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Infant sleep and negative reactivity: The role of maternal adversity and perinatal sleep
Abstract
Sleep during infancy contributes to the development and maintenance of infant regulatory functioning and may be an early risk marker for more difficult temperamental traits like negative reactivity. Further, maternal adverse childhood experiences (ACEs) may predispose individuals to greater sleep disturbances in adulthood and have been linked with sleep disturbances in both mothers and infants. Thus, examining maternal history of ACEs and maternal sleep difficulties during pregnancy and postpartum may provide insight into underlying risk factors affecting infant sleep difficulties and early temperament development. Fifty-nine mothers from a diverse, community sample (44% white) completed questionnaires on ACEs, maternal sleep, infant sleep, and infant temperament at 30-weeks gestation, 6-weeks postpartum, and 16-weeks postpartum. Results indicated that maternal ACES and sleep problems during pregnancy have long term implications for infant negative reactivity at 16-weeks, with significant indirect effects through maternal and infant sleep problems at 6-weeks. Addressing psychosocial functioning and prenatal sleep during pregnancy, particularly among women with high ACEs, may be a target of intervention to improve maternal and infant sleep health during the postpartum, and reduce the risk for difficult infant temperament.
... Only a handful of studies have looked at the associations between prenatal maternal sleep and postnatal outcomes in humans. Prenatal maternal sleep predicts newborn event related potential (ERP) responses to auditory stimuli (Lavonius et al., 2020), infant negative affectivity (Ciciolla et al., 2022), and socioemotional development (Trauman et al., 2015). Recent reviews have identified prenatal maternal sleep health as an understudied and potentially critical process that may influence the developing fetus (Johnson and Louis, 2022;Mindell et al., 2015;Moreno-Fernandez et al., 2020). ...
... Notably, associations persisted after covarying intracranial volume, age at scan, birth weight percentile, and biological sex at birth. Despite evidence that poor sleep quality is a pervasive public health problem, only a few prior studies evaluate the impact on postnatal function in humans (Ciciolla et al., 2022;Lavonius et al., 2020;Trauman et al., 2015). The present findings provide novel evidence suggesting that sleep disruptions early Note: ICV = intracranial volume, BWP = birthweight percentile, INR = income to needs ratio, QC = quality control. ...
Background
The rapid maturation of the fetal brain renders the fetus susceptible to prenatal environmental signals. Prenatal maternal sleep quality is known to have important health implications for newborns including risk for preterm birth, however, the effect on the fetal brain is poorly understood.
Method
Participants included 94 pregnant participants and their newborns (53% female). Pregnant participants (Mage = 30; SDage= 5.29) reported on sleep quality three times throughout pregnancy. Newborn hippocampal and amygdala volumes were assessed using structural magnetic resonance imaging. Multilevel modeling was used to test the associations between trajectories of prenatal maternal sleep quality and newborn hippocampal and amygdala volume.
Results
The overall trajectory of prenatal maternal sleep quality was associated with hippocampal volume (left: b = 0.00003, p = 0.013; right: b = 0.00003, p =.008). Follow up analyses assessing timing of exposure indicate that poor sleep quality early in pregnancy was associated with larger hippocampal volume bilaterally (e.g., late gestation left: b = 0.002, p = 0.24; right: b = 0.004, p =.11). Prenatal sleep quality was not associated with amygdala volume.
Conclusion
These findings highlight the implications of poor prenatal maternal sleep quality and its role in contributing to newborn hippocampal development.
Using samples of twins and singletons totaling 715 individuals, the authors document heritable influences on various temperamental dimensions during the toddler and preschooler age ranges, which have been somewhat understudied relative to infants and older adolescents. In contrast to instruments on which prior literature is based, the Toddler Behavior Assessment Questionnaire and the Children’s Behavior Questionnaire offer assessment of positive affectivity (separately from negative affectivity) and of emotional regulation. Positive affect reveals substantial shared environmental influence, and emotion regulation reveals additive genetic influence. Evidence for genetic variance in temperament is strengthened because intraclass correlations from many of these questionnaire scales show no evidence of “too-low” dizygotic correlations that imply contrast effects. Suggestive evidence is offered that psychometric characteristics of the questionnaires can affect biometric inferences.
Epidemiological and interventional research has highlighted sleep as a potentially modifiable risk factor associated with poor physical and mental health. Emerging evidence from (behavioral) genetic research also shows that sleep characteristics are under strong genetic control. With this study we aimed to meta-analyze the literature in this area to quantify the heritability of sleep duration and sleep quality in the general population. We conducted a systematic literature search in 5 online databases on January 24th 2020. Two authors independently screened 5,644 abstracts, and 160 complete articles for the inclusion criteria of twin studies from the general population reporting heritability statistics on sleep duration and/or quality, and written in English. We ultimately included 23 papers (19 independent samples: 45,328 twins between 6 months to 88 years) for sleep duration, and 13 papers (10 independent samples: 39,020 twins between 16 and 95 years) for sleep quality. Collectively, we showed that 46% of the variability in sleep duration and 44% of the variability in sleep quality is genetically determined. The remaining variation in the sleep characteristics can mostly be attributed to the unique environment the twins experience, although the shared environment seemed to play a role for the variability of childhood sleep duration. Meta-analyzed heritability estimates for sleep duration, however, varied substantially with age (17% infancy, 20-52% childhood, 69% adolescence and 42-45% adulthood) and reporter (8% parent-report, 38-52% self-report). Heritability estimates for actigraphic and PSG-estimated sleep were based on few small samples, warranting more research. Our findings highlight the importance of considering genetic influences when aiming to understand the underlying mechanisms contributing to the trajectories of sleep patterns across the lifespan.
Child sleep disorders are increasingly prevalent and understanding early predictors of sleep problems, starting in utero, may meaningfully guide future prevention efforts. Here, we investigated whether prenatal exposure to maternal psychological stress is associated with increased sleep problems in toddlers. We also examined whether fetal brain connectivity has direct or indirect influence on this putative association. Pregnant women underwent fetal resting-state functional connectivity MRI and completed questionnaires on stress, worry, and negative affect. At 3-year follow-up, 64 mothers reported on child sleep problems, and in the subset that have reached 5-year follow-up, actigraphy data (N = 25) has also been obtained. We observe that higher maternal prenatal stress is associated with increased toddler sleep concerns, with actigraphy sleep metrics, and with decreased fetal cerebellar-insular connectivity. Specific mediating effects were not identified for the fetal brain regions examined. The search for underlying mechanisms of the link between maternal prenatal stress and child sleep problems should be continued and extended to other brain areas.
Background
It has been proposed that adverse childhood experiences (ACEs) can put women at risk for mental illness in the pregnancy and postpartum periods. While some studies have found strong support for this proposition, others have found weak or no support. This study is a meta-analysis of the association between ACEs and maternal mental health to resolve between-study discrepancies, and to examine potential moderators of associations.
Methods
Three electronic databases (i.e., MEDLINE, Embase, and PsycINFO) were searched up to November 2018 by a health sciences librarian. A hand search was conducted in January 2020 and relevant studies were added. Included studies reported on associations between ACEs and maternal depression and/or anxiety in the perinatal period (pregnancy to 1-year postpartum). Pregnancy and postpartum outcomes were examined separately for both depression and anxiety. Random-effect meta-analyses were conducted. Moderator analyses were conducted using meta-regression. Study quality was evaluated using a 15-point scale.
