Michael J. Shanahan

Previous brain-wide association studies (BWAS) have linked specific environmental and behavioral variables to brain variability. In this work, we mapped 649 variables to children’s brains and compared the resultant BWAS maps with each other and with neurobiological reference patterns. Socioeconomic status (SES) showed the strongest brain-wide associations. The SES associations were strongest in motor and sensory but not cognitive regions, a pattern shared across many BWAS maps, including intelligence quotient (IQ). A single, common BWAS brain pattern existed across variables that was most reflective of a child’s socioeconomics. Adjusting for SES weakened brain-IQ associations, eliminating the BWAS motor and sensory pattern. Brain-with-IQ associations also did not generalize when trained on higher-SES subsamples. Thus, children’s brains vary the most with SES, potentially through SES-dependent sleep deprivation and stress.

Background: Peer victimization (PV) in adolescence—verbal, social, and physical aggression—may disrupt normative developmental processes and is associated with psychosocial difficulties. Although previous research has established associations between early adversity and altered attention and cognitive-affective processing, the specific mechanisms of information-processing through which adolescent PV may affect later social functioning remain unclear. Methods: We conducted a counterfactual multimethod study in a sample of young adults (age 22; n = 191; 47.1% female), comparing individuals with and without a history of PV between ages 11–20. Specifically we employed: (1) an eye tracking task using a free-viewing paradigm to assess spontaneous threat-related attention; (2) a longitudinal analysis of changes in hostile attribution and reactive aggression using baseline data collected prior to PV exposure and follow-up data in young adulthood; and (3) a morph-based task assessing facial emotion discrimination capabilities between happy and angry expressions. Results: Relative to controls, victims exhibited a vigilance–avoidance attentional pattern and blunted affective responses; they showed reduced initial gaze allocation, repeated returns to angry faces, and a tendency to rate more angry faces as neutral. Over adolescence, a flatter decline in hostile attribution and a steeper drop in reactive aggression led to elevated hostile attribution and reduced reactive aggression. Conclusions: These results suggest a victim profile characterized by impaired attentional processing with biased social threat perception, a more hostile view of the social world, and blunted affect. Our study offers preliminary evidence that adolescent PV may induce enduring changes in social information processing, with implications for maladaptive social cognition and increased risk for psychopathology.

BACKGROUND Adolescent peer victimization (PV) is a prevalent social stressor associated with potential long-term psychological and physiological consequences. Yet, the mechanisms underlying enduring alterations in stress-regulatory systems remain underexplored. This multimodal study examines autonomic, endocrine, and affective reactivity in young adults with a history of severe PV. METHODS Eyeblink startle electromyograms, pupil dilation, hair cortisol, resting heart rate variability, and self-reported state anxiety were assessed in 182 young adults (age 22) with longitudinal data on adolescent PV (ages 11–20). Effects were estimated using a counterfactual framework with genetically informed inverse probability weighting—leveraging polygenic risk scores and genetic ancestry—and adjustment for time-varying confounders. RESULTS Victims exhibited heightened startle amplitudes compared to controls, with negative stimuli (angry faces) further exaggerating amplitude and prolonging latency. Pupil dilation increased in response to negative stimuli, but was otherwise blunted. Victims also showed reduced resting heart rate variability, elevated hair cortisol, and slower state anxiety recovery across the session. Depression moderated several effects; more depressed victims showed hypocortisolism and reduced autonomic reactivity. CONCLUSIONS Findings provide converging evidence and mechanistic insight into potential links between PV and trauma-like physiological effects, suggesting sustained alterations into young adulthood. Targeted interventions are needed to reduce PV and its stress-related dysregulation, preventing potential long-term psychiatric and societal sequelae.

