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Background Benefits of elevated high-density lipoprotein cholesterol (HDL-C) levels are challenged by reports demonstrating U-shaped relations between HDL-C levels and all-cause mortality; the association with cause-specific mortality is less studied. Methods A total of 344 556 individuals (20–79 years, 52 % women) recruited from population-based health screening during 1985–2003 were followed until the end of 2018 for all-cause and cause-specific mortality by serum HDL-C level at inclusion of 99 mg/dl (< 0.78, 0.78–1.01, 1.04–1.27, 1.30–1.53, 1.55–1.79, 1.81–2.04, 2.07–2.31, 2.33–2.56, >2.56 mmol/L). Hazard ratios (HRs) were adjusted for sex, age, calendar period, smoking, total cholesterol, triglycerides, systolic blood pressure, physical activity, educational length, body mass index and ill health. Results During a mean follow-up of 22 years, 69 505 individuals died. There were U-shaped associations between HDL-C levels and all-cause, cancer and non-cardiovascular disease/non-cancer mortality (non-CVD/non-cancer), whereas for CVD there was increased risk of death only at lower levels. With HDL-C stratum 50–59 mg/dl (1.30–1.53 mmol/L) as reference, HRs [95% confidence intervals (CIs)] for levels >99 mg/dl (>2.56 mmol/L) were 1.32 (1.21–1.43), 1.05 (0.89–1.24), 1.26 (1.09–1.46) and 1.68 (1.48–1.90) for all–cause, CVD, cancer and non–CVD/non–cancer mortality, respectively. For HDL-C levels Conclusions Higher HDL-C levels were associated with increased mortality risk of several diseases which also have been associated with heavy drinking, and lower HDL-C levels were associated with increased mortality from IHD, other CVDs, gastric cancer and diabetes.

Background Several studies have shown that women and men with two children have lower mortality than the childless, but there is less certainty about mortality, including CVD mortality, at higher parities and meagre knowledge about factors underlying the parity–mortality relationship. Methods The association between parity and CVD mortality was analyzed by estimating discrete-time hazard models for women and men aged 40–80 in 1975–2015. Register data covering the entire Norwegian population were used, and the models included a larger number of relevant sociodemographic control variables than in many previous studies. To analyze the relationship between parity and seven CVD risk factors, logistic models including the same variables as the mortality models were estimated from the CONOR collection of health surveys, linked to the register data. Results Men (but not women) who had four or more children had higher mortality from CVD than those with two, although this excess mortality was not observed for the heart disease sub-group. Overweight, possibly in part a result of less physical activity, seems to play a role in this. All CVD risk factors except smoking and alcohol may contribute to the relatively high CVD mortality among childless. Conclusions Childbearing is related to a number of well-known CVD risk factors, and becoming a parent or having an additional child is, on the whole, associated with lower—or at least not higher—CVD mortality in Norway. However, for men family sizes beyond three children are associated with increased CVD mortality, with risks of overweight one possible pathway.

Aims Alcohol consumption has been linked to colorectal cancer (CRC) and also to the high-density lipoprotein cholesterol level (HDL-C). HDL-C has been associated with the incidence of CRC. The aim of this study was to investigate the association between self-reported alcohol consumption, HDL-C and incidence of CRC, separately for the two sites. Methods Altogether, 250,010 participants in Norwegian surveys have been followed-up for an average of 18 years with respect to a first-time outcome of colon or rectal cancer. During follow-up, 3023 and 1439 colon and rectal cancers were registered. Results For men, the HR per 1 drink per day was 1.05 with 95% confidence interval (0.98–1.12) for colon and 1.08 (1.02–1.15) for rectal cancer. The corresponding figures for women were 1.03 (0.97–1.10) and 1.05 (1.00–1.10). There was a positive association between alcohol consumption and HDL-C. HDL-C was inversely associated with colon cancer in men (0.74 (0.62–0.89) per 1 mmol/l) and positively associated with rectal cancer, although not statistically significant (1.15 (0.92–1.44). A robust regression that assigned weights to each observation and exclusion of weights ≤ 0.1 increased the HRs per 1 drink per day and decreased the HR per 1 mmol/l for colon cancer. The associations with rectal cancer remained unchanged. Conclusion Our results support a positive association between alcohol consumption and colon and rectal cancer, most pronounced for rectal cancer. Considering the positive relation between alcohol consumption and HDL-C, the inverse association between HDL-C and colon cancer in men remains unsettled., Short Summary: This study showed that the relation between alcohol consumption is somewhat stronger for rectal cancer than for colon cancer. Although there is a positive relation between levels of HDL and alcohol consumption, the relation between HDL and colon cancer in men is inverse. This finding warrants further studies.

