Adipokines measured during pregnancy and at birth are associated with infant negative affect.

BACKGROUND: Increased adiposity during pregnancy may be related to offspring risk for mental health disorders, although the biological mechanisms are poorly understood. One promising hypothesis is that factors secreted from adipocytes such as leptin and adiponectin may explain this association. The current study examined whether pregnancy or umbilical cord blood concentrations of leptin and/or adiponectin a) predict elevated infant negative affect at 6 months (an early life marker of risk for psychopathology); and b) help explain the association between pregnancy adiposity and increased infant negative affect. METHODS: Data came from a prospective cohort (N = 305) of pregnant individuals and their offspring. Second trimester adiposity was assessed using air displacement plethysmography. Concentrations of leptin and adiponectin were measured in second trimester plasma and umbilical cord plasma. Infant negative affect was assessed by standardized observation at 6 months. Second trimester inflammation was assessed using a comprehensive panel of cytokines. RESULTS: Lower second trimester adiponectin was associated with elevated infant negative affect, and mediated the effect of pregnancy adiposity on infant negative affect. This association was independent of the effect of second trimester inflammation. Umbilical cord leptin also predicted higher infant negative affect and mediated the association between pregnancy adiposity and infant negative affect. CONCLUSIONS: This is the first study to link pregnancy adiponectin or cord blood leptin to infant markers of risk for psychopathology, and the first to demonstrate that these adipokines mediate the association between pregnancy adiposity and offspring behavioral outcomes, suggesting novel markers of risk and potential mechanisms of effect.

Maternal diet and obesity shape offspring central and peripheral inflammatory outcomes in juvenile non-human primates.

The obesity epidemic affects 40% of adults in the US, with approximately one-third of pregnant women classified as obese. Previous research suggests that children born to obese mothers are at increased risk for a number of health conditions. The mechanisms behind this increased risk are poorly understood. Increased exposure to in-utero inflammation induced by maternal obesity is proposed as an underlying mechanism for neurodevelopmental alterations in offspring. Utilizing a non-human primate model of maternal obesity, we hypothesized that maternal consumption of an obesogenic diet will predict offspring peripheral (e.g., cytokines and chemokines) and central (microglia number) inflammatory outcomes via the diet's effects on maternal adiposity and maternal inflammatory state during the third trimester. We used structural equation modeling to simultaneously examine the complex associations among maternal diet, metabolic state, adiposity, inflammation, and offspring central and peripheral inflammation. Four latent variables were created to capture maternal chemokines and pro-inflammatory cytokines, and offspring cytokine and chemokines. Model results showed that offspring microglia counts in the basolateral amygdala were associated with maternal diet (ß = -0.622, p < 0.01), adiposity (ß = 0.593, p < 0.01), and length of gestation (ß = 0.164, p < 0.05) but not with maternal chemokines (ß = 0.135, p = 0.528) or maternal pro-inflammatory cytokines (ß = 0.083, p = 0.683). Additionally, we found that juvenile offspring peripheral cytokines (ß = -0.389, p < 0.01) and chemokines (ß = -0.298, p < 0.05) were associated with a maternal adiposity-induced decrease in maternal circulating chemokines during the third trimester (ß = -0.426, p < 0.01). In summary, these data suggest that maternal diet and adiposity appear to directly predict offspring amygdala microglial counts while maternal adiposity influences offspring peripheral inflammatory outcomes via maternal inflammatory state.

Associations between childhood maltreatment, poor sleep, and prenatal distress in pregnant adolescents.

