Conceptualisation, design and development of a primary school based child healthy weight intervention

INTRODUCTION: In common with much of the developed world, Scotland has a severe and well established problem with overweight and obesity in childhood with recent figures demonstrating that 31% of Scottish children aged 2-15 years old were overweight including obese in 2014. This problem is more pronounced in socioeconomically disadvantaged groups and in older children across all economic groups (Scottish Health Survey, 2014). Children who are overweight or obese are at increased risk of a number of adverse health outcomes in the short term and throughout their life course (Lobstein and Jackson-Leach, 2006). The Scottish Government tasked all Scottish Health Boards with developing and delivering child healthy weight interventions to clinically overweight or obese children in an attempt to address this health problem. It is therefore imperative to deliver high quality, affordable, appropriately targeted interventions which can make a sustained impact on children’s lifestyles, setting them up for life as healthy weight adults. This research aimed to inform the design, readiness for application and Health Board suitability of an effective primary school-based curricular child healthy weight intervention. METHODS: the process involved in conceptualising a child healthy weight intervention, developing the intervention, planning for implementation and subsequent evaluation was guided by the PRECEDE-PROCEED Model (Green and Kreuter, 2005) and the Intervention Mapping protocol (Lloyd et al. 2011). RESULTS: The outputs from each stage of the development process were used to formulate a child healthy weight intervention conceptual model then develop plans for delivery and evaluation. DISCUSSION: The Fit for School conceptual model developed through this process has the potential to theoretically modify energy balance related behaviours associated with unhealthy weight gain in childhood. It also has the potential to be delivered at a Health Board scale within current organisational restrictions.

Tackling health inequalities in primary care: an exploration of GPs’ experience at the frontline

In Scotland, life expectancy and health outcomes are strongly tied to socioeconomic status. Specifically, socioeconomically deprived areas suffer disproportionately from high levels of premature multimorbidity and mortality. To tackle these inequalities in health, challenges in the most deprived areas must be addressed. One avenue that merits attention is the potential role of general medical practitioners (GPs) in helping to address health inequalities, particularly due to their long-term presence in deprived communities, their role in improving patient and population health, and their potential advocacy role on behalf of their patients. GPs can be seen as what Lipsky calls ‘street-level bureaucrats’ due to their considerable autonomy in the decisions they make surrounding individual patient needs, yet practising under the bureaucratic structure of the NHS. While previous research has examined the applicability of Lipsky’s framework to the role of GPs, there has been very little research exploring how GPs negotiate between the multiple identities in their work, how GPs ‘socially construct’ their patients, how GPs view their potential role as ‘advocate’, and what this means in terms of the contribution of GPs to addressing existing inequalities in health. Using semi-structured interviews, this study explored the experience and views of 24 GPs working in some of Scotland’s most deprived practices to understand how they might combat this growing health divide via the mitigation (and potential prevention) of existing health inequalities. Participants were selected based on several criteria including practice deprivation level and their individual involvement in the Deep End project, which is an informal network comprising the 100 most deprived general practices in Scotland. The research focused on understanding GPs’ perceptions of their work including its broader implications, within their practice, the communities within which they practise, and the health system as a whole. The concept of street-level bureaucracy proved to be useful in understanding GPs’ frontline work and how they negotiate dilemmas. However, this research demonstrated the need to look beyond Lipsky’s framework in order to understand how GPs reconcile their multiple identities, including advocate and manager. As a result, the term ‘street-level professional’ is offered to capture more fully the multiple identities which GPs inhabit and to explain how GPs’ elite status positions them to engage in political and policy advocacy. This study also provides evidence that GPs’ social constructions of patients are linked not only to how GPs conceptualise the causes of health inequalities, but also to how they view their role in tackling them. In line with this, the interviews established that many GPs felt they could make a difference through advocacy efforts at individual, community and policy/political levels. Furthermore, the study draws attention to the importance of practitioner-led groups—such as the Deep End project—in supporting GPs’ efforts and providing a platform for their advocacy. Within this study, a range of GPs’ views have been explored based on the sample. While it is unclear how common these views are amongst GPs in general, the study revealed that there is considerable scope for ‘political GPs’ who choose to exercise discretion in their communities and beyond. Consequently, GPs working in deprived areas should be encouraged to use their professional status and political clout not only to strengthen local communities, but also to advocate for policy change that might potentially affect the degree of disadvantage of their patients, and levels of social and health inequalities more generally.

