scholarly journals Evidence for Causal Effects of Smoking Initiation and Alcohol Consumption on Substance Use Outcomes

2021 ◽  
Author(s):  
Zoe E. Reed ◽  
Robyn E. Wootton ◽  
Marcus R. Munafò
Keyword(s):  
Substance Use ◽  
Risk Factor ◽  
Alcohol Consumption ◽  
Opioid Dependence ◽  
Smoking Initiation ◽  
Cannabis Use ◽  
Causal Effects ◽  
P Value ◽  
Gateway Hypothesis ◽  
Shared Risk

AbstractBackground and AimsThe ‘gateway’ hypothesis proposes that initial use of drugs such as tobacco and alcohol can lead to subsequent more problematic drug use. However, it is unclear whether true casual pathways exist, or whether there is instead a shared underlying risk factor. We used bidirectional Mendelian Randomisation (MR) to test these two competing hypotheses.MethodsWe conducted two-sample MR analyses, using genome-wide association data for smoking initiation, alcoholic drinks per week, cannabis use and dependence, cocaine and opioid dependence. We used several MR methods that rely on different assumptions: inverse-variance weighted (IVW), MR-Egger, weighted median, simple mode and weighted mode. Consistent results across these methods would support stronger inference.ResultsWe found evidence of causal effects from smoking initiation to increased drinks per week (IVW: β=0.06; 95% CI 0.03 to 0.09; p-value=9.44×10-06), cannabis use (IVW: OR=1.34; 95% CI 1.24 to 1.44; p-value=1.95×10-14), and cannabis dependence (IVW: OR=1.68; 95% CI 1.12 to 2.51; p-value=0.01). We also found evidence of an effect of cannabis use on increased likelihood of smoking initiation (IVW: OR=1.39; 95% CI=1.08 to 1.80; p-value=0.01). We did not find evidence of an effect of drinks per week on substance use outcomes, except for weak evidence of an effect on cannabis use. We also found evidence of an effect of opioid dependence on increased drinks per week (IVW: β=0.002; 95% CI=0.0005 to 0.003; p-value=8.61×10-03).ConclusionsOverall, we found evidence suggesting a causal pathway from smoking initiation to alcohol consumption, and both cannabis use and dependence, which may support the gateway hypothesis. However, we also found causal effects of cannabis use on smoking initiation, and opioid dependence on alcohol consumption, which suggests the existence of a shared risk factor. Further research should explore whether this is the case, and in particular the nature of any shared risk factors.

scholarly journals Is there a causal relationship between executive function and liability to mental health and substance use? A Mendelian randomisation approach

2022 ◽  
Author(s):  
Sabrina M.I Burton ◽  
Hannah M Sallis ◽  
Alexander S Hatoum ◽  
Marcus R Munafo ◽  
Zoe E Reed
Keyword(s):  
Mental Health ◽  
Substance Use ◽  
Executive Function ◽  
Alcohol Consumption ◽  
Causal Relationship ◽  
Causal Effect ◽  
Smoking Initiation ◽  
Mendelian Randomisation ◽  
P Value ◽  
Causal Relationships

