Acute cannabis intoxication is associated with a statistically significant increase in motor vehicle crash risk. The increase is of low to medium magnitude. Remaining selection effects in the studies used may limit causal interpretation of the pooled estimates.

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Population intelligence quotients increased throughout the 20th century—a phenomenon known as the Flynn effect—although recent years have seen a slowdown or reversal of this trend in several countries. To distinguish between the large set of proposed explanations, we categorize hypothesized causal factors by whether they accommodate the existence of within-family Flynn effects. Using administrative register data and cognitive ability scores from military conscription data covering three decades of Norwegian birth cohorts (1962–1991), we show that the observed Flynn effect, its turning point, and subsequent decline can all be fully recovered from within-family variation. The analysis controls for all factors shared by siblings and finds no evidence for prominent causal hypotheses of the decline implicating genes and environmental factors that vary between, but not within, families.

Does cannabis use have substantial and permanent effects on neuropsychological functioning? Renewed and intense attention to the issue has followed recent research on the Dunedin cohort, which found a positive association between, on the one hand, adolescent-onset cannabis use and dependence and, on the other hand, a decline in IQ from childhood to adulthood [Meier et al. (2012) Proc Natl Acad Sci USA 109(40):E2657-E2664]. The association is given a causal interpretation by the authors, but existing research suggests an alternative confounding model based on time-varying effects of socioeconomic status on IQ. A simulation of the confounding model reproduces the reported associations from the Dunedin cohort, suggesting that the causal effects estimated in Meier et al. are likely to be overestimates, and that the true effect could be zero. Further analyses of the Dunedin cohort are proposed to distinguish between the competing interpretations. Although it would be too strong to say that the results have been discredited, the methodology is flawed and the causal inference drawn from the results premature. marijuana | longitudinalT o what extent does cannabis use have permanent and substantial effects on neuropsychological functioning? The question has received renewed and worldwide attention with the recent evidence of correlations between, on the one hand, persistent cannabis use initiated in adolescence and, on the other hand, a decline in IQ-scores between the ages of 13 and 38 (1). Although Meier et al. (1) note the possibility of remaining confounders, they conclude that the findings are suggestive of a neurotoxic effect of cannabis on developing brains that permanently lowers IQ. This conclusion seems premature in light of likely confounding from socioeconomic status (SES). After a brief description and discussion of the Meier et al. study design, I present evidence regarding the relationship between IQ trajectories and SES. Simulation results indicate that SES-correlated cognitive decline is sufficient to reproduce the Meier et al. results. I conclude by sketching empirical analyses that can distinguish between the causal and confounding model. Meier et al., 2012: Study Design and Methodological IssuesThe Meier et al.(1) study uses data from the high-quality Dunedin cohort, a "prospective study of a birth cohort of 1,037 individuals followed from birth (1972/1973) to age 38 y." As part of this study, participants were scored for use of-and dependence on-cannabis at ages 18, 21, 26, 32, and 38. Using these data, Meier et al. sort participants into cannabis-exposure groups: nonusers, users who never scored as dependent, and users who scored as dependent once, twice, or three or more times. Controlling for sex, ordinary least-squares regressions find IQ-declines increasing linearly with cannabis exposure (a dose-response relationship). The correlations persist within a number of subsets cleared of various possible confounders (e.g., subsamples with no alcohol dependence or no schizophrenia), and are driven ...

The main objective of "Lifebrain" is to identify the determinants of brain, cognitive and mental (BCM) health at different stages of life. By integrating, harmonising and enriching major European neuroimaging studies across the life span, we will merge fine-grained BCM health measures of more than 5000 individuals. Longitudinal brain imaging, genetic and health data are available for a major part, as well as cognitive and mental health measures for the broader cohorts, exceeding 27,000 examinations in total. By linking these data to other databases and biobanks, including birth registries, national and regional archives, and by enriching them with a new online data collection and novel measures, we will address the risk factors and protective factors of BCM health. We will identify pathways through which risk and protective factors work and their moderators. Exploiting existing European infrastructures and initiatives, we hope to make major conceptual, methodological and analytical contributions towards large integrative cohorts and their efficient exploitation. We will thus provide novel information on BCM health maintenance, as well as the onset and course of BCM disorders. This will lay a foundation for earlier diagnosis of brain disorders, aberrant development and decline of BCM health, and translate into future preventive and therapeutic strategies. Aiming to improve clinical practice and public health we will work with stakeholders and health authorities, and thus provide the evidence base for prevention and intervention.

