Biological Sensitivity to the Effects of Childhood Family Adversity on Psychological Well-Being in Young Adulthood

Abstract

The theory of biological sensitivity to context may inform our understanding of why some children exposed to family adversity develop mental health problems in emerging adulthood whereas others demonstrate resilience. This study investigated the interactive effects of heart rate (HR) reactivity and childhood family adversity (maltreatment and changes in family structure) on depressive symptoms and positive affect among 150 undergraduate students (18–28 years old; 77% White, non-Hispanic; 61% female). Participants reported on childhood parental divorce or death, and child maltreatment, and current depressive symptoms and positive affect. HR reactivity was assessed in response to a laboratory interpersonal stressor. HR reactivity moderated the effects of child maltreatment on depressive symptoms and positive affect; higher maltreatment was associated with more depressive symptoms and less positive affect, but only among those with average and higher levels of HR reactivity. Results suggest that higher physiological reactivity may confer greater susceptibility to environmental contexts.

Keywords

physiological processes depression resilience child maltreatment

Childhood maltreatment and changes in family structure (e.g., parental divorce or bereavement) are robust risk factors predisposing children to psychological problems in emerging adulthood (Connolly, 2014; Dion et al., 2016; Gutman & Sameroff, 2004; Herrenkohl, Hong, Kilka, Herrenkohl, & Russo, 2013). Yet, there is significant variability in the developmental processes and outcomes of affected children. A prospective study by Herrenkohl, Hong, Kilka, Herrenkohl, and Russo (2013) found that adults who were abused or neglected as children reported higher levels of anxiety, depression, and worse general mental health than adults who were not abused or neglected as children. However, only approximately one quarter of adults who experienced child abuse or neglect reported moderate to severe depression or anxiety, and the average number of depressive and anxiety symptoms reported by these adults was below clinically significant levels (Herrenkohl et al., 2013). Given the variability in outcomes, more work is needed to identify factors promoting resilience in affected youth.

Youth who experience parental death also have increased vulnerability to psychopathology and physical health problems, but most bereaved children do not experience long-term problems, and some may even demonstrate enhanced adaptive abilities later in life (Luecken, 2008). Similarly, children of divorced families demonstrate more behavior and psychological maladjustment relative to children of nondivorced families (Amato & Keith, 1991), and these problems can persist into adulthood (Rutter, Kim-Cohen, & Maughan, 2006). However, although changes in family structure predispose youth to risk trajectories, the majority of youth are able to adjust to these circumstances without developing psychological problems later in life (Amato & Keith, 1991).

The theory of biological sensitivity to context (BSC; Boyce & Ellis, 2005; Ellis & Boyce, 2008; Ellis, Boyce, Belsky, Bakermans-Kranenburg, & van IJzendoorn, 2011; Ellis, Essex, & Boyce, 2005) may inform our understanding of why some children who experience family adversity demonstrate mental health problems in emerging adulthood whereas others demonstrate resilience. In contrast to stress–diathesis/dual-risk models that evaluate factors that confer heightened vulnerability to adverse conditions, BSC models suggest that there are susceptibility factors that not only confer heightened vulnerability to adverse conditions but also promote enhanced positive outcomes under supportive contexts. Although other theories (e.g., differential susceptibility; Belsky, 1997) similarly posit variation in the extent to which people are influenced by their environment, BSC is unique in offering a specific mechanism of context susceptibility: the magnitude of biological stress responses. Specifically, people with more reactive stress responses are thought to be more susceptible to the effects of their environment.

BSC theory’s central tenet, that highly physiologically reactive individuals who experienced environmental adversity are more likely to develop mental and physical health problems than their less reactive counterparts, has been supported across numerous physiological systems (Obradovic, 2012), especially the autonomic nervous system (ANS). The sympathetic branch (SNS) of the ANS initiates physiological arousal (e.g., increased heart rate [HR] and blood pressure, sweating) in response to environmental challenges. The parasympathetic branch (PNS) regulates rest and recovery and promotes autonomic homeostasis (e.g., decreases HR and blood pressure). A commonly studied method of assessing ANS activity uses HR reactivity, which captures both sympathetic and vagal influences on the heart (unlike other measures that focus solely on one branch of activation; Berntson, Cacioppo, & Quigley, 1993).