Results
The initial search yielded 4646 non-duplicate records and full text review occurred for 196 articles. A total of 15 studies ( N = 7788) were included in the meta-analyses, of which 2 were also described narratively. Publication year ranged from 1998 to 2019. Mothers were approximately 28.93 years of age when they retrospectively reported on their ACEs. All studies had maternal self-report questionnaires for the mental health outcomes. Study quality ranged from 7 to 12. The pooled effect sizes between ACEs and prenatal ( N = 12; r = .19; 95% CI= .13, .24) and postpartum ( N = 7; r = .23; 95% CI = .06 to .39) depressive symptoms were significant. The pooled effect size between ACEs and prenatal anxiety was also significant ( N = 5; r = .14; 95% CI= .07, .21). Moderator analyses indicated that timing of depressive and anxiety symptoms may be important for understanding associations.
Conclusions
ACEs confer risk to maternal mental health, albeit effect sizes are small to moderate in magnitude. Trauma-informed approaches, as well as increased mental health support during and after pregnancy, may help to offset the relative risk of ACEs on maternal mental health.
Sleep disturbances among pregnant women are increasingly linked to suboptimal maternal/birth outcomes. Few studies in the USA investigating sleep by pregnancy status have included racially/ethnically diverse populations, despite worsening disparities in adverse birth outcomes. Using a nationally representative sample of 71,644 (2,349 pregnant) women from the National Health Interview Survey (2004–2017), we investigated relationships between self‐reported pregnancy and six sleep characteristics stratified by race/ethnicity. We also examined associations between race/ethnicity and sleep stratified by pregnancy status. We used average marginal predictions from fitted logistic regression models to estimate prevalence ratios (PRs) and 95% confidence intervals (CIs) for each sleep dimension, adjusting for sociodemographic and health characteristics. Pregnant women were less likely than non‐pregnant women to report short sleep (PROverall = 0.75; 95% CI, 0.68–0.82) and more likely to report long sleep (PROverall = 2.06; 95% CI, 1.74–2.43) and trouble staying asleep (PROverall = 1.34; 95% CI, 1.25–1.44). The association between pregnancy and sleep duration was less pronounced among women aged 35–49 years compared to those <35 years. Among white women, sleep medication use was less prevalent among pregnant compared to non‐pregnant women (PRWhite = 0.45; 95% CI, 0.31–0.64), but this association was not observed among black women (PRBlack = 0.98; 95% CI, 0.46–2.09) and was less pronounced among Hispanic/Latina women (PRHispanic/Latina = 0.82; 95% CI, 0.38–1.77). Compared to pregnant white women, pregnant black women had a higher short sleep prevalence (PRBlack = 1.35; 95% CI, 1.08–1.67). Given disparities in maternal/birth outcomes and sleep, expectant mothers (particularly racial/ethnic minorities) may need screening followed by treatment for sleep disturbances. Our findings should be interpreted in the historical and sociocultural context of the USA.
Maltreatment increases risk for psychopathology in childhood and adulthood, thus identifying mechanisms that influence these associations is necessary for future prevention and intervention. Emotion dysregulation resulting from maltreatment is one potentially powerful mechanism explaining risk for psychopathology. This study tests a conceptual model that distinguishes deprivation and threat as distinct forms of exposure with different pathways to psychopathology. Here we operationalize threat as exposure to physical and/or sexual abuse and deprivation as exposure to neglect. We test the hypothesis that threat and deprivation differentially predict use of avoidant strategies and total regulation. Data were drawn from the Longitudinal Studies on Child Abuse and Neglect (LONGSCAN study; N = 866), which followed high-risk children from age 4 to 18. At age 6, children and their parents reported on adversity exposure. Case records documented exposure to abuse and neglect. At 18, adolescents reported on regulation strategies and psychopathology. Regression analyses indicated that greater exposure to threat, but not deprivation, predicted greater use of avoidant strategies in adolescence. Moreover, avoidance partially mediated the longitudinal association between exposure to threat in early childhood and symptoms of internalizing psychopathology in adolescence. Results suggest that abuse and neglect differentially predict regulation strategy use and that regulation strategy use predicts psychopathology.
The developmental origins of health and disease hypothesis applied to neurodevelopmental outcomes asserts that the fetal origins of future development are relevant to mental health. There is a third pathway for the familial inheritance of risk for psychiatric illness beyond shared genes and the quality of parental care: the impact of pregnant women's distress—defined broadly to include perceived stress, life events, depression, and anxiety—on fetal and infant brain–behavior development. We discuss epidemiological and observational clinical data demonstrating that maternal distress is associated with children's increased risk for psychopathology: For example, high maternal anxiety is associated with a twofold increase in the risk of probable mental disorder in children. We review several biological systems hypothesized to be mechanisms by which maternal distress affects fetal and child brain and behavior development, as well as the clinical implications of studies of the developmental origins of health and disease that focus on maternal distress. Development and parenting begin before birth. Expected final online publication date for the Annual Review of Clinical Psychology Volume 15 is May 7, 2019. Please see http://www.annualreviews.org/page/journal/pubdates for revised estimates.
Associations between stress, sleep, and functioning have been well-established in the general adult population, but not as well-established in the specific subpopulation of interest here-parents. To advance understanding of how maternal sleep is linked with both mothers' experiences of stress and their parenting, this study used actigraphic and mother-report measures of sleep, observed and mother reports of parenting, and measures of multiple stressors of relevance. In a community sample of mothers of toddlers (N = 314; child age M = 2.60, SD = 0.07 years), maternal stress was indexed with a cumulative risk score that combined sociodemographic risks and common parent stressors, including household chaos, role overload, parenting hassles, child misbehavior, negative life events, and lack of social support. We found that mothers who experienced shorter, later, and more variable sleep experienced higher levels of stress as indexed by the cumulative risk index. In addition, those with higher stress required longer to fall asleep and perceived more sleep problems. We also found that actigraphic measures of poor and insufficient maternal sleep were associated with less observed positive parenting, even when controlling for the cumulative risk index and maternal age, employment, and family size. Mothers who required longer to fall asleep also reported more dysfunctional parenting, with the same statistical controls. The findings, coupled with research showing that sleep is amenable to intervention, suggest that parental sleep may ultimately prove to be a useful intervention target for promoting positive parent involvement and responsiveness.
Sleep disturbance is the most prominent symptom in depressive patients and was formerly regarded as a main secondary manifestation of depression. However, many longitudinal studies have identified insomnia as an independent risk factor for the development of emerging or recurrent depression among young, middle‐aged and older adults. This bidirectional association between sleep disturbance and depression has created a new perspective that sleep problems are no longer an epiphenomenon of depression but a predictive prodromal symptom. In this review, we highlight the treatment of sleep disturbance before, during and after depression, which probably plays an important role in improving outcomes and preventing the recurrence of depression. In clinical practice, pharmacological therapies, including hypnotics and antidepressants, and non‐pharmacological therapies are typically applied. A better understanding of the pathophysiological mechanisms between sleep disturbance and depression can help psychiatrists better manage this comorbidity.
Introduction:
Adverse childhood experiences (ACEs) are common among pregnant women and contribute to increased risk for negative perinatal outcomes, yet few clinicians screen prenatal patients for ACEs. The purpose of this study was to evaluate the feasibility and acceptability of screening for ACEs in standard prenatal care.
