Summary Background Indices of cortisol activity, including the cortisol awakening response (CAR), diurnal slope, and cortisol output across the day (total daily output), are often studied as mechanistic indicators that could link stress with health. Yet there is a paucity of data speaking to their temporal features, particularly whether they behave in a more state- or trait-like manner across time. Methods To address this issue, data from 3 studies were used to assess CAR, diurnal slope and total daily output stability over different age groups and time spans: 130 healthy children and adolescents collected salivary cortisol samples 5 times/day (1, 4, 9 and 11 h after wake) over 2 days at 5 visits spaced 6 months apart (Study 1); 147 adolescent girls collected saliva 6 times/day (wake, 1, 4, 9 and 14 h after wake) for 2 days at 3 visits, each a year apart (Study 2); and 47 healthy, primarily middle age adults collected saliva 6 times/day (wake, 1, 4, 9 and 14 h after wake) for 3 days at 4 visits spaced 2–3 months apart (Study 3). Stability was estimated by multilevel model-derived intraclass correlation coefficients (ICCs). Results Across studies, approximately 50% of the variance in cortisol indices was attributable to day-to-day fluctuations, suggesting state-like properties. Of the indices, total daily output emerged as the most stable over time, followed by diurnal slope and CAR, but stability estimates were generally quite modest regardless of index and sample. Over time spans of >1 year, ICCs were ≤.13. Conclusions Most of the variance in CAR, diurnal slope and total daily output reflects day-to-day fluctuation; there was little evidence for more stable trait-like influences. These findings suggest that future research should focus on short-term fluctuations in stress, cortisol and health, as opposed to lengthy disease processes.

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Background Higher socioeconomic status (SES) has less impact on cardio-metabolic disease and preterm birth risk among Black women compared to White women, an effect called "diminishing returns." No studies have tested whether this also occurs for pregnancy cardio-metabolic disease, specifically preeclampsia, or whether preeclampsia risk could account for race-by-SES disparities in birth timing. Methods A sample of 718,604 Black and White women was drawn from a population-based California cohort of singleton births. Education, public health insurance status, gestational length, and preeclampsia diagnosis were extracted from a Statemaintained birth cohort database. Age, prenatal care, diabetes diagnosis, smoking during pregnancy, and pre-pregnancy body mass index were covariates. Results In logistic regression models predicting preeclampsia risk, the race-by-SES interaction (for both education and insurance status) was significant. White women were at lower risk for preeclampsia, and higher SES further reduced risk. Black women were at higher risk for preeclampsia, and SES did not attenuate risk. In pathway analyses predicting gestational length, an indirect effect of the race-by-SES interaction was observed. Among White women, higher SES predicted lower preeclampsia risk, which in turn predicted longer gestation. The same was not observed for Black women. Conclusions Compared to White women, Black women had increased preeclampsia risk. Higher SES attenuated risk for preeclampsia among White women, but not for Black women. Similarly, higher SES indirectly predicted longer gestational length via reduced preeclampsia risk among White women, but not for Black women. These findings are consistent with diminishing returns of higher SES for Black women with respect to preeclampsia.

Accumulating evidence suggests that the experience of early life adversity is a risk factor for a range of poor outcomes across development, including poor physical health in adulthood. The biological embedding model of early adversity (Miller, Chen, & Parker, 2011) suggests that early adversity might become embedded within immune cells known as monocytes/macrophages, programming them to be overly aggressive to environmental stimuli and insensitive to inhibitory signals, creating a “proinflammatory phenotype” that increases vulnerability to chronic diseases across the life span. We tested this hypothesis in the present study. Adolescent girls (n = 147) had blood drawn every 6 months across a 2.5-year period. To assess inflammatory responses to challenge, their monocytes were stimulated in vitro with a bacterial product, and production of the cytokine interleukin-6 was quantified. Hydrocortisone was added to cultures to assess the cells’ sensitivity to glucocorticoids’ anti-inflammatory signal. Using cluster analyses, we found that early life adversity was associated with greater odds of displaying a proinflammatory phenotype characterized by relatively larger interleukin-6 responses and relatively less sensitivity to glucocorticoids. In contrast, ongoing social stress was not associated with increasing odds of being categorized in the proinflammatory cluster. These findings suggest that early life adversity increases the probability of developing a proinflammatory phenotype, which, if sustained, could forecast risk for health problems later in life.