Childhood maltreatment (CM) is a known risk factor for adolescent pregnancy. Sleep disturbances and psychological distress, both common negative sequelae of CM, often co-occur during pregnancy, although directionality remains unclear. Furthermore, little is known about how CM affects sleep-distress associations during pregnancy. In pregnant adolescents, we examined: (a) whether there are significant predictive associations from CM to sleep quality and distress and (b) bidirectional influences of distress and sleep quality. Healthy pregnant adolescents (n = 204) were recruited before or during the 2nd trimester. CM was assessed at enrollment; sleep quality and distress were assessed in the 2nd and 3rd trimesters. Hypotheses were tested using path analysis. Findings revealed that CM was associated with worse 2nd trimester sleep quality and distress (ß = .19, p < .05 for sleep; ß = .30, p < .001 for distress). Higher levels of 2nd trimester distress were associated with lower 3rd trimester sleep quality (ß = .19, p < .05). Findings provide novel information about (a) associations from CM to prenatal mood and sleep in pregnant adolescents, and (b) sleep-distress directionality over the course of pregnancy. These results have implications for better understanding the ways in which CM potentially exerts influences later in life, and for targeting interventions to address physical and mental health during pregnancy.

Electroencephalogram aperiodic power spectral slope can be reliably measured and predicts ADHD risk in early development.

The aperiodic exponent of the electroencephalogram (EEG) power spectrum has received growing attention as a physiological marker of neurodevelopmental psychopathology, including attention-deficit/hyperactivity disorder (ADHD). However, its use as a marker of ADHD risk across development, and particularly in very young children, is limited by unknown reliability, difficulty in aligning canonical band-based measures across development periods, and unclear effects of treatment in later development. Here, we investigate the internal consistency of the aperiodic EEG power spectrum slope and its association with ADHD risk in both infants (n = 69, 1-month-old) and adolescents (n = 262, ages 11-17 years). Results confirm good to excellent internal consistency in infancy and adolescence. In infancy, a larger aperiodic exponent was associated with greater family history of ADHD. In contrast, in adolescence, ADHD diagnosis was associated with a smaller aperiodic exponent, but only in children with ADHD who had not received stimulant medication treatment. Results suggest that disruptions in cortical development associated with ADHD risk may be detectable shortly after birth via this approach. Together, findings imply a dynamic developmental shift in which the developmentally normative flattening of the EEG power spectrum is exaggerated in ADHD, potentially reflecting imbalances in cortical excitation and inhibition that could contribute to long-lasting differences in brain connectivity.

Trajectories of perinatal depressive symptoms in the context of the COVID-19 pandemic.

This study sought to advance understanding of the potential long-term consequences of the COVID-19 pandemic for child development by characterizing trajectories of maternal perinatal depression, a common and significant risk factor for adverse child outcomes. Data came from 393 women (86% White, 8% Latina; mean age = 33.51 years) recruited during pregnancy (n = 247; mean gestational age = 22.94 weeks) or during the first year postpartum (n = 146; mean child age = 4.50 months; 55% female). Rates of depression appear elevated, relative to published reports and to a pre-pandemic comparison group (N = 155). This study also provides evidence for subgroups of individuals who differ in their depressive symptom trajectories over the perinatal period. Subgroup membership was related to differences in maternal social support, but not to child birth outcomes.

Early development of negative and positive affect: Implications for ADHD symptomatology across three birth cohorts.

High levels of early emotionality (of either negative or positive valence) are hypothesized to be important precursors to early psychopathology, with attention-deficit/hyperactivity disorder (ADHD) a prime early target. The positive and negative affect domains are prime examples of Research Domain Criteria (RDoC) concepts that may enrich a multilevel mechanistic map of psychopathology risk. Utilizing both variable-centered and person-centered approaches, the current study examined whether levels and trajectories of infant negative and positive emotionality, considered either in isolation or together, predicted children's ADHD symptoms at 4 to 8 years of age. In variable-centered analyses, higher levels of infant negative affect (at as early as 3 months of age) were associated with childhood ADHD symptoms. Findings for positive affect failed to reach statistical threshold. Results from person-centered trajectory analyses suggest that additional information is gained by simultaneously considering the trajectories of positive and negative emotionality. Specifically, only when exhibiting moderate, stable or low levels of positive affect did negative affect and its trajectory relate to child ADHD symptoms. These findings add to a growing literature that suggests that infant negative emotionality is a promising early life marker of future ADHD risk and suggest secondarily that moderation by positive affectivity warrants more consideration.