Methods:
We evaluated a 4-month pilot (March 2016-June 2016) to screen pregnant women (at ∼14-23 weeks of gestation) for ACEs and resiliency in two Kaiser Permanente Northern California medical centers (N = 480). We examined the acceptability of the screening to patients through telephone surveys (N = 210) and to clinicians through surveys and focus groups (N = 26).
Results:
Most eligible patients (78%) were screened. Patients who received the screening were significantly more likely to be non-Hispanic White, Asian, or of "Other" or "Unknown" race/ethnicity than African American or Hispanic race/ethnicity (p = 0.02). Among those screened, 88% completed the questionnaires; 54% reported 0 ACEs, 28% reported 1-2 ACEs, and 18% reported ≥3 ACEs. Most patients were somewhat or very comfortable completing the questionnaires (91%) and discussing ACEs with their clinician (93%), and strongly or somewhat strongly agreed that clinicians should ask their prenatal patients about ACEs (85%). Clinicians reported significant pre- to postpilot increases in comfort discussing ACEs, providing education, and offering resources (ps < 0.01). Clinicians' willingness to screen for ACEs was contingent on adequate training, streamlined workflows, inclusion of resilience screening, and availability of mental health, parenting, and social work resources.
Conclusion:
ACEs screening as part of standard prenatal care is feasible and generally acceptable to patients. Women's health clinicians are willing to screen patients for ACEs when appropriately trained and adequate behavioral health referral resources are available.
Background
Difficult conditions during childhood can limit an individual’s development in many ways. Factors such as being raised in an at-risk family, child temperamental traits or maternal traits can potentially influence a child’s later behaviour. The present study investigated the extent of regulatory problems in 6-month-old infants and their link to temperamental traits and impact on externalizing and internalizing problems at 36 months. Moderating effects of maternal distress and maternal depressive symptoms were tested as well. Methods
In a quasi-experimental, longitudinal study, a sample of 185 mother-infant dyads at psychosocial risk was investigated at 6 months with SFS (infants’ regulatory problems) and at 3 years with CBCL (children’s behavioural problems), EAS (children’s temperament), ADS (maternal depressive symptoms) and PSI-SF (maternal stress). ResultsA hierarchical regression analysis yielded a significant association between infants’ regulatory problems and both externalizing and internalizing behaviour problems at age 3 (accounting for 16% and 14% variance), with both externalizing and internalizing problems being linked to current maternal depressive symptoms (12 and 9% of the variance). Externalizing and internalizing problems were found to be related also to children’s temperamental difficulty (18 and 13% of variance) and their negative emotionality. With temperamental traits having been taken into account, only feeding problems at 6 months contributed near-significant to internalizing problems at 3 years. Conclusions
Our results underscore the crucial role of temperament in the path between early regulatory problems and subsequent behavioural difficulties. Children’s unfavourable temperamental predispositions such as negative emotionality and generally “difficult temperament” contributed substantially to both externalizing and internalizing behavioural problems in the high-risk sample. The decreased predictive power of regulatory problems following the inclusion of temperamental variables indicates a mediation effect of temperamental traits in the path between early regulatory problems and subsequent behavioural problems. Our results support the main effects of a child’s temperament, and to some degree maternal depressive symptoms, rather than the diathesis stress model of interaction between risky environment and temperamental traits.Trial registration D10025651 (NZFH)
Objective:
Research has demonstrated that exposure to violence and adversity has negative effects on both mental health and biobehavioral outcomes, such as sleep health. Research examining the relationship between past and recent violence exposure and mental health suggests that the effects of childhood adversity are especially pernicious, but to date, no studies have attempted to disentangle the direct, indirect and relative effects of past year versus childhood exposure to violence and adversity on sleep. The objective of the current study was to examine the direct effects of adverse childhood experiences (ACEs) and past year intimate partner violence (IPV) on different aspects of sleep health in pregnant women.
Method:
A sample of high-risk pregnant women (n = 101) were interviewed. Mediation analysis with bias-corrected, bootstrapped confidence intervals was used to evaluate direct and indirect effects.
Results:
Findings indicated that while ACEs had significant direct effects on mental health, past year IPV had stronger effects on sleep quality, latency, and efficiency. ACEs did, however, indirectly affect subjective sleep quality via past year psychological IPV.
Conclusion:
These findings suggest that sleep disturbance may be a regulatory stress response that is most clearly linked to past year violence and trauma. That is, though long-term sleep disturbance may be evident following childhood adversity, it is likely that this relationship is better explained by the role of childhood adversity in predicting adulthood revictimization or due to long-term mental health difficulties associated with early trauma. (PsycINFO Database Record
Poor sleep in pregnancy is related to adverse neonatal health. Elevated maternal cortisol has been proposed as a pathway, yet the association in pregnancy is not well understood. The goals of the current study were to examine associations between (a) sleep and cortisol, (b) sleep, cortisol, and neonatal outcomes, and (c) variables that could explain these associations. Two hundred pregnant women completed the Pittsburgh Sleep Quality Index (PSQI; Buysse, Reynolds, Monk, Berman, & Kupfer, 1989) and provided diurnal salivary cortisol samples at two times over pregnancy. Poor sleep quality was associated with greater evening cortisol concentrations at 36 weeks’ gestation. This association was mediated by anxiety symptoms. Higher evening cortisol at 36 weeks’ gestation was associated with shorter gestation.
The aim of this study was to investigate the development of infant and toddler sleep patterns. Data were collected on 841 children (aged from birth to 36 months) via a free, publicly available, commercially sponsored iPhone app. Analyses were conducted on caregiver recordings of 156 989 sleep sessions across a 19-month period. Detailed visualizations of the development of sleep across the first 3 years of life are presented. In the first 3 months, sleep sessions primarily lasted less than 3.5 h throughout the day. Between 3 and 7 months old, sleep consolidated into two naps of about 1.5 h in length and a night-time sleep session of about 10.5 h. Across age groups, a negative relationship was observed between the start of bedtime and the length of the night-time sleep session (i.e. later bedtime is associated with a shorter night-time sleep period). The length of daytime sleep sessions (naps) varied with age, decreasing between 1 and 5 months old, and then increasing monotonically through 28 months. Morning wake time was observed to be invariant in children aged 5-36 months. Sleep patterns are ever-changing across the first few years with wide individual variability. Sleep patterns start to develop more clearly at 5-6 months, when longer night-time sleep duration begins and sleep consolidation occurs. Daytime sleep patterns appeared to become more consistent and consolidated later in age than night-time sleep. Finally, there is greater variability in bedtimes than wake times, with bedtimes having a greater influence on night-time sleep duration.
The most commonly used method to test an indirect effect is to divide the estimate of the indirect effect by its standard error and compare the resulting z statistic with a critical value from the standard normal distribution. Confidence limits for the indirect effect are also typically based on critical values from the standard normal distribution. This article uses a simulation study to demonstrate that confidence limits are imbalanced because the distribution of the indirect effect is normal only in special cases. Two alternatives for improving the performance of confidence limits for the indirect effect are evaluated: (a) a method based on the distribution of the product of two normal random variables, and (b) resampling methods. In Study 1, confidence limits based on the distribution of the product are more accurate than methods based on an assumed normal distribution but confidence limits are still imbalanced. Study 2 demonstrates that more accurate confidence limits are obtained using resampling methods, with the bias-corrected bootstrap the best method overall.
