Negative mood induction in children: An examination across mood, physiological, and cognitive variables.

Experimental mood induction procedures are commonly used in studies of children's emotions, although research on their effectiveness is lacking. Studies that support their effectiveness report sample-level changes in self-reported affect from pre- to post-induction, and a subset of children who do not self-report expected changes in affect (i.e., "nonresponders"). Given children's limited abilities to self-report their emotions, it is critical to know whether these paradigms also shift physiological and social-cognitive indices of emotion. We hypothesized increases in physiological reactivity and accuracy for discerning facial expressions of negative emotions from pre- to post-induction and smaller increases for nonresponders, Children (N = 80; 7- to 12-year-olds) completed a facial emotion recognition task and had an electrocardiogram recorded to index high-frequency heart rate variability (HF-HRV) before and after a mood induction procedure. The mood induction involved watching a 3-min sad film clip while attending to their feelings. In the sample overall, from pre- to post-mood induction, children self-reported significantly sadder affect, displayed significant increases in HF-HRV, and displayed significant increases in accuracy of recognizing facial emotion expressions congruent with the mood induced. One quarter (25%) of the sample did not self-report expected increases in sad affect. Contrary to expectations, responders and nonresponders did not differ in mood-induced changes in physiological reactivity or emotion recognition accuracy. These findings support that mood inductions are efficacious in shifting not only children's self-reported affect but also underlying physiological and social-cognitive processes. Furthermore, they are an effective methodology for research questions related to underlying processes even in self-reported nonresponders.

Signatures of emotional face processing measured by event-related potentials in 7-month-old infants.

The ability to distinguish facial emotions emerges in infancy. Although this ability has been shown to emerge between 5 and 7 months of age, the literature is less clear regarding the extent to which neural correlates of perception and attention play a role in processing of specific emotions. This study's main goal was to examine this question among infants. To this end, we presented angry, fearful, and happy faces to 7-month-old infants (N = 107, 51% female) while recording event-related brain potentials. The perceptual N290 component showed a heightened response for fearful and happy relative to angry faces. Attentional processing, indexed by the P400, showed some evidence of a heightened response for fearful relative to happy and angry faces. We did not observe robust differences by emotion in the negative central (Nc) component, although trends were consistent with previous work suggesting a heightened response to negatively valenced expressions. Results suggest that perceptual (N290) and attentional (P400) processing is sensitive to emotions in faces, but these processes do not provide evidence for a fear-specific bias across components.

The Antidepressant Duloxetine Inhibits Platelet Function and Protects against Thrombosis.

While cardiovascular disease (CVD) is the leading cause of death, major depressive disorder (MDD) is the primary cause of disability, affecting more than 300 million people worldwide. Interestingly, there is evidence that CVD is more prevalent in people with MDD. It is well established that neurotransmitters, namely serotonin and norepinephrine, are involved in the biochemical mechanisms of MDD, and consequently, drugs targeting serotonin-norepinephrine reuptake, such as duloxetine, are commonly prescribed for MDD. In this connection, serotonin and norepinephrine are also known to play critical roles in primary hemostasis. Based on these considerations, we investigated if duloxetine can be repurposed as an antiplatelet medication. Our results-using human and/or mouse platelets show that duloxetine dose-dependently inhibited agonist-induced platelet aggregation, compared to the vehicle control. Furthermore, it also blocked agonist-induced dense and α-granule secretion, integrin αIIbß3 activation, phosphatidylserine expression, and clot retraction. Moreover duloxetine-treated mice had a significantly prolonged occlusion time. Finally, duloxetine was also found to impair hemostasis. Collectively, our data indicate that the antidepressant duloxetine, which is a serotonin-norepinephrine antagonist, exerts antiplatelet and thromboprotective effects and inhibits hemostasis. Consequently, duloxetine, or a rationally designed derivative, presents potential benefits in the context of CVD, including that associated with MDD.

Exposure to prenatal maternal distress and infant white matter neurodevelopment.

The prenatal period represents a critical time for brain growth and development. These rapid neurological advances render the fetus susceptible to various influences with life-long implications for mental health. Maternal distress signals are a dominant early life influence, contributing to birth outcomes and risk for offspring psychopathology. This prospective longitudinal study evaluated the association between prenatal maternal distress and infant white matter microstructure. Participants included a racially and socioeconomically diverse sample of 85 mother-infant dyads. Prenatal distress was assessed at 17 and 29 weeks' gestational age (GA). Infant structural data were collected via diffusion tensor imaging at 42-45 weeks' postconceptional age. Findings demonstrated that higher prenatal maternal distress at 29 weeks' GA was associated with increased fractional anisotropy (b = .283, t(64) = 2.319, p = .024) and with increased axial diffusivity (b = .254, t(64) = 2.067, p = .043) within the right anterior cingulate white matter tract. No other significant associations were found with prenatal distress exposure and tract fractional anisotropy or axial diffusivity at 29 weeks' GA, nor earlier in gestation.

