Smoking contributes to a variety of neurodegenerative diseases and neurobiological abnormalities, suggesting that smoking is associated with accelerated brain aging. However, the neurobiological mechanisms affected by smoking, and whether they are genetically influenced, remain to be investigated.

Using structural magnetic resonance imaging data from the UK Biobank (n = 33 293), a brain age predictor was trained on non-smoking healthy groups and tested on smokers to obtain the BrainAge Gap (BAG). The cumulative effect of multiple common genetic variants associated with smoking was then calculated to acquire a polygenic risk score (PRS). The relationship between PRS, BAG, total gray matter volume (tGMV), and smoking parameters was explored and further genes included in the PRS were annotated to identify potential molecular mechanisms affected by smoking.

The BrainAge in smokers was predicted with very high accuracy (r = 0.725, MAE = 4.16). Smokers had a greater BAG (Cohen's d = 0.074, p < 0.0001) and higher PRS (Cohen's d = 0.63, p < 0.0001) than non-smokers. A higher PRS was associated with increased amount of smoking, mediated by BAG and tGMV. Several neurotransmitters and ion channel pathways were enriched in the group of smoking-related genes involved in addiction, brain synaptic plasticity, and some neurological disorders.

By using a simplified single indicator of the entire brain (BAG) in combination with the PRS, this study highlights the greater BAG in smokers and its linkage with genes and smoking behavior, providing insight into the neurobiological underpinnings and potential features of smoking-related aging.

Smoking and vaping are prohibited on Ireland's Health Service Executive (HSE) campuses. The HSE states that there is no evidence to suggest vaping is less damaging than cigarettes. Recent meta-analyses have shown that e-cigarettes are in fact less dangerous and can help smokers quit. Our study analyses the current smoking policies in place in mental health ‘approved centres’ in Ireland, what is being done to help smokers quit while in-patients and the level of support among staff for the introduction of e-cigarettes as a harm reduction tool. Clinical nurse managers from each mental health approved centre were surveyed to assess adherence to smoking policies.

Only 5% of surveyed units enforce the HSE's Tobacco Free Campus Policy; 55% of units supported the idea of using e-cigarettes to help patients quit cigarettes.

Ireland's hospital campuses are not tobacco free. Changes need to be made to our smoking policies and their enforcement.

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.

Prevalence of smoking in schizophrenia (SCZ) is larger than in general population. Genetic studies provided some evidence of a causal effect of smoking on SCZ. We aim to characterize the genetic susceptibility to SCZ affected by genetic susceptibility to smoking.

Multi-trait-based conditional and joint analysis was applied to the largest European SCZ genome-wide association studies (GWAS) to remove genetic effects on SCZ driven by smoking, estimated by generalized summary data-based Mendelian randomization. Enrichment analysis was performed to compare original v. conditional GWAS. Change in genetic correlation between SCZ and relevant traits after conditioning was assessed. Colocalization analysis was performed to identify specific loci confirming general findings.

Conditional analysis identified 19 new risk loci for SCZ and 42 lost loci whose association with SCZ may be partially driven by smoking. These results were strengthened by colocalization analysis. Enrichment analysis indicated a higher association of differentially expressed genes at prenatal brain stages after conditioning. Genetic correlation of SCZ with substance use and dependence, attention deficit-hyperactivity disorder, and several externalizing traits significantly changed after conditioning. Colocalization of association signal between SCZ and these traits was identified for some of the lost loci, such as CHRNA2, CUL3, and PCDH7.

Our approach led to identification of potential new SCZ loci, loci partially associated to SCZ through smoking, and a shared genetic susceptibility between SCZ and smoking behavior related to externalizing phenotypes. Application of this approach to other psychiatric disorders and substances may lead to a better understanding of the role of substances on mental health.

Asthma is the most common non-communicable chronic airway disease worldwide. Obesity and cigarette use independently increase asthma morbidity and mortality. Current literature suggests that obesity and smoking synergistically increase asthma-related wheezing.

