Your browser doesn't support javascript.
Mostrar: 20 | 50 | 100
Resultados 1 - 20 de 347
Filtrar
Mais filtros










Base de dados
Intervalo de ano de publicação
1.
Nicotine Tob Res ; 2019 Oct 05.
Artigo em Inglês | MEDLINE | ID: mdl-31586403

RESUMO

INTRODUCTION: There is an absence of evidence regarding the impact of treating tobacco smoking and vaping equivalently in workplace policies. We aimed to describe and compare smoking and vaping policies in acute non-specialist NHS Trusts (n=131) and Higher Education Institutions (HEIs) (n=131) in England. METHODS: We conducted a census of smoking and vaping policies through organisational websites searches and direct requests for information. We recorded whether and where smoking and vaping were permitted. RESULTS: Smoking was prohibited indoors in all organisations. No NHS Trust permitted smoking freely outdoors, in contrast with 60% of HEIs. In 27% of NHS Trusts and 33% of HEIs smoking was permitted in designated areas, while in 73% of NHS Trusts and 8% of HEIs smoking was prohibited anywhere on site. Vaping was prohibited indoors in all NHS Trusts and all but one HEI, but permitted freely outdoors in 18% of NHS Trusts and 75% of HEIs. Vaping was permitted in designated outdoor spaces in 23% of NHS Trusts: 21% had areas shared with smokers; 2% had separate vaping areas. Vaping was permitted in designated outdoor areas in 18% of HEIs, all of which were shared with smokers. Vaping was prohibited anywhere on site in 54% of NHS Trusts and 6% of HEIs. CONCLUSIONS: Policies vary considerably in whether vaping and smoking are treated equivalently. Smoking policies in most HEIs should be reviewed to include more effective tobacco control approaches. Evidence is needed on the impact of imposing shared or separate spaces on vapers and smokers. IMPLICATIONS: This report provides a comprehensive review of smoking and vaping policies in two types of organisation across England. It highlights key discrepancies between current public health recommendations for vaping and existing workplace policies, which often lead to smokers and vapers sharing spaces. The report identifies the need for evidence on the impact of imposing shared spaces on smokers and vapers to inform workplace policies that maximise public health benefit.

2.
Br J Psychiatry ; : 1-7, 2019 Sep 17.
Artigo em Inglês | MEDLINE | ID: mdl-31526406

RESUMO

BACKGROUND: 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. AIMS: 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. METHOD: 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. RESULTS: 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). CONCLUSIONS: 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. DECLARATION OF INTEREST: W.v.d.B received fees in the past 3 years from Indivior, C&A Pharma, Opiant and Angelini. G.M.G. is a National Institute for Health Research (NIHR) Emeritus Senior Investigator, holds shares in P1vital and has served as consultant, advisor or CME speaker in the past 3 years for Allergan, Angelini, Compass Pathways, MSD, Lundbeck (/Otsuka and /Takeda), Medscape, Minervra, P1Vital, Pfizer, Sage, Servier, Shire and Sun Pharma.

3.
Addiction ; 2019 Aug 02.
Artigo em Inglês | MEDLINE | ID: mdl-31376200

RESUMO

BACKGROUND: Very few countries regulate maximum cigarette pack size. Larger, non-standard sizes are increasingly being introduced by the tobacco industry. Larger portion sizes increase food consumption; larger cigarette packs may similarly increase tobacco consumption. Here we consider the evidence for legislation to cap cigarette pack size to reduce tobacco-related harm. AIMS AND ANALYSIS: We first describe the regulations regarding minimum and maximum pack sizes in the 12 countries that have adopted plain packaging legislation and describe the range of sizes available. We then discuss evidence for two key assumptions that would support capping pack size. First, regarding the causal nature of the relationship between pack size and tobacco consumption, observational evidence suggests that people smoke fewer cigarettes when using smaller packs. Secondly, regarding the causal nature of the relationship between reducing consumption and successful cessation, reductions in number of cigarettes smoked per day are associated with increased cessation attempts and subsequent abstinence. However, more experimental evidence is needed to infer the causal nature of these associations among general populations of smokers. CONCLUSION: Cigarette pack size is positively associated with consumption and consumption is negatively associated with cessation. Based on limited evidence of the causal nature of these associations, we hypothesize that government regulations to cap cigarette pack sizes would positively contribute to reducing smoking prevalence.

