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From the Department of Psychology, Arizona State University, Tempe, Arizona.
Address correspondence and reprint requests to Linda J. Luecken, PhD, Box 1104, Department of Psychology, Arizona State University, Tempe, AZ 85287. E-mail: Linda.Luecken{at}asu.edu
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ABSTRACT |
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Methods: The current study evaluated systolic blood pressure (SBP), diastolic blood pressure (DBP), and heart rate (HR) responses to a challenge task in 150 young adults from families characterized by parental loss, divorce, or intact marriages.
Results: Overall, higher-quality family relationships were associated with stronger recovery of SBP. For DBP and HR, interactions were found in which higher-quality family relationships were associated with stronger recovery in the loss group relative to the divorce and intact groups. Good support was found for a mediational model outlining self-regulatory abilities as a pathway linking family relationships to SBP reactivity and recovery.
Conclusions: Findings provide further evidence that family-of-origin relationship experiences can affect cardiovascular responses to later-life stress.
Key Words: family • blood pressure • divorce • heart rate
Abbreviations: BMI = body mass index; DBP = diastolic blood pressure; FR = family relationships; HR = heart rate; SBP = systolic blood pressure; SEM = structural equation modeling.
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMETHODSRESULTSDISCUSSIONNOTESREFERENCES |
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The identification of developmental factors capable of influencing the patterning of cardiovascular stress responses has powerful implications for understanding long-term vulnerability to stress-related illnesses. Animal models provide convincing evidence that early caregiving experiences directly affect the development of physiological stress response systems (8). For nonhuman primates, maternal separation results in long-term physiological changes, including increased heart rate (9) and elevated physiological reactivity to stress (10). In contrast, models involving rat pups show that higher-quality parenting promotes the development of adaptive stress responses (11). Although the evidence with humans is less extensive, it is consistent that the primary caregiver plays a critical role in regulation of stress responses by modulating physiological arousal and soothing an overly aroused child (12).
Family characteristics that may be associated with elevated risk of physiological dysregulation include parental death or divorce. Approximately 3.5% of children experience the early death of a parent (13), and approximately 1.5 million children per year will experience parental divorce (14). Adults who experienced the death of a parent during childhood or adolescence were shown to have elevated blood pressure relative to those from intact, married families (15). Long-term physical health outcomes have also been associated with parental divorce (16), although findings have been inconsistent. Despite these risks, it is clear that many children from divorced or bereaved homes adjust well and do not develop symptoms of physiological or psychologic disorder. Good-quality parent–child relationships are an important buffer against the stress and psychosocial risk associated with parental death or divorce (17,18) and may also moderate the impact of family disruption on physiological outcomes. The quality of family relationships may also independently influence the development of physiological stress responses. For example, elevated cardiovascular stress responses have been demonstrated in children from homes characterized by high conflict or low cohesion (19,20).
We have previously outlined a number of pathways by which adversity in the family-of-origin may increase the risk of physiological dysregulation in adulthood, including genetic, cognitive–affective, and psychosocial processes (8). A cognitive–affective pathway suggests that parenting experiences influence the development of cognitive or emotional self-regulatory responses to stress, which then influence physiological responses. Self-regulatory processes include regulation of emotions and attempts to cope with stress. Coping responses are deliberate, controlled strategies used to moderate the impact of stress and typically involve engagement with or disengagement from the source of stress and one’s emotional reactions to the stressor (21). The development of self-regulatory abilities is strongly influenced by parenting experiences in the family-of-origin (22,23). Harsh parenting is associated with impaired self-regulatory abilities, as evidenced by poor emotion-regulation and maladaptive coping styles, which may result in a long-term pattern of dysregulated physiological stress responses (8,24).
