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Background and Aims The concern that alcohol advertising can have detrimental effects on vulnerable viewers has prompted the development of codes of responsible advertising practices. This paper evaluates critically the concept of vulnerability as it applies to (1) susceptibility to alcohol-related harm and (2) susceptibility to the effects of marketing, and describes its implications for the regulation of alcohol marketing. Method We describe the findings of key published studies, review papers and expert reports to determine whether these two types of vulnerability apply to population groups defined by (1) age and developmental history; (2) personality characteristics; (3) family history of alcoholism; (4) female sex and pregnancy risk; and (5) history of alcohol dependence and recovery status. Results Developmental theory and research suggest that groups defined by younger age, incomplete neurocognitive development and a history of alcohol dependence may be particularly vulnerable because of the disproportionate harm they experience from alcohol and their increased susceptibility to alcohol marketing. Children may be more susceptible to media imagery because they do not have the ability to compensate for biases in advertising portrayals and glamorized media imagery. Conclusion Young people and people with a history of alcohol dependence appear to be especially vulnerable to alcohol marketing, warranting the development of new content and exposure guidelines focused on protecting those groups to improve current self-regulation codes promoted by the alcohol industry. If adequate protections cannot be implemented through this mechanism, statutory regulations should be considered.

Background and aims Despite decades of research on co-occurring smoking and depression, cessation rates remain consistently lower for depressed smokers than for smokers in the general population, highlighting the need for theory-driven models of smoking and depression. This paper provides a systematic review with a particular focus on psychological states that disproportionately motivate smoking in depression, and frame an incentive learning theory account of smoking-depression co-occurrence. Methods We searched PubMed, Scopus, PsychINFO, and CINAHL through December 2014, which yielded 852 articles. Using pre-established eligibility criteria, we identified papers focused on clinical issues and motivational mechanisms underlying smoking in established, adult smokers (i.e., maintenance, quit attempts, and cessation/relapse) with elevated symptoms of depression. Two reviewers independently determined whether articles met review criteria. We included 297 articles in qualitative synthesis. Results Our review identified three primary mechanisms that underlie persistent smoking among depressed smokers: low positive affect, high negative affect, and cognitive impairment. We propose a novel application of incentive learning theory which posits that depressed smokers experience greater increases in the expected value of smoking in the face of these three motivational states, which promotes goal-directed choice of smoking behavior over alternative actions. Conclusions The incentive learning theory accounts for current evidence on how depression primes smoking behavior and provides a unique framework for conceptualizing psychological mechanisms of smoking maintenance among depressed smokers. Treatment should focus on correcting adverse internal states, and beliefs about the high value of smoking in those states, to improve cessation outcomes for depressed smokers. This article is protected by copyright. All rights reserved.

Author(s): Guydish, Joseph; Passalacqua, Emma; Pagano, Anna; Martinez, Cristina; Le, Thao; Chun, JongSerl; Tajima, Barbara; Docto, Lindsay; Garina, Daria; Delucchi, Kevin | Abstract: AimsSmoking prevalence is higher among people enrolled in addiction treatment compared with the general population, and very high rates of smoking are associated with opiate drug use and receipt of opiate replacement therapy (ORT). We assessed whether these findings are observed internationally.MethodsPubMed, PsycINFO and the Alcohol and Alcohol Problems Science Database were searched for papers reporting smoking prevalence among addiction treatment samples, published in English, from 1987 to 2013. Search terms included tobacco use, cessation and substance use disorders using and/or Boolean connectors. For 4549 papers identified, abstracts were reviewed by multiple raters; 239 abstracts met inclusion criteria and these full papers were reviewed for exclusion. Fifty-four studies, collectively comprising 37,364 participants, were included. For each paper we extracted country, author, year, sample size and gender, treatment modality, primary drug treated and smoking prevalence.ResultsThe random-effect pooled estimate of smoking across people in addiction treatment was 84% [confidence interval (CI) = 79, 88%], while the pooled estimate of smoking prevalence across matched population samples was 31% (CI = 29, 33%). The difference in the pooled estimates was 52% (CI = 48%, 57%, P l .0001). Smoking rates were higher in programs treating opiate use compared with alcohol use [odds ratio (OR) = 2.52, CI = 2.00, 3.17], and higher in ORT compared to out-patient programs (OR = 1.42, CI = 1.19, 1.68).ConclusionsSmoking rates among people in addiction treatment are more than double those of people with similar demographic characteristics. Smoking rates are also higher in people being treated for opiate dependence compared with people being treated for alcohol use disorder.