Background: Executive function consists of several cognitive control processes that are able to regulate lower level processes. Poorer performance in tasks designed to test executive function is associated with a range of psychopathologies such as schizophrenia, major depressive disorder (MDD) and anxiety, as well as with smoking and alcohol consumption. Despite these well-documented associations, whether they reflect causal relationships, and if so in what direction, remains unclear. We aimed to establish whether there is a causal relationship between a latent factor for performance on multiple executive function tasks - which we refer to as common executive function (cEF) - and liability to schizophrenia, MDD, anxiety, smoking initiation, alcohol consumption, alcohol dependence and cannabis use disorder (CUD), and the directionality of any relationship observed. Methods: We used a two-sample bidirectional Mendelian randomisation (MR) approach using genome-wide association study (GWAS) summary data from large cohorts (N=17,310 to 848,460) to examine whether causal relationships exist, and if so in which direction. Results: We found evidence of a causal effect of increased cEF on reduced schizophrenia liability (IVW: OR=0.10; 95% CI 0.05 to 0.19; p-value=3.43x10-12), reduced MDD liability (IVW: OR=0.52; 95% CI 0.38 to 0.72; p-value=5.23x10-05), decreased drinks per week (IVW: β=-0.06; 95% CI -0.10 to -0.02; p-value=0.003), and reduced CUD liability (IVW: OR=0.27; 95% CI 0.12 to 0.61; p-value=1.58x10-03). We also found evidence of a causal effect of increased schizophrenia liability on decreased cEF (IVW: β=-0.04; 95% CI -0.04 to -0.03; p-value=3.25x10-27), as well as smoking initiation on decreased cEF (IVW: β=-0.06; 95%CI -0.09 to -0.03; p-value=6.11x10-05). Conclusion: Our results indicate a potential bidirectional causal relationship between a latent factor measure of executive function (cEF) and schizophrenia liability, a possible causal effect of increased cEF on reduced MDD liability, CUD liability, and alcohol consumption, and a possible causal effect of smoking initiation on decreased cEF. These results suggest that executive function should be considered as a potential risk factor for some mental health and substance use outcomes, and may also be impacted by mental health (particularly schizophrenia). Further studies are required to improve our understanding of the underlying mechanisms of these effects, but our results suggest that executive function may be a promising intervention target. These results may therefore inform the prioritisation of experimental medicine studies (e.g., of executive function interventions), for both mental health and substance use outcomes, to improve the likelihood of successful translation.

scholarly journals Investigating causal pathways between liability to ADHD and substance use, and liability to substance use and ADHD risk, using Mendelian randomization

2019 ◽  
Author(s):  
Jorien L Treur ◽  
Ditte Demontis ◽  
George Davey Smith ◽  
Hannah Sallis ◽  
Tom G Richardson ◽  
...  
Keyword(s):  
Substance Use ◽  
Alcohol Use ◽  
Genetic Variants ◽  
Mendelian Randomization ◽  
Smoking Initiation ◽  
Cannabis Use ◽  
Causal Effects ◽  
Sensitivity Analyses ◽  
Genome Wide Association Studies ◽  
Causal Pathways

ABSTRACTBackgroundAttention-deficit hyperactivity disorder (ADHD) has consistently been associated with substance (ab)use, but the nature of this association is not fully understood. In view of preventive efforts, a vital question is whether there are causal effects, from ADHD to substance use and/or from substance use to ADHD.MethodsWe applied bidirectional Mendelian randomization using summary-level data from the largest available genome-wide association studies (GWASs) on ADHD, smoking (initiation, cigarettes/day, cessation, and a compound measure of lifetime smoking), alcohol use (drinks/week and alcohol use disorder), cannabis use (initiation and cannabis use disorder (CUD)) and coffee consumption (cups/day). Genetic variants robustly associated with the ‘exposure’ were selected as instruments and then identified in the ‘outcome’ GWAS. Effect estimates from individual genetic variants were combined with inverse-variance weighted regression and five sensitivity analyses were applied (weighted median, weighted mode, MR-Egger, generalized summary-data-based MR, and Steiger filtering).ResultsWe found strong evidence that liability to ADHD increases likelihood of smoking initiation and also cigarettes per day among smokers, decreases likelihood of smoking cessation, and increases likelihood of cannabis initiation and CUD. In the other direction, there was evidence that liability to smoking initiation and CUD increase ADHD risk. There was no clear evidence of causal effects between liability to ADHD and alcohol or caffeine consumption.ConclusionsWe find evidence for causal effects of liability to ADHD on smoking and cannabis use, and of liability to smoking and cannabis use on ADHD risk, indicating bidirectional pathways. Further work is needed to explore causal mechanisms.

Exploring a causal model in observational cohort data: The role of parents and peers in shaping substance use trajectories

2020 ◽  
Author(s):  
Christopher Greenwood ◽  
George Joseph Youssef ◽  
Primrose Letcher ◽  
Elizabeth Spry ◽  
Lauryn Hagg ◽  
...  
Keyword(s):  
Substance Use ◽  
Cannabis Use ◽  
Causal Effects ◽  
Deviant Peers ◽  
Adolescent Relationships ◽  
Cohort Data ◽  
Observational Cohort ◽  
Peer Affiliations ◽  
Role Of Parents ◽  
Adolescent Relationship

