441 research outputs found

    Weight change over eight years in relation to alcohol consumption in a cohort of continuing smokers and quitters

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    INTRODUCTION: Stopping smoking results in weight gain. Avoidance of alcohol is often advocated to reduce cues to smoking, but the effect of alcohol consumption on body weight is unclear. METHODS: We used regression models to examine weight change by baseline alcohol consumption in quitting and continuing smokers. Weight was measured at baseline and at 8 years, and weekly alcohol consumption was reported at baseline in participants from the Oxfordshire general practices nicotine patch/placebo trial. Of 698 smokers attempting to stop smoking, 85 were abstinent for 8 years and 613 continued to smoke. RESULTS: The association between baseline alcohol consumption and weight change depended upon smoking status (p for interaction = .019). In smokers, there was no association with weight change, 0.005 (95% CI: -0.037 to 0.056) kg per UK unit (U) (8 g of ethanol) consumed each week. This was unmodified by gender and baseline body mass index (BMI). In quitters, there was a negative association with weight change, -0.174 (95% CI: -0.315 to -0.034) kg per U consumed each week (unmodified by gender and baseline BMI). Quitters who consumed 14 U (112 g ethanol) a week weighed a mean 2.4 kg less than quitters who did not drink. CONCLUSIONS: Quitting smokers who drink more alcohol appear to gain less weight after quitting than those who do not drink. This is consistent across studies, it may be accounted for by unmeasured confounders or it may be that alcohol reduces weight gain. If alcohol reduces weight gain, the advice for quitting smokers must balance the benefits and hazards of alcohol consumption. However, there is currently insufficient evidence to advise quitters who drink little or no alcohol to increase consumption

    Slimming World in Stop Smoking Services (SWISSS): Study protocol for a randomized controlled trial

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    BACKGROUND: Quitting smokers gain weight. This deters some from trying to stop smoking and may explain the increased incidence of type 2 diabetes after cessation. Dieting when stopping smoking may be counterproductive. Hunger increases cravings for smoking and tackling two behaviours together may undermine quitting success. A meta-analysis of randomized controlled trials (RCTs) showed individualized dietary support may prevent weight gain, although there is insufficient evidence whether it undermines smoking cessation. Commercial weight management providers (CWMPs), such as Slimming World, provide individualized dietary support for National Health Service (NHS) patients; however, there is no evidence that they can prevent cessation-related weight gain.Our objective is to determine whether attending Slimming World from quit date, through referral from NHS Stop Smoking Services, is more effective than usual care at preventing cessation-related weight gain. METHODS: This RCT will examine the effectiveness of usual cessation support plus referral to Slimming World compared to usual cessation support alone. Healthy weight, overweight and obese adult smokers attending Stop Smoking Services will be included. The primary outcome is weight change in quitters 12 weeks post-randomization. Multivariable linear regression analysis will compare weight change between trial arms and adjust for known predictors of cessation-related weight gain.We will recruit 320 participants, with 160 participants in each arm. An alpha error rate of 5% and 90% power will detect a 2 kg (SD = 2.5) difference in weight gain at 12 weeks, assuming 20% remain abstinent by then. DISCUSSION: This trial will establish whether referral to the 12-week Slimming World programme plus usual care is an effective intervention to prevent cessation-related weight gain. If so, we will seek to establish whether weight control comes at the expense of a successful quit attempt in a further non-inferiority trial.Positive results from both these trials would provide a potential solution to cessation-related weight gain, which could be rolled out across England within Stop Smoking Services to better meet the needs of 0.75 million smokers stopping with NHS support every year. TRIAL REGISTRATION: Current Controlled Trials ISRCTN65705512

    A Delphi study to strengthen research methods training in undergraduate psychology programmes

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    Psychology programmes often emphasise inferential statistical tests over a solid understanding of data and research design. This imbalance may leave graduates under-equipped to effectively interpret research and employ data to answer questions. We conducted a two-round modified-Delphi to identify the research methods skills that the UK psychology community deems essential for undergraduates to learn. Participants included 103 research methods instructors, academics, students, and non-academic psychologists. Of 78 items included in the consensus process, 34 reached consensus. We coupled these results with a qualitative analysis of 707 open-ended text responses to develop nine recommendations for organisations that accredit undergraduate psychology programmes—such as the British Psychological Society (BPS). We recommend that accreditation standards emphasise (1) dataskills, (2) research design, (3) descriptive statistics, (4) critical analysis, (5) qualitative methods, and (6) both parameter estimation and significance testing; as well as (7) give precedence to foundational skills, (8) promote transferable skills, and (9) create space in curricula to enable these recommendations. Our data and findings can inform modernised accreditation standards to include clearly-defined, assessable, and widely-encouraged skills that foster a competent graduate body for the contemporary world