4.
Int J Behav Nutr Phys Act ; 16(1): 75, 2019 08 28.
Artigo em Inglês | MEDLINE | ID: mdl-31462252

RESUMO

BACKGROUND: There is considerable uncertainty regarding the impact of tableware size on food consumption. Most existing studies have used small and unrepresentative samples and have not followed recommended procedures for randomised controlled trials, leading to increased risk of bias. In the first pre-registered study to date, we examined the impact on consumption of using larger versus smaller plates for self-served food. We also assessed impact on the underlying meal micro-structure, such as number of servings and eating rate, which has not previously been studied. METHODS: The setting was a purpose-built naturalistic eating behaviour laboratory. A general population sample of 134 adult participants (aged 18-61 years) was randomly allocated to one of two groups varying in the size of plate used for self-serving lunch: large or small. The primary outcome was amount of food energy (kcal) consumed during a meal. Additionally, we assessed impact on meal micro-structure, and examined potential modifying effects of executive function, socio-economic position, and sensitivity to perceptual cues. RESULTS: There was no clear evidence of a difference in consumption between the two groups: Cohen's d = 0.07 (95% CI [- 0.27, 0.41]), with participants in the large plate group consuming on average 19.2 (95% CI [- 76.5, 115.0]) more calories (3%) compared to the small plate group (large: mean (SD) = 644.1 (265.0) kcal, versus small: 624.9 (292.3) kcal). The difference between the groups was not modified by individual characteristics. There was no evidence of impact on meal micro-structure, with the exception of more food being left on the plate when larger plates were used. CONCLUSIONS: This study suggests that previous meta-analyses of a low-quality body of evidence may have considerably overestimated the effects of plate size on consumption. However, the possibility of a clinically significant effect - in either direction - cannot be excluded. Well-conducted trials of tableware size in real-world field settings are now needed to determine whether changing the size of tableware has potential to contribute to efforts to reduce consumption at population-level. TRIAL REGISTRATION: The study protocol ( https://osf.io/e3dfh/ ) and data analysis plan ( https://osf.io/sh5u7/ ) were pre-registered on the Open Science Framework.

6.
Nicotine Tob Res ; 2019 Jul 10.
Artigo em Inglês | MEDLINE | ID: mdl-31289809

RESUMO

OBJECTIVE: We conducted a prospective cohort study of the Clinical Practice Research Database to estimate rates of varenicline and nicotine replacement therapy (NRT) prescribing and the relative effects on smoking cessation, and mental health. METHODS: We used multivariable logistic regression, propensity score matched regression, and instrumental variable analysis. Exposure was varenicline or NRT prescription. Mental disorders were bipolar, depression, neurotic disorder, schizophrenia, or prescriptions of antidepressants, antipsychotics, hypnotics/anxiolytics, mood stabilizers. Outcomes were smoking cessation, and incidence of neurotic disorder, depression, prescription of antidepressants, or hypnotics/anxiolytics. Follow-ups were 3, 6, and 9 months, and at 1, 2, and 4 years. RESULTS: In all patients, NRT and varenicline prescribing declined during the study period. Seventy-eight thousand four hundred fifty-seven smokers with mental disorders aged ≥18 years were prescribed NRT (N = 59 340) or varenicline (N = 19 117) from September 1, 2006 to December 31, 2015. Compared with smokers without mental disorders, smokers with mental disorders had 31% (95% CI: 29% to 33%) lower odds of being prescribed varenicline relative to NRT, but had 19% (95% CI: 15% to 24%) greater odds of quitting at 2 years when prescribed varenicline relative to NRT. Overall, varenicline was associated with decreased or similar odds of worse mental health outcomes than NRT in patients both with and without mental disorders, although there was some variation when analyses were stratified by mental disorder subgroup. CONCLUSIONS: Smoking cessation medication prescribing may be declining in primary care. Varenicline was more effective than NRT for smoking cessation in patients with mental disorders and there is not clear consistent evidence that varenicline is adversely associated with poorer mental health outcomes. IMPLICATIONS: Patients with mental disorders were less likely to be prescribed varenicline than NRT. We triangulated results from three analytical techniques. We found that varenicline was more effective than NRT for smoking cessation in patients with mental disorders. Varenicline was generally associated with similar or decreased odds of poorer mental health outcomes (ie, improvements in mental health) when compared with NRT. We report these findings cautiously as our data are observational and are at risk of confounding.

