The Burden of Bereavement: Early-Onset Depression and Impairment in Youths Bereaved by Sudden Parental Death in a 7-Year Prospective Study
This article has been corrected.
VIEW CORRECTIONPublication: American Journal of Psychiatry
Abstract
Objective:
The authors sought to determine the long-term impact of sudden parental death on youths and pathways between youth bereavement and impairment.
Methods:
Youths (N=216) who lost a parent to suicide, accident, or sudden natural death and nonbereaved youths (N=172) were followed periodically for up to 7 years. The incidence and prevalence of disorder and of functional impairment, as well as pathways to impairment, were assessed using Cox and mixed-effects logistic regression and structural equation modeling.
Results:
Prior to parental death, bereaved youths had higher rates of psychiatric disorder, parental psychiatric disorder, and maltreatment. Even after adjustment for predeath risk factors, bereavement was associated with an increased incidence of depression, posttraumatic stress disorder, and functional impairment. The peak incidence of depression was in the first 2 years postbereavement, with incident depression occurring mainly in those who lost a parent at age 12 or younger. Youths bereaved by all three causes of death showed higher rates of impairment at all time points. Structural equation modeling found that bereavement had a direct effect on impairment and was also linked to impairment via its effects on early and later depression and through negative life events. Child psychiatric disorder prior to parental loss also contributed to functional impairment.
Conclusions:
Parental death increased the incidence of depression in offspring early in the course of bereavement. Early identification and treatment of depression in bereaved youths and augmentation of family resilience may protect against later sequelae of functional impairment.
The loss of a parent is one of the most stressful events that a child can experience (1). There is less clarity about the short- and longer-term sequelae of parental bereavement. Reports of enduring effects of parental bereavement are often based on assessments of adults who report a history of parental death. In contrast, longitudinal studies have usually been limited to the first 2 years postbereavement, so that the longer-term effects of parental bereavement and the mechanisms linking bereavement and later outcomes are not well understood.
Adults who were parentally bereaved as children report increased depressive symptoms, diminished self-confidence, educational underattainment, and dissatisfaction with their interpersonal relationships (1–3). However, these studies did not adjust for risk factors for impairment that antedated the death of the parent and that are more common in bereaved families, such as parental or personal psychopathology (4, 5).
Longitudinal studies of parentally bereaved youths have found an increased risk for psychopathology up to 2 years after parental death, even after adjusting for predeath risk factors (4–7). Youths who lost a parent to a natural disaster have reported long-lasting sequelae of depression and posttraumatic stress disorder (PTSD) (8), although these conditions may also be attributable to the effects of dislocation and loss of a home (1, 8). Registry studies of parental bereavement find a peak incidence of adverse outcomes within the first 2 years but also report more enduring psychological sequelae (9, 10).
To address the impact and mechanisms of the sequelae of parental death, we conducted a 7-year longitudinal study of youths whose parents died suddenly and of demographically similar nonbereaved comparison subjects. We posited, per extant theoretical models (1), that the loss of a parent increased the risk for psychiatric disorder and functional impairment in children through three interrelated pathways: children of parents who die prematurely are already at higher risk than their nonbereaved peers because of preexisting vulnerability prior to the death, namely, personal and family history of psychopathology and exposure to adversity; parental loss decreases family resources that protect children from the effects of other negative events, due to functional impairment and psychiatric disorder in the surviving parent; and as a result of the first two pathways, youths develop maladaptive coping styles and experience an increased risk of new-onset psychopathology that in turn results in functional impairment over time.
In previous reports, we found that deceased parents, who were middle-aged and, as such, died prematurely, had higher rates of psychiatric disorders compared with nonbereaved subjects (4). Parentally bereaved youths had an increased incidence of depression and PTSD 9 months after parental death, even after controlling for predeath risk factors (4). Bereaved offspring had a higher rate of depression nearly 2 years postdeath, mediated by higher rates of incident depression 9 months after the loss (6). Enduring depression was more common in those bereaved offspring who had a previous history of depression, increased exposure to negative life events, and lost a mother rather than a father (6). Five years postdeath, bereaved offspring showed attenuated developmental competence in work, career planning, and relationships, mediated by family climate and functional impairment in both the surviving parent and the child (11). We report here on a 7-year follow-up of this cohort to determine transient and enduring sequelae of parental bereavement relative to nonbereaved comparison subjects, inquiring about the peak incidence and subsequent course of depression, PTSD, and other conditions; the incidence and course of functional impairment; and the pathways by which bereavement leads to enduring impairment.
