Øyvind Næss

Cohort Profile: Cohort of Norway (CONOR)

A number of large population-based cardiovascular surveys have been conducted in Norway since the beginning of the 1970s. The surveys were carried out by the National Health Screening Service in cooperation with the universities and local health authorities. All surveys comprised a common set of questions, standardized anthropometric and blood pressure measurements and non-fasting blood samples that were analysed for serum lipids at the Ulleval Hospital Laboratory. These surveys provided considerable experience in conducting large-scale population-based surveys, thus an important background for the Cohort of Norway (CONOR). In the late 1980s the Research Council of Norway established a programme in epidemiology. This also gave stimulus to the idea of establishing a cohort including both core survey data and stored blood samples. In the early 1990s, all universities, the National Health Screening Service, The National Institute of Public Health and the Cancer Registry discussed the possibility of a national representative cohort. The issue of storing blood samples for future analyses raised some concern and it was discussed in the parliament. In 1994, the Ministry of Health appointed the Steering Committee for the CONOR collaboration. In 1994–95, the fourth round of the Tromso Study was conducted, and became the first survey to provide data and blood samples for CONOR. During the years 1994–2003, a number of health surveys that were carried out in other counties and cities also provided similar data for the network. So far, 10 different surveys have provided data and blood samples for CONOR (Figure 1). The administrative responsibility for CONOR was given to the Norwegian Institute of Public Health (NIPH) in 2002. The CONOR collaboration is currently a research collaboration between the NIPH and the Universities of Bergen, Oslo, Tromso and Trondheim.

Educational inequalities in mortality over four decades in Norway: prospective study of middle aged men and women followed for cause specific mortality, 1960-2000.

Objectives To determine the extent to which educational inequalities in relation to mortality widened in Norway during 1960-2000 and which causes of death were the main drivers of this disparity. Design Nationally representative prospective study. Setting Four cohorts of the Norwegian population aged 45-64 years in 1960, 1970, 1980, and 1990 and followed up for mortality over 10 years. Participants 359 547 deaths and 32 904 589 person years. Main outcome measures All cause mortality and deaths due to cancer of lung, trachea, or bronchus; other cancer; cardiovascular diseases; suicide; external causes; chronic lower respiratory tract diseases; or other causes. Absolute and relative indices of inequality were used to present differences in mortality by educational level (basic, secondary, and tertiary). Results Mortality fell from the 1960s to the 1990s in all educational groups. At the same time the proportion of adults in the basic education group, with the highest mortality, decreased substantially. As mortality dropped more among those with the highest level of education, inequalities widened. Absolute inequalities in mortality denoting deaths among the basic education groups minus deaths among the high education groups doubled in men and increased by a third in women. This is equivalent to an increase in the slope index of inequality of 105% in men and 32% in women. Inequalities on a relative scale widened more, from 1.33 to 2.24 among men (P=0.01) and from 1.52 to 2.19 among women (P=0.05). Among men, absolute inequalities mainly increased as a result of cardiovascular diseases, lung cancer, and chronic lower respiratory tract diseases. Among women this was mainly due to lung cancer and chronic lower respiratory tract diseases. Unlike the situation in men, absolute inequalities in deaths due to cardiovascular causes narrowed among women. Chronic lower respiratory tract diseases contributed more to the disparities in inequalities among women than among men. Conclusion All educational groups showed a decline in mortality. Nevertheless, and despite the fact that the Norwegian welfare model is based on an egalitarian ideology, educational inequalities in mortality among middle aged people in Norway are substantial and increased during 1960-2000.

Air pollution, social deprivation, and mortality: a multilevel cohort study.

Background: It is becoming increasingly evident that exposure to air pollution and its adverse effects are not equitably distributed. Our goal was to investigate the role of social deprivation in explaining the effect of neighborhood differences in level of air pollution fine particulates (PM2.5) on mortality when the indicators of social deprivation are measured at both individual level and at neighborhood level. Methods: All inhabitants registered in Oslo, Norway on 1 January 1992 in the age group 50–74 years (n = 105,359) constitute the study base. We used an air dispersion model (AirQUIS) to estimate levels of exposure in the period 1992–1995 in all 470 administrative neighborhoods. These data were linked to Census, educational, and death registries. Deaths were recorded in the period 1992–1998. Main Results: PM2.5 was associated with most neighborhood-level indicators of deprivation, as was most clearly seen for type of dwelling and ownership of dwelling. The effect of PM2.5 on mortality was to some extent explained by these indicators independently of the corresponding individual-level indicators. Conclusions: Findings from this study suggest that socially deprived neighborhoods have higher exposure to air pollution. Deprivation at both the individual and neighborhood level is associated with air pollution, accounting for some of the excess mortality associated with air pollution in these neighborhoods.

