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. Author manuscript; available in PMC: 2020 Feb 1.
Published in final edited form as: Health Psychol. 2018 Dec 20;38(2):103–112. doi: 10.1037/hea0000699

Parental Depression and Diabetes-Specific Distress After the Onset of Type 1 Diabetes in Children

Amy E Noser 1,2, Hongying Dai 3, Arwen M Marker 1,2, Jennifer K Raymond 4, Shideh Majidi 5, Mark A Clements 2,6, Kelly R Stanek 5, Susana R Patton 2,7
PMCID: PMC6407701  NIHMSID: NIHMS1015523  PMID: 30570283

Abstract

Objective:

To examine trajectories of two types of type 1 diabetes (T1D) specific distress (i.e., daily T1D management and worries about the future and long-term complications) and the moderating role of parental depression in parents of children newly diagnosed with T1D.

Methods:

A total of 126 families of five- to nine-year-olds with new-onset T1D enrolled in the study. One-hundred and twenty-five families completed study measures at baseline, 102 at six-month follow-up, and 89 at twelve-month follow-up. Parents completed measures of depression and T1D-specific distress concerning daily T1D management and worries about the future and long-term complications at baseline and at six- and twelve-month follow-ups. We used multilevel modeling to examine twelve month trajectories of daily and long-term T1D-specific distress and to examine if parental depression modified these trajectories.

Results:

Results showed a significant reduction in daily T1D-specific distress from baseline to six-month follow-up and maintenance of daily T1D-specific distress from six- to twelve-month follow-up. The significant interaction of baseline parental depression and Time indicated that parents with depressive symptoms had a smaller reduction in daily T1D-specific distress from baseline to six-month follow-up compared to parents without depressive symptoms. Findings for long-term T1D-specific distress indicated that parents with depressive symptoms reported higher distress across all assessment points, with peak long-term T1D-specific distress for depressed parents occurring at six months.

Conclusion:

Many parents experienced significant T1D-specific distress for a period of time following their child’s initial diagnosis and this distress appears to be exacerbated by parental depressive symptoms.

Keywords: Type 1 diabetes, depression, parents, distress, new-onset

A diagnosis of type 1 diabetes (T1D) is life-changing. Treatment of T1D involves a rigorous daily regimen, including insulin therapy, blood glucose monitoring, carbohydrate counting, and physical activity. Moreover, failure to adequately care for T1D can lead to serious short- and long-term complications and premature death (Chiang, Kirkman, Laffel, & Peters, 2014). Current clinical care guidelines recommend that parents assume the majority of daily diabetes self-care during childhood (Chiang et al., 2014). Thus, parents of children with new-onset T1D face the challenging task of learning to manage insulin and make diet and physical activity adjustments in relation to their child’s glycemic status (Wennick & Hallström, 2006). These new found responsibilities as well as concerns about long-term complications are described by parents as “all-consuming” (Whittemore, Jaser, Chao, Jang, & Grey, 2012), and often result in high levels of diabetes-specific distress (Kovacs et al., 1985; Rankin et al., 2016; Streisand et al., 2008). In an early study of parents of children newly diagnosed with T1D, 64% of mothers and 41% of fathers reported moderate to considerable levels of worry and preoccupation about their child and T1D self-cares (Kovac et al., 1985). More recent cross-sectional studies have also shown that parents report elevated levels of emotional distress and parenting stress following their child’s T1D diagnosis (e.g., Haugstvedt, Wentzel-Larsen, Graue, Søvik, & Rokne, 2010; Streisand et al., 2008). Similarly, themes from qualitative studies indicate that for parents the new-onset period is a time of overwhelming distress with the short- and long-term implications of T1D dominating their thoughts (Lowes, Gregory, & Lyne, 2005; Lowes, Lyne, & Gregory, 2004).

While many parents report elevated levels of T1D-specific distress following initial diagnosis (Rankin et al., 2016; Streisand et al., 2008), we have a limited understanding of variation in parents’ T1D-specific distress over time nor have we considered factors that may impact the course of T1D-specific distress in parents of newly diagnosed children with T1D. Kovacs et al. (1985) is the only study to prospectively examine parental T1D-specific distress in parents of children newly diagnosed with T1D, and they found a decline in distress over twelve months. However, a significant limitation of this study was its measurement of distress, which consisted of a non-validated two-item measure that assessed 1) the extent of parental worry and concern about their child’s T1D and 2) degree of parental involvement in T1D self-cares. Thus, additional research examining parents’ levels of T1D-specific distress is necessary to better understand the need for interventions to improve parental adjustment to the demands and realities of a T1D diagnosis. Identifying factors that modify the course of T1D-specific distress can also provide valuable information about for whom and under what circumstances targeted interventions may be most beneficial.

