It is not clear to what extent associations between schizophrenia, cannabis use and cigarette use are due to a shared genetic etiology. We, therefore, examined whether schizophrenia genetic risk associates with longitudinal patterns of cigarette and cannabis use in adolescence and mediating pathways for any association to inform potential reduction strategies.

Associations between schizophrenia polygenic scores and longitudinal latent classes of cigarette and cannabis use from ages 14 to 19 years were investigated in up to 3925 individuals in the Avon Longitudinal Study of Parents and Children. Mediation models were estimated to assess the potential mediating effects of a range of cognitive, emotional, and behavioral phenotypes.

The schizophrenia polygenic score, based on single nucleotide polymorphisms meeting a training-set p threshold of 0.05, was associated with late-onset cannabis use (OR = 1.23; 95% CI = 1.08,1.41), but not with cigarette or early-onset cannabis use classes. This association was not mediated through lower IQ, victimization, emotional difficulties, antisocial behavior, impulsivity, or poorer social relationships during childhood. Sensitivity analyses adjusting for genetic liability to cannabis or cigarette use, using polygenic scores excluding the CHRNA5-A3-B4 gene cluster, or basing scores on a 0.5 training-set p threshold, provided results consistent with our main analyses.

Our study provides evidence that genetic risk for schizophrenia is associated with patterns of cannabis use during adolescence. Investigation of pathways other than the cognitive, emotional, and behavioral phenotypes examined here is required to identify modifiable targets to reduce the public health burden of cannabis use in the population.

There is a wealth of literature on the observed association between childhood trauma and psychotic illness. However, the relationship between childhood trauma and psychosis is complex and could be explained, in part, by gene–environment correlation.

The association between schizophrenia polygenic scores (PGS) and experiencing childhood trauma was investigated using data from the Avon Longitudinal Study of Parents and Children (ALSPAC) and the Norwegian Mother, Father and Child Cohort Study (MoBa). Schizophrenia PGS were derived in each cohort for children, mothers, and fathers where genetic data were available. Measures of trauma exposure were derived based on data collected throughout childhood and adolescence (0–17 years; ALSPAC) and at age 8 years (MoBa).

Within ALSPAC, we found a positive association between schizophrenia PGS and exposure to trauma across childhood and adolescence; effect sizes were consistent for both child or maternal PGS. We found evidence of an association between the schizophrenia PGS and the majority of trauma subtypes investigated, with the exception of bullying. These results were comparable with those of MoBa. Within ALSPAC, genetic liability to a range of additional psychiatric traits was also associated with a greater trauma exposure.

Results from two international birth cohorts indicate that genetic liability for a range of psychiatric traits is associated with experiencing childhood trauma. Genome-wide association study of psychiatric phenotypes may also reflect risk factors for these phenotypes. Our findings also suggest that youth at higher genetic risk might require greater resources/support to ensure they grow-up in a healthy environment.

Smoking prevalence is higher amongst individuals with schizophrenia and depression compared with the general population. Mendelian randomisation (MR) can examine whether this association is causal using genetic variants identified in genome-wide association studies (GWAS).

We conducted two-sample MR to explore the bi-directional effects of smoking on schizophrenia and depression. For smoking behaviour, we used (1) smoking initiation GWAS from the GSCAN consortium and (2) we conducted our own GWAS of lifetime smoking behaviour (which captures smoking duration, heaviness and cessation) in a sample of 462690 individuals from the UK Biobank. We validated this instrument using positive control outcomes (e.g. lung cancer). For schizophrenia and depression we used GWAS from the PGC consortium.

There was strong evidence to suggest smoking is a risk factor for both schizophrenia (odds ratio (OR) 2.27, 95% confidence interval (CI) 1.67–3.08, p < 0.001) and depression (OR 1.99, 95% CI 1.71–2.32, p < 0.001). Results were consistent across both lifetime smoking and smoking initiation. We found some evidence that genetic liability to depression increases smoking (β = 0.091, 95% CI 0.027–0.155, p = 0.005) but evidence was mixed for schizophrenia (β = 0.022, 95% CI 0.005–0.038, p = 0.009) with very weak evidence for an effect on smoking initiation.

These findings suggest that the association between smoking, schizophrenia and depression is due, at least in part, to a causal effect of smoking, providing further evidence for the detrimental consequences of smoking on mental health.

There is increasing evidence that smoking is a risk factor for severe mental illness, including bipolar disorder. Conversely, patients with bipolar disorder might smoke more (often) as a result of the psychiatric disorder.

We conducted a bidirectional Mendelian randomisation (MR) study to investigate the direction and evidence for a causal nature of the relationship between smoking and bipolar disorder.