Time series analyses are statistical methods used to assess trends in repeated measurements taken at regular intervals and their associations with other trends or events, taking account of the temporal structure of such data. Addiction research often involves assessing associations between trends in target variables (e.g. population cigarette smoking prevalence) and predictor variables (e.g. average price of a cigarette), known as a multiple time series design, or interventions or events (e.g. introduction of an indoor smoking ban), known as an interrupted time series design. There are many analytical tools available, each with its own strengths and limitations. This paper provides addiction researchers with an overview of many of the methods available (GLM, GLMM, GLS, GAMM, ARIMA, ARIMAX, VAR, SVAR, VECM) and guidance on when and how they should be used, sample size det ermination, reporting and interpretation. The aim is to provide increased clarity for researchers proposing to undertake these analyses concerning what is likely to be acceptable for publication in journals such as Addiction. Given the large number of choices that need to be made when setting up time series models, the guidance emphasizes the importance of pre-registering hypotheses and analysis plans before the analyses are undertaken.

Background and aims Estimated alcohol consumption from national self-report surveys is often only 30-40% of official estimates based on sales or taxation data. Global burden of disease (GBD) estimates for alcohol adjust survey estimates up to 80% of total per capita consumption. This assumes that cohort studies needed to estimate relative risks for disease suffer less from under-reporting than typical national surveys. However, there is limited evidence on which to base that assumption. This paper aims to assess the extent of underestimation of alcohol consumption in cohort studies concerning alcohol and mortality compared with official total consumption estimates. Design Comparisons of estimated per capita consumption from a comprehensive sample of cohort studies against official estimates by country and year. Participants A total of 1 876 046 participants in 40 cohort studies from 18 countries on alcohol use and all-cause mortality identified by systematic review. Measurements Alcohol consumption data from the cohort studies were converted into usual grams of ethanol per day and then to total age 15+ per capita consumption. Matched estimates were sourced from the World Health Organization (WHO) Global Health Observatory. Findings The cohort studies had mean coverages of age 15+ per capita alcohol consumption of 61.71% (ranging from 29.19% for Russia to 96.53% for Japan), after weighting estimates by sample size for within-country estimates and by number of studies per country for the overall estimate. Regional estimates were higher for the United States (66.22%) and lower for western European countries (55.35%). Conclusions Underestimation of alcohol consumption in cohort studies is less than in typical population surveys. Because some under-coverage is caused by under-sampling heavier drinkers, the current practice of uplifting survey estimates to 80% of total population consumption in global burden of disease studies appears to be appropriate.

