Structural Racism and Lessons Not Heard: A Rapid Review of the Telepsychiatry Literature During the COVID-19 Public Health Emergency.

Objective: To assess the extent to which articles examining telepsychiatry after the start of the COVID-19 pandemic provided racial and sociodemographic characteristics for people receiving audiovisual (video) versus audio-only telepsychiatry.Data Sources, Study Selection, and Data Extraction: We employed the keyword telepsychiatry and screened all peer-reviewed articles in PubMed published from March 1, 2020, until November 23, 2022, prior to the federal government's announcement of the impending end to the COVID-19 public health emergency. We retrieved and reviewed the full-text articles of 553 results for potential inclusion, of which 266 were original research articles.Results: We found that 106 of 553 articles had any mention of differences between audio-only and audiovisual telepsychiatry. Twenty-nine of 553 articles described potential socioeconomic differences in the distribution of people receiving audio-only versus audiovisual telepsychiatry, and 20 of 553 described potential racial/ethnic differences. Among research articles, most (213/266) did not differentiate between videoconferencing and audio-only/telephone-based telehealth services. A total of 4 research articles provided racial and sociodemographic characteristics of individuals who received audio-only versus audiovisual telepsychiatry services during the COVID-19 pandemic, all of which were conducted in relatively small regional samples that could not be generalized to the US as a whole.Conclusions: Overall, this analysis underscores that empirical data are lacking on racial and sociodemographic distribution of audio-only versus audiovisual telepsychiatry services since the COVID-19 pandemic.Prim Care Companion CNS Disord 2023;25(6):23r03563. Author affiliations are listed at the end of this article.

Editorial: Considerations and Implications of a Nuanced Understanding of Neonatal Intensive Care Unit Distress for the Long-term Mental Health of Diverse Mothers and Children.

The perinatal period (pregnancy up to 1 year postpartum) is one of immense psychological and physical changes, many of which increase the risk for psychopathology for parent-child dyads. Families with infants requiring neonatal intensive care unit (NICU) interventions face additional challenges and distress in both the short and long term. Approximately 7% to 12% of infants require NICU admission for many factors including prematurity and neonatal complications1; 2% to 30% experience postpartum depression.2 Although something is known about NICU distress, a nuanced understanding of the experiences of NICU families is lacking, including their effects on longer-term mental health for parents and children. This is particularly true for families of minoritized groups, who often experience additional stressors, including interpersonal and systemic racism as well as differential Social Determinants of Health (SDoH)-the conditions in which people are born, grow, live, work, and age.

Using Digital Technology to Overcome Racial Disparities in Child and Adolescent Psychiatry.

Racial inequity in mental health care quality is influenced by many systems-level factors, as elucidated by critical race theory, structural competency, and other keystone frameworks.1 A growing body of literature also suggests provider-level bias to be a key driver.1-3 There is specific evidence that racism is an important driver of health inequities among youth4 and that it is mediated, in part, by provider-level processes related to diagnosis and treatment.2 For example, in child and adolescent psychiatry, youth who are Black, Indigenous, and People of Color (BIPOC) experience disproportionate rates of delayed diagnosis and treatment of autism spectrum disorder, overdiagnosis of conduct disorder, and underdiagnosis of attention-deficit/hyperactivity disorder.4 Black and multiracial adolescents are at highest risk of suicide,5 yet are least likely to receive preventive psychotherapy.4.

Genetic architecture of reciprocal social behavior in toddlers: Implications for heterogeneity in the early origins of autism spectrum disorder.

Impairment in reciprocal social behavior (RSB), an essential component of early social competence, clinically defines autism spectrum disorder (ASD). However, the behavioral and genetic architecture of RSB in toddlerhood, when ASD first emerges, has not been fully characterized. We analyzed data from a quantitative video-referenced rating of RSB (vrRSB) in two toddler samples: a community-based volunteer research registry (n = 1,563) and an ethnically diverse, longitudinal twin sample ascertained from two state birth registries (n = 714). Variation in RSB was continuously distributed, temporally stable, significantly associated with ASD risk at age 18 months, and only modestly explained by sociodemographic and medical factors (r2 = 9.4%). Five latent RSB factors were identified and corresponded to aspects of social communication or restricted repetitive behaviors, the two core ASD symptom domains. Quantitative genetic analyses indicated substantial heritability for all factors at age 24 months (h2 ≥ .61). Genetic influences strongly overlapped across all factors, with a social motivation factor showing evidence of newly-emerging genetic influences between the ages of 18 and 24 months. RSB constitutes a heritable, trait-like competency whose factorial and genetic structure is generalized across diverse populations, demonstrating its role as an early, enduring dimension of inherited variation in human social behavior. Substantially overlapping RSB domains, measurable when core ASD features arise and consolidate, may serve as markers of specific pathways to autism and anchors to inform determinants of autism's heterogeneity.

Patterns and predictors of family environment among adolescents at high and low risk for familial bipolar disorder.