Most of the empirical support for BSC has demonstrated that elevated ANS reactivity operates as a susceptibility factor to the effects of early family environments on childhood outcomes. Boyce and colleagues (1995) demonstrated that high mean arterial pressure (MAP) reactivity to a laboratory stress test in early childhood interacts with childcare quality to prospectively predict respiratory illnesses. Consistent with BSC, children with higher MAP reactivity demonstrated elevated rates of respiratory illnesses if raised under stressful conditions but fewer respiratory illnesses if raised in low-stress conditions. Recently, Obradovic, Bush, Stamperdahl, Adler, and Boyce (2010) found that respiratory sinus arrhythmia reactivity to laboratory challenges interacted with a composite measure of early family adversity to predict concurrent psychological and psychosocial adjustment and short-term change in academic competence among kindergartners. Similarly, among older children, high SNS reactivity (indexed by skin conductance level [SCL] reactivity) during a cognitive challenge conferred risk for increases in psychological problems among those exposed to high levels of marital conflict but protected against large increases in these problems among children from less conflictual homes (El-Sheikh, Keller, & Erath, 2007).

Despite converging evidence that high ANS reactivity confers susceptibility to the effects of childhood environments on adjustment, there remain inconsistencies and limitations in the literature. First, some studies find buffering effects of biological reactivity against the effects of family adversity on behavioral problems, without promoting exceptional well-being among children raised in nonadverse families, which is more consistent with stress–diathesis/dual-risk models than with BSC (e.g., El-Sheikh & Whitson, 2006); other studies find that less reactivity confers susceptibility (e.g., El-Sheikh, Harger, & Whitson, 2001). Second, few researchers have assessed sensitivity to multiple contexts among the same sample. Most empirical investigations have focused on the family environment; however, it is not known whether high reactivity confers susceptibility to stressful but potentially supportive family environments (e.g., parental divorce or loss, which have not been represented in the literature) or only to more severe adversity (e.g., child maltreatment). Third, although BSC suggests highly physiologically reactive people are more susceptible to environmental influences, for better and for worse, researchers have primarily focused on psychological and physical health problems, with limited consideration of positive outcomes.

Finally, more work is needed to assess whether support for BSC found in early childhood research can be replicated in adolescence and emerging adulthood. Adolescence and young adulthood are particularly important periods to study biological susceptibility due to the dramatic physiological, emotional, cognitive, social, and academic changes that occur; these changes confer unique challenges that have implications for stress responsivity and the development of psychopathology (Dahl & Gunnar, 2009). A combination of unique stressors and increased autonomy to navigate problems make these developmental periods times of increased risk for poor psychological outcomes; in fact, the incidence of psychopathology increases during the transition to adulthood (Tanner et al., 2007). Recent cross-sectional studies provide limited evidence that ANS reactivity moderates concurrent associations between family environments and psychological well-being in adolescence and emerging adulthood. Wagner and Abaied (2016) demonstrated that parental psychological control during adolescence was associated with reactive relational aggression in emerging adulthood only among participants with high SCL reactivity, consistent with BSC. In contrast, Sijtsema and colleagues (2013) found that among boys (14–18 years old) with less HR reactivity during a stressful speech task, family cohesion was positively associated with prosocial behavior and negatively associated with aggressive/rule-breaking behavior.

The current study assessed the role of ANS reactivity in moderating the associations between childhood family adversity and psychological problems and well-being in emerging adulthood. The study builds on prior research in several ways. First, we assessed sensitivity to two forms of family adversity: changes in family structure (specifically, parental divorce and loss), which has not been studied in the susceptibility literature thus far, and child maltreatment. Second, we evaluated whether ANS reactivity (indexed by HR reactivity) acts as a susceptibility factor in emerging adulthood. Finally, we assessed indicators of psychological problems (depressive symptoms) and of resilience (positive affect). We hypothesized that (a) more highly reactive participants who experienced higher child maltreatment would report more depressive symptoms and less positive affect than less reactive participants and those who reported lower maltreatment and (b) highly reactive participants who experienced changes in family structure (parental bereavement or parental divorce) would report more depressive symptoms and less positive affect than less reactive participants and those who did not experience changes in family structure during childhood.

Method

Participants

Participants included 150 undergraduate students (18–28 years of age, M = 19.7, SD = 2.1) from continuously married, parentally bereaved, or parentally divorced families. Sample demographics are displayed in Table 1. The current analyses use data from the first day of participation in a broader study of the effects of child adversity on physical and mental health. Eligibility criteria for participants from continuously married families (n = 51) included two living, married, and biological parents; bereaved families (n = 49) experienced the death of one biological parent prior to the participant’s 16th birthday; and divorced families (n = 50) included two living biological parents who divorced before the participant’s 16th birthday. Exclusion criteria included a history of serious illness, acute illness, or use of medications that affect neuroendocrine or cardiovascular functioning (although hormone-based oral contraceptives were allowed) and parental divorce or death that occurred after the participant’s 16th birthday.

Table 1.

Sample Descriptives.