Parasympathetic response to challenge in infancy moderates the effects of sociodemographic risk on academic achievement at school entry.

Exposure to higher levels of sociodemographic risk is associated with lower levels of academic achievement among young children. However, there is variability in the strength of this association, which may be traced to individual differences in physiological processes underlying self-regulation. In the current study, we examined whether the response of the parasympathetic nervous system to challenge, indexed by change in respiratory sinus arrhythmia (RSA), moderated the association between risk and school readiness at 5 years of age in a diverse sample of young children. We found that parasympathetic response to the Still-Face Paradigm moderated the effects of risk on a measure of school readiness, such that there was no association between risk and school readiness among children who exhibited RSA decreases during challenge at 6 months of age, a purported index of self-regulation at this age. For those infants who did not exhibit RSA withdrawal during this challenge, exposure to early cumulative risk was associated with lower scores on achievement assessment. These results speak to the possibility that certain patterns of parasympathetic response can serve as a protective factor for young children growing up in disadvantaged environments.

Evaluation of maternal inflammation as a marker of future offspring ADHD symptoms: A prospective investigation.

Early life predictors of attention-deficit/hyperactivity disorder (ADHD) are critically needed; they could inform etiological theory and may help identify new prevention targets. The current study examined prospectively whether maternal cytokine levels during pregnancy predict offspring ADHD symptoms at age 4-6 years. Secondarily, we evaluated maternal cytokine levels as a possible common pathway through which prenatal risks exert influence on child ADHD. Data came from a sample of women recruited during the 2nd trimester of pregnancy (N = 62) and followed postnatally until children were 4-6 years old. Maternal inflammation was assessed using 3rd trimester plasma concentrations of three indicators of nuclear factor kappa B signaling: interleukin-6, tumor necrosis factor-alpha, and monocyte chemoattractant protein-1 which were combined into a latent variable. Mothers and teachers reported on child ADHD symptoms, negative affect, and externalizing behaviors at 48-72 months of age. Maternal inflammation in the 3rd trimester predicted ADHD symptoms when children were 4-6 years old (ß = 0.53, 95% CI = 0.154, 0.905, p = 0.006). Further, maternal inflammation mediated the effect of prenatal distress on child ADHD (ß = 0.21, 95% CI = 0.007, 0.419, p = 0.04). The inflammation effect on ADHD was not explained by concurrent child negative affect, externalizing behavior, or familial ADHD status. This is the first human study to prospectively link maternal pregnancy cytokine levels and offspring ADHD symptoms, suggesting that cytokine levels are a possible marker of ADHD risk. Results also provide new evidence that maternal prenatal inflammation may be one common pathway by which prenatal risk factors influence offspring mental health outcomes.

Evaluating chronic emotional dysregulation and irritability in relation to ADHD and depression genetic risk in children with ADHD.

BACKGROUND: A central nosological problem concerns the etiological relationship of emotional dysregulation with ADHD. Molecular genetic risk scores provide a novel method for informing this question. METHODS: Participants were 514 community-recruited children of Northern European descent age 7-11 defined as ADHD or non-ADHD by detailed research evaluation. Parents-rated ADHD on standardized ratings and child temperament on the Temperament in Middle Childhood Questionnaire (TMCQ) and reported on ADHD and comorbid disorders by semi-structured clinical interview. Categorical and dimensional variables were created for ADHD, emotional dysregulation (implicating disruption of regulation of both anger-irritability and of positive valence surgency-sensation seeking), and irritability alone (anger dysregulation). Genome-wide polygenic risk scores (PRS) were computed for ADHD and depression genetic liability. Structural equation models and computationally derived emotion profiles guided analysis. RESULTS: The ADHD PRS was associated in variable-centered analyses with irritability (ß = .179, 95% CI = 0.087-0.280; ΔR2  = .034, p < .0002), but also with surgency/sensation seeking (B = .146, 95%CI = 0.052-0.240, ΔR2 =.022, p = .002). In person-centered analysis, the ADHD PRS was elevated in the emotion dysregulation ADHD group versus other ADHD children (OR = 1.44, 95% CI = 1.03-2.20, Nagelkerke ΔR2  = .013, p = .033) but did not differentiate irritable from surgent ADHD profiles. All effects were independent of variation in ADHD severity across traits or groups. The depression PRS was related to oppositional defiant disorder but not to ADHD emotion dysregulation. CONCLUSIONS: Irritability-anger and surgency-sensation seeking, as forms of negative and positively valenced dysregulated affect in ADHD populations, both relate principally to ADHD genetic risk and not mood-related genetic risk.