Parental depression is one factor that may be particularly salient for understanding the onset and course of parents’ T1D-specific distress during the new-onset period. Depression is a mood disorder identified by disturbances in affect (e.g., anhedonia, depressed mood), cognition (e.g., suicidal ideation, feelings of worthlessness), and behavior (e.g., insomnia or hypersomnia, psychomotor agitation or retardation) that cause significant impairment in daily functioning (American Psychiatric Association, 2013). A clinician formulates a diagnosis of depressive disorders based on well-defined symptoms scales and associated functional impairment for a specified period of time (American Psychiatric Association, 2013; Snoek, Bremmer, & Hermanns, 2015). Moreover, depressive disorders differ from T1D-specific distress because to diagnose a depressive disorder the patient does not need to endorse a specific content-related stressor associated with their symptoms (American Psychiatric Association, 2013; Snoek et al., 2015). In contrast, measures of T1D-specific distress aim to assess the worries, concerns, and fears associated with the emotional and behavioral demands of T1D, and unlike a depressive disorder, T1D-specific distress is not considered pathological (Fisher, Gonzalez, & Polonsky, 2015; Snoek et al., 2015). Further, while the existing literature has shown moderate to strong associations between diabetes-specific distress and depression, findings suggest that a large portion of the variance in diabetes-specific distress remains unexplained after accounting for depression, suggesting they are related, yet unique constructs (e.g., Hessler, Fisher, Polonsku, & Johnson, 2016; Reddy, Wilhelm, & Campbell, 2013; Van Bastelaar et al., 2010).

Previous studies have demonstrated elevated rates of depression among parents of children newly diagnosed with T1D, with up to 74% of parents reporting elevated depressive symptoms during the new-onset period (Streisand et al., 2008). According to cognitive theories, depression is characterized by dysfunctional cognitive structures and biased information processing (Beck, 1987, 2008) and has been shown to be associated with maladaptive coping strategies (Luyckx, Vanhalst, Seiffge-Krenke, & Weets, 2010). Thus, parents with depressive symptoms may perceive the complexities of T1D and the challenges associated with treatment as more negative and distressing and may lack the necessary coping skills to manage their distress. Indeed, studies have shown that parental depression negatively impacts the psychosocial functioning, coping, and adherence behaviors of families of children with T1D (e.g., Jaser, Linsky, & Grey, 2014; Jaser, Whittemore, Ambrosino, Lindemann, & Grey, 2009; Luyckx et al., 2010; Whittemore et al 2012). Moreover, in a study of mothers of adolescents with T1D, maternal depressive symptoms were associated with higher parent T1D-specific distress, use of disengagement coping strategies, and poorer adolescent quality of life (Jaser et al., 2014). Taken together, these findings indicate that depressive symptoms are common among parents of children newly diagnosed with T1D and appear to negatively impact parents’ functioning and well-being. However, it remains unknown how parental depression impacts T1D-specific distress during the new-onset period.

Our goals for the current study were to examine changes in the level of two sources of parent-reported T1D-specific distress: daily T1D tasks and worries about the future and long-term complications, over the course of twelve months. Additionally, we sought to examine the impact of baseline parental depression on the level and course of each source of T1D-specific distress. We hypothesized that parents’ levels of T1D-specific distress due to daily T1D tasks would be highest at baseline and that it would decline across six-month and twelve-month assessment points as parents gained experience and confidence in their ability to successfully complete daily T1D tasks. For parents’ levels of distress due to concerns about the future (e.g., worries about my child living with diabetes) and risk of long-term complications, we hypothesized a similar pattern with smaller declines across assessment points. We expected there would be smaller declines because we anticipated that parents would have limited direct experience either reducing risk of long-term complications or working through any worries about the future during the new-onset period, thereby leading to less normalization of these concerns and smaller declines in distress. Further, we hypothesized that elevated depressive symptoms would be associated with higher levels of daily and long-term T1D-specific distress at all assessment points and that parental depressive symptoms would modify the course of both sources of T1D-specific distress. Specifically, we hypothesized that parents with depressive symptoms would perceive daily T1D tasks and concerns about the future and long-term complications as more distressing than parents without depressive symptoms at all assessment points. Additionally, because individuals with depression are more inclined to ruminate, have negative biases, and use maladaptive coping skills (Baucom et al., 2015; Freckleton, Sharpe, & Mullan, 2014; Jaser et al., 2014; Jaser et al., 2009), we hypothesized that parents with depressive symptoms would show smaller declines in distress due to both daily T1D tasks and worries about the future and long-term complications across all assessment points.

Method

Participants

We recruited parent-children dyads through two pediatric diabetes centers in the Midwestern United States by telephone and in-clinic solicitation to participant in a 30-month longitudinal study examining individual and family factors that impact adherence and glycemic control in 5 to 9 year olds with new-onset T1D. The current study focuses on an early subset of this project and outcomes of the first twelve months of study participation. Eligible participants had a T1D diagnosis of ≤ 12 months, were between 5 and 9 years old, used either basal/bolus or insulin pump therapy, and were English speaking. Exclusion criteria included a diagnosis of developmental delay (i.e., autism, cerebral palsy, or intellectual disability), presence of a severe psychiatric disorder or comorbid chronic condition (e.g., renal disease), evidence of type 2 or monogenic diabetes, and chronic use of medication that may impact glycemic control (e.g., systemic steroids). Subsequently, we recruited the parents of eligible children.

