Higher Rates of Sleep Disturbance Among Offspring of Parents With Recurrent Depression Compared to Offspring of Nondepressed Parents

Jessica L. Hamilton, PHD; Cecile D. Ladouceur, PHD; Jennifer S. Silk, PHD; Peter L. Franzen, PHD; Lauren M. Bylsma, PHD

Disclosures

J Pediatr Psychol. 2020;45(1):1-11. 

In This Article

Discussion

Offspring of parents with recurrent depression are at heightened risk for mental health problems (Weissman et al., 2016), including earlier onset, poorer course, and more severe depression (Lieb et al., 2002). Using a multimethod approach of parent and child-reported sleep disturbance and 9-day sleep diary-based measures of sleep duration and sleep midpoint, our study examined differences between offspring of parents with recurrent depression and offspring of parents without psychopathology. Our findings indicate that per both self- and parent-report, high-risk youth had more sleep disturbance than low-risk youth, controlling for demographic characteristics (age, sex, pubertal status, SES, and timing of study completion) and youth internalizing symptoms. In contrast, there were no significant differences between high- and low-risk youth on sleep duration and midpoint assessed via sleep diary. Further, our study is the first to include both male and female offspring of parents with recurrent depression and examine potential sex differences. Our exploratory analyses found that high-risk female offspring had more parent-reported sleep disturbance compared to high-risk boys and low-risk girls. There were no sex differences for child-reported sleep disturbance, duration, or midpoint.

Overall, our findings support prior research that subjective reports of sleep disturbance but not sleep duration or midpoint, differentiate high- and low-risk youth based on parent history of depression, even prior to youth onset of psychopathology (Chen et al., 2012). These findings suggest that there may be specific differences between high and low risk youth on sleep disturbance, which broadly encompasses prebedtime and night-time behaviors (e.g., difficulty falling/staying asleep, nightmares) and daytime sleepiness. High-risk youth may be more likely to have sleep disturbance due to genetic risk (as the parents were biologically related in the current study), parenting styles (Kopala-Sibley et al., 2017), emotion regulation impairments (Silk et al., 2006), and other environmental factors (e.g., stress, neighborhood environment) associated with parental depression (Marco, Wolfson, Sparling, & Azuaje, 2011). Indeed, in the current study, high-risk youth were more likely to receive public assistance, an indicator of SES, which may be associated with environmental factors that disrupt sleep such as inconsistent schedules, noise, and air pollution (Marco et al., 2011). These factors, along with vulnerability for emotion dysregulation, may also make high-risk youth more susceptible to both experience more sleep disturbance and the cognitive-affective impact of disturbed sleep (Karazsia & Berlin, 2018), thereby increasing risk for subsequent psychopathology.

Consistent with prior studies (Chen et al., 2012), our findings were specific to subjective measures of sleep quality, and extend these findings to both youth and parent-reported sleep disturbances. There may be several reasons for our study results. First, our findings may suggest that high-risk offspring have more biased cognitive information processes and attend more to negative information (Sfärlea et al., 2019). Although depressed parents also reported more offspring sleep disturbance, particularly for females, this finding may reflect shared cognitive and affective biases among parents and offspring that contribute to perception of poor sleep quality. Further, depressed parents are more likely to have disturbed sleep, which may contribute to higher levels of youth sleep disturbance or overestimation by parents of their child's sleep disturbance (Ronnlund, Elovainio, Virtanen, Matomaki, & Lapinleimu, 2016). Second, it could be that our sleep diary did not capture more habitual sleep patterns that reflect differences in sleep duration and midpoint between high- and low-risk youth. Our study was conducted continuously throughout the year, which may not fully capture critical school-year versus school-break differences in sleep and underestimate potential group differences. For instance, nearly 40% of the sample had short weekday sleep (defined as < 9 hrs for youth under 13 years old), which is comparable to national averages (Wheaton, Jones, Cooper, & Croft, 2018), though sleep duration did not differ between youth who were studied in the school year versus school break. Importantly, there also was considerable variability within individuals on sleep duration and midpoint, suggesting other factors may be more important than risk status in determining these sleep characteristics. Third, it is also possible that sleep disturbances may be more closely linked to risk for psychopathology than sleep duration and midpoint. For instance, sleep disruptions such as delayed sleep onset latency or nighttime awakenings may be more problematic or indicative of future psychopathology among high-risk youth, whereas shorter sleep duration and midpoint may reflect more developmental patterns in sleep that affect most youth.