7.
Artigo em Inglês | MEDLINE | ID: mdl-31315910

RESUMO

BACKGROUND: The 5-year mortality rate for pancreatic cancer is amongst the highest of all cancers. Greater understanding of underlying causes could inform population-wide intervention strategies for prevention. Summary genetic data from genome-wide association studies (GWAS) have become available for thousands of phenotypes. These data can be exploited in Mendelian randomization (MR) phenome-wide association studies (PheWAS) to efficiently screen the phenome for potential determinants of disease risk. METHODS: We conducted an MR-PheWAS of pancreatic cancer using 486 phenotypes, proxied by 9124 genetic variants, and summary genetic data from a GWAS of pancreatic cancer (7,110 cancer cases; 7,264 controls). Odds ratios and 95% confidence intervals per 1 SD increase in each phenotype were generated. RESULTS: We found evidence that previously reported risk factors of body mass index (1.46; 1.20 to 1.78) and hip circumference (1.42; 1.21 to 1.67) were associated with pancreatic cancer. We also found evidence of novel associations with metabolites that have not previously been implicated in pancreatic cancer: fibrinogen-cleavage peptide (1.60; 1.31 to 1.95) and O-sulfo-L-tyrosine (0.58; 0.46 to 0.74). An inverse association was also observed with lung adenocarcinoma (0.63; 0.54 to 0.74). CONCLUSIONS: Markers of adiposity (BMI and hip circumference) are potential intervention targets for pancreatic cancer prevention. Further clarification of the causal relevance of fibrinogen cleavage peptides and O-sulfo-L-tyrosine in pancreatic cancer aetiology is required, as is the basis of our observed association with lung adenocarcinoma. IMPACT: For pancreatic cancer, MR-PheWAS can augment existing risk factor knowledge and generate novel hypotheses to investigate.

8.
J Affect Disord ; 257: 461-469, 2019 Oct 01.
Artigo em Inglês | MEDLINE | ID: mdl-31310908

RESUMO

OBJECTIVE: Cognitive theories suggest people with depression interpret self-referential social information negatively. However, it is unclear whether these biases precede or follow depression. We investigated whether facial expression recognition was associated with depressive symptoms cross-sectionally and longitudinally. METHODS: Prospective cohort study of people who had visited UK primary care in the past year reporting depressive symptoms (n = 509). Depressive symptoms were measured using the Patient Health Questionnaire (PHQ-9) at four time-points, 2 weeks apart. A computerised task assessed happy and sad facial expression recognition at three time-points (n = 505 at time 1). The unbiased hit rate measured ability to recognise emotions accounting for any general tendency to identify the emotion when it was not present. RESULTS: The sample included the full range of depressive symptom severity, with 45% meeting diagnostic criteria for depression. There was no evidence that happy or sad unbiased hit rates were associated with concurrent or subsequent depressive symptoms. There was weak evidence that, for every additional face incorrectly classified as happy, concurrent PHQ-9 scores reduced by 0.05 of a point (95% CI = -0.10 to 0.002, p = 0.06 after adjustment for confounders). This association was strongest for more ambiguous facial expressions (interaction term p<0.001). LIMITATIONS: This was an observational study with relatively short follow-up (6 weeks) and small changes in depressive symptoms and emotion recognition. Only 7% of invited patients consented to participate. CONCLUSIONS: Reduced misclassifications of ambiguous faces as happy could be a state marker of depression, but was not associated with subsequent depressive symptoms. Future research should focus on the interpretation of ambiguous social information.