Of the 126 families recruited, 125 completed baseline assessment (99.2%), 102 completed the six-month assessment (81.0%), and 89 completed the twelve-month assessment (70.6%). At baseline, children had a mean time since diabetes diagnosis of 4.61±3.19 months and a mean age of 7.45±1.34 years with the majority of parents identifying their child as non-Hispanic White (89.3%) and approximately half the sample identifying their child as female (52%). Mean child HbA1c at baseline was 7.63±1.37 (Table 1). Children of parents with depressive symptoms had a slightly higher mean HbA1c (t = 2.09; p = 0.04) than parents without depressive symptoms at baseline. Caregivers had a mean age of 36.62±6.40 years, 88.8% were mothers, and 80.8% were married (Table 1).

Table 1.

Baseline Demographics.

Full Sample
(n=126)		 Parents with depressive symptoms
(n=32)		 Parents without depressive symptoms
(n=92)
Child age, Mean (SD) years 7.45 (1.34) 7.25 (1.24) 7.50 (1.37)
Duration of diagnosis, Mean (SD) months 4.61 (3.19) 5.21 (3.68) 4.45 (3.01)
HbA1c, Mean (SD) % 7.63 (1.37) 8.06 (1.33) 7.48 (1.36)
Female, % 52.0 46.9 54.3
Non-Hispanic White, % 89.3 90.0 88.9
Parent age, Mean (SD) years 36.62 (6.40) 36.78 (6.06) 36.48 (6.54)
Mother, % 88.8 93.8 87.0
CES-D score ≥16, % 25.8 100 0
Daily T1D-specific distress, Mean (SD) 30.77 (6.56) 27.70 (6.22) 31.76 (6.37)
Long-term T1D-specific distress, Mean (SD) 27.59 (8.30) 31.02 (8.89) 26.32 (7.79)
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Note: Two participants did not complete the CES-D at baseline and have been omitted from moderator analyses. One participant did not complete baseline T1D-specific distress measures, however completed measures at subsequent assessment points.

CES-D=Center for Epidemiologic Studies – Depression Scale.

Of the 37 families who did not complete all three-assessment points, 27 did not have data at subsequent assessment points because they had not been enrolled in the study long enough yet and 10 families had already withdrawn from the study (e.g., family relocated). Families who completed all three assessment points did not differ from parents with missing assessment points based on baseline measures of T1D-specific distress, parental depressive symptoms, or demographic variables. Children of families who completed all three assessment time points had a shorter duration of T1D than children of families who had withdrawn from the study (t = 2.86, p = 0.005). No other differences on baselines measures and demographics emerged between the families who had completed all three assessment points compared to the families who had withdrawn from the study. Of the 89 parents who completed all three assessment time points, one parent had incomplete data.

Measures

Demographic and medical information.

Parents provided family and child demographic data and child’s medical history (e.g., T1D history and events) at baseline. We verified medical data through medical record review.

Parental distress.

The Problem Areas in Diabetes Survey – Parent Revised Version (PAID-PR; Markowitz et al., 2012) is an 18-item self-report measure of parents’ T1D-specific distress. Parents rated items using a 5-point scale ranging from 1 (not a problem) to 5 (serious problem). The PAID-PR assesses two domains of parents’ T1D-specific distress: immediate burden, which comprises present, concrete concerns (9 items; e.g., “I worry whether or not my child will remember to eat his/her snack”) and theoretical burden, which comprises negative emotions and worries about the future (9 items; e.g., “I feel scared when thinking about my child having/living with diabetes”). For the present study, we used the immediate burden subscale to assess parents’ distress about daily T1D tasks (daily T1D-specific distress) and the theoretical burden subscale to assess parents’ distress about the future and long-term complications (long-term T1D-specific distress). One item of the immediate burden subscale (“I feel “burned out” by the constant effort to manage diabetes”) was mistakenly omitted from all surveys, thus scores at each time point were calculated based on 8 items. The internal consistency of the PAID-PR immediate burden subscale was α = .59 at baseline, α = .77 at six-month follow-up, and α = .80 at twelve-month follow-up. For the PAID-PR theoretical burden subscale, internal consistency was α = .71 at baseline, α = .89 at six-month follow-up, and α = 0.89 at twelve-month follow-up. We demonstrated similar internal consistency as Markowitz et al. (2012), who found an alpha of .78 for the PAID-PR immediate burden subscale and an alpha of .83 for the PAID-PR theoretical burden subscale.