BACKGROUND AND AIMS: Chronic skin and soft tissue infections (SSTI) among people who inject drugs (PWID) can lead to AA-amyloidosis: a serious, yet neglected, multi-organ disease. We aim to synthesise findings on the epidemiology, risk factors, clinical outcomes, screening recommendations, and challenges to treatment for AA-amyloidosis among PWID. METHODS: A systematic review was conducted in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA). We searched the following bibliographic databases in July 2017: CINAHL Plus, Embase, Global Health, MEDLINE, PsycEXTRA, PsycINFO, and SCOPUS. Studies were included if they investigated AA-amyloidosis in PWID. Studies were not restricted to location, study type, year, or language of publication. Study heterogeneity precluded meta-analysis (I2: 86%); we present a narrative review of the literature. RESULTS: Thirty-seven papers from eight countries met inclusion criteria. A total of 781 PWID are reported on, of whom 177 had AA-amyloidosis. Where disease causality is established, it is attributed to chronic inflammation caused by injecting-related SSTIs. Most (88.7%) PWID with AA-amyloidosis had SSTIs. Proportions of PWID with AA amyloidosis at post-mortem range from 1.6% (Germany) to 22.5% (Serbia). Biopsy studies report from 5.26% (Portugal) to 50% (Germany) of AA-amyloidosis in PWID with suspected or known kidney disease. Following diagnosis, the typical trajectory for PWID with AA-amyloidosis was rapid deterioration of renal function requiring haemodialysis (32.8%). Treatment difficulties, end-stage renal failure (40%), and premature death from sepsis (33%) were observed. Good outcomes, including reversibility of AA-amyloidosis are attributed to rapid treatment of the underlining inflammation and injecting cessation. Notably, given the population in question, no studies were published in addiction or harm reduction journals; most (92%) appear in specialist nephrology and medical journals. CONCLUSION: There is strong evidence of an association between skin and soft tissue infections (SSTIs) and AA-amyloidosis. Among people who inject drugs, injecting-related SSTIs are a significant cause of morbidity and premature mortality and there is evidence of increasing SSTI prevalence. Limitations in the literature make it difficult to estimate AA-amyloidosis prevalence among people who inject drugs.

Aims To conduct a systematic review and meta-analysis of studies in order to estimate the effect of US medical marijuana laws (MMLs) on past-month marijuana use prevalence among adolescents. Methods A total of 2999 papers from 17 literature sources were screened systematically. Eleven studies, developed from four ongoing large national surveys, were meta-analyzed. Estimates of MML effects on any past-month marijuana use prevalence from included studies were obtained from comparisons of pre–post MML changes in MML states to changes in non-MML states over comparable time-periods. These estimates were standardized and entered into a meta-analysis model with fixed-effects for each study. Heterogeneity among the study estimates by national data survey was tested with an omnibus F-test. Estimates of effects on additional marijuana outcomes, of MML provisions (e.g. dispensaries) and among demographic subgroups were abstracted and summarized. Key methodological and modeling characteristics were also described. Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines were followed. Results None of the 11 studies found significant estimates of pre–post MML changes compared with contemporaneous changes in non-MML states for marijuana use prevalence among adolescents. The meta-analysis yielded a non-significant pooled estimate (standardized mean difference) of −0.003 (95% confidence interval = −0.012, +0.007). Four studies compared MML with non-MML states on pre-MML differences and all found higher rates of past-month marijuana use in MML states pre-MML passage. Additional tests of specific MML provisions, of MML effects on additional marijuana outcomes and among subgroups generally yielded non-significant results, although limited heterogeneity may warrant further study. Conclusions Synthesis of the current evidence does not support the hypothesis that US medical marijuana laws (MMLs) until 2014 have led to increases in adolescent marijuana use prevalence. Limited heterogeneity exists among estimates of effects of MMLs on other patterns of marijuana use, of effects within particular population subgroups and of effects of specific MML provisions.

