376 research outputs found

    How Can Technology Support Smoking Cessation Interventions?

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    Navigating an open road

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    Current incentives for scientists lead to underpowered studies with erroneous conclusions

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    We can regard the wider incentive structures that operate across science, such as the priority given to novel findings, as an ecosystem within which scientists strive to maximise their fitness (i.e., publication record and career success). Here, we develop an optimality model that predicts the most rational research strategy, in terms of the proportion of research effort spent on seeking novel results rather than on confirmatory studies, and the amount of research effort per exploratory study. We show that, for parameter values derived from the scientific literature, researchers acting to maximise their fitness should spend most of their effort seeking novel results and conduct small studies that have only 10%-40% statistical power. As a result, half of the studies they publish will report erroneous conclusions. Current incentive structures are in conflict with maximising the scientific value of research; we suggest ways that the scientific ecosystem could be improved

    Causal inference with observational data:the need for triangulation of evidence

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    Variation in health warning effectiveness on cigarette packs:a need for regulation?

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    The Tobacco Products Directive allows the possibility of strategic placement of health warnings on cigarette packs by manufacturers to reduce overall warning effectiveness. Information regarding health warning effectiveness was assessed in an online survey, and the prevalence of warnings on cigarette packs was assessed in a shop survey. Although we find no evidence of a strong correlation between health warning effectiveness ratings and their frequency on cigarette packs (r = −0.17, P = 0.56), there may be other ways this possibility is exploited. We suggest that this potential loophole is addressed and monitoring of the placement of health warnings on cigarette packs is continued

    Anxiety sensitivity and trait anxiety are associated with response to 7.5% carbon dioxide challenge

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    The 7.5% carbon dioxide (CO(2)) inhalation model is used to provoke acute anxiety, for example to investigate the effects of anxiety on cognitive processes, or the efficacy of novel anxiolytic agents. However, little is known about the relationship of baseline anxiety sensitivity or trait anxiety (i.e., anxiety proneness), with an individual’s response to the 7.5% CO(2) challenge. We examined data from a number of 7.5% CO(2) challenge studies to determine whether anxiety proneness was related to subjective or physiological response. Our findings indicate anxiety proneness is associated with greater subjective and physiological responses. However, anxiety-prone individuals also have a greater subjective response to the placebo (medical air) condition. This suggests that anxiety-prone individuals not only respond more strongly to the 7.5% CO(2) challenge, but also to medical air. Implications for the design and conduct of 7.5% CO(2) challenge studies are discussed

    Schizophrenia and neighborhood deprivation

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    Biased facial emotion perception in mental health disorders:a possible target for psychological intervention?

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    Our perception of emotion in the faces of others affects our own behavior and mood. Indeed, individuals with mood disorders such as depression and aggression often show biases in facial-emotion perception. Here, we review recent and ongoing research suggesting that biased emotion perception may be on the causal pathway of the onset and maintenance of mood disorders, and hence a potential target for intervention. Simple cognitive-bias modification tasks that change participants’ perception of facial expressions of emotion have shown some promise as a therapeutic technique. We outline further directions for continued research investigating the robustness and clinical impact of emotion-bias modification in real-world settings. </jats:p

    Using Mendelian randomization to explore the gateway hypothesis:possible causal effects of smoking initiation and alcohol consumption on substance use outcomes

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    BACKGROUND AND AIMS: Initial use of drugs such as tobacco and alcohol may lead to subsequent more problematic drug use—the ‘gateway’ hypothesis. However, observed associations may be due to a shared underlying risk factor, such as trait impulsivity. We used bidirectional Mendelian randomization (MR) to test the gateway hypothesis. DESIGN: Our main method was inverse‐variance weighted (IVW) MR, with other methods included as sensitivity analyses (where consistent results across methods would raise confidence in our primary results). MR is a genetic instrumental variable approach used to support stronger causal inference in observational studies. SETTING AND PARTICIPANTS: Genome‐wide association summary data among European ancestry individuals for smoking initiation, alcoholic drinks per week, cannabis use and dependence, cocaine and opioid dependence (n = 1749–1 232 091). MEASUREMENTS: Genetic variants for exposure. FINDINGS: We found evidence of causal effects from smoking initiation to increased drinks per week [(IVW): β = 0.06; 95% confidence interval (CI) = 0.03–0.09; P = 9.44 × 10(−06)], cannabis use [IVW: odds ratio (OR) = 1.34; 95% CI = 1.24–1.44; P = 1.95 × 10(−14)] and cannabis dependence (IVW: OR = 1.68; 95% CI = 1.12–2.51; P = 0.01). We also found evidence of an effect of cannabis use on the increased likelihood of smoking initiation (IVW: OR = 1.39; 95% CI = 1.08–1.80; P = 0.01). We did not find evidence of an effect of drinks per week on other substance use outcomes, except weak evidence of an effect on cannabis use (IVW: OR = 0.55; 95% CI = 0.16–1.93; P‐value = 0.35). We found weak evidence of an effect of opioid dependence on increased drinks per week (IVW: β = 0.002; 95% CI = 0.0005–0.003; P = 8.61 × 10(−03)). CONCLUSIONS: Bidirectional Mendelian randomization testing of the gateway hypothesis reveals that smoking initiation may lead to increased alcohol consumption, cannabis use and cannabis dependence. Cannabis use may also lead to smoking initiation and opioid dependence to alcohol consumption. However, given that tobacco and alcohol use typically begin before other drug use, these results may reflect a shared risk factor or a bidirectional effect for cannabis use and opioid dependence
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