Study Variable	Full Sample (n = 150)	Loss (n = 49)	Divorced (n = 50)	Continuously Married (n = 51)	p Value
Demographic N
Sex					.992
Male	59	19	20	20
Female	91	30	30	31
Ethnicity					.983
White, non-Hispanic	115	37	39	39
Other	34	11	11	12
Income					.008
US$0–29,999	19	12	7	0
US$30,000–44,999	19	7	9	3
US$45,000–59,999	17	7	6	4
US$600,000–79,999	15	4	4	7
US$80,000–99,999	25	7	8	10
US$100,000 and above	50	10	14	26
Continuous variable mean (standard deviation)
Age	19.7 (2.1)	19.1^a (1.4)	20.2^b (2.4)	19.9^ab (2.3)	.028
Maltreatment	2.2 (2.2)	2.21^ab (2.1)	3.20^b (2.5)	1.3^a (2.2)	.000
Heart rate
Baseline	73.8 (10.6)	73.5 (10.2)	75.4 (11.2)	72.5 (10.6)	.937
Task	89.6 (14.3)	90.0 (15.3)	90.7 (12.6)	88.2 (15.1)	.391
Depressive symptoms	9.8 (7.9)	10.3 (8.5)	10.0 (8.2)	9.0 (7.1)	.449
Positive affect	23.4 (6.3)	23.0 (4.9)	24.3 (6.7)	22.8 (7.0)	.416

Note. Superscript letters represent Tukey's honest significant difference (HSD) test post hoc analyses of homogenous subsets; means with the same superscript do not significantly differ. Analyses with ethnicity compared Caucasian, non-Hispanic participants to non-Caucasian or Hispanic participants.

Procedures

The study protocol was approved by the (Arizona State University) institutional review board prior to study inception. Upon arriving to the lab, participants read and signed informed consent forms. Participants were asked to refrain from alcohol the night before participation, cold medication the day of participation, and caffeine, energy drinks, eating, smoking, or exercise for at least 2 hrs prior to participation. Participants who were not compliant with these instructions were rescheduled. A trained research assistant applied a blood pressure cuff to the participant’s nondominant arm and sampled HR for a 10-min baseline period, after which participants completed an interpersonal stressor (speech) task. Following the task, participants completed survey measures. Participants were not financially compensated for completing this component of the study; however, most participants completed a larger, 2-day study for which they received US$75.

Interpersonal stressor task

The task was adapted from Saab, Matthews, Stoney, and McDonald’s (1989) speech task, in which participants were given 4 min to prepare and 4 min to deliver a speech to defend themselves from a false accusation of shoplifting. Participants were told the strength and clarity of their arguments would be rated relative to speeches given by similar participants. The speech was videotaped and given in front of both the experimenter and the “lab supervisor.” Prior reports demonstrate that this task elicits significant cardiovascular reactivity (Luecken, Rodriguez, & Appelhans, 2005).

Measures

Child maltreatment

Child maltreatment was assessed using the 25-item Childhood Trauma Questionnaire (CTQ; Bernstein et al., 1994; α = .90). Participants rated the extent to which they experienced emotional, physical, and sexual abuse and emotional and physical neglect prior to age 16. Items are rated for the frequency of occurrence on a 5-point scale, with 0 indicating never and 4 indicating very frequent. Scores on each of the five subscales were averaged, and then the mean scores on each subscale were added to form a composite of total maltreatment experiences. Higher scores indicate a greater frequency of maltreatment. Due to its late addition to the larger study, the CTQ was completed by a subset (n = 129) of the full sample.

Depressive symptoms

Depressive symptoms were assessed using the 21-item Beck Depression Inventory II (Beck, Steer, & Brown, 1996; α = .89). Each item is rated on a 4-point scale, and responses are summed to form a total score ranging from 0 to 63. Higher scores represent a greater level of depressive symptomatology.

Positive affect

Positive affect in the past week was assessed using the 10-item Positive Affect Scale of the Positive Affect and Negative Affect Schedule (Watson, Clark, & Tellegen, 1988; α = .83). The Positive Affect Scale has good internal consistency and excellent convergent and divergent validity (Watson et al., 1988). Items are rated on a 5-point scale, and responses are summed to form a total score; higher scores represent a higher positive affect.

HR reactivity

HR was sampled every minute using an Omega 5600 adult blood pressure monitor (Invivo Research, Orlando, FL); automated blood pressure (BP) monitors are commonly used, reliable methods of obtaining HR data (e.g., Smith & Jordan, 2015). Seven participants were missing HR data due to participant movement or experimenter error. The first 5 min of readings were discounted to allow adaptation to the novel laboratory setting, and the following 5 min of readings were averaged for a baseline. Readings taken during the 4-min speech delivery were averaged for a measure of HR during the stressor. HR reactivity was assessed as the standardized residual change score from the baseline activity to the speech task.