The current article examines cardiovascular responses during a stressful speech task in young adults who experienced parental death or divorce during childhood or adolescence as well as those from intact married families. There were two basic goals to our analyses. First, we evaluated the interaction of family context (intact, divorced, bereaved) and relationship quality on cardiovascular stress responses. The key question is whether poor family relationships or separation experiences exert independent effects on physiological outcomes, or if effects of poor family relationships are unique within family contexts. For example, strong relationships may exert a more powerful beneficial impact in a family characterized by severe disruption (e.g., death of a parent). Therefore, one theoretical comparison of interest included those from intact families relative to those who experienced separation from a parent either by death or divorce to evaluate if separation from a parent contributed an independent risk for maladaptive outcomes. It was also important to directly compare the effects of parental loss and parental divorce on cardiovascular stress responses. The experiences and psychosocial concomitants of parental loss and divorce are considerably different (25), and it is unknown whether the long-term physiological consequences are comparable. We hypothesized that for both parental loss and divorce, cardiovascular dysregulation would be evident only in the absence of high-quality family relationships. As evidence of dysregulation, we were particularly interested in the magnitudes of cardiovascular reactivity and recovery.
The second goal of our analyses was to evaluate a preliminary model of a cognitive–affective pathway linking family relationships to cardiovascular reactivity and recovery. We included coping strategies and indicators of emotion regulation as potential mediators in this model. Anxiety, depression, and hostility were chosen as indicators of emotion regulation based on strong research literature linking these variables to cardiovascular reactivity and long-term cardiovascular health (26,27).
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METHODS |
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Family Groups
Participants included 49 students from bereaved families, 50 from divorced families, and 51 from maritally intact families. Criteria for bereaved families included the death of one biologic parent up to the participant’s age of 16. Participants in the loss group were eligible even if their surviving parent had remarried. Participants’ ages at the time of the death ranged from 0 to 16 years (mean = 8.2 years, standard deviation [SD] = 4.9). Criteria for divorced families included two married, biologic parents who divorced up to the participant’s age of 16. Remarriage of either parent did not affect eligibility for the study. Ages at the time of divorce ranged from 1 to 16 years (mean = 7.8 years, SD = 3.7). At least 2 years must have elapsed since the death or divorce, and no death or divorce could have occurred after the age of 16 in any of the groups. Criteria for intact families included two living, married, biologic parents.
Recruitment and Selection Criteria
Participants were recruited from Introduction to Psychology classes and advertisements in the student newspaper. Respondents completed a large screening survey, and those who were eligible were invited to participate. Participants did not know why they had been selected, and family experiences were not known to the experimenter until all data were collected. Exclusionary criteria included a history of heart problems, other serious illness, or acute illness. Participants were asked to refrain from use of alcohol the night before participation, cold medication the day of participation, and caffeine, energy drinks, eating, smoking, or exercise for at least 2 hours before participation. Compliance was queried before participation, and those who did not comply were rescheduled.
Measures
Questionnaires
The Moos Family Environment Scale (28) assessed retrospective accounts of the quality of family relationships. Participants were asked to rate specific aspects of family relationship experiences before their age of 16. As recommended by the FES scale manual, a Family Relationships score ("FR"; 
= 0.85) was calculated consisting of the combined scores from the Cohesion, Expressiveness, and Conflict subscales. This score was treated as a continuous variable in all analyses. The Responses to Stress Questionnaire (RSQ (29)) served as a multidimensional measure of voluntary coping responses. Two coping scales of the RSQ were selected for analyses: Primary Control Engagement Coping (problem-solving, emotional regulation, emotional expression; 9 items; = 0.74), and Effortful Disengagement Coping (avoidance, wishful thinking, denial; 9 items; = 0.76). The State-Trait Anxiety Inventory ((30); state anxiety = 0.87) and the Beck Depression Inventory II ((31); = 0.89) were also completed. Hostility was measured with the Cook-Medley Hostility Scale ((32); = 0.75).