AimsWhile investigators have typically quantified the health risk of passive smoking by utilising self-reported exposure, prospective studies with objective ascertainment, which are less liable to measurement error, are rare. Using data pooling, we examined the relation of a biochemical assessment of passive smoking, salivary cotinine, with mortality from a range of causes.MethodsWe combined data from twelve cohort studies from England and Scotland initiated between 1998 and 2008. Study members were linked to national death registries. A total of 36 584 men and women aged 16 to 85 years of age reported that they were non-smoking at baseline, provided baseline salivary cotinine, and consented to mortality record linkage.ResultsA mean of 8.1 years of mortality follow-up of 36 584 non-smokers (16 792 men and 19 792 women) gave rise to 2367 deaths (775 from cardiovascular disease, 780 from all cancers, and 289 from smoking-related cancers). After controlling for a range of covariates, a 10 ng/ml increase in salivary cotinine level was related to an elevated risk of total (hazard ratios; 95% confidence interval: 1.46; 1.16, 1.83), cardiovascular (1.41; 0.96, 2.09), cancer (1.49; 1.00, 2.22) and smoking-related cancer mortality (2.92; 1.77, 4.83).ConclusionsPassive smoking assessed biomedically was a risk factor for a range of health outcomes known to be causally linked to active smoking.

Aim The aim of this study was to investigate whether the coffee brewing method is associated with any death and cardiovascular mortality, beyond the contribution from major cardiovascular risk factors. Methods and results Altogether, 508,747 men and women aged 20–79 participating in Norwegian cardiovascular surveys were followed for an average of 20 years with respect to cause-specific death. The number of deaths was 46,341 for any cause, 12,621 for cardiovascular disease (CVD), 6202 for ischemic heart disease (IHD), and 2894 for stroke. The multivariate adjusted hazard ratios (HRs) for any death for men with no coffee consumption as reference were 0.85 (082–0.90) for filtered brew, 0.84 (0.79–0.89) for both brews, and 0.96 (0.91–1.01) for unfiltered brew. For women, the corresponding figures were 0.85 (0.81–0.90), 0.79 (0.73–0.85), and 0.91 (0.86–0.96) for filtered, both brews, and unfiltered brew, respectively. For CVD, the figures were 0.88 (0.81–0.96), 0.93 (0.83–1.04), and 0.97 (0.89–1.07) in men, and 0.80 (0.71–0.89), 0.72 (0.61–0.85), and 0.83 (0.74–0.93) in women. Stratification by age raised the HRs for ages ≥60 years. The HR for CVD between unfiltered brew and no coffee was 1.19 (1.00–1.41) for men and 0.98 (0.82–1.15) for women in this age group. The HRs for CVD and IHD were raised when omitting total cholesterol from the model, and most pronounced in those drinking ≥9 of unfiltered coffee, per day where they were raised by 9% for IHD mortality. Conclusion Unfiltered brew was associated with higher mortality than filtered brew, and filtered brew was associated with lower mortality than no coffee consumption.

Surprisingly few attempts have been made to quantify the simultaneous contribution of well-established risk factors to CVD mortality differences between countries. We aimed to develop and critically appraise an approach to doing so, applying it to the substantial CVD mortality gap between Russia and Norway using survey data in three cities and mortality risks from the Emerging Risk Factor Collaboration. We estimated the absolute and relative differences in CVD mortality at ages 40–69 years between countries attributable to the risk factors, under the counterfactual that the age- and sex-specific risk factor profile in Russia was as in Norway, and vice-versa. Under the counterfactual that Russia had the Norwegian risk factor profile, the absolute age-standardized CVD mortality gap would decline by 33.3% (95% CI 25.1–40.1) among men and 22.1% (10.4–31.3) among women. In relative terms, the mortality rate ratio (Russia/Norway) would decline from 9–10 to 7–8. Under the counterfactual that Norway had the Russian risk factor profile, the mortality gap reduced less. Well-established CVD risk factors account for a third of the male and around a quarter of the female CVD mortality gap between Russia and Norway. However, these estimates are based on widely held epidemiological assumptions that deserve further scrutiny.