Aims: To explore the process of applying counterfactual thinking in examining causal predictors of substance use trajectories in observational cohort data. Specifically, we examine the extent to which quality of the parent-adolescent relationship and affiliations with deviant peers are causally related to trajectories of alcohol, tobacco, and cannabis use across adolescence and into young adulthood. Methods: Data were drawn from the Australian Temperament Project, a population-based cohort study that has followed a sample of young Australians from infancy to adulthood since 1983. Parent-adolescent relationship quality and deviant peer affiliations were assessed at age 13-14 years. Latent curve models were fitted for past month alcohol, tobacco, and cannabis use (n = 1,590) from age 15-16 to 27-28 years (5 waves). Confounding factors were selected in line with the counterfactual framework. Results: Following confounder adjustment, higher quality parent-adolescent relationships were associated with lower baseline cannabis use, but not alcohol or tobacco use trajectories. In contrast, affiliations with deviant peers were associated with higher baseline binge drinking, tobacco, and cannabis use, and an earlier peak in the cannabis use trajectory. Conclusions: Confounding adjustments weakened several estimated associations and the interpretation of such associations as causal is not without limitations. Nevertheless, findings suggested causal effects of both parent-adolescent relationships and deviant peer affiliations on the trajectory of substance use. Causal effects were however more pervasive (i.e., more substance types) and protracted for deviant peer affiliations. The current study encourages the exploration of causal relationships in observational cohort data, when relevant limitations are transparently acknowledged.

scholarly journals Hubungan antara Perilaku Merokok Anggota Rumah Tangga dengan Perilaku Merokok Remaja di Indonesia

2020 ◽  
Vol 23 (2) ◽  
pp. 80-88
Author(s):  
Olwin Nainggolan ◽  
Ika Dharmayanti ◽  
A Yudi Kristanto
Keyword(s):  
Alcohol Consumption ◽  
Service Providers ◽  
Economic Status ◽  
Smoking Behavior ◽  
Secondary Data ◽  
Smoking Initiation ◽  
Adolescent Smoking ◽  
P Value ◽  
Consumption Behavior ◽  
Confounding Variables

This study aimed to know the association and risk levels of household other members and adolescent smoking behaviors in Indonesia. As confounding variables of study involving Alcohol Consumption Behavior, Lived Area, and Social-Economics Status Variables. A study hypothesis declared that there was a signifi cant correlation between smoking behavior of household other members as a smoker with the smoking behavior of 15 to 18 years old after being controlled by other variables. Furthermore, this study using a Basic Health Research Secondary Data of 2018 aged 15 until 18 years and a multivariable analyzed uses logistic regression. The results showed a signifi cant correlation (p-value 0,000) between Household Other Members as a Smoker with smoking behavior of 15 to 18 years old after being controlled by confounding variables with OR 1,449 (95% CI 1,346-1,56-0). Smoker Variable not as a Head of Household was signifi cantly correlated (p-value 0,007) with OR 2,002 (95% CI 1,211-3,377), Alcohol Consumption Behavior was signifi cantly correlated (P-value 0,000) with OR 20,602 (95% CI 17,611-24,101), Lived Area with OR 1,129 (95% CI 1,051-1,212), also Social Economic Status with OR 1,098 (95%CI 1,024-1,178). An Alcohol Consumption Behavior Variable was the most dominant variable in determining Adolescent Smoking Behavior. We should focalize on areas identity is driven by health service providers, stakeholders, and policymakers. Accordingly, formulate awareness programs and education, particularly adolescents, to eliminate smoking initiation.  Abstrak Penelitian ini bertujuan untuk mengetahui hubungan dan besaran risiko perilaku merokok anggota rumah tangga lain dengan perilaku merokok remaja berusia 15 sampai dengan 18 tahun di Indonesia. Variable perancu pada penelitian ini meliputi perilaku konsumsi alkohol, wilayah tempat tinggal, serta status sosial ekonomi responden. Hipotesis penelitian ini adalah ada hubungan yang bermakna antara perilaku merokok anggota rumah tangga lain sebagai perokok, dengan perilaku merokok remaja usia 15 sampai dengan 18 tahun setelah dikontrol oleh variabel lain. Penelitian ini menggunakan data sekunder Riset Kesehatan Dasar (Riskesdas) tahun 2018 dengan rentang usia 15-18 tahun dan data di analisis secara multivariabel menggunakan regresi logistik. Hasil penelitian diperoleh bahwa terdapat hubungan yang bermakna (p value 0,000) antara anggota rumah tangga lain sebagai perokok dengan dengan perilaku merokok pada remaja usia 15 sampai dengan 18 tahun setelah dikontrol oleh variabel perancu dengan OR 1,449 (95% CI 1,346-1,56-0). Variabel perokok bukan sebagai kepala rumah tangga berhubungan bermakna (p value 0,007) dengan OR 2,002 (95% CI 1,2113,377), perilaku minum alkohol berhubungan bermakna (p value 0,000) dengan OR 20,602 (95% CI 17,611-24,101), wilayah tempat tinggal responden dengan OR 1,129 (95% CI 1,051-1,212), serta status sosial ekonomi dengan OR 1,098 (95%CI 1,024-1,178). Variabel perilaku minum alkohol adalah variabel yang paling besar pengaruhnya terhadap perilaku merokok pada remaja. Perlu fokus identifi kasi area oleh penyedia layanan kesehatan serta para stake holder pembuat kebijakan dalam merumuskan program kesadaran dan pendidikan khususnya pada remaja untuk eliminasi inisiasi merokok.

