A1 Refereed original research article in a scientific journal
Neighbourhood socioeconomic disadvantage from childhood to midlife and carotid atherosclerosis.
Authors: Raitakari, Olli; Pentti, Jaana; Koskinen, Juhani S.; Mykkänen, Juha; Rovio, Suvi; Pahkala, Katja; Juonala Markus; Lehtimäki, Terho; Kähönen, Mika; Kawachi, Ichiro; Kivimäki, Mika; Viikari, Jorma; Vahtera, Jussi
Publisher: Elsevier
Publication year: 2026
Journal: International Journal of Cardiology
Article number: 134216
Volume: 450
ISSN: 0167-5273
eISSN: 1874-1754
DOI: https://doi.org/10.1016/j.ijcard.2026.134216
Publication's open availability at the time of reporting: Open Access
Publication channel's open availability : Partially Open Access publication channel
Web address : https://doi.org/10.1016/j.ijcard.2026.134216
Self-archived copy’s web address: https://research.utu.fi/converis/portal/detail/Publication/509012636
Self-archived copy's licence: CC BY
Self-archived copy's version: Publisher`s PDF
Background
Neighbourhood socioeconomic disadvantage correlates with cardiovascular disease risk. However, its relationship with subclinical atherosclerosis from childhood to midlife is not well-defined. We examined whether cumulative neighbourhood disadvantage is associated with carotid artery plaques, a measure of subclinical atherosclerosis.
MethodsWe analysed data from 1998 participants in the Cardiovascular Risk in Young Finns Study, a cohort followed from childhood (mean age 10.7 years in 1980) to adulthood (mean age 48.6 years in 2018–2020). Neighbourhood disadvantage was derived from national grid-based socioeconomic data and computed cumulatively across the life course. The number of carotid artery plaques (mean plaque count) was assessed by standardized ultrasound imaging. Multivariable Poisson regression models were used to evaluate the associations. Mediation analyses were used to assessed the role of ideal cardiovascular health (CVH) metrics.
ResultsHigher cumulative neighbourhood disadvantage from childhood to mid-adulthood was associated with a 1.24-fold increase in mean plaque count for every 1 standard deviation increase in cumulative disadvantage. This relationship persisted after controlling for parental carotid artery plaques, polygenic coronary artery disease risk score, and Framingham risk score. The association was partially explained by ideal CVH metrics, particularly smoking and blood pressure, which collectively accounted for almost half of the association.
ConclusionsLong-term exposure to neighbourhood socioeconomic disadvantage beginning in childhood is associated with subclinical atherosclerosis in midlife, independently of achieved socioeconomic position. These findings highlight the importance of cumulative socioeconomic environments across the life course and suggest that behavioural risk factors may partly explain observed neighbourhood-level associations with atherosclerosis.
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Funding information in the publication:
The Young Finns Study has been financially supported by the Academy of Finland: grants 356,405, 322098, 286284, 134309 (Eye), 126925, 121584, 124282, 129378 (Salve), 117797 (Gendi), and 141,071 (Skidi); the Social Insurance Institution of Finland; Competitive State Research Financing of the Expert Responsibility area of Kuopio, Tampere and Turku University Hospitals (grant X51001); Juho Vainio Foundation; Paavo Nurmi Foundation; Finnish Foundation for Cardiovascular Research; Finnish Cultural Foundation; The Sigrid Juselius Foundation; Tampere Tuberculosis Foundation; Emil Aaltonen Foundation; Yrjö Jahnsson Foundation; Signe and Ane Gyllenberg Foundation; Diabetes Research Foundation of Finnish Diabetes Association; EU Horizon 2020 (grant 755,320 for TAXINOMISIS and grant 848,146 for To Aition); European Research Council (grant 742,927 for MULTIEPIGEN project); Tampere University Hospital Supporting Foundation; Finnish Society of Clinical Chemistry; the Cancer Foundation Finland; pBETTER4U_EU (Preventing obesity through Biologically and bEhaviorally Tailored inTERventions for you; project number: 101080117); CVDLink (EU grant nro. 101,137,278) and the Jane and Aatos Erkko Foundation. MK was supported by the Wellcome Trust (221,854/Z/20/Z), the UK Medical Research Council (MR/Y014154/1), the National Institute on Aging (National Institutes of Health), USA (R01AG056477, R01AG062553), and the Research Council of Finland (350426).