Observational studies consistently report associations between tobacco use, cannabis use and mental illness. However, the extent to which this association reflects an increased risk of new-onset mental illness is unclear and may be biased by unmeasured confounding.

A systematic review and meta-analysis (CRD42021243903). Electronic databases were searched until November 2022. Longitudinal studies in general population samples assessing tobacco and/or cannabis use and reporting the association (e.g. risk ratio [RR]) with incident anxiety, mood, or psychotic disorders were included. Estimates were combined using random-effects meta-analyses. Bias was explored using a modified Newcastle–Ottawa Scale, confounder matrix, E-values, and Doi plots.

Seventy-five studies were included. Tobacco use was associated with mood disorders (K = 43; RR: 1.39, 95% confidence interval [CI] 1.30–1.47), but not anxiety disorders (K = 7; RR: 1.21, 95% CI 0.87–1.68) and evidence for psychotic disorders was influenced by treatment of outliers (K = 4, RR: 3.45, 95% CI 2.63–4.53; K = 5, RR: 2.06, 95% CI 0.98–4.29). Cannabis use was associated with psychotic disorders (K = 4; RR: 3.19, 95% CI 2.07–4.90), but not mood (K = 7; RR: 1.31, 95% CI 0.92–1.86) or anxiety disorders (K = 7; RR: 1.10, 95% CI 0.99–1.22). Confounder matrices and E-values suggested potential overestimation of effects. Only 27% of studies were rated as high quality.

Both substances were associated with psychotic disorders and tobacco use was associated with mood disorders. There was no clear evidence of an association between cannabis use and mood or anxiety disorders. Limited high-quality studies underscore the need for future research using robust causal inference approaches (e.g. evidence triangulation).

Substance use is a complex condition with multidimensional determinants. The present study aims to find the prevalence and determinants of substance use among young people attending primary healthcare centers in India.

A multicentric cross-sectional study was conducted across 15 states in India on 1,630 young people (10–24 years) attending primary health centers. The Alcohol, Smoking, and Substance Involvement Screening Test (ASSIST) was used to capture data on substance use. The degree of substance involvement was assessed and multivariate regression analysis was conducted to determine the risk factors of substance use.

The prevalence of substance use was 32.8%, with a median substance initiation age of 18 years. Among the substance users, 75.5% began before completing adolescence. Tobacco (26.4%), alcohol (26.1%) and cannabis (9.5%) were commonly consumed. Sociodemographic determinants included higher age, male gender, urban residence, positive family history, northeastern state residence and lower socioeconomic class. Over 80% of users had moderate or high involvement.

High substance use prevalence among young people in Indian healthcare centers underscores the urgency of targeted intervention. Insights on determinants guide effective prevention strategies for this complex public health issue.

Tobacco is a highly prevalent substance of abuse in patients with psychosis. Previous studies have reported an association between tobacco use and schizophrenia. The aim of this study was to analyze the relationship between tobacco use and first-episode psychosis (FEP), age at onset of psychosis, and specific diagnosis of psychosis.

The sample consisted of 1105 FEP patients and 1355 controls from the European Network of National Schizophrenia Networks Studying Gene–Environment Interactions (EU-GEI) study. We assessed substance use with the Tobacco and Alcohol Questionnaire and performed a series of regression analyses using case-control status, age of onset of psychosis, and diagnosis as outcomes and tobacco use and frequency of tobacco use as predictors. Analyses were adjusted for sociodemographic characteristics, alcohol, and cannabis use.

After controlling for cannabis use, FEP patients were 2.6 times more likely to use tobacco [p ⩽ 0.001; adjusted odds ratio (AOR) 2.6; 95% confidence interval (CI) [2.1–3.2]] and 1.7 times more likely to smoke 20 or more cigarettes a day (p = 0.003; AOR 1.7; 95% CI [1.2–2.4]) than controls. Tobacco use was associated with an earlier age at psychosis onset (β = −2.3; p ⩽ 0.001; 95% CI [−3.7 to −0.9]) and was 1.3 times more frequent in FEP patients with a diagnosis of schizophrenia than in other diagnoses of psychosis (AOR 1.3; 95% CI [1.0–1.8]); however, these results were no longer significant after controlling for cannabis use.

Tobacco and heavy-tobacco use are associated with increased odds of FEP. These findings further support the relevance of tobacco prevention in young populations.

