Faculty Bibliography

Despite major anatomical differences with other mammalian sensory systems, olfaction shares with those systems a modulation by sleep/wake states. Sleep modulates odor sensitivity and serves as an important regulator of both perceptual and associative odor memory. In addition, however, olfaction also has an important modulatory impact on sleep. Odors can affect the latency to sleep onset, as well as the quality and duration of sleep. Olfactory modulation of sleep may be mediated by direct synaptic interaction between the olfactory system and sleep control nuclei, and/or indirectly through odor modulation of arousal and respiration. This reciprocal interaction between sleep and olfaction presents novel opportunities for sleep related modulation of memory and perception, as well as development of non-pharmacological olfactory treatments of simple sleep disorders.

Despite the speedy development of vaccines for COVID-19, their rollout has posed a major public health challenge, as vaccine hesitancy (VH) and refusal are high. Addressing vaccine hesitancy is a multifactorial and context-dependent challenge. This perspective focuses on VH in the world region of Latin America and the Caribbean (LAC) and includes people suffering from severe mental illness, therefore covering populations and subpopulations often neglected in scientific literature. We present an overview of VH in LAC countries, discussing its global and historical context. Vaccine uptake has shown to widely vary across different subregions of LAC. Current data points to a possible correlation between societal polarization and vaccination, especially in countries going through political crises such as Brazil, Colombia, and Venezuela. Poor accessibility remains an additional important factor decreasing vaccination rollout in LAC countries and even further, in the whole Global South. Regarding patients with severe mental illness in LAC, and worldwide, it is paramount to include them in priority groups for immunization and monitor their vaccination coverage through public health indicators.

OBJECTIVE:Children with ADHD often exhibit marked impairment in their social skills, but evidence-based psychosocial interventions for ADHD have shown limited efficacy in remediating these deficits. Co-occurring psychopathology exacerbates social deficits in children with ADHD and is a plausible moderator of treatment response. To identify factors contributing to variable social skills treatment response, we examined co-occurring externalizing, depression, and anxiety symptoms as moderators of social skills outcomes in a randomized controlled trial of the Collaborative Life Skills (CLS) program, an evidence-based collaborative school-home ADHD intervention. METHOD:age = 8.35 years, 28.3% female) at 27 schools in an urban public school district. Twenty-three schools were randomly assigned to CLS or usual services, with an additional four schools assigned to Spanish-adapted CLS or usual services. Multi-informant measures of co-occurring psychopathology and social skills were collected at baseline and post-treatment. RESULTS:Parent-rated externalizing and depression symptoms moderated treatment effects on social skills, whereby higher symptomatology in each domain was unrelated to social skills improvement in the CLS group but predicted worsening social skills in response to usual services. In contrast, teacher-rated anxiety moderated treatment effects on social skills, whereby higher anxiety predicted greater social skills improvement in response to CLS but was unrelated to social skills outcomes following usual services. CONCLUSIONS:Findings reflect novel evidence that child psychopathology domains exhibit unique moderating effects on social skills treatment response in children with ADHD. We discuss implications for optimizing evidence-based interventions to target social impairment in this population.

Introduction/UNASSIGNED:Adults who have histories of childhood trauma have been noted to display greater somatization, dissociative symptoms and affect dysregulation. What happens in the parent-child relationship when those traumatized children become parents? A potential link to somatization in the child has been suggested by several prior studies. Children who have early attachment disturbances had more physical complaints if their mothers displayed less maternal sensitivity during observed parent-child interactions. Yet, the intergenerational link between maternal and child somatization has not been sufficiently explored in a longitudinal study in order to understand the potential impact of maternal trauma history and related psychopathology on subsequent child somatization and psychopathology. Methods/UNASSIGNED:This paper examined prospective, longitudinal data of 64 mother-toddler dyads (mean age = 2.4 years, SD = 0.7) who were later studied when children had a mean age of 7 years. Mothers with and without histories of interpersonal violence (IPV; physical/sexual abuse and/or family violence exposure) were included. Mothers with IPV histories were oversampled. Linear and Poisson regression models were used to test the associations between maternal IPV-related post-traumatic stress disorder (PTSD) with maternal somatization severity when children were toddlers, and between maternal somatization and maternal interactive behaviors with child somatization by maternal report and clinician-rated assessment at school-age. Results/UNASSIGNED:= 0.007) when children were school-aged. No association was found between maternal somatization and child-reported psychopathology. The study did not find that maternal alexithymia, caregiving behaviors or child exposure to violence contributed significantly to the model examining the association between maternal and child somatization. Conclusion/UNASSIGNED:The results are in line with the hypothesis of intergenerational transmission of somatization in the context of IPV and related maternal PTSD during formative early development. We interpret this as an expression of psychological distress from mother to child, as maternal trauma and pathology affect the caregiving environment and, thus, the parent-child relationship. The authors conclude with a discussion of implications for parent-infant and early childhood intervention.

Introduction/UNASSIGNED:Interpersonal violent (IPV) experiences when they begin in childhood and continue in various forms during adulthood often lead to chronic post-traumatic stress disorder (PTSD) that is associated in multiple studies with hypocortisolism and lower percentage of methylation of the promoter region of the gene coding for the glucocorticoid receptor (NR3C1). This prospective, longitudinal study examined the relationship of NR3C1 methylation among mothers with IPV-related PTSD and their toddlers and then looked at the relationship of maternal NR3C1 methylation and child psychopathology at school age. Methods/UNASSIGNED:structured clinical interview when their children were ages 12-42 months (mean age 26.7 months, SD 8.8). Their children's psychopathology in terms of internalizing symptoms and externalizing behaviors was evaluated using the Child Behavior Checklist at ages 5-9 years (mean age 7 years, SD 1.1). Percentage of methylation for the NR3C1 gene promoter region was assessed from DNA extracted from maternal and child saliva using bisulfite pyrosequencing. Data analysis involved parametric and non-parametric correlations and multiple linear and logistic regression modeling. Results/UNASSIGNED:Logistic regression models using child NR3C1 methylation as the dependent variable and maternal NR3C1 methylation and PTSD group status as predictors, as well as the interaction indicated that all three of these significantly predicted child NR3C1 methylation. These findings remained significant when controlling for child age, sex and maternal child abuse history. Overall, maternal NR3C1 methylation when children were toddlers was negatively and significantly associated with child externalizing behavior severity at school age. Discussion/UNASSIGNED:We found that correlations between mothers and their children of NR3C1 methylation levels overall and at all individual CpG sites of interest were significant only in the IPV-PTSD group. The latter findings support that NR3C1 methylation in mothers positively and statistically significantly correlates with NR3C1 methylation in their children only in presence of IPV-PTSD in the mothers. This maternal epigenetic signature with respect to this glucocorticoid receptor is significantly associated with child behavior that may well pose a risk for intergenerational transmission of violence and related psychopathology.