Physiological Measures
Blood pressure and heart rate were measured every minute using an Omega 5600 adult blood pressure monitor (In vivo Research, Orlando, FL) with the cuff positioned on the participant’s nondominant arm. The Omega 5600 uses an oscillometric method of measurement to provide systolic blood pressure (SBP), diastolic blood pressure (DBP), and heart rate (HR). The first 5 minutes of readings were discarded to account for novelty effects of the laboratory environment, and the following 10 were averaged for a baseline. Readings were averaged for four experimental periods (baseline, speech preparation, speech delivery, and recovery).
Speech Task
The speech task was modeled after the procedure of Saab et al. (33) in which participants were given 4 minutes to prepare and 4 minutes to deliver a speech to defend themselves from a false accusation of shoplifting. The speech was videotaped and was given in front of an "audience" consisting of the experimenter and the "lab supervisor."
Procedure
On arriving at the lab, participants first read and signed informed consent forms. The blood pressure cuff was then applied and readings were taken at 1-minute intervals throughout the baseline period, the speech task, and a 7-minute recovery period. Questionnaires were completed after the task.
Data Analysis
Preliminary Analyses
Family groups were compared for equivalence on demographic variables and potential covariates (see Table 1). Chi-square and analysis of variance found no group differences in gender (p = .99), smoking status (p = .63), ethnicity (p = .41), caffeine use (p = .51), or body mass index (BMI; p = .88). Differences were found for income (F[2,142] = 12.5, p < .001) and age (F[2,147] = 3.8, p = .02), in which the intact group had the highest incomes and the divorced group was older on average than the loss group (see Table 1). Only gender and BMI were related to mean SBP and DBP. Men had higher mean SBP (F[1,143] = 25.6, p < .001) and DBP (F[1,143] = 3.8, p = .05) than women. Higher BMI was associated with higher mean SBP (F[1,143] = 35.9, p < .001) and DBP (F[1,143] = 16.3, p < .001). None of the demographic variables were related to SBP, DBP, or HR reactivity or recovery. Ages at the time of parental death or divorce and the amount of time that had elapsed since the death or divorce were not related to any of the cardiovascular measures. There was a significant repeated-measures (time) effect for SBP (p < .001; baseline mean = 109.5, SD = 9.6; preparation mean = 117.3, SD = 10.7; speech mean = 126.9, SD = 12.5; recovery mean = 114.4, SD = 10.9), DBP (p < .001; baseline mean = 67.0, SD = 7.2; preparation mean = 73.6, SD = 8.9; speech mean = 80.8, SD = 10.1; recovery mean = 67.5, SD = 8.5), and HR (p < .001; baseline mean = 74.0, SD = 10.5; preparation mean = 83.4, SD = 12.8; speech mean = 89.7, SD = 14.2; recovery mean = 74.2, SD = 10.5), in the sample as a whole, indicating significant reactivity and recovery of cardiovascular measures in response to the task.
Primary Analytic Strategy
Evaluation of differences in the pattern of cardiovascular responses to the speech task were conducted with repeated-measures general linear models (GLM; SPSS 11.0) with four repeated-measures (baseline, preparation, speech, recovery) of SBP, DBP, or HR as dependent variables. Family group (loss, divorce, or intact), the quality of family relationships (FR), and the interaction of group and FR served as independent variables. FR was treated as a continuous variable in all models. Gender and BMI were covariates in models predicting SBP and DBP. Greenhouse-Geisser corrections were used for all repeated-measures analyses to correct for sphericity. Following significant omnibus tests of differences in the overall pattern of responses, planned within-subjects contrasts evaluated reactivity (the change from baseline to speech level) and recovery (the change from speech to recovery levels). Also following a significant omnibus test, planned orthogonal contrasts compared the intact group with the divorce and loss groups, and the divorce with the loss group.
Structural equation modeling (SEM) with AMOS 5.0 was used to evaluate the proposed structural model shown in Figure 1, which was based on the theoretical model outlined by Luecken and Lemery (8). Separate models were evaluated for SBP, DBP, and HR. For SEM models, "reactivity" was calculated by subtracting baseline levels from speech levels, and "recovery" was calculated by subtracting recovery levels from speech levels. Maximum likelihood estimation was used, and model fit was examined using cumulative fit index (CFI), root mean square error of approximation (RMSEA), chi-square goodness-of-fit test, and AIC to compare alternative models. A search for multivariate outliers using Mahalonobis distance identified one potential outlier. When analyses were repeated with that case removed, results were not affected. Therefore, all cases were retained in analyses.
