Current incentives for scientists lead to underpowered studies with erroneous conclusions

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

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

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

Effects of Electronic Cigarette E-Liquid Flavouring on Cigarette Craving

This experimental study, conducted remotely, investigated the effects of vaping nicotine-containing flavoured e-liquid, compared with unflavoured e-liquid, on (a) general cigarette craving, and (b) cue-elicited cigarette craving in response to smoking-related cues, among abstinent daily smokers. Participants (n = 84) were randomised to use an e-cigarette with nicotine-containing fruit/sweet-flavoured e-liquid (blackcurrant, strawberry, vanilla, caramel) or unflavoured e-liquid, for one week

Mendelian randomization studies of coffee and caffeine consumption

Habitual coffee and caffeine consumption has been reported to be associated with numerous health outcomes. This perspective focuses on Mendelian Randomization (MR) approaches for determining whether such associations are causal. Genetic instruments for coffee and caffeine consumption are described, along with key concepts of MR and particular challenges when applying this approach to studies of coffee and caffeine. To date, at least fifteen MR studies have investigated the causal role of coffee or caffeine use on risk of type 2 diabetes, cardiovascular disease, Alzheimer’s disease, Parkinson’s disease, gout, osteoarthritis, cancers, sleep disturbances and other substance use. Most studies provide no consistent support for a causal role of coffee or caffeine on these health outcomes. Common study limitations include low statistical power, potential pleiotropy, and risk of collider bias. As a result, in many cases a causal role cannot confidently be ruled out. Conceptual challenges also arise from the different aspects of coffee and caffeine use captured by current genetic instruments. Nevertheless, with continued genome-wide searches for coffee and caffeine related loci along with advanced statistical methods and MR designs, MR promises to be a valuable approach to understanding the causal impact that coffee and caffeine have in human health

Neural correlates of cigarette health warning avoidance among smokers

AbstractBackgroundEye-tracking technology has indicated that daily smokers actively avoid pictorial cigarette package health warnings. Avoidance may be due to a pre-cognitive perceptual bias or a higher order cognitive bias, such as reduced emotional processing. Using electroencephalography (EEG), this study aimed to identify the temporal point at which smokers’ responses to health warnings begin to differ.MethodNon-smokers (n=20) and daily smokers (n=20) viewed pictorial cigarette package health warnings and neutral control stimuli. These elicited Event Related Potentials reflecting early perceptual processing (visual P1), pre-attentive change detection (visual Mismatch Negativity), selective attentional orientation (P3) and a measure of emotional processing, the Late Positive Potential (LPP).ResultsThere was no evidence for a difference in P1 responses between smokers and non-smokers. There was no difference in vMMN and P3 amplitude but some evidence for a delay in vMMN latency amongst smokers. There was strong evidence for delayed and reduced LPP to health warning stimuli amongst smokers compared to non-smokers.ConclusionWe find no evidence for an early perceptual bias in smokers’ visual perception of health warnings but strong evidence that smokers are less sensitive to the emotional content of cigarette health warnings. Future health warning development should focus on increasing the emotional salience of pictorial health warning content amongst smokers

Prospective Investigation of Video Game Use in Children and Subsequent Conduct Disorder and Depression Using Data from the Avon Longitudinal Study of Parents and Children

There is increasing public and scientific concern regarding the long-term behavioural effects of video game use in children, but currently little consensus as to the nature of any such relationships. We investigated the relationship between video game use in children, degree of violence in games, and measures of depression and a 6-level banded measure of conduct disorder. Data from the Avon Longitudinal Study of Parents and Children were used. A 3-level measure of game use at age 8/9 years was developed, taking into account degree of violence based on game genre. Associations with conduct disorder and depression, measured at age 15, were investigated using ordinal logistic regression, adjusted for a number of potential confounders. Shoot-em-up games were associated with conduct disorder bands, and with a binary measure of conduct disorder, although the strength of evidence for these associations was weak. A sensitivity analysis comparing those who play competitive games to those who play shoot-em-ups found weak evidence supporting the hypothesis that it is violence rather than competitiveness that is associated with conduct disorder. However this analysis was underpowered, and we cannot rule out the possibility that increasing levels of competition in games may be just as likely to account for the observed associations as violent content. Overall game exposure as indicated by number of games in a household was not related to conduct disorder, nor was any association found between shoot-em-up video game use and depression