To assess whether increased serum cotinine and obesity act synergistically to increase the likelihood of having an asthma exacerbation, emergency department (ED) visit, or hospitalization.

A cross-sectional analysis of the 2011–2015 iterations of NHANES database was performed. Patients aged 18 years or greater with asthma were included. Serum cotinine was utilized as an accurate measurement of cigarette use. Logistic regression models were constructed to determine whether elevated serum cotinine and obesity were associated with self-reported asthma exacerbations, asthma-specific ED usage, and hospitalizations for any reason in the past year. Odds ratios were adjusted for age, gender, race, and ethnicity. Interactions were assessed by multiplying the adjusted effect sizes for elevated cotinine and obesity.

We identified 2179 (N = 32,839,290) patients with asthma, of which 32.2% were active smokers and 42.7% were obese. Patients with an elevated cotinine and asthma were significantly more likely to have had an asthma-related ED visit in the past year (adjusted odds ratio [AOR] 1.82; 95% CI 1.19–2.79), have a physician-prescribed asthma medication (AOR 2.04; 95% CI 1.11–3.74), and have a hospitalization for any reason (AOR 3.65; 95% CI 1.88–7.07) compared to those with low cotinine. Patients with asthma and obesity were more likely to have an asthma-related ED visit (AOR 1.67; 95% CI 1.06–2.62) or hospitalization for any reason in the past year compared to non-obese patients (AOR 2.76; 95% CI 1.69–4.5). However, a statistically significant interaction between obesity and cotinine was only identified in patients who currently have asthma compared to a previous asthma diagnosis (AOR 1.76; 95% CI 1.10–2.82). There were no synergistic interactions among ED usage or asthma exacerbations.

Nearly one-third of patients with asthma were current smokers, and almost half were obese. This study identified elevated serum cotinine, a metabolite of cigarette use, and obesity as key risk factors for asthma exacerbations, asthma-related ED visits, and hospitalizations for any reason. Elevated serum cotinine and obesity were not found to act synergistically in increasing asthma exacerbations or ED visits. However, the presence of both risk factors increased the risk of currently having asthma (compared to a previous diagnosis) by 76%. Serum cotinine may be useful in predicting asthma outcomes.

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.

Depression as a public health concern highlights the importance of prevention. The nature of the disease is complex, linked to numerous biopsychosocial factors. However, it was found that healthiest lifestyle reduced 67% the risk of depressive symptoms.

To review evidence on how exercise, diet, and smoking impact on the risk of depression.

Non-systematic review of literature through search on PubMed/MEDLINE following the terms “Lifestyles”,“risk” and “depression”.

Several studies have shown that exercise reduces the incidence of depressive symptoms and major depressive disorder regardless of intensity, geographic region, age, gender, or follow-up period. Smoking significantly increases the risk of depression, including the ones exposed to second-hand smoking and pregnant women in which prenatal smoking was associated with a three-fold increased risk of postpartum depression. The Mediterranean diet rich in complex carbohydrates, omega-3 fatty acids, B-group vitamins and several amino acids have shown a negative association with the incidence of depression. A high frequency of breakfast consumption, an increased intake of fruits, vegetables, and some specific nutrients (zinc, iron, magnesium, vitamins, and folate) was also inversely correlated with prevalence of depressive symptoms. On the other hand, western dietary patterns, with sweetened beverages, processed food, and foods rich in saturated fatty acids, have been linked to an increased risk. Skipping meals and snacking on unhealthy food also contributes to depressive symptoms.

Relatively modest changes in population diet, tobacco consumption and levels of exercise may have important public mental health benefits preventing a substantial number of new cases of depression.

No significant relationships.

Tobacco smoking is one of the leading causes of preventable morbidity and mortality worldwide (WHO, 2020). Smoking cessation campaigns have been effective at reducing smoking in the general population, but not in individuals with mental illness (Lê Cook et al., 2014). A downward trend in smoking has been noted in EU countries but smoking rates have remained stable in Malta (Country Health Profile, 2019).