Parental depression.

The Center for Epidemiologic Studies – Depression Scale (CES-D; Radloff, 1977) is a 20-item survey that assesses depressive symptoms. Participants indicated the frequency with which they experienced each symptom over the past week using a 4-point scale ranging from 0 (none of the time) to 3 (all of the time) and scores were summed to calculate a total score. For the present analyses, we treated parental depressive symptoms as a categorical variable, with parents classified into two groups based on Radloff’s (1977) suggested cutoff score of 16 to indicate elevated depressive symptoms. The internal consistency for parental depression in this study was α = .89 at baseline, which is similar to internal consistencies reported in previous samples of parents of children with T1D (α = .87, Clayton et al., 2013; α = .88, Driscoll et al., 2010).

HbA1c.

HbA1c is an indicator of average blood glucose concentration over the previous three months. The recommended HbA1c level for children is < 7.5% (American Diabetes Association, 2018; Chiang et al., 2014). In the present study, we reported child HbA1c at baseline, which on average represents children’s HbA1c levels at 4.61±3.19 months post diagnosis. Following initial diagnosis, many patients with new-onset T1D experience a six- to twelve-month remission period (i.e., honeymoon phase), which has been shown to be associated with small insulin dose requirements and good metabolic control (Abdul-Rasoul, Habib, & Al-Khouly, 2006; Cengiz et al., 2014). Therefore, due to this confounding factor, we choose not to examine change in child HbA1c across study assessments. We sent children’s blood samples to a central laboratory for processing using automated high performance liquid chromatography (reference range 4.0–6.0%; Tosoh Corporation, San Francisco, CA). This method is traceable to Diabetes Control and Complications Trial standards (Lenters-Westra & Slingerland, 2014; NGSP, 2016).

Procedure

Parents who agreed to participate in the study completed a written informed consent form and children completed a written assent form. Parents completed study measures using a clinic tablet and children had their hemoglobin A1c (HbA1c) level drawn at each assessment point. All study procedures took place during families’ routine clinic appointments. The present study used parents’ report of depression at baseline and T1D specific distress at baseline and six-month and twelve-month follow-ups. We used baseline characteristics and child HbA1c to describe the study sample. At each time point, the same parent completed study measures and received a monetary payment for participation and children received a toy valued at $10 for the blood assays used to assess HbA1c. Children’s Mercy Hospital Pediatric Institutional Review Board and the Colorado Multiple Institutional Review Board both approved all study procedures prior to participant recruitment.

Analytic Plan

We summarized demographic variables by percent, mean, and standard deviation and conducted t-tests and chi-square tests to compare the demographic variables between parents with and without depressive symptoms. We conducted one-sample t-test with unequal variances to compare mean scores on the PAID-PR in our sample with published data. We used multilevel modeling to examine twelve month trajectories of daily and long-term T1D-specific distress in parents of children with new-onset T1D, and to examine whether baseline parental depression modified distress trajectories. For daily T1D-specific distress, we specified change over time as a function of time-in-study (i.e., baseline, six-month, and twelve-month assessment points) and centering time-in-study at the baseline assessment. The final model included Time, baseline parental depression, and the interaction between baseline parental depression and Time. We also considered duration of T1D diagnosis as a study covariate. For all models, we took the within subject correlation into account by constructing a random intercept variance-covariance matrix. We conducted a similar set of analyses for long-term T1D-specific distress. Notably, we chose multilevel modeling in order to account for our nested data structure (e.g., measurement occasions nested within participant) and varying sample sizes across measurement occasions (Hoffman, 2015; Raudenbush & Bryk, 2002; Snijders & Bosker, 2012). We calculated correlations among distress and depression variables using Pearson correlation coefficients. We conducted all trajectory analyses using SAS GLIMMIX (version 9.4; SAS Institute, Cary NC) and the restricted maximum likelihood estimator to report all model parameters. We used p-values < 0.05 to determine statistical significance.

Results

Measure Descriptives

Table 1 includes the mean and standard deviation of study measures. Twenty-six percent of caregivers reported clinical levels of depressive symptoms at baseline, 23% at six-month assessment, and 19% at twelve-month assessment. At baseline, caregivers’ mean (SD) level of daily T1D-specific distress was 30.77±6.56 and their mean level of long-term T1D-specific distress was 27.59±8.30. Mean (SD) daily and long-term T1D-specific distress at baseline, six-month, and twelve-month assessments for parents with and without depressive symptoms are reported in Table 2. We found no significant differences in the percentage of the sample with clinical levels of depressive symptoms across the baseline, six-month, and twelve-month assessment points (p = 0.51).

Table 2.

Descriptives and Comparisons of Mean Daily and Long-term T1D-specific Distress and Depression Variables in Parents with and without Elevated Depressive Symptoms.