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RESULTS |
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Cardiovascular Response Patterns During the Speech Task
Systolic Blood Pressure
The hypothesis was examined that family context (group) and FR would interact to predict the pattern of SBP responses to the speech task. The group by FR by time interaction was not significant (p = .12) and was subsequently dropped from the model to evaluate independent effects of family group and FR. Family group was not significantly associated with SBP measures. However, a significant FR by time interaction on SBP was found (F[2,303] = 4.2, p = .01). Follow-up tests of within-subjects contrasts revealed that higher-quality FR was associated with significantly greater decreases from speech to recovery level SBP (F[1,140] = 13.2, p < .001) and near-significant greater increases from baseline to speech level SBP (F[1,140] = 3.5, p = .06). Thus, higher-quality family relationships were associated with stronger recovery of SBP and a trend for greater reactivity to the task.
Diastolic Blood Pressure
The hypothesis was examined that family context and FR would interact to predict the pattern of DBP responses to the task. The three-way interaction of family group by FR by time interaction was significant (F[5,346] = 2.5, p = .03) (see Fig. 2. Although FR was a continuous variable in all models, results are graphically displayed for values set at one SD above and below the mean for ease of interpretation. Tests of within-subjects contrasts were significant for the change from speech to recovery levels (F[2,137] = 3.4, p = .04), suggesting that the magnitude of DBP recovery differed by family group and FR (see Fig. 3). The magnitude of reactivity did not differ by the interaction of family group and FR (p = .22).
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Because of the significant omnibus test of the family group by FR by time interaction on DBP, planned orthogonal contrasts directly compared the intact group with the divorce and loss groups, and the divorce with the loss group. The contrast comparing the intact group with the loss and divorce groups was not significant (p = .38). For the contrast of the divorce and loss groups, a significant group by FR by time interaction (F[3,239] = 4.2, p = .01) was found, in which the divorce and loss groups significantly differed on the effects of FR on the change from speech to recovery level DBP (F[1,91] = 9.5, p < .01). For the loss group, higher FR was associated with stronger recovery, and for the divorce group, higher FR was associated with lower magnitude of recovery. As a follow-up test, we conducted a univariate analysis of covariance (ANCOVA) with the change score for recovery (speech DBP – recovery DBP) as the dependent variable, family group by FR as the independent variable, and speech level DBP as a covariate. The family group by FR interaction remained significant (F[1,93] = 5.5, p = .02).
Heart Rate
The interaction of family group and FR on HR responses to the task was evaluated. Findings were similar to those for DBP. The group by FR by time interaction was significant (F[3,242] = 3.8, p = .007) (see Fig. 4). Tests of within-subjects contrasts evaluating reactivity and recovery were significant for the change from baseline to speech levels (F[2,139] = 5.2, p < .01), and for the change from speech to recovery levels (F[2,139] = 5.3, p < .01), suggesting that both HR reactivity and HR recovery differed by the interaction of family group and FR.
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The planned contrast comparing the intact group with the loss and divorce groups was significant overall (F[2,244] = 4.6, p = .01) and was significant for both reactivity (F[1,141] = 6.0, p = .02) and recovery (F[1,141] = 6.9, p < .01). The pattern of findings was such that higher FR was associated with both stronger reactivity and stronger recovery for participants in either the loss or divorce group relative to those in intact group. The overall contrast comparing the divorce with the loss group was also significant (F[2,170] = 3.1, p = .05), which was significant for reactivity (F[1,93] = 4.6, p = .03) and near-significant for recovery (F[1,93] = 3.8, p = .06). Higher FR was associated with greater reactivity and a trend for stronger recovery for those in the loss group relative to those in the divorce group.
