There is growing evidence for yoga's neurobiological effects in people with psychiatric disorders. Postulated mechanisms of action include: (a) modulation of the hypothalamic–pituitary–adrenal (HPA) axis; (b) enhancement of GABAergic neurotransmission; (c) autonomic modulation; and (d) neuroendocrinological effects. Yoga as a therapeutic intervention in psychiatric disorders appears promising and merits further attention in clinical practice and research.

There is strong evidence linking adverse childhood experiences (ACEs) and poor outcomes in adulthood both in terms of mental and physical health. Gaps in both the evidence base and research priorities still exist. These include understanding how to identify and assess risk in children who have experienced ACEs, and also the development and, importantly, the evaluation of interventions. Outstanding gaps include whether there are sensitive periods during childhood, the role of resilience/protective factors, the causal relationships, biological mechanisms and relative risk of ACEs for particular negative outcomes. ACEs affect individual children differently and chronic exposure appears to increase the risk of poor outcomes in adulthood, meaning interventions should also be tailored to the individual children, families and communities. Generally, there needs to be better evaluation of interventions and dissemination of this information to ensure that their use is evidence based. More input from affected communities, clinicians, funding bodies and Government departments is required to identify research priorities and ensure gaps in the evidence base are addressed.

Background: Transdiagnostic Cognitive Behaviour Therapy (CBT) seeks to identify core cognitive-behavioural processes hypothesized to be important across a range of disorders and to develop a treatment that targets these. This contrasts with standard CBT approaches that are disorder-specific. Proponents of transdiagnostic CBT suggest that it may offer advantages over disorder-specific CBT, but little is known about the effectiveness of this approach. Aims: The review aimed to summarize trial-based clinical and cost-effectiveness data on transdiagnostic CBT for anxiety and depression. Method: A systematic review of electronic databases, including peer-reviewed and grey literature sources, was conducted (n = 1167 unique citations). Results: Eight trials were eligible for inclusion in the review. There was evidence of an effect for transdiagnostic CBT when compared to a control condition. There were no differences between transdiagnostic CBT and active treatments in two studies. We found no evidence of cost-effectiveness data. Conclusions: Quality assessment of the primary studies indicated a number of methodological concerns that may serve to inflate the observed effects of transdiagnostic approaches. Although there are positive signs of the value of transdiagnostic CBT, there is as yet insufficient evidence to recommend its use in place of disorder-specific CBT.

Beyond the well-accepted effects on the skeleton, low vitamin D status has been linked to increased risk of several non-skeletal disease, including CVD. If low serum 25-hydroxyvitamin D (25(OH)D) concentration is causally linked to risk of CVD then this is important not only because low vitamin D status is quite common particularly in winter in countries above 40°N, but also of key relevance is the fact that such low vitamin D status can be improved by food-based strategies. The overarching aim of the present paper is to review the current evidence-base to support a link between low vitamin D status and CVD risk. The review initially briefly overviews how mechanistically vitamin D may play a role in CVD and then reviews the current available evidence-base to support a link between low vitamin D status and CVD risk, with particular emphasis on data from the randomised control trials, cohort studies and recent meta-analysis data as well as to the conclusions of a number of authoritative agencies/bodies. Finally, the review summarises current serum 25(OH)D concentrations within a select number of adult populations in the context of different definitions of vitamin D status proposed recently, and then briefly highlights food-based strategies for increasing vitamin D intake and status. In conclusion, at present the data for a causal link between low vitamin D status and CVD are mixed and ambiguous; however, should causality be affirmed by ongoing and future studies, there are food-based strategies for enhanced vitamin D status in the population which could ultimately lower risk of CVD.