Parent-Offspring Body Mass Index Associations in the Norwegian Mother and Child Cohort Study: A Family-based Approach to Studying the Role of the Intrauterine Environment in Childhood Adiposity

In the present study, the authors investigated the role of the intrauterine environment in childhood adiposity by comparing the maternal-offspring body mass index (BMI) association with the paternal-offspring BMI association when the offspring were 3 years of age, using parental prepregnancy BMI (measured as weight in kilograms divided by height in meters squared). The parent-offspring trios (n = 29,216) were recruited during pregnancy from 2001 to 2008 into the Norwegian Mother and Child Cohort Study conducted by The Norwegian Institute of Public Health. Data from self-administered questionnaires were used in linear regression analyses. Crude analyses showed similar parental-offspring BMI associations; the mean difference in offspring BMI was 0.15 (95% confidence interval: 0.13, 0.16) per each 1-standard-deviation increase in maternal BMI and 0.15 (95% confidence interval: 0.13, 0.17) per each 1-standard-deviation increase in paternal BMI. After all adjustments, the mean difference in offspring BMI per each 1-standard-deviation increment of maternal BMI was 0.12, and the mean difference in offspring BMI per each 1-standard-deviation increment of paternal BMI was 0.13. There was no strong support for heterogeneity between the associations (P > 0.6). In conclusion, results from the present large population-based study showed similar parental-offspring BMI associations when the offspring were 3 years of age, which indicates that the maternal-offspring association may be explained by shared familial (environmental and genetic) risk factors rather than by the intrauterine environment.

Four indicators of socioeconomic position: relative ranking across causes of death:

Objective: A study was undertaken to examine the relative ability of occupational class, education, household income, and housing conditions to discriminate all cause and cause-specific mortality-risk in Oslo, and to see if this relative ability is consistent across the 12 most common causes of death. Design and setting: Census records of inhabitants in Oslo 1990 aged 45 to 64 were linked to death records 1990—98 (n=88,159). All inhabitants were included except those who lacked census data on the independent variables. The relative index of inequality (RII) for each indicator was calculated. Main results: Education, occupation, and housing conditions had similar RIIs for all-cause mortality in both sexes. Household income had low RIIs, particularly in men. For the 12 most common causes of death some heterogeneity in the relative ranking between the four indicators was observed, with causes of death known to be related to early-life social circumstances (stomach cancer, cardiovascular disease, chronic obstructive pulmonary disease) being particularly strongly related to education, and causes of death which were likely to be determined by adult social circumstances (violence, sudden unexpected death) being particularly strongly related to occupation and housing conditions. Conclusions: Education, occupational class, and housing conditions all seemed to discriminate all-cause mortality to a similar degree. However, the cause-specific analysis revealed a heterogeneous pattern.

Ambient air pollution exposure, residential mobility and term birth weight in Oslo, Norway.

Environmental exposure during pregnancy may have lifelong health consequences for the offspring and some studies have association between maternal exposure to air pollution during pregnancy and offsprings birth weight. However, many of these studies do not take into account small-scale variations in exposure, residential mobility, and work addresses during pregnancy. We used information from the National Birth Registry of Norway to examine associations between ambient environmental exposure such as air pollution and temperature, and offsprings birth weight taking advantage of information on migration history and work address in a large population-based cohort. A dispersion model was used to estimate ambient air pollution levels at all residential addresses and work addresses for a total of 25,229 pregnancies between 1999 and 2002 in Oslo, Norway. Ambient exposure to traffic pollution for the entire pregnancy was associated with a reduction in term birth weight in crude analyzes when comparing children of the highest and lowest exposed mothers. No evidence for an association between exposure to traffic pollution at home and work addresses and term birth weight after adjustment for covariates known to influence birth weight during pregnancy. After stratification, small statistically non-significant reductions were present but only for multiparious mothers. This group also had less residential mobility and less employment during pregnancy. The overall findings suggest no clear association between term birth weight and traffic pollution exposure during pregnancy. However, mobility patterns could introduce possible confounding when examining small-scale variations in exposure by using addresses. This could be of importance in future studies.