Our goal was to examine associations of infant sleep and feeding patterns with maternal sleep and mood among women at risk for postpartum depression. Participants were 30 women (age ± SD = 28.3 ± 5.1 years) with a history of MDD (but not in a mood episode at enrollment) who completed daily sleep diaries, wore wrist actigraphs to estimate sleep, and had their mood assessed with the Hamilton Depression Rating Scale (HAM-D-17) during four separate weeks of the perinatal period (33 weeks pregnancy and weeks 2, 6, and 16 postpartum). They logged their infants' sleep and feeding behaviors daily and reported postnatal stress on the Childcare Stress Inventory (CSI) at week 16. Mothers' actigraphically estimated sleep showed associations with infant sleep and feeding patterns only at postpartum week 2. Shorter duration of the longest infant-sleep bout was associated with shorter maternal sleep duration (p = .02) and lower sleep efficiency (p = .04), and maternal sleep efficiency was negatively associated with the number of infant-sleep bouts (p = .008) and duration of infant feeding (p = .008). Neither infant sleep nor feeding was associated with maternal sleep at 6 or 16 weeks, but more disturbed infant sleep and more frequent feeding at 6 weeks were associated with higher HAM-D scores at 6 and 16 weeks and higher CSI scores. Sleep in the mother-infant dyad is most tightly linked in the early postpartum weeks, but mothers continue to experience disturbed sleep and infant sleep and feeding behaviors continue to be associated with mothers' depressive symptoms and stress ratings as long as 16 weeks postpartum. These data imply that interventions designed to improve maternal sleep and postpartum mood should include both mothers and infants because improving infant sleep alone is not likely to improve maternal sleep, and poor infant sleep is linked to postpartum depression and stress.
Objective
To examine maternal childhood adversity in relation to increased risk for maternal and infant perinatal complications and newborn Neonatal Intensive Care Unit (NICU) admittance.
Methods
A sample of 164 women recruited at their first prenatal appointment participated in a longitudinal study through 6 weeks postdelivery. Participants self-reported on their adverse childhood experiences (ACEs), negative health risks (overweight/obesity, smoking, and alcohol use), adverse infant outcomes, NICU admittance, and maternal perinatal complications across three pregnancy assessments and one post-birth assessment. Logistic binomial regression analyses were used to examine associations between maternal ACEs and adverse infant outcomes, NICU admittance, and maternal perinatal complications, controlling for pregnancy-related health risks.
Results
Findings showed that women with severe ACEs exposure (6+ ACEs) had 4 times the odds of reporting at least one adverse infant outcome (odds ratio [OR] = 4.33, 95% CI: 1.02–18.39), almost 9 times the odds of reporting a NICU admission (OR = 8.70, 95% CI: 1.34–56.65), and 4 times the odds of reporting at least one maternal perinatal outcome (OR = 4.37, 95% CI: 1.43–13.39).
Conclusions
The findings demonstrate the extraordinary risk that mothers’ ACEs pose for infant and maternal health outcomes over and above the associations with known maternal health risks during pregnancy, including overweight/obesity, smoking, and alcohol use. These results support a biological intergenerational transmission framework, which suggests that risk from maternal adversity is perpetuated in the next generation through biophysical and behavioral mechanisms during pregnancy that negatively affect infant health outcomes.
Introduction
Poor sleep quality is common during pregnancy and can increase the risk of adverse obstetric and fetal outcomes. Existing research on the association between prenatal sleep and infant sleep is scarce and has focused on other aspects of prenatal sleep such as sleep duration, chronotype, and insomnia symptoms. To our knowledge, no studies have examined the association between prenatal sleep quality and infant sleep outcomes. Thus, this study aimed to investigate whether maternal sleep quality during pregnancy was prospectively associated with infant sleep dimensions, independent of relevant covariates.
Methods
Participants were a subset of 272 mother-infant dyads enrolled in an ongoing cohort study. Maternal prenatal sleep quality was assessed with the Pittsburgh Sleep Quality Index (PSQI) in early to mid- (M gestational age = 15.12 ± 3.56 weeks) and late- (M gestational age = 32.44 ± 0.99 weeks) pregnancy. Mothers completed the Brief Infant Sleep Questionnaire (BISQ) at 3, 6, and 12 months postpartum. The following infant sleep parameters were assessed: sleep duration (day, night, 24-hour), number of night awakenings, and wake after sleep onset. Prenatal depressive symptoms were assessed with the Edinburgh Postnatal Depression Scale (EPDS) at both pregnancy time points. Other covariates included maternal age at enrollment, infant age, parity, and co-sleeping status.
Results
Generalized estimating equations (GEE) models revealed that poorer maternal sleep quality during early-to-mid pregnancy did not significantly predict infant sleep parameters after adjustment for covariates (p > .05). However, in late pregnancy, poorer maternal sleep quality significantly predicted shorter 24-hour sleep duration and longer wake after sleep onset, but not daytime sleep duration, nighttime sleep duration, and number of night awakenings (p < .05).
Conclusion
Study findings advance our understanding of the prospective link between maternal prenatal sleep quality and infant sleep. Results indicate that maternal sleep quality during late gestation may play a role in the development of infant sleep patterns. These findings have important implications for intervention efforts targeting maternal sleep quality during pregnancy. Future research should use objective measures of sleep, such as actigraphy, to better elucidate the effects of prenatal sleep quality on infant sleep outcomes.
Support (if any)
The Canadian Institutes of Health Research (CIHR)
Study objectives:
To investigate whether the interaction between infant negative affectivity and maternal depressive symptoms is associated with the degree to which mothers perceive infant sleep to be problematic at six months postpartum, independent of infant sleep and sociodemographic factors.
Methods:
Infant negative affectivity and maternal depressive symptoms were assessed in a sample of 59 mother-infant dyads at 6 months postpartum using standardized measures. Mothers reported the degree to which they perceived their infant's sleep to be problematic via an item composite of the Sleep Practices Questionnaire. Nocturnal infant sleep variables (duration, number of awakenings) were retrieved from a two-week infant sleep diary (maternal report).
Results:
There was a significant interaction between infant negative affectivity and maternal depressive symptoms in predicting mothers' perceived extent of infant sleep problems. Simple slope analysis showed that high levels of depression were related to higher maternal perception of infant sleep problem scores only among mothers of infants with high levels of negative affectivity. Moreover, infant negative affectivity and maternal depressive symptoms positively predicted perception scores after adjustment for infant sleep, maternal age, and parity (p<.05).
Conclusions:
The current study provides evidence that high levels of maternal depression combined with high levels of infant negative affectivity may contribute to mothers' perceptions of infant sleep problems, independent of infant sleep duration and awakenings. These findings highlight the importance for pediatricians and other health professionals to consider infant temperament in conjunction with mother's depressive symptoms when addressing mothers' concerns about infant sleep problems.
Temperament and sleep in infants are related but also distinct concepts. The longitudinal effects of temperament on sleep in infancy remain unclear, although this information is potentially important for the prevention and treatment of early sleep problems. We examined how various temperament features influence sleep development during the first year of life in a large birth cohort. This study comprised mother-infant dyads with complete longitudinal data on sleep, temperament and sociodemographic measurements at six and 12 months (N = 1436). We observed that higher infant Negative Affectivity was related to several sleep problems, and that many subscales of Negative Affectivity and Orienting/Regulation predicted worse sleep and deterioration in sleep problems from six to 12 months. Few associations between Surgency and sleep were found. Our findings highlight especially Negative Affectivity as a risk factor for persistent and increasing sleep problems, and also the specific importance of the fine-grained aspects of temperament in predicting infant sleep development.