Outcome Variables Baseline Six months Twelve months Baseline to Six months Baseline to Twelve months Six to Twelve months
Parents with depressive symptoms (N=32) (N=26) (N=23)
Daily T1D-specific distress, Mean (SD) 27.70 (6.22) 20.96 (6.31) 21.47 (6.39) p≤0.001 p≤0.001 ns
Long-term T1D-specific distress, Mean (SD) 31.02 (8.89) 35.72 (9.26) 33.10 (8.78) 0.012 ns ns
CES-D, Mean (SD) 23.38 (6.94) 16.33 (9.87) 16.39 (10.10) p≤0.001 p≤0.001 ns
Parents without depressive symptoms (N=92) (N=74) (N=64)
Daily T1D-specific distress, Mean (SD) 31.76 (6.37) 15.71 (5.38) 16.77 (6.24) p≤0.001 p≤0.001 ns
Long-term T1D-specific distress, Mean (SD) 26.32 (7.79) 26.83 (8.33) 27.03 (8.90) ns ns ns
CES-D, Mean (SD) 6.77 (4.43) 8.07 (6.70) 7.40 (6.90) ns ns ns
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Note: Two participants did not complete the CES-D at baseline and have been omitted from moderator analyses. Separate linear mixed models were performed for the outcome variables. In each model, the explanatory variables included main effects of Time and baseline depressive status and the interaction between these two variables. CES-D=Center for Epidemiologic Studies – Depression Scale.

Correlations of Daily and Long-term T1D-specific Distress

Parent report of daily T1D-specific distress was positively associated for the six-month and twelve-month assessments (r = 0.69, p ≤ 0.001). Parent report of long-term T1D-specific distress was positively associated for the baseline and six-month follow-up (r = 0.40, p ≤ 0.001) and for the six-month and twelve-month follow-up (r = 0.71, p ≤ 0.001). At baseline, there was no correlation between daily and long-term T1D-specific distress. At six-month follow-up, we observed a significant positive correlation between daily and long-term T1D-specific distress (r = 0.77, p ≤ 0.001). This correlation was similar at twelve-month follow-up (r = 0.79, p ≤ 0.001). Parental depressive symptoms were negatively associated with parent report of daily T1D-specific distress at baseline (r = −0.27, p = 0.002) and positively associated with parent report of daily T1D-specific distress at six-month (r = 0.38, p ≤ 0.001) and twelve-month (r = 0.32, p = 0.003) follow-ups. Parental depressive symptoms were positively associated with parent report of long-term T1D-specific distress at baseline (r = 0.25, p = 0.005), six-month follow-up (r = 0.42, p ≤ 0.001), and twelve-month follow-up (r = 0.29, p = 0.006).

Change in Daily T1D-specific Distress

Adjusted means and standard deviations for all study variables are presented in Table 2. Overall, our results showed a significant Time effect (p ≤ 0.001). Specifically, we found a significant reduction in daily T1D-specific distress from baseline to six-month follow-up (β = 11.39, SE = 0.94, p < 0.001) and from baseline to twelve-month follow-up (β = 10.61, SE = 0.97, p < 0.001). We observed no significant change in daily T1D-specific distress from six-month follow-up to twelve-month follow-up (β = −0.78, SE = 1.02, p = ns).

Next, we examined the role of baseline parental depressive symptoms and its interaction with Time (Figure 1). Results of this analysis showed main effects of Time (p ≤ 0.001) and parental depressive symptoms (p = 0.015) that were qualified by the two-way interaction of Time and parental depressive symptoms (p ≤ 0.001). Post-hoc analyses found different patterns of change based on parental depressive symptoms. At baseline, parents with depressive symptoms had lower daily T1D-specific distress as compared to parents without depressive symptoms (β = 4.06, SE = 1.25, p = 0.001). Both parents with depressive symptoms (β = −6.74, SE = 1.61, p ≤ 0.001) and parents without depressive symptoms (β = −16.05, SE = 0.95, p ≤ 0.001) showed a significant decrease in daily T1D-specific distress from baseline to six-month follow-up. But parents with depressive symptoms had a smaller reduction in daily distress from baseline to six-month follow-up (p ≤ 0.001) than parents without depressive symptoms at baseline. As such, parents with depressive symptoms at baseline had higher daily T1D-specific distress at six-month follow-up (β = 5.25, SE = 1.39, p ≤ 0.001) than parents who reported no depressive symptoms at baseline. For all parents, we observed no change in daily T1D-specific distress from six-month to twelve-month follow-up. Thus, daily T1D-specific distress at twelve-month follow-up remained higher among parents with depressive symptoms (β = 4.70, SE = 1.48, p = 0.002) than parents who reported no depressive symptoms at baseline.

Figure 1.

Figure 1.

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Twelve month trajectories of daily T1D-specific distress in parents with and without depressive symptoms. Data are presented as least square means, and error bars depict the standard error of the mean.