Data Analyses

Missing data

Of the 150 cases, 27 (18.0%) were missing on either the measure of HR reactivity or child maltreatment. Participants with missing data did not differ from participants with complete data with respect to body mass index, age, family group, family income, or ethnicity. The percentage of participants with missing data did differ by sex, χ2 (1, N = 150) = 5.61, p = .02, such that male participants were more likely to have missing data than female participants. Participant sex was included as a covariate in analyses. All analyses were conducted with Mplus Version 7.2 which uses all available values and maximum likelihood estimation, which is superior to pairwise or listwise deletion (Enders, 2001).

Preliminary analyses

Primary study variables were assessed for skewness, kurtosis, and outliers, and none exceeded recommended cutoffs of 2 for skewness and 7 for kurtosis (West, Finch, & Curran, 1995). Two potential outliers were identified with child maltreatment values 3 SD above the sample mean. When analyses were repeated removing these two participants, results were not significantly affected. Therefore, all data were retained for analyses.

Correlations were analyzed between potentially relevant covariates and HR reactivity, including age, ethnicity, family income, average caffeine intake, smoking, medication use, and body mass index. None reached statistical significance, and therefore, these variables were not considered further in the analyses. One-way analysis of variances were conducted to assess for differences on continuous study variables, and χ² tests were conducted to assess whether there were differences on categorical study variables for continuously married families, bereaved families, and divorced families. Independent samples t tests and χ² tests were conducted to assess whether there were differences in study variables between male and female participants.

Primary analyses

Two regression models were evaluated to estimate the main and interactive effects of family group and HR reactivity, and child maltreatment and HR reactivity on mental health outcomes. First, family group¹ (parentally bereaved and parentally divorced codes), HR reactivity, and their interaction were entered into a model predicting depressive symptoms and positive affect, adjusting for child maltreatment and participant sex. Second, child maltreatment, HR reactivity, and their interaction were entered in a model to predict depressive symptoms and positive affect (Model 2), adjusting for family group and participant sex.

Results

Preliminary Analysis

Table 1 presents descriptive statistics. Family income was higher in continuously married families than in parentally divorced or bereaved families. Youth from parentally divorced families were younger than youth from parentally bereaved families, and youth from parentally divorced families endorsed more exposure to child maltreatment than youth from continuously married families. There were no statistically significant differences in participant sex, ethnicity, HR reactivity, depressive symptoms, or positive affect by family group. Bivariate correlations are presented in Table 2. Males reported fewer depressive symptoms (M _depress = 8.2, SD _depress = 7.0) than females (M _depress = 10.8, SD _depress = 8.3), t(148) = −2.0, p = .047, and more positive affect (M _pos = 24.9, SD _pos = 5.4) than females (M _pos = 22.4, SD _pos = 6.6), t(148) = 2.45, p = .015.

Table 2.

Bivariate Correlations Between Study Variables.

Study Variables	1	2	3	4	5	6	7
1. Heart rate reactivity	—
2. Age	−0.11	—
3. Ethnicity^a	−0.13	0.08	—
4. Childhood maltreatment	−0.14	0.16	0.18	—
5. Sex^b	0.05	−0.12	−0.03	0.02	—
6. Depressive symptoms	−0.07	−0.14	−0.07	0.33	0.16	—
7. Positive affect	−0.01	0.10	0.05	−0.19	−0.20	−0.53	—

Note. Correlation coefficients in boldface are statistically significant, p < .05.

^aCoded 1 = White, non-Hispanic and 2 = nonWhite. ^bCoded 0 = male and 1 = female.

There were no sex differences in age, ethnicity, family income, child maltreatment, or HR reactivity. Child maltreatment was not significantly associated with HR reactivity.

Primary Results

Model 1: Effects of parental death or divorce

The first model predicted depressive symptoms and positive affect from family group, HR reactivity and their interaction, adjusting for sex and child maltreatment. As shown in Figure 1, sex (p = .043) and maltreatment (p < .001) were the only statistically significant predictors of depressive symptoms, such that women and those with more child maltreatment exposure reported more depressive symptoms. Family group (bereaved, p = .921; divorced, p = .176), HR reactivity (p = .842), and their interactions (HR Reactivity × Bereaved Group, p = .176; HR Reactivity × Divorced Group, p = .318) were not significant predictors of depressive symptoms.

Figure 1.

Structural equation model of depressive symptoms and positive affect regressed on family group, heart rate reactivity, and their interaction, adjusting for sex and child maltreatment. Covariances between exogenous variables and error terms not shown for visual clarity. Covariates are shown in boxes with dashed lines. * Statistically significant pathways (at p < .05) are shown in bold, with their parameter estimates and standard errors above the arrow.

