To answer this, we need to understand both determinants of declines of rates in CVD in general in the population and trends in the patterning of CVD risk between social groups. Since the 1970 s the ...trends in CVD in high-income countries have most likely been driven by declines in important behavioral risk factors (such as smoking, physical inactivity, unhealthy diet and excessive alcohol use), physiological risk factors (such as blood pressure and cholesterol both of which are partly determined by healthy behavior) and pharmacological treatments for hypertension and dyslipidemia 4. A key question when trying to relate general trend rates in CVD to changes in the social environment is to what extent social inequalities in incident cases of CVD are mediated by established cardiovascular risk factors or if there are additional factors to look for 5. ...there is a question if general preventive measures lead to increased inequalities or not 10. Because socially deprived people experience more of the CVD burden, preventive measures that reach everyone will in principle both lead to decreased mortality rates and decreased inequalities – if the uptake of these measures is equitable.
Psychotic-like experiences (PLE) have been associated with the subsequent emergence of psychotic disorders as well as several other domains of psychopathology. In this twin study, we estimated the ...genetic and environmental correlations between PLE and 10 personality disorders (PD).
Diagnoses of 10 PDs according to the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) and PLE from the Composite International Diagnostic Interview (CIDI) were retrieved for 2793 young adult twins from the Norwegian Twin Registry. Risk for having a PD and PLEs was modeled using item response theory. Biometric twin models were fitted to estimate the genetic and environmental correlations between PDs and PLEs. Co-twin control analysis was performed to estimate additional within-family risk for PLEs when having a PD.
Phenotypic overlap between PDs and PLEs ranged from 14% to 44% in males and from 11% to 39% in females, with the highest overlap for borderline PD in both sexes. In general, we found higher genetic correlations (r = 0.14-0.72) than environmental correlations (r = 0.06-0.28) between PDs and PLEs. The highest genetic correlations between PLE and PDs were found for borderline (r = 0.72), paranoid (r = 0.56), schizotypal (r = 0.56) and antisocial PD (r = 0.49).
We found that the co-occurrence between PDs and PLE is the best explained by shared genetic determinants, with minor contributions from environmental factors. Interestingly, borderline PD was highly genetically correlated with PLE, warranting molecular genetic studies of this association.
Background
Individuals suffering from schizophrenia have a reduced life expectancy with cardiovascular disease (CVD) as a major contributor. Low educational attainment is associated with ...schizophrenia, as well as with all‐cause and CVD mortality. However, it is unknown to what extent low educational attainment can explain the increased mortality in individuals with schizophrenia.
Aim
Here, we quantify associations between educational attainment and all‐cause and CVD mortality in individuals with schizophrenia, and compare them with the corresponding associations in the general population.
Method
All Norwegian citizens born between January 1, 1925, and December 31, 1959, were followed up from January 1, 1990, to December 31, 2014. The total sample included 1,852,113 individuals, of which 6548 were registered with schizophrenia. We estimated hazard ratios (HR) for all‐cause and CVD mortality with Cox models, in addition to life years lost. Educational attainment for index persons and their parents were included in the models.
Results
In the general population individuals with low educational attainment had higher risk of all‐cause (HR: 1.48 95% CI: 1.47–1.49) and CVD (HR: 1.59 95% CI: 1.57–1.61) mortality. In individuals with schizophrenia these estimates were substantially lower (all‐cause: HR: 1.13 95% CI: 1.05–1.21 and CVD: HR: 1.12 95% CI: 0.98–1.27). Low educational attainment accounted for 3.28 (3.21–3.35) life years lost in males and 2.48 (2.42–2.55) years in females in the general population, but was not significantly associated with life years lost in individuals with schizophrenia. Results were similar for parental educational attainment.
Conclusions
Our results indicate that while individuals with schizophrenia in general have lower educational attainment and higher mortality rates compared with the general population, the association between educational attainment and mortality is smaller in schizophrenia subjects than in the general population.
This study investigated the concentration-response relation between air pollution (nitrogen dioxide and particulate matter pollutants PM10 and PM2.5) and cause-specific mortality. The population ...included all inhabitants of Oslo, Norway, aged 51–90 years on January 1, 1992 (n = 143,842) with follow-up of deaths from 1992 to 1998. An air dispersion model (AirQUIS; Norwegian Institute for Air Research (NILU), Oslo, Norway) was used to estimate levels of exposure in 1992–1995 in all 470 administrative neighborhoods. These data were linked to census, education, and death registries. A consistent effect on all causes of death was found for both sexes and age groups by all indicators of air pollution. The effects appeared to increase at nitrogen dioxide levels higher than 40 μg/m3 in the youngest age group and with a linear effect in the interval 20–60 μg/m3 for the oldest. An effect of all indicators on cardiovascular causes, lung cancer, and chronic obstructive pulmonary disease was also found in both age groups and sexes. The effects were particularly strong for chronic obstructive pulmonary disease, which appeared to have linear effects, whereas cardiovascular causes and lung cancer seemed to have threshold effects. Results show that vulnerable persons with chronic obstructive pulmonary disease and the elderly seem to be susceptible to air pollution at lower levels than the general population.