Children's perceptions are important to understanding family environment in the bipolar disorder (BD) high-risk context. Our objectives were to empirically derive patterns of offspring-perceived family environment, and to test the association of family environment with maternal or paternal BD accounting for offspring BD and demographic characteristics. Participants aged 12-21 years (266 offspring of a parent with BD, 175 offspring of a parent with no psychiatric history) were recruited in the US and Australia. We modeled family environment using latent profile analysis based on offspring reports on the Conflict Behavior Questionnaire, Family Adaptability and Cohesion Evaluation Scales, and Home Environment Interview for Children. Parent diagnoses were based on the Diagnostic Interview for Genetic Studies and offspring diagnoses were based on the Schedule for Affective Disorders and Schizophrenia for School-Aged Children. Latent class regression was used to test associations of diagnosis and family environment. Two-thirds of all offspring perceived well-functioning family environment, characterized by nurturance, flexibility, and low conflict. Two 'conflict classes' perceived family environments low in flexibility and cohesion, with substantial separation based on high conflict with the father (High Paternal Conflict), or very high conflict and rigidity and low warmth with the mother (High Maternal Conflict). Maternal BD was associated with offspring perceiving High Maternal Conflict (OR 2.8, p = 0.025). Clinical care and psychosocial supports for mothers with BD should address family functioning, with attention to offspring perceptions of their wellbeing. More research is needed on the effect of paternal BD on offspring and family dynamics.

Editorial: Elevating the Narrative About Adverse Events During Development.

United States middle- or high-school-age children are taught about the perils of cyber bullying in health classes. They learn that they are at risk of suicide because of online harassment behaviors and that resources are being expanded to prevent, report, or interrupt such bullying. However, the perspective that suicide victims likely have other salient predisposing or precipitating risk factors (eg, summarized comprehensively by Turecki and Brent1) is usually not emphasized simultaneously. In the context of an abundance of studies documenting clear associations between childhood or adolescence adverse experiences and many aspects of health, as reviewed recently in The Lancet Public Health,2 it is not an exaggeration to observe that a crucial axiom of first science classes, correlation is not causation, can be overlooked when a small number of specific adverse events emerges narratively as the major etiologic cause of much of psychopathology, including youth suicide. However, traumatic events, such as youth sexual victimization3 or physical punishment/maltreatment,4 have long been known to correlate to social contexts and/or heritable genotypes, which also might mediate or co-mediate the risk for adverse outcomes. That some methodologic designs are superior to others to disentangle such confounds and examine causation is well known in behavior genetics.5 This was highlighted 2 decades ago, in this very journal, by Dr. Naimah Weinberg of the National Institutes of Health, in an article reviewing the cognitive and behavioral deficits associated with parental alcohol use,6 where she noted the growing field of behavior genetics offers an approach to understanding such complex problems. This is a necessary perspective to move the science of child psychiatry forward.

Editorial: Could a Treatment for Youth Anxiety Specifically Prevent the Emergence of Depression 2 Years Later?

The comorbidity of depression and anxiety is a major global health problem. A 2015 report examining response patterns of 74,000 adults across 27 World Mental Health surveys in 24 countries showed a very high comorbidity between a diagnosis of lifetime DSM-IV1 major depressive disorder and a diagnosis of any anxiety disorder in the past 12 months or lifetime anxiety disorder at similar rates in high-income and mid- to low-income countries. In addition, the report highlighted that almost 70% of people with lifetime depression and anxiety first developed anxiety and that the course and burden of lifetime depression comorbid with anxiety was usually more impairing than depression without anxiety.2.

Salivary melatonin onset in youth at familial risk for bipolar disorder.

Melatonin secretion and polysomnography (PSG) were compared among a group of healthy adolescents who were at high familial risk for bipolar disorder (HR) and a second group at low familial risk (LR). Adolescent participants (n = 12) were a mean age 14 ± 2.3 years and included 8 females and 4 males. Saliva samples were collected under standardized condition light (red light) and following a 200 lux light exposure over two consecutive nights in a sleep laboratory. Red Light Melatonin onset (RLMO) was defined as saliva melatonin level exceeding the mean of the first 3 readings plus 2 standard deviations. Polysomnography was also completed during each night. HR youth, relative to LR, experienced a significantly earlier melatonin onset following 200 lux light exposure. Polysomnography revealed that LR youth, relative to HR, spent significantly more time in combined stages 3 and 4 (deep sleep) following red light exposure. Additionally, regardless of the group status (HR or LR), there was no significant difference in Red Light Melatonin Onset recorded at home or in the laboratory, implying its feasibility and reliability.

Early Origins of Autism Comorbidity: Neuropsychiatric Traits Correlated in Childhood Are Independent in Infancy.

Previous research has suggested that behavioral comorbidity is the rule rather than the exception in autism. The present study aimed to trace the respective origins of autistic and general psychopathologic traits-and their association-to infancy. Measurements of autistic traits and early liability for general psychopathology were assessed in 314 twins at 18 months, ascertained from the general population using birth records. 222 twins were re-evaluated at 36 months. Standardized ratings of variation in social communication at 18 months were highly heritable and strongly predicted autistic trait scores at 36 months. These early indices of autistic liability were independent from contemporaneous ratings of behavior problems on the Brief Infant-Toddler Social and Emotional Assessment (which were substantially environmentally-influenced), and did not meaningfully predict internalizing or externalizing scores on the Achenbach Scales of Empirically Based Assessment at 36 months. In this general population infant twin study, variation in social communication was independent from variation in other domains of general psychopathology, and exhibited a distinct genetic structure. The commonly-observed comorbidity of specific psychiatric syndromes with autism may arise from subsequent interactions between autistic liability and independent susceptibilities to other psychopathologic traits, suggesting opportunities for preventive amelioration of outcomes of these interactions over the course of development.