Maternal prenatal depression predicts infant negative affect via maternal inflammatory cytokine levels.

Maternal depressive symptoms during pregnancy are associated with risk for offspring emotional and behavioral problems, but the mechanisms by which this association occurs are not known. Infant elevated negative affect (increased crying, irritability, fearfulness, etc.) is a key risk factor for future psychopathology, so understanding its determinants has prevention and early intervention potential. An understudied yet promising hypothesis is that maternal mood affects infant mood via maternal prenatal inflammatory mechanisms, but this has not been prospectively examined in humans. Using data from a pilot study of women followed from the second trimester of pregnancy through six months postpartum (N = 68) our goal was to initiate a prospective study as to whether maternal inflammatory cytokines mediate the association between maternal depressive symptoms and infant offspring negative affect. The study sample was designed to examine a broad range of likely self-regulation and mood-regulation problems in offspring; to that end we over-selected women with a family history or their own history of elevated symptoms of attention-deficit/hyperactivity disorder. Results supported the hypothesis: maternal pro-inflammatory cytokines during the third trimester (indexed using a latent variable that included plasma interleukin-6, tumor necrosis factor-alpha and monocyte chemoattractant protein-1 concentrations as indicators) mediated the effect, such that higher maternal depressive symptoms were associated with higher maternal inflammation, and this mediated the effect on maternal report of infant negative affect (controlling for maternal affect during the infant period). This is the first human study to demonstrate that maternal inflammatory cytokines mediate the association between prenatal depression and infant outcomes, and the first to demonstrate a biological mechanism through which depressive symptoms impact infant temperament.

Major depressive disorder during pregnancy: Psychiatric medications have minimal effects on the fetus and infant yet development is compromised.

Psychotropic medication use and psychiatric symptoms during pregnancy each are associated with adverse neurodevelopmental outcomes in offspring. Commonly, studies considering medication effects do not adequately assess symptoms, nor evaluate children when the effects are believed to occur, the fetal period. This study examined maternal serotonin reuptake inhibitor and polypharmacy use in relation to serial assessments of five indices of fetal neurobehavior and Bayley Scales of Infant Development at 12 months in N = 161 socioeconomically advantaged, non-Hispanic White women with a shared risk phenotype, diagnosed major depressive disorder. On average fetuses showed the expected development over gestation. In contrast, infant average Bayley psychomotor and mental development scores were low (M = 84.10 and M = 89.92, range of normal limits 85-114) with rates of delay more than 2-3 times what would be expected based on this measure's normative data. Controlling for prenatal and postnatal depressive symptoms, prenatal medication effects on neurobehavioral development were largely undetected in the fetus and infant. Mental health care directed primarily at symptoms may not address the additional psychosocial needs of women parenting infants. Speculatively, prenatal serotonin reuptake inhibitor exposure may act as a plasticity rather than risk factor, potentially enhancing receptivity to a nonoptimal postnatal environment in some mother-infant dyads.

Associations between early caregiving and rural, low-SES, African-American children's representations of attachment relationships.

Little research has examined the legacy of early maternal care for later attachment representations among low-income and ethnic minority school-aged children. Using data from a sample of 276 rural, low-income, African-American families, this study examined associations between maternal care in infancy and children's representations of attachment figures in middle childhood. Maternal care was coded from 10-min home-based observations at 6, 15, and 24 months of age. Representations of attachment figures were assessed using the Manchester Child Attachment Story Task at 6 years of age. Sensitive maternal care in infancy was not significantly related to attachment security or episodic disorganized behaviors in children's representations. However, children exposed to more harsh-intrusive parenting during infancy displayed less secure representations of attachment figures in middle childhood and more episodic disorganized behaviors, even after controlling for numerous child and family contextual covariates. Findings inform conceptualizations of attachment formation among rural, low-income, African-American parent-child dyads.

