For 20 years the UK Government has recognised that food advertising plays a part in food choices and hence diets of the population, particularly for children. In 2007 the UK brought in regulations to stop the advertising of less healthy foods on television (TV) during child-specific programming. Less healthy foods were defined using the 2004/2005 nutrient profiling model (NPM) as products high in saturated fat, salt and sugar (HFSS). Evaluations showed that children were still seeing and being affected by the adverts for less healthy foods. To try to mitigate childhood obesity, in 2018, the UK Government announced its intention to consult on further restrictions on the advertising of HFSS products on TV and online. Two years later, the intention to implement a 9pm advertising ban on TV and a further consultation on restricting online advertising of HFSS products was announced. New legislative controls on the advertising of HFSS foods are expected to be brought into legislation in the UK in January 2024. In the present paper, the history of advertising restrictions in the UK and the evidence informing them is reviewed. There will also be a reflection on where further actions might be needed in due course.

The Winter Conference 2021 focused on the theme of obesity and the brain, with symposia on the consequences of obesity on brain function, developments in behavioural change interventions, neurobiology of appetite regulation and obesity treatment, and personalised medicine for obesity prevention and treatment. The first plenary lecture discussed sweetness perceptions and how non-nutritive sweeteners may lead to a mismatch between metabolic signals and reward systems in the brain, and the second plenary lecture presented novel approaches to the treatment of binge-eating disorders. This short report summarises the content of these scientific sessions.

The liver is a key metabolic organ that undertakes a multitude of physiological processes over the course of a day, including intrahepatic lipid and glucose metabolism which plays a key role in the regulation of systemic lipid and glucose concentrations. It serves as an intermediary organ between exogenous (dietary) and endogenous energy supply to extrahepatic organs. Thus, perturbations in hepatic metabolism can impact widely on metabolic disease risk. For example, the accumulation of intra-hepatocellular TAG (IHTG), for which adiposity is almost invariably a causative factor may result in dysregulation of metabolic pathways. Accumulation of IHTG is likely due to an imbalance between fatty acid delivery, synthesis and removal (via oxidation or export as TAG) from the liver; insulin plays a key role in all of these processes.

The association between maternal metabolic status at the time of conception and subsequent embryogenesis and offspring development has been studied in detail. However, less attention has been given to the significance of paternal nutrition and metabolism in directing offspring health. Despite this disparity, emerging evidence has begun to highlight an important connection between paternal metabolic well-being, semen quality, embryonic development and ultimately adult offspring health. This has established a new component within the Developmental Origins of Health and Disease hypothesis. Building on the decades of understanding and insight derived from the numerous models of maternal programming, attention is now becoming focused on defining the mechanisms underlying the links between paternal well-being, post-fertilisation development and offspring health. Understanding how the health and fitness of the father impact on semen quality is of fundamental importance for providing better information to intending fathers. Furthermore, assisted reproductive practices such as in vitro fertilisation rely on our ability to select the best quality sperm from a diverse and heterogeneous population. With considerable advances in sequencing capabilities, our understanding of the molecular and epigenetic composition of the sperm and seminal plasma, and their association with male metabolic health, has developed dramatically over recent years. This review will summarise our current understanding of how a father's metabolic status at the time of conception can affect sperm quality, post-fertilisation embryonic and fetal development and offspring health.

Environmental features such as the ‘foodscape’ defined as the physical, sociocultural and economic space in which people encounter meals and foods, might be associated with dietary intake and health outcomes. This review focuses mainly on the spatial approach of the foodscape, i.e. all the local shops, markets, restaurants and sales outlets that provide food supplies in a given area. This review aims to explore the evidence on relationships of urban foodscape with diet and health outcomes and to highlight the limitations in studying these relationships as well as suggestions for future studies. Many systematic reviews on characteristics of the foodscape in relation to weight status outcomes emerged over the last decade and results are equivocal. There is not a direct association between the foodscape and weight status of the individual, rather any association is a distant one. Therefore, it is more appropriate to focus on associations between foodscape and intermediate, more proximal outcomes, such as dietary behaviours. Research on the role of the foodscape in promoting or hindering healthy dietary behaviours are also numerous, and results are again mixed. The diversity of methodologies might partly explain the heterogeneity of these results. Focusing on overall diet quality rather than fruit and vegetable consumption, taking into account multiple characteristics of the foodscape, as well as socioeconomic and contextual differences, might be part of the solution for more consistent results. Consequently, results of such studies could help shape foodscapes, which present a great opportunity for promoting healthier and eventually more sustainable diets.

