Relationship of early life stress and psychological functioning to blood pressure in the CARDIA study.

Hypertension is a serious and prevalent medical problem, with one in three U.S. adults estimated to have high blood pressure (Fields et al., 2004). Hypertension is a primary risk factor for coronary artery disease, the major cause of death in the U.S., yet nearly 90 percent of hypertension is essential, that is, of unknown origin. Hypertension is especially prevalent in African-American communities, an association that is believed to result in part from stressors related to low socioeconomic status (SES) (Bell, Adair, & Popkin, 2004). A propensity for high blood pressure can be evident at an early age. For example, Woodall and Matthews (1989) documented that boys (but not girls) from families characterized as unsupportive had stronger heart rate responses during a series of laboratory stressors, compared with boys from more supportive families. Matthews, Gump, Block, and Allen (1997) reported that high levels of background stress were associated with larger increases in diastolic blood pressure and total peripheral resistance during laboratory stressors in children aged 8 to 17. Matthews, Salomon, Brady, and Allen (2003) found that increases in blood pressure reactivity related to stress predicted future blood pressure rises in adolescence. As a group, these results suggest that early childhood environment likely contributes to high blood pressure Understanding how and why is an important research priority. The goal of the present study was to test a model of pathways that may relate childhood socioeconomic status and family environment to blood pressure and blood pressure change over ten years in a large cohort study of African-American and White men and women (the Coronary Artery Risk Development in Young Adults (CARDIA) study). As presented in Figure 1, the model posits links among low childhood SES, an early family environment marked by harsh parenting, poor emotional functioning, and poor health behaviors as predictors of blood pressure. We describe it here in more detail. Figure 1 Sample standardized path coefficients for the model of SBP. Solid lines indicate the pathways included in the initial test of the model. The dotted lines and values in the dotted boxes indicate estimates when CSES is linked directly with blood pressure. ... The first link in the model is childhood SES. Health-related risks of low SES begin in early childhood (Adler, Marmot, McEwen, & Stewart, 2000), and family environment is implicated in these processes (Repetti, Taylor, & Seeman, 2002). Considerable research links economic adversity in the family to poor or deteriorating quality of parenting, including higher levels of family conflict, a harsh restrictive parenting style, and chaotic or neglectful parenting (Emery & Laumann-Billings, 1998; McLoyd, 1998). Research also indicates that multiple early life environmental factors, including low socioeconomic status and a harsh family environment, can have a cumulative negative effect on children’s psychosocial functioning, health behavior, and physical health (Larson, Russ, Crall, & Halfon, 2008). Low SES is associated with elevated risk for hypertension (e.g., Karlamangla et al 2005; Lawlor & Smith, 2005), and this association may contribute to the SES gradient in coronary heart disease (Owen, Poulton, Hay, Mohamed-Ali, & Steptoe, 2003). Parental education is one indicator of childhood SES (Adler et al., 2000). The next variable in the model, a harsh early family environment (FE), is temporally prior to the subsequent variables in the model and has been independently correlated with each of the subsequent steps. Early family environments marked by harsh or chaotic parenting are reliably associated with deficits in offspring emotion regulation skills, including both internalizing and externalizing behavior in children (Repetti et al., 2002). A risky family environment has been related to more negative emotions (Repetti et al., 2002); to poor health behavior (Kertesz et al., 2007); to preclinical risk factors for illness, including elevated autonomic and cortisol responses to stress (Luecken, Rodriguez, & Appelhans, 2005; Taylor, Lerner, Sage, Lehman, & Seeman, 2004), to major physical health disorders (Felitti et al., 1998); and indirectly to compromised metabolic functioning (Lehman, Taylor, Kiefe, & Seeman, 2005) and elevated C-reactive protein (Taylor, Lehman, Kiefe, & Seeman, 2006). With respect to negative emotionality (NE), the next step in the model, indicators of chronic negative emotions, such as depression, anxiety, and hostility, have been tied to increased body mass index (BMI) (Pine, Goldstein, Wolk, & Weissman, 2001) to poor health behavior, (Caspi et al., 1997), and to hypertension (Davidson et al, 2000; Yan et al., 2003). Empirical and conceptual reviews suggest that negative emotions are linked to cardiovascular risk, and that examining NE as a construct, as opposed to merely one or more of its components, is appropriate, at least in prospective studies (Suls & Bunde, 2005). The fact that the behavioral and emotional consequences of growing up in low socioeconomic environment or in a harsh family environment are seen early in life, coupled with the relation of these variables to risks for health disorders later in life, makes them potentially useful in understanding the links between childhood SES, family environment, and blood pressure. Likewise, physical inactivity, risky health behaviors, and high BMI predict elevated blood pressure (Whelton, Chin, Xin, & He, 2002), and risk for mortality (Willcox et al., 2006). Because it is possible that health behaviors further contribute to the relation of childhood SES and family environment to elevated blood pressure they were assessed in the model. We tested whether the proposed model (see Figure 1) would be substantiated in its entirety and hypothesized support for each of the proposed pathways by which emotional and behavioral risk factors may influence blood pressure. In addition, because CARDIA is a large sample, relatively evenly balanced between African-Americans and Whites and between men and women, the research afforded an opportunity to examine whether the model would be supported in each of the four race-sex subgroups, and whether the rate of longitudinal change in blood pressure was consistent across groups.