PREPP: postpartum depression prevention through the mother-infant dyad.

Most interventions to prevent postpartum depression (PPD) focus on the mother rather than the mother-infant dyad. As strong relationships between infant sleep and cry behavior and maternal postpartum mood have been demonstrated by previous research, interventions targeted at the dyad may reduce symptoms of PPD. The goal of the current study was to examine the effectiveness of Practical Resources for Effective Postpartum Parenting (PREPP). PREPP is a new PPD prevention protocol that aims to treat women at risk for PPD by promoting maternally mediated behavioral changes in their infants, while also including mother-focused skills. Results of this randomized control trial (RCT) (n = 54) indicate that this novel, brief intervention was well tolerated and effective in reducing maternal symptoms of anxiety and depression, particularly at 6 weeks postpartum. Additionally, this study found that infants of mothers enrolled in PREPP had fewer bouts of fussing and crying at 6 weeks postpartum than those infants whose mothers were in the Enhanced TAU group. These preliminary results indicate that PREPP has the potential to reduce the incidence of PPD in women at risk and to directly impact the developing mother-child relationship, the mother's view of her child, and child outcomes.

Maternal dietary fat intake during pregnancy is associated with infant temperament.

Research with rodents and nonhuman primates suggests that maternal prenatal dietary fat intake is associated with offspring behavioral functioning indicative of risk for psychopathology. The extent to which these findings extend to humans remains unknown. The current study administered the Automated Self-Administered 24 hr Dietary Recall Questionnaire three times in pregnancy (n = 48) to examine women's dietary fat intake in relation to infant temperament assessed using the Infant Behavior Questionnaire at 4-months old. The amount of saturated fat that the mother consumed was considered as a moderator of the association between total fat intake and child temperament. Results from a series of multiple linear regressions indicate that greater total fat intake was associated with poorer infant regulation and lower surgency. However, this second effect was moderated by maternal saturated fat intake, such that total fat intake was only related to infant surgency when mothers consumed above the daily recommended allowance of saturated fat. Under conditions of high total fat and high saturated fat, infants were rated as lower on surgency; under conditions of low total fat yet high saturated fat, infants were rated as higher on surgency. There were no associations between maternal prenatal fat intake and infant negative reactivity. These findings provide preliminary evidence that pregnant women's dietary fat intake is associated with infants' behavioral development, though future research is needed to address this report's limitations: a relatively small sample size, the use of self-report measures, and a lack of consideration of maternal and infant postnatal diet.

Associations between Computationally Derived Parent Emotional Sentiment Scores and Child ADHD and ODD Over Time.

Family emotional climate is often assessed as expressed emotion (EE) using the five-minute speech sample (FMSS). Parent EE is related to child externalizing behavior, but the relationship with ADHD apart from externalizing is unclear. We report the largest ADHD-non-ADHD study of EE to date, introduce computational scoring of the FMSS to assay parent negative sentiment, and use this to evaluate reciprocal parent-child effects over time in ADHD while considering comorbid ODD. Parents of 810 children (nADHD = 509), aged 7-13 years old, completed the FMSS at three points. The FMSS was expert-coded for EE-Criticism at Time 1 and Time 2, negative sentiment was scored at all three time points. Sentiment and EE-Criticism were moderately correlated (r =.39, p <.001, 95% CI [0.32, 0.46]), and each was similarly correlated with baseline ADHD symptoms (r's range 0.31-0.33, p <.001) and ODD symptoms (r(ODD-EE) = 0.35, p <.001; r(ODD-sentiment = 0.28, p <.001). A longitudinal, cross-lagged panel model revealed that increases over time in parental negative sentiment scores led to increased ODD symptoms. Parent sex (namely fathers, but not mothers) showed an interaction effect of sentiment with ADHD. ADHD and ODD are independently and jointly associated with parental EE-Criticism and negative sentiment assessed by the FMSS cross-sectionally. A recursive effects model is supported for ODD, but for ADHD effects depend on which parent is assessed. For fathers, ADHD was related to negative sentiment in complex manners but for mothers, negative sentiment was related primarily to ODD.