Methods
Participant Recruitment
Adults who died by suicide, accident, or sudden natural death and had at least one biological child between the ages of 7 years and 17 years and 11 months were identified through medical examiner reports (45.1%) or via newspaper advertisements (54.9%). The parental death needed to have occurred within 24 hours of the initial incident, and families with multiple deaths or injuries were excluded. Of those who were eligible, 71% consented to participate.
Living, nonbereaved parents were recruited by random-digit dialing or by newspaper advertisements, and one of the parents was frequency-matched to the deceased parents by neighborhood, age, and gender, with a participation rate of 55%. Comparison offspring could not have had a death in a first- or second-degree relative within the past 2 years.
This study was approved by the University of Pittsburgh institutional review board. All participants in the study gave written consent or assent.
Assessments
Participants were interviewed by experienced clinical interviewers 9, 21, 33, 62, and 84 months after the death; clinicians interviewing the offspring and parents were blind to bereavement status. Retrospective assessment was used to determine whether the offspring’s and surviving parent’s disorders had their onset before or after parental death. For nonbereaved offspring and their parents, “new-onset disorder” was defined as having occurred within 9 months of the baseline assessment. The equivalent of “predeath psychiatric disorders” in the nonbereaved offspring and parents was defined as disorders that occurred at least 9 months before the baseline assessment.
Socioeconomic status was assessed using Hollingshead’s scale at intake and by recording household income at each subsequent assessment (12). The Schedule for Affective Disorders and Schizophrenia for School-Age Children–Present and Lifetime Version (13) and the Structured Clinical Interview for DSM-IV Axis I Disorders (14) were used for the diagnostic assessment of youths and adults, respectively. Deceased parents’ lifetime disorders were assessed by psychological autopsy (15). Personality disorders in adult participants were assessed with the Structured Clinical Interview for DSM-IV Personality Disorders (16). The Longitudinal Interview for Follow-Up Evaluations was used to document the course of disorders in offspring (17). Functional impairment was assessed using the Global Assessment Scale (GAS) for children and adults (18, 19). The distribution of GAS scores was highly skewed (Shapiro-Wilk W=0.92, p<0.001), so we used impairment as a dichotomous outcome with a score <70 corresponding to impairment in school, with peers, or in family domains. High interrater reliability was maintained for the assessment of psychiatric diagnoses (kappa=0.74–0.85; N=107) and impairment (intraclass correlation=0.92, 95% CI=0.90, 0.93; N=734). Additional assessments of youths and adults for symptomatology, suicidal ideation, aggression, history of maltreatment, life events, coping, social support, and family climate are listed in Table S1 in the data supplement that accompanies the online edition of this article (20–35).
Data Analyses
The incidence of disorders was compared between bereaved and comparison offspring using Kaplan-Meier survival analysis. Cox proportional hazard models were used to assess the effects of bereavement on incident disorders after controlling for demographic variables and predeath risk variables. Predeath risk variables were child and parental psychiatric disorder and history of physical or sexual abuse that antedated the death. These variables differentiated between bereaved and nonbereaved samples and were related to postbereavement incident disorder. We tested for interactions of bereavement with demographic and predeath risk variables and subsequently conducted stratified analyses when interactions were significant. When the proportional hazards assumption was not met, a time-varying covariate that was an interaction between bereavement and survival time was included. The prevalence of disorders at each time point, which included disorders that occurred since the previous assessment, was also compared between bereaved and nonbereaved offspring using the chi-square statistic or Fisher’s exact test. To examine changes in the prevalence of outcomes over time, we used mixed-effects logistic regression, adjusting for predeath risk variables.
For statistical analyses with missing data, we conducted multivariate imputation by chained equations. Results using the original and imputed data set were similar, so only the latter are reported here. Analyses were conducted using Stata/IC, version 12.1.
Structural equation modeling in Mplus, version 8.0 (36), was used to examine the direct and indirect effects of bereavement on impairment 7 years after parental death. Logistic regression was employed to identify the variables at baseline and follow-up time points associated with impairment at 7 years to be included in structural equation modeling. We reduced the longitudinal data for the middle three time points after the baseline assessment by averaging across these three time points.
When different measures were used in youths and adults to assess the same domain, scores were standardized. To adjust for the effects of having multiple participants from the same family, all multivariate analyses included a term for clustering. Six bereaved and seven comparison subjects experienced the death of a family member or close relationship during the study. The findings were the same including or excluding these subjects, so we report the results on the full sample.