    Improving research quality: the view from the UK Reproducibility Network institutional leads for research improvement

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    The adoption and incentivisation of open and transparent research practices is critical in addressing issues around research reproducibility and research integrity. These practices will require training and funding. Individuals need to be incentivised to adopt open and transparent research practices (e.g., added as desirable criteria in hiring, probation, and promotion decisions, recognition that funded research should be conducted openly and transparently, the importance of publishers mandating the publication of research workflows and appropriately curated data associated with each research output). Similarly, institutions need to be incentivised to encourage the adoption of open and transparent practices by researchers. Research quality should be prioritised over research quantity. As research transparency will look different for different disciplines, there can be no one-size-fits-all approach. An outward looking and joined up UK research strategy is needed that places openness and transparency at the heart of research activity. This should involve key stakeholders (institutions, research organisations, funders, publishers, and Government) and crucially should be focused on action. Failure to do this will have negative consequences not just for UK research, but also for our ability to innovate and subsequently commercialise UK-led discovery

    Statistical power in clinical trials of interventions for mood, anxiety, and psychotic disorders

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    BACKGROUND: Previous research has suggested that statistical power is suboptimal in many biomedical disciplines, but it is unclear whether power is better in trials for particular interventions, disorders, or outcome types. We therefore performed a detailed examination of power in trials of psychotherapy, pharmacotherapy, and complementary and alternative medicine (CAM) for mood, anxiety, and psychotic disorders.METHODS: We extracted data from the Cochrane Database of Systematic Reviews (Mental Health). We focused on continuous efficacy outcomes and estimated power to detect predetermined effect sizes (standardized mean difference [SMD] = 0.20-0.80, primary SMD = 0.40) and meta-analytic effect sizes (ESMA). We performed meta-regression to estimate the influence of including underpowered studies in meta-analyses.RESULTS: We included 256 reviews with 10 686 meta-analyses and 47 384 studies. Statistical power for continuous efficacy outcomes was very low across intervention and disorder types (overall median [IQR] power for SMD = 0.40: 0.32 [0.19-0.54]; for ESMA: 0.23 [0.09-0.58]), only reaching conventionally acceptable levels (80%) for SMD = 0.80. Median power to detect the ESMA was higher in treatment-as-usual (TAU)/waitlist-controlled (0.49-0.63) or placebo-controlled (0.12-0.38) trials than in trials comparing active treatments (0.07-0.13). Adequately-powered studies produced smaller effect sizes than underpowered studies (B = -0.06, p ⩽ 0.001).CONCLUSIONS: Power to detect both predetermined and meta-analytic effect sizes in psychiatric trials was low across all interventions and disorders examined. Consistent with the presence of reporting bias, underpowered studies produced larger effect sizes than adequately-powered studies. These results emphasize the need to increase sample sizes and to reduce reporting bias against studies reporting null results to improve the reliability of the published literature.</p

    Prefrontal cortex stimulation does not affect emotional bias, but may slow emotion identification

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    Transcranial direct current stimulation (tDCS) has recently garnered attention as a putative depression treatment. However, the cognitive mechanisms by which it exerts an antidepressant effect are unclear: tDCS may directly alter ‘hot’ emotional processing biases, or alleviate depression through changes in ‘cold’ (non-emotional) cognitive function. Here, 75 healthy participants performed a facial emotion identification task during 20 minutes of anodal or sham tDCS over the left dorsolateral prefrontal cortex (DLPFC) in a double-blind, within-subject crossover design. A subset of 31 participants additionally completed a task measuring attentional distraction during stimulation. Compared to sham stimulation, anodal tDCS of the left DLPFC resulted in an increase in response latency across all emotional conditions. Bayesian analysis showed definitively that tDCS exerted no emotion-dependent effect on behaviour. Thus, we demonstrate that anodal tDCS produces a general, rather than an emotion-specific, effect. We also report a preliminary finding in the subset of participants who completed the distractibility task: increased distractibility during active stimulation correlated significantly with the degree to which tDCS slowed emotion identification. Our results provide insight into the possible mechanisms by which DLPFC tDCS may treat symptoms of depression, suggesting that it may not alter emotional biases, but instead may affect ‘cold’ cognitive processes

    Association Between Genetic Variants on Chromosome 15q25 Locus and Objective Measures of Tobacco Exposure