scholarly journals 24-h Movement Guidelines and Substance Use among Adolescents: A School-Based Cross-Sectional Study

2021 ◽  
Vol 18 (6) ◽  
pp. 3309
Author(s):  
Hugues Sampasa-Kanyinga ◽  
Ian Colman ◽  
Gary S. Goldfield ◽  
Ian Janssen ◽  
JianLi Wang ◽  
...  
Keyword(s):  
Physical Activity ◽  
Substance Use ◽  
Alcohol Consumption ◽  
Cigarette Smoking ◽  
Sleep Duration ◽  
Screen Time ◽  
Vigorous Physical Activity ◽  
Cross Sectional Study ◽  
Cannabis Use ◽  
Cross Sectional

Children and youth are recommended to achieve at least 60 min/day of moderate-to-vigorous physical activity, no more than 2 h/day of recreational screen time, and a sleep duration of 9–11 h/night for 11–13-year-olds or 8–10 h/night for 14–17-year-olds. Meeting the physical activity, screen time, and sleep duration recommendations have previously been associated with substance use among adolescents. However, previous research has mainly examined these factors individually rather than looking at how these indicators could concurrently relate to substance use in this age group. Therefore, this study examined the associations between meeting the 24-h movement guidelines for screen time, sleep duration, and physical activity (independent variables) with substance use outcomes including alcohol consumption, cannabis use, and cigarette smoking (dependent variables) among adolescents. Self-reported data from a cross-sectional and representative sample of 10,236 students (mean age = 15.1 years) in Ontario, Canada were analyzed. Logistic regression models stratified by gender were adjusted for potential confounders. Combinations of 24-h movement guidelines was differentially associated with substance use in boys and girls. Overall, findings showed that meeting 24-h movement guidelines is associated with lower odds of alcohol consumption, cannabis use, and cigarette smoking differentially with type of recommendation met and gender. Given that the associations between 24-h movement guidelines and substance use differ between boys and girls, future efforts should take this into consideration.

scholarly journals Causal relationships between substance use and insomnia

2020 ◽  
Author(s):  
Joëlle A. Pasman ◽  
Dirk J.A. Smit ◽  
Lilian Kingma ◽  
Jacqueline M. Vink ◽  
Jorien L. Treur ◽  
...  
Keyword(s):  
Substance Use ◽  
Alcohol Use ◽  
Alcohol Dependence ◽  
Strong Evidence ◽  
Smoking Initiation ◽  
Causal Effects ◽  
Sensitivity Analyses ◽  
Poor Sleep ◽  
A Genome ◽  
Bidirectional Effects