Results
Sample Description
Participants were 216 offspring from 143 families bereaved by suicide, accident, or sudden natural death who were between the ages of 7 years and 17 years and 11 months at the time of the parent’s death, and 172 nonbereaved offspring from 98 families who were also between the ages of 7 years and 17 years and 11 months (Table 1).
| Characteristic | Total | Nonbereaved | Bereaved | Test | df | p | |||
|---|---|---|---|---|---|---|---|---|---|
| Offspring | |||||||||
| N | 388 | 172 | 216 | ||||||
| Mean | SD | Mean | SD | Mean | SD | ||||
| Age (years)a | 12.0 | 3.0 | 12.0 | 2.8 | 12.0 | 3.1 | t=–0.05 | 386 | 0.96 |
| N | % | N | % | N | % | ||||
| Female | 188 | 48.5 | 84 | 48.8 | 104 | 48.1 | χ2=0.02 | 1 | 0.89 |
| White | 311 | 80.2 | 144 | 83.7 | 167 | 77.3 | χ2=2.47 | 1 | 0.12 |
| History of psychiatric disordersb | |||||||||
| Depression diagnosis | 42 | 10.9 | 14 | 8.2 | 28 | 13.0 | χ2=2.30 | 1 | 0.13 |
| Bipolar disorder diagnosis | 3 | 0.8 | 0 | 0.0 | 3 | 1.4 | Fisher’s | — | 0.26 |
| Anxiety diagnosis | 33 | 8.5 | 12 | 7.0 | 21 | 9.7 | χ2=0.90 | 1 | 0.34 |
| Posttraumatic stress disorder diagnosis | 4 | 1.0 | 1 | 0.6 | 3 | 1.4 | Fisher’s | — | 0.63 |
| Attention deficit hyperactivity disorder diagnosis | 56 | 14.6 | 19 | 11.2 | 37 | 17.2 | χ2=2.78 | 1 | 0.10 |
| Behavioral disorder diagnosis | 21 | 5.5 | 6 | 3.5 | 15 | 7.0 | χ2=2.19 | 1 | 0.14 |
| Alcohol or substance abuse diagnosis | 4 | 1.0 | 2 | 1.2 | 2 | 0.9 | Fisher’s | — | >0.99 |
| Any psychiatric history | 111 | 28.8 | 39 | 22.9 | 72 | 33.5 | χ2=5.15 | 1 | 0.02 |
| Physical or sexual abuse | 21 | 5.4 | 3 | 1.7 | 18 | 8.3 | χ2=8.12 | 1 | 0.004 |
| Psychiatric disorders at baseline | |||||||||
| Depression diagnosis | 45 | 11.6 | 7 | 4.1 | 38 | 17.6 | χ2=17.08 | 1 | <0.001 |
| Bipolar disorder diagnosis | 8 | 2.1 | 2 | 1.2 | 6 | 2.8 | Fisher’s | — | 0.31 |
| Anxiety diagnosis | 41 | 10.6 | 14 | 8.1 | 27 | 12.5 | χ2=1.93 | 1 | 0.17 |
| Posttraumatic stress disorder diagnosis | 18 | 4.6 | 0 | 0.0 | 18 | 8.3 | χ2=15.03 | 1 | <0.001 |
| Attention deficit hyperactivity disorder diagnosis | 53 | 13.7 | 19 | 11.1 | 34 | 15.7 | χ2=1.79 | 1 | 0.18 |
| Behavioral disorder diagnosis | 18 | 4.6 | 6 | 3.5 | 12 | 5.6 | χ2=0.92 | 1 | 0.34 |
| Alcohol or substance abuse diagnosis | 2 | 0.5 | 1 | 0.6 | 1 | 0.5 | Fisher’s | — | >0.99 |
| Any psychiatric disorder at baseline | 116 | 29.9 | 33 | 19.2 | 83 | 38.4 | χ2=16.91 | 1 | <0.001 |
| Mean | SD | Mean | SD | Mean | SD | ||||
| Functioningc | 78.6 | 11.8 | 82.2 | 10.1 | 75.7 | 12.2 | t=5.72 | 384.6 | <0.001 |
| Self-reported clinical measures | |||||||||
| Depression z score | 0.23 | 1.09 | –0.04 | 0.94 | 0.48 | 1.16 | t=–4.64 | 349.5 | <0.001 |
| Anxiety z score | 0.25 | 1.05 | 0.13 | 0.98 | 0.36 | 1.10 | t=–2.09 | 355.8 | 0.04 |
| Suicidal ideation | 21.5 | 11.4 | 19.7 | 9.9 | 23.0 | 12.41 | t=–2.75 | 345.5 | 0.01 |
| Impulsive aggression | 69.6 | 22.4 | 66.6 | 20.4 | 72.2 | 23.9 | t=–2.38 | 354 | 0.02 |
| Posttraumatic stress disorder | 2.98 | 5.86 | 0.47 | 2.22 | 5.72 | 7.23 | z=–11.46 | — | <0.001 |