Parental divorce (p = .015), sex (p = .009), and maltreatment (p = .003) were significant predictors of positive affect, such that parental divorce, male sex, and less maltreatment were associated with more positive affect. Parental bereavement (p = .421), HR reactivity (p = .618), and their interactions (HR Reactivity × Bereaved Group, p = .772; HR Reactivity × Divorced Group, p = .218) were not significant predictors of positive affect.

Model 2: Effects of child maltreatment

The second model predicted depressive symptoms and positive affect from child maltreatment, HR reactivity, and their interaction, adjusting for sex and family group. As shown in Figure 2, the HR Reactivity × Child Maltreatment interaction predicted positive affect, p = .009, and depressive symptoms, p = .018.

Figure 2.

Structural equation model of depressive symptoms and positive affect regressed on childhood maltreatment, heart rate reactivity, and their interaction, adjusting for sex and family group. Covariances between exogenous variables and error terms not shown for visual clarity. Covariates are shown in boxes with dashed lines. * Statistically significant pathways (at p < .05) are shown in bold, with their parameter estimates and standard errors above the arrow.

Post hoc probing was conducted by evaluating the simple slopes at the means of child maltreatment and HR reactivity and 1 SD above and below the means of the two variables (Aiken & West, 1991). The simple slopes of the effect of maltreatment on depressive symptoms were significant for above average HR reactivity, p < .001, and for average HR reactivity, p < .001, but not for below average HR reactivity, p = .362. As shown in Figure 3, participants with below average reactivity showed similar levels of depressive symptoms at each level of child maltreatment. In contrast, participants with above average reactivity showed the least depressive symptoms when they reported few maltreatment experiences, but the most depressive symptoms when they reported higher levels of maltreatment experiences.

Figure 3.

Simple slopes of the effect of maltreatment on depressive symptoms at high, average, and low levels of heart rate reactivity.

The simple slope of the effect of maltreatment on positive affect was significant for above average HR reactivity, p < .001, and average HR reactivity, p = .001, but not for below average HR reactivity, p = 0.885. As shown in Figure 4, participants with above average HR reactivity showed the most positive affect when they reported few maltreatment experiences but the least positive affect when they reported higher maltreatment.

Figure 4.

Simple slopes of the effect of maltreatment on positive affect at high, average, and low levels of heart rate reactivity.

Discussion

Experiences of parental divorce, parental death, and maltreatment during childhood are established risk factors for poor psychological adjustment later in life (Connolly, 2014; Dion et al., 2016). However, there is considerable variability in the extent to which these experiences affect children (Amato & Keith, 1991; Luecken, 2008). We evaluated whether heightened HR reactivity acts as a biological susceptibility factor to the effects of maltreatment and parental loss or divorce during childhood on depressive symptoms and positive affect in emerging adulthood.

Results supported the anticipated crossover interactions, such that youth who had higher HR reactivity and experienced greater maltreatment exhibited the most depressive symptoms and least positive affect. On the other hand, youth who had higher HR reactivity and were raised in a nonabusive context demonstrated fewer depressive symptoms and more positive affect than youth who had lower HR reactivity. Further, youth who had lower HR reactivity showed similar levels of depressive symptoms and positive affect regardless of maltreatment experiences. Contrary to expectations, associations between family structure and mental health problems and resilience in young adulthood were not moderated by HR reactivity.

Our results add to an emerging body of work demonstrating that the variability in the extent to which child maltreatment influences psychological well-being may be explained by biological sensitivity (e.g., Hagan, Roubinov, Mistler, & Luecken, 2014). These results build on prior research that has largely focused on susceptibility in childhood, and suggest HR reactivity may also operate as a susceptibility factor in emerging adulthood, which has heretofore been neglected in the literature. Emerging adulthood is an especially important period to study biological sensitivity to mental health risk, given the increased rates of psychopathology during this developmental period (Tanner et al., 2007). HR reactivity may increase susceptibility to maltreatment by influencing an individual’s ability to mount a “fight-or-flight” response to environmental challenges, which may lead to physiologically driven behavioral adaptations to these contexts. Whereas results from prior studies differ across different types of stressor paradigms (Obradovic, 2012), physiological reactivity to an interpersonal stressor may be a particularly salient marker of biological sensitivity to the effects of social environments characterized by low social support and high threat (as may be indicated in maltreatment experiences). The paradigm used in the present study, in which participants had to defend themselves against a false accusation of shoplifting, offers an ecologically valid simulation of a real-world scenario characterized by social threat. Experimental designs are also needed to determine whether experientially induced changes in physiological reactivity can upregulate or downregulate susceptibility to environmental contexts. Overall, our results add to a growing body of research that suggests the utility of assessing HR reactivity, a noninvasive measure of ANS reactivity, as a biological susceptibility factor to adverse family contexts.

