuated the benefits of moderate activity. Low RHR was a risk factor for AF. Our results support the hypothesis that moderate and vigorous physical activity may affect AF risk via different pathophysiological mechanisms.

Postmenopausal hormone therapy and the risk of breast cancer in Norway.

There is convincing evidence that combined estrogen-progestin therapy (EPT) increases the risk of breast cancer. However, the effect of different formulations, preparations and routes of administration is largely unknown. Estrogen only-therapy (ET) is, in general, not associated or weakly associated with breast cancer risk. We investigated the effect of hormone therapy (HT) with ET, EPT, and tibolone on risk of invasive breast cancer. Information on HT use was obtained from the Norwegian Prescription Database, and breast cancer incidence from the Cancer Registry of Norway. Poisson regression was used to estimate the incidence rate ratios (RR). We analyzed data from 686,614 Norwegian women, aged 45-79 years in January 2004, followed until December 2008, of whom 178,383 (26%) were prescribed HT. During the average 4.8 years of follow-up, 7,910 invasive breast cancers were registered. Compared with nonusers, current users of estradiol-norethisterone acetate (NETA)(EPT) had a RR of 2.74 (95% CI: 2.55-2.95). Users of the high dose estradiol-NETA formulation Kliogest(®) had a RR of 3.26 (95% CI: 2.84-3.73), while users of the low dose Activelle(®) had a RR of 2.76 (95% CI: 2.51-3.04). Current users of tibolone had a RR of 1.91 (95% CI: 1.61-2.28). Current users of ET with oral or transdermal estradiol had a RR of 1.40 (95% CI: 1.16-1.68), and 1.40 (95% CI: 1.00-1.95), respectively. The increased incidence rates approximates one extra invasive breast cancer case diagnosed for every 259 women using estradiol-NETA for one year, and one extra case for every 475 women using tibolone. In conclusion, use of estradiol-NETA and tibolone preparations is associated with an increased breast cancer risk.

Physical activity, symptoms, medication and subjective health among veteran endurance athletes with atrial fibrillation.

BACKGROUND: Atrial fibrillation (AF) is highly prevalent, but has not previously been characterized in detail in veteran athletes. We aimed to describe physical activity (PA), symptoms, medication and subjective health in relation to AF subtype and co-morbidity among veteran cross-country skiers with AF. METHODS: In total, 4952 Norwegian men and women aged 53-85 years took part in this cohort study, 2626 veteran cross-country skiers and 2326 from the general population. PA, endurance exercise, functional capacity, co-morbidity, drug use and subjective health were self-reported by questionnaires. AF was self-reported and confirmed by electrocardiograms in a medical record review. RESULTS: The prevalence of self-reported AF among veteran skiers was 12.3%. AF was confirmed in 140 skiers and 118 individuals from the general population. Among skiers with AF (mean age 69 years), 52% had paroxysmal, 23% persistent and 24% permanent AF. AF was associated with poor subjective health, but 89% of the veteran skiers were physically active and 64% engaged in regular endurance exercise after the onset of AF. While 59% had experienced palpitations during the past year, 32% reported reduced functional capacity. Two out of three with AF and a CHA2DS2-VASc score ≥ 2 used oral anticoagulants (OACs). CONCLUSIONS: AF was associated with poor subjective health, but the vast majority of veteran athletes engaged in regular PA and endurance exercise also after the onset of AF. This is important, as PA and exercise might reduce AF symptoms, mortality and morbidity. Many veteran skiers with AF were not optimally treated with OACs.

Do repeated risk factor measurements influence the impact of education on cardiovascular mortality?

OBJECTIVE: It has been questioned if the excess cardiovascular disease (CVD) mortality by lower educational level can be fully explained by conventional modifiable CVD risk factors. Our objective was to examine whether repeated measures over time of risk factors (smoking, physical inactivity, blood pressure, total cholesterol and body mass index) explain more of the socioeconomic gradient in CVD mortality than if they are measured only once. METHODS: A cohort of 34 884 men and women attended all three screenings (1974-1978, 1977-1983 and 1985-1988) in the Norwegian Counties Study and were followed for CVD mortality through 2009 by linkage to the Norwegian Cause of Death Registry. RESULTS: Age-adjusted and sex-adjusted HR of CVD mortality was 2.32 (95% CI 1.93 to 2.80) for basic relative to tertiary educated individuals. The HR was attenuated by 48% (HR 1.54 (1.28 to 1.87)) when adjusted for CVD risk factors measured at baseline and by 56% (HR 1.45 (1.20 to 1.75)) when two repeated measurements ascertained 5 years apart were added to the model. Similarly, absolute risk difference in CVD mortality by education was attenuated by 62% when adjusted for baseline and by 72% when adjusted for repeated measurements of risk factors. CONCLUSIONS: In this cohort, repeated measurements of risk factors seemed to explain more of the educational gradient in CVD mortality. This suggests that a substantial part of the excess CVD mortality among those with lower education might be explained by conventional risk factors.

