Harsh parenting and adolescent health: a longitudinal analysis with genetic moderation.

A growing body of research has tested the hypothesis that harsh interactions with one’s parents during childhood may contribute to vulnerability to chronic diseases later in life (Repetti, Taylor, & Seeman, 2002; Shonkoff, Boyce, & McEwen, 2009). For example, the Adverse Childhood Experiences Study assessed the medical histories of more than 17,000 adults and found that the rates of cardiovascular disease, autoimmune disorders, and premature death were 1.5 to 2.0 times higher among respondents who were exposed to family violence than among those who were not exposed (Dube et al., 2009). Other studies reveal that adults reared in harsher home environments evince higher blood pressure, worse metabolic profiles, greater inflammatory activity, and higher levels of depressive symptoms than do adults reared in less harsh households (Miller, Chen, & Parker, 2011; Repetti et al., 2002). The present study was designed to advance understanding of the association between harsh parenting practices and health status by testing hypotheses involving prospective pathways among harsh parenting, anger, and health outcomes among a representative sample of rural African American adolescents. This study was designed specifically to address several conceptual and design issues. Research to date has often confounded the operationalization of harsh parenting with other adversity processes including family conflict, conflict among adult caregivers, family violence, neighborhood violence, and low socioeconomic status (SES). Also, all but one of these studies (Danese et al., 2009) measured harsh parenting using retrospective reports. The present study addressed these issues by assessing exposure to harsh parenting across preadolescence (ages 11–13), anger across adolescence (ages 16–18), and a health phenotype at age 19 to test hypothesized links across time between the receipt of harsh parenting across preadolescence and poor health outcomes. The health phenotype assessment included three indicators that not only index physical health and emotional well-being at age 19 but also have prognostic significance for health at midlife and beyond. The three indicators included a biomarker of chronic inflammation, C Reactive Protein (CRP); self-reported health problems; and depressive symptoms. CRP was selected because mounting evidence indicates that elevated levels of CRP are associated with heightened risk for age-related diseases, included hypertension, cardiovascular disease (CVD), stroke, diabetes, and cancer in adulthood (Chung et al., 2009; Singh & Newman, 2011). Consequently, CRP is used in clinical settings to evaluate risk of CVD and other chronic diseases of aging (Ridker, 2009; Yeh, 2005). Another emerging body of evidence indicates that stress can increase inflammation; the stimulation of the hypothalamic-pituitary-adrenal (HPA) axis and the sympathetic nervous system by stress can increase inflammatory processes as indicated by higher levels of CRP (Miller et al., 2011). Relevant to the present study are recent findings demonstrating that life stress during adolescence is positively associated with contemporaneous CRP levels (Fuligni et al., 2009). The second indicator, self-reported health problems, consistently shows a positive association with life stress (Sutin, Costa, Wethington, & Eaton, 2010) and forecasts mortality over and above current health status (Idler & Benyamini, 1997). Depressive symptoms, the third indicator, have been found to heighten risk for morbidity and mortality from chronic diseases associated with aging, including CVDs, autoimmune conditions, and metabolic disorders (Evans et al., 2005; Hemingway et al., 2003). Growing up in harsh rearing environments has been found to increase vulnerability to the development of depressive symptoms across the lifespan (Heim & Nemeroff, 2001). The following sections focus on the hypothesized prospective contributions that harsh parenting, anger, and genetic sensitivity make to the adolescent health phenotype. Harsh Parenting, Anger, and Health The literature on determinants of parenting chronicles the ways in which the strains and multiple demands imposed by socioeconomic stressors tax even the most concerned caregivers and lead them to use harsh parenting practices that, by design, quickly terminate aversive child and adolescent behavior (Belsky, 1984; Brody et al., 2008). These findings generalize across racial and ethnic groups (Conger & Donnellan, 2007). Harsh parenting is often part of a set of parenting practices that also includes high levels of vigilance and control. These practices are used particularly by parents living in dangerous contexts to protect their children against neighborhood dangers, risk behaviors, and the influence of delinquent peers (R. H. Bradley et al., 2000; Brody & Flor, 1998; Brody et al., 2001; J. Taylor, Spencer, & Baldwin, 2000). Generally, however, research suggests that growing up with a large dose of harsh parenting does not lead to positive physical and mental health outcomes (Repetti et al., 2002). Its most prominent legacy concerns problems with emotion regulation, particularly with respect to elevated levels of anger and its expression (Davies, Winter, & Cicchetti, 2006; Simons et al., 2011). Research indicates that youths who receive harsh parenting over time become more likely to maintain a heightened state of vigilance for signs of anger and to respond with anger to incidents in which anger is expressed (Cicchetti & Rogosch, 2009; Dodge, Pettit, & Bates, 1994). We predict that exposure to harsh parenting during preadolescence will be positively associated with anger during adolescence and health problems at age 19. Episodic and chronic anger states are hypothesized to trigger reactions from the sympathetic-adrenal-medullary (SAM) and HPA axis systems, which results in frequent releases of catecholamines and cortisol (Chorpita & Barlow, 1998; Matthews, Woodall, Kenyon, & Jacob, 1996). Although this chain reaction is adaptive in the short term, continuous exposure to cortisol and catecholamines over time exacts a toll by promoting the development of glucocorticoid resistance, disruptions in the glucocorticoid anti-inflammatory system, and, eventually, elevated levels of systemic inflammation (Black, 2006). The same stress physiology pathways have been hypothesized to contribute to the development of depressive symptoms (McEwen, 1998); recent findings tend to support this hypothesis (Miller & Cole, 2012). Thus, relatively higher levels of anger across adolescence are predicted both to forecast a poor health phenotype and to serve as a mediator connecting harsh parenting with health at age 19. The Serotonin Transporter Gene as a Moderator Stressful events have been shown to increase the probability of a wide variety of physical and mental health problems, and yet many individuals exposed to environmental or negative emotional stressors do not become sick or emotionally dysregulated. During the past decade, much research investigated the hypothesis that particular genetic polymorphisms increase an individual's response to stress and enhance the probability of compromised physical and mental health functioning (Way & Taylor, 2010). Much of this research has focused on a genetic marker of differential functioning in the serotonin system, the 5-HTTLPR. This polymorphism has two principal alleles, long (l, 16 repeats) and short (s, 14 repeats). The s allele is associated with reduced serotonergic neurotransmission; low central serotonergic transmission has been linked to robust activity in the amygdala (Heinz et al., 2005), a brain region involved in the processing of verbal and nonverbal threats (Isenberg et al., 1999), and with enhanced reactivity to punishment cues in the environment (Battaglia et al., 2005; Hariri, Drabant, & Weinberger, 2006; Hariri et al., 2002). Recent research has extended these findings by demonstrating that ss and sl allele carriers direct preferential attention toward, and have difficulty in disengaging from, threat-related stimuli; they also engage in more rumination about such stimuli (Beevers, Wells, Ellis, & McGeary, 2009; Osinsky et al., 2008). In addition, researchers have recently investigated the interactions of stressful life events and family characteristics with the 5-HTTLPR genotype (Petersen et al., 2012). Findings demonstrate that stress may affect the likelihood that adolescents with a genotype associated with low serotonin activity will experience symptoms of anxiety or depression. Together, this literature suggests that the effects of the 5-HTTLPR s allele may place youths at greater risk for the negative effects of harsh parenting and anger by increasing vigilance, reactivity, rumination, anxiety, and depressive symptoms.