However, HR reactivity did not modulate the effects of childhood experiences of parental divorce or death. For children, the experience of parental divorce or bereavement may be qualitatively different from maltreatment in several meaningful ways. The persistent presence of a neglectful or an abusing caregiver, and lack of protection against the abuser, may create a consistently unsafe environment and prevent opportunities for social support (Luthar, Crossman, & Small, 2015). Divorce and bereavement experiences, albeit potentially highly stressful, are not directly targeted at the child, and children’s experiences of stress and social support in these contexts may be more variable. Not all experiences of parental divorce are negative; parents may offer warmth and support that buffers the potential adverse effects of divorce. Research also suggests divorce may be beneficial for youth when marital discord is high (Amato, 2001). Alternatively, interparental conflict may continue after the divorce, resulting in loss of time or contact with one parent or children acting as intermediaries between feuding parents. Although parental death is an acute traumatic experience involving the permanent loss of an attachment figure, there is tremendous variability in bereavement experiences (Luecken, 2008). Parental loss can occur in a family that was high-functioning prior to the loss, and youth may be well supported by the other, living parent, and/or extended family members. Other sources of variability include the cause of death and the child’s age at the time of parental divorce or bereavement, which may moderate the long-term effects of these experiences.

The experiences of parental loss or divorce were not directly related to young adult’s depressive symptoms or positive affect. However, when examining the effects of parental loss or divorce in the full model, we statistically adjusted for maltreatment, which revealed a positive association between parental divorce and positive affect. Maltreatment appears to act as a suppressor variable in the relation between parental divorce and positive affect such that a relation is statistically stronger after accounting for maltreatment (for a description of suppressor variables, see MacKinnon, Krull, & Lockwood, 2000). In general, the circumstances surrounding parental death or divorce, such as maltreatment, interparental conflict, economic support, and social support, may be more salient predictors of long-term mental health than the death or divorce itself and may be a better focus for studies examining context sensitivity.

The current results were evident in a young adult sample that was not specifically selected for child maltreatment, suggesting that even among young adults who experienced less extreme forms of adversity, child maltreatment predicts psychological problems to varying degrees based on HR reactivity. Larger interactive effects between stress reactivity and child family adversity may be detected at the extreme ends of environmental conditions (Obradovic, Bush, Stamperdahl, Adler, & Boyce, 2010), and clinical samples with more severe exposure to maltreatment may increase power to detect biological susceptibility to these experiences. With greater variability in maltreatment experiences, researchers would also be able to address outstanding questions regarding whether differences in type and duration of maltreatment experience (e.g., physical vs. sexual abuse, and cumulative effects of experiencing several types of maltreatment) are associated with different levels of sensitivity to these effects.

There are several limitations to the current analyses. Maltreatment was assessed retrospectively, potentially raising concerns about biased associations between maltreatment and psychological problems. However, longitudinal research on the validity of retrospective recall of childhood maltreatment suggests that recall bias does not significantly affect estimates of child maltreatment’s impact on mental health (Fergusson, Horwood, & Boden, 2011). Parental divorce and bereavement were reported retrospectively, but these events are unlikely to be subject to recall bias. The study evaluated a college student sample, and our results may not generalize to other populations.

Although we did not find evidence that HR reactivity in the current sample was related to child maltreatment, parental divorce, or parental loss, our use of a cross-sectional design cannot rule out the possibility that childhood experiences may have affected ANS reactivity. Although susceptibility is often interpreted as a constitutional factor, early environments may influence stress reactivity later in life; theoretical extensions of BSC, such as the adaptive calibration model (Del Giudice, Ellis, & Shirtcliff, 2011), maintain that physiological stress response systems adapt to either promote or reduce susceptibility based on early environmental exposure. Researchers have only recently begun to identify which children, under what conditions, will develop upregulated physiological reactivity in response to early environmental adversity or exceptional nurturing (Obradovic, 2012). Research is needed that incorporates multiple measures of stress responsivity and employs longitudinal designs that can address whether (and if so, how) stress response systems are influenced by early environmental contexts. In addition, the present study was only able to address biological sensitivity to the effects of adverse family environments. Thorough tests of BSC should assess whether HR reactivity also operates as a susceptibility factor to the benefits of positive family environmental contexts.

Results of this study suggest it is important to assess physiological indicators in order to understand the variability in outcomes of maltreated youth. Our study builds on recent work (Hagan et al., 2014) that suggests adult’s cortisol reactivity moderates the effects of child maltreatment on internalizing problems in young adulthood by replicating this pattern in a unique sample with a different physiological domain (i.e., ANS reactivity) and extending analyses to consider an indicator of resilience (positive affect). Future interventions may benefit from awareness that maltreated children with high levels of physiological reactivity may be more sensitive to the adverse effects of their experiences, may be more in need of intervention, or may respond to strategies targeting elevated physiological reactivity.