Background and Aims The time post-release from prison involves elevated mortality, especially overdose deaths. Variations in overdose mortality both by time since release from prison and time of release has not been investigated sufficiently. Our aims were to estimate and compare overdose death rates at time intervals after prison release and to estimate the effect on overdose death rates over calendar time. Design, Setting, Participants, Measurements This 15-year cohort study includes all individuals (n = 91 090) released from prison (1 January 2000 to 31 December 2014) obtained from the Norwegian prison registry, linked to the Norwegian Cause of Death Registry (2000–14). All-cause and cause-specific mortality were examined during different time-periods following release: first week, second week, 3–4 weeks and 2–6 months, and by three different time intervals of release. We calculated crude mortality rates (CMRs) per 1000 person-years and estimated incidence rate ratios (IRR) by Poisson regression analysis adjusting for time intervals after prison release, release periods and time spent in prison. Findings Overdose deaths accounted for 85% (n = 123) of all deaths during the first week following release (n = 145), with a peak during the 2 days immediately following release. Compared with week 1, the risk of overdose death was more than halved during week 2 [IRR = 0.43; 95% confidence interval (CI) = 0.31–0.59] and reduced to one-fifth in weeks 3–4 (IRR = 0.22; 95% CI = 0.16–0.31). The risk of overdose mortality during the first 6 months post-release was almost twofold higher in 2000–04 compared with 2005–09 (IRR = 0.53; 95% CI = 0.43–0.65) and 2010–14 (IRR = 0.47; 95% CI = 0.37–0.59). The risk of overdose death was highest for those incarcerated for 3–12 months compared with those who were incarcerated for shorter or longer periods, and recidivism was associated with risk of overdose death. Conclusions There is an elevated risk of death from drug overdose among individuals released from Norwegian prisons, peaking in the first week. The risk has reduced since 2000–04, but is greatest for those serving 3–12 months compared with shorter or longer periods.

Background Guidelines for the prevention of cardiovascular disease recommend the estimation of an individual's total risk. We have developed a new model for the prediction of the 10-year risk of incident acute myocardial infarction or cerebral stroke based on Norwegian data, NORRISK 2. Design The model was based on 10-year follow-up of a large population-based cohort (CONOR) through linkage to the CVDNOR project, a database of cardiovascular disease hospital discharge diagnoses and mortality in Norway in 1994-2009. Methods We used the Fine and Gray regression model to estimate the 10-year risk adjusting for competing risk. The model population consisted of participants in 1994-1999 and the external validation population of participants in 2000-2003. We validated the model by area under the receiver operating characteristic curves, calibration plots and analyses of sensitivity and specificity. Results The model population consisted of 31,445 men and 35,267 women aged 40-79 years with 3658 endpoints in men and 2459 in women. The external validation population consisted of 19,980 men and 19,309 women, of whom 1858 men and 874 women had an endpoint during follow-up. The area under the curve was 0.79 (0.79-0.80) in men and 0.84 (0.83-0.85) in women in the model population and was slightly lower in the external validation population. Calibration plots showed good agreement between observed and predicted risk. The sum of sensitivity and specificity was greatest around the suggested risk thresholds. Conclusion The NORRISK 2 model showed good validity in an external dataset and will be a valuable tool to guide decisions about preventive interventions in people without known previous cardiovascular disease.

Purpose To study the association between coffee and alcoholic beverage consumption and alcoholic liver disease mortality. Methods In total, 219,279 men and women aged 30–67 years attended cardiovascular screening in Norway from 1994 to 2003. Linkage to the Cause of Death Registry identified 93 deaths from alcoholic liver disease. Coffee consumption was categorized into four levels: 0, 1–4, 5–8, and greater than or equal to 9 cups/d and alcohol consumption as 0, greater than 0 to less than 1.0, 1.0 to less than 2.0, and greater than or equal to 2.0 units/d, for beer, wine, liquor, and total alcohol consumption. Results The hazard ratios per one category of consumption were 2.06 (95% confidence interval 1.62–2.61), 0.68 (0.46–1.00), and 2.54 (1.92–3.36) for beer, wine, and liquor, respectively. Stratification at 5 cups/d (the mean) revealed a stronger association between alcohol consumption and alcoholic liver disease at less than 5 versus 5 or more cups/d. With less than 5 cups/d, 0 alcohol units/d as reference, the hazard ratio reached to 25.5 (9.2–70.5) for greater than or equal to 2 units/d, whereas with greater than or equal to 5 cups/d, it reached 5.8 (1.9–17.9) for greater than or equal to 2 units/d. A test for interaction was significant (P = .01). Conclusions Coffee and wine consumption were inversely associated with alcoholic liver disease death. Total alcohol consumption was adversely associated with alcoholic liver disease mortality and the strength of the association varied with the level of coffee consumption.