We used publicly available summary statistics from genome-wide association studies on bipolar disorder, smoking initiation, smoking heaviness, smoking cessation and lifetime smoking (i.e. a compound measure of heaviness, duration and cessation). We applied analytical methods with different, orthogonal assumptions to triangulate results, including inverse-variance weighted (IVW), MR-Egger, MR-Egger SIMEX, weighted-median, weighted-mode and Steiger-filtered analyses.

Across different methods of MR, consistent evidence was found for a positive effect of smoking on the odds of bipolar disorder (smoking initiation ORIVW = 1.46, 95% CI 1.28–1.66, P = 1.44 × 10−8, lifetime smoking ORIVW = 1.72, 95% CI 1.29–2.28, P = 1.8 × 10−4). The MR analyses of the effect of liability to bipolar disorder on smoking provided no clear evidence of a strong causal effect (smoking heaviness betaIVW = 0.028, 95% CI 0.003–0.053, P = 2.9 × 10−2).

These findings suggest that smoking initiation and lifetime smoking are likely to be a causal risk factor for developing bipolar disorder. We found some evidence that liability to bipolar disorder increased smoking heaviness. Given that smoking is a modifiable risk factor, these findings further support investment into smoking prevention and treatment in order to reduce mental health problems in future generations.

Herd immunity, a concept normally applied in vaccinated populations, is a preventative measure to determine if a significant portion of a population can protect vulnerable individuals against a certain disease. Like vaccines, tourniquet education can be a form of herd immunity to protect vulnerable individuals in a population and prevent the loss of life from a peripheral hemorrhage. The authors have identified a deficiency in simple, quick, and effective hemorrhage control education. Therefore, to maximize herd immunity, the novel educational platform evaluates the efficacy of “Just-in-Time” (JiT) tourniquet application training.

The authors hypothesize that the utilization of JiT training will be effective in promoting both competence and confidence for individuals to utilize tourniquets in response to a disaster environment.

This Institutional Review Board-approved study recruited medical students who were trained in hemorrhage control measures at a Level 1 Trauma Center. Tourniquet training sessions were held, and naïve civilians received tourniquet education. The subjects received a five- to ten-minute lesson on indications, contraindications, and application techniques of commercial and improvisational tourniquets. Participants subsequently applied a tourniquet to an instructor’s arm to demonstrate proper tourniquet application for a brachial artery hemorrhage. Pre- and post-educational surveys were completed to test participant competency and confidence.

Of the 104 subjects who completed the course, 97 had no prior training in hemorrhage control techniques, including commercial and improvisational tourniquet application. The mean pre-test score was 2.27/5.00 and the mean post-test score was 4.38/5.00, P <.001 (n = 97). When queried “How competent would you feel applying a tourniquet (commercial or improvisational) on an individual with a bleeding wound?” 92/97 felt confident (95%), one felt less confident, and four felt no difference in confidence levels (P <.001).

Just-in-Time training is an effective method in teaching naïve civilians proper tourniquet application. This platform could serve as an alternative to more extensive training programs and requires less time, costs, and resources. If a significant number of individuals in a local community can effectively apply a tourniquet in a disaster scenario, a “herd immunity” effect could be achieved to control peripheral hemorrhages.

Lower cognitive ability in childhood is associated with increased risk of future schizophrenia, but its relationship with adult psychotic-like experiences and other psychopathology is less understood.

To investigate whether this childhood risk factor is shared with adult subclinical psychiatric phenotypes including psychotic-like experiences and general psychiatric morbidity.

A population-based sample of participants born in Great Britain during 1 week in March 1946 was contacted up to 20 times between ages 6 weeks and 53 years. Cognition was assessed at ages 8, 11 and 15 years using a composite of age-appropriate verbal and non-verbal cognitive tests. At age 53 years, psychotic-like experiences were self-reported by 2918 participants using four items from the Psychosis Screening Questionnaire and general psychiatric morbidity was assessed using the scaled version of the General Health Questionnaire (GHQ-28).

Psychotic-like experiences were reported by 22% of participants, and were highly comorbid with other psychopathology. Their presence in adults was significantly associated with poorer childhood cognitive test scores at ages 8 and 15 years, and marginally so at age 11 years. In contrast, high GHQ scores were not associated with poorer childhood cognition after adjustment for the presence of psychotic-like experiences.

Psychotic and non-psychotic psychopathologic symptoms are highly comorbid in the general population. Lower childhood cognitive ability is a risk factor for psychotic-like experiences in mid-life; these phenomena may be one end of a continuum of phenotypic expression driven by variation in early neurodevelopment.