IJE Advance Access originally published online on December 3, 2007
International Journal of Epidemiology 2008 37(2):290-298; doi:10.1093/ije/dym244
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When do social inequalities in C-reactive protein start? A life course perspective from conception to adulthood in the Cardiovascular Risk in Young Finns Study
1 Department of Epidemiology and Public Health, International Institute for Society and Health, UCL Medical School, London, UK.
2 Department of Psychology, University of Helsinki, Helsinki, Finland.
3 National Research and Development Centre of Welfare and Health (STAKES), Helsinki, Finland.
4 Department of Microbiology and Immunology, Tampere University Hospital and University of Tampere Medical School, Tampere, Finland.
5 Department of Clinical Chemistry, Tampere University Hospital and University of Tampere Medical School, Tampere, Finland.
6 Department of Health and Functional Capacity, National Public Health Institute, Turku, Finland.
7 Department of Medicine, University of Turku, Turku, Finland.
8 Department of Clinical Physiology, University of Turku, Turku, Finland.
*Corresponding author. Department of Epidemiology and Public Health, International Institute for Society and Health, University College London, 1-19 Torrington Place, London WC1E 6BT, UK. E-mail: d.gimeno{at}ucl.ac.uk
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Background It is unclear when in the life course do social inequalities in inflammation emerge. We examined whether the association between socioeconomic position (SEP) and C-reactive protein (CRP) is determined at conception, in childhood, adolescence or adulthood in 1484 participants from the population-based Cardiovascular Risk in Young Finns Study.
Methods Five variants of the CRP gene were used to investigate whether SEP differences in CRP levels are determined at conception. SEP and serum CRP were assessed in childhood (age 3–9), adolescence (age 12–18) and in adulthood (age 24–39). SEP was measured using parental education and occupational status in childhood and adolescence, and participants own education and occupational status in adulthood. Participants with CRP > 10 mg/l were excluded.
Results All CRP gene variants were associated with circulating CRP concentrations in childhood, but there were no differences in the distribution of these variants by SEP. No strong evidence was found of associations between parental SEP and CRP. A graded association between higher SEP and lower CRP was observed in adulthood for education (P = 0.0005) but not for occupational status. Trajectories that led to high educational achievement both in the participants and their parents were associated with lower (P
0.047) CRP levels in adulthood. Excluding participants with infectious diseases, pregnant or lactating women and women using oral contraceptives did not change the findings.
Conclusion In this cohort, SEP differences in CRP concentrations seen in adulthood appear not to be determined at conception or evident in childhood or adolescence.
Keywords Inflammation, social class, population studies, cumulative risk
Accepted 30 October 2007
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