A major task of contemporary cognitive neuroscience of aging is to explain why episodic memory declines. Change in resting-state functional connectivity (rsFC) could be a mechanism accounting for reduced function. We addressed this through 3 studies. In study 1, 119 healthy participants (20-83 years) were followed for 3.5 years with verbal recall testing and magnetic resonance imaging. Independent of atrophy, recall change was related to change in rsFC in anatomically widespread areas. Striking age-effects were observed in that a positive relationship between rsFC and memory characterized older participants while a negative relationship was seen among the younger and middle-aged. This suggests that cognitive consequences of rsFC change are not stable across age. In study 2 and 3, the age-dependent differences in rsFC-memory relationship were replicated by use of a simulation model (study 2) and by a cross-sectional experimental recognition memory task (study 3). In conclusion, memory changes were related to altered rsFC in an age-dependent manner, and future research needs to detail the mechanisms behind age-varying relationships.

Normative thinking about addiction has traditionally been divided between, on the one hand, a medical model which sees addiction as a disease characterized by compulsive and relapsing drug use over which the addict has little or no control and, on the other, a moral model which sees addiction as a choice characterized by voluntary behavior under the control of the addict. Proponents of the former appeal to evidence showing that regular consumption of drugs causes persistent changes in the brain structures and functions known to be involved in the motivation of behavior. On this evidence, it is often concluded that becoming addicted involves a transition from voluntary, chosen drug use to non-voluntary compulsive drug use. Against this view, proponents of the moral model provide ample evidence that addictive drug use involves voluntary chosen behavior. In this article we argue that although they are right about something, both views are mistaken. We present a third model that neither rules out the view of addictive drug use as compulsive, nor that it involves voluntary chosen behavior.

BackgroundPandemic mortality rates in 1918 and in 2009 were highest among those with the lowest socioeconomic status (SES). Despite this, low SES groups are not included in the list of groups prioritized for pandemic vaccination, and the ambition to reduce social inequality in health does not feature in international and national pandemic preparedness plans. We describe plans for a systematic review and meta-analysis of the association between SES and pandemic outcomes during the last five pandemics.MethodThe planned review will cover studies of pandemic influenza that report associations between morbidity, hospitalization, or mortality with socioeconomic factors such as education and income. The review will include published studies in the English, Danish, Norwegian, and Swedish languages, regardless of geographical location. Relevant records were identified through systematic literature searches in MEDLINE, Embase, Cinahl, SocIndex, Scopus, and Web of Science. Reference lists of relevant known studies will be screened and experts in the field consulted in order to identify other additional sources. Two investigators will independently screen and select studies, and discrepancies will be resolved through discussion until consensus is reached. Covidence will be used. Results will be summarized narratively and using three meta-analytic strategies: coefficients expressing the difference between the highest and lowest socioeconomic groups reported will be pooled using (a) fixed and random effects meta-analysis where studies involve similar outcome and exposure measures and (b) meta-regression where studies involve similar outcome measures. In addition, we will attempt to use all reported estimates for SES differences in (c) a Bayesian meta-analysis to estimate the underlying SES gradient and how it differs by outcome and exposure measure.DiscussionThis study will provide the first systematic review of research on the relation between SES and pandemic outcomes. The findings will be relevant for health policy in helping to assess whether people of low socioeconomic status should be prioritized for vaccines in preparedness plans for pandemic influenza. The review will also contribute to the research literature by providing pooled estimates of effect sizes as inputs into power calculations of future studies.Systematic review registration PROSPERO 87922