Children's recognition of happy, sad, and angry facial expressions across emotive intensities.

Sharing emotional experiences is a key task that requires accurate recognition of peers' emotions during middle childhood. Existing research suggests that children are proficient at discerning emotion from facial expressions during middle childhood, but this research has focused on recognition of adults' intense emotional expressions. In this study, facial emotion recognition for children's happy, sad, and angry expressions across low, medium, and high intensities was measured in a sample of 7- to 10-year-old children (N = 80; 53% female) to quantify overall accurate recognition as well as inaccuracies, including identifying an emotion as present when it is not (false alarms) and failing to identify an emotion when present (miss rate). Children's recognition accuracy for low-threshold happiness, sadness, and anger was quite poor but improved in a cubic fashion as expression intensity increased, with dramatic improvements across medium-intensity expressions, and little further improvement across high-intensity expressions. A positivity bias was evident; children were more accurate at recognizing happiness than at recognizing sadness and anger, rarely failed to identify happiness when present, and tended to mislabel expressions as happy rather than as angry or sad. Children were generally better at recognizing anger compared with sadness but were more accurate at recognizing subtle sadness compared with anger, which appeared to be due to children missing subtle anger when present. The findings are discussed with regard to the functionality of others' happiness for signaling positive socializing opportunities, anger for signaling threatening interactions, and sadness for prompting prosocial action and with regard to how children's facial emotion recognition may affect general socioemotional development.

Does Prenatal Maternal Distress Contribute to Sex Differences in Child Psychopathology?

PURPOSE OF REVIEW: Prenatal maternal psychological distress is an established risk factor for the development of psychopathology in offspring. The purpose of this review is to evaluate whether sex differences in fetal responses to maternal distress contribute to sex differences in subsequent psychopathology. RECENT FINDINGS: Male and female fetuses respond differently to stress signals. We review recent evidence that demonstrates a sex-specific pattern of association between prenatal maternal distress and pathways associated with risk for psychopathology including offspring hypothalamic pituitary adrenocortical (HPA) axis regulation, brain development, and negative emotionality. Prenatal maternal distress exerts sex-specific consequences on the fetus. These differences may contribute to the well-established sex differences in psychopathology and in particular to greater female vulnerability to develop internalizing problems.

Children's empathy responses and their understanding of mother's emotions.

This study investigated children's empathic responses to their mother's distress to provide insight about child factors that contribute to parental socialisation of emotions. Four- to six-year-old children (N = 82) observed their mother's sadness and anger during a simulated emotional phone conversation. Children's facial negative affect was rated and their heart rate variability (HRV) was recorded during the conversation, and their emotion understanding of the conversation was measured through their use of negative emotion words and perspective-taking themes (i.e., discussing the causes or resolution of mother's emotions) in narrative accounts of the conversation. There were positive quadratic relationships between HRV and ratings of facial affect, narrative references to mother's negative emotions and perspective-taking themes. High and low HRV was associated with high facial negative affect, suggesting well-regulated sympathy and poorly regulated personal distress empathic responses, respectively. Moderate HRV was associated with low facial negative affect, suggesting minimal empathic engagement. High and low HRV were associated with the highest probabilities of both emotion understanding indicators, suggesting both sympathy and personal distress responses to mother's distress facilitate understanding of mother's emotions. Personal distress may motivate attempts to understand mother's emotions as a self-soothing strategy, whereas sympathy-related attempts to understand may be motivated by altruism.

Experiences of Discrimination and Depression Trajectories over Pregnancy.

INTRODUCTION: Research on risk factors for prenatal depression is critical to improve the understanding, prevention, and treatment of women's psychopathology. The current study examines the relation between experiences of racial discrimination and trajectories of depression symptoms over the course of pregnancy. METHOD: Participants completed standardized measures regarding symptoms of depression at four timepoints during pregnancy and reported on experiences of racial discrimination at one timepoint. Latent growth curve modeling was used to examine the relation between discrimination and initial levels (intercept) and trajectories (slope) of depression symptoms over pregnancy. RESULTS: Participants were 129 pregnant individuals recruited from obstetric clinics and oversampled for elevated depression symptoms. Thirty-six percent of the participants were living at or below 200% of the federal poverty line. Fifty-four percent of the sample identified as non-Latinx White, 26% as Latinx, and 13% as non-Latinx Black. An unconditional latent growth curve modeling revealed a negative quadratic trajectory of depression symptoms during pregnancy. When women's report of discrimination was added as a predictor of depression trajectories, discrimination predicted the initial value (intercept) of depression symptoms, but not change over the course of pregnancy (slope). Specifically, higher levels of experiences of discrimination were associated with higher levels of depression symptoms. When sociodemographic and contextual covariates were included in the model, a low family income-to-needs ratio was also related to higher levels of depression symptoms. CONCLUSIONS: These findings provide evidence that women's experiences of racial discrimination and family financial strain are risk factors for prenatal depression, with implications for screening, treatment, and policy.

