Early childhood socioeconomic status is associated with circulating interleukin-6 among mid-life adults

被引:72
作者
Carroll, Judith E. [1 ,3 ]
Cohen, Sheldon [2 ]
Marsland, Anna L. [3 ]
机构
[1] Univ Calif Los Angeles, Cousins Ctr Psychoneuroimmunol, Dept Psychiat & Biobehav Sci, Semel Inst Neurosci & Human Behav, Los Angeles, CA 90095 USA
[2] Carnegie Mellon Univ, Dept Psychol, Pittsburgh, PA 15213 USA
[3] Univ Pittsburgh, Dept Psychol, Behav Immunol Lab, Pittsburgh, PA 15260 USA
关键词
Childhood socioeconomic status; Inflammation; Interleukin-6; Early biological programming; Immune phenotype; SC childhood interview; ARTERY RISK DEVELOPMENT; CAUSE-SPECIFIC MORTALITY; C-REACTIVE PROTEIN; LOW-BIRTH-WEIGHT; EARLY-LIFE; CARDIOVASCULAR-DISEASE; PROINFLAMMATORY PHENOTYPE; PHYSICAL-ACTIVITY; INFANT-HEALTH; SOCIAL-CLASS;
D O I
10.1016/j.bbi.2011.05.016
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
It is proposed that socioeconomic conditions in early childhood effect immune programming, with poorer conditions resulting in adult phenotypes that are prone to inflammation. Recent evidence supports this possibility, showing an inverse association of childhood SES with adult markers of systemic inflammation. In this study, we further investigate this association, extending prior studies to include an examination of multiple indices of SES across distinct periods of childhood. Subjects were 112 men and women, 40-60 years of age (88.6% Caucasian). Childhood SES was indexed by a composite of three indicators of parental wealth (parental home and vehicle ownership, and number of bedrooms per child in the family home) averaged across 2 year periods of childhood between 1 and 18 years old. Higher adult serum concentrations of interleukin (1L)-6 were associated with lower SES in early childhood (years 1-2) (beta = -.05, p <.05), associations that were independent of adult age, personal income, educational attainment, gender, race, body mass index, and physical activity. These associations support recent suggestions that the early environment may program immune phenotypes that contribute to disease risk. (C) 2011 Elsevier Inc. All rights reserved.
引用
收藏
页码:1468 / 1474
页数:7
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