Background Socioeconomic status (SES) is associated with many chronic diseases, indicators of senescence and mortality. However, the changing salience of SES in the prediction of adult health is not well understood. Using mRNA-seq abundance data from wave V of the National Longitudinal Study of Adolescent to Adult Health (Add Health), we examine the extent to which SES across the early life course is related to gene expression-based signatures for chronic diseases, senescence and inflammation in the late 30s. Methods We use Bayesian methods to identify the most likely model of life course epidemiology (critical, sensitive and accumulation models) that characterises the changing importance of parental SES and SES during young (ages 27–30) and mid-adulthood (ages 36–39) in the prediction of the signatures. Results For most signatures, SES is an important predictor in all periods, although parental SES or SES during young adulthood are often the most predictive. For three signatures (components of diabetes, inflammation and ageing), critical period models involving the exclusive salience of SES in young adulthood (for diabetes) or parental SES (for inflammation and ageing) are most probable. The observed associations are likely mediated by body mass index. Conclusion Models of life course patterns of SES may inform efforts to identify age-specific mechanisms by which SES is associated with health at different points in life and they also suggest an enhanced approach to prediction models that recognise the changing salience of risk factors.

Social adversity downregulates antiviral genes and upregulates inflammatory genes, altering cytokine levels. This study investigated the effects of peer victimization (PV) during adolescence on gene expression, cellular dynamics, and cytokine profiles in young adulthood. Data from the Zurich Brain and Immune Gene Study (z-GIG, n = 200; 47% female) captured PV between ages 11 and 20, with mRNA and plasma cytokines analyzed in 144 participants at age 22. A counterfactual design with genetically informed inverse probability weighting adjusted for baseline confounders in individual and environmental characteristics. In silico deconvolution revealed altered leukocyte composition in victims, including an M2-like monocyte–skewed profile. Differentially expressed genes in victims were enriched in preselected Reactome pathways, including Interferon signaling, Metabolism and Signal transduction . Exploratory Reactome-wide queries confirmed pathways in the Immune System and Metabolism , highlighted their downregulation, and identified additional pathways, such as those involved in Chromatin organization and Metabolism of proteins . Transcription factors STAT2, IRF2, and NF-κB emerged as key regulators in victims, with target genes prominently mapped to Interferon signaling and Chromatin organization pathways. Victims exhibited altered cytokine levels, including pro-inflammatory CCL4, TNF, CXCL9, and CXCL10. These findings suggest that adolescent PV can lead to changes in gene regulation and cytokine levels, potentially altering the immune profile into young adulthood. The results underscore the importance of health policies aimed at prevention, building resilience, and mitigating the long-term effects of PV.

Since the 1990s, terms such as ‘parasite singles’, ‘the kangaroo generation’ and ‘NEET’ (Not in Employment, Education or Training) have been used by the mass media of Japan, South Korea and China to address the topic of whether young adults of this generation are refusing to grow up. This topic has aroused heated discussion. Japanese scholar Yamada coins the term ‘parasite singles’ to refer to the many unmarried adults in Japan who continue to live with their parents. These young adults resemble parasites by living off their parents with low ...

Many common chronic diseases of aging are negatively associated with socioeconomic status (SES). This study examines whether inequalities can already be observed in the molecular underpinnings of such diseases in the 30s, before many of them become prevalent. Data come from the National Longitudinal Study of Adolescent to Adult Health (Add Health), a large, nationally representative sample of US subjects who were followed for over two decades beginning in adolescence. We now have transcriptomic data (mRNA-seq) from a random subset of 4,543 of these young adults. SES in the household-of-origin and in young adulthood were examined as covariates of a priori -defined mRNA-based disease signatures and of specific gene transcripts identified de novo . An SES composite from young adulthood predicted many disease signatures, as did income and subjective status. Analyses highlighted SES-based inequalities in immune, inflammatory, ribosomal, and metabolic pathways, several of which play central roles in senescence. Many genes are also involved in transcription, translation, and diverse signaling mechanisms. Average causal-mediated effect models suggest that body mass index plays a key role in accounting for these relationships. Overall, the results reveal inequalities in molecular risk factors for chronic diseases often decades before diagnoses and suggest future directions for social signal transduction models that trace how social circumstances regulate the human genome.