Denny Vågerö

Reduced fetal growth rate and increased risk of death from ischaemic heart disease: cohort study of 15 000 Swedish men and women born 1915-29.

Abstract Objective: To establish whether fetal growth rate (as distinct from size at birth) is associated with mortality from ischaemic heart disease. Design: Cohort study based on uniquely detailed obstetric records with 97% follow up over the entire life course and linkage to census data in adult life. Subjects: All 14 611 babies delivered at the Uppsala Academic Hospital, Sweden, during 1915-29 followed up to end of 1995. Main outcome measures: Mortality from ischaemic heart disease and other causes. Results: Cardiovascular disease showed an inverse association with birth weight for both men and women, although this was significant only for men. In men a 1000 g increase in birth weight was associated with a proportional reduction in the rate of ischaemic heart disease of 0.77 (95% confidence interval 0.67 to 0.90). Adjustment for socioeconomic circumstances at birth and in adult life led to slight attenuation of this effect. Relative to the lowest fourth of birth weight for gestational age, mortality from ischaemic heart disease in men in the second, third, and fourth fourths was 0.81 (0.66 to 0.98), 0.63 (0.50 to 0.78), and 0.67 (0.54 to 0.82), respectively. The inclusion of birth weight per se and birth weight for gestational age in the same model strengthened the association with birth weight for gestational age but removed the association with birth weight. Conclusions: This study provides by far the most persuasive evidence of a real association between size at birth and mortality from ischaemic heart disease in men, which cannot be explained by methodological artefact or socioeconomic confounding. It strongly suggests that it is variation in fetal growth rate rather than size at birth that is aetiologically important.

Failure to realise growth potential in utero and adult obesity in relation to blood pressure in 50 year old Swedish men

Abstract Objectives: To clarify the type of fetal growth impairment associated with increased blood pressure in adult life, and to establish whether this association is influenced by obesity and is mediated through impairment of insulin action. Design: Cross sectional survey with retrospective ascertainment of size at birth from obstetric archives. Subjects: 1333 men resident in Uppsala, Sweden, who took part in a 1970 study of coronary risk factors at age 50 and for whom birth weight was traced. Main outcome measures: Systolic and diastolic blood pressure at age 50. Results: In the full study population for a 1000 g increase in birth weight there was a small change in systolic blood pressure of −2.2 mm Hg (95% confidence interval −4.2 to −0.3 mm Hg) and in diastolic blood pressure of −1.0 mm Hg (−2.2 to 0.1 mm Hg). Much stronger effects were observed among men who were born at term and were in the top third of body mass index at age 50, for whom a 1000 g increase in birth weight was associated with a change of −9.1 mm Hg (−16.4 to −1.9 mm Hg) systolic and −4.2 mm Hg (−8.3 to −0.1 mm Hg) diastolic blood pressure. Men who were light at birth (<3250 g) but were of above median adult height had particularly high blood pressure. Adjustment for insulin concentrations reduced the associations of birth weight with systolic and diastolic blood pressure. Conclusions: A failure to realise growth potential in utero (as indicated by being light at birth but tall as an adult) is associated with raised adult blood pressure. Impaired fetal growth may lead to substantial increases in adult blood pressure among only those who become obese. Metabolic disturbances, possibly related to insulin resistance, may provide a pathway through which fetal growth affects blood pressure.

Education, income, and occupational class cannot be used interchangeably in social epidemiology. Empirical evidence against a common practice

Study objective: Education, income, and occupational class are often used interchangeably in studies showing social inequalities in health. This procedure implies that all three characteristics measure the same underlying phenomena. This paper questions this practice. The study looked for any independent effects of education, income, and occupational class on four health outcomes: diabetes prevalence, myocardial infarction incidence and mortality, and finally all cause mortality in populations from Sweden and Germany. Design: Sweden: follow up of myocardial infarction mortality and all cause mortality in the entire population, based on census linkage to the Cause of Death Registry. Germany: follow up of myocardial infarction morbidity and all cause mortality in statutory health insurance data, plus analysis of prevalence data on diabetes. Multiple regression analyses were performed to calculate the effects of education, income, and occupational class before and after mutual adjustments. Setting and participants: Sweden (all residents aged 25–64) and Germany (Mettman district, Nordrhein-Westfalen, all insured persons aged 25–64). Main results: Correlations between education, income, and occupational class were low to moderate. Which of these yielded the strongest effects on health depended on type of health outcome in question. For diabetes, education was the strongest predictor and for all cause mortality it was income. Myocardial infarction morbidity and mortality showed a more mixed picture. In mutually adjusted analyses each social dimension had an independent effect on each health outcome in both countries. Conclusions: Education, income, and occupational class cannot be used interchangeably as indicators of a hypothetical latent social dimension. Although correlated, they measure different phenomena and tap into different causal mechanisms.