COVID-19 pandemic-related trauma symptoms are associated with postpartum alcohol consumption.

OBJECTIVE: The COVID-19 pandemic has led to escalations in substance use, including alcohol consumption. Of particular concern are the potential impacts during the postpartum period, a time of heightened vulnerability to stress and potential transmission of the negative sequelae of substance use to offspring. However, postpartum alcohol consumption during the COVID-19 pandemic has not been well characterized. METHOD: Postpartum drinking habits and COVID-19-related stress were repeatedly assessed (every two weeks for 12 weeks, and at one-, six-, and 12-months postpartum) from N = 378 individuals during the COVID-19 pandemic. Average alcohol use trajectories as well as heterogeneity in trajectories were characterized. COVID-19-related trauma symptoms and coping were examined in relation to alcohol use over time. RESULTS: Average postpartum alcohol use included an initial quadratic increase from one-to-four-months postpartum, followed by a plateau between four-to-12-months. Higher (15.08%), moderate (26.90%), and lower consumption (57.90%) subgroups were identified. Endorsement of COVID-19-related trauma symptoms and using alcohol to cope with stress predicted higher consumption. CONCLUSIONS: Findings suggest a potential sensitive period in establishing postpartum alcohol use patterns from one-to-four-months postpartum. Findings further suggest that postpartum alcohol use is heterogenous and that individual response to major traumatic stressors, like the COVID-19 pandemic, may influence emerging patterns of postpartum alcohol use.

The association between food desert severity, socioeconomic status, and metabolic state during pregnancy in a prospective longitudinal cohort.

Poor metabolic health during pregnancy is associated with health concerns for pregnant individuals and their offspring. Lower socioeconomic status (SES) is one risk factor for poor metabolic health, and may be related to limited access to healthful and affordable foods (e.g., living in a food desert). This study evaluates the respective contributions of SES and food desert severity on metabolic health during pregnancy. The food desert severity of 302 pregnant individuals was determined using the United States Department of Agriculture Food Access Research Atlas. SES was measured using total household income adjusted for household size, years of education, and amount of reserve savings. Information about participants' glucose concentrations one hour following an oral glucose tolerance test during the second trimester was extracted from medical records and percent adiposity during the second trimester was assessed using air displacement plethysmography. Information about participants' nutritional intake during the second trimester was obtained by trained nutritionists via three unannounced 24-h dietary recalls. Structural equation models showed that lower SES predicted higher food desert severity (ß = - 0.20, p = 0.008) and higher adiposity (ß = - 0.27, p = 0.016) and consumption of a more pro-inflammatory diet (ß = - 0.25, p = 0.003) during the second trimester of pregnancy. Higher food desert severity also predicted higher percent adiposity during the second trimester (ß = 0.17, p = 0.013). Food desert severity significantly mediated the relationship between lower SES and higher percent adiposity during the second trimester (ßindirect = - 0.03, 95% CI [- 0.079, - 0.004]). These findings indicate that access to healthful and affordable foods is a mechanism by which SES contributes to adiposity during pregnancy and may inform interventions intended to improve metabolic health during pregnancy.

Delineating early developmental pathways to ADHD: Setting an international research agenda.