Change in Long-term T1D-specific Distress

Adjusted means and standard deviations for all study variables are presented in Table 2. Overall, our results showed a significant Time effect (p = 0.039). Specifically, we found a significant increase in long-term T1D-specific distress from baseline to six-month follow-up (β = 2.56, SE = 1.04, p = 0.015), a marginally significant increase in long-term T1D-specific distress from baseline to twelve-month follow-up (β = 1.87, SE = 1.09, p = 0.088), and no change from six-month to twelve-month follow-up (β = 0.70, SE = 1.13, p = ns).

Next, we examined the role of baseline parental depressive symptoms and its interaction with Time (Figure 2). Results of this analysis showed main effects of Time (p = 0.039) and parental depressive symptoms (p ≤ 0.001); however, the two-way interaction of Time and parental depressive symptoms was not significant (p = 0.16). Post-hoc analyses showed that parents with depressive symptoms at baseline consistently had higher long-term T1D-specific distress at baseline (β = 4.69 SE = 1.74, p = 0.008), six-month follow-up (β = 8.70, SE = 1.90, p < 0.001), and 12-month follow-up (β = 6.60, SE = 2.00, p = 0.001) than parents without depressive symptoms. Parents with depressive symptoms showed a slight increase in long-term T1D-specific distress from baseline to six-month follow-up and no change from six-month to twelve-month follow-up. Parents without depressive symptoms showed no change in long-term T1D-specific distress across assessment points.1

Figure 2.

Figure 2.

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Twelve month trajectories of long-term T1D-specific distress in parents with and without depressive symptoms. Data are presented as least square means, and error bars depict the standard error of the mean.

PAID-PR Total Score Comparisons with Published Outcomes

No existing studies provide mean scores for the PAID-PR subscales, thus to allow for comparisons of T1D-specific distress with existing studies we calculated a mean item score for the PAID-PR total score.2 The mean PAID-PR total item score for our sample was 3.43±0.65 at baseline, 2.73±0.86 at six-month follow-up, and 2.77±0.89 at twelve-month follow-up. For parents with depressive symptoms the mean PAID-PR total item score was 3.45±0.68 at baseline, 3.33±0.83 at six-month follow-up, and 3.21±0.85 at twelve-month follow-up. Parents without depressive symptoms had a mean PAID-PR total item score of 3.42±0.64 at baseline, 2.50±0.76 at six-month follow-up, and 2.58±0.84 at twelve-month follow-up. The mean PAID-PR total item score from published studies of children with longer duration T1D has ranged from 2.3 to 2.6 (Giani, Snelgrove, Volkening, & Laffel, 2017; Katz, Volkening, Dougher, & Laffel, 2017; & Markowitz et al., 2012).

Results of a series of one-sample t-tests with unequal variances showed significantly higher PAID-PR total item scores for parents in the present sample at baseline when compared to the original validation study of parents of youth with a longer T1D duration (p ≤ 0.001; Mean PAID-PR total item score = 2.6; Mean age = 12.9±2.7 year; Mean duration of T1D = 6.3±3.5 years; Markowitz et al., 2012). We also found significantly higher PAID-PR total item scores for parents without depressive symptoms at baseline and parents with depressive symptoms at baseline, six-month follow-up, and twelve-month follow-up when compared to published data from the original validation study (p’s ≤ 0.01; Markowitz et al., 2012).

Discussion

We examined the twelve-month trajectories of parental T1D-specific distress about daily T1D tasks and worries about the future and long-term complications, as well as the impact of parental depression on the level and course of each type of T1D-specific distress in a cohort of parents of five- to nine-year-olds recently diagnosed with T1D. Consistent with our hypotheses and the extant literature (Kovacs et al., 1985), we found that parents’ daily T1D-specific distress was highest at baseline, declined from baseline to six-month follow-up, but showed no change from six-month to twelve-month follow-up. Contrary to our hypothesis, we found a negative association between parental depressive symptoms and daily T1D-specific distress at baseline. Further, parents with depressive symptoms reported lower levels of daily T1D-specific distress than parents without depressive symptoms at baseline. However, parents with depressive symptom at baseline also showed a smaller reduction in distress over the initial six months and thus, had higher subsequent levels of distress at the six-month and twelve-month assessment points, as compared to parents without depressive symptoms. Taken together, these findings indicate that parents experience notable distress when first learning to perform daily T1D tasks, however as they gain experience and likely confidence in their ability to carry out these tasks, they also show a reduction in associated daily T1D-specific distress. Further, we found that parents with elevated depressive symptoms at baseline were at increased risk of experiencing prolonged levels of distress regarding daily T1D management tasks. This finding may be explained by use of maladaptive coping strategies that are common in individuals with depression (Luyckx et al., 2010). That is, parents with depressive symptoms may lack the necessary coping skills to manage their distress about daily T1D tasks and thus, show smaller reductions in T1D-specific distress than parents without depressive symptoms. Future studies are needed to understand if our findings extend beyond the new-onset stage and should also consider the potential impact of stress trajectories on child outcomes (e.g., glycemic control, psychosocial well-being).