10.
Nat Commun ; 10(1): 2949, 2019 07 03.
Artigo em Inglês | MEDLINE | ID: mdl-31270314

RESUMO

Recent analyses have shown educational attainment to be associated with a number of health outcomes. This association may, in part, be due to an effect of educational attainment on smoking behaviour. In this study, we apply a multivariable Mendelian randomisation design to determine whether the effect of educational attainment on smoking behaviour is due to educational attainment or general cognitive ability. We use individual data from the UK Biobank study (N = 120,050) and summary data from large GWA studies of educational attainment, cognitive ability and smoking behaviour. Our results show that more years of education are associated with a reduced likelihood of smoking that is not due to an effect of general cognitive ability on smoking behaviour. Given the considerable physical harms associated with smoking, the effect of educational attainment on smoking is likely to contribute to the health inequalities associated with differences in educational attainment.


Assuntos
Cognição/fisiologia , Escolaridade , Análise da Randomização Mendeliana , Fumar/genética , Viés , Estudo de Associação Genômica Ampla , Humanos , Razão de Chances
11.
Nicotine Tob Res ; 2019 Jul 11.
Artigo em Inglês | MEDLINE | ID: mdl-31294817

RESUMO

INTRODUCTION: FTND (FagerstrÓ§m test for nicotine dependence) and TTFC (time to smoke first cigarette in the morning) are common measures of nicotine dependence (ND). However, genome-wide meta-analysis for these phenotypes has not been reported. METHODS: Genome-wide meta-analyses for FTND (N = 19,431) and TTFC (N = 18,567) phenotypes were conducted for adult smokers of European ancestry from 14 independent cohorts. RESULTS: We found that SORBS2 on 4q35 (p = 4.05 × 10-8), BG182718 on 11q22 (p = 1.02 × 10-8), and AA333164 on 14q21 (p = 4.11 × 10-9) were associated with TTFC phenotype. We attempted replication of leading candidates with independent samples (FTND, N = 7010 and TTFC, N = 10 061), however, due to limited power of the replication samples, the replication of these new loci did not reach significance. In gene-based analyses, COPB2 was found associated with FTND phenotype, and TFCP2L1, RELN, and INO80C were associated with TTFC phenotype. In pathway and network analyses, we found that the interconnected interactions among the endocytosis, regulation of actin cytoskeleton, axon guidance, MAPK signaling, and chemokine signaling pathways were involved in ND. CONCLUSIONS: Our analyses identified several promising candidates for both FTND and TTFC phenotypes, and further verification of these candidates was necessary. Candidates supported by both FTND and TTFC (CHRNA4, THSD7B, RBFOX1, and ZNF804A) were associated with addiction to alcohol, cocaine, and heroin, and were associated with autism and schizophrenia. We also identified novel pathways involved in cigarette smoking. The pathway interactions highlighted the importance of receptor recycling and internalization in ND. IMPLICATIONS: Understanding the genetic architecture of cigarette smoking and ND is critical to develop effective prevention and treatment. Our study identified novel candidates and biological pathways involved in FTND and TTFC phenotypes, and this will facilitate further investigation of these candidates and pathways.

