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Background and hypothesisChildren exposed to socioenvironmental adversities (eg, urbanicity, pollution, neighborhood deprivation, crime, and family disadvantage) are more likely to subsequently develop subclinical psychotic experiences during adolescence (eg, hearing voices, paranoia). However, the pathways through which this occurs have not been previously investigated. We hypothesized that cognitive ability and inflammation would partly explain this association.Study designData were utilized from the Environmental-Risk Longitudinal Twin Study, a cohort of 2232 children born in 1994-1995 in England and Wales and followed to age 18. Socioenvironmental adversities were measured from birth to age 10 and classified into physical risk (defined by high urbanicity and air pollution) and socioeconomic risk (defined by high neighborhood deprivation, neighborhood disorder, and family disadvantage). Cognitive abilities (overall, crystallized, fluid, and working memory) were assessed at age 12; and inflammatory markers (C-reactive protein, interleukin-6, soluble urokinase plasminogen activator receptor) were measured at age 18 from blood samples. Participants were interviewed at age 18 regarding psychotic experiences.Study resultsHigher physical risk and socioeconomic risk were associated with increased odds of psychotic experiences in adolescence. The largest mediation pathways were from socioeconomic risk via overall cognitive ability and crystallized ability, which accounted for ~11% and ~19% of the association with psychotic experiences, respectively. No statistically significant pathways were found via inflammatory markers in exploratory (partially cross-sectional) analyses.ConclusionsCognitive ability, especially crystallized ability, may partly explain the association between childhood socioenvironmental adversity and adolescent psychotic experiences. Interventions to support cognitive development among children living in disadvantaged settings could buffer them against developing subclinical psychotic phenomena.

Background: Women who experience adverse pregnancy outcomes (APOs; gestational hypertension, preeclampsia (PE), gestational diabetes (GD), preterm birth (PTB), small or large for gestational age, miscarriage, multiple miscarriages, stillbirth, and offspring with major congenital anomalies) have increased risk of developing cardiovascular disease (CVD). We aimed to compare cardiometabolic health trajectories across the life course between women with and without APOs. Methods: We studied 187,186 women with a registered pregnancy in the UK Clinical Practice Research Datalink (CPRD) GOLD linked to Hospital Episode Statistics. Fractional polynomial multilevel models were used to compare trajectories of cardiometabolic risk factors (body mass index [BMI], blood pressure [BP], cholesterol, and glucose) between women with and without a history of APOs (individual APOs in any pregnancy and number of APOs). We explored two underlying time axes: (1) time relative to first pregnancy (from 10 years before first pregnancy to 15 years after) and (2) age. Models controlled for age at first pregnancy, residential area deprivation, non-singleton pregnancy, parity, smoking status, ethnicity, and medications use. Results: Women with a history of PE, gestational hypertension, or GD had higher BMI, BP, and glucose 10 years before first pregnancy compared to women without these APOs. These differences persisted 15 years post-first pregnancy. Women with a history of GD had a steeper post-partum rise in glucose. Women who experienced multiple (3 +) miscarriage, stillbirth, and/or medically indicated PTB had higher BP and BMI before and after pregnancy, with BP trajectories converging 15 years after first pregnancy. Women who experienced multiple APOs had the most adverse measurements across all cardiometabolic risk factors, with more unfavourable mean levels with each additional APO. There was little difference in cardiometabolic trajectories between women with and without a history of 1 or 2 miscarriages or congenital anomalies. Conclusions: Women with APOs had adverse cardiometabolic profiles before first pregnancy, persisting up to 15 years post-pregnancy. Findings highlight the potential for targeted public health interventions to promote good cardiometabolic health in young adults transitioning from contraceptive use to planning pregnancies. APOs may identify young women who could benefit from monitoring CVD risk factors and interventions to improve cardiometabolic health. [ABSTRACT FROM AUTHOR]

Introduction: Socioeconomic disadvantage has been associated with cannabis use and poor mental health. It is therefore hypothesised that lower maternal education, a proxy for socioeconomic disadvantage, may increase the risk of cannabis‐related mental health and substance use consequences. Methods: A total of 5099 participants from the Avon Longitudinal Study of Parents and Children reported cannabis use via questionnaires at 16 or 18. Logistic regression was used to examine the relationship between any and regular (weekly or more) adolescent cannabis use with depression, anxiety, psychotic experiences, and problematic cannabis use at age 24. Maternal education was included as an effect modifier. Missing data were addressed through multiple imputation using chained equations. Results: In total, 36.5% of participants reported adolescent cannabis use and, of these, 14% reported regular use. Adolescent cannabis use was associated with an increased likelihood of anxiety and problematic cannabis use; however, there was little evidence of moderation by maternal education. Regular cannabis use was associated with an increased likelihood of problematic cannabis use, with little evidence of moderation by maternal education. There was weak evidence that the association between regular cannabis use and depression (interaction p‐value = 0.024) and anxiety (interaction p‐value = 0.056) was stronger in people with high maternal education. Discussion and Conclusions: Adolescent cannabis use is associated with increased risk of anxiety and cannabis use disorder, but there was insufficient evidence that childhood socioeconomic position (proxied by maternal education) modifies this relationship. Improved public health messages for all adolescents about these risks may be warranted. [ABSTRACT FROM AUTHOR]

Background: Adverse childhood experiences (ACEs) are well‐established risk factors for self‐harm and depression. However, despite their high comorbidity, there has been little focus on the impact of developmental timing and the duration of exposure to ACEs on co‐occurring self‐harm and depression. Methods: Data were utilised from over 22,000 children and adolescents participating in three UK cohorts, followed up longitudinally for 14–18 years: the Avon Longitudinal Study of Parents and Children (ALSPAC), the Millennium Cohort Study (MCS) and the Environmental Risk (E‐Risk) Longitudinal Twin Study. Multinomial logistic regression models estimated associations between each ACE type and a four‐category outcome: no self‐harm or depression, self‐harm alone, depression alone and self‐harm with co‐occurring depression. A structured life course modelling approach was used to examine whether the accumulation (duration) of exposure to each ACE, or a critical period (timing of ACEs) had the strongest effects on self‐harm and depression in adolescence. Results: The majority of ACEs were associated with co‐occurring self‐harm and depression, with consistent findings across cohorts. The importance of timing and duration of ACEs differed across ACEs and across cohorts. For parental mental health problems, longer duration of exposure was strongly associated with co‐occurring self‐harm and depression in both ALSPAC (adjusted OR: 1.18, 95% CI: 1.10–1.25) and MCS (1.18, 1.11–1.26) cohorts. For other ACEs in ALSPAC, exposure in middle childhood was most strongly associated with co‐occurring self‐harm and depression, and ACE occurrence in early childhood and adolescence was more important in the MCS. Conclusions: Efforts to mitigate the impact of ACEs should start in early life with continued support throughout childhood, to prevent long‐term exposure to ACEs contributing to risk of self‐harm and depression in adolescence. [ABSTRACT FROM AUTHOR]