| Negative coping strategies z score | 0.16 | 1.00 | 0.16 | 0.98 | 0.15 | 1.02 | t=0.12 | 336 | 0.91 |
| Family climate | 52.7 | 8.9 | 53.8 | 8.3 | 51.7 | 9.3 | t=2.22 | 343 | 0.03 |
| Intercurrent life events z score | 0.82 | 1.15 | 0.55 | 1.00 | 1.03 | 1.21 | t=–4.29 | 383.5 | <0.001 |
| Social support z score | –0.05 | 1.02 | 0.11 | 1.00 | –0.18 | 1.02 | t=2.70 | 353 | 0.01 |
| Surviving caretaking adult | |||||||||
| N | 240 | 99 | 141 | ||||||
| Mean | SD | Mean | SD | Mean | SD | ||||
| Age (years) | 43.3 | 7.7 | 42.4 | 6.3 | 43.8 | 8.4 | t=–1.37 | 226 | 0.17 |
| Hollingshead scale score | 43.5 | 12.4 | 45.8 | 10.7 | 42.1 | 13.2 | t=1.81 | 154 | 0.07 |
| N | % | N | % | N | % | ||||
| Female | 195 | 81.3 | 75 | 75.8 | 120 | 85.1 | χ2=3.34 | 1 | 0.07 |
| White | 203 | 84.6 | 86 | 86.9 | 117 | 83.0 | χ2=0.67 | 1 | 0.41 |
| Spouse or significant other of the deceased | 173 | 75.9 | 80 | 92.0 | 93 | 66.0 | χ2=19.87 | 1 | <0.001 |
| History of psychiatric disordersb | |||||||||
| Depression diagnosis | 99 | 41.4 | 31 | 31.6 | 68 | 48.2 | χ2=6.56 | 1 | 0.01 |
| Bipolar disorder diagnosis | 7 | 2.9 | 1 | 1.0 | 6 | 4.3 | Fisher’s | 1 | 0.25 |
| Psychosis diagnosis | 1 | 0.4 | 1 | 1.0 | 0 | 0.0 | Fisher’s | — | 0.41 |
| Anxiety diagnosis | 61 | 25.4 | 15 | 15.2 | 46 | 32.6 | χ2=9.37 | 1 | 0.002 |
| Posttraumatic stress disorder diagnosis | 25 | 10.4 | 9 | 9.1 | 16 | 11.3 | χ2=0.32 | 1 | 0.57 |
| Alcohol or substance abuse diagnosis | 66 | 27.8 | 28 | 28.3 | 38 | 27.5 | χ2=0.02 | 1 | 0.90 |
| Personality disorder diagnosis | 8 | 3.3 | 2 | 2.0 | 6 | 4.3 | Fisher’s | — | 0.48 |
| Any psychiatric history | 150 | 63.0 | 51 | 52.0 | 99 | 70.7 | χ2=8.63 | 1 | 0.003 |
| Mean | SD | Mean | SD | Mean | SD | ||||
| Functioningc | 76.8 | 12.2 | 82.0 | 9.2 | 73.6 | 12.7 | t=5.78 | 219.2 | <0.001 |
| Deceased parent | |||||||||
| N | 241 | 98 | 143 | ||||||
| Mean | SD | Mean | SD | Mean | SD | ||||
| Age (years) | 43.9 | 7.7 | 43.4 | 7.0 | 44.3 | 8.2 | t=–0.86 | 239 | 0.39 |
| Hollingshead scale score | 43.4 | 13.4 | 46.6 | 11.4 | 41.0 | 14.3 | t=2.67 | 150.02 | 0.01 |
| N | % | N | % | N | % | ||||
| Male | 186 | 77.5 | 74 | 76.3 | 112 | 78.3 | χ2=0.14 | 1 | 0.71 |
| White | 199 | 82.9 | 84 | 86.6 | 115 | 80.4 | χ2=1.56 | 1 | 0.21 |
| History of psychiatric disordersb | |||||||||
| Depression diagnosis | 93 | 39.1 | 31 | 32.3 | 62 | 43.7 | χ2=3.11 | 1 | 0.08 |
| Bipolar disorder diagnosis | 18 | 7.5 | 2 | 2.0 | 16 | 11.2 | χ2=7.04 | 1 | 0.01 |
| Psychosis diagnosis | 3 | 1.3 | 0 | 0.0 | 3 | 2.1 | Fisher’s | — | 0.28 |
| Anxiety diagnosis | 56 | 23.6 | 25 | 26.0 | 31 | 22.0 | χ2=0.52 | 1 | 0.47 |
| Posttraumatic stress disorder diagnosis | 23 | 9.6 | 13 | 13.4 | 10 | 7.0 | χ2=2.74 | 1 | 0.10 |
| Alcohol or substance abuse diagnosis | 131 | 54.4 | 43 | 43.9 | 88 | 61.5 | χ2=7.31 | 1 | 0.01 |
| Personality disorder diagnosis | 39 | 16.2 | 4 | 4.1 | 35 | 24.5 | χ2=17.83 | 1 | <0.001 |
| Any psychiatric history | 177 | 73.8 | 66 | 68.0 | 111 | 77.6 | χ2=2.74 | 1 | 0.10 |
a
Age at time of parental death for bereaved youths, and age at 9 months prior to the baseline assessment for nonbereaved youths.