12.
Nat Neurosci ; 22(7): 1196, 2019 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-31168101

RESUMO

Several occurrences of the word 'schizophrenia' have been re-worded as 'liability to schizophrenia' or 'schizophrenia risk', including in the title, which should have been "GWAS of lifetime cannabis use reveals new risk loci, genetic overlap with psychiatric traits, and a causal effect of schizophrenia liability," as well as in Supplementary Figures 1-10 and Supplementary Tables 7-10, to more accurately reflect the findings of the work.

13.
Addiction ; 114(8): 1487-1488, 2019 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-31222838
14.
Int J Epidemiol ; 2019 May 10.
Artigo em Inglês | MEDLINE | ID: mdl-31074779

RESUMO

BACKGROUND: Smoking is an important cause of mortality and recent studies have suggested that even low-intensity smoking might be associated with increased mortality. Still, smoking is associated with lower socio-economic status as well as other potential risk factors, and disease onset might motivate smoking cessation, thus residual confounding and reverse causality might bias results. We aimed to assess the evidence of a causal relationship between smoking intensity and cause-specific as well as all-cause-mortality using Mendelian randomization analyses. METHODS: We included 56 019 participants from the Norwegian HUNT2 Study and 337 103 participants from UK Biobank, linked to national registry data on causes of death. We estimated associations of self-reported smoking as well as the genetic variant rs1051730 as an instrument for smoking intensity with all-cause and cause-specific mortality. We subsequently meta-analysed the results from the two cohorts. RESULTS: Each effect allele of the rs1051730 was associated with a 9% increased hazard of all-cause mortality [95% confidence interval (CI) 6-11] among ever smokers. Effect alleles were also associated with death by neoplasms [hazard ratio (HR) 1.11, 95% CI 1.06-1.15], circulatory diseases (HR 1.06, 95% CI 1.01-1.11) and respiratory diseases (HR 1.15, 95% CI 1.05-1.26) among ever smokers. The association was stronger among ever than never smokers for all-cause mortality (p < 0.001), neoplasms (p = 0.001) and respiratory diseases (p = 0.038). CONCLUSIONS: Our results indicate a causal effect of smoking intensity on all-cause mortality and death by neoplasms and respiratory diseases. There was weaker evidence of a causal effect of smoking intensity on death by circulatory diseases.

15.
BMJ ; 365: l1855, 2019 05 22.
Artigo em Inglês | MEDLINE | ID: mdl-31122926

RESUMO

OBJECTIVES: To investigate the role of body mass index (BMI), systolic blood pressure, and smoking behaviour in explaining the effect of education on the risk of cardiovascular disease outcomes. DESIGN: Mendelian randomisation study. SETTING: UK Biobank and international genome-wide association study data. PARTICIPANTS: Predominantly participants of European ancestry. EXPOSURE: Educational attainment, BMI, systolic blood pressure, and smoking behaviour in observational analysis, and randomly allocated genetic variants to instrument these traits in mendelian randomisation. MAIN OUTCOMES MEASURE: The risk of coronary heart disease, stroke, myocardial infarction, and cardiovascular disease (all subtypes; all measured in odds ratio), and the degree to which this is mediated through BMI, systolic blood pressure, and smoking behaviour respectively. RESULTS: Each additional standard deviation of education (3.6 years) was associated with a 13% lower risk of coronary heart disease (odds ratio 0.86, 95% confidence interval 0.84 to 0.89) in observational analysis and a 37% lower risk (0.63, 0.60 to 0.67) in mendelian randomisation analysis. As a proportion of the total risk reduction, BMI was estimated to mediate 15% (95% confidence interval 13% to 17%) and 18% (14% to 23%) in the observational and mendelian randomisation estimates, respectively. Corresponding estimates were 11% (9% to 13%) and 21% (15% to 27%) for systolic blood pressure and 19% (15% to 22%) and 34% (17% to 50%) for smoking behaviour. All three risk factors combined were estimated to mediate 42% (36% to 48%) and 36% (5% to 68%) of the effect of education on coronary heart disease in observational and mendelian randomisation analyses, respectively. Similar results were obtained when investigating the risk of stroke, myocardial infarction, and cardiovascular disease. CONCLUSIONS: BMI, systolic blood pressure, and smoking behaviour mediate a substantial proportion of the protective effect of education on the risk of cardiovascular outcomes and intervening on these would lead to reductions in cases of cardiovascular disease attributable to lower levels of education. However, more than half of the protective effect of education remains unexplained and requires further investigation.


