Journal: The American journal of psychiatry
OBJECTIVE The authors examined midlife outcomes of childhood bullying victimization. METHOD Data were from the British National Child Development Study, a 50-year prospective cohort of births in 1 week in 1958. The authors conducted ordinal logistic and linear regressions on data from 7,771 participants whose parents reported bullying exposure at ages 7 and 11 years, and who participated in follow-up assessments between ages 23 and 50 years. Outcomes included suicidality and diagnoses of depression, anxiety disorders, and alcohol dependence at age 45; psychological distress and general health at ages 23 and 50; and cognitive functioning, socioeconomic status, social relationships, and well-being at age 50. RESULTS Participants who were bullied in childhood had increased levels of psychological distress at ages 23 and 50. Victims of frequent bullying had higher rates of depression (odds ratio=1.95, 95% CI=1.27-2.99), anxiety disorders (odds ratio=1.65, 95% CI=1.25-2.18), and suicidality (odds ratio=2.21, 95% CI=1.47-3.31) than their nonvictimized peers. The effects were similar to those of being placed in public or substitute care and an index of multiple childhood adversities, and the effects remained significant after controlling for known correlates of bullying victimization. Childhood bullying victimization was associated with a lack of social relationships, economic hardship, and poor perceived quality of life at age 50. CONCLUSIONS Children who are bullied-and especially those who are frequently bullied-continue to be at risk for a wide range of poor social, health, and economic outcomes nearly four decades after exposure. Interventions need to reduce bullying exposure in childhood and minimize long-term effects on victims' well-being; such interventions should cast light on causal processes.
The purpose of the present study was to address 1) whether exercise provides protection against new-onset depression and anxiety and 2) if so, the intensity and amount of exercise required to gain protection and, lastly, 3) the mechanisms that underlie any association.
The authors examined the prospective relationship between physical activity and incident depression and explored potential moderators.
In addition to N-methyl-d-aspartate receptor antagonism, ketamine produces opioid system activation. The objective of this study was to determine whether opioid receptor antagonism prior to administration of intravenous ketamine attenuates its acute antidepressant or dissociative effects.
Alcohol and cannabis misuse are related to impaired cognition. When inferring causality, four nonexclusive theoretical models can account for this association: 1) a common underlying vulnerability model; 2) a neuroplasticity model in which impairment is concurrent with changes in substance use but temporary because of neuroplastic brain processes that restore function; 3) a neurotoxicity model of long-term impairment consequential to substance use; and 4) a developmental sensitivity hypothesis of age-specific effects. Using a developmentally sensitive design, the authors investigated relationships between year-to-year changes in substance use and cognitive development.
The authors conducted a genome-wide association study of anorexia nervosa and calculated genetic correlations with a series of psychiatric, educational, and metabolic phenotypes.
Cigarette smoking during pregnancy is a major public health problem leading to adverse health outcomes and neurodevelopmental abnormalities among offspring. Its prevalence in the United States and Europe is 12%-25%. This study examined the relationship between prenatal nicotine exposure (cotinine level) in archived maternal sera and schizophrenia in offspring from a national birth cohort.
Interest in candidate gene and candidate gene-by-environment interaction hypotheses regarding major depressive disorder remains strong despite controversy surrounding the validity of previous findings. In response to this controversy, the present investigation empirically identified 18 candidate genes for depression that have been studied 10 or more times and examined evidence for their relevance to depression phenotypes.
DNA methylation has been proposed as an epigenetic mechanism by which early-life experiences become “embedded” in the genome and alter transcriptional processes to compromise health. The authors sought to investigate whether early-life victimization stress is associated with genome-wide DNA methylation.
The authors sought to demonstrate that schizophrenia is a heterogeneous group of heritable disorders caused by different genotypic networks that cause distinct clinical syndromes.