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Wiley Open Access, Journal of the American Heart Association, 8(6), 2017

DOI: 10.1161/jaha.117.005925

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Socioeconomic position is associated with carotid intima-media thickness in mid-childhood: The longitudinal study of Australian children

This paper is made freely available by the publisher.
This paper is made freely available by the publisher.

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Data provided by SHERPA/RoMEO

Abstract

Background Lower socioeconomic position ( SEP ) predicts higher cardiovascular risk in adults. Few studies differentiate between neighborhood and family SEP or have repeated measures through childhood, which would inform understanding of potential mechanisms and the timing of interventions. We investigated whether neighborhood and family SEP , measured biennially from ages 0 to 1 year onward, was associated with carotid intima–media thickness ( IMT ) at ages 11 to 12 years. Methods and Results Data were obtained from 1477 families participating in the Child Health CheckPoint study, nested within the Longitudinal Study of Australian Children. Disadvantaged family and neighborhood SEP was cross‐sectionally associated with thicker maximum carotid IMT in separate univariable linear regression models. Associations with family SEP were not attenuated in multivariable analyses, and associations with neighborhood SEP were attenuated only in models adjusted for family SEP . The difference in maximum carotid IMT between the highest and lowest family SEP quartile measured at ages 10 to 11 years was 10.7 μm (95% CI , 3.4–18.0; P =0.004), adjusted for age, sex, pubertal status, passive smoking exposure, body mass index, blood pressure, and arterial lumen diameter. In longitudinal analyses, family SEP measured as early as age 2 to 3 years was associated with maximum carotid IMT at ages 11 to 12 years (difference between highest and lowest quartile: 8.5 μm; 95% CI , 1.3–15.8; P =0.02). No associations were observed between SEP and mean carotid IMT . Conclusions We report a robust association between lower SEP in early childhood and carotid IMT in mid‐childhood. Further investigation of mechanisms may inform pediatric cardiovascular risk assessment and prevention strategies.