In sum, this study provides support for biological sensitivity to the effects of child family adversity on psychological well-being in emerging adulthood. Our results suggest that young adults with high levels of HR reactivity to interpersonal stress are more sensitive to the effects of child maltreatment on depressive symptoms and positive affect than youth with lower HR reactivity. HR reactivity did not alter associations between childhood experiences of parental divorce or death and depressive symptoms or positive affect. Whereas most studies have focused on one specific form of environmental adversity (Obradovic et al., 2010), the present study suggests biological sensitivity may not be uniformly present across environmental contexts.

Footnotes

Declaration of Conflicting Interests

The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Funding

The author(s) disclosed receipt of the following financial support for the research, authorship, and/or publication of this article: This research was supported by grant 0130024N (principal investigator: Linda Luecken) from the American Heart Association and by a National Science Foundation Graduate Research Fellowship to Jennifer Somers.

Note

References

Aiken

L. S.

West

S. G.

(1991). Multiple regression: Testing and interpreting interactions. Thousand Oaks, CA: Sage.

Amato

P. R.

(2001). Good enough marriages: Parental discord, divorce, and children’s well-being. Virginia Journal of Social Policy & the Law, 9, 71–94.

Amato

P. R.

Keith

(1991). Parental divorce and the well-being of children: A meta-analysis. Psychological Bulletin, 110, 26–46.

Beck

A. T.

Steer

R. A.

Brown

G. K.

(1996). Manual for the Beck Depression Inventory-II. San Antonio, TX: Psychological Corporation.

Belsky

(1997). Variation in susceptibility to rearing influence: An evolutionary argument. Psychological Inquiry, 8, 182–186.

Bernstein

D. P.

Fink

Handelsman

Lovejoy

Wenzel

Sapareto

, & Gurriero

(1994). Initial reliability and validity of a new retrospective measure of child abuse and neglect. American Journal of Psychiatry, 151, 1132–1136.

Berntson

G. G.

Cacioppo

J. T.

Quigley

K. S.

(1993). Respiratory sinus arrhythmia: Autonomic origins, physiological mechanisms, and psychophysiological implications. Psychophysiology, 30, 183–196. doi:10.1111/j.1469-8986.1993.tb01731.x.

Boyce

W. T.

Chesney

Alkon

Tschann

J. M.

(1995). Psychobiologic reactivity to stress and childhood respiratory illnesses: Results of two prospective studies. Psychosomatic Medicine, 57, 411–422.

Boyce

W. T.

Ellis

B. J.

(2005). Biological sensitivity to context: I. An evolutionary developmental theory of the origins and functions of stress reactivity. Development and Psychopathology, 17, 271–301.

10.

Connolly

(2014). Outcomes in emerging adulthood for maltreated youth: A clinical developmental approach. Child Maltreatment, 19, 270–274.

11.

Dahl

R. E.

Gunnar

M. R.

(2009). Heightened stress responsiveness and emotional reactivity during pubertal maturation: Implications for psychopathology. Development and Psychopathology, 21, 1–6. doi:10.1017/S0954579409000017

12.

Del Giudice

Ellis

B. J.

Shirtcliff

E. A.

(2011). The adaptive calibration model of stress responsivity. Neuroscience & Biobehavioral Reviews, 35, 1562–1592.

13.

Dion

Matte- Gagné

Daigneault

Blackburn

Hébert

McDuff

… Perron

(2016). A prospective study of the impact of child maltreatment and friend support on psychological distress trajectory: From adolescence to emerging adulthood. Journal of Affective Disorders, 189, 336–343.

14.

Ellis

B. J.

Boyce

W. T.

(2008). Biological sensitivity to context. Current Directions in Psychological Science, 17, 183–187.

15.

Ellis

B. J.

Boyce

W. T.

Belsky

Bakermans-Kranenburg

M. J.

van IJzendoorn

M. H.

(2011). Differential susceptibility to the environment: An evolutionary-neurodevelopmental theory. Development and Psychopathology, 23, 7–28.

16.

Ellis

B. J.

Essex

M. J.

Boyce

W. T.

(2005). Biological sensitivity to context: II. Empirical explorations of an evolutionary-developmental theory. Development and Psychopathology, 17, 303–328.

17.

El-Sheikh

Harger

Whitson

S. M.

(2001). Exposure to interparental conflict and children’s adjustment and physical health: The moderating role of vagal tone. Child Development, 72, 1617–1636.

18.

El-Sheikh

Keller

P. S.

Erath

S. A.

(2007). Marital conflict and risk for child maladjustment over time: Skin conductance level reactivity as a vulnerability factor. Journal of Abnormal Child Psychology, 35, 715–727.

