A life course approach to explore the multi-layer biological embedding of socioeconomic position through the inflammation

2016 ◽  
Vol 2016 (1) ◽  
Author(s):  
Raphaele Castagné ◽  
Michelle Kelly-Irving ◽  
Paolo Vineis ◽  
Marc Chadeau ◽  
Cyrille Delpierre*
2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Raphaële Castagné ◽  
Cyrille Delpierre ◽  
Michelle Kelly-Irving ◽  
Gianluca Campanella ◽  
Florence Guida ◽  
...  

2018 ◽  
Vol 107 ◽  
pp. 29-35 ◽  
Author(s):  
Gregore I. Mielke ◽  
Wendy J. Brown ◽  
Ulf Ekelund ◽  
Soren Brage ◽  
Helen Gonçalves ◽  
...  

2006 ◽  
Vol 163 (suppl_11) ◽  
pp. S67-S67
Author(s):  
M.M Glymour ◽  
M Avendano ◽  
L.F Berkman

Author(s):  
José Aparecido Soares Lopes ◽  
Luana Giatti ◽  
Rosane Harter Griep ◽  
Antonio Alberto da Silva Lopes ◽  
Sheila Maria Alvim Matos ◽  
...  

Abstract Background Life course epidemiology is a powerful framework to unravel the role of socioeconomic position (SEP) disparities in hypertension (HTN). This study investigated whether life course SEP is associated with HTN incidence. Specifically, to test whether cumulative low SEP throughout life and unfavorable intergenerational social mobility increased HTN incidence. METHODS Longitudinal analysis of 8,754 ELSA-Brasil participants without HTN or cardiovascular in visit 1 (2008–2010). The response variable was the incidence of HTN between visits 1 and 2 (2012–2014). The explanatory variables were childhood, youth, and adulthood SEP, cumulative low SEP, and intergenerational social mobility. Associations were estimated by incidence rate ratios (IRRs) obtained by generalized linear models, with Poisson distribution and logarithmic link function, after adjustment for sociodemographic, behavioral, and health factors. RESULTS The incidence of HTN was 43.2/1,000 person-years, being higher in males, elderly (70–74 years), self-declared black, and low SEP individuals. After considering sociodemographic factors, low SEP in childhood, youth, and adulthood remained statistically associated with increased HTN incidence. Individuals in the third (IRR: 1.26; 95% confidence interval (CI): 1.11–1.44) and fourth top quartiles (IRR: 1.29; 95% CI: 1.11–1.49) of cumulative low SEP, vs. first, as well as those with low stable intergenerational trajectory (IRR: 1.29; 95% CI: 1.16–1.43), vs. high stable, also had increased HTN incidence rates. Conclusions Socioeconomic disparities at all phases of the life cycle appear to raise HTN incidence rates, being the individuals with greater accumulation of exposure to low SEP and with more unfavorable intergenerational mobility at greatest risk, even in a short follow-up time.


2005 ◽  
Vol 93 (05) ◽  
pp. 955-963 ◽  
Author(s):  
George Smith ◽  
Ann Rumley ◽  
Gordon Lowe ◽  
Shah Ebrahim ◽  
Debbie Lawlor

SummaryA cross sectional and prospective analysis of 3,745 British women aged 60–79 years at baseline was undertaken. Among these women there were 570 prevalent cases of coronary heart disease (CHD) and 151 new cases among 12,641 person-years of follow up of women who were free of CHD at baseline. Both fibrinogen and CRP were associated with indicators of socioeconomic position in childhood and adulthood and there was a cumulative effect of socioeconomic position from across the life course. The age-adjusted odds ratio (95% confidence interval) of prevalent CHD for a 1 unit (1 g/L) increase in fibrinogen was 1.29 (1.12, 1.49); with full adjustment for all potential confounding factors this attenuated to 1.09 (0.93, 1.28). The hazards ratio for incident CHD among those free of disease at baseline was 1.28 (1.00, 1.64); with full adjustment for all potential confounding factors this attenuated to 1.09 (0.84, 1.44). Similar effects of adjustment for confounding factors were seen for the associations between CRP and both prevalent and incident CHD. By contrast, the strong positive association between smoking (an established causal risk factor for CHD) and CHD was not attenuated by adjustment for life course socioeconomic position or other risk factors. We conclude that fibrinogen and CRP predict CHD but may not be causally related to it.


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