AbstractBackgroundPoor sleep quality and insomnia have been associated with the use of tobacco, alcohol, and cannabis, but it is unclear if there is a causal link. In this Mendelian Randomization (MR) study we examine if insomnia causes substance use and/or if substance use causes insomnia.MethodsMR uses summary effect estimates from a genome-wide association study (GWAS) to create a genetic instrumental variable for a proposed ‘exposure’ variable and then identifies that same genetic instrument in an ‘outcome’ GWAS. With data of GWAS of insomnia, smoking (initiation, heaviness, cessation), alcohol use (drinks per week, dependence), and cannabis initiation, bi-directional causal effects were tested. Multiple sensitivity analyses were applied to assess the robustness of the findings.ResultsThere was strong evidence for positive causal effects of insomnia on all substance use phenotypes (smoking traits, alcohol dependence, cannabis initiation), except alcohol per week. The effects on alcohol dependence and cannabis initiation were attenuated after filtering out pleiotropic SNPs. In the other direction, there was strong evidence that smoking initiation increased chances of insomnia (smoking heaviness and cessation could not be tested as exposures). We found no evidence that alcohol use per week, alcohol dependence, or cannabis initiation causally affect insomnia.ConclusionsThere were unidirectional effects of insomnia on alcohol dependence and cannabis initiation, and bidirectional effects between insomnia and smoking measures. Bidirectional effects between smoking and insomnia might give rise to a vicious circle. Future research should investigate if interventions aimed at insomnia are beneficial for substance use treatment.

scholarly journals M25. CLINICAL CORRELATES OF SUBSTANCE USE IN HEALTHY ADOLESCENTS: ASSOCIATIONS WITH PSYCHOTIC EXPERIENCES AND COGNITIVE BIASES

2020 ◽  
Vol 46 (Supplement_1) ◽  
pp. S143-S143
Author(s):  
Elena Estefania Gago Quintela ◽  
Berta Blasco ◽  
Maria José Miñano ◽  
Meritxell Tost Bonet ◽  
Sara Pérez ◽  
...  
Keyword(s):  
Substance Use ◽  
Alcohol Consumption ◽  
Alcohol Use ◽  
Tobacco Use ◽  
Peer Relations ◽  
Cognitive Biases ◽  
P Value ◽  
Psychotic Experiences ◽  
Psychometric Scales ◽  
Jumping To Conclusions

Abstract Background Substance use (tobacco, cannabis and alcohol consumption) is associated with the risk of developing a psychotic disorder as well as the risk of presenting psychotic experiences. We aimed to study the associations between substance use and psychotic-like experiences in a sample of healthy adolescents aged between 14 and 15 years. We also aimed to study potential relationships with bullying and cognitive biases. Methods A sample of 207 adolescents born in 2004 and studying in high schools from Sabadell. After excluding 33 participants who were receiving mental health care, a final sample of 174 adolescents (102 girls; 72 boys, mean ± standard deviation age: 14.4 ± 0.5 years) was included in the analyses. Before participating in the study, all participants and their parents signed a full written consent. The study was approved by the local Ethics Committee. All participants completed on-line questionnaires to explore psychotic-like experiences (15-item Community Assessment of Psychic Experiences – Positive Scale [CAPE-P15]), cognitive biases (Cognitive Biases Questionnaire for Psychosis [CBQp], with some items adapted for adolescents) and bullying (Adolescent Peer Relations Instrument [APRI]). Substance use was registered for tobacco, cannabis and alcohol consumption (sporadic or continuous). Statistical analysis were conducted with SPSS v 23.0 (IBM, USA). Substance use was recoded in dichotomic variables (use vs no use). All psychometric scales by these two groups were compared with non-parametric tests (U Mann Whitney). A p value <0.05 was considered to be significant. Results Of all 174 participants, 24 (13.8%) reported tobacco consumption, 49 (28.2%) alcohol consumption and 5 (2.9%) cannabis consumption. Differences in psychometric scales were tested for tobacco and alcohol use. Tobacco use was associated with more cognitive biases (total CBQp score [p=0.036] and dichotomic thinking [p=0.018]) but not with psychotic-like experiences or bullying. Alcohol use was associated with more cognitive biases (total CBQp score [p= 0.033] and jumping to conclusions [p= 0.025]) and more psychotic-like experiences (total CAPE-P15 score [p=0.008] and paranoid ideation subscore [p= 0.002]). Alcohol consumption was not associated with reported bullying. Discussion Our findings suggest that alcohol use in healthy adolescents aged between 14 and 15 years old is associated with psychotic-like experiences, and that this association could also involve cognitive biases (a ‘jumping to conclusions’ thinking style). Tobacco use was also associated with cognitive biases, although no effect was found on psychotic-like experiences. Bullying did not appear to have a relationship with substance use. Some limitations of our study include the cross-sectional design (no causal relationship might be inferred) and the low proportion of cannabis use. Future longitudinal studies also including a wider range of adolescent ages are needed to overcome our limitations. Our study underscores the need to monitor the potential psychopathological risks of alcohol consumption on adolescents.