19.

El-Sheikh

Whitson

S. A.

(2006). Longitudinal relations between marital conflict and child adjustment: Vagal regulation as a protective factor. Journal of Family Psychology, 20, 30–39.

20.

Enders

C. K.

(2001). A primer on maximum likelihood algorithms available for use with missing data. Structural Equation Modeling, 8, 128–141.

21.

Fergusson

D. M.

Horwood

L. J.

Boden

J. M.

(2011). Structural equation modeling of repeated retrospective reports of childhood maltreatment. International Journal of Methods in Psychiatric Research, 20, 93–104.

22.

Gutman

L. M.

Sameroff

A. J.

(2004). Continuities in depression from adolescence to young adulthood: Contrasting ecological influences. Development and Psychopathology, 16, 967–984.

23.

Hagan

M. J.

Roubinov

D. S.

Mistler

A. K.

Luecken

L. J.

(2014). Mental health outcomes in emerging adults exposed to childhood maltreatment: The moderating role of stress reactivity. Child Maltreatment, 19, 156–167.

24.

Herrenkohl

T. I.

Hong

Kilka

J. B.

Herrenkohl

R. C.

Russo

M. J.

(2013). Developmental impacts of child abuse and neglect related to adult mental health, substance use, and physical health. Journal of Family Violence, 28, 191–199.

25.

Luecken

L. J.

(2008). Long-term consequences of parental death in childhood: Psychological and physiological manifestations. Handbook of Bereavement Research and Practice: 21st Century Perspectives.

26.

Luecken

L. J.

Rodriguez

A. P.

Appelhans

B. M.

(2005). Cardiovascular stress responses in young adulthood associated with family-of-origin relationship experiences. Psychosomatic Medicine, 67, 514–521.

27.

Luthar

S. S.

Crossman

E. J.

Small

P. J.

(2015). Resilience in the face of adversities. In Lamb

(Ed.), Handbook of child psychology and developmental science (Vol. III, 7th ed., pp. 247–286). New York, NY: Wiley.

28.

MacKinnon

D. P.

Krull

J. L.

Lockwood

C. M.

(2000). Equivalence of the mediation, confounding and suppression effect. Prevention Science, 1, 173–181.

29.

Obradovic

(2012). How can the study of physiological reactivity contribute to our understanding of adversity and resilience processes in development? Development and Psychopathology, 24, 371–387.

30.

Obradovic

Bush

N. R.

Stamperdahl

Adler

N. E.

Boyce

W. T.

(2010). Biological sensitivity to context: The interactive effects of stress reactivity and family adversity on socio-emotional behavior and school readiness. Child Development, 81, 270–289.

31.

Rutter

Kim-Cohen

Maughan

(2006). Continuities and discontinuities in psychopathology between childhood and adult life. Journal of Child Psychology and Psychiatry, 47, 276–295.

32.

Saab

P. G.

Matthews

K. A.

Stoney

C. M.

McDonald

R. H.

(1989). Premenopausal and postmenopausal women differ in their cardiovascular and neuroendocrine responses to behavioral stressors. Psychophysiology, 26, 270–280.

33.

Sijtsema

J. J.

Nederhof

Veenstra

Ormel

Oldehinkel

A. J.

Ellis

B. J.

(2013). Effects of family cohesion and heart rate reactivity on aggressive/rule-breaking behavior and prosocial behavior in adolescence: The Tracking Adolescents’ Individual Lives Survey study. Development and Psychopathology, 25, 699–712.

34.

Smith

T. W.

Jordan

K. D.

(2015). Interpersonal motives and social-evaluative threat: Effects of acceptance and status stressors on cardiovascular reactivity and salivary cortisol response. Psychophysiology, 52, 269–276.

35.

Tanner

J. L.

Reinherz

H. Z.

Beardslee

W. R.

Fitzmaurice

G. M.

Leis

J. A.

Berger

S. R.

(2007). Change in prevalence of psychiatric disorders from ages 21 to 30 in a community sample. The Journal of Nervous and Mental Disease, 195, 298–306.

36.

Wagner

C. R.

Abaied

J. L.

(2016). Skin conductance level reactivity moderates the association between parental psychological control and relational aggression in emerging adulthood. Journal of Youth and Adolescence, 45, 687–700.

37.

Watson

Clark

L. A.

Tellegen

(1988). Development and validation of brief measures of positive and negative affect: The PANAS scales. Journal of Personality and Social Psychology, 54, 1063–1070.

38.

West

S. G.

Finch

J. F.

Curran

P. J.

(1995). Structural equation models with nonnormal variables. Problems and remedies. In Hoyle

R. H.

(Ed.). Structural equation modeling: Concepts, issues and applications (pp. 56–75). Newbury Park, CA: Sage.