Mother's prenatal and postpartum depression have been associated with infant's sleep problems. This study aimed to analyze (a) the effects of mother's prenatal and postpartum depression symptoms, including the effects of prenatal and postpartum anxiety and depression scores of the Edinburgh Postnatal Depression Scale (EPDS), on infant's sleep problems at 6 months, and (b) the interaction effect between mother's prenatal and postpartum depression symptoms and infant's sex on infant's sleep problems at 6 months. The sample was comprised of 164 mother-infant dyads whose mothers completed measures of depression at the third trimester of pregnancy, 2 weeks, 3 and 6 months postpartum and a measure of infant's sleep problems at 6 months (CSHQ-I). Mother's prenatal depression symptoms, specifically depression scores of the EPDS, predicted more infant's sleep anxiety and daytime sleepiness, while mother's depression symptoms at 2 weeks postpartum, specifically anxiety scores of the EPDS, predicted more bedtime resistance and CSHQ-I total scores at 6 months. Boys of mothers with more prenatal depression symptoms presented more sleep anxiety at 6 months. Both mother's prenatal and early postpartum depression symptoms have a negative effect on the emergence of infant's sleep problems. Additionally, boys seem more vulnerable to mother's prenatal depression symptoms.
Introduction
Childhood sleep problems are associated with increased risk of psychiatric conditions later in life. Sleep disturbances are prevalent during pregnancy and associated with postpartum depression and persistent sleep disturbance. Although maternal sleep and mood likely contribute to infant sleep problems, relationships between these factors are understudied. The present study examined associations of prenatal maternal sleep and postpartum depression with infant sleep patterns.
Methods
The sample included 235 women (29.2±5.8 years old), who were enrolled in a longitudinal study beginning in the first trimester of pregnancy. Maternal sleep and mood were assessed with the Pittsburgh Sleep Quality Index, the Center for Epidemiologic Studies Depression Scale, and the Edinburgh Postnatal Depression Scale during 3 prenatal and 2 postpartum visits. Infant sleep patterns were assessed with the Brief Infant Sleep Questionnaire at 2-, 6-, and 12-months. Mixed model repeated measure analyses were conducted to examine changes in maternal and infant sleep across time. Partial correlation adjusted for age, depression, and postpartum maternal sleep was performed to estimate the association between prenatal maternal sleep and infant sleep. ANCOVAs controlling for age were conducted to assess the effect of postpartum depression on infant sleep.
Results
Maternal sleep quality deteriorated during the third trimester and 2-months postpartum, and improved at 6-months postpartum (ps< .001). Infant sleep became more consolidated with age, with decreased nocturnal awakenings (frequency and duration) and increased nighttime sleep duration (ps< .001). Poorer prenatal maternal sleep was associated with shorter infant sleep duration at 6 months (r=-0.33, p<.001). Mothers with persistent postpartum depression reported their child as having longer daytime sleep compared to their counterparts (F=3.55, p<.05).
Conclusion
Prenatal sleep problems and persistent postpartum depression are associated with poorer infant sleep. Our findings suggest that screening and preventive interventions for sleep problems during pregnancy may have beneficial impact on infant sleep.
Support
Research supported by National Institutes of Health MH-96889.
Objective:
Maternal depression is associated with infant and child sleep patterns, and with infant temperament. Here, we examine whether infant temperament mediated an association between maternal antenatal depression and toddler sleep.
Method:
Within the prebirth longitudinal cohort Growing Up in New Zealand, symptoms of antenatal and postnatal depression were measured in 5,568 women using the Edinburgh Postnatal Depression Scale (EPDS). Infant temperament was measured at age 9 months using the Very Short Form of Infant Behavior Questionnaire-Revised (IBQ-R VSF). Sleep duration and nighttime awakenings were reported by parents when children were 2 years old.
Results:
Independent associations of maternal depression with child sleep patterns at age 2 years, adjusted for maternal demographics, physical health, family relationships, and child health and feeding, were determined using multivariate logistic regression analysis. The odds of having ≥2 nighttime awakenings were increased for children whose mothers had antenatal (1.36, 1.07-1.73) but not postnatal (1.22, 0.88-1.68) or both antenatal and postnatal depression (0.89, 0.56-1.36). There was no association of maternal depression with shorter sleep duration. Two of five dimensions of infant temperament (fear and negative affect) were associated with both antenatal depression scores and increased nighttime awakenings. Mediation analyses controlling for postnatal depression and other predictors of child sleep supported an indirect pathway of antenatal depression to child sleep through infant temperamental negative affectivity.
Conclusion:
Antenatal depression is independently associated with more frequent nighttime awakenings in early childhood. Findings support an indirect pathway through infant negative affect characteristics.
Sleep patterns change dramatically across the earliest years of life and play an important role in children’s daytime functioning. As a result, psychological research has taken an increasing interest in unpacking the many intrinsic (i.e., child characteristics) and extrinsic (i.e., environmental input) factors that influence children’s sleep development. Considerably less attention has been given to understanding the transactional relationships among intrinsic and extrinsic factors, or to the underlying mechanisms, that both initiate and maintain individual differences in infant sleep development. In the current review, we begin by summarizing what is known about the development of sleep across the first two years of life, making explicit reference to the dual-process model of sleep consolidation and regulation. Next, we synthesize existing literature on the intrinsic and extrinsic factors that influence the development of sleep consolidation and regulation in infants. Finally, we reconsider extant findings in the infant sleep literature using theories and concepts from developmental science, posing new hypotheses about the ways in which environmental input both shapes infant sleep patterns and modulates the effects of sleep on later developmental outcomes. We conclude with an examination of current challenges in this field and a suggested roadmap for future research.
Previous studies of the relationship between temperament and psychopathology have been limited by focusing on main effects of temperament on psychopathology, reliance solely on maternal reports of child temperament, and predominately using cross-sectional designs. This study extended this work by focusing on interactions between reactive (positive emotionality/PE; negative emotionality/NE) and regulatory (effortful control) dimensions of temperament, using laboratory observations of temperament, and focusing on longitudinal prediction of internalizing and externalizing behavior problems. 536 children (46.1% Female, 92.4% White) were followed in a prospective, longitudinal study of the relationship between temperament and psychopathology. Temperament was assessed using laboratory observations when children were at age 3. Mothers and fathers reported on internalizing and externalizing symptoms in their children at ages 3, 6, and 9. Multilevel modeling analyses examined associations between the interaction of temperament traits and patterns of change in internalizing and externalizing psychopathology. Interactions between reactive PE traits (Sociability, Exuberance), but not NE traits (Dysphoria, Fear), and regulatory temperament (Disinhibition) were associated with the slope of maternal-reported internalizing and paternal-reported externalizing symptoms such that youth low in PE traits and high in effortful control experienced a greater decline in symptoms over time. In conclusion, among children with lower levels of PE traits, strong regulatory abilities are associated with greater reductions in internalizing and externalizing symptoms over time. These models highlight the complex interaction between reactive and regulatory temperament and expand current understanding of temperamental risk for psychopathology.