Controlling for High-Density Lipoprotein Cholesterol Does Not Affect the Magnitude of the Relationship Between Alcohol and Coronary Heart Disease

Background— This study tested the hypothesis that moderate alcohol intake exerts its cardioprotective effect mainly through an increase in the serum level of high-density lipoprotein cholesterol. Methods and Results— In the Cohort of Norway (CONOR) study, 149 729 adult participants, recruited from 1994 to 2003, were followed by linkage to the Cause of Death Registry until 2006. At recruitment, questionnaire data on alcohol intake were collected, and the concentration of high-density lipoprotein cholesterol in serum was measured. Using Cox regression, we found that the adjusted hazard ratio for men for dying from coronary heart disease was 0.52 (95% confidence interval, 0.39–0.69) when consuming alcohol more than once a week compared with never or rarely. The ratio changed only slightly, to 0.55 (0.41–0.73), after the regression model included the serum level of high-density cholesterol. For women, the corresponding hazard ratios were 0.62 (0.32–1.23) and 0.68 (0.34–1.34), respectively. Conclusions— Alcohol intake is related to a reduced risk of death from coronary heart disease in the follow-up of a large, population-based Norwegian cohort study with extensive control for confounding factors. Our findings suggest that the serum level of high-density cholesterol is not an important intermediate variable in the possible causal pathway between moderate alcohol intake and coronary heart disease.

Midlife vascular risk factors and their association with dementia deaths: results from a Norwegian prospective study followed up for 35 years.

There is growing evidence that midlife risk factors for vascular disease also are risk factors for dementia, but there is still need for long-term observational studies to address this. Our objective was to investigate the association of midlife vascular disease risk factors with dementia death. Participants were included in The Norwegian Counties Study (NCS) in the period 1974-78, aged 35-50 years at baseline. Information from NCS was linked with the Cause of Death Registry through the year 2009 using the unique personal identification number. The study included 48,793 participants, 1.5 million person years and 486 dementia deaths (187 Alzheimers; 299 non-Alzheimers dementia). Cox regression for cause-specific hazards was used. Dementia death was associated with increased total cholesterol levels (>7.80 vs. <5.20 mmol/l: HR=2.01, 95% confidence interval 1.37-2.93); diabetes (HR=2.43, 95% CI 1.40-4.32) and low body mass index (<20 kg/m(2) vs. 20-25 kg/m(2): HR=1.76, 95% CI 1.15-2.68) in midlife. The associations remained after adjustment for other vascular risk factors and educational level. Smoking status or blood pressure in midlife was not significantly associated with risk of dementia death, although the results indicate a possible increased risk in heavy smokers. People suffering from high cholesterol levels, diabetes or underweight in midlife are at increased risk of dying from or with dementia later in life. Our findings add to previous results suggesting that intervention in midlife may be important. To better understand the mechanisms involved in the associations between midlife underweight, diabetes, and elevated cholesterol level and late-life dementia death, these links need to be further investigated.

Cumulative deprivation and cause specific mortality. A census based study of life course influences over three decades

Objective: To examine whether increasing cumulative deprivation has an incremental effect on total as well as cause specific mortality. Design: Census data on housing conditions as indicators of deprivation from 1960, 1970, and 1980 were linked to 1990–98 death registrations. Relative indices of inequalities were computed for housing conditions to measure the cumulative impact of differences in social conditions. Participants: 97 381 (71.1%) 30–49 year old and 70 701 (80.0%) 50–69 year old inhabitants of Oslo, Norway, in 1990 with census information on housing conditions and recorded length of education. Main results: Mortality risk was increased when all censuses’ housing conditions were summed in both age groups and sex. The cause specific analysis indicated such an effect particularly for coronary heart disease, chronic obstructive lung disease, and smoking related cancers. Violent deaths were essentially associated with housing conditions closer to the time of death in men in both age groups and in young women. Conclusions: To fully account for socially mediated risk of death, a full life course approach should be adopted. The relative importance of each stage seems to vary by cause of death.

Childhood and adulthood socioeconomic position across 20 causes of death: a prospective cohort study of 800 000 Norwegian men and women

Objective: To assess the impact of childhood and adulthood socioeconomic position (SEP) across 20 causes of death in a large population-wide sample of Norwegian men and women. Methods: Census data on parental occupational class from 1960 and data from the tax register on household income in 1990 were linked to the death register for 1990–2001, and 20 causes of death were studied. Relative indices of inequalities were computed. Norwegians in the age group 0–20 years in 1960 and still alive in 1990 were followed for deaths in 1990 to 2001. This follow up involved 795 324 individuals (78%) and 20 887 deaths. Main results: In men most support for an effect of childhood socioeconomic position was found for stomach cancer, lung cancer, coronary heart disease, “other violent death”, and all causes of death. In women similar effects were found for lung cancer, cervical cancer, coronary heart disease, chronic obstructive pulmonary disease, and all causes of death. Conclusions: The effect of childhood socioeconomic position relative to adulthood varies by cause of death. Although there are some exceptions, the patterns in men and women are generally similar.