b
History of psychiatric disorders prior to death in the bereaved group, and lifetime history of psychiatric disorders that occurred prior to 9 months from the baseline assessment in the nonbereaved group.
c
Functioning was assessed using the Global Assessment Scale.
The deceased parents were middle-aged, predominantly men and white, and had died from suicide (N=50), accident (N=35), or sudden natural death (N=58). The causes of sudden natural death were myocardial infarction (N=23), other cardiac conditions (N=21), pneumonia (N=3), and other conditions (N=11) (aneurysm, blood clot, cancer, complications from gastric bypass surgery, diabetes mellitus, infection, stroke). Those bereaved families recruited via medical examiners were less likely to be bereaved by sudden natural death (32.8% compared with 54.7%, χ2=6.34, df=1, p=0.01) and to be white (71.7% compared with 86.3%, χ2=4.36, df=1, p=0.04); the surviving parent was more likely to have had a history of depression (78.9% compared with 47.6%, χ2=4.18, df=1, p=0.04), and the offspring were more likely to have been physically or sexually abused prior to the death (23.1% compared with 3.4%, p=0.04, Fisher’s exact test).
Compared with their living counterparts, deceased parents had higher lifetime rates of bipolar disorder (11.2% compared with 2.0%, χ2=7.04, df=1, p=0.01), alcohol or substance use disorder (61.5% compared with 43.9%, χ2=7.31, df=1, p=0.01), and personality disorders (24.5% compared with 4.1%, χ2=17.83, df=1, p<0.001). The surviving caretaking adults were middle-aged and predominantly women (81.3%), and compared with their nonbereaved peers, had higher predeath rates of lifetime depression (48.2% compared with 31.6%, χ2=6.56, df=1, p=0.01) and anxiety disorders (32.6% compared with 15.2%, χ2=9.37, df=1, p=0.002).
The 68% of offspring who completed the 7-year assessment, compared with those not retained, were less likely to have been bereaved (60.2% compared with 76.7%, χ2=11.97, df=1, p=0.001), to be black or Hispanic (13.4% compared with 33.3%, χ2=21.34, df=1, p<0.001), and to have had a parent with a history of bipolar disorder (3.4% compared with 16.7%, χ2=20.88, df=1, p<0.001) (see Table S2 in the online data supplement ), although the median duration of follow-up was similar between bereaved and nonbereaved offspring (6.6 compared with 6.4 years, χ2=3.10, df=1, p=0.08, Wilcoxon rank sum test).
Incidence
Compared with nonbereaved offspring, bereaved offspring showed an increased incidence of depression (incidence rate ratio=2.08, 95% CI=1.45, 3.03) during the first 2 years postbereavement (incidence rate ratio=3.13, 95% CI=1.89, 5.40), but not thereafter (incidence rate ratio=1.24, 95% CI=0.70, 2.20). Bereavement increased the incidence of depression, even after adjusting for predeath risk variables (hazard ratio=2.67, 95% CI=1.58, 4.51) (see Table S3a in the online data supplement ). For incident depression, there was a significant interaction between bereavement and the offspring’s age at the time of parental death (hazard ratio=0.85, 95% CI=0.75, 0.97) (see Table S3b in the data supplement ). The adjusted hazard ratio for incident depression was increased in offspring who lost a parent at age 12 or younger (hazard ratio=4.92, 95% CI=2.04, 11.87) but not in those who lost a parent during adolescence (hazard ratio=1.15, 95% CI=0.69, 1.90) (Figure 1; see also Table S3c and S3d in the data supplement ). Relative to comparison subjects, there was a significantly increased incidence of depression in offspring whose parents died by suicide (hazard ratio=2.26, 95% CI=1.39, 3.66) and by sudden natural death (hazard ratio=2.19, 95% CI=1.26, 3.83), but not in offspring bereaved by accidental death (hazard ratio=1.59, 95% CI=0.88, 2.85).