OBJECTIVE To quantify concentrations of cartilage oligomeric matrix protein (COMP) and fibromodulin in synovial fluid from the tarsocrural joints (TCJs) of horses with osteochondritis dissecans (OCD) of the distal intermediate ridge of the tibia and determine whether concentrations would change following arthroscopic removal of osteochondral fragments. ANIMALS 115 client-owned horses with OCD of the TCJ and 29 control horses euthanized for unrelated reasons. PROCEDURES COMP and fibromodulin concentrations were measured in synovial fluid from the TCJs of the affected horses before and after osteochondral fragments were removed arthroscopically and in synovial fluid from the TCJs of the control horses after euthanasia. Synovial biopsy specimens from the TCJs of affected and control horses were examined histologically for evidence of inflammation. RESULTS Synovial fluid COMP and fibromodulin concentrations prior to surgery in horses with OCD were not significantly different from concentrations in control horses. Fibromodulin, but not COMP, concentration in horses with OCD was significantly decreased after surgery, compared with the concentration before surgery. Fibromodulin concentration was significantly correlated with joint effusion score but not with lameness score or results of a flexion test and was correlated with histologic score for number of synoviocytes on the surface of the synovium but not with score for degree of infiltration of inflammatory cells in the synovium. Synovial fluid COMP concentration was not significantly correlated with clinical or histologic findings. CONCLUSIONS AND CLINICAL RELEVANCE Results suggested that fibromodulin, but not COMP, could potentially be a biomarker of joint inflammation in horses with OCD of the TCJ.

We tested whether teetotalism explains the upturn in cardiovascular risk for non-drinkers and whether wine is a more favorable alcohol type. We studied 115,592 men and women aged 40–44 years who participated in the age 40 program in Norway in 1994–1999 and were followed for an average of 16 years with 550 cardiovascular deaths. Self-reported number of glasses of beer, wine and spirits during 14 days was transformed to alcohol units/day. One unit is approximately 8 grams of pure alcohol. The mean and median number of alcohol units/day were 0.70 and 0.46. Teetotallers had higher risk of dying from cardiovascular disease than alcohol consumers, multivariate adjusted hazard ratio (95% CI) 1.97 (1.52–2.56). The use of alcohol-related deaths as endpoint substantiated a selection of previous alcohol users to the teetotal group. Without teetotallers there was no association between alcohol consumption and cardiovascular disease mortality. However, the multivariate adjusted hazard ratio per one unit/day of wine was 0.76 (0.58–0.99). The corresponding figures for beer and spirits were 1.04 (0.94–1.15) and 0.98 (0.75–1.29). The upturn in risk for non-drinkers could be explained by a higher risk for teetotallers who likely included previous alcohol users or teetotalers who started to drink during follow-up. Wine gave the most favorable risk estimates.

Background: There is insufficient epidemiological evidence on the relationship between type of coffee and the risk of prostate cancer. Methods: The risk of prostate cancer by use of boiled vs not boiled coffee were assessed in a prospective study of 224,234 men 20–69 years. 5740 incident prostate cancers were identified. Results: With no coffee as reference group the hazard ratios of