Somewhat surprisingly, we found a negative association between depressive symptoms and daily T1D-specific distress at baseline. While a previous study in adolescents with T1D has found a similar association, this result was counter to our expectation that parents with depressive symptoms would demonstrate a negative response bias (Baucom et al 2015). We can only speculate that the negative association we found at baseline may be due to blunted stress reactivity or the possibility that parents who were experiencing depressive symptoms at baseline exhibited lower distress reactivity to the daily demands of T1D because of their depressive symptoms (Baucom et al 2015; Oldehinkle & Bouma, 2010). In the future, studies should consider collecting parents’ daily report of distress and depressive symptoms in the new-onset period to better understand this association.

Results for parents’ long-term T1D-specific distress showed minimal change over time. However, there were notable differences in the levels of long-term T1D-specific distress between parents with and without depressive symptoms, such that parents with depressive symptoms reported significantly higher levels of distress compared to parents without depressive symptoms across all assessment points. Further, despite an overall non-significant change in long-term T1D-specific distress, parents with depressive symptoms showed a slight increase in distress from baseline to six-month follow-up that appeared to level off between six-month and twelve-month assessments. In contrast, parents without depressive symptoms reported minimal changes in distress across all assessment points. These findings suggest that parents with depressive symptoms experience elevated levels of long-term T1D-specific distress compared to parents without depressive symptoms and that this distress may increase following the time of initial diagnosis.

One possible explanation for increased risk of prolonged elevated levels of long-term T1D-specific distress in parents with depressive symptoms is that these parents are more likely to engage in ruminative thought patterns, which could make it difficult for them to direct their attention away from stressful thoughts and toward more proactive coping strategies (Brinker & Dozois, 2009; Smyth, Zawadzki, & Gerin, 2013; Zawadzki, 2015). Additionally, these ruminative thought patterns may contribute to feelings of hopelessness, as well as negative evaluations about one’s current circumstances (Lavender & Watkins, 2004; Lyubomirsky, Tucker, Caldwell, & Berg, 1999; Nolen-Hoeksema, 2000; Nolen-Hoeksema, Wisco, & Lyubomirsky, 2008). That is, parents with depressive symptoms may be more likely to ruminate about their child’s T1D diagnosis and its associated implications, as well as lack the necessary cognitive resources to redirect their attention to more effective coping strategies (e.g., active or problem-focused coping). Future research is necessary to discern the specific cognitive and/or behavioral strategies contributing to prolonged elevated long-term T1D-specific distress in parents with depressive symptoms and whether parents with depressive symptoms continue to experience similar distress levels beyond the first year of diagnosis.

Study findings for both types of T1D-specific distress and parental depressive symptoms highlight the need for additional research concerning the clinical management of families during the new-onset stage. From an assessment standpoint, findings indicate a need for future research to establish clinical cut-off scores, as well as minimal clinically important differences in T1D-specific distress. Establishing these clinical indicators of change is necessary to determine the need for assessing and monitoring parental levels of T1D-specific distress at routine diabetes clinic visits during the new-onset stage. Moreover, because the majority of parents appear to have elevated levels of distress, particularly surrounding daily T1D management tasks for a period of time following their child’s T1D diagnosis, parents may benefit from social support to normalize their experiences and intervention to learn coping strategies to effectively manage distress. While many endocrine clinics may provide families with external referrals for parent support groups or facilitate their own parent support groups, a recent qualitative study of parents of youth newly diagnosed with T1D suggest that parents may find these services inadequate (Rankin et al., 2016). Specifically, the findings of this study suggest that parents desire additional support from other parents and their child’s health care provider as well as help, encouragement, and daily advice on T1D self-cares when first learning to manage T1D (Rankin et al., 2016). As a direction for future research, it would be important to assess the effectiveness of existing and standard support services available to parents of youth newly diagnosed with T1D. In this area, it may also prove helpful to employ study designs (e.g., sequential multiple assignment randomized trials) that can examine the optimal type, timing, and duration of support services for parents during the new-onset stage (Noser, Cushing, McGrady, Amaro, & Huffhines, 2017).