Family history of premature myocardial infarction, life course socioeconomic position and coronary heart disease mortality--A Cohort of Norway (CONOR) study.

BACKGROUND/OBJECTIVES: To investigate self-reported family history (FH) of premature myocardial infarction (MI) in first-degree relatives as a risk factor for coronary heart disease (CHD) mortality, and assess whether any observed effect could be explained by current or life course socioeconomic position. METHODS: 130,066 participants from Cohort of Norway were examined during 1994-2003. A subgroup (n=84,631) had additional life course socioeconomic data. Using Cox proportional hazard analyses, we calculated hazard ratios (HR) for CHD mortality, assessed by linkages to the Norwegian Cause of Death Registry through 2009. For subgroup analyses, we created an index of life course socioeconomic position, and assessed its role as a potential confounder in the association of FH with CHD. RESULTS: For men, MI in parents and siblings were both a significant risk factor for CHD mortality after adjusting for established risk factors and current socioeconomic conditions; the highest risk was with MI in siblings (HR: 1.44 [1.19-1.75]). For women, FH constituted significant risk after similar adjustment only for those with MI in parents plus siblings (HR: 1.78 [1.16-2.73]). Adjusting for current and life course socioeconomic conditions only marginally lowered the estimates, and those with FH did not have worse life course socioeconomic position than those without. CONCLUSIONS: FH of premature MI is an independent risk factor for CHD mortality that differs in magnitude of effect by the sex of the index person and type of familial relationship. Life course socioeconomic position has little impact on the association between FH and CHD, suggesting the effect is not confounded by this.

Road traffic noise and markers of obesity - a population-based study.

BACKGROUND: Noise has been found to be associated with endocrine changes and cardiovascular disease. Increased cortisol levels and chronic sleep problems due to noise may increase the risk of obesity. OBJECTIVES: We investigated the relationship between road traffic noise and obesity markers. Furthermore, we explored the modifying role of noise sensitivity, noise annoyance, and sleep disturbances. METHODS: We used data from a population-based study, HUBRO (N=15,085), and its follow-up study HELMILO (N=8410) conducted in Oslo, Norway. Measurements were used to define body mass index (BMI), waist circumference (WC), waist-hip ratio (WHR), and these binary outcomes: BMI≥30kg/m(2), WC≥102cm (men)/88cm (women), and WHR≥0.90 (men)/0.85 (women). Modelled levels of road traffic noise (Lden) were assigned to each participant's home address. Linear and logistic regression models were used to examine the associations. RESULTS: The results indicated no significant associations between road traffic noise and obesity markers in the total populations. However, in highly noise sensitive women (n=1106) a 10dB increase in noise level was associated with a slope (=beta) of 1.02 (95% confidence interval (CI): 1.01, 1.03) for BMI, 1.01 (CI: 1.00, 1.02) for WC, and an odds ratio (OR) of 1.24 (CI: 1.01, 1.53) for WHR ≥0.85. The associations appeared weaker in highly noise sensitive men. We found no effect modification of noise annoyance or sleep disturbances. In a sub-population with bedroom facing a road, the associations increased in men (e.g. an OR of 1.25 (CI: 0.88, 1.78) for BMI ≥30kg/m(2)), but not in women. Among long-term residents the associations increased for BMI ≥30kg/m(2) (OR of 1.07 (CI: 0.93, 1.24) in men and 1.10 (CI: 0.97, 1.26) in women), but not for the other outcomes. CONCLUSION: In an adult urban Scandinavian population, road traffic noise was positively associated with obesity markers among highly noise sensitive women. The associations appeared stronger among men with bedroom facing a street, representing a population with more accurately assigned exposure.