Exploring the role of miR-34a in regulating adipose inflammation during obesity

Background: Obesity is not a new disease, with roots that can be traced back to 400 BC. However, with the staggering increase in individuals that are overweight and obese since the 1980s, now over a quarter of individuals in Europe and the Americas are classed as obese. This presents a global health problem that needs to be addressed with novel therapies. It is now well accepted that obesity is a chronic, low-grade inflammatory condition that could predispose individuals to a number of comorbidities. Obesity is associated with cardiovascular diseases (CVDs) and type 2 diabetes (T2D) as part of “the metabolic syndrome,” and as first identified by Dr Vauge, central distribution of white adipose tissue (WAT) is an important risk factor in the development of these diseases. Subsequently, visceral WAT (vWAT) was shown to be an important factor in this association with CVDs and T2D, and increasing inflammation. As the obese WAT expands, mainly through hypertrophy, there is an increase in inflammation that recruits numerous immune cells to the tissue that further exacerbate this inflammation, causing local and systemic inflammatory and metabolic effects. One of the main types of immune cell involved in this pathogenic process is pro-inflammatory M1 adipose tissue macrophages (ATMs). MicroRNAs (miRNAs) are a species of small RNAs that post-transcriptionally regulate gene expression by targeting gene mRNA, causing its degradation or translational repression. These miRNAs are promiscuous, regulating numerous genes and pathways involved in a disease, making them useful therapeutic targets, but also difficult to study. miR-34a has been shown to increase in the serum, liver, pancreas, and subcutaneous (sc)WAT of patients with obesity, non- alcoholic fatty liver disease (NAFLD) and T2D. Additionally, miR-34a has been shown to regulate a number of metabolic and inflammatory genes in numerous cell types, including those in macrophages. However, the role of miR-34a in regulating vWAT metabolism and inflammation is poorly understood. Hypothesis: miR-34a is dysregulated in the adipose tissue during obesity, causing dysregulation of metabolic and inflammatory pathways in adipocytes and ATMs that contribute to adipose inflammation and obesity’s comorbidities, particularly T2D. Method/Results: The role of miR-34a in adipose inflammation was investigated using a murine miR-34a-/- diet-induced obesity model, and primary in vitro models of adipocyte differentiation and inflammatory bone marrow-derived macrophages (BMDMs). miR-34a was shown to be ubiquitously expressed throughout the murine epididymal (e)WAT of obese high-fat diet (HFD)-fed WT mice and ob/ob mice, as well as omental WAT from patients with obesity. Additionally, miR-34a transcripts were increased in the liver and brown adipose tissue (BAT) of ob/ob and HFD-fed WT mice, compared to WT controls. When miR-34a-/- mice were fed HFD ad libitum for 24 weeks they were significantly heavier than their WT counterparts by the end of the study. Ex vivo examinations showed that miR-34a-/- eWAT had a smaller adipocyte area on chow, which significantly increased to WT levels during HFD-feeding. Additionally, miR-34a-/- eWAT showed basal increases in cholesterol and fatty acid metabolism genes Cd36, Hmgcr, Lxrα, Pgc1α, and Fasn. miR-34a-/- iBAT showed basal reductions in Cebpα and Cebpβ, with increased Pgc1α expression during HFD- feeding. The miR-34a-/- liver additionally showed increased basal transcript expression of Pgc1α, suggesting miR-34a may broadly regulate PGC1α. Accompanying the ex vivo changes in cholesterol and fatty acid metabolism genes, in vitro miR-34a-/- white adipocytes showed increased lipid content. An F4/80high macrophage population was identified in HFD-fed miR-34a-/- eWAT, with increased Il-10 transcripts and serum IL-5 protein. Following these ex vivo observations, BMDMs from WT mice upregulated miR-34a expression in response to TNFα stimulation. Additionally, miR-34a-/- BMDMs showed an ablated CXCL1 response to TNFα. Conclusion: These findings suggest miR-34a has a multi-factorial role in controlling a susceptibility to obesity, by regulating inflammatory and metabolic pathways, potentially through regulation of PGC1α.