BACKGROUND AND AIMS: Estimating 'return on investment' (ROI) from smoking cessation interventions requires reach and effectiveness parameters for interventions for use in economic models such as the EQUIPT ROI tool (http://roi.equipt.eu). This paper describes the derivation of these parameter estimates for England that can be adapted to create ROI models for use by other countries. METHODS: Estimates were derived for interventions in terms of their reach and effectiveness in: 1) promoting quit attempts, and 2) improving the success of quit attempts (abstinence for at least 12 months). The sources were systematic reviews of efficacy supplemented by individual effectiveness evaluations and national surveys. FINDINGS: Quit attempt rates were estimated to be increased by the following percentages (with reach in parentheses): 20% by tax increases raising the cost of smoking 5% above the cost of living index (100%); 10% by enforced comprehensive indoor public smoking bans (100%); 3% by mass media campaigns achieving 400 gross rating points (100%); 40% by brief opportunistic physician advice (21%); and 110% by use of a licensed nicotine product to reduce cigarette consumption (12%);. Quit success rates were estimated to be increased by the following ratios: 60% by single-form nicotine replacement therapy (NRT) (5%); 114% by NRT patch plus a faster acting NRT (2%);124% by prescribed varenicline (5%); 60% by bupropion (1%); 100% by nortriptyline (0%), 10) 298% by cytisine (0%); 40% by individual face-to-face behavioural support (2%); 37% by telephone support (0.5%); 88% by group behavioural support (1%); 63% by text messaging (0.5%); and 19% by printed self-help materials (1%). There was insufficient evidence to obtain reliable, country-specific estimates for interventions such as websites, smartphone apps and e-cigarettes. CONCLUSIONS: Tax increases, indoor smoking bans, brief opportunistic physician advice, and use of nicotine replacement therapy (NRT) for smoking reduction can all increase population quit attempt rates. Quit success rates can be increased by provision of NRT, varenicline, bupropion, nortriptyline, cytisine and behavioural support delivered through a variety of modalities. Parameter estimates for the effectiveness and reach of these interventions can contribute to return on investment estimates in support of national or regional policy decisions.

AIMS: This paper estimates how far monthly changes in prevalence of cigarette smoking, motivation to quit and attempts to stop smoking have been associated with changes in prevalence of high-risk drinking, and motivation and attempts to reduce alcohol consumption in England. DESIGN: Data were used from the Alcohol and Smoking Toolkit Studies between April 2014 and June 2016. These involve monthly household face-to-face surveys of representative samples of ~1700 adults in England. MEASUREMENTS: ARIMAX modelling was used to assess the association over time between monthly prevalence of a) smoking and high-risk drinking; b) high motivation to quit smoking and high motivation to reduce alcohol consumption; and c) attempts to quit smoking and attempts to reduce alcohol consumption. FINDINGS: Mean smoking prevalence over the study period was 18.6% and high-risk drinking prevalence was 13.0%. A decrease of 1% of the series mean smoking prevalence was associated with a reduction of 0.19% of the mean prevalence of high-risk drinking (95%CI 0.03 to 0.34, p = 0.017. A statistically significant association was not found between prevalence of high motivation to quit smoking and high motivation to reduce alcohol consumption (β 0.324 95%CI -0.371 to 1.019, p = 0.360) or prevalence of attempts to quit smoking and attempts to reduce alcohol consumption (β -0.026 95%CI -1.348 to 1.296, p = 0.969). CONCLUSION: Between 2014 and 2016, monthly changes in prevalence of smoking in England were positively associated with prevalence of high-risk drinking. There was no significant association between motivation to stop and motivation to reduce alcohol consumption, or attempts to quit smoking and attempts to reduce alcohol consumption.

Background and aims There is increasing research evidence about the causal role of alcohol in cancer, accompanied by unclear and conflicting messages in the media. This paper aimed to clarify the strength of the evidence for alcohol as a cause of cancer, and the meaning of cause in this context. Methods Recent epidemiological and biological research on alcohol and cancer was reviewed and summarized, drawing upon published meta-analyses identified from the Medline database and the archives of the International Agency for Research on Cancer. More recent epidemiological studies not included in these publications were also reviewed. A brief description of the nature of causal inference in epidemiology was used to frame discussion of the strength of the evidence that alcohol causes cancer, and contrast this with the case for a protective association of alcohol with cardiovascular disease. Results The usual epidemiological understanding of a cause is a factor that increases the incidence of a condition in the population. In the context of a body of epidemiological evidence of an association of alcohol consumption with a disease, the inference that it is a causal association requires alternative explanations of the observed finding to be judged unlikely. Even without complete knowledge of biological mechanisms, the epidemiological evidence can support the judgement that alcohol causes cancer of the oropharynx, larynx, oesophagus, liver, colon, rectum and breast. The measured associations exhibit gradients of effect that are biologically plausible, and there is some evidence of reversibility of risk in laryngeal, pharyngeal and liver cancers when consumption ceases. The limitations of cohort studies mean that the true effects may be somewhat weaker or stronger than estimated currently, but are unlikely to be qualitatively different. The same, or similar, epidemiological studies also commonly report protection from cardiovascular disease associated with drinking but a high level of scepticism regarding these findings is now warranted. Conclusions There is strong evidence that alcohol causes cancer at seven sites in the body and probably others. Current estimates suggest that alcohol-attributable cancers at these sites make up 5.8% of all cancer deaths world-wide. Confirmation of specific biological mechanisms by which alcohol increases the incidence of each type of cancer is not required to infer that alcohol is a cause.