Bereaved offspring showed an increased incidence of PTSD (incidence rate ratio=7.27, 95% CI=2.58, 28.29) (Figure 2), which was increased in the first 2 years after the loss (incidence rate ratio=10.41, 95% CI=2.57, 91.10). The incidence of PTSD in bereaved youths compared with nonbereaved youths did not reach significance thereafter (incidence rate ratio=4.14, 95% CI=0.86, 39.34). Bereavement increased the incidence of PTSD, even after adjusting for predeath risk variables (adjusted hazard ratio=5.66, 95% CI=1.95, 16.40) (see Table S4 in the online data supplement ). Relative to comparison subjects, those bereaved by suicide (hazard ratio=6.11, 95% CI=1.94, 19.29) and by sudden natural death (hazard ratio=8.00, 95% CI=2.39, 26.83) showed elevated hazard ratios for PTSD, but offspring bereaved by accidental death did not (hazard ratio=2.93, 95% CI=0.69, 12.43).
Bereaved offspring had a higher incidence of clinically significant suicidal ideation (defined as a Suicidal Ideation Questionnaire score ≥31; incidence rate ratio=1.89, 95% CI=1.20, 3.03) (Figure 3). Bereavement did not have a significant effect on increased suicidal ideation in the first 24 months (incidence rate ratio=1.72, 95% CI=0.96, 3.19), but it did thereafter (incidence rate ratio=2.18, 95% CI=1.04, 4.92). The effect of bereavement on suicidal ideation became nonsignificant after controlling for predeath risk variables (see Table S5 in the data supplement ).
There were no significant effects of bereavement on the incidence of anxiety (hazard ratio=1.44, 95% CI=0.86, 2.40), alcohol or drug abuse (hazard ratio=0.97, 95% CI=0.55, 1.69), bipolar disorder (hazard ratio=1.34, 95% CI=0.45, 3.99), or behavioral disorders (conduct disorder, oppositional defiant disorder) (hazard ratio=1.02, 95% CI=0.48, 2.15).
Prevalence
The prevalence of psychiatric disorders and suicidal ideation was compared between bereaved and nonbereaved offspring at each time point (Figure 4). Although bereaved offspring showed an increased prevalence of depression at early time points, mixed-effects logistic regression indicated that over time, the rates of depression in the bereaved and nonbereaved offspring converged (bereavement-by-time interaction, odds ratio=0.62, 95% CI=0.48, 0.81, p<0.001; see Table S6 in the data supplement ). The prevalence of clinically significant suicidal ideation was elevated in bereaved offspring at four out of five time points, including the assessment at 7 years, but the increased prevalence in bereaved offspring was accounted for by greater loading of predeath risk variables. In contradistinction to earlier findings (4), the sex of the deceased parent did not significantly affect the prevalence of depression or other disorders at 7 years.
FIGURE 4. Prevalence of Disorders and Impairment in Bereaved and Nonbereaved Youths Between Assessment Pointsa
a ADHD=attention deficit hyperactivity disorder; PTSD=posttraumatic stress disorder.
*p<0.05. **p<0.01. ***p<0.001.
Incidence and Course of Impairment
Compared with nonbereaved offspring, bereaved offspring had an increased incidence of impairment (incidence rate ratio=2.93, 95% CI=2.10, 4.14) even after adjusting for demographic and predeath risk variables (hazard ratio=2.07, 95% CI=1.43, 2.99) (Table 2; see also Figure S1 in the data supplement ). Impairment related to bereavement was increased over the first 2 years (incidence rate ratio=2.63, 95% CI=1.72, 4.13) and thereafter (incidence rate ratio=2.56, 95% CI=1.47, 4.61), and it was also increased in all three types of parental death: suicide (hazard ratio=1.69, 95% CI=1.05, 2.74), accident (hazard ratio=1.73, 95% CI=1.10, 2.72), and sudden natural death (hazard ratio=2.71, 95% CI=1.78, 4.14). Mixed-effects logistic regression indicated that the prevalence of impairment was consistently increased in bereaved offspring (odds ratio=6.60, 95% CI=2.66, 16.32, p<0.001), with no change in this relationship over time (nonsignificant bereavement-by-time interaction, p=0.23).
