Subhi Arafat

Methods sections are often missing critical details needed to reproduce an experiment. Methodological shortcut citations, in which authors cite previous papers instead of describing the method in detail, may contribute to this problem. This meta-research study used three approaches to systematically examine the use of shortcut citations in neuroscience, biology and psychiatry. First, we examined papers to determine why authors use citations in the methods section and to assess how often shortcut citations were used. Common reasons for using citations in the methods section included explaining how something was done by citing a previous resource that used the method (methodological shortcut citation), giving credit or specifying what was used (who or what citation), and providing context or a justification (why citation). Next, we reviewed 15 papers to determine what can happen when readers follow shortcut citations to find methodological details. While shortcut citations can be used effectively, problems encountered included difficulty identifying or accessing the cited materials, missing or insufficient descriptions of the cited method, and chains of shortcut citations. Third, we examined journal policies. Fewer than one quarter of journals had policies describing how authors should report methods that have been described previously or asking authors to explain modifications of previously described methods. We propose that methodological shortcut citations should meet three criteria; cited resources should describe a method very similar to the authors’ method, provide enough detail to allow others to implement the method, and be open access. We outline actions that authors and journals can take to use shortcut citations responsibly, while fostering a culture of open and reproducible methods reporting.

The Barker hypothesis states that low birth weight (BW) is associated with higher risk of adult onset diseases, including mental disorders like schizophrenia, major depressive disorder (MDD), and attention deficit hyperactivity disorder (ADHD). The main criticism of this hypothesis is that evidence for it comes from observational studies. Specifically, observational evidence does not suffice for inferring causality, because the associations might reflect the effects of confounders. Mendelian randomization (MR) — a novel method that tests causality on the basis of genetic data — creates the unprecedented opportunity to probe the causality in the association between BW and mental disorders in observation studies. We used MR and summary statistics from recent large genome-wide association studies to test whether the association between BW and MDD, schizophrenia and ADHD is causal. We employed the inverse variance weighted (IVW) method in conjunction with several other approaches that are robust to possible assumption violations. MR-Egger was used to rule out horizontal pleiotropy. IVW showed that the association between BW and MDD, schizophrenia and ADHD is not causal (all p > .05). The results of all the other MR methods were similar and highly consistent. MR-Egger provided no evidence for pleiotropic effects biasing the estimates of the effects of BW on MDD (intercept = -0.004, SE = 0.005, p = .372), schizophrenia (intercept = 0.003, SE = 0.01, p = .769), or ADHD (intercept = 0.009, SE = 0.01, p = .357). Based on the current evidence, we refute the Barker hypothesis concerning the fetal origins of adult mental disorders. The discrepancy between our results and the results from observational studies may be explained by the effects of confounders in the observational studies, or by the existence of a small causal effect not detected in our study due to weak instruments. Our power analyses suggested that the upper bound for a potential causal effect of BW on mental disorders would likely not exceed an odds ratio of 1.2.