Tobacco use is common in subjects with schizophrenia (SZ) and has sometimes been associated with better functioning in short-term studies. Only few studies embrace an extensive examination of tobacco influence on clinical, cognitive and therapeutic characteristics in stabilized SZ outpatients. The objective of the present study was to assess the association between cognitive performances and smoking status in SZ subjects.

In total, 1233 SZ participants (73.9% men, mean age 31.5) were included and tested with a comprehensive battery. Tobacco status was self-declared (never-, ex-, or current smokers). Multivariable analyses including principal component analyses (PCA) were used.

In total, 53.7% were smokers with 33.7% of them nicotine-dependent. Multiple factor analysis revealed that current tobacco smoking was associated with impaired general intellectual ability and abstract reasoning (aOR 0.60, 95% IC 0.41–0.88, p = 0.01) and with a lifetime alcohol use disorder (p = 0.026) and a lifetime cannabis use disorder (p < 0.001). Ex- and never-smokers differed for age, mean outcome, cannabis history and medication [ex-smokers being older (p = 0.047), likely to have higher income (p = 0.026), a lifetime cannabis use disorder (p < 0.001) and higher CPZeq doses (p = 0.005)]. Premorbid IQ in the three groups significantly differed with, from higher to lower: ex-smokers, never-smoker, current smokers (all p < 0.001).

This study is the largest to date providing strong evidence that chronic smoking is associated with cognitive impairment in SZ, arguing against the self-medication hypothesis as a contributor to the high prevalence of smoking in SZ. Ex-smokers may also represent a specific subgroup. Longitudinal studies are warranted to determine the developmental impact of tobacco on neurocognition.

Evidence from epidemiological studies indicated that intrauterine exposure to alcohol and tobacco is linked with a number of adverse outcomes in offspring. However, few studies have linked prenatal alcohol and tobacco exposures to offspring depressive symptoms with mixed results.

The objective of this study was to examine the link between maternal prenatal alcohol and tobacco exposures and depressive symptoms in offspring.

Using data from the Raine Study, a prospective multigenerational observational study, we examined the associations between maternal prenatal alcohol and tobacco use and the risk of depressive symptoms in offspring at age 17 years (N=1168). Depressive symptoms in offspring were measured using the Beck Depression Inventory for Youth. Log-binomial regression was used to estimate relative risk (RR) for associations between exposures and outcome. To better investigate the role of potential confounders, risk factors were sequentially added as adjustment variables in separate models.

After adjustment for potential confounders, depressive symptoms in offspring remained related to maternal alcohol use of six or more standard drinks per week during the first trimester of pregnancy [RR 1.59 (95% CI: 1.11-2.26)]. Further, the risk of depressive symptoms was 50% higher for offspring exposed to prenatal tobacco use when compared to non-exposed. The Associations did not appear to be mediated by the effects of prenatal alcohol and tobacco use on adverse pregnancy outcomes.

Early screening and prevention of these exposures could possibly reduce depressive symptoms in offspring. Moreover, future examinations such as Mendelian Randomization that allow a stronger causal inference is warranted.

No significant relationships.

Caffeine acts as a competing antagonist of adenosine receptors, increasing the release of norepinephrine and the activation of noradrenergic neurons. Long-standing schizophrenia patients frequently develop a comorbidly high daily caffeine intake. This could be explained by its relationship with smoking [1,2].

To determine caffeine consumption in schizophrenia and predisposing factors.

Cross-sectional study designed on a sample of 68 outpatients with a follow-up of at least 5 years at the Mental Health Unit, aged between 18 and 65 years, diagnosed with schizophrenia (ICD-10). Average daily caffeine intake was quantified by reference values for each beverage: coffee (66.7mg/100ml), tea (30mg/100ml), soft or energy drinks (11.5mg/100ml). High intake was defined as a consumption of ≥200mg of caffeine per day. Retrospective review of medical records revealed tobacco use and negative symptoms observed on the PANSS scale. Statistical analysis were performed using SPSS v21.0 (significance p<0.05).

88.2% of the subjects were daily caffeine consumers with a mean intake of 146.7mg/day (SD=5.8), and a mean consumption time of 6.2 years. Coffee was the predominant beverage in 66.7% of the cases, followed by soft or energy drinks (25%) and tea (0.1%). 45% of participants also had a high caffeine intake of ≥200 mg/day. Comorbid smoking was found in 93% of these patients. Negative symptomatology prevailed among caffeine consumers (PANSS-N= 41.3).

Xanthine abuse seems to be highly prevalent in people with schizophrenia, and there may be a relationship with smoking and negative psychotic symptoms.

No significant relationships.