HEALTH INEQUALITIES IN BRITAIN AND SWEDEN

Health differences between social classes are greater in Britain than in Sweden, but persist in both countries despite central Government interventions aimed at the reduction of such differences.

Ischaemic heart disease and low birth weight: a test of the fetal-origins hypothesis from the Swedish Twin Registry.

Twins constitute a population with lower than average birth weight for reasons that are not a consequence of social disadvantage. The hypothesis that ischaemic heart disease (IHD) is linked to low birth weight was tested by analysing whether or not 8174 female and 6612 male Swedish twins had a higher mortality compared to the general Swedish population. The association between adult body height and IHD mortality was also analysed in a nested case-control study among monozygotic and dizygotic twins. Ischaemic heart disease mortality was not higher among twins (women: relative risk [RR] 0.99; 95% confidence limits [CL] 0.89-1.10; men: RR 0.85; CL 0.79-0.92). However, the shorter twin in a twin pair was more likely to die of heart disease than the taller (odds ratio [OR] 1.15, CL 1.03-1.25). We suggest that postnatal influences may well be as important as prenatal influences in producing any effect on ischaemic heart disease mortality and that the type of growth retardation in utero experienced by twins may not constitute a risk for ischaemic heart disease in adulthood.

Global health equity and climate stabilisation: a common agenda

Although health has improved for many people, the extent of health inequities between and within countries is growing. Meanwhile, humankind is disrupting the global climate and other life-supporting environmental systems, thereby creating serious risks for health and wellbeing, especially in vulnerable populations but ultimately for everybody. Underlying determinants of health inequity and environmental change overlap substantially; they are signs of an economic system predicated on asymmetric growth and competition, shaped by market forces that mostly disregard health and environmental consequences rather than by values of fairness and support. A shift is needed in priorities in economic development towards healthy forms of urbanisation, more efficient and renewable energy sources, and a sustainable and fairer food system. Global interconnectedness and interdependence enable the social and environmental determinants of health to be addressed in ways that will increase health equity, reduce poverty, and build societies that live within environmental limits.

Long term mortality after severe starvation during the siege of Leningrad: prospective cohort study

Abstract Objectives To determine whether starvation during periods of increased growth after birth have long term health consequences. Design Analysis of cardiovascular risk factors and mortality in a longitudinal follow up after the 1941-4 siege of Leningrad. Mortality measured from 1975 up to the end of 1999. Setting St Petersburg, Russia (formerly Leningrad). Participants 5000 men born 1916-35 who lived in Leningrad, randomly selected to take part in health examinations in 1975-7. Of the 3905 men who participated, a third had experienced the siege. Main outcome measures Relative risk of ischaemic heart disease and mortality from stroke by siege exposure. Odds ratios and means for several cardiovascular risk factors. Results Three to six decades after the siege, in men who experienced the siege around the age of puberty blood pressure was raised (mean difference in systolic 3.3 mm Hg, in diastolic 1.3 mm Hg) as was mortality from ischaemic heart disease (relative risk 1.39, 95% confidence interval 1.07 to 1.79) and stroke (1.67, 1.15 to 2.43), including haemorrhagic stroke (1.71, 0.90 to 3.22). The effect on mortality was partly mediated via blood pressure but not by any other measured biological, behavioural, or social factor. Conclusions Starvation, or accompanying chronic stress, particularly at the onset of or during puberty, may increase vulnerability to later cardiovascular disease.