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    Background: Two single-nucleotide polymorphisms, rs1051730 and rs16969968, located within the nicotinic acetylcholine receptor gene cluster on chromosome 15q25 locus, are associated with heaviness of smoking, risk for lung cancer, and other smoking-related health outcomes. Previous studies have typically relied on self-reported smoking behavior, which may not fully capture interindividual variation in tobacco exposure. / Methods: We investigated the association of rs1051730 and rs16969968 genotype (referred to as rs1051730–rs16969968, because these are in perfect linkage disequilibrium and interchangeable) with both self-reported daily cigarette consumption and biochemically measured plasma or serum cotinine levels among cigarette smokers. Summary estimates and descriptive statistical data for 12 364 subjects were obtained from six independent studies, and 2932 smokers were included in the analyses. Linear regression was used to calculate the per-allele association of rs1051730–rs16969968 genotype with cigarette consumption and cotinine levels in current smokers for each study. Meta-analysis of per-allele associations was conducted using a random effects method. The likely resulting association between genotype and lung cancer risk was assessed using published data on the association between cotinine levels and lung cancer risk. All statistical tests were two-sided. / Results: Pooled per-allele associations showed that current smokers with one or two copies of the rs1051730–rs16969968 risk allele had increased self-reported cigarette consumption (mean increase in unadjusted number of cigarettes per day per allele = 1.0 cigarette, 95% confidence interval [CI] = 0.57 to 1.43 cigarettes, P = 5.22 × 10−6) and cotinine levels (mean increase in unadjusted cotinine levels per allele = 138.72 nmol/L, 95% CI = 97.91 to 179.53 nmol/L, P = 2.71 × 10−11). The increase in cotinine levels indicated an increased risk of lung cancer with each additional copy of the rs1051730–rs16969968 risk allele (per-allele odds ratio = 1.31, 95% CI = 1.21 to 1.42). / Conclusions: Our data show a stronger association of rs1051730–rs16969968 genotype with objective measures of tobacco exposure compared with self-reported cigarette consumption. The association of these variants with lung cancer risk is likely to be mediated largely, if not wholly, via tobacco exposure

    Behavioral tasks sensitive to acute abstinence and predictive of smoking cessation success:a systematic review and meta-analysis

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    BACKGROUND AND AIMS: Performance on cognitive tasks may be sensitive to acute smoking abstinence and may also predict whether quit attempts fail. Our aim was to conduct a systematic review and meta-analysis to identify cognitive tasks sensitive to acute abstinence and predictive of smoking cessation success.METHODS: Embase, Medline, PsycInfo and Web of Science were searched up to March 2016. Studies were included if they enrolled adults and assessed smoking using used a quantitative measure. Studies were combined in a random effects meta-analysis.RESULTS: We included 42 acute abstinence studies and 13 cessation studies were included. There was evidence for an effect of abstinence on delay discounting [d = 0.26, 95% CI 0.07 to 0.45, p = 0.005], response inhibition [d = 0.48, 95% CI 0.26 to 0.70, p &lt; 0.001], mental arithmetic [d = 0.38, 95% CI 0.06 to 0.70, p = 0.018], and recognition memory [d = 0.46, 95% CI 0.23 to 0.70, p &lt; 0.001]. In contrast performance on the Stroop [d =0 .17, 95% CI -0.17 to 0.51, p = 0.333] and smoking Stroop [d = 0.03, 95% CI -0.11 to 0.17, p = 0.675] task was not influenced by abstinence. We found only weak evidence for an effect of acute abstinence on dot probe task performance [d = 0.15, 95% CI -0.01 to 0.32, p = 0.072]. The design of the cessation studies was too heterogeneous to permit meta-analysis.CONCLUSIONS: Compared with satiated smokers, acutely abstinent smokers display higher delay discounting, lower response inhibition, impaired arithmetic, and recognition memory performance. However, reaction time measures of cognitive bias appear to be unaffected by acute tobacco abstinence. Conclusions about cognitive tasks that predict smoking cessation success were limited by methodological inconsistencies.</p

    Genetic variation at CHRNA5-CHRNA3-CHRNB4 interacts with smoking status to influence body mass index

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    Cigarette smoking is associated with lower body mass index (BMI), and a commonly cited reason for unwillingness to quit smoking is a concern about weight gain. Common variation in the CHRNA5-CHRNA3-CHRNB4 gene region (chromosome 15q25) is robustly associated with smoking quantity in smokers, but its association with BMI is unknown. We hypothesized that genotype would accurately reflect smoking exposure and that, if smoking were causally related to weight, it would be associated with BMI in smokers, but not in never smokers
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