scholarly journals Comorbid substance use and age at onset of schizophrenia

2006 ◽  
Vol 188 (3) ◽  
pp. 237-242 ◽  
Author(s):  
Thomas R. E. Barnes ◽  
Stanley H. Mutsatsa ◽  
Sam B. Hutton ◽  
Hilary C. Watt ◽  
Eileen M. Joyce
Keyword(s):  
Substance Use ◽  
Risk Factor ◽  
Alcohol Use ◽  
Strong Association ◽  
Age At Onset ◽  
Cannabis Use ◽  
First Episode ◽  
Recent Onset ◽  
And Gender ◽  
Reported Data

BackgroundSubstance use may be a risk factor for the onset of schizophrenia.AimsTo examine the association between substance use and age at onset in a UK, inner-city sample of people with recent-onset schizophrenia.MethodThe study sample consisted of 152 people recruited to the West London First-Episode Schizophrenia Study. Self-reported data on drug and alcohol use, as well as information on age at onset of psychosis, were collected. Mental state, cognition (IQ, memory and executive function) and social function were also assessed.ResultsIn total, 60% of the participants were smokers, 27% reported a history of problems with alcohol use, 35% reported current substance use (not including alcohol), and 68% reported lifetime substance use (cannabis and psychostimulants were most commonly used). Cannabis use and gender had independent effects on age at onset of psychosis, after adjusting for alcohol misuse and use of other drugs.ConclusionsThe strong association between self-reported cannabis use and earlier onset of psychosis provides further evidence that schizophrenia may be precipitated by cannabis use and/or that the early onset of symptoms is a risk factor for cannabis use.

scholarly journals A genetically-informed study disentangling the relationships between tobacco smoking, cannabis use, alcohol consumption, substance use disorders and respiratory infections, including COVID-19

2021 ◽  
Author(s):  
Daniel B. Rosoff ◽  
Joyce Yoo ◽  
Falk W. Lohoff
Keyword(s):  
Substance Use ◽  
Alcohol Consumption ◽  
Substance Use Disorders ◽  
Genome Wide Association Study ◽  
Respiratory Infections ◽  
Study Data ◽  
Cannabis Use ◽  
European Ancestry ◽  
Future Research ◽  
Increased Risk

ABSTRACTBackgroundObservational studies suggest smoking, cannabis use, alcohol consumption, cannabis use, and substance use disorders (SUDs) may play a role in the susceptibility for respiratory infections and disease, including coronavirus 2019 (COVID-2019). However, causal inference is challenging due to comorbid substance use.MethodsUsing genome-wide association study data of European ancestry (data from >1.7 million individuals), we performed single-variable and multivariable Mendelian randomization to evaluate relationships between smoking, cannabis use, alcohol consumption, SUDs, and respiratory infections.ResultsGenetically predicted lifetime smoking was found to be associated with increased risk for hospitalized COVID-19 (odds ratio (OR)=4.039, 95% CI 2.335-6.985, P-value=5.93×10−7) and very severe hospitalized COVID-19 (OR=3.091, 95% CI, 1.883-5.092, P-value=8.40×10−6). Genetically predicted lifetime smoking was also associated with increased risk pneumoniae (OR=1.589, 95% CI, 1.214-2.078, P-value=7.33×10−4), lower respiratory infections (OR=2.303, 95% CI, 1.713-3.097, P-value=3.40×10−8), and several others. Genetically predicted cannabis use disorder (CUD) was associated with increased bronchitis risk (OR=1.078, 95% CI, 1.020-1.128, P-value=0.007).ConclusionsWe provide strong genetic evidence showing smoking increases the risk for respiratory infections and diseases even after accounting for other substance use and abuse. Additionally, we provide find CUD may increase the risk for bronchitis, which taken together, may guide future research SUDs and respiratory outcomes.

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