Assuntos
Doenças Cardiovasculares/etiologia , Escolaridade , Adulto , Idoso , Pressão Sanguínea , Índice de Massa Corporal , Feminino , Humanos , Masculino , Análise da Randomização Mendeliana , Pessoa de Meia-Idade , Análise Multivariada , Razão de Chances , Fatores de Risco , Fumar/efeitos adversos , Fatores Socioeconômicos , Reino Unido
16.
Tob Control ; 2019 Apr 01.
Artigo em Inglês | MEDLINE | ID: mdl-30936390

RESUMO

OBJECTIVES: To examine whether during a period of limited e-cigarette regulation and rapid growth in their use, smoking began to become renormalised among young people. DESIGN: Interrupted time-series analysis of repeated cross-sectional time-series data. SETTING: Great Britain PARTICIPANTS: 248 324 young people aged approximately 13 and 15 years, from three national surveys during the years 1998-2015. INTERVENTION: Unregulated growth of e-cigarette use (following the year 2010, until 2015). OUTCOME MEASURES: Primary outcomes were prevalence of self-reported ever smoking and regular smoking. Secondary outcomes were attitudes towards smoking. Tertiary outcomes were ever use of cannabis and alcohol. RESULTS: In final models, no significant change was detected in the pre-existing trend for ever smoking (OR 1.01, CI 0.99 to 1.03). There was a marginally significant slowing in the rate of decline for regular smoking (OR 1.04, CI 1.00 to 1.08), accompanied by a larger slowing in the rate of decline of cannabis use (OR 1.21, CI 1.18 to 1.25) and alcohol use (OR 1.17, CI 1.14 to 1.19). In all models and subgroup analyses for smoking attitudes, an increased rate of decline was observed after 2010 (OR 0.88, CI 0.86 to 0.90). Models were robust to sensitivity analyses. CONCLUSIONS: There was a marginal slowing in the decline in regular smoking during the period following 2010, when e-cigarettes were emerging but relatively unregulated. However, these patterns were not unique to tobacco use and the decline in the acceptability of smoking behaviour among youth accelerated during this time. These analyses provide little evidence that renormalisation of youth smoking was occurring during a period of rapid growth and limited regulation of e-cigarettes from 2011 to 2015. TRIAL REGISTRATION NUMBER: Research registry number: researchregistry4336.

17.
Addiction ; 114(6): 968-982, 2019 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-30891835

RESUMO

BACKGROUND AND AIMS: Despite a wealth of literature, the relationship between anxiety and alcohol use remains unclear. We examined whether (a) child and adolescent anxiety is positively or negatively associated with later alcohol use and disorders and (b) study characteristics explain inconsistencies in findings. DESIGN AND SETTING: We conducted a systematic review of 51 prospective cohort studies from 11 countries. Three studies contributed to a meta-analysis. We searched PubMed, Scopus, Web of Science and PsycINFO databases, and studies were included if they met the following criteria: English language publication, human participants, anxiety exposure (predictor variable) in childhood or adolescence and alcohol outcome at least 6 months later. PARTICIPANTS: Study sample sizes ranged from 110 to 11 157 participants. Anxiety exposure ages ranged from 3 to 24 years, and alcohol outcome ages ranged from 11 to 42 years. MEASUREMENTS: Ninety-seven associations across 51 studies were categorized by anxiety exposure (generalized anxiety disorder, internalizing disorders, miscellaneous anxiety, obsessive compulsive disorder, panic disorder, separation anxiety disorder, social anxiety disorder and specific phobias) and alcohol use outcome (drinking frequency/quantity, binge drinking and alcohol use disorders). FINDINGS: The narrative synthesis revealed some evidence for a positive association between anxiety and later alcohol use disorders. Associations of anxiety with later drinking frequency/quantity and binge drinking were inconsistent. Type and developmental period of anxiety, follow-up duration, sample size and confounders considered did not appear to explain the discrepant findings. The meta-analysis also showed no clear evidence of a relationship between generalized anxiety disorder and later alcohol use disorder (odds ratio = 0.94, 95% confidence interval = 0.47-1.87). CONCLUSIONS: Evidence to date is suggestive, but far from conclusive of a positive association between anxiety during childhood and adolescence and subsequent alcohol use disorder.