The time post-release from prison involves elevated mortality, especially overdose deaths. Variations in overdose mortality both by time since release from prison and time of release has not been investigated sufficiently. Our aims were to estimate and compare overdose death rates at time intervals after prison release and to estimate the effect on overdose death rates over calendar time.This 15-year cohort study includes all individuals (n = 91 090) released from prison (1 January 2000 to 31 December 2014) obtained from the Norwegian prison registry, linked to the Norwegian Cause of Death Registry (2000-14). All-cause and cause-specific mortality were examined during different time-periods following release: first week, second week, 3-4 weeks and 2-6 months, and by three different time intervals of release. We calculated crude mortality rates (CMRs) per 1000 person-years and estimated incidence rate ratios (IRR) by Poisson regression analysis adjusting for time intervals after prison release, release periods and time spent in prison.Overdose deaths accounted for 85% (n = 123) of all deaths during the first week following release (n = 145), with a peak during the 2 days immediately following release. Compared with week 1, the risk of overdose death was more than halved during week 2 [IRR = 0.43; 95% confidence interval (CI) = 0.31-0.59] and reduced to one-fifth in weeks 3-4 (IRR = 0.22; 95% CI = 0.16-0.31). The risk of overdose mortality during the first 6 months post-release was almost twofold higher in 2000-04 compared with 2005-09 (IRR = 0.53; 95% CI = 0.43-0.65) and 2010-14 (IRR = 0.47; 95% CI = 0.37-0.59). The risk of overdose death was highest for those incarcerated for 3-12 months compared with those who were incarcerated for shorter or longer periods, and recidivism was associated with risk of overdose death.There is an elevated risk of death from drug overdose among individuals released from Norwegian prisons, peaking in the first week. The risk has reduced since 2000-04, but is greatest for those serving 3-12 months compared with shorter or longer periods.

Background: While hypertension still is a major health problem worldwide, some studies have indicated that the blood pressure level has decreased in some populations. This population based cohort study aims at analysing blood pressure changes in a large Norwegian population over a 22 year period. Methods: Data is acquired from three comprehensive health surveys of the HUNT Study conducted from 1984–86 to 2006–08. All citizens of Nord-Trøndelag County, Norway, >20 years were invited: 74,549 individuals participated in 1984–86; 64,523 in 1995–97; and 43,905 in 2006–08. Results: Both systolic and diastolic blood pressure levels decreased substantially from mid 1980s to mid 2000s, with the most pronounced decrease from 1995–97 to 2006–08 (from 136.0/78.9 to 128.3/70.9 mmHg in women and from 140.1/82.1 to 133.7/76.5 mmHg in men). Although the use of blood pressure lowering medication increased, there was a considerable decrease even in those who reported never use of medication (mean decrease 6.8/7.2 mmHg in women and 6.3/5.3 mmHg in men), and the decrease was most pronounced in the elderly (mean decrease 16.1/12.4 mmHg in women and 14.7/10.4 mmHg in men aged 80+). Mean heart rate, total cholesterol and daily smoking decreased, self-reported hard physical activity increased, while body weight and the prevalence of diabetes increased during the same period. Conclusions: The BP decrease might seem paradoxically, as body weight and prevalence of diabetes increased during the same period. Salt consumption might have decreased, but no salt data is available. The parallel decrease in mean heart rate might indicate reduction in the white-coat phenomenon, or increased use of beta blockers or calcium channel blockers for other diagnosis than hypertension. Additionally, the data could support the “healthy obese” hypothesis, i.e., that subgroups in the population can sustain obesity without serious health consequences. © 2016 Holmen et al. Open Access. This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

Estimation of cardiovascular disease risk, using SCORE (Systematic COronary Risk Evaluation) is recommended by European guidelines on cardiovascular disease prevention. Risk estimation is inaccurate in older people. We hypothesized that this may be due to the assumption, inherent in current risk estimation systems, that risk factors function similarly in all age groups. We aimed to derive and validate a risk estimation function, SCORE O.P., solely from data from individuals aged 65 years and older.20,704 men and 20,121 women, aged 65 and over and without pre-existing coronary disease, from four representative, prospective studies of the general population were included. These were Italian, Belgian and Danish studies (from original SCORE dataset) and the CONOR (Cohort of Norway) study. The variables which remained statistically significant in Cox proportional hazards model and were included in the SCORE O.P. model were: age, total cholesterol, high-density lipoprotein cholesterol, systolic blood pressure, smoking status and diabetes. SCORE O.P. showed good discrimination; area under receiver operator characteristic curve (AUROC) 0.74 (95% confidence interval: 0.73 to 0.75). Calibration was also reasonable, Hosmer-Lemeshow goodness of fit test: 17.16 (men), 22.70 (women). Compared with the original SCORE function extrapolated to the ≥65 years age group discrimination improved, p = 0.05 (men), p 0.001 (women). Simple risk charts were constructed. On simulated external validation, performed using 10-fold cross validation, AUROC was 0.74 and predicted/observed ratio was 1.02.SCORE O.P. provides improved accuracy in risk estimation in older people and may reduce excessive use of medication in this vulnerable population.