Background:
Trauma-exposed women may be at magnified risk for posttraumatic stress (PTSS) and depression symptoms in the perinatal period, but few studies have examined symptomatology across the perinatal period in high-risk samples. Further, the role of sleep in perinatal symptomatology has been largely neglected in the violence literature, despite its well-established associations to mental health in other samples. This study aimed to examine the trajectory of PTSS and depression symptoms across the perinatal period and the effects of childhood adversity, intimate partner violence and prenatal sleep impairment on PTSS and depression symptoms across the perinatal period.
Method:
In a longitudinal, prospective study, 101 low-income pregnant women were interviewed during pregnancy, at 6-weeks postpartum, and 4 months postpartum. N = 83 women completed at least 2 interviews and were included in the analyses. Prenatal sleep, childhood adversity, and IPV exposure were assessed at the prenatal interview; PTSS and depression were assessed at all interviews.
Results:
Past year IPV was associated with elevated prenatal mental health symptoms and prenatal sleep difficulties were associated with a worsening trajectory in perinatal PTSS.
Conclusions:
Screening for IPV and prenatal sleep difficulties may be paramount in identifying those at risk for the development or exacerbation of mental health symptoms in the perinatal period.
After childbirth, most American women are not scheduled for follow up care for 6 weeks, and this visit is poorly attended. Many new mothers feel unprepared for the common health issues they encounter and are uncertain of whom to contact. To improve care, the 4(th) Trimester Project is bringing together mothers, health care providers, and other stakeholders to explore what families need most from birth to 12 weeks postpartum. Eighty-seven individuals convened in March 2016 in Chapel Hill, NC. Four major topic areas emerged: (1) the intense focus on women's health prenatally is unbalanced by infrequent and late postpartum care; (2) medical practice guidelines often do not align with women's experiences and constraints; (3) validation of women as experts of their infants and elevating their strengths as mothers is necessary to achieve health goals; and (4) mothers need comprehensive care, which is difficult to provide due to numerous system constraints. Considerations for improving postpartum services include enabling more convenient care for families that is holistic, culturally appropriate, conversation-based, and equitable. Maternal health issues in the 4(th) Trimester intersect and can compound one another. Enhanced collaboration among health care providers may improve the focus clinical interactions to address the interrelated health issues most important to women.
Infant sleep problems have been the focus of a growing literature over the last few years. The current review is based on literature searches of Pubmed and PsycInfo for studies published over the last few years including randomized controlled trials, systematic reviews and meta-analyses on infant sleep problems and resulting developmental effected, risk factors and interventions. Several risk/protective factors for sleep problems have been identified including health literacy, TV in the room, feeding, close contact and arousing activities at bedtime, intolerance for infant crying, co-sleeping, maternal depression and infant temperament. Cross-cultural differences have been noted both for infant sleep problems and parents’ perceived distress by those problems. A number of interventions have been tried to ameliorate infant sleep problems including consultations, teaching sessions on extinction and bedtime fading, internet-based interventions and nighttime massages by parents. Some of these studies have shown improvements and others have suggested only short-term or negligible effects. Significant methodological problems exist with this literature including the almost sole use of parent report as well as the mixed age samples and the potential confounding variables.
Objective
Growing evidence suggests the deleterious consequences of exposure to childhood maltreatment (CM) not only might endure over the exposed individual’s lifespan but also might be transmitted across generations. The time windows, mechanisms, and targets of such intergenerational transmission are poorly understood. The prevailing paradigm posits that mother-to-child transmission of the effects of maternal CM likely occurs after her child’s birth. The authors seek to extend this paradigm and advance a transdisciplinary framework that integrates the concepts of biological embedding of life experiences and fetal origins of health and disease risk.
Method
The authors posit that the period of embryonic and fetal life represents a particularly sensitive time for intergenerational transmission; that the developing brain represents a target of particular interest; and that stress-sensitive maternal-placental-fetal biological (endocrine, immune) pathways represent leading candidate mechanisms of interest.
Results
The plausibility of this model is supported by theoretical considerations and empirical findings in humans and animals. The authors synthesize several research areas and identify important knowledge gaps that might warrant further study.
Conclusion
The scientific and public health relevance of this effort relates to achieving a better understanding of the “when,” “what,” and “how” of intergenerational transmission of CM, with implications for early identification of risk, prevention, and intervention.
The influence of the lifespan approach has been an important feature of recent research in developmental psychology, as has a growing interest in the relationship between personality and development. This important new book, edited by two distinguished psychologists, explores the relationship between personality and development from a life-course perspective. The book presents current theoretical approaches and new empirical findings from ongoing studies conducted by leading researchers in North America and Europe. It is unique in focussing on successful personality development, where developmental psychology in the past seems to have focussed almost entirely on problem behaviour and risk of maladaption. The book has a multidisciplinary appeal and will be of interest to students and researchers in the fields of developmental psychology, adult development and aging, and personality and social psychology.
Objective:
To evaluate the feasibility and efficacy of a home-based cognitive-behavioral training program for sleep during late pregnancy.
Methods:
A nonrandomized quasiexperimental sample of nulliparous women who received the intervention during pregnancy (n=25) was compared with two control groups (n=76 and n=48) from other intervention studies at similar postintervention time points: approximately 1 month before childbirth and 1-2 months after childbirth. The home-based Sleep Enhancement Training System for Pregnancy consisted of 4 weeks of sound-enhanced audio relaxation programs, readings, and daily sleep diaries. Both control groups received dietary recommendations for improving sleep. Sleep duration (total sleep time) and sleep disruption (wake after sleep onset) were measured using wrist actigraphy for a minimum of 48 hours on consecutive weekdays.
Results:
The intervention group had significantly longer sleep duration and less sleep disruption than both control groups, particularly at the postpartum assessment. Intervention participants slept an average of 430 (95% confidence interval [CI] 397-464) minutes during pregnancy compared with 420 (95% CI 403-438) and 417 (95% CI 395-439) minutes for the two control groups. At the postpartum assessment, the intervention group slept 446 (95% CI 415-478) minutes compared with 390 (95% CI 373-408) and 370 (95% CI 348-393) minutes for those in the control groups. In terms of sleep disruption, women in the intervention group had 16.1% (95% CI 11.9-20.2%) wake after sleep onset during pregnancy, whereas women in the control groups had 13.4% (95% CI 11.2-15.5%) and 20.4% (95% CI 17.7-23.0%). Postpartum, the intervention group had 20.3% (95% CI 16.4-24.1%) wake after sleep onset compared with 26.6% (95% CI 24.5-28.8%) and 28.7% (95% CI 26.0-31.5%) among women in the control groups. Participant feedback about the intervention was generally positive, although intervention adherence was variable.
Conclusion:
This study provides evidence of the feasibility and efficacy of the Sleep Enhancement Training System for Pregnancy intervention for enhancing sleep that typically worsens during late pregnancy and after childbirth.
The aim of this study was to examine the cross-sectional and longitudinal relationships among variables related to sleep patterns and both social-emotional problems (i.e., internalizing, externalizing, and dysregulation) and healthy social development (i.e., social competence). Assessments were completed at 6, 12, and 18 months across 5 cohorts of children for a total of 117 mother-child dyads. Mothers completed the Brief Infant Sleep Questionnaire at 6, 12, and 18 months, as well as the Infant Toddler Social Emotional Assessment at 12 and 18 months. Later bedtimes and less total sleep across the 24-hr period predicted higher internalizing problem scores, which includes indices of depression/withdrawal, general anxiety, separation distress, and inhibition. In contrast, sleep fragmentation was minimally associated with decreased social competence but not with any negative social-emotional outcomes. These results indicate that sleep patterns, primarily later bedtimes and less total sleep, appear to be associated with and predictive of social-emotional problem areas, namely, internalizing issues, in infants and toddlers. These findings add to the growing literature on the role of sleep in early social-emotional development and suggest that sleep schedule and duration should be addressed in clinical assessment and interventions for infant sleep.
