This Viewpoint discusses social health, which refers to the quality and quantity of social interactions, relationships, and support networks, as an important independent component of overall health alongside physical and mental health.
Abstract Background Elevated loneliness experiences characterise young people. While loneliness at this developmental juncture may emerge from age‐typical upheaval in social relationships, there is little data on the extent to which young people experience high and persistent levels of loneliness, and importantly, who is most vulnerable to these experiences. Using the widespread social restrictions associated with the COVID‐19 pandemic, which precipitated loneliness in many, we aimed to examine adolescents' loneliness profiles across time and the demographic predictors (age, sex, and country) of more severe trajectories. Methods Participants aged 12–18 years, recruited into a multi‐wave study ( N = 1039) across three sites (UK, Israel, and India) completed a 3‐item loneliness measure fortnightly across 8 timepoints during the pandemic. Results Latent class growth analysis suggested 5 distinct trajectories: (1) low stable (33%), (2) low increasing (19%), (3) moderate decreasing (17%), (4) moderate stable (23%), and (5) high increasing (8%). Females and older adolescents were more likely to experience persistently high loneliness. Conclusions These findings indicate a need for interventions to reduce loneliness in adolescents as we emerge from the pandemic, particularly for those groups identified as being at highest risk.
Abstract Purpose of Review Adolescent depression is a major public health concern associated with severe outcomes. A lack of efficacious interventions has triggered an increase in cognitive neuropsychology research to identify relevant treatment targets for new interventions. This review summarises key neurocognitive findings in adolescent depression and explores the potential of neurocognitive markers as treatment targets in new interventions. Recent Findings Studies support difficulties in the voluntary deployment of attention towards and away from emotional stimuli, negative interpretation biases and overgeneralised autobiographical memories in adolescent depression; however, little evidence is given to a general decline in executive function. There is consistent evidence for abnormalities in several distributed neural networks in adolescent depression, including dysfunction in and between the amygdala, medial prefrontal cortex and ventral striatum. Summary The relationships between different cognitive biases and abnormalities in specific neural networks remain unclear. Several new experimental interventions targeting these neurocognitive markers await evaluation.
This study set out to establish the novel use of the go/no-go Overlap task for investigating the role of attentional control capacities in the processing of emotional expressions across different age-groups within adolescence: at the onset of adolescence (11-12 year-olds) and toward the end of adolescence (17-18 year-olds). We also looked at how attentional control in the processing of fearful, happy, and neutral expressions relates to individual differences in trait anxiety in these adolescent groups. We were able to show that younger adolescents, but not older adolescents had more difficulties with attention control in the presence of all faces, but particularly in the presence of fearful faces. Moreover, we found that across all groups, adolescents with higher trait anxiety exhibited attentional avoidance of all faces, which facilitated relatively better performance on the primary task. These differences in reaction time emerged in the context of comparable accuracy level in the primary task across age-groups. Our results contribute to our understanding of how attentional control abilities to faces but in particular fearful expressions may mature across adolescence. This may affect learning about the environment and the acquisition of behavioral response patterns in the social world.
Childhood depressive symptoms may arise from genetic and environmental risks, which act to bias the ways in which children process emotional information. Indeed previous studies show that several “cognitive biases” are heritable and share genetic and environmental risks with depressive symptoms. Intriguingly, past research suggests that many cognitive biases only reflect genetic risks for depressive symptoms from adolescence. The present study aimed to identify (i) when interpersonal cognitions mature as risk factors for depressive symptoms by examining whether these factors are stable and predict symptoms across time in childhood, (ii) the extent to which interpersonal cognitions reflect inherited/environmental risks on children’s depressive symptoms. Results showed that compared to age 8, interpersonal cognitive biases were becoming more stable across time (from age 8 to 10 years: r’s = 0.32 to 0.43) but only the absence of positive self/other perceptions, and negative peer and mother expectations at age 8 predicted depressive symptoms at age 10 (after controlling for depressive symptoms at age 8). The absence of positive self/other perceptions shared genetic influences with depressive symptoms within and across time. Across middle to late childhood, interpersonal cognitions begin to operate as vulnerability-trait factors for depressive symptoms, gradually reflecting distal genetic risks on symptoms.
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