Background: Attention-deficit/hyperactivity disorder (ADHD) is a prevalent, impairing, and highly heritable condition typically diagnosed in middle childhood. However, it is now recognized that symptoms emerge much earlier in development. Research focused on understanding-using multiple units of analysis-the cascade of early-life (i.e., prenatal-infant-toddler) developmental changes that will later emerge as ADHD has the potential to transform early identification, prevention, and intervention. To this end, we introduce the recently established Early ADHD Consortium, an international network of investigators engaged in prospective, longitudinal studies of risk for ADHD beginning early in life, conducted within a developmental framework, and which incorporate multimethod approaches. This network seeks to harmonize measures and methodological approaches to increase the potential for data sharing and subsequent impact. Methods: This perspective paper highlights the importance of investigating pre-diagnostic markers of ADHD, and potential models and mechanisms of ADHD risk and development, with the long-term objective of facilitating development of preemptive interventions that will minimize the impact of ADHD symptoms on everyday functioning and maximize health and developmental outcomes. Results: We selectively describe key challenges and questions for this field related to theoretical models and developmental mechanisms in ADHD and recommend next steps for the science, including methodological, measurement, and study design considerations. We then describe potential implications for preemptive intervention development. We conclude by considering other issues including ethical concerns and the critical value of incorporating stakeholder input. Conclusions: It is hoped that this perspective puts forth a research agenda that will enhance collaborative efforts and accelerate progress in understanding developmental mechanisms and the early ADHD phenotype, with implications for early intervention enhancement of healthy development for infants, young children, and their families.

Developmental trajectories of toddler sleep problems: can a person-centered approach help identify children at risk?

STUDY OBJECTIVES: Previous research examining toddler sleep problems has relied almost exclusively on variable-centered statistical approaches to analyze these data, which provide helpful information about the development of the average child. The current study examined whether person-centered trajectory analysis, a statistical technique that can identify subgroups of children who differ in their initial level and/or trajectory of sleep problems, has the potential to inform our understanding of toddler sleep problems and their development. METHODS: Families (N = 185) were assessed at 12, 24, 30, and 36 months of child age. Latent class growth analysis was used to test for subgroups that differed in their 24-36 month sleep problems. Subgroups were compared on child 36-month externalizing, internalizing, and total problem behaviors, and on 12 month maternal mental health, inter-parental conflict, and maternal parenting behaviors. RESULTS: Results support a four-class solution, with "low, stable," "low, increasing," "high, increasing," and "high decreasing" classes. The classes whose sleep problems persisted or worsened over time had worse behavioral problems than those whose symptoms improved or remained stably low. Additionally, 12 month maternal depression and global symptom severity, intimate partner violence, and maternal harsh-intrusive parenting behaviors discriminated between the classes that had similar levels of 24 month sleep disturbance but who had diverging trajectories over time. CONCLUSIONS: This statistical approach appears to have the potential to increase understanding of sleep problem trajectories in the early years of life. Maternal mental health, intimate partner violence, and parenting behaviors may be clinically useful markers of risk for the persistence or development of toddler sleep problems.

Effects of Maternal Psychological Stress During Pregnancy on Offspring Brain Development: Considering the Role of Inflammation and Potential for Preventive Intervention.

Heightened psychological stress during pregnancy has repeatedly been associated with increased risk for development of behavior problems and psychiatric disorders in offspring. This review covers a rapidly growing body of research with the potential to advance a mechanistic understanding of these associations grounded in knowledge about maternal-placental-fetal stress biology and fetal brain development. Specifically, we highlight research employing magnetic resonance imaging to examine the infant brain soon after birth in relation to maternal psychological stress during pregnancy. This approach increases capacity to identify specific alterations in brain structure and function and to differentiate between effects of pre- versus postnatal exposures. We then focus on the extensive preclinical literature and emerging research in humans that have found that heightened maternal inflammation during pregnancy as a mechanism through which maternal stress influences the developing fetal brain. We place these findings in the context of recent work identifying psychotherapeutic interventions that have been found to be effective for reducing psychological stress among pregnant individuals and that also show promise for reducing inflammation. We argue that a focus on inflammation, among other mechanistic pathways, may lead to a productive and necessary integration of research focused on the effects of maternal psychological stress on offspring brain development and on prevention and intervention studies aimed at reducing maternal psychological stress during pregnancy. In addition to increasing capacity for common measurements and understanding potential mechanisms of action relevant to maternal mental health and fetal neurodevelopment, this focus may inform and broaden thinking about prevention and intervention strategies.