To investigate the association between subfertility and risk of cardiovascular disease (CVD) outcomes.
Prospective study.
Population-based cohort.
We studied 31,629 women and 17,630 men participating ...in the Trøndelag Health Study.
Self-reported subfertility. As men were not directly asked about fertility, male partners of female participants were identified through linkage to the Medical Birth Registry of Norway and assigned the fertility information obtained from their partners.
The primary outcomes were stroke and coronary heart disease in women and men with and without a history of subfertility. The secondary outcomes were myocardial infarction and angina (subgroups of coronary heart disease) and any CVD (stroke or coronary heart disease). Information on CVD was available by linkage to hospital records. We used Cox proportional hazards models adjusted for age at participation in the Trøndelag Health Study (linear + squared), birth year, smoking history, cohabitation, and education. Cardiometabolic factors were assessed in separate models.
A total of 17% of women and 15% of men reported subfertility. In women, subfertility was modestly associated with an increased risk of stroke (age-adjusted hazard ratio aaHR, 1.19; 95% confidence interval CI, 1.02-1.39; adjusted hazard ratio aHR; 1.18; 95% CI, 1.01-1.37) and coronary heart disease (aaHR, 1.19; 95% CI, 1.06-1.33; aHR, 1.16; 95% CI, 1.03-1.30) compared with fertile women. In men, we observed a weak positive association for stroke (aaHR, 1.11; 95% CI, 0.91-1.34; aHR, 1.10; 95% CI, 0.91-1.33) and a weak inverse association for coronary heart disease (aaHR, 0.92; 95% CI, 0.81-1.05; aHR, 0.93; 95% CI, 0.81-1.06).
We observed modestly increased risks of CVD outcomes in women and some weak associations in men, although with no strong statistical evidence on sex differences. We acknowledge that we were only able to include men linked to pregnancies ending at 12 completed gestational weeks or later, potentially resulting in selection bias and misclassification of history of subfertility in analyses of male partners. Despite the large sample size, our results indicate the need for larger studies to obtain precise results in both sexes and determine whether there are true sex differences.
Individuals with schizophrenia or substance use disorder have a substantially increased mortality compared to the general population. Despite a high and probably increasing prevalence of comorbid ...substance use disorder in people with schizophrenia, the mortality in the comorbid group has been less studied and with contrasting results. We performed a nationwide open cohort study from 2009 to 2015, including all Norwegians aged 20-79 with schizophrenia and/or substance use disorder registered in any specialized health care setting in Norway, a total of 125,744 individuals. There were 12,318 deaths in the cohort, and total, sex-, age- and cause-specific standardized mortality ratios (SMRs) were calculated, comparing the number of deaths in patients with schizophrenia, schizophrenia only, substance use disorder only or a co-occurring diagnosis of schizophrenia and substance use disorder to the number expected if the patients had the age-, sex- and calendar-year specific death rates of the general population. The SMRs were 4.9 (95% CI 4.7-5.1) for all schizophrenia patients, 4.4 (95% CI 4.2-4.6) in patients with schizophrenia without substance use disorder, 6.6 (95% CI 6.5-6.8) in patients with substance use disorder only, and 7.4 (95% CI 7.0-8.2) in patients with both schizophrenia and substance use disorder. The SMRs were elevated in both genders, in all age groups and for all considered causes of death, and most so in the youngest. Approximately 27% of the excess mortality in all patients with schizophrenia was due to the raised mortality in the subgroup with comorbid SUD. The increased mortality in patients with schizophrenia and/or substance use disorder corresponded to more than 10,000 premature deaths, which constituted 84% of all deaths in the cohort. The persistent mortality gap highlights the importance of securing systematic screening and proper access to somatic health care, and a more effective prevention of premature death from external causes in this group.
Despite substantial geographical variation in cardiovascular (CVD) mortality within countries, little is known about whether this variation can be explained by individuals' life course socioeconomic ...position (SEP) or differences in family history of premature CVD deaths. Cox proportional hazards models were used to investigate the association between the county of residence at ages 50–59 and CVD death in Norwegians born between 1940 and 1959 and survived to at least age 60, using national data. Individual life course SEP and family history of premature CVD death reduced the geographical variation in CVD mortality across Norwegian counties, but some significant differences remained. Furthermore, CVD risk varied by residents' migration histories between two counties with distinct CVD and socioeconomic profiles.
•Individual life course SEP and family history of premature CVD death reduced the regional variation of CVD death.•Despite the attenuation, the variation persisted in a few counties with distinct CVD and socioeconomic profiles.•CVD mortality varied by different domestic migration histories in these counties.
