Background
Cardiovascular disease is a major cause of morbidity and mortality in developed and increasingly, developing countries. The aetiology of cardiovascular disease is multifactorial, with lifestyle, environmental and genetic factors implicated. There is evidence to suggest that early life exposures may also influence cardiovascular disease risk. The work of Barker and colleagues (eg. BMJ 1995, 311:171-4) suggests that fetal nutrition during pregnancy can influence the risk of chronic diseases in adulthood, by a process known as 'programming'. However, further studies investigating the relationship between fetal growth and risk of adult cardiovascular disease are inconclusive and many do not account for possible confounding factors, such as socio-economic status. Also, a study by Hattersley et al. (Nat Genet 1998,19(3):268-70) indicated that the impact of poor fetal growth on, for example, type 2 diabetes and insulin resistance, could be mediated via the genes affecting fetal growth.
More recently the 'programming' hypothesis has been questioned (Lancet 2002; 360(9334):659-665 and Journal of Hypertension 2003; 21(2):273-279), and with discussion over publication and other potential biases in research, it remains a controversial area. Longitudinal studies investigating the relationship between maternal and fetal factors as well as factors operating throughout the life course are needed in order to further understand the aetiology of cardiovascular disease and develop potential preventative and therapeutic measures. The EURO-BLCS study sets out to explore the evolution of cardiovascular morbidity, mortality and intermediate disease markers throughout the lifecourse in children, adolescents, young adults, middle-aged and elderly people as a means of identifying high risk groups and biological markers amenable to early intervention and prevention.
objectives are
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study population
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Through our collaboration, we have access to a unique cohort collection from several european populations |
| population | year of birth | cohort size | |
| northern finland birth cohort (NFBC 66) | Finland | 1966 | 12231 |
| northern finland birth cohort (NFBC 86) | Finland | 1985-6 | 9479 |
| national survey of health and development (NSHD) | UK | 1946 | 5362 |
| ALSPAC cohort | UK | 1991-2 | 14,062 |
| greek national perinatal survey | Greece | 1983 | 11,000 |
| faroe islands cohort | Faroe islands | 1927-37 | 6379 |
These cohorts have been followed prospectively either since birth, or early in gestation. Extensive data is available on family background, maternal characteristics during pregnancy (blood pressure, BMI, smoking, diet, socioeconomic factors, pregnancy complications), clinical characteristics at birth (birth weight and length, gestational length, neonatal hospitalisations) and throughout the lifecourse (blood pressure, biochemical factors, hospitalisations) and lifestyle factors (smoking, exercise, diet, socioeconomic factors).
For the greek national cohort and NFBC 86 new outcome data (social background, health status, blood pressure, blood biochemistry, diet, fitness, physical activity) will be collected during the course of the study. Methods of collection will be harmonised between the cohorts, to allow data comparisons and pooling. For more details go to harmonised data collection.
work packages
Five main work packages will be carried out
1 identifying maternal and fetal markers in the evolution of CVD risk in existing datasets
2 gene markers of disorders of insulin, glucocorticoid and androgen metabolism and their relation to prenatal growth
3 pre-eclampsia and high blood pressure – association with mother’s own lipid and insulin profile as markers of future CVD risk
4 harmonization of measurement and techniques between centres, new outcome data collection and data analyses
5 dissemination to the european community
expected achievements
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This project is expected to clarify the relative roles of genetic, biological and environmental variation in explaining the association between low birthweight and adult disease, and thereby to have a major impact on our understanding of the aetiological mechanisms responsible for the evolution of chronic diseases. In public health terms this is likely to influence development of therapeutic and preventive strategies for these conditions, including screening.
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