The current study prospectively examined the ways in which goodness of fit between maternal and infant sleep contributes to maternal depressive symptoms and the mother-child relationship across the first years of life. In a sample of 173 mother-child dyads, maternal prenatal sleep, infant sleep, maternal depressive symptoms, and mother-child attachment security were assessed via self-report, actigraphy, and observational measures. Results suggested that a poor fit between mothers’ prenatal sleep and infants’ sleep at 8 months (measured by sleep diary and actigraphy) was associated with maternal depressive symptoms at 15 months. Additionally, maternal depression mediated the association between the interplay of mother and infant sleep (measured by sleep diary) and mother-child attachment security at 30 months. Findings emphasize the importance of the match between mother and infant sleep on maternal wellbeing and mother-child relationships and highlight the role of mothers’ perceptions of infant sleep.
Maternal adverse childhood experiences (ACEs) have been associated with negative physical and mental health outcomes in adulthood. Less is known regarding how maternal ACEs relate to perinatal depressive symptoms or the intergenerational effect of maternal childhood trauma history on birth outcomes and infant functioning. To address this gap, an at-risk sample of 398 pregnant women was recruited from Women, Infants, and Children health clinics. Participants completed a prenatal (M = 4.84 months before due date) and postnatal (M = 6.76 months after birth) assessment and provided birth outcome data. At the prenatal assessment, mothers completed an ACEs measure which assessed experiences of childhood maltreatment and household dysfunction. Self-report measures of maternal depressive symptoms were obtained at both time points. Mothers reported on infant socioemotional functioning at 6 months. Maternal ACEs predicted higher levels of prenatal depressive symptoms. Childhood maltreatment experiences, in particular, predicted higher postnatal depressive symptoms and a smaller reduction in depressive symptoms across the perinatal period. Regarding intergenerational associations, maternal childhood maltreatment directly predicted higher levels of maladaptive infant socioemotional symptoms, whereas maternal household dysfunction indirectly related to infant socioemotional symptoms through maternal age at first pregnancy and infant birth weight. Limitations and future directions are discussed.
Infant sleep consolidates rapidly during the first half year of life in the context of a dynamic, bidirectional exchange between infant characteristics and the caregiving environment. The current study examined the relationship between mothers' emotional availability (EA) at bedtime and infant temperament, and objectively assessing infant sleep development from one to six months, particularly focus on whether infant temperament moderated linkages between EA at bedtime and infant sleep development. The sample consisted of 72 mother–infant dyads, and the measures included actigraphy-assessed infant sleep at one and six months, observed maternal EA coded from bedtime videos at 3 and 6 months, and maternal reports of infant temperament at three and six months. The analysis showed significant positive effects of maternal EA at bedtime on developmental changes in infant sleep minutes. Additionally, infant temperamental surgency moderated the influence of EA at bedtime on the increase in infant sleep minutes. In other words, highly surgent infants whose mothers were emotionally available at bedtime showed a greater increase in their sleep time than other infants. The results are discussed in terms of the transactional model of infant sleep development.
The notion of an average expectable environment for promoting normal development proposes that there are species-specific ranges of environmental conditions that elicit normative developmental processes. This chapter provides a review of child maltreatment. Of particular salience is the growing contribution of neurobiological and genetic research to the study of child maltreatment, such that ontogenic development can be considered from both psychological and neurobiological perspectives. The ecological-transactional model of child maltreatment explains how processes at each level of ecology exert reciprocal influences on each other and shape the course of child development. The extent of variation in personality characteristics and personality organization among maltreated children represents an area of investigation that has recently gained attention in the maltreatment literature. The maladaptive trajectories of maltreated children diverge from those of nonmaltreated children over time such that maltreated children's problems become more severe as children get older, especially in peer relationships.
Objective:
This article presents a new formulation of the relationship between stress and the processes leading to disease. It emphasizes the hidden cost of chronic stress to the body over long time periods, which act as a predisposing factor for the effects of acute, stressful life events. It also presents a model showing how individual differences in the susceptibility to stress are tied to individual behavioral responses to environmental challenges that are coupled to physiologic and pathophysiologic responses.Data Sources:
Published original articles from human and animal studies and selected reviews. Literature was surveyed using MEDLINE.Data Extraction:
Independent extraction and cross-referencing by us.Data Synthesis:
Stress is frequently seen as a significant contributor to disease, and clinical evidence is mounting for specific effects of stress on immune and cardiovascular systems. Yet, until recently, aspects of stress that precipitate disease have been obscure. The concept of homeostasis has failed to help us understand the hidden toll of chronic stress on the body. Rather than maintaining constancy, the physiologic systems within the body fluctuate to meet demands from external forces, a state termed allostasis. In this article, we extend the concept of allostasis over the dimension of time and we define allostatic load as the cost of chronic exposure to fluctuating or heightened neural or neuroendocrine response resulting from repeated or chronic environmental challenge that an individual reacts to as being particularly stressful.Conclusions:
This new formulation emphasizes the cascading relationships, beginning early in life, between environmental factors and genetic predispositions that lead to large individual differences in susceptibility to stress and, in some cases, to disease. There are now empirical studies based on this formulation, as well as new insights into mechanisms involving specific changes in neural, neuroendocrine, and immune systems. The practical implications of this formulation for clinical practice and further research are discussed.(Arch Intern Med. 1993;153:2093-2101)
Insomnia disorder is characterized by chronic dissatisfaction with sleep quantity or quality that is associated with difficulty falling asleep, frequent nighttime awakenings with difficulty returning to sleep, and/or awakening earlier in the morning than desired. Although progress has been made in our understanding of the nature, etiology, and pathophysiology of insomnia, there is still no universally accepted model. Greater understanding of the pathophysiology of insomnia may provide important information regarding how, and under what conditions, the disorder develops and is maintained as well as potential targets for prevention and treatment. The aims of this report are (1) to summarize current knowledge on the pathophysiology of insomnia and (2) to present a model of the pathophysiology of insomnia that considers evidence from various domains of research. Working within several models of insomnia, evidence for the pathophysiology of the disorder is presented across levels of analysis, from genetic to molecular and cellular mechanisms, neural circuitry, physiologic mechanisms, sleep behavior, and self-report. We discuss the role of hyperarousal as an overarching theme that guides our conceptualization of insomnia. Finally, we propose a model of the pathophysiology of insomnia that integrates the various types of evidence presented.
Growing evidence suggests that toxic stressors early in life not only convey developmental impacts but also augment risk of proliferating chains of additional stressors that can overwhelm individual coping and undermine recovery and health. Examining trauma within a life course stress process perspective, we posit that early childhood adversity carries a unique capacity to impair adult psychological well-being both independent of and cumulative with other contributors, including social disadvantage and stressful adult experiences. This study uses data from a representative population-based health survey (N=13,593) to provide one of the first multivariate assessments of unique, cumulative, and moderated effects of adverse childhood experiences (ACEs) toward explaining 3 related yet distinct measures of adult mental health: perceived well-being, psychological distress, and impaired daily activities. Results demonstrate support for each set of hypothesized associations, including exacerbation and amelioration of ACEs effects by adult stress and resilience resources, respectively. Implications for services and future research are discussed.