As a follow up, we conducted a univariate ANCOVA with the change score for recovery (calculated as speech HR – recovery HR) as the dependent variable, family group by FR as the independent variable, and speech level HR as a covariate, and the family group by FR interaction remained significant (F[2.140] = 4.6. p = .01). A similar test was conducted with reactivity (calculated as speech HR – baseline HR) as the dependent variable, controlling for baseline HR. The family group by FR interaction remained significant (F[2,138] = 4.3, p = .02).
Mediational Model Testing
First, a confirmatory factor analysis of the hypothesized measurement model was conducted that sought to quantify the latent construct of a self-regulation, with depressive symptoms, anxiety, hostility, engagement coping, and disengagement coping as indicators. Because of the expected correlation between depressive symptoms and anxiety, their disturbances were allowed to covary. The model was of good fit (CFI = 0.99, 
2 (4) = 5.2, p = .26, RMSEA = 0.047 [0.0; 0.142]). All factor loadings were significant at p < .01.
Next, the proposed model shown in Figure 1 examined the hypothesis that family relationship quality would be associated with self-regulatory abilities and cardiovascular reactivity and recovery. Separate models were evaluated for SBP, DBP, and HR. For SBP, the model was of good fit (CFI = 0.993, 2 (18) = 20.2, p = .32, RMSEA = 0.03 [0.0; 0.08], AIC = 72.2), and all paths were significant at p < .05. As a test for mediation, the model was repeated with direct paths included from FR to SBP reactivity and recovery. Although fit indices remained good (CFI = 0.999, 2 (16) = 16.3, p = .43, RMSEA = 0.012 [0.0; 0.08], AIC = 72.3), the direct paths from FR to SBP reactivity (p = .40) and recovery (p = .09) were not significant, providing evidence for mediation. In addition, the small increase in AIC suggested that the more parsimonious proposed model was preferable to this alternative model.
For DBP and HR, although fit indices were good (DBP: CFI = 0.99, 2 (11) = 13.1, p = .29, RMSEA = 0.04 [0.0;0.10]; HR: CFI = 1.0, 2 (11) = 10.8, p = .47, RMSEA = 0.00 [0.0; 0.09]), none of the paths to DBP (reactivity p = .85; recovery p = .61) or HR (reactivity p = .24; recovery p = .18) were significant. Therefore, the models were not good for predicting DBP or HR indices of response to the stress task.
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DISCUSSION |
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In contrast, intriguing family group differences emerged in the relations of family-of-origin relationship quality to DBP and HR responses. Higher-quality relationships were associated with significantly stronger recovery of DBP stress responses for participants who experienced early parental loss and lesser magnitude of recovery for those from divorced families, although the magnitude of reactivity was not different between the groups. For the loss group, these findings support our hypotheses. However, our results for the divorce group were unexpected and demonstrate that the experience of divorce exerts a long-term impact on cardiovascular stress responses that is different from the experience of parental death. Although for some children the divorce may cause feelings of loss, for others, it may provide relief from chronic conflict and a stressful family environment (17) and in this case may contribute to better physiological outcomes for those who experienced high conflict exposure. For HR, higher-quality family relationships were associated with both higher reactivity and stronger recovery for those from the loss group relative to the other groups. Our findings reinforce that parental loss is unique from separation from a parent by divorce in the impact of family relationship quality on DBP and HR responses to stress. In combination, these findings show the importance of considering family context when evaluating the long-term impact of childhood adversity.
The impact of family-of-origin relationships on later physiological outcomes evident in the current findings raises the need to identify the causal mechanisms underlying this effect. Eisenberg and colleagues (34) suggest that through their expression of emotion and reactions to children’s emotions, caregivers play a large role in socializing a child’s self-regulatory abilities. Eisenberg et al. (34) also point out that the socialization context interacts with parental influences. Death of a parent likely increases opportunities for socializing regulatory responses to high-magnitude negative emotions. Our finding that those who experienced parental loss and reported strong family relationships had stronger recovery of DBP and HR stress responses suggests that the combination of parental loss and positive parenting may shape adaptive self-regulatory ability, thus contributing to resilience in the face of later challenges.
