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Socioeconomic status in childhood and C reactive protein in adulthood: a systematic review and meta-analysis
  1. Richard S Liu1,2,
  2. Allison E Aiello3,
  3. Fiona K Mensah1,2,4,
  4. Constantine E Gasser1,2,
  5. Kuna Rueb1,
  6. Billie Cordell1,
  7. Markus Juonala5,6,
  8. Melissa Wake1,2,4,
  9. David P Burgner1,2,7
  1. 1Murdoch Childrens Research Institute, Parkville, Victoria, Australia
  2. 2Department of Paediatrics, The University of Melbourne, Parkville, Victoria, Australia
  3. 3Department of Epidemiology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, USA
  4. 4The Royal Children's Hospital, Parkville, Victoria, Australia
  5. 5Department of Medicine, University of Turku, Turku, Finland
  6. 6Division of Medicine, Turku University Hospital, Turku, Finland
  7. 7Department of Paediatrics, Monash University, Clayton, Victoria, Australia
  1. Correspondence to Professor David Burgner, Murdoch Childrens Research Institute, Royal Children's Hospital, 50 Flemington Road, Parkville, Victoria 3052, Australia; david.burgner{at}mcri.edu.au

Abstract

Background Inflammation plays a central role in cardiometabolic disease and may represent a mechanism linking low socioeconomic status (SES) in early life and adverse cardiometabolic health outcomes in later life. Accumulating evidence suggests an association between childhood SES and adult inflammation, but findings have been inconsistent.

Methods We conducted a systematic review and meta-analysis of observational studies to quantify the association between childhood (age <18 years) SES and the inflammatory marker C reactive protein (CRP) in adulthood. Studies were identified in Medline and Embase databases, and by reviewing the bibliographies of articles published from 1946 to December 2015. Study-specific estimates were combined into meta-analyses using random-effects models.

Results 15 of 21 eligible studies (n=43 629) were ultimately included in two separate meta-analyses. Compared with those from the most advantaged families, participants from the least advantaged families had 25% higher CRP levels (ratio change in geometric mean CRP: 1.25; 95% CI 1.19 to 1.32) in minimally adjusted analyses. This finding was attenuated by the inclusion of adult body mass index (BMI) in adjusted models, suggesting BMI has a strong mediating role in CRP levels.

Conclusions We observed an inverse association between childhood SES and adulthood CRP, potentially mediated through BMI. Investigating how childhood SES is associated with childhood BMI and CRP would provide insight into the effective timing of social and clinical interventions to prevent cardiometabolic disease.

  • Social and life-course epidemiology
  • OBESITY
  • Cardiovascular disease
  • SOCIAL INEQUALITIES

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Footnotes

  • Contributors RSL and DPB contributed to study conception and design, directed the study implementation, acquisition, analysis and interpretation of data, and drafted the initial manuscript and approved the final manuscript submitted. AEA and FKM contributed to study design, analysis and interpretation of data, and critically revised the initial manuscript and further drafts for important intellectual content, and approved the final manuscript submitted. BC, KR and CEG contributed to acquisition and analysis of data, drafting and reviewing the manuscript and further drafts, and approved the final manuscript as submitted. MJ and MW contributed to the analysis and interpretation of the data, critically revising drafts for important intellectual content, and approved the final manuscript as submitted.

  • Funding This work was supported by the Australian National Health and Medical Research Council (Postgraduate Scholarship 1114567 to RSL, Senior Research Fellowships 1046518 to MW and 1064629 to DPB, Early Career Fellowship 1037449 and Career Development Fellowship 1111160 to FKM); by the Center for Integrative Approaches to Health Disparities (P60MD002249 to AEA); NIH National Institute of Diabetes, Digestive, and Kidney Diseases (R01DK087864 to AEA); the Carolina Population Center and its NIH Center grant (P2C HD050924 to AEA); the Australian Government (an Australian Postgraduate Award to CEG); and the Murdoch Childrens Research Institute (Murdoch Childrens Research Institute Top Up Scholarship to CEG). Research at the Murdoch Childrens Research Institute is supported by the Victorian Government's Operational Infrastructure Program.

  • Disclaimer The funding bodies did not play any role in the study.

  • Competing interests None declared.

  • Provenance and peer review Not commissioned; externally peer reviewed.

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