The time between early adulthood and midlife is important for obesity development. There is paucity of studies using objectively measured body mass index (BMI) at both time points with full range of ...midlife cardiovascular risk factors. We aimed to investigate the risk of cardiovascular disease (CVD) mortality associated with different levels of objectively measured change in body weight from early adulthood to midlife, and to assess whether risk is primarily explained by midlife cardiovascular risk factors.
Pooled data from Norwegian health surveys (1985-2003), Tuberculosis screenings, Conscript data and the Norwegian Educational database were linked to the Cause of Death Registry. Health survey participants with data on objectively measured weight and height in both early adulthood (18-20 years) and midlife (40-50 years) were included, n = 148,021. Cox regression models were used to assess associations between weight change and CVD mortality.
Total analysis time included 2,841,174 person years. Mean follow-up was 19 (standard deviation 4) years. Participants being normal weight in early adulthood and obese in midlife had a hazard ratio (HR) of CVD mortality of 2.09 (95% CI 1.74-2.50) relative to those who were normal weight at both times. The corresponding HR of those being obese at both times was 5.15 (3.61-7.36). Adjustment for CVD risk factors attenuated these associations. Gaining ≥15 kg between early adulthood and midlife was associated with higher CVD mortality after adjustment for early adulthood weight (HR 1.51 (1.20-1.89)), and for smoking and education (HR 1.63 (1.30-2.04)), however not after adjustment for mediating CVD risk factors.
Obesity both in early adulthood and in midlife was associated with CVD mortality. Weight gain of ≥15 kg from early adulthood to midlife was also associated with CVD mortality, but not after adjustment for mediating CVD risk factors.
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).
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 (<once/month), moderately frequent consumption (2-3 times per week) was associated with a lower risk of CVD mortality (HR = 0.78, 95% CI 0.72, 0.84) overall. HRs for the high, middle, and low strata of SEP were 0.66 (95% CI 0.58, 0.76), 0.87 (95% CI 0.78, 0.97), and 0.79 (95% CI 0.64, 0.98), respectively, compared with infrequent users in each stratum. HRs for effect modification were 1.30 (95% CI 1.10, 1.54, p = 0.002; middle versus high), 1.23 (95% CI 0.96, 1.58, p = 0.10; low versus high), and 0.96 (95% CI 0.76, 1.21, p = 0.73; low versus middle). In the group with data on binge drinking, 2,284 deaths (15 years) from CVDs occurred. In comparison to consumers who did not binge during the past year, HRs among frequent bingers (≥1 time per week) were 1.58 (95% CI 1.31, 1.91) overall, and 1.22 (95% CI 0.84, 1.76), 1.71 (95% CI 1.31, 2.23), and 1.85 (95% CI 1.16, 2.94) in the strata, respectively. HRs for effect modification were 1.36 (95% CI 0.87, 2.13, p = 0.18; middle versus high), 1.63 (95% CI 0.92, 2.91, p = 0.10; low versus high), and 1.32 (95% CI 0.79, 2.20, p = 0.29; low versus middle). A limitation of this study was the use of a single measurement to reflect lifetime alcohol consumption.
Moderately frequent consumers had a lower risk of CVD mortality compared with infrequent consumers, and we observed that this association was more pronounced among participants with higher SEP throughout their life course. Frequent binge drinking was associated with a higher risk of CVD mortality, but it was more uncertain whether the risk differed by life course SEP. It is unclear if these findings reflect differential confounding of alcohol consumption with health-protective or damaging exposures, or differing effects of alcohol on health across socioeconomic groups.
Abstract
Background
Previous Mendelian randomization (MR) studies using population samples (population MR) have provided evidence for beneficial effects of educational attainment on health outcomes ...in adulthood. However, estimates from these studies may have been susceptible to bias from population stratification, assortative mating and indirect genetic effects due to unadjusted parental genotypes. MR using genetic association estimates derived from within-sibship models (within-sibship MR) can avoid these potential biases because genetic differences between siblings are due to random segregation at meiosis.
Methods
Applying both population and within-sibship MR, we estimated the effects of genetic liability to educational attainment on body mass index (BMI), cigarette smoking, systolic blood pressure (SBP) and all-cause mortality. MR analyses used individual-level data on 72 932 siblings from UK Biobank and the Norwegian HUNT study, and summary-level data from a within-sibship Genome-wide Association Study including >140 000 individuals.
Results
Both population and within-sibship MR estimates provided evidence that educational attainment decreased BMI, cigarette smoking and SBP. Genetic variant–outcome associations attenuated in the within-sibship model, but genetic variant–educational attainment associations also attenuated to a similar extent. Thus, within-sibship and population MR estimates were largely consistent. The within-sibship MR estimate of education on mortality was imprecise but consistent with a putative effect.
Conclusions
These results provide evidence of beneficial individual-level effects of education (or liability to education) on adulthood health, independently of potential demographic and family-level confounders.
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