In an attempt to better understand the role of self-regulatory processes for those from adverse family environments, a path model evaluated cognitive and emotional mediators of cardiovascular reactivity and recovery. Good-quality relationships within the family-of-origin were associated with indices of adaptive self-regulatory ability, which were associated with higher SBP reactivity and stronger recovery. Because of the moderating effect of the quality of family relationships for DBP and HR responses, the linear path model was not a good fit for DBP and HR. The finding for recovery of SBP supports previous research that has found stronger cardiovascular recovery after stress to be a resilience factor associated with positive emotions (35,36). The association of self-regulatory ability with greater SBP reactivity was contrary to predictions. However, physiological responses to challenge may be affected by task engagement and coping efforts. Our model shows increased engagement coping in those reporting higher-quality family-of-origin relationships, suggesting that greater reactivity may be at least partly explained by engagement with the task. This explanation is consistent with a recent report by Maier et al. (37) in which positive affect and greater task engagement were associated with elevated blood pressure reactivity in young adults. Similarly, Piferi and Lawler (38) reported that women low in hostility had elevated SBP stress reactivity, which was explained by greater engagement coping. It will be important in future studies to more closely examine the role of coping processes in moderating physiological stress responses.
There are several limitations to the current study. Self-report, retrospective measures of family-of-origin relationships were used. Although there is evidence that retrospective reports are not inherently inaccurate (39), the accuracy of participants’ reports cannot be determined. Current theories of the impact of childhood experiences on health outcomes emphasize cognitive and psychologic variables as mediating mechanisms. Therefore, perceptions of adversity may be more valid predictors of physiological outcomes than the objective events. The sample included healthy, young adults pursuing a college education and may not be representative of the general population. Participants were not selected for high psychologic distress; therefore, those for whom family-of-origin experiences led to clinical levels of distress were not represented. Because the sample was limited in age to 18 to 29 year olds, the long-term stability of the physiological alterations demonstrated in this study is not known. It is unclear why the moderating effect of family relationships was apparent only for DBP and HR and not for SBP. In the current findings, DBP and HR responses appear to be more sensitive to effects of family context than SBP responses, which were predicted by relationship quality independent of context. Future studies with a larger sample size may be necessary to understand how mediating and moderating factors affect different aspects of cardiovascular function during stress. Although our SEM model provides intriguing preliminary evidence for mediation of the impact of family-of-origin relationships by self-regulatory abilities, our sample size limited more extensive modeling of the many emotional and cognitive factors that may be influenced by family environment. Finally, given the wide range of physiological responses to stress, future studies should consider the long-term impact of family-of-origin experiences on other important indicators of allostatic load.
The current findings lend further support to the theory that relationship experiences within the family-of-origin can influence the pattern of self-regulatory and physiological responses to later-life challenges. Higher-quality relationships were associated with stronger SBP recovery after a challenge task for the sample as a whole. For DBP and HR, higher-quality family relationships were associated with stronger recovery for those who experienced parental loss. Parental loss and divorce were not directly associated with blood pressure reactivity, suggesting that the quality of family relationships is a significant moderator of the potential for long-term dysregulations in cardiovascular responses to stress. Good support was found for a mediational model in which the impact of family-of-origin relationships on SBP reactivity and recovery was mediated by indicators of self-regulatory ability. The implications of these findings are that attention to family relationships and children’s emotional well-being after family disruption may have long-term benefits for physiological as well as psychologic outcomes.
We are grateful for the research assistance of Jessica Tartaro, Heather Gunn, and Nidhi Bhalla.
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NOTES |
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This research was supported by grant 0130024N (L.J.L.) from the American Heart Association.
DOI:10.1097/01.psy.0000160466.10397.18
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