| Variable | Hazard Ratio | 95% CI | t | p |
|---|---|---|---|---|
| Bereavement | 2.07 | 1.43, 2.99 | 3.89 | <0.001 |
| Age at parent’s death | 0.95 | 0.90, 0.99 | –2.19 | 0.03 |
| Female | 1.34 | 0.98, 1.82 | 1.85 | 0.06 |
| White | 0.59 | 0.40, 0.88 | –2.57 | 0.01 |
| Socioeconomic status | 0.99 | 0.98, 1.01 | –0.94 | 0.35 |
| History of psychiatric disorder (offspring) | 4.02 | 2.86, 5.66 | 7.97 | <0.001 |
| History of psychiatric disorder (parent) | 1.17 | 0.71, 1.94 | 0.62 | 0.54 |
| Physical or sexual abuse | 1.48 | 0.93, 2.36 | 1.64 | 0.10 |
Pathways for the Relationship Between Bereavement and Impairment
Logistic regression identified the most parsimonious set of variables at baseline and the average score over the next three time points associated with impairment at 7 years (see Table S7 in the data supplement ), and they were used to fit a structural equation model (Figure 5).
FIGURE 5. Path Analysis of Functional Impairment (Average of Intermediate Time Points) in a Study of Bereaved Youthsa
a Standardized coefficients are represented by β. The model controls for age, sex, and race (test of model fit, χ2=12.61, df=10, p=0.25; comparative fit index=0.994; Tucker-Lewis index=0.970; weighted root mean square residual=0.37; root mean square error of approximation=0.03, 90% CI=0.00, 0.08). The indirect effects of bereavement were mediated via self-reported depression at 9 months and the average of self-reported depression at 21, 33, and 62 months (β=0.04, SE=0.02, p=0.02); via self-reported depression at 9 months and the average of negative life events at 21, 33, and 62 months (β=0.02, SE=0.01, p=0.03); and via negative life events at 9 months and the average of negative life events at 21, 33, and 62 months (β=0.03, SE=0.01, p=0.02). The indirect effects of offspring history of psychiatric disorder were mediated via social support at 9 months (β=0.13, SE=0.06, p=0.02); via self-reported depression at 9 months and the average of self-reported depression at 21, 33, and 62 months (β=0.11, SE=0.04, p=0.01); via self-reported depression at 9 months and the average of negative life events at 21, 33, and 62 months (β=0.04, SE=0.02, p=0.01); and via negative life events at 9 months and the average of negative life events at 21, 33, and 62 months (β=0.05, SE=0.02, p=0.02).
There was a significant direct effect of bereavement on impairment (standardized coefficient [β]=0.19, SE=0.09, p=0.04). The indirect effects of bereavement on impairment were mediated by self-reported depression at 9 months and the average of self-reported depression over the next three time points (β=0.04, SE=0.02, p=0.02); by negative life events at 9 months and the average over the next three time points (β=0.03, SE=0.01, p=0.02); and by self-reported depression at 9 months and the average of negative life events over the next three time points (β=0.02, SE=0.01, p=0.03). A history of predeath child psychiatric disorder was more common in bereaved offspring and showed indirect pathways to impairment via its impact on self-reported depression (β=0.11, SE=0.04, p=0.01), social support (β=0.13, SE=0.06, p=0.02), and negative life events (β=0.05, SE=0.02, p=0.02), as well as through self-reported depression at 9 months and the average of negative life events over the next three time points (β=0.04, SE=0.02, p=0.01). This model showed a good fit to the data (test of model fit: χ2=12.61, df=10, p=0.25; comparative fit index=0.994; Tucker-Lewis index=0.970; weighted root mean square residual=0.37; root mean square error of approximation=0.03, 90% CI=0.00, 0.08).
Discussion
In this 7-year controlled follow-up study, parentally bereaved offspring showed an increased incidence of depression and PTSD. The increased incidence of depression occurred mainly in the first 2 years after parental death and in youths whose parents died when they were age 12 or younger. Bereavement had a direct effect on impairment and was linked to impairment through its impact on earlier depression and continued depression in offspring at subsequent time points, and also through its impact on negative life events. Predeath psychiatric disorder in offspring was also related to impairment via its effects on social support, negative life events, and depression.
This study has several unique strengths. Both parents and children were carefully assessed for factors antecedent and subsequent to the death. Psychiatric disorder was also assessed in the deceased parent. The 7-year follow-up is considerably longer than most comparable longitudinal studies, and the multiple time points provide a detailed view of the unfolding sequelae of bereavement over time (1, 5, 7). The sample of youths bereaved by suicide and accidents is likely representative, given the participants’ high recruitment acceptance rate and demographic similarities to accidents and suicides in the region. Limitations include sample size, which, while large for a longitudinal study, precludes a definitive assessment of the impact of differing causes of parental death. It is difficult to determine the representativeness of the cases of sudden natural death because they were not routinely referred to medical examiners. While those cases obtained via advertising had lower family loading for psychopathology and abuse, the effects of bereavement appeared to be similar regardless of referral source.
