Lower SES in childhood may be associated with an increased risk for MetS, IFG, and type 2 diabetes in adulthood. Special attention could be paid to children of low SES families to decrease the prevalence of MetS in adulthood.
These results show that childhood SES associates with several lifestyle factors 31 years later in adulthood. Therefore, attention could be paid to lifestyle behaviors of children of low SES families to promote cardiovascular health.
IMPORTANCEIncreased left ventricular (LV) mass and diastolic dysfunction are associated with cardiovascular disease. Prospective data on effects of childhood socioeconomic status (SES) on measures of LV structure and function are lacking. OBJECTIVE To examine whether family SES in childhood was associated with LV mass and diastolic function after adjustment for conventional cardiovascular disease risk factors in childhood and adulthood. DESIGN, SETTING, AND PARTICIPANTSThe analyses were performed in 2016 using data gathered in 1980 and 2011 within the longitudinal population-based Cardiovascular Risk in Young Finns Study. The sample comprised 1871 participants who reported family SES at ages 3 to 18 years and were evaluated for LV structure and function 31 years later.EXPOSURES Socioeconomic status was characterized as annual income of the family and classified on a 3-point scale. MAIN OUTCOMES AND MEASURESLeft ventricular mass indexed according to height at the allometric power of 2.7 and the E/e′ ratio describing LV diastolic performance at ages 34 to 49 years. RESULTSThe participants were aged 3 to 18 years at baseline (mean [SD], 10.8 [5.0] years), and the length of follow-up was 31 years. Family SES was inversely associated with LV mass (mean [SD] LV mass index, 31.8 [6.7], 31.0 [6.6], and 30.1 [6.4] g/m 2.7 in the low, medium, and high SES groups, respectively; differences [95% CI], 1.7 [0.6 to 2.8] for low vs high SES; 0.8 [−0.3 to 1.9] for low vs medium; and 0.9 [0.1 to 1.6] for medium vs high; overall P = .001) and E/e′ ratio (mean [SD] E/e′ ratio, 5.0 [1.0], 4.9 [1.0], and 4.7 [1.0] in the low, medium, and high SES groups, respectively; differences [95% CI], 0.3 [0.1 to 0.4] for low vs high SES; 0.1 [−0.1 to 0.3] for low vs medium; and 0.2 [0 to 0.3] for medium vs high; overall P < .001) in adulthood. After adjustment for age, sex, and conventional cardiovascular disease risk factors in childhood and adulthood, and participants' own SES in adulthood, the relationship with LV mass (differences [95% CI], 1.5 [0.2 to 2.8] for low vs high SES; 1.3 [0 to 2.6] for low vs medium; and 0.2 [−0.6 to 1.0] for medium vs high; P = .03) and E/e′ ratio (differences [95% CI], 0.2 [0 to 0.5] for low vs high SES; 0.1 [−0.1 to 0.4] for low vs medium; and 0.1 [0 to 0.3] for medium vs high; P = .02) remained significant.CONCLUSIONS AND RELEVANCE Low family SES was associated with increased LV mass and impaired diastolic performance more than 3 decades later. These findings emphasize that approaches of cardiovascular disease prevention must be directed also to the family environment of the developing child.
Increasing evidence supports the importance of socioeconomic factors in the development of atherosclerotic cardiovascular disease. However, the association of childhood socioeconomic status (SES) with arterial stiffness in adulthood has not been reported. Our aim was to determine whether higher childhood family-level SES is associated with lower arterial stiffness in adulthood. The analyses were performed using data gathered within the longitudinal Young Finns Study. The sample comprised 2566 participants who had data concerning family SES at ages 3 to 18 years in 1980 and arterial pulse wave velocity and carotid artery distensibility measured 21 or 27 years later in adulthood. Higher family SES in childhood was associated with lower arterial stiffness in adulthood; carotid artery distensibility being higher ( value±SE, 0.029±0.0089%/10 mm Hg; =0.001) and pulse wave velocity lower ( value±SE, -0.062±0.022 m/s; =0.006) among those with higher family SES in a multivariable analysis adjusted with age, sex, and conventional childhood cardiometabolic risk factors. The association remained significant after further adjustment for participant's SES in adulthood ( value±SE, 0.026±0.010%/10 mm Hg; =0.01 for carotid artery distensibility and value±SE, -0.048±0.023 m/s; =0.04 for pulse wave velocity) but attenuated after adjustment for adulthood cardiometabolic risk factors ( value±SE, 0.015±0.008%/10 mm Hg; =0.08 for carotid artery distensibility and value±SE, -0.019±0.02 m/s; =0.38 for pulse wave velocity). In conclusion, we observed an association between higher family SES in childhood and lower arterial stiffness in adulthood. Our findings suggest that special attention could be paid to children from low SES families to prevent cardiometabolic diseases primordially.
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