Background and aims Addictive behaviours are among the greatest scourges on humankind. It is important to estimate the extent of the problem globally and in different geographical regions. Such estimates are available, but there is a need to collate and evaluate these to arrive at the best available synthetic figures. Addiction has commissioned this paper as the first of a series attempting to do this. Methods Online sources of global, regional and national information on prevalence and major harms relating to alcohol use, tobacco use, unsanctioned psychoactive drug use and gambling were identified through expert review and assessed. The primary data sources located were the websites of the World Health Organization (WHO), the United Nations Office on Drugs and Crime (UNODC) and the Alberta Gambling Research Institute. Summary statistics were compared with recent publications on the global epidemiology of addictive behaviours. Results An estimated 4.9% of the world's adult population (240 million people) suffer from alcohol use disorder (7.8% of men and 1.5% of women), with alcohol causing an estimated 257 disability-adjusted life years lost per 100 000 population. An estimated 22.5% of adults in the world (1 billion people) smoke tobacco products (32.0% of men and 7.0% of women). It is estimated that 11% of deaths in males and 6% of deaths in females each year are due to tobacco. Of ‘unsanctioned psychoactive drugs’, cannabis is the most prevalent at 3.5% globally, with each of the others at

Aims The purpose of this paper is to discover patterns of drug use initiations over time through a multiple event process survival mixture model (MEPSUM model), a novel approach for substance use and prevention research. Design The MEPSUM model combines survival analysis and mixture modeling—specifically latent class analysis—to examine individual differences in the timing of initiation and cumulative risk of substance use over time, and is applied to cross-sectional survey data on drug initiations. Setting Data are drawn from the 2009 National Survey on Drug Use and Health. Participants The survey includes responses from 55 772 individuals (52.05% female). Measurements The age of first use of nine different types of substances are examined, including alcohol, tobacco, cocaine and non-medical use of prescription drugs. Findings It is argued that six patterns parsimoniously describe the population's risk of initiating different substances over time, described colloquially as general abstainers; early, late and progressive soft drug users; and early and late hard drug users. Both gender and ethnicity significantly predict the patterns, with Caucasians and males having a higher risk for the hard drug-using patterns. The MEPSUM model produced stable results in this application, as the patterns are validated in a split-sample design. Conclusions The MEPSUM model provides a statistical framework from which to evaluate patterns of risk for drug initiations over time and predict substance use trajectories relevant to public health interventions. The patterns that result from the model can be used as outcomes for subsequent investigations of etiological and mediating mechanisms.

This paper describes three important strands in the career of Griffith Edwards that define him as a leader and an innovator. Believing that education and science were critical for the development of addiction as a profession and as a field of inquiry, his approach was multi-faceted: educating all doctors to appreciate the fundamental issues in addiction; training psychiatrists in the complexity of 'dual diagnosis' and specific specialist intervention; and teaching that addiction could be a chronic condition which required care management over the life course. These three inter-related areas are directly related to the need for a range of practitioners to have an understanding of addiction so that patients can be properly managed. The greater our understanding of the nature of addiction behaviour, the more likely the potential to optimize treatment and train practitioners from different professional disciplines.