Understanding associations between negatively biased attention and depression and social anxiety: positively biased attention is key.

Background and objectives: Although research supports the premise that depressed and socially anxious individuals direct attention preferentially toward negative emotional cues, little is known about how attention to positive emotional cues might modulate this negative attention bias risk process. The purpose of this study was to determine if associations between attention biases to sad and angry faces and depression and social anxiety symptoms, respectively, would be strongest in individuals who also show biased attention away from happy faces. Methods: Young adults (N = 151; 79% female; M = 19.63 years) completed self-report measures of depression and social anxiety symptoms and a dot probe task to assess attention biases to happy, sad, and angry facial expressions. Results: Attention bias to happy faces moderated associations between attention to negatively valenced faces and psychopathology symptoms. However, attention bias toward sad faces was positively and significantly related to depression symptoms only for individuals who also selectively attended toward happy faces. Similarly, attention bias toward angry faces was positively and significantly associated with social anxiety symptoms only for individuals who also selectively attended toward happy faces. Conclusions: These findings suggest that individuals with high levels of depression or social anxiety symptoms attend preferentially to emotional stimuli across valences.

Quadratic Associations Between Empathy and Depression as Moderated by Emotion Dysregulation.

Empathic tendencies have been associated with interpersonal and psychological benefits, but empathy at extreme levels or in combination with certain personal characteristics may contribute to risk for depression. This study tested the moderating role of cognitive emotion regulation in depression's association with empathy using nonlinear models. Young adults (N = 304; 77% female; M = 19 years) completed measures of cognitive emotion regulation strategies, depression, and affective and cognitive empathy. Individuals with good regulation had low levels of depression overall and their depression symptoms were lowest when levels of affective empathy were average. Individuals with poor regulation had high levels of depression overall, particularly when levels of empathy were moderate to high. Extremely high and low levels of cognitive empathy were associated with elevated depression, and this association was not moderated by regulation. These findings suggest tendencies to respond empathically to others' needs is neither an adaptive nor maladaptive characteristic but rather moderate empathy, particularly in the context of good regulation, may offer the greatest protection against depression.

Genetic and environmental influences on affiliation with deviant peers during adolescence and early adulthood.

Adolescence and early adulthood is a time when peer groups become increasingly influential in the lives of young people. Youths exposed to deviant peers risk susceptibility to externalizing behaviors and related psychopathology. In addition to environmental correlates of deviant peer affiliation, a growing body of evidence has suggested that affiliation with deviant peers is heritable. This study examined the magnitude of genetic and environmental influences on affiliation with deviant peers, changes in the relative importance of these factors, and which of these factors contribute to the stability of affiliation across this critical developmental period using a longitudinal twin study design that assessed same-sex twins (485 monozygotic pairs, 271 dizygotic pairs) at 3 discrete ages: 15, 18, and 21 years of age. Biometric models revealed that genetic influences increased with age. New genetic influences appeared during late adolescence, and no new genetic influences emerged by age 21. Environmental influences shared by sibling pairs decreased with age, while the proportion of nonshared environmental effects unique to each individual remained relatively stable over the course of development. Shared environmental influences were largely age-overlapping, whereas nonshared environmental influences were largely age-specific. In summary, this study found variance in affiliation with deviant peers is explained by shared and nonshared environment effects as well as by genetic influences (46% by age 21), supporting the role of genetically influenced selection factors. The shared environment was almost exclusively responsible for the stability in late adolescence, while genetic influences were primarily responsible for stability in early adulthood.

Changes in genetic and environmental influences on trait anxiety cfrom middle adolescence to early adulthood.

BACKGROUND: Middle adolescence to early adulthood is an important developmental period for the emergence of anxiety. Genetically-influenced stable traits are thought to underlie internalizing psychopathology throughout development, but no studies have examined changes in genetic and environmental influences on trait anxiety during this period. METHOD: A longitudinal twin study design was used to study same-sex twin pairs (485 monozygotic pairs, 271 dizygotic pairs) at three ages, 14, 18, and 21 years, to examine developmental shifts in genetic and environmental effects on trait anxiety. RESULTS: The heritability of trait anxiety increased with age, particularly between ages 14 and 18, no significant new genetic influences emerged after age 14, and the genetic influences were highly correlated across the three ages, supporting developmentally stable genetic risk factors. The environmental effects shared by members of a family decreased in influence across adolescence, while the influence of environmental effects unique to each individual twin remained relatively stable over the course of development and were largely age-specific. LIMITATIONS: The twin study design does not inform about specific genes and environmental risk factors. CONCLUSIONS: Genetic influences increased in importance from middle to late adolescence but common genetic factors influenced trait anxiety across the three ages. Shared environmental influences decreased in importance and demonstrated negligible influence by late adolescence/early adulthood. Nonshared environmental effects were almost entirely age-specific. These findings support the importance of developmentally-sensitive interventions that target shared environmental factors prior to middle adolescence and shifting non-shared environmental risks at each age.