Copyright © 2015 Elsevier Ltd. All rights reserved.
Sleep patterns and temperament in the first year of life are closely related. However, research utilizing objective, rather than subjective measurements of sleep and temperament is scarce and results are inconsistent. In addition, a relative lack of longitudinal data prevents inference of causality between the two constructs. In this study, infant sleep was objectively assessed among 95 infants at 3, 6, and 12 months-of-age with an actigraph in the home setting. Reactivity to sound, light, and touch, a specific aspect of temperament, was behaviorally assessed at 3 and 6 months, both during sleep (at home) and during waking (at the laboratory). Expected maturational trends were recorded in sleep, with a temporal increase in sleep efficiency and percent of motionless sleep. Quadratic (i.e., inverse U shape) relations were found, especially among girls, when predicting change in sleep by reactivity thresholds, suggesting that both hyposensitive and hypersensitive infants are at risk for poor sleep quality. These are the first research findings suggesting that low reactivity in infancy might be associated with compromised sleep quality. The observed nonlinear effects may account for null or inconsistent results in previous studies that explored only linear associations between temperament and sleep. Future studies should address both extremes of the temperament continuum when exploring relations with sleep patterns.
© 2015 The Society for Research in Child Development, Inc.
The aims of this longitudinal study were to examine (a) development of infant sleep and maternal sleep from 3 to 6 months postpartum; (b) concomitant and prospective links between maternal sleep and infant sleep; and (c) triadic links between paternal involvement in infant caregiving and maternal and infant sleep. The study included 57 families that were recruited during pregnancy. Maternal and infant sleep was assessed using actigraphy and sleep diaries for 5 nights. Both fathers and mothers completed a questionnaire assessing the involvement of fathers relative to mothers in infant caregiving. The results demonstrated moderate improvement in infant and maternal sleep percent between 3 and 6 months. Maternal sleep percent at 3 months significantly predicted infant sleep percent at 6 months. Greater paternal involvement in infant daytime and nighttime caregiving at 3 months significantly predicted more consolidated maternal and infant sleep at 6 months. These findings suggest that maternal sleep is an important predictor of infant sleep and that increased involvement of fathers in infant caregiving responsibilities may contribute to improvements in both maternal and infant sleep during the first 6 months postpartum.
© 2015 The Society for Research in Child Development, Inc.
Adverse childhood experiences (ACEs) represent substantial threats to public health and affect about 58% of youth in the US. In addition to their acute effects such as injury and physical trauma, ACEs are associated with an increased risk of several negative health outcomes throughout the life course. Emerging evidence suggests that sleep disorders may be one such outcome, but existing studies have not been systematically reviewed and summarized. We conducted a systematic review to summarize the evidence concerning the relationship between ACEs and sleep disorders and disturbances, with a focus on adult women. Original publications were identified through searches of the electronic databases MEDLINE, Embase, and Web of Science using the keywords "childhood," "adversity," "abuse," and "sleep" as well as searches of the reference lists of eligible studies. Studies evaluating ACEs that occurred before 18 years of age and sleep outcomes that were assessed at 18 years or older were adjudicated and included. A total of 30 publications were identified. Of the 30 studies, 28 were retrospective analyses and there was vast heterogeneity in the types of ACEs and sleep outcomes measured. The majority of retrospective studies (N = 25 of 28) documented statistically significant associations between sleep disorders including sleep apnea, narcolepsy, nightmare distress, sleep paralysis, and psychiatric sleep disorders with a history of childhood adversity. In many studies, the strengths of associations increased with the number and severity of adverse experiences. These associations were corroborated by the two prospective studies published to date. Notably, investigators have documented statistically significant associations between family conflict at 7-15 years of age and insomnia at 18 years of age (odds ratio, OR = 1.4; 95% confidence interval, CI = 1.2-1.7) and between childhood sexual abuse and sleep disturbances 10 years later in adult women (β = 0.24, p <0.05). There is a growing scientific body of knowledge suggesting an association between ACEs and multiple sleep disorders in adulthood. The available evidence indicates the need to develop treatment strategies such as trauma-informed care for survivors of abuse who suffer from sleep disorders and disturbances. Further, longitudinal studies among diverse populations are needed to improve the overall understanding of this association and to investigate potential gender and racial/ethnic disparities in the strength of the association.
Copyright © 2014 Elsevier B.V. All rights reserved.
Emotions are biologically-based responses that help an organism meet challenges and opportunities, and involve changes in subjective experience, behavior, and physiology. Emotions arise when something important to us is at stake. Although many factors have been associated with healthy emotional regulation, the role of sleep in this process has been largely ignored. Recent studies, however, have begun to delineate how sleep critically affects emotional functioning. Nighttime sleep affects daytime mood, emotional reactivity and the capacity to regulate positive and negative emotions; conversely, daytime experiences affect sleep. Hence, there is a complex interplay between sleep and emotional regulation. The objective of this article is to examine this interplay in adults. This objective is addressed by utilizing a framework that identifies key aspects of the relationship between sleep and emotion. We propose that the connectivity between the emotional centers of the brain - the prefontal cortex and the amygdala - is in part dependent on the homeostatic sleep system such that connectivity between these brain networks is higher when rested and lower when sleep deprived. High connectivity drives more efficient executive functioning, while a disconnect leads to poor executive functioning capacity including emotional reactivity and impulsivity. The cognitive effects of the homeostatic system are couple with the mood regulation effects of the circadian system together dictating the degree to which one experiences emotional regulation or dysregulation. Further, the affective brain systems of individuals with clinical symptomology and/or pathology are suggested to be more vulnerable to homeostatic pressure and circadian lows or misalignment resulting in increased affective clinical symptomology. We review empirical evidence that supports this framework and explore the implications of this framework. Finally, we describe future directions for this type of work.
Background:
Pregnant women with complications including pregnancy-induced hypertension (PIH) and gestational diabetes mellitus (GDM) often experience disrupted sleep patterns because of activation of the sympathetic nervous system. These pathologies are aggravated by sympathetic nervous system activation and may be related to stress. The present study aimed to clarify the characteristics of and changes in sleep quality and stress in pregnant women with PIH and GDM during the second and third trimesters.
Methods:
We enrolled 56 women in their second or third trimesters who were diagnosed with PIH or GDM. Participants completed questionnaires, including the Pittsburgh Sleep Quality Index (PSQI) and the Perceived Stress Scale (PSS). Secretory immunoglobulin A (SlgA) concentrations were measured as a biological indicator of stress.
Results:
PSS scores and subjective stress parameters were significantly higher than those reported from previous studies of healthy pregnant women (15.2 points and 15.1 points for the second and third trimesters, respectively). Mean one-day values for SIgA were 168.3 and 205.7 μg/mL for the second and third trimesters, respectively. During the second and third trimesters, SIgA scores were higher than those reported for healthy pregnant women in previous studies. The PSQI component scores sleep disturbance (C5) and sleep duration (C3) in follow up case were significantly higher in the third trimester than in the second trimester.
Discussion:
This investigation suggests that pregnant women with PIH and GDM experience higher stress levels than do non-pregnant women and healthy pregnant women. Further, our results indicate that sleep quality worsens during the third trimester compared with the second trimester.