With approximately two in three UK adults overweight or obese, one in five living in poverty and our emergence from the Covid-19 pandemic with implications for employment and income status there is an urgent need to understand what it costs to eat healthily and the role that promotions can play in helping householders manage food budgets. The literature suggests that, in affluent countries, price promotions appear to increase consumer food purchases and are applied more frequently to less healthy products than their healthy counterparts. This review discusses the cost of a healthy diet, identifies the prevalence of promotions in both the supermarket setting generally and a typical shopping basket specifically, and discusses the barriers to affording a healthy diet. Given the current policy focus on the cost of living and population health emphasising the need for food shopping to represent health and value for money for better public health outcomes, this review contributes to the evidence base for retailers' and policymakers' consideration as policy solutions are sought to reduce population obesity levels, while ensuring the affordability and accessibility of nutritious food. It is important, given the shift in consumer purchasing behaviour to online shopping as a result of self-isolating or reticence to physically access stores in response to the Covid-19 pandemic, that retail food promotions are available irrespective of the chosen mode of shopping (in-store or online).

Parkinson's disease (PD) is the second most common neurodegenerative disease after Alzheimer's disease and affects about 1% of the population over the age of 60 years in industrialised countries. The aim of this review is to examine nutrition in PD across three domains: dietary intake and the development of PD; whole body metabolism in PD and the effects of PD symptoms and treatment on nutritional status. In most cases, PD is believed to be caused by a combination of genetic and environmental factors and although there has been much research in the area, evidence suggests that poor dietary intake is not a risk factor for the development of PD. The evidence about body weight changes in both the prodromal and symptomatic phases of PD is inconclusive and is confounded by many factors. Malnutrition in PD has been documented as has sarcopaenia, although the prevalence of the latter remains uncertain due to a lack of consensus in the definition of sarcopaenia. PD symptoms, including those which are gastrointestinal and non-gastrointestinal, are known to adversely affect nutritional status. Similarly, PD treatments can cause nausea, vomiting and constipation, all of which can adversely affect nutritional status. Given that the prevalence of PD will increase as the population ages, it is important to understand the interplay between PD, comorbidities and nutritional status. Further research may contribute to the development of interventional strategies to improve symptoms, augment care and importantly, enhance the quality of life for patients living with this complex neurodegenerative disease.

Obesity, excess adipose tissue accumulation that may impair health, is a major global healthcare challenge that increases the risk of several life-limiting diseases, reduces quality of life and leads to premature mortality. Weight loss improves or leads to the resolution of obesity-related diseases. Lifestyle interventions are the cornerstone for all weight management programmes and lead to health benefits. However, for the majority of people with severe obesity, lifestyle interventions and currently available anti-obesity medications lead to insufficient weight loss to improve their health. For these patients the only effective treatment option is bariatric surgery, which whilst highly effective, is difficult to access and not suitable for everyone, leaving a ‘treatment gap’ between lifestyle interventions and bariatric surgery. Unfortunately, the history of development of drugs to treat obesity has been marred by poor efficacy and safety issues. This is now set to change as a result of scientific advancements, which have increased the understanding of the role that gut hormones play in regulating energy and glucose homoeostasis. This has led to the development of effective, safe drugs based on gut hormones that target the body's own appetite regulating systems that herald a new era of treatments for people living with obesity.

There is an ever increasing prevalence of maternal obesity worldwide such that in many populations over half of women enter pregnancy either overweight or obese. This review aims to summarise the impact of maternal obesity on offspring cardiometabolic outcomes. Maternal obesity is associated with increased risk of adverse maternal and pregnancy outcomes. However, beyond this exposure to maternal obesity during development also increases the risk of her offspring developing long-term adverse cardiometabolic outcomes throughout their adult life. Both human studies and those in experimental animal models have shown that maternal obesity can programme increased risk of offspring developing obesity and adipose tissue dysfunction; type 2 diabetes with peripheral insulin resistance and β-cell dysfunction; CVD with impaired cardiac structure and function and hypertension via impaired vascular and kidney function. As female offspring themselves are therefore likely to enter pregnancy with poor cardiometabolic health this can lead to an inter-generational cycle perpetuating the transmission of poor cardiometabolic health across generations. Maternal exercise interventions have the potential to mitigate some of the adverse effects of maternal obesity on offspring health, although further studies into long-term outcomes and how these translate to a clinical context are still required.