Most parents in our study did not report clinically significant depressive symptoms, which suggests that many parents are resilient to the emotional distress that often accompanies first learning of their child’s T1D diagnosis (e.g., Haugstvedt et al., 2010; Kovac et al., 1985; Streisand et al., 2008; Whittemore et al., 2012). However, because our findings suggest that depressive symptoms exacerbate T1D-specific distress during the new-onset period, providers should consider screening for parental depression at the time of diagnosis and at follow-up clinic appointments. Parents who screen positive for depression could then receive intensive support and treatment while they learn about T1D management and the risk for long-term complications. With regard to intervention, previous research in T1D has shown promise for some family-based interventions (e.g., Behavioral Family Systems Therapy, Multisystemic Therapy) aimed at reducing parent-child conflict, increasing communication, and learning adherence behaviors (e.g., McBroom & Enriquez, 2009; Whittemore et al., 2012). However, the majority of these studies have focused on child health outcomes, rather than improvements in caregiver depression or distress. Research suggests that cognitive-behavioral therapy is the most efficacious treatment to improve psychological health in parents of children with a chronic illness (Eccleston et al., 2012). Yet, before these treatments can become standard of care for diabetes clinics, additional research is needed to determine if targeted interventions, such as cognitive-behavioral therapy or brief skills-training, can successfully reduce caregiver depression in T1D and if these treatments can also have indirect impacts on reducing T1D-specific distress and improving child health outcomes. Finally, related to intervention development in parents of children with new-onset T1D, there is a need for studies that examine parents’ and providers’ perceptions of the benefit as well as the optimal timing and delivery of such interventions.

The study presents some limitations. First, our sample was predominantly non-Hispanic, white mothers. Therefore, study findings may not generalize to families from other racial or ethnic backgrounds or other caregivers (e.g., fathers). While this racial/ethnic breakdown is generally representative of families of children with T1D living in the United States (Mayer-Davis et al., 2009), future studies should examine these relations in a more racially and ethnically diverse sample and other caregivers. Second, we relied exclusively on parents’ self-report of distress and depression, which introduces the risk of response bias. Although self-report provides a reasonable initial step when examining perceived distress and depressive symptoms, future research may benefit from clinical interviews or behavioral observation. Third, our measure of parental depression only accounted for parents’ baseline report of depressive symptoms. Although, we found no differences in the percent of parents with depressive symptoms across assessment points, future studies should consider whether change in depression status impacts distress trajectories. Additionally, because we were interested in examining clinical levels of depressive symptoms, we coded parental depression as a categorical moderator based on clinical cutoff scores on the CES-D (Radloff, 1977). However, this approach limits our understanding of potential differences based on symptom severity (e.g., subthreshold and severe depressive symptoms). Future studies may consider examining these relations using a dimensional measure of depressive symptoms. Fourth, the internal consistency of daily T1D-specific distress at baseline was relatively low (α = .59). One possible explanation is that this subscale had lower internal consistency at baseline because there was higher variability in how parents responded to the subscale items due to less time managing T1D. That is, parents gave lower distress ratings to items that happen relatively infrequently (e.g., communicating to school staff about T1D management) and greater distress ratings to items that happen daily (e.g., treating a low blood sugar) because of a cumulative effect and that parents needed more time managing T1D for parents to respond more consistently to these subscale items. Fifth, at the time of data analyses only 71% of our sample had completed all three assessment points and 8% of our sample had already withdrawn from the larger study. Although, we found no differences in baseline daily and long-term T1D-specific distress and parental depression between those who had completed all three assessment points, those who had not completed all assessment points, and those who had withdrawn from the study, future research using larger samples may be warranted to confirm our longitudinal associations. Sixth, because we did not collect data about parents’ use of mental health services, it remains unknown if some parents were receiving services that may account for changes in T1D-specific distress or their baseline depressive symptoms. However, it is notable that while all families received basic T1D education and management skills at diagnosis, these services did not target parental distress or emotional reactions to a T1D diagnosis and it is unlikely that families received mental health services through the hospitals’ endocrinology clinics given long waitlists.

Our study is the first to provide data examining trajectories of two types of parental T1D-specific distress prospectively over twelve-months using validated instruments. Additionally, we identified differences in the level and course of each type of T1D-specific distress between parents with and without depressive symptoms. Our results indicate that although parents initially experience elevated distress about daily T1D management, they show a significant reduction over the course of six months. However, for parents with depressive symptoms reductions in daily T1D-specific distress appear blunted. Our data also suggest that parents with depressive symptoms report significantly higher distress about long-term T1D complications compared to parents without depressive symptoms, and experience a slight increase in long-term T1D-specific distress from baseline to six-month follow-up. Our findings highlight the need for additional research on screening and referral for parental depression in parents of children recently diagnosed with T1D. Given that T1D-specific distress appears to be pervasive among parents of children newly diagnosed with T1D, future studies should also examine the benefit of providing brief intervention or additional resources about distress management to parents at diagnosis and during routine clinic visits.

Acknowledgments

This research was supported by a grant R01-DK100779 (to S.R.P.) from the National Institutes of Health/National Institute of Diabetes and Digestive and Kidney Diseases.

The authors wish to thank the parents and children who and contributed the data for the current analyses.

Footnotes

1

Adjusting models for duration of T1D diagnosis did not impact findings for daily or long-term T1D-specific distress, therefore we removed this covariate for parsimony.

2

We accounted for the missing item of the PAID-PR when calculating the mean item score for the sample.

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