Importantly, our study examined sex differences in sleep among female and male offspring of parents with recurrent depression, which represents a unique contribution to the field. Our findings indicate that depressed parents reported higher levels of sleep disturbance specifically among female offspring, but there were no self-reported sleep differences by sex. While these findings may reflect sex-specific mechanisms of risk for high-risk girls compared to high-risk boys, there are other possible explanations for these findings. There may be sex differences in parental awareness of sleep disturbances for high-risk females due to more observable or verbalized disturbances (e.g., parents awakened in nighttime) or specific bias in parental perception of sleep among female offspring. For instance, it could be that parents (especially mothers given the study composition) may be more attune to the health behaviors of their female child given their own history of recurrent depression, and be more likely to notice specific difficulties in sleep behaviors or daytime sleepiness among female offspring. Given limitations in power and a relatively small sample size, it will be important for future studies to replicate these findings and estimate potential mechanisms through which high-risk girls may or may not have more sleep disturbances.

Our study has notable strengths, such as the use of both parent and youth report, sleep diary design, and high-risk youth of parental recurrent depression in a developmental stage of heightened risk. However, several methodological limitations should be noted. First, we did not record the timing of parents' most recent depressive episode, which limits the ability to determine whether youth were exposed to parental depression during the youth's lifetime. Second, paternal depression was relatively rare in our sample, which limited examination of differences between maternal and paternal depression and pathways of risk for offspring to sleep disturbances. Our sample also was relatively small, and we had limited power to detect associations for between-person effects of multilevel models, particularly sex differences. Interaction analyses should be considered exploratory, and future studies should be designed with sufficient power to test these hypotheses. This study also did not have objective measures of sleep to evaluate specificity of findings to subjective estimates of sleep. Several subscales of sleep measures had low internal reliability in our sample, which limited examination of specific areas of sleep disturbance. In our sample, younger youth were more likely to report sleep disturbance than older youth, which may reflect developmental differences or perceptions of sleep. Further, our sleep measures domains are not independent and may capture overlapping sleep characteristics (e.g., sleep disturbance includes sleep duration). It will be important for future research to examine specific aspects of sleep using multiple measures and methods, including actigraphy and the gold-standard of polysomnography to inform intervention targets.

Our findings identify differences in sleep disturbance between offspring of parents with depression, which may reflect a potential transdiagnostic risk factor for subsequent psychopathology (Harvey, 2009; Harvey et al., 2016). However, the current study did not evaluate this directly, which remains an important area of future investigation. Despite advances in the field and understanding of potential mechanisms of risk among high-risk youth, existing interventions are still limited in their prevention of disorder. Existing treatments primarily focus on cognitive and emotional skills (Loechner et al., 2018). Sleep disturbance impairs emotion regulation (Palmer & Alfano, 2017) and executive functioning skills that facilitate skill acquisition, consolidation, and recall (Walker, 2009), which may impair the ability of youth to learn and implement these cognitive-behavioral strategies. Thus, it is possible that targeting sleep may enhance existing intervention and prevention programs (Harvey, 2009; Harvey et al., 2016). Although existing literature of sleep within high-risk youth is emerging, a body of research indicates that sleep disturbance predicts a range of psychopathology (Dolsen, Asarnow, & Harvey, 2014), including risk for depression and suicidality (Liu et al., 2019). Thus, sleep disturbance may be an actionable target for prevention and intervention among high-risk youth because: (a) it is a risk factor associated with physical and mental health that is modifiable compared to other known factors (e.g., genetic risk), (b) high-risk youth may be even more susceptible to the impact of sleep, particularly given that these youth are more likely to have emotion dysregulation (Silk et al., 2006), and (c) there are well-validated and publicly available self-report sleep measures, such as the CSHQ (Owens, Spirito, McGuinn, et al., 2000), that can be efficiently administered to identify sleep disturbance. Promoting healthy sleep practices and intervening on nighttime disturbances may be valuable targets among these vulnerable youth, with the long-term potential to improve early prevention and intervention efforts. Future research is needed to examine whether differences in sleep disturbance between high- and low-risk youth and sex differences within high-risk youth persist over time and confer risk for subsequent psychopathology. It will also be important to determine which aspects of sleep disturbance are present among high-risk youth and should be prioritized in treatments. Future studies are needed to examine whether targeting sleep disturbance among high-risk youth serves as a critical early intervention to prevent the intergenerational transmission of psychopathology (Soehner et al., 2019).

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