Our finding of an increased incidence of depression early in the course of bereavement is consistent with other studies, as is the result that younger children are more vulnerable to the negative sequelae of parental bereavement (9, 10). The incidence pattern for PTSD was more ambiguous but was consistent with other work showing a long-lasting vulnerability to incident PTSD after a traumatic event (37).
The loss of a parent conveyed an early and enduring negative impact on the functioning of offspring that was in part mediated by the onset of depression beginning early in the course of bereavement. The deleterious impact of early depression on later functioning occurred despite the convergence of rates of depression in bereaved and nonbereaved offspring over time, with similar findings in prevention trials showing long-term functional sequelae of early-onset depression (38).
There were increased rates of clinically significant suicidal ideation at nearly all time points in bereaved offspring compared with nonbereaved offspring, consistent with other reports finding that parental bereavement was associated with an increased risk for suicidal behavior (9, 10). While it appears that antecedent risk factors associated with bereavement, rather than bereavement per se, increased the risk of suicidal ideation in bereaved youths, clinicians should be aware that parentally bereaved youths are at increased risk for clinically significant suicidal ideation.
These findings serve as a reminder that parents with a psychiatric disorder are at increased risk for premature death (4). Better identification and treatment of parental psychiatric disorder, and attendance to the increased comorbid medical problems associated with mood disorders, such as cardiovascular disease, could help prevent premature death in parents and hence protect families from the sequelae of parental bereavement (39).
These findings partially support the conceptual model outlined in the introduction of the article, in which predeath risk factors, postbereavement child disorder, and erosion of familial social support, along with the impact of negative life events, contribute to enduring impairment. While offspring coping was related to impairment in univariate analyses, this variable did not survive logistic regression and hence did not play a role in our path analysis. Our model was influenced by that developed for the Family Bereavement Program, a preventive intervention for families that have lost a parent. In that model, parental bereavement negatively affected children’s adaptive coping and the surviving parent’s ability to provide consistent discipline and maintain a positive relationship with the child (1, 40). The Family Bereavement Program offers parallel group sessions for children that teach optimal coping responses and for parents to promote consistent discipline, augmenting parent-child relationships and encouraging, as appropriate, children’s expression of grief (40). Youths whose families were assigned to the program experienced both fewer negative life events and a diminished impact of those events when they occurred (40). The Family Bereavement Program protected bereaved children from negative sequelae via the promotion of adaptive coping and through the augmentation of the parent-child relationship (1, 40).
This study supports improved detection and management of parental psychiatric disorder and comorbid medical conditions in order to prevent the sequelae of parental bereavement. These findings also highlight the importance of careful monitoring, early identification and treatment of psychiatric disorder in bereaved children and the surviving parent, assessment of family psychiatric and environmental risk factors, and augmentation of family resilience through promotion of positive parenting. These steps in early identification and intervention can attenuate the impact of parental loss and help these youths become functional adults despite the burden of bereavement.
Acknowledgments
The authors acknowledge John T. Chen, Ph.D., for his statistical assistance, and the editorial assistance of Mr. Joseph Park. The authors thank the participants who made this study possible.
Footnote
Drs. Melhem and Brent are joint senior authors.
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Information & Authors
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Published In
History
Received: 18 July 2017
Revision received: 15 November 2017
Revision received: 14 February 2018
Revision received: 1 March 2018
Accepted: 5 March 2018
Published online: 20 June 2018
Published in print: September 01, 2018
Keywords
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Funding Information
American Foundation for Suicide Prevention10.13039/100001455: Young Investigator Award
National Institute of Mental Health10.13039/100000025: MH018951, MH065368
University of Pittsburgh Clinical Scientist Training Program from the Clinical and Translation Science Institute grant: UL1TR001857
Supported by NIMH grants MH-065368 to Dr. Brent and MH-018951 to Dr. Pham, by an American Foundation for Suicide Prevention Young Investigator Award to Dr. Melhem, and by grant UL1TR001857 from the University of Pittsburgh Clinical Scientist Training Program from the Clinical and Translational Science Institute to Dr. Pham.Dr. Brent receives royalties from Guilford Press, has received or will receive royalties from the electronic self-rated version of the Columbia–Suicide Severity Rating Scale from eResearch Technology, is on the editorial board of UpToDate, is a reviewer for Healthwise, and is a consultant for McKesson. The other authors report no financial relationships with commercial interests.Metrics & Citations
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