This audit aims to assess smoking status, provision of smoking cessation advice and psychotropic dose adjustment depending on smoking status by the Bormla Mental Health Team.

Patient health records were reviewed for patient demographics, psychiatric diagnosis, medical co-morbidities, smoking status and cessation advice and changes in psychiatric medication according to smoking status.

Of the 171 patients studied, 35% (n=61) were smokers, 33% (n=58) were non-smokers while in 30% (n=52) the smoking status was undocumented. Smokers had a mean age of 50 years with an almost equal gender distribution (49% (n=30) male and 51% (n=31) female). The most common documented psychiatric diagnoses were depression (52.5% (n=32)) and anxiety (34.5% (n=21)), while 59% (n=36) had documented medical co-morbidities. Only 14% (n=9) where given smoking cessation advice and one patient was referred to the smoking cessation clinic. One third of smokers (n=20) were prescribed psychotropic medications which are affected by smoking status but only two patients had their doses adjusted.

Improved smoking cessation advice, referral to services, consideration of smoking cessation while prescribing and documentation are need to better patient care.

No significant relationships.

More than half patients with schizophrenia are smokers. Heavy smoking has been correlated to more severe positive symptoms, a higher number of hospitalizations and a less efficiency of antipsychotics. Unfortunately, abstinence is difficult to achieve in these patients, therefore it is importance of understanding the link between smoking and psychosis.

Analyzing the complex relationship between schizophrenia and nicotine’s effects on the human brain.

The study was a review of literature over the past 10 years based on the pubmed database.

Smoking might be a precipitating factor in the development of schizophrenia since it preceded the onset of this illness for several years.Shared genetic background was also emphasized establishing a complex biological link between nicotine and schizophrenia.

In another approach, the “self-medication hypothesis” has been proposed suggesting a beneficial effect of nicotine on both cognitive impairment and negative symptoms in schizophrenia, related to the regulation of the dopamine and nicotinic receptor systems. But this conclusion is controversial since other studies concluded to a more neurocognitive impairment in smokers compared to controlled population.

Smoking in schizophrenia is a complex “phenomenon” that remains, so far, misunderstood. Greater differences might exist between heavy and light smokers making it more difficult to point out the exact effect of nicotine on the brain. Smoking cessation therapies taking into account the specificity of patients with schizophrenia should be more developed.

No significant relationships.

Smoking is the leading cause of preventable death in the world. Studies have shown that the frequency of its use in schizophrenic patients is significantly higher than in the general population,which hinders both treatment strategies and the efficacy of antipsychotics.

The objectives of our study are to highlight the prevalence of smoking in this population,to assess their nicotine dependence as well as to support the difficulties of their management.

We conducted a cross-sectional study of 92 male patients, hospitalized at Ar-razi Hospital in Salé, using the Fagerström scale, associated with a questionnaire that included age, marital status, educational level, somatic comorbidities, current treatment, other substances used, withdrawal attempts, age of first cigarette, family history of smoking, and finally,number of cigarettes per day before and after psychiatric diagnosis.

All our patients were male,the average age was 31 years, 84.8% of our patients were single, 73.9% were without a profession, only 23.9% were under classic neuroleptics while 4.3% were under Clozapine, the most of our patients were also using Cannabis,52.2% attempted a withdrawal, with an average duration of 6 months.69.6% of our patients had a family history of smoking and only 21.7% had somatic comorbidities.The average daily consumption was 12 cigarettes per day before the onset of psychiatric symptoms, rising to 18 cigarettes per day after the psychiatric diagnosis.

The frequency of smoking in schizophrenic patients is high. Unfortunately, these patients remain poorly aware of the harms of smoking, hence the need to integrate a smoking control strategy into the management of schizophrenia.

No significant relationships.