18.
Drug Alcohol Depend ; 197: 344-353, 2019 04 01.
Artigo em Inglês | MEDLINE | ID: mdl-30827758

RESUMO

BACKGROUND: High levels of alcohol use in pregnancy have been shown to be associated with negative physical health consequences in offspring. However, the literature is less clear on the association of alcohol use in pregnancy and offspring mental health, specifically for low levels of prenatal alcohol exposure. We conducted a systematic review to evaluate studies examining this association. METHODS: Studies were identified by searching PsycINFO, PubMed and Web of Science, and were included if they examined alcohol use during pregnancy as an exposure and offspring mental health at age 3 or older as an outcome. We excluded non-English language publications and studies of fetal alcohol syndrome. RESULTS: Thirty-three studies were included and were categorized by mental health outcomes: anxiety/depression, emotional problems, total internalizing problems, total problem score, and conduct disorder. Over half of the analyses reported a positive association of prenatal alcohol exposure and offspring mental health problems. CONCLUSIONS: Our review suggests that maternal alcohol use during pregnancy is associated with offspring mental health problems, even at low to moderate levels of alcohol use. Future investigation using methods that allow stronger causal inference is needed to further investigate if these associations shown are causal.


Assuntos
Consumo de Bebidas Alcoólicas/efeitos adversos , Alcoolismo/psicologia , Transtornos do Neurodesenvolvimento/induzido quimicamente , Complicações na Gravidez/psicologia , Efeitos Tardios da Exposição Pré-Natal/psicologia , Pré-Escolar , Feminino , Humanos , Gravidez , Efeitos Tardios da Exposição Pré-Natal/induzido quimicamente
19.
J Psychopharmacol ; 33(3): 326-334, 2019 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-30717614

RESUMO

BACKGROUND:: Research suggests that acute alcohol consumption alters recognition of emotional expressions. Extending this work, we investigated the effects of alcohol on recognition of six primary expressions of emotion. METHODS:: We conducted two studies using a 2 × 6 experimental design with a between-subjects factor of drink (alcohol, placebo) and a within-subjects factor of emotion (anger, disgust, sadness, surprise, happiness, fear). Study one ( n = 110) was followed by a direct replication study ( n = 192). Participants completed a six alternative forced choice emotion recognition task following consumption of 0.4 g/kg alcohol or placebo. Dependent variables were recognition accuracy (i.e. hits) and false alarms. RESULTS:: There was no clear evidence of differences in recognition accuracy between groups ( ps > .58). In study one, there were more false alarms for anger in the alcohol compared to placebo group ( n = 52 and 56, respectively; t(94.6) = 2.26, p = .024, d = .44) and fewer false alarms for happiness ( t(106) = -2.42, p = .017, d = -.47). However, no clear evidence for these effects was found in study two (alcohol group n = 96, placebo group n = 93, ps > .22). When the data were combined we observed weak evidence of an effect of alcohol on false alarms of anger ( t(295) = 2.25, p = .025, d = .26). CONCLUSIONS:: These studies find weak support for biased anger perception following acute alcohol consumption in social consumers, which could have implications for alcohol-related aggression. Future research should investigate the robustness of this effect, particularly in individuals high in trait aggression.

SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA