摘要:Objectives. We examined the association of childhood and adult socioeconomic status with longitudinal change in allostatic load (AL), a measure of biological dysfunction. Methods. The study sample included 6135 participants from the Multi-Ethnic Study of Atherosclerosis, aged 45 to 84 years, recruited in 2000 from 6 US counties; 3 follow-up examinations took place through September 2011. We calculated standardized scores for several metabolic and cardiovascular components relative to accepted clinical cut points for “higher risk” and then summed them to create an overall index of AL. We used mixed effects growth curve models to assess the relationship between socioeconomic status and AL as a linear function of time passed since the baseline examination; we included random effects for the intercept and slope. Results. Among those with lower baseline AL (< median), high adult education was associated with a significantly slower increase in AL over time, whereas there was no significant association among those with higher baseline AL. Conclusions. The relationship between socioeconomic status and patterns of change in health parameters may vary over time and with the accumulation of biological risk. Researchers have proposed multiple biological pathways by which socioeconomic status (SES) might influence health. A large and growing body of evidence documents SES gradients in major cardiovascular disease risk factors such as obesity, high blood pressure, abnormal lipid profiles, and diabetes 1–7 as well as markers of inflammation. 8–10 Researchers have also begun to examine the relationship between SES and a cumulative, multisystem biological risk index, allostatic load (AL), that might better capture the full biological impact resulting from low SES. Those studies have found that lower SES is associated with higher AL. 11–13 A few studies have examined the association of SES with AL at multiple time points through the life course; these were limited in racial/ethnic diversity and measured AL at 1 time point. 14–16 No study, to our knowledge, has examined the relationship between life course SES and the development of AL over multiple time points. We examined the relationship of both childhood and adult SES with longitudinal change in AL over time. Three major theories have been suggested regarding the influence of life course SES on cardiovascular disease, including the critical period, cumulative risk, and social mobility models. 17 The first suggests that exposure to low SES at critical stages of life plays a role in the development of disease. The second postulates that cumulative socioeconomic exposure plays an influential role in the development of disease. The third suggests that socioeconomic downward mobility, or decline in SES over time, is associated with increased health risks in adulthood. We tested these 3 models as potential contributors to the increased accumulation of biological stress over time as measured by AL. AL is a cumulative measure of physiologic dysregulation and an indicator of the overall “wear and tear” on physiological regulatory systems. The concept of AL focuses on the multisystems nature of biological risk, stating that multiple biological regulatory systems contribute to overall health risks. 11 A cumulative measure of biological risk such as AL may thus serve as a particularly relevant outcome when examining the effects of the accumulation of life course exposure to low SES, because it focuses on cumulative physiological effects across multiple major regulatory systems. Consistent with this perspective, research has shown that AL has a stronger association with SES than with any of its individual components. 11 To date, although multiple studies have examined the relationship between SES and AL at specific time points, none has considered longitudinal changes in AL over time or the relationship of such changes to SES. A longitudinal assessment of AL change addresses whether greater exposure to low SES is associated with a greater accumulation of AL over time. We sought to extend prior work by examining the associations of SES at childhood and adulthood, as well as socioeconomic intergenerational mobility, with longitudinal changes in cumulative biological dysregulation, as measured by AL. The Multi-Ethnic Study of Atherosclerosis (MESA) data are unique in their availability of AL measures over a 7-year period, 18 enabling us to assess a longitudinal measure of AL in a multiethnic cohort.