Educational inequalities in mortality in four Eastern European countries: divergence in trends during the post-communist transition from 1990 to 2000

BACKGROUND Post-communist transition has had a huge impact on mortality in Eastern Europe. We examined how educational inequalities in mortality changed between 1990 and 2000 in Estonia, Lithuania, Poland and Hungary. METHODS Cross-sectional data for the years around 1990 and 2000 were used. Age-standardized mortality rates and mortality rate ratios (for total mortality only) were calculated for men and women aged 35-64 in three educational categories, for five broad cause-of-death groups and for five (seven among women) specific causes of death. RESULTS Educational inequalities in mortality increased in all four countries but in two completely different ways. In Poland and Hungary, mortality rates decreased or remained the same in all educational groups. In Estonia and Lithuania, mortality rates decreased among the highly educated, but increased among those of low education. In Estonia and Lithuania, for men and women combined, external causes and circulatory diseases contributed most to the increasing educational gap in total mortality. CONCLUSIONS Different trends were observed between the two former Soviet republics and the two Central Eastern European countries. This divergence can be related to differences in socioeconomic development during the 1990s and in particular, to the spread of poverty, deprivation and marginalization. Alcohol and psychosocial stress may also have been important mediating factors.

Social class differences in infant mortality in Sweden: comparison with England and Wales.

OBJECTIVES--To investigate social class differences in infant mortality in Sweden in the mid-1980s and to compare their magnitude with that of those found in England and Wales. DESIGN--Analysis of risk of infant death by social class in aggregated routine data for the mid-1980s, which included the linkage of Swedish births to the 1985 census. SETTING--Sweden and England and Wales. SUBJECTS--All live births in Sweden (1985-6) and England and Wales (1983-5) and corresponding infant deaths were analysed. The Swedish data were coded to the British registrar generals social class schema. MAIN OUTCOME MEASURES--Risk of death in the neonatal and postneonatal period. RESULTS--Taking the non-manual classes as the reference group, in the neonatal period in Sweden the manual social classes had a relative risk for mortality of 1.20 (95% confidence interval 1.02 to 1.43) and those not classified into a social class a relative risk of 1.08 (0.88 to 1.33). In the postneonatal period the equivalent relative risks were 1.38 (1.08 to 1.77) for manual classes and 2.14 (1.65 to 2.79) for the residual; these are similar to those for England and Wales (1.43 (1.36 to 1.51) for manual classes, 2.62 (2.45 to 2.81) for the residual). CONCLUSIONS--The existence of an equitable health care system and a strong social welfare policy in Sweden has not eliminated inequalities in post-neonatal mortality. Furthermore, the very low risk of infant death in the Swedish non-manual group (4.8/1000 live births) represents a target towards which public health interventions should aim. If this rate prevailed in England and Wales, 63% of postneonatal deaths would be avoided.

The length of unemployment predicts mortality, differently in men and women, and by cause of death: A six year mortality follow-up of the Swedish 1992-1996 recession

This study examines the relationship between the total amount of accumulated unemployment during the deep Swedish recession of 1992-1996 and mortality in the following 6 years. Nearly 3.4 million Swedish men and women, born between 1931 and 1965 who were gainfully employed at the time of the 1990 census were included. Almost 23% of these individuals were unemployed at some point during the recession. We conduct a prospective cohort study utilizing Cox proportional hazard regression with a mortality follow-up from January 1997 to December 2002. We adjust for health status (1982-1991), baseline (1991) social, family, and employer characteristics of individuals before the recession. The findings suggest that long-term unemployment is related to elevated all-cause mortality for men and women. The excess mortality effects were small for women and attributable to a positive, linear increase in the hazard of alcohol disease-related mortality and external causes-of-death not classified as suicides or transport accidents. For men, the excess hazard of all-cause mortality was best represented by a cubic, non-linear shape. The predicted hazard increases rapidly with the shortest and longest accumulated levels of unemployment. However, the underlying pattern differed by cause-of-death. The cancer, circulatory, and alcohol disease-related analyses suggest that mortality peaks with mid-levels of accumulated unemployment and then declines with longer duration unemployment. For men, we observed a positive, linear increase in the hazard ratios associated with transport and suicide mortality, and a very steep non-linear increase in the excess hazard ratio associated with other external causes of death that were not classified as suicide or transport accidents. In conclusion, mortality risk increases with the duration of unemployment among men and women. This was best described by a cubic function for men and a linear function for women. Behind this pattern, different causes-of-death varied in their relation to the accumulation of unemployment.